LAPORAN PRAKTIKUM FARMASI KLINIS: GANGGUAN PADA KARDIOVASKULER

 I.  THEORETICAL BASIS

Coronary heart disease (CHD), also known as coronary artery disease (CAD), is caused by the buildup of plaque in the arteries that supply oxygen-rich blood to the heart. Plaque, a mixture of fat, cholesterol, and calcium deposits, can build up in the arteries over many years. Over time, this plaque can cause the narrowing and hardening of the coronary arteries, a condition called atherosclerosis (Figure 1). Coronary heart disease can often be symptom-free but people with CHD have an increased risk of angina (chest pain or discomfort), heart attack, heart failure, and cardiac arrhythmias. Angina and heart attacks are caused by reduced or blocked blood flow to the heart. Stable angina will typically intensify with physical exertion and subside with rest but a heart attack can cause heart muscle death and requires emergency attention (National Heart Lung and Blood Institute, 2011).

Figure 1 (Centers for Disease Control and Prevention)

 

 

Pathophysiology of coronary heart disease CHD mainly occurs due to atherosclerosis and its progression is associated with environmental and genetic factors. Atherosclerosis is a chronic process, characterized by progressive accumulation of lipids, fibrous elements, and inflammatory molecules in the walls of the large arteries. Atherosclerosis starts with the efflux of low density lipoprotein (LDL) cholesterol to the sub-endothelial space, which can be changed and oxidized by various agents. Oxidized/modified LDL particles are powerful chemotactic molecules that prompt expression of vascular cell adhesion molecules and intercellular adhesion molecules at the surface of endothelium, and stimulate monocyte adhesion and migration to the subendothelial space. Monocytes transform into macrophages in the intima media. Macrophages enchain oxidized LDL thru scavenger receptors to become foam cells and release pro inflammatory cytokines including interleukins and tumor necrosis factor. The development of fatty streak which foam cells appear in the sub-endothelial space it is the final result of this process. Moreover, in the subendothelial space accumulate other forms of leukocytes, including lymphocytes and mast cells. The interaction between monocytes, macrophages, foam cells and T-cells induce a cellular and humoral immune response (inflammatory cascade) with the production of several pro inflammatory molecules such as interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) (Themistocleous, et al., 2017).

Stroke is not only a multifactorial disease but also a gamma of different pathologies with markedly varied etiology that manifest themselves in a clinically similar way. For this reason, the accurate diagnosis of the stroke patient involves not only differentiating a stroke from other diseases with comparable clinical features, but also determining the type of stroke and its etiology. Stroke can be classified as ischemic or hemorrhagic. The latter implies the rupture of intracranial vessels leading, in a very generalized sense, to mass effect, compression, and inflammation leading to neuronal death (Mestre, et al., 2013).

The core of acute ischemic stroke (AIS) pathophysiology is the complete interruption of cerebral blood flow (CBF) leading to energy depletion and oxygen starvation with necrotic neuronal death within the first couple of minutes. Modern day therapeutic strategies are aimed at arterial recanalization in order to reestablish CBF. This rapid return to normal CBF is the turning point in salvaging the surrounding tissue of the focal necrotic core. This area lies above the threshold of cell death and below functional levels of CBF, and is commonly known as the penumbra. The penumbra is the principal target of all pharmacological treatments in AIS. The goal of AIS therapeutics is a strategy that will encompass the four cornerstones previously mentioned. The first step depends on the prompt diagnosis of AIS and the treatment aimed at preventing and treating secondary complications of the disease. The second is a fast and effective recanalization of the occluded vessel (i.e. thrombolysis) in order to ameliorate the hypoperfusion of the penumbra. Drugs that target arterial recanalization have the goal of quickly reestablishing CBF and alleviating this area of ischemia allowing the tissue to return to homeostasis. Third, are specific neuroprotective strategies that will intervene in the apoptotic cascade, excitotoxicity, reactive oxygen species (ROS) production and lipid peroxidation further protecting the ischemic tissue or reversing its damage. This branch of interventional AIS research is aimed at discovering compounds that will allow the neural tissue to better survive this period of limited oxygen and nutrients. The fourth and final step is to modulate the inflammatory response to abolish the deleterious effects of unrestrained inflammation (Mestre, et al., 2013).

