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UWorld mixed > test #41 4.30 > Flashcards

test #41 4.30 Flashcards

1
Q

immunoglobulins made by Salk polio vaccine?

A

killed – only IgG

injected intramuscularly, unable to stimulate mucosal secretory IgA

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2
Q

immunoglobulins made by Sabin polio vaccine?

A

live – both IgG and IgA on (mucosal surfaces)

will colonize natural site of viral entry, producing a greater & more prolonged immune response there.

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3
Q

difference between Salk & Sabin’s polio vaccine

A

Salk - killed. less effective in generating prolonged oropharyngeal & intestinal IgA
(not serum)

Sabin - live, will be able to colonize mucosal surface and secrete IgA

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4
Q

two primary sites of poliovirus replication

A

oropharynx & intestine

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5
Q

common sites of psoriasis

A

elbow, knees, gluteal cleft, lumbosacral area, glans penis, scalp

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6
Q

nail changes associated w/ psoriasis

A

yellow-brown discoloration w/ pitting, thickening, or crumbling

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7
Q

type of arthritis w/ psoriasis

A

often deforming, upper extremity, small joint

dactylitis (sausage fingers), pencil-in-cup defomity on x-ray

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8
Q

HLA subtype associated w/ psoriasis

A

HLA C

HLAB27 too bc of psoriatic arthritis

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9
Q

who makes angiotensin converting enzyme?

A

pulmonary vascular endothelial cells

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10
Q

three direct effects of antgiotensin II

A
  1. sodium retention (direct)
  2. aldosterone production
  3. vasconstriction
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11
Q

negative predictive value.

“what’s the probability that negative test results truly mean absence of disease”

A

of the people who tested negative, how many don’t have the disease

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12
Q

relationship of NPV and prevalence

A

NPV decreases as prevalence increases

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13
Q

Gardos channel blockers for Sickle-cell anemia

A

Ca2+ dependent K+ channel blockers, reduces K+ & H2O efflux from erythrocytes

prevents dehydration & sickling in Sickle-cell anemia

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14
Q

which substances increase gastric acid production from parietal cells? block

A

increase: histamine, Ach, gastrin
block: PGE2

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15
Q

predominant source of TGF-alpha

A

CARCIMONAS

also, mac

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16
Q

cachexia cytokines

A

TNF-alpha, IFN-gamma, IL-6

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17
Q

what can severely impair cardiac output in patients w/ aortic stenosis

A

sudden drop in preload w/ loss of atrial contraction (i.e. atrial fibrillation)

bc left heart needs to generate lots of pressure to get blood out in aortic stenosis, now relies on atrial contraction for maximal preload (max LV filling)

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18
Q

in which pts is atrial contraction importrant

A

patients w/ poorly compliant left ventricles. needed to maintain adequate LV filling.

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19
Q

definition of preload

A

end-diastolic volume in ventricle

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20
Q

definition of afterload

A

arterial resistance

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21
Q

where does CN I olfactory bundles enter skull?

A

cribiform plate

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22
Q

what goes through optic canal

A
  1. CN II
  2. central retinal vein
  3. opthalmic artery
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23
Q

what goes through superior orbital fissure?

A
  1. CN III
  2. CN IV
  3. CN VII
  4. CN V1
  5. opthalmic vein
  6. sympathetic fibers
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24
Q

foramen rotundum

A

CN V2

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25
Q

foramen ovale

A

CN V3

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26
Q

foramen spinosum

A

middle meningeal artery & vein

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27
Q

internal acoustic meatus

A

CN VII

CN VIII

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28
Q

jugular foramen

A

CN IX,
CNX,
CN XI,
jugular vein

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29
Q

foramen magnum

A

spinal root of CN XI
brain stem
vertebral artery

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30
Q

hypoglossal canal

A

CN XII

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31
Q

jugular foramen (vernet) syndrome

A

loss of CN IX, X, XI

  • loss of taste from posterior 1/3 tongue (CN IX)
  • reduce parotid gland secretion (CN IX)
  • loss of gag reflex (CN IX, X)
  • dysphagia (CN IX, X)
  • dysphonia/hoarseness (CN X)
  • soft palate drop w/ deviation of uvula to normal side (CN X)
  • SCN and trapezius paralysis (CN XI)
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32
Q

air in the gallbladder biliary tree suggests

A

gallstone ileus

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33
Q

where does gallstone lodge in gallstone ileus

A

trapped behind the ileocecal valve.

see it in ileum

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34
Q

choledocolithiasis

A

obstruction of cystic or common bile duct by gallstone

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35
Q

mechanism of genomic imprinting

A

DNA methylation by DNA methytransferases

transfer methy from donors, like S-adenosyl-methionine (SAM) to CYSTEINE residues

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36
Q

describe airway resistance

A

upper respiratory tract: nasal passage, mouth, pharynx, larynx = 1/2

trachea & mainstem bronchus: HIGH

increases in MEDIUM-sized bronchi bc of highly turbulent flow (generation 2-5)

falls in smaller airways bc high cross-sectional area is combined high.

