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135 Cards in this Set

  • Front
  • Back
diff in structure of large arteries vs musclar arteries?
large arteries: elastin
muscular arteries: musle
what are the 3 layers of blodd vssls?
intima, media, adventia
intiima: single layer of endo cells
internal elatic lamina separates intima from media
media: sm m cells
adventia: connective tissue
with age what happens to the aorta?
loss elastin thus the arteries bcome tortuous and dilated
fxn of large arteries vs musclar artery?
large artery: storage and propulsion
muscular artery: regulatio of pressure
diamter of capillaries? flow rate?
dimater= RBC size
slow flow rate
endothelial cell lining but no media
compare the veins to arteries
veins: larger diamters, larger lumens, thinner less well organized walls and bc of this are predisposed to irregular dilation, compression and easy penetration
job of post capiillary venules?
site of fliuid/cell transfer to tissues in inflammation
what do endothlail cells contain?
Weibel Palade bodies: membrane bound storage organelles that contain vWF
how do we ID endothlial cells?
vWF contiained inside Weibel Palade bodies
what are some impt activators of endothlial cells?
cytokines, complement, hypoxia
what are some induced produces of EC"s
adhesion molecules, MHC
where do SMCs migrate in injury?
from media to intima to cause intimal thickening
how are ECs involved in transport?
the allow small molcues to cross, large to cross if pressure is high, stop proteins
how are EC's involved in synthesis?
collagen prodxn
how are EC's involved in coagulation regulation?
anti coagulands, prothrombotics, **vWF
what happes to SMC after they migrate into intima?
lose ability to contract and they gain the capacity to divide
decrase in contractile filametns and an incrase in organelles involved in protein syn
may lead to narrowing of lumen
*intimal thickening can also occur in normal arteries as a result of aging
how do EC's regulate blood flow?
produce endothelin to cause vascoconstriction
produce NO to cause vasodilation
what is an AV fistula?
rare abnormal communication b/n arteries and vv
arise as developemental defects
problematic b/c in CV could lead to high output cardiac failure b/c they cause the heart to pump additional volume
CNs: irritation
CNS: rupture and cause stroke
hardening of ARTERIOLES
thickening of vssl walls with with luminal narrowing that may cause downstream ishcemic injury
*most often associated with hypertension and DM
Monkeberg medial calcific stenoiss?
calcific deposits in musclar arteries in persons older than 50
media is inovlved
what are three patterns of ateriosclerosis?
arteriosclerosis=hardening of ateries
Monkeberg medial calcfic stenois
what problem is responsbile for 50% of all deaths?
what problem is responsibe for 25% of all deaths?
what are the earliest lesions of atherosclerosis?
fatty streaks:lipid filled foam cells
not raised, do not cause disturbance in blood flow
begin as fatty dots that coalesce into steaks
what are fatty dots?
intial lesion
foam cells: few intimal macrophages: begining of atherosclerosis
all childran older than age 10 have what?
fatty streaks
ppl of age 30 and up are most likely to have what atherosclerotic change?
complicated plaque or fibroatheroma
at which stage in atherosclerosis is lipid entirely intracellular?
fatty streak
in this stage the plaque is not raised
where do athromas tend to occur?
at exit pts that leave the aorta, fatty streaks are not seen here
where do fatty streaks normally form?
in areas of vaculature that are not susceptible to developing atheromas later in life
what are the major complications of atherosclerosis?
MI, cerebral infarction, aortic aneurysm, peripheral vascular disease
what changes occur in intermediate lesion?
this leasion is after fatty streak
small extracellular lipid pools but most is still intracellular
what is an eccentric lesion?
atheroma that involves only a partial circumference of the arterial wall and are patchy and variable
what forms after an intermediate lesion? waht is it composed of?
atheroma: central core of extracellular lipid
what forms after an atheroma?
fibrous tissue is laid down
calification occurs (dystrophic)
*the fibrous tissue provides stability to plaque thus won't form thrombus as easlity
what is a complicated plque? what is this pt at risk for?
the most advanced lesion of atherosclerosis at risk for:
rupture, ulceration, erosion
hemorrhage into a plaque
thrombus (most feared) that may occlude lumen
aneurysmal dialation
what are the most heaveily involved vessles in atherosclerosis?
coronary arteries
popliteal arteries
internal carotid
vssls of cirle of willis
what will you see in the necrotic center of a complicated plaque?
cell debris
cholesterol crystals that look like needles
foam cells
how does mortality from IHD in US differ from Japan?
