test #43 4.30 Flashcards

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

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2
Q

when are the papillary muscles placed under tension

A

during ventricular systole

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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

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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.

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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

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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

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7
Q

primary energy source for sperm

A

fructose

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8
Q

where is the polyol pathway particularly prominent

A

seminal vesicles, make fructose for sperm

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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!

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10
Q

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

A

sorbitol accumulation -> osmotic damage

NADPH depletion: oxidative damage

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11
Q

xylulose

A

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

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12
Q

presentation of klinefelters

A

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

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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

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14
Q

congenital absence of GnRH-neurons called

A

Kallmann syndrome

decreased LH, FSH, testosteone, and sperm count

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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.

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16
Q

hormonal problems in cryptoorchidism

A

high FSH, normal LH, normal testosterone, decreased sperm

sertoli cells susceptible to heat, poor inhibin, high FSH

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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

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18
Q

peak murmur intensity of mitral regurg

A

greatest pressure diff in ventricle and atria.

early systole. opening of aortic valve

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19
Q

peak murmur intensity of aortic stenosis

A

greatest pressure diff in aorta and ventricle.

peak of systole

crescendo-descrescendo

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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

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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

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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
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23
Q

bronchial epithelium

A

columnar

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24
Q

relative risk reduction

A

absolute risk (control) - absolute risk (treatment)

