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UWorld mixed > test #36 4.27 > Flashcards

test #36 4.27 Flashcards

1
Q

4 A’s of Ataxia-telengectiasia

A

B & T cell immunodeficiency
autosomal recessive

  • ATM gene (repair double stranded breaks)
  • spider Angiomas
  • IgA deficiency (bc need double stranded DNA breaks for class switching)
  • increased AFP

radiation sensitivity, recurrent sinopulmonary infxn

also increased risk of hematological malignancy

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2
Q

bare lymphocyte syndrome

A

autosomal recessive form of SCI

immunodeficiency resulting form a defect in expression of HLA class II antigens on APC

no MHC class II to present foreign antigens to T cells & have both cell mediated & humoral response

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3
Q

how does cisplatin exert chemotherapeutic effects? how can this be prevented (2 ways)

A

generates reactive oxygen species that can cross-link DNA

  1. amifostine = free radical scavenger. can prevent nephrotoxity and acoustic nerve damage.
  2. establishing chloride diuresis (IV normal saline) bc cisplatin stays in nonreactive state when in high Cl- concentration
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4
Q

N-acetylcysteine for influenza, bronchitis, cystic fibrosis?

A

mucolytic agent
-cleaves DISULFIDE bones in mucous glycoproteins

also

  • enhances glutathione production
  • conjugates NAPQI
  • prevents radiocontrast-induced nephropathy

4 main effects

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5
Q

filgrastim

A

G-CSF analong.

stimulate prolif and diff of granulocytes

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6
Q

fomepizole

A

antidote in methanol (rubbing alcohol) or ethylene glycol (antifreeze) posioning

competitive antagonist of alcohol dehydrogenase (prevents conversion into toxic metabolites)

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7
Q

methanol is in..

A

rubbing alcohol

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8
Q

ethylene glycol is in…

A

antifreeze

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9
Q

dexrazoxane

A

iron-chelating agent, help prevents anthracycline-induced (doxorubicin) toxicity

CHF

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10
Q

anthracycline fxn

A

generate free radicals –> intercalate DNA –> cause breaks

antitumor antibiotic

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11
Q

congenital hypothyroidism (cretinism)

A

6 P’s

  • pot-bellied
  • pale
  • puffy-faced (myxedema – edema of skin and subcut fat)
  • protruding UMBILICUS
  • protuberant TONGUE
  • poor brain development

mental retardation, short, coarse facial features, prolonged jaundice, hypotonic

increased incidence of congenital heart defects like ASD and VSD

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12
Q

what can cause congenital hypothyroidism (4)

A
  • maternal hypothyroidism,
  • thyroid agenesis,
  • thyriod dysgenesis (most common in US
  • dyshormonogenic goiter
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13
Q

4 general effects of thyroid hormones

A

4 B’s

  1. brain maturation
  2. bone growth (increased osteoclast activity
  3. b-adrenergic (upregulate B1 in heart)
  4. increased BMR
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14
Q

phenothiazine

A

antipsychotic / antihistamine

block D2 receptor –> relieves inhibition –> cause hyperprolactinemia at certain doses

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15
Q

how does dopamine inhibit prolactin secretion?

A

binds to D2 receptor on prolactin-producing cells

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16
Q

competence defined as..

A

ability to understand a situation and the possible CONSEQUENCES of decisions made in a situation

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17
Q

who makes medical decisions if there is no next of kin?

A

judge / court will appoint a guardian to act on the patient’s behalf

[hospital ethics committee makes recommendations, but cannot act]

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18
Q

describe how sunlight increases vitamin D

A

7-dehydrocholesterol (provitamin D3) in skin absorbs UVB –> opens up B-ring, forming previtamin D3 –> undergoes isomerization induced by heat to form vitamin D3 (cholecalciferol)

physiologically-produced D3 or plant-derived D2 undergoes the 2 hydroxylation steps

1st: cytochrome P450 enzyme 25-hydroxylase converts vitamin D into 25-hydroxyvitamin D (calcidiol)
2nd: 1-alpha-hydroxylase in kidney converts calcidiol to calcitriol (active vitamin D3)

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19
Q

how is excess 1,25-vitamin D dealt w/

A

kidney has enzyme 24 hydroxylase, converts 25 hydroxy-vitamin D to inactive 24,25 dihydrox vitamin D

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20
Q

vitamin D2. vitamin D3. cholecalciferol. calcidiol. calcitriol. 24,25-dihydrocholecalciferol

A
  • vitamin D2: plant-derived
  • vitamin D3: cholecalciferol; physiologically produced
  • calcidiol: 25-hydroxy vitamin D
  • calcitriol: 1,25-dihydroxy vitamin D
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21
Q

precision and reliability

A

essentially equivalent. low variability when measuring same thing.

