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UWorld mixed > #3 3/8 > Flashcards

#3 3/8 Flashcards

1
Q

describe a koilocyte

A

sign of HPV infection; immature squamous cell w/ dense, irregularly staining cytoplasm, perinuclear clearing. enlarged nucleus w/ undulating ‘rasinoid’ membrane, perinuclear vacuoles. pynknotic

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2
Q

HPV infection presentation (3 possibilities)

A
  1. skin warts (verruca vulgaris) HPV 1-4
  2. genital warts (condylomata acuminatum) HPV 6,11
  3. Intraepithelial neoplasia of cervix (CIN) and vulva: HPV 16, 18, 31, 33, 35
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3
Q

describe endometrial cells

A

resemble histiocytes: small dark nuclei, no perinuclear clearing

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4
Q

describe parabasal cells in Pap smear

A

epithelial cells: round with a basophillic cytoplasm & finely granular chromatin in nuclei, no visible nucleoli, high N/C ratio. predominate in Pap from post-menopausal and post-partum women

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5
Q

describe glandular endocervical cells in Pap smear

A

indicate good sample: columnar with prominent cell borders. cluster = honeycomb

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6
Q

how much atherosclerotic blockage is needed for stable angina? unstable angina?

A

> 75% for stable angina. >90% for unstable angina

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7
Q

4 conditions associated w/ Down’s syndrome

A
  1. Alzheimer’s (extra copy of APP)
  2. acute leukemia: AML and ALL
  3. congenital heart disease: endocardial cushion defects
  4. GI defects: duodenal atresia and Hirschsprung
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8
Q

clinical presentation of Creutzfeldt-Jacob disease

A

rapidly progressive dementia and myoclonic jerks

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9
Q

Nesiritide

A

recombinant brain natriuretic peptide (BNP). used in patients w/ decompensated left ventricle dysfunction leading to CHF. activate guanylyl cyclase. vasodilate, diuresis/natriuresis, decrease BP. counteract sympathetics, endothelin, and ANG II

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10
Q

where is endorphin made?

A

endogenous narcotic, made by corticotrophs in

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11
Q

three effects of TGF-beta

A
  1. inhibition of cell cycle
  2. promotion of angiogenesis
  3. stimulation of fibroblasts
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12
Q

bradykinin; where is it made, what does it cause?

A

kidney, locally constricts veins and dilates arterioles (increase renal perfusion). implicated in angioedema (rx: ace inhibitors)

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13
Q

3 possible causes of acute orchitis

A

1&2 in young pts: c. trachomatis & n. gonorrhea. 3 in older: e. coli

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14
Q

predisposition to testicular torsion

A

congenitally-horizontal positioning of testes “bell-clapper deformity”permits rotation of testes around spermatic cord

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15
Q

hypospadias caused by..

epispadias caused by..

A
  • incomplete closure of urethral folds

- faulty positioning of the genital tubercle

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16
Q

t-sample T test

A

determine if the means of 2 populations are equal/not.

need two means, sample variance, and sample size. calculate T-statistic and then p-value

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17
Q

linear regression

A

relationship between dependent and independent variable

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18
Q

correlation coefficient

A

measure of strength and direction of a linear relationship

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19
Q

meta-analysis

A

epidemiological method of analyzing pooled data from several studies, increasing statistical power beyond that of individual studies

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20
Q

generalized anxiety disorder criteria

A

excessive and uncontrollable worry w/ 3+ non-worry symptoms (irritability, disturbed sleep, poor concentration, muscle tension, easy fatiguability, restlessness)

for at least 6 months

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21
Q

classic presentation of acute intermittent porphyria (AIP)

A

abdominal pain, neurpsychiatric manifestations, and colour change in urine upon standing (excess prophyrinogen in urine –> light-induced formation of porphyrins)

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22
Q

where is heme produced (2)

A

85% in bone marrow erythroid cells for hemoglobin. 15% in liver for cytochrome p450 detox enzyme system

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23
Q

enzyme deficiency in acute intermittent porphyria & toxic agents (2)? Rx?