5x greater in US
how has the deat rate from IHD changed in US since 1960s
50% reduction in IHD deaths
70% reduction in stoke
due to lifestye changes, diet, cigs
how does MI incidence change b/n ages of 40 and 60?
5x greater risk
who is more prode to atherosclerosis
uncommon in premeno females
what single gene defect can play impt role in atherosclerosis?
familial hypercholesterolemia
risk involved in HDL and LDL levels
LDL=bad delivry of cholesterol to peripheral tissues
HDL=good moves cholesterol from atheromas to liver
higher HDL=lower risk
what can incrse HDL? waht can decrase HDL?
increse: exercise
decraes: obesity, smoking
how does dietary intake contribue to hyperlipidemia?
omega 3 lipids in fish=good
trans fats= bad
statsin: good, lower circulating cholesterol by inhibiting HMG CoReducatase
how impt is BP in atherosclerosis
if BP exceeds 169/95 5x greater risk than 140/90
increasing incidence of IHD in women is due to what?
incrased risk of atherosclerosis with DM?
2x increased risk
higher LDL levels
prone to strokes
100x risk of foot gangrene
ingestion of what can reduce the incidence of CV disease in pts with hyperhomocystinemia?
folate and B6
therefore give to pts with incrased homocystine
what are the big 4 risk factors for atherosclerosis
what is the first step in pathogenesis of atherosclerosis
endothelial injury
LDL accumulation in intima
LDL become oxidized
waht are the 3 cell types involved in atherosclerosis after endothelial injur
monocytes bind to damaged endo to become foam cells
platelets adhere to damaged intima and release factors taht cause migration of SMCs
SMCs proliferate in intima and produce matrix, lipids accumulate in SMcells
what damages teh endothelium in atherosclerosis
hemodynamic trauma
elevated cholesterol
how do the monocytes attach to the damaged EC to migrate into intima?
they bind to VCAM on endo cells and migrate into imtima
in intima they turn into macrophages and engulf oxidized LDLs
the lesion then incresaes in size b/c of cytokines released for recruitemen
the major lipids in atheromatous plques are what?
cholesteral and cholesterl esters
how is Familal hypercholesterolemia involved in lipids in atherosclerosis
defect in LDL R leading to inadquate hepatic uptake of LDL and incrsed circulaign LDL
how does hypercholestolemia direcly impair EC fxn
through increased prodxn of O2 free radicals that deactivate NO
how do macrophages cause chemical change in lipids?
macrophages and EC's make free radicals that change lipid to make it oxidize
the oxidized LDL is then ingested by macrophages through the scavenger R (not the LDL R) forming foam cels
what growth factors are involved in the proliferation of SMC?
TGF alph
what is the oligoclonality theroy of atherogenesis?
plques equi to bengin neoplastic growth
what are the most common atherosclerosis aneurysms?
abdominal aortic aneurysm
what is an AAA and where do they occur?
pulsatile abdominal mass
below renal arteries
above aota bifurcation
thromus present in lumen
in who do AAA occur?
after 50
genetic susceptibility
what is thought to be the pathogenesis concerning AAA
MMPs throught incrased proteolysis of ECM..degrade all compoents of ECM inlcuding collagen, elastin
there is a decreese in TIMP in AAA pts
how do AAA's present? what are the consequences associated with them?
present as a pulsatile abdominal mass that simulates a tumor
may obstruct local renal structurs, embolism from atheroma to legs, rupture
risk of rupture of AAA is related to what?
size of AAA
bigger = higher chance of rupture
what is a leutic aneurysm?
