test #43 4.30 Flashcards Preview

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1
Q

S4 heart sound results from

A

suddent rise in end diastolic ventricular pressure caused by atrial contraction against a ventricle that has reached the limit of its capacitance.

stiff ventricle

presystolic sound, precedes S1

2
Q

when are the papillary muscles placed under tension

A

during ventricular systole

3
Q

describe axoneme in flagella and cilia

A

circular array of microtubule doublets anchored at basal body and surrounding 2 central microtubules (9+2)

doublets connected by ATP-splitting dynein arms

4
Q

primary ciliary dyskinesia

A

autosomal recessive

impaired ciliary & flagellar motility due to dynein protein defect

about 1/2 develop kartagener: male infertility, situs inversus, recurrent sinusitis/otitis, and bronchiectasis.

5
Q

reaction formation

A

behavior pattern in which person does opposite of what he feels/desires

usu: person uses excessive havior to cover up how she/he really feels bc feeling that might be perceived as unacceptable by others in society.

wants to do crack, gives talks about how people who do crack should be shunned

(diff from altruism bc here, hope is to cover up a desire)

or angry at wife, tells her she looks great

short-term, immature, eventually breaks down

6
Q

describe polyol pathway

A

glucose -> sorbitol
consume NADPH -> NADP+
via: aldose reductase

sorbitol -> fructose
consume NAD+ -> NADH
via: sorbitol dehydrogenase

note: retina, renal papilla, schwann cells have much less sorbitol dehydrogenase activity: prone to osmotic damage w/ glucose overload

lens has significant sorbitol dehydrogenase, but can still be overwhelmed.

note: oxidative stress from NADPH depletion also plays a role

7
Q

primary energy source for sperm

A

fructose

8
Q

where is the polyol pathway particularly prominent

A

seminal vesicles, make fructose for sperm

9
Q

how does hyperglycemia lead to cataracts

A

overwhelm sorbitol dehydrogenase ability to convert sorbitol to fructose

sorbitol generates osmotic prssure, influx of water into lens cells –> hydropic lens fibers that degenerate. lens opacification.

oxidative stress from NADPH depletion also plays a role!

10
Q

2 ways damage induced w/ hyperglycemia in lens, retina, schwann cells, renal papillae..

A

sorbitol accumulation -> osmotic damage

NADPH depletion: oxidative damage

11
Q

xylulose

A

end product of glucoronic acid metabolism, and intermediate in pentose phosphate pathway

12
Q

presentation of klinefelters

A

hypogonadism, eunuchoid habitus, small firm testes, genotype 47 XXY. have barr body

13
Q

hormonal abnormalities in klinefelter

A

high LH, FSH.
low inhibin, testosterone

sperm count is decreased

seminferous tubules progressively destroyed & hyalinized –> small firm testes.

results in low inhbin & low testosterone (leydig cells also hurt)

results in high LH and FSH

14
Q

congenital absence of GnRH-neurons called

A

Kallmann syndrome

decreased LH, FSH, testosteone, and sperm count

15
Q

why is sperm count low w/ exogenous steroids

A

high LOCAL concentration of androgens needed for spermatogenesis.

exogenous steroids decrease LH production, reducing local testosterone in testes.

ends up w/ testicular atrophy over time.

16
Q

hormonal problems in cryptoorchidism

A

high FSH, normal LH, normal testosterone, decreased sperm

sertoli cells susceptible to heat, poor inhibin, high FSH

17
Q

when is aortic regurg heard loudest (peak murmur intensity)

A

greatest pressure difference,
when incompetent aortic valve closes

early diastolic, high-pitched, blowing descrendo.

mid to late diastole, intensity of murmur would be less bc magnitude of the gradient diminished.

left sternal border, patient leaning forward (valve to wall), end expiration

18
Q

peak murmur intensity of mitral regurg

A

greatest pressure diff in ventricle and atria.

early systole. opening of aortic valve

19
Q

peak murmur intensity of aortic stenosis

A

greatest pressure diff in aorta and ventricle.

peak of systole

crescendo-descrescendo

20
Q

peak murmur intensity of mitral stenosis

A

greatest pressure diff in atria and ventricle

mid-diastole. low pitch rumble after the opening snap

21
Q

low grade vs. high grade tumors

A

low grade: well differentiated. morphologically and architecturally similar to normal cells in tissue of origin

high grade: poorly differentiated, lack most characteristic feature of original tissue.

complete lack of differentiation: anaplastic

22
Q

features of anaplastic (high-grade, poorly differentiated) tumors

A

pleomorphic cells w/ large, hyperchromatic nuclei, grow in disorganized fashion. contain numerous mitoses, and giant multinucleated cells.

