test #43 4.30 Flashcards Preview

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Flashcards in test #43 4.30 Deck (165):
1

S4 heart sound results from

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

when are the papillary muscles placed under tension

during ventricular systole

3

describe axoneme in flagella and cilia

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

doublets connected by ATP-splitting dynein arms

4

primary ciliary dyskinesia

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

reaction formation

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

describe polyol pathway

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

primary energy source for sperm

fructose

8

where is the polyol pathway particularly prominent

seminal vesicles, make fructose for sperm

9

how does hyperglycemia lead to cataracts

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

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

sorbitol accumulation -> osmotic damage

NADPH depletion: oxidative damage

11

xylulose

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

12

presentation of klinefelters

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

13

hormonal abnormalities in klinefelter

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

congenital absence of GnRH-neurons called

Kallmann syndrome

decreased LH, FSH, testosteone, and sperm count

15

why is sperm count low w/ exogenous steroids

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

hormonal problems in cryptoorchidism

high FSH, normal LH, normal testosterone, decreased sperm

sertoli cells susceptible to heat, poor inhibin, high FSH

17

when is aortic regurg heard loudest (peak murmur intensity)

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

peak murmur intensity of mitral regurg

greatest pressure diff in ventricle and atria.

early systole. opening of aortic valve

19

peak murmur intensity of aortic stenosis

greatest pressure diff in aorta and ventricle.

peak of systole

crescendo-descrescendo

20

peak murmur intensity of mitral stenosis

greatest pressure diff in atria and ventricle

mid-diastole. low pitch rumble after the opening snap

21

low grade vs. high grade tumors

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

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

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

bronchial epithelium

columnar

24

relative risk reduction

absolute risk (control) - absolute risk (treatment)

divided by

absolute risk control

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