im Flashcards
(355 cards)
emergent tx for hyperkalemia
hyperkalemia is treated emergently when ECG changes (peaked t waves, widened QRS, bradycardia, disappearance of p waves, sinus node dysfunction and av node block) or when K+ is really high (like >6.5) or rises really fast. Calcium is used to stabilize cardiac membrane. Since it’s faster to shift K+ intracellular than get it out of the body, insulin is given. Glucose is also given to prevent hypoglycemia.

acute epididymitis usually due to bladder obstruction and the organism ______ in men >35 and due to ________ in men <35
men >35: e coli men < 35 N gonorrhea, Chlamydia
dermatomyositis antibodies
anti RNP, anti JO 1, anti Mi2 bonus: highly elevated creatinine kinase
in patients wither dermatomyositis, you need to screen for…
internal malignancy! they are at much higher risk for cancer also interstitial lung disease, myocarditis, dysphagia
seen with heliotrope rash, proximal muscle weakness, rash on shoulders

dermatomyositis
anti RNP, anti Jo 1, anti Mi2
give high dose glucocorticoid steroid plus glucocorticoid steroid sparing agent and screen for malignancy
how do you tell the difference between IgA nephropathy and acute post infectious glomerulonephritis?
both are nephritic syndrome (blood in urine, htn). Ig A nephropathy will affect Adults (20s-30s usually men) while postinfectious GN usually affects kids ages 6-10. IgA nephropathy shows up 5ish days after an infection while postinfectious GN takes weeks after an infection and it’s usally strep throat or impetigo so check their antistretolysin O titers. Also in IgA nephropathy complement levels are normal while in postinfectious GN complement levels are low. both tend to have benign course but IgA nephropathy can cause rapidly progressive glomerulonephritis and postinfectious GN can possibly lead to CKD in adulthood
triad of paroxysmal nocturnal hemoglobinuria
- hemolytic anemia
- pancytopenia
- thrombosis (especially in weird places like in abdomen, hepatic, cerebral)
usually in middle age b/c acquired mutation, lack CD55, CD 59 on RBCs, tx: prednisone and eculizumab
describe cardinal symptoms of ACA, MCA, posterior, opthalmic, lacunar stroke syndromes

high fever, severe polyartheritis, lymphopenia & thrombopenia, macular rash 3-7 days after travel to tropical/subtropical regions of central/south america, asia, africa
chikungunya fever
transmitted by mosquito (Aedes)
supportive care
often causes chronic arthritis, may have to give methotrexate
opening snap with mid diastolic rumble heard best at the apex
mitral stenosis,
most commonly due to rheumatic fever (usually in immigrants)
-can cause right sided, heart failure, dyspnea, left atrium dilation –> bronchus elevation and afib
Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with new onset afib with RVR?
- Are the symptomatic? Presumably yes or you wouldnt get called
- Are they unstable? Like will they die in seconds? If yes, you shock – synchronous cardioconversion. They will need anticoag for a month afterwards
- Much more likely scenario: symptomatic and stable: You need to RATE CONTROL. Goal: below 110. Here’s the all important question: are they in heart failure exacerbation or not?
Acute decomp HF: Give Digoxin or Amiodirone
No HF: CCB like diltiazam or beta blocker like metopropolol

Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with chronic afib
per AFFIRM trial, you can either do rate or rhythm control. Really the only time you’ll do rhythm control is for somebody who has “no good reason”to be in afib and won’t hop right back into if you convert them out and you’ll for sure anticoag those peeps.
For rate control: diltiazem or metroprolol.
Anticoag? CHA2DS2VAS score >2
for score of 1, maybe, maybe aspirin, maybe nothing
Anticoag:
Warfarin: No bridge needed for afib. Reversible. Inconvenient. Have to worry about diet. INR 2-3.
NOACs: Dabigatran, Apixiban, Rivaroxaban: easier, no reversal, insurance?

most common site of ectopic electrical foci causing afib
pulmonary veins
most common anatomic origin of atrial flutter

tricuspid annulus
status of pt with + Anti-HepB surface antibody and +Anti HepB core antibody and -HebBeAg
AntiHepB core antibody is present in acute or chronic infection but NOT after immunization; Anti-HepB surface antibody is present after immunization or succesfully clearing an infection so this person succesfully cleared an infection.
HepB e Ag indicates active infection and viral replication, infectivity
You have a patient with atypical community acquired pneumonia, GI symptoms and confusion – what tests would be really helpful besides the usual labs?
likely Legionnaire’s disease, especially if history of travel
Sputum culture Gram stain: lots of neutrophils, no organisms
Urinary legionella antigen
also low Na+ on BMP
acute symmetric arthritis in a school teacher/day care worker, maybe fever, fatigue, diarrhea
Parvovirus B19
describe areas of referred abdominal pain

test for suspected urolithiasis
abdominal US or noncontrast spiral CT
why is colonoscopy usually not performed in pts with acute abdominal pain
risk of perforation
what are 3 most common causes of esophogitis in patients with HIV?
- Herpes simplex virus
- candida
- CMV
How do you tell the difference? In Candida albicans, they will usually have oral thrush as well so that one is easy. For VIRAL esophogitis, the primary complaint is PAIN with swallowing but they can still swallow.
HSV: usually ulcers around mouth, round volcano-like ulcers in esophagus
CMV: linear ulcerations in esophagus
symptoms of hemorrhagic stroke in cerebellum
ipsilateral ataxia
nystagmus
occiputal headache, maybe neck stiffness
NO hemiparesis
facial weakness
symptoms of hemorrhagic stroke in Thalamus
contralateral hemiparesis and hemisensory loss
eyes deviate Toward hemiparesis
upgaze palsy
nonreactive miotic pupils
















