  1. loss of cell polarity, complete disruption of normal tissue architecture, cells coalsce into sheets / islands in a disorganized, infiltrative fashion
  2. significant variation in shape & size (cellular pleomorphism) and nuclei (nuclear pleomorphism)
  3. disproportionately large nuclei (high NC ratio) often deep staining (hyperchromatic) w/ abdunfant coarsely clumped chromatin and nucleoli
  4. numerous, abnormal, mitotic figues
  5. giant, multinucleated tumor cells
23
Q

bronchial epithelium

A

columnar

24
Q

relative risk reduction

A

absolute risk (control) - absolute risk (treatment)

divided by

absolute risk control

25
Q

musculocutaneous n

A

C5-7
major upper arm flexors
biceps brachii, coracobrachialis, brachialis muscles.

continues as lateral cutaneous nerve of forearm, sensory to lateral forearm

26
Q

sensory innervation to the foot

A

mostly superficial peroneal n.

deep only: region between 1st & 2nd digits

27
Q

impt strxr near medial malleolus

A

saphenous n & great saphenous vein; course anteriorly

posterior tibial artery, tibial n, tendons of flexor digitorum longus, flexor hallucis longus, tibialis posterior; course posteriorly

28
Q

anastrozole, letrozole, exemestane

A

aromatase inhibitor

29
Q

describe how the lens is attached to eye

A

lens is attached to suspensory ligaments, which are attached to the ciliary muscle.

ciliary muscle relaxes->
suspensory fibers are taut
lens flatten

ciliary muscle contracts ->
suspensory fibers are loose
lens thicken

30
Q

age related changes in lens –? ]

A

presbyopia, inability of lens to focus on near objects

lens is hardened; loose elasticity as proteins undergo progressive degeneration

also, ciliary muscle less strong.

when contract ciliary muscle
loosen suspensory ligaments
lens no longer thickens

loose accomodation

31
Q

presbyopia is most people? in myopic people?

A

most: loose ability to read fine print, eye strain after reading, need to hold objects farther from eye.

myopic (near-sighted): will retain ability to see up close w/o refractive correction & experience some improved distance vision

32
Q

cause of skin aging (wrinkles: rhytides)

A

reduced elasticity, decreased amounts if supporting subdermal fat

  • thinning of dermis and epidermis w/ flattening of dermoepidermal junction,
  • decreased FIBROBLASTS
  • reduced synthesis & increased breakdown of collagen & elastin
33
Q

what position allows for S3 hearing?

A

low frequency

lie in left lateral decubiitus, fully exhale (bring heart close to chest wall)

34
Q

what forms s-adenosyl-methionine SAM?

A

added adenosine from ATP to methionine

35
Q

role of s-adenosyl-methionine SAM

A

methyl donor (methyltransferases take its methy & give to others)

becomes s-adenosyl-homocysteine –> homocysteine + adenosine

36
Q

what is the precursor to homocysteine

A

s-adenosyl-homocysteine

which forms after SAM gives away a methyl

37
Q

what are 2 fates of homocysteine

A

cystathione or methionine

cystathione -> cysteine

38
Q

what converts homocysteine to cystathione

A

cystathione synthetase

+ B6 & serine

39
Q

how does B12 help form homocysteine -> methionine

A

homocysteine -> methionine requires conversion of n5-methyl-THF to THF.

N5-methyl-THF -> THF requires B12.

w/o B12, accumulate N5-methyl-THF ‘folate trap’. can’t make methionine

40
Q

methylmalonylCoA -> succinyl-CoA requires

A

methylmalonyl-CoA mutase, B12 cofactor.

