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Flashcards in UW Internal Medicine Deck (1117)
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Lady has history of chest pain worse with emotional stress. No change with deep inspiration or exercise, no syncope, no SOB. Vitals, heart/ lung sounds, and EKG are all normal. Order an echo or stop testing for CAD?

Stop testing for CAD

-She’s a low-risk patient (no cardiac risk factors), so even if we did a stress test and it came back positive, it would likely be a false positive
-A transthoracic echo (TTE) would test for wall motion abnormalities during chest pain/ stress test or valvular abnormalities (like aortic stenosis) in a patient with exertional chest pain and a murmur


Old guy has problems with his central vision. Peripheral vision is good. History of cataracts, but otherwise healthy. Diagnosis?

Age-related macular degeneration (AMD)

*This is seen in patients >50 y.o.
Results from degeneration and atrophy of the central retina (macula) and surrounding structures.

**Macula= center of retina (the light-sensitive tissue that lines the inside of the eye and allows us to see in color)


Lady with stabbing pain on cheek when lightly touched, radiates from ear to jaw line. Treatment?

Carbamazepine (if this causes adverse effects: Oxcarbazepine, Baclofen, or surgical decompression of the trigeminal nerve)

This is trigeminal neuralgia (neuropathic pain along the V2/ maxillary and V3/ mandibular branches of the trigeminal nerve)


Monitor what in a patient on Carbamazepine?

Blood count

Carbamazepine can cause leukopenia (low WBC count) and aplastic anemia


What does chemosis mean?

Swelling/ edema of the conjunctiva


Normal platelet count?

150,000- 400,000


Guy traveled to Mexico. Came back with abdominal pain, vomiting, and diarrhea. These symptoms went away, but then the guy got a fever, swelling around the eyes, double vision, and splinter hemorrhages. Has eosinophilia and elevated creatine kinase. Diagnosis?

Trichinellosis (aka Trichinosis) caused by the roundworm Trichinella (“porky trickster”)

Eat undercooked pork with cysts-> gastric acid releases larvae from cysts (intestinal stage)-> female worms release new larvae a few weeks later that migrate into striated muscle (muscle stage)

*most common presentation: eosinophilia + periorbital edema + myositis (inflamed, weak muscles)
**since the larvae migrate, patients may get systemic symptoms like fever and splinter hemorrhages


Dengue fever usually presents with pain where?

Behind the eye (retro-orbital pain)


Why might shistocytes/ helmet cells show up on blood smear in a patient with a replaced heart valve?

Prosthetic heart valves can destroy RBCs that cross the valve-> schistocytes/ helmet cells (fragmented RBCs)


Is haptoglobin increased or decreased in hemolytic anemia?


Haptoglobin binds up free hemoglobin (Hb). In hemolytic anemia, there’s a lot of broken up RBCs, so there’s a lot of free Hb for haptoglobin to pick up. Since haptoglobin is getting used up, it is decreased.


Meaning of conjunctival pallor?

Pale conjunctiva


Patient has macrocytic anemia, shiny tongue, SOB on exertion, and depigmented areas over the arm suggestive of vitiligo. Cause of the anemia?

Pernicious anemia (antibodies against intrinsic factor)-> vitamin B12 deficiency

*Macrocytic= B12 or folate deficiency. Glossitis is seen in both these, since these deficiencies impair DNA synthesis (and therefore impair epithelial replication). Folate deficiency is usually seen in alcoholics or malnourished. Having vitiligo makes pernicious anemia more likely- if you have 1 autoimmune dz you’re at greater risk for another since your immune system sucks


Patient went to the Caribbean and came back with fever, malaise, rash, lymphadenopathy, and polyarthralgias (pain in joints). Diagnosis?

Chikungunya fever

*caused by the Aedes mosquito in the Caribbean
*supportive treatment


Patient has aortic dissection (tearing chest pain) + orthopnea (SOB when lying down) to the point that he refuses to lay down. Most likely cause of the SOB?

Aortic regurg

-Aortic dissection can lead to aortic regurg if blood from the intimal tear extends to the aortic valve
-This can cause 4 symptoms:
1. Hypotension (blood is regurging backwards, so less blood is being pumped forwards)
2. Sudden onset worsening chest pain
3. Pulmonary edema
4. Orthopnea (SOB lying down)
(2-4 are due to: blood from aorta-> LV and backing up into lungs)

**aortic dissection can also cause cardiac tamponade (if blood from the intimal tear enters into the pericardium and restricts filling of the heart). This would NOT cause pulmonary edema.


Patient just took Bactrim for a UTI. She is on Phenytoin for seizures. Recently, she has had an unsteady gait and nystagmus. What’s going on?

Phenytoin toxicity (ataxia and nystagmus are side effects of Phenytoin)

-Bactrim (TMP-SMX)= P450 inhibitor, so it blocks P450 metabolism in the liver—> drug stays in body longer. Phenytoin working in the body longer—> toxicity.


40 y.o. Lady from India has episodes of upper abdominal pain and burning that waxes and wanes. Feels bloated after meals. Positive stool guaiac (occult blood in stool). Most likely diagnosis?

H. Pylori

*dyspepsia (indigestion/ heartburn) can be—> from NSAIDs, GERD, H Pylori, etc.
GERD wouldn’t cause blood in stool. Since she has blood in stool and from India (low-income), H. Pylori is most likely.

**diagnose with urea breath test or stool antigen test. Endoscopy is reserved for patients >55 y.o. Or those with alarm symptoms (weight loss, bleeding, anemia, dysphasia, persistent vomiting).


What is dyspepsia?

Indigestion/ heartburn


What is bradyarrhythimia?

Bradycardia <60 bpm


TIA vs. stroke?

TIA (transient ischemic attack or “mini stroke”)- blockage is temporary and blood flow returns on its own. Stroke symptoms go away on their own

Stroke- “brain attack” where blockage is permanent


Lady with a hx of MS and hyperlipidemia has speech arrest and right arm weakness for <30 minutes. What are 2 meds we should give her?

Aspirin (ASA) and a statin

Why? She had a TIA (classic stroke symptoms for <24 hrs that resolved on their own). The treatment for TIA is to address the risk factors- so give aspirin (to prevent platelet aggregation and stroke) and give a statin (to lower her cholesterol).

**This presentation is NOT an MS exacerbation (MS attacks last for days or weeks). If it were, we could treat the flare up with glucocorticoids, immunoglobulins, or plasma exchange therapy (since MS is an autoimmune condition and we want to decrease the immune system’s damage).


Women has burning upper abdominal pain, constipation, and blood in stool. Calcium is high, phosphorus is low. What syndrome does she likely have?

MEN 1 (multiple endocrine neoplasia type 1)= “pans of pitted pears”
-pancreatic, pituitary, and parathyroid tumors

*Has a pancreatic tumor (ZE syndrome)—> burning upper abdominal pain and GI bleed (tumor can invade into duodenum).
*Has a parathyroid tumor—> release PTH (primary hyperparathyroidism), which increases calcium absorption and phosphorus wasting.
*That’s 2/3, so MEN 1 is likely and we would want to check for a pituitary tumor also.


Sarcoidosis effect on calcium levels?

Can cause hypERcalcemia

(Due to increased conversion to 1,25 active vitamin D—> more calcium and phosphorous reabsorption)


What is Milk-alkali syndrome?

Hypercalcemia + metabolic alkalosis + AKI due to taking too much calcium (can be from taking too many Tums pills...since Tums= calcium carbonate)

**too much calcium has multiple effects on the kidneys and ultimately causes diuresis and stimulates bicarb reabsorption-> met alkalosis


What is a plantar reflex?



Old guy with memory loss and muscle spasms when startled. He also has nystagmus, hypokinesia, and positive Babinski (plantar reflex). EEG shows periodic sharp-wave complexes. Diagnosis?

Creutzfeldt-Jakob disease (CJD)

*prion disease (usually sporadic, but can be due to contaminated corneal transplants).
*key findings: startle response and sharp waves on EEG
**as it progresses, patients may lose ability to move and speak (txt is supportive)


Lady has temporal (giant cell) arteritis and gets treated. 6 months later her muscles are weak and she has trouble going up stairs or standing from a chair. Most likely cause?

Drug-induced myopathy

-glucocorticoids (used to treat giant cell arteritis) can cause myopathy (think of Cushing’s secondary to too much glucocorticoid use...skin thinning, fat redistribution, and muscle thinning!)


What are the pneumonia vaccine guidelines for seniors 65+?

One 13-valent pneumococcal conjugate vaccine (PCV13) +

One 23-valent pneumococcal polysaccharide vaccine (PPSV23) at least 6-12 months later

*give add’l PCV13 and PPSV23 vaccines to high-risk patients (CSF leaks, sickle cell, cochlear implants, asplenia/ immunocompromised)

**give one PPSV23 before age 65 too for some patients (smokers or chronic medical problems like heart/ lung/ liver dz or DM)


What’s a normal pupil size?

2-4 mm in light


How would Phenytoin toxicity present?

Nystagmus, ataxia, confusion


Decreased sensation over 4th and 5th digits and weak grip. What nerve is probably damaged and where?

Ulnar nerve
At the elbow (medial epicondylar groove)

*ulnar nerve syndrome can be caused by prolonged compression on the ulnar nerve from leaning on the elbows while working at your desk


Incidence vs. prevalence?

Incidence= # new cases

Prevalence= total cases


If a man abuses steroids (testosterone), will his levels of GnRH, LH, and FSH be high or low?

All low

-the exogenous testosterone will feedback and inhibit GnRH, LH, and FSH production (-> low endogenous testosterone, small testes, possible infertility)


After treatment with Dapsone, a patient developed fatigue and dark urine. Why?

G6PD deficiency

-in this condition, RBCs can’t make enough NADPH to protect against oxidative injury. Some meds (Dapsone, TMP/SMX, Primaquine), foods (Fava beans), and infections cause oxidative damage and bring on anemia attacks in patients with this
**hemolytic anemia-> blood in urine (dark urine)


What type of drug is Enoxaparin?

Low-molecular weight heparin (LMWH)


Patient has a DVT. Is treated with Enoxaparin (LMWH). Platelet count goes down. Why?

This is heparin-induced thrombocytopenia (HIT)

-bad reaction to heparin where heparin binds to platelet factor 4 (PF4) and antibodies form against the hep-PF4 complex. These antibodies attack platelets—> thrombocytopenia (low platelets) and stick them together—> clotting (opposite of what you’d expect when giving an anti-coagulant).

*discontinue the hep immediately and pick another anticoagulant to treat with!


Reg chest X-rays, what does “bilateral basilar lucency” mean?

Lucency= shows up dark on x-ray
-means it’s less dense (like air-filled lungs in emphysema)—> more X-rays pass through

Basilar= bottom of lungs (opposite of apex, which is the pointy top of the lungs)

So...”bilateral basilar lucency” means the bottom of both lungs appears darker (air-filled) on X-ray


38 y.o. man with SOB and cough, worse on exertion. Smoked 2 years, otherwise no medical hx. Breath sounds are decreased on the bottom of both lungs. Diagnosis?

Alpha-1 antitrypsin deficiency—> panacinar emphysema (destruction of lower lobes *vs. emphysema due to smoking alone would be centriacinar and cause destruction of upper lobes “smoke rises”)


How do you diagnose Alpha-1 antitrypsin (AAT) deficiency (besides going off the history and physical)?

Measure serum AAT levels (should get pulmonary function tests too)


What is nephrolithiasis?

Kidney stones


Alcoholic is having seizures. Cr is 2.4. RBCs are found in his urine. Diagnosis?


*seizures-> skeletal muscles overexertion-> release of myoglobin into the blood-> clogs up renal tubules and causes renal injury


Normal Cr? Normal BUN? Normal BUN:Cr ratio?

Cr- 0.6-1.2
BUN- 7-25

BUN/CR- around 15


Normal calcium levels?



Normal potassium (K+) level?



Normal Na+ level?



Paraneoplastic syndromes in small cell lung CA (4) vs. squamous cell lung CA (1)?

Small cell:
2. Lambert-Eaton
3. ACTH (Cushing’s)
4. Anti-Hu antibodies

Squamous cell:
1. PTHrP (-> hypercalcemia)


Former smoker has a lung mass and calcium level of 14.5. Why is calcium at this level?

Calcium is high (normal would be 8.5-10ish...14 is very high)

This is due to squamous cell carcinoma of the lung-> PTHrP (paraneoplastic syndrome)-> excess calcium reabsorption (and phosphorous wasting)
-This is also known as “hypercalcemia of malignancy”


How do we treat hypercalcemia in the short-term? Long-term?

Short term: Give normal saline (and calcitonin)

*why? Hypercalcemia-induced DI (high calcium interferes with renal channels that allow ADH to work to retain water)-> hypercalcemia patients pee a lot and are volume depleted, so you have to restore volume/ hydrate
*may also give Calcitonin (directly blocks osteoC’s from breaking down bone and releasing calcium-> so, they lower calcium levels in the blood)
**don’t give loop diuretics (even though they can lower calcium levels) unless they have HF (not worth the side effect of worsening volume depletion)

Long term: Give bisphosphonates

*why? Bisphosphonates stimulate apoptosis of osteoClasts (they stop osteoC’s from breaking down bone and releasing calcium-> so, they lower calcium levels in the blood)


Normal platelet count?

150,000- 400,000


Normal Hb in male? Female?

Normal Hb in males= 13.5- 17.5

Normal Hb in females= 12-16
(a little lower due to bleeding once a month/ menstrual cycles)


Treatment for botulism?

Horse-derived (equine) antitoxin therapy


Treatment for Guillain-Barre?

Plasmaphoresis (therapeutic plasma exchange)

*GB occurs when the immune system attacks nerves (can be after Campylobacter or a flu shot...)


What is antiphospholipid antibody syndrome?

The presence of antiphospholipid antibodies + you have blood clots (DVT, PE, stroke, or MI) or pregnancy problems (miscarriages or premature birth from placental insufficiency or preeclampsia)

**Antiphospholipid antibodies are seen in SLE (lupus) (though not specific to it). They can cause 3 problems: (1) antiphospholipid antibody syndrome, (2) increased PTT, (3) false positive syphilis test (RPR/ VDRL)


What is spontaneous bacterial peritonitis (SBP)?

A bacterial infection of the ascitic fluid of the peritoneum
(So, it’s when a patient has ascites, usually secondary to cirrhosis, and that fluid gets infected)


Man with hx of cirrhosis secondary to chronic hep C presented with confusion. He was found to have hepatic encephalopathy and spontaneous bacterial peritonitis (infection of ascitic fluid). He was given Lactulose and Cefotaximine. Since admission and all of this, his Creatinine has gone up. Most likely cause?

Hepatorenal syndrome


Most likely diagnosis in a Mississippi patient who was initially thought to have sarcoidosis (cough, hilar lymphadenopathy, erythema nodosum, and non-caseating granulomas)?


*Blasto is also seen in the Mississippi region, but usually does not involve hilar lymphadenopathy


Where are these fungi found?
1. Histoplasmosis
2. Blastomycoses
3. Coccidioides
3. Paracoccidioides

1. Histoplasmosis- Mississippi/ Ohio river valley (Midwest)

2. Blastomycoses- Great Lakes/ Ohio river valley (Midwest)

3. Coccidioides- Southern US (Cali, Arizona, northern Mexico)

3. Paracoccidioides- South America, Brazil


Guy has a hx of IV drug abuse, endocarditis, and stroke (made him wheelchair-bound). Presents with right calf pain and swelling. On physical exam, there is hepatosplenomegaly. Abdomen is distended with shifting dullness suggestive of ascites. Most likely cause of the ascites?

Chronic liver disease

-IV drug use= high-risk for hep C w/ chronic liver dz (cirrhosis)—> ascites (the portal HTN causes fluid to accumulate in the peritoneum)

*IV drug use also—> endocarditis with embolic stroke. Stasis (wheelchair-bound) following the stroke—> DVT. But DON’T be distracted by everything going on w/ this patient! The question is just asking why does he have ascites? 80% of ascites is due to liver failure and you can trace this to his IV drug abuse.


Man with hx of IV drug abuse has dark urine and jaundice. Total bilirubin, direct (conjugated) bilirubin, alk phos, and AST are all high. Abdomen is not tender. Next best step to diagnose?

Ultrasound the abdomen

(High serum alk phos suggests cholestasis/ reduced bile flow, possibly due to an obstruction/ stone. U/S will help you look for intrahepatic or extrahepatic causes of biliary obstruction.)


50 year old lady with hx of GERD. Has episodes of hands turning bluish in the cold. Her hands are puffy and lungs have crackles. Diagnosis? Associated with what 2 antibodies?

Systemic sclerosis (diffuse type)
1. anti-Scl-70 antibody (aka anti-DNA topoisomerase-1 antibody)
2. anti-RNA polymerase III

*Systemic sclerosis= autoimmunity + non inflammatory vasculopathy + collagen deposition w/ fibrosis.
2 sub-types: (1) diffuse (involves the skin all over and early visceral involvement- interstitial lung dz), (2) limited aka CREST syndrome (face and fingers)

**CREST= Calcinosis (calcium deposits) and anti-Centromere antibody
Raynaud’ s phenomenon
Esophageal dysmotility (GERD0
Sclerodactyly (thickened skin on hands and feet)
Telangiectasia (dilated blood vessels)


What does CREST syndrome stand for?

Calcinosis (calcium deposits) and anti-Centromere antibody
Raynaud’ s phenomenon
Esophageal dysmotility (GERD0
Sclerodactyly (thickened skin on hands and feet)
Telangiectasia (dilated blood vessels)


What is the drug Memantine used for?

Severe Alzheimer’s disease

-it blocks NMDA glutamate receptors
-may improve cognitive symptoms


Lady just flew home from Central Asia. Has SOB, chest pain, and hemoptysis. HR is 106, RR is 28. Most likely diagnosis?

Pulmonary embolism (PE)

*She was on a long flight, has SOB, and is coughing up blood. Red flags!

*typical PE presentation= tachypnea (rapid breathing) and tachycardia in addition to SOB. This is because she has the pulm artery occluded-> dec oxygenation-> heart tries to compensate.


Patient is anxious, confused, has conjunctival injection. What substance?


(Conjunctival injection= bloodshot eyes)
*increases appetite, HR, breathing, causes dry mouth, and bloodshot eyes. Also slows reaction time-> car accidents.


What acid-base disturbance can AKI cause?

Non-nation gap metabolic acidosis

-from retention of uremia and impaired acid excretion (if you can’t pee out the acid, it accumulates in the blood)


Why might hypoventilation cause fatigue?

Breathing less= less oxygen being delivered to organs in the body to provide energy


In nephrogenic DI (like due to lithium), will sodium levels go up or down? Will blood or urine have a higher osmolarity?

Nephrogenic DI (not responding to ADH)-> not retaining water-> pee more-> [Na+] will go up-> HYPERNATREMIA (high Na+)

Blood will be more concentrated (HIGHER OSMOLARITY) than the urine (urine is more dilute since you’re peeing more)


How can sodium levels differentiate nephrogenic DI vs. psychogenic polydipsia?

Nephrogenic DI (not responding to ADH)-> not retaining water-> pee more-> [Na+] will go up-> HYPERNATREMIA (high Na+)

Psychogenic polydipsia (drinking water like a crazy person)-> you’re putting so much water into the body that it dilutes [Na+]-> HYPONATREMIA (low Na+)


What is the DASH diet?

DASH= Dietary Approaches to Stop Hypertension
-this is the diet you put HTN patients on
(Involves eating fruits, veggies, whole grains, low-fat, low salt, high potassium foods)


What is UP/Cr?

Urine protein over creatinine ratio
(A way to estimate how much protein is being spilled in the urine per day)


What is ankle-brachial index?

Ratio of BP at the ankle to BP in the upper arm (brachial)

-If BP in the ankle is lower than in the arm, it suggests blocked arteries in the ankle due to peripheral vascular disease (PAD)

*used to check when patient has claudication, dermal atrophy, and absent distal pulses


A patient had a previous MI complicated by LV systolic dysfunction (the heart isn’t pumping so well anymore-> ejection fraction <30%). What deadly condition is this patient at risk of?

Sudden cardiac death (SCD) due to ventricular arrhythmia


Guy is brought in by his GF for confusion. He moved into a mobile home yesterday and had headache, nausea, and dizziness. This morning she went over to check on him and found him confused in bed in his urine. What test will most likely diagnose him?

Measuring carboxyhemoglobin level

*this is likely carbon monoxide (CO) poisoning from an old heater. Hb binds CO instead of oxygen (CO has a greater affinity)—> carboxyhemoglobin. Less oxygen delivered to tissues (left shift).


What is Well’s criteria?

A calculator to assess the probability a patient has a PE (pulmonary embolism)

*if total score (based on clinical signs of DVT, previous DVT/ PE, tachycardia, recent surgery, hemoptysis/ cancer) is >4, a PE is likely


If PE is on your differential but is unlikely (based on Wells criteria), what test can you do to rule it out completely?

Check the D-dimer (make sure it’s less than 500)

*D-dimer is sensitive, but not specific for PE. So, you get this to make sure you can rule out PE.
**If PE is likely (based on Wells criteria), don’t get a D-dimer...go straight to CT pulmonary angiogram (aka spiral CT) (or V/Q scan if you can’t do the pulmonary angiogram bc the patient has bad kidneys and can’t handle the contrast) to diagnose.


If PE is on your differential and is LIKELY (based on Wells criteria), what test do you do?

Get a CT pulmonary angiogram (aka spiral CT) to diagnose

Unless your patient has kidney problems (in which case they can’t handle the IV contrast needed to do the pulmonary angiogram)—> then get a V/W scan to diagnose


What number is an elevated D-dimer?

> 500


What antibiotic can you give as empiric treatment of traveler’s diarrhea (ETEC)?

Ciprofloxacin (short-course)

*if symptoms fail to improve, test for something else (ex: may be parasitic like Giardia and require Metronidazole)


35 year old guy with PMH of Bipolar (on Risperidone) comes in for fatigue, headache, and decreased libido.
Testosterone- low
TSH- low
T4- low
Prolactin- high
Most likely diagnosis?

Pituitary adenoma

*anterior pituitary—> FLAT PiG (FSH, LH, ACTH, TSH, Prolactin, GnRH)
*mass effect—> headache and visual disturbance. Production of most hormones will be decreased due to compression of normal pituitary cells. But, prolactin is high due to anatomic disruption of the dopamine brake onto prolactin.

**NOT Hashimotos/ hypothyroidism bc T4 would be low, but TSH would be high due to negative feedback.
**NOT Risperidone side effect bc that’s an anti-dopamine drug-> takes brake off prolactin-> high prolactin, but does not affect these other hormones.


What valvular problem is common in ankylosing spondylitis?

Aortic regurg

*Ankylosing spondylitis= a seronegative spondyloarthritis (FA pg 461- lack of Rheumatoid factor, axial skeleton involvement, HLA-B27) with spinal fusion—> bamboo spine. Patients can also get uveitis and aortic regurg (aortic inflammation-> aortic aneurysm-> pulls on valve-> regurg).

**These patients are at risk for vertebral fractures with minimal trauma! (Increased osteoclast activity in the setting of chronic inflammation)


A patient has a MI of the LAD. 4 days later, she is hypotensive with tachycardia. There are crackles over her lungs and her extremities are cold. EKG shows deep T wave inversion in leads V1-V5. Most likely cause of her deterioration?

Interventricular septum rupture (complication 3-5 days post-MI)

-> cardiogenic shock (hypotension, pulm edema, confusion due to poor pumping and poor organ perfusion). Cold extremities due to shunting of blood to core vital organs.


Male patient undergoing chemo for Seminoma comes to the ED for fever and chills, nothing else going on. He has mucosal pallor (pale skin), low Hb and Hct, and low leukocytes and neutrophils. Diagnosis and treatment?

Febrile neutropenia (fever + low neutrophils, specifically absolute neutrophil count <1500)

Treat with an anti-pseudomonas beta-lactam agent (these bugs are often responsible)—
Cefepime (4th gen cephalosporin), Meropenem (carbapenem), or Piperacillin-Tazobactam (extended-spectrum penicillin)

*Chemo patients are at higher risk for this and you need to give emergent empiric antibiotics to prevent progression to sepsis!


Patient with PMH of Genital herpes comes in with scaley rashes looking like psoriasis. What screening test should you offer him?

HIV test

*HIV is associated with flares of psoriasis. Other things that can worsen psoriasis— skin trauma, withdrawal from glucocorticoids, and certain meds (anti-malaria, indomethacin, propranolol)


AIDS patients are at greatest risk for a CMV (cytomegalovirus) infection with a CD4 count less than what?

CD4 < 50
(“Charity drive 50 cents”)


Treatment for CMV esophagitis (AIDS patient with CD4 <50 with linear ulcerations)?


*Herpes Simplex esophagitis (well-circumscribed, round ulcers as opposed to linear ulcers in CMV) is treated with Acyclovir


HIV patient has a CD4 count of 300. She has a lobular pneumonia, diagnosed by symptoms and chest X-ray. What is the most likely organism responsible for the pneumonia?

Strep pneumo

*Don’t assume it’s PCP pneumonia just bc she has HIV! That is seen in HIV patients with CD4 <200. Still, step pneumo is the no. 1 cause of lobular CAP!


AIDS patient with CD4 <50 and bloody diarrhea. Most likely cause?

Cytomegalovirus (CMV colitis)

*common causes of diarrhea in HIV patients:
1) Cryptosporidium—CD4 <180 (severe watery diarrhea, low-grade fever)
2) Microsporidium—CD4 <100 (crampy watery diarrhea, usually no fever)
3) MAC—CD4 <100 (watery diarrhea and high fever)
4) CMV—CD4 <50 (bloody diarrhea, abdominal pain, low-grade fever)


HIV patient has had a cough for 2 months, no hemoptysis. Was hospitalized 6 months ago for seizures. CXR shows cavitation in the right upper lobe. Most likely diagnosis?

Reactivation TB (affects upper lobes)

*not likely to be aspiration pneumonia bc that is found in lower lobes (due to gravity)
*you do not HAVE TO HAVE hemoptysis for it to be TB!!! Also, note this guy’s HIV status puts him at increased risk for TB


What the heck is Strep Sanguinus?

It’s in the family of Step Viridans

*think of it when there is a patient with a heart problem who gets a dental procedure done!


Lady has painful swelling of the left face. There is a raised red rash with sharply-demarcated borders including the left ear. She also have fever + chills. What bug is responsible?

Group A strep (Strep Pyogenes)

This is Erysipelas (superficial skin infection of the upper dermis *like cellulitis but more superficial)


When is Toxoplasma prophylaxis indicated?

In HIV patients with CD4 <100


When is CMV prophylaxis indicated?

In some organ transplant recipients


HIV patient not taking his meds. Has had weight loss, fever, night sweats, cough, and SOB for 3 weeks. There are small ulcers on his hard palate, enlarged lymph nodes, and lung crackles. What test should you order?

Urine Histoplasma antigen
(This sounds like disseminated histoplasmosis)

*treat with Amp B


What is the most appropriate empiric antibiotic to start an endocarditis patient on with a hx of IV drug abuse?


-it is broad spectrum and has MRSA coverage


Wisconsin guy has fever, night sweats, productive cough, and weight loss. Also has crusty skin lesions, lytic lesions on ribs, and consolidation on his left upper lung. Diagnosis?


*seen in the Mississippi/ Ohio river valley (Wisconsin has the highest infection rate)


Teenager has episodes of “chest fluttering.” BP is normal, but pulse is 210. EKG shows narrow complex tachycardia. What diagnosis should be on the differential?

Wolff-Parkinson-White syndrome

-going through an accessory “secret pathway” (bundle of Kent) that bypasses the rate-slowing AV node-> ventricles get depolarized before they should (shows up on EKG as delta waves).


What is long QT syndrome?

When you have a long QT interval (QT= ventricular depolarization + depolarization, so the entire systole)

* >450 mace in males or >470 mace in females
*can be congenital or acquired
*risk for sudden cardiac death (due to Torsades or polymorphic ventricular tachycardia)


What is micturition?



What is an electrocardiogram?

ECG! (Same thing as EKG)


Old guy felt like he was going to pass out while running. He had a similar episode before. You did a physical exam, significant for a systolic ejection murmur at the right 2nd intercostal space. You order an EKG, which showed LV hypertrophy. Next step?

Order an echocardiogram

This guy most likely has aortic stenosis (exertional syncope, systolic murmur, LV hypertrophy). Get an echo any time you suspect a structural/ valvular heart disease (aortic stenosis, HOCM, LV dysfunction, cardiac tamponade, etc.)
*do NOT stress test symptomatic severe aortic stenosis


20 year old lady with episodes of sharp chest pain for 3 weeks. Has systolic murmur at the apex that shortens with squatting. Diagnosis?

Mitral valve prolapse

*Apex= mitral region
Systolic murmur= MVP or mitral regurg
Squatting= increased preload (kink veins in legs-> more ‘milking’ of blood to heart)
Murmur is softer with squatting= MVP (more preload helps the valve to be more crisp as opposed to floppy where it doesn’t align well)

**Do an echo to confirm the diagnosis. Symptoms are benign.


Guy comes in with sudden onset palpitations. He is found to be in a-fib. BP is 112/70 and O2 sat is 92. He is full code.
He suddenly becomes unresponsive. Cardiac monitor still shows a-fib, but there’s no palpable pulse and he has agonal breathing (gasping). What do you do next?

Chest compressions

-The heart has an abnormal rhythm going on, but it is not effectively pumping blood out to the extremities, so you can’t feel a pulse (this is called pulseless electrical activity).
-ACLS guidelines say do CPR and give epi (beta>alpha agonist, so helps improve contractility and is a vasopressor-> vasoconstricts to improve cerebral and coronary perfusion).

*Although we should cardiovert new a-fib patients (had it <48 hrs) or a-fib patients who are unstable, if they are so unstable they go into a non-perfusing rhythm, you follow ACLS guidelines!


Asystole vs. Pulseless electrical activity (PEA)?

Asystole- Cardiac arrest
No electrical activity
Monitor is flat-lined

Pulseless electrical activity (PEA)- A non-perfusing rhythm
There is an abnormal heart rhythm (ex: a-fib), but the heart isn’t effectively pumping blood out, so there’s no palpable pulse (or measurable BP)
Monitor shows the abnormal rhythm

**NOTE: 3 rhythms cannot be PEA: (1) V-fib, (2) V-tach, (3) Asystole. Why? Bc we don’t expect a pulse with these rhythms. PEA is an organized electrical activity where we expect to see a pulse but we don’t have one.


What does ACLS stand for? What does CPR stand for?

ACLS= Advanced Cardiac Life Support

(guidelines on what to do if a patient is in cardiac arrest)

CPR= Cardiopulmonary Resuscitation


What are the reversible causes of asystole/ pulseless electrical activity? “5 H’s and 5 T’s”

(You want to consider these when doing chest compressions and giving epi...if you figure out the source of the problem, you may be able to correct the heart’s rhythm and save the patient’s life!)

Hydrogen ions (acidosis)
HypOkalemia/ HyPERkalemia

Tension pneumothorax
Tamponade, cardiac
Toxins (narcotics, benzos)
Thrombosis (pulmonary or coronary)


Can you shock a patient in Asystole?


Asystole= they are flat-lined. There is ZERO electrical activity in the heart, so shocking them will not work (shocks work by feeding off of electrical activity). Do chest compressions, give epi (every 3-5 min), and try to figure out why the patient went into asystole bc there may be a reversible cause.


2 shockable rhythms? 2 non-shockable rhythms?

1. V-fib (ventricular fibrillation)
2. V-tach (ventricular tachycardia)
**note: Torsades is a subcategory of ventricular tachycardia- shock it.

