Preparation for UTS & UAS

05 March 2022 7:31

Goal: A. ACUTE CORONARY SYNDROME E. Chronic Kidney Disease (maaf Tuhan dan penulis buku2 yg dibawah ini, F. Stroke
saya minta maaf saya potong2 bukunya, karena saya butuh) saya gak ada uang G. EPILEPSY
1. Read the Lecturer slide Notes: buat beli gambar2 di OSMOSIS. Terima kasih.  Stroke
2. Understand it
3. Make a notes  Throughout the body, cells continually perform a variety of metabolic
https://drive.google.com/drive/folders/1v6yTfjcKFcXN9XSE8ZFDFKo5h7D3n ○ A Sudden and Severe attack => Called also Ictus
4. Make a question processes. Each of these processes produces waste as a by product.
XuT : Guidelines ○ Stroke Involves Abrupt onset of focal (pertaining to or occupying focus deficit)
5. Do Spaced repetition Cleansing the blood of these toxic substances is the job of the kidneys.
 Kidney also: adjust the water content of blood
Cardiomyctes. => get O2 from blood. When ischemia => Hungry for O2.  Tweak levels of Na& K 
they send pain signal to brain.  Adjust pH levels
QUESTION  Regulation of Blood Pressure
Brain trigger adrenaline realese to blood. Adrenalone causes heart to race.  Production of red blood cells ○
A. Acute coronary syndrome => plaque is bigger => cardiomyctes work slowly and then stop to beat  GFR => The Amount of Fluid Filtered by both kidney
 Most of the Ca, Fe, Thyroid Hormone in the blood is bound to Plasma Proteins,
 Why nerve, cardiovascular and nerve are related each other? Membran of cardiomytes start rupture and release the troponins.
which Prevents these solutes from being filtered out of the blood in the  PATHOPHYSIOLOGY
○ Because in the cardiovascular center in Medulla oblongata receives glomerulus
input from cerebral cortex, limbic system, proprioceptors, When your heart isn't pumping well. => blood flow back up => shortness ○ Hemorrhagic stroke => because of rupture artery. => Hemorrhagic stroke => because of blood high
baroreceptors, and chemoreceptors. Therefore Increased of breath => because blood isn't pumping well. pressure, etc.
sympathetic stimulation and decreased parasympathetic
○ Apa itu Subarachnoid hemmorrhage?
stimulation. Cardiomytes can't be replaced. ○ intracranial hemorrhage into the subarachnoid space; the most common cause is rupture of an
 Where is the location of Cerebral cortex, limbic system, proprioceptors, aneurysm.
baroreceptors, and chemoreceptors? Full thickness infartct (transmural )
 What is major adverse cardiac events?
 What is a P2Y inhibitor?  
Healing after Myocardial Infarct
 Apa perbedaan Heart failure dan Heart attack?
 Bagaiamna treadmill bisa mendeteksi penyakit jantung koroner? Necrosis => death of our cell
 Fungsi kalium dalam tubuh?
○
 Diuretika untuk apa? Neutrophil lysing the death cardiomyctes.
 Apa fungsi calcium channel blocker?
 Kenapa Isosorbid dinitrate harus diberikan pada perut kosong? Macrophages eat the death neutrophils. All necrotic area is being
 Jadi isosorbid itu dipakenya sebelum angina atau pada saat angina? phagocytosis.  Renin-Angiotensin-Aldosterone System => A Key Mechanism for maintaining
 Kenapa antiplatelet dimakannya sesudah makan?
blood pressure
 Kenapa captopril dimakan dengan perut kosong? There's new blood vessel and colagen => granulation tissue forms.
 Apa tujuan penggunaan ACE inhibitor pada pasien ACS? ○ Ischemic Strokes => 87%. Hemorrhagic Strokes => 13%
 Apa itu nitrat sublingual ○ Kalau TIA => Yang disumbat pembuluh darah kecil => durasi nya hanya 30 menit => Stroke kecil =>
There's a scar tissue after 1 months => it's not as strong as heart muscle Warning untuk mencegah terjadinya stroke yg Sebenarnya
 Apa tujuan diuretika, beta blocker, CCB, Vasodilator, antiplatelet
○ Affected regions with cerebral blod flow < 10 ml/100 g of tissue/minute → core → these cells are
aggregasi, ACE inhibitor pada pasien ACS? Psychological healing: presumed to die within minutes of stroke onset
 WHAT IS CORONARY ARTERY REOCCLUSION? -new medication
 Cardiogenic shock? -risk of depression
 What's the meaning of negative inotropes? -loved ones

B. Dislipidemia ○ 

 What is phytosterolemia?
○ phy•tos•ter•ol•emia (fi-tos00ter-ol-e0me-e) sitosterolemia
Sitosterolemia => excessive levels of sitosterols in the blood and
tissues, caused by a hereditary defect in intestinal and biliary ○ Warning Signs of Stroke
sterol transport that results in the absorption of all sterols, 1.Sudden weakness or numbness
including those from plants. Sitosterol accumulation results in 2.Sudden change in vision
hemolysis and xanthomatosis, with tuberous and tendon 3.Sudden difficulty in speaking or understanding
xanthomas appearing in childhood. Called also phytosterolemia. 4.Sudden dizziness or loss of balance
5.Sudden headache  PATHOPHYSIOLOGY
○ Sitosterol =>
si•tos•ter•ol (si-tos0ter-ol) 1. a generic term for a group of closely
related natural plant sterols, the individual compounds being  Many Diuretics work by blocking tubular reabsorption of sodium, which also
designated by Greek letters, and sometimes subscript numerals, blocks the reabsorption of water.
as a1, a2, a3, b, and c, on the basis of differing characteristics. 2. a
pharmaceutical preparation consisting of b-sitosterol and related
plant sterols, used as an anticholesterolemic agent

○ ster•ol (ster0ol) [stereo- + -ol ] any of a group of steroids with a ○ ○

long (8–10 carbons) aliphatic side-chain at position 17 and at least
one alcoholic hydroxyl group, usually at position 3; sterols have
lipidlike solubility. Examples are cholesterol and ergosterol. Complications after a heart attack

