Hypertension

Question 1

Explain Guyton’s theory of hypertension

Answer 1

Increased BP causes pressure natriuresis in normal people due to increased perfusion pressure (GFR unchanged though)

thick ascending loop is important

Problem arises when pressure natriuresis threshold is altered through genetic inheritance of angiotensin II issues

Question 2

Explain Brenner’s theory of hypertension

Answer 2

Low birthweight or impaired renal development causes reduced nephron mass that causes systemic and glomerular hypertension, leading to glomerular sclerosis which further exacerbates the reduction in nephron mass (necrosis/fibrosis, etc.).

Question 3

Explain Laragh’s hypothesis of hypertension

Answer 3

Nephron heterogeneity - some nephrons are ischemic and produce high renin, which acts on even those nephrons which are not ischemic, resulting in an overall effect of constant RAAS effect, though ‘diluted’

Question 4

Explain secondary hypertension from unilateral RAS

Answer 4

RAAS increases in hypotensive kidney, causing, increased SVR in both, right shift pressure natriuresis in the other, normal kidney which is available to excrete excess Na

Volume is not an issue

ACE inhibitors are helpful

Question 5

Explain secondary hypertension from bilateral RAS

Answer 5

Total kidney hypoperfusion leads to increased RAAS with no ability to get rid of retained sodium

Edema

ACE inhibitors do NOT help; ATII needed!

Question 6

Most common cause of RAS?

Answer 6

Athersclerosis

Question 7

Common features of secondary hypertension disorders

Answer 7

Hypokalemia (except Gordon)
Metabolic alkalosis (except Gordon)
Low RAAS (except aldo excess)

Question 8

Cushing’s pathogenesis in brief

Answer 8

Excess cortisol overpowers ability of 11B-HSD2 to degrade it to cortisone. Cortisol activates MR receptor in collecting duct causing increased sodium retention and BP up

can be caused by exogenous steroids too

Question 9

Pseudohyperaldosteronism in brief

Answer 9

11B-HDS2 deficiency so cortisol is not converted to cortisone; cortisol activates aldosterone MR receptor leading to more Na reabsorption in collecting duct

Question 10

Liddle’s syndrome fast facts

Answer 10

AD
ENaC always on in distal tubule

treat with ENaC blockers triamterene and amiloride

Question 11

What are the two contributing factors to metabolic alkalosis in secondary hypertension?

Answer 11

Hypokalemia
Aldosterone (H secretion)

Question 12

Pseudohypoaldosteronism II other name

Answer 12

Gordon syndrome

Question 13

Gordon syndrome fast facts

Answer 13

Salt-sensitive hypertension
Hyperkalemia
metabolic ACIDOSIS

Na/Cl transporter in DCT always on due to WNK4 or WNK1 mutation causes distal Na delivery decrease, and thus less potassium decrease