41
Q

fibroadenoma histology

A

cellular, myxoid stroma, encircles (and sometimes compresses) epithelium-lined glandular & cystic spaces.

42
Q

sclerosing adenosis

A

proliferative breast disease

increased acini & intralobular fibrosis. associated w/ calcifications. often confused w/ cancer.

central acinar compression & distortion (by surrounding fibrotic tissue) & peripheral duct diitation

increase risk 1.5-2x of cancer.

43
Q

paget’s disease of nipple

A

malignant cells spread from DCIS into nipple (w/o crossing basement membrane)

still in epidermis. will see large cells in epidermis w/ clear halo “paget cells”

unilateral erythema & scale crust

44
Q

mammary duct ectasia

A

ductal dilation, inspissated breast secretion, chronic granulomatous inflammation in periductal / interstitial areas

45
Q

medullary breast carcinoma (invasive)

A

fleshy, cellular, lymphocytic infiltrate.

good prognosis, associated w/ BRCA1

solid sheets of vesicular, pleomorphic, mitotically active cells w/ significant lymphoplasmacytic infiltrate around & within the tumor & a pushing, non-infiltrating border.

46
Q

units of the breast anatomy

A

deep -> out

lobule, terminal duct, major duct, lactiferous sinus, nipple

47
Q

intraductal papilloma

A

benign breast tumor, occurs in lactiferous duct, typically beneath areola

serous/blood nipple discharge,
slight risk w/ carcinoma

48
Q

phyllodes tumor

A

large bulky mass of connective tissue & cysts. biphasic. may become malignant.

49
Q

invasive ductal carcinoma

A

worst, most invasive.
most common of all breast cancer

firm, fibrous, rock-hard mass. sharp margins, small, glandular, duct-like cells.

gross: stellate

50
Q

invasive lobular carcinoma

A

often e-cadherin mutation in in situ form –> “floating”

oderly row of cells

often bilateral, multiple lesions

51
Q

inflammatory invasive breast cancer

A

dermal lymphatic invasion by carcinoma.

peau d’orange: due to lymphedema –> pitting, skin thickening.

neoplastic cells block lymphatic drainage

50% survival in 5 years

presents like acute mastitis that won’t get better w/ antibiotics

52
Q

what causes nipple inversion? skin retraction

A

nipple inversion: tumor invades central part of breast

skin retraction: cancer infiltrates coopers suspensory ligament –> focal dimpling

53
Q

legionella infection leading to legionnaire’s disease

A

very HIGH fever in a smoker w/ 1. diarrhea,

  1. confusion,
  2. cough (slightly productive)

lab: hyponatremia

54
Q

radiographic evidence of pneumonia, high fever, GI symptoms; suspect

A

legionella (legionaire’s disease)

HYPONATREMIA

55
Q

testing for legionella

A

antigen in urine

lab: hyponatremia

56
Q

rx for legionella

A

respiratory fluoroquinolines: levofloxacin.

or new macrolide: azithromycin

57
Q

sputum stain of legionella? detection

A

will be negative, unless using silver stain

ANTIGEN in URINE

58
Q

water sources of legionella

A

aersolized water: air conditioning, hot water tanks

no person to person

59
Q

pontiac fever vs. legionaire’s disease

A

legionnaire: severe pneumonia, fever, GI, CNS
pontiac: mild flu-like. no pneumonia

60
Q

pneumonia w/ mild anemia

A

consider mycoplasma: cold hemolytic anemia

61
Q

chest radiography that looks must more severe than patient

A

consider mycoplasma

diffuse bilateral infiltrate

62
Q

M. kansasii

A

atypical mycobacterium
causes disease like TB

similar to legionella bc water contaminant.

a particular contaminant of municipal drinking water system. not frequently found in nature.

63
Q

M. avium intracellulare

A

disseminated non-TB disease in AIDS.