1. Asystole
2. Pulseless electrical activity (PEA)

Rap song: “Defib for V-fib and pulseless V-tach. Don’t defib asystole, you won’t get them back!”


Define orthostatic hypotension.

Decrease in BP by 20 systolic or 10 diastolic when standing
*may be accompanied by an increase in HR


Why are old people more likely to get orthostatic hypotension (big drop in BP when they stand, making them momentarily lightheaded)?

Aging-> some baroreceptor activity is lost

*normally: you stand-> gravity is working against you so vessels have to constrict in the lower extremities to ‘milk’ blood up to the heart so it can pump enough to maintain BP. For the moment that BP is dropped right when you stand, baroreceptors (on carotid sinus) respond to decreased stretch-> decrease firing-> this increases sympathetic stimulation to raise the BP to baseline.


Young man faints when exercising. Has a crescendo-decrescendo systolic murmur in the left sternal border. Diagnosis?


(Basically a functional aortic stenosis, since the intraventricular septum is in the way of aortic outflow)


IV drug user had an episode of syncope. Has a diastolic murmur at the left sternal border. Platelet count is elevated and EKG shows 2nd degree AV block. Diagnosis?

Perivalvular abscess

*Be suspicious of perivalvular abscess anytime a patient has endocarditis + conduction abnormalities on EKG (the abscess can extend into the conduction pathway, messing it up). Endocarditis alone wouldn’t cause AV block or syncope.


Man comes in for palpitations and SOB on exertion. He recently binge drank. HR is 130. EKG shows no clear P waves. Echo shows EF=35%, mitral regurg, and dilated LA and LV with global hypokinesis. What’s going on?

Alcohol-> A-fib w/ RVR (rapid ventricular response)-> tachycardia-mediated cardiomyopathy (the prolonged arrhythmia and rapid ventricular rate is causing HF)

*treat with aggressive rate and rhythm control

**note: the mitral regurg in this patient is just due to the fact that the ventricles are overloaded


What is tachycardia-mediated cardiomyopathy? How do you treat it?

When you have a tachyarrhythmia (heart is beating super fast, out of rhythm for a while) that leads to HF
(*can be due to a-fib, a-flutter, v-tach, etc.)

Treat with aggressive rate or rhythm control
(*AV nodal blocking agents, antiarrhtymic drugs, ablation of arrhythmia, etc.)


37 year old lady who immigrated from Cambodia presents with stroke symptoms. Over the past several months, she has had palpitations, SOB on exertion, and hemoptysis. Most likely explanation?

Rheumatic heart disease-> mitral stenosis-> a-fib-> stroke

*remember that mitral stenosis (MS) over time-> increased LA pressure. This predisposes to a-fib. This also leads to pulmonary vascular congestion, explaining the hemoptysis.


What is “flash pulmonary edema?”

Acute pulmonary edema secondary to increased cardiac filling pressures (such as after an MI)


What is micturition?



What is an electrocardiogram?

ECG! (Same thing as EKG)


Old guy felt like he was going to pass out while running. He had a similar episode before. You did a physical exam, significant for a systolic ejection murmur at the right 2nd intercostal space. You order an EKG, which showed LV hypertrophy. Next step?

Order an echocardiogram

This guy most likely has aortic stenosis (exertional syncope, systolic murmur, LV hypertrophy). Get an echo any time you suspect a structural/ valvular heart disease (aortic stenosis, HOCM, LV dysfunction, cardiac tamponade, etc.)
*do NOT stress test symptomatic severe aortic stenosis


20 year old lady with episodes of sharp chest pain for 3 weeks. Has systolic murmur at the apex that shortens with squatting. Diagnosis?

Mitral valve prolapse

*Apex= mitral region
Systolic murmur= MVP or mitral regurg
Squatting= increased preload (kink veins in legs-> more ‘milking’ of blood to heart)
Murmur is softer with squatting= MVP (more preload helps the valve to be more crisp as opposed to floppy where it doesn’t align well)

**Do an echo to confirm the diagnosis. Symptoms are benign.


Guy comes in with sudden onset palpitations. He is found to be in a-fib. BP is 112/70 and O2 sat is 92. He is full code.
He suddenly becomes unresponsive. Cardiac monitor still shows a-fib, but there’s no palpable pulse and he has agonal breathing (gasping). What do you do next?

Chest compressions

-The heart has an abnormal rhythm going on, but it is not effectively pumping blood out to the extremities, so you can’t feel a pulse (this is called pulseless electrical activity).
-ACLS guidelines say do CPR and give epi (beta>alpha agonist, so helps improve contractility and is a vasopressor-> vasoconstricts to improve cerebral and coronary perfusion).

*Although we should cardiovert new a-fib patients (had it <48 hrs) or a-fib patients who are unstable, if they are so unstable they go into a non-perfusing rhythm, you follow ACLS guidelines!


Asystole vs. Pulseless electrical activity (PEA)?

Asystole- Cardiac arrest
No electrical activity
Monitor is flat-lined

Pulseless electrical activity (PEA)- A non-perfusing rhythm
There is an abnormal heart rhythm (ex: a-fib), but the heart isn’t effectively pumping blood out, so there’s no palpable pulse (or measurable BP)
Monitor shows the abnormal rhythm

**NOTE: 3 rhythms cannot be PEA: (1) V-fib, (2) V-tach, (3) Asystole. Why? Bc we don’t expect a pulse with these rhythms. PEA is an organized electrical activity where we expect to see a pulse but we don’t have one.


What does ACLS stand for? What does CPR stand for?

ACLS= Advanced Cardiac Life Support

(guidelines on what to do if a patient is in cardiac arrest)

CPR= Cardiopulmonary Resuscitation


What are the reversible causes of asystole/ pulseless electrical activity? “5 H’s and 5 T’s”

(You want to consider these when doing chest compressions and giving epi...if you figure out the source of the problem, you may be able to correct the heart’s rhythm and save the patient’s life!)

Hydrogen ions (acidosis)
HypOkalemia/ HyPERkalemia

Tension pneumothorax
Tamponade, cardiac
Toxins (narcotics, benzos)
Thrombosis (pulmonary or coronary)


Can you shock a patient in Asystole?


Asystole= they are flat-lined. There is ZERO electrical activity in the heart, so shocking them will not work (shocks work by feeding off of electrical activity). Do chest compressions, give epi (every 3-5 min), and try to figure out why the patient went into asystole bc there may be a reversible cause.


2 shockable rhythms? 2 non-shockable rhythms?

1. V-fib (ventricular fibrillation)
2. V-tach (ventricular tachycardia)
**note: Torsades is a subcategory of ventricular tachycardia- shock it.

1. Asystole
2. Pulseless electrical activity (PEA)

Rap song: “Defib for V-fib and pulseless V-tach. Don’t defib asystole, you won’t get them back!”


Define orthostatic hypotension.

Decrease in BP by 20 systolic or 10 diastolic when standing
*may be accompanied by an increase in HR


Why are old people more likely to get orthostatic hypotension (big drop in BP when they stand, making them momentarily lightheaded)?

Aging-> some baroreceptor activity is lost

*normally: you stand-> gravity is working against you so vessels have to constrict in the lower extremities to ‘milk’ blood up to the heart so it can pump enough to maintain BP. For the moment that BP is dropped right when you stand, baroreceptors (on carotid sinus) respond to decreased stretch-> decrease firing-> this increases sympathetic stimulation to raise the BP to baseline.


Young man faints when exercising. Has a crescendo-decrescendo systolic murmur in the left sternal border. Diagnosis?


(Basically a functional aortic stenosis, since the intraventricular septum is in the way of aortic outflow)


IV drug user had an episode of syncope. Has a diastolic murmur at the left sternal border. Platelet count is elevated and EKG shows 2nd degree AV block. Diagnosis?

Perivalvular abscess

*Be suspicious of perivalvular abscess anytime a patient has endocarditis + conduction abnormalities on EKG (the abscess can extend into the conduction pathway, messing it up). Endocarditis alone wouldn’t cause AV block or syncope.


Man comes in for palpitations and SOB on exertion. He recently binge drank. HR is 130. EKG shows no clear P waves. Echo shows EF=35%, mitral regurg, and dilated LA and LV with global hypokinesis. What’s going on?

Alcohol-> A-fib w/ RVR (rapid ventricular response)-> tachycardia-mediated cardiomyopathy (the prolonged arrhythmia and rapid ventricular rate is causing HF)

*treat with aggressive rate and rhythm control

**note: the mitral regurg in this patient is just due to the fact that the ventricles are overloaded


What is tachycardia-mediated cardiomyopathy? How do you treat it?

When you have a tachyarrhythmia (heart is beating super fast, out of rhythm for a while) that leads to HF
(*can be due to a-fib, a-flutter, v-tach, etc.)

Treat with aggressive rate or rhythm control
(*AV nodal blocking agents, antiarrhtymic drugs, ablation of arrhythmia, etc.)


Lady presents with stroke symptoms. Over the past several months, she has had palpitations, SOB on exertion, and hemoptysis. Most likely explanation?

Rheumatic heart disease-> mitral stenosis-> a-fib-> stroke

*remember that mitral stenosis (MS) over time-> increased LA pressure. This predisposes to a-fib. This also leads to pulmonary vascular congestion, explaining the hemoptysis.


What is “flash pulmonary edema?”

Acute pulmonary edema secondary to increased cardiac filling pressures (such as after an MI)


Patient has episodes of squeezing chest pain at rest. EKG and exercise stress test are normal. Most likely diagnosis?



Gold standard for diagnosing type 2 DM in PCOS patients?

Oral glucose tolerance test

(It is more sensitive in PCOS patients than fasting glucose and A1c standard screenings tests)


Pathophys of PCOS?

Inc LH (related to insulin resistance)—> theca cells in ovaries use this to make androgens, then granulosa cells of ovaries take the androgens and make estrogen (estradiol).

With all the excess LH, there’s too many androgens for the granulosa cells to convert to estradiol, so excess androgens circulate in the blood and go into the peripheral fat—> fat cells make it into estrone and this feeds back onto the GnRH axis, inhibiting it.

Excess androgens—> hirsutism
Inhibition of GnRH—> anovulatory, infertile


55 year old guy has urinary frequency, urgency, hesitancy, and low back pain + perineal pain during ejaculation. The prostate is smooth but slightly enlarged. Urine culture is negative. Most likely diagnosis?

Chronic prostatitis
(Noninfectious chronic prostate inflammation)

*this is a diagnosis of exclusion based on urinary symptoms + perineal or genital pain + pain or blood with ejaculation in the setting of a negative urine culture
*antibiotics (fluoroquinolones) can help (even though a bacteria is not identified)
*alpha-adrenergic inhibitors (Tamsulosin) and 5-alpha-reductase inhibitors (Finasteride) can also help


How does epididymitis (inflammation of the epididymis of the testicles) typically present?

Urinary/ voiding symptoms + scrotum pain/ swelling + purulent (pus) urethral discharge


Why would you test a patient with Raynaud phenomenon for autoantibodies and inflammatory markers (ex: ANA)?

It can occur in the setting of an autoimmune or systemic disease (ex: CREST syndrome)


What drugs may be helpful for Raynaud phenomenon?

Dihydropyridine CCBs
(Vasodilate, so help improve perfusion to the fingertips)


Lichen planus (pruritic, purple, papules, plaques) is associated with what disease?

Hepatitis C


If FENa (fraction of excreted sodium) is >2%, what does that tell you?

It’s either post-renal (later stage) or intrinsic AKI
(Normal FeNa= <1%. If FeNa is higher, you know the kidneys are not working to reabsorb Na+)


Lady has pyelonephritis. Later develops intrinsic AKI. What agent was she likely treated with?

An aminoglycoside

-these drugs treat serious gram-negative infections (pyelonephritis is often due to E-coli—a bladder infection that ascends) and are nephrotoxic


Minimal bright red blood per rectum (not mixed in stool) is most often due to benign disorders such as __________ and __________.

Hemorrhoids (varicose veins in the rectum that can cause bleeding)
Anal fissures (aka anal ulcer) (small tear in the lining of the anal wall)


What is a barium enema?

They give you a contrast solution and then take an x-ray of the colon


Patient under 40 years old has minimal bright red blood per rectum. What test should you do first?

Anoscopy (anal speculum)

Why? This is minimally invasive and allows you to look in there for hemorrhoids (varicose veins) or rectal fissures (ulcer/ tear in anal wall). If you don’t find the cause with the anoscopy, then consider a sigmoidoscopy or colonoscopy.
*If the patient were 40-49, you may consider a sigmoidoscopy. If the patient were 50+ and it’s been 2-3 years since the last colonoscopy, you’d want to do a colonoscopy.


How long does a seizure have to go on for there to be risk of permanent brain injury?

>5 minutes

*Status epilepticus used to be defined as a seizure <30 min, but recent studies show all it takes is 5+ minutes of seizing for there to be risk of permanent brain injury (from the excitatory cytotoxicity)


How do we get rid of Basal Cell Carcinoma (pearly nodules) on the face and other cosmetically sensitive areas?

Mohs micrographic surgery

(Sequential removal of thin layers of skin with microscopic inspection to confirm that the margins have been cleared of malignant tissue)


Name for brown plaques/ nodules with “stuck-on” appearance?

Seborrheic keratosis


Drug-induced acne is a common side effect of what drugs?



If a patient cannot run on a treadmill, how do we do a stress test?

Give them Adenosine (vasodilator)

-to normal coronary arteries—> this causes a big increase in blood flow (dilates them a lot)
-to stenotic coronary arteries—> this does not cause an increase in blood flow (the body’s mechanisms have already dilated these stenotic vessels to the max, so adding in a vasodilator doesn’t do a thing)
-the difference in blood flow allows us to diagnose CAD


Guy has an MI. You also notice an S3 heart sound and crackles in the lungs on examination. He’s already been given ASA, Clopidogrel, and Atorvostatin. What should you give him next?


-Diuretics are recommended for acute pulmonary edema (“flash pulmonary edema”) secondary to an MI.

*Although beta-blockers are part of the therapy for MI (“MONA BASH”), do NOT give a beta-blocker to a patient with decompensated CHF (dilated cardiomyopathy) or bradycardia
(This guy has this based on S3 and crackles—fluid overloaded). Why? Beta-blockers cause decreased contractility and HR...if you already got a pumping problem, this will worsen it!


What lung conditions are associated with CREST syndrome?

Interstitial fibrosis and pulmonary HTN

*if pulm HTN, would expect a RV heave (impulse palpated immediately left of the sternum that suggests RV enlargement) and/or a loud pulmonary component of the 2nd heart sound


Girl with hx of depression and chronic back pain overdosed on meds in a suicide attempt. Has a seizure on her way to the ED. She’s tachy, hypotensive, skin is warm and flushed, pupils dilated, bowel sounds decreased, and QRS prolonged.
What did she overdose on and what are you going to do about it?

TCA (tricyclic antidepressants) overdose
Give sodium bicarbonate

*Can cause QRS prolongation (or QT prolongation-> Torsades). Also causes anti-cholinergic effects.


Calcium gluconate is given in what arrhythmia?

Hyperkalemia (peaked T waves)


Homeless guy comes in smelling like alcohol. BP is 90/60, HR 95, RR 5. Has normal pupil size. Extremities are cool to touch. Decreased bowel sounds and muscular tone. Diagnosis? What is your priority in managing this patient?

Opioid overdose
Priority= airway protection—intubate and give Naloxone (mu-opioid antagonist to reverse acute opioid toxicity)

-What gives it away is the respiratory depression (RR=5)!
-Other findings also support this diagnosis (extremities cool to touch is due to hypothermia from impaired thermogenesis)

*don’t rule out opioid use just cuz the pupils are normal sized (not pinpoint)! They can be normal (could even be dilated if the patient took amphetamines too, for example)


What do you give for beta-blocker overdose/ intoxication?



What’s a “scaphoid stomach?”

A sunken in stomach


Teenage girl has constipation and says her stomach is “puffed up.” She has cold intolerance. BP and HR are low. BMI is 18. On exam, abdomen is non-distended and normal bowel sounds. Diagnosis?

Anorexia nervosa

BMI <18.5 + distorted body image (thinks stomach is “puffed up” when it is not)

*Constipation and cold intolerance are also consistent with hypOthyroidism. BUT, in hypOthyroidism you’d expect weight GAIN (everything is slowed down) and HTN (not low BP).
*In Anorexia, electrolyte abnormalities—> slowed bowels and constipation. Malnutrition—> loss of muscle mass (which includes the heart)—> heart shrinks and beats slower to conserve energy (think of it as the heart is weakened bc it is starving)


Treatment options for psoriasis?

Topical glucocorticoids (betamethasone, fluocinonide) or Vitamin D derivatives


Another name for esophagogastroduodenoscopy (EGD)?


(Tube that goes down the mouth-> esophagus-> stomach-> duodenum)


Guy with HTN (taking a Thiazide diuretic) is peeing all the time, thirsty all the time. Glucose is 90, Na+ is 150, serum osmolality is 300, urine osmolality is 125. Most likely diagnosis?

Diabetes insipidus (DI)

-glucose is normal, so rule out DM
-Na+ is high, so rule out side effect of the Thiazide diuretic alone (this causes hypOnatremia)
-the blood is more concentrated than the urine...in DI, you are not making/ responding to ADH, so you cannot retain water and just pee it all out, makes sense


Lady complains of daily headaches. She used to get migraines a lot and uses over-the-counter analgesics (pain relievers for headache, like Tylenol) each day. What advice should you give her?

Stop taking the over-the-counter headache meds!

Using these too often—> medication overuse headaches (like a caffeine headache, these occur do to getting addicted to the meds)


Why do you get chills with fever?

Fever-> cytokines cause the hypothalamus to change the body’s setpoint to a higher level-> to reach this new setpoint, peripheral blood vessels vasoconstrict (to shunt blood to the core) and this can make a person feel cold

*also, muscles may contract (shivering) during this process


Patient comes in for recurrent sinusitis. He also has hematuria, found on urinalysis. Past medical history is significant for chronic joint and back pain. Likely diagnosis and next best step?

Granulomatosis with polyantiitis (Wagner’s)
-small-vessel vasculitis involving the nasopharynx, lungs (but not in this patient), and kidneys
-systemic symptoms are common (anemia, fatigue, fever, joint pains)

Next step= check for c-ANCA (autoantibodies against neutrophils)
*tissue biopsy is the confirmatory test


What test can you do to confirm lactose intolerance and how does it work?

Hydrogen breath test

-Lactose intolerance= you lack lactase, a brush border enzyme that breaks down lactose in dairy products (decreases with age, esp in Asians). Since lactose doesn’t get broken down into simple carbs, its draws in water-> osmotic diarrhea.

-Since it’s not broken down, more stomach acid will try to compensate to digest it—> positive H+ breath test.


High, low, or normal osmotic gap in lactose intolerance?



Old lady just diagnosed with colon cancer comes in complaining of intermittent pressure-like chest pain since the morning. EKG shows T wave inversion in leas V2-V4. Angiogram shows no blockage. Diagnosis?

Stress-induced (takotsubo) cardiomyopathy
Aka “broken heart syndrome”

*believed to be brought on by a catecholamine surge from a stressor-> microvascular spasm and impaired contraction of the heart (hypokinesis).

*EKG usually shows evidence of ischemia (ST elevation, T wave inversion, etc.) in the anterior precordial leads (V1-V4) and troponin may be a little high. But, angiogram shows no CAD.

*self-limiting in weeks


EKG changes in:
1. Panic attack
2. Stress-induced cardiomyopathy (“broken heart syndrome”)?

1. Panic attack—> no EKG abnormalities

2. Broken heart syndrome—> ischemic EKG symptoms (ST elevation, T wave inversion, moderately elevated troponin, etc.)


Are the following levels high, low, or normal in Paget’s dz of the bone?
1. Serum calcium
2. Serum phosphorus
3. Alkaline phosphatase
4. Urgent hydroxyproline

1. Serum calcium- NORMAL
2. Serum phosphorus- NORMAL
3. Alkaline phosphatase- HIGH
4. Urgent hydroxyproline- HIGH (an elevated bone turnover marker)

*Paget disease of the bone- imbalance between osteoclast and osteoblast function (osteoC’s go crazy breaking down bone w/o the regulation of osteoB’s-> osteoB’s rush to compensate and lay down bone, but do a poor job of it-> thick bone that fractures easily)
*Symptoms: bone pain, increasing hat size, hearing loss, lion face, isolated elevated alk phos (due to activation of osteoB’s)


Lady in the ED has an S3 and bilateral crackles. O2 sat is 78% with 40% oxygen, so she is intubated for respiratory failure and given nitrates and diuretics. Breath sounds on the left continue to be decreased. How can you restore them?

Reposition the endotracheal tube

(When you intubate, the goal is to get the tube just before the carina, where the main bronchus bifurcates into the right and left bronchus. If only one lung is expanding after intubation, you advanced the tube too far into either the right bronchus or the left bronchus.)


Patient had a URI 2 weeks ago that resolved. Now he has tingling in his foot, bilateral muscle weakness, and absent knee and ankle reflexes. No headache or photophobia. Diagnosis?

Guillain-Barré syndrome

-ascending paralysis from a URI or diarrheal illness (Campylobacter jejuni)


Will the following be high, low, or normal on examination of CSF in a patient with Guillain-Barré syndrome?

Protein- HIGH
Glucose- NORMAL

*CSF protein may be high due to increased permeability of the blood-nerve-barrier
*treat with IV Ig or plasmapheresis
*takes patients months to recover (can be chronic too- I saw a patient like this in the hospital)


When is it ok to accept a gift from a medical conference?

When the gift directly benefits patient care and it is of low monetary value


What are the indications for long-term home oxygen therapy? What about in patients with cor pulmonale, right HF, or hematocrit >55%?

1. PaO2 < 55 or oxygen sat SaO2 < 88%

2. In patients with cor pulmonale, right HF, or hematocrit >55%, PaO2 < 59 or oxygen sat SaO2 < 89%

**PaO2= Oxygen in blood, not bound to Hb
**SaO2= Percent of oxygen that is bound to Hb (saturated)


What do you do with a patient who has an epidural hematoma?

Emergent neurosurgery to get rid of the hematoma


A patient is having an MI. What’s the max time you can take to place that stent (PCI)?

90 min


Middle age man has nerve palsy, low-grade fevers, enlarged parotid glands, enlarged cervical lymph nodes. Labs are normal, except calcium is high. He is sexually active with multiple women. Diagnosis?


-systemic granulomatous disease that can involve the nervous system (Bell’s palsy), lymphadenopathy, parotid gland swelling, hypercalcemia (1-alpha hydroxylase activity)


What EKG chance does TCA (tricyclic antidepressant) overdose cause?

TCAs block fast sodium channels—> slower conduction speed= QRS prolongation
(*can also lead to Torsades)

*Treat with sodium bicarb bc it increases serum pH (more alkaline) and extracellular sodium. Both the increased pH and extra extracellular Na+ decrease the drug’s binding to cardiac Na+ channels.


Normal calcium level?


(For simplicity, remember about 8.5-10)


Patient has breast cancer that metastasized to bone. She had a mastectomy and is undergoing chemo.
She is having vague bone pain. Has a palpable supraclavicular lymph node and high calcium.
What is this and how do you treat it?

Hypercalcemia of malignancy


*She has metastatic breast cancer to the bone—> more bone breakdown—> bone pain and higher levels of calcium in the blood (*you can also get hypercalcemia of malignancy if you have a tumor secreting PTHrP).
Bisphosphonates cause osteoClast apoptosis so they can’t keep breaking down bone


Patient has an adrenal mass, high BP, headache, and hypokalemia. Diagnosis?

Primary hyperaldosteronism due to adrenal adenoma

*aldosterone-> Na+ reabsorption, K+ and H+ wasting, so hypokalemia makes sense

**treat with an aldosterone antagonist (Spironolactone, Eplerenone) or surgery


Old man has weakness and pain in his shoulders since shoveling snow 3 weeks ago. There is weakness on shoulder aBduction and decreased sensation on left forearm. Next step?

Get an MRI of the cervical spine

-He most likely has C5-6 nerve root impingement (cervical radiculopathy) from underlying cervical spondylitis (wear and tear of spinal disks in neck/ cervical spine degeneration)


Man has 1 year history of diarrhea, cramps, flushing, systolic murmur over left sternal border that increases with inspiration, and high LFTs. Diagnosis?

Carcinoid syndrome

-Serotonin-secreting tumor
-Usually in the GI tract, but if Mets to the liver, it can’t be broken down and serotonin travels through the bloodstream causing systemic effects. Can affect right heart only (tricuspid regurg in this patient) bc lungs (like the liver) have the enzyme to break down serotonin.
-Symptoms= diarrhea, flushing, tricuspid regurg, bronchospasm


How can Carcinoid tumors lead to Niacin (vit B3) deficiency?

Carcinoid= serotonin-secreting tumor
Tryptophan gets used up to make serotonin
Since tryptophan (and vit B6) are required to make niacin (vit B3), you’ll get a niacin deficiency as a result


Lady with hx of DM presents with sudden-onset double vision and ptosis of her right eye. The right eye is down and out. Pupils are responsive and there are no other neuro defects. Most likely diagnosis?

Diabetic ophthalmoplegia- poorly controlled DM—> ischemic neuropathy (tiny blood vessels that supply CN 3 are damaged)—> CN 3 palsy


Tendon vs. ligament?

Tendon- muscle to bone

Ligament (“Like”)- bone to bone


What is enthesitis?

Inflammation and pain at sites where tendons (muscle to bone) and ligaments (bone to bone) attach to bone

*most often at the Achilles’ tendon (but also can be at the costosternal junction, shoulders, elbows, hips, iliac crests, tibial tuberosities, etc.)
*can be part of an isolated disorder (like plantar fasciitis) or in spondyloarthropathies (like ankylosing spondylitis)


30 year old guy has low back pain that improves with use. He has limited spine flexion and sacroiliac joint inflammation. Has also had diarrhea going on. Diagnosis?

IBD (Crohn’s or Ulcerative Colitis)

*remember they are associated with arthritis, including spondylarthritis or sacroilitis


What does a positive pronator drift test tell you?

There is upper motor neuron (UMN) or pyramidal/ CST (corticospinal tract) disease

*UMN lesions cause more weakness in supinator muscles compared to pronator muscles of the upper limb—> affected arm drifts down and the palm turns (pronates) toward the floor


Middle aged woman is having strong urges to urinate and sometimes leaks urine on her way to the bathroom. What med can you give her?

Oxybutynin (anti-muscarinic for treatment of urinary incontinence)


What is presbycusis?

Age-related hearing loss

*due to cochlear hair cell loss (and cochlear neuron degeneration)


What can you advise patients to do when they get vasovagal syncope episodes- when they feel fainting coming on (prodromal phase)?

Cross legs, tense calf muscles, handgrip, and tense arm muscles with clenched fists...)
-These maneuvers increase venous return to the heart (more ‘milking’ of blood to heart)—> more CO, which can stop the syncope from happening


Fever and chills 1-6 hrs after blood transfusion. What reaction is this?

Febrile nonhemolytic transfusion reaction
(Due to cytokines in stored blood products)

*prevention of this is by leukoreduction of blood products (filter out most the WBCs after blood collection, before storage to prevent cytokine production within the packed RBC product)


What 2 medication classes can lead to severe hypotension if combined with a PDE-5 inhibitor like Sildenafil (Viagra) for ED?

1. Nitrates
2. Alpha blockers (ex: Doxazosin)


Patient has fever and new holosystolic murmur at the apex. He was treated empirically with vancomycin. Blood culture results came back sensitive to penicillin. What should you change his antibiotics to (2 options)?

IV Penicillin G or IV Ceftriaxone

-Fever + murmur suggests endocarditis
-Initial emperic treatment with Vanco is appropriate to cover MRSA (just in case)
-Now we got cultures back and know it is not MRSA (it is sensitive to penicillin), so switch to IV penicillin or Ceftriaxone (easier to administer due to once daily dosing vs. every 4-6 hrs)
*Do not use oral Penicillin- should treat IV for endocarditis


Do you have a high A-a gradient in PE (pulmonary embolism)?


You have a high A-a in any V/Q mismatch where there is impaired gas exchange!
-in the case of PE, the problem is with Q (perfusion)
-oxygen is getting from the alveoli fine, but the blood isn’t there to pick it up bc it is stuck (there’s a clot in major pulmonary vessels)


Do patients with PE typically have a high or low PaCO2?


PE—> hyperventilation (in effort to compensate)—> blowing off more CO2, so less CO2 stays behind in the blood


1st line treatment for female pattern hair loss?

Topical Minoxidil

(A vasodilator that increases blood flow to the scalp)
*side effects: irritation and itching


Old lady with PMH of DM and HTN has began having difficulty planning meetings for 9 months. She can no longer cook for herself. Gait is unsteady. She is sad. Diagnosis?

Vascular dementia
(Stepwise/ gradual decline, often presents with motor, gait, urinary, and psych symptoms)

*not likely to be Alzheimer’s bc that starts with memory problems and other stuff goes later


Patient flexes right hip and knee and slaps foot to ground w/ each step. He is complaining of recurrent falls. Cause of gait abnormality?

Common peroneal neuropathy
(L5 radiculopathy-> back pain radiating to the foot and weakness on foot inversion and plantar flexion)

*remember the common peroneal (fibular) nerve:
PED= Peroneal Everts and Dorsiflexes
If injured-> foot dropPED


Patients with SOB due to CHF have high BNP levels, typically above what number?

BNP >400

(Remember BNP is released by the heart in response to stretch, which there is more of when you have CHF and are fluid overloaded)

*BNP is a highly sensitive test for CHF. Clinical signs (JVD, crackles, lower extremity edema) are highly specific, but not sensitive.


Why might a male with a prolactinoma have decreased testosterone levels?

HIGH prolactin will feedback on GnRH, making it LOW (negative feedback)—> LOW testosterone production


35 year old guy has recurrent headaches. BP is 190/100 and you hear a S4 and continuous murmur. Diagnosis?

Coarctation of the aorta

-narrowing of descending aorta-> pressure overload in proximal part of aorta-> HTN in arms (where BP is normally measured), headaches (pressure goes back to carotids-> head)
*murmur for coarctation is systolic (blood through constricted aorta like aortic stenosis) or continuous (if collateral vessels are present)
*S4 may be heard due to LV hypertrophy (induced by HTN)


What may be seen on CXR of a patient with coarctation of the aorta?

Notching of the ribs (erosions of inferior costal surfaces)

-this finding is due to collateral vessel formation


Patient has watery diarrhea, flushing, and low K+ causing muscle cramps. CT shows a mass in the pancreatic tail. Diagnosis?


-rare tumor of pancreatic cells—> releases vasoactive intestinal peptide (VIP)


Patient has fever, acute-onset respiratory distress, hypoxemia, and bilateral opacities on CXR. Diagnosis?

ARDS (Acute Respiratory Distress Syndrome)

*acute inflammatory response w/ cytokines in the lungs-> epithelial damage/ necrosis of alveolar cells + endothelial damage/ inc capillary permeability leaking proteins-> hyaline membranes


What happens in ARDS?

Acute inflammatory response w/ cytokines in the lungs-> epithelial damage/ necrosis of alveolar cells + endothelial damage/ inc capillary permeability leaking proteins-> hyaline membranes
(The release of cytokines/ overreactive inflammatory response to a stressor like sepsis, PNA, whatever is the problem...causes damage to lung tissue)

**rarely can lead to irreversible pulmonary fibrosis (from too much collagen deposition as endothelial cells, pneumocytes, and fibroblasts proliferate to repair damaged lung)


What are the 2 ways to improve oxygenation in a ventilated patient?