thoracic aorta aneurysm characteristic of tertiary syphillis that can include the aorta annulus
less likely to rupture
can encroach on mediastinal structures
resp difficulties
difficuly in swallowing
sypphiic endarteritis obliterans involves what?
aneurysm of VASA VASORUM of the arotic wall
narrowing of lumina of vasa causes ischemia and destrxn of media, aorta now loses elasticity and dilates forming aneurysm (**loss of elastin fibers and replae with fibrin)
fibrous scars lead to "tree barking"
tree barking is seen in ?
syphillic endarteritis obliterans
caused by the loss of elastin fibers and replaced with fibrin..the scarring looks like tree bark
waht is destroyed in sphyilic endarteritis obliterans?
narrowing of the vasa vasorum causes ishcmea to media..destrxn of MEDIA
are aortic dissections associated with aortic dilatation/
NO not always but they are called aneurysm anywas
what is an aortic dissection/
dissection of blood bn and along the laminar planes of the media with a formation of blood filled channel w/n aortic wall which often ruptures outward cuasing massive hemoorhage
in who do aortic dissections occur?
90% men b/n 40 and 60 with hypertension
or in Marfan younger pts
waht will you think if aortic dissection occurs in young pts? older?
where do aortic dissections occur?
extends into but not through the media of asc aorta w/n 10cm of aortic valve
spreads along the laminar planes of the aorta* bn middle and outer 1/3 of media
what is the major risk factor in dissectoin?
trigger for intimal tear is unkonwn but once it is torn incrased BP accelerates teh problem
**antihypertensive therapy
when is an aortic dissection most dangerous?
from the aortic valve to the arch
what does severe pain, radiating through to back and progresses downwards indicate?
aortc dissection
what type of dissection is more common?
proximal involving the asc aorta
into what 3 body cavities can rupture ofa dissection enter?
how is the prognosis of arotic dissection?
improved b/c of surgical repair success after operaion is 65-75%
is a berry aneurysm a congenital disorder?
no it is a congenital defect present at birth...congential predispostion
the berry aneurysm is not present at birth
what are the 3 categorires of mutations?
genome: loss or gain of whole chromosomes giving rising to monosomy or trisomy
chromosome: rearrangemnt of genetic material
Gene: partial or complete deletion of a gene or affect single base
result of nondisjxn in MI? MII?
MI: 2 disomic, 2 nullsomic
MII: 1 disomic, 1 nullisomic, 2 normal
what is pleitropy?
single mutant gene may lead to many end effects ex: sickle cell anemia
charactristics of AD inheritance
50:50 chance of transmitting phenotype to each offsrping
males and femals eqally effected
male to male transmission
vertical transmission
which diseae results from complete or partial monosomy of the X and is characterized by hypogonadism in phenotypic females?
what percent of Turners are mosaics?
30%: they have a 45X population along with one or more karytypically normal or abnromal cell types such as 45X/46XX
*all surviviing Turners might be mosaics
classic characteristics of Turners
webbing of neck
coarctation of aorta**killer
failure to develop normal secondary sexual characteristics
waht is the single most impt cause of amenorrhea?
what is an impt gene involved in Turner phenotype?
SHOX short stature homeobox gene on the X chromosome-one of the genes that remains active in both X chormosoms and its has a homolgoe on short arm of Y
haplo of this gene = short stature
SHOX is located in PAR region
what is a malformation?
structural defect b/c of intrinsically abnromal developmental process like a cleft lip
what is a disruption?
structral defect resulting from breakdown of or interference with an orgininally nl developemental procese
structral defect resulting from breakdown of or interference with an orgininally nl developemental procese is what?
