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UWorld mixed > test #45 5.4 > Flashcards

test #45 5.4 Flashcards

1
Q

when to involve ethics committee or risk management?

A

basically never on USMLE. handle it on your own.

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2
Q

sudden onset headache and nuchal rigidity

A

subarachnoid hemorrhage

meningeal irritation from blood

can also see papilledema and pupillary dilation, but no other focal neurological signs

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3
Q

xanthochromia

A

blood in CSF

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4
Q

diff between intracerebral hemorrhage & subarachnoid hemorrhage

A

intracerebral: focal neurological impairment
subarachnoid: no focal issues

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5
Q

carrier frequency for mom 1/30
carrier frequency for dad: 1/100

chance child will have disease?

A

(1/30 x 1/2) x (1/100 x 1/2)

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6
Q

what % of observations fall in 1 standard deviation of mean

A

68%

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7
Q

what % of observations fall in 2 standard deviations of mean

A

95%

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8
Q

what % of observations fall in 3% of standard deviation of mean

A

99.7%

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9
Q

normal pulmonary arterial pressure

A

< 20mmHg

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10
Q

definition of pulmonary artery hypertension

A

> 25mmHg

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11
Q

major causes of pulmonary artery HTN

A
  • hereditary (AD: BMPR2 mutation)
  • left heart failure
  • chronic hypoxia: obstructive sleep apnea, COPD
  • chronic thromboembolism
  • HIV infxn
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12
Q

idiopathic pulmonary artery HTN inheritence

A

autosomal dominant w/ variable penetrance

2 hit:

  1. mutation in BMPR2. normally suppresses smooth muscle proliferation
  2. activates disease process (i.e. infxn, drug)
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13
Q

cardiac sounds that can arise w/ pulmonary HTN (2)

A
  1. accentuated S2

2. holosystoic tricuspid regurg (diastolic) due to increased ‘afterload’

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14
Q

etiology of pulmonary HTN in COPD, obstructive sleep apnea, interstitial lung disease

A

hypoxic vasoconstriction

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15
Q

compensation for chronic respiratory acidosis

A

3-5 days
(at least 24hr)

kidney excrete acid & retain HCO3-

> 30

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16
Q

Kussmal breathing

A

shallow breathing seen in diabetic ketoacidosis, attempt to blow off CO2 to compensate for metabolic acidosis (low bicarb, low CO2, low pH)

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17
Q

adverse effects of succinylcholine (3)

A
  1. malignant hyperthermia in genetically susceptible people
  2. hyperkalemia in pts w/ burns, myopathy, crush injury, denervation -> quadriplegia, guillan-barre

(due to upregulation of muscle nAChR & rhabdomyolysis –> increase K+ efflux)

  1. bradycardia, from parasympathetic stimulation or tachycardia, from sympathetic ganglion effects
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18
Q

side effects of atracurium

A
  1. release histamine ->
    bp drop, flushing, bronchoconstriction
  2. spontaneous degradation to laudanosine –> seziure

but, good for renal/hepatic insufficiency

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19
Q

baclofen mechanism

A

GABAb at level of spinal cord

CNS

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20
Q

phase I of succinylcholine

A

strong agonist of nAChR
binds & depolarizies
insensitive to AChE, so prolonged depolarization –> twitching

potentiate: AchE inhibitors, bc Ach will help further depolarize & inactivate muscle.

eventually degraded by plasma cholinesterases

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21
Q

phase II of succinylcholine

A

w/ continuous infusion or SLOW metabolizers

eventually nAChR insensitive to succinylcholine, which can bind & block site, but can no longer depolarize

–> becomes nondepolarizing blocker

antidote: AChE inhibitors (increase Ach concentration)