1. Increase FiO2 (fraction of inspired oxygen)

2. Increase PEEP (positive end-expiratory pressure)
*This is the best way to improve hypoxemia in a patient with ARDS bc it additionally prevents alveolar collapse


If high levels (>60%) of FiO2 are required to maintain oxygenation in a patient on a ventilator, what setting should you increase?

PEEP (positive end-expiratory pressure)

*There are 2 ways to improve oxygenation of a ventilated patient:
1. Increase FiO2 (fraction of inspired oxygen)
2. Increase PEEP (positive end-expiratory pressure)


Patient has nasal breathing, stuffy nose, dry cough for more than a year. No allergies. Diagnosis and treatment (2 options)?

Nonallergic rhinitis (aka vasomotor rhinitis)

Treat with an intranasal antihistamine and/or intranasal glucocorticoid


Man comes in after long plane flight with LUQ pain. Has high indirect bilirubin (UCB), high reticulocyte count, and splenomegaly. Most likely cause of his symptoms?

Splenic infarction
(Acute occlusion of splenic artery, causing LUQ pain)

*High retic count and UCB= Intravascular hemolysis
*Could be due to sickle cell trait (usually asymptomatic, but can get Intravascular hemolysis and splenic infarction in stressors like a long flight- do Hb electrophoresis to diagnose


What is “salvage therapy?”

Treating a disease a different way when the standard treatment fails

(Ex: guy gets radical prostatectomy for prostate adenocarcinoma and PSA is undetectable. Months later, PSA is high and he gets radiation= a salvage therapy)


Old guy has progressive loss of vision in his right eye. Vertical lines look bent and wavy to him. Diagnosis?

Macular degeneration

-often age-related, the macula (center of retina in back of eye responsible for visual acuity) wears down
-early finding= straight lines look wavy
-eventually they loose central vision

*most common cause of blindness in industrialized nations


How do we confirm a diagnosis of Scabies and how do we treat it (2 drug options)?

Diagnosis: light microscopy of skin scrapings

Treatment: topical permethrin or oral ivermectin


30 y.o. African American woman
Painful, stiff hands/ wrists, esp in morning
Muscle aches
Ulcer on buccal mucosa
Low Hb (anemia), low platelets (thrombocytopenia)


Lupus (SLE)

Diagnosis if 4+ of these criteria:
1. Butterfly rash
2. Photosensitivity
3. Oral/ nasopharyngeal ulcers
4. Discoid rash (coin-shaped, worse with sun exposure)
5. Arthritis
6. Pericarditis
7. Hematologic dz (anemia, leukopenia, thrombocytopenia)
8. Renal disease (proteinuria, casts)
9. CNS- seizures, psychosis
10. Immuno markers (false positive Syphilis, anti-dsDNA, anti-Smith Ab)
11. ANA

*She has: (1) arthritis, (2) oral ulcer, (3) lymphadenopathy, (4) anemia and thrombocytopenia


What is Felty syndrome?

Triad of:
RA + splenomegaly + neutropenia (low neutrophils-> high-risk for bacterial infections)

*"SANTA's suit is felty" Splenomegaly, Anemia, Neutropenia, Thrombocytopenia, Arthritis (Rheumatoid)


Patient who got a liver transplant 5 months ago (taking immunosuppressants, no antibiotics) comes in with SOB, nonproductive cough, fever, chills. O2 sat is 82%, has bilateral crackles, diffuse interstitial infiltrates, elevated lactate dehydrogenase (LDH).
What test should you order?

Bronchoalveolar lavage

This is likely PCP (Pneumocystis) pneumonia
*immunosuppressed/ organ transplant patients are at high risk for PCP and CMV pneumonia. Therefore, they should be on prophylactic Bactrim (for PCP) and Ganciclovir-Valganciclovir (for CMV in seropositive patients)


What does recumbent mean?

Lying down


Guy smoker has blood in urine and fever for 4 weeks. Family hx of blood disorder. Has a left-sided varicocele even when lying down.
Next test?

Abdominal CT

-Patient most likely has RCC (renal cell carcinoma) (*classic triad: flank pain, hematuria, palpable abdominal mass is in few patients)
-smoking is a risk factor
-varicocele is due to tumor pressing against left renal vein and left testicular vein, impairing venous drainage from testicle
-fever is a nonspecific cancer finding (also weight loss, anorexia, fatigue, night sweats)
-ectopic production of EPO by kidney tumor-> polycythemia


Increased QRS voltage (really high QRS peaks) tells you what?

LV hypertrophy


Guy has narrowed retinal vessels and blurred vision and increased QRS voltage on EKG and T wave inversion. BP is 130/80.
What’s going on?

Isolate ambulatory HTN (aka masked HTN)

-even though BP is okay rn, it is probably high on average (avg over day of >135/85= HTN)
-he has evidence of end-organ failure from HTN (retinal AV nicking aka hypertensive retinopathy and LV hypertrophy shown by peaked QRS’s)


Woman had 2 miscarriages. Positive VDRL. Low platelets (thrombocytopenia). High PTT.

Anti-phospholipid antibody syndrome
Treat/ prophylaxis with aspirin and LMWH (low molecular weight heparin) to avoid clotting problems and pregnancy loss

-the presence of antiphospholipid antibodies + you have blood clots (DVT, PE, stroke, MI) or pregnancy problems (miscarriages or premature birth from placental insufficiency or preeclampsia)

-antiphospholipid antibodies are seen in SLE (but not specific to it). They can cause 3 problems: (1) antiphospholipid antibody syndrome, (2) increased PTT, (3) false positive syphilis test (RPR, VDRL)


Guy has cough, fatigue, unintentional weight loss, enlarged mediastinum, enlarged hilar and mediastinal lymph nodes.
PET (positron emission tomography) scan with 18-fluorodeoxyglucose shows uptake in the brain, kidneys, bladder, supraclavicular and mediastinal lymph nodes.

Hodgkin lymphoma

-B symptoms
-painless lymphadenopathy
-mediastinal mass
-PET scan radiotracer is taken up by cancer cells w/ a high metabolic rate (supraclavicular and mediastinal LN’s) and healthy organs with high metabolic rates (brain, kidneys, bladder)


Guy has diverticulitis and gets treated. A couple days later, he develops acute pain and redness in his right ankle (had a similar episode before). Diagnosis?


-usually occurs in big toe, but can occur in ankle or knee too
-triggers: alcohol, surgery/ trauma, dehydration, some meds (diuretics)


Explain what goes down when the RAA System is activated.
(*triggers that activate RAAS: low BP, low NaCl delivery to macula densa, sympathetic NS kicks in)

1. Liver releases AT
2. Kidney JGA cells release Renin, which converts AT-> AT I
3. Lungs release ACE (angiotensin converting enzyme), which converts AT I-> AT II
*ACE also breaks down bradykinin
4. AT II has multiple effects on the body to raise BP:
-constricts efferent arteriole (raise GFR)
-aldosterone release from adrenal gland-> reabsorption of Na+ (wasting of K+, H+)
-ADH (retains water) and thirst


Explain amaurosis fugax.

Temporary loss of vision (in 1 or both eyes)

-For example, due to emboli from severe carotid stenosis can cause ischemia to the optic nerve-> transient (on/off) vision loss


Young woman comes in with really high BP of 165/100 and transient (on/off) vision loss in an eye. She has a right carotid bruit. Renin and aldosterone levels are high. Next step?

CT Angiogram of the abdomen (look at the renal arteries)

Why? She has such a high BP that it is causing transient vision loss (amaurosis fugax- emboli from severe ipsilateral carotid stenosis can cause ischemia to the optic nerve), so you need to work it up. High Renin and Aldosterone means it’s secondary hyperaldosteronism. This is most likely due to FIBROMUSCULAR DYSPLASIA (developmental defect in blood vessel wall-> irregular thickening of renal, carotid, vertebral arteries)-> kidneys read low BP-> activate RAAS-> increased renin, aldosterone, and BP.


Atrioventricular (AV) nodal reentrant tachycardia (AVNRT) is a sub-type of what tachycardia?

Paroxysmal supraventricular tachycardia (PSVT)


What is the diving reflex? (Our body’s response to immersion in cold water)

Reflex on immersion in cold water that slows HR and causes peripheral vasoconstriction to divert blood flow to central, vital organs (brain, heart, lungs) to conserve oxygen until breathing resumes and to delay potential brain damage

(*the body knows it cannot breathe in oxygen while underwater, so it slows the HR down so that the body can survive longer with the blood/ oxygen it already has to pump)

*colder water (drops core temp super fast)= stronger diving reflex response (and therefore better chance of survival if you drown in ice cold water vs. a pool)
(*supraventicular means it is coming from the atria)


How would immersion in cold water relieve heart palpations? (state mechanism involving baroreceptors)

Vagal maneuver (cold water immersion/ diving reflex, carotid sinus massage, Valsalva, eyeball pressure)—> increased stretching and firing of baroreceptors—> more parasympathetic response—> lowered HR

*diving reflex (immersion in cold water slows the heart to conserve energy/ so you could survive longer + vasoconstricts to shunt blood to central, vital organs)


In hypovolemic shock, are the following values high or low?
1. pulmonary capillary wedge pressure (PCWP)
2. cardiac output (CO)
3. blood pressure (BP)
4. systemic vascular resistance (SVR)

1. PCWP (=LA pressure)- LOW (due to decreased preload)
2. CO- LOW (due to decreased preload)
3. BP- LOW (due to deceased CO)
4. SVR- HIGH (vasoconstriction in attempt to raise BP and maintain CO)


Why might an inferior MI (ST elevations in II, III, aVF) cause AV block (prolonged PR intervals w/ dropped QRS’s)?

Inferior MI—> occluded RCA, which supplies the AV node—> since the AV node has cut off blood supply, it won’t be able to do a good job of delaying the signal from the atria to ventricles—> AV block
(prolonged PR’s= impulse from atria to ventricles gets too delayed, dropped QRS’s= part of the AV node is blocked so failing to send the impulse from the atria to ventricles)


60 y.o. smoker has sudden-onset chest pain, diaphoresis, and N/V. BP is 85/55 and HR is 50 bpm. EKG shows ST-elevations in leads II, III, aVF. Diagnosis?

Inferior MI- occlusion of the RCA

*His vitals tells you he’s in cardiogenic shock (really low HR and BP). This makes sense bc MI-> heart not getting fed enough blood to pump well


In pericarditis, what do you see on EKG?

Diffuse ST-segment elevations


Guy had an MI 3 days ago. Now he’s coming in with sharp pain on his left chest that improves with leaning forward. Diagnosis?

Acute pericarditis (aka fibrinous pericarditis aka peri-infarction pericarditis)

*EKG would show diffuse ST-segment elevation


Woman with history of rheumatic heart dz has acute onset SOB. She has a mid-diastolic rumble at the apex, crackles over the lungs, and EKG shows irregularly, irregular rhythm and no P waves. What’s going on?

She has mitral stenosis (from rheumatic heart disease which causes mitral regurg, later mitral stenosis)—> increased pressure in LA causes the LA to dilate—> predisposes to a-fib—> worsening flow through the stenotic mitral valve—> more backing up of blood/ congestion to lungs, explaining the SOB

*up to 70% of patients with mitral stenosis will develop a-fib from the significant LA dilation


Most reliable finding to differentiate between an epileptic seizure and syncope?

Tongue biting

(*95% specificity for epileptic seizure, esp if on the lateral tongue- bc rarely syncope can cause frontal tongue biting)


What are these EKG findings suggestive of?
High-voltage QRS complexes, lateral ST segment depression, and lateral T wave inversion

LV hypertrophy


30 year old guy has a nosebleed requiring nasal packing. His BP is 180/120. EKG shows high-voltage QRS complexes, ST-segment depression, and T-wave inversion. Most likely diagnosis?

Coarctation of the aorta

-high-voltage QRS’s, ST-segment depression, and T-wave inversion= LV hypertrophy from long-standing HTN
-prob not essential HTN bc that rarely causes end-organ damage in young patients <40
-coarctation of the aorta (narrowing at distal aorta) usually causes asymptomatic HTN, but can cause headache, nosebleeds, lower extremity claudication

*check bilateral arm and leg BP measurements


Old lady has acute-onset epigastric pain associated with N/V. What test should you do 1st?


*You need to rule out acute coronary syndrome (STEMI, NSTEMI, unstable angina), which could have an atypical presentation like this! Once ruled out, then you can consider GI things like pancreatitis

**women, elderly, and diabetes patients are more likely to have atypical heart symptoms


How is vasospastic (Prinzmetal) angina similar to Raynaud phenomenon?

Vasospastic (Prinzmetal) angina- due to episodic vasospasm of pulmonary vessels

Raynaud phenomenon- due to episodic vasospasm in fingers and toes


What is the screening protocol for AAA?

One-time abdominal ultrasound screen for men 65+ who have ever smoked


How do you treat Wolff-Parkinson White syndrome patients with A-fib with RVR:
-if unstable?
-if stable?

Unstable—> immediate cardioversion

Stable—> IV procainamide or Ibutilide (rhythm control)

*do NOT use AV node blockers like adenosine, beta blockers, CCBs, digoxin—they would promote conduction across the accessory ‘secret’ pathway, causing a-fib—> v-fib


Meniere disease is a disorder of the inner ear (too much endolymph/ fluid) characterized by what triad?

1. Episodes of vertigo (20 min- 24 hrs, associated with nausea/ vomiting)

2. Sensorineural hearing loss (fluctuates)

3. Tinnitus (ringing of ear)


Woman comes in for episodes of dizziness (room spinning) associated with ringing in the ears, improved with lying down and eyes closed. When you do Rinne test, air conduction > bone conduction on both ears. When you do Webber test, the sound is heard better on the left. Diagnosis?

Meniere Disease (disorder of inner ear where you have too much volume/ pressure of endolymph fluid)

1. Episodes of vertigo
2. Sensorineural hearing loss
3. Tinnitus


You need 2/3 criteria to diagnose acute pancreatitis. What are they?

1. Acute-onset epigastric pain radiating to the back

2. Increased amylase or lipase >3x the upper limit of normal (lipase more specific)

3. Abdominal imaging suggestive of pancreatitis- CT of abdomen (pancreatic enlargement)

*NOTE: you do NOT need CT to make the diagnosis...epigastric pain radiating to back + lipase >3x upper limit of normal is sufficient!

**U/S is not used (gas prevents visualization) and X-ray is not used (poor test for pancreatitis)


Guy has an NSTEMI (substernal chest pain w/ diaphoresis, ST depressions, up-trending troponin) so he gets a stent placed. Besides ASA, a beta-blocker, statin, ACE inhibitor, what do you need to give him?

A P2y12 receptor blocker
(like Clopidogrel aka Plavix)

*normally, ADP binds this receptor on platelets to promote platelet aggregation (we block it to stop platelet aggregation)

Dual Anti-Platelet Therapy (DAPT) (ASA + P2y12 receptor blocker) is given to patients with stents for 12 mo to reduce the risk of stent thrombosis. Also, it reduces risk of recurrent MI in NSTEMI compared to ASA alone!


If a patient gets a stent, how long do they need to be on DAPT (Dual Anti-Platelet Therapy= Aspirin + P2y12 receptor blocker like Clopidogrel/ Plavix)?

At least 12 months
(Significantly reduces risk of stent thrombosis and recurrent MI)


Younger guy who has a sore throat for 4 days is coming in due to hematuria. U/A shows protein and RBCs in his urine. Diagnosis?

IgA nephropathy

-protein in urine= nephrotic syndrome
-most common nephrotic syndrome in adults= IgA nephropathy, esp after a URI (“sore throat”)


Lady has right ear pain, red vesicles in the ear canal, and right facial droop. Diagnosis?

Herpes zoster oticus
aka Ramsay Hunt syndrome

Varicella zoster (VZV) reactivates—> Herpes zoster. If the herpes occurs in the dermatome of the geniculate ganglion (collection of sensory nerves from the facial nerve in the facial canal of the head), you get this. It disrupts CN 7/ facial nerve motor fibers and spreads to CN 8/ vestibulocochlear nerve—> facial paralysis and ear pain there.


Old man presents with worsening SOB and nonproductive cough. Has had an ongoing fever, headache, sore throat, runny nose, anorexia, and body aches since Christmas shopping at a mall 5 days ago. He has crackles. Diagnosis?

Influenza virus
(Muscle aches + nonspecific flu symptoms after shopping in a germy mall)

*pneumonia is the most common complication of the flu


Most common complication of influenza?


-This can be from secondary bacterial infection (ex: Strep pneumo, Staph a.) or from direct viral attack (influenza pneumonia)

*give oxygen support and oseltamivir (Tamiflu) + treat the pneumonia with Abx


50 y.o. Guy has nausea, fatigue, bilateral flank pain over the last couple yrs. BP is 160/100. Liver is large, mass is felt on palpation of flank, prostate is enlarged. BUN and Cr are high. Diagnosis?

Autosomal Dominant Polycystic Kidney Disease (ADPKD)—> chronic kidney dz (CKD)

-evidence of ADPKD: flank pain, HTN (would be due to excess renin release), large liver (cysts)
-evidence of CKD: nausea, fatigue, high Cr (due to structural degeneration of the kidneys)
*NOTE: BPH is a separate issue here


Car crash victim is having severe pain from a leg fracture. He is a former heroin addict. You give him ketorolac (NSAID) for pain management, but it doesn’t cut it. What do you give now?

IV Morphine

*INITIAL management for acute pain (including opioids) is about the same for all patients—regardless of addiction history (you will just need to monitor this guy closely to avoid relapse)


Why do you get the following in aortic stenosis?
1. Diminished and delayed carotid pulse (“pulsus parvus et tarsus”)
2. Systolic murmur (late-peaking, crescendo-decrescendo)
3. Soft and single S2

1. Diminished and delayed carotid pulse (“pulsus parvus et tarsus”)—> since you have a stenotic aortic valve, there’s less blood flow making it through

2. Systolic murmur (crescendo-decrescendo)—> aortic valve opens during systole so makes sense that aortic stenosis (problem opening) is heard during systole

3. Soft and single S2—> normally, you have physiologic split of S2 (inspiration-> more blood to right heart-> pulmonic valve takes slightly longer to close than aortic valve in S2)...with aortic stenosis, the stenotic aortic valve takes longer to close too so they close at the same time= single S2


40 y.o. guy comes in for a physical. He has fatigue, muscle aches, weight gain. His total cholesterol and triglycerides are high. What is the next best step to manage his dyslipidemia?

Order TSH

Fatigue, muscles aches, weight gain-> suspicious for hypothyroidism, which can cause lipid abnormalities!

You need to confirm this diagnosis—if it is in fact hypothyroidism, you will need to treat the underlying cause with Levothyroxine (will improve lipid levels, but does take a few months). Don’t jump straight to a statin (can worsen myopathy) or another anti-lipid drug until you do the work-up.


Mechanism responsible for angina pain relief with nitrates?

Decreased LV wall stress (afterload)

Nitrates-> venodilate-> decrease preload/ blood in heart-> decrease demand on the heart (heart has to pump less blood) to match decreased supply (heart fed less blood) from angina

*they also vasodilate, resulting in less pressure (afterload) the heart has to pump against

**nitrates-> decreased LV end diastolic volume and wall stress-> decreased myocardial oxygen demand


What is a proctocolectomy?

Surgical removal of the rectum and colon
(Done in FAP and UC, for example)


Kid has FAP (familial adenomatous polyposis). How do you manage it?

Frequent colonoscopic surveillance

-screening sigmoidoscopies for kids starting at 10-12 yrs
-once you detect adenoma (or if >50 yrs) do annual colonoscopies
-do proctocolectomy (surgical removal of rectum + colon) if they initially present bad with high-grade dysplasia or adenomas or once they get into their 20’s (prophylactic since nearly 100% FAP patients will get colon cancer)


Lady has sudden onset left-sided weakness. Has positive Babinski. Has fatigue and a mitral regurg murmur (holosystolic at apex). ANA (antinuclear antibody) and RPR (rapid plasma regain) are positive. Diagnosis?

Antiphospholipid antibody syndrome
(These antibodies are present in SLE/ lupus and we call it a syndrome if you also have blood clots or miscarriages/ placental problems)

-sudden-onset left-sided weakness= stroke
(Babinski= UMN signs)
-fatigue and mitral regurg are lupus symptoms (antibodies can damage valves-> exposure of subendothelial collagen-> vegetations of platelets/ clotting factors form)
-ANA is non-specific to autoimmune dz’s
-false positive Syphilis (RPR/ VDRL) is a thing with antiphospholipid antibody syndrome (*as well as high PTT)


What 2 types of pneumonia should you be suspicious of in an immunocomprimised pneumonia patient?

1. CMV (cytomegalovirus)
2. PCP (pneumocystis)


Narrow QRS, what is it?
Wide QRS, what is it?

Narrow QRS—> SVT (supraventricular tachycardia) or A-fib
*In SVT, the fast rhythm is coming from the atria. QRS is narrow (shorter ventricular contraction) bc it the atria send a rapid signal to the ventricles-> ventricles contract faster, keeping up with incoming signals.

Wide QRS—> V-tach (ventricular tachycardia) or Torsades
*In V-tach, the fast rhythm is coming from a rapid-firing pacemaker in the ventricles. QRS is wide (takes longer for ventricular contraction) bc it takes longer for a signal to go from ventricular myocyte to myocyte over the normal conduction pathway. That said, since it’s not paying attention to atrial signals and the ventricle is just going crazy on its own, the overall pace is fast/ tachy.


How do you treat SVT (supraventricular tachycardia) (narrow QRS) if the patient is stable? Unstable?

Stable SVT—> Adenosine (x3, rate control)

Unstable SVT—> shock

*Sketchy: Adenosine (swing dancing) is the agent of choice of SVT
**Valsalva, carotid sinus massage, breath holding, and immersion in cold water may help temporarily by lowering HR


How do you treat V-tach (wide QRS) if the patient is stable? Unstable?

Stable V-tach—> Amiodarone

Unstable V-tach—> shock


Panic attacks usually cause what type of tachycardia?

Sinus tachycardia

(Normal P waves followed by QRS’s)
*do NOT cause narrow QRS= supraventricular tachy (PSVT) or wide QRS= V-tach


In paroxysmal supraventricular tachycardia (PSVT) will you see P-waves?

No, probably not

You get narrow QRS complexes and can have “hidden P-waves”


Lady had an MI of the LAD. Got a stent. On day 4 of hospitalization, she develops SOB, confusion, cold extremities, JVD, crackles. Has a loud systolic murmur at the left sternal border with a palpable thrill. What happened?

Rupture of the interventricular septum

*can happen 3-5 post-MI of the LAD or RCA
*when the interventrciular septum ruptures you basically get a VSD with flow from the LV-> RV, which explains the holosystolic murmur and cardiogenic shock presentation (too much backward flow of blood, not enough forward flow)


Where is aortic regurg heard best?

The left sternal border

(Not the usual right 2nd intercostal space where you hear many aortic murmurs echo best...aortic regurg is actually heard best directly over the aortic valve)


What should you think of when you hear flashes, floaters, or curtain across vision?

Retinal detachment


Does the retina share a blood supply with the macula?

No! They have their own blood supply


Patient has both a metabolic acidosis from AKI (kidneys not working to reabsorb bicarb-> low bicarb in blood) and respiratory acidosis from hypoventilation (breathe less-> blow off less CO2-> high CO2 in blood). The patient feels lethargic. What is the lethargy due to?

The respiratory acidosis/ CO2 retention (hypercapnia)


Why can AKI cause metabolic acidosis?

The kidneys aren’t working to reabsorb bicarb-> less bicarb in the blood


What is the CURB-65 scoring?

MD Calc tool to determine whether a pneumonia patient should be admitted to the hospital

C- confusion (+1)
U- urea >20 (+1)
R- respirations >30/ min (+1)
B- BP, hypotensive <90/60 (+1)
Age >65 (+1)

If CURB-65 score is 3 or greater—> admit to hospital (*if 1-2 you might still admit)

**basically you’re looking at their vitals (is this a sepsis-like picture, really sick patient?) to determine if they need inpatient vs outpatient care


What should you give a patient with CAP admitted to the hospital floor (bc they are really sick)?

Beta-lactam + macrolide (ex: Ceftriaxone + Azithromycin)


Fluoroquinolone (ex: Moxifloxacin)


Reg respiratory settings on a ventilator, what 2 things should you think of changing when oxygenation is a problem? Ventilation?

Oxygenation is a problem—> consider changing FiO2 or PEEP (the percent oxygen in the air you are giving to the person or the positive end expiratory pressure to keep the alveoli from collapsing)

Ventilation is a problem—> consider changing Tv (tidal volume) (mL of air the patient is getting in/out) or the RR (respiratory rate) (how fast they are breathing/ blowing off CO2)


Patient has been taking Naproxen (Aleve) for years to manage chronic back pain. Labs show her kidney function is getting worse. What is the cause of her renal failure?

Analgesic nephropathy (too many NSAIDs damaged the kidneys)
-most often—> Tubulointerstitial nephritis or Papillary necrosis

*Naproxen (Aleve)= NSAID
Remember that NSAIDs block PG’s (PG’s dilate the afferent)—> constriction of afferent—> decreased GFR and RPF (decrease blood flow to kidneys/ put more pressure on the kidneys)

**chronic NSAID use also can cause premature aging, atherosclerotic valvular disease, and urinary tract cancer


If you suspect a chest pain patient may have aortic dissection, should you give them aspirin?

NO! Aspirin is an antiplatelet agent-> stops clotting, and therefore causes bleeding, which would worsen aortic dissection. In fact, aspirin can kill a patient with aortic dissection.


Mechanism of action of Aspirin (ASA)?

Blocks COX-1 (and COX-2)—> decreased production of TXA2 (thromboxane A2) (*and PGs) within platelets—> decreased platelet aggregation
(It is an NSAID/ antiplatelet agent that stops platelets from sticking)


What should you give chest pain patients with possible ACS (acute coronary syndrome) (and low risk for aortic dissection) ASAP?


(Blocks COX-1-> TXA2-> platelet aggregation)


Guy has fatigue, lower extremity edema, dark urine. U/A shows protein and blood in the urine. Kidney biopsy shows dense deposits in the glomerular BM. Immunofluorescene is positive for C3, not Ig’s. Diagnosis?

Membranoproliferative glomerulonephritis (nephrotic syndrome)

*complement gets activated/ used up—> decreased C3 protein


FEV1/FVC ratio in restrictive vs obstructive lung dz?

Restrictive= problem getting air IN
FEV1 low/ FVC low= NORMAL or HIGH (less air in means less air out)

Obstructive= problem getting air OUT
FEV1 lower/ FVC low= LOW

*remember FEV1= max air you can blow out in 1 second; FVC= max air you can blow out after max inspiration


Middle aged guy has SOB on exertion. CXR shows mediastinal fullness and scattered reticular opacities in the upper lungs. Labs show calcium is high. Diagnosis?

Sarcoidosis-associated lung disease (restrictive pattern, so problem breathing in)

*Clues: he’s young, “mediastinal fullness and scattered reticular opacities”= hilar lymphadenopathy, hypercalcemia (vit D conversion by lung macrophages)


Are the following values high, low, or normal in sarcoidosis-associated lung disease?
TLC (total lung capacity)
DLCO (diffusion capacity for carbon monoxide)

Restrictive= problem breathing in (less air in= less air out)

FEV1 (max air you can breathe out in 1 sec)= normal to low

TLC= low (problem breathing in, so lungs hold less air)

DLCO= low (inflammation and scarring interfere with gas exchange)


In ARDS, would you want to put the patient on high or low tidal volume (Vt) ventilator support?

Low tidal volume ventilation (LTVV)
-to prevent overdistention of alveoli


Lady who recently underwent chemo presents with right-sided severe abdominal pain that is constantly burning. No other symptoms, but when you touch the area it hurts a lot and no NSAIDs or antacids have helped. Likely diagnosis?

Herpes Zoster (Shingles)

*The pain can come before the vesicular rash by several days!


Patient with surgical history of gastrectomy presents with fatigue and SOB on exertion. He has a shiny tongue, low Hb, high LDH. Diagnosis?

Vitamin B12 deficiency

-gastrectomy (surgical removal of part or all of the stomach)—> loss of intrinsic factor, which is needed to absorb vit B12–> vit B12 deficiency, which is a macrocytic anemia

*why hemolysis (inc LDH)? Vit B12 is needed for DNA synthesis. If it is deficient, you get ineffective erythropoiesis (making of RBCs in the bone marrow)-> intramedullary hemolysis


Lady is having difficulty swallowing solid foods (not liquids). Lost weight, has oral thrush, dental caries, and firm submandibular nodules. Only 1 sexual partner. Next step to diagnose?

Get antibodies to Ro/SSA and La/SSB

-this sounds like Sjogren syndrome (autoimmune disorder of exocrine glands)—> dry mouth (leading to difficulty swallowing, thrush, and dental carries)

-to diagnose you need (1) evidence of dry mouth/ eyes (positive Schirmer test for decreased lacrimation) and (2) histologic evidence of lymphocytic infiltration of the salivary glands OR serum antibodies against SSA (Ro) and/or SSB (La)


Old guy with hx of metastatic squamous cell cancer has had low back pain for 2 months. In the last 2 weeks, he’s had progressive leg weakness and dribbling of urine. He has decreased strength and sensation in the lower extremities. Diagnosis?

Cauda equina syndrome

-compression of 2+ spinal nerve roots in the lumbar cistern (in his case, likely due to a tumor *other cases: large lumbar disc herniation or abscess in the region)
-the urinary incontinence is due to damage to S3-S5 (can also get sexual dysfunction)

*get an urgent MRI of the lumbosacral spine
*emergency surgical decompression within 1-2 days is required to prevent irreversible neuro damage


Most common cause of primary adrenal insufficiency in developed countries (US)?

Autoimmune adrenalitis (autoantibodies against the adrenal gland)


If you suspect lupus, what antibody should you check first?

ANA (antinuclear antibody)

-this is sensitive, so it is the best screening test. Anti-dsDNA and anti-Sm (smith) antibodies are specific, so they are confirmatory tests.


What disease do you associate each of the following antibodies with?
1. Anti-cyclic citrullinated peptide
2. Anti-histone
3. Anti-neutrophil cytoplasmic (ANCA)
4. Anti-Ro/SSA
5. Anti-Scl-70 (anti-topoisomerase)

1. Anti-cyclic citrullinated peptide—> Rheumatoid arthritis

2. Anti-histone—> drug-induced lupus (from hydralazine, procainamide, etc.)

3. Anti-neutrophil cytoplasmic (ANCA)—> vasculitis

4. Anti-Ro/SSA—> Sjogren syndrome

5. Anti-Scl-70 (anti-topoisomerase)—> scleroderma (systemic sclerosis)


What is serositis?

Inflammation of the serous membranes in the body (for example, the pleural lining of the lungs or the pericardium lining of the heart)

*can cause positional chest pain and SOB
*if this is part of the presentation along with fatigue, polyarthritis, etc. you would suspect lupus (SLE)


When/ how often should you do colonoscopy screening for patients with Ulcerative Colitis?

8 years after initial diagnosis and every 1-2 years thereafter


Initial treatment of frostbite?

Rapid rewarding with warm water (37-39*C/ 98.6-102.2*F)
*also give pain meds (rewarming tissue is painful)

*frostbite= freezing of tissue-> disruption of cell membranes, ischemia, vascular thrombosis, inflammatory changes (usually involves face, ears, distal limbs)

**do NOT do hot air rewarming (not good enough control over the temp) or rewarm by placing the limb near your abdomen in the field if there’s the possibility of refreezing before getting definitive care (freezing-> warm-> freezing can cause more damage than just freezing-> warm)


Lady twisted her ankle a month ago. The swelling improved, then got worse over the last couple weeks. Her foot, ankle, and calf are really painful now all the time. There is erythema, warmth, edema up to the calf and imaging shows patchy area of osteopenia. Diagnosis?

