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UWorld mixed > test #38 4.28 > Flashcards

test #38 4.28 Flashcards

1
Q

triple test (maternal serum)

A
  1. AFP
  2. estriol
  3. hCG

between weeks 16-18
abnormal values –> ultrasound
if no abnormalities found –> amniocentesis

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2
Q

AFH in triple test? elevated? low?

A

synthesized by fetal liver, GI tract, and yolk sac (early gestation only).

maternal serum aFP levels increase w/ gestation age

elevated:

  1. dating error (underestimation)
  2. neural tube defects
  3. anterior abdominal wall defects (omaphalocele, gastrochisis)
  4. multiple gestatoin

decrease: Down’s syndrome

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3
Q

most common cause of elevated AFP in triple test?

A

dating error (underestimation of gestational age).

confirm w/ ultrasound

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4
Q

estriol levels in triple test? decreased levels suggest?

A

reflect placental and fetal function (both necessary for synthesis)

decrease:
1. placental insufficiency

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5
Q

hCG in triple test? increased levels associated w/?

A

synthesized by trophoblastic tissue.

increased levels:

  1. multiple gestation,
  2. hydatidiform mole,
  3. choriocarcinoma
  4. down’s syndrome
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6
Q

placental abnormalities & intrauterine growth retardation are associated w/ decreased..

A

estriol

placental insufficiency!

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7
Q

infection, pain, and sleep deprivation all increase..

A

blood glucose!

stress: increase catecholamines
decreased insulin, increase glycogenolysis, increased gluconeogenesis

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8
Q

isolation (defense mechanism

A

removing disturbing feelings from an event.

combat veterans who describes friends dying in cold and distant tones. isolating the fear and sadness from event

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9
Q

bifid carotid pulse w/ brisk upstroke “spike & dome” associated w.

A

hypertrophic obstructive cardiomyopathy

collapse in pulse, followed by secondary rise

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10
Q

three cytogenetic abnormalities that can lead to downs syndrome

A
  1. trisomy 21: meotic nondisjunction (usu mama)
  2. unbalanced robertsonian translocations (2-3%)
    - normal number of chromosomes, but extra arm of chromosome 21 is attached to another chromosome
  3. mosaicism: one w/ normal genotype, one with trisomy 21
    - postfertilization mitotic error
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11
Q

uniparental disomy

A

when fetus inherits two copies of homologous chromosomes from one parent and no copy from other parent

(occurs in complete hydatidiform mole)

consider when child inherits a recessive condition when only 1 parent is carrer

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12
Q

heterodisomy and isodisomy

A

heterodisomy: uniparental disomy in meiosis I

isodisomy (homozygous): in meiosis II or postzygotic duplicatino of one & deletion in one

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13
Q

cytokines involved in asthma

A

IL4: class-switch to IgE
IL5: recruit eosinophils
IL10: block Th1, encourage Th2

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14
Q

charcot-leyden crystals

A

asthma sputum: eosinophil membrane protein

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15
Q

TGF-beta is important for..

A

tissue regeneration and repair

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16
Q

anti-inflammatory cytokines

A

IL-10 and TGF-beta

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17
Q

loss of CNIII to the eye results in.. (3)

A

somatic:
1. ptosis (levator palpebrae)
2. down & out (only maintain superior oblique and lateral rectus)

  1. loss of iris spincter
    (fixed dilated)
  2. loss of acommodation
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18
Q

describe light pathway (reflex)

A

afferent in one eye:

ipsilateral optic nerve -> bilateral post optic chiasm -> bilateral pretectal area -> bilateral edingerwestphal nucleus

efferent:
bilateral edingerwestphal nucleus -> travel w/ oculomotor n -> bilateral ciliary ganglion -> bilateral pupillary sphincter

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19
Q

2 ways to get lung abscess

A
  1. aspiration of oropharyngeal contents (most common)

2. right sided endocarditis -> septic emboli

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20
Q

Marcus Gunn pupil

A

defect in CN II
“swinging flashlight test”

affected eye will have consensual pupillary constriction, but will appear to ‘dilate’ when light is on affected eye

– can’t detect light

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21
Q

differentiate lesion in LGN and optic tract

A

both will have contralateral hemianopsia

optic tract: has Marcus Gunn pupil (loss of direct pupillary constriction w/ light)

LGN: light reflex should be fine (does not go through LGN, instead straight to pretectal -> edingerwestphal -> ciliary ganglion -> iris sphincter

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22
Q

Marcus-Gunn pupil in optic nerve lesion? optic tract?

