Unit 4 - Wk 5 Pharmacology

Front 1

Hydrochlorothiazide

Back 1

Diuretic; decrease volume of blood; block renal Na resoprtion (natriuresis) and thereby causing dieresis (loss of water) from the blood.

Front 2

Amlodipine

Back 2

Vasodilation; calcium channel blocker; calcium channel blocker that directly acts in the vascular smooth muscle to cause vasodilation and also acts in the heart to decrease cardiac output.

Front 3

Captopril

Back 3

Decrease blood volume AND vasodilation; ACE inhibitor; Angiotensin converting enzyme (ACE) inhibitor which blocks the formation of antiotensin II and blocks the inactivation of bradykinin. The blockade on angiotensin II formation limits the vasoconstriction and stimulation of aldosterone release while the blockade of bradykinin inactivation allows continued bradykinin-induced vasodilation.

Front 4

Losartan

Back 4

Angiotensin receptor blocker; decreases blood volume AND vasodilation; Angiotensin II receptor antagonist (or blocker also called ARB for Angiotensin Receptor blockers) that blocks the actions of angiotensin II to cause vasoconstriction and aldosterone release.

Front 5

Clonidine

Back 5

Central acting alpha-2 agonist; decrease sympathetic stimulation to heart and vasculature; alpha-2 adrenergic agonist that works within the CNS to decrease overall (heart, resistance arterioles and capacitance venules) cardiovascular sympathetic stimulation from the CNS (sympathoplegics).

Front 6

Prazosin

Back 6

Alpha 1 antagonist; decrease sympathetic stimulation to vasculature; alpha-1 adrenergic antagonist that decreases blood pressure by blocking alpha-1 receptors in resistance arterioles and capacitance venules and thereby affecting both cardiac output and total peripheral resistance.

Front 7

Metoprolol

Back 7

Beta adrenergic antagonist (beta blocker); decrease sympathetic stimulation to the heart;beta-1 adrenergic antagonist that decreases blood pressure by blocking beta-1 receptors primarily in the heart and secondarily in the kidney.

Beta blockers can also block release of renin (secondary affect)

Front 8

Hydralazine

Back 8

Direct vasodilator; acts directly on smooth muscle cells of arterioles (much more than veins);a direct acting arteriole-specific vasodilator that may cause nitric oxide release and that causes decreases in blood pressure by effects on total peripheral resistance.

Front 9

Nitroprusside

Back 9

NO releasing drugs; vasodilation; powerful dilator of both veins and arterioles; breaks down to release nitric oxide (NO) which directly acts on vascular smooth muscle relaxation.

Front 10

Adverse effects/antihypertensive clinical uses of aliskirin/renin inhibitor?

Back 10

Front 11

Adverse effects/antihypertensive clinical uses of amlodipine/Ca channel blockers?

Back 11

Front 12

Adverse effects/antihypertensive clinical uses of captopril/ACEinhibitor?

Front 13

Adverse effects/antihypertensive clinical uses of captopril/ACEinhibitor?

Back 13

Front 14

Adverse effects/antihypertensive clinical uses of clonidine/sympathoplegics?

Back 14

Front 15

Adverse effects/antihypertensive clinical uses of hydralazine/vasodilators?

Back 15

Front 16

Adverse effects/antihypertensive clinical uses of hydrochlorothiazide?

Back 16

Front 17

Adverse effects/antihypertensive clinical uses of losartan/ARB?

Back 17

Front 18

Adverse effects/antihypertensive clinical uses of metoprolol/B-blockers?

Back 18

Front 19

Adverse effects/antihypertensive clinical uses of nitroprusside?

Back 19

Front 20

Adverse effects/antihypertensive clinical uses of prazosin/alpha antagonists?

Back 20

Front 21

What are two pathological reasons for poor response to antihypertensive therapy?

Back 21

Sleep apnea and secondary hypertension

Front 22

What are some pharmacological reasons for poor response to antihypertensive therapy?

Back 22

Non adherence, suboptimal antihypertensive dose, suboptimal choice of drugs, dietary components that promote hypertension (salt, licorice)

Front 23

What is the target HTN tx blood pressure in absence of complicating comorbidities?

Back 23

< 140/90 mmHg

Front 24

What is the target HTN tx blood pressure in presence of complicating comorbidities

Back 24

< 130/90 mmHg

In presence of heart failure = < 120/80 mmHg

Front 25

What are some complicating comorbidities to hypertension?

Back 25

Diabetes, kidney disease, coronary heart disease, heart failure

Front 26

Why does dopamine act on adrenergic receptors?

