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Flashcards in Robbins pg. 332-342 Deck (57)
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What is hypertension defined as systolically and diastolically?

diastolic pressures greater than 90 mm Hg, or sustained systolic pressures in excess of 140 mm Hg-- associated with an increased risk of atherosclerosis


What is malignant hypertension?

A small percentage of hypertensive patients (approximately 5%) present with a rapidly rising blood pressure that, if untreated, leads to death in within 1 to 2 years.

Such malignant hypertension usually is severe (i.e., systolic pressures over 200 mm Hg or diastolic pressures over 120 mm Hg) and associated with renal failure and retinal hemorrhages, with or without papilledema. It can arise de novo but most commonly is superimposed on preexisting benign hypertension.


What are the major causes of hypertension?

- idiopathic (95%)- aka essential hypertension
- 'secondary hypertension'


What are the major causes of secondary hypertension?

- Primary renal disease
- Endocrine dysfunction
- CV
- Neurologic


Some relatively rare single-gene disorders cause hypertension (and hypotension) by affecting renal sodium resorption. Name some.

• Gene defects in enzymes involved in aldosterone
metabolism, leading to increased aldosterone secretion, increased salt and water resorption, and plasma volume expansion

• Mutations in proteins that affect sodium resorption
(as in Liddle syndrome, which is caused by mutations in ENaC, leading to increased distal tubular resorption of sodium induced by aldosterone)


Although the specific triggers are unknown, what are some of the main processes involved in essential hypertension?

• Reduced renal sodium excretion in the presence of normal arterial pressure. At the new higher blood pressure, the kidneys excrete additional sodium.

• Increased vascular resistance may stem from
vasoconstriction or structural changes in vessel
walls. These are not necessarily independent factors, as chronic vasoconstriction may result in permanent thickening of the walls of affected vessels.

• Genetic factors
Hypertension has been linked to specific angiotensinogen
polymorphisms and angiotensin II receptor variants; polymorphisms of the renin-angiotensin system also may contribute to the known racial differences in blood pressure regulation.

• Environmental factors, such as stress, obesity, smoking, physical inactivity, and high levels of salt consumption, modify the impact of genetic determinants.


How does reduced sodium excretion increase blood pressure?

Decreased sodium excretion causes an obligatory increase in fluid volume, increasing filling pressure, and thus increased cardiac output, thereby elevating AP.


Does hypertension cause atherogenesis?

Yes, it accelerates atherogenesis but also causes degenerative changes in the walls of large and medium sized arteries that can lead to aortic dissection and cerebrovascular hemorrhage.


What are two forms of small blood vessel disease that are hypertension-related?

-hyaline arteriolosclerosis
-hyperplastic arteriolosclerosis


What is hyaline arteriolosclerosis?

A condition associated with benign hypertension that is marked by homogeneous, pink hyaline thickening of arteriolar walls and lumenal narrowing


What causes hyaline arteriolosclerosis?

Leakage of plasma components across injured endothelial cells into vessel walls results in increased ECM production by smooth muscle cells in response to chronic hemodynamic stress.


How is the kidney affected by hyaline arteriolosclerosis?

The arteriolar narrowing caused by hyaline arteriosclerosis leads to diffuse vascular compromise and nephrosclerosis (glomerular scarring).


What is hyperplastic arteriosclerosis?

a condition associated with severe hypertensions in which vessels exhibit "onionskin" concentric laminated thickening of arteriolar walls and luminal narrowing

In malignant hypertension these changes are accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing
arteriolitis), which are particularly prominent in the kidney


Vascular injury leading to endothelial cell loss or dysfunction stimulates what?

smooth muscle cell growth and associated matrix synthesis.


T or F. Intimal thickening is a stereotypical response of the vessel wall to any insult

T. With persistent or recurrent insults, further thickening can occur that leads to the stenosis of small and medium-sized blood vessels


What is different about neointimal smooth muscle cells from medial smooth muscle cells in the media?

neointimal smooth muscle cells lack the capacity to contract like medial smooth muscle cells, but do have the capacity to divide and have a considerably greater synthetic capacity than their medial colleagues


How are neointimal smooth muscle cells formed?

- previously thought to arise from dedifferentiated medial smooth muscle cells
- increasing evidence suggests that at least a subset is derived from circulating precursor cells


Intimal thickening is an invariable consequence of endothelial insult. When else does it occur?

Intimal thickening appears to be a part of normal aging.

Such age-related intimal change typically is of no consequence, in part because compensatory outward remodeling of the vessel results in little net change in the luminal diameter.


What is arteriosclerosis?

“hardening of the arteries”; it is a generic term reflecting arterial wall thickening and loss of elasticity.


What are the three types of arteriosclerosis?

• "Arteriolosclerosis" affects small arteries and arterioles and may cause downstream ischemic injury. The two variants are hyaline and hyper plastic arteriolosclerosis.

• "Mönckeberg medial sclerosis" is characterized by the presence of calcific deposits in muscular arteries, typically in persons older than 50. The lesions do not encroach on the vessel lumen and usually are not clinically significant

• "Atherosclerosis" is the most frequent and clinically important pattern


What is Atherosclerosis?

a condition characterized by the presence of intimal
lesions called atheromas (or atheromatous or atherosclerotic plaques). Atheromatous plaques are raised lesions composed of soft grumous lipid cores (mainly cholesterol and cholesterol esters, with necrotic debris) covered by fibrous caps.


What are some possible complications of atherosclerotic plaque?

- can mechanically obstruct vascular lumina and are prone to rupture, resulting in catastrophic vessel thrombosis.

- Plaques also weaken the underlying media, sometimes leading to aneurysm formation.


Where in the world is atherosclerosis common?

-US and Europe
-less common in Central and South America, Africa, and parts of Asia


T or F. The risks (constitutional or environmental/acquired) of MI have a multiplicative effect

T, Thus, two factors increase the risk of myocardial infarction approximately four-fold, and three (i.e., hyperlipidemia, hypertension, and smoking), increase the rate by a factor of 7


What are some constitutional risk factors for atherosclerosis?

-gender (premenopausal women are slightly protected)

After menopause, however, the incidence of atherosclerosis-related diseases increases and, in old age, even exceeds that in men


T or F. Postmenopausal estrogen replacement appears
to decrease cardiovascular risk.

F. it increases it


What are some acquired risk factors for atherosclerosis?

- hyperlipidemia (hypercholesterolemia)
- hypertension
- cigs
- diabetes mellitus


What does LDL do? HDL?

LDL distributes cholesterol to peripheral tissues. When LDL is too high, some cholesterol is deposited into vessel walls.

By contrast, high-density lipoprotein (HDL) mobilizes cholesterol from developing and existing vascular
plaques and transports it to the liver for biliary excretion. Consequently, higher levels of HDL correlate with reduced risk.


Is hypertension really associated with heart disease?

Yes, it can increase the risk of IHD by 60%. Hypertension also is the major cause of left ventricular hypertrophy (LVH),
which also can contribute to myocardial ischemia


Why would diabetes mellitus increase IHD risk?

Diabetes mellitus is associated with raised circulating
cholesterol levels and markedly increases the risk of atherosclerosis. Other factors being equal, the incidence of MI is twice as high in diabetics as in non-diabetics.

In addition, this disorder is associated with an increased risk of stroke and a 100-fold increase in atherosclerosis-induced gangrene of the lower extremities.