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Drug Action I > Block 2 - Anti-HTN Drugs Pharm > Flashcards

Block 2 - Anti-HTN Drugs Pharm Flashcards

1
Q

What is BP? Why is it important?

A

Mathematical product of CO and total peripheral resistance (TPR)

BP/MAP → CO x TPR

The sustain a consistent amount of blood to maintain perfusion

Systemic arterial pressure is BP while venous system is low pressure system

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2
Q

Why do we use arterial to calculate BP?

A

Higher pressure system compared to veins

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2
Q

Why do we use arterial to calculate BP?

A

Higher pressure system compared to veins

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3
Q

How do you calculate cardiac output?

A

Stroke volume x HR

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4
Q

What is mean arterial pressure?

A

BP/MAP → CO x TPR

Average pressure in arterial system during ventricular contraction and relaxation → good indicator of tissue perfusion

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5
Q

What are the short term mechanisms of regulating BP? What are its components?

A
  1. Neural mechanisms: ANS (para and sym)
  2. Humoral mechanism: RAAS and vasopressin (ADH)
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6
Q

What neural mechanism is most predominate in the heart?

A

Sympathetic

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7
Q

What are the long term mechanisms of regulating BP?

A

Regulation of ECF volume by the kidneys

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8
Q

What is HTN?

A

Consistent elevation of arterial BP above the normal range

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9
Q

What are the types of HTN?

A

Primary and secondary

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10
Q

What is primary HTN?

A
  1. 90% of cases
  2. Essential or idiopathic HTN (cause is uncertain)
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11
Q

What is secondary HTN?

A
  1. 5-10% of cases
  2. Cause is clearly defined
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12
Q

What abnormalities of pathophysiology that may cause HTN?

A
  1. Malfunctions in RAAS
  2. Over-activity of SNS
  3. Disturbances in Na+, Ca2+, and natriuretic hormone
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13
Q

Why is RAAS important?

A
  1. Most influential contributor to the regulation of BP
  2. Influences vascular tone and SNS activity
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14
Q

What are the Sympatholytics used for the RAAS?

A

ß blockers
a2 agonists

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15
Q

What are some vasodilators used for the RAAS?

A
  1. CCB
  2. a1 blockers
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16
Q

What are the types of ACEIs?

A
  1. Captopril
  2. Enalapril (Vasotec)
  3. Lisinopril (Prinivil, Zestril)
  4. Benazepril (Lontensin)
  5. Quinapril (Accupril)
  6. Fosinopril (Monopril)
  7. Trandolapril
  8. Perindopril
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17
Q

What -prils are sulfhydryl containing?

A

Captopril

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18
Q

What -prils are dicarboxyl containing?

A

Enalapril, Lisinopril, Benazepril, Ramipril

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19
Q

What -pril is phosphorous containing?

A

Fosinopril

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20
Q

How are ACEIs similar?

A
  1. MOA
  2. Indications
  3. ADRs
  4. CIs
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21
Q

How do ACEis differ from one another?

A
  1. Potency
  2. PK
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22
Q

What ACEis are NOT prodrugs?

A

Captopril and Lisinopril

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23
Q

What is the pharmacological action of ACEis in HTN?

A

Cause vasodilation → lover PVR → reduce BP

Reduce aldosteron secretion → decrease Na+ and water retention → Reduce BP

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24
Q

What is the pharmacological action of ACEis in Left ventricular systolic dysfunction (HF)?

A

Reduce after load and systolic wall stress → CO and cardiac index increase

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25
Q

What is the pharmacological action of ACEis in DM and Renal failure?

A

ACEI are reno protective and delay the progression of renal disease in diabetic neuropathy

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26
Q

What is the pharmacological action of ACEis in DM and Renal failure?

A
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27
Q

Why is ACEis considered reno protective?

A

Through increased glomerular capillary pressure inducing glomerular injury, ACEis reduce parameter by decreasing arterial BP and dilating renal referent arterioles

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28
Q

What are the indications of ACEis?

A

HTN, LVSD, Acute MI, Diabetic neuropathy

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29
Q

What ACEis ADRs?

A
  1. Hypotension
  2. Cough
  3. Wheezing
  4. Angioedema
  5. Hyperkalemia
  6. Acute Renal failure
  7. Skin rash
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30
Q

Why does ACEis cause coughing?