A

porphobillinogen deaminase (hydroxymethylbilane synthase) deficiency. accumulation of ALA and PBG, which are toxic to human tissue

Rx: intravenous heme preps and glucose –> inhibits ALA synthase activity

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24
Q

distinguish enzyme deficiency in early steps of porphyrin synthesis vs. latter steps (after condensation of porphobilinogen)

A

early (AIP): neurologic abnormalities w/o photosensitivity, darkening of urine when standing, increased urinary ALA and PBG

later: photosensitivity.

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25
Q

coronary steal phenomenon

A

collateral blood flow and maximal vasodilation in ischemic areas allows for maintenance of perfusion (low pressure drives flow through collaterals). normal myocardium has normal vascular size

selective coronary vasodilators (adenosine & dipyridamole) vasodilate blood flow to normal myocardium, but can’t vasodilate vasculature to ischemic tissue anymore. blood flow through collaterals reduce. hypoperfusion, worsening ischemia.

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26
Q

explain the use of selective coronary vasodilators in myocardial perfusion studies

A

ADENOSINE and DIPYRIDAMOLE:
simulate coronary steal phenomenon. reveal changes that would occur w/ exercise (vasodilation of normal coronary vasculature –> ischemia in regions w/ collateral flow / obstruction

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27
Q

burkitt lymphoma translocation

A 
typically t(8,14) c-myc w/ IgG heavy chain enhancer
but can be t(8,2) w/kappa light chain 
or t(8,22)  w/ lambda light chain
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28
Q

CML translocation

A

t(9,22) bcr-abl fusion protein

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29
Q

follicular lymphoma

A

t(14,18) bcl-2 (anti-apoptotic) and IgG heavy chain enhancer element

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30
Q

mantle cell lymphoma

A

t(11,14) CD-1 with IgG heavy chain enhancer

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31
Q

Erb2, HER2, neu are all the same name for..

A

epidermal growth factor over expressed in many breast cancers

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32
Q

Li-Fraumeni syndrome

A

autosomal dominant cancer syndrome caused by inherited mutation in p53. p53 inactivation often occurs as one of the two ‘hits’ in human malignancies

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33
Q

tibial collateral ligament (medial collateral ligament)

A

spans medial femoral epicondyle to medial condyle of tibia. attaches to medial meniscus

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34
Q

anterior cruciate ligament

A

attaches ANTERIOR portion of tibia (intercondylar) to posteriormedial side of LATERAL femoral condyle. prevents anterior movement of tibia

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35
Q

posterior cruciate ligament

A

attaches POSTERIOR part of intercondylar area of tibia and anterolateral surface of MEDIAL epicondyle of femor.

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36
Q

transverse genicular ligament

A

attaches medial and lateral menisci anteriorly on proximal articular surface of tibia

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37
Q

patellar ligament

A

spans from patella to tibial tuberosity. continuation of quadriceps femoris tendon

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38
Q

pasturella, borrelia, treponema rx:

A

penicillin, can get the little peptidoglycan that is there

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39
Q

drugs used for MRSA (3)

A

(1) Vancomycin, (2) Daptomycin (depolarization of cellular membrane), (3) Linezolid (inhibit bacterial protein synthesis by binding to 50s)

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40
Q

side-effects of daptomycin (1)

A

(1) myopathy w/ CPK elevation

note: it is inactivated by pulmonary surfactant (not good for pneumonia or gram negs)

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41
Q

side effects of linezolid (3)

A

(1) thrombocytopenia (2) optic neuritis (3) serotonin syndrome

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42
Q

micturition reflex (3 centers of regulation)

A

(1) sacral micturition center - S2-S4, responsible for bladder contraction. parasympathetic fibers travel from S2-S4 ventral white matter within pelvic nerves, stimulate cholinergic receptors in bladder wall
(2) pontine micturition center - pontine reticular formation. coordinates relaxation of of external urethral sphincter w/ bladder contraction in voiding
(3) cerebral cortex – inhibits sacral micturition center

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43
Q

which brain regions are affected by normal pressure hydrocephalus (& which 3 are not)

A

corona radiata in of cerebral cortex. spares: cerebellum, basal ganglia (despite being right next to ventricle), pontine reticular formation

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44
Q

long thoracic nerve 1. enervation and 2. damage causes..?