 Kenapa Trigliserida papa tinggi banget dibandingkan LDL, HDL nya? Complication => another disease
 How High Cholesterol cause Alzheimer's disease? 
 Why 70-80% of Individuals with Dyslipidemia do not meet LDL Mycordial infarct cause => decrease in contratility, electrical instability,
Cholesterol targets despite lipid therapy?
tissue necrosis.  Increased excitatory ( Glutamat ) & Decreased
 Apakah kadar gula darah tidak terkontrol juga dapat  Diagnosis inhibitory (GABA)
 Coagulation studies ( prothrombin time, INR, clotting factors) might be needed if the patient is on warfarin,  Clinical Presentation
menyebabkan peningkatan VLDL? After a heart attack => the contratility is unstable, electrical instability, heparin or antithrombotic agents (e.g dabigatran, rivaroxaban
 What's the example of trans fat? tissue necrosis  Cardiac biomarkers (e.g CK-MB, CPL, troponin) are important due to association of cerebral vascular
 What is NLA? disease (coronary artery disease.
 How Niacin can cause Hyperglycemia? Low contratility=> Hypotensionn => decrease in vessel perfusion. =>  Brain imaging is essential for confirming diagnosis of ischemic stroke
 Why a combination with a statin fenofibrate is the preferred option? ○ CT scans => menggunakan sinar X untuk melihat bagian dalam otak => Choosen for rapid action
ischemia => cardiogenic shock => there would be a clot. => the trombus
can travel trough the body. If its stuck on cerebrovascular => it would ○ MRI (Magnetic resonance Imaging) => menggunakan gelombang elektromagnetik.
 Goals of Treatment 
cause stroke.
○ Reduce ongoing neurologic injury and decrease mortality & long-term disability
○ Prevent complications secondary to immobility and neurologic dysfunction
Electrical instability => due to conduction system migh be compromised.
○ Prevent stroke recurrence
=> aritmia.
 Treatment
Tissue necrosis => inflammation => pericarditis ○ Fibrinolytics (causing fibrinolysis)  2 BAD SEIZURES IN ONE DAY (OCTOBER 23)
○ Fibrinolytics restore cerebral blood flow → lead to improvement or resolution of neurologic
Necrosis => refer to the death of tissue. deficits

○ Fibrinolysis: The dissolution of fibrin by enzymatic
Necrosis of septum => Hypoxemia => low oxygen on the blood. Blood Action.
from the left ventricle Fibrin: the insoluble protein formed from fibrinogen by the
proteolytic action of thrombin during normal clotting of blood; it forms
the essential portion of the blood clot
Necrosis at outer wall => tissue necrosis can cause rupture of ventricle. =>
cardiac tamponade.  Diagnosis
○ Alteplase
 Electroencephalographic (EEG) is used
How to prevent complication after heart attack ? to record the electrical activity of the
brain.
Low contractility, mitral regurgitation, ventricular septal defect => run the  MRI is very useful (especially imaging of
the temporal lobes), CT scan typically is
risk of congestive heart failire
 DEFINITION □ not helpful except in the initial
 CKD defined as => Kidney Damage for >3 months, as defined by evaluation for a brain tumor or cerebral
structural/functional abnormalities of the kidney with or without decreased bleeding.
GFR => Manifest by either => Pathophysiological abnormalities or marker of  Desired Outcome
kidney damage including abnormalities in the composition of the blood or -control or reduce the frequency of seizures,
urine -minimize side effects, and
 Marker of Kidney Damage (One or more) from KDIGO □
The only fibrinolytic agents showing benefit in acute ischemic stroke patients -ensure compliance,
□ Albuminuria (Albumin Excretion Rate) ≥ 30 mg/24 hours , □
Adverse effects: intra/extracranial hemorrhage, angioedema or allergic reactions -allowing the patient to live as normal a life as possible
Albumin to Creatinine ratio 30 mg/g □
Streptokinase => Increase risk of intracranial hemorrhage & death ischemic stroke  International Classification of Epileptic Seizures
□ Urine Sediment Abnormalities □
Alteplase is given within 4.5 hours after symptom onset. Dose: 0.9 mg/kg (max 90 mg)  Partial Seizures
□ Electrolyte & other abnomarlities due to tubular disorders infused IV over 1 hr with 10% given a initial bolus over 1 minute  Generalized Seizures
□ Abnormalities detected by Histology □ Avoid anticoagulant and antiplatelet therapy for 24 hours.  Unclassified Seizures
□ Structural abnormalities detected by imaging □ Can't be given at/on:  Status epilepticus
□ History kidney of transplantation  Lewat 4,5 jam udah gaboleh dikasih alteplase.
 pasien lansia => gaboleh dikasih alteplase. Lebih dari 80 tahun
 CKD can also defined as => GFR <60 ml/min/1.73 m2 for ≥ 3 months with or  Mengkonsumsi antikoagulan
without Kidney damage  History of DM & Stroke.
 Exclusion criteriaa 
◊ Receiving heparin within 48 hr and elevated aPTT (Activated Partial
Thromboplastin Time)
◊ Recent use of anticoagulant (eg warfarin) & elevated PT (>15 second)/INR (> 1.7)
 Betablocker yang non selektif tidak boleh diberikan pada pasien yang ◊ SBP>185 mmHg or DBP>110 mmHg at time of treatment (Krisis Hipertensi)
juga memiliki asma karena nanti obat2 kek salbutamol akan saingan ◊ Recent acute myocardial infarction within 3 months
 Treatment
◊ Evidence of intracranial hemorrhage
untuk saling bekerja.
 ○ Antiplatelet Agennt
○ Aspirin 160-325 mg/day started between 24-48 hour after completion of alteplase → reduces
 Isosorbid => vasodilator long-term disability and death.
 Namun, dalam beberapa tahun terakhir, rekomendasi untuk Aspirin 50-325 mg daily 
penggunaan rutin beberapa terapi ini (misalnya, morfin, oksigen) telah Clopidogrel 75 mg daily
dikurangi. Aspirin 25 mg + extended-release dipyridamole 200 mg twice daily
○ Anticoagulant
 NITRATES ○ Currently, data are inadequate to support the routine use of heparin or other anticoagulants in the
 Nitrates promote the release of nitric oxide from the endothelium,  GFR is one of key to predict the Chronic Kidney Disease
acute management of ischemic stroke
which results in venous and arterial vasodilation ○ Patients with embolic stroke with other indication for anticoagulation (e.g atrial fibrillation) →
may receive therapy nonemergently as secondary prevention → the potential benefit should be
 ex•trap•o•la•tion (ek-strap00o-la0shen) inference of one or more
 Etiology weighed against the risk of hemorrhage
unknown values on the basis of that which is known or has been  The susceptibility factors to CKD may include: ○ Immobilized stroke patients incresed risk of deep venous thrombosis → recommended to use
observed; usually applied to estimation beyond the upper and lower  advanced age, low molecular weight heparin or low dose unfractionated heparin (eg enoxaparin SC)
ranges of observed data  low income or education, ○ Blood Pressure

