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Daily Flashcard Quizzes > 7/17 > Flashcards

7/17 Flashcards

1
Q

what’s a possible side effect of a pt taking dapsone

A

possible hemolytic anemia if pt is G6PD deficient

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2
Q

what type of test do you want to rule out a life-threatening disease

A

highly sensitive,
because it’s able to correctly identify those with the disease.

the identification of every person with the disease is important here.

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3
Q

what provides local defense against candida

A

T cells

localized Candida is common in HIV pts

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4
Q

what provides systemic defense against candida

A

neutrophils,
prevent hematogenous spread

neutropenic pts are likely to have systemic candidiasis

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5
Q

distinguish between conductive, sensorineural, and noise-induced hearing loss

A

conductive:
mechanical damage
(Weber localizes to affected ear; abnormal Rinne)

Sensorineural:
loss of hair cells/nerve
(Weber test localized to unaffected ear; nl Rinne)

noise-induced:
damaged to stereo ciliated cells in ORGAN OF CORTI
loss of high-frequency hearing first

suddenly extreme loud noises: tympanic membrane rupture
causes unilateral conductive hearing loss

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6
Q

what does LH do in a male

A

stimulates release of testosterone from Leydig cells,

which produces negative feedback on LH

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7
Q

what does FSH do in a male

A

stimulates release of inhibin B from Sertoli cells, which produces negative feedback on FSH

FSH also stimulates sertoli cells to produce androgen-binding protein locally (ABP)

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8
Q

what does ABP do

A

ABP from the sertoli cells is responsible for keeping high levels of local testosterone, necessary for spermatogenesis

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9
Q

which male cells are and are not temp sensitive

A

Sertoli cells support sperm synthesis and are sensitive to temperature!

Leydig cells secrete testosterone and are unaffected by temperature

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10
Q

what does the pathogenicity of H influenzae depend on

A

the presence of an antiphagocytic polysaccharide capsule.

type B strain is most invasive

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11
Q

what is leukocytoclastic vasculitis

A

a cutaneous small vessel vasculitis, often associated with medication for a recent infection (penicillins, cephalosporins)

typically presents w/ palpable purpora in lower extremities

characteristic histology:
marked perivascular inflammation of small blood vessels
fibrinoid necrosis
predominance of neutrophils and fragmented neutrophilic nuclei

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12
Q

what is erythema nodosum

A

form of panniculitis (inflamm of subcutaneous fat)

typically presents as painful erythematous nodules in the lower extremities

histology:
widening of CT septa due to neutrophilic infiltration and fibrin exudation
histiocyte and giant cell infiltration with septal fibrosis

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13
Q

what histology do you see in giant cell vasculitis

A

focal granulomatous inflammation of the media and internal elastic lamina fragmentation

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14
Q

what is polyarteritis nodosa

A

transmural medium-vessel vasculitis

pts typically present with systemic symptoms, renal failure, and abdominal pain
from ischemia of involved organs

lungs/pulmonary arteries are spared

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15
Q

what does urticaria histology look like

A

superficial dermal edema with a mild perivascular infiltrate (rare neutrophils) and dilated lymphatic channels

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16
Q

what happens in a type 1 hypersensitivity

A

mediated by the interaction of the allergen with preexisting IgE bound to basophils and mast cells

this facilitates cross-linking of the surface IgE molecules that signals the cell to degranulate, releasing chemical mediators (histamine, heparin)

described as “cell surface-bound antibody bridging by antigen”

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17
Q

how would you describe type 2 hypersensitivity

A

antibody-dependent cell-mediated cytotoxicity

IgM or IgG binds to antigens expressed on the cell surface. these antibodies are then recognized by Fc receptors on immune cells, triggering the release of perforin and granzymes that ultimately leads to cell lysis/death

