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Block 9; Week 1 & 2-M > Anti-hypertensive Therapy > Flashcards

Anti-hypertensive Therapy Flashcards

1
Q

What are the BP classifications for Normal, Pre-HTN, HTN Stage 1, HTN Stage 2?

A 
Normal: less than 120/80
Pre-HTN: 120/180-139/89
HTN Stage 1: 140/90-159/99
HTN Stage 2: 160/100 & above
**NOTE: if the systolic or diastolic requirement is met-->belong to that stage
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2
Q

What are the therapeutic goals for patients with HTN that are less than 60 yo?

A

less than 140/90

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3
Q

What are the therapeutic goals for patients with HTN that are over 60 yo?

A

less than 150/90

guidelines loosened for this pop b/c of the side effects elderly people were experiencing.

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4
Q

What are the therapeutic goals for patients with HTN also have kidney disease or diabetes?

A

less than 140/90

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5
Q

WHat is essential HTN? What % of HTN patients belong in this category?

A

cause isn’t known

85-90%

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6
Q

What are some causes of secondary HTN?

A 
Sleep apnea
Drug-induced or related causes
Chronic kidney disease
Primary aldosteronism
Renovascular disease
Chronic steroid therapy and Cushing’s syndrome
Pheochromocytoma
Coarctation of the aorta
Thyroid or parathyroid disease
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7
Q

What are some contributing factors to essential HTN?

A 
Obesity
Stress
Lack of exercise
Diet (excess dietary salt)
Alcohol intake
Smoking
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8
Q

What is the prevalence of HTN? Gender difference? Age difference?

A

30% of adults
men & women equal
more common in elderly

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9
Q

Which ethnicity has the highest rates of HTN?

A

African AMericans–42%

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10
Q

Are people aware of their HTN? Which ethnicity & age group is least aware?

A

83% of people with HTN were aware, 76% of them are on meds

Asians & young people are least aware

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11
Q

What are some complications of HTN?

A

risk of cardiovascular disease, renal damage, retinal damage increases with HTN
risk double for heart disease w/ each increase of 20/10 mmHg

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12
Q

What is the treatment strategy for HTN?

A

Lifestyle modification

Antihypertensive drugs

Follow-up and monitoring

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13
Q

What are some lifestyle modifications used in the treatment of HTN?

A 
Reduce weight to normal BMI, <25
DASH eating plan (8-14 mmHg)
Reduce your salt intake! (2-8 mmHg)
Increase your activity! (4-9 mmHg)
Stop smoking & reduce your drinking.
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14
Q

For each 10 kg loss in weight…how much reduction do you get in your systolic BP?

A

5-20 mmHg

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15
Q

What is the DASH diet?

A

similar to Mediterranean
fruits, veggies, low fat dairy, low salt
whole grains, poultry, fish, nuts
LESS red meat, sugar, saturated fat

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16
Q

What is the formula for mean arterial pressure?

A

MAP=CO X PVR

CO=HR X SV

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17
Q

What are some factors that affect cardiac output?

A

Heart rate & contractility

  • Autonomic Nervous system
  • Blood Volume
  • Venous Tone
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18
Q

What are some factors that can affect peripheral vascular resistance?

A

determined by the radius of resistance of arteries & arterioles
circulating factors: NE, ANG II, Sympathetic Nervous System, Local Reactions

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19
Q

T/F Blocking the NE receptor will increase BP.

A

False. Will decrease by decreasing PVR.

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20
Q

GIve the different types of antihypertensive medications.

A
  1. Diuretics
  2. Agents affecting adrenergic function
  3. vasodilators
  4. RAAS target
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21
Q

What are the 3 types of diuretics?

A

Thiazides
Loop Diuretics
Potassium sparing diuretics

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22
Q

Which of the diuretics are most commonly used? What are 2 examples?

A

thiazides

ex: chlorothiazide, hydrochlorothiazide

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23
Q

Give 3 examples of loop diuretics? When are they usu used?

A

Ex: Furosemide, bumetanide, ethacrynic acid

used for severe HTN & heart failure

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24
Q

Give 3 examples of potassium sparing diuretics. What is the usual indication for this?

A

spironolactone, triamterene, amiloride

Reduction in heart failure mortality

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25
Q

What is the initial effect of diuretics? Effect after 6-8 weeks?

A

Initially: increase excretion of sodium & water
decrease blood volume–decrease CO–>decrease MAP
After some time: CO returns to normal, but PVR decreases (vasodilation)

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26
Q

How much do diuretics usu lower BP?

A

usu lower by 10-15 mmHg

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27
Q

What are some possible toxic effects of diuretics?