 In two studies randomizing more than 77,000 patients with suspected  low birth weight, ○ Elevated BP should remain untreated in the acute period (first 7 days) after ischemic stroke →
 dikurangi.
 NITRATES
 Nitrates promote the release of nitric oxide from the endothelium,
which results in venous and arterial vasodilation
 ex•trap•o•la•tion (ek-strap00o-la0shen) inference of one or more
unknown values on the basis of that which is known or has been
observed; usually applied to estimation beyond the upper and lower
ranges of observed data
 In two studies randomizing more than 77,000 patients with suspected
MI, neither IV NTG (for 24 hours) followed by daily transdermal NTG
nor daily isosorbide mononitrate reduced the incidence of MACE.
 major adverse cardiac events
 Major adverse cardiac events (MACE) were defined as the composite
of total death; MI; stroke, hospitalization because of HF; and
revascularization, including percutaneous coronary intervention, and
coronary artery bypass graft.
 prevention of additional MACE, including reinfarction, stroke, and HF
 Lower rates of inhospital death and MACE have been associated with
increased utilization of percutaneous coronary intervention (PCI)
 Initially, SL NTG should be administered every 5 minutes for up to
three doses as needed for angina
 The most significant adverse effects of nitrates are flushing, headache,
hypotension, and tachycardia
MORPHINE
 anx•io•lyt•ic (ang00ze-o-lit0ik) 1. antianxiety. 2. antianxiety agent.
 he•mo•dy•nam•ic (he00mo-di-nam0ik) pertaining to the movements
involved in the circulation of the blood
 non-Stsegment elevation acute coronary syndrome
Aspirin 25 mg + extended release dipyridamole 200 mg twice daily
○ Anticoagulant
○ Currently, data are inadequate to support the routine use of heparin or other anticoagulants in the
 GFR is one of key to predict the Chronic Kidney Disease
acute management of ischemic stroke
○ Patients with embolic stroke with other indication for anticoagulation (e.g atrial fibrillation) →
may receive therapy nonemergently as secondary prevention → the potential benefit should be
 Etiology weighed against the risk of hemorrhage
 The susceptibility factors to CKD may include: ○ Immobilized stroke patients incresed risk of deep venous thrombosis → recommended to use
 advanced age, low molecular weight heparin or low dose unfractionated heparin (eg enoxaparin SC)
 low income or education, ○ Blood Pressure

 low birth weight, ○ Elevated BP should remain untreated in the acute period (first 7 days) after ischemic stroke →
 family history of CKD, avoid decreasing cerebral blood flow & worsening symptoms
 reduced kidney mass, ○ For patients who are not candidates for fibrinolytric → moderate hypertension is allowed. BP
 systemic inflammation and should be lowered if > 220/120 mmHg
 dyslipidemia. => Why? ○ If BP is treated in the acute phase → short-acting parenteral agents (eg labetalol, nicardipine,
nitroprusside) are preferred. The goal is lowering BP by 15% during the first 24 hr after stroke
onset. Care must be taken not to lower BP aggresively → worsen perfusion in the penumbra.
○ Patients with elevated BP & are eligible for alteplase → BP carefully lowered to <185/110 mmHg
before starting alteplase
○ Blood Glucose Control
○ Persistent hyperglycemic patients receive standardized intravenous insulin protocol to improve
□
blood glucose control for at least the first 24 to 48 h of hospitalization
○ Pada saat kena stroke dan ga ada riwayat DM => tapi hiperglikemia => ini karena respon tubuh.
Kalau kadar glukosa terlalu tinggi => biasanya diberi infus intravena.
○ They should then be transitioned to a subcutaneous insulin regimen that includes basal long- 
acting insulin along with correction rapid-acting insulin for glucose that is out of range.
○ Seizure Control
□ Dislipidemia => Atherosclerosis => Low Renal blood flow to Kidney
=> Hypertension (Because our body want to maintain Homeostatis) ○ Seizures occur in 2-23% of patients within the first days after ischemic stroke →usually focal but
=> Chronic Kidney Disease may be generalized
○ Benzodiazepines (typically diazepam and lorazepam) are the first line drugs for ongoing seizures.
 Three most common causes => DM, Hypertension & Glomerular disease
→ should be augmented(ditambah) by longer-acting anticonvulsants (eg phenytoin, phenobarbital
○ Cerebral edema control
 Some Antiepileptic drug => Low Therapeutic Index Drug
○ No evidence exists supporting the use of corticosteroids to decrease cerebral edema in acute
ischemic stroke
○ NON PHARMACOLOGIC THERAPY

 One analysis of registry data from 57,039 patients found that patients
treated for NSTE-ACS with IV morphine had higher rates of in-hospital 
death 
○
 More recently, while the use of IV morphine had no effect on in-
hospital outcomes in patients with STEMI, it was associated with
longer hospital stays and larger infarct sizes in patients with NSTEMI in
an observational analysis of 3,027 patients
 While nausea and vomiting are common, the most serious adverse ○ When Fibrinolisis is Ineffective or Contraindicated
 Excess Glucose => Non Enzymatic Glycation => Efferent arteriole become
effects to monitor are hypotension and respiratory depression.  PREVENTION 
stiff and narrow => Increased Pressure => Glomerulosclerosis => CKD
 pRIMARY  Side Effect
OXYGEN Antiplatelet (recommended only in patients with at least 6-10% risk of cardiovascular events over
 A recent pooled Cochrane review of five studies revealed that routine 10 yr
use of supplemental oxygen to patients treated for MI was of no Statins
benefit with signals suggesting infarct size may be increased Smoking cessation