A

optic nerve: marcus gunn pupil when light is shone into affected eye (IPSILATERAL relative afferent pupillary defect)

optic tract: marcus gunn pupil when light is shone on eye CONTRALATERAL to side of lesion.

bc nasal fibers contribute more to prectal afferents. optic tract will have more contralateral ‘nasal’ fibers. less afferents

both have contralateral homonymous hemianopsia

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23
Q

rabies virus is..

A

killed vaccine

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24
Q

Live vaccines (6)

A

live! small yellow chickens get vaccinated w/ mmr and sabin’s polio! it’s INcredibly

  1. smallpox
  2. yellow fever
  3. VZV chicken pox
  4. MMR (measles, mumps, rubella)
  5. sabin’s polio (IgA and IgG)
  6. infuenza intranasal
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25
Q

Killed vaccines (4)

A

SalK = killed
RIP Always

  1. rabies
  2. influenza (intramuscular)
  3. salk polio
  4. hepatitis A
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26
Q

recombinant vaccines (2)

A
  1. HBV (recombinant HBsAg)

2. HPV (6, 11, 16, 18)

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27
Q

path of rabies viruses

A

deposit in wound:

rabies binds to nicotinic AchR in striated muscle -> binds NCAM -> enters motor neuron // DRG?

  • rabies virus travels retrograde via peripheral nerves to DRG
  • then to brain
  • massive replication in CNS
  • rabies then spreads to other organs via neural pathways
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28
Q

recommendation for rabies vaccine

A

prophylatic for certain populations: veterinarians, 30+ days in country w/ lots of rabid dogs)

inactivated (killed) virus w/ beta-propiolactone

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29
Q

clinical presentation of rabies

A

restlessness, agitation, dysphagia progressing to coma 30-50 days following exposure

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30
Q

chromosome of NF2

A

chr. 22

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31
Q

chromosome of p53

A

chr. 17

breast, sarcoma, brain tumor, leukemia, adrenocortical tumor

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32
Q

gene implicated in NF-1

A

von Reclinghausen disease, chr. 17

tumor supressor gene: neurofibromin

(cafe au lait, neurofibromas, lisch nodules)

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33
Q

gene implicated in NF-2

A

central neurofibromatosis, chr. 22

tumor supressor gene: merlin

bilateral acoustic neuromas

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34
Q

chromosome of APC

A

chr. 5

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35
Q

chromosome of Rb

A

chr. 13

osteoscarcoma, retinoblastoma

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36
Q

chromosome of VHL

A

chr. 3

renal cysts, renal cell carcinoma, hemangioblastoma of cerebellum and retina

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37
Q

ureteral constriction / obstruction causes..

A

decreased GFR, normal RPF = decreased filtration fraction

FF = GFR/RPF

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38
Q

amino acid w/ 3 titratable protons (3 pKA) (7)

A

histidine, arginine, lysine, aspartic acid, glutamic acid, cysteine, tyrosine

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39
Q

histidinemia

A

rare autosomal recessive disorder

deficience of histidase (required for catabolism of histidine)

speech defects, psychomotor & generalized retardation, emotional disturbance

most frequent inborn metabolic error in Japan

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40
Q

how much coronary blood flow occurs in systole

A

30%

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41
Q

critical factor in determining coronary blood flow, esp in exercise

A

duration of diastole

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42
Q

single most important risk factor for development of aortic dissection

A

hypertension!

next: cystic medial degeneration, connective tissue disorder

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43
Q

diabetes mellitus is an important risk factor for developing which 2 major diseases

A
  1. atherosclerosis

2. hypertension

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44
Q

most impt factor for development of aortic aneurysm?

