Path: Hypertension and Congestive HF
Terms
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- General characteristics of Hypertension
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Elevated blood pressure, may be defined operationally, convetionally, or realistically but point is "the lower the better"
major cause of morbiddity and mortality, affects multiple organ systems
single most prevelant risk factor for developing heart disease and stroke (20% of US)
most common heritable disease among blacks (35% have HT) - what are the 3 major determinants of blood pressure?
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BP = CO x TPR
CO = SV x Heart rate
...so they are CO, SV, and Heart rate
*TPR is controlled at arteriol level - What are genetic determinants of HT?
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family history, prevelance in people of african descent
single gene mutations have been linked to HT
angiotensin gene has been linked to essential HT - What are some environmental determinants of HT?
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increased dietary sodium intake
stress
lifestyle = obesity, cigarette smoking, physical inactivity
*metabolic syndrome = obesity, type II diabetes, dyslipidemia often with HT all increase the risk of Heart disease - What are the 2 types of HT?
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Essential HT: of unknown etiology accounts for majority of cases; represents interaction of predisposing determinants w/ a number of exogenous factors
Secondary HT: several known casuses inc renal, endocrine, renovascular, neurogenic, and iatrogenic pathology - Essential HT may take 2 forms, describe them?
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BENIGN: most common, slow progressing asymptomatic
MALIGNANT: only about 5% of all cases, fulminant course with extreme elevations in BP; associated w/ acute organ dysfunction; in absence of treatment patients may die w/in a year
*Hypertensive emergency - fibrinoid necrosis, thrombotic arteritis, organs suffer ischemic injury - What structural changes occur at the level of the small vessels during HT?
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Endothelium --> inc. permeability, decreased vasodilatory, damage/ denudation in arterioles
Vascular Smooth Muscle --> medial hypertrophy, medial hyperplasia in arterioles, increased synthesis of ECM components,
accelerated intimal proliferation in artherosclerosis - What anatomical changes occur in the elastic amd muscular arteries as a result of HT?
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accelerated artherosclerosis
inc. frequency of aortic dissection - What anatomical changes occur in the small muscular arteries and arterioles as a result of HT?
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intimal and medial thickening due to smooth muscular proliferation and/or increased ground substance
Hyaline sclerosis: thickening of the vesssel wall w/ deposition of a variety of proteins and lipids <-- benign neprhosclerosis
Hyperplastic arteriosclerosis, fibrinoid necrosis and necrotizing arteriolitis <-- malignant neprhosclerosisis
microaneurysm formation - What is Benign nephrosclerosis?
- renal disease associated with benign HT = hyaline sclerosis, arterial intimal hyperplasia, changes of chronic ischemia
- describe malignant nephrosclerosis?
- renal disease associated with malignant HT = hyperplastic arteriosclerosis (onion skinning)
- What anatomical changes occur in the kidney as a result of HT?
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nephrosclerosis
2 types - benign and malignant - What pathological changes occur in the brain as a result of HT?
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increased incidence of intracerebral hemorrhage (CVA, stroke)
hypertensive encephalopathy - What disease states can HT cause in the eyes?
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hypertensive retinopathy --> blindness
vascular sclerosis
hemorrhages (flame shaped)
exudates (macular star)
microaneurysms
foci of axonal degeneration (cotton-wool spots)
necrotizing arteriolotis in malignant HT
Keith-Waggoner classification is based on the severity of the above changes - What disease states occur in the heart as a result of HT?
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accelerated coronary artherosclerosis
left ventricular hypertrophy
predisposition to MI, angina pectoris, cardiac failure - What is cardiac failure?
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the condition in which cardiac output is inadequate to meet the metabolic requirements of the body
typically accompanied by organ congestion and thus termed congestive heart failure (CHF) - What are syptoms of CHF?
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dyspnea (shortness of breath) most common
orthopnea(dyspnea on lying down)
paraxosymal nocturnal dyspnea - What are the basic causes of CHF?
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hemodynamic overload from too much pressure or volume
disorders of contractility
disturbances of ventricular filling --> dont allow diastole to occur - Describe the pathogenesis of CHF?
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increased end diastolic volume producing dilation
adaptive changes to minimize wall stress
hypertrophy of myocardial cells
changes in gene expression and cellular biochemistryto accomodate hypertrophy (growth factors) - What are the mechanisms by which CHF produces organ dysfunction?
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forward effect: decreased arterial perfusion and hypoxia of peripheral organs esp kidney and brain
backward effect: increased vascular pressure of pulmonary and systemic venous circulation resulting in congestion and angina - What are compensatory mechanisms that occur in response to CHF?
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increased heart rate
increased in blood volume
increase in peripheral vascular resistance
redistrubution of blood flow - What are causes of clinical manisfestations of Left sided heart failure?
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ischemic heart disease
hypertension
aortic and mitral valvular disease
myocardial diseases
first affects the pulmonary circulation
leads to dyspnea and orthopnea, pleural effusion with hydrothorax, reduction in renal perfusion, cerebral anoxia - What are the causes and clinical manisfestations of Right sided heart failure?
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left sided heart failure
left sided lesions
pulmonary HT
cardiomyophathyand diffuse myocarditis
tricuspid or pulmonary valvular disease
pure RV failure caused by hemodynamic overlaod, smoking related diseases
effects are congestion, edema, focal hemorrhage in systemic organs but not in lung