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Pharmacology > Cardiovascular III - Treatment of Hypertension > Flashcards

Cardiovascular III - Treatment of Hypertension Flashcards

1
Q

Definition of hypertension?

Hypertension is the key risk factor in ____ and a major risk factor for?

A

Consistent resting arterial BP in excess of 140/90

Stroke; myocardial ischemia, MI, cardiac arrhythmias, and the progression of atherosclerosis

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2
Q

Two complete clinical consensus?

Goal of physician treating hypertension?

A

a. Failure to treat will cause harm
b. Sucessful treatment of hypertension is a benefit

Get the pressure down any way you can

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3
Q

First line medical treatment of hypertension?

A

NOT drugs: employs weight loss, excercise, salt restriction, cessation of smoking and limiting alcohol consumption

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4
Q

First line pharmacological treatment:

What are the 5 first line agents?

A

Thiazide Diuretics

Beta blockers

Alpha 1 blockers

ACE Inhibitors

Calcium channel blockers

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5
Q

Thiazide Diuretics:

Why are they used so widely? (3 main reasons)

A

a. They lower blood pressure by themselves
b. They potentiate the actions of other antihypertensive agents
c. ***They reduce the incidence of stroke associated with hypertension

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6
Q

Thiazide Diuretics:

Mechanism of action:

  1. Initial effects?
  2. What happens after 6 weeks?
A
  1. Effects are initially related to diuresis and natriuresis with resultant decrease in ECVF (extracellular fluid volume) –> decrease in CO
  2. Volume and CO return to normal
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7
Q

Thiazide Diuretics:

Mechanism of action:

What are the chronic effects?

A

Reduction of vascular resistance

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8
Q

Thiazide Diuretics:

Side effects:

What are the three side effects?

A

Hypokalemia, glucose intolerance, hyperlipidemia

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9
Q

Thiazide Diuretics:

Side effects: Hypokalemia

  1. What pathology is associated with hypokalemia?
  2. How can this be managed?
A
  1. ventricular ectopy, ventricular tachycardia, and ischemic ventricular fibrillation
  2. Lower the dose, K+ supplement, or K+ sparing diuretic
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10
Q

Thiazide Diuretics:

Side effects: Glucose intolerance

How is glucose intolerance generated?

A

Hypokalemia suppresses insulin secretion

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11
Q

Thiazide Diuretics:

Side effects: Hyperlipidemia

What occurs to the lipid profiles?

A

DECREASED HDL

INCREASED cholesterol, triglycerides, and LDL

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12
Q

Thiazide Diuretics:

Side effects:

  1. May increase mortality in what patients?
  2. What serious event is positively correlated with thiazide diuretic dose?
A
  1. Coronary artery disease patients: but more likely in geriatric hypertensive patients and when K+ wasting is associated with diuretic administration
  2. Sudden cardiac death
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13
Q

Thiazide Diuretics:

Current recommendations:

  1. Low doses of what drugs are beneficial either alone or in combination with other drugs?
  2. What is important to note about greater doses?
A
  1. Chlorthalidone or hydrochlorothiazide
  2. It will cause greater diuresis but NOT greater antihypertensive effect while at the same time will produce K+ wasting and hypokalemia
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14
Q

Thiazide Diuretics:

  1. Why are loop diuretics NOT recommended as first line agents?
  2. Why are K+ sparing diuretics NOT recommended as first line agents?
A
  1. Single doses are potent but short acting and increasing the dose to twice a day greatly increases risk of side effects
  2. Side effects
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15
Q

Beta Adrenergic Antagonists:

  1. What beta-adrenergic antagonists are effective? What grades of hypertension?
  2. They reduce what two adverse events associated with hypertension?
A
  1. ALL are effective for ALL grades of hypertension
  2. CV disease and death
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16
Q

Beta Adrenergic Antagonists:

  1. Examples of antagonists without intrinsic sympathomimetic activity (ISA)?
A
  1. Atenolol, Betaxolol, Bisoprolol, Metoprolol, Nadolol, Propranolol, Timolol
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17
Q

Beta Adrenergic Antagonists:

When are beta adrenergic agonists without ISA recommended? Why?

A

After MI because of long term cardioprotective effects

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18
Q

Beta Adrenergic Antagonists:

When are beta-adrenergic antagonists the PREFERRED DRUG OF CHOICE?

A

For hypertensive patients with MI, MYOCARDIAL ISCHEMIA, or HEART FAILURE

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19
Q

Beta Adrenergic Antagonists:

4 proposed mechanisms of action?

