Cardio-path-hypertension

Question 1

Kidney damage from HTN can result in low renal pressure, what can be the result of this?

Answer 1

A false sense that there is low blood pressure throughout the body which can lead to release of renin that converst angiotensinogen to angiotensin I then II that promotes release of aldosterone and smooth muscle vasoconstriction and then increase BP

Question 2

Renin is produced by

Answer 2

renal juxtaglomerular cells.

Question 3

Kidneys influence peripheral resistance and sodium excretion/retention primarily through?

Answer 3

the renin-angiotensin system.

Question 4

Renin is released in response to 3 things:

Answer 4

low blood pressure in afferent arterioles, elevated levels of circulating catecholamines, or low sodium levels in the distal convoluted renal tubules

Question 5

low sodium levels in the distal convoluted renal tubules are sensed in response to

Answer 5

when the glomerular filtration rate falls (eg, when the cardiac output is low) because a higher fraction of the filtered sodium is resorbed in the proximal tubules.

Question 6

What converst angiotensin I to II?

Answer 6

angiotensin-converting enzyme (ACE) in the periphery.

Question 7

Where does the angiotensin I to II conversion mostly take place?

Answer 7

endothelium of the lungs

Question 8

Angiotensin II raises blood pressure by:

Answer 8

1. Inducing vascular smooth muscle cell contraction,
2. Stimulating aldosterone secretion by the adrenal gland, and
3. Increasing tubular sodium resorption.

Question 9

Aldosterone increases blood pressure by its effect on blood volume; aldosterone increases sodium resorption (and thus water) in the distal convoluted and collecting tubules, what effect does it have on K+?

Answer 9

driving potassium excretion into the urine.

Question 10

What hormones are released by from atrial and ventricular myocardium in response to volume expansion?

Answer 10

Natriuretic peptides

Question 11

What is the role of natriuretic peptide?

Answer 11

these inhibit sodium resorption in the distal renal tubules, thus leading to sodium excretion and diuresis.

๏ They also induce systemic vasodilation.

Question 12

Vascular resistance is regulated at the level of which vessel?

Answer 12

arterioles

Question 13

What is essential HTN?

Answer 13

manifests in an acute aggressive form, high blood pressure is typically asymptomatic for many years.

Question 14

HTN can increase the risk for :

and lead to:

Answer 14

risk for stroke and atherosclerotic coronary heart disease

cardiac hypertrophy and heart failure, aortic dissection, multi-infarct dementia, and renal failure.

Question 15

What results from the interplay of several genetic polymorphisms and environmental factors, which conspire to increase blood volume and/or peripheral resistance?

Answer 15

essential hypertension

Question 16

What is the cutoff BP for diagnosing HTN?

Answer 16

130/80

Question 17

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 called?

Answer 17

malignant hypertension

Question 18

malignant hypertension usually is severe, ie, systolic pressures over mmHg or diastolic pressures over 120mmHg, and frequently is associated with failure and hemorrhages, with or without papilledema.

Answer 18

200; renal; retinal

Question 19

Concerning pathogenesis, most cases of hypertension are:

Answer 19

primary (idiopathic) or essential

Question 20

Secondary hypertension, are due to:

Answer 20

primary renal disease, renal artery narrowing (renovascular hypertension), or adrenal disorders.

Question 21

renovascular hypertension can cause renal artery , which causes increased/decreased glomerular flow and pressure in the afferent arteriole of the glomerulus.

Answer 21

stenosis; decreased

Question 22

Because of the false sense of systemic blood pressure brought on by renovascular hypertension, this can induce secretion, which, as already discussed, increases vascular tone and blood volume via the angiotensin-aldosterone pathway

Answer 22

renini

Question 23

Rare forms of HTN can be caused by gene disorders

Answer 23

single

Question 24

Gene defects affecting which enzymes involved in aldosterone metabolism can lead to hypertension?

Answer 24

1. aldosterone synthase
2. 11β-hydroxylase
3. 17α-hydroxylase

Question 25

Gene defects affecting enzymes involved in aldosterone metabolism (e.g., aldosterone synthase, 11β-hydroxylase, 17α-hydroxylase) can lead to an **increase/decrease** e in secretion of aldosterone, increased salt and water resorption, plasma volume expansion and, ultimately, hypertension.

Answer 25

increase

Question 26

There are also mutations affecting proteins that influence sodium reabsorpton caused by **gain-of-function** mutations in an **epithelial Na + channel protein** that **increase distal tubular reabsorption of sodium in response to aldosterone** called:

Answer 26

Liddle syndrome

Question 27

Although the specific triggers are unknown, it appears that both **altered renal sodium** **handling** and **increased vascular resistance** contribute to hypertension.\*

Answer 27

essential

Question 28

What is the key pathogenic feature of essential hypertension?

Answer 28

Reduced renal sodium excretion in the presence of normal arterial pressure, which can lead to high BP

Question 29

Increased vascular resistance may stem from:

Answer 29

vasoconstriction or structural changes in vessel walls

Question 30

not only accelerates atherogenesis

Answer 30

๏ HTN

Question 31

HTN causes degenerative changes in the walls of large- and medium-sized arteries that can lead to dissection and hemorrhage.

Answer 31

aortic; cerebrovascular

Question 32

Which small blood vessel disease is associated with benign hypertension?

Answer 32

**Hyaline arteriolosclerosis** -homogeneous, pink hyaline thickening of the arteriolar walls, and luminal narrowing

Question 33

How does hyaline arteriolosclerosis form:

Answer 33

lesions stem from **leakage of plasma components** across injured endothelial cells into vessel walls, and **increased ECM production** by smooth muscle cells in **response to hemodynamic stress**

Question 34

What happens to the kidneys with hylaline arteriosclerosis in the small blood vessels:

Answer 34

leads to diffuse vascular compromise and nephrosclerosis (glomerular scarring) Which can also cause false sense of low BP leading to RAS

Question 35

hyaline arteriolosclerosis is found in older and those with HTN but also with people diagnosed with

Answer 35

**diabetic microangiopathy** however, in this disorder, the underlying etiology is **hyperglycemia associated EC dysfunction.**

Question 36

Hyperplastic arteriolosclerosis is more typical of hypertension.

Answer 36

severe

Question 37

What is being demonstrated in this example of Hyperplastic arteriolosclerosis?

Answer 37

“onion skin”, concentric, laminated thickening of arteriolar walls and luminal narrowing.

Question 38

What do the onion skin layers of this artery related to “onion skin” Hyperplastic arteriolosclerosis consist of:

Answer 38

laminations consist of **SMCs** and thickened, reduplicated **basement membrane.**

Question 39

In malignant hypertension, these changes are accompanied by fibrinoid deposits and vessel wall necrosis called:

Answer 39

**necrotizing arteriolitis**- which occurs mainly in the kidney note: the dark pink surrounding the vessel are fibrin deposits