A

atherosclerosis (high cholesterol)

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45
Q

what 4 things increase risk for atherosclerosis (2)

A
  1. high cholesterol
  2. smoking
  3. HTN
  4. diabetes mellitus
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46
Q

t. pallidium infects what part of aorta

A

vasa vasorum in adventitia of ascending thoracic aorta

weakens wall -> predispose to ascending aortic aneursym

dissection = rare w/ syphillis

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47
Q

rx for status epilepticus (4 steps)

A

1st line: IV lorazepam
2nd. simultaneous phenytoin.

if still seizing:
3rd: phenobarbital

if still seizing
4: intubate / general anesthesia

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48
Q

definition of status epilepticus?

A

generalized tonic clonic seizure lasting for more than 30min w/o return to consciousness.

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49
Q

mechanism of valproic acid

A

increase Na+ channel inactivation
block NMDA receptor
affect K+ current
GABA Cl- receptors

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50
Q

rx for myoclonic seizure

A

valproate -> first line

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51
Q

definition of myoclonic seizure

A

repetitive seizures, consisting of brief, symmetric muscular contractions w/ loss of body tone causing patient to fall or slump forward.

usu morning and ppt by stress / sleep deprivation

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52
Q

myoclonic seziure vs. tourette tics

A

tourette: motor tics are nonrhythmic, temporarily suppressible, often preceeded by urge to make stereotyped movement

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53
Q

rx for tourette

A

typical & atypical antipsychotics, like haloperidol

54
Q

describe tonic clonic

A

generalized tonic extension, followed by clonic rhythmic motions

rx: PVC

55
Q

which DNA pol has 5’-3’ exonuclease activity

A

DNA pol I (remove primer)

also have 3’-5’ corrective abilities

56
Q

cyanide toxicity

A

binds to many iron containing enzymes.

most importantly: cytochrome a-a3 complex (in complex IV)

toxicity: inhibits aerobic metabolism –> rapid death

57
Q

complex I of ETC is known as? inhibited by?

A

NADH oxidase

inhibited by: rotenone

58
Q

complex II of ETC is known as? inhibited by?

A

succinate dehydrogenase

nothing!

59
Q

complex III of ETC is known as? inhibited by?

A

has coenzyme Q

blocked by amtimycin A

60
Q

complex IV of ETC known as?

inhibited by?

A

has cytochrome C (between it and complex III)

cyanide + CO

cytochrome a a-a3 complex blocked by cyanide

61
Q

complex V also known as? inhibited by?

A

ATP synthase

oligomycin

62
Q

why make methemeglobin in cyanide toxicity (w/ nitrites)

A

methemoglobin can’t bind oxygen, but can bind & sequester cyanide (keeps poision away from mitochondria, etc)

cyanide binds ferric iron more than mitochondrial cytochrome enzymes

63
Q

Dubin-Johnson problem? gross? histology?

A

defect in hepatic excretion of (conjugated) bilirubin across canalicular membrane.

gross: liver is black
histology: features are normal, though dense pigment of epinephrine metabolites within lysosomes can be seen

64
Q

histology of liver: dense pigments of epinephrine metabolites in lysosomes?

A

dubin-johnson

65
Q

diagnosis of dubin johnson

A

conjugated hyperbilirubinemia w/ direct bilirubin > 50%

otherwise normal liver function profile must be present

confirmation: unusually high levels of coproporphyrin I

66
Q

Ras-MAP kinase signalling cascade

A

growth factor
autophosphorylation of RTK
–> interact w/ SH2 domain protein & SOS protein

leads to Ras activation (G protein) + GTP
–> phosphorylates Raf kinase

all leads to MAP kinase (enters nucleus to influence gene transcription

67
Q

what kind of protein is Ras

A

G-protein, activated w/ RTK

68
Q

PI3K pathway associated w.