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18
Q

how would you describe type 4 hypersensitivity

A

CD8 T cell-mediated hypersensitivity

no antibodies

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19
Q

what antibody is the most efficient in initiating complement

A

IgM in types 2 and 3 hypersensitivities

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20
Q

where can enhancer sequences be located

A

upstream, downstream, or within a transcribed gene

it functions to increase (or decrease, if it’s a silencer) transcription

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21
Q

what are promoter sequences

A 
typically 25-75 bases upstream of their associated genes
function to initiate transcription
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22
Q

distinguish between HUS and TTP

A

both are thrombotic microangiopathies,
characterized by microvascular lesions with platelet aggregation
both have abnormal BLEEDING TIMES because of LOW PLATELETS
normal PT/PTT because it’s a platelet problem, not a coagulation problem

HUS:
more common in children
prominent renal involvement

TTP:
more common in adults
associated with pregnancy, HIV, cancer, bacterial infections, vasculitis, bone marrow transplant, drugs
TTP will have schistocytes on a blood smear

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23
Q

distinguish between TTP and ITP

A

TTP will have neuro findings

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24
Q

distinguish between TTP/HUS and hemophilias and VWF

A

TTP/HUS will have abnormal bleeding times
(problem with platelets)

Hemophilias will have prolonged PTT/PT
(abnormal coagulation factors)

VWF:
has both abnormal PTT and prolonged bleeding times

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25
Q

how will a hemophilia vs VWF pt present

A

Hemophilia:
deep tissue bleeding (hemarthrosis)

VWF:
menorrhagia
mucosal bleeding (GI, hematuria, epistaxis, gingival bleeds)

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26
Q

what are the phases of Pagets disease of the bone

A

Lytic: osteoclasts
Mixed: clasts + blasts
Sclerotic: blasts
Quiescent: minimal of either

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27
Q

how does Pagets bone disease present

A

abnormal bone remodeling forming poor-quality bone

elevated Alk Phos,
all other labs normal

Mosaic pattern of woven and lamellar bone

long bone chalk-stick fractures

Hat size may be increased (skull thickening)

hearing loss (narrow auditory foramen)

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28
Q

what are the segmented viruses, and what’s their significance

A 
BOAR:
Bunyavirus
Orthomyxovirus 
Arenavirus
Rotavirus

can undergo reassortment (genetic shift) and exchange entire segments, causing a dramatic mutation and an epidemic or pandemic.

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29
Q

what characteristics cause a drug to remain inside of a plasma compartment

A

high molecular weight
high plasma protein binding
high charge
hydrophilic

these all give the drug a lower Vd

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30
Q

what heart rhythm is commonly seen after excessive alcohol consumption

A

a fib

absent P waves, irregularly irregular rhythm, and varying R-R intervals

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31
Q

what would cause a high QRS voltage

A

ventricular hypertrophy, commonly 2/2 prolonged HTN

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32
Q

what can cause widened QRS complex

A

delay in intraventricular conduction due to fascicular or bundle branch block

the heart rhythm remains regular in this abnormality

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33
Q

what is prolonged QT interval associated with

A

risk of torsades de pointes (polymorphic V tach)

sudden cardiac death

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34
Q

how does chlamydia trachomatis present

A

L1-L3 cause lymphogranuloma venerum,
initially a painless ulcer
progresses to painful inguinal lymphadenopathy (buboes) and ulceration

see chlamydial cytoplasmic inclusion bodies

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35
Q

what are Councilman bodies

A

AKA acidophilic bodies, and apoptotic bodies

seen in pts with acute Hepatitis, which causes hepatocyte apoptosis and necrosis.
Apoptotic hepatocytes shrink, undergo nuclear fragmentation, and become intensely eosinophilic.

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36
Q

what does an elevated creatinine kinase suggest

A

underlying myopathy

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37
Q

what should be excluded in all pts with unexplained CK elevation

A

hypothyroidism,
via checking of TSH levels

myopathy can often be the first manifestation of hypothyroidism, so you should rule this out

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38
Q

what are common causes of myopathies

A

hypothyroidism
muscular dystrophies
inflammatory muscle diseases
mendications (statins)

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39
Q

describe the anatomy/pathway of the ureters

A

ureters pass posterior to ovarian/gonadal vessels in the retroperitoneum off the aorta and SVC
then anterior to the common/external iliac arteries

then reach the true pelvis:
anterior to internal iliac artery
medial to ovarian vessels
crosses under the uterine artery (water under the bridge)