Life style interventions (low fat low salt diet, exercise, weight loss
 Secondary
B-blockers

I. ANXIETY DISORDERS 
 Type of Anxiety
 Generalized anxiety disorder
○ The patients suffer from somatic anxiety symptoms as well as from restlessness, irritability,
difficulty concentrating, muscle tension, sleep disturbances and being easily fatigued.
 Because β-blockers not only possess beneficial anti-ischemic effects
but also lower the risk of MACE, their use is recommended for all
 Panic disorder
patients with ACS without contraindications
○ Panic disorder is characterized by recurrent panic attacks.
 palpitations, sweating, trembling,
 β-blockers effective anti-ischemic medications in patients
dyspnoea , choking sensations, chest
with ACS. => The reduction in myocardial oxygen demand coupled
pain, nausea,abdominal distress, dizziness, feeling of
with improved coronary blood flow to ischemic areas unreality, fear of dying, etc
 The risk of reinfarction and post-infarction angina is reduced in
patients with MI treated with β-blockers  Social anxiety disorder
 Additionally, β-blockers have been shown to improve survival in 
patients with MI, although this benefit has been questioned in recent  Other causes: autoimmune disease, polycystic kidney disease, systemic
years. Propranolol was studied in one of the earliest, large-scale infections, urinary tract infections, urinary stones and drug toxicity.
clinical trials to demonstrate that the long-term use of β-blockers  The most important predictors of progressive CKD are the persistence of
reduced mortality underlying initiation factors e.g:
 the most commonly used agents are metoprolol and carvedilol largely □ DM,
due to the mortality benefit associated with their use in the treatment □ hypertension,
□ glomerulonephritis,
○  Drug Interaction
of HF, a common complication of ACS
 The most serious adverse effects observed in patients with ACS □ polycystic kidney disease)
□ the progression factors of proteinuria,
treated with β-blockers include HF, hypotension, bradycardia, and
□ hyperlipidemia,
cardiogenic shock
□ obesity and smoking.
 in•tox•i•ca•tion (in-tok00sı˘-ka0shen) [L. in intensive + Gr. toxikon
poison] 1. stimulation, excitement, or stupefaction produced by a  Clcr = [ 140 – umur (tahun)] x berat badan/ 72 x Ccr
chemical substance, or as if by one. 2. substance i., particularly that in  Kalau cewe x 0,8  Posttraumatic stress disorder 
which the substance is alcohol (see alcohol i.). 3. poisoning.  Sbg respon thdp stimulus yg mengancam berbahaya , maka LC (locus
ceruleus ) sbg pusat alarm, akan mengaktivasi release NE dan menstimulasi
Calcium Channel Blockers  PATHOPHYSIOLOGY sistem saraf simpatik & parasimpatik

□ The majority of pathway of renal disease progression to renal
 CCBs cause arterial vasodilation, including coronary  Obat2 anxiogenik misal yohimbin & isoproterenol) akan menstimulasi LC
parenchymal damage involved 3 key elements:
vasodilation, decreasing peripheral resistance, afterload, blood dan meningkatkan aktivitas NE memicu gangguan ansietas & panik
 Loss of nephron  \
 Sebaliknya obat2 anxiolytic atau antipanic misal BZs, antidepresan ,
pressure, and myocardial oxygen demand  Glomerular capillary hypertension
klonidin ) akan menghambat LC, menurunkan aktivitas NE dan
 Proteinuria
menghambat efek obat2 anxiogenik
 Clopidogrel : P2Y12 Inhibitors  Renal parenchymal => the functional tissue of the kidney,
 Diagnosis
 Loading Dose animation consisting of the nephrons
 Symptoms, Physical and mental status examination
 Appropriate laboratory test
 CLINICAL PRESENTATION  Terapi Non Farmakologi
□ Asymptomatic.  Psikoeukasi: Konseling jangka pendek, manajemen stress, psikoterapi, meditasi, latihan.
□ People who need screening => people with 
 Terapi
DM/Hypertension/Genitourinary abnormalities & autoimmune
disease/familyy history
□ Recommended Screening Studies
 Serum Creatinine (up) => why?

