rosh review questions Flashcards
what are the different mechanism of action between PPIs and H2 receptor blockers?
Proton-pump inhibitors directly block the hydrogen-potassium ATPase action on parietal cells to effectively decrease acid suppression.
H2 Blockers: competitively bind with gastric parietal cells to inhibit gastric acid secretion
Proton-pump inhibitors have greater effectiveness in treating esophagitis because they act on the final pathway of acid secretion rather than one of its receptors.
what is pre-tibial myedema?
it is a skin condition in Grave’s disease- hyperthyroidism- looks like peripheral vascular disease - it is caused by the deposition of hyaluronic acid (hydrophilic glycosaminoglycans in the dermis)
when do you add dextrose to IV fluid replacement in DKA treatment?
when anion gap is still elevated but glucose is < 200.
when would you give sodium bicarb in DKA?
if pH is < 6.9. otherwise it’s controversial to add this when bicarb level is low.
how is anion gap calculated?
Anion Gap = Sodium - (Chloride + Bicarbonate).
Potassium may or may not be included in anion gap calculation- if it is, it changes the normal range.
what are physical barriers of innate immune system?
physical barriers which include the skin, sweat, oral secretions, stomach acid, and mucosa
what are physical exam findings of bacterial infective endocarditis?
fever, Roth spots, Osler nodes, murmur, Janeway lesions, anemia, nailbed hemorrhages, emboli (FROM JANE)
what are Roth spots
retinal changes from infective endocarditis
what are osler nodes vs janeway lesions
infective endocarditis
osler nodes- on hands, more like hard bumps or moles
janeway lesions- hemorrhagic lesions
what are the most common bacteria for endocarditis- mechanical vs. natural valve
IVDA: Staphylococcus aureus, tricuspid
Native valve: Staphylococcus aureus, viridans streptococci (most common in previously diseased), mitral
Pneumopericardium- what are the impacts on hemodynamic status? what’s the severe complication?
increased pulmonary capillary wedge pressure, decreased cardiac output, and increased systemic vascular resistance.
can develop into cardiac tamponade and cardiogenic shock
what is risk with succinylcholine? which patients to avoid this for rapid sequence intubation?
succinylcholine (suxamethonium) is a rapid-acting depolarizing skeletal muscle relaxant that can cause fatal hyperkalemia and, less commonly, malignant hyperthermia
avoid in ESRD
what does positive Murphy’s sign indicate?
acute cholecystitis- RUQ pain
imaging recommendations for acute cholecystitis workup
initial: ultrasound- better detection of gallstones compared to CT scan
gold standard: HIDA scan
basal cell carcinoma defining features
translucent, pearly nodule and rolled raised edge.
thyroid storm medication regimen
propranolol, propylthiouracil, potassium iodide, dexamethasone
Grave’s disease
propranolol first because decreasing peripheral conversion of T4 to T3. Propylthiouracil- block synthesis of thyroid hormone potassium iodide- prevent release of stored thyroid. dexamethasone- concern for adrenal insufficiency and decrease peripheral conversion of T4 to T3
Beta-blocker (propranolol)
Thioamide (propylthiouracil or methimazole)
Iodine solution
Glucocorticoids
what is treatment for 3rd degree HB?
electrophysiology consult: permanent pacemaker placement
what anticoagulant is approved during/after pregnancy
enoxaparin- low molecular weight heparin
describe hyperparathyroidism
Labs will show high PTH, high calcium, low phosphorus
Most commonly caused by an adenoma with unregulated overproduction of PTH
hereditary angioedema
deficiency of C1 inhibitor- part of the compliment system
excessive bradykinin
Tx: replase C1 esterase inhibitor- FFP