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40
Q

how does estrogen affect bone and other tissues

A

estrogen decreases bone resorption
so low estrogen causes osteoporosis risk

unopposed estrogen exposure (estradiol therapy) can cause excessive endometrial proliferation, resulting in endometrial hyperplasia/cancer

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41
Q

what are Raloxifene and tamoxifen

A

SERMs

selective estrogen receptor modulators

they bind to estrogen receptors and exhibit estrogen antagonist or agonist properties in a tissue-specific manner

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42
Q

what is Raloxifene’s specific use

A

estrogen agonist at bone (to decrease resorption)
improves bone mineral density

estrogen antagonist at breast
prevents breast cancer

estrogen antagonist at uterus
does not increase risk for endometrial cancer

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43
Q

what is Tamoxifen’s specific use

A

strong estrogen antagonist in breast
used in treating ER-positive breast cancer

estrogen agonist at bone (protective)

however, also agonist activity at uterus, increasing risk for endometrial hyperplasia/cancer

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44
Q

alendronate’s use

A

bisphosphonate that inhibits bone resorption

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45
Q

leuprolide’s use

A

GnRH analog with estrogen agonist properties when administer pulsatile
estrogen antagonist properties when administer continuously

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46
Q

medroxyprogesterone’s use

A

reduces incidence of endometrial hyperplasia and risk of cancer in postmenopausal women on estrogen replacement therapy

prolonged use of this as a contraceptive is associated with decreased bone mineral density

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47
Q

what parameter is increased in CHF

A

arteriolar resistance

via angiotensin 2 causing vasoconstriction.
this exacerbates HF because the heart is now pumping against against a higher arterial resistance (after load)

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48
Q

what do pts with deficient C5b-C9 have problems with

A

unable to form membrane attack couplex MAC

often experience recurrent infections with Neisseria

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49
Q

which anti fungal targets mitosis

A

griseofulvin

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50
Q

which anti fungal targets DNA and RNA synthesis

A

flucytosine

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51
Q

which anti fungal targets cell wall polysaccharide synthesis

A

capsofungin

note, it’s the WALL not plasma membrane

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52
Q

which anti fungal inhibits ergosterol synthesis

A

azoles

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53
Q

which anti fungal damages cell membrane

A

amphotericin B and nystatin

they bind ergosterol and “tear holes” in it

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54
Q

what is congenital long-QT syndrome

A

mutated K channel,
causing a delayed re-polarizing rectifier current (Ik) of the cardiac AP

Jervell and Lange-Nielsen syndrome is the recessive form that also has sensorineural hearing loss

increased risk of sudden cardiac death 2/2 Torsades de pointes

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55
Q

what is the pathology of achondroplasia

A

exaggerated inhibition of chondrocyte proliferation

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56
Q

how does superior vena cava syndrome present

A

impaired venous return from the upper body:
dyspnea
facial swelling
dilated collateral veins in the upper trunk
possible headache, dizziness, confusion

most commonly caused by lung cancer as a mediastinal mass compressing SVC

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57
Q

what is a superior sulcus tumor

A

pan coast tumor

arises at lung apex and frequently causes shoulder pain 2/2 compression of brachial plexus

commonly involves cervical sympathetic ganglia, leading to Horner’s syndrome

may cause SVC syndrome, but the shoulder pain and Horner’s are most common manifestation

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58
Q

what is seen on NF-1:

A

cafe-au-lait spots

Neurofibromas (short, sessile, or pedunculate lesions varying in size)

optic gliomas

Lisch nodules (asymptomatic hamartomas of the iris)

mutations in NF1 on chromosome 17 (Von Recklinghausen)
auto dominant

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59
Q

what is seen on NF-2

A

bilateral acoustic schwannomas
juvenile cataracts
meningiomas
ependymomas

NF2 gene on chromosome 22
auto dominant

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60
Q

what does spherocytosis come from

A

mutation in spectrin or ankyrin, two plasma-membrane scaffolding proteins

61
Q

what are 2 complications of spherocytosis

A

pigmented gallstones

aplastic crisis from parvovirus B19 infection

62
Q

what are fava bean reactions a buzzword for

A

G6PD deficiency

gives you bite cells, Heinz bodies, all from eating some fava beans :)

