Overview of Hypertension

Question 1

3 key features of all hypertension (HTN)?

Answer 1

Systemic arterial pressure is at sustained increased levels.
SVR is too high, and too much Na+ and H2O is retained.
Abnormal fibrosis.

Question 2

2 broad groups of hypertension?

Answer 2

Primary (essential) HTN - resistance or compliance HTN.

Secondary HTN.

Question 3

Why is HTN bad for the LV?

Answer 3

Increased afterload means LV has more wall stress -> hypertrophy, fibrosis -> impaired diastolic relaxation and general function.

Question 4

Why is HTN bad for the arterial system?

Answer 4

Increased pressure -> increased wall stress.
Aneurysms, accelerated atherosclerosis.
Esp. obliterative destruction of systemic arterioles -> higher SVR -> more HTN.
(and strokes)

Question 5

Why is HTN bad for the kidney?

Answer 5

Arteriolar destruction.

HTN is made worse because reduced GFR -> reduced ability to excrete sodium.

Question 6

How does blood pressure change with age?

Answer 6

With increasing age, there’s increasing BP, especially systolic BP.

Question 7

Is there a threshold effect for the relationship between BP and morbidity/mortality?

Answer 7

Nope, it’s pretty much continuous (until you hit hypotension) - where lower is better.

Question 8

What might drive much of the hypertension in modern society?

Answer 8

Sodium consumption.

Question 9

What are the cut offs for classifying normal, prehypertension, stage 1 HTN, and stage 2 HTN?

Answer 9

Normal: < 120 systolic, and < 80 diastolic.
Prehypertension: 120 - 139 SBP, or 80-89 DBP.
Stage 1 HTN: 140 - 159 SBP, or 90-99 DBP.
Stage 2 HTN: >160 SBP, or >100 DBP.

(note that whether these line up with thresholds for treatment depends on concurrent risk factors, eg. with diabetes one might treat at 130/90.)

Question 10

4 mechanisms for secondary hypertension?

Answer 10

Kidney disease.
Adrenal disease (primary aldosteronism, Cushing’s, pheochromocytoma).
CNS (corticotroph pituitary adenoma -> ACTH)
Drug intake.

Question 11

What are 3 mechanisms that should prevent hypertension?

Answer 11

Baroreceptor reflexes.
Pressure-natriuresis.
RAAS should shut off.

Question 12

Are there racial/ethnic differences in HTN prevalence?

Answer 12

Yep. Higher in African-Americans, Africans in the UK, and Asians…
(heredity or environment?)

Question 13

Does Na+ restriction work well for HTN?

Answer 13

Yes, very well. But it’s hard to get people to do it..

Question 14

Does stress increase BP?

Answer 14

Yep.

Question 15

Does alcohol increase BP?

Answer 15

Yep.

Question 16

How do blood pressures vary between resistance hypertension and compliance hypertension?

Answer 16

Resistance HTN: problem is w. regulation of SVR -> increase in both systolic and diastolic BP.
Compliance HTN: problem is loss of compliance in great vessels “stiff pipes” -> increase in systolic BP, but diastolic BP is normal to low.

Question 17

Consequences of compliance HTN?

Answer 17

Severe LV pressure overload ->
LV hypertrophy.
Aneurysms (in aortic and brain)

Question 18

Describe the deWardener & MacGregor model for essential HTN.

Answer 18

Normally, when plasma volume is expanded, a natriuretic peptide (not identified) inhibits Na+/K+ pumps… in the kidney, this causes Na+ excretion.
However, in pts with HTN, the kidneys don’t respond normally, so natriuretic peptide levels stay high. Na+/K+ pumps on vascular smooth muscle cells are blocked. Na+ buildup intracellularly -> activation of Na+/Ca++ exchanger -> Ca++ buildup -> more vascular smooth muscle contraction -> increased SVR and BP.

Question 19

So… what’s the deal with this mysterious natriuretic peptide?

Answer 19

Still not found. It’s not any of the atrial natriuretic peptides.
Ouabain may be an analogue of it.

Question 20

In HTN, renal sympathetics might be overactive.

Answer 20

okay

Question 21

What effects does adrenergic agonism have on renal functions related to HTN?

Answer 21

alpha 1 agonism on afferent arteriole -> decreased renal blood flow and GFR.
alpha 1 agonism on renal tubules -> more Na/K pump activity -> increased Na+ and water reabsorption.
beta 1 on juxtaglomerular cells -> more renin production.
(in people with kidneys removed, or renal sympathetics severed, BP is lowered)