HTN physio and background

Question 1

Stage I and Stage II HTN defined as; what are the types of HTN?

Answer 1

Stage I: 140-159/90-99; stage II: >160 systolic, >100 diastolic;
Essential/idiopathic HTN 95%, secondary is other problems, but MINORITY of patients

Question 2

BP goes up ___ in men as we get older, and in women goes up; who tolerates HTN better?

Answer 2

linearly; with an inflection around the perimenopausal period since change in hormones could affect this;
Men do!!

Question 3

Causes of secondary HTN?

Answer 3

1. Renal (chronic kidney disease with high volume state with too much Na and water in vasculature; renal artery stenosis means high renin, small kidney, maybe hypokalemia)
2. Drugs (EtOH, oral contraceptives, NSAIDS which inhibit prostaglandins at afferent arteriole which constricts if people use this mechanism) EON
3. Endocrine: pheochromocytoma for catecholamines, Cushings, hyperaldosteronism, hypo/hyperthyroidism, hyperparathyroidism (PC HHH)
4. Pulmonary (obstructive sleep apnea)

Question 4

Factors that aren’t modifiable in HTN; modifiable?

Answer 4

Nonmod: genetics, race, gender, age (RAGG);
mod: Na intake, obesity, Heavy EtOH intake, meds, sedentary lifestyle, physiologic stress, diets lower in potassium and calcium (Write SOHP note to Say to MD)

Question 5

The more cardiovascular risks; the younger you are; list of cardiac risk factors

Answer 5

the more aggressive you should be with treatment;
the longer you have to live with the disease so consider treating more aggressively;
hyperlipidemia, diabetes, smoking, FH of vascular disease

Question 6

Examples of end organ disease;

risk of end organ disease higher in

Answer 6

1. Brain (stroke and small vessel disease)
2. eyes (retina)
3. vascular tree (vascular stiffness, atherosclerosis, aneurysm)
4. heart (CAD and LV hypertrophy)
5. kidneys nephrosclerosis
   (related to extent of BP elevation and HTN duration);
   AA’s and premenopausal women

Question 7

Two patients: one with end organ disease and one without; who gets the pharmacotherapy?

Answer 7

Give it to person with end organ disease since benefit of lowering BP increases (eg LV hypertrophy)

Question 8

Diuretics action regarding five categories

Answer 8

Diuretics help shrink plasma volume, lowering PVR and leading to increased plasma renin

Question 9

Central acting sympatholytics

Answer 9

decrease symp tone (HR and CO), decreasing PVR; increase the plasma volume and the lack of symp tone blocks renin release

Question 10

Alpha blockers act by

Answer 10

decreasing PVR, which then leads to increased plasma volume and compensation of symp tone to increase HR and CO; no effect on plasma renin

Question 11

No ISA beta-blockers leads to

Answer 11

decrease in CO, leading to decreased volume to the kidney and decreased GFR and the retention of Na and water in the plasma volume, increasing plasma volume and decreasing plasma renin; PVR and HR decrease;

Question 12

ISA beta blockers lead to

Answer 12

decrease in PVR, and increase in plasma volume and decrease in plasma renin, but WON’T affect HR or CO (CO minimally)

Question 13

Arteriolar vasodilators:

Answer 13

decrease in PVR, see increase in plasma volume AND plasma renin; HR and CO both increase

Question 14

ACE i and ARB both lead to

Answer 14

decrease in PVR, and increase in plasma renin with less AII; no appreciable changes in plasma volume and no real changes in HR or CO (in long run, can get increased forward CO)

Question 15

What do the dihydropyridines do relative to non-dihydros? Terms of BP, antianginal, SA node, AV node conduction, inotropy?

Answer 15

Dihydros: decrease BP big time, some anti-angial, nothing else;
non-dihyros: decrease in BP, anti-anginal BIG TIME, big decreases in SA node, AV node conduction, inotropy!!

Question 16

Ca channel blockers can lead to

Answer 16

decrease in PVR; plasma volume AND plasma renin both increase; your CO or HR can EITHER increase OR decrease