divided by

absolute risk control

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25
musculocutaneous n
C5-7 major upper arm flexors biceps brachii, coracobrachialis, brachialis muscles. continues as lateral cutaneous nerve of forearm, sensory to lateral forearm
26
sensory innervation to the foot
mostly superficial peroneal n. deep only: region between 1st & 2nd digits
27
impt strxr near medial malleolus
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
anastrozole, letrozole, exemestane
aromatase inhibitor
29
describe how the lens is attached to eye
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
age related changes in lens --? ]
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
presbyopia is most people? in myopic people?
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
cause of skin aging (wrinkles: rhytides)
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
what position allows for S3 hearing?
low frequency lie in left lateral decubiitus, fully exhale (bring heart close to chest wall)
34
what forms s-adenosyl-methionine SAM?
added adenosine from ATP to methionine
35
role of s-adenosyl-methionine SAM
methyl donor (methyltransferases take its methy & give to others) becomes s-adenosyl-homocysteine --> homocysteine + adenosine
36
what is the precursor to homocysteine
s-adenosyl-homocysteine | which forms after SAM gives away a methyl
37
what are 2 fates of homocysteine
cystathione or methionine | cystathione -> cysteine
38
what converts homocysteine to cystathione
cystathione synthetase | + B6 & serine
39
how does B12 help form homocysteine -> methionine
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
methylmalonylCoA -> succinyl-CoA requires
methylmalonyl-CoA mutase, B12 cofactor.
41
fibroadenoma histology
cellular, myxoid stroma, encircles (and sometimes compresses) epithelium-lined glandular & cystic spaces.
42
sclerosing adenosis
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
paget's disease of nipple
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
mammary duct ectasia
ductal dilation, inspissated breast secretion, chronic granulomatous inflammation in periductal / interstitial areas
45
medullary breast carcinoma (invasive)
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
units of the breast anatomy
deep -> out lobule, terminal duct, major duct, lactiferous sinus, nipple
47
intraductal papilloma
benign breast tumor, occurs in lactiferous duct, typically beneath areola serous/blood nipple discharge, slight risk w/ carcinoma
48
phyllodes tumor
large bulky mass of connective tissue & cysts. biphasic. may become malignant.
49
invasive ductal carcinoma
worst, most invasive. most common of all breast cancer firm, fibrous, rock-hard mass. sharp margins, small, glandular, duct-like cells. gross: stellate
50
invasive lobular carcinoma
often e-cadherin mutation in in situ form --> "floating" oderly row of cells often bilateral, multiple lesions
51
inflammatory invasive breast cancer
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
what causes nipple inversion? skin retraction
nipple inversion: tumor invades central part of breast skin retraction: cancer infiltrates coopers suspensory ligament --> focal dimpling
53
legionella infection leading to legionnaire's disease
very HIGH fever in a smoker w/ 1. diarrhea, 2. confusion, 3. cough (slightly productive) lab: hyponatremia
54
radiographic evidence of pneumonia, high fever, GI symptoms; suspect
legionella (legionaire's disease) HYPONATREMIA
55
testing for legionella
antigen in urine lab: hyponatremia
56
rx for legionella
respiratory fluoroquinolines: levofloxacin. or new macrolide: azithromycin
57
sputum stain of legionella? detection
will be negative, unless using silver stain ANTIGEN in URINE
58
water sources of legionella
aersolized water: air conditioning, hot water tanks no person to person
59
pontiac fever vs. legionaire's disease
legionnaire: severe pneumonia, fever, GI, CNS pontiac: mild flu-like. no pneumonia
60
pneumonia w/ mild anemia
consider mycoplasma: cold hemolytic anemia
61
chest radiography that looks must more severe than patient
consider mycoplasma diffuse bilateral infiltrate
62
M. kansasii
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
M. avium intracellulare
disseminated non-TB disease in AIDS.
64
hemodynamic findings in cardiac tamponade
pulsus paradoxus & arterial hypotension usu when pericardial pressure > 10mmHg
65
pulsus paradoxus
exaggeration in normal drop in systolic pressure w/ inspiration >10mmHg drop
66
gross diagnosis of pulsus paradoxus
grossly diagnose w/ radial pulse disappearing w. inspiration
67
pulsus alternans
in patients w/ left ventricular dysfunction beat-to-beat variation in magnitude of pulse pressure in presence of regular cardiac rhythm
68
dicrotic pulse
pulse w/ 2 distinct peaks (one in systole, one in diastole) best palpated in carotids in patient w/ severe systolic dysfunction
69
pulsus parvus et tardus
aortic stenosis low magnitude pulse w/ delayed peak
70
hyperkinetic pulse
rapid ejection of large stroke volume against decreased afterload during fever / exercise in normal or patient w/ high-output condition (AV fistula, PDA)
71
halothane, enflurane, isoflurane, sevoflurane..
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
microvesicular fatty change in liver
reyes syndrome | children 5-10 w/ salicylate
73
drug induced cholestasis