64
Q

hemodynamic findings in cardiac tamponade

A

pulsus paradoxus & arterial hypotension

usu when pericardial pressure > 10mmHg

65
Q

pulsus paradoxus

A

exaggeration in normal drop in systolic pressure w/ inspiration
>10mmHg drop

66
Q

gross diagnosis of pulsus paradoxus

A

grossly diagnose w/ radial pulse disappearing w. inspiration

67
Q

pulsus alternans

A

in patients w/ left ventricular dysfunction

beat-to-beat variation in magnitude of pulse pressure in presence of regular cardiac rhythm

68
Q

dicrotic pulse

A

pulse w/ 2 distinct peaks (one in systole, one in diastole)

best palpated in carotids

in patient w/ severe systolic dysfunction

69
Q

pulsus parvus et tardus

A

aortic stenosis

low magnitude pulse w/ delayed peak

70
Q

hyperkinetic pulse

A

rapid ejection of large stroke volume against decreased afterload

during fever / exercise in normal

or patient w/ high-output condition (AV fistula, PDA)

71
Q

halothane, enflurane, isoflurane, sevoflurane..

A

halogenated inhalation anestheics

think: massive hepatic necrosis!
esp: halothane

presents 2d-4wks post exposure w/ liver tenderness, hepatomegaly, increased LFT

80% mortality; no therapy
rare, but severe

72
Q

microvesicular fatty change in liver

A

reyes syndrome

children 5-10 w/ salicylate

73
Q

drug induced cholestasis

A

oral contraceptive, anabolic steroid, chlorpromazine

74
Q

hepatic granulomatosis

A

associated w/ methyldopa, hydralazine, quininde

75
Q

base excision repair

A
  1. make apurinic/apyrimidinic site (remove base)
    - glycosylase
  2. cleave 5’end phosphodiester bond
    - endonuclease
  3. cleave 3’ end phosphodiester bond
    - lyase
  4. fill in single gap
    - DNA polymerase
    - ligase
76
Q

UV on DNA? ionizing radiation?

A

UV: thymidine dimers

ionizing radiation: double stranded DNA break & oxidative changes

77
Q

deamination of cytosine

A

leads to uracil

78
Q

demaination of adenine

A

xanthine

79
Q

deamination of guanine

A

hypoxanthine

80
Q

methylation of uracil

A

thymine

81
Q

where is total pulmonary vascular resistance lowest?

A

at functional residual capacity

end of tidal volume

82
Q

what are the determinants of pulmonary vascular resistance?

A

both alveolar & extraalveolar pulmonary vascular resistance, which have opposite relationships w/ increasing lung volumes

83
Q

what increases alveolar pulmonary vascular resistance?

A

increased lung volume stretches alveoli –> reduces diameter & lengths vessel –> increasing resistance

84
Q

what increases extraalveolar pulmonary vascular resistance?

A

decreased lung volumes reduce radial traction holding vessels open & increases intrathoracic pressure –> compresses extraalveolar vasculature –> increasing resistance

85
Q

effect of competitive antagonist on maximum drug effect

A

just requires higher dose of drug (shifts to right)

does not change Vmax

86
Q

effect of noncompetitive // or irreversible competitive antagonist on maximum drug effect

A

reduces vmax

87
Q

bosentan (2 effects)

A

oral endothelin receptor antagonist, blocks pulmonary hypertension

  1. decrease pulmonary arterial pressure
  2. lessens progression of vascular & right ventricular hypertrophy
88
Q

endothelin

A

potent vasoconstrictor and stimulant of endothelial proliferation.

89
Q

mycobacterium leprae infects..

A

cold temp: skin, nerves (schwann cells), eyes & testes

transmission: armadillo

90
Q

what should be checked before giving etanercept

A

PPD

TNF-alpha inhibitor.

TNF-alpha needed to keep latent TB in check.

worry about reactivation TB

91
Q

what must be checked before given methotrexate & leflunomide?

A

liver function test

can cause hepatotoxicity

92
Q

hydroxychloroquine can cause..

A

irreversible retinal damage

must have baseline & follow up opthalmologic exam

93
Q

rx for CHF and HTN?

A

best: ACE inhibitors

inhibit myocardial remodeling * associated deterioration of ventricular contractile function.