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22
Q

PCA territory? symptoms expected?

A
  • contralateral hemianopia w/ macular sparing
  • contralateral paraesthesia & numbness: face, trunk, limbs (involvement of lateral thalamus)
  • cranial nerves III and IV (midbrain)
  • lateral thalamus
  • medial temporal lobe
  • splenium of corpus callosum
  • parahippocampal gyrus
  • fusiform gyrus
  • occipital lobe
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23
Q

ACA covers..

A
  • frontal: inferior and medial
  • parietal: medial
  • anterior 4/5 of corpus callosum
  • olfactory bulb and tract
  • anterior basal ganglia (caudate)
  • anterior limb internal capsule
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24
Q

anterior choroidal

A

last branch off internal carotid before it trifurcates.

supplies posterior limb of internal capsule, optic tract, LGN, choroid plexus, uncus, hippocampus, amygdala

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25
Q

artery of percheron

A

branches off either right or left of PCA.

supplies bilateral thalami and dorsal midbrain

rare normal variant, seen in patients w/ bilateral thalamic or dorsal midbrain stroke

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26
Q

MCA covers

A
  • lateral convexity of frontal, parietal, temporal lobe
  • deep subcortical structures, like internal capsule, basal ganglia.

usu contralateral motor & sensory defects

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27
Q

exogenous cortisol suppresses what part of HPA axis?

A

all! CRH, ACTH, and cortisol

bilateral adrenal cortical atrophy

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28
Q

unilateral of adrenal cortex can result from..

A

adrenocortical adenoma

autonomous production of cortisol from one adrenal gland suppresses CRH, ACTH. less stimulation of the OTHER gland.

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29
Q

triggers for atopic dermatitis? presentation in young children? older children

A

chronic inflammatory skin disorder. HALLMARK: intense pruritus (if not itching, not AD)

CHILDREN!

triggered by:
environmental antigens
- FOOD, irritants

usu present by 5 y/o:
red, weeping/crusted lesions involving face, scalp, extensor surfaces. diaper area usu spared.

older:
manifests as lichenification in flexural distribution (neck, wrists, antecubital, popliteal fossa)

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30
Q

cause of atopic dermatitis

A

mutations affecting proteins like filaggrin or other components of epidermis (impairment of skin’s barrier function)

–> increases immunologic exposure to environmental allergens & microbial antigens –> immune HSR.

patients have:

  1. high serum levels of IgE,
  2. peripheral eosinophilia,
  3. high cAMP phosphodiesterase in leukocytes
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31
Q

allergic triad

A

allergic rhinitis
asthma
atopic dermatitis

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32
Q

gluten enteropathy & dermatitis herpetiformis presentation

A

usually in 4th-5th decades of life. UNCOMMON in children!

pruritic vesicles & plaques on buttocks & extensor surfaces.

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33
Q

erythematous, well-demarcated papules and plaques w/ silvery scale

A

psoriasis

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34
Q

dermatitis herpetiformis vs. atopic dermatitis

A

atopic dermatitis: usu kids

dermatitis herpetiformis: usu presents in 4th-5th decade of life, uncommon in kids.

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35
Q

acute viral hepatitis on hepatocyte (2)

A
  1. hepatocyte injury

2. hepatocyte death

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36
Q

travel to foreign country (overcrowing & poor sanitation) & return w/ liver problems

A

think acute hepatitis A

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37
Q

hepatocyte injury vs. hepatocyte death

A

injury: ballooning degeneration
- cytoplasm appears empty w/ only occasional eosinophillic organelle remnant remaining

death: lobular architecture disruption, cytolysis, apoptosis, confluent hepatocyte necrosis.

damage attracts mononuclear inflammation in sinusoids & portal tracts

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38
Q

bridging necrosis

A

regions of adjacent lobules are interconnected by swatches of dead hepatocytes

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39
Q

presentation of viral A hepatitis

A

acute.

fever, malaise, fatigue, anorexia, nausea & vomiting, mild abdominal pain.