oral contraceptive, anabolic steroid, chlorpromazine
74
hepatic granulomatosis
associated w/ methyldopa, hydralazine, quininde
75
base excision repair
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
UV on DNA? ionizing radiation?
UV: thymidine dimers ionizing radiation: double stranded DNA break & oxidative changes
77
deamination of cytosine
leads to uracil
78
demaination of adenine
xanthine
79
deamination of guanine
hypoxanthine
80
methylation of uracil
thymine
81
where is total pulmonary vascular resistance lowest?
at functional residual capacity | end of tidal volume
82
what are the determinants of pulmonary vascular resistance?
both alveolar & extraalveolar pulmonary vascular resistance, which have opposite relationships w/ increasing lung volumes
83
what increases alveolar pulmonary vascular resistance?
increased lung volume stretches alveoli --> reduces diameter & lengths vessel --> increasing resistance
84
what increases extraalveolar pulmonary vascular resistance?
decreased lung volumes reduce radial traction holding vessels open & increases intrathoracic pressure --> compresses extraalveolar vasculature --> increasing resistance
85
effect of competitive antagonist on maximum drug effect
just requires higher dose of drug (shifts to right) does not change Vmax
86
effect of noncompetitive // or irreversible competitive antagonist on maximum drug effect
reduces vmax
87
bosentan (2 effects)
oral endothelin receptor antagonist, blocks pulmonary hypertension 1. decrease pulmonary arterial pressure 2. lessens progression of vascular & right ventricular hypertrophy
88
endothelin
potent vasoconstrictor and stimulant of endothelial proliferation.
89
mycobacterium leprae infects..
cold temp: skin, nerves (schwann cells), eyes & testes transmission: armadillo
90
what should be checked before giving etanercept
PPD TNF-alpha inhibitor. TNF-alpha needed to keep latent TB in check. worry about reactivation TB
91
what must be checked before given methotrexate & leflunomide?
liver function test can cause hepatotoxicity
92
hydroxychloroquine can cause..
irreversible retinal damage must have baseline & follow up opthalmologic exam
93
rx for CHF and HTN?
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
rx for HTN and diabetes
best: ACE inhibitors
95
rx for essential HTN (w/o diabetes or CHF)
hydrochlorothiazide
96
rx for HTN and benign prostatic hyperplasia
can give terazosin alpha-blocker
97
what agents produce bad myocardial remodeling?
angiotensin II - give ace inhibitors aldosterone - give spironolactone
98
positive long term effects of b-blockers
improve mortality in patients w/ systolic CHF & MI w/ HTN
99
what produces ring-enhancing lesions in brain (4)
multiple 1. toxoplasmosis 2. neurocystercersosis from taenia solium eggs 3. CNS lymphoma single: 4. glioblastoma (usu solitary & butterfly) distinguish w/ story & biopsy
100
prepubertal eggs are stuck in..
prophase meiosis I | primary oocyte
101
postovulatory eggs are stuck in..
metaphases meiosis II
102
when does gametogenesis begin
4 weeks ovulation. primordial germ cells migrate from yolk sac to developing gonadal region & undergo mitosis
103
progression of germ cells in females
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
when is a woman's full complement of oocytes developed?
by 5 months gestational age. from that point on, oocytes deplete
105
coagulative necrosis on histology
structure maintained. NO NUCLEUS in heart, occurs w/ >30min ischemia
106
fibrinoid necrosis
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
when does dystrophic calficiation occur
in areas of necrosis that escape removal by phagocytes microscopic: amorphous BASOPHILIC material on H&E
108
where are cysts found in ADPKD
kidney, liver
109
differentiate cysts in liver & kidney from solid mets on CT
cysts: homogenous w/ regular outlines, nonenhacing on CT solid med: irregular, enhancing
110
life span of ARPKD
manifest in INFANT die shortly after birth, or first years of life
111
Kearns-Sayre syndrome
mitochondrial disease: aka oculocraniosomatic neuromuscular disease w/ ragged red fibers mitochondrial myopathy
112
pleomorphism, nuclear abnormalities, abundant mitoses, disordered maturation, changes in cell polarity occur in what cell change?
BOTH dysplasia and carcinoma
113
what differentiates dysplasia from carcinoma?
dysplasia: reversible | carcinoma: IRREVERSIBLE once breach BM -> irreversible
114
dysplasia
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
high-grade dysplasia is synonymous with
carcinoma in situ dysplasia throughout epithelium. does not penetrate. once breach = invasive carcinoma
116
low grade vs. high grade dysplasia
low grade: does not involve entire thickness of epithelium. high grade: entire = carcinoma in situ
117
epithelial malignancy progression
low grade dysplasia -> high-grade dysplasia/carcinoma in situ -> invasive carcinoma
118
what types of plaques are more prone to rupture
1. think fibrous cap 2. rich lipid core 3. high degree of inflammation (metalloproteinases: destabilize mechanical integrity) all promote rupture & superimposed thrombosis
119
important determinant of whether a coronary plaque --> myocardial necrosis
RATE of arterial occlusion slow: allow development of adequate collateral circulation
120
blood supply to upper 1/3 ureter? | lower 2/3?