63
Q

what does ubiquitin ligase do

A

ubiquitin ligase recognizes specific protein substances and attach a ubiquitin tag

the proteins are degraded to an appropriate size,
then coupled with MHC 1 protein complex in the ER

then they’re presented on cell surface for recognition by CD8 lymphocytes

all part of the ubiquitin proteasome pathway

64
Q

what is a suggestive asthma presentation

A

intermittent resp symptoms

normal CXR

sputum eosinophils

reduced FEV1

65
Q

what can you use to treat recurrent C diff

A

fidamoxicin

macrocyclic (related to macrolide)

66
Q

how do you remember 30s vs 50s inhibitors

A

“buy AT 30; CCEL at 50”

30:
Aminoglycosides
Tetracyclines

50:
Chloramphenicol
Clindamycin
Erythromycin (macrolides)
Linezolid
67
Q

what would give you a winged scapula

A

damage to long thoracic nerve,
possibly during axillary lymph node dissection

unable to abduct shoulder past horizontal because the serrates anterior muscle is paralyzed and cannot rotate scapula upward

68
Q

what do you see 0-4 hours post MI

A

gross:
none

micro:
none

complications: decreased organ perfusion:
cariogenic shock
CHF
arrhythmia

69
Q

what do you see up to 1 day post MI

A

gross:
dark discoloration
(pyknosis, karyorrhexis, karyolysis)

micro:
coagulative necrosis
(anuclear cells)

complications:
arrhythmia
(damaged conducting system will show up early, or not at all)

70
Q

what do you see up to 1 week post MI

A

gross:
yellow pallor
(WBCs within myocardium

micro:
neutrophils 
(acute inflamm always follows necrosis)
then macrophages
(eat dead/necrotic debris; the wall is weakest here)

complications:
fibrinous pericarditis- presenting as chest pain with friction rub (neutrophils infiltrate past the entire wall into pericardium)
RUPTURE:
of ventricular free wall (leads to tamponade)
interventricular septum (leads to shunt)
papillary muscle (leads to mitral insufficiency)

71
Q

what vessel supplies papillary muscle

A

RCA

72
Q

what do you see up to 1 month post MI

A

gross:
red border emerges as granulation tissue enters from edge of infarct

micro:
granulation tissue with plump fibroblasts, collagen, and blood vessels (neovascularization)
all healing and forming a scar

73
Q

what do you see >1 month post MI

A

gross:
white scar

micro:
fibrosis

complications:
aneurysm
mural thrombus
Dressler syndrome

74
Q

what is Dressler syndrome

A

pericardium inflammation
expose antigens to immune system
Ab’s against own pericardium develop

results in pericarditis 6-8 weeks post MI

75
Q

what does neutrophil elastase do

A

it’s the major protease of extracellular elastin degradation

released by neutrophils and macrophages

76
Q

what inhibits elastase

A

alpha-1 antitrypsin

smokers can permanently inactivate AAT through oxidation of crucial methionine residue

77
Q

what is projection

A

the misattribution of one’s unacceptable feelings or thoughts to another person who does not actually have them

boy is mad at parents for divorcing, but avoids them because he thinks they’re mad at him

(vs reaction formation, where boy would be overly nice to his parents)

78
Q

what labs do you see in parotitis

A

elevated amylase without pancreatitis

normal lipase

79
Q

what is the defect in Kartageners

A

dynein arm,

causing primary ciliary dyskinesia

80
Q

how does Kartageners present

A

situs inversus
chronic sinusitis
bronchiectasis

81
Q

what causes SCID

A

defects in T cell IL-2 recepotrs

82
Q

what does deficiency in C1 complement component

A

increased susceptibility to encapsulated bacteria

and predisposes pts to SLE

83
Q

what is immunoglobulin gene rearrangement impaired in

A

hyper-IgM syndrome

B cells produce high IgM but are unable to class switch

84
Q

what is tryptase

A

an inflammatory mediator, similar to histamine
relatively specific for mast cells (marker for mast cell activation)

released from degranulation of mast cells and basophils in anaphylaxis

85
Q

when do you see elevated myeloperoxidase

A

following inflammation and infection, because it’s found in neutrophils

(not seen in anaphylaxis)