A
  1. DECREASED CO
  2. DECREASED plasma renin activity
  3. Central hypotensive activity
  4. Presynaptic INHIBITION of sympathetic nerve activity
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20
Q

Beta Adrenergic Antagonists:

Without ISA initially DECREASES ___ and ___ and cause a ____ INCREASE in ___ ___ ___.

Inpatients that see a BP lowering effect with these drugs their resistance eventually?

A

HR; CO; reflex; periperal vascular resistance

Resistance eventually returns to normal or lower than normal values (it decreases)

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21
Q

Beta Adrenergic Antagonists:

Beta adrenergic antagonists WITH ISA produce ____ DECREASE ___ and ___ compared to those without ISA. Their anti-hypertensive effects are correlated with lowering of ___ ___ below normal through activation of ____ receptors.

A

less; HR; CO; vascular resistance; beta2

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22
Q

Beta Adrenergic Antagonists:

Side effects:

  1. Severe ____ and decreased ___
  2. What does extremity vasoconstriction cause?
  3. What can specifically occur with patients on non-selective beta blockers?
  4. What can specifically occur in beta blockers without ISA?
A
  1. bradycardia; CO
  2. cold extremities
  3. Epinepherine mediated hypertension and bradycardia during hypoglycemia
  4. Increased triglycerides and decreased HDL
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23
Q

Beta Adrenergic Antagonists:

Contraindications?

A

Patients with diabetes, asthma, SA/AV node conduction disorders, or with drugs that reduce AV conduction

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24
Q

Beta Adrenergic Antagonists:

Why are they contraindicated in diabetics?

Why are they contraindicated in asthmatics?

A

Beta blockers prolong hypoglycemia after an insulin reaction. They exacerbate glucose intolerance

Beta blockers cause bronchoconstriction

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25
Q

Alpha 1 Antagonists:

  1. Primarily ____ dilators. How?
  2. NOT first choice monotherapy: when are they used?
A
  1. Arterial (but still provide some venodilation) by antagonizing catecholamine receptors
  2. Alpha antagonists are used in combination with beta blockers when that agent and a diuretic cannot lower BP OR when beta blockers are contraindicated
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26
Q

Alpha 1 Antagonists:

Initially cause?

What are advantages of alpha 1 blockers?

A

Alpha 1 blockers initially cause reflex tachycardia and INCREASED plasma renin activity (return to normal over time)

Cause little postural hypotension (except after first dose) and do not adversely affect lipid profiles

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27
Q

Alpha 1 Antagonists:

Side effects?

A

Alpha 1 Antagonists have infrequent and mild side effects including dizziness, palpitations, headache, and lethargy

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28
Q

ACE Inhibitors:

These are effective even when what is not present?

What do they lower?

A

ACE Inhibitors are effective even if high renin levels are not present

ACE inhibitors lower TPR (unclear mechanism)

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29
Q

ACE Inhibitors:

They improve prognosis of what patients?

They blunt the rise in ___ and ___ loss following ___ administration and thus potentiate the anti-hypertensive effects of?

A

ACE Inhibitors improve the pronosis of patients with severe loss of left ventricular bunction

aldosterone; K+; diuretic; diuretics

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30
Q

ACE Inhibitors:

When are they PREFERRED? Why?

A

ACE Inhibitors are good for patients whose hypertension is complicated by DIABETES because they exert RENAL PROTECTIVE effects

31
Q

ACE Inhibitors:

Side effects? What could be taken for the side effects? Example?

A

ACE inhibitors ahve few notable side effects. However, some cases present with cough and angioedema

Can be treated with an AII blocker such as Losartan

32
Q

Calcium channel blockers:

Which class/drug should be avoided? Why?

A

Calcium channel blockers like DHPs/nifedipine should be avoided because their rapid onset and short action can cause risk of sudden cardiac death

33
Q

K+ channel openers:

Drug?

A

Minoxidil

34
Q

K+ channel openers:

When is it used? Why?

A

K+ channel openers are only used for hypertensive emergencies because of their undesireable side effects

35
Q

K+ channel openers:

Mechanism of action:

How do they reduce BP?

At the cellular level, action?

A

K+ channel openers relax vascular smooth muscle directly thus lower vascular resistance

They open ATP activated K+ channels resulting in hyperpolarization and causing inactivation of the Ca++ channels

36
Q

K+ channel openers:

Side effects that are an extension of pharmacological effects?