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37
Q

what constitutes “upper” respiratory tract

A

nasal passage, mouth, pharynx, larynx

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38
Q

what constitutes “lower” respiratory tract

A

trachea & 23 generation of airways

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39
Q

where is lower respiratory airway resistance highest

A

MEDIUM-sized bronchi (generation 2-5) bc of turbulent flow

moderately high in trachea too. falls after medium sized bronchi (bc summation of cross-sectional area = low)

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40
Q

antipseudomonal penicillins

A

ticarcillin, piperacillin

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41
Q

antipseudomonal cephalosporins

A

ceftazidime (3rd gen)

cefepime (4th gen)

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42
Q

antipseudomonal aminoglycosides

A

amikan, gentamycin, tobramycin

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43
Q

antipseudomonal fluroquinolones

A

ciprofloxacin

levofloxacin

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44
Q

antipseudomonal monobactam

A

aztreonam

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45
Q

antipseudomonal carbapenem

A

imipenem

meropenem

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46
Q

azetreonam works on

A

aerobic gram negatives

bad against gram positive and anerobes

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47
Q

what type of haemophilus produces ear infxn

A

noncapsular, nontypable

h. flu vaccine won’t prevent it

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48
Q

what kind of illness can nontypable h. flu cause?

A

part of upper respiratory normal flora

otitis media
sinusitis
bronchitis

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49
Q

type of immunity conferred by conjugated vaccine

A

humoral.
adding protein helps it be presented on MHC II.

doesn’t stimulate a cell-mediated response (not on MHC I)

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50
Q

time frame for ischemic-related brain injury

A

hypoxia > 1 min = cessation of neuronal fxn

permanent damage to brain tissue in 4-5min

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51
Q

gingival hyperplasia

A

phenytoin, nifedipine, verapamil,

52
Q

adverse effects of phenytoin

A

CNS: cerebeullum & vestibular, ataxia & nystagmus

gingival hyperplasia, coarsening facial features, hirsitism

interfere w/ folic acid absorption

induces P450

teratogen: fetal hydantoin syndrome

53
Q

mechanism of gingival hyperplasia w/ phenytoin

A

increases expression of PDGF, stimulating prolif of gingival cells & alveolar bone.

54
Q

how are the 3 genes in lac operon coordinated to be made in equal amounts

A

prokaryotic mRNA can be polycistronic (on mRNA codes for several proteins)

3 genes regulated by SINGLE promoter, operator & regulatory elements

55
Q

duodenal atresia occurs due to..

A

failure of duodenum to recanalizein early embryonic life

56
Q

malrotation in gut

A

failure of midgut to rotate counterclockwise as it returns to abdominal cavity

57
Q

when does vitelline duct normally obliterate

58
Q

aminoglycoside resistance (i.e. via enterococci)

A

aminoglycoside-modifying agents that transfer diff chemical groups – acetyl, adenyl, phosphate

outside of bacteria, so it can no longer bind to ribosomes.

aqcuired by plasmid / transposons

59
Q

penicillin resistance

A

(1) b-lactamase

(2) penicillin-binding proteins

60
Q

vancomycin resistance

A

mutation in cell wall precursor turning D-ala-D-ala to D-ala-D-lactate

(altered target)

61
Q

tetracycline resistance

A
  1. mutation in ribosome

2. increased efflux, influx

62
Q

fluoroquinolone resistance

A

mutations in gyrase / topoisomerase gene

63
Q

what is hepatic encephalopathy acutely triggered by

A

often GI bleed, increasing ammonia & nitrogen in gut for absorption

64
Q

relationship between alpha-ketoglutarate, glutamate, and glutamine

A

alpha-ketoglutarate + NH3 –> glutamate
(via glutamate dehydrogenase, both ways)

glutamate + NH3 –> glutamine
(via glutamine synthase)

glutamine —> glutamate + NH3
glutaminase

65
Q

describe glutamate-glutamine cycle

A

in neuron:

glutamate made 2 ways
1. glutamine -> glutamate + NH3
(via glutaminase)
2. alpha-ketoglutarate + NH3 --> glutamate
(via glutamate dehydrogenase)

in synaptic cleft, glutamate is taken up by astrocytes
1. glutamate + NH3 –> glutamine
(via glutamine synthase)

glutamine is shuttled back into neurons

66
Q

how does hyperammonia affect glutamate-glutamine cycle

A
  1. in astrocyte, excess NH3 creates toxic accumulation of glutamine
  2. in neuron, excess NH3 promotes excess consumption of alpha-ketoglutarate –> glutamate

this leaves less alpha-ketoglutarate for TCA in neurons!

