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20 Cards in this Set
- Front
- Back
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Describe the relative beta1 selectivity, intrinsic sympathomimetic activity, local anesthetic activity, GI absorption, Bioavailability, Lipid solubility, Elimination t1/2, Route of elimination of Propranolol
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Relative beta1 selectivity: 0
Intrinsic sympathomimetic activity:0 Local anesthetic activity: ++ GI absorption: >90% Bioavailability: ~30% of dose Lipid solubility: high Elimination t1/2: 3.5-6hrs Route of elimination: Hepatic metabolism |
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Describe the relative beta1 selectivity, intrinsic sympathomimetic activity, local anesthetic activity, GI absorption, Bioavailability, Lipid solubility, Elimination t1/2, Route of elimination of Metoprolol
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Relative beta1 selectivity: +
Intrinsic sympathomimetic activity:0 Local anesthetic activity: 0 GI absorption: >95% Bioavailability: ~50% of dose Lipid solubility: mod Elimination t1/2: 3-4hrs Route of elimination: Hepatic metabolism |
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Describe the relative beta1 selectivity, intrinsic sympathomimetic activity, local anesthetic activity, GI absorption, Bioavailability, Lipid solubility, Elimination t1/2, Route of elimination of Pindolol
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Relative beta1 selectivity: 0
Intrinsic sympathomimetic activity:+ Local anesthetic activity: + GI absorption: >90% Bioavailability: ~90% of dose Lipid solubility: mod Elimination t1/2: 3-4hrs Route of elimination: Renal (40% unchanged) and hepatic metabolism |
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What are the important vasodilators?
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-Hydralazine
-Nifedipine, nicardipine -Sodium nitroprusside -Fenoldopam |
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Describe the mechanism of action of Hydralazine
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-The principal action of hydralazine is considered to be a direct relaxation of vascular smooth muscle. In vitro, hydralazine relaxes only arteries with intact endothelium. Thus, the vasodilating effect is most likely through a release of endothelium derived relaxing factor (EDRF). Precapillary vessels are preferentially affected and, therefore, the drug does not cause venodilation, venous pooling or postural hypotension
-The drug has a central site of action. It is unclear, however, whether this contributes to the hypotensive effect |
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Describe the untoward effects of Hydralazine
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a. Cardiac stimulation (palpitation, tachycardia, increased CO). Often this is referred to as a "hyperdynamic state", The exact underlying mechanism is unclear but the reflex increase in sympathetic activity definitely contributes to its occurrence. Cardiac stimulation can be minimized by concurrent use of a beta blocker or a drug which modifies sympathetic function
b. Na+ and water retention c. Effects in the CNS - Headache, dizziness, acute psychotic episodes d. GI effects - Nausea, vomiting, anorexia, constipation e. Acute rheumatoid state of LE-like syndrome may be seen in patients taking high doses of the drug, especially in "slow acetylators" and women |
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Describe the effectiveness of Hydralazine
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-Hydralazine is a potent antihypertensive drug when it is used alone in high doses, but under these circumstances the incidence of side effects is always very high. Presently it is used in lower doses combined with other drugs to treat moderately severe to severe hypertension. The addition of propranolol or another drug which modifies the sympathetic function not only alleviates the undesired cardiac stimulating effects of hydralazine, but also increases the antihypertensive efficacy
-Other desirable properties of hydralazine include a decrease in supine as well as standing BP and a relatively greater decrease of renal vascular resistance than that found in other vascular beds |
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Describe Calcium Channel Blocking Drugs
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-3 major classes: phenylalkylamines, dihydropyridines, benzothiazines
-All classes are effective in causing vasodilation and are used to lower BP |
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Describe the mechanism of action of Ca channel blocking drugs
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-These drugs act by reducing Ca influx through the L-type voltage gated Ca2+ channel membranes of cardiac and smooth muscle and nerve cells. Only the effects on smooth muscle in the vasculature are discussed in this lecture
-Dihydropyridines are used primarily for their vascular effects. Nifedipine shows a large component of tonic block (because it is not ionized) in smooth muscle. Tonic block is strongest at more depolarized levels of membrane potential characteristic of smooth muscle cells |
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Describe the effects of Ca channel blocking drugs on vascular smooth muscle
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-All Ca channel blockers decrease transmembrane Ca current in vascular smooth muscle.
-Block of the Ca channels prevents contraction (vasoconstriction) and promotes relaxation (vasodilation). -Effects on atrial vasculature are greater than on venous smooth muscle |
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Describe the effects of Ca channel blocking drugs on the peripheral resistance and BP
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-Ca channel blockers decrease peripheral resistance but may not lower BP in normotensive subjects because of the reflex activation of the sympathetic nervous system. They do lower BP in patients with hypertension
-The hypotensive effect is prompt. The magnitude of the pressure drop is a function of the diastolic pressure, i.e., the higher the pretreatment pressure, the greater the fall in pressure. Supine as well as standing pressure is decreased -Different drugs have different pharmacokinetic properties necessitating different dosing schedules -Combined use with a beta blocker or a drug modifying sympathetic function has been advocated to lessen the reflex cardiac stimulating effect of nifedipine |
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Describe the untoward effects of Ca channel blocking drugs
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Dihydropyridines: tachycardia (reflexly induced from fall in BP) and palpitation are much less prominent than with hydralazine
Other effects reported in the short period of drug trial include headache, burning sensation in the face and extemities, and lower extremity edema -Verapamil can depress the heart |
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What are the important saluretics?
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-Chlorothiazine
-Hydrochlorothiazide |
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Describe saluretics
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Diuretics
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Describe the mechanism of action of saluretics
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-All have antihypertensive action. Na and water depletion appear to be the basis of these drugs' action. Site of action is the distal tubule where they block Na-Cl symport and prevent the reabsorption of Na from the renal tubule. During chronic treatment, there is a small but persistent decrease in extracellular water and plasma volume. These drugs lower BP only in hypertensive subjects, with or without edema
-Drug actions can be reversed if the patient consumes a high salt diet -Vascular smooth muscle is less sensitive to angiotensin II in the Na+ depleted state |
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Describe the untoward effects of saluretics
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1. Hypokalemia - Most troublesome with long-term use. It can be prevented using the lowest effective dose and careful dietary K+ supplement. Can lead to drug-induced long QT
2. Glucose intolerance may accompany prolonged therapy due to reduced insulin secretion 3. Hyperuricemia 4. Drug interactions - their effectiveness is reduced by NSAIDs 5. Erectile dysfunction - limits use in some patients |
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Describe the effectiveness of saluretics
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1. Benzothiadiazine saluretics can reliably lower BP in mild hypertensives. The action, however, is relatively weak and limited. The response plateaus after a certain dose is reached. These drugs do not lower the BP of normotensives
2. This class of drugs is extensively used in the treatment of hypertension: saluretics have been the principal drug used alone for mild hypertensives; in moderately severe and severe hypertensives, they are used in combination with other antihypertensive drug(s) 3. Salt sensitivity in African-American population - renal regulation of sodium |
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Describe the desirable effects of saluretics
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1. Tolerance does not develop with chronic use
2. The drug brings about a decrease in supine as well as standing BP 3. There is little or no hemodynamic alteration associated with chronic use |
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Describe the uses of saluretics
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1. CHF
2. Hypertension |
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Describe angiotensinogen
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-Renin substrate, a globulin, present in plasma
-Polymorphisms within the angiotensinogen gene have been genetically linked with some familial hypertension |