A

Minoxidil can cause hypotension, dizziness, flushing, fluid retention, reflex tachycardia, and decrease renal perfusion

37
Q

K+ channel openers:

Major unique side effect?

A

K+ channel openers can cause hypertrichosis (increased hair growth)

38
Q

K+ channel openers:

What else can Minoxidil be used for?

A

Male pattern baldness (rogaine) due to hypertrichosis

39
Q

Direct vasodilator:

Drug?

A

Hydralazine

40
Q

Direct vasodilator:

Hydrazaline has been attributed to the stimulation of? or direct production of?

Preferentially dilates?

A

Hydrazaline stimulates EDRF or direct production of NO from the drug

Arteries over veins

41
Q

Direct vasodilator:

These can only be used in conjunction with?

Duration of action?

A

Hydrazaline can only be used in conjunction with drugs that counteract sodium/fluid retention and that counteract reflex tachycardia

Up to 12 hours

42
Q

Direct vasodilator:

  1. Hydrazaline side effects?
  2. Biggest drawback?
  3. What is seen with long-term administration?
A
  1. headache, hypotension, dizziness, and flushing
  2. Hydrazaline has reflex activation of the SNS and fluid retention (is thus bad monotherapy)
  3. Lupus syndrome (after more than 6 months)
43
Q

Nitrodilators - Sodium Nitroprusside:

  1. Actions are same as?
  2. __ stimulated ___ mediated vasorelaxation
  3. When is it used?
A
  1. Nitric oxide
  2. NO; cGMP
  3. Sodium nitroprusside is used for hypertensive emergencies or to cause purposeful acute hypotension in surgery
44
Q

Dopamine Receptor Agonists:

Drug?

A

Fenoldopam

45
Q

Dopamine Receptor Agonists:

  1. Fenoldopam acts as ___ vasodilator
  2. Duration of action?
  3. Given for what?
A
  1. Fenoldopam acts as an arterial vasodilator
  2. Short duration
  3. Fenoldopam is given for hypertensive emergencies (with poor renal perfusion) and post-operative hypertension.
46
Q

Dopamine Receptor Agonists:

Fenoldopam side effects?

Contraindications? Why?

A

Similar to other direct vasodilators: flushing, tachycardia, headache, hypotension, dizziness

Fenoldopam is contraindicated in patients with glaucoma because it increases IOP.

47
Q

Catecholamine metabolism modifiers:

Two drugs?

A

alpha-methyltyrosine and methyldopa

48
Q

Catecholamine metabolism modifiers:

Alpha-methyltyrosine seves as? and thus inhibits?

A

Alpha-methyltyrosine is a false substrate for tyrosine hydroxylase and inhibits synthesis of NE

49
Q

Catecholamine metabolism modifiers:

Alpha-methyltyrosine reduces synaptic __ ____ and reduces effects on ___ end organs.

Clinical application?

A

Alpha-methyltyrosine reduces synaptic NE concentration and thus reduces effects on autonomic end organs

For severe hypertension associated with phochromocytoma

50
Q

Catecholamine metabolism modifiers:

Methyldopa is metabolized to what? Where?

What does this metabolite do? What receptor?

Clinical application?

A
  1. Methyldopa is metabolized to alpha-methylnorepinepherine in the brain
  2. Alpha-methylnorepinepherine activates the central alpha2 receptors to lower arterial BP
  3. Originally it was an antihypertensive but has since been replaced
51
Q

Inhibitors of catecholamine storage/reuptake:

  1. Eventually deplete vesicular stores of ___.
  2. What do these cause initially? Why is this important
A
  1. NE
  2. First displace NE from the nerve terminals causing a burst of NE mediated effects (indirect sympathomimetic effects) and this burst can be dangerous
52
Q

Inhibitors of catecholamine storage/reuptake:

3 drug examples?

A

Guanethidine, Guanadrel, and Reserpine

53
Q

Inhibitors of catecholamine storage/reuptake:

Guanethidine and Guanadrel:

What occurs with acute administration?

A

Guanethidine and Guanadrel when administered acutely acts as an indirect sympathomimetic because it displaces NE stored in the synaptic vesicles and results in a massive efflux of NO through the NET acting in reverse (there is too much NE for the MAO to handle); it thus floods the synapse causing a huge increase in sympathetic stimulation

54
Q

Inhibitors of catecholamine storage/reuptake:

Guanethidine and Guanadrel:

What occurs when they are administered chronically?

