Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ICOM-Cardio > Cardio-pharm-antihypertensives I- Mortensen > Flashcards

Cardio-pharm-antihypertensives I- Mortensen Flashcards

1
Q

What type of drug is adenosine?

A

antidysrhythmic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is adenosine so susceptible to degradation in the body?

A

It is a purine nucleoside, it has a very short half-life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adenosine subtype receptor A1 is found on which type of cells?

A

AV nodal cells which stimulate opening of membrane K+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Adenosine stimlates A1 receptors on AV nodal cells which open K+ channels, what happens to the AV nodal tissue?

A

AV nodal hyperpolarization and complete AV nodal block, it becomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is adenosine used for in its capacity of a short acting AV nodal blocker?

A

conversion of reentrant SVT (PAT, PSVT and WPW) to NSR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the preferred route of administration of adenosine?

A

IV • rapid bolus at 6-12 mg, proximal to heart (brachial vein, antecubital) because of rapid half-life of 15 s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why are we not too concerned about ADEs of adenosine?

A

too fast to be concerning

: hypotension, flushing, complete heart block, CNS effects, dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

There are two important MOAs for digoxin: What are they and which MOA is useful as an AV nodal blocker or sifter?

A
  1. CHF – Na+/K+-ATPase inhibition- increases contractility by keeping Ca2+ inside cell
  2. Atrial Fib. – vagal stimulation effect resulting in a negative dromotropic effect at the AV node resulting in prolonged refraction (↑ERP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which type of medicine is preferred as AV nodal blockers for treating AFIB over digoxin?

A

Calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which antihypertensive is considered a cardiac glycoside and has 2 MOAs:

  • CHF – Na+/K+-ATPase inhibition
  • Atrial Fib. – vagal stimulation effect resulting in a negative dromotropic effect at the AV node resulting in prolonged refraction (↑ERP)
A

digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

• in atrial flutter/fibrillation, digoxin slows ventricular rate by decreasing the number of P-wave depolarizations that reach the ventricles, however, stimulation may over-ride this therapeutic effect because of the dual MOAs.

A

sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

As concerning pharmacokinetics: Digoxin is soluble and can access the CNS and placenta

A

lipid soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Some of the main ADEs of digoxin include :

A

• highly dysrhythmogenic (prodysrhythmic) due to effects on plasma potassium (hypokalemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which categories of antidhysryhtmics are useful in treating digoxin induced dysrhythmia?

A

Class IB and Class II agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 3 treatments for bradycardia?

A

atropine – produces a vagal block to increase HR •

isoproterenol – β1-stimulated increase in HR •

pacemaker – morphologic AV nodal bloc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the MOA of atropine?

A

– produces a vagal block to increase HR, blocks parasympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Isoproterenol is a agonist and can HR and can treat bradycardia

A

B1; increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pacemakers mainly treat ?

A

bradycardia which can be caused by morphologic AV nodal block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some non pharmacologic ways to treat sinus tachycardia?

A

vagal stimulation through carotid sinus massage or Valsalva maneuver- causing baro-reflex and reducing HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which nerve is mainly involved with the carotid sinus?

A

glossopharyngeal nerve (IX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which other elements are involved with the carotid sinus and the baroreceptor reflex?

A

Nucleus tractus solitarus, area postrema, rostral and caudal ventral lateral medulla, and CN IX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What elements are involved with the efferent part of the baroreceptor reflex?

A

Info comes back through the vagus nerve (X), cardiac accelerans, and other medullary efferents to increase or decrease HR, vasocontsriction, and renal function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

• eclampsia/preeclampsia • endocrine disorders (e.g. Cushing’s Syndrome) • pheochromocytoma • renal disease • essential hypertension are all causes of blood pressure

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

There are 2 major types of HTN which are:

A

Non-essential/secondary (10%) • a clinically identifiable cause (e.g. renal disease, endocrine tumors, aortic stenosis, etc.) • primary management is usually surgical

• Essential/primary (90%) • idiopathic • a genetic basis for incidence most often found in middle-aged adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

First line recommendations for HTN is not medications, but ?

A

lifestyle modifications

Lose weight if overweight •

Limit alcohol intake to ≤1 oz (30mL) per day •

Aerobic physical activity (30-45 min per day) •

Reduce Na+ intake to ≤100mmol (6g) per day •

Maintain intake of K+ to ~90mmol (7g) per day •

Maintain intake of Ca+2 and Mg+2 •

Stop smoking and reduce dietary intake of sugar, saturated fat and cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What level of BP is the pharmacological tx goal for HTN:

A

<130/85

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

• Chronic hypertension usually ‘resets’ the baroreflex such that the pressure is considered normal.