A

PI3K / Akt / mTOR

69
Q

activation and inactivation of RAS

A

activated by RTK

inactivated by GAP (GTPase activating protein) 00> hydrolysis

70
Q

ETEC toxin is like..

A

cholera toxin, especially heat labile

(heat labile & stabile toxin)
plasmid encoded

LT – like cholera (activates Gs –> adenylate cyclase –> cAMP)

ST – increase cGMP (binds & activates guanylate cyclase on apical membranes of gut mocsal cells)

FIMBRIAE // pilli allow for adhesion

watery diarrhea

71
Q

invasive gastroenteritis (5)

A 
Salmonella
Shigella
EIEC
Camplyobacter jejuni
Entamoeba histolytica
72
Q

stacked-brick intestinal adhesion

A

characterestic of enteroaggregative E. coli
EAEC

adhere to jejunal, ileal, and colonic mucosa

do not invade

persistent diarrhea in infants in developing countries

73
Q

2 risks w/ fibrates

A
  1. myositis (esp w/ statin)
  2. cholesterol stones

use to treat hypertriglyceridemia

74
Q

side effect w/ ezetimibe?

A

rare LFT increase, diarrhea

75
Q

side effect w/ cholestyramine?

A

taste bad
GI discomfort
decrease absorption of fat soluble vitamins
maybe cholesterol gallstones

76
Q

statin toxicity

A

hepatoxicity

myositis (esp w/ niacin & fibrates)

77
Q

what combination of lipid lowering agents increases myositis

A

statin + fibrate + niacin

78
Q

hydroxymethylglutaryl coenzyme A reductase

A

HMG CoA reductase

convert HMG CoA to cholesterol

79
Q

statin w/ highest myopathy

A

simvastatin

80
Q

jimson weed is similar to

A

atropine! causes gardener’s mydriasis (anticholinergic crisis)

81
Q

blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel and bladder loose their tone, and the heart runs alone

A

anticholinergic crisis

  • mydriasis & cylcloplegia
  • CNS hallucinations, agitation, delirium
  • hyperthermia –> cutaneous vasodilation
  • loss of secretions (salvation, lacrimation, sweating)
  • decreased GI motility & secretion, urinary retention via detrusor relaxation & constriction of external urethral sphincter
  • tachycardia (diminshed vagal tone)
82
Q

clasp knife spasticity

A

sign of upper motor neuron lesion:

initial jerking resistance to passive extension followed by sudden release of resistence

due to lack of UMN inhibitory control on spine muscle stretch reflex arc

cortisospinal tracts of spinal cord, medulla, pons & midbrain, internal capsule, precentral gyrus

83
Q

‘watershed areas’ of bowel (2)

A

splenic flexure: between SMA and IMA

distal sigmoid colon: between IMA and hypogastric

84
Q

side effects of colchicine?

A

binds to tublin & blocks its polymerization

GI ISSUES: many get diarrhea. some, nausea and vomiting (effects on gastric mucosa)

recommended for patients who cannot take NSAIDs (i.e. renal failure, peptic ulcer disease)

85
Q

which drugs are contraindicated in acute gouty arthritis?

A

probenecid and allopurinol!

can ppt acute attacks!

86
Q

describe thiopental mechanism

A

used for INDUCTION.
highly lipid soluble.
equilibrates w/ brain within 1 minute.

accumulation in brain followed by rapid “redistribution” into skeletal muscles & adipose tissue (within 5-10min)

87
Q

what is responsible for rapid awakening after thiopental

A

REDISTRIBUTION (into skeletal and adipose tissue)

NOT metabolism.

88
Q

carcinoid tumor on histology

A

eosinophilic cytoplasm, oval-to-round nuclei

minimal to no variation in shape and size of tumor cells.

gland, nests, rows, or sheets may form

EM: dense core granules

ECL cells

89
Q

APUD system

A

Amine Precursor Uptake and Decarboxylation

the ECL cells (that become malignantly transformed into carcinoid tumors)

90
Q

most common location for carcnoid tumor

A

ileum.

also appendix and rectum.

