test #27 4.16 Flashcards
why does C. perfringens make gas necrosis?
rapid metabolism of muscle tissue carbohydrate –> gas
osmium tetroxide
fat = black
fat embolism syndrome
(1) respiratory distress
(2) nonfocal neurological disturbance
(3) chest lesions consistent w/ thrombocytopenia
describe path of fat emboli
dislodge from bone marrow, enter marrow vascular sinusoids,
- occlude pulmonary microvessels –> impair gas exchange
- occlude vasculature in CNS
describe promotion of parenchymal destruction w/ fat emboli (2)
- platelet & mediators coat & adhere to emboli –> thrombocytopenia
- systemic activation of LPL (lipoprotein lipase) releases oleic acid systemically –> toxic levels
wright stain
often hemotological stain. purple platelets
iron stain // hemosiderin
brown on H&E
dark blue on prussian blue
second trimester quad screen for down’s syndrome:
increased: b-HCG, inhibin A.
decreased: AFP, estriol
first trimester findings in down’s syndrome:
ultrasound:
increased nuchal translucency &
hypoplastic nasal bone.
serum:
increased b-HCG
decreased PAPP-A
edward’s syndrome (trisomy 18) screening findings
everything is down.
1st trimester:
DOWN: PAPP-A and b-HCG
quad screen:
DOWN: AFP, b-HCG, estriol, inhibin-A (could be normal)
elevated b-HCG and inhibin in 2nd semester?
[low estriol and AFP]
down’s syndrome
low bHCG, inhibin, estriol, and ADP
edward’s syndrome
patau syndrome screening findings
first trimester:
DOWN: bHCG, PAPP-A
increased nuchal translucency
low b-HCG and PAPP-A w/ nuchal translucency? without nuchal translucency
nuchal translucency: patau
w/o nuchal translucency: edwards
vast majority of trisomy 21 occur due to..
nondisjunction in meiosis I
failure of homologous chromosomes to separate
nondisjunction in meiosis I due to? nondisjunction in meiosis II due to?
meiosis I: failure of homologous chromosomes to separate
meiosis II: failure of sister chromatids to separate
lagging strand is CONSTRUCTED in which direction? SYNTHESIZED in which direction?
constructed in 3’->5’ direction.
synthesized in 5’->3’ direction
elder abuse
FIRST: try to speak to patient alone – to avoid intimidation.
ask:
1. do you feel safe at home
2. who prepares your meals
3. who handles your checkbook
REPORT only after information is collected
anovulatory cycles
common in early menarche years.
immature HPA-axis
longer menstrual cycles and irregular bleeding patterns due to presence of anovulatory cycles
no ovulation -> no corpus luteum -> no progesterone -> continuous estrogen
results in continued proliferation.
becomes disorganized, fragile, w/ unstable venous capillaries –> irregular periods of stromal breakdown w/ variable (spotting) & heavy bleeding.
three major causes of valvular aortic stenosis. most common world-wide? in USA?
(1) congenitally abnormal valve w/ calcification (i.e. biscuspid)
(2) calcified normal valve
(3) rheumatic heart disease
world-wide: rheumatic heart disease.
US: calcific aortic valve (either bicuspid/tricuspid)
right horn of sinus venosus
originally receives blood from IVC. l
becomes smooth part of right atrium.
(smooth part of left from primitive pulmonary vein)
bulbos cordis
forms beginning of ventricular outflow tract in embryonic heart. later –> smooth portion of left and right ventricles (adjacent to aorta and pulmonary artery, respectively)
primitive atrium
receives blood from sinus venosus in embryonic heart, transmits to primitive ventricle.
primitive atrium –> rough portions of left and right atria
close PDA? keep it open?
close: indomethacin.
keep open: PGE2