farmakologi kardiovaskuler
DESCRIPTION
DASTRANSCRIPT
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FARMAKOLOGI KARDIOVASKULER
EVI SOVIA
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Antihipertensi
Diuretik
Antihiperlipidemia
Obat-obat yang mempengaruhi darah
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Pengertian
Hipertensi : - Sistolik > 140 mmHg dan atau
- Diastolik > 90 mmHg
Mrp kondisi yg terjadi akibat tonus otot polos vaskular perifer resistensi arteri
kapasitas vena
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Mekanisme Pengontrolan Tekanan Darah
Faktor- faktor Penentu Tekanan Darah :
TD = CO X PR
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Faktor-faktor yang menurunkan tekanan darah
Peningkatan pelepasan renin
Stimulasi sistim saraf simpatis
Angiotensin I
Ginjal
Otot polos vaskuler
Resistensi perifer
Retensi air dan Na
Volume intravaskuler
Jantung CO
Angiotensin II
Pelepasan vasopresin
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Memulai atau meneruskan modifikasi gaya hidup
Tidak mencapai target tekanan darah (<140/90 mmHg). Target lebih rendah pada pasien dengan DM, gagal jantung dan gagal ginjal
Pilihan terapi inisial
Hipertensi tanpa komplikasi Penyakit penyerta-Diuretic DM tipe I dengan pruteinuria- blocker -ACE inhibitors
Gagal jantungIndikasi spesifik untuk obat lain -ACE inhibitors-ACE inhibitors -Diuretik -Angiotensin II blocker Infark miokard- blocker - blocker (non ISA)- blocker -ACE inhibitors (dengan disfungsi sistolik)-Ca antagonis Hipertensi sistolik terisolasi-Diuretik -Diuretik
-Dihidrofiridin Ca antagonis kerja lama
Target tidak tercapai
Respon inadekuat tapi ditoleransi baik
Tidak ada respon atau terjadi efek samping
Ganti dengan obat lain dari kelas yang berbeda Tambahkan obat kedua dari kelas yang berbeda (diuretik bila belum digunakan)
Target tidak tercapai
Teruskan menambah obat dari kelas lainPertimbangkan merujuk ke ahli hipertensi
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Obat-obat antihipertensi
I. DIURETIK THIAZIDE Pemakaian sangat luas Hidroklorotiazid MK : meningkatkan ekskresi Na dan air
Volume ekstraseluler menurun
CO menurun
Resistensi perifer menurun
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Efek samping :
hipokalemi, hipomagnesemi, hiperkalsemi, hiperlipidemi, hiperuricemia dan hiperglikemia
perlu observasi :
- kadar K serta tanda-tanda aritmia
- monitoring ketat pada kombinasi dengan digitalis
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II. OBAT-OBAT YG MENGUBAH FUNGSI SISTEM SARAF SIMPATIS
Umumnya dipakai pada pasien-pasien dgn hipertensi sedang –berat.
1. Obat-obat simpatolitik sentral ( Metildopa, Clonidin )
- MK : mengurangi aliran simpatis dari pusat vasomotor di otak, menurunkan tekanan darah dgn menurunkan HR, CO dan PR. Efek ini lebih kuat pada Clonidin ~ metildopa. Aliran darah ke ginjal tetap dipertahankan.
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Metildopa & clonidin tidak mengurangi aliran darah ke ginjal
- Efek Samping : Gol obat ini yg bekerja pada CNS
cenderung menyebabkan sedasi , mulut kering, depresi mental, gangguan tidur, serta mimpi buruk.
Postural hipotensi penghentian tiba-tiba dari clonidin
sering menyebabkan rebound phenomenon.
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2. Penghambat saraf simpatis
( Guanethidin, Reserpin )
MK : Menurunkan tekanan darah dengan menurunkan pelepasan norefinefrin dari neuron postganglionik simpatis. Menurunkan HR, CO dan PR.