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Must find a HTN treatment plan that will best combat the effects of the .

A

Baroreflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

sodium and water retention by the kidneys and sympathetically-induced increases in peripheral vascular resistance, heart rate and cardiac output are all mechanisms by which the can try to increase BP to what it considers normal (but is acutally high BP) while the provider trys to lower BP

A

baroreflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

According to the formulas:

MAP = CO × TPR

CO = HR × SV

you can lower BP (MAP) by decreasing HR, SV, and/or TPR (systemic vascular resistance)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diuretics are used to treat which type of BP?

A

moderate HTN as a monotherapy

but also augments antihypertensive effects of other drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What 3 types of diuretics have been discussed?

A

• thiazides, loop diuretics, K+-sparing diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Efficacy of diuretics is greater in which two populations?

A

African-American and elderly patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the effect of diuretics on CO and TPR?

A

initial ↓CO followed by sustained ↓TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When do you expect to see peak effects after starting diuretics?

A

3-4 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What 2 contraindications are important in the use of diuretics?

A
  • diabetics : may induce hyperglycemia
  • hyperlipidemia: tend to elevate plasma LDL and TG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What type of pharmacologic agent is propranolol?

A

β-adrenergic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The main effect of B blockers is at which receptor in order to lower BP?

A

B1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the MOAs of β-adrenergic antagonists (B-blockers) like propranolol?

A
  • heart: ↓HR/contractility ⇒ ↓blood pressure
  • kidney: ↓renin release ⇒ ↓Angiotensin II formation

both lower BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Beta blockers work at which parts of the heart to be effective?

A

The nodes and the conductile tissues of the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Like diuretics, the efficact of monotherapy with b blockers is and it works better in a combination therapy

A

moderate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

B blockers and are often used together, to lower the dose of each and get a broad and wide range of antihypertensive effects

A

diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Which population responds poorly to β-adrenergic antagonists (B blockers)?

A

smokers

44
Q

There are several ADEs to β-adrenergic antagonists as there are B receptors all over the body:

A
  • minor GI and CNS nausea
  • asthma: exacerbation with non-specific antagonists (B2)
  • hyperlipidemia (↑TG, ↓HDL)
  • male sexual dysfunction (vasodilation)
  • diabetes: β-blockade masks signs and symptoms of hypoglycemia (dysrhythmia, tachycardia, tremor, diaphoresis) leading to ↑coma and death incidence
  • may exacerbate CHF
45
Q

Why are we so concerned with the use of b blockers and those with diabetes?

A

symptoms of hypoglycemia can include dysrhythmias and diaphoresis that can be masked by B blockers

46
Q

How could B blockers exacerbate CHF?

A

By reducing contractility of ventricle

47
Q

How are the β-adrenergic antagonists, labetalol and carvedilol, different from others in their class (eg. propranolol)?

A

they can block β1, β2, α1 receptors, in this case, they are very potent vasodilators

48
Q

Which antihypertensives are administered PO for long-term management of CHF and hypertension and IV for hypertensive emergencies?

A

(labetalol and carvedilol)

(labetalol only)

49
Q

What are the centrally-acting sympatholytics?

A

clonidine and a-methyldopa

50
Q

Clonidine is a centrally acting sympatholytic and it acts on the receptor as an agonist.

A

a2

51
Q

What is the MOA of clonidine, a centrally-acting sympatholytic?

A
  • post-synaptic α2-agonist in CNS: inhibits sympathetic outflow at the level of the NTS resulting in ↓HR/TPR
  • pre-synaptic α2-agonist in periphery: decreases NE release from post-ganglionic nerve terminals
  • since actual catecholamine storage is not effected, orthostatic hypotension is not prominent
52
Q

How effective is clonodine at lowering blood pressure as a centrally acting sympatholytic?

A

It is quite effective as a monotherapy, 35/20, it is common to use in combination with a diuretic.

53
Q

Like clonidine, α-methyldopa is centrally-acting sympatholytics, which receptors does it stimulate?

A

stimulates inhibitory presynaptic α2 receptors

acts as a ‘false transmitter’ at post-synaptic terminals

54
Q

What is the drug of choice for treatment of chronic hypertension in women in their childbearing years?

A

α-methyldopa

55
Q

What is the drug of choice for lowering blood pressure for ecclampsia, preeclampsia?

A

a-methyldopa

56
Q

Which centrally acting sympatholytic ADEs include:

+ direct Coombs test (presence of auto-antibodies to RBCs) producing a frank hemolytic anemia

and more minor ADEs

prominent sexual dysfunction, dry mouth, sedation

A

a-methyldopa

57
Q

Which two peripherally acting sympatholytics are no longer used as blood pressure lowering agents due to their ADEs?