Complex regional pain syndrome

-can happen 4-6 wks post-trauma due to inflammatory cytokine effects

-causes burning/ tingling pain out of proportion to the injury

-associated with erythema, edema, skin changes, X-ray may show patchy demineralization


Lady on OCPs explains she has been having severe migraines with aura. What should you tell her to do?

Give off the OCPs!

Women with migraines, esp with aura, are at increased risk for ischemic stroke. OCPs (and other estrogen-containing contraceptives) increase risk for stroke too. So you don’t want to have both these stroke risk factors at once! OCPs are contraindicated in migraine sufferers for this reason.


How do you treat symptomatic prolactinoma?

Dopamine agonist (Cabergoline, Bromocriptine)

*remember that dopamine puts the break on prolactin, so by giving a dopamine agonist, you are stopping prolactin (helps normalize prolactin levels and reduce tumor size)

**only do surgery (transsphenoidal resection) if the tumor is really large (>3 cm) or not responding to meds


Patient was diagnosed with adrenal insufficiency and got put on hydrocortisone. She continues to have light-headedness and salt cravings. Next step in her management?

Add fludrocortisone (a synthetic mineralcorticoid/ aldosterone)

-she is already taking hydrocortisone (a synthetic glucocorticoid/ cortisol)...since this doesn’t do much for the mineralcorticoid/ aldosterone deficiency, she gets those symptoms (hypOnatremia/ salt cravings/ light-headedness, hyperkalmeia)


Guy was wearing contact lenses for a week straight. Is having difficulty removing the contact lenses now. He woke up with eye pain and discharge. The cornea is hazy and there is sclera injection (red/ bloodshot). Diagnosis?

Contact lens associated keratitis
-usually due to Pseudomonas and serratia (gram-neg) and require removal of contacts and antibiotics emergently! (Otherwise can-> corneal perforation, scarring, permanent vision loss)


You do a CXR on a girl with a shoulder sprain and find an incidental coin-sized lesions on the upper lobe of her lung. 1st step to work it up?

Compare to a previous CXR

Most likely it’s a solitary pulmonary nodule (SPN)= benign nodule

*no further testing if it’s stable in size >2 yrs
*if it’s changed, move on to a CT and continue to rule out or rule in cancer


Patient has rash, joint pain, fatigue. Has palpable purpura, hepatosplenomegaly. Bun and Cr are elevated, complement is low, anti-HCV (hep C) and Rheumatoid factor are both positive. Diagnosis?

Mixed cryoglobulinemia

Vasculitis (from immune complexes)
-palpable purpura on legs, joint pain, liver involvement, kidney disease/ glomerulonephritis
-associated with hep C and hypocomplementemia (depleted complement levels)


What is an AV fistula (used in dialysis) and how can it cause high-output cardiac failure?

AV fistulas connect the arteries to the veins directly

Rather than the normal path: arteries-> arterioles-> capillaries-> venous system, AV fistulas directly connect arteries-> veins (blood can dump right into the venous system at the top of the arm where the fistula is placed for dialysis access). Now the lower arm isn’t getting good perfusion-> heart makes up for it by pumping harder. This constant increase in contractility (heart having to work harder)-> high-output cardiac failure.


Upper abdominal systolic-diastolic bruit indicates what?

Renal artery stenosis

**A bruit does not usually indicate AAA (abdominal aortic aneurysm)- this would be a pulsatile mass (in <50% of patients) or picked up on screening Doppler U/S.


Reduced systemic vascular resistance (SVR) means what?



Most patients with AAA (abdominal aortic aneurysm) present with what symptoms?

Most are asymptomatic! (Trick Q)


Guy has CABG (coronary artery bypass grafting) and aortic valve replacement done. 2 days later gets sudden-onset weakness, chest tightness, SOB. He is hypotensive and tachy. EKG shows irregularly irregular rhythm. Diagnosis and treatment?


Cardiovert (it is <48 hrs plus he is hemodynamically unstable)


Defibrillation vs. cardioversion?

Defibrillation= unsynchronized shock
-“drops a bomb”/ shocks at a random point in the cardiac cycle
-use for V-fib and V-tach (Rap: “defib for V-fib and pulseless V-tach. Don’t defib asystole you won’t bring em back”)

Cardioversion= SYNCHRONIZED shock (press that sync button)
-shock is given at the QRS complex (purpose is to minimize shock occurring during depolarization, which could throw the patient into V-fib)
-example: use for a-fib if unstable, onset <48 hrs, or in a young person with a structurally normal heart after anti-coagulating with Warfarin for 3 weeks and do TEE right before to make sure there’s no clots (don’t want to throw a clot with the CV-> stroke)


Lady with HTN (on Lisinopril) and OSA (on CPAP during sleep) presents with leg swelling, worse in evenings. She has pitting edema in the bilateral ankles, dilated and tortuous superficial veins, and a small ulcer noted on the left medial ankle. All pulses are normal. Diagnosis and solution?

Chronic venous insufficiency (CVI)
(Incompetent venous valves-> backflow of blood and pooling in legs)
*ankles often appear hyperpigmented, may have ulcers

Leg elevation, compression stockings, exercise
**patients who don’t respond to these conservative treatments should get venous duplex U/S to confirm the diagnosis (by retrograde venous blood flow)


What 4 drugs improve survival in patients with LV systolic HF?

1. ACE inhibitors
2. ARBs
3. Beta-blockers
4. Mineralcorticoid receptors antagonists (Spironolactone/ Eplerenone)

*also hydralazine + nitrates in African American patients


What are electrical alternans?

Varying amplitude (height) of QRS complexes

Suggests cardiac tamponade


Holosystolic murmur beast heard over the cardiac apex with radiation to the axilla

Mitral regurg

*clinical features: SOB on exertion (dec CO due to the regurg and inc LA pressure) and fatigue...can lead to a-fib (stretched LA) and HF


Man has MI of his LAD and gets a stent placed. 10 days later presents with another MI (mid sternal chest pain, diaphoresis, SOB) with ST-elevation in leads V1-V4. Cause of this?

Medication non adherence

He’s having stent thrombosis. To prevent this, patients should be on ASA + Clopidogrel (Plavix)= dual anti-platelet therapy (DAPT). Most common cause of stent thrombosis= not taking these meds as instructed.

How do you know this is stent thrombosis, not a recurrent MI? LAD= leads V1-V4 where the stent was placed! So this is far more likely.


Young guy with HTN and alcohol abuse comes into the ED with SOB for 2 days, worse last night. BP is 220/110. He has crackles, S4, and cotton-wool spots on eyes. Cr is 2.1. He is given IV furosemide + Nitroprusside with improvement of symptoms but the next day he has a seizure. Diagnosis?

Hypertensive emergency—> next day Cyanide (CN) toxicity

Really high BP + end-organ damage (CHF, renal failure, and eye signs/ symptoms)
*cotton-wool spots= white patches on retina (high pressure damages blood supply to the nerve fibers)
IV Nitroprusside is given in HTN emergency, but gives off nitric oxide and cyanide byproducts. CN toxicity= neurologic change (seizure, altered mental status, lactic acidosis, coma)


Man with CAD and HTN is brought to the ED after a suicide attempt. BP is 75/40, HR is 40 bpm. Extremities are cold and clammy. EKG shows sinus Brady with 1st degree AV block. He is given IV fluids + Atropine w/o improvement. Next thing to give him?

-Bradycardia, AV block, hypotension and wheezing suggests beta-blocker overdose

*Remember that beta-blockers dec HR (block beta-1 on heart), can cause AV block (AV node is slowing the signal from atria to ventricles too much), can cause hypotension (block beta-1, which causes renin release), and can cause wheezing (block beta-2, which bronchodilates-> bronchoconstriction)

**extremities are cold due to peripheral vasoconstriction (inc BP, dec blood flow) to shunt blood to centrally located vital organs

***also, the fact he has CAD and HTN tells you he prob was prescribed a beta-blocker and has it available to overdose on in a suicide attempt


Guy with CAD, hx of MI comes in for retrosternal chest pain and burning, worse at night (not w/ exercise). He has cough and occasional hoarseness. Resting EKG is normal. Exercise EKG shows ST depression in the inferior leads, but myocardial perfusion study shows no evidence of stress-induced ischemia. Treatment?

PPI (like Omeprazole)
-this is GERD

*GERD symptoms mimic angina, worse at night bc acid can reflux easier when laying down
*cough and hoarseness from laryngeal irritation (from the acid)

*Although the exercise EKG shows ST depression (subendocardial ischemia), evidence of ischemia when exercising at 90% of maximal HR is NOT unusual in patients with known CAD


In terms of the EKG, how is uremic pericarditis different from other etiologies of pericarditis?

Does not typically cause diffuse ST elevation (or PR depression)

*this is bc the inflammation doesn’t affect the myocardium
**uremic pericarditis presents in patients with advanced renal failure requiring dialysis (they come in with pleuritic chest pain and pericardial friction rub)


What is the CHADS-VASC score? What do each of the letters stand for and how do you interpret the results?

CHADS-VASC score is used to determine whether an a-fib patient should be started on lifelong anticoagulation

A- Age >75 (*2 points)
S- Stroke/ TIA (*2 points)
V- Vascular dz (prior MI, PAD, aortic plaque)
A- Age 65-74
Sc- Sex (female)
*everything positive counts as 1 point except age >75 and stroke count as 2 points

0–> no anticoagulation
1–> none, ASA, or oral anticoagulation
2+-> oral anticoagulation


44 year old guy with no medical hx presented with new-onset a-fib w/ RVR. Echo showed mildly dilated LA, but no valvular abnormalities. Should we have him on long-term anticoagulation, like ASA and/or Warfarin?

His CHADSVASc score is 0 so it is not indicated.

A- Age >75 (*2 points)
S- Stroke/ TIA (*2 points)
V- Vascular dz (prior MI, PAD, aortic plaque)
A- Age 65-74
Sc- Sex (female)
*everything positive counts as 1 point except age >75 and stroke count as 2 points

0–> no anticoagulation
1–> none, ASA, or oral anticoagulation
2+-> oral anticoagulation


Pregnant lady present with SOB, S3, and holosystolic murmur at the apex. U/A shows trace protein and she has a little ankle edema. EKG shows sinus tachy. Next best step?


You need to check for peripartum cardiomyopathy (dilated cardiomyopathy that can occur during or up to 5 mo. after pregnancy). It is often associated with mitral regurg (holosystolic murmur at the apex).


Patient comes in after a car crash. Vitals are stable and physical exam is unremarkable. 30 min after arrival, his BP is 80/50 and HR is 120. Now he is having trouble breathing and has a erythematous rash and wheals over his chest and abdomen. Most likely cause?

Latex allergy (anaphylactic shock)


Fat embolism presents with what type of rash? How long does is occur after a long-bone fracture?

Petechial rash (also SOB and confusion)

12-24 hrs later! Not immediate


An aortic regurg patient is asymptomatic. How does his heart adapt to explain this?

Increased LV compliance

(The LV undergoes eccentric hypertrophy of myocardial fibers in series, meaning it stretches out/ dilates in response to the backflow of blood)


We start a patient on a statin if their ASCVD (atherosclerotic cardiovascular disease) score is what?

> 7.5-10%

(Depends on the resource you’re looking at)


Most common cardiac manifestation of lupus (SLE)?


(*typically presents as pleuritic chest pain, pericardial friction rub, and diffuse EKG changes w/ other SLE symptoms such as joint pain)


Systolic murmur at the sternal border

Tricuspid regurg


Normal range for total bilirubin?



Alcoholic has obvious signs of cirrhosis (ascites, spider angiomas, hemorrhoids, AST:ALT >2:1). Do you need to do a liver biopsy to confirm the diagnosis of cirrhosis?

-though liver biopsy is the gold standard for diagnosis of cirrhosis, if the history and physical is obvious for cirrhosis, do not put the patient through this

*you also don’t need to do unnecessary work-up for rare causes of cirrhosis like alpha-1 antitrypsin deficiency or hemochromatosis. This guy is an alcoholic so you can say with confidence that the cirrhosis resulted from alcohol intake.


What screening test should you do in a patient with liver cirrhosis?

Endoscopy (EGD= EsophagoGastroDuodenoscopy)

-you need to check for esophageal varices, determine their risk for variceal hemorrhage, and come up with strategies for prevention of variceal hemorrhage (these patients bleed so much it’s life threatening!)


How do you manage acute diverticulitis (presents as LLQ pain and confirmed by CT)? Be specific about the antibiotics used. What do you need to follow up with?

Antibiotics- Ciprofloxacin + Metroniadazole (Flagyl)
And bowel rest

Follow up with colonoscopy (4-8 wks later) since colon cancer can mimic the presentation and CT findings of diverticulitis!
*also advice patients to increase fiber intake and exercise and lose weight and stop eating red meats, smoking, and straining on the toilet

**Cipro is a fluoroquinolone that is broad spectrum and good for gram neg GI bugs + Metronidazole is good for anaerobic coverage


50 y.o. heavy alcoholic presents with SOB, even at rest. He has an S3 and crackles. CXR shows pulmonary venous congestion. Echo shows dilated LV and EF of 25%. He has no history of any heart problems. What is the most likely cause of his symptoms?

Alcoholic dilated cardiomyopathy

-he has evidence of systolic dysfunction in the setting of alcohol abuse. Know that dilated CM from alcohol is a dx of exclusion (he had no prior CAD or valvular heart dz and heavy alcoholism is evident)

*abstinence from alcohol should improve or normalize LV function over time


Peripheral vascular dz vs. acute arterial occlusion? What are they

Peripheral vascular dz- blood flow is reduced to a limb (same concept as angina)

Acute arterial occlusion- blood flow is cut off to a limb (same concept as MI, emergency!)


Old man ex-smoker has worsening cramping in his left leg. He has decreased pulses in the left leg and a reduced ankle-brachial index. Diagnosis and treatment?

Peripheral artery disease

Treat with smoking cessation, graduated exercise program (walk until claudicaiton/ pain from ischemia, then rest, then do 1 more cycle), atherosclerotic risk factor reduction, avoid temperature extremes, aspirin + a stain, can also give Clopidogrel, cilostazol (surgery- angioplasty or bypass grafting- if severe)

*this usually occurs with CAD/ is a manifestation of atherosclerotic cardiovascular dz (ASCVD)
**do not confuse with acute arterial occlusion- this is an emergency where blood flow through an artery to a limb is fully cut off! Presents with 6 P’s: pain, pallor, polar (cold), paralysis, paresthesias, and pulselessness (not just reduced pulse/ blood flow...none at all!)


Patient complains of on/off epigastric abdominal pain for 1 year, worse with eating. Hb is low, MCV is >100. Diagnosis?

Autoimmune gastritis—> pernicious anemia

(Antibodies against parietal cells—> cannot absorb vit B12–> macrocytic anemia)

*look for hypochlorhydria (decreased stomach acid- since parietal cells produce acid) and elevated gastrin (gastrin stimulates parietal cells to release acid, so it will get up-regulated in response to the low acid as feedback)


Name some functions of the liver.

1. Synthetic (makes stuff)
-clotting factors
-proteins (ex: protein c and s, albumin)

2. Metabolic
-metabolism of drugs and corticosteroids (P450 system)
-breaks down estrogen

3. Excretory
-bile excretion


40 y.o guy has chronic diarrhea with fat in it (no pathogens or WBCs). He’s given a oral D-xylose solution. Urinary excretion of the D-xylose is low. He is treated with Rifaximin and D-xylose test is repeated but results didn’t change. Diagnosis?

He is peeing out a LOW amount of D-xylose (monosaccharide), meaning he has a mucosal reabsorption problem like celiac dz or SIBO...but it’s not SIBO since that’s treated with Rifaximin and that did not help...so it’s celiac
(problem with reabsorption due to flattened villi-> less of the monosaccharide pushed into the blood-> less filtered through the kidneys and peed out)

*patients with malabsorption due to enzyme deficiencies would have normal absorption and urinary output of D-xylose (bc their problem is with enzymes breaking polysaccharides into monosaccharides and D-xylose is already a monosaccharide)


Explain how the D-xylose test can be used to distinguish pancreatic insufficiency from mucosal causes of malabsorption (celiac dz, bacterial overgrowth, etc.).

D-xylose is a monosaccharide and gets fully absorbed into the blood.

Pancreatic insufficiency (not getting enough pancreatic enzymes into the duodenum to break down polysaccharides-> monosaccharides)—since D-xylose is already a monosaccharide it doesn’t need the help of pancreatic enzymes, so all the D-xylose gets appropriately absorbed into the blood and a normal amount is peed out

Celiac dz (flattened villi/ problem at small intestine level with pushing nutrients into the blood/ reabsorption)—so some D-xylose does NOT get reabsorbed into the blood as it should and a low amount is peed out


Mechanism of spider angiomas and palmar erythema in cirrhosis?

Both due to hyperestrinism

Liver not working to break down estrogen—> too much estrogen


Mechanism of caput medusae in cirrhosis?

Caput medusae= dilation of superficial veins on the abdominal wall DUE TO PORTAL HTN
(Backs up portal vein-> periumbilical vein)


Truck driver comes in with SOB and sharp chest pain for 10 hrs, relieved by taking shallow breaths. BP is normal, HR is tachy, RR is 30. EKG is normal. Most likely diagnosis?

PE (pulmonary embolism)

*presents with SOB, pleuritic chest pain, tachypnea, tachycardia (CXR may appear normal)


Guy with long extremities, flexible joints, and pectus carinatum has sudden-onset chest and neck pain. Diagnosis?

Aortic dissection

-this guy has Marfan syndrome (mutation of fibrillin-1-> connective tissue integrity problems throughout the body, including aortic root dilation)


20 y.o guy is having depression and involuntary movements. Total bili, direct bili, AST, and ALT are elevated. Diagnosis?

Wilson disease

-rare AR disease in which copper transport is impaired—> copper accumulation in tissues
-consider this when there is liver dysfunction + neuro psych symptoms!


Which has a greater impact on BP reduction: following the DASH diet or reducing sodium in your diet?

DASH diet

*the following can decrease BP by this much:
Weight loss—5-20 per 10kg loss
DASH diet—8-14
Dietary sodium reduction—2-8
Limiting alcohol—2-4

**tell patients to do all of the above, but losing weight and eating a DASH diet (all-around healthy diet rich in fruits and veggies, low in saturated and total fats) is key to lowering BP, more so than limiting salt


Patient has S3 and SOB. Best initial therapy?

Loop diuretics

He has LV failure (backing up to lungs). Taking off fluid is the first step in providing symptomatic relief.

*yes, drugs like beta-blockers are helpful in the long-term and reduce mortality, but this wouldn’t be the best initial therapy—wouldn’t take the excess fluid off to make the patient feel better


What heart problem can amyloidosis cause?

Restrictive cardiomyopathy

(Amyloidosis= misfolded protein that deposits around the body)


Diarrhea + leukocytosis. Think of what?

C diff


What is SBP?

Spontaneous bacterial peritonitis

-infection of the ascitic fluid

*presents as abdominal discomfort in a cirrhosis patient, possibly mental status change
*diagnose by PMN (neutrophil) count >250 + positive peritoneal fluid culture


Woman with SLE on Prednisone comes in for fever, chills, fatigue, cough, and SOB. Pulse ox is 86% and she’s using accessory muscles to breathe. LDH is elevated. CXR shows bilateral interstitial infiltrates. Diagnosis?

PCP pneumonia

*it’s associated with AIDS, but also immunosuppressed people (she’s taking glucocorticoids/ steroids, which block the immune system)


Patient has burning chest pain for 2 hrs. Lungs sound clear. EKG shows ST elevation in leads II, III, and aVF. You give him nitroglycerin. A few minutes later, he’s lightheaded and his BP dropped from normal to 75/50. What happened? Next step?

ST elevation in II, III, aVF= inferior STEMI (occlusion of the RCA). Inferior wall MI’s have a 50% chance of involving the RV. Since he has clear lungs (meaning left heart is good), it probably did involve the right heart.

In a right sided MI, you don’t give nitrates bc the right heart is preload dependent and this will drop BP too much!

Since you already gave nitros and his BP did drop too much, give a normal saline bolus (IV fluids) to get the preload back up (which will improve CO and BP).


Normal CD4+ count?

>500 (*10^6/ L)


Does it help if alcoholic cirrhosis patients stop drinking?

Yes! Alcoholic cirrhosis-> liver inflammation after drinking involving fibrosis and nodule formation. This fibrogenesis improves with abstinence from alcohol.
Although advanced cirrhosis is irreversible, avoiding alcohol still carries a huge survival benefit.


How does disseminated MAC (mycobacterium avium complex) infection present?

Constitutional (fever, night sweats, fatigue, malaise, weight loss) and GI (diarrhea, abdominal pain) symptoms


Normal AST? Normal ALT?

8-40 is the normal range for both AST and ALT


Obese patient has high AST of 80 and high ALT of 90 + mild hepatomegaly. Not an alcoholic. No other signs/ symptoms. Diagnosis?

Nonalcoholic fatty liver disease (NAFLD)

*we see a mild elevation in liver enzymes in these patients (AST/ALT ratio <1) and mild hepatomegaly. Alk phos may also be on the high side. Albumin and bili are typically normal.
*diagnose by labs and U/S showing hyperechoic texture of the liver (liver biopsy would confirm but we don’t do this for fatty liver)
*treat with weight loss/ manage metabolic risk factors


Regarding class I antiarrhythmic drugs, what is “use dependence?”

Class I anti-arrhythmic drugs block Na+ channels in depolarization (phase 0)

In patients with faster heart rates, the drug has less time to dissociate from the Na+ channels—> longer effect of the drug (more widening of the QRS interval/ ventricular contraction)

**this is why class I anti arrhythmic drugs (esp class IC) are good at treating supraventricular tachyarrhythmias


What happens to SVR (systemic vascular resistance) and afterload in HF?

SVR goes up (vasoconstriction)
Afterload goes up

*Here’s the cycle of hemodynamics in HF:
Dec contractility-> dec CO-> poor perfusion to kidneys activates RAAS-> vasoconstriction (inc SVR)-> inc afterload (the vasoconstriction/ inc BP increases the pressure the heart now has to pump against)-> decreases the contractility even more since the extra afterload makes it harder to pump...so its a nasty cycle


Why might a HF patient have mitral regurg (holosystolic murmur at the cardiac apex)?

LV dilation (due to decreased CO)/ remodeling—> functional mitral regurg


What is cardiac index?

Basically the same as cardiac output, but takes into account the person’s body weight

*Cardiac Index (CI)= CO/ body surface area


Septic shock and anaphylactic shock both fall under what category of shock?

Distributive shock

(“Warm shock” from vasodilation)


Most common cause of mitral regurg?

Mitral valve prolapse (MVP)

(Myxomatous degeneration of the mitral valve)


Patient with known HFrEF on ASA, Digoxin, Lasix, Metoprolol, Lisinopril, and Atorvostatin presents with worsening SOB and lower extremity edema. You give her IV Lasix and edema improves but a few days later she has a few beats of wide complex V-tach. Next step?

Check serum electrolytes!

If a patient is stable in V-tach, you need to find out why there are having this arrhythmia (if unstable defibrillate)! She likely has electrolyte imbalance due to the IV Lasix/ Fuorosemide, which is a loop diuretic and causes hypokalemia and hypomagnesemia. Low K+ and Mg can lad to V-tach. If this is the case, you need to correct her electrolytes.


What is another name for vasospastic angina?

Variant angina or Prinzmetal angina


Mechanism and treatment for Vasospastic/ Variant/ Prinzmetal angina?

Mechanism= the intima layer of the artery smooth muscle is hyperactive—> intermittent coronary artery vasospasm (ST elevation during chest pain episodes lasting <15 min)

Treatment= CCB’s (Diltiazem, Amlodipine)
-cause coronary artery vasodilation to prevent vasospasm
*Nitrates given to stop chest pain during an episode


Guy comes in with sudden-onset severe left-sided chest pain. Has HR of 125, BP of 160/90, ST depression and T-wave inversion in leads V4-V6. He is agitated, pupils are dilated, and nasal mucosa is atrophic. What should you give him?

IV Benzo (like Diazepam)

This guy is on cocaine (tachy, HTN, signs of MI specifically NSTEMI, dilated pupils, nose jacked up from snorting cocaine) having cocaine-induced MI.
Benzos bind to GABA and enhance its inhibitory CNS activity-> less sympathetic activity so reduced agitation, improved HR and BP, improvement in cardiac symptoms.

*also give ASA (antiplatelet to stop thrombus formation enhanced by cocaine), nitrates, and CCBs to vasodilate. Do NOT give beta-blockers due to unopposed alpha-1 constriction-> worsening vasoconstriction!!

**Remember cocaine blocks NET and DAT (NE and dopamine reuptake)-> inc NE and dopamine in the cleft. NE= alpha-1> beta-1 agonist, so causes vasoconstriction (including coronary vasoconstriction).
**Use alpha-blockers in cocaine toxicity where BP is super high


Patient is found to have premature atrial complexes (PACs) on EKG. Is not symptomatic. Drinks 1-2 beers/ day. Best way to manage this patient?

Advise quitting alcohol

PACs are early beats from the atria firing on its own, you see early P waves (QRS is normal bc conduction below the atria is normal). Usually asymptomatic and does not require treatment, however advice to quit tobacco, alcohol, caffeine, stress bc these things can be what’s causing it!
*if symptomatic (palpitations) a beta-blocker can be given


Old guy comes into the ED with the worst pain in his life in his chest and back. He has a diastolic decrescendo murmur at the sternal border and is tachy. Has nonspecific ST-segment elevation and T-wave changes. CXR shows widening of the mediastinum. Diagnosis?

Acute Aortic Dissection

*Diastolic murmur at sternal border= aortic regurg (dissection can pull apart at aortic valve)


What fasting blood glucose and hemoglobin A1c do you need to meet criteria for a diagnosis of diabetes?

Fasting blood glucose >125

Hb A1c of 6.5% or more


For patients <40 yo with ASCVD or >40 yo with DM, what med do you give?

A statin! (Long-term)


Asthma patient in respiratory distress is given nebulized albuterol, IV methylprednisolone, and supplemental O2. Repeat labs show leukocytosis (high WBCs). Why?

Glucocorticoids (methylprednisolone) cause mobilization of marinated neutrophils-> inc WBCs
(Medication effect)


What are the 4 severity levels of asthma? State the frequency of symptoms (times they need to use SABA albuterol rescue inhaler) for each.

1. Intermittent- symptoms 2 or less days/ week (treatment= SABA prn)

2. Mild persistent- symptoms >2 days/ week but not daily (SABA prn + low-dose ICS)

3. Moderate persistent- symptoms daily (SABA prn + low-dose ICS + LABA (or medium-dose ICS))

4. Severe persistent- symptoms throughout the day (SABA prn + medium-dose ICS + LABA)

*if worse: SABA prn + high-dose ICS + LABA + oral corticosteroid and/or Omalizumab (if allergies too)


Smoker guy is planning to get a knee replacement surgery in a month. He has COPD and HTN. What will decrease his risk of post-operative pulmonary complications the most?

Quitting smoking right now

There is no evidence that drugs (such as Moxifloxacin) or anything else decreases PNA risk in the setting of surgery. There is, however, evidence that quitting smoking 1-2 months prior to surgery decreases post-op pulmonary risk by a lot!


What valvular issue can cause hemoptysis?

Mitral stenosis

(Mitral valve has a hard time opening-> blood backs up to LA and lungs-> pulmonary edema and that extra pressure in the lungs can burst capillaries-> cough up blood)


Another name for bronchogenic carcinoma?

Lung cancer!


Most common cause of hemoptysis?

Pulmonary airway disease
(Chronic bronchitis, bronchiectasis, lung CA)

-Chronic bronchitis (the constant coughing and irritation from mucus plugs can cause bursting of blood vessels in the bronchus), Bronchiectasis (same reason- you also have chronic coughing and mucus trapping from the abnormal dilation of the bronchus), and Bronchogenic carcinoma/ Lung cancer (likely due to coughing and maybe related to the rich vascular supply of the tumor)


Asthma patient comes in with worsened SOB and cough (asthma attack). Pulse ox= 88%. Patient is wheezing and using accessory muscles to breathe. ABG shows: pH of 7.43, PaO2 of 65, PaCO2 of 40. CXR shows hyperinflated lungs. What is most concerning and indicates the patient is getting worse?

Most concerning= the fact that PaCO2 is normal-high

-Why? The normal response to an asthma exacerbation is hyperventilation (compensation for not breathing well)—> blowing off more CO2–> low PaCO2 (<40). If you are not hyperventilating in an asthma attack, you are not blowing off as much CO2 and PaCO2 will be high >40–this suggests respiratory muscle fatigue or severe air trapping suggesting RESPIRATORY COLLAPSE.

*CXR showing hyperinflation is expected in an asthma exacerbation (obstructive= hard to breathe out= air trapping)


Patient with PMH of leukemia who got stem cell transplantation and developed neutropenia presents with fever, pleuritic chest pain, hemoptysis. CXR shows right upper lobe infiltrate. CT of chest shows nodular lesions surrounded by ground-glass opacities in the right upper lobe. Sputum gram stain shows inflammatory cells but no organisms. Diagnosis and treatment?

Invasive aspergillosis
(Fever, pleuritic chest pain, and hemoptysis in immunocompromised)

Voriconazole + an echinocandin (Caspofungin)


Most common cause of Cor-pulmonale in the US?

COPD (accounts for 25% of cases)

(Widespread vasoconstriction in pulmonary vasculature to shunt blood to areas where there’s better oxygen...but problem is all areas are diseased, so this just creates a greater pressure that the right heart has to pump against-> right-sided HF)


HIV patient off his meds presents with fever, cough, SOB. Has bilateral lung crackles. CXR shows bilateral interstitial infiltrates. Patient is given antibiotics and IV NS (normal saline) at 150mL/hr. 2 days later his SOB improved but he is confused and Na+ levels are lower than on admission. Cause of his hypOnatremia?


-He has PCP pneumonia (HIV, classic fever + cough + SOB symptoms, crackles, CXR infiltrates)
-SIADH can happen from PNA= too much retention of water-> low sodium concentration
-Giving normal saline will worsen this kind of hypOnatremia (although it’s salty and you’re giving back some Na+, it is FLUID and that fluid dilutes the [Na+] more)


When you suspect lung CA what should you do?

CT of the chest


How can cirrhosis cause lower extremity edema?

Bad liver—> not making albumin like it should—> low oncotic pressure holding fluid in vessels—> peripheral edema


What is Spontaneous bacterial peritonitis (SBP)?

An infection of the ascitic fluid

*usually occurs in patients with underlying chronic liver disease and ascites. Spontaneous bacterial peritonitis (SBP) is often associated with fever and abdominal pain (can also present with hepatic encephalopathy alone)


What does “serial” mean in medicine?


For example, “serial troponin” means you are measuring troponin several time (usually q8 hrs). “Serial CT scan” for lung cancer screening means you are doing a CT annually.


What is empyema?

Collection/ pocket of pus in the pleural space

*empyema often results from untreated exudative pleural effusion (usually secondary to bacterial PNA)
*give antibiotics and do aggressive draining of the pleura with thoracentesis. If that doesn’t do it, do throacotomy (surgical opening up of the chest to gain access to the pleural space/ open drainage)


Renal failure= GFR of less than what?

