Pathology of HTN Flashcards
Right failure associated with more impairment because
no removal of waste and metabolites
morphogenesis of HTn in large/medium arteries
accelerated ahterogenesis
degenerative change in vasc walls
risk of aortic disection and cerbrovascular hemorrhage
morphology of HTN in small arteries and arterioles
hyaline arterioloscleosis
hyperplastic ateriolosclerosis
Hyaline arteriolosclerosis
leakage of plasma across endotheliaum due to HTN
excess matrix production by SMC secondary
pink collagen fibrosis/sclerosis
benign neprhosclerosis
hyperplastic arteriolosclerosis
characteristic of malignant HTN
onion skinnig cocentric luminal walls with luminal narrowing
due to replicated basement mem. + smooth muscle
termed used in malignant HTN when arteriol changes are associated with fibrinoid necrosis
necrotizing arteriolitis
systemic HTN heart disease is ___ sided
left
concentric left ventricular hypertrophy in absence of other cardio path
evidence of HTN >140/90
systemic hypertensive heart disease
morphology of systemic HTN heart disease
cardiomegaly - 1.5cm wall thickiness
thickiness of LV impairs filling > LA dilatation
Myocyte hypertrophy and nucelar enlargement
HTN encephalopathy
Headaches, confusion vomiting convulsions
increased CSF pressure
Renal damage of benign HTN
Kidney atrophy with pitted surface
hyaline arteriolosclerosis of vessels > ischemia + atrophy
glommeruli sclerosed
renal damage of malignant HTN
pinpoint petechial hem. on surface
fibrinoid necrosis of arterioles
hyperplastic arteriolosclerosis and microthrombi > global ischemia
cause and morpholohy COr pulmonaue
Acute due to massive pul embolism
Chronic - secondary to Pul HTN or lung disease
RV hypertrophy
obstruction of pul vessels
mechanism of CHF pathogenesis
abnml load on heart (fluid, MI valve dysfunction, ischemic HD, HTN, Dilated CM)
Impaired vent filling: (acute: pericarditis or tamponade, chronic: restrictive CM, severe LV hyper)
obstruction due to valve stenosis (chronic rheumatic mitral)
systolic dysfunction in CHF
progressive deterioration of contractilitiy
iscehmic HD, pressure or volume overload, Dilated CM
diastolic dysfunction in CHF
inability to relax and fill
LVH
amyloidosis
myocardial fibrosis (from infarct, radiation ect)
consstrictive pericarditis
rapidly occuring compensatory mechanisms
Frank starling (increased end diastolic filling vol)
NE release by cardiac nerves (HR, contract, vasc R)
Rening angiotensin aldosterone
atrial natriuretic peptide (dilation, diuresis)
pattern of hypertrophy, Pressure overload leads to (morphology)
HTN, aortic stenosis
concentraic hypertrophy
paterns of hypertrophy, volume overload leads to (morphology)
mitral or aortic regurgitation
cells found in pulmonary edema of left sided failure
heart failure cells (macrophages)
physical exam left sided heart failure
dyspnea
orthopenea
paroxysmal nocturnal dyspnea
rales
in left sided failure, if kidney perfusion deficiency is severe >
pereneal azotemia (impaired function)
cerebral effects of left sided failure
cerebral hypoxia
encepalopathy
causes of right sided failure
**secondary to left side **
Pul HTN
Primary myocardial disease
Tricuspid or Pulmonary valve disease
Right sided failure kidney impact
congestion, fluid retention, peripheral edea, azotemia more marked than with left sided failure
heart impact of right sided failure
RV hypertrophy and dilatation
hepatic impact right sided failure
elevated portal pressure > congestive hepatosplenomegaly
cardiac cirrhosis
ascites
eventual anscara of Right sided failure
massive edma