A

Accumulation of BK, substance P, and/or PG in lungs

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31
Q

What are ACEis BBI?

A
  1. Antacids reduce absorption
  2. NSAIDs reduce AHTN response
  3. K+ sparing diuretic and K+ supplement → exacerbated hyperkalemia
32
Q

What are the types of ARBS?

A
  1. Losartan (Cozaar)
  2. Valsartan (Diovan)
  3. Candesartan (Atacand)
  4. Olmesartan (Benicar)
  5. Irbesartan (Avapro)
  6. Telmisartan (Micardis)
  7. Eprosartan
33
Q

What is the MOA of ARBs?

A

Angiotensin II → AT1 receptor in vascular smooth muscle → ARB is AT1&raquo_space;> AT2 receptors → slow dissociation kinetics → receptor internalization

34
Q

What are the ADRs of ARBs?

A
  1. Less angioedema and cough risk than ACEIs
  2. Hypotension, oliguria, azotemia, acute renal failure
  3. Hyperkalemia (CI with K+ supplement and sparing diureics)
35
Q

Why are ARBs slightly more favorable than ACEIs?

A
  1. ARBs increase Arc receptor activation → vasodilation
  2. Greater AT1 inhibitor effect than ACEIs
  3. Favorable adverse-effect profile
  4. ACEIs increase BK → coughing
    (ACEIs don’t inhibit alternative non-ACE angiotensin II generating pathways)
36
Q

Why are ACEIs used to treat HTN?

A

Prevents angiotensin 2 from causing vasodilation

37
Q

Which drugs is more likely to cause cough? Why?

A

ACEis due to accumulation of BK

38
Q

Which receptors do ARB selectively bind to? Why?

A

Strongly binds to receptor leading to longer DOA and slow dissociation

39
Q

Why do ACEIs cause hyperkalemia and acute renal injury?

39
Q

What are approved indications for ARBs? Specific drugs?

A

All ARBs → HTN
Avapro and Cozaar → Diabetic neuropathy
Cozaar → Stroke prophylaxis
Diovan → HF

39
Q

What are the pharmacological action of ARBs?

A
  1. Block the effects of AT 2 decreasing → vascular contraction, aldosterone secretion, vasopressin release, catecholamine release from adrenal decreasing sympathetic tone and neurotransmission
40
Q

What is the role to Ca2+ in the body?

A
  1. Excitation, contractions of cardiac, skeletal, and smooth muscle, enzyme activity and coagulation
  2. Stabilizes cell membranes
  3. Neurotransmitters release from neurons
  4. Hormones release from endocrine glands
41
Q

What causes Ca2+ influx?

A

L-type and to some extent T-type of voltage gated Ca2+ channels promotes vascular smooth muscle contraction

42
Q

Describe how Ca2+ cause contractions in vascular smooth muscle Figure

43
Q

What are the types of CCB DHP?

A
  1. Nifedipine (Adalat CC, Procardia XL)
  2. Amlodipine (Norvasc)
  3. Felodipine (Plendil)
  4. Isradipine
  5. Lacidipine
  6. Lercanidipine
  7. Nicardipine
  8. Nisoldipine
44
Q

What is the MOA of DHP?

A

(Long lasting) Block Ca2+ effects on vascular smooth muscles causing relaxation → peripheral vasodilation

Little effect on myocardium

45
Q

What are examples of non-DHP?

A

Phenylalkymine
Benzothiazepine

46
Q

What are examples of phenylakylamine?

A

Verapamil (Calan, Calan SR)

47
Q

What are examples of benzothiazepine?

A

Diltiazem (Cardizem, Cartia XT, Dilacor XR, Dilt-XR, Taztia XT, Tiazac)

48
Q

What is the MOA of non-DHP?

A

Block Ca2+ effects on SA and AV nodes and cardiac cells → decreasing cardiac conduction and contractility

Less potent vasodilator

49
Q

What mechanism that blocks Ca2+ influx?

A

Block the voltage gated Ca2+ channels predominately the L and T type → prevent entry Ca2+ into vascular smooth muscles and heart

51
Q

How does CCBs effect the cardiac tissues? DHP?

A

Negative inotropic, chronotropic, dromotropic effects

DHP: Negative inotropic is off set by baroreflex-mediated increased sympathetic tone

52
Q

How does CCBs effect the vascular smooth muscle? All CCBs?

