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Cardiovascular System > Hypertension - Pharmacology > Flashcards

Hypertension - Pharmacology Flashcards

1
Q

Increasing blood pressure is associated with a progressive increase in the risk of _____ and _______ _____

A

Stroke; cardiovascular disease

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2
Q

As blood pressure rises, does HTN risk rise linearly or exponentially?

A

exponentially

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3
Q

Hypertension is most common in _____ _____

A

older women

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4
Q

Of those with uncontrolled hypertension, what percentage are aware and treated? Aware and untreated? Unaware?

What percentage of hypertensive individuals have controlled HTN?

A

Aware/treated: 44.8%

Aware/Untreated: 15.8%

Unaware: 39.4%

Controlled: 46.5%

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5
Q

What are the JNC 8 recommendations for target SBP and DBP in individuals…

≥60 years

<60 years

> 18 years with chronic kidney disease

> 18 years with diabetes

A

≥60 years: less than 150/90

<60 years: less than 140/90

> 18 years with chronic kidney disease: less than 140/90

> 18 years with diabetes: less than 140/90

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6
Q

Classifications of ANtihypertensive Drugs

A

Vasodilators

Agents affecting adrenergic function

Agents affecting RAS

Diuretics

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7
Q

What are the direct arterial vasodilators?

A
  1. Hydralazine
  2. Minoxidil
  3. Diazoxide
  4. Nitroprusside
  5. Fenoldopam
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8
Q

How do direct arterial vasodilators cause antihypertensive effect?

A

Cause smooth muscle relaxation of vessels

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9
Q

How can vasodilators lead to increased heart rate? How is this counteracted?

A
  • Potent reductions in perfusion pressure activate baroreceptor reflexes
  • Baroreceptor activation leads to compensatory increase in sympathetic outflow - reflex release of renin
  • Counteract with concurrent ß-blocker
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10
Q

What blood pressure is used to determine a hypertensive crisis?

What is the best way to treat this (duration)?

A

BP> 180/120

Gradual injection of vasodilators (nitroprusside) to allow organs to adjust to change in blood pressure

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11
Q

What is the difference between hypertensive urgency and a hypertensive emergency?

A

Hypertensive urgency - elevated BP with no acute or progressing organ injury

Hypertensive emergency - Acute or progressing target-organ damage

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12
Q

What pathway to nitric oxide drugs activate?

A

Guanylate cyclase pathway leading to increase in cGMP and protein kinase G → vasodilation

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13
Q

Why don’t you use nitroprusside for long periods?

A

Can cause damage to kidneys with cyanide toxicity

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14
Q

What are some adverse effects of direct arterial vasodilators?

How are these adverse effects reduced?

A
  • Adverse effects
    • Sodium/water retention
    • Tachycardia and angina
    • Hydralazine can cause lupus like syndrome
    • Minoxidil can cause hair growth (not used with women)
  • Use with diuretic (thiazide) and ß-blocker to reduce fluid retention and reflex tachycardia
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15
Q

Why do calcium channel blockers cause less reflex tachycardia than vasodilators?

A

Smaller HR increase due to the calcium channels that exist on the heart (CCBs don’t only affect vascular system)

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16
Q

What are the calcium channel blockers?

A
  • Nifedipine
  • Diltiazem
  • Verapamil
  • Amlodipine
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17
Q

Calcium Channel blockers - what are the differences between dihydropyridines and non-dihydropyridines?

A
  • Dihydropyridines
    • Baroreceptor mediated reflex tachycardia due to potent vasodilating effects
    • Do not alter conduction through AV node
  • Non-dihydropyridines decrease HR and slow AV node conduction
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18
Q

What are the two non-dihydropyridines?

A

Verapamil and diltiazem

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19
Q

What are some CCB side effects?

A
  • Flushing
  • Headaches
  • Negative inotropic effect(V>D>N)
  • Constipation (V>D or N)
  • Decreased AV conduction (V = D)
  • Edema (N>V or D)
  • Refractoriness (N)

* N = nifedipine, V = verapamil, D = Diltiazem

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20
Q

Which SNS receptors are responsible for the following…

  • Increased contractility
  • Increased HR
  • Vasoconstriction
  • Vasodilation
  • Bronchodilation
  • Increased renin
A

Increased contractility: beta-1
Increased HR: beta-1
Vasoconstriction: alpha-1
Vasodilation: beta-2
Bronchodilation: beta-2
Increased renin: alpha-1, beta-1

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21
Q

What are the α1/α2 blockers and what do they do?

A

Phenoxybenzamine and Phentolamine

Inhibit smooth muscle catecholamine uptake in peripheral vasculature: Vasodilation and BP lowering

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22
Q

What are the α1 blockers and how are they different than α1/α2 blockers?

A

Prazosin, Terazosin, and Doxazosin

  • Smaller increase in heart rate
  • Arterial vasodilation
  • No stimulation in Renin release
  • Does not block α2 thus NE can inhibit its own release
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23
Q

What is the first dose effect of α1 blockers? How do you minimize this effect?