86
Q

how does an allergic reaction trigger substance release

A

“receptor aggregation”

the high affinity IgE receptor is found on the surface of mast cells and basophils.
It normally binds to the Fc portion of circulating IgE antibodies.
Cross-linking of multiple membrane-bound IgE antibodies by a multivalent antigen results in aggregation of the high-affinity IgE receptors,
causing degranulation and release of preformed mediators that initiate the allergic response

87
Q

what does the ureteric bud turn into

A

collecting system, including collecting tubules, ducts, major/minor calyces, renal pelvis, and ureters

88
Q

what does the metanephric mesoderm turn into

A

structures from the glomerulus through to the DCT

AKA metanephric blastema

89
Q

what does the mesonephros turn into

A

interim kidney and male genitals

90
Q

which murmur goes with the buzzword head bobbing/ bounding pulses

A

aortic regurg

91
Q

which murmur radiates to cartotids

A

aortic stenosis

92
Q

which murmur radiates forward axilla

A

mitral/tricuspid regurg

93
Q

which murmur causes mid systolic click

A

mitral valve prolapse

the click is sudden tensing of chord tenidnae

94
Q

what is a holosystolic, harsh murmur

A

VSD

95
Q

which murmur has an opening snap

A

mitral stenosis

due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips

delayed rumbling late diastolic murmur

96
Q

what murmur has continuous machine-like murmur

A

PDA

97
Q

what is Edwards syndrome

A

Trisomy 18
“election age”

CLENCHED HANDS with overlapping fingers
micrognathia
low-set Ears
rocker-bottom feet

98
Q

what do Edwards Syndrome labs show

A 
low PAPP-A  (same as 13,21)
low beta-hCG
low alpha-fetoprotein
low estriol
low/nl Inhibin A
99
Q

what is Patau syndrome

A

Trisomy 13
“Puberty”

MIDLINE DEFECTS
CLEFT LIP/PALATE
POLYDACTYLY
omphalocele
microphthalmia
microcephaly/holoprosencephaly 
cutis aplasia
cardiac defects
rocker bottom feet
100
Q

what do Patau syndrome labs show

A

low PAPP-A (same as 13,21)

low free beta-hCG

101
Q

what do Down Syndrome labs show

A

high nuchal translucency
hypoplastic nasal bone

low PAPP-A (same as 13,18)
HIGH BETA-HCG!!!
HIGH INHIBIN A!!!
low alpha-fetoprotein
low estriol
102
Q

what can paraneoplastic cerebellar degeneration come from

A

small cell lung cancer
Female cancers

an immune response against tumor cells cross-reacts with Purkinje neuron antigens

antibodies involved:
Anti-Yo
Anti-P/Q
Anti-Hu

103
Q

what is P-glycoprotein

A

AKA multidrug resistance protein 1 (MDR1)

used to pump out toxins, including chemotherapeutic agents

an “ATP-dependent transporter”

classically seen in adrenal cell carcinoma

104
Q

what does Inulin estimate

A

GFR

105
Q

what does PAH estimate

A

RPF

106
Q

what’s a general explanation for heavy proteinuria or edema

A

decrease in serum albumin and total protein concentrations

this lowers the plasma oncotic pressure, and increases net plasma filtration in capillary beds

107
Q

what causes Zenker diverticulum

A

abnormal spasm or diminished relaxation of cricopharyngeal muscles during swallowing, causing increased intraluminal pressure in the oropharynx.

the mucosa will herniate through the zone of muscle weakness, forming a Zenker diverticulum (FALSE diverticulum)

