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MSII Pharmacology > Unit 4 - Hypertensives > Flashcards

Unit 4 - Hypertensives Flashcards

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1
Q

what are causes of secondary HTN?

A
  1. renal
    - chronic kidney disease (high volume, high renin)
    - renal artery stenosis
  2. drugs
    - ETOH, OCP, and NSAIDs are most common
    - appetite duppressants
    - TCA, MAOi
  3. endocrine
    - pheochromocytoma (uncommon)
    - Cushing’s disease
    - hyperaldosteronism
    - hypo/hyperthyroidism
    - hyperparathyroidism
  4. pulmonary
    - obstructive sleep apnea

usually HTN decreases if treat the underlying cause

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2
Q

what are BP factors that aren’t modifiable?

A
  • genetics (FH of vascular disease in men >50 or women >60)
  • race (African-Americans have higher)
  • gender (females)
  • age
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3
Q

what are BP factors that are modifiable?

A
  • Na+ intake (largest controllable variable)
  • obesity, sedentary
  • heavy ETOH
  • meds
  • physiologic stress
  • diets low in K+ and Ca++
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4
Q

where does end-organ disease occur? in who is it most common?

A

related to extent of BP elevation and duration of HTN; higher in African-Americans and premenopausal women

  • brain (stroke, small vessel disease)
  • eyes (retina)
  • vascular tree (vascular stiffness, atherosclerosis, aneurysm)
  • heart (coronary artery disease, LV hypertrophy)
  • kidneys (nephrosclerosis)
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5
Q

what is the most important, and earliest manifestation of end-organ disease?

A

LV hypertrophy

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6
Q

when is secondary prevention more beneficial?

A

before end-organ damage sets in

  • if only essential HTN w/o damage, then can take slow approach to decreasing HTN
  • if has many end-organ damage (or even just LV hypertrophy), then must take very swift action
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7
Q

in a black VS white patient, what is their essential HTN most likely caused by?

A

black: increased peripheral vascular resistance
white: higher renin

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8
Q

how come most people don’t faint when standing up?

A

catecholamines are released to vasoconstrict and cause tachycardia
-thus the dip in BP is less, and one can compensate once upright

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9
Q

what is the most potent vasoconstrictor and what does it act on?

A

angiotensin II

-acts on small afferent arteriole and larger arteries/veins

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10
Q

what is the basic mech for diuretics?

A

decrease intravascular volume

-initial decrease in BP and CO, but over time CO returns to normal

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11
Q

what is the basic mech for angiotensin blockers?

A

inhibit production/action of AII (vasoconstrictor) to decrease peripheral vascular resistance

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12
Q

what is the basic mech for direct vasodilators?

A

relax vascular smooth muscles, and thereby reduce peripheral vascular resistance

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13
Q

what is the basic mech for sympathoplegic agents?

A

decrease peripheral vascular resistance by decreasing sympathetic tone (beta-blockers, alpha-blockers, and central/peripheral sympathetic blockers)

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14
Q

what is the main effect of diuretics?

A

plasma volume decreases

  • decreased peripheral resistance
  • increased renin (due to decreased renal perfusion)
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15
Q

what is the main effect of central acting sympatholytics and adrenergic blockers?

A

decreased sympathetic system causes decreased CO and TPR

-increased renin (due to decreased CO causing decreased renal perfusion)

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16
Q

what is the main effect of alpha blockers?

A

decreased peripheral resistance (due to vasodilation)

  • increased CO and HR (due to catecholamines)
  • -increased plasma volume (may cause edema and CV mortality)
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17
Q

what is the main effect of beta blockers w/o intrinsic sympathomimetic activity? what is it used for now?

A

decreased CO

  • increased plasma volume
  • -decreased renin (would initially increase due to decreased CO, but then normalizes to decreased renin)

used for AV node blocking in afib

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18
Q

what is the main effect of beta blockers w/ intrinsic sympathomimetic activity? what is it used for now?

A

decreased peripheral resistance

used for heart failure

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19
Q

what is the main effect of arteriolar vasodilators?

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A

decreased TPR

-increased CO and HR (due to catecholamines)

20
Q

what is the main effect of ACEi and ARBs?

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A

decreased TPR (due to decreased AII)

21
Q

what is the main effect of renin inhibitors?

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A

decrease renin only (don’t work very well)

22
Q

what are the most, less, and least commonly used anti-HTNs?

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A

most: thiazides, ACEi, ARBs (angiotensin receptor blockers), CCBs
less: beta-blockers, alpha-blockers
rare: central-acting a2 agonists and adrenergic blocking agents

23
Q

what are high, medium, and low potency diuretics? when are they used?

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A

high: loops (competitively inhibit Na/K/Cl2 transporters in TAL)
- for severe HTN, in setting of CHF or cirrhosis, and with renal insufficiency (GFR < 30-40)
medium: thiazide (inhibits exchange of NaCl in distal ascending loop)
- for most mild-moderate HTN
low: K+ sparing diuretics (inhibit Na+ reabsorption in distal tubule)
- in combo with above 2 to help prevent hypokalemia

24
Q

why are loop and thiazide diuretics contraindicated in DM?