91
Q

meningiomas arise from cells of..

A

arachnoid villi

92
Q

Arnold-Chiari malformation.

type I vs. type II

A

congenital issue
underdeveloped posterior fossa

parts of cerebellum & medulla herniate through foramen magnum

type 1:

  • low lying cerebellar TONSILS extend below foramen magnum into vertebral canal
  • infant: asymptomatic
  • adult: headache & ataxia

type 2

  • more severe; evident in neonate
  • abnormally formed cerebellum & medulla
  • TONSIL and VERMIS herniate through
  • hydrocephalous (aqueductal stenosis) & lumbosacral myelomeningocele (paralysis)
  • medulla compression: dysphagia, dysphonia, stridor, apnea
93
Q

Dandy walker

A

agenesis of cerebellar vermis w/ cystic enlargement of 4th ventricle (occupies the enlarged posterior fossa)

associated w/ spina bifida and hydrocephalous

94
Q

all antidepressants carry risk of..

A

inducing mania in susceptible patients!

especially TCA and venlafaxine

95
Q

carbamazepine, lithium and valproate as all

A

mood stabilizers!

used in acute mania and maintence of bipolar disorder

96
Q

genetic components of type I and type II diabetes

A

DM2: strong, but we don’t know gene
DM1: weak, but we know MHC related

twin studies
50% DM1
80% DM2

genes:
DM1: polymorphism in MHC (HLA-DQ and DR)

DM2: polygenic, unknown

97
Q

HLA-DQ & DR associated with

A

type 1 diabetes mellitus

type 2: polygenic, unknown

98
Q

genetics of friedrich’s ataxia

A

autosomal recessive
chr. 9
frataxin protein – essential for normal mitochondrial fxn

trinucleotide repeats in frataxin gene -> diminished levels pf protein

99
Q

presentation of friedrich’s ataxia

A
  1. ascending / descending spinocerebellar tract degeneration –> ATAXIA
  2. degeneration of dorsal columns and DRG –> loss of position & vibration sensation
  3. kyphoscoliosis and foot abnormalities: characteristic skeletal deformity
  4. hypertrophic cardiomyopathy
  5. DM in 10%
100
Q

diffuse medium-sized lymphocytes & high proliferation index (represented by high Ki-67 fraction –> 100%)

A

burkit lymphoma
EBV related
t(8,14) overexpression of c-MYC

101
Q

50% of B-cell lymphoma and almost all primary CNS lymphoma in HIV infxn associated w/

A

Burkitt Lymphoma

102
Q

4 stages of syphillis

A

PRIMARY: chancre
1-3wks after contact
resolves in 3-6 wks

SECONDARY: bacteremic stage.
5-10wks following chancre resolution
diffuse macular rash including palms and soles
condylomata lata

LATENT: asymptomatic period.
early latent: 1 year after resolution of secondary symptoms
late latent: more than 1 yr after asymptomatic state

TERTIARY: years after infection.
neurosyphillis: subacute meningoencephalitis, tabes dorsalis, etc

gummas: commonly cutaneous, but also subcut, bones, liver, etc
aortitis: vasovasorum of ascending sorta

103
Q

painless induration on genitals w/ headaches & memory loss

A

NOT a chancre bc neuro involvement!

has to be a gumma

104
Q

describe a chancre

A

painless ulceration w/ raised, indurated borders.

develops at site of t. pallidum inoculation in 1-3wks. resolves in 3-6 wks.

PRIMARY SYPHILLIS

105
Q

condylomata lata

A

large gray wart-like growths that occur in genital / perineal regions

typical manifestation of secondary syphillis

106
Q

gumma

A

painless, indurated granulomatous lesions that progress to white-rubbery lesions that may ulcerate.

commonly cutaneous, but also on subcutaneous tissue, bones, liver, other organs.