 ACE inhibitors/ARB => Following MI, the benefit of ACE inhibitors has 
 Specific Antileptic Drug
been demonstrated through reductions in mortality, reinfarction rates,
 Carbamazepin
and HF, most likely through prevention of adverse cardiac remodeling  it is considered an AED of first choice for newly diagnosed partial
seizures and for primary
B. Dislipidemia The reference range for serum creatinine is 0.7 to 1.4 mg/dL GTC seizures that are not considered an emergency.
(62 to 125 μmol/L).  Neurosensory side effects (e.g., diplopia, blurred vision, nystagmus ,
 What is phytosterolemia? Creatinine is a waste product of creatine ataxia, dizziness, and
phosphate, a substance stored in muscle and used for energy. headache) are the most common, occurring in 35% to 50% of patients
 ste•no•sis (ste-no0sis) pl. steno0ses [Gr. steno¯sis] an abnormal
Creatinine is excreted by the kidney. initially.
narrowing of a duct or canal; called also arctation, coarctation, and
When renal function is impaired, blood creatinine levels rise, 
stricture. stenot0ic
but more than 50% of kidney function must be lost before this Rashes may occur in 10% of patients. Other side effects include hepatitis,
 Methods section as the probability that the effect of LDL-C
happens. Creatinine levels are not affected by diet or hormone  osteomalacia ,
differs between statin and non-statin trials relative to the
levels. Increases occur when urine formation or excretion is cardiac conduction defects, and lupus like reactions.
probability that the effect is the same, given the published data.
impaired, which occurs in renal disease, water imbalance, or  Nystagmus => pupil mata nya muter2.
Thus, the value of 7.3 10 6 provides very strong evidence
ureter blockage. From Basic Clinical Laboratory Techniques  Diplopia => melihaat benda ada 2
that there is no difference between the statin and non-statin
 GFR (down)  metabolite without affecting the concentration of carbamazepine. The
trials included in our analysis, assuming a prior probability
 Urinalysis interaction of erythromycin and clarithromycin (CYP3A4 inhibition) with
distribution that assigns equal weight to the two hypotheses.
 Imaging of Kidney carbamazepine is particularly significant.
 Cholesterol => manufactured in the liver.
 Kreatinin Klirensnya turun  Ethosuximide
□ General Symptomps stage 1-4 :  It is a first line treatment for absence seizures.
 Cholesterol to be absorbed it must be taken up by cholesterol
 General symptoms associated with stages 1-4: edema, cold  Ca channels Blockers
transporter.
intolerance, shortness of breath, fatigue, depression, muscle  Felbamate
 Defect in ABCG5/G8 transporter causes phytosterolemia
pain, palpitations and sexual dysfunction  AMPA Blockers
 High Cholesterol is one of the major risk factors for coronary artery
 Let's find out! It is approved for treating atonic seizures in patients with Lennox
disease, heart attacks and strokes, it also appears to boost the risk
◊ Edema => karena penurunan GFR juga menyebabkan Gastaut
of Alzheimer's disease 
penurunan konsentrasi air yang masuk ke Glomerulus syndrome and is effective for partial seizures as well.
 High Cholesterol leads to a build up of plaque that narrows the
dan menyebabkan imbalance air/cairan => jadinya ada  Because of the reports of aplastic anemia (1 in 3,000 patients) and
arteries.
penumpukan darah (retensi air) dan masuk ke berbagai hepatitis (1 in 10,000 patients), it is now recommended only for patients
 Majority of patients with atherosclerosis have some form of
organ seperti kaki, paru-paru. (edema pulmonal, refractory to other AEDs.
dyslipidemia
Hipertensi, edema perifer)  Phenobarbital
 70-80% of individuals with dyslipidemia do not meet LDL Cholesterol
 Phenobarbital is the drug of choice for neonatal seizures, but in other
targets despite lipid therapy Laboratory test &
situations
 High Cholesterol does not cause any symptomps, too much Other Diagnostic
it is reserved for patients who have failed other AEDs.
cholesterol may lead to atherosclerosis. Procedures
 Phenobarbital may act by interacting with GABA receptors, blocking
Increased sCr, BUN, K, phosphorus, BP, glucose high
 Dyslipidemia is the most prevalent and important modifiable risk (uncontrolled diabetes as the cause), voltage activated Ca channels, and blocking α amino 3 hydroxy 5
factor atherosclerosis LDL and triglycerides, T4 methylisoxazole 4 propionic acid and kainate receptors.
 VLDL is a precursor of LDL. (hypothyroidism), calcium (in ESRD)
  Phenytoin
 A total cholesterol score of under 200 => considered healthy in most
Decreased creatinin clearance, bicarbonate  Phenytoin is a first line AED for primary generalized convulsive seizures
cases
(metabolic acidosis), Hb/hematocrit and
 Target of lipid profile & Information
(anemia), iron stores, Vit D, albumin for partial seizures.
○ Total cholesterol => <200
(malnutrition), glcose (decreased  Phenytoin is metabolized in the liver mainly by CYP2C9, but CYP2C19 is
HDL => >40
 High Cholesterol does not cause any symptomps, too much
cholesterol may lead to atherosclerosis.
 Dyslipidemia is the most prevalent and important modifiable risk
factor atherosclerosis
 VLDL is a precursor of LDL.
 A total cholesterol score of under 200 => considered healthy in most
cases
 Target of lipid profile & Information
○ Total cholesterol => <200
○ HDL => >40
○ LDL => <100
○ Tryglyceride => <150
○ People with heart disease need to aim lower the level of LDL
not just below 100
○ Tryglycerides score of 150 or higher puts you at risk for
metabolic syndrome, linked to heat disease and diabetes.
○ Elevated triglycerides => independent risk factor for Coronary
Heart Disease.
○ If triglycerides >500 => do an prevention of acute pancreatitis!
○ If triglycerides >1000 => acute pancreatitis can happen
 The major core lipids of VLDL is a Triglyceride. VLDL is a precusor of
LDL
 A diet high in saturated fats and trans fats tends to raise the level of
LDL Cholesterol
 Statin and non statin don't have a significant different in reduce
Coronary artery disease death and non fatal Myocardial infarction
 HDL helps remove bad Cholesterol
 People who are overweight, inactive and those eat a very high
carbohydrate => tend to have high triglycerides.
 Dietary Carbohydrate => Plasma Triglyceride (VLDL)
 Diabetes, renal failure, nephrosis, physical inactivity => causes of
high triglycerides in the general population.
 CHOLESTEROL
○ Several factors can make you more likely to develop high
cholesterol => A diet high in saturated fats & cholesterol, getting
older
○ Way to lower cholesterol =>
 Dietary modifications,
 lifestyle modifications (lose weight, quit smoking)
 and also medications ( Statin & Non statin (Cholesterol
Absorption inhibitor, nicotinic acid, bile acid sequestrants,
Fibric acid Derivatives, omega 3 fatty acids)
○ Dietary modifications include
 Eat more fiber (fruit, oatmeal, cereal, vegetables)
 low-carb diet, know youf fats (no more than 35% of your
daily calories should come from fat)
○ Saturated fats => from animal products and tropical oils => Raise
LDL Cholesterol.
○ Trans fats => Increased bad cholesterol and lowers the good
cholesterol
○ Unsaturated fats => may lower LDL when combined with other
healthy diet changes => They're found in Avocados, Olive oil &
Peanut Oil
○ Trans fat and saturated fats =>found in Doughnuts, french fries,
chips, stick margarine and cookies.
 Therapy
○ Fibrate/nicotinic acid
 First line therapy for lowering triglycerides.
○ Statin
 THE MOST EFFECTIVE AND SAFE FIRST LINE OF
TREATMENT
 Statin therapy doesn't eliminate CV Risk Associated with TG
level
 Atorvastatin, Rosuvastatin, Simvastatin, Lovastatin,
Fluvastatin, Lovastatin
 Statins decrease LDL => 18-55%
 Increase HDL => 5-15%
 Decrease TG by 7-30%
 Drug of choice for elevated LDL levels.
 Prevent Cardiovascular & Cerebrovasvular events.
 Side effect
□ Myopathy and Rhabdomyolisis are associated with
statin therapy. Elevated creatine kinase (CK) => levels
may indicate statin-induced muscle damage.
□ Very rare case reports of liver failure have occurred
in patients receiving statin therapy
□ There is no evidence that statin use leads to renal
glomerular damage.
□ Monitoring CK levels is recommended only for
symtomatic patients
○ Non statin
 Cholesterol Absorption Inhibitor