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Karena Reserpin dapat dengan mudah masuk ke CNS, reserpin menyebabkan sedasi, mental depresi dan parkinsonism.
Mekanisme kompensasi dari obat2 pengubah fungsi simpatis adalah retensi cairan, sehingga obat-obat tersebut cocok digunakan bersama-sama dengan diuretik.
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III. BETA BLOKER ( Prototipe: Propranolol)
MK :
1. Menurunkan aktivasi Beta1 adrenoceptor jantung
Menurunkan CO2. Menurunkan Renin Angiotensin
Retensi
Na&H2O Aldosteron PR
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Contoh obat: nadolol, pindolol, timolol, labetolol, atenolol, metoprolol
Kontra indikasi :Bradikardi
Ashma
Diabetes
Periferal Vask. Disease
SE : bradikardi, abnormalitas konduksi atrioventrikular, congestive heart failure (dosis tinggi)
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IV. ALFA 1 ADRENERGIK BLOKER
( Prazosin, terazosin)
MK : Memblok reseptor alfa 1 di pembuluh darah arteri dan vena.
Retensi air cenderung terjadi bila diberikan tanpa diuretik.
Sangat baik bila dikombinasi dgn diuretik atau Beta bloker.
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V. VASODILATOR
( Hidralazin, Minoksidil )
- MK : direct acting smooth muscle relaxant vasodilatasi arteri perifer penurunan tekanan darah
merangsang refleks takhikardi, retensi cairan.
- dapat memprovokasi angina pectoris, infark miocard pada ‘ predisposed patient’.
- baik digunakan bersama-sama beta bloker dan diuretik
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VI. ANTAGONIS KALSIUM Verapamil, diltiazem, dihidrofiridin (amlodipin, felodipin,
isradipin, nicardipin, nifedipin, nisoldipin)
- MK : Menghambat influks kalsium pada sel otot polos arteri → vasodilatasi
- Terdapat perubahan hemodinamik yang berbeda dari masing-masing obat
Nifedipin : Kronotropik positif / normal Verapamil, diltiazem : Kronotropik negatif- Ketiganya punya efek vasodilatasi koroner
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VI. ACE INHIBITOR ( Captopril )
-MK: Angiotensinogen
Renin Bradikinin
Angiotensin I
ACE Inh.
Angiotensin II
ARB inaktif
Vasokonstriksi Sekresi aldosteron
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- EFEK SAMPING :
hipotensi, batuk, wheezing, angioedema. (akibat peningkatan aktivitas bradikinin )
- KI : Kehamilan ( hipotensi, anuria, renal failure pada fetus)
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VII. ANGIOTENSIN RESEPTOR BLOKER ( ARB) ( Losartan, Valsartan)
MK : Memblok pada tempat pengikatan angiotensin II di pembuluh darah dan jaringan.
Efektivitas = ACE Inh
Efek samping : <<, karena metabolisme bradikinin dan prostaglandin tidak terpengaruhi.
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ANTI HIPERLIPIDEMIA
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HIPERLIPIDEMIA : Kelainan metabolisme lipid yang ditandai
dengan keadaan hiperkolesterolemia (kolesterol total, kolesterol LDL), hipertrigliseridemia atau kombinasi antara keduanya
DISLIPIDEMIA :
Idem, disertai penurunan kadar kolesterol HDL
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OBAT ANTIHIPERTLIPIDEMIA(Lipid Lowering Drugs)
Niasin (Asam nikotinat)
Sequestran asam empedu
Derivat asam Fibrat
HMG ko A inhibitor (Statin)
Probukol
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NIASIN (asam nikotinat)
Moa : menghambat lipolisis pd jar adiposa
me↓ transport asam lemak ke hepar
me↓ sintesis VLDL
me↓ sintesis LDL
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Triasilgliserol
Asam lemakNIASIN
(-)
Asam lemak
Triasilgliserol
VLDL VLDL LDL
jaringan adiposa
Hepar
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ESO : flushing, pruritus, ggn gastrointestinal, hiperurikemi
membatasi penggunaan niasin !!