II. ALGORITHM THERAPY

a.    Coronary Heart Disease Therapy Algorithm

 

INFORMATION:

·       Identification of patients:

1.   Patients with CAD often first present dramatically with symptoms of acute disease primary care should have protocols in place, including education of reception staff, to ensure patients with symptoms of acute coronary disease are taken directly to hospital by paramedics: 

a.        uncomfortable pressure, squeezing, or fullness in the chest 

b.        pain or discomfort in one or both arms, the back, the neck, and the jaw  

c.        cold sweat, nausea, or lightheadedness 

2.   Patients who present in primary care reporting exertional chest pain, particularly older high-risk patients with new or increasing symptoms, will require referral to secondary care for formal diagnosis and consideration of disease in all vascular beds.

3.   Some patients may decline referral to secondary care and should be managed within primary care as having suspected CAD, as long as this was an informed decision.

 

·       All patients with CAD should be prescribed:

1.   Statins

2.   Antiplatelet and Anticoagulant Drugs 

3.   Angiotensin-Converting Enzyme (Ace) Inhibitors 

4.   Antihypertensive Agents 

 

b.     Acute Ischemic Stroke Therapy Algorithm

  

INFORMATION:

1.     Low-dose (50-100 mg daily) aspirin is prescribed typically as a prophylactic in the prevention of cardiovascular and cerebrovascular disease. Taken daily, it effectively reduces platelet efficiency despite adequate platelet concentration in the full blood count. Due to the irreversible inactivation of platelet enzymes, adequate platelet function is only restored upon production of new platelets after halting aspirin treatment. Since platelets have an average lifespan of 10 days it is estimated that 10% of platelets are replaced every day; moreover for proper hematological function it is required that approximately 20% of platelets be functional. Thus, normal blood clotting is achieved two days after discontinuing a low-dose aspirin regimen. Although high-dose aspirin (above 300 mg daily) provides a similar inhibition time window of platelet function and recovery after cessation of treatment; nonetheless, the incidence of gastrointestinal adverse effects (i.e. gastritis) is much higher than on low-dose aspirin. However, if the formulation of high-dose aspirin includes an enteric coating, the therapeutic time window and recovery are significantly prolonged. This effect however is not seen with enteric-coated low-dose aspirin.

2.     The use of other antiplatelet medication such as clopidogrel, ticlopidine and dipyridamole has not been as formally evaluated in trials, as has aspirin. The routine use of these drugs is not recommended, however it is reasonable to suggest the use of, for example, clopidogrel at an initial dose of 300 mg, as it will efficiently inhibit platelet aggregation, when aspirin is not tolerated by the patient. Likewise, a subsequent daily dose of 75 mg of clopidogrel will maintain platelet aggregation at bay. Furthermore, the guidelines provided by the American College of Chest Physicians recommend the use of aspirin in combination with dipyridamole or clopidogrel over aspirin therapy alone.

  

d. FARM

 

CKD STAGE 5

 

CKD refers to all five stages of kidney damage, from very mild damage in stage 1 to complete kidney failure in stage 5. The stages of kidney disease are based on how well the kidneys can filter waste and extra fluid out of the blood. In the early stages of kidney disease, kidneys are still able to filter out waste from blood. In the later stages, kidneys must work harder to get rid of waste and may stop working altogether. Uremic pruritus is a common discomfort of hemodialysis patients/dialysis dependent end-stage renal disease (ESRD) (Lau et al., 2016).

