Path EXAM III D5

angiotensinogen by liver
renin
angiotensin I
acd
angiotensin II
ADH secretion but post pit
Adolsterone by adrenal cortex
systemic arteriole vasoconstriciton
increase water and sodium absroptin
increased mean arterial pressure

blood volume
peripheral resistance

kinins prostaglandins
NO
parasymp stimulation

cardiac output
total peripheral resistance
vasoncstrictors
genetic factors
environmental factors

abdominal aortic aneurysms
syphilitic luetic aneuryms
dissecting aneurysms

ATH
over 50
males
genetic liek marfans

tertiary syhpilis

root of aorta and ascending aorta into late devleopment

older men
younger with CT disorder liek marfans

blood dissect betweent he planes of the media and ruptures outward

inflammatory
autoimmune

giant cell or temporal arteritis

granuloamtous inflammation fo large to small arteries principally the arteries in the head

T cell mediated
HLA DR antigens

usually age over 50
fatigue
malaise
tneder temporal arteries
sudden onset blindness if ophthalmic artery involved

ESR erythrocyte sedimentation rate an indiriect measure of inflammatory proteins epseiclaly fibringoen

high doses of corticosteroids

ishcemic ehart disease

60 in males
70 in females

HTN
DM
smoking
high LDL

angina pectoris
acute myocardial infarction
sudeen cardiac death
chronic ishcemic heart disease with heart failure

intermittnet caused by transient MI

acute thrombosis
necrosis begins

subendocardial where there is the poorest circulation

sudden cardiac death

failure of the heart to pump sufficient lood to meet hte body's metabolic needs,m usually reuslting in accumulation of interstitial fluid

sever MI
severe valvular disease
myocarditis
cardiomyopahty
cardiac tamponade
cardaic metabolis derrangements usually from chemic or poison

heart damage
decreased blood volume
increased afterload
fluid overload
other rare disorders

hemorrhage
sever dehydration
sever anemia

hypertension
systemic hypertension or obesity
lung disease

congestion
activation of circulatory compensatory mechniams
increased renin

bacup of blood in vessels up[stream from teh heart because the heart cannot miantina forward flow

hypertension and edema of congested tissues

increased EDV
frank starling inreases cardiac stroke volume
myocardium is stretched and begisn to thina dn lose elasticity
stroke volume compromised

increases productio of renin

increases stimulation SA node
increases pb
increases strength of contraction

result is increased co but also increase bp

systolic
diastoic
diminshed co
damming of blood in venous system

correct underlying problem ie valve replacement
decrease thrombus formation ex. aspirin
diuretics to reduce afterload
adrenergic agents ie. alpha beta
inotoropic agents ie digitalis

vasolilators that cuase sm relaxation and cuase bp to decrease ex minipress

cause vasoilation fo the coronary a ex. dobutamine

alter myocardial contractility and thus stroke volume es. digitalis

derivatives of diogxina nd ditoxin that increase myocardial contractility

increase in afterload
hypertrophy

greater metabolic reqauirements due to work load and size

heart cannot meet its own needs

right

elevated blood pressure in pulmonary circuit
pulmonary hypertension
usually PE

chornic disease of lungs pulmonary vessels restricted chest movement and artreriorlar constriction

rheumatic heart disease
mitral valve prolapse

cross reactivity between heart and M proteins in the cell walls of certain strep

floppy mitral valve in which one or both cusps everts during systole

cardiomyopathies

dilated/congested
hypertrophic
restrictive

alochol toxic insult
hereditary
coxsacievirus

restrict ventircular filling

1/2 autosomal dominant disorder

ventricular septal defect
root of aorta overrides
narrowed pa
hypertrophied right ventricle

blood flows from L back to R ventricle

some of blood entering the body has not been oxygenated