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SEQUESTRAN ASAM EMPEDU
Moa : mencegah reabsorpsi asam empedu ke hati
konversi kolesterol ke asam empedu di hati ↑
kdr kolesterol hati ↓ up regulasi reseptor LDL hati
kadar LDL plasma ↓
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Hepar
Kolesterol
Asam empedu
Asam empedu
Sequestran asam empedu
Ekskresi melalui feses
UsusReseptor LDL
LDL plasma
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ESO : gangguan gastrointestinal, gangguan absorpsi vitamin A,C,D,E,K, asam folat dan obat lain
Obat : Kolestiramin, kolestipol
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DERIVAT ASAM FIBRAT
Efek (NCEP 2001, ATP III) : LDL me ↓ 5 – 20% HDL me ↑ 10 – 35%
Trigliserida me ↓ s/d 50%1. KLOFIBRAT
MK : - Me ↑ aktivitas & sintesis lipoprotein lipase - Menghambat sintesis kolesterol - Me ↑ ekskresi kolesterol melalui empedu
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ESO : ggn GIT, myopathi, rhabdomyolisis,
keganasan, pbtkn batu empedu
2. GEMFIBROZIL
MK : sama dgn klofibrat, ttp gemfibrozil jg dpt menghambat sintesis VLDL
ESO : ggn GIT, rash
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HMG KO-A REDUKTASE INHIBITOR (Statin)
Clinical Trial : Paling efektif, ditoleransi plg baik
moa : menghambat sintesis kolesterol endogen di hati
HMG koa mevalonat ↓ HMG ko A reduktase kolesterol hepar ↓
me ↓ LDL , VLDL plasma up regulasi Reseptor LDL di hati
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HMG ko A
Mevalonat ↓↓
Kolesterol ↓↓
HMG ko A reduktase(-)STATIN
Hepar
Reseptor LDL
LDL plasma
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ESO : - minimal - pe↑ transaminase hati
- myopathi, rhabdomiolisis ( dosis tinggi ) - insufisiensi ginjal,
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PROBUKOL
MK : mencegah atherosklerosis dengan cara mencegah oksidasi kolesterol LDL
Tdk me↓ trigliserida, dapat me↓ kadar kolesterol HDL (!!!)
ESO : ggn GIT ringan, memperpanjang interval QT
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DIURETIC DRUGS
Evi SoviaLab. Farmakologi FK UNJANI
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Diuretics
Drugs inducing a state of increased urine flow
Carbonic Anhydrase Inhibitors
Loop Diuretics
Thiazide Diuretics
Potassium-sparing Diuretics
Osmotic Diuretics
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Carbonic Anhydrase InhibitorsMOAAcetazolamide inhibits carbonic anhydrase intracellularly on apical membrane of proximal tubular epithelium
H2O + CO2 H2CO3 H+ + HCO3 –
HCO3 – retained in lumen urinary pH
Loss of HCO3 – metabolic acidosis & diuretic efficacy following several days of therapy
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Therapeutic UsesP.O. once daily
Glaucoma
Epilepsy
Mountain sickness
Adverse EffectsMetabolic acidosis (mild), potassium depletion, renal stone formation, drowsiness
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Loop/High-Ceiling Diuretics
Bumetanide, furosemide, torsemide, ethacrynic acidOn ascending limb of the loop of HenleHighest efficacy in mobilizing Na & Cl
MOAInhibit Na+/K+/Cl- cotransportReabsorption of Na, K,Cl , Ca++ urine Most efficacious of diureticsRenal vasc. resistance , renal blood flowGood in poor renal function
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Therapeutic UsesDOC in acute pulmonary edema of CHDHypercalcemia
PharmacokineticsP.O., I.V., rapid onset, DOA 1-4 hrs
Adverse EffectsOtotoxicityHyperuricemiaAcute hypovolemiaPotassium depletion