Finding	Assessment	Resolution and Monitoring
Vital sign: ·       10/7: Temperature: 360 (normal: 360-370) HR: 111 (normal: 80-85x/minute) RR: 22 (normal: 20x/minute) BP: 112/65 (normal: 120/80 mmHg) SPO2: 99 ·       11/7: Temperature: 360 HR: 92 RR: 18 BP: 120/70 ·       12/7: Temperature: 360 HR: 100 RR: 20 BP: 100/60 ·       13/7: Temperature: 370 HR: 80 RR: 20 BP: 128/76 ·       14/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70 ·       15/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70   Clinical signs: ·        10/7: tingling pain in the legs, nausea and vomiting, DOE. ·       11/7: tingling pain in the legs, DOE. ·       12/7: tingling pain in the legs, DOE. ·       13/7: tingling pain in the legs. ·       14/7: tingling pain in the legs, itchy. ·       15/7: tingling pain in the legs, itchy.   Lab data: ·       Albumin= 2,28 g/dL (normal value= 3,5-5,5 g/dL) ·       Sodium= 128 Mmol/L (normal value= 136-145 Mmol/L) ·       Potassium= 3,21 Mmol/L (normal value= 3,5-5,5 Mmol/L) ·       Phospor= 8,5	CKD STAGE 5     GABAPENTIN   ·     Pharmacologic Category: Anticonvulsant. ·     Mechanism of Action: Gabapentin is structurally related to GABA. However, it does not bind to GABAA or GABAB receptors, and it does not appear to influence synthesis or uptake of GABA. High affinity gabapentin binding sites have been located throughout the brain; these sites correspond to the presence of voltage-gated calcium channels specifically possessing the alpha-2-delta-1 subunit. This channel appears to be located presynaptically, and may modulate the release of excitatory neurotransmitters which participate in epileptogenesis and nociception.	·       Gabapentin is an antiepileptic agent that has analgesic properties in neuropathic pain. ·       Gabapentin is recognized as a second- or third-line agent for generalized uremia pruritis refractory to topical emollients and/or oral antihistamines (Lau et al., 2016). ·       The dose is correct: 300 mg daily (Stiff & Lewis, 2010).

 

HYPERTENSION

Blood pressure is the force exerted by circulating blood against the walls of the body’s arteries, the major blood vessels in the body. Hypertension is when blood pressure is too high. Blood pressure is written as two numbers. The first (systolic) number represents the pressure in blood vessels when the heart contracts or beats. The second (diastolic) number represents the pressure in the vessels when the heart rests between beats. Modifiable risk factors include unhealthy diets (excessive salt consumption, a diet high in saturated fat and trans fats, low intake of fruits and vegetables), physical inactivity, consumption of tobacco and alcohol, and being overweight or obese. Non-modifiable risk factors include a family history of hypertension, age over 65 years and co-existing diseases such as diabetes or kidney disease (WHO).

Finding	Assessment	Resolution and Monitoring
Vital sign: ·       10/7: Temperature: 360 (normal: 360-370) HR: 111 (normal: 80-85x/minute) RR: 22 (normal: 20x/minute) BP: 112/65 (normal: 120/80 mmHg) SPO2: 99 ·       11/7: Temperature: 360 HR: 92 RR: 18 BP: 120/70 ·       12/7: Temperature: 360 HR: 100 RR: 20 BP: 100/60 ·       13/7: Temperature: 370 HR: 80 RR: 20 BP: 128/76 ·       14/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70 ·       15/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70   Clinical signs: ·        10/7: tingling pain in the legs, nausea and vomiting, DOE. ·       11/7: tingling pain in the legs, DOE. ·       12/7: tingling pain in the legs, DOE. ·       13/7: tingling pain in the legs. ·       14/7: tingling pain in the legs, itchy. ·       15/7: tingling pain in the legs, itchy.   Lab data: ·       Albumin= 2,28 g/dL (normal value= 3,5-5,5 g/dL) ·       Sodium= 128 Mmol/L (normal value= 136-145 Mmol/L) ·       Potassium= 3,21 Mmol/L (normal value= 3,5-5,5 Mmol/L) ·       Phospor= 8,5	HYPERTENSION   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. ·  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. ATORVASTATIN   ·  Pharmacologic Category: Antilipemic Agent, HMG-CoA Reductase Inhibitor. ·  Mechanism of Action: Inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism.	·       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 correct.: 1x 10 mg (Lacy, 2009).                       ·       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. ·       The purpose given furosemide is for fluid retention. ·       The dose of furosemide given by i.v. route already correct.     ·       “pleiotropic” effects of statins involve improving endothelial function, enhancing the stability of atherosclerotic plaques, decreasing oxidative stress and inflammation, and inhibiting the thrombogenic response. Furthermore, statins have beneficial extrahepatic effects on the immune system, CNS, and bone (Liao & Laufs, 2005). ·       The dose of atorvastatin given by p.o. route already correct.: 1x 40 mg (Lacy, 2009).

 

 

HYPERPHOSPATEMIA

 

Hyperphosphatemia is associated with significant pathophysiology in chronic kidney disease (CKD). Kidney injury impairs the ability of mammals to maintain phosphorus balance, and in human chronic kidney disease, phosphorus homeostasis is lost and positive phosphate balance occurs in the later stages (4 and 5) of kidney diseases. Loss of phosphorus homeostasis due to excretion failure in chronic kidney disease results in hyperphosphatemia due to positive balance increasing the concentration in the exchangeable phosphorus pool, often when the pool size is reduced as in the adynamic bone disorder

Information:   Phosphorus homeostasis is lost in chronic kidney disease due to failure of excretion. Despite reductions in the fraction of filtered phosphorus that is reabsorbed, eventually the filtered load becomes insufficient to maintain homeostasis, and positive phosphorus balance ensues. Kidney disease decreases the exchangeable phosphorus pool size by inhibiting bone formation. The skeletal mineralization fronts at the sites of new bone formation are significant components of the exchangeable phosphorus pool. Positive phosphate balance is associated with establishment of heterotopic mineralization sites in soft tissue organs and the vasculature. Exit from the exchangeable phosphorus pool into the vasculature is portrayed as a bidirectional process because we have been able to demonstrate that stopping the exit into the vasculature results in diminishment of established vascular calcification levels (Hruska et al., 2008).

 

Finding	Assessment		Resolution and Monitoring
Vital sign: ·       10/7: Temperature: 360 (normal: 360-370) HR: 111 (normal: 80-85x/minute) RR: 22 (normal: 20x/minute) BP: 112/65 (normal: 120/80 mmHg) SPO2: 99 ·       11/7: Temperature: 360 HR: 92 RR: 18 BP: 120/70 ·       12/7: Temperature: 360 HR: 100 RR: 20 BP: 100/60 ·       13/7: Temperature: 370 HR: 80 RR: 20 BP: 128/76 ·       14/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70 ·       15/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70   Clinical signs: ·        10/7: tingling pain in the legs, nausea and vomiting, DOE. ·       11/7: tingling pain in the legs, DOE. ·       12/7: tingling pain in the legs, DOE. ·       13/7: tingling pain in the legs. ·       14/7: tingling pain in the legs, itchy. ·       15/7: tingling pain in the legs, itchy.   Lab data: ·       Albumin= 2,28 g/dL (normal value= 3,5-5,5 g/dL) ·       Sodium= 128 Mmol/L (normal value= 136-145 Mmol/L) ·       Potassium= 3,21 Mmol/L (normal value= 3,5-5,5 Mmol/L) ·       Phospor= 8,5	HYPERPHOSPATEMIA     CALCIUM CARBONATE ·     Pharmacologic Category: Antacid; Antidote; Calcium Salt; Electrolyte Supplement, Oral. ·     Mechanism of Action: As dietary supplement, used to prevent or treat negative calcium balance; in osteoporosis, it helps to prevent or decrease the rate of bone loss. The calcium in calcium salts moderates nerve and muscle performance and allows normal cardiac function. Also used to treat hyperphosphatemia in patients with advanced renal insufficiency by combining with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces. Calcium salts as antacids neutralize gastric acidity resulting in increased gastric and duodenal bulb pH; they additionally inhibit proteolytic activity of peptic if the pH is increased >4 and increase lower esophageal sphincter tone.		·       Labeled Indications: As an antacid; treatment and prevention of calcium deficiency or hyperphosphatemia (eg, osteoporosis, osteomalacia, mild/moderate renal insufficiency, hypoparathyroidism, postmenopausal osteoporosis, rickets); has been used to bind phosphate (Lacy, 2009). ·       The dose of the phosphate binder was adjusted regularly so that the serum phosphorus levels were below 1.8 mmol/l. The mean dose of calcium carbonate 4.96 g/day.

 

CRTITICAL LIMB ISCHEMIA

 

Critical limb ischemia (CLI) is defined as ischemic rest pain, tissue loss, or gangrene in the presence of peripheral artery disease (PAD) and hypoperfusion of the lower extremity. CLI has a high short-term risk of limb loss and cardiovascular events (Kinlay, 2016).