DARK URINE = increase serum bilirubin.

hepatomegaly & jaundice

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40
Q

prolonged pruritus and fatigue suggests

A

primary sclerosing cholangitis (diffuse inflammation and fibrosis of biliary tract)

recall pruitus – bile acid mediated

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41
Q

acholic stools and bone pain suggests

A

chronic cholestatis process, like primary biliary cirrhosis

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42
Q

liver lobule

A

functional anatomical unit of liver.

hexagonal structure centered on central vein

portal triad at each corner

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43
Q

liver acinus

A

diamond connecting 2 central veins (across) and 2 portal triads (vertically) of 2 different lobules

creates ‘zones’ of oxygenation

zone 1: vertical closest to 2 portal triads.

  • oxygen dependent processes (gluconeogenesis, beta oxidation, cholesterol synthesis)
  • site of viral hepatis

zone 3: closest to each central vein
- metabolic toxin removal (p450 system)

  • site of alcoholic hepatitis
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44
Q

acute hepatitis primary affects what part of liver? chronic?

A

acute: lobule & portal tract
chronic: predominantly portal tract

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45
Q

formula for resistance

A

R = nL / r^4

n = viscosity
L = length
r = radius
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46
Q

facies of potter syndrome

A

suborbital creases
depressed nasal tip
low set eats
retrognathia

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47
Q

common intraabdominal infections (i.e. post perforated appendix)

A

usu polymicrobial:

  1. b. frag
  2. ecoli

most common

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48
Q

candida can be isolated from an intraabdominal infection related to.

A

perforation of proximal bowel, like perforated peptic ulcer

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49
Q

what does EBV bind to in order to enter cell?

A

CD21 on B-lymphocytes

EBV glycoprotein gp350 binds to C3d complement component receptor CD21

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50
Q

where is CD21 expressed

A
  1. B cell surface

2. nasopharyngeal epithelial cells

51
Q

how does parvovirus enter erythroid cells

A

blood group P antigen

expressed on mature erythrocytes, erythroid progenitors, megakaryoctes, palcenta, fetal liver and heart

immature erythroid cells most vulnerable (adult bone marrow & fetal liver are principle targets)

52
Q

how does CMV bind to cells

A

like other herpesvirus, via glycosaminoglycans

53
Q

how does adenovirus enter cells

A

rodlike structures from its penton base capsomeres mediate adsorption to host cells.

receptor: transmembrane protein member of immunoglobulin superfamily

54
Q

kozack sequence

A

on mRNA
initiator for translation

gcc(A or G)ccAUGG

purine 3 bases upstream AUG = very important

55
Q

shrine dalgarno

A

8bp upstream AUG

help recruit ribosome to mRNA

56
Q

3 steps of translation (note where energy is used)

A
  1. initiation (IF, uses GTP)
    - assemble 40s subunit w/ initiator tRNA. wait for mRNA & 60s to bind
  2. elongation
    - charged tRNA (used ATP) binds
    - ribozyme catalyzes peptidyl-transferase (no energy)
    - translation of ribosome 3 nucleotides towards 3’ end of mRNA (uses GTP and EF2)
  3. termination, stop codon – recognized by release factor. polypeptide released
57
Q

what are the three end products of the nonoxidative (reversible) part of HMP shunt

A
  1. ribose 5-phosphate
  2. glyceraldehyde 3-phosphate
  3. fructose 6-phoshate
58
Q

NADPH vs. NADH

A

NADPH used as reducing equivalent in cytosol

NADH used as energy source for ATP synthesis (electron transport chain)

59
Q

how can ribose be synthesized by fructose-6-phosphate or glyceraldehyde-3-phosphate

A

ribose 5-phosphate glyceraldehyde 3-phosphate
(via transketolase)

[simultaneously xylucose 5-phosphate sedoheptulose 7-phosphate]

glyceraldehyde 3-phosphate fructose 6-phosphate
(via transaldolase)

[simultaneously sedoheptulose 7-phosphate erythrose 4-phosphate

60
Q

what reaction do transketolase do? transaldolase?

A

transketolase: transfers 2 carbon groups
transaldolase: transfers 3 carbon groups

61
Q

which cells produce NADPH (3 main uses)

A
  1. NADPH consumed in fatty acid & steroid synthesis.
  2. cytochrome p450 pathway
  3. generation of superoxide in phagocytes

so liver, adrenal cortex, gonads, adipose tissue, erythrocytes

62
Q

making MPO in phagocytes

A
  1. NADPH oxidase (O2-> superoxide
  2. superoxide dismutase (superoxide -> hydrogen peroxide
  3. myeloperoxidase (hydrogen peroxide -> MPO)
63
Q

enolase

A

converts 2-phosphoglycerate -> phosphoenolpyruvate in glycolysis

64
Q

aconitase

A

citrate -> isocitrate in TCA

65
Q

green pigment in echhymoses

A

biliverdin

heme -> biliverdin
via HEME OXYGENASE

66
Q

continuous leuprolide on testosterone and DHT levels

A

concordant transient increase, followed by decrease in both

67
Q

B12 + R protein? B-12 + intrinsic factor

A

R protein protects B12 from acid in stomach (released by pancreatic enzymes

intrinsic-factor protects B12 from pancreatic proteolysis + permits absorption in terminal ileum (bind to intrinsic factor receptor

68
Q

r protein

A

haptocorrin – made in salvia
-binds B12, protects from stomach acid

degraded by pancreatic enzymes

69
Q

most cases of B12 deficiency

A

unrelated to intake.. usu poor absorption.

b12 often needs to be taken parenterally

70
Q

elderly patient w/ chronic anemia and unknown underlying cause?

A

prob B-12 malabsorption.

elderly:
- poor absorption due to gastric atrophy –> achlorhydia and decreased release of B12 from food proteins
- also pernicious anemia can be common in elderly
- or terminal ileal disease (IBD)
- or bacterial overgrowth syndrome

71
Q

in what form is diet more readily absorpbed

A

dietary meat: iron in heme form –> more readily absorbed

iron from vegetable sources –> less absorbed

72
Q

endocarditis

A

inflammation of endocardium caused by

  1. infectious agents:
    - s. aureus or s. viridans
  2. inflammatory processes:
    - rheumatic fever or SLE
  3. other: metastatic cancer, carcinoid, etc
73
Q

culture negative endocarditis

A 
bartonella
coxiella
mycoplasma
histoplasma
chylamydia
HACEK organisms
haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
74
Q

aging heart changes

A

decrease in left ventricular chamber size (particular apex to base dimension)
- causes basal ventricular septum to bulge into left ventricular outflow tract: “sigmoid septum”

atrophy of cardiac myocytes
- increase interstitial connective tissue

progresive accumulation of brown cytoplasmic granules
- lipofuscin pigment: ingestible byproducts of subcellular membrane lipid peroxidation

75
Q

cystic fibrosis fertility

A

male infertility – bilateral absence of vas deferens

76
Q

GI agents that slow gastric motility

A

opiates like loperamide

77
Q

loperamide

A

opiod agents that slow down gastric motility (decrease volume of diarrhea, slow intestinal transit time, increase net reabsorption)

78
Q

symptomatic rx for cystic fibrosis

A
  1. n-acetylcysteine: cleaves disulfide bonds in glycoproteins of mucus
  2. dornase alfa (DNAse) to clear leukocytic debris
79
Q

dornase alfa

A

DNAse for cystic fibrosis, cleave leukocytic debris

80
Q

prognosis of colorectal cancer related to

A

STAGE (spread / expansion)

not grade (differentiation)

81
Q

most impt red cell index in hereditary spherocytosis?