A
  • Orthostatic hypotension
  • Transient dizziness, faintness, palpitations, syncope (w/in 1-3 hours of 1st dose)
  • Reflex tachycardia
  • First dose at bedtime to minimize effect
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24
Q

What are α1/ß1/ß2 blockers and how are they different than α1 blockers in terms of adverse effects?

A

Carvedilol and Labetalol - less orthostatic hypotension and headaches (mild)

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25
Q

What are the ß-blockers?

A

Propanalol (ß1 and ß2)

Metropolol (ß1)

Atenolol (ß1)

Labetalol (ß1/ß2/α1)

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26
Q

What are the locations and functions of ß1 receptors? ß2 receptors?

A
  • ß1 receptors
    • found in the heart and the kidney
    • stimulation increases heart rate, contractility and renin release
  • ß2 receptors
    • Found in the lungs, liver, pancrease, arterioloar smooth muscle
    • Stimulation causes bronchodilation and vasodilation and mediates insulin secreation and glycogenolysis
27
Q

ß-blockers work better in _____ ______ and in _____ _____ when combined with a diuretic

A

young adults; older adults

28
Q

Low renin levels in a patient make them ____ (more/less) responsive to beta blockers

A

less

29
Q

Which ß blockers have greater affinity for ß1 receptors than ß2 receptors and how does this relate to their dose?

A

Metropolol and atenolol - cardioselective ß-blockers

These drugs inhibit ß1 receptors at low to moderate doses

At higher doses they block ß2 blockers

30
Q

In what types of patients are metroprolol and atenolol safer to use?

A

Safer in patients with bronchospastic disease, peripheral arterial disease, and diabetes

Generally preferred ß-blockers for hypertension

31
Q

What are some potential adverse effects of ß-blockers?

A
  • Glucose intolerance
  • Bradycardia
  • Bronchospasm
  • Incresed TGs and HDL
  • CNS - depression, fatigue, and sleep disturbance
  • Reduced CO
  • Impotence
  • Exercise intolerance
32
Q

What are the central α2 agonists and what do they do?

A

Clonidine, Guanabenze and α-methyldopa

Stimulate α-2 adrenergic receptors in the brain which reduces sympatetic outflow from the brains vasomotor center and increase vagal tone

33
Q

What are the central α2 agonist’s adverse effects?

A
  • Sodium/water retention
  • Abrupt discontinuation may cause rebound hypertension
  • Depression
  • Orthostatic hypotension
  • Dizziness
34
Q

What are specific side effects associated with clonidine and methyldopa?

A

Clonidine - anticholinergic side effects

Methyldopa - can cause hepatitis hemolytic anemia

35
Q

What are the neuronal and ganglionic blockers?

A

Guanethidine

Guanadrel

Reserpine

Trimethaphan (ganglionic)

36
Q

What are some adverse effects for Reserpine and Guanethidine and how do you avoid these side effects?

A
  • Sedation (reserpine)
  • Depression (reserpine)
  • Decreased CO
  • Na+/H2O retention
  • Increased gastric acid secretion (reserpine)
  • Diarrhea
  • Bradycardia
  • Orthostatic Hypotension (Guanethidine)

* Use with diurtic (thiazide) to avoid fluid retention

37
Q

What are the diuretics?

A

Hydrochlorothiazide

Furosemide

Amiloride

38
Q

What are the causes and consequences of initial diuretic use?

What happens with chronic use?

A
  • Initial (BP drop)
    • Reduced plasma and stroke volume decreases CO
    • Causes compensatory increase increase in peripheral vascular resistance
  • Chronic use
    • Extracellular and plasma volume return to near pretreatment levels
    • Peripheral vascular becomes lower than pretreatment values (chronic antihypertensive effect)
39
Q

What are some potential adverse effects of diuretics?

A

Electrolyte disturbances

Hyperglycemia

Hypotension, orthostasis

Lipid abnormalities

Photosensitivity

Ototoxicity

Hyperuricemia, gout flare

40
Q

What are aldosterone antagonists and what do they do?

A

Spironolactone and Eplerenone

  • Inhibit the renal (sodiuma and water retention) and extra-renal (fibrosis/inflammation) actions of aldosterone
41
Q

What are the Renin Angiotensin System Inhibitors?

A
  • Aliskiren (Renin inhibitor)
  • Losartan (AT1 blocker)
  • Captopril
  • Enalapril
  • Lisinopril
42
Q

What do ACE inhibitors do? (Captopril, Lisinopril, Enalapril)

A

Block angiotensin I to angiotensin II conversion

Block bradykinin degeneration

Stimulate synthesis of other vasodilating substances such as prostaglandin E2 and prostacyclin

Prevent or regress left ventricular hypertrophy

43
Q

What do you monitor when giving ACE inhibitors?