A

resperine and trimethaphan

58
Q

prazosin, terazosin, and doxazosin are all examples of ?

A

peropherally-acting sympatholytics selective antagonist at vascular smooth muscle α1 receptors

59
Q

Not only can peripherally acting sympatholytics that are selective antagonists of a1 receptors, but can also lowere LDL, triglycerides, and total cholesterol, what are they called?

A

prazosin, terazosin, doxazosin

60
Q

What are the ADEs of prazosin, terazosin, doxazosin as selective a1 antagonists?

A

• mild tolerance development to antihypertensive effect

• reflex tachycardia

• sexual dysfunction

61
Q

Why do peripherally-acting sympatholytics prazosin, terazosin, doxazosin a1 antagonists possibly cause relex tachycardia?

A

the baroreceptor reflex will kick in, activating sympathetics, and lead to reflex tachycardia

62
Q

What can we do to combat the ADE of reflex tachycardia from taking selective a1 antagonists prazosin, terazosin, doxazosin?

A

use a B1 blocker simultaneously which combats the baroreceptor relex

63
Q

Which type of drug is often prescribed along with a1 antagonists prazosin, terazosin, doxazosin?

A

B1 antagonists (b blockers) to combat the baroreceptor reflex

64
Q

Which are the 2 main calcium channel antagonists?

A

verapamil and diltiazem

65
Q

Which calcium channel antagonists (blockers) have direct vasodilator activity by inhibiting both Ca+2 entry into vascular smooth muscle and Ca+2 release from the sarcoplasmic reticulum?

A

verapamil and diltiazem

66
Q

The vasoconstrictor and vasodilator nature of vascular smooth muscle is determined mostly by which ion?

A

movement of Ca2+

67
Q

What is the efficacy of calcium channel blockers verapamil and diltiazem?

A

verapamil, 30/20; diltiazem, 20/15

68
Q

What are the ADEs of the calcium channel antagonists verapamil and diltiazem?

A

cardiodepression (may counteract reflex tachycardia)

others as in “Drugs for Dysrhythmia

69
Q

Why do the calcium channel blockers verapamil and diltiazem sometimes cause cardiodepression?

A

They work on calcium channels in nodal tissue and ventricular contractile cells and may also block possible baroreflex actions from vasodilation

70
Q

What is an example of a dihydropyridine specific calcium channel blocker?

A

nifedipine

71
Q

dihydropyridine focused calcium channel blockers (nifedipine) work soley on which calcium channels?

A

direct vasodilator activity by inhibiting both Ca+2 entry into vascular smooth muscle and Ca+2 release from the sarcoplasmic reticulum

72
Q

Are dihydropyridine focused calcium channel blockers (nifedipine) used as antidysrhythmics like verapamil and diltiazem?

A

No, they have a greater vascular effect that verapamil/diltiazem • significantly less cardiodepressant activity

73
Q

Nifedipine as a dihydropyridine calcium channel antagonists can cause a prominent reflex tachycardia, how do we combat this?

A

By useing a B blocker

74
Q

Which drug promotes direct vasodilation via guanylate cyclase stimulation (similar to nitrovasodilators)?

A

hydralazine

75
Q

Which direct acting vasoldilator will be prescribed orally for long term management of moderate to severe hypertension?

A

hydralazine

76
Q

What happens when hydralazine stimulates of guanylate cylase aas a direct acting vasoldilator?

A
  • ↑intracellular cGMP activation
  • ↑Ca+2 sequestration ⇒ smooth muscle relaxation
77
Q

Where is the primary effect occur with the use of hydralazine, a direct-acting vasodilators and how effective is it?

A

primary effect on arterioles (afterload) with little effect on venous tone (preload); efficacy, 25/25

78
Q

What is tachyphylaxis and which drug can result with this?

A

hydralazine -It is tolerance development with a prominent baroreflex perturbation leading to ↑HR, ↑CO, ↑Na+/water retention (sympathetic stimulation of renin release)

79
Q

Because of the potential tolerance development of hydralazine : (full reversal of the antihypertensive effect of hydralazine may occur if baroreflex-mediated cardiac and renal effects are not inhibited) what can we use as a co-therapy?

A

• β-blockers and diuretics as concomitant therapy

80
Q

Because of the huge drop of blood pressure we can get from hydralazine (direct acting vasodilator), it’s use is limited to:

A

limited to resistant, fulminant hypertension and management of hypertensive emergency

81
Q

What are some ADEs for hydralazine?

A
  • SLE-like syndrome (metabolism by N-acetylation)
  • palpitation, tachycardia
82
Q

Which 2 medications can cause SLE-like symptoms as an ADE?

