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Clin Med-Cardio pt 2 > Hypertension lecture > Flashcards

Hypertension lecture Flashcards

1
Q

what is defined as HTN?

A

equal or above 140/90

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2
Q

What percentage of HTN is secondary? (i.e. because of renal, endocrine, congenital etiologies)

A

5%

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3
Q

____% of cases of HTN are etiology unknown

A

95%

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4
Q
  • Environmental factors
  • Sympathetic hyperactivity
  • RAA axis

can all lead to…

A

Hypertension

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5
Q 
Obesity
Excess Na intake
Cigarette smoking
NSAIDs
Excess alcohol
A

Exacerbating factors of HTN

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6
Q 
Estrogen use 
Renal dz
Renal vascular HTN
Endocrine disorders
Coarctation of aorta (congenital)
HTN in pregnancy
A

All secondary causes of HTN

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7
Q

Hypertension accelerates progression of..

A

Renal insufficiency

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8
Q

Any form of chronic renal parenchymal disease can result in..

A

Hypertension

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9
Q

Marked increase of renin
2 forms:
Fibromuscular hyperplasia
Atherosclerosis

A

Renal artery stenosis

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10
Q

Fibomuscular hyperplasia (FMH) usually presents in who?

BP markedly elevated; renal function preserved; arteriography diagnostic; angioplasty/stent beneficial in treatment.

A

Young adults

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11
Q

Athersclerosis renal artery stenosis presents in..

(BP elevated and unresponsive to meds; renal function often impaired; intervention may or may not help; long term med Rx necessary.)

A

Older adults

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12
Q

Heart’s response to pressure overload

A

Hypertrophy

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13
Q

Powerful predictor of prognosis, morbidity, mortality, and cardiac events once present.

A

LVH and hypertension

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14
Q

HTN is major predisposing cause of stroke. What part of BP is most closely correlated with stroke?

A

Systolic is correlated more with strokes

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15
Q

Retinal changes: 
Narrowing of arterioles (A/V over .50)
A-V nicking- (arteriosclerosis) 
Silver or copper wired appearance
Hemorrhages or exudates
Papilledema

A

signs of HTN

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16
Q

Creatinine
BUN
Potassium levels

A

MUST CHECK IN HTN PATIENTS! (among other things)

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17
Q

Why must you check potassium levels in HTN?

A

Bc will most likely put the pt on a diuretic, which can cause HYPOKALEMIA!*

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18
Q

if LVH seen on EKG, what next tests can you run?

A

Cardiac/echo doppler

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19
Q

DOC for diabetics with HTN

A

ACE inhibitor (or ARB) along with thiazide or CCB

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20
Q

Focus primarily on ______ as this is the most important target for reducing morbidity and mortality.

A

Systolic BP

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21
Q

Initial therapy for most HTN patients…

A

Thiazide diuretics

cost effective, lower systolic BP

22
Q

Diuretics are most potent in…

A

Blacks, elderly and obese

more effective in smokers

23
Q

is Chlorthalidone more or less potent than HCTZ?

A

MORE!

24
Q

Avoid diuretics with…

A

Hypokalemia

Gout

25
Q

Beta blockers are less effective in…

A

Black populations

Elderly

26
Q

New (2008) selective β-blocker with vasodilating properties.
Nitric oxide mediated vasodilation
Loses selectivity in high doses

A

Nebivolol

27
Q

What drug class is preferred for blacks and elderly?

A

calcium channel blockers

28
Q

Progressive renal insufficiency; more common in black populations, especially in the presence of DM.

A

Nephrosclerosis

29
Q

Usually asymptomatic. A.M. headaches may occur.
Late findings include:
-Symptoms related to LVH: Diastolic dysfunction (SOB, DOE).
-Symptoms related to cerebral involvement- *TIA, stroke, hemorrhage.
-Symptoms related to cardiac involvement- MI, angina, HF.

A

Nephrosclerosis

30
Q

DOC for HTN and angina?

A

beta blocker or CCB

31
Q

DOC for HTN and HF?

A

ACE inhibitor

32
Q

DOC for HTN and diabetes? or for HTN and renal dz?

A

ACE inhibitor/ARB

33
Q

Goals of treating HTN?

A

decrease endpoints!

endopoints= MI, Stroke, LVH, PAD, all cause/cardiac mortality, HF and renal failure

34
Q

MI, Stroke, LVH, PAD, all cause/cardiac mortality, HF and renal failure.

A

Endpoints (what you are trying to avoid when treating HTN)

35
Q

Focus primarily on _____ BP as this is the most important target for reducing morbidity and mortality.

A

systolic

36
Q

1 DOC for HTN

A

Thiazide diuretics

37
Q
  • Initial effects via decreased plasma volume

- chronic effects via decreased SVR.

A

Diuretics

38
Q

Avoid in patients with hyponatremia and gout

A

Diuretics

39
Q

More potent in blacks, elderly and obese. More effective in smokers.

A

Diuretics

40
Q

Decrease BP by decreasing CO (-inotropic effect and ↓HR). SVR increases, renin levels decrease.
Less effective in black populations and in elderly.

A

Beta blockers

41
Q

Very useful in patients with HTN and other co-morbid conditions: angina pectoris, post MI→↓mortality, HF→↓mortality, essential tremor, migraine headaches, arrhythmias/sudden death (class II anti-arrhythmic)

A

Beta blockers

42
Q

selective β-blocker with vasodilating properties.
Nitric oxide mediated vasodilation
Loses selectivity in high doses

A

Nebivolol (Bystolic)

43
Q

Mortality and other “end-point” benefits (post MI, HF) applicable primarily to….

A

lipid soluble beta blockers

44
Q

Are beta blockers as successful in LVH regression compared to other treatments?

A

NO

45
Q

May worsen acute HF; but clearly beneficial for patients with chronic compensated & stable HF and low ejection fraction- ↓mortality.
May worsen advanced PAD and rest pain.
Mask signs of hypoglycemia in Type I diabetics.
CNS: Fatigue, nightmares, depression, sexual dysfunction-

A

Beta blockers

46
Q

Inhibit renin-angiotensin-aldosterone system and:
Inhibit Bradykinin degradation
Stimulate vasodilating prostaglandin synthesis.
Useful as initial Rx or when added to other drugs for HTN.

A

ACE inhibitors

47
Q

ACE inhibitors Anti-hypertensive efficacy significantly improved when combined with…

A

diuretic

synergistic effects

48
Q

May be useful for heart failure in patients who cannot take ACEI; do not inhibit bradykinin breakdown.
Renoprotective in diabetics.
Few side effects, and no cough.

A

ARBs

49
Q

Act by peripheral vasodilation
Effective in all demographic groups, and are preferable in blacks and the elderly.
Additional protection against stroke

A

Ca channel blockers

50
Q

In addition to vasodilation these drugs have negative inotropic, chronotropic and dromotropic (slow A-V conduction) effects.
Can exacerbate heart failure and cause SA and AV nodal dysfunction.
Also used as anti-anginals and in Rx of arrhythmias.

A

Nondihydro CCBs

51
Q

Significant vasodilation, reduction in SVR.
Fluid retention and reflex tachycardia occur (role of ß-blockers and diuretics).
Unlikely to cause heart failure and conduction problems (in vivo).
Must use long acting preparations.
2nd or 3rd line agents in diabetics.

A

Dihydro CCBs

52
Q

SE= headaches, periph edema

A

CCBs

Clin Med-Cardio pt 2 (11 decks)

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