Study These Flashcards
A

can cause impaired glucose tolerance

25
what is the basic mech for ACEi?
blocking endothelial ACE from converting AI to AII | -inhibits breakdown of bradykinin (potent vasodilator)
26
what is the basic mech for ARBs?
competitive receptor binding of AII to vascular endothelium
27
what three things cause renin production?
1. high CO 2. high plasma volume 3. sympathetic catecholamines
28
what are short-acting ACEi? long-acting? prodrug?
short: captopril (older, not used much) long: lisinopril, benazepril, quinapril, ramipril (more typical) prodrug: enalapril (converted to more active metabolite enalaprilat)
29
what are ARBs?
losartan, valsartan, irbesartan
30
what are ASE of ACEi and ARBs?
- cough (only ACEi, not ARBs) due to bradykinin vasodilator - hypotension - decreased renal function (acute) - rarely angioedema
31
contraindications of ACEi and ARBs?
- renal artery stenosis - hyperkalemia - ACUTE renal failure - pregnancy (category X stroke)
32
when are ACEi and ARBs beneficial?
- CHRONIC kidney disease and proteinuria - CHF - LV remodeling post MI - LV hypertrophy - may reduce risk of diabetes
33
what are the types of CCBs?
dihydropyridines - amlodipine - nifedipine non-dihydropyridines - verapamil - diltiazem
34
other than BP, what can CCBs treat?
angina -dihydropyridines: cause reflex tachycardia and may worsen angina by increasing O2 demand -non-DHP: decrease HR (chronotropic benefit), thus decreasing myocardial O2 demand Raynaud's syndrome
35
what is the mechanism of CCBs?
inhibit contraction of vascular smooth muscles by blocking Ca entry into the cell --> reduced systemic vascular resistance
36
what are side effects of CCBs? which ones are worse, short or long-acting?
- constipation and leg edema (biggest ones) - heart failure (non-DHP are negative inotropes) - bradycardia - AV nodal block - reflex tachycardia or dihydropyridines - short-acting CCBs worsen side effects (higher likelihood of hypotension), thus use long-acting CCB
37
what is the mechanism of BBs?
reduced CO (primary reason for BP lowering) - inhibiting renin release - reducing NE release from neurons - decreasing central vasomotor activity (less sympathetic tone) - overall, very modest BP improvement from BBs
38
what is propranolol? ASE?
nonselective BB - decreased exercise capacity - bronchospasm - bradycardia (negative chronotrope) - CHF (negative inotrope) - masks symptoms of hypoglycemia in diabetics - crosses BBB and can cause depression - worsening symptoms of peripheral vascular disease
39
what are metoprolol and atenolol? nadolol and bisoprolol?
moderately selective BB (block B1 >> B2); N/B are longer acting - widely used in clinical medicine - less likely to cause bronchospasm, hypoglycemia, depression
40
what are carvedilol, labetalol, and esmolol?
unique BB with sympathomimetic properties - potent anti-HTN used in ICU and CCU for BP control - -hypertensive urgency = labetalol - -acute coronary syndromes, CHF, HTN = carvedilol - -short half-life, for AV nodal blocking in unstable patients = esmolol
41
what is the mechanism of terazosin and doxazosin? ASE?
a1 antagonists - reduce vascular resistance by blocking vascular smooth muscles - ASE: orthostatic hypotension, fluid retention, worsening angina (secondary to reflux tachycardia) - -more likely to cause cardiac complications, thus only 2nd tier
42
what is the mechanism of hydralazine and minoxidil?
vasodilators (relax smooth muscles of peripheral arterioles) - M: used for refractory HTN and men with hair loss (rogaine) - H: used IV in ICUs for acute HTN urgency or chronic CHF
43
what is the mechanism of clonidine, alpha-methyl-dopa, and guanabenz?
central acting sympathoplegic drugs - stimulation of a2 adrenergic receptors reducing sympathetic outflow from vasomotor centers in brainstem - -decreased sympathetic tone inhibits renin release - clonidine: only one routinely used - AMD: used in pregnancy
44
what are side effects of sympathoplegic drugs?
- sedation - dry mouth - fatigue/depression - moderate orthostatic hypotension - sudden discontinuation --> severe rebound HTN
45
what is the mechanism of guanethidine? what is this equivalent to?
ganglion (adrenergic neuron) blocking agent - reduce BP by blocking release of NE from post-ganglionic symapthetic nerve terminals - pharmacologic "sympathectomy" that leads to postural hypotension, diarrhea, and impaired ejaculation
46
what is the mechanism of reserpine? ASE?
ganglion-blocking agent - depletes NE, DA, and 5-HT in central and peripheral nerves - decreases CO and systemic vascular resistance - ASE: sedation, mental depression, parkinsonism
47
what anti-HTN drug is good if one has an essential tremor?
non-cardioselective beta-blockers

MSII Pharmacology (43 decks)

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