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Thiazides & Related Agents
Sulfonamide derivates like acetazolamide, w/ greater activity
Affect distal tubules, w/ equal max diuretic effect, differing on potency
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A. Clorotiazide
Prototype thiazide diuretic
MOA
Inhibit Na/Cl cotransporter Na reabsorption very hyperosmolar urine
Not effective in renal function impairment
Loss of K+
Ca++ excretion
peripheral vascular resistance
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PharmacokineticsEffective orallyT1/2 40 hrsSecreted by organic acid secretory system1-3 weeks to stabilize blood pressure reduction
Therapeutic UsesHypertentionCHDRenal impairmentHypercalciuriaDiabetes insipidus
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Adverse EffectsPotassium depletion
Hyperuricemia
Volume depletion
Hypercalcemia
Hyperglycemia
Hypersensitivity
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B. HydrochlorotiazideThiazide derivative
Less ability to inhibit carbonic anhydrase
More potent, less dose than thiazide
Same efficacy as thiazide
C. ChlorthalidoneThiazide dervative
Very long DOA once daily
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D. Thiazide analogsMetolazone
More potent than thazideUnlike thiazide, causes Na excretion in advanced renal failure
IndapamideA lipid soluble, non thiazide diureticLong DOASignificant antihypertensive action w/ minimal diuretic effectsUsed in advanced renal failureMetabolized & excreted by GIT & kidneys
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Potassium-Sparing Diuretics
Act in collecting tubule
Inhibit Na reabsorption, K secretion, H secretion
Used primarily when aldosterone in in excess
In combination w/ thiazide
Stop exogenous potasium supplementation
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A. SpironolactoneMOA
A Synthetic aldosterone antagonistCompete w/ aldosterone for intracellular cytoplasmic receptor
Prevents translocation of receptor complex into target’s cell nucleus not bind to DNA
Not produce protein that response to aldosterone
Excretion of Na, retention of K, no diuretic effect
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Osmotic diuretic
Indikasi: gagal ginjal akut, menurunkan tekanan intraokuler atau intrakranial preoperasi
Manitol, urea, gliserol, isosorbid
Site of action: tubulus proksimal
MK: menurunkan resorpsi Na melalui kerja osmotiknya
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OBAT-OBAT YANG MEMPENGARUHI DARAH
EVI SOVIA
LAB. FARMAKOLOGI FK UNJANI
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OBAT YANG MEMPENGARUHI DARAH
= Obat yang digunakan untuk terapi keadaan disfungsi darah
TROMBOSIS BLEEDING
ANTITROMBOTIKANTIKOAGULANTROMBOLITIK
ASAM TRANEKSAMATASAM AMINO KAPROAT
VITAMIN K
ANEMIA
ZAT BESIASAM FOLATVITAMIN B12
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OBAT YANG DIGUNAKAN PD TROMBOSIS/ TROMBOEMBOLI
ANTITROMBOTIK/ PLATELET INHIBITORS
ANTIKOAGULAN
Mencegah agregasi trombosit
Menghambat faktor pembekuan darah
AspirinSulfinpyrazoneDipyridamoleClopidogrelTiclopidine
GPIIa/IIIa Receptor Inhibitor
HeparinWarfarinDikumarol
TROMBOLITIK
Melisiskan trombus
UrokinaseStreptokinaseTissue Plasminogen- Activator (TPA)
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ANTITROMBOTIK
1. ASPIRINMenghambat enzim sikooksigenase yang berperan dalam sintesis tromboxan A2 yang menyebabkan agregasi trombosit
Dosis : 160 – 320 mg/hr
Indikasi : profilaksis tromboemboli pada : transient cerebral ischemia, angina pectoris, myocard infark, deep vein trombosis dll