A
  1. serratus anterior 2. winged scapula
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45
Q

describe axonal reaction (when axon is severed- 3)

A

enlargement of cell body, movement of nucleus to periphery, dispersion of Nissl

46
Q

describe acute neuronal injury (transient severe insult i.e. ischemia, hypoxia, toxicity, hypoglycemia, that is irreversible) – red neuron (4 things)

A

12-24 hr post injury. shrinkage, pyknosis, loss of Nissl, eosinophilic cytoplasm

47
Q

Niemann-Pick disease type A, inheritance, common demographic, clinical presentation

A

autosomal recessive, infants, ashkenazi jewish descent. loss of previously acquired motor capabilities (after normal development) –> progress to hypotonia and blindness by 1y/o. death by 3 y/o

cherry-red macular spot )also seen in tay-sachs & hepatosplenomegaly

48
Q

Niemann-Pick disease

A

deficiency of sphingomyelinase. sphingomyelin accumulation within phagocytes. accumulate ‘foamy histiocytes’ in liver, spleen, and skin, and gradually in CNS (neurodegeneration).

49
Q

which two diseases have cherry-red macular spot

A

tay-sachs and niemann-pick disease

niemann-pick also has hepatosplenomegaly

50
Q

tay sachs enzyme deficiency

A

hexosaminidase A (causes GM2 ganglioside accumulation)

51
Q

Hurler syndrome

A

mucopolysaccharidosis
deficiency of alpha-L-iduronidase.
heparan sulfate and dermatan sulfate accumulate.

52
Q

gaucher disease

A

deficiency of glucocerebrosidase

glucocerebroside accumulates within phagocytes

53
Q

von gierke disease

A

glycogen storage disease; deficiency of glucose-6-phosphatase

54
Q

pompe disease

A

glycogen storage disease; deficiency of lysosomal-alpha-1,4-gluosidase

55
Q

fabry disease

A

deficiency of alpha-galactosidase A, causes ceramide trihexoside to accumulate. disease manifestation: angiokeratoma, acroparesthesia, hypohidrosis, renal failure

56
Q

lesch-nyhan

A

deficiency of HGPRT (hypoxanthine guanine phosphoribosyl transferase), disorder of uric acid metabolism

57
Q

describe two ways CO causes hypoxemia

A
  1. CO 220x more affinity for hemoglobin than O2 (occupies oxygen binding spot)
  2. when bound, forms carboxygemoglobin, alters hemoglobin conformation to relaxed state, which has high affinity for oxygen (leftward shift of oxygen dissociation)

rx: 100% or hyperbaric oxygen

58
Q

timeframe of postpartum blues, postpartum depression, postpartum psychosis

A
  1. postpartum blues: 2-3 days, resolves within 10
  2. postpartum depression: 2wks-12months
  3. postpartum psychosis: days to 6wks postpartum
59
Q

thiamine deficiency syndromes (3)

A
  • infantile beri beri
  • adult beri beri (dry or wet)
  • wernicke-korsakoff syndrome in alcoholics
60
Q

infantile beri beri presentation (thiamine deficiency)

A

appear between 2-3 months, include fulminant cardiac syndrome: cardiomegaly, tachycardia, cyanosis, dyspnea, vomitting

61
Q

adult beri beri (dry vs wet) thiamine deficiency

A

dry: symmetrical peripheral neuropathy w/ sensory & motor impairments, esp distal extremities
wet: this neuropathy + cardiac involvement (cardiomegaly, cardiomyopathy, CHF, peripheral edema, tachycardia)

62
Q

vitamin A deficiency

A

night blindness, xeropthalmia, vulnerability to infxn (esp measles)

63
Q

vitamin B2 (riboflavin) deficiency

A

cheilosis, stomatitis, glossitis, dermatitis, corneal vascularization, ariboflavinosis

64
Q

pyridoxine (vit B6) deficiency

A

cheilosis, glossitis, dermatitis, peripheral neuropathy

65
Q

niacin deficiency

A

pellagra (dementia, dermatitis, diarrhea, and death)

66
Q

ascorbic acid (vit C) deficiency

A

scurvy (hemorrhages, bleeding into joint spaces, gingival swelling, impaired wound healing, weakened immune system to local infxn)

67
Q

classic presentation of pernicious anemia

A

older, mentally slow woman of northern European descent who is “lemon-coloured” anemic & icteric, smooth shiny tongue indicative of atrophic glossitis, shuffling broad-based gait.

