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MB 3 Flashcards

1
Q

patient comes in with paralysis of her lower right face, where is the damage?

A

UMN damage of CN7 on contralateral side

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2
Q

which chewing muscles are responsible for closing the mouth?

A

masseter, medial pterygoid, temporalis

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3
Q

patient comes in with paralysis of entire right side of face, where is the damage?

A

CN7 or facial nerve nucleus on ipsilateral side

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4
Q

of the gram negative rods, which are lactose fermenters?

A

klebsiella, e coli, enterobacter (slow are citrobacter, serratia)

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5
Q

how is shigella different than salmonella?

A

non-motile and does NOT produce H2S

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6
Q

once invaded, how does shigella spread to neighboring cells?

A

via protrusions created through host-cell actin polymerization

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7
Q

some strains of shigella produce shiga toxin, how does this work?

A

inactivating the 60S ribosomal subunit, halting cellular protein synthesis which damages intestinal mucosa

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8
Q

first pharyngeal arch

A

first aortic arch and trigeminal nerve

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9
Q

first aortic arch progress

A

regresses mostly but does contribute somewhat to the maxillary artery

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10
Q

second pharyngeal arch

A

second aortic, facial nerve, muscles facial expression, some ear and hyoid-associated structures

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11
Q

second aortic arch progress

A

regresses

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12
Q

third pharyngeal arch

A

third aortic arch and glossopharyngeal nerve, hyoid bone, sylopharngeus muscle

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13
Q

third aortic arch

A

common and proximal internal carotid arteries

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14
Q

fourth pharyngeal arch

A

fourth aortic arch, superior laryngeal branch of the vagus, many muscles of the pharynx and soft palate, few of the laryngeal muscles

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15
Q

fourth aortic arch

A

part of the true aortic arch and subclavian arteries

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16
Q

which pharyngeal and aortic arches are obliterated during fetal development?

A

fifth

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17
Q

sixth pharyngeal arch

A

sixth aortic arch, recurrent laryngeal branches of the vagus nerve, muscles of the larynx

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18
Q

sixth aortic arch

A

pulmonary arteries and ductus arteriosus

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19
Q

hyperthermia, muscle rigidity, confusion

A

neuroleptic malignant syndrome

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20
Q

drugs that cause NMS?

A

antipsychotics, which are also commonly neuroleptics

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21
Q

when is lithium use appropriate?

A

mood stabilizer, commonly in bipolar. NOT acute control of agitation and psychosis

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22
Q

acute lithium toxicity?

A

nausea, vomiting, diarrhea

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23
Q

propofol distribution and redistribution

A

first to areas of high blood flow (brain, rapid onset of drug) then fat and muscle tissues (rapid termination)

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24
Q

propofol vs inhaled anesthetic elimination?

A

propofol = liver, inhaled anesthetics = lung

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25
Q

what is the function of dextrans produce by strep viridans?

A

adherence to fibrin and platelets that are deposited at sites of endothelial trauma, providing a site for bacterial adherence and colonization during bacteremia

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26
Q

linkage disequilibrium

A

pair of alleles inherited together in the same gamete (haplotype) more often or less often than would be expected given random pairing

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27
Q

when does linkage disequilibrium most often occur?

A

when the genes are in close physical proximity on the same chromosome

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28
Q

6 classes of HIV anti-retroviral medications?

A

NRTI, NNRTI, PI, integrase inhibitor, fusion inhibitor, CCR5 antagonist

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29
Q

how do NRTI and NNRTIs work?

A

inhibit HIV DNA synthesis from RNA template by terminating DNA chain elongation - NRTI is a compteitive nucleoside/tide, NNRTI = allosteric inhibitor

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30
Q

PI anti-retroviral tx MOA

A

inhibits HIV polyprotein cleavage

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31
Q

Dolutegravir, raltegravir

A

inhibits HIV DNA integration into host genome

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32
Q

enfuvirtide

A

inhibits HIV fusion with target cell membrane by binding to HIV gp41

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33
Q

CCR5 antagonist

A

inhibits HIV entry by allosteric blocking of HIV gp120 interaction with CCR5

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34
Q

maraviroc

A

CCR5 antagonist

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35
Q

atazanavir, darunavir

A

PI - inhibits HIV polyprotein cleavage

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36
Q

efavirenz, nevirapine

A

NNRTI

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37
Q

pellagra

A

photosensitive dermatitis, diarrhea, dementia

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38
Q

niacin (vitamin B3) is involved in which enzymatic reactions?

