Mon June 29 Flashcards

1
Q

how may ethylene glycol lead to kidney damage?

A

ethylene glycol is metabolized to glycolic acid and oxalic acid.

  • Glycolic acid causes direct tubular cytotoxicity
  • oxalate precipitates and causes tubular obstruction
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2
Q

pyruvate carboxylase function?

A

Converts pyruvate to oxaloacetate for gluconeogenesis

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3
Q

What deposits in Henoch-Schlonlein purpura?

A

IgA and C3 deposition

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4
Q

what is amlodipine?

A

Ca channel blocker

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5
Q

What is diltiazem?

A

Ca channel blocker

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6
Q

does bicarb increase with vomiting?

A

yes - you have loss of H which is used to produce the buffer H2CO3, resulting in a relative increase in HCO3-
The dehydratio also leads to impaired HCO3- excretion

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7
Q

how does potassium contribute to the increased bicarb that occurs with metabolic alkalosis?

A

hypokalemia from loss of vomiting results in more uptake of H, as it is exchanged for K
(K goes extracellular for H which goes intracellular)

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8
Q

what is choroidal nevus?

A

an eye freckle

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9
Q

is choroidal nevus genetic?

A

NO

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10
Q

which pathway is responsible for crude touch?

A

spinothalamic

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11
Q

what fungus appears as sphagetti and meatballs on KOH prep?

A

malessezia

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12
Q

the dose of local anesthetic to achieve adequate anesthesia is higher in….

A

infected tissue - increased acidity at infected sites renders the anesthetic to its charged form, which does not cross the cell membranes

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13
Q

morphine is predominantly cleared in the. …

whereas fentanyl and hydromorphone are primarily cleared…

A

kidneys

in the liver

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14
Q

what is eplerenone?

A

a mineralocorticoid blocker that has less anti-androgenic effects than spironolactone

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15
Q

what do tRNA molecules have at their 3’ end? (the acceptor stem)?

A

a CCA tail -used for other molecules to recognize them

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16
Q

buproprion MOA

A

inhibits reuptake of NE and dopamine

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17
Q

buproprion A/E?

A

seizures

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18
Q

who is buproprion contraindicated in ?

A

those with seizure disorders and eating disorder (electrolyte imbalances increase risk for seizures)

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19
Q

which radiation-related skin changes may be present acutely post radiation (within 3 months?)

A

apoptosis and epidermal edema
erythema, desquamation
pigment changes and loss of skin appendages (hair, glands)

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20
Q

which radiation-related skin changes may be present in the late stage post radiation (over 3 months?)

A
  • Fibrosis - from homogenization of dermal collagen (due to fibroblast activation by TGF-B released from dying cells)
  • vascular damage -> chronic hypoxia and ulceration
  • abnormal microvasculature (telangiectasias)
21
Q

which organisms form pink colones on macconkey agar?

A

organisms that ferment lactose (E coli, Klebsiella, Enterobacter)

22
Q

what is the major virulence factor of E coli that cause neonatal meningitis?

A

K1 capsular antigen

23
Q

When do you start prophylaxis for pneumocystitis jiroveci?

A

CD4 <200

24
Q

When do you start prophylaxis for toxoplasmosis gondii?

A

CD4<100

25
Q

When do you start prophylaxis for M avium?

A

CD4< 50

26
Q

Uterine fundus abnormalities result from…

A

failed lateral fusion of the paramesonephric ducts

27
Q

Failure of the involution of the paramesonephric ducts would result in what?

A

a longitudinal uterine septum

28
Q

what does heteroplasmy mean?

A

it refers to having different mitochondrial genomes within a single cell (each cell has 100s of mitochondria)

29
Q

dysthmia AKA

A

persistant depressive disorder

30
Q

how does persistant depressive disorder differ from major depressive disorder?

A

its a chronic form of depression that lasts for years but is less severe than MDD

31
Q

diagnosis criteria of MDD vs persistant depressive disordeR?

A

MDD - 5 criteria met for at least 2 weeks with severely impaired functioning

Persistant depressive disorder - 3 criteria met, lasts for at least 2 years, milder impairment in functioning

32
Q

which enzyme is absent in Gauchers disease?

A

lysosomal beta-glucocerebrosidase

33
Q

what accumulates in Gauchers disease?

A

glucocerebrosidase

34
Q

how do you treat Gauchers disease?

A

recombinant glucocerebrosidase

35
Q

how do you administer recombinant glucocerebrosidase?

A

IV
-its a polypeptide (peptide drugs undergo extensive cleavage in the stomach and duodenem, and also arent effectively absorbed across the intestine)

36
Q

recombinant glucocerebrosidase MOA?

A

binds to mannose-6-phosphate receptor on the cell, and gets endocytosed into lysosomes where it degrades accumulated glucocerebrosidase

37
Q

presentation of Gauchers diseasE?

A

hepatosplenomegaly, bone pain, pancytopenia (from accumulation of lipid laden macrophages)

38
Q

how does infusion of excess normal saline lead to non anion gap metabolic acidosis?

A

the excess chloride causes bicarb to shift inside of cells -> decreased blood pH

Also the increase blood volume causes the kidneys to secrete Na, increasing urinary Na

39
Q

what repeats in huntingtons disease?

A

CAG

40
Q

In huntingtons disease, there is atrophy of. ..

A

the caudate nucleus

41
Q

what causes hemiballismus?

A

decreased activity in the subthalamic nucleus

42
Q

which 2 factors are important for osteoclast differentiation?

A

M-CSF (macrophage colony stimulating factor)

receptor for activated nuclear factor kappa-b ligand (RANKL)

43
Q

what will the osteoclasts look like in pagets disease?

A

Osteoclast multinucleated giant cells have up to 100 nuclei (opposed to the normal 2-5)

44
Q

what causes juvenile pagets disease ?

A

OPG loss of function mutations (the decoy receptor for RANKL)

45
Q

kinesin moderates ____ transport

A

anterograde

46
Q

dynein moderates ____ transport

A

retrograde

47
Q

Which movement is the infraspinatous muscle responsible for?

A

external rotation (attaches from the scapula to the humeral head, on the back)

48
Q

the subscapularis helps with which movements of the arm?

A

ADDuction and internal rotation

49
Q

what movement does the supraspinatous perform?

A

ABduction of the arm