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22
Q

infective dose of shigella, salmonella, and vibrio cholera, ETEC

A 
least --> most
shigella -- 10 - 10^2
salmonella -- 10^ 7
vibrio cholera: 10^5- 10^7
ETEC: 10^ 8-10^ 10
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23
Q

why is shigella so infective? when does infxn start

A
  • survive stomach acid & bile
  • uniquely bind to mucosal M cells in peyer’s patches

24-72 hrs incubation

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24
Q

tenesmus

A

painful spasm of rectum associated w/ urge to defecate, yet little passage of stool occurs

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25
Q

infective dose of c. perfinges

A

500 organisms

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26
Q

organisms that can cause diarrhea w/ small innoculum

A
  • camplyobacter jejuni - 500
  • entamoeba histolytica - as few as 1
  • giardia lamblia - as few as 1
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27
Q

TB virulence factor: cord factor

A
  • inhibit macrophage & neutrophil maturation
  • induce release of TNF-alpha
  • damages mitochondria

mycoside (2 mycolic acid molecules bound to disaccharide trehalose)

correlates w/ virulence.

no cord factor -> no disease.

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28
Q

TB virulence factor: sulfatides (surface glycolipids)

A
  • inhibit phagolysosomal fusion
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29
Q

thick, ropelike cords of mycobacterial organisms in twisted “serpentine” pattern

A

TB, consistent w/ presence of cord factor

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30
Q

eyes, lies, and capsize

A

wernicke encephalopathy

-opthalmoplegia / nystagmus:

anterograde amnesia: mamillary body
ataxia : cerebellum

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31
Q

what nutrient is often deficient in alcoholics

A

thiamine!
wernicke korsakoff

give IV dextrose & thiamine

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32
Q

wernicke encephalopathy is exacerbated when..

A

IV dextrose WITHOUT THIAMINE

thiamine needed for pyruvate dehydrogenase (pyruvate –> acetyl CoA for glycolysis -> TCA)

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33
Q

Wernicke encephalopathy?

Korsakoff psychosis?

A

acute thiamine def:
Wernicke encephalopathy
ataxia, nystagmus, opthalmoplegia, anterograde amnesia

chronic thiamine def:
Korsakoff
- anterograde & retrograde amnesia, apathy, lack of insight, confabulation

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34
Q

what brain structure is most affected by thiamine deficiency

A

mammillary body, undergoes necrosis.

papez circuit, neural pathway of limbic system involved in cortical control of emotion & memory.

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35
Q

fornix

A

originate from hippocampal subiculum, projects to mamillary body

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36
Q

alexia w/o agraphia

A

suggests corpus callosum lesion

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37
Q

before giving dextrose to alcoholic / malnourished, must give..

A

THIAMINE! to avoid ppt of wernicke encephalopathy.

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38
Q

virus w/ nuclear membrane envelope

A

herpesfamily!

herpes, CMV, EBV, etc

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39
Q

how do antithyroid drugs work (3)

A
  1. oxidation of iodine
  2. iodination of tyrosine residues
  3. coupling of iodotyosine molecules
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40
Q

different between PTU and methimazole (3)

A
  1. propylthiouracil also blocks peripheral conversion of T4 -> T3
  2. PTU shorter half life
  3. PTU for pregnancy!

methimazole = teratogen

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41
Q

both PTU and methimazole as associated with..

A

agranulocytosis.

both: thioamides

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42
Q

preferred rx for hyperthyroidism in US

A

radioactive iodine

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43
Q

definition of agranulocytosis

A

absolute neutrophil count of less than 500/mL

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44
Q

presentation of agranulocytosis

A

fever & sore-throat

often induced by medication

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45
Q

drugs that cause agranulocytosis

A

drugs cccrush myeloblasts & promyeloblasts

dapsone
clozapine
carbamazepine
colchicine
methimazole
propylthiouracil
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46
Q

how to check for agranulocytosis?

A

WBC & differential

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47
Q

patient w/ hyperthyroidism w/ fever & throat pain?

