2013-08-23 Hypertension Flashcards
(43 cards)
What president died of cerebral hemorrhage 2° to HTN while in office?
FDR in 1945
What is the prevalence of HTN?
Increases with age (44% of those 50-59, 54% of 60-69 y/o’s, plateaus at ~65 >70 y/o)
- -higher incidence in blacks (maybe only African Americans?) than whites; dz course is also faster and more severe in blacks
- -historically men>women, but in 2006 white women>WM
Draw the R-A-A-S system with Sympathetic inputs
See Slide 17 and 18
What are most important causes of 2° HTN?
- hyperaldosteronism
- pheochromocytoma
- renal artery stenosis
What are the consequences of hypertension?
stroke, chronic renal disease, atherosclerosis (retinopathy)
How do anti-hypertensive drugs work?
.
What are the three classic RCTs of HTN tx?
.
What is the relationship between severity of HTN and the benefit of therapy?
.
When do you start treatment of HTN?
SBP >140 or DBP >90 - confirm in 2 months –>tx
SBP >160 or DBP >100 - eval/tx w/in 1 mo
SBP >180 or DBP > 110 - eval/tx w/in 1 wk
SBP >210 or DBP >120 - eval/tx STAT
What is prehypertension? What are recommendations to do with pts who are pre-HTN?
SBP 120-139 AND DBP 80-89
–Re-check in one year.
What are the hemodynamic patterns seen in 2° (and perhaps some 1°) HTN?
What will [renin] be in each?
What’s an example of each?
How do you tx?
- incr total blood volume (tx w/ diuretics)
- -expect low renin because A.A. is sensing high P
- -Cushing’s, other hyperaldosteronism, renal dz, excessive salt intake
- -tx w/ diuretics - incr cardiac function (CO)
- -doesn’t say re: renin; guessing nl w/o hyperthyroidism
- -hyperthyroidism (β1 stimulation), hyperkinetic heart syndrome, ? the early phase of 1° HTN
- -tx w/ β-blockers - incr Periph venous tone
- -expect incr renin
- -renovascular HTN, hyperthyroidism (excess catecholamines), hypothyroidism (decr β2 receptors on periph arterioles), malignant HTN, late phase of essential HTN
- -tx w/ vasodilators
What factors affect total blood volume?
@ Kidney: renal blood flow, ADH, aldosterone and ANP, renal arteriolar symp tone, Angiotensin II
@vasculature: ADH (=vasopressin)
What factors affect CO?
Blood volume (preload) cardiac symp tone (contractility, HR) arteriolar symp tone (TPR) venous symp tone (∆s distrib of blood ) Angiotensin II (?) hypertrophy
How does peripheral venous tone ∆ BP?
shifts blood to and from periph and pulm beds; ∆s preload by ∆ing Venous return
What factors affect peripheral arteriolar tone?
autoregulation
arteriolar symp tone
AII
(Endothelin?)
What is one affect of OCPs on BP?
Increase production of angiotensinogen in liver.
Sktech the JGA
see slide 19
What factors increase Renin secretion?
- Decr pressure at afferent arteriolar stretch receptors (renal artery stenosis, hypovolemia, hypotension)
- Beta-receptor Increased sympathetic tone
- Reduced [Na+] at the distal tubule which the macula densa senses and feedback via JGA (hyponatremia or hypovolemia)
Why can ACEIs and ARBs cause nephropathy?
AII constricts the efferent arteriole to help maintain glomerular pressure. If you block this effect, the glomeruli can become hypoperfused.
Is morbidity and mortality more dependent on SBP or DBP?
SBP
Where is A.C.E. distributed in body?
lung endothelium (other endothelium, too)
Why do ACE inhibitors cause cough?
“A persistent dry cough is a relatively common adverse effect believed to be associated with the increases in bradykinin levels produced by ACE inhibitors, although the role of bradykinin in producing these symptoms has been disputed.[13] Patients who experience this cough are often switched to angiotensin II receptor antagonists.” Wikipedia
Name the effects of AII?
vasoconstriction stimulates adrenals to release aldosterone increased inotropy increased cardiac hypertrophy negative feedback on renin release
What is the prevalence of primary vs. secondary HTN?
5-10% secondary
>90% primary