A

as NAD and NADP, cofactors of many dehydrogenase and reductase enzymes

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39
Q

list enzymes that use NAD

A

citric acid cycle! majorly catabolic. isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, malate dehydrogenase

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40
Q

NK cells

A

destruction of cells with decreased or absent MHC class I proteins on their surfaces - virus infected cells, tumor cells

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41
Q

NK cell MOA

A

cytoplasmic granules with perforins to make holes in target cell membranes, and granzyme, chemicals that induce target cell apoptosis

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42
Q

NK activation

A

INF-gamma and IL-12

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43
Q

NK express what on cell surface?

A

CD 16 or CD 56

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44
Q

do neutrophils directly kill malignant cells?

A

NO

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45
Q

functions of macrophages

A

phagocytosis, antigen presentation to T-helped lymphocytes in association with MHC II molecules, secretion of immuno-modulatory cytokines, like TNF and IL-1

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46
Q

dendritic cells

A

avid antigen presenting cells that constantly sample their environment by endocytosis and become activatedupon encoutering a foreign antigen. When activated, DC migrante to the lymph nodes and spleen where they display antigen with MHC II and co-stimulatory molecules to activate T and B cells

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47
Q

CD4+ T-lymphocytes

A

activated by antigen presented in associated with MHC11 molecules and can promote cell-mediated (macs and CD8+ cells) and/or humoral (B-cell) responses

48
Q

B cell transformation to plasma cells?

A

activated by Th cells, plasma cells are ready to secrete ag-specific immunoglobulins

49
Q

how to NK cells kill target cells?

A

by inducing apoptosis

50
Q

cases of GVHD

A

1) allogeneic bone marrow transplantation, 2) transplantation of organs rich in lymphocytes (liver), 3) transfusion of non-irradiated blood

51
Q

how does GVHD happen?

A

donor T cells from graft survive due to donor immunosuppression and migrate into host tissues where they recognized host MHC antigens as foreign and become sensitized ; activated donor CD4+ and CD8+ T cells participate in host cell destruction

52
Q

common affected areas in GVHD

A

skin, liver, GI

53
Q

immature defense mechanisms

A

acting out, denial, displacement, intellectualization, passive aggression, projections, rationalization, reaction formation, regression, splitting

54
Q

mature defense mechanisms

A

sublimation, suppression

55
Q

acting out

A

expressing unacceptable feelings through actions

56
Q

displacement

A

transferring feelings to a more acceptable object

57
Q

intellectualization

A

using intellect to avoid uncomfortable feelings

58
Q

passive aggression

A

avoiding conflict by expressing hostility covertly

59
Q

projection

A

attributing one’s own feelings to others

60
Q

rationalization

A

justing behavior to avoid difficult truths

61
Q

reaction formation

A

responding in a manner opposite to one’s actual feelings

62
Q

regression

A

reverting to earlier developmental stage

63
Q

splitting

A

seeing others as all bad or all good; all or nothing thinking, unable to integrated positive and negative qualities into a cohesive and realistic whole; common in borderline personality disorder

64
Q

sublimation

A

channeling impulses into socially acceptable behaviors

65
Q

suppression

A

putting unwanted feelings aside to cope with reality

66
Q

somatic symptom disorder

A

excessive anxiety and preoccupation with one or more unexplained symptoms

67
Q

illness anxiety disorder

A

fear of having a serious illness despite few or no symptoms and consistently negative evaluations

68
Q

conversion disorder (functional neurologic symptom disorder)

A

neurologic symptom incompatible with any known neurologic disease; often acute onset associated with stress

69
Q

factitious disorder

A

intentional falsification or inducement of symptoms with goal to assume sick role

70
Q

malingering

A

falsification or exaggeration of symptoms to obtain external incentives (secondary gain)

71
Q

what is the SVC derived from embryologically?

A

common cardinal veins

72
Q

what does each of the 3 embryo vein groups go on to become/?

A

umbilical vein degenerates, vitelline veins = portal system, cardinal veins = constituents of the systemic venous circulation

73
Q

truncus arteriosus

A

ascending aorta and pulmonary trunk

74
Q

esophagus

A

endodermal foregut

75
Q

how does HCV have a lot of variation?

A

the virion-encoded RNA dependent RNA polymerase has no proofreading 3 –>5 exonuclease activity = many errors during replication’ marked variety in antigenic structure of envelope proteins so that host ab production continually lags behind new mutant HCV strains

76
Q

differential diagnosis of vaginitis

A

bacterial vaginosis (gardnerella vaginalis), trichomoniasis (trichomonas vaginalis), candida vaginitis (candida albicans)

77
Q

cottage cheese vaginal discharge

A

candida albicans

78
Q

pseudohyphae

A

candida albicans

79
Q

yellow-green frothy discharge

A

trichomonas vaginalis

80
Q

tx for trichomoniasis

A

metronidazole and treat partner

81
Q

tx for candida vaginalis

A

fluconazole

82
Q

tx for bacterial vaginosis

A

metronidazole or clindamycin

83
Q

x-ray shows hyper-inflated lungs and flattened diaphragm

A

COPD

84
Q

emphysema

A

destruction of alveolar wallas and decreased lung elastic recoil, leading to increased residual volume, increased FRC and increased TLC

85
Q

how do erythrocytes produce energy?