 

Finding	Assessment	Resolution and Monitoring
Vital sign: ·       10/7: Temperature: 360 (normal: 360-370) HR: 111 (normal: 80-85x/minute) RR: 22 (normal: 20x/minute) BP: 112/65 (normal: 120/80 mmHg) SPO2: 99 ·       11/7: Temperature: 360 HR: 92 RR: 18 BP: 120/70 ·       12/7: Temperature: 360 HR: 100 RR: 20 BP: 100/60 ·       13/7: Temperature: 370 HR: 80 RR: 20 BP: 128/76 ·       14/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70 ·       15/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70   Clinical signs: ·        10/7: tingling pain in the legs, nausea and vomiting, DOE. ·       11/7: tingling pain in the legs, DOE. ·       12/7: tingling pain in the legs, DOE. ·       13/7: tingling pain in the legs. ·       14/7: tingling pain in the legs, itchy. ·       15/7: tingling pain in the legs, itchy.   Lab data: ·       Albumin= 2,28 g/dL (normal value= 3,5-5,5 g/dL) ·       Sodium= 128 Mmol/L (normal value= 136-145 Mmol/L) ·       Potassium= 3,21 Mmol/L (normal value= 3,5-5,5 Mmol/L) ·       Phospor= 8,5	CRTITICAL LIMB ISCHEMIA     CILOSTAZOL ·    Pharmacologic Category: Antiplatelet Agent; Phosphodiesterase Enzyme Inhibitor. ·    Mechanism of Action: Cilostazol and its metabolites are inhibitors of phosphodiesterase III. As a result, cyclic AMP is increased leading to reversible inhibition of platelet aggregation, vasodilation, and inhibition of vascular smooth muscle cell proliferation.             PARACETAMOL ·     Pharmacologic Category: Analgesic. ·     Mechanism of Action: Inhibits the synthesis of prostaglandins in the central nervous system and peripherally blocks pain impulse generation; produces antipyresis from inhibition of hypothalamic heat-regulating center.     GABAPENTIN ·     Pharmacologic Category: Anticonvulsant. ·     Mechanism of Action: Gabapentin is structurally related to GABA. However, it does not bind to GABAA or GABAB receptors, and it does not appear to influence synthesis or uptake of GABA. High affinity gabapentin binding sites have been located throughout the brain; these sites correspond to the presence of voltage-gated calcium channels specifically possessing the alpha-2-delta-1 subunit. This channel appears to be located presynaptically, and may modulate the release of excitatory neurotransmitters which participate in epileptogenesis and nociception.	·       Labeled Indications: Symptomatic management of peripheral vascular disease, primarily intermittent claudication. ·       The dose is correct: 2x 100 mg (p o.) (Lacy, 2009). ·       Take on empty stomach (30 minutes before or 2 hours after meals). Do not take with grapefruit juice (Lacy, 2009).   ·       DRP: Serious- Use Alternative (omeprazole+cilostazol) omeprazole will increase the level or effect of cilostazol by affecting hepatic enzyme CYP2C19 metabolism. Avoid or Use Alternate Drug (Medscape). ·       With the increasing effect of cilostazol as an antiplatelet, meaning that blood will not stop flowing and has a risk of bleeding (need monitoring).                   ·       The administration of cilostazol must be combined with analgesics, in this case paracetamol is chosen.   ·       Labeled Indications: Treatment of mild-to-moderate pain and fever (antipyretic/analgesic); does not have antirheumatic or anti-inflammatory effects. ·       The dose is correct: 325-650 mg every 4-6 hours or 1000 mg 3-4 times/day; do not exceed 4 g/day (Lacy, 2009).       ·       Management of chronic pain in adults. Use of gabapentin as an analgesic in the management of CLI and leads to significant reductions in pain scores and also improves night pain for the majority of patients (Stiff & Lewis, 2010). ·       The dose is correct: 300 mg daily (Stiff & Lewis, 2010).

 

POTASSIUM DEFFICIENCY

 

Potassium disorders are common. Hypokalemia (serum potassium level less than 3.6 mEq per L [3.6 mmol per L]). Hypokalemia results from abnormal losses, transcellular shifts, or insufficient intake. Abnormal losses are most common. Hypokalemia is often asymptomatic. Evalu­ation begins with a search for warning signs or symptoms warranting urgent treatment. Most cases of hypokalemiainduced rhythm disturbances occur in individuals with underlying heart disease (Viera & Wouk, 2015).