A

INCREASED MCHC
mean corpuscular hemoglobin concentration

  • indicates membrane LOSS and red cell DEHYDRATION

(as evidence by osmotic fragility test)

82
Q

MCV in hereditary spherocytosis

A

LOW to normal, bc membrane loss

83
Q

howell-jolly bodies & pappenheimer bodies

A

associated w/ splenectomy

howell-jolly: nuclear fragments, DNA

pappenheimer bodies: iron

84
Q

eoisin-5-maleimide binding test

A

screening for hereditary spherocytosis

also see splenomegaly & increased osmotic fragility test

85
Q

Heinz bodies

A

ppt hemoglobin

- oxidation of sulfhydryl groups

86
Q

renal cell carcinoma most commonly? comes from? gross?

A

clear cell carcinoma

from PCT

golden-yellow: high glycogen and lipid content

usu has paraneoplastic (epo, acth, pthrp)

87
Q

renal oncocytomas

A

RARE tumors originating from COLLECTING DUCT cells

not clear cell!

large, well-differentiated neoplastic cells w/ numerous mitochondria

usu no paraneoplastic

88
Q

renal tumor from PCT? from collecting duct? renal pelvis?

A

PCT: clear cell carcinoma

CD: oncocytoma (rare)

pelvis: transitional cell carcinoma

89
Q

transitional cell carcinoma

A

90% of tumors involving renal pelvis.

often forms papillary tumors, composed of urothelium supported by thin fibrobvascular stalk

90
Q

prognosis of renal cell carcinoma (clear cell)

A

resistant to chemo and radiation, need to resect. if spread hematogenously already, which is common, it is bad.

91
Q

wilms tumor originates from..

A

embryonic glomerular structure.

due to loss of function mutation in WT1 or 2 on chr. 11

92
Q

beckwith-wierdman syndrome, or WAGR?

A

wilms tumor
aniridia
genitourinary malformation
mental retardation

93
Q
  1. unique feature of listera monocytogenes
A

facultative intracellular, able to

  1. multiply at 4 degrees (cold enrichment)
  2. tumbling motility

gram positive rod (distinguish from cornybacterium)

94
Q

location of pudendal nerve block

A

S2-S4 nerve roots

  1. sensory to perineum and genitals
  2. motor to sphincter urethrae and external anal sphincter.

palpate intravaginally for ischial spines –> inject there

95
Q

genitofermoral nerve

A

L1-L2

  • courses anterior surface of psoas muscle
  • splits into genital and femoral branches
  • innervates scrotum / labia majora & cutaneously femoral triangle, respectively
96
Q

iliohypogastric nerve

A

T12/L1

courses in that dermatome to innervate skin overlying iliac crests

97
Q

lateral femoral cutaneous

A

L2-L3
courses deep to inguinal ligament.
innervate skin on anterolateral thigh

98
Q

obturator n

A

L3-L4

motor innervation to medial thigh (adductor)

99
Q

inferior gluteal n

A

L5-S2

motor innervation to gluteus maximus

100
Q

krukenberg tumor

A

malignant ovarian tumor w/ mucous.

mucin-secreting signet cell adenocarcinoma

metastasis from gastric cancer / GI

101
Q

metastasis of gastric cancer can present as.. (3)

A
  1. virchow node
    - involvement of left supraclavicular node by metastasis from stomach
  2. sister mary joseph nodule
    - subcutaneous periumbilical metastasis
    - (seen w/ intestinal type)
  3. krukenberg tumor of ovary
    - bilateral metastases to ovaries. abundant mucus signet ring cells
    - (seen w/ diffuse type)
102
Q

what might decrease effectiveness of levodopa/carbidopa in parkinson’s patient

A

B6 supplementation.

DOPA –> dopamine
via dopamine decarboxylase
cofactor: B6

this enzyme is blocked peripherally by carbidopa

103
Q

possible side effect of cimetidine

A

H2 receptor blocker

can cause gynecomastia!! +

104
Q

first recommendation for high LDL, high TG, and low HDL?

A

exercise and diet!!

105
Q

rx for hypertriglyceridemia (4)

A
  1. diet, exercise, weight loss, abstinence from smoking & alcohol
  2. fibrates (PPAR-alpha & lipoproteinlipase)
  3. niacin (decreasing synthesis of TG and VLDL)
  4. fish oil containing omega 3-fatty acids (decreases VLDL and triglyceridesn
106
Q

actinic keratosis

A

3-6mm scaly, erythematous lesions occuring on sun-exposed areas

histology:
- hyperkeratosis (hyperplasia of stratum corneum
- parakeratosis (retention of nuclei in stratum corneum)

pigment irregularities & dilated vessels bc associated w/ sun exposure!

small percentage progress to squamous cell carcinoma

107
Q

psoriasis presentation. location histology.