A

glycolysis - do not have mitochondria and thus cannot use the citric acid cycle; erythrocytes convert 1,3BPG to 2,3 BPG by way of a mutase enzyme, and2,3BPG is increased in hypoxia and chronic anemia alosterically decreasing Hg affinity for O2 so body can get as much as possible

86
Q

what are 2 ways to decrease Hg affinity for oxygen?

A

lower blood oxygen concentrations and higher 2,3 BPG levels (indicating more energy being expended by erythrocytes

87
Q

patient appearance turner syndrome

A

webbed neck, broad chest with widely spaced nipples, cubitus valgus, short status and primary amerrhea in woman

88
Q

risks with bicuspid aortic valve

A

infectious endocarditis due to abnormal leaflet structure and turbulent flow

89
Q

cardiac abnormalities in down syndrome

A

complete atrioventricular canal, ASD, VSD

90
Q

sound with ASD

A

fixed splitting of the second heart sound

91
Q

sound with VSD

A

holosystolic murmur at the left lower sternal border

92
Q

sound mitral stenosis

A

mid-diastolic, low-pitched, rumbling that may being with an opening snap

93
Q

sound with mitral valve prolapse

A

mid systolic click, often accompanied by a late systolic murmur

94
Q

Marfan and Ehlers-Danlos syndrome accompanied with which heart malfunction?

A

mitral valve prolapse

95
Q

turner heart abnormalities

A

aorta - bicuspid aortic valve, which are at risk of stenosis, insufficiency, infection; aortic root dilation

96
Q

turner syndrome karyotype

A

45X

97
Q

cytoplasmic inclusions in oligodendrocytes

A

Progressive multifocal leukoencephalopathy (PML)

98
Q

passive congestion of the spleen

A

portal HTN, splenic vein thrombosis, CHF

99
Q

can infective endocarditis lead to circulating immune complexes which can be deposited into the kidney and spleen?

A

YES

100
Q

how does pyruvate kinase deficiency lead to hemolytic anemia?

A

failure of glycolysis and resultant failure to generate sufficient ATP to maintain erythrocyte structure, thus they lyse and end up in red pulp of speeln (remember: reythrocytes do not have own mitochondrion since they don’t want to consume the oxygen they carry, so instead they produce ATP through glycolysis)

101
Q

ataxia telangiectasia

A

triad = cerebellar ataxia, telangiectasis, increased risk of sinopulmonary infections; risk of hematologic malignancies; causes immune deficiency of cell-mediated and humoral (especially IgA deficiency), predisposing to upper and lower airways

102
Q

what is telangiectasias

A

widened venules which cause thread-like red lines on the skin

103
Q

ataxia telangiectasia inheritance?

A

AR; ATM gene mutation, responsible for DNA break repair

104
Q

how does lead intoxication cause hypochromic anemia?

A

inhibition of mitochondrial iron transport important for here synthesis

105
Q

Lesch Nyhan Syndrome

A

x-linked recessive results in HGPRT enzyme deficiency = defective purine catabolism = severe hyperuricemia and gout

106
Q

behavior of someone with Lesch Nyhan Syndrome

A

self-mutilating, mental retardation, choreoathetoid movements, spasticity

107
Q

bare lymphocyte syndrome

A

immunodeficiency resulting from a defect in expression of HLA class II antigens on the surface of APCs, result = no cell-mediated response and no humoral response

108
Q

Niemann-Pick disease

A

AR, defect in sphingomyelinase leading to accumulation of sphingomyeling within monocytic cells leading to death in early childhood

109
Q

two disease with a cherry red spot on the macula

A

niemann-pick disease and tay-sachs disease

110
Q

gag protein

A

p24 = capsule for HIV

111
Q

env protein

A

gp 41 (transmembrane protein of envelope) and gp 120 (outer glycoprotein that gets in touch with host)

112
Q

pol protein

A

RT polymerase to transfer positive RNA to DNA

113
Q

what microbes infect macrophages?

A

HIV and mycobacterium

114
Q

CD4 < 200

A

HIV progresses to AIDS

115
Q

HIV caused CA

A

diffuse large B cell lymphoma

116
Q

HIV virus interacts with what host cell proteins?

A

early = CCR5, later = CXCR4

117
Q

HIV diagnosis?

A

Eliza first with follow-up western blot

neuro (34 decks)

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