Back 26

It's chemically similar to norepinephrine and epinephrine since it's a catecholamine; thus has some binding affinity for adrenergic receptors

Front 27

Dose dependent nature of dopamine

Back 27

Low dose - D1
Higher dose - B1 agonist (increases cardiac output, opposite of beta blockers)
Very high dose - A1 (peripheral vasoconstriction)

Front 28

Aliskirin

Back 28

Renin inhibitor which limits the formation of Angiotensin I. This blockade limits angiotensin II vasoconstriction and angiotensin II stimulation of aldeosterone secretion.

Front 29

Explain why diuretics are an appropriate 1st line therapy for most patients confirmed as having essential hypertension not responding to lifestyle interventions

Back 29

Reducing the Na load decreases mean blood pressure by 10 to 15 mm Hg in most patients. Other agents that affect either vasoconstriction and/or sympathetic nervous system components tend to become compensated for by increasing Na load. Thus, in mild to moderate hypertension diuretics tend to function alone better than other agents.

Front 30

Low DA dose

Back 30

'pure' dopamine respeonse; vasodilation of arterioles of the renal and splanchnic region; this is due to binding of DA to D1R in those vascular regions

Front 31

Intermediate DA dose

Back 31

this dose is high enough to allow binding to DAR and B1R; this causes cardiac manifestations of increased force and rate of heart contractions

Front 32

High DA dose

Back 32

Additional stimulation of alpha-1 adrenergic receptors and vasoconstriction throughout the body

Front 33

Digoxin

Back 33

Cardiac glycoside; Inhibitors of Na+, K+ ATPase cause cardiac cells to
accumulated Na+ inside the cell. This increases the movement of Na+ out and Ca+2
into the cell by the antiport exchanger on the cardiac cell surface. The increased
Ca+2 causes increased force of contraction. Thus cardiac glycosides force the heart
to work harder. These agents are used as a 4th stage of therapy when the patient
is in Class III or IV (Stage C or D) heart failure. They have been shown to decrease
hospitalizations but not decrease death rate.

Front 34

Dobutamine

Back 34

Beta adrenergic agonist; stimulation of the beta receptor of the heart forces the heart to increase rate and force of contraction. These agents increase
cardiac oxygen demand and may initiate arrhythmias due to the beta adrenergic
receptor activation.

Front 35

Carvedilol

Back 35

Beta adrenergic antagonist; decrease HR and FOC;

second step of therapy when added to ACE inhibitors or in combo with ACE inhibitors a component of the first step of therapy

Front 36

Furosemide

Back 36

Loop diuretic; decrease blood volume thus decrease preload; most efficacious diuretics available;

Can cause hyponatremia, hypokalemia and electrolyte imbalances

Front 37

Furosemide

Back 37

Loop diuretic; decrease blood volume thus decrease preload; most efficacious diuretics available;

Can cause hyponatremia, hypokalemia and electrolyte imbalances

Front 38

Spironolactone

Back 38

Aldosterone antagonist; act in collecting tubules of kidney at aldosterone R to cause mild diuresis and block K+ excretion. Can minimize potential for hypokalemia caused by other diuretics.

Can cause hyperkalemia an care must be taken when used in combination with ACE inhibitors

Front 39

Captopril

Back 39

ACE Inhibitors; Inhibit formation of AII, decrease breakdown of bradykinin; decrease vasoconstriction (by decreased AII) and stimulate vasodilation (by increased bradykinin) as well as decrease blood volume (by decreasing AII and thus less release of aldosterone).

First choice therapy in omst causes of heart failure

Front 40

When are beta adrenergic antagonists appropriate to use to tx heart failure?

Back 40

Chronic heart failure - need to let heart rest and decrease oxygen demand

Front 41

Explain why β‐adrenergic receptor antagonists must not be discontinued abruptly and why it is important monitoring heart rate, blood pressure, and body weight while taking these agents.

Back 41

BAR antagonists increase # BARs (upregulation) on heart -> abrupt discontinuation = excess stimulation by unopposed NE (or Epi) - Arrythmia and Heart Failure

Front 42

Give example of select heart failure patient situations where cardiac glycoside could be beneficial but why monitoring serum potassium is important when they are used.

Back 42

Examples
To support renal, hepatic or coronary perfusion.
If need positive inotrope with negative chronotrope
Monitoring of K+
Therapeutic Index very low (- ~ 2)

Front 43

Identify heart failure patient situations where a loop diuretic could be beneficial over thiazide diuretic and why potassium sparing diuretics such as aldosterone receptor antagonists should be considered to be used.

Back 43

Loops versus thiazide diuretics
Efficaciousness
Addition of potassium sparing diuretics
With digoxin – avoid hypokalemia-induced problems
Severe CHF – add on to therapy – increase survival & reduce hospitalization