108
Q

how does Zenker diverticulum present

A

“Elder MIKE has bad breath”

Elderly 
Male
Inferior pharyngeal constrictor
Killian triangle
Esophageal dysmotility
Halitosis!!!
109
Q

what is VHL

A

deletion or mutation of the VHL tumor suppressor gene on chromosome 3p

110
Q

how does VHL present

A

cerebellar hemangioblastoma
clear cell renal carcinoma!!
pheochromocytomas

111
Q

distinguish between Wilms tumor and neuroblastoma

A

Wilms:
nephroblastoma (renal)
large, palpable, smooth, UNILATERAL flank mass and/or hematuria
WT1/2 on chromosome 11

Neuroblastoma:
adrenal medulla
from neural crest cells
firm, irregular mass that CAN cross the midline
can present with “opsoclonus-myoclonus syndrome
N-myc over expression

112
Q

what are Homer-Wright rosettes characteristic for

A

Neuroblastoma (adrenal)

and Medulloblastoma

113
Q

what does LMWH bind to

A

Antithrombin 3

Antithrombin3 binds to Factor 10a, and stops 10a from converting prothrombin to thrombin

114
Q

how do beta blockers treat open-angle glaucoma

A

open-angle glaucoma is from elevated IOP.

BBs diminish the SECRETION of aqueous humor by the ciliary epithelium
Acetazolamide also does the

115
Q

how do prostaglandin F2alpha and cholinomimetics treat glaucoma

A

PF2alpha:
latanoprost, travoprost

Cholinomimetics:
pilocarpine, carbachol

both decrease IOP by increasing OUTFLOW of aqueous humor

116
Q

what does vaccination conjugation cause

A

protein conjugation causes a T cell-mediated immune response,
leading to long-term immunity through production of memory B cells

117
Q

what is the most common cause of native valve infective endocarditis in developed nations

A

mitral valve prolapse with regurgitation

rheumatic heart disease causes IE in developing nations

118
Q

what is secretin

A

secreted from duodenal S cells in response to H+ concentrations

it increases pancreatic HCO3 secretion

119
Q

what are pulsion diverticula

A

false diverticula that develop 2/2 increased intraluminal pressure created during straining bowel movements (chronic constipation)

out pouching of mucosa and submucosa through the muscularis

120
Q

what is a traction diverticula

A

created by inflammation and subsequent scarring of the gut wall,
which typically results in pulling and out pouching of all gut wall waters (true)

may occur in the mid esophagus due to mediastinal lymphadenitis caused by TB or fungal infection

121
Q

what stone is crohn disease associated with

A

oxalate

2/2 impaired bile acid absorption in terminal ileum and loss of bile acids in feces

lipids bind Ca ions, and the resulting soap complex is excreted

free oxalate (normally bound to Ca) is absorbed and forms urinary stones

122
Q

how does pancreatitis cause ARDS

A

pancreas releases lots of inflammatory cytokines which activates neutrophils in alveolar tissues

interstitial and intraalveolar edema, inflammation, and fibrin deposition cause the alveoli to become lined w/ waxy HYALINE MEMBRANES

123
Q

what is pseudotumor cerebri

A

AKA idiopathic intracranial hypertension

increased ICP with no apparent cause

headache, diplopia without change in mental status
papilledema
increased opening pressure
in an obese female of childbearing age; possible Vita A excess

the ICP compresses the optic neves, causing an impaired axoplasmic flow and optic disc edema

124
Q

what is optic neuritis

A

associated with MS

monocular vision loss over several weeks w/ painful eye movement

afferent pupillary defect w/ hyperemia and swelling of the optic disc

125
Q

what’s a common finding in gallstone ileus

A

pneumobilia

air in biliary tract

126
Q

how can Crohn disease cause a bleeding problem

A

an ileal resection/involvement cause cause bile acid malabsorption,
which may lead to impaired absorption of fat soluble vitamins,
including Vitamin K.

vit K deficiency presents as impaired coagulation with easy bruising, large hematoma formation in deep tissues/joints after minor trauma, and prolonged bleeding after surgery