67
Q

which 2 substances are depleted in the brain during hyperammonia? accumulated?

A

deplete:
1. glutamate
(too much glutamine formation in astrocytes

  1. alpha-ketoglutarate
    (used to make more glutamate)

accumulate: glutamine in astrocytes! swell

68
Q

oxindole

A

tryptophan derivative

formed by bacteria in gut & normally cleaved by liver. elevated in hepatic encephalopathy.

69
Q

milrinone

A

strong ionotropic agent
inhibit phosphodiesterase

increase cardiac cAMP, increased contractility

70
Q

rx: during angioplasty in patients w/ acute coronary syndrome

71
Q

deciding between uricosuric (probenicid) agents vs. allopurinol/febuxostat?

A

if has uric stones, don’t want to add more uric acid in urine. give febuxostat / allopurinol.

72
Q

sudden liver failure after surgery?

A

consider hepatic necrosis caused by halothane!

73
Q

halothane side effects

A

type 1: aminotransferase elevation, mild syptoms

type 2: fulminant hepatitis. extensive hepatocellular damage.

RAPID ATROPHY - widespread centrilobular hepatocellular necrosis & inflammation of portal tracts & parenchyma

74
Q

decreased albumin levels is a sign of..

A

chronic liver injury. NOT aute.

half-life of 20 days.

75
Q

presentation of fulminant hepatitis caused by halothane

A

elevated aminotransferases
prolonged prothrombin
eosinophilia

(albumin takes 20 days to rise)

76
Q

anti-topoisomerase I specific for..

A

scleroderma (anti Scl-70)

77
Q

characterestics of esophageal motility

A

fibrosis of distal esophagus

  1. esophageal hypomotlity
  2. loss of tone in LES

manifests as GERD

78
Q

drug induced lupus

A

procainamide, hydralazine, isoniazid, d-penicillamine

79
Q

presentation of sjogren

A

keratoconjunctivitis sicca (dry eye)

xerostomia (dry mouth

may be parotid enlargement

increased risk of non-hodgkin lymphoma

80
Q

anomaly in antiphospholipid syndrome

A

thombophilia w/ paradoxical increased PTT

81
Q

hydronephrosis vs. autosomal dominant polycystic kidney disease

A

hydronephrosis: smooth surface

ADPKD: cyst bumps visualized on surface

82
Q

cysts in ADPKD and ARPKD

A

ADPKD: large cysts, from anywhere.
-lumpy bumpy cysts seen on gross exam of surface

ARPKD: small cysts in collecting duct.
- generally smooth surface

83
Q

shrunken kidney on ultrasound can suggest?

A

medullary cystic disease – inherited

tubulointerstitial fibrosis, progressive renal insufficiency. medullary cysts usu NOT visualized.

(shrunken, as opposed to polycystic kidney –> large)

84
Q

mucosa in lactase deficiency

85
Q

pancreatic pseudocyst

A

potential complication of pancreatitis.

leakage of pancreatic secretions – induce inflammatory response –> granulation tissue & fibrosis forms to trap fluid

86
Q

cyst vs. pseudocyst

A

cyst: lined w/ epithelial cells
pseudocyst: granulation tissue

87
Q

most common location for pancreatic pseudocyst:

A

lesser peritoneal sac, bordered by stomach, duodenum, transverse colon

88
Q

the only radiolucent stone

A

uric acid stones

89
Q

colorless octahedron crystals

A

calcium oxalate or calcium phosphate

90
Q

rectangular prism “coffin-lid” crystal

A

struvite (AMP or triple phosphate

proteus mirabilis / vulgaris, klebsiella, staphlococcus

91
Q

yellow, red-brown, diamond or rhombus

92
Q

flat, yellow, hexagonal crystals

93
Q

which 2 stones ppt in basic environment

A

calcium phosphate (or neutral)

AMP

94
Q

inheritance of alpha-1 antitrypsin

A

co-dominant, affects lung and liver

95
Q

genotype in alpha-1-antitrypsin deficiency

A

homozygous for Z allele - decrease secretion of A1AT secondary to abnormal protein folding.

STUCK IN ER

96
Q

liver consequences in alpha-1-antitrypsin deficiency

A

accumulation of anti 1-antitrypsin.

liver issues before lung issues usually

leads to..