B blocker also good: improves mortality in patients w/ systolic CHF & MI

94
Q

rx for HTN and diabetes

A

best: ACE inhibitors

95
Q

rx for essential HTN (w/o diabetes or CHF)

A

hydrochlorothiazide

96
Q

rx for HTN and benign prostatic hyperplasia

A

can give terazosin

alpha-blocker

97
Q

what agents produce bad myocardial remodeling?

A

angiotensin II
- give ace inhibitors

aldosterone
- give spironolactone

98
Q

positive long term effects of b-blockers

A

improve mortality in patients w/ systolic CHF & MI

w/ HTN

99
Q

what produces ring-enhancing lesions in brain (4)

A

multiple

  1. toxoplasmosis
  2. neurocystercersosis from taenia solium eggs
  3. CNS lymphoma

single:
4. glioblastoma (usu solitary & butterfly)

distinguish w/ story & biopsy

100
Q

prepubertal eggs are stuck in..

A

prophase meiosis I

primary oocyte

101
Q

postovulatory eggs are stuck in..

A

metaphases meiosis II

102
Q

when does gametogenesis begin

A

4 weeks ovulation.

primordial germ cells migrate from yolk sac to developing gonadal region & undergo mitosis

103
Q

progression of germ cells in females

A

primordial germ cells –> oogonia (46, 2N)

begin meiosis I –> primary oocyte (46, 4N)

stays until puberty. ovulation, finish meiosis I: secondary oocyte & polar body, both (23, 2N)

halt at metaphase of meoisis II until fertilization, when it divides into mature oocyte & second polar body

104
Q

when is a woman’s full complement of oocytes developed?

A

by 5 months gestational age.

from that point on, oocytes deplete

105
Q

coagulative necrosis on histology

A

structure maintained.
NO NUCLEUS

in heart, occurs w/ >30min ischemia

106
Q

fibrinoid necrosis

A

histologic pattern of injury seen in blood vessel walls

  1. polyarteritis nodosa (vasculitis
  2. malignant HTN
  3. diabetes

results from 1. immune complex deposition and/or 2. plasma protein (fibrin) leaking through damaged intima

histology: circumferential ring of pink, amorphous material

107
Q

when does dystrophic calficiation occur

A

in areas of necrosis that escape removal by phagocytes

microscopic: amorphous BASOPHILIC material on H&E

108
Q

where are cysts found in ADPKD

A

kidney, liver

109
Q

differentiate cysts in liver & kidney from solid mets on CT

A

cysts: homogenous w/ regular outlines, nonenhacing on CT

solid med: irregular, enhancing

110
Q

life span of ARPKD

A

manifest in INFANT
die shortly after birth, or
first years of life

111
Q

Kearns-Sayre syndrome

A

mitochondrial disease:
aka
oculocraniosomatic neuromuscular disease w/ ragged red fibers

mitochondrial myopathy

112
Q

pleomorphism, nuclear abnormalities, abundant mitoses, disordered maturation, changes in cell polarity occur in what cell change?

A

BOTH dysplasia and carcinoma

113
Q

what differentiates dysplasia from carcinoma?

A

dysplasia: reversible

carcinoma: IRREVERSIBLE
once breach BM -> irreversible

114
Q

dysplasia

A

abnormal cell growth confined to epithelium

cells: uniform and organized, but nuclei: pleomorphic, loss of alignment on BM, no longer grouped right, hyperchromatic, increased NC ratio, bizarre mitoses

115
Q

high-grade dysplasia is synonymous with

A

carcinoma in situ

dysplasia throughout epithelium. does not penetrate.

once breach = invasive carcinoma

116
Q

low grade vs. high grade dysplasia

A

low grade: does not involve entire thickness of epithelium.

high grade: entire = carcinoma in situ

117
Q

epithelial malignancy progression

A

low grade dysplasia -> high-grade dysplasia/carcinoma in situ -> invasive carcinoma

118
Q

what types of plaques are more prone to rupture

A
  1. think fibrous cap
  2. rich lipid core
  3. high degree of inflammation (metalloproteinases: destabilize mechanical integrity)

all promote rupture & superimposed thrombosis

119
Q

important determinant of whether a coronary plaque –> myocardial necrosis

A

RATE of arterial occlusion

slow: allow development of adequate collateral circulation

120
Q

blood supply to upper 1/3 ureter?

lower 2/3?

