2013-08-23 Hypertension Flashcards
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
List causes of 2° HTN.
ENDOCRINE-RELATED
- primary hyperaldosteronism
- pheo
- Cushing’s dz
- Thyroid dz
- OCPs
- Preg-induced HTN
ANATOMICAL-ISH
- renal a. stenosis
- renal parenchymal dz
- coarctation of the aorta
OTHER
8. EtOH
1° hyperaldosteronism
- -presentation
- -dx
- -tx
present: usu asmyp; dx w/ low K+
dx: expect high aldo and low renin
tx: surg or aldosterone agonists
pheo
- -presentation
- -dx
- -tx
neuro-ecotodermal tumor that arises from chromaffin cells in sympatho-adrenal system (celcia, mesenteric, renal, adrenal, hypogastric, testicular and paravertebral sym nerv plex; though 90% at adrenals)
present: w/ intermittent HTN + sx of excess of either NE or epi
dx: metanephrines in serum or urine + CT scan
tx: surgery
What does excess Norepi (from a pheo) present as?
paroxysms of HTN w/ vasconstriction, pallor and brady
What does excess epi (from a pheo) present as?
tachy + orthostatic
renal artery stenosis
- -subtypes
- -presentation
- -dx
- -tx
subtypes: atherosclerotic; fibromuscular (young females)
- -present: bruit in 50%; may also have hypokalemia
- -dx: duplex, renal scans, arteriograms and renal venous renin levels
- -angioplasty, bypass surgery, or meds
renal parenchymal dz
- -pathophys
- -present/dx
inability to excrete volume —>incrs blood vol
incr renin secretion (we don’t know why)
–present/dx w/ high creatinine (BUN?)
Coarctation of the aorta
- -dx
- -tx
dx: BP high in UE than LE; CXR shows rib notching
tx: surg?
Cushing’s dz briefly
cortisol excess; has mieralocorticoid properties similar to aldo;
–present: Cushingoid appearance
thyroid dz
hyperthy: b/c T4 induces heart muscle to make more Na/K-ATPases and beta-1 receptors
hypo: b/c of incr Periph vasc resist
EtOH
unclear why; likely symp-mediated
withdrawls cause HTN, too
OCPs
- -expected lab values
- -epidemiology
estrogens incr synth of angiotensinogen
- -incr AII leads to feedback suppress of renin so overall:
- —high AII, high alod, low renin
- -rises a little in most; <5% see significant incr
pregnancy-induced HTN
pre-eclampsia
- -assoc’d w/ 3rd trimester edema, wt gain, renal comps (like proteinuria)
- -BP normal after delivery
Name the two hemodynamic phases that 1° HTN goes through over time
Early: hyperkinetic heart and incr blood volume and low periph renin levels and labile BPs
–tx w/ beta-blockers or diuretics
Late: high PVR; BP fixed (not labile) w/ high periph [renin]
–tx: add vasodilators
complications of htn
MOST IMPORTANT CAUSES OF M&M: renal dz, CVAs, MIs
VASCULAR: atherosclerosis, aortic dissection
HEART: CAD, LVH
BRAIN: cerebrovasc athero, aneurysms, and hemorrhage
KIDNEY: nephrosclerosis, which along w/ RAS can lead to end-stage renal dz (HTN is most common causes of needing dialysis)
EYES: htnsive retinopathy (hemorrhage, arteriolar narrowing, exudate + cotton wool spots); papilledema in crisis
MALIGNANT HTN:
Diet ∆s
- -clear evidence losing weight in obese pts lowers HTN
- -salt for sure makes existing HTN worse; controversy over whether or not it causes HTN
- -decr EtOH
Exercise
evidence is better that it prevents development in previously sedentary and unfit normotensives than evidence that it can lower BP once htn
Relaxation Therapy
studies show short-term effects
Studies
there are three or four classic studies that show tx’ing HTN (especial moderate to severe HTN) has dramatic decrease in M&M
