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).
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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). |
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).
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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
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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 |
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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. |
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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. |
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).
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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). |
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Finding |
Assessment |
Resolution and Monitoring |
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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: ·
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. |
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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 |
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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.
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