A

worry about methimazole / PTU induced agranulocytosis

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48
Q

PO2 in venous blood

PCO2 in venous blood

A

PO2: 40mmHg
PCO2: 47 mmHg

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49
Q

PO2 in arterial blood

PCO2 in arterial blood

A

PaO2: 104
PaCO2: 40

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50
Q

describe bronchial arterial supply

A

left & right arise from descending thoracic aorta

oxygenated to bronchi & bronchioles

w/ pulmonary artery, form dual blood supply to lungs

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51
Q

describe bronchial drainage

A

drainage:
- part to right heart via azygous, accessory hemiazygous, intercostal veins
- MOST drain to left heart via pulmonary veins

DEOXYGENATED blood into LEFT ventricle

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52
Q

explain why pO2 (100) in left ventricle is lower than pO2 (104) in pulmonary capillaries

A

bc admixture w/ venous blood from bronchial VEINS

most drain into right heart via pulmonary vein

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53
Q

what normally limits blood gas exchange in alveoli

A

CO2 & O2: usu perfusion limited

CO2 equilibrates really fast
O2 also does

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54
Q

perfusion limited

A

CO2, N2O

also O2

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55
Q

diffusion limited

A

CO

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56
Q

what shifts hemoglobin curve to the right

A

unload O2

high temp, pCO2, 2,3DPG

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57
Q

degenerate code

A

more codons (61) than there are amino acids (20)

each tRNA molecule = specific for an AA

multiple tRNA can code for same aa

wobble

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58
Q

explain basis of wobble in tRNA

A

5’ tRNA has different spatial orientation than other 2 bases

may be inosine, which can hydrogen bond w/ uracil, adenine, and cytosine

allows for different codons to = same amino acid

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59
Q

3 categories of vitamin A toxicity

A

think: intracranial HTN, skin changes, hepatosplenomegaly

  1. acute
    - n/v, vertigo, blurred vision
  2. chronic
    - alopecia, dry skin, hyperlipidemia, hepatoxicity, hepatosplenomegaly, visual difficulty, papilledema (pseudotumor cerebri)
  3. teratogenic
    1st trimester: microcephally, cardiac anomalies, fetal death
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60
Q

thiamine deficiency associated w/

A

beri beri wet & dry

wernicke korsakoff

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61
Q

large doses of vitamin C associated w/

A

diarrhea, abdominal bloating

false negative stool guaiac results

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62
Q

large doses of vitamin E

A
  • hemorrhagic stroke in adult

- necrotizing enterocolitis in infants

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63
Q

major use of ELISA

A

quantiative

to measure AMOUNT of protein in body fluid

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64
Q

indirect vs. direct ELISA

A

indirect: test antigen to see if patient has antibody

indirectly assume if you Ab, you must have antigen

direct: test antibody to see if patient has antigen

[directly see if you have antigen]

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65
Q

HIV ELISA

A

look for patient antibody

indirect

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66
Q

name loop diuretics (4) & major use

A

furosemide, toresemide, bumetanide, ethacrynic acid

use for volume overloaded state: CHF

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67
Q

name thiazide diuretic (4) & major use (2)

A

hydrochlorothiazide, chlorthalidone, indapamide, metolazone

use: HTN, calcium nephrolithiasis prophylaxis

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68
Q

ENaC blockers (2)

A

amiloride, triamterene

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69
Q

mineralcorticoid receptor antagonist (2)

A

spironolactone, eplerenone

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70
Q

which diuretic is most likely to produce hyponatremia

A

thiazides

have normal corticomedullary concentration, better able to retain free water in response to ADH

(loop diuretics loose some corticomedullar gradient in TAL, less able to absorb free water in loop of henle & CD)

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71
Q

diuretic causing hypocalcemia?

A

loop (furosemide etc)

BAD for renal nephrolithiasis

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72
Q

hepatitis w/ isoniazid presentation

A

fever, anorexia, nausea

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73
Q

how can isoniazid peripheral neuropathy be averted?

A

administer vitamin B6

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74
Q

fever, urticaria, arthalgia, proteinuria, lymphadenopathy 5-10 days after drug exposure

A

serum sickness

type III HSR

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75
Q

fatigue & new onset cardiac murmur in young adult

A

bacterial endocarditis

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76
Q

nephritic issues with bacterial endocarditis?

A

can have circulating immune complexes –> diffuse proliferative glomerulonephritis

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77
Q

inheritance of hemophilia A? hemophilia B?

A

A: factor 8; X-linked recessive

B: factor 9; X-linked recessve -> christmas disease

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78
Q

difference between hemophilia A & B

A

clinically indistinguishable

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79
Q

common cause of PT prolongation

A

warfarin therapy

80
Q

common causes of increased bleeding time

A

von willebrand disease

NSAID use

81
Q

general side effect of sulfonylurea?
1st generation risk?
2nd generation risk?

A

general: hypoglycemia w/ renal failure
1st gen: disulfram-like rxn
2nd gen: hypoglycemia

82
Q

risk of rapid acting insulin

A

hypoglycemia, rare HSR

83
Q

side effect of metformin

A

lactic acidosis

CONTRAINDICATED in renal failure

84
Q

diabetes drug contraindicated w/ renal failure

A

metformin!

can cause lactic acidosis

85
Q

side effect of thiazolidinediones (4)

A
  1. weight gain (fluid)
  2. edema
  3. hepatotoxicity
  4. heart failure (bc of fluid retention)
86
Q

which diabetes drug can cause weight gain, edema, hepatoxicity, and heart failure

A

thiazolidinediones

87
Q

which diabetes drugs can cause hypoglyemia

A

insulin & sulfonylureas

not TZD or metformin

88
Q

drugs associated w/ pulmonary fibrosis

A

amiodarone, bleomycin, mitomycin C, busulfan, methysergide

89
Q

how to identify lunate on X-ray

A

most medial articulation w/ radius!

be careful when counting!

90
Q

how to identify scaphoid on X-ray

A

lateral articulation w/ radius

be careful when counting

91
Q

what carpal bone articulates w/ thumb?

A

trapezium

thumb swings on trapezium

92
Q

linitis plastica

A

stomach wall grossly thickened & leathy, diffuse stomach adenocarcinoma

93
Q

progression of gastric adenocarcinoma

A

early aggrssive local spread & node/liver mets

recall

  1. virchow node
  2. krukenberg tumor
  3. sister mary joseph node
94
Q

signet cells in stomach

A

diffuse adenocarcinoma, associated w/ linitis plastica

95
Q

nodular, polypoid-well demarcated masses in stomach.

microscopy: well-formed glands w/ columnar/cuboidal cells

A

intestinal-type adenocarcinoma

resembles colon cancer

96
Q

prognostic factors of gastric adenocarcinoma

A

depth of invasion through gastric wall & regional lymph involvement

97
Q

what type of gastric carcinoma can ulcerate

A

intestinal type, can present as upper GI bleed

98
Q

rugal thickening w/ acid hypersecretion in stomach

A

think zollinger-ellison; bc gastrin increases acid secretion & parietal cell growth factor

99
Q

hypertrophy of brunner’s gland

A

suggests peptic ulcer disease

brunner gland in duodenum –> secrete mucous via crypts of lieberkuhn

100
Q

bicarbonate in small intestine comes from.. (2)

A
  1. pancreatic duct secretions

2. brunner’s gland (only in duodenum)

101
Q

brunner gland. where am i?

102
Q

crypt of lieberkuhn. where am i?

A

anywhere from small intestine to colon.

stomach: has gastric glands

103
Q

CCK and secretin on pancreatic secretions

A

CCK stimulates mostly acinar cells (enzymes)

secretin stimulates mostly ductal cells (bicarb)

104
Q

CCK and secretin on gallbladder

A

CCK stimulates gallbladder contraction & sphincter of Odi opening

secretin stimulates bile secretion

105
Q

chronic gastritis w/ h. pylori leads to..

A

diffuse gland atrophy & intestinal emtaplasia

increase risk of gastric carcinoma

106
Q

resistance to rifampin

A

mutation in DNA-dep RNA pol

107
Q

best indicator of MR severity?

A

presence of S3 gallop

reflects increase rate of left ventricular filling due to large volume of regurgitant flow re-entering ventricle during mid diastole

108
Q

functional diastolic rumbling?

A

suggests mitral regurg leading to high rate of regurgitant flow across MV in diastole

109
Q

is intensity of murmur a good indicator of mital regurg?

A

no, bc low intensity means larger regurg orifice –> worse!

110
Q

what causes mid systolic click in MVP?

A

tensing of chordae tendineae as they are being pulled taut by valve leaflets into atrium.

111
Q

chordae tendinae

A

connect papillary muscles to AV valves leaflets (mitral & tricuspid)

collagen & elastin

112
Q

most common cause of aortic stenosis?

A

degenerative senile calcification of valves

result of prolonged hemodynamic stress on valves

common >65 y/o

113
Q

physical exam of aortic stenosis (3)

A
  1. pulsus parvus et tardus:
    - small & slow rise in carotid pulse
  2. diminished aortic component to S2
  3. harsh systolic crescendo-decrescendo murmur right upper border
114
Q

valve issues w/ rheumatic fever (3)

A
  1. mitral stenosis (late)

2. mitral & aortic regurg

115
Q

what type of valvular issue is caused by infectious endocarditis

A

insufficiency of any valve
(regurg)

NOT stenosis

116
Q

cystic medial necrosis can lead to what valve issue

A

aortic regurg

dilation of ascending aorta

117
Q

non-musculoskeletal issues associated w/ ankylosing spondylitis

A

peripheral enthesopathies
uveitis
apical pulmonary fibrosis
aortic insufficiency

118
Q

medical to prevent calcium stone formation

A

DON’T GET CONFUSED

thiazides!!

reduce calcium in tubules

119
Q

diuretic that worsens calcium stones

A

furosemide!

looses Ca2+ means more in the tubules

120
Q

how to thiazides reduce hypercalciuria (2)

A
  1. block Na/Cl –>
    - less Na+ in tubular cell, activates basolateral Na/Ca2+ antiporter, which pumps Na into cell in exchange for Ca2+

-this increases uptake of Ca2+ across apical membrane

  1. hypovolemia –?
    increases Na and H20 absorption in PCT, leading to passive Ca2+ too
121
Q

acetazolamide on calcium levels

A

induces metabolic acidosis -> increase bone release of Ca2+ PO4-

hypercalciuria, worsens calcium stones

122
Q

comedocarcinoma

A

DCIS w. solid sheets of pleomorphic, high grade cells w/ central necrosis

chroni inflammation & periductal concentrib fibrosis

calcify necrosis –> mammographic detection

123
Q

paget’s disease of nipple

A

malignant cells spread from DCIS into nipple w/o having crossed basement membrane

erythema and scale crust

124
Q

medullary breast carcinoma

A

good prognosis

invasive, lymphocytic infiltrate

solid sheets of vesicular, pleomorphic, mitotically active cells w/ lymphoplasmacytic infiltrate around & within tumor & pushing noninfiltrating border

125
Q

sclerosing adenosis

A

central acinar compression & distortion by surrounding fibrotic tissue w/ peripheral ductal dilation

fibrocystic change

slight association w/ carcinoma risk

126
Q

breast ductal dilation, inspissated breast secretion, chronic granulomatous inflammation in periductal & interstitial area

A

mammary duct ectasia

127
Q

phyllodes tumor

A

like fibroadenoma but increased cytological atypia & stromal cellularity & overgrowth

biphasic

leaflike

128
Q

how long will myocardium look normal on histology post MI

A

up until 4 hours post MI.