GFR <30 mL/min


You have a patient that needs to be started on anticoagulation (for PE, for example). The patient has a GFR of 20mL/min. Which initial anticoagulation med is best and why?
A) Enoxaparin
B) Fondaparinux
C) RivaroXaBAN
D) Unfractionated heparin
E) Warfarin

D) Unfractionated heparin

A) Enoxaparin= low-molecular-weight heparin (LMWH)
B) Fondaparinux= IV factor Xa inhibitor
C) RivaroXaBAN= oral factor Xa inhibitor
E) Warfarin
Cannot use A, B, C, E^ because the patient has renal failure (GFR <30) and these anticoagulants are not recommended for patients with renal insufficiency (takes too long to clear them-> increased factor X activity and bleeding risk)
*Remember that LMWH (IV) is the best choice for renal insufficient patients and bridge to Warfarin (PO)!


Small cell lung cancer patient has SIADH (paraneoplastic syndrome) causing hypOnatremia. What’s the best initial treatment for the patient’s hypOnatremia?

Fluid restriction

SIADH-> too much ADH-> too much retention of fluid diluting [Na+] so that it is low
Less fluid will help this concentration come back up
*SIADH drugs (Vaptans and Demeclocycline) can be used to block V2 ADH receptors, but start with fluid restriction and see if that is enough


Most common side effect of Beclomethasone?

Most common side effect of inhaled corticosteroids (ICS) like Beclomethasone (in asthma, COPD)= OROPHARYNGEAL THRUSH (oral candidiasis)


Patient takes the following meds at home: Aspirin, Diltiazem, Atorvostatin, and Albuterol as needed. Was recently diagnosed with stable angina and recently had a nasal polyp removed. Present with SOB and wheezing. Diagnosis?

Aspirin-exacerbated respiratory distress (AERD)

*ASA and all NSAIDs block COX—> more shunting toward LOX in AA pathway—> more leukotriene synthesis, which causes bronchoconstriction and can bring on an asthma attack


What is a parapneumonic effusion?

A pleural effusion that arises as a result of a pneumonia

*subtypes: uncomplicated, complicated, and empyema


Light’s criteria?

P:S (pleural: serum ratios)—

Protein >0.5
LDH >0.6
Pleural LDH > 2/3rds the upper limit of normal for serum LDH

If any of these are true, it is exudative (“extra shit in it”) vs. transudative (fluid only)


What are the 3 types of Aspergillus infections and their presentations?

1. Allergic Bronchopulmonary Aspergillosus (ABPA)
-Pulm infiltrates, wheezing, IgE in an asthma or CF patient

2. Aspergilloma (fungal ball)
-Gravity-dependent lung cavitation, fever, hemoptysis in a patient with prior TB

3. Invasive pulmonary Aspergliosis
-Fever, hemoptysis, chest pain, SOB-> kidney failure, endocarditis, ring-enhancing lesions in brain, and sinus tissue necrosis in an immunocomprimised/ neutropenic patient


How do you diagnose Aspergilloma?

Will present as a lung cavitation in a patient with prior TB (seen on chest CT) and you get Aspergillus IgG serology to confirm


Does lung compliance increase or decrease in ARDS?

Decreased lung compliance

-ARDS= inflammatory condition in the setting of infection (sepsis, PNA, etc.), trauma, or other conditions (pancreatitis, massive transfusion). Lung injury causes the release of proteins, inflammatory cytokines, and neutrophils into the alveolar space (hyaline membranes). This leads to leakage of bloody and proteinaceous fluid into the alveoli, alveolar collapse due to loss of surfactant, and DIFFUSE ALVEOLAR DAMAGE-> inability to expand/ stiff lungs/ dec compliance


What happens to the ratio of arterial oxygen tension to fraction of inspired oxygen in ARDS?

It decreases

Arterial oxygen (PaO2) to fraction of inspired oxygen (FiO2) ratio:
PaO2/ FiO2 (also called P/F ratio)
Decreases (<300) bc the lung injury/ hyaline membranes impair gas exchange-> decreases PaO2 and raises the FiO2 requirement (the oxygen that you have to give them through the ventilator)


70 y.o. man has a history of attacks of dyspnea on exertion. He has an ejection-type systolic murmur along the left sternal border that decreases with squatting. What does he have?


*remember that HOCM is a SYSTOLIC murmur at the left sternal border (systolic bc the problem is when the blood is being pumped out through the aorta)

*remember that squatting increases preload (compress leg veins= more ‘milking’ of blood to heart), which makes the problem better (more blood to push septal defect out of the way)


Inheritance pattern of HOCM?

Autosomal dominant

*caused by mutations in sarcomere genes (ex: cardiac myosin binding protein C and cardiac beta-myosin heavy chain gene) for the myocardial contractile proteins of the heart


If you suspect aortic dissection, what imaging do you do?

TEE (trans esophageal echocardiogram) is preferred

But you can also do a chest CT with contrast (if patient’s kidneys are ok/ can tolerate contrast) or an MRI (if non-emergency and patient can lie still)
*do whichever of these is available at the time


What is the recommendation for AAA screening?

Abdominal ultrasound once on men 65+ who EVER smoked


What is the recommendation for breast cancer screening?

Mammogram every 2 years on women 50-74


What is the recommendation for cervical cancer screening?

Pap smear every 3 years on women 21-65

*women 30-65 may substitute w/ HPV testing every 5 yrs


What is the recommendation for colon cancer screening?

Fecal occult blood test (FOBT) or fecal immunochemical test (FIT) every year
Colonoscopy every 10 years


What is the recommendation for HIV screening?

Do HIV antibody screen once in adults 15-65


What is the recommendation for lung cancer screening?

Low-dose CT scan every year in adults 55-80, 30+ pack-years of smoking, current smoker, or quit in last 15 years


What is the recommendation for osteoporosis screening?

DEXA scan in women 65+


Patient presents with worsening SOB, pitting edema in legs, hepatojugular reflux. Has a pleural effusion—what is it most likely due to?


-CHF—> increased hydrostatic pressure pushing fluid out of vessels—> transudative pleural effusion

*you’d expect:
Pleural protein: serum ratios to be...
Protein <0.5
LDH <0.6
LDH < upper 2/3rds limit of normal serum


A glucose of <60 (or pleural: serum glucose ratio of <0.5) represents what type of pleural effusion?

Complicated parapneumonic effusion (exudative pleural effusion in the setting of pneumonia)


Criteria for extubation (of a person on a ventilator)?

1. pH > 7.25

2. Adequate oxygen on minimal support (FiO2 less than or equal to 40%, PEEP less then or equal to 5)

3. Intact inspiratory effort and sufficient mental alertness to protect the airway

*if a patient is ready to be exubated based on the above criteria, do a spontaneous breathing trial (keep them intubated but turn off ventilator support to check that they breathe on their own and ABG remains normal throughout this effort)!


Symptoms of CHF + peeing out protein. Think about what?

Cardiac amyloidosis
(Amyloid, a misfolded protein, deposits in various tissues, including the heart-> restrictive CM and you pee out some excess protein)


Patient has sharp chest pain worse with deep breathing, better with leaning forward. BUN and Cr are elevated a lot. Diagnosis and treatment?

Uremic pericarditis
(Toxins accumulate and cause inflammation of the heart sac)



How does acute HIV infection present?

Mono-like symptoms (fever, lymphadenopathy, sore throat, athralgias) 2-4 weeks post-exposure

*Viral load is really high (>10,000 copies/mL) (but HIV antibody testing may be negative adn CD4 still normal)


Patient has fatigue, SOB on exertion, lower extremity edema, proteinuria, easy bruising. Echo shows concentric thickening of ventricular walls w/ diastolic dysfunction. Diagnosis?


-Causes a restrictive CM + peeing out protein
-Remember, it’s a misfolded protein that deposits in various places (systemic dz)


What is dumping syndrome?

Seen in gastric bypass patients

The stomach is now so small that food, esp simple carbs, gets dumped into the intestines really fast-> diarrhea (can also cause abdominal pain, nausea, hypotension, tachycardia, lightheadedness)


Mechanism of vasovagal syncope?

Severe dehydration, etc.-> dec preload to heart-> dec CO-> cardiopulmonary receptors recognize there’s less volume in the heart-> initially this causes inc sympathetic activity, so inc HR and contractility to raise CO to normal-> contortion/ weird twisting of the LV (bc it’s pumping normal but there’s not enough blood to pump out)-> messes up cardiopulmonary receptors so that they have the opposite effect (they think the heart is over full)-> dec sympathetic activity, so dec HR and contractility-> lack of blood to brain-> body faints to inc preload back again (gravity isn’t against you when you’re laying on the floor)


What is a pericardial knock and when do you hear it?

Mid-diastolic sound associated with constrictive pericarditis

Remember, constrictive pericarditis= fibrotic, scarred pericarditis (from repeated inflammation/ recurrent pericarditis). This restricts diastolic filling of the heart-> “pericardial knock” during diastole.


What screening do you need to do for cirrhosis patients?

EGD (endoscopy) to screen for esophageal varices


What med can you give for esophageal varices?

Non-selective beta blocker (Propranolol or Nadolol)

-Block beta-2 (vasodilates)-> vasoconstricts-> reduces portal blood flow


Would you expect PT and albumin to be high or low in a cirrhosis patient?

PT- High (liver makes clotting factors. If the liver is bad, it’s not making as many clotting factors and PT goes up bc takes longer to clot)

Albumin- Low (liver makes albumin. If the liver is bad, makes less of it)


Besides in B12 and folate deficient individuals, we see macrocytic anemia in what population of patients?



Explain high-output cardiac failure in a hemodialysis patient with an AV fistula.

AV fistula= direct connection between artery and vein (blood goes in arteries away from heart and meets up right away with vein back to heart rather than having to journey through tiny vessels first)

Way more blood in venous system to heart—> heart has to deal with more blood, so a preload overload—> high-output cardiac failure

*these patients get a wide pulse pressure (ex: 160/90) bc in systole the heart pumps out a huge amount of blood (due to having more preload) and during diastole blood is shunting across the AV fistula to VEINS so the pressure drops a lot in the ARTERIES


Patient had penetrating injury to right eye which resulted in blindness in the right eye. 2 weeks later presents with “floating spots” and blurry vision in his left eye. Most likely cause?

“Spared eye injury”

Damage to eye-> exposes antigens your body has never seen (‘hidden antigens’)-> immune system responds to them and attacks other eye


Guy presents with SOB, cough, hemoptysis for 2 days. He has had weight loss and rhinosinusitis. Labs show low Hb, high BUN and Cr, high WBCs. CXR shows lung nodules. Diagnosis?

Granulomatosis with polyangiitis (Wegner’s)

-systemic vasculitis that involves nasopharynx + lungs + kidneys


Patient flexes his right hip and knee and slaps his foot to the floor with each step. What gait is this?

“Steppage gait”

L5 radiculopahty adn compression peroneal neuropathy are common causes


Lady had a liver transplant 2 weeks ago (is on immunosuppressant meds). Has fever, chills, weakness, vomiting. Fever, low BP, tachy. Most likely cause of her presentation?

Bacterial infection

*most infections within the first month are bacterial causes, during months 1-6 opportunistic (in setting of immunosuppression)
*hemodynamic instability (look at the vital signs) makes bacterial infection more likely than transplant rejection


What med can treat an actively bleeding esophageal varices?



Lady comes in with periorbital edema and proteinuria. She is started on diuretics and the edema improves. Then she gets severe right-sided abdominal pain, fever, and gross hematuria. Why?

Renal vein thrombosis

Remember that nephrotic syndrome (esp membranous GN)-> peeing out protein, including antithrombin III-> hypercoagulable state


60 year old man has diarrhea w/ blood and mucus. Has not been on antibiotics. Colonoscopy 4 years ago was normal. Has elevated WBC count and ESR, low Hb. Sigmoidoscopy shows erythematous friable mucosa from the rectum to sigmoid colon. Diagnosis?

Ulcerative colitis (UC)

*has a bimodal distribution- more common in young (15-40) and old (50-80)

**NOT colon cancer...although low Hb in elderly is colon cancer until proven otherwise, the colonoscopy 4 years ago did prove otherwise (only need 1 every 10 years). Plus, the sigmoidoscopy showing involvement of just the distal colon is constituent with UC (bleeding-> low Hb from that)


Patient has coffee ground emesis + black, tarry stools. What are you thinking?

Upper GI bleed

*look for elevated BUN (due to increased GI digestion/ breakdown of Hb)


Lady with osteoarthritis (takes NSAIDs) has conjunctival pallor. Most likely cause of her anemia?

Iron deficiency anemia from NSAIDs (block GI protective prostaglandins-> gastritis and/or gastric ulcers leading to chronic GI blood loss and depletion of iron stores)

*osteoarthritis does NOT cause anemia of chronic dz!


Patient with BMI of 55 and extensive smoking history has SOB, clear lungs, distant heart sounds, low-voltage QRS complexes on EKG, Hb 16, pH 7.3, PaCO2 60. Diagnosis?

Obesity hypoventilation syndrome

-BMI >30 (obese)
-Lungs are clear
-Distant heart sounds and low-voltage QRS= heart is further away due to excess fat in between (*think of this and pericardial effusion)
-Reactive polycythemia (poor oxygenation due to shallow breaths-> kidneys inc EPO-> inc Hb to try to compensate by having more O2 binding sites)
-Respiratory acidosis (retained CO2 from shallow breathing)


In a patient with poor oxygenation, why might you see inc Hb?

Reactive polycythemia

Poor oxygenation-> kidneys pump out more EPO-> more Hb to try to compensate by providing more oxygen binding sites


3 diagnostic criteria for obesity hypoventilation syndrome?

1. Obesity with BMI >30
2. Daytime hypercapnia (PaCO2>45)
3. No alternate explanation of their hypoventilation

*work it up by getting ABG (hypercapnia, normal A-a gradient), r/o pulm disease w/ CXR, restrictive pattern on PFTs (all the fat restricts them from expanding their lungs), normal TSH, polysomnography
*treat with weight loss/ bariatric surgery, nocturnal positive-pressure ventilation
**most of these patients have coexisting OSA


Patient with cardiomyopathy is on Furosemide (Lasix), Carvedilol, Lisinopril, and Digoxin. She presents with a-fib w/ RVR and you treat her with RivaroXaBAN and Amiodarone. 2 weeks later, she comes back with anorexia, nausea, weakness. Why?

Digoxin toxicity (causes GI symptoms)

She was already taking Digoxin. You added Amiodarone (anti-arrhythmic) to her regime, which blocks the P450 system (broken chrome bumper in uno, does, tres sketchy)-> inc Digoxin in blood.


Normal leukocyte (WBC) count?


*just remember it as roughly <10,000


What is Myasthenia Gravis and how do meds like Pyridostigmine work for it?

MG= antibodies against the nicotinic ACh receptors on the post-synaptic at the motor end plate (skeletal muscle NMJ)-> proximal muscle weakness worse w/ use, ptosis, diplopia

Pyridostigmine= ACh-esterase inhibitor-> blocks the breakdown of ACh-> more ACh in the cleft to outcompete MG antibodies


What is a Myasthenic crisis?

Exacerbation of Myasthenia Gravis (antibodies going crazy against post-synaptic nicotinic ACh receptors-> muscle weakness)

*can be brought on by infection, surgery, pregnancy/ childbirth, tapering off immunosuppressant drugs, some meds (aminoglycosides, beta blockers)

*presents with oropharyngeal and general weakness, respiratory insufficiency

*intubate, plasmapheresis or IVIG + corticosteroids


Lady with Myasthenia Gravis and Hypothyroidism presents with SOB, productive cough, and choking sensation. T 101, BP 130/80, HR 110, RR 22. She takes shallow breaths and has crackles at lung bases. High WBCs, resp acidosis (low pH, high CO2). Diagnosis and next step?

Myasthenia crisis
Endotracheal intubation

-This patient has PNA (SOB, productive cough, shallow breathing, crackles, WBC count). Resp acidosis (low pH, high CO2) explained by not breathing deep-> less air getting down into lungs for gas exchange. This was a trigger for MG crisis/ exacerbation.

-Do elective intubation bc of evidence of impending respiratory failure (ill-appearing, tachypnea/ breathing rapid and shallow, muscle weakness, difficulty clearing secretions/ choking sensation, and respiratory acidosis).


We should do elective intubation in patients with evidence of impending respiratory failure. What kind of subjective and objective signs serve as evidence that they’re going to lose ability to support their airway and you should intubate?

-they look really sick
-tachypnea (breathing fast and shallow)
-muscle weakness
-can’t clear secretions/ choking

-low vital capacity (after max inspiration, the max air you can exhale/ breathe out) *low means they have a weak ability to exhale
-respiratory acidosis (retaining CO2 from poor gas exchange)


You see low Na+ and high K+ in the labs. What should you automatically think of?

A problem with aldosterone!

Remember, aldosterone-> Na+ absorption, K+ and H+ wasting. If aldosterone is low, you get dec Na+ in the blood and inc K+, H+ in the blood-> hypOnatremia, hypERkalemia, and metabolic acidosis.


Normal fasting glucose?



Guy from Southeast Asia has lightheadedness, cough, unexpected weight loss. Has fever, low BP. Labs show low Na+, high K+, low glucose, eosinophilia. CXR shows airspace disease in upper lung w/ lymphadenopathy. Diagnosis?

Military TB-> infectious adrenalitis/ primary adrenal insufficiency (Addison’s disease)

*Remember, no.1 cause of Addison’s in the US= autoimmune destruction of adrenal glands. But no.1 cause of Addison’s in developing countries= TB! The inflammation from military TB destroys adrenal glands so that they stop producing hormones.
*Addison’s= adrenal glands aren’t making aldosterone and cortisol-> low Na+ in blood (low BP, weakness/ lightheadedness, hypOnatremia), high K+ in blood (hypERkalemia).


Girl is treated for asthma exacerbation with albuterol nebulization + IV methylprednisolone. Her asthma symptoms improve, but now she has severe muscle weakness and hand tremor. Next step?

Check serum electrolyte panel

Albuterol= beta-2 agonist-> hypokalemia (stimulates sodium potassium pumps, so brings K+ into cells). HypOkalmeia can cause muscle weakness and tremor.
*Another side effect is palpitations (speed up the heart bc has some agonist effects on beta-1 too)


Old lady has lethargy and SOB. Hypotension, tachycardia, reduced breath sounds and crackles. Systolic ejection murmur at right upper sternal border. High cardiac index, normal RA pressure, normal pulmonary capillary wedge pressure (LA pressure). Low SVR. What clinical picture does this fit?

Septic shock

*note: you can’t meet all the SIRS criteria based off this question, have to roll with just the info they give you. But the clinical picture is septic shock- possible PNA for infection source (crackles and SOB), hemodynamic instability (low BP, tachy), low SVR= widespread vasodilation in response to inflammatory cytokines.

*high CI (which is CO taking into account body size) and no problems with the heart, so not a cardiogenic shock picture (inc CO is the heart trying to compensate for low BP).

**do NOT get thrown off by the murmur (systolic at right upper sternal border). This is aortic stenosis- a lot of old people have it due to calcifications!


What types of shock present with cold extremities?

1. Cardiogenic shock
(Heart is not pumping blood out well to extremities and vasoconstriction to divert blood to vital organs)

2. Hypovolemic shock (hemorrhagic shock)
(Body vasoconstricts to divert blood away from extremities and toward vital organs)


Do “bounding pulses” always indicate aortic regurg?


Just means the heart is working overtime (inc CO)


Usually use BiPAP or CPAP in:
1. COPD exacerbation
2. Obstructive Sleep Apnea

COPD exacerbation—> BiPAP

Obstructive Sleep Apnea—> CPAP


What is the goal for O2 sat in a COPD exacerbation patient?


*if higher, you will inhibit their respiratory drive (based on low oxygen, not high CO2 like normal people since they have chronic CO2 retention and are desensitized to it)-> hypoventilation (slows or stops their breathing)


Patient is treated for COPD exacerbation. Treatment includes noninvasive ventilation (BiPAP), which is stopped. Patient has improved respiratory symptoms, but now has altered mental status. O2 sat is 96%, vitals normal. Next step?

Get an ABG (arterial blood gas analysis) to confirm acute hypercapnic respiratory failure

-remember our O2 sat goal in COPD’ers is 88-92% due to their respiratory drive being controlled by low O2 (vs. high CO2)...giving too much O2 will stop their respiratory drive to breathe
-also, too much O2 may encourage hypercapnia (CO2 retention) and worsened VQ mismatch (in COPD you have vasoconstriction in lungs to shunt blood to better oxygenated areas...if you flood in the oxygen, there will be areas that vasodilate thinking the oxygenation is good now, so blood will be sent to this damaged tissue but can’t gas exchange well so the CO2 just builds up more)
-hypercapnia (CO2 retention)-> delirium, confusion, lethargy, eventually coma and seizures


Increased or decreased lung compliance in COPD?

Increased lung compliance (more stretchy lungs)

*remember COPD is obstructive= hard to get air out. The lungs are filling well, but not pushing air out well.


Patient with PMH of HTN, CAD (recent CABG), recent hospitalization for PNA, and 35 pack-year smoking hx presents with SOB. Has decreased breath sounds at both lung bases, crackles, and wheezing. ABG shows high pH, low O2, low CO2. Diagnosis?

CHF exacerbation

-Given his hx of CAD and smoking, be thinking of COPD or CHF exacerbation
-High pH, low O2, low CO2= respiratory alkalosis (hyperventilating/ blowing off more CO2)
-NOT COPD exacerbation (that would have CO2 retention)
-NOT PE (this may have a unilateral, not bilateral pleural effusion and would have more history like recent travel or surgery, tachycardia)
-CHFe makes sense—bilateral pleural effusions (dec breath sounds), crackles from backing up of fluid from left heart to lungs. Pumping problem, so patient hyperventilates to compensate and get more oxygen in


Why might a patient with shallow/ restricted breathing have low O2, high CO2 (respiratory acidosis)?

Not expanding lungs well-> air not reaching as many alveoli for gas exchange-> low O2 into blood, high CO2 in blood bc cannot get out


Can you hear an S4 in a patient with a prior MI?

Yes, sometimes

Think of S4 as “stiff heart”
Can be due to diastolic dysfunction/ filling problem/ hypertrophy/ thick LV wall OR scar tissue making the heart stiff


Reg ventilator settings, FiO2 should usually be less than what?

FiO2 <60%

*for comparison, normal air has roughly 20% oxygen content in it
*don’t go higher than FiO2 of 60% long-term or else you risk oxygen toxicity to the patient (pro inflammatory oxygen free radicals-> atelectasis/ collapsing of alveoli)


High or low Tv (tidal volume) and PEEP (positive end-expiratory pressure) in a patient with ARDS?

High PEEP (prevent alveolar collapse)

Low Tv (Tv= the air going into the lungs. You don’t want to shove too much air into the lungs at once or you cause alveoli to pop open and slam shut. Goal is to have LOW trauma to alveoli)


What is the ‘rule’ for how high to make tidal volume (Tv) on a ventilator?

6 mL per kg

Ex: patient weighs 50kg. Make Tv 6*50= 300 mL

**Tv= the air going into the lungs. The reason you don’t want it too high is to avoid trauma to alveoli. If you shove too much air into the lungs at once or you cause alveoli to pop open and slam shut.


Do you always see a low RR in obesity hypoventilation syndrome?

No, not necessarily (RR can be within normal range)

Obesity-> fat restricts lungs from expanding well-> not as much air reaches alveoli for gas exchange (more dead space)-> CO2 retention= respiratory acidosis due to ‘hypoventilation’


What would chloride and bicarb levels look like in a patient with obesity hypoventilation syndrome (OHS) and obstructive sleep apnea (OSA)?

Chronic CO2 retainers (impaired gas exchange)-> high CO2 (respiratory acidosis)-> body compensates by increasing HCO3/ bicarb retention...
So, INCREASED bicarb and DECREASED chloride (for every negatively charged bicarb you keep, you get rid of a negatively charged Chloride)


Are transudative pleural effusions usually unilateral or bilateral?


Transudative= due to high hydrostatic pressure or low oncotic pressure driving fluid out (no other inflammatory cells in the effusion)
-CHF, nephrotic syndrome, cirrhosis
-these things don’t just target one side like a pneumonia does, so you’d expect if there’s a pleural effusion from it, it is bilateral


What is a hepatic hydrothorax?

Right-sided pleural effusion in cirrhosis patient (ruled out other causes)

*Pathophys is incompletely understood, but is thought to happen from ascites crossing the diaphragm (travels from the peritoneal cavity into the pleural cavity through small diaphragmatic defects)
-increased permeability of right hemidiaphragm


If pleural effusion fluid has glucose <60, consider what cause?

Rheumatoid arthritis (RA can rarely lead to inflammation affecting the lungs= pleuritis/ pleurisy, and that inflammation can cause effusion)

*StepUpToMed page 82, 2nd quick hit box
*But when glucose is low, still consider other causes of pleural effusion (complicated parapneumonic effusion, empyema, malignant effusion, TB pleurisy, lupus pleuritis, esophageal rupture)! (Just put this in the differential)


Patient with CHF and cirrhosis has SOB and dullness to percussion at right lung base. CXR shows right sided pleural effusion. Thoracentesis shows pleural fluid has glucose of 30 and LDH of 250. Cause?

Pneumonia (this is a parapneumonic effusion, or pleural effusion 2/2 PNA)
-Specifically, it’s likely an empyema (low glucose due to high metabolic activity of WBCs and bacteria in the pleural fluid)

-LDH of fluid= 250, which is >2/3rds upper limit of normal serum LDH (45-90), so EXUDATIVE
-NOT a pleural effusion due to CHF (high hydrostatic pressure) or cirrhosis (low albumin= low oncotic pressure) bc these are transudative (plus would expect them to cause bilateral, not unilateral, pleural effusions—these disease processes don’t isolate to one side) *hepatic hydrothorax (right-sided pleural effusion in cirrhosis patients from ascites crossing diaphragm is also usually transudative)


Think of what causes if a pleural effusion has elevated amylase?

Pleural effusion due to pancreatitis, esophageal rupture, or malignancy


Inflammatory conditions can cause pleural effusions by increasing what?

Pleural membrane and capillary permeability


Patient has epigastric pain radiating to back associated with nausea/ vomiting. Elevated alk phos, ALT (>150), AST, lipase, WBCs. RUQ U/s shows gallstones w/o gallbladder wall thickening. She is given supportive care (pain control, IV fluids), NPO. Enzymes trend down over a couple days. Next step?


-This patient has acute pancreatitis from a gallstone (*ALT>150 is pretty specific for it—plus patient has high lipase, AST, alk phos)
-Early cholecystectomy is recommended in stable patients who receiver from acute pancreatitis
*ERCP would have been the answer (to remove obstructing stone) if we saw common bile duct dilation/ obstruction on U/S (gallstone pancreatitis), or if liver enzymes keep rising

**Note: My surgery patient had choledocolithiasis (stone lodge in common bile duct) so we did—
1. RUQ U/S
2. MRCP (MRI of the biliary tract to prove it)
3. ERCP (to remove the stone blocking the common bile duct)
4. Wait for the pancreas to cool down/ labs to downtrend (bc inflammation complicates surgery)
5. Cholecystectomy (take out the gallbladder to avoid this happening again)


Patient with cirrhosis has worsening renal function during his hospital stay. Cr and urine output are both down-trending. U/A shows minimal hematuria, no casts. Renal U/S shows no hydronephrosis. Renal function is not improving with IV fluids. Diagnosis?

Hepatorenal syndrome

-Kidney function is declining in the setting of cirrhosis
-You know it’s not just AKI because: no casts (not ATN/ intrinsic), no hydronephrosis/ obstruction (not post-renal), no improvement with fluids (not pre-renal)

*treat with stopping alcohol, liver transplant if possible (if not, can try splanchnic vasoconstrictors like Octreotide, NE, Midodrine or albumin or dialysis, but may not help too much)


“Splanchnic arterial dilation” should make you think what?

Hepatorenal syndrome


Patient has foul smelling stools and weight loss over the last 6 mo. Has iron def anemia. Immunoglobulin A anti-tissue transglutaminase antibody is negative. Small-bowel biopsy shows villous atrophy. Diagnosis?

Celiac disease

-IgA anti-tissue transglutaminase and IgA anti-endomysial antibodies are screening tests, but can be negative in a person with celiac dz + IgA deficiency (if negative but clinical suspicion is high, order total IgA to check for IgA def or do IgG-based serologic testing)
-Biopsy showing villous atrophy is the confirmatory test
*associated with iron def anemia (not absorbing enough iron from the food they eat)


Low Hb and low ferritin. What type of anemia?

Fe deficiency

*Ferritin= Fe in storage site (this will be the first thing depleted in iron deficiency anemia)


Guy with cirrhosis comes in with bloating. There is shifting dullness and fluid wave. Diagnostic parade tests shows stay-colored fluid. In addition to abstinence from alcohol, what treatment do you recommend?

Low-sodium diet (restricting Na+= less water will follow) and diuretics, specifically Furosemide (Lasix) + Spironolactone (loop and K+ sparing)

*you always do diagnostic paracentesis, but only do regular therapeutic paracentesis if the patient is having symptoms from the ascites (SOB, tense, early satiety)


A patient has ascites. You do diagnostic paracentesis. If the ascites is due to portal HTN (from cirrhosis), what would you expect in the ascites fluid?

-yellow or straw-colored
-low total protein in it (<2.5 g/dL)
-high SAAG (serum-ascites albumin gradient) (>1.1)

*if SAAG <1.1 ascites is likely due to another cause (CHF, CKD, massive fluid overload, TB peritonitis, malignancy, hypoalbuminemia, hepatorenal syndrome)
*get cell count and differential—if neutrophils >250, spontaneous bacterial peritonitis (SBP)


How can you determine the cause of ascites based on SAAG (serum ascites albumin gradient) (from doing diagnostic paracentesis)?

SAAG >1.1 means portal HTN (due to cirrhosis)

SAAG <1.1 means the ascites is due to another cause (CHF, CKD, massive fluid overload, TB peritonitis, malignancy, hypoalbuminemia, hepatorenal syndrome)


Patient is positive for Anti-HBs and Anti-HBc. What does this mean?

Recovered from a past Hep B infection

*remember “SpECiES”
HBsAg: 1st marker of infection
HBeAg: marker of infectivity
Anti-HBc: core antibody
Anti-HBe: e antibody
Anti-HBs: surface antibody (indicates vaccination if alone, recovery if with anti-HBc)


If you suspect acute cholecystitis and RUQ U/S is inconclusive, what should you do?

HIDA scan


Lady with PMH of HTN (recently put on hydrochlorothiazide and amlodipine) has epigastric pain radiating to the back associated with N/V. RUQ U/S shows no gallstones or duct dilation. She doesn’t drink alcohol. TAGs are normal. Next step?

Discontinue hydrochlorothiazide

*Most common causes of pancreatitis=
1. Gallstones
2. Alcohol abuse
3. Triglycerides >1,000
-Once you rule out these 3 causes, consider less common causes including drug-induced pancreatitis. Loop and Thiazide diuretics can cause pancreatitis as a side effect.


Lady has thyroid nodule. Calcitonin is elevated. Ultrasound-guided biopsy shows malignant cells. Next step to work-up this patient?

DO A PLASMA METANEPHRINE ASSAY (may also do RET mutation testing)

Thyroid nodule w/ malignant cells and high calcitonin= Medullary Carcinoma of the thyroid. This is associated with MEN II (2a and 2b have Medullary Carcinoma + Pheochromocytoma. 2a also has parathyroid cancer. 2b also has acoustic neuromas/ marfanoid habitus). So you need to screen for Pheochromocytoma!

*this is important bc a pheochromocytoma can be asymptomatic at the time of diagnosis, but cause life-threatening HTN crisis during surgical procedures (thyroidectomy) if not caught and respected!