A

usu on knees and elbows and nape

hyperkeratotic plaques

histology: clubbed rete ridges, hyperkeratosis, neutrophils in stratum corneum (monroe abscesses), and perivascular lymphocytic infiltrate

108
Q

dermatofibroma

A

superficial benign fibrous histiocytoma
unknown etiology

benign proliferation of fibroblasts.
common on lower extremities as solitary nodules

109
Q

most common skin cancer

A

basal cell carcinoma

110
Q

metastasis of basal cell carcinoma? melanoma?

A

basal cell: low tendency to metastasize

melanoma: high tendency to metastazie

111
Q

presentation of basal cell carcinoma

A

usu pearly papule w/ central depression or ulceration

histology: nests of basaloid cells and peripheral palisaiding nuclei

112
Q

most common cause of renal papillary necrosis

A

diabetes mellitus

113
Q

causes of renal papillary necrosis

A

SO sAAD

  • sickle cell anemia / trait
    obstruction of small kidney vessels, predispose to ischemia.
  • obstruction
  • acute pyelo
    both: edematous interstitium of pyelonephritic kidney compresses medullary vasculature –> predisposing to ischemia
  • analgesic: phenacetin, acetaminophen, aspirin, caffeine, codeine
    inhibit renal blood flow by decreasing prostaglandins.
  • diabetic mellitus
    nonenzymatic glycosylation –> alter vascular walls –> compromised renal vasculature
114
Q

abrupt onset of gross hematuria in a pt w/ family history of sickle cell suggests…

A

renal papillary necrosis

115
Q

gross & microscopic renal papillary necrosis

A

gross: gray yellow/white necrosis of tips or distal 2/3 of renal pyramids
microscopic: coagulative infarct necrosis, preserved tubule outlines. later- -> fibrous depressions

116
Q

condition that causes low complement levels

A

poststreptococcal glomerulonephritis

117
Q

thrombin time measures

A

rate of conversion of fibrinogen to fibrin

prolonged by heparin and dysfibrinogenemia

118
Q

what causes mallory-weiss tears?

A

longitudinal mucosal tears at esophagogastric-squamocolumnar junction.

secondary to rapid intraabdominal & intraluminal gastric pressures (retching & vomitting)

also: coughing, hiccuping

predisposing factor: hiatal hernias.

119
Q

evidence of steroid use

A

suspect in athlete w/ erythrocytosis, abnormal testicular size & fxn, hepatic abnormalities, & acne

  1. high hematocrit (androgen stimulate RBC production)
    [reason why males have higher hematocrit]
  2. small testicular size, decreased sperm production, decreased endogenous testosterone
  3. acne, voice deepening, male pattern baldness

hepatic side effects

120
Q

rx for hep C (chronic infection)

A

ribavarin and IFN-alpha

121
Q

ribavarin is used for..

A

chronic hep C infxn

RSV

122
Q

mechanism of ribavarin (5)

A

nucleoside antimetabolite.
interferences w/ duplication of viral genetic material

lethal hypermutation, inhibiting RNA pol and inosine monophosphate dehydrogenase (depleting GTP), causing defective 5’ cap formation on mRNA transcrips, and modulates a more effective immune response.

  1. phosphorylated, incorporated into RNA & pairs w. uracil or cytosine –> hypermutation during RNA dep RNA replication
  2. direct inhibition of HCV RNA pol (by ribavarin triphosphate)
  3. ribavarin monophosphate inhibits cellular monophosphate dehydrogenase (depleting GTP pools)
    [needed to convert IMP to GMP)
  4. inhibits viral RNA guanylyltransferase and methytransferase, resulting in defective 5’ cap formation on mRNA –> ineffective translation
  5. enhances Th1-cell mediated immunity while inhibiting Th2 cytokine production –> modulates a more effective immune response
123
Q

which two drugs block IMP dehydrogenase? what step is blocked

A

purine de novo synthesis

IMP -> GMP

mycophenolate & ribavarin

UWorld mixed (60 decks)

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