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MSII Pharmacology > Unit 4 - Hypertensives > Flashcards

Unit 4 - Hypertensives Flashcards

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?

A

decreased TPR

-increased CO and HR (due to catecholamines)

20
Q

what is the main effect of ACEi and ARBs?

A

decreased TPR (due to decreased AII)

21
Q

what is the main effect of renin inhibitors?

A

decrease renin only (don’t work very well)

22
Q

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

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?

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?

A

can cause impaired glucose tolerance

25
Q

what is the basic mech for ACEi?

A

blocking endothelial ACE from converting AI to AII

-inhibits breakdown of bradykinin (potent vasodilator)

26
Q

what is the basic mech for ARBs?

A

competitive receptor binding of AII to vascular endothelium

27
Q

what three things cause renin production?

A
  1. high CO
  2. high plasma volume
  3. sympathetic catecholamines
28
Q

what are short-acting ACEi? long-acting? prodrug?

A

short: captopril (older, not used much)
long: lisinopril, benazepril, quinapril, ramipril (more typical)
prodrug: enalapril (converted to more active metabolite enalaprilat)

29
Q

what are ARBs?

A

losartan, valsartan, irbesartan

30
Q

what are ASE of ACEi and ARBs?

A
  • cough (only ACEi, not ARBs) due to bradykinin vasodilator
  • hypotension
  • decreased renal function (acute)
  • rarely angioedema
31
Q

contraindications of ACEi and ARBs?

A
  • renal artery stenosis
  • hyperkalemia
  • ACUTE renal failure
  • pregnancy (category X stroke)
32
Q

when are ACEi and ARBs beneficial?

A
  • CHRONIC kidney disease and proteinuria
  • CHF
  • LV remodeling post MI
  • LV hypertrophy
  • may reduce risk of diabetes
33
Q

what are the types of CCBs?

A

dihydropyridines

  • amlodipine
  • nifedipine

non-dihydropyridines

  • verapamil
  • diltiazem
34
Q

other than BP, what can CCBs treat?

A

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
Q

what is the mechanism of CCBs?

A

inhibit contraction of vascular smooth muscles by blocking Ca entry into the cell –> reduced systemic vascular resistance

36
Q

what are side effects of CCBs? which ones are worse, short or long-acting?

A
  • 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
Q

what is the mechanism of BBs?

A

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
Q

what is propranolol? ASE?

A

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
Q

what are metoprolol and atenolol? nadolol and bisoprolol?

A

moderately selective BB (block B1&raquo_space; B2); N/B are longer acting

  • widely used in clinical medicine
  • less likely to cause bronchospasm, hypoglycemia, depression
40
Q

what are carvedilol, labetalol, and esmolol?

A

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
Q

what is the mechanism of terazosin and doxazosin? ASE?

A

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
Q

what is the mechanism of hydralazine and minoxidil?

A

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
Q

what is the mechanism of clonidine, alpha-methyl-dopa, and guanabenz?

A

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
Q

what are side effects of sympathoplegic drugs?

A
  • sedation
  • dry mouth
  • fatigue/depression
  • moderate orthostatic hypotension
  • sudden discontinuation –> severe rebound HTN
45
Q

what is the mechanism of guanethidine? what is this equivalent to?

A

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
Q

what is the mechanism of reserpine? ASE?

A

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
Q

what anti-HTN drug is good if one has an essential tremor?

A

non-cardioselective beta-blockers

MSII Pharmacology (43 decks)

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