  1. cirrhosis (2nd most common cause of death) and
  2. hepatocellular carcinoma
97
Q

histology of liver w/ alpha 1-antitrypsin deficiency

A

intracellular granules of unsecreted A1AT.

stain reddish pink w/ PAS

resist digestion by diastase

98
Q

symptoms of scurvy

A

impaired collagen formation

hemorrhage
SUBPERIOSTEAL HEMATOMA
bleeding into JOINT SPACE
GINGIVAL swelling
secondary peridontal infection
anemia
hyperkeratotic papular rash
impaired wound healing
weakened immune response
99
Q

vitamin K deficiency vs. vitamin C deficiency

A

both have bleeding diathesis, but vitamin K usu doesn’t present w/ PAINFUL GUMS

100
Q

acrodermatitis enteropathica, growth retardation, infertility

A

zinc deficiency

101
Q

b-blocker overdose?

A

glucagon

increase cAMP, increase Ca2+ release during contraction. increases HR & contractility (independent of adrenergic receptors)

102
Q

histological diagnosis of celiac

A

small intestine: MOST: duodenum and proximal jejuneum

flattening of mucosa w/ loss of villi and chronic inflammatory infiltration of lamina propria

103
Q

antibodies seen in celiac (3)

A

anti-endomysial
anti-reticulin
anti-transglutaminase

104
Q

common finding in GI malabsorption?

A

steatorrhea: foul, smelling, bulky, floating, greasy stoof

105
Q

dfiferential of steatorrhea (3)

A
  1. pancreatic insufficiency
    - chronic pancreatitis, cystic fibrosis
  2. intestinal mucosal defect
    - celiac, tropical spru, whipple, chron.
  3. bacterial proliferation
    small bowel diverticulosis, diabetic neuropathy. bacteria eat nutrients
106
Q

differentiate cause of steatorrhea?

A

stool sample

  1. sudan III stool stain: identidy fat
  2. quantitative analysis of amt of fat

then bariums studies to see what caused it.

107
Q

what do you need for diagnosis of malabsorption

A

STOOL SAMPLE

108
Q

major pathophysiology w/ prolonged NSAID use

A

chronic interstitial nephritis

clinically: see modest elevation in serum creatinine, evidence of tubular dysfxn, fanconi syndrome (aminoaciduria, glycosuria, hypophosphatemia, hypouricemia)

109
Q

fibromyalgia

A

key: multiple symmetrically distributed tender spots over patients’ muscles, joints, tendons (spine of scapula, lateral epicondyle, medial fat pad of knee)
demo: 20-50y/o. mostly women

widespread musculoskeletal pain w. stiffness, paresthesia, poor sleep, emotional disturbance.

muscle pain & stiffness severe in morning. exacerbated w/ exercise.

110
Q

polymyalgia rheumatica

A

> 50 y/o.

morning stiffness of neck, shoulder, pelvic girdle.

weight loss, fever, increased ESR

111
Q

presentation of ankylosing spondylitis

A

low back stiffness, resolves w/ exercise.

usu affects males

PE: decrease anterior flexion of spine.

112
Q

formula for clearance

A

urine concentration x urine flow rate

over

plasma concentration

113
Q

normal filtration rate

114
Q

common side effects of first-generation anti-histamine

A

anti-muscarinic
anti-5HT
anti-alpha-adrenergic

and lipophilic –> sedation / cognitive dysfxn

115
Q

second generation antihistamine

A

NO anti-muscarininc, anti-5HT, anti-alpha-adrenergic.

not lipohilic –> no sedation / cognitive dysfxn

116
Q

hydroxyzine, promethazine, chlorpheniramine, diphenhydramine

A

1st gen anti-histamine

side effects!

117
Q

fexofenadine

A

2nd gen anti-histamine

minimal sedation & anti-muscarinic

118
Q

wax & waning lymphadenopathy

A

follicular lymphoma!

119
Q

follicular lymphoma

A

most common indolent non-hodgkin lymphoma in adults

indolent course, marked by remission & recurrence

wax & wane

t(14,18) bcl-2 overexpression

120
Q

diffuse large cell lymphoma often involves..

A

waldeyer ring (oropharyngeal lymphoid tissue)

GI tract

most common aggressive non-hodgkin’s lymphoma in adult

121
Q

mycosis fungoides

A

cutaneous T-cell lymphoma

proliferating CD4+ T cell infiltrate dermis & epidermis –> PAUTRIER MICROABSCESSES.

manifest w/ plaques that may be confused w/ psoriasis or eczema

generalized erythema, scaling, thickening of skin

122
Q

clinical presentation of hairy cell leukemia

A

splenomegaly & pancytopenia in older men

123
Q

BRAF mutation w/ glutamic acid for valine at position 600 (V600E)

124
Q

antibody rx for mutant BRAF in melanoma?

A

vemurafenib

125
Q

vemurafenib

A

inhibitor of mutant BRAF in melanoma

126
Q

most common AGGRESSIVE non-hodgkin lymphoma

A

diffuse large B cell lymphoma

rapidly enlarging mass

127
Q

most common INDOLENT non-hodgkin lymphoma?

A

follicular lymphoma, wax & wane

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