then waviness in myofibrils (due to relaxation) will start, w/ edema, hemorrhage, early coagulative necrosis

129
Q

earliest sign of coagulative necrosos of cardiac myocytes

A

cytoplasmic hypereosinophilia

also: punctate hemorrhage & edema

130
Q

when do neutrophils come into myocardium post MI

131
Q

when do macrophages come into myocardium post MI

132
Q

when does granulation tissue form post MI

A

10-14 days post MI

133
Q

when does collagen start to lay down post MI

A

2 weeks post MI -> 2 months

134
Q

causes of acute pancreatitis (common & uncommon)

A

usu gallstones & alcoholism

also

  1. drugs: azathioprine, sulfasalazine, furosemide, valproic acid
  2. infxn: mumps, coxsackie virus, mycoplasma pneumoniae
  3. hypertriglyceridemia
  4. structure abnormalities of pancreatic duct (stricture, cancer, divisum) or ampulla (choledochal / bile duct cyst, stenosis of sphincter of odi)
  5. hypercalcemia
  6. surgery of stomach / bilary tree
  7. recent endoscopic retrograde cholangiopancreatography
135
Q

repeated acute pancreatitis that resolves on fasting w/ no risk factors in young patient?

A

consider hypertriglyceridemia

136
Q

how does hypertriglyceridemia lead to acute pancreatitis

A

DIRECT TISSUE TOXICITY

high TG -> increased production of free fatty acids within pancreatic capillaries via pancreatic lipase

normally is bound to albumin

when TG >1000mg/dl -> will exceed albumin’s binding capacity & directly injure pancreatic acinar cells

137
Q

increased cholesterol predisposes to.. (3)

A
  1. coronary artery disease
  2. peripheral vascular disease
  3. stroke
138
Q

hemachromatosis on pancreas

A

pancreatic fibrosis –> secondary diabetes

does NOT cause pancreatitis

139
Q

things that can cause pancreatitis mnemonic

A

GET SMASHED

  1. gallstones
  2. ethanol
  3. trauma (seat belt)
  4. steroids
  5. mumps
  6. autoimmune
  7. scorpion sting
  8. hypercalcemia / hypertriglyceridemia
  9. ERCP
  10. drugs (esp sulfa)
140
Q

wilson disease signs

A

Copper is Hella BAD

unable to loose Cu2+ in bile

  1. low ceruloplasmin, cirrhosis, corneal deposit (kaiser-fleisher ring), hepatocellular carcinoma
  2. hemolytic anemia
  3. basal ganglia degeneration (parkinsonian)
  4. asterixis
  5. dementia, dyskinesia, dysarthria
141
Q

turbid plasma

A

suggests lots of chylomicrons in blood stream

think: turbid blood 30min post hamburger!

142
Q

lipoprotein lipase deficiency

A

1 form of hyperchylomirconemia:

autosomal recessive

childhood: hyperlipidemia, abdominal pain (pancreatitis), lipema retinalis, xanthomas, hepatosplenomegaly

reduced LPL response to heparin

143
Q

what converts nascent HDL to mature HDL

A

LCAT: which esterifies cholesterol

144
Q

role of CETP

A

cholesterol ester transfer protein: transfers cholesterol liporotein particles from mature HDL to VLDL, IDL, LDL

145
Q

hyperchylomicronemia can develop with what 2 deficiencies

A

autosomal recessive.

  1. deficiency of lipoprotein lipase
  2. mutation in apo C-II

recall, apo C-II activates LPL

146
Q

hypertriglyceridemia results from..

A

autosomal dominant.
hepatic overproduction of VLDL

CAUSES PANCREATITIS

increased blood levels of VLDL and TG

147
Q

presentation of hyperchylomicronemia

A

increased chylomicrons & TG

PANCREATITIS, hepatosplenomegaly, eruptive/pruritic xanthoma

no increase risk of atherosclerosis

148
Q

heparin on lipase activity

A

heparin releases endothlium-bound lipases, encourage triglyceride clearance from circulation.

