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SBM Cardio JXC > 2013-08-23 Hypertension > Flashcards

2013-08-23 Hypertension Flashcards

1
Q

What president died of cerebral hemorrhage 2° to HTN while in office?

A

FDR in 1945

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2
Q

What is the prevalence of HTN?

A

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
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3
Q

Draw the R-A-A-S system with Sympathetic inputs

A

See Slide 17 and 18

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4
Q

What are most important causes of 2° HTN?

A
  1. hyperaldosteronism
  2. pheochromocytoma
  3. renal artery stenosis
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5
Q

What are the consequences of hypertension?

A

stroke, chronic renal disease, atherosclerosis (retinopathy)

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6
Q

How do anti-hypertensive drugs work?

A

.

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7
Q

What are the three classic RCTs of HTN tx?

A

.

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8
Q

What is the relationship between severity of HTN and the benefit of therapy?

A

.

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9
Q

When do you start treatment of HTN?

A

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

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10
Q

What is prehypertension? What are recommendations to do with pts who are pre-HTN?

A

SBP 120-139 AND DBP 80-89

–Re-check in one year.

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11
Q

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?

A
  1. 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
  2. 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
  3. 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
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12
Q

What factors affect total blood volume?

A

@ Kidney: renal blood flow, ADH, aldosterone and ANP, renal arteriolar symp tone, Angiotensin II

@vasculature: ADH (=vasopressin)

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13
Q

What factors affect CO?

A 
Blood volume (preload)
cardiac symp tone (contractility, HR)
arteriolar symp tone (TPR)
venous symp tone (∆s distrib of blood )
Angiotensin II (?)
hypertrophy
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14
Q

How does peripheral venous tone ∆ BP?

A

shifts blood to and from periph and pulm beds; ∆s preload by ∆ing Venous return

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15
Q

What factors affect peripheral arteriolar tone?

A

autoregulation
arteriolar symp tone
AII
(Endothelin?)

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16
Q

What is one affect of OCPs on BP?

A

Increase production of angiotensinogen in liver.

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17
Q

Sktech the JGA

A

see slide 19

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18
Q

What factors increase Renin secretion?

A
  1. Decr pressure at afferent arteriolar stretch receptors (renal artery stenosis, hypovolemia, hypotension)
  2. Beta-receptor Increased sympathetic tone
  3. Reduced [Na+] at the distal tubule which the macula densa senses and feedback via JGA (hyponatremia or hypovolemia)
19
Q

Why can ACEIs and ARBs cause nephropathy?

A

AII constricts the efferent arteriole to help maintain glomerular pressure. If you block this effect, the glomeruli can become hypoperfused.

20
Q

Is morbidity and mortality more dependent on SBP or DBP?

A

SBP

21
Q

Where is A.C.E. distributed in body?

A

lung endothelium (other endothelium, too)

22
Q

Why do ACE inhibitors cause cough?

A

“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

23
Q

Name the effects of AII?

A 
vasoconstriction
stimulates adrenals to release aldosterone
increased inotropy
increased cardiac hypertrophy
negative feedback on renin release
24
Q

What is the prevalence of primary vs. secondary HTN?

A

5-10% secondary

>90% primary

25
Q

List causes of 2° HTN.

A

ENDOCRINE-RELATED

  1. primary hyperaldosteronism
  2. pheo
  3. Cushing’s dz
  4. Thyroid dz
  5. OCPs
  6. Preg-induced HTN

ANATOMICAL-ISH

  1. renal a. stenosis
  2. renal parenchymal dz
  3. coarctation of the aorta

OTHER
8. EtOH

26
Q

1° hyperaldosteronism

  • -presentation
  • -dx
  • -tx
A

present: usu asmyp; dx w/ low K+
dx: expect high aldo and low renin
tx: surg or aldosterone agonists

27
Q

pheo

  • -presentation
  • -dx
  • -tx
A

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

28
Q

What does excess Norepi (from a pheo) present as?

A

paroxysms of HTN w/ vasconstriction, pallor and brady

29
Q

What does excess epi (from a pheo) present as?

A

tachy + orthostatic

30
Q

renal artery stenosis

  • -subtypes
  • -presentation
  • -dx
  • -tx
A

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

31
Q

renal parenchymal dz

  • -pathophys
  • -present/dx
A

inability to excrete volume —>incrs blood vol
incr renin secretion (we don’t know why)
–present/dx w/ high creatinine (BUN?)

32
Q

Coarctation of the aorta

  • -dx
  • -tx
A

dx: BP high in UE than LE; CXR shows rib notching
tx: surg?

33
Q

Cushing’s dz briefly

A

cortisol excess; has mieralocorticoid properties similar to aldo;
–present: Cushingoid appearance

34
Q

thyroid dz

A

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

35
Q

EtOH

A

unclear why; likely symp-mediated

withdrawls cause HTN, too

36
Q

OCPs

  • -expected lab values
  • -epidemiology
A

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
37
Q

pregnancy-induced HTN

A

pre-eclampsia

  • -assoc’d w/ 3rd trimester edema, wt gain, renal comps (like proteinuria)
  • -BP normal after delivery
38
Q

Name the two hemodynamic phases that 1° HTN goes through over time

A

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

39
Q

complications of htn

A

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:

40
Q

Diet ∆s

A
  • -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
41
Q

Exercise

A

evidence is better that it prevents development in previously sedentary and unfit normotensives than evidence that it can lower BP once htn

42
Q

Relaxation Therapy

A

studies show short-term effects

43
Q

Studies

A

there are three or four classic studies that show tx’ing HTN (especial moderate to severe HTN) has dramatic decrease in M&M

SBM Cardio JXC (6 decks)

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