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MS3 > Internal Med 12 > Flashcards

Internal Med 12 Flashcards

1
Q

How do you diagnose gastroparesis

A

Emptying study

Will have >60% of stomach contents after 2 hours or >10% after 4 hours

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2
Q

Tx of gastroparesis

A 
•	Avoid opiates
•	Blood glucose control
•	Prokinetic agents
o	Metaclopramide (PO) in stable disease
o	Erythromycin (IV) in acute flare
•	Low fiber, small volume meals
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3
Q 
Describe the association you should make to determine which of the following organisms caused diarrhea (e.g. what will the clinical vignette look like)
o	C. Diff  
o	ETEC  
o	Vibro Cholera  
o	Staph aureus  
o	B. Cerreus 
o	Giardia
A 
o	C. Diff  abx use
o	ETEC  traveller’s diarrhea (Mexico)
o	Vibro Cholera  3rd world countries / no boiling water
o	Staph aureus  proteinatious foods
o	B. Cerreus  reheated rice
o	Giardia  camping / fresh water
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4
Q 
Describe the association you should make to determine which of the following organisms caused diarrhea (e.g. what will the clinical vignette look like)
o	Salmonella  
o	Shigella  
o	EHEC (O157-H7)  
o	Campylobacter  
o	Amoeba histolytica
A 
o	Salmonella  chickens, eggs
o	Shigella  HUS
o	EHEC (O157-H7)  HUS, uncooked meat
o	Campylobacter  most common
o	Amoeba histolytica  HIV/AIDs
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5
Q

What are Light’s criteria

A

If these are true then it is EXUDATIVE pleural effusion:

  • Pleural fluid protein/serum protein >. 0.5
  • Pleural fluid LDH/serum LDH >0.6
  • Pleural fluid LDH >2/3 upper limit of normal serum LDH
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6
Q

What causes isolated elevation of alk phos

A

Paget disease

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7
Q

Treatment of frostbite

A
  • Rapid rewarming in warm water bath

- Analgesia and wound care

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8
Q

What is the difference between the two pneumoccocal vaccines (23 vs 13)

A

o Pneumococcal polysaccharide vaccine (PPSV23)
♣ Contains capular material from 23 serotypes that have historically been responsible for the majority of pneumonoccal infections
♣ Because polysaccharides alone cannot be presented to T-cells, the vaccine induces a relatively T-cell-independent B-cell response that is less effective in young children and the elderly

o Pneumococcal conjugate vaccine (PCV13)
♣ Consists of capsular polysaccharides from 13 of the most common serotypes that have been covalently attached to the inactivated diphtheria toxin protein
♣ This polysaccharide-protein conjugate induces a T-cell-depended B-cell response, resulting in improved immunogenicity due to the formation of higher-affinity antibodies and memory cells

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9
Q

What are the indications for urgent dialysis

A 
A = acidosis
E = electrolyte abnormalities
I = ingestion
O = overload
U = symptomatic Uremia
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10
Q

What is the biggest environmental risk factor for pancreatitis

A

Smoking

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11
Q

What are the cancers involved in Lynch syndrome

A

o Associated with colon (non-polyposis), endometrial, ovarian, and skin cancers

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12
Q

Describe Turcot syndrome

A

o FAP + malignant CNS tumor (medulloblastoma)

♣ THINK: TURcot = TURban

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13
Q

What is Wilson disease

A

♣ Mutation in hepatocyte copper-transporting ATPase (ATP7B gene)
♣ Inadequate copper excretion into bile and blood

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14
Q

How does Wilson disease present

A
  • Copper accumulation in: liver, brain, cornea, kidney, joints
  • Liver disease, Kayser-Fleischer rings, renal disease (Fanconi syndrome), neurologic manifestations (behavioral changes, dementia, chorea, parkinsonian sx)
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15
Q

Diagnosis of Wilson disease

A
  • Low ceruloplasmin

* Increased urinary copper excretion

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16
Q

Tx of Wilson disease

A

• Chelation with Penicillamine

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17
Q

What is the cause of hemochromatosis

A

Gene mutation leads to abnormal iron sensing, which causes increased intestinal iron absorption

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18
Q

Presentation of hemochromatosis

A

o Cirrhosis
o Diabetes mellitus
o Skin pigmentation

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19
Q

Treatment of hemochromatosis

A 
•	Phlebotomy (blood-letting)
•	Chelation with Deferoxamine  
o	THINK: Undo the iron from me
♣	Undo = De
♣	Iron = Fe
♣	From me = mine
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20
Q

Describe presentation of alpha-1-antitrypsin deficiency

A
  • Early COPD (uninhibited elastase causes increased breakdown of elastic tissue in lung
  • Cirrhosis (misfolded proteins aggregate in the liver)
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21
Q

Describe the effect of cirrhosis of steroids

A 
Liver is usually responsible for metabolizing steroids
- Cirrhosis = elevated estrogen
•	Testicular atrophy, gynecomastia 
•	Spider telengiectasias
•	Palmar erythema
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22
Q

Tx of non-bleeding esophageal varices

A

♣ Propranolol or Nadolol

• To reduce portal pressure

23
Q

Tx of bleeding varices

A
  • Endoscopic banding
  • Octreotide – reduces portal pressure acutely
  • Ceftriaxone

OR

♣ TIPS procedure: Transjugular intrahepatic portosystemic shunt
• Shunt between the portal vein and hepatic vein relieves portal HTN by shunting blood to the systemic circulation, bypassing the liver

24
Q

Describe how you can evaluate the cause of ascites

A

o Serum-Ascites Albulim Gradient (SAAG) – used to determine cause of ascites
♣ SAAG = (serum albumin) – (ascites albumin)