Lady had diarrhea after a picnic that resolved. Now presents with ptosis, diplopia, weakness with upward gaze, loss of deep tendon reflexes, and dysmetria (lack of coordination) with heel-to-shin testing bilaterally. Diagnosis?

Guillain-Barre syndrome
Specifically, the sub-type Miller Fisher syndrome (abnormal muscle coordination, absent tendon reflexes, and paralysis of eye muscles)


40 year old guy has tinea corporis, with widespread fungal “ringworm” rash. You’ll give him oral fluconazole to treat, but what other screening should you offer?

HIV screening

Tinea corporis with extensive skin involvement raises the question of whether the patient is immunocompromised


Old guy with recent MI two months ago (on ASA, Clopidogrel (Plavix), Metoprolol, Lisinopril, and Atorvostatin) presents with SOB. Has crackles in lower lung fields and systolic murmur over cardiac apex. Deep Q waves in leads I, aVL, V2-V5. Most likely cause?

Ventricular aneurysm

*Months post-MI there are 3 complications to remember:
1. Aneurysm (scar tissue outpouches bc it is weaker than the myocardium)
2. Mural thrombus (clotting within the wall-> blood clot thrown elsewhere)
3. Dressler syndrome (autoantibodies against the pericardium)


Concentric vs. Eccentric LV hypertrophy?

-LV hypertrophy (thickened LV)
-myocardial contractile fibers are in parallel (stacked up)

-LV dilation/ dilated cardiomyopathy (stretched out LV)
-myocardial contractile fibers are in series (stacked out)


What defines typical angina/ chest pain?

1. Substernal
2. Provoked by exercise or emotional stress
3. Relieved by rest or nitroglycerin

*3/3= typical/ classic angina
*2/3= atypical
*<2= non-anginal


Old guy has substernal chest discomfort when walking, better with rest. Echo shows normal EF, mild LA dilation. Aortic valve is calcified with aortic valve area of 1.6 cm^2. What condition is most likely responsible for his symptoms?

Coronary artery disease (CAD)

-he has typical angina symptoms (substernal, with exercise, better with rest)

*Although he also has aortic stenosis and this too can be a cause of angina, it’s unlikely to be the cause unless it’s severe aortic stenosis (valve area <1 cm^2). Since his aortic valve is 1.3 cm^2 and the angina is mild-moderate, its most likely CAD causing it.


20 year old guy is having a resting tremor, muscle rigidity, clumsy gait, slurred speech recently. He also has hepatomegaly, high total bili, alk phos, ALT, and AST. Liver biopsy shows inflammation, portal fibrosis, hepatocyte necrosis, macrovesicular steatosis, vacuolated hepatocellular nuclei, and Mallory bodies. Diagnosis?

Wilson disease

AR mutation in copper transporting channel-> accumulation of copper in liver, eyes (Kayser-Flesher corneal deposits), and brain (psychosis, Parkinson’s and behavior symptoms)
*diagnose with decreased serum ceruloplasmin (copper transporter) and increased urinary copper


Guy who’s been binge drinking and using cocaine comes in for weakness. His thighs and calves are swollen and tender, strength decreased. What complication is he at risk for over the next couple days in the hospital?

AKI secondary to rhabdomyolysis

-binge drinking and cocaine-> acute alcohol myopathy esp in lower extremities= drug-induced rhabdo-> myoglobin gets released into blood-> can block renal tubules-> AKI


What does tumor lysis syndrome do to the following electrolytes?
-uric acid

-uric acid: INCREASED (nucleic acids are released and metabolized to uric acid)

-potassium (K+): INCREASED (released from lysed cells)

-phosphate (P): INCREASED (released from lysed cells)

-calcium (Ca2+): DECREASED (the extra phosphate binds it up-> decreased free calcium levels in the blood)


What is type 2 heparin induced thrombocytopenia (HIT)?

A bad reaction to heparin where the heparin binds to PF4 (platelet factor 4) and then antibodies get made against that complex (hep-PF4). The antibodies attack platelets-> thrombocytopenia and cause platelets to stick/ aggregate (leading to paradoxical blood clots/ thrombosis).

*usually happens in 5-10 days post-heparin administration, stop heparin and give another anticoagulant (Argatroban, Fondaparinux)!

**type 1 HIT is milder (nonimmuned-mediated platelet aggregation) and doesn’t require treatment


35 year old lady has dry cough. CXR shows bilateral hilar lymphadenopathy. Diagnosis?


(Chronic non-caseating granulomatous inflammation)


Man with hyperlipidemia (on Simvastatin) and gout (on Colchicine) presents with muscle pain/ weakness and dark urine. Labs show elevated K+, BUN, Cr. U/A shows blood. What should you order to establish the diagnosis?

Creatinine phospholipase (CPK)
(Marker of skeletal muscle damage)

-Sounds like Rhabdo! Statin + Colchicine-> drug-induced rhabdomyolysis (both are myotoxins and muscle breakdown is more likely in combination)
-Dark Urine, blood on U/A w/o RBCs on urine microscopy (myoglobinuira), high BUN and Cr all point to AKI 2/2 rhabdo


How do you treat a mild tinea corporis infection (ringworm)?

Topical terbinafine or azoles (like Miconazole)


Lady has been having fever and malaise for 2 weeks. Has systolic murmur at cardiac apex. Today she presents with sudden-onset right-sided flank pain. CT abdomen shows wedge infarct. What’s going on?

Renal infarction due to embolization of valvular vegetation

(Fever, mitral regurg point to infective endocarditis. A vegetation embolized/ got thrown to infarct the kidney- an ‘MI’ of the kidney causing sudden pain and wedge on CT)


ARDS patient is intubated and ventilated with high PEEP, low FiO2. He begins to deteriorate, vital signs because unstable and breath sounds absent on one side. Most likely reason for this?

-This is a complication of PEEP

*Remember, in ARDS inflammation and edema-> alveolar collapse. PEEP maintains airway pressure at the end of expiration to prevent alveolar collapse. But, since the lung tissue is already weak and predisposed to barotrauma, PEEP can rupture alveoli-> leakage of air to pleural space-> pneumothorax (sudden-onset SOB, hypotension, tachy, tracheal deviation, unilateral absence of breath sounds).


What is the FeNa (fraction of excreted sodium) and BUN/Cr ratio in pre-renal AKI?

FeNa <1% (normal- the kidneys reabsorb most Na+)

BUN/Cr >20:1 (high- blood flow to the kidneys is slowed, so there is more time for Na+ to get reabsorbed at the PCT)


Patient has meningococcal meningitis and wants to leave the hospital AMA. The patient understands the risks and is mentally normal. What do you do?

Hospitalize and isolate the patient against his wishes

You cannot let a patient leave AMA when the patient is a risk to public health! This is highly contagious and serious.


Patient is treated for severe asthma exacerbation. He has diminished breath sounds and faint wheezing. ABG shows pH 7.3, PaO2 65, PaCO2 50. Next step?

Endotracheal intubation

This patient has signs of impending respiratory failure (need to intubate to maintain adequate oxygenation and ventilation)
-Diminished breath sounds/ wheezing
-Respiratory acidosis (low pH, high CO2)
*Note that a normal response to an asthma exacerbation is hyperventilation (blow off more CO2)-> decreased CO2. So, CO2 retention is a bad sign that they’re not maintaining their airway well!
-Low PaO2/ hypoxia


What does lymphocyte pleocytosis mean?

Increase in cell count, so more lymphocytes/ WBCs (lymphocytosis)


CSF findings in bacterial vs viral vs fungal meningitis?

Bacterial- neutrophils + decreased CSF glucose

Viral- lymphocytes + normal CSF glucose (elevated protein)

Fungal- lymphocytes + decreased CSF glucose


Patient has herpes simplex viral meningitis and is treated with high-dose IV acyclovir. His neurologic status improves, but 2 days later he develops AKI (rise in BUN, Cr). Most likely cause?

IV Acyclovir-> Crystalline Nnephropathy (type of intrinsic AKI where crystals obstruct renal tubules)

*note: this is NOT the same as acute interstitial nephritis—drug (NSAID, Penicillin, diuretic)—> fever, rash, and dec urine output


Guy with drinking history (no other med hx) presents with altered mental status. Labs show low bicarb (10), normal Na (140), normal Cl (100), high BUN and Cr. ABG shows low pH (7.2), low PaCO2 (30). U/A shows rectangular, envelope-showed crystals. Diagnosis?

Ethylene glycol poisoning

-low pH, low bicarb, low PaCO2 means metabolic acidosis
-calculate anion gap: AG= Na-Cl-HCO3= 140-100-10= 30. This is >12, so anion-gap met acidosis
-keep in mind “MUDPILES”: Methanol, Uremia, DKA, Porpylene glycol, Iron tablets or INH, Lactic acidosis, Ethylene glycol, Salicylates
-Ethylene glycol blocks alcohol dehydrogenase (competitive inhibitor)-> build up of toxic metabolites-> Ca2+ oxalate kidney stones (envelope-shaped) an AG met acidosis


What are your “MUDPILES”—causes of anion gap metabolic acidosis?

Porpylene glycol
Iron tablets or INH
Lactic acidosis
Ethylene glycol


Equation for calculating anion gap?

AG= Na-Cl-HCO3

(Sodium minus chloride minus bicarb)


1st line medication for Restless Leg Syndrome?

Dopamine agonists (Pramipexole)

*Also check for iron deficiency anemia and treat that with Fe supplementation
*Alpha-2-delta calcium channel ligand (gapapentin) may also help


Guy with BPH comes in due to more difficulty urinating over the last day. The last 2 days he’s been taking diphenhydramine for cough, otherwise no changes in medical hx. Cause?

Diphenhydramine (1st gen anti-histamine)-> anticholinergic side effects, including urinary retention from detrusor hypOcontractility

*BPH wouldn’t cause urination to go downhill more so in just one day


Middle aged woman has abdominal pain (esp over RLQ) and non-bloody diarrhea for 4 months. Lost some weight. Has oral ulcers. Hb is low, WBCs and ESR high. Diagnosis?

Crohn’s disease

-Inflammatory markers are suggestive of inflammatory bowel dz rather than celiac or IBS
-Crohn’s inflames anywhere along GI tract from mouth (mouth ulcers) to anus (*vs UC affects only distal GI tract-> LLQ pain, bloody diarrhea)
-IBD associated with iron def anemia (malabsorption of iron)


30 year old woman had an episode of hand numbness 5 months ago. Now presents with bilateral shooting facial pain triggered by the cold, brushing her teeth, chewing, or touching her cheeks. NSAIDs do not help. What condition does she have?

Trigeminal neuralgia most likely due to MS (multiple sclerosis), one of the few conditions that causes BILATERAL trigeminal neuralgia (due to demyelinating of the trigeminal nerve axon/ root)

*hand numbness was probably her first MS symptom


Always start with what to rule out brain bleeds?


(No contrast bc contrast appears white and so does blood)


Guy falls to the ground and has a seizure leaving a bar. He’s confused, but fully responsive. You order a CBC, serum electrolytes, echo, cervical spine imagine, and urine tox screen. Now what?


CT of brain w/o contrast is the initial imaging choice to r/o acute neuro problems (intracranial or subarachnoid bleeds). Note that MRI is more sensitive than CT is identifying structural causes of epilepsy but takes longer, so this is the choice if non-emergent.
*EEG is a good test for helping to decide course of antiepileptic agents, but ruling out brain bleeds is the 1st imaging step!


Most common cause of peripheral neuropathy?

Diabetes mellitus!

*don’t jump straight to rare junk like Charcot-Marie-Tooth disease


60 year old man with T2DM and PMH of diabetic retinopathy presents for evaluation of recurrent falls. He sways when standing with eyes closed, has bilateral hammer toe deformities, decreased proprioception and vibration sense in his feet, and absent ankle reflexes. Diagnosis (be specific)?

Large fiber neuropathy secondary to DM

*small fiber neuropathy-> positive symptoms such as pain, paresthesias, allodynia (pain out of proportion like light touching of the skin makes you scream out in pain)
-pain and temp
-burning and stabbing pain

*large fiber neuropathy-> negative symptoms such as numbness, loss of proprioception/ vibration, diminished reflexes (this guys’ symptoms fit this picture)
-pressure/ proprioception/ balance
-numbness and poor balance


Old lady presents with productive cough and low-grade fever, crackles over lung base. She’s been getting a lot of upper respiratory infections lately. ROS is significant for weakness and right-sided chest pain. Labs show low Hb, high WBCs. CXR shows consolidation in lower lung and osteo lytic lesions with fractures in ribs. Diagnosis?

Multiple myeloma

malignancy of plasma cells
-cytokines activate osteoClasts-> lytic lesions
-inc serum protein (M spike)
-inc infection risk (monoclonal antibody lacks antigenic diversity)
-Rouleaux formation of RBCs
-primary amyloidosis from light chains depositing in tissue
-proteinuria (Bence Jones proteins)-> kidney failure
-normocytic anemia (bone marrow replaced by plasma cells + renal failure so dec EPO to drive production of RBCs)


Treatment for cluster headaches (severe unilateral periorbital pain sometimes with autonomic symptoms)?

Oxygen facemask or Sumatriptan


Cancer patient with Mets to vertebrae is having uncontrolled pain. Right now is only on ibuprofen 3-4x/ day for pain. What med should you prescribe at this time for pain management?

Short-acting opioid (morphine, hydromorphone)

*If the pain is still bad, you can add a long-acting opioid (morphine, fentanyl) for help with sleep, but he’s never been on opiods before so do not start him right away on long-acting due to risk of respiratory depression! Start with short-acting to determine appropriate dosing for the patient.


Old guy comes in due to urinary frequency waking him up throughout the night. Has no burning when peeing. Has diffusely enlarged, smooth prostate on digital rectal exam. Next step?

Get a urinalysis (U/A)

-Seems he has BPH, but all patients with urinary symptoms (frequency, nocturia, hesitancy) should get a U/A to check for hematuria and infection.
*Also get a PSA as prostate cancer screening unless predicted life expectancy is <10 yrs.


What is osteopenia?

Bone loss/ weakened bones


Guy with PMH of Crohn’s disease s/p small bowel resection (on Mesalamine and Infliximab) presents with generalized bone pain. Radiographs show osteopenia of the spine w/ pseudo fractures in femoral necks. Diagnosis? Effect on serum calcium, phosphate, PTH?

Osteomalacia (vit D deficiency)

-Crohn’s disease-> inflammation esp at terminal ileum-> impaired reabsorption of bile acids-> malabsorption of fats and fat-soluble vitamins, including vit D-> DECREASED calcium + P, INCREASED PTH (to try to compensate)


Lady who abuses heroin daily presents with arm swelling w/ needle marks. She is treated with clindamycin. The next day she feels awful with congestion, myalgia, nausea/ vomiting, loose stools. WBC count is low. Next step?

This is opioid withdrawal (she is off her heroin and has symptoms within ~12 hrs of last use)

-N/V, cramps, diarrhea (opposite of constipation from opioids), restlessness, rhinorrhea, lacrimation, myalgia, arthralgia, HTN, tachy, mydriasis (dilated pupils), hyperactive bowel sounds

Give OPIOID WITHDRAWAL MEDS: Methadone (done timer) or Buprenorphine (blueprint)
*long half-life


From Sketchy, what drug is used for acute opioid toxicity? What 2 used for opioid withdrawal?

Opioid toxicity—> Naloxone (no lax zone)

Opioid withdrawal—> Methadone (done timer) or Buprenorphine (blueprint)
*long half-life


HIV patients with CD4 <100 should be on what med for Toxoplasmsis prophylaxis?

HIV patients with CD4 <200 should be on what med for PCP (pneumocystis pneumonia) prophylaxis?

Bactrim (TMP-SMX, trimethoprim-sulfamethoxazole)

*Bactrim reduces the risk of toxo in CD4<100 so that getting toxoplasmosis is only 0-2%! Bactrim also reduces the risk of PCP PNA in CD4 <200.


Triple therapy for H Pylori?

PPI + Amoxicillin (Metronidazole if allergic) + Clarithromycin


Alcoholic has epigastric pain radiating to the back. He is given opioids for pain + IV fluids. On day 2 of hospitalization his BP drops to 80/60, HR tachy at 120. He is satting at 92% on 2L O2 nasal canula and has crackles. BUN, Cr aare high, urine output is low. Diagnosis?

Acute severe pancreatitis

-premature release of pancreatic enzymes-> inflammation and increased vascular permeability around the pancreas-> widespread vasodilation-> septic shock with multisystem organ dysfunction (respiratory and renal failure)

*old people >75, alcoholics, obese, CRP>150 at 48 hrs, and inc BUN/CR in 48 hrs at higher risk for this (most other patients with acute pancreatitis have mild dz and recover in 3-5 days with fluids/ conservative treatment)


Patient presents with urinary frequency, fever of 102, nausea. Costovertebral angle tenderness. WBC count. U/A shows nitrate, WBCs, bacteria in urine. Diagnosis?

Pyelonephritis (kidney infection)

-presents as cystitis (bladder infection/ UTI symptoms) + flank pain, costovertabral angle tenderness, fever, and/or nausea/ vomiting

*get urine culture and treat empirically with antibiotics that cover gram-neg organisms (ex: Fluoroquinolones)


You have a patient with pyelonephritis. When is a CT of the abdomen/ pelvis indicated?

-Patient does not clinically improve within 72 hours (3 days)

-Has history of nephrolithiasis (kidney stones)

-Has complicated pyelonephritis (progression to renal abscess, emphysematous pyelonephritis where there’s gas accumulation in the tissues, papillary necrosis, or sepsis)

-Has unusual urinary findings (gross hematuria, suspicion for urinary obstruction)


Patient with Hodgkin lymphoma on chemo (last dose 3 days ago) presents with crampy abdominal pain and vomiting. Labs show mild anemia and thrombocytopenia. What can you do for this paitent?

Give Ondansatron (serotonin 5HT receptor antagonist/ anti-emetic)

*mild anemia and thrombocytopenia is normal for a patient with a lymphoproliferative disorder on chemo—she’s just having N/V from chemo


Old guy with PMH of HTN, DM, hyperlipidemia, PVD, and recent MI has sudden, painless loss of vision in the right eye. Hours ago, he had similar loss of vision in the same eye but only for 5 min. On exam, he has retinal whitening and a carotid bruit. Diagnosis and next step?

Retinal artery occlusion (from embolism)

Treat with high-flow oxygen and ocular massage

*he has all the risk factors for retinal artery occlusion
*note: episode of vision loss for 5 min is “amaurosis fugax” (like TIA of retinal artery) and then persisting loss of vision is retinal artery occlusion (like stroke of retinal artery)


Middle aged woman with PMH of RA (on Methotrexate) has unilateral knee pain with edema and fever/ chills. Treatment?


This is septic arthritis
Do synovial fluid analysis to confirm diagnosis (and blood cultures)
Gram (+)—> Vanco
Gram (-)—> 3rd gen cephalosporin


Alcoholic stumbles into the ED with muscle cramps and perioral numbness. He is found to have hypOcalcemia. Labs also significant for: low Hb, high MCV, low Mg, low Phosphorus. Most likely cause of his hypOcalcemia?


Low Mg (common in alcoholics)—> decreases PTH secretion and decreases responsiveness to it—> Low calcium (bc PTH increases calcium and you don’t have as much of it)
(**PTH also dumps Phosphorus, so you’d think with less PTH you’d get higher Phosphorus levels, but oddly Phosphorus levels are normal-low, possibly due to intracellular P depletion)


Woman with SLE (on Prednisone and Hydroxychloroquine) has pain in her right hip that is worse with weight bearing. She denies trauma to the hip. Range of motion is normal. X-ray of hip is normal. Next step?

Get an MRI of the hip

-This sounds like avascular necrosis (risk is increased with SLE and glucocorticoid use)
-MRI is more specific than X-ray (can visualize the boundary between normal and ischemic bone)
*note that in the first few months of having this, range of motion and x-rays may be normal but this will decline later on


What effect can Trimethoprim (in TMP-SMX aka Bactrim) have on potassium and creatinine levels?

Trimethorpim—> hyperkalemia (by blocking Na+ channel in CD) and artificial increase in Cr (w/o affecting GFR)


What is carotid endarterectomy?

A vascular surgical procedure done to reduce the risk of stroke by correcting stenosis in the internal carotid artery

-indicated in patients with TIA/ stroke with high-grade carotid stenosis (>70%)


Patient has right shoulder pain for 2 months. Cannot raise arms. Has decreased passive and active aBduction, flexion, and rotation of the right shoulder. Palpation does not cause pain. X-ray normal. Diagnosis?

Adhesive capsulitis aka “Frozen shoulder”
Thickened, tight shoulder (glenohumeral joint) capsule

-due to chronic inflammation, fibrosis, and contracture

-pain with aBduction, external rotation
-decreased passive and active range of motion


50 year old guy with T2DM comes in for follow-up lab work. His total cholesterol is normal, LDL normal, TAGs are elevated. What med should you start him on?

A statin

Give statins to any patient >40 years old with DM regardless of LDL level!
*Although a fibrate (like gemfibrozil) seems reasonable to reduce the elevated TAGs, statins are 1st line in ASCVD prevention (you would give a fibrate just to reduce TAGs in someone with TAGs>1000 at risk for acute pancreatitis)


Can Dermatomyositis be a paraneoplastic syndrome (seen in lung cancer)?



Heat stroke can be exertional or non-exertional. What does this mean?

Exertional- when heat stroke happens to patients who have over exerted themselves

Non-exertional- when heat stroke happens to patients with chronic medical conditions (have underlying impaired thermoregulation)

*HEAT STROKE: Too hot-> blood is shunted away from central organs and to skin to sweat and cool down body-> distributive shock, where organs lack adequate perfusion-> organs suffer and die
-SIGNS/ SYMPTOMS: temp >105, altered mental status, hypotension, tachycardia, tachypnea


Guy is going to die at your ED unless you give him a blood transfusion. His fiancé tells you at the scene he is Jehovah’s Witness, don’t give the transfusion. He doesn’t have a card on him/ advance directive/ living will that states this. What do you do?

Give the blood transfusion

In the absence of an advance directive, a life-saving blood transfusion can be given to a Jehovah’s Witness who lacks decision-making capacity


50 year old woman with hypothyroidism presents with itching and fatigue. She has hepatomegaly and bilateral xanthelasma and skin excoriations. Labs are notable for high total cholesterol, total bili, and alk phos. RUQ U/S is normal. Next step?

Check anti-mitochondrial antibodies

For Primary Biliary Cholangitis (autoimmune destruction of intrahepatic bile ducts)
*classically in middle-aged women and associated with other autoimmune conditions (hypothyroidism)


To treat Wernicke encephalopathy (encephalopathy + ocular dysfunction + gait ataxia) what do you give IN WHAT ORDER?

Give thiamine before glucose! Do NOT give glucose, then thiamine.
(Pixorize: don’t eat sugar before you work out your thighs)


Lady presents with fatigue, weight loss. Has splenomegaly. Has anemia and thrombocytosis. FISH shows abnormality in chromosome 22. What is the disease and treatment target?

Chronic myeloid leukemia (CML) t(9,22), BCR-ABL
*too many granulocytes in myeloid path, esp basophils

Treatment target= tyrosine kinase inhibitor (imatinib)


60 year old man presents with scrotal pain. Only sexually active with his wife. Has a tender mass in the left scrotum and erythema. Cremasteric reflex is intact and no discharge. Diagnosis and cause?

Acute epididymitis (swelling of the epididymis around the testicle), most likely due to E.coli (from bladder outlet obstruction)

*In age <35 it would be most likely due to chlamydia, gonorrhea from STD


Patient has elbow pain radiating to the forearm, worse with activity like after baggage handling work. Pain is reproduced by flexion of the wrist. Diagnosis?

Lateral epicondylitis= tennis elbow= swollen extensor tendon (where extensor muscles insert into lateral epicondyle of the humerus)

*remember from anatomy: Medial-> flexors. Lateral-> extensors.


40 year old guy with alcoholic history has epigastric pain, especially after meals. He has ascites and paracentesis shows serosanguinous fluid with high total protein, high amylase, low serum-ascites albumin gradient (SAAG <1.1). Most likely cause of his ascites?


-he has chronic pancreatitis (recurrent episodes)

-pancreatic ascites is a rare complication of pancreatitis! (Repeated inflammation damages pancreatic duct-> leakage of pancreatic juice into peritoneal space-> ascites)

-serosanguinous fluid= straw-colored ascites fluid (yellow w/ blood streaks)—pancreatic ascites is usually this color

-pancreatic ascites has high amylase (>1000), high total protein (>2.5), and low SAAG (<1.1 means NOT due to portal HTN from cirrhosis)


30 year old guy who recently traveled and had unprotected sex presents with RUQ pain and fever. Breath sounds are decreased on the right lung base, liver is palpable. Labs show WBC count, high alk phos, high ALT and ALT (in the 90’s). U/S of abdomen shows a hypoechoic lesion in the right liver lobe. Diagnosis?

Entamoeba histolytica
(A parasite, protozoan that causes liver abscess)

-RUQ pain, fever, hepatomegaly, transaminases (*but note that ALT, AST are not SUPER high in the hundreds or thousands as in viral hepatitis)
-recent travel and sex
-hypoechoic lesion= dark on U/S (less dense, fluid-filled, consistent with liver abscess)

*But why decreased right lung breath sounds?? Don’t get hung up in this—possibly due to a small right-sided pleural effusion due to the inflammation in the nearby liver


Lady has hyperthyroidism w/ a nodule in the left thyroid gland. Radioactive iodine scan shows uptake only in the nodule. If she gets pregnant, will baby get hyperthyroidism?


Remember the most common causes of hyperthyroid are:
1. Graves dz (TSI autoantibodies that stimulate TSH receptors)
2. Toxic adenoma
3. Toxic multi-nodular goiter
(Toxic adenoma and goiter caused by activating mutation in TSH receptor)

She has a single “hot nodule” (radioactive iodine uptake) suggestive of toxic adenoma. Baby won’t get this. *If Graves were the reason she had hyperthyroidism, then the autoantibodies would cross the placenta and baby would be affected.


If you don’t treat hyperthyroidism, what can happen to the bones?

Bone loss

-excess thyroid hormone increases osteoclast activity-> more bone resorption (breakdown)
(-> hypercalcemia-> dec PTH-> more urinating/ wasting of calcium)


How can atelectasis lead to pneumonia?

Atelectasis= deflated/ collapsed alveoli—> allows for formation of mucus plugs—> inc risk of infection (always a higher risk of infection when any tube is blocked- from Pathoma)

*spirometers help patients breathe deeper to avoid shallow breathing-> atelectasis-> possible PNA as a complication. So, spirometers are used in the hospital for prevention of atelectasis and indirect prevention of PNA.


Rib fracture can be deadly in the elderly because it can lead to pneumonia. Explain how a fractured rib can lead to pneumonia.

Rib fracture-> pain-> hypoventilation (hurts to take deep breaths, so patient takes shallow breaths)-> atelectasis (alveolar collapse)-> allows for formation of mucus plugs (and any time you block a tube you inc infection risk)-> pneumonia


40 year old lady comes in due to abnormal LFTs (AST is 450, ALT is 512). She has no symptoms. Family history is negative for liver disease and she does not drink. Most likely diagnosis?

Autoimmune hepatitis

-more common in women than men (esp consider if they have another autoimmune disorder)
-initial presentation varies—can involve abdominal pain, pruritus (itching), possibly cirrhosis (jaundice, ascites), but 25% are asymptomatic!

*positive serology (anti-smooth muscle antibody, anti-liver/ kidney microsomal type 1, antinuclear antibodies)
*may have high gamma gap (serum protein-serum albumin of >4) prob due to bad liver producing less albumin


Old man with past hospitalization for necrotizing pancreatitis due to alcohol use presents with loose, watery stools that are hard to flush and intermittent epigastric pain for 2 months. He also lost weight unintentionally. Most likely diagnosis?

Chronic pancreatitis
(Progressive inflammatory disease of the pancreas)

-epigastric pain (worse w/ meals and intermittent, but may become constant later on)
-steatorrhea (loose, fatty stools) (pancreas isn’t functioning well to release enzymes that will help break down fat)
-weight loss
-history of pancreatitis episode(s)

*treatment involves pancreatic enzyme replacement


What can you look for in the stool to aid in diagnosing chronic pancreatitis?

Low fecal ELASTASE

-this is an inactive enzyme (zymogen) that is released by the pancreas and normally activated by trypsin in the duodenum
-low levels= exocrine insufficiency


Explain how vitamin B12 gets digested/ absorbed (what things does it get bound to)?

1. In mouth, vit B12 is bound to amylase (salivary protein)

2. In stomach, the acid (pepsin) breaks up vit B12—amylase and vit B12 binds to R-binder

3. In duodenum, pancreatic proteases break up vit B12—R-binder and vit B12 binds to IF (intrinsic factor), which is made by parietal cells in the stomach

4. vit B12—IF gets absorbed in the ileum


25 year old with PMH of asthma presents with difficulty swallowing solids and liquids. He’s had heartburn lately (doesn’t respond to antacids), but this swallowing problem is new. He has a piece of steak stuck in his throat, and when given water to swallow, he vomits it right back up. Diagnosis?

Eosinophilic esophagitis-> food impaction (food stuck in the esophagus due to underlying problem)

*history of asthma and refractory heartburn makes eosinophilic esophagitis the most likely thing predisposing to food getting stuck


40 year old man has fatigue, abdominal pain, and bloody diarrhea. Two years ago, he has a colonoscopy w/ biopsy that showed pseudopolyps, mucosal ulcerations, and crypt abscesses. 5-ASA helped his symptoms then. But now he has LLQ tenderness. T. Bili and alk phos are elevated. ALT and AST are mildly elevated. Most likely diagnosis and next step?

Primary sclerosing cholangitis
(Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts)
*highly associated with UC (ulcerative colitis), which this guy has

Get a MRCP (magnetic resonance cholangiopancreatography, MRI of bile ducts)
-will show you the “bead on a string” appearance of bile ducts from “onion-skinning” fibrosis


35 year old lady with PMH of T1DM (not always compliant with insulin) presents with abdominal pain + confusion. The abdominal pain is worse in the RUQ and epigastrium and is associated with vomiting. She has fever, hypotension, tachycardia. Labs show leukocytosis, glucose of 400, low bicarb, high total and direct bili, mildly elevated ALT, and U/A shows glucose (no ketones) in urine. Diagnosis?

Acute (ascending) cholangitis

Charcot triad: (1) RUQ pain, (2) fever, (3) jaundice
Reynolds pentad: (4) hypotension/ shock, (5) altered mental status
*this patient has it all except jaundice is not noted (but bili is high and it jaundice may develop as this worsens)
*anion gap metabolic acidosis due to lactic acidosis from severe sepsis
**no ketones so no DKA. Her hyperglycemia is likely due to infection

Life-threatening emergency! Sepsis-> death happens fast. Give broad-spectrum antibiotics, aggressive IV fluids, and relief of common bile duct obstruction with ERCP or percutaneous drainage


How would acetaminophen toxicity present?

RUQ pain, nausea/ vomiting, elevated bilirubin, maybe anion gap metabolic acidosis, and SUPER high liver enzymes (AST, ALT in the thousands)


50 year old man complains of black stools and occasional epigastric abdominal discomfort. Food makes it better, it is worse at night. A right-sided carotid bruit is noted on exam. Fecal occult blood testing is positive. Most likely diagnosis?

Peptic ulcer disease (most likely due to H. Pylori)

-epigastric abd pain + melena (black stool from digested blood)
-food makes it better and worse at night when not eating, which suggests a duodenal ulcer (acid-neutralizing enzymes are released there)

*peptic ulcer dz is one of the most common causes of GI bleeds! Think of it and diagnose it with upper GI endoscopy

**he has a carotid bruit, suggesting atherosclerosis. This is a throw-off here


Crohn’s vs. UC—which is more likely to present with melana vs. hematochezia?