A

procainamide and hydralazine

83
Q

Which direct acting vasoldilator acts on stimulation of vascular smooth muscle K+ channel opening causing arteriolar vasodilation, and also regrows hair?

A

monoxidil

84
Q

Monoxidil, a direct acting vasodilator that stimulates vascular smooth muscle K+ channel opening resulting in membrane hyperpolarization, is used only for r severe, refractory hypertension?

A

monoxidil

85
Q

What is the use for minoxidil, other than regrowing hair?

A

severe, refractory (unrelenting) hypertension

86
Q

Like hydralazine, monoxidial can cause which ADE due to baroreflex-mediated increases in sympathetic tone?

A

tachyphylaxis (rapidly diminishing response to successive doses of drugs)

87
Q

Along with other direct-acting vasodilators, they can be used in combination with?

A

β-blockers and diuretics

88
Q

What type of drug is sodium nitroprusside?

A

direct-acting vasodilators, very potent vasodilator with rapid onset and short duration of action (1-10 minutes after cessation)

89
Q

Which direct-acting vasodilators decreases both afterload and preload (venodilation)?

A

sodium nitroprusside

90
Q

How is sodium nitoprusside, a direct-acting vasodilators, normally administered and in which situations?

A

• parenterally infused agent used in hypertensive emergencies and the rapid management of CHF

91
Q

What is the MOA of sodium nitroprusside?

A

donates NO (EDRF) ⇒ cGMP-mediated Ca+2 sequestration

92
Q

What is the strongest vasodilator that we know of?

A

NO

93
Q

What are the concerning ADEs of the direct-acting vasodilators, sodium nitroprusside?

A

extended continuous infusion may produce methemoglobinemia, cyanide poisoning and cell death due to inhibition of cellular respiration

• Formula: Na2Fe(CN)5NO

94
Q

A very large class of blood pressure medicatons that include captopril, enalapril, linsinopril, etc. are the ?

A

angiotensin converting enzyme inhibitors or ACE inhibitors.

95
Q

ACE inibitors (angiotensin converting enzyme inhibitors) all end in the suffix:

A

-pril

96
Q

What role do B blockers have on the kidneys and JGA complex?

A

They can inhibit the release of renin which converts Angiotensinogen to Angiotensin I to Angiotensin II

97
Q

What is the MOA of ACE inhibitiors (angiotensin converting enzyme inhibitors)?

A

they inhibit the conversion of Angiotensin I to Angiotensin II, which blocks vascular constriction and blocks release of aldosterone which causes Na+ and water retention

98
Q

ACE inhibitiors have a more recently discovered MOA involving bradykinin which?

A

ACE/Kininase II inhibitors inhibit the breakdown of bradykinin, which is also a vasodilator

bradykinins stay elevated

99
Q

What are the 2 important MOAs for ACE (angiotensin converting enzyme inhibitors) as concerning the treatment of high BP?

A

inhibits the conversion of angiotensin I to II

inhibits the breakdown of bradykinin (vasodilator)

100
Q

Which population has less efficacy with ACE inhibitors as a monotherapy and what do we do to combat that?

A

less efficacy in African-Americans as monotherapy, must be combined with diutretic and/or B blocker

101
Q

About a quarter to a third of those who take ACE inhibitiors will complain of which symptom?

A

dry, persistent cough -you need to discontinue as this indicates a buld up of bradykinin in the circulation which can stimulate respiratory pathways

102
Q

ACE inhibitiors are contraindicated in which population?

A

pregnancy or those who will become pregnant - teratogenic

103
Q

What is the newest antihypertensive drug that works directly on arterioles by blocking the AT1 receptors?

A

angiotensin receptor blockers:

losartan, candesartan, irbesartan, valsartan, etc.

104
Q

What is the MOA for the angiotensin receptor blockers?

A

specific antagonists of angiotensin II at AT1 receptors on vascular smooth muscle, adrenal cortex, brain, spinal cord, heart, etc.

105
Q

Which neurotransmitters/hormones are associated with a1 receptors, A1 receptors, and AT1 receptors?

A

a1- norepi, epi

A1- adenosine

AT1- angtiotensin II

106
Q

As angiotensin receptor blockers (losartan, candesartan, irbesartan, valsartan, etc) do not alter ACE (angiotensin converting enzyme) inhibitors, bradykinins are not effected and there is no prominent , a prominant ADE of ACE inhibitors.

A

cough

107
Q

Like ACE ihibitors, angiotensin receptor blockers (-artans) are contraindicated in which population?

A

pregnancy

ICOM-Cardio (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions