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Terms in this set (19)
Age: Elderly - due to isolated systolic hypertension.
Sex: Men until 45, Equal 45-54, Women after 55.
Other: Obesity and weight gain. Dietary NaCl intake, heavy alcohol consumption, pyschosocial stress, sedentary lifestyle.
Clinical Manifestations of Hypertension
Blood pressure: an elevated blood pressure (≥ 140/90 mm Hg) has been documented on at least 2 or more separate occasions.
Sx: None unless severe.
Severe - 'hypertensive headache',dizziness, palpitations, easy fatigability, and impotence.
Clinical evaluation of hypertension
Look for end organ damage:
-hypertensive retinopathy: increased arteriolar light reflex, arteriovenous crossing defects, flame-shaped hemorrhages and cotton wool exudates. Papilledema in malignant hypertension.
- Palpation of all peripheral pulses
- Auscultation should be performed for renal artery bruit -
renal artery stenosis
(cause for secondary hypertension)
check for L ventricular hypertrophy
Lab Evaluation for Hypertension
UA, a full blood
count, serum electrolytes, glucose and uric acid, and electrocardiography.
Hypokalemia: Primary hyperaldosteronism
UA VMA - exculeds pheochomocytomas, adrenal function tests to check for steroid excess and renal angiography to exclude renal artery stenosis.
Vascular Pathology in Hypertension
Vascular remodeling: adaptive-hypertrophied vascular wall attempts to normalize arterial wall stress.
Maladaptive: remodelling makes increased peripheral resistance and blood pressure elevation.
lesions in the large and small arteries and arterioles
Large arteries: increased lumen size and thickened tunica media, accelerated atherosclerosis
aortic dissection due to degeneration of tunica media
Small arteries: increased wall thickness in tunica media
: homogeneous, pink hyaline thickening with associated luminal narrowing. (Hyaline refers to the glassy, homogenous appearance of the blood vessels).
more apparent in kidneys ->benign nephrosclerosis
Necrotizing arteriolitis and hyperplastic arteriolosclerosis
: Malignant hypertension is a syndrome caused by a severe and generalized arteriolar spasm (vasoconstriction) and characterized by severe, generalized changes in arterioles of kidney, brain, retina and other organs. Endothelial integrity
"hyperplastic arteriolosclerosis" results in a striking concentric increase in the number of layers of smooth muscle cells, which yields the so-called "onion-skin" lesion.
Hypertension and the Heart
- Hypertension as a risk factor for cardiovascular diseases.
Heart disease is the most common cause of death in hypertensive patients
pressure overload and LV hypertrophy.
- Left ventricular concentric hypertrophy - The wall thickness increases initially without ventricular dilation.
- LV diastolic dysfunction (left atrial enlargement and pulmonary congestion or even pulmonary edema (diastolic heart failure).
Clinical manifestations of hypertensive heart disease: Usually asymptomatic or atrial fibrillation induced by left atrial enlargement or pulmonary edema. - they can die from ischemic heard disease or experience progressive heart failure. Toward the end ventricle may dialate and decrease L ventricular performance.
D) Reversibility of LV hypertrophy after therapeutic blood pressure reduction w/ meds or exercise.
Hypertension and the Brain
- Risk factor for brain infarction and intracerebral hemorrhage.
: occur in the deeper structures of
the brain such as subcortical nuclei and internal capsule. Lipohyalinosis (cerebral vessels develop hyaline arteriolosclerosis associated with accumulation of lipid-laden macrophages and cholesterol deposits).
2. Intracerebral hemorrhage: when in basal ganglia (ganglionic hemorrhages), when in lobes of cerebral hemispheres (lobar hemorrhages).
: Arteriolohyalinosis of the lenticulostriate arteries gives rise to microaneurysms termed Charcot-Bouchard microaneurysms- occur in
lenticulostriate arteries from trunk of MCA
(supply basal ganglia). (not to be confused w/ berry aneyursms (circle of Willis).
Hypertension and the Kidney
Causes chronic kidney disease
-pathological changes in the kidney.
Due to focal ischemia and glomerular hyperfiltration
- manefestations of renal damage due to hypertension.
(B) Fibroelastic hyperplasia and hyaline arteriolosclerosis.
-Kidney is smaller. he cortical surfaces have a fine, even granularity that resembles grain leather. On cut section the cortex is thin and there are fine depressions of the cortical surface alternating with small granular elevations.
Hyalinization, hypertrophic nephrons, enlargment of glomeruli and incresased diameter of tubules. Narrowing of arterioloar luminia.
- clinical syndrome of minimal proteinuria and progressive renal insufficiency.
Benign nephrosclerosis is the second most common cause of end- stage renal disease
small, petechial-type hemorrhages on cortical surface that can give the kidneys a characteristic "flea-bitten" appearance
peripheral arterial disease (PAD)
peripheral arterial disease (PAD). Hypertension is a risk factor for premature atherosclerosis of the peripheral arteries of the lower extremities
- Most common cuase of hypertension. Famililar, environmental.
(A) Inherited defect in renal handling of sodium.
: Sodium retention: hypervolemia, increased CO, excess vascoconstriction, hypertension.
Low and high renin types of essential hypertension.
Low renin hypertension: Volume-dependent hypertension, excess sodium retention. Use diuretics to treat.
High renin hypertension: vasconstrictor hypertension. ACE Inhibitors, b-blockers work best. High renin (increased sympathetic activity).
Secondary Hypertension - Renal hypertension
(A) Renal parenchymal diseases. Renal parenchymal diseases are the most common cause of secondary hypertension.
(B) Renovascular hypertension. Renovascular hypertension is blood pressure elevation due to partial or complete occlusion of one or more renal arteries or their branches.
Secondary Hypertension - Endocrine Hypertension
A. Primary hyperaldosteronism - aldosterone-producing adrenal adenoma (Conn syndrome). Or bilateral adrenocortical hyperplasia.
sodium retention, expansion in the extracellular volume, volume-dependent hypertension, hypokalemia, and suppression of renin production.
(B) Cushing syndrome: prolonged exposure to elevated levels of glucocorticoids due to exogenous glucocorticoid administration, or to endogenous production from an ACTH-secreting pituitary adenoma or adrenocortical adenoma/carcinoma.
(C) Pheochromocytoma.: catecholamine-secreting tumor derived from chromaffin cells. adrenal medulla (pheochromocytoma) or in extra-adrenal paraganglion tissue (paraganglioma). High BP is due to arteriolar spasm due to catecholamine excess.
(D) Thyroid disease, acromegaly, and hyperparathyroidism:
Secondary Hypertension: Miscellaneous causes
(A) Obstructive sleep apnea
(B) Coarctation of the aorta. Occurs in children w/ Turner's syndrome. Congenital.
Severe elevation of blood pressure > 180/120 mm Hg. Risk of rapid deterioration of target-organs.
Urgency of Emergency
Rapid deterioration of one or more target-organs (such as CNS, cardiovascular system and kidney). A hypertensive emergency poses an immediate threat to life.
Situation where the blood pressure is severely elevated but there is no associated organ damage.
Pathophysiology of Hypertensive emergency
Incompletely understood....initial severe vasoconstriction leading to abrupt rise in vascular resistance, release of vasoconstricting substances, endothelial failure, release of proinflammatory mediators, increases in endothelial permeability, inhibit local endothelial fibrinolytic activity, and activate the coagulation cascade. Platelet aggregation --> further inflammation, thrombosis, and vasoconstriction.
Due to increased cerebral perfusion from the loss of blood-brain barrier integrity, resulting in
exudation of fluid into the brain
. With persistent elevation of the systemic blood pressure, arteriolar damage and necrosis occur. leads to generalized vasodilatation, cerebral edema, and papilledema --> Altered mentation.
Sx: Anterior headache, confusion, visual disturbances, seizures, nausea, and vomiting.
Findings: Retinal findings of hypertension.
Bilateral areas of low attenuation on CT scan and increased T2 signal on MRI studies usually in brain regions supplied by posterior circulation. Occipital lobes often involved.
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