What are some adverse effects of ACE inhibitors?

A

Monitor serum K+ and SCr within 4 weeks of initiation or dose increase

  • Adverse effects
    • Cough (increased bradykinin)
    • Angioedema
    • Hyperkalemia: particularly in patients with CKD or DM
    • Neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure
44
Q

What are adverse effects of Angiotensin II receptor blockers?

A

Orthostatic hyptension

Renal insufficiency

Hyperkalemia

45
Q

What are the different roles of the AT2 and AT1 receptors

A
  • AT2
    • ​Vasodilation
    • Antiproliferation
    • Apoptosis
  • AT1
    • ​Vasoconstriction
    • Vascular proliferation
    • Aldosterone secretion
    • Cardiac myocyte proliferation
    • Increased Sympathetic tone
46
Q

Angiotensin receptor blockers have higher affinity for which receptor (AT1 or AT2)?

A

AT1

47
Q

What are the functions and adverse effects of Aliskiren (Renin inhibitor)?

A
  • Inhibits angiotensinogen to angiotensin I conversion
  • Antihypertensive
  • Does not block bradykinin breakdown
  • Adverse effects
    • Orthostatic hypotension
    • Hyperkalemia
48
Q

What are some precautions to using ACE inhibitors or ARBs

A

Can cause acute kidney failure in patients with severe bilateral renal artery stenosis or stenosis in artery to solitary kidney

Should not be used with pregnancy

49
Q

What are some potential drug interactions with ACE inhibitors and ARBs

A
  • Medications that promote hyperkalemia
  • Medications that have activity which is sensitive to changes in serum K+
  • Medications that cause additive antihypertensive effects
  • NSAIDs
50
Q

______ and ____ together have an additive effect

A

Diuretics; ARBs

51
Q

Which drug is only 35% effective in Blacks and 67% effective in non-blacks - how do you overcome this disparity?

A

Enalapril - give with hydrochlorothiazide

52
Q

What are the Lifestyle modifications associated with JNC7 regulation hypertension treatment?

A
  • Reduce weight to normal BMI
  • DASH eating plan
  • Dietary sodium reduction
  • Increase physical activity
  • Reduce alcohol consumption
53
Q

What are some differences between the JNC7 and JNC8 guidelines?

A
  • JNC8
    • Systematic review
    • Randomized, controlled trials only (vs. range of study designs in JNC7)
    • Graded recommendations
    • No specific lifestyle recommendations
    • Racial, CKD, and diabetic subgroups addressed
54
Q

Grading in JNC8

A:

B:

C:

E:

A

A: Strong recommendation - high certainty net benefit is substantial

B: Moderate recommendation - moderate certainty net benefit is moderate to substantial

C: Weak recommendation - at least moderate certainty of small net benefit

E: Expert opinion - insufficient or unclear/conflicting evidence

55
Q

In JNC7 the BP goal is ______ regardless of age

In JNC8 the BP goal is _______ in patients 60 and older

A

<140/90

<150/90 (Grade A)

56
Q

JNC8 recommendations and grades for…

General populations:

Black population:

DM:

CKD:

A
  • General populations: Thiazide, CCB, ACEi, ARB (Grade B)
  • Black population: CCB or Thiazide (Grade B)
    • Grade C if Black and DM
  • DM: Thiazide, CCB, ACEi, ARB (Grade B)
  • CKD: ACEi or ARB (Grade B)
57
Q

JNC8 treatment strategies (Grade E)…

If goal BP not met after 1 month treatment:

If goal BP not met with 2 medications:

A
  • If goal BP not met after 1 month treatment:
    • increase dose of inital drug or add a second drug (Thiazide, CCB, ACEi, or ARB)
  • If goal BP not met with 2 medications:
    • Add and titrate a third medication
    • DO NOT USE ACE and ARB together
58
Q

When adminstering Diuretics what should be monitored?

ß-blockers?

ACEi and ARBs?

CCBs?

A
  • Diuretics: BP, BUN/serum Creatinine, electrolytes, uric acid
  • ß-blockers: BP and HR
  • ACEi and ARBs: BP, BUN/serum creatinine, potasisum
  • CCBs: BP and HR
59
Q

What drugs are better in African Americans and why?

A

Diuretics and CCB > ACEi, ARBs and ß-blockers (these cause 2-4 fold risk for angioedema)

60
Q

What drugs are not used for LVH

A

Hydralazine and minoxidil

61
Q

What drugs are better tolerated in the elderly?

A

Thiazide or CCB

62
Q

What drugs are used in pregnant patients?

What drugs are avoided?

A

Use: Methyldopa, beta-blockers, vasodilators

Avoid: ACEi and ARBs

63
Q

In combination therapy, at least one of the agents should be a ______ _______

A

thiazide diuretic

64
Q

What is resistant hypertension

A

Failure to achieve BP goal on full doses of 3 drug regimen including a diuretic

Cardiovascular System (35 decks)

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