Finding	Assessment	Resolution and Monitoring
Vital sign: ·       10/7: Temperature: 360 (normal: 360-370) HR: 111 (normal: 80-85x/minute) RR: 22 (normal: 20x/minute) BP: 112/65 (normal: 120/80 mmHg) SPO2: 99 ·       11/7: Temperature: 360 HR: 92 RR: 18 BP: 120/70 ·       12/7: Temperature: 360 HR: 100 RR: 20 BP: 100/60 ·       13/7: Temperature: 370 HR: 80 RR: 20 BP: 128/76 ·       14/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70 ·       15/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70   Clinical signs: ·        10/7: tingling pain in the legs, nausea and vomiting, DOE. ·       11/7: tingling pain in the legs, DOE. ·       12/7: tingling pain in the legs, DOE. ·       13/7: tingling pain in the legs. ·       14/7: tingling pain in the legs, itchy. ·       15/7: tingling pain in the legs, itchy.   Lab data: ·       Albumin= 2,28 g/dL (normal value= 3,5-5,5 g/dL) ·       Sodium= 128 Mmol/L (normal value= 136-145 Mmol/L) ·       Potassium= 3,21 Mmol/L (normal value= 3,5-5,5 Mmol/L) ·       Phospor= 8,5	POTASSIUM DEFFICIENCY   KSR ·    KSR is a film-coated preparation of potassium chloride formulated for slow release. ·    Each sustained-release film-coated tablet contains potassium chloride 600 mg which is equivalent to 8 mEq each of potassium (K-) and chloride (Cl-) (Mims).   ·    Mechanism of Action: The slow- and sustained-release over a period of 6 hrs precludes high concentrations of potassium chloride against a localized area of the gut wall which might irritate or damage the mucosa. The sustained release provides conditions of maximum gastric tolerance and effective absorption for the treatment of all types of potassium deficiency, whether hypochloraemic or hypokalaemic alkalosis. KSR does not alter normal kidney function; can be used in all age groups; replaces the essential chloride anion and potassium, and so prevents hypochloraemic alkalosis (Mims).	·     Giving ksr is a premedication treatment in furosemide treatment. ·     The dose is correct: 1 or 2 tab 2-3 times daily (Mims). ·     Administration: KSR tablet should be swallowed whole with a little water preferably during meals. ·     During KSR administration, laboratory monitoring of serum electrolyte levels should be done periodically. ·     Patients with a history of congestive heart failure or myocardial infarction should maintain a serum potassium concen­tration of at least 4 mEq per L (4 mmol per L) (Viera & Wouk, 2015).

 

Finding	Assessment		Resolution and Monitoring
Vital sign: ·       10/7: Temperature: 360 (normal: 360-370) HR: 111 (normal: 80-85x/minute) RR: 22 (normal: 20x/minute) BP: 112/65 (normal: 120/80 mmHg) SPO2: 99 ·       11/7: Temperature: 360 HR: 92 RR: 18 BP: 120/70 ·       12/7: Temperature: 360 HR: 100 RR: 20 BP: 100/60 ·       13/7: Temperature: 370 HR: 80 RR: 20 BP: 128/76 ·       14/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70 ·       15/7: Temperature: 370 HR: 82 RR: 20 BP: 100/70   Clinical signs: ·        10/7: tingling pain in the legs, nausea and vomiting, DOE. ·       11/7: tingling pain in the legs, DOE. ·       12/7: tingling pain in the legs, DOE. ·       13/7: tingling pain in the legs. ·       14/7: tingling pain in the legs, itchy. ·       15/7: tingling pain in the legs, itchy.   Lab data: ·       Albumin= 2,28 g/dL (normal value= 3,5-5,5 g/dL) ·       Sodium= 128 Mmol/L (normal value= 136-145 Mmol/L) ·       Potassium= 3,21 Mmol/L (normal value= 3,5-5,5 Mmol/L) ·       Phospor= 8,5	OMEPRAZOL   ·     Pharmacologic Category: Proton Pump Inhibitor. ·     Mechanism of Action: Proton pump inhibitor; suppresses gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump.                                           METOKLOPRAMID   ·  Pharmacologic Category: Antiemetic, Gastrointestinal Agent.   · Mechanism of Action: Blocks dopamine receptors and (when given in higher doses) also blocks serotonin receptors in chemoreceptor trigger zone of the CNS; enhances the response to acetylcholine of tissue in upper GI tract causing enhanced motility and accelerated gastric emptying without stimulating gastric, biliary, or pancreatic secretions; increases lower esophageal sphincter tone.		·       Labeled Indications: Short-term (4-8 weeks) treatment of active duodenal ulcer disease or active benign gastric ulcer; treatment of heartburn and other symptoms associated with gastroesophageal reflux disease (GERD); short-term (4-8 weeks) treatment of endoscopically-diagnosed erosive esophagitis; maintenance healing of erosive esophagitis; long-term treatment of pathological hypersecretory conditions; as part of a multidrug regimen for H. pylori eradication to reduce the risk of duodenal ulcer recurrence. ·     The dose is correct. ·     Dosing: Renal Impairment No adjustment is necessary (Lacy, 2009).                               ·       Labeled Indications: Symptomatic treatment of diabetic gastric stasis; gastroesophageal reflux. ·     The dose is correct.