127
Q

what causes an elevated ESR

A

high levels of circulating fibrinogen (ACUTE PHASE REACTANTS) increase ESR

it’s a nonspecific marker of inflammation

128
Q

what 3 cytokines mediate systemic inflammatory responses and acute phase reactant release

A

IL-1
IL-6
TNF-alpha

129
Q

what does AAT deficiency look like histologically

A

reddish-pink, PAS (+) granules of unsecreted, polymerized AAT in the periportal hepatocytes

130
Q

what does acute tubular necrosis look like when alcohol is the culprit

A

generic:
vacuolar degeneration and ballooning of the proximal tubular cells

specific to alcohol:
calcium oxalate crystals

131
Q

how does Hepatitis B cause damage

A

Hep B virus itself doesn’t have cytotoxic effect
the presence of viral HBsAg and HBcAg on cell surface
stimulate the host’s cytotoxic CD8+ T cells to destroy the infected hepatocytes

132
Q

what are muddy brown casts pathognomonic for

A

acute tubular necrosis

133
Q

how does CO poisoning affect blood

A

CO binds Hb with stronger affinity than O₂,
which reduces the number of Heme binding sites available for O₂.

the levels of CO-bound Hb (carboxyhemoglobin) increase

CO decreases the oxygen carrying capacity and oxygen content of blood, but
NOT the amount of oxygen dissolved in plasma, which is the partial pressure PaO2 of oxygen

134
Q

what murmur is heard best with pt leaning forward

A

aortic regurg

135
Q

distinguish between rheumatic heart disease and infectious endocarditis

A

Infectious endocarditis:
aortic or mitral regurgitation

Rheumatic heart disease:
most common cause of aortic stenosis in developing world
always accompanied by mitral valve disease (stenosis/regurg)
uncommon cause of aortic stenosis in developed world

136
Q

what does GFAP indicate

A

astrocytomas

137
Q

what does vimentin indicate

A

it’s an intermediate filament found within cells of mesenchymal origin

used in diagnosing sarcomas

138
Q

what is neural cell adhesion molecule indicate

A

a cell with a neuroendocrine origin, such as small cell lung carcinoma

139
Q

what is a cavernous hemangioma

A

most common benign liver tumor

consist of cavernous, blood-filled vascular spaces lined by single epithelial layer

do not biopsy- expected to bleed and cause fatal hemorrhage

140
Q

what can help the regression of hepatic adenoma

A

discontinue oral contraceptives

141
Q

which cancer is associated with hemochromatosis

A

HCC

142
Q

what is positive in a neuroendocrine tumor

A

chromogranin A

synaptophysin

143
Q

what does HER2 do

A

oncogene that encodes for a transmembrane glycoprotein with intrinsic tyrosine kinase activity

member of the epidermal growth factor receptors

over expression accelerates cell proliferation

144
Q

what is paroxysmal nocturnal hemoglobinuria

A

complement-mediated intravascular RBC lysis

caused by absent GPI anchor for DAF and MIRL (CD55/59) that protect RBC membranes from complement destruction

145
Q

what does portal vein thrombosis cause

A

portal HTN
splenomegaly
varicosities at portocaval anastomoses

does not cause histologic changes to the hepatic parenchyma
(ascites is rare)

146
Q

what is Budd Chiari

A

thrombosis or compression of hepatic veins

biopsy shows centrilobular congestion and necrosis

leads to congestive liver disease (ascites)

absence of JVD

may cause nutmeg liver

147
Q

what do metalloproteinases do

A

they’re zinc-containing enzymes that degrade the extracellular matrix

they participate in normal tissue remodeling and in tumor invasion through the basement membrane and connective tissue

148
Q

what do NSAIDs do to kidneys

A

chronic interstitial nephritis and papillary necrosis

149
Q

what may determine the stability of a vessel plaque

A

plaque stability largely depends on mechanical strength of fibrous cap.

inflammatory macrophages in the intima may reduce plaque stability by secreting metalloproteinases,
which degrade extracellular matrix proteins (collagen)

Daily Flashcard Quizzes (21 decks)

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