Crohn’s (affects anywhere in GI tract, skip lesions)- MELENA
(Upper GI tract bleeding-> digested blood= black stool)

UC (affects distal colon/ rectum)- HEMATOCHEZIA (lower GI tract bleeding-> bright red blood per rectum)


Is ischemic colitis more associated with hematochezia or melena?

Hematochezia (bright red blood per rectum)


“Hot nodule” (hyperthyroid symptoms with low TSH + single palpable nodule). Diagnosis?

Toxic adenoma of the thyroid

*not Graves, even though that’s the most common cause of hyperthyroidism—Graves affects the thyroid in a diffuse manner (TSI thyroid-stimulating antibodies stimulate the entire thyroid), so wouldn’t just be a single hot nodule


Nitrofurantoin (Macrobid) is a medication used for what?


(It is a bactericidal antibiotic)


HIV patient presents with all the signs and symptoms of TB and CXR shows a upper lobe cavitary lesion. But, his PPD test is negative. Can you rule out TB?


PPD test can be false negative in an immunocompromised patient! (Their immune system sucks, so does not mount the appropriate response to the injected antigen)


Lady presents with weight loss, irritability, insomnia, and palpitations. Exam shows lid retraction, dry skin, and hand tremor. Diagnosis?

Thyrotoxicosis/ hyperthyroidism

*lid retraction likely is referring to the protruding eyes seen in Graves dz, the most common cause of hyperthyroidism


WHY does hyperthyroidism/ thyrotoxicosis cause HTN?

Due to increased myocardial contractility

Thyroid hormone (T3) acts on cardiac myocytes-> increased cardiac output (more blood is getting pumped out, so more blood is in circulation= hyperdynamic circulation)-> so inc BP!


Old lady presents with constipation and abdominal pain. She also has urinary frequency and thirst. PMH includes a-fib (on Diltiazem and Rivaroxaban) and osteoporosis (refused medical treatment, taking vitamins and minerals instead). Mucous membranes are dry, no tenderness on palpation of abdomen. Normal urine dipstick. Diagnosis?

Milk-alkali syndrome
(Excessive intake of calcium/ inflammation absorbable alkali like calcium carbonate)
*she has osteoporosis, so makes sense she’d take calcium as the vitamin

-symptoms of hypercalcemia: abdominal pain, constipation, polydipsia (urinary frequency) (*too much calcium-> kidneys have to work harder to filter it. Causes renal vasoconstriction and dec GFR)

-Milk-alkali syndrome often presents as symptomatic hypercalcemia + metabolic alkalosis + AKI


You do a thyroid ultrasound to look at a high-risk thyroid nodule. When should you go onto doing a FNA (fine needle aspiration)?

If the nodule is >2 cm or >1 cm with high-risk U/S features

(microcalcifications, irregular margins, internal vascularity)


Man has right shoulder and arm pain after playing golf all day. His arm is weak, especially when lifting objects. On exam, he has decreased right biceps reflex with cervical paraspinal muscle spasm. His pain improves when he is asked to lift his right arm above his head and rest his hand on his head. Diagnosis?

Cervical radiculopathy (of C6 nerve root)

-caused by disc herniation-> compression of nerve root
(*could also be caused by spondylosis/ osteoarthritis of neck-> compression of nerve root, but this would be chronic not acute)

-acute right shoulder/ arm pain, biceps weakness, diminished biceps reflex with cervical muscle spasm

*shoulder aBduction w/ hand on head provides relief bc it takes tension off the impinged nerve root (diagnostic and therapeutic!)


Lady gets treated for TB. Two months later on follow-up exam her sputum is clear (no longer has acid-fast bacilli), but she has fatigue, malaise, nausea, tender hepatomegaly. T bili, ALT (350), AST (400) are elevated, viral hep panel is negative. Liver biopsy shows mononuclear infiltrates and hepatic cell necrosis. Diagnosis?

Hepatitis secondary to Isoniazid (causes liver injury that presents similarly to viral hep)


Patient with PMH of Crohn’s disease s/p intestinal surgery presents with worsening fatigue and painful paresthesia in her feet. Hb is 8 (low) and MCV is 98 (normal). Next step?

Serum vitamin B12 level (test for vitamin B12 deficiency)
**Methylmalonic acid and homocysteine if inconclusive

*Remember that vit B12 is reabsorbed at the terminal ileum (“iron fist bro”- iron at duodenum, folate/ B9 at jejunum, B12 at ileum) and Crohn’s disease affects the terminal ileum (and his surgery was likely removal of the ileum, which means no B12 reabsorption).

*Vit B12 is needed for DNA synthesis and myelin formation, so B12 deficiency-> macrocytic anemia + neuro demyelination (causing paresthesias).

**Why is his anemia normocytic? He prob has iron deficiency too (due to GI bleeding from Crohn’s). Vit B12 def (macrocytic) + Fe def (microcytic)= normocytic.


What neuro problems can vitamin B12 deficiency cause?

Subacute combined degeneration- demyelination of dorsal column (DC-ML)-> dec vibration and proprioception AND lateral corticospinal tracts (CST)-> spastic paresis, enhanced reflexes.
*Peripheral nerves often affected first-> lower extremity paresthesias.


60 year old man with MI complicated by cardiogenic shock is in the ICU. He now has acute renal failure and lower GI bleeding from anticoagulation therapy. He has no previous history of thyroid disease, but T3 is low (TSH and T4 are normal). Thyroid diagnosis?

Euthyroid sick syndrome (“low T3 syndrome”)

-Any patient with acute, severe illness may have abnormal thyroid function tests w/ low T3 (less conversion of T4-> T3 due to caloric deprivation, inflammation, and FFA’s/ meds that inhibit 5’-deiodinase)

*It is not recommended to test thyroid function in sick patients for this reason.


What lobe are Broca’s and Wernicke’s areas in?

Broca’s—> frontal lobe

Wernicke’s—> temporal lobe

*both on dominant side of brain (if right-handed, on right brain)


What lobe is Broca’s area in? A lesion here will cause what?

Broca’s is in the frontal lobe.

Nonfluent aphasia (can’t talk well, but can understand)


What lobe is Wernicke’s area in? A lesion here will cause what?

Wernicke’s is in the temporal lobe.

Fluent aphasia (can talk, but can’t understand—“Wernicke word salad,” words you say don’t make sense)


70 year old man with PMH of alcohol use disorder is brought in due to falls over the past 6 months. He is also forgetful to the point where his wife thinks he forgets to use the bathroom bc he urinates on himself. Mini-mental state exam score is low. Diagnosis?

Normal pressure hydrocephalus

“Wet, wobbly, and wacky”
-Urinary incontinence (urinating on self)
-Gait dysfunction (falls)
-Dementia (forgetful)

*It is a type of communicating hydrocephalus (decreased CSF absorption) in elderly-> more CSF in ventricles-> stretching of corona radiata (nerve fibers running along edge of ventricles)-> motor neurons are disrupted
(Normal pressure means the CSF opening pressure is normal)


What would CT of the brain show in a patient with normal pressure hydrocephalus?

Large ventricles (ventriculomegaly) with normal sulci

*It is a type of communicating hydrocephalus (decreased CSF absorption) in elderly-> too much CSF in ventricles (elevated central pressure, improvement with LP)-> stretching of corona radiata (nerve fibers running along edge of ventricles)-> motor neurons are disrupted
(Normal pressure means the CSF opening pressure is normal)


Management of a myasthenic crisis patient (severe respiratory weakness-> respiratory failure)?

1. Intubate to protect airway
2. Hold AChE inhibitors (Pyridostigmine) to reduce excess airway secretions and reduce aspiration risk
3. Give IV plasmapheresis (or IVIG) + corticosteroids


What kind of diarrhea does nocturnal diarrhea (diarrhea waking you up from your sleep) suggest?

Secretory diarrhea

*causes: chronic infection, microscopic colitis, bile salt diarrhea, hormone secreting tumor (gastrinoma, VIPoma)


Patient comes in with IBS symptoms (fluctuating diarrhea and constipation relieved with a bowel movement, worse with stress). Her diarrhea has become more persistent- she has 6 loose stools/ day and they frequently wake her up at night. Why should we do further testing on this patient?

This patient has alarm symptoms, specifically nocturnal diarrhea (this suggests secretory diarrhea, as it occurs during the night when fasting)

*IBS is a clinical diagnosis and involves limited work-up (CBC, serological for celiac dz, inflammatory markers) and reassurance. However, you need to do further testing on patients with alarm features: older age of onset (>50), GI bleeding, nocturnal diarrhea, worsening pain, unintended weight loss, concerning labs (Fe def anemia, elevated CRP), or family hx of IBD or colon CA.


Lady has an adrenal mass. She has dark hair growth on her face, acne, clitoromegaly, LMP was 12 wks ago. Will levels of testosterone and LH be high, low, or normal?

Adrenal mass with hirsutism (androgen excess)—> HIGH testosterone, LOW LH (due to negative feedback)


65 year old with PMH of T2DM (diagnosed 6 mo ago, diet controlled) presents with a progressive rash. It was initially painful, itchy red spots. Now it is crusty. ROS is positive for watery stools and weight loss. On exam, there are erythematous plaques with central clearing and eroded borders on the thigh. There are scattered papules with crusting over the lower abdomen. Labs significant for Hb of 10 and glucose of 175. Next step?

Order a glucagon level

-She likely has glucagonoma (DM, weight loss, watery diarrhea, rash)

-The rash is “necrolytic migratory erythema” (red blistering rash that spreads across the skin), seen in 70% of glucagonoma patients

*normocytic anemia likely due to anemia of chronic disease
**glucagon >500 confirms the diagnosis + CT abdomen will localize the tumor and check for metastasis


50 year old man who works for a new battery manufacturing plant comes in due to frequent stumbling and falls. He also has abdominal pain, constipation, recurrent headaches, and a “pins and needles sensation” in his palms and soles. His wife says he’s more forgetful lately. BP is 160/90, HR is 85. Neuro exams shows reduced pinprick sensation in the hands and feet bilaterally and a wide-based gait. Labs show Hb of 9, MCV of 65, Cr of 2, uric acid of 13 (high). Diagnosis?

Lead poisoning

-Microcytic anemia with basophilic stippling (lead toxicity blocks ALAD, an enzyme needed for heme synthesis)

-Hyperuricemia (due to impaired purine metabolism)

-Neuropsych manifestations (memory loss, sensorimotor neuropathy, headaches, ataxia)

-GI manifestations (abdominal pain, constipation)

-HTN and possible nephrotoxicity (elevated creatinine)

*remember that it causes anemia, GI and kidney disease + Kids (lead paint)-> mental deterioration. Adults (batteries, environmental exposure)-> headache, memory loss, demyelination.


Gross, painless hematuria. What 2 differential diagnoses should come to mind w/o any further information?

Gross, painless hematuria= BLADDER CANCER or KIDNEY CANCER (RCC) until proven otherwise!


Old man with PMH of non-small cell lung carcinoma s/p surgical resection comes in after having a seizure. MRI brain shows a solitary cortical mass at the right hemisphere grey-white matter junction. It is consistent with metastasis, but CT chest shows no evidence of recurrent malignancy. He is started on Phenytoin. Next step?

Surgical resection of brain mass

*Metastatic brain tumors= most common brain tumors, often seen at the grey-white matter junction (grey matter= neuron cell bodies, white matter= axons)
*Single brain metastasis-> surgery is the best choice if possible!
**Multiple brain metastasis-> whole brain radiation therapy (or supportive care, but then expectation is that the person will live <2 mo.)


Patient has a pleural effusion. Pleural fluid has LDH of 300. Serum LDH is 100. Is this transudative or exudative? Note that normal serum LDH is 45-90.


*Remember Light’s criteria based on Pleural: Serum ratios. Exudative if:
1. LDH >0.6
2. Protein >0.5
3. LDH > 2/3rds the upper limit of normal

P:S LDH is 300/100= 3 >0.5, so exudative (by the 2nd criteria)

Pleural LDH is 300, which is more than 2/3rds the upper limit of normal Serum LDH (upper limit of the normal serum LDH is 90...2/3rds of 90 is 60...300 >60), so exudative (by the 3rd criteria)


70kg patient on a ventilator has the following settings. Next best step?
RR of 18
Tidal Volume of 450
FiO2 of 40%
PEEP of 5
pH of 7.5
pCO2 of 22
pO2 of 120

Decrease the RR (18 is too high)

-His pH is 7.5 and CO2 is low= respiratory alkalosis (due to hyperventilation-> blowing off too much CO2)

Ventilation settings (CO2):
-Tidal Volume of 4-8 mL/kg is appropriate (may go lower for COPD or ARDS)
-RR of 10-12 breaths/ min is appropriate

Oxygenation settings (O2):
-Start with FiO2 of 100% and titrate down to <60% (you want the lowest FiO2 to maintain PaO2 of 50-60 or O2 sat of >90%)
-PEEP around 5 cm H2O is appropriate


Regarding ventilator settings, what are “rules” about appropriate settings? Give specific numbers on what we generally want to keep Tidal Volume, RR, FiO2, and PEEP at.

Ventilation settings (CO2):
-Tidal Volume of 4-8 mL/kg is appropriate (may go lower for COPD or ARDS)
-RR of 10-12 breaths/ min is appropriate

Oxygenation settings (O2):
-Start with FiO2 of 100% and titrate down to <60% (you want the lowest FiO2 to maintain PaO2 of 50-60 or O2 sat of >90%)
-PEEP around 5 cm H2O is appropriate


Generally, what do we want to keep Tidal Volume at for a patient on a ventilator?

4-8 mL/kg is appropriate (may go lower for COPD or ARDS)


Generally, what do we want to keep RR at for a patient on a ventilator?

10-12 breaths/ min is appropriate


Generally, what do we want to keep FiO2 at for a patient on a ventilator?

Start with FiO2 of 100% and titrate down to <60% (you want the lowest FiO2 to maintain PaO2 of 50-60 or O2 sat of >90%)


Generally, what do we want to keep PEEP at for a patient on a ventilator?

Around 5 cm H2O is appropriate

*PEEP keeps alveoli propped open, but too high of PEEP increases risk of barotrauma (injury to alveoli) and can lead to pneumothorax and decreased CO (inc intrathoracic pressure-> dec venous return)


20 year old obese woman has headaches for 6 wks that wake her from sleep. Fundoscopy shows papilledema. CT brain is normal. LP shows elevated opening pressure, otherwise CSF analysis is normal. Diagnosis and next step?

Idiopathic Intracranial Hypertension (IIH) aka Psuedotumor Cerebri

Give Acetazolamide

-High ICP (papilledema is a sign), high CSF opening pressure, otherwise normal neuro exam (may have CN6 palsy), CT, and CSF analysis
-Often seen in young, obese females
*We don’t use Mannitol- that’s used in inpatient setting for increased ICP due to cerebral edema (given IV and requires close monitoring for renal function and electrolytes)


What are the neoplasias/ findings in MEN 1, MEN 2a and MEN 2b?

MEN 1: “pans of pitted pears”
1. Pancreatic tumors
2. Pituitary tumors
3. Parathyroid tumors

MEN 2a:
1. Medullary thyroid CA
2. Pheochromocytoma
3. Parathyroid tumors

MEN 2b:
1. Medullary thyroid CA
2. Pheochromocytoma
3. Mucosal neuromas/ marfanoid habitus


Crazy patient insists on being seen right now for an urgent breast exam with only the male doctor in the room because it’s a “private matter.” She doesn’t have an appointment. What do you do?

Have the receptionist instruct the patient to schedule an appointment

(Stay professional, she has to make an appointment like everyone else, but don’t blow her off either...obviously you’ll have to tell her a chaperone is required at her appointment if a private exam is indicated)


Cavernous hemangioma (benign vascular tumor w/ dilated blood vessels) is associated with what disease?

Von Hippel-Lindau Disease


IV drug user presents with acute-onset right-sided weakness. She also has fever, HTN, tachycardia. MRI brain shows acute infarct of the left MCA. TEE shows an aortic valve vegetation with mild aortic regurg. You order blood cultures and start her on IV antibiotics for bacterial endocarditis. Should you continue current care with observation, start her on aspirin, or start her on IV heparin?

Continue current care with observation

IV antibiotics significantly reduce risk of septic cardioembolism (thrown vegetation-> stroke). Aspirin would only be indicated in ischemic stroke due to atherosclerotic thrombosis or embolism. Heparin is NEVER indicated in stroke due to risk of hemorrhagic stroke (and no proof it helps in the acute setting)/


What kind of drug is Amiloride?

K+ sparing diuretic

(“Almonds” in Sketchy)


IV drug user has bacterial endocarditis affecting the aortic valve. When would you consider aortic valve surgery?

If there is significant valvular dysfunction-> Heart Failure (or if infection persists/ septic embolization is recurrent)


30 year old comes in due to epigastric abdominal discomfort and 2 episodes of vomiting a little blood. The patient had an alcohol and cocaine party last night and took aspirin tablets this morning due to headache. Most likely cause of his hematemesis?

Gastritis (stomach inflammation) aka Acute erosive gastropathy (or gastric mucosal erosion)

-alcohol-> stomach mucosal injury
-cocaine-> vasoconstriction-> dec gastric blood flow to sweep away acid-> stomach mucosal injury
-aspirin blocks protective prostaglandins-> gastric mucosal injury

*NOT pancreatitis (this is usually associated with chronic alcohol abuse- not one binge drinking party and doesn’t include hematemesis)
*NOT esophageal varices (he is young, no signs of cirrhosis)
*NOT Mallory-Weiss esophageal tear (he hasn’t had multiple vomiting/ retching episodes)


Why are diabetic patients at increased risk for non-alcoholic fatty liver disease (NAFLD)? (May present as RUQ fullness, transaminitis.)

NAFLD is associated with insulin resistance!

Insulin resistance (body not responding to insulin)-> increased lipolysis (break down of fats for energy, since glucose is not getting into cells), more triglyceride synthesis, and hepatic uptake of fatty acids


23 year old with PMH of asthma comes into the ED with difficulty breathing “feels like an asthma attack.” She is non-compliant with her ICS (inhaled corticosteroid) but takes albuterol as needed. She was recently diagnosed with sinusitis and started antibiotics this morning. Her BP is 80/50, HR 120. Exam is significant for bilateral wheezing, prolonged expiration, and urticarial (hives) rash on trunk and arms, and arms are warm to touch. Next step?

Give intramuscular epi- this is anaphylaxis!

-likely caused by the antibiotic she started in the morning for sinusitis

*epi is a beta > alpha agonist, so causes bronchodilation (beta-2) and vasoconstriction to inc BP (alpha-1). The perfect drug for anaphylactic shock!


Explain what anaphylaxis is. Give details.

Severe, life-threatening allergic reaction. IgE-> mast cell degranulation-> MASSIVE histamine release-> systemic vasodilation-> hypotension-> poor organ perfusion. Also, causes edema (due to histamine + complement), which compromises the airway.

*Give epi (beta > alpha agonist) to cause bronchodilation (beta-2) and vasoconstriction to inc BP (alpha-1)
*Order: give IM epi (if airway compromise)-> antihistamines-> steroids


IV drug user presents with difficultly walking and “funny” sensations in his feet. He recently had a URI and is sexually active. He is afebrile, vitals are normal. On exam, he has reduced sensation and muscle strength bilaterally in the legs. He also has mild hyperreflexia and positive Babinski. What test do you need to order?

MRI of the spine

-He is presenting with signs and symptoms of spinal cord compression (bilateral in just lower extremities means you can localize to spinal cord. No UMNs below compression-> UMN signs).
-Since he’s an IV drug user, an epidural abscess (even w/o fever) is a concern.

**if you were thinking Guillain-Barre, you’d do an LP. But that wouldn’t cause UMN signs or sensory deficit. Bad idea to do LP when abscess is in the differential bc that can introduce more bacteria.


Patient with hx of anemia and dark brown urine (did not go to doctor for diagnosis) comes in for abdominal pain, vomiting, fatigue. He has fever, RUQ tenderness worse with deep inspiration, splenomegaly, and jaundice. Labs significant for high WBC count, low Hb, normal MCV, high MCHC, high reticulocytes, high total bili, and high LDH. Cause of anemia?

Hereditary spherocytosis

-Classic triad is: (1) hemolytic anemia, (2) jaundice, (3) splenomegaly

*RBC protein (Ankrin, band 3) deficiency-> RBCs are spherical instead of donut-shaped-> spleen kills them-> hemolytic anemia, splenomegaly, and jaundice is due to too much bilirubin (UCB) for the liver to conjugate.
**inc MCHC (mean corpuscular Hb concentration) is due to membrane loss and RBC dehydration

*Patient is presenting with RUQ pain worse with deep inspiration (positive Murphy’s sign) wi nausea/ vomiting. This is due to bilirubin (pigmented) gallstones, which he has increased risk for due to his underlying disease (hemolysis).


30 year old woman has worsening SOB after vacation. It started with SOB on exertion, and now she wakes up at night with a choking sensation until she sits up. On exam, she has bilateral pitting ankle edema, hepatomegaly, decreased breath sounds at the bilateral lung bases, and an S3. EKG shows nonspecific ST segment changes. CXR shows enlarged cardiac silhouette and bilateral pleural effusions. Most likely diagnosis?

Viral myocarditis

-presents with CHF symptoms (usually a few weeks after a viral prodrome of fever, malaise, myalgias)
-EKG shows nonspecific ST changes, echo shows 4 chamber dilation
-common cause of dilated cardiomyopathy in young adults
*can be caused by parvovirus B19, HHV 6, coxsackievirus, adenovirus, influenza, HIV
*thought to happen due to an initially inadequate immune response to viral infection-> virus invades cardiac myocytes-> cytotoxicity (toxic to cells) and impaired contractile function
*gold standard to diagnose is endomyocardial biopsy with PCR (but cardiac MRI is noninvasive and can help)


30 year old lady has a few weeks of feeling sick (fever, myalgia). Now she presents with CHF symptoms. You suspect viral myocarditis. What is the gold standard diagnostic test?

Endomyocardial biopsy with PCR (but cardiac MRI is noninvasive and can help)


Patient with renal transplant and recently diagnosed paroxysmal a-fib comes in for decreased urine output and fatigue for 2 weeks. Meds include Diltiazem, Apixaban, Prednisone, Tacrolimus, and Mycophenolate. She is hypertensive. Labs show Cr of 2.3 (increased from baseline of 1.4) and Tracrolimus level is elevated. Cause of worsening renal function?

AKI due to acute calcineurin inhibitor (CNI) renal toxicity
(*calcineurin= protein that activates T-cells and is targeted by immunosuppressant agents like Tacrolimus)

She was recently diagnosed with a-fib, so recently started Diltiazem (CCB), which blocks P450-> allows other drugs like Tacrolimus to stay in the system longer-> increased Tacrolimus levels-> vasoconstriction and AKI


70 year old lady has leg swelling and fatigue. She has had bilaterally lower extremity edema and joint pains for years, which she attributes to old age. She has pitting edema, scattered ecchymoses, and deformed hands. Hb is 11, albumin is 3. U/A shows proteinuria. Diagnosis?

AA amyloidosis nephrotic syndrome (peeing out protein, pitting edema)

-rheumatoid arthritis (deformed hands, joint pains, fatigue)-> chronic inflammation-> release of the acute phase protein serum amyloid associated protein-> AA amyloidos is (that protein misfolds and deposits in tissue)

*diagnose with renal biopsy showing Congo-red glomerular deposits


How do you diagnose AA amyloidosis-> nephrotic syndrome?

Renal biopsy showing Congo-red glomerular deposits

*suspect this is patients with nephrotic syndrome (peeing out protein, pitting edema) with history of rheumatoid arthritis (or other chronic inflammatory disease)


Name the 6 nephrotic syndromes.

1. Minimal change dz
2. Focal segmental GN
3. Membranous GN
4. Membranoproliferative GN
5. DM nephrotic syndrome
6. Amyloidosis (AL in multiple myeloma, AA in chronic inflammation like RA)


Name the 4 nephritic syndromes.

1. Post-strep GN
2. Rapidly progressive GN
-Goodpastrues, post-strep GN, diffuse proliferative GN, Wegner’s, microscopic polyangiits, or Churg Strauss
3. IgA nephropathy (Bergers)
4. Alport syndrome


Proliferative glomerularnephritis is associated with what condition?

SLE (lupus)

*also called DIFFUSE proliferative GN (most common nephritic syndrome in lupus with “wire-looping”)
**renal biopsy would show glomerular immune deposits on histo


25 year old female presents with acute pain in her left knee joint. A few days ago, she had pain in her wrist, then in her ankle. She is sexually active on OCPs. She has a fever and synovial fluid analysis shows elevated WBC count and predominance of neutrophils. Diagnosis?

Gonococcal septic arthritis (from Disseminated Gonococcal Infection)

-asymmetric polyarthralgias (hers is migratory), fever, high neutrophil count in synovial fluid
*confirm diagnosis with gram stain of synovial fluid, blood cultures, and genital NAAT (PCR) for Neisseria Gonorrhea


30 year old man has worsening low back pain and tightness for 3 months. It improves throughout the day with activity. Exam is unremarkable (no tenderness over spine, no weakness, negative straight leg test). Most likely diagnosis?

Ankylosing spondylitis

(Joint disorder that affects the sacroiliac joints-> fusion “bamboo spine”)


What is enthesitis? What seronegative spondyloarthropathy is this seen in?

Inflammation of entheses, the sites where tendons (attaching bone to muscle) or ligaments (attaching bone to bone) insert into bone

-this is seen in ankylosing spondylitis!


What is radiculopathy?

Compression of a spinal nerve root/ “pinched nerve”


What is the treatment for Rosacea?

Topical Metronidazole (gel form)
(Other options: Azelaic acid or Ivermectin)

*2nd line: oral tetracyclines


35 year old woman has a spinning sensation associated with N/V. 2 weeks ago, she had a URI and “muffled hearing.” PMH includes mild asthma and she takes OCPs. Diagnosis?

Vestibular neuritis
(Inflammation of vestibular nerve/ CN8-> vertigo)

-it is a self-limited disorder that follows a viral URI
*vestibular neuritis + unilateral hearing loss= labyrinthitis


50 year old man is in the ICU for septic shock from PNA. He is treated with IV fluids, antibiotics, and vasopressors. 4 days later, his lungs are doing better but he has anemia and positive occult blood in his stool. Most likely cause?

Stress-induced ulcer

-common in ICU patients w/ severe physiologic stress (risk factors: shock, sepsis, coagulopathy, mechanical ventilation, traumatic spinal cord/ brain injury, burns, high-dose corticosteroids)

-multifactorial: due to poor blood flow to abdomen (splanchnic hypoperfusion) and kidneys-> uremic toxins accumulate and impair formation of the protective mucosal layer of the stomach-> mucosal injury and bleeding

*this is the very reason we give GI prophylaxis (PPIs) to patients at high-risk! (*but don’t just throw them at everybody either, as PPIs inc risk for C diff)


35 year old man presents with substernal pain and palpitations. BP is 160/110, HR 110, pupils are dilated and reactive to light. EKG shows sinus tachy with ST elevations in leads V1-V4. Most likely explanation?

STEMI 2/2 cocaine abuse


60 year old man has sudden-onset pain and redness in his left eye associated with severe headache and photophobia. He has been getting over a cold and taking over-the-counter decongestants. Exam shows a non reactive, dilated left pupil that is red. Next step?

Tonometry (measure that IOP)

-This is acute angle-closure glaucoma, possibly triggered by decongestant use (alpha-1 agonists like Phenylephrine-> pupillary dilation, which can completely close the anterior chamber angle in a person who’s predisposed bc of their anatomy/ already has a narrower angle)

**don’t confuse alpha-1 and alpha-2. Alpha-1-> pupillary dilation. Alpha-2-> decreases aqueous humor production. When we treat open angle glaucoma with alpha agonists (“activate alpha, block beta”), that’s alpha-2 agonists**


29 year old man presents with weakness in the legs. He recently had trigeminal neuralgia and a URI. Exam shows increased resistance to passive flexion and extension of the legs and decreased vibration and proprioception in the left arm. What will LP likely show?

Oligoclonal bands (this is MS)

-He has neurologic deficits separated by time and space (trigeminal neuralgia, lower limb motor loss, upper limb sensory loss)

*For diagnosis, do an MRI (expect to see demyelinating lesions affecting white matter). If not classic, follow-up with LP (expect to see oligoclonal bands of Ig).


What is albuminocytologic dissociation and what condition is it associated with?

Elevated CSF protein w/ normal cell count (on LP CSF analysis)

Characteristic of Guillain-Barré syndrome


What does pleocytosis mean?

Increased cell count


Presence of 14-3-3 protein in CSF analysis (from LP) indicates what?

Prison disease (Creutzfeldt-Jakob disease)

*these patients have rapid, profound deterioration of mental status (dementia, behavioral changes) with startle myoclonus


50 year old lady with PMH of breast cancer s/p mastectomy presents with worsening SOB for 2 wks. She denies fever and cough. CXR shows white on the bottom right lobe. What is going on?

Right-sided pleural effusion

*given her history of breast cancer, this raises concern for a malignant effusion due to breast cancer recurrence


In a pleural effusion, what would you expect on exam:
1. Breath sounds (inc or dec)?
2. Tactile fremitus (in or dec)?
3. Percussion (dull, resonant, or hyperresonant)?

1. Breath sounds- DECREASED
2. Tactile fremitus- DECREASED
3. Percussion (dull, resonant, or hyperresonant)- DULL

-There’s fluid between you and the lungs, so lung sounds are more distant
-There’s fluid between you and the lungs, os vibrations from the lung will be felt less
-Fluid causes dullness to percussion (vs air creates a hollow, hyperresonant sound)


80 year old has muscle pain and morning stiffness in the shoulders and hips. ROS is positive for fatigue and fever. On exam, aBduction of shoulders worsens pain. Labs show high ESR. In 1 week, patient responds well to glucocorticoid therapy. What additional tests, if any, do you need to confirm the diagnosis?


This is Polymyalgia rehumatica (pain and stiffness in shoulders/ hips/ neck, fatigue, weight loss, low-grade fever)
-classic symptoms, elevated inflammatory markers, and response to glucocorticoids-> no further testing needed

*a small number of cases are associated with giant cell (temporal) arteritis (headache, temporal tenderness, jaw claudication, visual disturbance)


70 year old man with hx of chronic constipation has rectal bleeding that is bright red and lightheadedness. NG tube returns nonbilious stomach contents w/o blood. Most likely cause of the rectal bleeding?

Diverticulosis (diverticulum hemorrhage)

-the most common cause of large-volume rectal bleed in adults (painless, but can be associated with lightheadedness or hemodynamic instability)
*usually resolves on its own, but occasionally requires endoscopic or surgical evaluation

**diverticulosis is most common in the sigmoid colon, but diverticular bleeding is more common in the right colon


What is the most common cause of large-volume rectal bleed in adults?

Diverticulosis (diverticular hemorrhage)

*painless, but can be associated with lightheadedness or hemodynamic instability
*usually goes away on its own, but may require endoscopic or surgical intervention


Patient presents with joint pain and fat fingers that look like sausages (“sausage digits”). Diagnosis?

Psoriatic arthritis

-psoriasis + arthritis
-characteristic “sausage digits” (also called dactylitits, meaning inflammation of the fingers and toes) w/ nail pitting may be present


High, low, or normal DLCO and FEV1/FVC ratio in interstitial lung dz?