68
Q

most important cause of thrombocytopenia in hospitalized patients

A

heparin (heparin induced thrombocytopenia HIT) – leading to paradoxical thrombosis

69
Q

name 3 direct thrombin inhibitors. used for?

A

hirudin, lepirudin, agratroban. drug of choice for HIT

70
Q

aspirin mechanism & indication

A
  • irreversibly acetylates platelet cyclooxygenase I, leading to decreased foramtion of thromboxane A2.
  • primary and secondary prevention of MI and stroke
71
Q

ticlopidine and clopidogrel mechanism & indication (3)

A
  • block ADP receptors (block aggregation)
  • percutaneous coronary intervention (PCI), treatment of unstable in unstable angina and non-Q-wave myocardial infarction
72
Q

dipyridamole and cilostazol

A

inhibit phosphodiesterase activity, increase cAMP, inhibit platelet aggregation

73
Q

glycoprotein IIb/IIIa inhibitors (name & indication [1])

A

abciximab, eptifibatide, tirofiban; use post percutaneous intervention in acute coronary syndrome (PCI)

74
Q

cardiac tissue conduction velocity

A

fastest to slowest: purkinje system, atrial muscle, ventricular muscle, AV node (park at ventura avenue)

75
Q

pentazocine mechanism

A

opioid narcotic, partial agonist activity and weak antagonist activity at mu receptors. when used in combination w/ opiods, act as antagonist –> withdrawal symptoms

76
Q

how much perfusion of myocardial capillaries of LV occurs during systole?

A

10%

77
Q

neurophysins are..? where is ADH made? oxytocin?

A

carrier proteins for oxytocin and vasopressin (ADH), produced in paraventricular and supraoptic nuclei, respectively

78
Q

mechanism for autosomal dominant hereditary hypothalamic diabetes insipidus

A

neurophysin II might shuttle/package vasopressin through ER and golgi into neurosecretory granules.

point mutation in neurophysin II, result in abnormal protein folding, removal from ER (along w/ bound vasopressin), decreasing availability of vasopressin for neurosecretory release.

79
Q

Addison’s disease primary defect

A

in adrenal cortisol production (of the adrenal cortical neurons, low cortisol is the only one needed to spike ACTH)

80
Q

ACTH and MSH are derivived from which common protein

A

POMC (pro-opiomelanocortin)

81
Q

corticosteroids

A

demargination of leukocytes (neutrophils)

82
Q

visual impairment in an HIV-infected patient

A

secondary to CMV-retinitis

83
Q

rx: CMV retinitis

A

ganciclovir, foscarnet, cidofovir

84
Q

side effects of foscarnet

A

pyrophosphate analog that can chelate Ca++. nephrotoxic renal Mg+ wasting, and reduction in the release of PTH (further hypocalcemia)

85
Q

acyclovir toxicity

A

crystal nephropathy and neurotoxicity (delirium and/or tremor)

86
Q

ganclicovir side effect

A

severe neutropenia

87
Q

indinavir (protease inhibitor side effects)

A

fat redistribution, insulin resistance (hyperglycemia) and hypertriglyceridemia, kidney stones

88
Q

lamivudine side effects (though rare)

A

peripheral neuropathy and lactic acidosis

89
Q

common causes of UTI

A

e. coli, s. saprophyticus, p. mirabilis, klebsiella, and eneterococci

90
Q

after ligating coronary artery, how long does it take for myocardium to stop contracting? when does ischemia become irreversible?

A

ischemia –> cessation of aerobic glycolysis & initiation of anaerobic glycolysis. inadequate production of ATP & creatine phosphate, build up deleterious metabolites inclu lactate.

although total ATP levels remain relatively normal during first few minutes of ischemia, ATP is rapidly depleted from areas with high metabolic demand (cytosol surrounding contraction fibers and electrolyte transport pumps).

loss of contractility within about 60 seconds

ischemia that lasts less than 30min, restoration of blood flow leads to reversible contractile dysfunction (myocardial stunning) w/ contractility gradually returning to normal over the next several hours to days.

irreversible after 30min

91
Q

hypoglycemia; presentation and rx in a nonmedical or medical setting

A

pallor and sweaty skin, can progress to bizarre behavior, convulsions, and unconsciousness.

early: mild to moderate rx: 15-30grams of fast-acting carbohydrates
when severe enough to be unconscious, need parenteral treatment

rx: glucagon intramuscularly or subcutaneously. corrects hypoglycemia by increasing hepatic glycogenolysis and gluconeogenesis. return to consciousness 10-15 min

IM glucagon can be done by a friend or relative
hospital –> IV glucose

92
Q

low dose aspirin? high does?