□ Decrease LDL by 18-20%
□ Safe and effective adjunct to statins when further LDL
loweing is required.
□ Ezetimibe
 Niacin
□ Decrease Trygliceride by 20-50%
□ Adverse effects => Hyperglycemia, Hyperuricemia,
Hepatotoxicity ( when use slow release formulations)
□ Niacin is useful for the treatment of the dyslipidemia
of diabetes mellitus
□ Minor increases (4-5% on average) in glucose levels
result from niacin-induced insulin resistance
□ Glucose levels 125 mg/dl or posprandial glucose
levels 200 mg/dl => consider dosage reduction,
withdrawal
□ Niacin coadministration with statin does not
potentiate statin-related myopathic reactions
□ Palpitations and tachycardia are potential adverse
experiences with niacin
□ Active gout => contraindication with niacin => niacin
competes with uric acid for secretion by kidney
tubules.
 Bile Acid Sequestrants
□ Decrease LDL-> 30%
□ Trglycerides usually not affected but may increase
□ Colesevelam, Cholestyramine, Colestipol
 Fibrates
□ Decrease Triglycerides 20-50%
□ Gemfibrozil, fenofibrate, clofibrate
□ Measure serum creatinine first!
□ Consider medication if patietn has impaired renal
function or taking another medications (Metformin)
□ High dose of Statin and fibrate => increased risk for
myopathy
□ Gemfibrozil => for renal insufficiency
□ Fenofibrate/Gemfibrozil + Anticoagulants => could
prolong the PT and INR
 Omega-3 Fatty Acids
□ Decrease TG by 45%
□ Increase LDL by 44%
□ Major use is in hypertriglyceridemia (>500 mg/dL)
□ Monitor patients treated with fish oils and
anticoagulants => potential bleeding adverse
experiences
□ Clinicians need to educate patients of the wide
variance in fish oils therapies regarding efficacy,
tolerability and perhaps even safety
C. HYPERTENSION
 Cushing sydrome
Other Diagnostic
Procedures
Increased sCr, BUN, K, phosphorus, BP, glucose
(uncontrolled diabetes as the cause),
LDL and triglycerides, T4
(hypothyroidism), calcium (in ESRD)
Decreased creatinin clearance, bicarbonate
(metabolic acidosis), Hb/hematocrit
(anemia), iron stores, Vit D, albumin
(malnutrition), glcose (decreased
degradation of insulin with impaired
kidney function or poor oral intake),
Calcium (eary stages), HDL cholesterol
□ Complications
 Anemia => karena salah satu kerja ginjal untuk produksi sel
darah merah. Melalui pembentukan hormon eritropoetin
(stimulasi sumsum tulang untuk menjalankan eritropoesis) =>
sehingga pasien rentan mengalami Anemia. Anemia => Hb < 13
(Male), Hb < 12 (Female)
◊ Pathophysiology
◊ Anemic ESRD → normocytic normochromic anemia.
However, if the CKD patients have concomitant iron
deficiency → microcytic anemia
 Cardiovascular disease =>
◊ Complications e.g anemia and metabolic disorders
(abnormalities of Ca, P, PTH) contribute to CVD.
◊ The primary types of CVD found in CKD patients may
include arterial vascular diseases (e.g atherosclerosis)
and cardiomyopathy lead to development of ischemic
heart disease and its manifestation including myocardial
infarction.
 Metabolic bone disease
 Malnutrition
 Disorders of fluid & Electrolytes
◊ Pathophysiology
 noc•tu•ria => urinary frequency at night; called also
nycturia. => Present relatively early in the course of
CKD. (Stage 3)
 Total renal Na Excretion decreases (Stage 4-5) =>
Systemic hypertension (↑intravascular volume) and
volume overload with pulmonary edema can occur
 FUN FACT !??? => CKD bikin hipertensi bisa karena
eksresi Na dan air yang menurun… COOOLLLL..
 Serum K is usually maintained in the normal range
until the GFR is < 20 ml/min/1.73 m2 → at which mild
hyperkalemia is likely to develop.
 Secondary Hyperparathyroidism & Renal Osteodystrophy
◊ inhibitor (selegiline, rasagiline), agonis dopamin
◊ Renal osteodystrophy is the term used to describe the
many different patterns of the skeletal abnormalities
that occur in patients with chronic kidney disease.
Osteitis fibrosa is a manifestation of the effects of high
levels of parathyroid hormone (PTH) on bone and is
associated with a high bone turnover.
◊ Ketika pospat dalam darah meningkat => kalsium dalam
bentuk bebas jadi tuurun => terjadilah hipokalsemia. =>
kadar kalsium dalam darah turun.. Dikoreksi dengan
peningktakan aktivitas hormon PTH. Untuk mengkoreksi
kadar kalsium normal kembali dalam darah. Atau
meningkatkan reasbopsi kalsium. Kalau fosfat banyak =>
akan mengikat kalsium. Kalau kalsium nya diambil dari
tulang => tulang akan keropos.
Osteodystrophy => kondisi tulang rapuh.
 Metabolic Acidosis
◊ Pada ginjal salah satau fungsinya adalah menghasilkan
ion H+, berfungsi juga untuk menghasilkan amonia
sehingga bisa dibuffer dengan bikarbonat dan ammonia
itu pada kondisi yang normal => ketika kondisi ginjal
terjadi penurunan. Karena produksi nya kurang. ion H+
hanya bisa dinetralkan oleh bikarbonat. Akibatnya pH
darah akan turun => terjadilah asidosis.
◊ In severe CKD, all filtered bicarbonate is reclaimed but
the ability of kidney to synthesize ammonia is impaired.
◊ A clinically significant metabolic acidosis is commonly
seen when the GFR < 20 ml/min (stage 4)→ in these
patients plasma bicarbonate tends to stabilize at 15-20
mEq/L.
□ TREATMENT FOCUS
◊ Delaying or halting the CKD Progression
Treatment of the underlying condition if possible
•Aggressive blood pressure control
•Treatment of hyperlipidemia
•Aggressive glycemic control
•Avoidance of nephrotoxin (e.g., NSAIDs,
aminoglycosides, IV radiocontrast etc)
 Treatment of Hypertension in CKD without DM
 Treatment of Hypertension in CKD with DM
–
 Apa itu loop diuretika?
 Kenapa kalau albumin excretion <30 mg/24 hour itu
opsinya naikin dosis dari ACEi/ARB?
 With DM => ACEi/ARB => increase doses & or +
Diuretics => Add Dihydropiridine CCB => add minoxidil
◊ Diagnosing & Treating the CKD manifestations
 Anemia
– With ESA (Erythropoietic-Stimulating Agent)
– Why we have to check iron stores before give
ESA?
– Before starting ESA => Check Iron Stores =>
Target Iron Saturation 30-50% & Ferritin
200-500 ng/mL
– Hb should be monitored at least monthly or
more frequently after intitian of ESA and dose
change until Hb is stable.
it is reserved for patients who have failed other AEDs.
 Phenobarbital may act by interacting with GABA receptors, blocking
high
voltage activated Ca channels, and blocking α amino 3 hydroxy 5
methylisoxazole 4 propionic acid and kainate receptors.
  Phenytoin
 Phenytoin is a first line AED for primary generalized convulsive seizures
and
for partial seizures.
 Phenytoin is metabolized in the liver mainly by CYP2C9, but CYP2C19 is
also involved. Zero order kinetics occurs within the usual therapeutic
range, so any change in dose may produce disproportional changes in
serum concentrations.
 Valproic Acid
 PARKINSON
 Penyakit saraf yang mempengaruhi bagian otak
yang berfungsi mengoordinasikan gerakan
tubuh.
Akibatnya, penderita kesulitan mengatur
gerakan tubuhnya, tremor, termasuk saat
berbicara, berjalan, dan menulis.
 Parkinson => Ada Tremor pada tangan, kehilangan keseimbangan.
 Pada orang parkinson. Dopaminnya yg berkurang, Asetilkolin yang berlebih yang
 menyebabkan gangguan
 Penyebab Parkinson => Degenerasi sel-sel Dopaminergik sehingga Produksi Dopamin
Menurun => Keseimbangan dalam ganglia basalis terganggu => terjadi Kelebihan
Asetilkolin.
 Pada umumnya penyebab penyakit Parkinson tidak diketahui
 Etiology Parkinson dikenal 3 jenis
 Parkinson yang terjadi setelah
ensefalitis virus
 Parkinson setelah pemberian obat
seperti Fenotiazin dan Haloperidol
 Parkinson idiopatik
 Gejala Klinis
• 1. Merasakan tubuh kaku dan berat
• 2. Gerakan lebih kaku dan lambat
 SSRIs are indicated (first line)for the anxiety disorders and PTSD.
• 3. Tulisan tangan mengalami mengecil dan tidak
terbaca
• 4. Ayunan lengan berkurang saat berjalan
• 5. Kaki diseret saat berjalan
• 6. Suara bicara pelan dan sulit dimengerti
• 7. Tangan atau kaki gemetar
• 8. Merasa goyah saat berdiri
 • 9. Merasakan kurang bergairah
• 10. Berkurang fungsi penghidu / penciuman
• 11. Keluar air liur berlebihan
 Treatment
 Terapi hanya bersifat simptomatis, karena sel-sel
otak yang sudah rusak tidak bisa diperbaiki
lagi dan progres penyakit tidak bisa dihentikan
 Non Farmakologi
 Aktifitas : edukasi, aerobik, penguatan, peregangan,
Latihan keseimbangan
 Terapi simptomatis awal (motorik) : Levodopa, MAO-B
(pramipexol, ropinirole, rotigotine).
 Farmakologi