25
Q

What are the causes of high SAAG

A

• SAAG > 1.1
o This occurs when there is not a lot of stuff in the ascites, meaning it was caused by hydrostatic pressure pushing fluid out
o Causes: portal HTN, R-sided heart failure

26
Q

What are the causes of low SAAG

A

• SAAG < 1.1
o This occurs when there is a lot of stuff in the ascites meaning it was caused by oncotic pressure pulling fluid into the belly
o Causes: cancer, nephrotic syndrome, tuberculosis, pancreatitis, biliary disease, connective tissue disease

27
Q

Tx of ascites

A

o Diuresis = Furosemind + Spironolactone

o Paracentesis

28
Q

How do you diagnose SBP

A

• Tap shows neutrophils >250

29
Q

Tx of SBP

A

IV CTX

30
Q

How do you diagnose hepatocellular carcinoma

A

o Confirmatory test = triple phase CT
♣ Cancer is supplied by arteries, so during arterial phase of the CT, the cancer will light up
♣ Liver is supplied by the portal vein so it will not light up in the arterial phase of the CT but will light up in the venous phase, whereas cancer will not light up in venous phase

31
Q

First step in evaluating a GI bleed

A

1st step = EGD
• If find source = upper GI bleed = treat appropriately
• If negative = lower GI bleed = follow steps below

32
Q

What is next step if EGD showed nothing aka lower GI bleed

A

o If bleed has stopped
♣ Colonoscopy

o If bleeding is ongoing but not brisk
♣ Tagged RBC scan

o If brisk bleeding
♣ Arteriogram to visualize bleed and embolize

o If none of these work:
♣ Pill-cam endoscopy – swallow a pill that is also a camera and when you poop it out we can watch the film and figure out where bleed is

33
Q

What is the difference between Mallory Weiss tear and Boerhaave Syndrome

A

Mallory Weiss = superficial tear; self-limited

Boerhaave syndrome = esophageal rupture; surgical emergency

34
Q

What is the difference between mesenteric ischemia and ischemic colitis

A

Mesenteric ischemia
- Caused by a clot/blockage of the blood supply to the gut

Ischemic colitis
- Caused by lack of blood flow secondary to hypovolemia, usually occurs in watershed areas

35
Q

Causes of pancreatitis

A

• I GET SMASHED:
o Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypertriglyceridemia/Hypercalcemia, ERCP, Drugs (e.g. Sulfa, NRTIs, protease inhibitors)

36
Q

What are the basic criteria of bundle branch block

A

♣ 1. Wide QRS
♣ 2. inverted T-waves in precordial leads
• So T will go opposite way of QRS
♣ 3. No q-wave in V5 or V6

37
Q

Diagnose this EKG:

  • Diffuse ST segment elevations
  • Depressed PR segments
A

Pericarditis

38
Q

Tx of pericarditis

A

NSAIDs + Colchicine

39
Q

Tx of pericardial effusion

A
  • Treat the underlying pericarditis

- If that fails, then do a pericardial window (put hole in pericardium to let fluid drain)

40
Q

Tx of cardiac tamponade

A

Pericardiocentesis (drain the fluid)

41
Q

Tx of vasovagal syncope

A

Beta blockers (block the vagal response to the brain)

42
Q

Describe EPO levels in polycythemia vera

A

♣ Normally, RBC production is depended on EPO released by the kidney and liver in response to tissue hypoxia
♣ EPO activates JAK2 tyrosine kinase, which differentiates late myelid cells into erythrocytes
♣ In PV, RBC production is driven by a constitutively active JAK2 gene rather than by tissue hypoxia; therefore, EPO levels tend to be low

43
Q

What is methemoglobinemia and its causes

A 
♣	Methemoglobin = hemoglobin with oxidized form of Hb (Fe3+) that does not bind to O2 readily but has increased affinity for cyanide
♣	Causes:
•	Nitrates and nitrites
•	Antimalarial drugs
•	Sulfonamides
44
Q

Presentation of methemoglonemia

A
  • Cyanosis
  • Chocolate-colored blood
  • Skin flushing
  • HA, AMS, seizures, coma
  • Arrythmias
  • Tachypnea followed by respiratory depression, pulmonary edema
  • Abd pain, N/V
  • Metabolic acidosis (from lactic acidosis), renal failure
45
Q

Describe the major complication in T2DM

A

o Hyperosmolar hyperglycemic nonketotic syndrome (HHS)
♣ Hyperglycemia = excessive osmotic diuresis = dehydration = HHNS
♣ Symptoms: thirst, polyuria, lethargy, focal neurological deficits (e.g. seizures), can progress to coma and death

46
Q

Tx of torsades

A

Magnesium

47
Q

Adverse effects of Statins

A

Hepatitis, Rhambdo

48
Q

Tx of diabetic nephropathy

A

ACEi

49
Q

Drug tx of supraventricular tachycardias (aka tx of narrow QRS tachycardias)

A

Adenosine

50
Q

Drug tx of V-tch (aka tx of wide QRS tachycardia)

A
  • Amiodorone if stable

- Shock if unstable

51
Q

Tx of A-fib

A
  • Rate control > rhythm control if stable

- Shock if unstable

52
Q

What drugs are used to tx rate control in A-fib

A

CCB (verapamil, diltiazem) = BB

53
Q

What medication can you use to treat 1st and 2nd degree AV block

A

Atropine

54
Q

What is the most dramatic tx that should be used for a fast rhythm vs a slow rhythm

A
  • Fast = shock

- Slow = pace

MS3 (88 decks)

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