A

upper 1/3rd: renal artery
- transplanted w/ kidney!

lower 2/3rd: branches of aorta & iliac: gonadal & vesical artery

121
Q

kidney transplant

A

usually leave old kidney. anastomose..
-donor renal artery & vein -> external iliac artery & vein

also transplant upper 1/3 of ureter

122
Q

3 microscopic changes in alzheimers

A
  1. neurofibrillary tangles
  2. senile plaques
  3. amyloid angiopathy
123
Q

biochemical changes in Alzheimers

A

decreased Ach in

  1. hippocampus
  2. nucleus basalis of meynert

due to deficiency of choline acetyltransferase (ChAT)

124
Q

basal nucleus of meynert

A

participates in memory & cognition

base of forebrain, widely projects to neocortex

in alzheimers, see deficiency in ChAT (low Ach)

125
Q

what is depleted in huntington’s

A

NMDA receptors depleted in striatum –> loss of GABA release

126
Q

EML4-ALK fusion protein associated w/

A

non-small cell lung cancer
chromosomal rearragement

constitutive active tyrosine kinase

usu nonsmoking adenocarcinoma who lack k-ras gene or EGF-R mutation

rx: crizotinib

127
Q

what structures derive from ventral pancreas bud? dorsal?

A

main pancreatic duct
uncinate process, and piece of head

dorsal?
everything else, inclu: accessory pancreatic duct

128
Q

pancreatic divisum

A

ventral and dorsal bud don’t fuse (should in 8th wk of fetal life)

not a big deal. pancreas drain via 2 ducts now.

accessory pancreatic duct will not degenerate, so that pancreas can still drain dorsal via minor papilla.

ventral: drain via main pancreatic duct; major papilla

129
Q

embryonic origin of pancreas

A

from foregut outpouching

endodermal

130
Q

anti-snRNP antibodies

A

mixed connective tissue disease

131
Q

how to snRNP cleave introns

A

cleave 5’ end of intron & joining that end to branch point. then cleave 3’ end

ligate remaining exon mRNA w/ phosphodiester

132
Q

peroxisomes

A

cytoplasmic organelles containing oxidative enzymes

catalase, D-amino oxidase, uric acid oxidase.

most abundant in liver & kidney.

detox of ingested materials.

ALSO breakdown FATTY ACIDS

133
Q

proteosome vs. lysosomes

A

both degrade proteins

proteosome: intracellular protein degrade
lysosome: mostly extracellular

134
Q

PCOS hormones

A

high everything, except FSH normal/low

(high: testosterone, LH, estrogen)

LH/FSH ratio > 3

135
Q

long term risk of PCOS

A

high unopposed estrogen –> endometrial hyperplasia / adenocarcinoma

136
Q

histology of ovaries in PCOS

A

exam: bilaterally enlarged
histology: multiple enlarged, sclerotic, cystic follicles

137
Q

vaginal adenosis

A

replacement of squamous epithlelium w/ glandular columnar epithelium

associated w. female offspring exposed to DES (diethylstilbestrol)

precursor for clear cell adenocarcinoma of vagina

138
Q

DES (diethylstilbestrol) exposure in utero

A

vaginal adenosis

precursor: clear cell adenocarcinoma of vagina

139
Q

histology of abetalipoproteinemia

A

normal intestinal mucosal architecture,

but enterocytes contain clear / foamy cells:

more promiment at tips

140
Q

dietary lipids are processed in enterocytes as..

A

chylomicrons B-48

141
Q

endogenosly produced lipids are secreted from hepatocytes as..

A

VLDL B-100

142
Q

what is missing in abetalipoproteinemia

A

autosomal recessive, loss of function in MTP gene.