149
Q

pain w/ hyperchylomicronemia / hypertriglyceridemia?

pain w/ hypercholesterolemia?

A

high chylomicron & TG –> abdominal pain –> PANCREATITIS

high LDL cholesterol –> chest pain –> MI

150
Q

hallmark of familial hypercholesterolemia

A

tubular xanthomas (tendon)

also have: xathelasma & acrus cornea

151
Q

what increases risk of pancreatic cancer?

A
  • tobacco smoke

- obesity

152
Q

what increases risk of gastric cancer?

A
  • dietary nitrates (smoked food)
  • alcohol & tobacco
  • h. pylori
153
Q

what increases risk of liver cancer?

A
  • hep B & C
  • liver cirrhosis
  • hemochromatosis
  • wilson’s
  • aflatoxin
  • carbon tetrachloride
154
Q

what increases risk of colorectal cancer?

A
  • hereditary colorectal cancer
  • inflammatory bowel disease
  • obesity
  • charred / fried food
155
Q

what increases risk of renal cancer?

A
  • tobacco smoke
  • obesity
  • hypertension
156
Q

what increases risk of bladder cancer

A
  • tobacco smoke
  • occupational exposure to..
  • rubber
  • aromatic amine-containing dyes (benzidine, 2-napthylamine,
  • textiles
  • leather
  • aniline dye
  • phenacetin
157
Q

what increases risk of breast cancer

A
  • early menarche
  • late menopause
  • nulliparity
  • BRCA mutation
158
Q

what increases risk of prostate cancer

A

age

african american race

159
Q

what increases risk of leukemia / lymphoma

A

alkylating agents

160
Q

what increases risk of angiosarcoma in liver

A

arsenic

vinyl chloride

161
Q

what increases risk of papillary thyroid cancer?

A

ionizing radiation

162
Q

2nd leading cause of lung cancer?

A

radon exposure

163
Q

angiosarcoma prognosis

A

aggressive & difficult to treat

164
Q

gross appearance of transitional cell carcinoma of bladder?

histology

A

gross cystoscopy: multifocal sessile or papillary tumors

histology: pleomorphic, hyperchromatic nuclei, increased NC ratio, disrupted oritentation & polarity

165
Q

how does cyclophosphamide & ifosfamide cause hemorrhagic cystitis

A

acrolein – irritates bladder mucosa

166
Q

carcinoma, mesothelioma, thymoma, sarcoma, trophoblastic tumor, desmoplastic small round cell tumor all..

A

stain positive for ketatin!

167
Q

desmin, caldesmon, actin +

A

muscle tissue stain

168
Q

stain for endothlium

A

CD34+, von willebrand factor

169
Q

presentation of dermatomyositis (3)

A

grotton papule
- red violaceous fat-topped papules w/ light scale. over bony prominences.

heloptrope rash: erythematous or violaceous edematous eruption on upper eye-lid & periorbital skin

proximal muscle weakness!

170
Q

serum findings in dermatomyositis

A 
ANA +
anti-Jo1 +
anti-SRP
anti-Mi2
elevated creatinine kinase
171
Q

prognosis of dermatomyositis

A

if present after age 50 –> increased risk of underlying occult malignancy

172
Q

dermatomyositis is associated w/ underlying

A

lung cancer!

173
Q

lichen sclerosis

A

elevated white lesion near vagina

174
Q

acute pyelonephritis pathogenesis

A

must have vesicoureteral reflux in some way

175
Q

fat embolism syndrome triad

A
  1. acute onset neuro issues
  2. hypoxemia
  3. petechial rash

trauma of long bone/pelvis

176
Q

pathogenesis of fat embolism syndrome

A
  1. trauma dislodge fat in marrow
  2. travels in bone marrow sinusoud
  • pulmonary vasculature
  • CNS (via AV shunt)
  • thrombocytopenia & petechial rash due to platelet coating fat microglobules
177
Q

why see petechial rash in fat embolism syndrome?