• levodopa,
• agonis dopamin (pramipeksol,
ropinirol, rotigotin),
• MAO-B inhibitor (selegilin,
rasagilin),
• COMT inhibitor (entacapon),
• antivirus (amantadin),
• antikolinergik
 Terapi Simptomatik lanjut
-Demensia : rivastigmin, donepezil,
galantamin, memamtin
-Psikosis : clozapine, olanzapin, quetiapin,
risperidon
-Depresi : antidepresan trisiklik
(amitriptilin), SSRIs
-Hipotensi ortostatik : midodrine,
fludrokortison
-Mual dan muntah : donperidon,
ondasentron


 Dopaminergic Drug
 menstimulasi pelepasan dopamin dan
menghambat reuptake di ujung saraf
-> amantadin
 Levodopa mengurangi semua gejala parkinson kecuali Tremor
 Levodopa tidak bisa menembus blood brain barrier
 Levodopa + Karbidopa/Benserazide
Efek levodopa pada SSP dapat diperkuat
oleh pemberian Karbidopa, suatu inhibitor
dekarboksilase dopamin yang tidak
menembus sawar darah otak.
Karbidopa mengurangi metabolisme
levodopa dalam saluran cerna dan akan
meningkatkan ketersediaan levodopa di SSP.
 Levodopa =>
Waktu paruh 1-2 jam dan harus diminum pada
keadaan perut kosong, 45 menit sebelum makan