MTP (microsomal triglyceride transfer protein) = chaperone protein needed for

  1. proper folding of apo B
  2. loading lipids into chylomicrons & VLDL
143
Q

presentation of abetalipoproteinemia

A

first year of life: malabsorption (abdominal distention, foul smelling stools).

lab: very low plasma triglycerides and cholesterol. chylomicons, VLDL, and apoB missing.

poor absorption of fat soluble vitamins & essential fatty acids.

RBC: thorny projections: acanthocytes

neuro abnormalities: progressive ataxia, retinitis pigmentosa

144
Q

mutation in MTP gene causes

A

microsomal triglyceride transfer protein

abetalipoproteinemia
no chylomicrons, VLDL

145
Q

histology of whipple’s disease

A

distended macrophages in lamina propria of small intestine

macrophage: PAS+ diastase resistance granules & rod shapped tropheryma whippelii bacilli

146
Q

granules in whipple are..

A

PAS +

diastase resistane

147
Q

greatest risk of abestos exposure

A

greatest risk: bronchogenic carcinoma!

mesothelioma is rare! if had mesothelioma, most likely related to abestos exposure

148
Q

abestosis

A

fibrocalcific plaques on parietal pleura. subsequence diffuse pleural thickening & fibrosis of lower lobe.

histology: interstitial fibrosis & asbestos bodies

149
Q

most common cause of death in asbestos workers

A

bronchogenic carcinoma

2nd: mesothelioma

150
Q

what increases risk of mesothelioma

A

asbestos exposure

smoking does NOT

151
Q

direct alkylating agents associated w/

A

acute leukemia

152
Q

nitrosamines and amide exposure associated w/

A

stomach carcinoma

153
Q

beta-napthylamine exposure assoaciated w/

A

(in aniline dyes & rubber)

bladder carcinoma

154
Q

neonatal complications w/ gestational diabetes

A
  • premature
  • fetal macrosomia
  • neural tube defects: caudal regression
  • hypoglycemia
  • hypocalcemia
  • polycythemia
  • respiratory distress
  • transient hypertrophic cardiomyopathy
155
Q

neonates exposed to high glucose in utero develop..

A

glucose crosses, insulin doesn’t

baby makes more insulin from pancreas.

after birth, continue to make extra insulin –> HYPOGLYCEMIA

will eventually downregulate

156
Q

redistribution of fat from extremities to trunk associated with (2)

A
  1. glucocorticoids
    - cushing syndrome
  2. HAART therapy - protease inhibitors
    (highly active antiretroviral therapy)
    - lipodystrophy
157
Q

lipodystrophy

A

redistribution of body fat from extremities to trunk

occurs w/ protease inhibitors in HAART therapy

158
Q

pathogenesis of drug-induced lipodystrophy

A

protease inhibitor: impair hepatic chylomicron uptake & triglyceride clearance

excess accumulation of fat in abdominal viscera, breast, posterior neck “buffalo hump”, supraclavicular area

dysmetabolic profile: hyperglycemia, hyperlipidemia, hyperinsulinemia

159
Q

short-term relief of osteoarthritis

A

intra-articular glucocortoids
(NOT oral)

which has very low chance of producing cushing syndrome

160
Q

in the first month after a vasectomy

A

can still find viable sperm in ejaculate

can have sperm proximal to ligation

20% still have viable sperm after 3 months and at least 20 ejaculations

need sperm sample to confirm azoospermia

161
Q

path of vas deferens

A

up abdominal wall, around top part of bladder, down posterior wall of bladder, connects to prostate near seminal vesicle

162
Q

vas deferens does not affect

A
  1. sexual desire, satisfaction

2. ejaculate volume: semen mostly seminal vesicle & prostate fluid

163
Q

monitor DIC occurance

A

D-dimers and serum fibrinogen

164
Q

dead fetus in utero for 6 wks can cause

A

release of thomboplastin (tissue factor) from placenta – consumptive coagulopathy

165
Q

findings of DIC (5)

A
  1. prolonged PTT and PT
  2. thrombocytopenia & microangiopathic hemolytic anemia
  3. low fibrinogen
  4. elevated fibrin split products (D-dimer)
  5. low factor V and VIII