Decreased DLCO (diffusion problem)
Normal FEV1/FVC ratio (restrictive lung dz= problem getting air in, so less air in= less air out, so FEV1 and FVC are both lower, but ratio is maintained)


COPD involves what type of emphysema- panacinar or centriacinar?



Is DLCO high, low, or normal in chronic bronchitis? Emphysema?

Chronic bronchitis- DLCO is normal

Emphysema- DLCO is low (alveolar destruction impairs diffusion capacity)


Name the 4 types of pneumoconioses (interstitial lung disease due to occupational exposure) and their associated jobs.

1. Coal workers pneumoconiosis (coal miners)

2. Silicosis (sandblasters and silica miners)

3. Asbestosis (construction workers, plumbers, and shipyard workers)

4. Berylliosis (beryllium miners and aerospace workers like in NASA)


Patient with PMH of hypothyroidism (on Levothyroxine) is going through menopause, having bad insomnia, hot flashes, and mood swings. If you treat her with estrogen therapy, what will change in terms of her Levothyroxine dosage?

Requirement for Levothyroxine would increase (you’d have to up her dose)

*if hypothyroid patient is pregnant or on estrogen therapy, you need to up the thyroid dose. Why? Pregnancy/ estrogen increases TBG (thyroid-binding globulin)-> more TH will bind it-> less free TH (will require more to be at normal levels).


Which antiemetic drug can cause extrapyramidal symptoms?


(Remember the D2 rings in Sketchy)


50 year old man with PMH of HTN and hypercholesterolemia feels “dizzy” like the room is spinning when he turns over in bed or looks up. On exam, he has an ejection murmur at the left sternal border. Most likely diagnosis?

Benign paroxysmal positional vertigo (BPPV)

-vertigo episodes triggered by head positional changes
-caused by calcium debris in the semicircular canal-> disruption of normal fluid flow through the vestibular system
-diagnose with Dix-Hallpike maneuver (quickly lie patient down with head rotated 45 degrees)-> will reproduce vertigo and nystagmus
-treat with Epley/ canalith repositioning maneuvers

*murmur is unrelated! Ejection murmur at left sternal border= still murmur aka functional murmur (an innocent murmur)


70 year old lady has confusion, memory loss, and poor sleep. She has also been walking more slowly, has fallen, and is seeing “strangers in the backyard” that don’t exist. MRI brain shows cortical atrophy. Diagnosis?

Dementia with Lewy bodies

-dementia with Parkinsonism and visual hallucinations (the dementia may come first or at the same time as the other symptoms)

*treat with carbidopa-levodopa for Parkinsonism and anticholinergics for cognitive impairment
*on autopsy: Lewy bodies (eosinophilic inclusion bodies of alpha-synuclein protein) in brain


50 year old man has fever/ chills, low back pain, and urinary frequency/ urgency. He is not sexually active and has no discharge. Digital rectal exam reveals anterior tenderness. Diagnosis?

Acute bacterial prostatitis
(Most likely due to E. Coli)

-presents as a flu-like illness w/ lower urinary tract symptoms


Equation for anion gap?

AG= sodium- bicarb- chloride


Patient undergoes a lung biopsy. After the procedure, he develops severe SOB and chest pain. BP is 70/40, HR 120, RR 30. He is diaphoretic with cold, clammy skin. CO is low and PCWP is high. Most likely diagnosis?

MI-> cardiogenic shock

-He’s in shock
-cold skin= vasoconstriction diverts blood away from extremities to vital organs + lack of perfusion
-CO is low, so heart isn’t pumping well
-PCWP is high, so LA is extra full since heart isn’t pumping forward well


32 year old man comes in for palpitations. He has a family hx of sudden death at a young age due to “heart issues.” Exam reveals decrescendo early diastolic murmur at the left sternal border. Likely diagnosis?

Bicuspid aortic valve (causing aortic regurg)

*bicuspid aortic valve is often associated with aortic STENOSIS, but can also be a cause of aortic regurg (from aortic root dilation)!

*remember the 3 murmurs best heard at the left sternal border: (1) aortic regurg, (2) pulmonary regurg, (3) HOCM


What 3 murmurs best heard at the left sternal border?

1. aortic regurg
2. pulmonary regurg


What patients should get an annual low-dose CT scan for lung CA screening?

Smokers age 55-80

*start earlier if 30+ pack year history comes before age 55

*stop earlier if 15+ years w/o smoking comes before age 80


Lady is on Phenytoin for a general tonic-clonic seizure she had 5 yrs ago. She is contemplating pregnancy. Next step?

Slowly taper her off Phenytoin and discontinue it

-she’s been seizure free >2 yrs, so discontinuation of anti-seizure medication is reasonable (wein her off bc rapid withdrawal could cause seizure reoccurrence)
-Phenytoin is a teratogen! Causes fetal hydantoin syndrome (group of defects due to Phenytoin): cleft palate, microcephaly, nail/ digit hypoplasia, cardiac defects, facial feature abnormalities


Lady complains of excessive urination at night for 2 wks. She has a PMH of hypothyroidism (on Levothyroxine) and bipolar (on Lithium). Labs show high serum osmolality, lower urine osmolality, and high TSH. What’s going on?

Nephrogenic DI 2/2 Lithium use

-Lithium accumulation in renal collecting ducts-> ADH resistance (kidneys not responding to ADH, so not retaining water-> pee out the water too much)
*will have concentrated blood, dilute urine (since you’re peeing out the water)


30 year old man is brought into the ED after being found confused in his garage. His pulse is 48 bpm. He is lethargic, diaphoretic, drooling, has constricted pupils, and is wheezing. Next best step?

Give Atropine

This is organophosphate poisoning (cholinergic toxicity).
*remember DUMBBELS (Diarrhea, Urination, Miosis/ constricted pupils, Bronchospasm and Bradycardia, Emesis, Lacrimation, Salivation)
-PNS symptoms

*Manage A,B,Cs (airway, breathing, circulation), give Atropine (anti-muscurinic), also give Pralidoxime if neuromuscular dysfunction is present


Car crash victim is unconscious. CT/ MRI head shows numerous small hemorrhages with blurring of the gray-white matter interface. Most likely diagnosis?

Diffuse axonal injury

-traumatic brain injury that results in unconsciousness-> vegetative state-> death


75 year old man with T2DM is brought in for weakness and blurry vision. He’s had a cough and sore throat over the last week. Patient appears dry and weak. Labs are significant for high K+, high BUN and Cr, and high glucose of 1,070. Diagnosis?

Hyperosmolar hyperglycemic state

-state of severe hyperglycemia (>600), hyperosmolarity, and dehydration in T2DM patients

*they have such high blood sugar (body not responding to insulin to pull glc into cells)-> hyperosmolarity and glc is spilling out into urine, water follows-> dehydration.
*hyperkalemia is an issue (lack of insulin to pull K+ into cells and hyperosmolarity also pushes K+ out of cells). Giving insulin to treat can then rapidly shift K+ back into cells-> hypokalemia, so watch it.


Huntington disease causes atrophy in what area of the brain?

The caudate nucleus and putamen


What do ACE inhibitors do to the renal arteries (mechanism)?

ACE inhibitors dilate the efferent arteriole
(Angiotensin II constricts the efferent and ACE i’s block that-> dilation of efferent-> dec GFR, inc RPF)

*since they decrease GFR (reduce glomerular hydrostatic pressure, while still preserving renal perfusion flow), they take pressure off the kidneys and are important in preventing nephrotic syndrome (DM nephropathy) in diabetics


Lady has altered mental status. She has had headaches and intermittent vision changes over the last week. BP is 220/115. On exam, she has shiny thickened skin with multiple telangiectasias. Cr is high and she has 1+ proteinuria. Next step?

Start her on an ACE inhibitor

-She has systemic sclerosis (diffuse scleroderma)

-Widespread fibrosis of multiple organ systems (autoimmune vasculopathy involving collagen deposition)-> thick skin, telangiectasias, HTN emergency and acute renal failure from renal vascular injury (scleroderma renal crisis)

-ACE inhibitors are used to prevent and treat renal HTN crisis (StepUp2Med pg 249), they reduce RAAS activation (*the high Cr is not a contraindication for ACEi’s in this population)


Guy has worsening weakness and exertional dyspnea. He had a URI 3 wks ago, symptoms never fully went away. BP is 90/60, HR 110. JVP is 11 cm. Heart sounds are muffled. Diagnosis?

Cardiac tamponade (likely 2/2 viral pericarditis)

Beck’s triad: (1) hypotension, (2) distended neck veins, (3) muffled heart sounds
*pulsus paradoxus (>10 drop in BP during inspiration) is another common finding

*normal JVP= 6-8 cm (11 is elevated!)


What’s a normal JVP?

6-8 cm


WHY does cardiac tamponade result in low BP?

Due to decreased LV preload

Fluid filling the pericardial sac RESTRICTS FILLING-> decreased preload-> decreased stroke volume-> decreased CO


25 year old with PMH of childhood asthma has dry cough since he contracted a URI 10 days ago. He is afebrile. On exam, he has wheezing. Next step?

Inhaled bronchodilator

-This is likely ACUTE BRONCHITIS (90% viral)
*cough can be dry or productive
*self-limited (lasts 3-4 wks), but treat with supportive therapy (throat lozenges, over-the-counter cough suppressants, albuterol in patients with underlying asthma)—NO antibiotics
*fever is not typical (if fever is present, think PNA)
*no need to get a CXR here to r/o PNA—do this for patients with high fever, tachypnea, crackles/ dullness on lung exam, or underlying COPD


68 year old woman with PMH of breast cancer and vertebral mets complains of general weakness and dizziness. Radiation + chemo are planned, but she hasn’t started yet. BP is 105/65 with orthostatic changes and HR is 102. Na+ is low and K+ is at the upper limit of normal. Diagnosis?

PRIMARY ADRENAL INSUFFICIENCY (lack of aldosterone and cortisol production by the adrenal glands)
-likely 2/2 metastatic breast cancer (adrenal glands are a common site of metastasis, and when they are destroyed by cancer, they stop working like they should)

-> low BP, low Na+ (not reabsorbing it), high K+ (not peeing it out)

*confirm the diagnosis by cosyntropin (synthetic ACTH) stimulation testing (after giving ACTH to stimulate the adrenal glands, her adrenals would still fail to produce cortisol)


How do you confirm a diagnosis of primary adrenal insufficiency?

Do a Cosyntropin (synthetic ACTH) stimulations test (after giving ACTH to stimulate the adrenal glands, adrenals will still fail to produce cortisol if adrenal insufficiency is present)

*this test is usually done in the morning when cortisol levels are normally most pronounced (body gets ready for the day of stress)
*remember adrenal insufficiency= lack of aldosterone and cortisol by the adrenals


Man got into a motorcycle crash, now has weakness + loss of pain and temp in both legs. Touch and vibration are intact. What spinal cord problem does this patient likely have?

Anterior cord syndrome

(Motor + pain/ temp are broken on both sides, since the anterior part of the spinal cord is where CST and STT fibers cross)

*from injury to anterior spinal artery in trauma


How does Anterior cord syndrome present?

Motor + pain/ temp are broken on both sides
(since the anterior part of the spinal cord is where CST and STT fibers cross)


How does central cord syndrome present?

Pain/ temp broken on both sides (affects STT crossing)
-paralysis and burning pain in upper extremities
-usually in old patients after forced hyperextension of the neck (whiplash)
*can be assoc with bladder dysfunction


35 year old obese woman complains of periodic visual disturbance. She goes blind for several seconds when standing up and has morning headaches. Visual testing reveals large blind spots. What eye condition do we call this?

Papilledema (swollen optic nerve due to elevated ICP)
-causes transient vision loss with change in head position
-headaches due to inc ICP are usually worse in the morning

*she may have idiopathic intracranial HTN (pseudotumor cerebri), given her young age, obesity, and lack of other comorbidities...next step would be neuroimaging (CT or MRI brain)


45 year old man has headache and confusion for 2 days. Hb is 8, BUN is 30, Cr is 2.2. Peripheral blood smear shows fragmented RBCs. PT is normal. Next best step?

Plasmapheresis (plasma exchange)

-This patient has TTP (Thrombotic Thrombocytopenic Purpura)
-Presents with thrombocytopenia, microangiopathic hemolytic anemia, renal insufficiency, neuro changes (headache, confusion, coma, stroke), fever

*autoantibody against ADAM 13, an enzyme that normally degrades vWF-> vWF stays there, clumping up platelets-> dec platelets/ thrombocytopenia (since they are getting used up forming microthrombi) + CNS abnormalities (tends to involve CNS vessels)
*fragmented RBCs= shistocytes/ helmet cells
*PT, PTT are normal (unlike in DIC)


Multiple people are brought into the ED from the shopping mall after smelling a fruity odor then having symptoms. Your patient developed rapid SOB. She is diaphoretic and drooling. Pupils are pinpoint and non reactive. She is wheezing. Likely diagnosis and test to confirm?

Organophosphate poisoning

RBC acetylcholinesterase activity test
*you can also just give Atropine and if it works in resolving the symptoms, you know your diagnosis was correct

-organophosphates block AChE in muscarinic and nicotinic synapses-> ACh can’t be broken down-> too much ACh-> overstimulation at the NMJ to where muscles stop responding

-PNS symptoms: DUMBBELS (Diarrhea/ Diaphoresis, Urination, Miosis, Bronchospasm/ Bradycardia, Emesis, Lacrimation, Salivation)

*think of this in an agricultural worker (pesticides) or in a group of people with similar symtpoms (nerve agent—these chemical weapons are used in terrorist attacks and the gas is colorless, tasteless, but has a slight fruity odor)


55 year old man comes in due to having many falls over the past few wks. He’s also had dry skin, dry mouth, erectile dysfunction, and resting tremor. BP is 120/80 supine, 90/60 standing. Exam shows rigidity and bradykinesia (slow movement). Most likely diagnosis?

Multiple system atrophy (Shy-Drager syndrome)
-degenerative disease w/ Parkinson’s symptoms + autonomic insufficiency

-this patient has Parkinson’s symptoms—resting tremor, rigidity, bradykinesia
-and autonomic dysfunction (postural hypotension, erectile dysfunction, dry skin, dry mouth)
*other autonomic symptoms may include: loss of bowel or bladder control, abnormal salivation or lacrimation, gastroparesis...


80 year old man with PMH of HTN (on Ramipril and Chlorthalidone) comes in due to sudden painless vision loss in his left eye. Funduscopic exam of the left eye shows swelling of the optic disk, retinal hemorrhages, dilated and tortuous veins, and cotton wool spots. Diagnosis?

Central retinal vein occlusion
(Blood not draining from the eye)

*this is describing a “blood and thunder” appearance (optic disk swelling, retinal hemorrhages, dilated and tortuous veins, cotton wool spots)


65 year old man with PMH of osteoarthritis (on naproxen for pain relief) presents with fatigue. Hb is 8.5, MCV is 72, rest of labs are normal. Would the following most likely be high, low, or normal?
Serum iron
Serum ferritin
TIBC (total iron binding capacity)
Transferrin saturation

*He has microcytic anemia= iron deficiency, anemia of chronic dz, sideroblastic anemia, or thalassemia. Most likely IRON DEFICIENCY (usually due to GI blood loss in men)- this is most common + he has no inflammatory disorders that point to anemia of chronic dz (osteoarthritis is wear and tear—it’s not autoimmune like rheumatoid)

Serum iron- LOW
Serum ferritin (iron in storage)- LOW
TIBC (total iron binding capacity) (Tf)- HIGH
Transferrin (Tf) saturation- LOW


What type of drug is Naproxen?


(Trade name= Aleve)


Man has burning pain and cramping in his feet and a pins and needles sensation in his toes. He works as a construction worker and is exposed to vibrating machinery. He doesn’t smoke, drinks 6 beers/ day. Exam shows loss of ankle reflex bilaterally and impaired touch and vibration sensation on the feet. Hb A1c and MMA levels are normal. Diagnosis?

Alcoholic peripheral neuropathy
(a toxic neuropathy)

-alcohol is neurotoxic-> symmetric distal polyneuropathy in a “stocking and glove pattern”
-loss of deep tendon reflexes begins with loss of ankle reflexes
*treat with stopping alcohol (improves symptoms), give thiamine supplements, and may give gabapentin or TCAs for refractory neuropathic pain


What hereditary polyneuropathy is slowly progressive and results in foot drop, muscle weakness, and lower leg atrophy?

Charcot-Marie-Tooth disease


Most common autoimmune neuropathy?

Guillain-Barré syndrome

-rapidly progressive, ascending
-usually follows a GI infection or URI


If a CHF patient has hypOnatremia, do we care?

Yes—hypOnatremia in patients with CHF parallels the severity of HF and is a predictor of clinical outcomes

-it is caused by increased ADH (more water retention-> dilutes [Na+]) and increased renin and NE (increase Na+ and water reabsorption in the distal tubules)


HIV patient presents with jerking movements of his arms and face. He also has been having headaches. MRI brain shows ring-enhancing lesions at the gray-white matter junction and basal ganglia. Diagnosis and treatment?

Toxoplasma encephalitis

Sulfadiazine + Pyrimethamine
(Sulfa dyed eggs + pyramid shape on dyed eggs)


60 year old patient with PMH of HTN and hyperlipidemia. 6 hrs ago he had weakness that resolved after 30 min. On exam, patient has an S4 and mild right-sided pronator drift. EKG shows T-wave inversion in leads I and V6. CT non con of brain is normal, MRI is pending. Next step?

Give Aspirin

*This is likely ischemic stroke and patient is not a TPA candidate (last normal was >4.5 hrs ago)
*ASA is the only antiplatelet agent hat is effective in reducing the risk of early ischemic stroke recurrence- give within 24 hrs!


What are the dietary recommendations to prevent recurrent calcium oxalate kidney stones?

1. Increase fluid intake
2. Decrease sodium intake
3. Normal calcium intake

*hydration always helps prevent kidney stones
*low sodium in the diet promotes sodium and calcium reabsorption (by pushing more calcium in the blood, you pee out less= less calcium kidney stones)
*calcium intake has no effect


65 year old man has unsteady gait and frequent falls for 2 months. His left side feels weak. He also has morning headaches. Exam shows swaying to the left when walking and increased resistance to passive flexion of the left upper and lower extremity. Most likely cause?

Brain tumor

-morning headaches + focal neuro deficits
*diagnose with MRI brain


Dullness to percussion and increased breath sounds. What does this indicate?

Consolidation of the lung

-dullness= trapped fluid
-increased breath sounds (bronchial, crackles)= fluid in lungs (**vs pleural effusion breath sounds are decreased bc the fluid is in the pleura b/w you and the lungs)


40 year old woman complains of palpitations. Over the past few months, she has had anxiety and weight loss. BP is 110/80, HR is 125 and irregular. Exam shows lid lag and fine tremor of the hands. EKG shows a-fib with RVR. What initial medical therapy should you give?

Beta blocker (Propranolol)

This is hyperthyroidism
-a-fib with RVR, tachycardia
-weight loss

*beta-blockers are used for initial treatment of a-fib 2/2 hyperthyroidism to control HR and sympathetic symptoms (they also block peripheral conversion of T4-> to active T3)
-continue beta-blockers until patient becomes euthyroid + treat hyperthyroidism with medication, radioactive ablation, and/or surgery


55 year old woman with PMH of HTN (on Lisinopril) presents with severe headache that got rapidly worse over a few minutes and hasn’t responded to analgesics. It is associated with vomiting and photophobia. Exam shows mild neck stiffness, but full neuro exam is normal. Non-con CT head is normal. Next step?

Lumbar puncture (LP)

This sounds like subarachnoid hemorrhage (*from ruptured berry aneurysms)
-thunderclap headache (reaches max intensity in few minutes) “worst headache of my life”
-associated with N/V, photophobia
-neck stiffness= meningeal irritation (from the blood)

You would expect a non-con CT to show bleeding, but if it comes back negative and you are highly suspicious of subarachnoid hemorrhage, do a LP to check!
Xanthochromia (yellow/ bloody CSF)= SAH

*NOT a migraine (migraine headaches don’t irritate the meninges)


A hospital undergoes review of malpractice claims. They tally up the number of missed or delayed diagnoses over the last 10 yrs and find the rate is 25% higher in their ER compared to other hospitals nationwide. Most likely underlying cause of these medical errors?

Communication failures between providers


What has been proven to most effectively improve communication of relevant information in patient transfers (signing off a patient from one doc to another)?

Implementing a signout checklist

*face-to-face handoffs w/o interruptions are also ideal, but not proven to be AS good as checklists in the signout procedure for improving medical outcomes


32 year old man is seen to “check up on my liver.” 2 yrs ago, he shared needles with another IV drug user and was positive for hep B surface antigen, negative for all other antigens and antibodies. He stopped doing IV drugs since. His hep B serology is most likely to show what—positive or negative?


*remember “SpECiES” (HBsAg, HBeAg, HBcAb, HBeAb, HBsAb)
-serum antigen, e antigen (infectivity), core antibody, e antibody, and serum antibody

This patient had the serum antigen at the time he presented with infection, but not the e antigen and no antibodies (hadn’t been produced yet)...so now he will have the core antibody (1st one that gets made- in “window period”) and serum antibody (may or may not have the e antibody)
(No antigens anymore bc the infection is resolved)


IV drug user gets hep B. What’s the most likely prognosis?

95% of hep B infections are self-limited (resolve on their own)

**vs. babies who get it from vertical transmission are likely to get the chronic form and children age 1-5 have a 30-50% chance of getting the chronic form


65 year old obese smoker man has high fevers, confusion, and productive cough for 2 days. On exam, his cervical lymph nodes are enlarged but not painful, he has rales at the R lung bases, and he has hepatosplenomegaly. CXR shows R lower lobe infiltrate. Labs show low Hct, low platelets, and leukocytosis (low neutrophils and monocytes, high lymphocytes). Blood cultures, antibiotics, and supportive care are initiated. Next step?

Get a FLOW CYTOMETRY of the peripheral blood
(To diagnose CLL—will show too many naive B-cells)

-Fever + cough + R lung infiltrate= PNA
-Note that most bacterial infections, including PNA, cause leukocytosis with neutrophil predominance—this guy has dramatic lymphocyte predominance
-Old patient + lymphocytosis (too many lymphocytes) + anemia + thrombocytopenia + hepatosplenomegaly= CLL (chronic lymphocytic leukemia) *the most common leukemia

**anemia and thrombocytopenia due to the B-cells crowding out other cell lines
**note that a peripheral blood smear could also aid in the diagnosis (would show smudge cells)


Rales vs. rhonchi vs. crackles vs. wheezing?

“Rales in the tails, rhonchi in the bronchi”

Rales= Crackles
-from the alveoli

Rhonchi= low-pitched wheezing
-from the bronchus


75 year old man comes in due to tremor when holding the newspaper or drinking his morning cup of coffee. He has an obvious tremor when touching his finger to the doctor’s finger. Diagnosis and treatment?

Essential tremor

-this is an action tremor (vs. the resting tremor you get in Parkinson’s)

*Propranolol is first-line, but other options are Primidone and Topiramate


Patient has colon cancer. You explain his treatment options, but he says he does not want treatment. He is mentally competent. Do you ask him why he doesn’t want treatment or respect his wishes?

Ask him why he doesn’t want to have treatment

-before you respect his decision to not have treatment, you need to explore why he feels this way...there’s a chance he’s just in denial or afraid and needs more clarification on treatment options or depressed...

Always discuss reasons for a patient’s decision to withhold treatment before honoring it!


45 year old man presents with daytime headaches, dizziness, and nausea. He doesn’t snore, he smokes, he works in an underground parking garage. Vitals are normal and pulse ox is 97%. Labs show Hct of 60% (normal is 40-53%). Most likely diagnosis?

Chronic CO poisoning
(Exposure to car exhaust in an enclosed space + has intermittent headaches, dizziness, nausea + polycythemia)

*CO has a greater affinity for Hb than oxygen-> carboxyhemoglobinemia. Less oxygen is able to bind to Hb to be delivered to tissues (left shift on Hb curve)-> hypoxia-> reactive polycythemia (kidneys release more EPO so more RBCs are made) to try to compensate.

**normal pulse ox bc pulse oximetry cannot differentiate between Hb bound to CO vs. oxygen
**diagnose with ABG (arterial blood gas)!


60 year old man has sudden-onset weakness in the lower extremities since swimming in a pool and cannot pee. Medical hx includes DM and he had back pain the last 2 months. Exam shows motor weakness in both legs. He has no sensation in the perineal are and rectal tone is absent. Next step?

Emergency neurosurgical evaluation!

This patient has acute spinal cord compression, likely due to vertebral metastasis (progressive back pain and activity brought on the onset of concerning symptoms)

*some causes of spinal cord compression are: fracture, trauma, disk herniation, malignancy, epidural abscess
*urinary retention occurs with lesion above S2 (autonomic tract involvement)
*regardless of the cause, when the spinal cord is compressed, you need to get a surgery consult for decompression 1st, do neuroimaging, and IV glucocorticoids may be given


HIV patient has severe watery diarrhea and lightheadedness and lost weight. He’s non-compliment with his HIV meds and last CD4 count was 95. He works at a horse breeding farm, denies recent travel. Most likely responsible organism?


-profuse watery diarrhea in AIDS (seen w/ CD4 count <180)
-get it from drinking contaminated water, animal contact (horse breeding), or person-to-person contact
*stool exam w/ modified acid-fast stain shows cryptosporidium oocytes


AIDS patient with severe watery diarrhea and low-grade fever. CD4 <180. What should you think of?



AIDS patient with watery diarrhea and crampy abdominal pain, no fever. CD4 count is <100. What should you think of?



AIDS patient with watery diarrhea and high fever. CD4 count is <50. What should you think of?

Mycobacterium avium complex (MAC)


AIDS patient with frequent, small-volume diarrhea w/ blood, abdominal pain, and low-grade fever. CD4 count is <50. What should you think of?

Cytomegalovirus (CMV colitis)


Patient who is being treated for TB complains of fatigue. His Hb is low, MCV is normal, serum iron is high, and TIBC is low. On microscopy, some RBCs are hypochromic and others are normochronic. Next step?

Give Vitamin B6 (Pyridoxine)
(*the bees w/ pyramid sticks in Pixorize)

-Isoniazid depletes Vit B6 stores. Since Vit B6 is needed to make protoporphyrin (and to make heme, since heme= Fe + protoporphyrin), this causes sideroblastic anemia (type of microcytic anemia, though it starts off normocytic).
-increased serum Fe (there is lack of protoporphyrin to combine with Fe, so excess free iron-> ringed sideroblasts)
-decreased TIBC (Tf)


30 year old man comes in for a check-up. He has had a lot of stress lately, otherwise no concerns. Labs show Hb of 10.5, MCV of 60, and high RBC count. Peripheral blood smear shows target cells. Diagnosis and treatment?

Thalassemia minor
No treatment needed

-mild microcytic anemia, target cells, high RBC count

*microcytic anemia means choices are: iron deficiency, anemia of chronic dz, sideroblastic anemia, or thalassemia (alpha or beta, minor or major)
*alpha thal is due to a gene mutation-> dec synthesis of beta globin chain
*target cells due to dec Hb (RBC “blebs up” like a deflated B-ball you can indent)
*inc RBC count (to compensate for having less functional Hb)


Young man comes into the ED for chronic tension headaches that are “debilitating.” He only gets partial relief with NSAIDs. He has no associated symptoms. He was evaluated for the same headaches last year and extensive neuro work-up was normal. He is worried about his schooling and constantly worried he may have an undiagnosed brain tumor. What med may help?

SSRI (like Fluoxetine)

This is somatic symptom disorder (when a patient has a minor symptom like a headache and is convinced they got brain cancer for sure). Manage with regular appointments and avoid unnecessary referrals and tests. SSRIs and cognitive-behavioral therapy may help too.


Lady had a TIA. She had a mitral valve replacement 5 years ago. In addition to neuroimaging, what test do you need to do?


-Look for evidence of Prosthetic Valve Thrombosis (PVT), a complication of artificial valve repair (patients can have a new murmur, HF due to stenosis/ valvular obstruction or regurg from valve not aligned perfectly, or a thromboembolic event like a TIA)


70 year old man with PMH of HTN, DM, CDK, and CAD presents with cough. CXR shows a R upper lung nodule. A CTA with IV contrast confirmed this. Patient is admitted and found to have worsening acute renal failure. BP remains 140s/90s, but BUN and Cr uptrend. What would have prevented this AKI?

IV hydration

He has CDK and you gave him IV contrast—stupid idea! -> contrast-induced nephropathy. If you have to give contrast for imaging, dilute the contrast with hydration to prevent injury to the kidneys.


Would you expect electrolytes (Mg, K+, Na+, P) to be high, low, or normal in anorexia nervosa?

All normal to low

*HypOkalemia is common particularly in the binge-purge type (vomit out K+-> low K+ in blood)


When is Metformin contraindicated?

In acute renal failure, liver failure, or sepsis—as these conditions increase risk of LACTIC ACIDOSIS


Duke criteria is a MDCalc tool/ objective way to define what disease?

Infective endocarditis

(*need 2 major + 1 minor or 3 minor criteria)


Patient with PMH of rheumatic fever, mitral stenosis, and recent dental procedure has fatigue and SOB. Cardiac exam is significant for a holosystolic murmur at the cardiac apex with a diastolic rumble and hemorrhages under a nail bed. Labs show leukocytosis, anemia, elevated Cr. U/A shows 1+ protein. Blood cultures are most likely to isolate what organism?

Strep viridans (includes strep mutants, mitis, oralis, and sanguinis)

-infective endocarditis following a dental procedure (previously affected heart valve)


Strep mutans belongs to what class of bacteria?

It is a strep viridans

*In the strep viridans family: strep mutants, mitis, oralis, and sanguinis


50 year old lady has a “stabbing” chest pain when taking a deep breath. She has also had frequent pain in her hands and feet. Exam reveals fine inspiratory crackles and decreased breath sounds over the L lung base. Wrist and hand joints are swollen and tender. Labs are normal, ANA is negative. CXR shows increased interstitial markings and L pleural effusion. Thoracentesis shows it’s exudative and pleural glucose is 10. Most likely cause of the pleural effusion?

Rheumatoid Arthritis (RA)

Pleural effusions due to RA have a low glc, high LDH
*if pleural glucose level is low (<60), consider RA as the cause of the pleural effusion! (StepUp2Med pg 82)
*exudative= due to inflammation
*fine crackles + increased interstitial lung markings= interstitial lung disease (ILD), a pulmonary manifestation of RA


25 year old military recruit with PMH of allergic rhinitis (on chlorpheniramine) suddenly collapsed at bootcamp. He lost consciousness, now he’s awake but confused. Temp 106, BP 90/60, HR 130, RR 22. He is sweating. On lung exam, he has rales (crackles) at both lung bases. Labs show thrombocytosis, leukocytosis, and slightly elevated PT (normal Hb, BUN, PTT). Most likely cause of his symptoms?

Exertional heat stroke

-heavy exercise (bootcamp) presenting with hyperthermia (>104 F), confusion, and multi-organ dysfunction

*way too hot-> vasodilation happens to shunt blood toward skin to sweat (though sweating is inadequate to cool the body at this temp)-> distributive shock (blood is not where it needs to be feeding the central organs)-> organs die and become ischemic-> tissue factor is released-> pathologic activation of coag cascade= DIC
*may also cause CNS dysfunction (confusion, seizures), ARDS (his lung crackles), hepatic failure, renal failure...end-organ damage from the distributive shock
*may present with anhidrosis (lack of sweating from dehydration) or sweating
*leukocytosis is from the severe stress
*this patient was taking an antihistamine, which has anti-cholinergic activity and can further impair heat dissipation (“hot as a hare”)