A

Guanethidine and Guanadrel, when administered chronically, is concentrated in synaptic vessels and replaces NE. In addition the MAO degrades the small pool of NE that remains in the cytoplasm.

55
Q

Inhibitors of catecholamine storage/reuptake:

What is Guanadrel specific for?

Why are they no longer first choice agents?

A

Guanadrel is specific for peripheral adrenergic neurons

Guanethidine and Guanadrel are no longer first choice because of the effects of initial massive NE release

56
Q

Inhibitors of catecholamine storage/reuptake:

Reserpine

Mecanism of action?

A

Reserpine irreversibly blocks the vesicular monoamine transporter in the nerve terminal and eventually depletes the terminal of its NE stores because MAO destroys free NE in the terminal. (cant package NE)

57
Q

Inhibitors of catecholamine storage/reuptake:

Reserpine:

What occurs if too much Reserpine is given?

What are the major side effects?

A

If too much Reserpine is diven the depletion process can be overwhelmed and force the NET to work in revers and essentially dump excessive NE out of the nerve terminal

MAJOR CNS side effects: can mimic paranoid schizophrenia, psychotic depression, and homocidal/suicidal ideation

58
Q

Alpha-antagonists used for other pathologies:

Drug?

A

Tamsulosin

59
Q

Tamsulosin:

  1. Selectivity for what receptor? Action?
  2. Clinical uses?
  3. Adverse effects?
A
  1. Tamsulosin has selectivity for alpha one receptors to relax muscles in the bladder neck and prostate
  2. Treatment of urinary tract symptoms of enlarged prostate and good for hypertensive patients with BPH
  3. dizziness, drowsiness, weakness, diarrhea, nasal congestion
60
Q

Preferred and least preferred drugs for:

African heritage?

Pregnancy?

A

African - give diuretics (with ACEI or angiotensin receptor blocker (ARB)) or CCB. DO NOT give Beta blocker

Pregnancy - give methyldopa, labetalol (beta blocker), or hydrazaline. CONTRAINDICATED: ACEI, ARB, aliskiren

61
Q

Preferred and least preferred drugs for:

Angina pectoris

Asthma

A

Angina: give Beta blocker or CCB CONTRAINDICATED: hydrazaline and minoxidil

Asthma: give CCB, ACEI, or ARB CONTRAINDICATED: Beta blocker

62
Q

Preferred Drug for:

MI?

CHF?

A

MI - Beta blocker, ACEI, ARB, aldosterone antagonist

CHF - ACEI, ARB, Beta-blocker, thiazide diuretic

63
Q

Preferred drugs for:

Stroke prevention?

Kidney disease?

A

Stroke prevention - Thiazide diuretic + ACEI/ARB

Kidney disease - ACEI or ARB

64
Q

Preferred drugs for:

Diabetes?

BPH?

A

Diabetes - ACEI or ARB

BPH - alpha-blocker

65
Q

Preferred drugs for:

Migraine?

Osteoporosis?

A

Migraine: Beta-blocker, CCB

Osteoporosis - thiazide diuretic

66
Q

Type of drug given to hypertensive patients with atrial fibrillation, supraventricular tachycardia, or sinus tachycardia?

A

non-ISA beta blocker, verapamil, or diltiazem

67
Q

Type of drug given for hypertensive patients with irritable bowel (with diarrhea)?

A

Verapamil

68
Q

Type of drug given for hypertensive patients with recurrent renal calculi?

A

Thiazide diuretics

69
Q

Type of drug given for hypertensive patients with senile tremor, cardiac awareness, or glaucoma?

A

Beta-blockers

70
Q

Multiple drug therapy:

Diuretics + ACE inhibitors =

A

Diuretics + ACEI = potentiates antihypertensive action and controls excessive reflex AII effect

71
Q

Multiple drug therapy:

Diuretics + hydralazine =?

A

Diuretics + hydralazine = diuretic to prevent fluid retention that occurs from hydralazine

72
Q

Multiple drug therapy:

Diuretic + Beta-blocker =?

A

Diuretic + Beta-blocker = the diuretic causes reflex activation of CV and RAS that is controlled by the beta-blocker

73
Q

What is the biggest problem with antihypertensive therapy? Why?

What class of drugs cause a negative effect on K+, total cholesterol, LDL, HDL, and triglycerides?

A

Noncompliance because the patient cant feel the problem until it is too late.

Thiazide and loop diuretics

Pharmacology (24 decks)

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