A

thrombocytopenia

platelet coats fat globule in vasculature

178
Q

presentation of epidural hematoma

A

talk and die

may loose consciousness after injury. then lucid interval -> loss of consciousness

179
Q

epicranial aponeurosis & periosteum cover..

A

outer surface of skull

180
Q

why is there a physiological drop in systolic pressure with inspiration

A

increased pulmonary vascular capacitance –> reduced left ventricle preload

181
Q

what is there a exacerbated drop in systolic pressure w/ inspiration w/ pulsus paradoxus?

A

physiologic: increased pulmonary capacitance -> reduced preload

+

increased filling of right heart, normally bulges into pericardium, but when filled will blood -> push against interventricular septum, reducing LV stroke volume

182
Q

low potency antipsychotics associated with

A

non neurologic:

histamine block: sedation
cholinergic block
alpha-1 block: orthostatic hypotension

183
Q

name 2 low potency 1st generation antipsychotics

A

chlorpromazine

thioridazine

184
Q

name 2 high potency 1st generation antipsychotics

A

haloperidol

fluphenazine

185
Q

migratory thrombophlebitis suggests

A

underlying visceral malignancy

trousseau’s sign

186
Q

explain trousseau’s sign

A

migratory thrombophlebitis

bc common paraneoplastic syndrome: hypercoagulability, esp adenocarcinoma (of pancreas, lung, colon)

secrete thromboplastin-like substance -> cause chronic intravascular coagulation –> disseminated & tend to migrate

187
Q

superficial venous thromboses that appear in one site, resolves & appears elsewhere

A

migratory thrombophlebitis –> underlying visceral malignancy

188
Q

WBC casts ppt by what in renal tubular cells

A

Tamm-Horsfall protein, secreted by tubular epithelial cells

189
Q

what will have highest rate of metabolism in glycolytic pathway: glucose 6-phosphate, mannose 6-phosphate, galactose 1-phosphate, fructose 1-phosphate, glucose 1-phosphate

A

fructose 1-phosphate, bypasses rate limiting step of PFK-1

all others enter before PFK-1

190
Q

rate limiting enzyme in glycolysis

A

phosphofructokinase

F 6-phosphate -> F 1,6 bisphosphate

191
Q

mannose metabolism

A

formed from metabolism of several polysaccharides & glycoproteins

phosphorylated to mannose 6-P, converted to fructose 6-P (by mannose isomerase) then acted on by PFK-1

192
Q

galactose metabolism

A

galactoskinase makes galatose 1-P

transfer of UDP to galactose 1-phosphate, then epimerization to UDP-glucose (by galactose 4-epimerase).

resultant glucose 1-P -> glucose 6-P via phosphoglucomutase

then PFK-1

193
Q

fructose metabolism

A

fructokinase
fructose 1-phosphate

F 1P–> DHAP & glyceradehyde
via aldolase B

glyceraldehyde -> glyceraldehyde 3-P
via tiokinase

becomes pyruvate eventually

bypass PFK-1

194
Q

gaucher disease

A

defect: glucocerebrocidase
accumulate: glucocerebroside

hepatosplenomegaly, aseptic necrosis, gaucher cells

195
Q

presentation of fabry’s

A
  1. peripheral neuropathy of hand and feet
  2. angiokeratoma
  3. cardiovascular / renal disease (COD)
196
Q

DNR means (3)

A
  1. no intubation or mechanical ventillation
  2. no defibrillation or IV drugs to acutely treat terminal rhythm
  3. no chest compressions

can otherwise specify additionally:

  • no artificial feeding
  • etc
197
Q

order of next of kin

A

spouse
adult children
parents
adult siblings

UWorld mixed (60 decks)

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