 

 

CALCULATION OF POTASSIUM NEEDS

	·       Sex: Male ·       Kmeasured= 3,21 Mmol/L ·       Knormal lower limit= 3,5 Mmol/L ·       Body weight= 55 kg   Kdeficit (in Mmol)  = (Knormal lower limit − Kmeasured) × kg body weight × 0.4 = (3,5-3,21) x 55 x 0,4 = 0,29 x 55 x 0,4 = 6,36/24 hours

 

CALCULATION OF SODIUM NEEDS

·       Sex: Male ·       Nameasured= 128 Mmol/L ·       Nanormal= 136-145 Mmol/L ·       Body weight= 55 kg   = 0,6 x 55 x (136-128) = 0,6 x 55 x 8 = 264/24 hours

 

 

CALCULATION OF ALBUMIN NEEDS

·       Sex: Male ·       Albuminmeasured= 2,28 g/dL ·       Albuminnormal= 3,5-5,5 g/dL ·       Body weight= 55 kg   = (10 x 5,5) - (2,28 x 55 x 0,3) = 55-37,62 = 17,38 gr albumin/100cc

 

 

CONCLUSION:

1.     Therapy is appropriate, but it is necessary to monitoring some ADR of drug which is expected to further improve the patient's condition due to the patient's poor condition.

2.     Some doses of the medicine may be adjusted related to the condition of patients who have stage 5 CKD.

3.     Therapy monitoring.

 

SUGGESTION:

1.     Increase cooperation between health workers such as doctors, pharmacy, nurses and nutrition to support the effectiveness of therapy and help improve the quality of life of patients.

 

DAFTAR PUSTAKA

 

Chopra, H.K. & Ram, S.V.C., 2019, Recent Guidelines for Hypertension A Clarion Call for Blood Pressure Control in India, Department of Cardiology, Moolchand Hospital, New Delhi,India (H.K.C.).

Falkenberg, K. & Olesen, J., 2018, Pre-Treatment With Sumatriptan For Cilostazol Induced Headache In Healthy Volunteers, The Journal of Headache and Pain, Headache Center and Department of Neurology, University of Copenhagen, Rigshospitalet Glostrup, Copenhagen, Denmark.

Hruska et al., 2008, Hyperphosphatemia of Chronic Kidney Disease, NIH Public Access, Renal Division, Department of Pediatrics, Washington University, St Louis, Missouri.

Kementerian Kesehatan Republik Indonesia, 2011, Pedoman Interpretasi Data Klinik, Jakarta.

Kinlay, S., 2016, Management of Critical Limb Ischemia, Circulation: Cardiovascular Interventions Volume 9, Issue 2, Cardiovascular Division, Department of Medicine, VA Boston Healthcare System, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA.

Kiss et al., 1990, Calcium Carbonate For The Treatment Of Hyperphosphatemia In Chronic Hemodialysis Patients, US National Library of Medicine.

Lacy, F.C., 2009, Drug Information Handbook 17^th Edition, Lexi Comp., New York, Amerika.

Lau et al., 2016, Gabapentin For Uremic Pruritus In Hemodialysis Patients: A Qualitative Systematic Review, Canadian Journal of Kidney Health and Disease, 3:14.

Liao, K.J. & Laufs, U., 2005, Pleiotropic Effects of Statins, NIH Public Access, Vascular Medicine Research, Brigham & Women’s Hospital, Cambridge, Massachusetts.

National Heart Lung and Blood Institute, 2011, Heart Disease and Stroke Prevention Program, America.

Mestre, H. et al., 2013, Pharmacological Treatment of Acute Ischemic Stroke, Faculty of Health Sciences, Universidad Anáhuac México Norte, Mexico.

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