upper 1/3rd: renal artery - transplanted w/ kidney! lower 2/3rd: branches of aorta & iliac: gonadal & vesical artery
121
kidney transplant
usually leave old kidney. anastomose.. -donor renal artery & vein -> external iliac artery & vein also transplant upper 1/3 of ureter
122
3 microscopic changes in alzheimers
1. neurofibrillary tangles 2. senile plaques 3. amyloid angiopathy
123
biochemical changes in Alzheimers
decreased Ach in 1. hippocampus 2. nucleus basalis of meynert due to deficiency of choline acetyltransferase (ChAT)
124
basal nucleus of meynert
participates in memory & cognition base of forebrain, widely projects to neocortex in alzheimers, see deficiency in ChAT (low Ach)
125
what is depleted in huntington's
NMDA receptors depleted in striatum --> loss of GABA release
126
EML4-ALK fusion protein associated w/
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
what structures derive from ventral pancreas bud? dorsal?
main pancreatic duct uncinate process, and piece of head dorsal? everything else, inclu: accessory pancreatic duct
128
pancreatic divisum
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
embryonic origin of pancreas
from foregut outpouching endodermal
130
anti-snRNP antibodies
mixed connective tissue disease
131
how to snRNP cleave introns
cleave 5' end of intron & joining that end to branch point. then cleave 3' end ligate remaining exon mRNA w/ phosphodiester
132
peroxisomes
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
proteosome vs. lysosomes
both degrade proteins proteosome: intracellular protein degrade lysosome: mostly extracellular
134
PCOS hormones
high everything, except FSH normal/low (high: testosterone, LH, estrogen) LH/FSH ratio > 3
135
long term risk of PCOS
high unopposed estrogen --> endometrial hyperplasia / adenocarcinoma
136
histology of ovaries in PCOS
exam: bilaterally enlarged histology: multiple enlarged, sclerotic, cystic follicles
137
vaginal adenosis
replacement of squamous epithlelium w/ glandular columnar epithelium associated w. female offspring exposed to DES (diethylstilbestrol) precursor for clear cell adenocarcinoma of vagina
138
DES (diethylstilbestrol) exposure in utero
vaginal adenosis precursor: clear cell adenocarcinoma of vagina
139
histology of abetalipoproteinemia
normal intestinal mucosal architecture, but enterocytes contain clear / foamy cells: more promiment at tips
140
dietary lipids are processed in enterocytes as..
chylomicrons B-48
141
endogenosly produced lipids are secreted from hepatocytes as..
VLDL B-100
142
what is missing in abetalipoproteinemia
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
presentation of abetalipoproteinemia
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
mutation in MTP gene causes
microsomal triglyceride transfer protein abetalipoproteinemia no chylomicrons, VLDL
145
histology of whipple's disease
distended macrophages in lamina propria of small intestine macrophage: PAS+ diastase resistance granules & rod shapped tropheryma whippelii bacilli
146
granules in whipple are..
PAS + | diastase resistane
147
greatest risk of abestos exposure
greatest risk: bronchogenic carcinoma! mesothelioma is rare! if had mesothelioma, most likely related to abestos exposure
148
abestosis
fibrocalcific plaques on parietal pleura. subsequence diffuse pleural thickening & fibrosis of lower lobe. histology: interstitial fibrosis & asbestos bodies
149
most common cause of death in asbestos workers
bronchogenic carcinoma 2nd: mesothelioma
150
what increases risk of mesothelioma
asbestos exposure | smoking does NOT
151
direct alkylating agents associated w/
acute leukemia
152
nitrosamines and amide exposure associated w/
stomach carcinoma
153
beta-napthylamine exposure assoaciated w/
(in aniline dyes & rubber) bladder carcinoma
154
neonatal complications w/ gestational diabetes
- premature - fetal macrosomia - neural tube defects: caudal regression - hypoglycemia - hypocalcemia - polycythemia - respiratory distress - transient hypertrophic cardiomyopathy
155
neonates exposed to high glucose in utero develop..
glucose crosses, insulin doesn't baby makes more insulin from pancreas. after birth, continue to make extra insulin --> HYPOGLYCEMIA will eventually downregulate
156
redistribution of fat from extremities to trunk associated with (2)
1. glucocorticoids - cushing syndrome 2. HAART therapy - protease inhibitors (highly active antiretroviral therapy) - lipodystrophy
157
lipodystrophy
redistribution of body fat from extremities to trunk occurs w/ protease inhibitors in HAART therapy
158
pathogenesis of drug-induced lipodystrophy
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
short-term relief of osteoarthritis
intra-articular glucocortoids (NOT oral) which has very low chance of producing cushing syndrome
160
in the first month after a vasectomy
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
path of vas deferens
up abdominal wall, around top part of bladder, down posterior wall of bladder, connects to prostate near seminal vesicle
162
vas deferens does not affect
1. sexual desire, satisfaction | 2. ejaculate volume: semen mostly seminal vesicle & prostate fluid
163
monitor DIC occurance
D-dimers and serum fibrinogen
164
dead fetus in utero for 6 wks can cause
release of thomboplastin (tissue factor) from placenta -- consumptive coagulopathy
165
findings of DIC (5)
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