Hypertension

Question 1

What is the primary determinant of CO in normal individuals?

Answer 1

volume status (Na+ content)

Question 2

True or false: An increase in CO is often the cause of persistent HTN.

Answer 2

False- increased CO may result in early phase HTN but is rarely the result of persistent HTN.

Question 3

What are 2 of the more important humoral factors that affect SVR?

Answer 3

angiotensin II and NE - cause vasoconstriction

Question 4

Increased ______ tone leads to HTN.

Answer 4

adrenergic

Question 5

Adrenergic tone increases:

Answer 5

• vascular tone
• Na+ retention
• cardiac inotropy

Question 6

Is primary essentialHTN monogenic or polygenic in most cases?

Answer 6

polygenic

Question 7

What is the Guyton Hypothesis?

Answer 7

It states that the fundamental mechanism of long-term control of BP is fluid volume feedback by the kidneys. Kidneys regulate arterial pressure by altering renal excretion of Na+ and water, thereby controlling circulatory volume and CO.

Question 8

What are some of the causes of monogenic HTN, and what do all of these conditions have in common?

Answer 8

• Glucocorticoid remedial aldosteronism (GRM)
• Syndrome of apparent mineralocorticoid excess (AME)
• Mineralocorticoid receptor mutation \
• Liddle Syndrome - gain of funct. ENaC
• T594M mutation (African American subtype) - incr. ENaC activity
• All involve retention of Na+

Question 9

With the progressive loss of kidney function, what percentage of patients become hypertensive?

Answer 9

nearly 100%

Question 10

What happens to patients with essential HTN vs. normal patients when saline is given?

Answer 10

• essential HTN pts: Na+ excretion is delayed and pressure increases
• normal pts: able to excrete volume load with little or no change in BP

Question 11

Autoregulation of blood flow and GFR depends primarily on 2 mechanisms:

Answer 11

• myogenic response (2/3)

- tubuloglomerular feedback (1/3)

Question 12

What is the autoregulatory range of the kidney?

Answer 12

60-160 mm Hg

Question 13

What is the myogenic response to increased afferent arteriolar pressure?

Answer 13

stimulates reflexive vasoconstriction by stimulating smooth muscle contraction; this minimizes the increase in glomerular capillary pressure that would otherwise occur in response to increased systemic arterial pressure, preventing damage to glomerular capillaries

Question 14

What is the myogenic response to decreased afferent arteriolar pressure?

Answer 14

stimulates reflexive vasodilation by stimulating vascular smooth muscle relaxation; this increases blood flow and filtration pressure in the glomerulus, thus helping maintain GFR

Question 15

Which hypertensive medication would NOT be a good choice in patients with advanced kidney disease?

Answer 15

dihydropyridine calcium channel blockers, as they relax/dilate blood vessels and therefore abolish renal autoregulation

Question 16

What happens to renal autoregulation in malignant hypertension?

Answer 16

BP level exceeds autoregulation limits

Question 17

What are the 2 patterns of hypertension injury to the kidneys?

Answer 17

• essential HTN: benign nephrosclerosis

- malignant HTN: intimal thickening, proliferative arteritis, fibrinoid necrosis

Question 18

What happens to kidney architecture in essential hypertension?

Answer 18

nephrosclerosis: contraction of kidneys and progressive reduction in size leading to cortical atrophy and diffuse fibrosis –> afferent arteriolar hyaline arteriosclerosis –> subintimal hyaline homogenous eosinophilic deposits –> ischemic atrophy

Question 19

What is the main reason for kidney failure in patients with essential HTN?

Answer 19

ischemic atrophy

Question 20

What is renovascular hypertension?

Answer 20

HTN resulting from unilateral or bilateral renal artery stenosis (usually >70%).

(however, keep in mind that “stenosis” does not necessarily mean “HTN”)

Question 21

What are the clinical presentations of renal artery stenosis?

Answer 21

• severe and difficult to control HTN
• kidney failure
• flash pulmonary edema

Question 22

What happens to pressure natriuresis in bilateral renal artery stenosis?

Answer 22

There is not pressure natriuresis because the total renal mass is hypoperfused. Due to bilateral stenoses, sodium excretion is impaired, leading to fluid retention.

Question 23

In unilateral renal artery stenosis, do patients respond to ACEIs?

Answer 23

yes

Question 24

In renal artery stenosis of a solitary kidney, do patients respond to ACEIs?

Answer 24

no

Question 25

In bilateral renal artery stenosis, do patients respond to ACEIs?

Answer 25

no

Question 26

A primary aldosterone tumor is relatively rare. How, then, can primary aldosteronism occur?

Answer 26

It may result from adrenal hyperplasia.

Question 27

What are the treatments of renal artery stenosis?

Answer 27

• Medical: antihypertensives
• Intervention: renal artery angioplasty (+/- stenting)
• Surgical: renal artery bypass

Question 28

How do patients with excess aldosterone present?

Answer 28

with HTN and hypokalemia

Question 29

What happens to electrolyte balance in CKD?

Answer 29

Na+ and H2O are retained, thus volume becomes an important factor

Question 30

Unilateral renal artery stenosis with a normal contralateral kidney is ______ - dependent and thus responsive to _______.

Answer 30

renin; ACEIs/ARBs (drugs that block RAAS)