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FOSFOLIPID MEMBRAN
Fosfolipase A2
ASAM ARACHIDONAT
siklooksigenaselipoksigenase
Leukotrien
(Cox)
PG
ASPIRIN
* PG = Prostaglandin, PGI2 = Prostasiklin, TXA2 = Tromboxan A2
PGI2 TXA2
sikloendoperoksid
(-) (-)(+)
5-HPETE
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2. DIPYRIDAMOLE (persantin®)
Meningkatkan c AMP, potensiasi dengan prostasiklin
Indikasi : profilaksis tromboemboli pada pasien dgn katup jantung buatan
Biasanya dikombinasi dengan warfarin
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3. CLOPIDOGREL
Menghambat pelepasan ADP yang berperan dalam proses agregasi trombosit
ESO : nausea, dyspepsia, diare
4. GPIIB/IIIA PLATELET RESEPTOR INHIBITORMenghambat reseptor GPIIB/IIIA pada platelet. Yaitu reseptor yang
berikatan dengan fibrinogen dan platelet yang lain
Obat : Ticlopidine
ESO : Bleeding, nausea, diare
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Antikoagulan diperlukan untuk
Penyakit dengan kecenderungan terjadinya tromboemboli
Mencegah pembekuan darah utk pemeriksaan lab
Mencegah pembekuan darah untuk transfusi
ANTIKOAGULAN
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FAKTOR PEMBEKUAN DARAH DAN OBAT YANG MEMPENGARUHINYA
FAKTOR PEMBEKUAN DARAH
SINONIM TARGET KERJA DARI
IIIIIIIVV
VIIVIIIIXXXI
XIIXIII
FibrinogenProtrombin
Tissue tromboplastinCalcium
ProaccelerinProconvertin
Antihaemofilic factorChristmas factor
Stuart-Prower FactorPlasma tromboplastin
antecedentHageman factor
Fibrin stabilizing factor
Heparin, warfarin
Warfarin
Warfarin, HeparinHeparin, warfarin
Heparin
HeparinHeparin
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TROMBOLITIK
1. STREPTOKINASE
2. TISSUE-TYPE PLASMINOGEN ACTIVATOR (tPA)
3. UROKINASE
Plasminogen
Plasmin
FibrinFibrin degradation product/ Lisis
Streptokinase
Urokinase
tPA
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Digunakan pada acute tromboembolic disease (MI, emboli paru, DVT)
Mekanisme kerja : Mengaktivasi proses fibrinolisis dengan merangsang perubahan plasminogen menjadi plasmin
tPA dosis rendah bersifat fibrin selective karena selektif bekerja pada plasminogen trombus
Streptokinase dan urokinase dapat menyebabkan sistemic fibrinolytic state
ESO : Bleeding, hipersensitivity (streptokinase)
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1. ASAM AMINOKAPROAT2. ASAM TRANEXAMAT (transamin®)
Mekanisme kerja : Menghambat aktivasi plasminogen (menghambat proses fibrinolisis)
3. VITAMIN K (menadion®)Mekanisme kerja : Meningkatkan sintesis protrombin dan faktor pembekuan darah
4. PROTAMIN SULFAT
OBAT YANG DIGUNAKAN PADA PERDARAHAN (HEMOSTATIK)
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OBAT UNTUK ANEMIA
Anemia: penurunan konsentrasi sel darah merah atau hemoglobinKriteria anemia:
Wanita: Hb < 12 g/dl atau hematokrit < 37%Laki-laki:Hb < 14 g/dl atau hematokrit < 40%
Zat besiVitamin B12 dan Asam folat
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Zat besi
Indikasi: anemia defesiensi besiPemberian zat besi → produksi sel darah merah ROA: p.o atau parenteralAbsorpsi meningkat bila diberikan bersama ascorbate (mereduksi besi dari bentuk ferri menjadi ferro)Distribusi: plasma transferin protein (glikoprotein)
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Vitamin B12 dan Asam folat
Vitamin B12 dan asam folat diperlukan untuk sintesis DNA dan protein
Defisiensi → anemia megaloblastik
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