LAPORAN PRAKTIKUM FARMASI KLINIS: REVIEW PENDAHULUAN (Analisis Kefarmasian Kasus CAP, COPD, HF)

 I.  THEORETICAL BASIS

 

 Community-acquired pneumonia is a leading cause of death. Risk factors include older age and medical comorbidi­ties. Diagnosis is suggested by a history of cough, dyspnea, pleuritic pain, or acute functional or cognitive decline, with abnormal vital signs (e.g., fever, tachycardia) and lung examination findings. Diagnosis should be confirmed by chest radiography or ultrasonography. Validated prediction scores for pneumonia severity can guide the decision between outpatient and inpatient therapy. Using procalcitonin as a biomarker for severe infection may further assist with risk stratification. Most outpatients with community-acquired pneumonia do not require microbiologic testing of sputum or blood and can be treated empirically with a macrolide, doxycycline, or a respiratory fluoroquinolone. Patients requiring hospitalization should be treated with a fluoroquinolone or a combination of beta-lactam plus mac­rolide antibiotics. Patients with severe infection requiring admission to the intensive care unit require dual antibiotic therapy including a third-generation cephalosporin plus a macrolide alone or in combination with a fluoroquinolone. Treatment options for patients with risk factors for Pseudomonas species include admin­istration of an antipseudomonal antibiotic and an aminoglycoside, plus azithromycin or a fluoroquinolone (Kaysin & Viera, 2016).

Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable lung disease. People with COPD must work harder to breathe, which can lead to shortness of breath and/or feeling tired. Early in the disease, people with COPD may feel short of breath when they exercise. As the disease progresses, it can be hard to breathe out (exhale) or even breathe in (inhale). A person with COPD may have obstructive bronchiolitis (bron-kee-oh-lite-is), emphysema, or a combination of both conditions. The amount of each of these conditions differs from person to person. Asthma is another disease that causes narrowing of the airways, making it hard to breathe at times, but asthma is not included in the definition of COPD. Some people do have a mix of both COPD and asthma (Lareau, dkk., 2019).

Heart failure (HF) is a clinical syndrome caused by structural and functional defects in myocardium resulting in impairment of ventricular filling or the ejection of blood. The most common cause for HF is reduced left ventricular myocardial function; however, dysfunction of the pericardium, myocardium, endocardium, heart valves or great vessels alone or in combination is also associated with HF. Some of the major pathogenic mechanisms leading to HF are increased hemodynamic overload, ischemia-related dysfunction, ventricular remodeling, excessive neuro-humoral stimulation, abnormal myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis and genetic mutations (Inamdar, A.A. & Inamdar, C.A., 2016).

 

II. ALGORITHM THERAPY

a.    Community-acquired Pneumonia Therapy Algorithm

 

b.   Chronic Obstructive Pulmonary Disease Therapy Algorithm (COPD)

 

c.    Heart Failure Therapy Algorithm

 

d. FARM

Finding	Assessment	Resolution and Monitoring
Patient progress notes: ·       GCS= 456: tgl 14-18 ·       Batuk dahak (kuning): tgl 14-18 ·       Sesak nafas: tgl 14-18 ·       Hematemesis: tgl 17-18 ·       Melena: tgl 17-18   Clinical signs: ·       TD Tgl 14/6: 130/70 Tgl 16/6: 130/70 Tgl 17/6: 130/80 Tgl 18/6: 130/80 ·       HR Tgl 14-18: di atas normal   Lab data: ·       Leukosit= 15.980 ·       Hematocrit= 35-50% ·       Ureum/BUN= 1,53 ·       Kreatinin= 1,49 ·       pCO2= 51,3 ·       HCO3= 34,9	Community Acquired Pneumonia (CAP)   Cefoperazon ·       Cephalosporin class of antibiotics, which are antibiotics for the treatment of gram-negative bacterial infections (third generation). ·       This drug works by inhibiting the formation of bacterial cell walls thereby preventing bacterial growth.   Levofloxacin ·       Quinolone class of antibiotics which are broad spectrum antibiotics for the treatment of gram-negative and gram-positive bacterial infections. ·       This drug works by cause bacterial cell death due to inhibition and increased concentration of the gyrase and topoisomerase enzymes.	·       It is recommended to use levofloxacin because of a broad-spectrum antibiotic. ·       The dose is correct: 750 mg every 48 hours (i.v.), adjusted for the patient's GFR value of 26.17 ·       GFR values ​​must be calculated because it is related to kidney function. The lower the GFR value means that the kidney condition is getting worse. ·       For all patients with kidney disorders, care should be taken to take the dosage of the drug to be given. ·       Antibiotics given (levofloxacin) are in accordance with first line therapy.
Finding	Assessment	Resolution and Monitoring
Patient progress notes: ·       GCS= 456: tgl 14-18 ·       Batuk dahak (kuning): tgl 14-18 ·       Sesak nafas: tgl 14-18 ·       Hematemesis: tgl 17-18 ·       Melena: tgl 17-18   Clinical signs: ·       TD Tgl 14/6: 130/70 Tgl 16/6: 130/70 Tgl 17/6: 130/80 Tgl 18/6: 130/80 ·       HR Tgl 14-18: di atas normal   Lab data: ·       Leukosit= 15.980 ·       Hematocrit= 35-50% ·       Ureum/BUN= 1,53 ·       Kreatinin= 1,49 ·       pCO2= 51,3 ·       HCO3= 34,9	Chronic Obstructive Pulmonary Disease (COPD)   Combivent ·       Contains Ipratropium Bromide, Salbutamol Sulphate. Salbutamol ·       Function as a bronchodilator. ·       Mechanism of action for muscle relaxation in the respiratory tract so that it stimulates adrenergic beta 2 receptors. Ipratropium bromide ·       It has a bronchodilating effect.     Pulmicort ·       Contains Budesonide. ·       Budesonide is a corticosteroid class of drugs.   NAC (Acetylcysteine) ·       Mechanism of Action: Exerts mucolytic action through its free sulfhydryl group which opens up the disulfide bonds in the mucoproteins thus lowering mucous viscosity. ·       Serves to reduce the viscosity of mucus, so it is expected that mucus can be eliminated.       Metil prednisolon ·       Corticosteroid drugs, which function to inhibit prostaglandins so it can treat inflammation of the lungs.	·       This drug is suitable for the treatment of COPD. ·       Frequency of drug use can be increased if needed. ·       The amount of puff applied depends on the strength of the active substance.                       ·       The dosage is correct.         ·       The dosage is correct.                           ·       Administration of high dose methyl prednisolone route i.v. at risk of causing hypotension and cardiac arrhythmias. ·       i.v. route dose conversion being oral by using body weight, with a conversion value of 0.5-1.7 mg/kg/day, so the maximum dose for patients with 52 kg body weight is 26-88.4 mg/kg/day.

 

 

Finding	Assessment	Resolution and Monitoring
Patient progress notes: ·       GCS= 456: tgl 14-18 ·       Batuk dahak (kuning): tgl 14-18 ·       Sesak nafas: tgl 14-18 ·       Hematemesis: tgl 17-18 ·       Melena: tgl 17-18   Clinical signs: ·       TD Tgl 14/6: 130/70 Tgl 16/6: 130/70 Tgl 17/6: 130/80 Tgl 18/6: 130/80 ·       HR Tgl 14-18: di atas normal   Lab data: ·       Leukosit= 15.980 ·       Hematocrit= 35-50% ·       Ureum/BUN= 1,53 ·       Kreatinin= 1,49 ·       pCO2= 51,3 ·       HCO3= 34,9	Heart Failure (HF)   Captopril ·       Pharmacologic Category: Angiotensin-Converting Enzyme (ACE) Inhibitor ·       Mechanism of Action: Competitive inhibitor of angiotensin-converting enzyme (ACE); prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion. ·       A persistent, dry cough in a patient using captopril as medical treatment, should be considered as an adverse effect. Lisinopril ·       Mechanism of Action: Competitive inhibitor of angiotensin-converting enzyme (ACE); prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion. ·       Labeled Indications: Treatment of hypertension, either alone or in combination with other antihypertensive agents; adjunctive therapy in treatment of heart failure (HF).       Amlodipine ·       Pharmacologic Category: Calcium Channel Blocker. ·       Mechanism of Action: Inhibits calcium ion from entering the slow channel or select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization, producing a relaxation of coronary vascular smooth muscle and coronary vasodilation; increases myocardial oxygen delivery in patients with vasospastic angina. Furosemide ·       Pharmacologic Category:  Loop Diuretic. ·       Labeled Indications: Management of edema associated with congestive heart failure and hepatic or renal disease; alone or in combination with antihypertensives in treatment of hypertension. ·       Mechanism of Action: Inhibits reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule, interfering with the chloride-binding cotransport system, thus causing increased excretion of water, sodium, chloride, magnesium, and calcium.	·       The patient has a history of COPD, which coughs, so if given captopril it will worsen the cough disease. ·       A suggestion is to stop using captopril, and only lisinopril is given.                                   ·       Lisinopril dose given to patients with kidney disorders is appropriate.                                         ·       Amlodipine selection is appropriate because it is selective in blood vessels and rarely causes tachycardia. ·       The dose of amlodipine given by p.o. route already right.                                     ·       The purpose given furosemide is for fluid retention. ·       The dose of furosemide given by i.v. route already right.

 

 

Finding	Assessment	Resolution and Monitoring
Patient progress notes: ·       GCS= 456: tgl 14-18 ·       Batuk dahak (kuning): tgl 14-18 ·       Sesak nafas: tgl 14-18 ·       Hematemesis: tgl 17-18 ·       Melena: tgl 17-18   Clinical signs: ·       TD Tgl 14/6: 130/70 Tgl 16/6: 130/70 Tgl 17/6: 130/80 Tgl 18/6: 130/80 ·       HR Tgl 14-18: di atas normal   Lab data: ·       Leukosit= 15.980 ·       Hematocrit= 35-50% ·       Ureum/BUN= 1,53 ·       Kreatinin= 1,49 ·       pCO2= 51,3 ·       HCO3= 34,9	Hematemesis and Melena   Sucralfat ·       Pharmacologic Category: Gastrointestinal Agent. ·       Mechanism of Action: Forms a complex by binding with positively charged proteins in exudates, forming a viscous paste-like, adhesive substance. This selectively forms a protective coating that acts locally to protect the gastric lining against peptic acid, pepsin, and bile salts. Lanzoprazole ·       Pharmacologic Category: Proton Pump Inhibitor. ·       Mechanism of Action: Decreases acid secretion in gastric parietal cells through inhibition of (H+, K+)-ATPase enzyme system, blocking the final step in gastric acid production.       Aspirin ·       Pharmacologic Category: Salicylate (NSID). ·       Labeled Indications: Treatment of mild-to-moderate pain, inflammation, and fever; may be used as prophylaxis of myocardial infarction; prophylaxis of stroke and/or transient ischemic episodes; management of rheumatoid arthritis, rheumatic fever, osteoarthritis, and gout (high dose); adjunctive therapy in revascularization procedures (coronary artery bypass graft [CABG], percutaneous transluminal coronary angioplasty [PTCA], carotid endarterectomy), stent implantation. ·       Mechanism of Action: Irreversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which result in decreased formation of prostaglandin precursors; has antiplatelet, antipyretic, analgesic, and anti-inflammatory properties.   Simvastatin ·       Pharmacologic Category: Antilipemic Agent, HMG-CoA Reductase Inhibitor. ·       Mechanism of Action: Simvastatin is a methylated derivative of lovastatin that acts by competitively inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis. ·       Secondary prevention of cardiovascular events in hypercholesterolemic patients with established coronary heart disease (CHD) or at high risk for CHD: To reduce cardiovascular morbidity (myocardial infarction, coronary revascularization procedures) and mortality; to reduce the risk of stroke and transient ischemic attacks. ·       Prophylaxis of atrial fibrillation among patients with stable coronary artery disease.	·       Hematemesis is bloody vomiting or material such as coffee grounds, whereas melena is black stool like tar and has a foul odor. ·       Sucralfate and lanzoprazole are given because the patient experiences hematemesis and melena. ·       The dose of sucralfate and lanzoprazole given is appropriate.                                           DRP: ·       Aspirin causes hematemesis. ·       Plan: treatment with ASA 75 mg/day to 100 mg/day for patients with non-ST-segment elevation myocardial infarction. US guidelines on reducing the gastrointestinal risks of anti-platelet therapy recommend that ASA doses >81 mg/day should not be used routinely.                                               DRP: ·       Simvastatin and amlodipine: rhabdomyolysis. ·       Amlodipine increases levels of simvastatin. Benefit of combination therapy should be carefully weighed against the potential risks of combination. Potential for increased risk of myopathy/rhabdomyolysis. ·       Plan: limit simvastatin dose to not more than 20 mg/day when use concurrently. ·       The dose of simvastatin given is appropriate.

DAFTAR PUSTAKA

 

Kaysin, A. & Viera, J.A., 2016, Community-Acquired Pneumonia in Adults: Diagnosis and Management, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

Inamdar, A.A. & Inamdar, C.A., 2016, Heart Failure: Diagnosis, Management and Utilization, Journal of Clinical Medicine, University Medical Center, Hackensack, NJ 07601, USA.

Lareau, S. dkk., 2019, Chronic Obstructive Pulmonary Disease (COPD), American Thoracic Society.