**previously normal
what is a deformation?
abnormaility in form of position of a body part by a non-disruptive mxnl force
uterine constriction
what is the most common underlying factor responsible for deformation?
uterine constrain
abnormal deveopmental process
waht is dysplasia? ex?
abnormal org of cells into tissues
waht is a sequence
pattern of cascade anomalies
structral defect or mechanical factor leading to multiple 2ndary effects
ex: potter sequence, pierre robin
potter seq also known as ?
oligohydraminos: decreaed amniotic fluid due to leakage, renal agenesis (fetal urine is a major constituent of amniotic fluid)
describe potter seq?
renal agenesis of fetus or urethral obstruction leads to reduced urinary output
nl the fetal urine contributes to amniotic fluid
oligohydraminos (or by chronic leakage)
result is sqashed facial features, pulmonary hyoplasia, dislocation of hips and talipes
oligohydramnios causes waht?
fetal compression: flattened facies and postitional abnormalities of hands and feet, dislocated hips
what is a syndrome?
multiple anomalies with SINGLE BASE cause hat occur independentaly rather than sequentaily
when is the embyo extremely susceptible to teratogenesis?
3-9 weeks
what percent of congenital abnormalities are caused by teratogens?
how does thalidomide cause congential malformations?
high freq of limb abnormalities by blocking the proliferation of mesenchymal cells in the limb bud
what kind of problems can anti-epileptic drugs cause?
learning difficulties
behavioural problems
mom's take antiepileptic drugs
broad nasal root, blunt nasal tip, thin upper lip
features of fetal alcohol syndrome?
short palpebral fissures
epianthal folds
low nasal bridge
2% of live births in US: strong coorelation with socio-economic status
*common in Native Ams
timing of CNS development
begin in 6th week
how much alcohol is safe for mom? session of binge drinking is as likely to cause FAS
later in preg decrased risk
what type of defecits occur with retinoic acid embryopathy?
changes in HOX gene expression..nature of malformation determined by dosage and timing
why retinoic acid embryopathy?
mom taking retinoic acid for acne
HOX genes have retinoid acid response elements
most common CV abnormality?
ventricular septal defect
most common CNS abnormality?
spina bifida
most common urogenital abnormality?
bilateral renal agenesis
waht perent of 1trimester miscarriage have structral abnormalities? 2nd trimester?
ist: 80-85%
2nd: 25%
15% of all recognzed conceptuses are structurally abnormal
are genetic causes or environmental cuases more common in congenital abnormalities?
genetic: 30-40
5% environment
50% unknown
gene involved in Tetraology of Fallot?
JAG1: single gene defect
Tetrology of Fallot?
aorta shifted right
right vent outflow obstruction
opening b/n ventricles
r ventricular hypertrophy
neural tube defects can be reduced to 75% by?
supplementation of folic acid
waht is a holoprosencephaly?
failure of cleavage of prosencephalon
get single ventricle
includes Smith-Lemi-Opitz syndrome (lack of cholesterol to combine with SHH)
mutations in SHH are freq cause of what
cleft lip and palate can be due to?
cig smoking + TGF alpha, MTHFR gene
what single gene shows 12-16% genetic predisposition for cleft lip/palate?
what is Pierre Robin Seq and what can it reuslt from?
alters 1st arch structures esp manible
can result from oligohydramnoiis
laterality defects are due to wha?
defects in cilia fxn
they sweep high concs of SHH and FGF8 towards the left resulting in asymmetric cascade of gene expression
*Lefty1 prevents diffusion to the right side
is dizygotic twinning genetic or monozygotic?
dizygotic: separate placenta and chorion or fusing placentas and fused chorions
what is reason for the major diff in gene number bn mammal and other animals?
number of TFs
what are teh 2 HOX genes that the Drosophila had no homologs for?
A13 and D13: for limb devleopment thus they are well characterized with human syndroms
mutations in HOXD13? A13?
D13: synpolydactly
A13: hand-foot-genital (affect distal ends of limb development)
waht are HOX genes involved in?
patterning of limbs, vertebrae and craniofacial structures
whare are PAX genes invlved in?
code for DNA-biding proteins taht code for TF's
what are the PAX genes?
paried box genes: code for paired structures like eyes, kidneys, thyroid
muations in PAX3 cause what?
Waardenburg sydnrome: mos common form of inherited congenital deafness
all AD disorders, No ethnic predispostion