A

Most sensitive

Relax vascular smooth muscles → vasodilation → reduction of BP

All CCBs: Arterial dilation&raquo_space;> venous → don’t significantly affect cardiac preload

53
Q

How does CCBs effect other smooth muscle besides vascular?

A

Relaxes bronchial, GI, and uterine

54
Q

What are DHP ADRs? How are they products of its MOA?

A
  1. HA, flushing, lightheadedness, hypotension → Peripheral vasodilation
  2. Reflex tachycardia and palpitations → secondary to SNS activation
  3. Nifedipine SR → lessen reflex tachycardia
  4. Peripheral edema
55
Q

What are the non-DHP ADRs?

A
  1. Bradycardia, AV conduction delay or block and cardiac arrest → direct cariac effects
  2. Constipation → Verapamil
  3. Vasodilation effects &laquo_space;DHP
56
Q

What are the indictions of CCBs?

A

HTN, Arrhythmia, Agina, Migranes

57
Q

What are the most popular non-selective 1st gen beta blockers?

A

Propranolol (Inderal)

58
Q

What are the most popular 2nd gen beta-1 blockers?

A

Atenolol (Tenormin)
Bisoprolol (Zebeta)
Metoprolol (Toprol XL)

59
Q

What are the most popular non-selective 3rd gen beta blockers?

A

Cavedilol (Coreg)
Labetalol (Normodyne)

60
Q

What are the most popular selective 3rd gen beta-1 blockers?

A

Nebivolol (Bystolic)

61
Q

What are the CV indications of beta blockers?

A

HTN, Ischemic heart disease, arrhythmias

62
Q

What are the non-CV uses of beta blockers?

A

Anxiety, hyperthyroidism

63
Q

What are the pharmacological effects of beta blockers on the heart? How?

A
  1. Decrease BP (suppress renin, negative inotropic and chronotropic effects)
  2. Reduce myocardial o2 demand on heart (negative inotropic and chronotropic)
  3. Decrease conduction velocity (slowed AV conduction with increased PR interval)
  4. Decrease secretion of renin in kidney (Suppress RAAS)
64
Q

What are the types of a1-antagonists used for the heart?

A
  1. Prazosin (Minipress)
  2. Terazosin (Hytrin)
  3. Doxazosin (Candura)
  4. Tamsulosin (Flomax)
65
Q

What is the pharmacological action of a1 blockers?

A

Vasodilation → Decreases arteriolar resistance and increase venous capacitance → stimulates sympathetically mediated reflex (increase HR and renin activity)

66
Q

Indication for a1 blockers?

A
  1. HTN (not as mono therapy)
  2. Pheochromocytoma
67
Q

What are the ADR of a1 blockers?

A
  1. First dose phenomenon
  2. Orthostatic hypotension
68
Q

What type of class is Clonidine?

A

Catapress is a centrally acting antihypertensive

69
Q

What is the MOA of Catapres?

A
  1. Stimulate ɑ2 (ɑ2A subtype) adrenergic receptors in the brainstem → Decrease sympathetic outflow from CNS and NE release in periphery
70
Q

What happens when a patient takes high doses of clonidine?

A

Activation of ɑ2 (ɑ2A subtype) receptors on vascular smooth muscle → vasoconstriction

71
Q

What are the ADRs of Catapres?

A
  1. Sedation
  2. Xerostomia
  3. Orthostatic hypotension
  4. ED
72
Q

What drug class in Hydralazine? Effects of use?

A

Apresoline is a direct vasodilator that releases arteriolar but not smooth muscle

  1. Associated with SNS reflexes
  2. Combined with sympatholytics and diuretics
73
Q

ADRs of Apresoline?

A

Severe hypertension

74
Q

What is the CIs of using ACEI, ARB, and renin inhibitors?

A

Second and third trimester of pregnancy due to FETAL TOXICITY

Discontinue asap when pregnancy is detected

75
Q

What is the CIs of using Nifedipine?

A
  1. IV admin and immediate release formulation
  2. Increased risk of MI, stroke, and arrhythmias
76
Q

What happens if beta-blockers aren’t slowly tapered?

A
  1. May cause exacerbations of angina or MI → ascetic heart disease
  2. Discontinues drug → reduce dosage over 1-2 weeks

Drug Action I (32 decks)

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