A

low dose, irrev acetylates cox1 alone.

high dose, irrev acetylates cox 1 and cox 2

93
Q

rofecoxib

A

selective cox2 inhibitor (cox 2 preferentially expressed at sites of inflammation, cox 1 constitutively expressed in platelets and in the GI tract where it is impt for normal physiological functioning)

94
Q

cox 1 and cox 2 expression

A

cox 2 preferentially expressed at sites of inflammation.

cox 1 constitutively expressed in platelets and GI tract. impt for normal physiological fxn

95
Q

glut transporter in skeletal muscle and adipocytes

A

glut4

96
Q

glut transporter in liver, small intestine, kidney and pancreas

A

glut 2

97
Q

when are MAOi used (i.e. phenelzine or tranylcypromine) [2]

A
  1. atypical depression

2. treatment-resistant depression

98
Q

describe atypical depression (4 features)

what makes it different from typical major depression?

A
  • mood reactivity
  • leaden fatigue (patients arms and legs feel extremely heavy)
  • rejective sensitivity (overly sensitive to slight criticism)
  • reversed vegetative signs of increased sleep and appetite

main diff from MDD – MOOD REACTIVITY; atypical depression will have improvement in mood in response to something positive.

99
Q

describe lung transplant rejection (hyperacute, acute, chronic). how is it different from renal rejection?

A
  1. hyperacute: graft blood vessel spasm and diffuse DIC w/ resultant ischemia. “white graft” rejection
  2. acute: vascular damage, perivascular and peribronchial lymphocytic infiltrates
  3. chronic rejection: inflammation of the small bronchioles –> BRONCHIOLITIS OBLITERANS. inflammation and fibrosis

vs. chronic rejection in renal transplant –> vascular obliteration

100
Q

granuloma formation (i.e. for TB)

A

Th1 releases IFNy

  1. formation of phagolysosome (harsh bactericidal acids) in infected macrophages
  2. release of iNOS (inducible nitric oxide synthase), ultimately produce reactive nitrogen intermediates and free radicals.

IFN-y activates macrophages, which then produce TNF
1. recruits monocytes that differentiate into epithelioid histiocytes, which cluster in a circular fashion around TB, hemming in. limits spread. caseating granuloma

101
Q

leukotriene C4, D4, E4 (3 things)

A

vasoconstriction, increased vascular permeability, bronchospasm

102
Q

thromboxane A2

A

platelet aggregator and vasoconstrictor

103
Q

platelet activating factor

A

platelet aggregation, vasoconstriction, bronchoconstriction, increased leukocyte adhesion to endothelium

104
Q

C3a

A

anaphylotoxin, from C3. stimulates mass cell histamine release. increased vascular permeability and vasodilation

105
Q

IL-4

A

Th2 differentiation, B cell growth, isotype switching, IgE formation

106
Q

IL5

A

B cell differentiation, eosinophil activation, igA formation

107
Q

which nerve is at risk during a thyroidectomy? which muscle would be affected?

A

external branch of superior laryngeal nerve, as it travels with the superior thyroid artery and vein. innervates cricothyroid muscle (the only muscle of the larynx not served by recurrent laryngeal)

108
Q

describe branches of the vagus nerve innervation to larynx

A

superior laryngeal n and recurrent laryngeal n.
- recurrent laryngeal: all laryngeal muscle except cricothyroid, and sensory below vocal cords

superior laryngeal

  • external branch: cricothyroid
  • internal branch: sensory above cords
109
Q

possible progression of CIN

A
  1. frank cervical cancer

2. most cases -> spontaneously resolve, immune survellience

110
Q

OCP has what effect on the risk of ovarian and endometrial cancer

A

decreased risk, bc suppression of ovulation

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