A

K+ Depletion (except K+-sparing diuretics)
Can be minimized by limiting Na+ intake

Mg2+ depletion, impaired glucose tolerance, and increase serum lipid concentration

Gout (increased uric acid)

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28
Q

What are the targets of drugs affecting the adrenergic system?

A

sympathetic nerves release NE that act on beta 1 receptors in the heart & alpha 1 receptors in blood vessels.
beta 1: causes increase in contractility, HR, & conduction velocity. Increase in CO, MAP.
alpha 1: increase in smooth muscle contraction in bv–>increase in PVR–>increase in MAP.

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29
Q

WHat is a good target to reduce NE release from sympathetic stimulation?

A

alpha 2

30
Q

Give 4 categories of drugs that decrease adrenergic function.

A
  1. Agents that prevent adrenergic transmission.
  2. selective alpha 1 blockers
  3. beta adrenergic blockers
  4. agents directly affecting the CNS
31
Q

What is an example of an agent preventing adrenergic transmission? What is its MOA?

A

depletes neurotransmitters (e.g. NE) in the nerve endings in the brain and periphery.
Main effects: depress SNS function centrally and peripherally  decreased HR, contractility and PVR
Ex: reserpine
used infrequently b/c of the side effects

32
Q

What are the negative side effects of reserpine? What are its pharmacokinetics?

A

Adverse effects: depression, insomnia, nightmares, ulcers, diarrhea, abdominal cramping, nasal stuffiness, orthostatic hypotension, dry mouth, impotence
Pharmacokinetics: onset is slow and full effect is seen in weeks

33
Q

What are some examples of alpha 1 blockers? What is its mechanism? WHen is this commonly used?

A

(prazosin, terazosin, doxazosin)

Mechanism: block 1 receptors in vasculature

Main effects: decreased PVR  decrease BP
stage 1 & 2 HTN used in conjunction w/ diuretics & beta blockers

34
Q

What are the adverse effects of alpha 1 blockers?

A

Adverse effects: 1st dose phenomenon, fluid retention, dizziness, headache
1st dose: when you first take it can have a dramatic reduction in BP…need to take before bed or something not while driving in your car.

35
Q

What are the 2 types of beta blockers?

A

nonselective, blocks beta 1 & beta2

cardioselective for beta 1

36
Q

What is the MOA for beta blockers?

A

Block cardiac beta1 receptors –> lower CO

Block renal beta 1 receptors –> lower renin, lower PVR

37
Q

Describe the characteristics of propranolol.

A

nonselective beta blocker
decrease HR
use in stage 1 & 2 HTN

38
Q

What are possible adverse effects of propranolol? Bad drug interactions?

A

bradycardia, depression, aggravates asthma (beta2 blockade in airways)

Drug Interactions: verapamil, diltiazem, digitalis (possible AV Block)

39
Q

What are the more commonly used beta blockers?

A

Metoprolol & Atenolol

Cardioselective
Most widely used β-blockers for hypertension
More selective for β1 vs. β2 (less bronco constriction)

40
Q

What is a good med to use for hypertensive emergencies?

A

Labetalol

Combined nonselective beta and alpha-1 blocker. Beta blocking action is more prominent

41
Q

What are some agents that act directly on the CNS? What is its mechanism?

A

alpha-methyldopa
clonidine
become alpha 2 agonists. Suppresses sympathetic output.
Effect: decreases PVR & HR

42
Q

What is the clinical indication for methyldopa? for clonidine? Adverse effects?

A

Methyldopa: HTN during pregnancy
Clonidine: Stage 1 & 2 HTN
Adverse effects: sedation, drowsiness, dry mouth, impotence, bradycardia, withdrawal syndrome (rebound HTN)

43
Q

What are 3 types of vasodilator drugs?

A
  1. calcium channel blockers
  2. direct acting vasodilators
  3. potassium channel openers
44
Q

What are 3 types of calcium channel blockers & examples of each? MOA?

A

mechanism: inhibit Ca2+ entry through L-type voltage gated Ca2+ channels

Phenylalkylamines: verapamil

Benzothiazepines: diltiazem

Dihydropyridines: amlodipine

45
Q

What is the category of meds that amlodipine belongs to? What is its MOA ?

A

calcium channel blocker, dihydropyridine
blocks vascular calcium channels
vasodilation–>lower PVR–>lower BP
Used for HTN & angina, effective in AA pop.

46
Q

What are the adverse effects of amlodipine?

A

headache, flushing, nausea, dizziness, ankle edema, reflex tachycardia

47
Q

What category do verapamil & diltiazem belong to?

A 
calcium channel blockers
verapamil-phelyalkylamine
diltiazem-benzothiazepine
MOA: block calcium in vasculature, heart muscle, AV node
Vasodilation-->lower PVR-->lower mAP
48
Q

What are the adverse effects &contraindications for verapamil & diltiazem?

