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CHF Case Study

CHF Case Study

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Published by Caren Chan

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Published by: Caren Chan on Mar 20, 2011
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08/05/2013

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Identify the therapeutic problem(s) where the pharmacist¶s intervention maybenefit the patient
.LM is a stage 1 (mild) hypertension patient is managed with an ACE inhibitor, enalapril.She has the signs and symptoms of congestive heart failure (CHF) namely by loss of appetite,constipation, ankle edema and slight hepatomegaly, indicative of right ventricular dysfunction. The incidence of CHF also increases markedly with age in this case; LM is an80 year old, black female. Plan treatment initiated by her physician is beneficial with acardiac glycoside or other positive inotropic agent and a diuretic, furosemide. Since ACEinhibitor is somewhat less effective in black patients (produce relatively lesser renin) inhypertension management, diuretic is used in combination. Digoxin is the only cardiacglycoside extensively reviewed because of its predominant use in clinical medicine.
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Identify and prioritize the patient specific factors that must be considered toachieve the desired therapeutic outcomes.
 
LM has congestive heart failure and high blood pressure is controlled by an ACEinhibitor in reducing the generation of a potent vasoconstrictor, angiotensin II. ACEinhibitor prolonged the survival of severe CHF patients and produce regression of leftventricular hypertrophy. Positive inotropic drugs are in use to increase cardiac outputin CHF patient.
 
LM¶s a black female patient may be of less effectiveness with the use of ACEinhibitor. Increase dosage of ACE inhibitor or use diuretic in combination for hypertension management.
 
The underlying reduction in cardiac output in CHF stimulates compensatorymechanisms, leading to sodium and water retention and increased sympatheticactivity; liberating symptom of ankle edema. Systemic congestion of hepatomegalyoccur secondary to failure of the right ventricle. Restriction of fluid is vital to preventfurther congestions. Loop diuretic may help excrete most fluid.
 
G
eneralized visceral edema may also occur, causing constipation, nausea (loss of appetite) and abdominal distension.
 
Age-related decreases in renal and hepatic function are normal in old people; mayrequire dose of drugs adjustment which are extensively metabolized by hepaticenzymes and/ or renal excreted.
 
 
 
 
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C
onduct a thorough and mechanistically oriented structure-activity analysis of all therapeutic alternatives provided in the case.
Compound 1, high-ceiling/loop diuretic, furosemide, a derivatice of anthranilic acid or o-aminobenzoic acid. The most active of a series of variously substituted derivatives arefurosemide. The sulphonamide group gives acidity to this molecure making possible for theformation of water-soluble sodium salt which can be used for intravenous administration.Replacement or removal of the sulphonamide group yields compound with little or nodiuretic activity. The chlorine and sulphonamide substitutions are features seen in other diuretics as well. An electron-withdrawing group is necessary for diuretic activity.Substitution with a lipophilic group on the aromatic amino group gives a marked increase indiuretic potency. Furosemide is a stronger acid than that of thiazide diuretics (pKa 3.9) due toits possession of a free carboxyl group. This drug is excreted primarily unchanged. A smallamount of metabolism (20%) may take place on the furan ring. Food affects its oralabsorption bioavailability. 80% is excreted in urine unchanged. It has a shorter duration of action, about 6-8 hours and better effect than that of thiazide diuretics in electrolyte and water excretion. Furosemide is effective in treatment of edemas connected with cardiac, hepatic,and renal sites and is also used in the treatment of hypertension. Dosage of furosemide is 20-80mg per day, and may be given in divided doses due to the short duration of action.Compound 2 is milrinone, ³non-glycoside´ produce both positive inotropic andconcentration-dependent vasodilatory effects. Milrinone is a specific phosphodiesteraseinhibitor (phosphodiesterase fraction III) in the myocardium. This inhibition leads to elevatedlevels of cAMP, increases in the intracellular calcium ions, followed by muscle contractility.It undergoes some conjugative metabolism in the liver and is excreted unchanged in theurine. Similar to its structurally related agent, inamrinone, it is of short-term intravenousadministration in patient with severe heart failure refractory to other measures. UnlikeMilrinon, inamrinone, orally active gives drawbacks of gastrointestinal disturbance,thrombocytopenia, and impairement of the liver function. Milrinone is of an more potent thaninamrinone, reported to be better tolerated, with no apparent thrombocytopenia or gastrointestinal disturbance. Renal impairment patients require reduced dosages of Milrinone.Compound 3, compound 4, and compound 5 are cardiac glycosides for they processedtwo portions; the sugar and the non-sugar (aglycone) moiety. The aglycone portion has a

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