TERTIARY SYPHILLIS

107
Q

positive VDRL and pleocytosis in CSF

A

diagnostic of NEUROSYPHILLIS (part of tertiary syphillis, w/ gummas)

NOT primary.

108
Q

granuloma inguinale

A

STD
klebsiella granulomatis

inguinal swelling, ulcers, abscesses, fistulas.

gram stain: cells w/ rod-shaped intracytoplasmic inclusions: Donovan bodies

109
Q

condyloma accuminata

A

anogenital wars by HPV (6, 11)

110
Q

painless ulcer w/ painful lymphadenopathy

A

lymphogranuloma venerum

C. trachoatis (L1-L3)

111
Q

chancroid

A

painful genital ulcer and inguinal adenopathy

haemophilus ducreyi

112
Q

donovan bodies

A

granuloma inguinale

klebsiella granulomatis

113
Q

interferon alpha & beta

A

innate host defect
secreted by virally infected HOST cells

act on locally unaffected cells “priming them” for viral defense

when infected, viral nucleic acids will activate

HALT PROTEIN SYNTHESIS

  1. RNAse L: degrade viral & host mRNA
  2. protein kinase: inhibit viral/host protein synthesis

essentially results in apoptosis (interrupting amplification)

114
Q

type II interferon (IFN-gamma)

A

secreted by Th1 and NK cell mainl

promote th1 differentiation, increase expression of class II MHC on APC, and improve intracellular killing of macrophages

115
Q

type 1 and 2 interferons generally.

A

increase MHC class I expression
increase NK cell
increase CD8+ cytotoxic

all aim to increase amt of virally infected cells that undergo apoptosis

116
Q

local pleural thickening w/ calcification (particularly of parietal pleura of posterolateral mid-lung zones & diaphragm)

A

hallmark of asbestosis

117
Q

pulmonary manifestation of silicosis

A

nodular densities & eggshell calcifications of hilar nodes

118
Q

pulmonary berylliosis

A

closely resembles sarcoidosis

nodular infiltrates, enlarged lymph nodes, non-caseating granulomas

119
Q

ITP in children vs. adult

A

children: acute & self-limited
adult: insidious & chronic course

120
Q

ITP considered when you DON’T have

A

signs & symptoms of TTP/HUS, pancytopenia, marrow failure, or splenomegaly (would be sequestration)

121
Q

what constitutes crescent in RPGN?

A

FIBRIN & monocytes

also: macrophages, proliferated glomerular parietal cells

eventually oblterate bowman’s space

122
Q

influenza A infection

A

can affect 50-75% of school-aged children, often pass on to family.

  • abrupt onset fever, headache, myalgia, malaise
  • gradually improve over 2-5 days.
123
Q

staph aureus pneumonia

A

bronchopneumonia:
most common cause of SECONDARY pneumonia

(bacterial pneumonia on top of influenza)
- recurrent fever, dyspnea, productive cough. see consolidation.

ELDERLY, particularly at risk.

124
Q

most common agents responsible for secondary bacterial pneumonia

A
  1. strep pneumoniae
  2. staph aureus
  3. haemophilus influenzae
125
Q

listeria in neonates

A

septicemia and purulent meningitis in neonates

126
Q

klebsiella pneumonia is most commonly responsible for..

A

nosocomial UTI
nosocomial pneumonia
pneumonia in alcoholics & IV drug

127
Q

mycobacterium scrofulaceum

A

cervical lymphadenitis in children

128
Q

mycobacterium kanasasii

A

pulmonary TB like symptoms

129
Q

effect modification

A

effect of main exposure on an outcome is modified by another variable

a chemo for breast cancer that only helps smokers

not a bias.

130
Q

MCD is thought to be caused by..

A

primary defect in immunologic function
(associated w/ respiratory infection, immunization, atopic disorders; helped by steroids)

overproduction of IL-13 –> damage podocytes.

selective albuminuria

UWorld mixed (60 decks)

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