A

headache, flushing, nausea, dizziness, ankle edema
contraindications: Caution for AV block when used with beta blockers, and digitalis (amlodipine does not have this effect)

49
Q

Does amlodipine carry increased risk for AV block, like verapamil & diltiazem?

A

Nope.

50
Q

What is a direct acting vasodilator? What is its MOA?

A

sodium nitroprusside
NO donor-vasodilator
vasodilation–>lower PVR–> lower BP

51
Q

What are possible adverse effects of sodium nitroprusside? PHarmacokinetics? What are its indications?

A

Adverse Effects: Reflex tachycardia, severe hypotension, possible cyanide poisoning

Pharmacokinetics: rapid acting, i.v. drip, short plasma half-life

Use: Hypertensive emergencies

52
Q

What is an example of a potassium channel opener? How does it work?

A 
minoxidil
Opens K+ channels
Smooth muscle hyperpolarization
smooth muscle relaxation
arterial dilation
decreased PVR
decreased BP
**adverse effect: hair growth
53
Q

What are 3 categories of drugs affecting the RAAS system?

A
  1. ACE inhibitors
  2. Angiotensin II Receptor Blockers
  3. Renin Inhibitors
54
Q

What are some examples of ACE inhibitors? What is its MOA?

A

(captopril, enalapril, lisinopril, rampiril)

Mechanism: inhibit ACE –> lower circulating Ang II Levels –>decreased PVR –>decreased BP

55
Q

Review the RAAS system.

A

Liver produces angiotensinogen.
Decreased renal perfusion (decreased BP) sensed by juxtaglomerular apparatus. Renin released.
Angiotensinogen + Renin–>Ang I.
Ang I + ACE–>Ang II
Ang II increases simp activity, tubular Na+ & H2O reabsorption, aldosterone secretion
vasoconstriction, ADH secretion
BP goes up mainly b/c of water & salt retention

56
Q

Adverse effects of ACE inhibitors? Indication?

A

Adverse effects: skin rash, taste, cough, hyperkalemia (decreased K+ excretion from aldosterone)

Use: Stage 1 and 2 HT; also for congestive heart failure

57
Q

What is the MOA of aldosterone & ADH?

A

Aldosterone: tubular Na+ & H2O retention. K+ excretion
ADH: increases collecting duct absorption

58
Q

T/F ACE inhibitors have negative effects on plasma lipids, glucose.

A

False.

59
Q

Which pop should ACE inhibitors be used in? Not be used in?

A

Should be used in: patients with diabetes

Not used in: pregnancy, less effective in AA

60
Q

What are different types of ARBs? What is its MOA?

A

(losartan, valsartan, irbesartan)

Mechanism: selectively block Ang II AT-1 receptor –> decrease PVR –> decrease BP

61
Q

Negative effects of ARBs?

A

skin rash, taste, hyperkalemia

fetal toxicity

62
Q

What’s the deal with renin inhibitors? Contraindications?

A

new drug, prevents the formation of Ang I
Aliskiren

Equally effective (or better) at lowering BP as ACE Inhibitors and ARBs.

Reported side effects: Diarrhea, stomach pain, heartburn, cough, rash, dizziness, headache, back pain. Fetal Toxicity.

Contraindicated for use with ARBs or ACE inhibitors in patients with diabetes and/or CKD

63
Q

What is resistant HTN?

A

BP > 140/90 mmHg (130/80 with diabetes and CKD) for patients prescribed 3 or more antihypertensive medications at optimal doses
or
BP controlled with 4 or more antihypertensive drugs

64
Q

What % of HTN patients have resistant HTN?

A

up to 40%

65
Q

What are the adherence rates for HTN treatment? How are adherence rates for lifestyle mod ?

A

Meds: 20-80% adherence
Lifestyle: 10-20% adherence

66
Q

What appear to be the med combos/strategies that elicit the highest adherence rates?

A

Adherence is higher for single drug and/or lower number of doses per day

Adherence may be higher for RAS drugs and Ca2+ channel blockers vs. diuretics and β-blockers.

67
Q

What is the BP goal for patients with CKD or diabetes?

A

less than 140/90

68
Q

With patients who have CKD…what are the meds used?

A

ACEI or ARB alone or in combo w/ another class

69
Q

With patients who have diabetes w/o CKD…what is the dosing strategy?

A

thiazide-type diuretic or ACEI or ARB or CCB
If African American: thiazide type diuretic or CCB
**same for all other HTN patients

70
Q

What are 3 titration dosing strategies?

A
  1. Max dose of 1st med before adding a second
  2. Add second med before reaching max dose of 1st
  3. Start with 2 meds @ the beginning

Block 9; Week 1 & 2-M (10 decks)

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