 Anemia
C. HYPERTENSION – With ESA (Erythropoietic-Stimulating Agent)
– Why we have to check iron stores before give
 Cushing sydrome ESA?
– Before starting ESA => Check Iron Stores =>
Target Iron Saturation 30-50% & Ferritin
200-500 ng/mL
– Hb should be monitored at least monthly or
more frequently after intitian of ESA and dose
change until Hb is stable.
○ – Pemberian ESA tidak akan efektif jika ga ada
besi. Cek dulu besi nya. Jadi penting dicek
kecukupan zat besi pasien => ukur saturasi besi
dan lakukan pemeriksaan ferritin.
 The Renin Angiotensin-Aldosterone system
 Blood Pressure in Adults Classification
○ Stage 1 Hypertension: >140/90
○ Stage 2 Hypertension: >160/100
 There's primary and secondary hypertension – 
 Drugs that may increase Blood pressure => Estrogens, NSAIDs,
Amphetamines, Erythropoietin
 Factors that contributing to development of Primary hypertension
○ Deficiency in Synthesis of Vasodilating substances (prostacyclin,
bradykinin, nitric oxide)
○ Excess Vasoconstricting susbtances (Angiotensin II, endothelin
I)
○ High Sodium intake  Management of Bone & Mineral Disorder
 In primary hypertension => asymptomatic initially. Secondary – As kidney disease progresses → renal
hypertension => symptoms of the underlying disorder. activation of vit D is impaired → reduces gut
 ACE inhibitors, Angiotensin II receptor blockers (ARBs), Calcium absorption of calcium → hypocalcemia
channel blockers (CCBs) & Thiazide diurectics => First line therapy stimulates secretion of PTH
 B-blockers => with or with out compelling indication – As renal function declines → serum calcium
 ACE inhibitors: Captopril, Fosinopril balance can be maintained only at the expense
 For stage 1 Hypertension with no compelling indications: ACE of increased of bone resorption → renal
inhibitor, ARB, CCB or thiazide thype diuretic osteodystrophy
 For stage 2 Hypertension with no compelling indications => ACE – Hubungan Ca dan P04?
inhibitor/ARB with a thiazide-type diuretic OR ACE inhibitor/ARB with  pospat yang meningkat didarah akan
CCB mengikat calcium akibatnya calcium
berkurang sehingga hormon Paratiroid
D. HEART FAILURE kerjanya naik. Hormon PTH => bisa ngambil
calcium dari tulang => Renalosteodistrofi.
 Ekskresi fospat menurun saat CKD
 – Phosphat binders => Decrease phosphorus
absorption from the gut => First line agents for
Controlling both serum phosphorous and
calcium level.
Levodopa + Karbidopa/Benserazide
Efek levodopa pada SSP dapat diperkuat
oleh pemberian Karbidopa, suatu inhibitor
dekarboksilase dopamin yang tidak
menembus sawar darah otak.
Karbidopa mengurangi metabolisme
levodopa dalam saluran cerna dan akan
meningkatkan ketersediaan levodopa di SSP.
 Levodopa =>
Waktu paruh 1-2 jam dan harus diminum pada
keadaan perut kosong, 45 menit sebelum makan
karena absorpsi terganggu oleh makanan
 Dopamin Agonis efeknya tidak lebih baik
dibandingkan levodopa.
 Dopamin Agnois =>
Untuk pasien yang mengalami dyskinesia dan
overdosis akibat levodopa
 Bromokriptin
 Selegiline
 Dapat meningkatkan kerja levodopa dan bila
dikombinasi akan menurunkan dosis levodopa

Rasagiline
 COMT Inhibitor
 Entacapone, Tolacapon
 Amantadin
 Berfungsi juga meningkatkan sintesis,
pengeluaran atau ambilan dopamin dari
neuron yang sehat (jika pengeluaran
dopamin sudah maksimum, amantadin tidak
bermanfaat)


– Combination of calcium and non-calcium

containing phosphate binders (e.g., sevelamer
HCl, lanthanum carbonate) may be necessary to
avoid hypercalcemia
– Adverse effects of all phosphate binders are
limited to GI effects (constipation,
diarrhoea,nausea, vomiting, abdominal pain

– The newer vit D analogues paricalcitol and

doxercalciferol may be associated with less
hypercalcemia and hyperphosphatemia
– Pengikat pospat with Ca=> Calcium carbonate
– Pengikat Pospat withput Ca => Sevelamer
Carbonate
– Penggunaan vitamin D3 yang aktif => bisa
menekan sintesis hormon paratiroid.
 Other CKD manifestations
•Volume overload → treat with loop diuretics or
ultrafiltration
•Uremia → dialysis
•Metabolic acidosis → bicarbonate
supplementation (e.g., sodium bicarbonate)
•Hypocalcemia: Treat with calcium supplements
with or without calcitriol
•Hyperkalemia: diuretic, potassium binder
 Cardiovascular risk
– Adults aged ≥50 years with GFR < 60
mL/min/1.73 m 2 who are not being treated with
long-term dialysis or kidney transplantation
should be treated with a statin or a statin plus
ezetimibe
– Treatment with statins or statin/ezetimibe
should not be initiated in adults with dialysis-
dependent CKD, but patients already being
treated with a statin at the time of dialysis
should continue
– Adult kidney transplant patients should be
treated with a statin because of an increased
risk for coronary events
– Adults aged 18-49 years with GFR < 60
mL/min/1.73 m 2 who are not being treated with
dialysis or kidney transplantation should be
treated with statins if they have coronary
disease, diabetes, prior ischemic stroke, or an
estimated 10-year incidence of coronary death
or nonfatal myocardial infarction exceeding 10%
◊ Renal Replacement Therapy
Severe metabolic acidosis
•Uremia
•Refractory Hyperkalemia
•Pericarditis
•Encephalopathy
•Uncontrollable volume overload
•Failure to thrive and malnutrition
•Peripheral neuropathy
•Uncontrollable gastrointestinal symptoms
•In asymptomatic adult patients → GFR 5-9
ml/min/1.73 m2 irrespective of the casue of CKD or
the presence/absence of other comorbidities.

 Terapi pengganti ginjal. => paling banyak digunakan

dialisis. Kalau transplantasi ginjal jarang => biaya
operasi mahal, penggunaan immunosupresan
sepanjang hidup.
◊ Non Pharmacology Management
A. Anxiety Disorder

B. Epilepsi

C. Parkinson.