UKDI

2015
PRAJOGO WIBOWO

Anti Hipertensi

JNC VII

ACE INHIBITORS
Captopril dkk menghambat
converting enzyme peptidyl dipeptidase
yang menghidrolisa angiotensin I ke
angiotensin II
inaktivasi bradikinin, potent
vasodilator, which works at least in part
by stimulating release of nitric oxide
and prostacyclin.

ACE-I & ARB

ACE-Inhibitor +
Diuretik

Target BP:
<140/90 mmHg
<130/80 mmHg if DM or
renal disease (+)
<125/75 if proteinuria >
1g/24h
If BP >20/10 mmHg above
target BP use two-drug
combination
HT + DM
BP 130-139/80-89:
lifestyle modification ~3
mo drug
BP >140/90: drug

Sources: The Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure. 2003.
Konsensus Pengendalian dan Pencegahan Diabetes Mellitus
Tipe 2 di Indonesia. 2006.

Diuretika antihipertensi
Biasa dipakai thiazide HCT single dose
25-50 mg/hari selama 2-4 minggu
(bila dosis dinaikkan sebelum 4 minggu
toksik)
Efek Hipokalemia (terapi suplemen K+),
dehidrasi, hiperurisemia (gout),
hiperglikemia, DE

CALCIUM CHANNEL BLOCKERS

CCB menurunkan PR & BP
Mekanisme kerja pada hipertensi (dan, pada
sebagian, angina) : hambat influks calcium
ke dalam sel otot polos arterial
Peningkatan risiko infark miokard, reinfarksi
& kematian, terutama oleh short acting CCB
(Nifedipine)
Pilihan Amlodipine
Nifedipine takikardi

 - BLOKER
Penurunan Cardiac Output
Metoprolol & Atenolol: 1-cardioselective
Betaxolol & bisoprolol : 1 -selective blockers yang
metabolisme primernya di hepar, tapi waktu paruhnya
lama
Nebivolol : 1 -selective blocker dan vasodilator
Labetalol : punya rasio 3:1 sebagai antagonis : per
oral tanpa pengaruh HR dan CO indikasi hipertensi
karena pheochromocytoma & hypertensive
emergencies
Carvedilol, antagonis dan (~ labetalol) indikasi
HT + heart failure

Obat HT dengan Indikasi Khusus

Source: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure. 2003.

Drug
combinations in
hypertension:
recommendations

Preferred
ACEInhibitor/diuretic
ARB/diuretic
ACE-Inhibitor/CCB
ARB/CCB

Acceptable
Beta-blocker/diuretic
CCB (dihydropyridine)/beta-blocker
CCB/diuretic
Renin inhibitor/diuretic
Renin inhibitor/CCB
Dihydopyridine CCB/non-dihydropyridine CCB

Unacceptable
ACE-Inhibitor/ARB
Renin inhibitor/ARB
Renin inhibitor/ACE-Inhibitor
RAS inhibitor/beta-blocker
CCB (non-dihydropyridine)/beta-blocker
Centrally acting agent/beta-blocker

Anti Angina

Unstable Angina

Source: European Heart Journal (European Society of Cardiology). 2006.

Lilly LS. Pathophysiology of Heart Disease. 4th ed. 2007.

Coronary Heart Disease

Source: Porths Essentials of Pathophysiology Concepts of Altered Health States

Acute Coronary Syndromes

Sources: ST-Segment Elevation Myocardial Infarction. Harrisons Principles of Internal Medicine. 17th Ed. 2008.
Lilly LS. Acute Coronary Syndromes. Pathophysiology of Heart Disease. 4th ed. 2007.

Lokasi sumbatan

Lead

Arteri Koroner

Inferior

II, III, aVF

RCA

Anteroseptal

V1-V2

LAD

Anteroapikal

V3-V4

LAD (distal)

Anterolateral

V5-V6, I, aVL

CFX

Posterior

V1-V2 (tall R wave, not

Q wave)

RCA

Sources: Lilly LS. Electrocardiogram. Pathophysiology of Heart Disease. 4th ed. 2007.

Nitrate

ANTI ANGINA

Indikasi

 Terapi spesifik untuk mencegah infark myocard dan

kematian mengandung antiplatelet (aspirin, ADP
receptor blockers) and lipid-lowering agents,
khususnya statin
Untuk terapi rumatan chronic stable angina, long-acting
nitrates, ccb, atau blockers bisa dipilih; drug of
choice tergantung individual response.
Pada HT, monotherapy dengan slowrelease atau longacting ccb or blockers mungkin adequate.
Pada normotensi, long-acting nitrates mungkin cocok.
Kombinasi blocker + ccb (eg, propranolol +
nifedipine) atau 2 CCB berbeda (eg, nifedipine and
verapamil) lebih efektif

Pembuluh darah

Emboli Paru ec DVT

Temuan klasik

Takikardia
Tanda2 disfungsi RV

Distensi vena juguler

Left parasternal lift
S2 komponen
pulmonal mengeras
Murmur sistolik yg
meningkat pada
inspirasi

Acute Limb Ischemia

Penurunan perfusi
ekstremitas secara
mendadak yang dapat
mengancam viabilitas
jaringan
Onset <2 minggu
6P Pain, pallor,
pulselessness,
paresthesia, poikilothermia,
paralisis
Golden period: 6 jam
Dx: arteriografi Doppler

Source: Inter-Society Consensus for the Management of PAD . TASC II Guidelines. 200

Chronic Limb
Ischemia
Insufisiensi arteri
perifer >2 minggu
Klaudikasio
intermitten
Dipicu aktivitas &
elevasi tungkai
Metabolisme
anaerob asam
laktat muscle
cramping
Nyeri atau
burning pada
plantar pedis

Dx: ABI

Source: Vascular Disease of The Extremities. Harrisons Principle of Internal Medicine. 17th ed. 200

Tromboangitis
Rx inflamasi non-ateromatosa (vasospasme) pada arteri &
obliterans (Buergers vena kecil ulkus atau gangren digiti
disease)
Laki-laki muda, perokok
Diabetic arteriopathy

Makrovaskuler: CAD, PAD, CVA

Mikrovaskuler: retinopati, nefropati, neuropati, gangren

Giant cell arteritis

Vaskulitis pada percabangan kranial arkus aorta, terutama a.

Temporalis (temporal arteritis) + demam, fatigue, BB turun,
anoreksia
Arteri-arteri wajah klaudikasio mandibula

Chronic limb ischemia

Terutama arteri ekstremitas bawah setelah keluar dari

percabangan aortoiliaka (a. Iliaka, a. Femoralis, a. Tibialis, a.
Dorsalis pedis)
Dx: ABI <0.9

Arteritis Takayasu

Vaskulitis granulomatosa sistemik aorta dan

percabangannya a. Subklavia & a. Brachiocephalica
Klaudikasio ekstremitas, pulsasi a. Brakhialis, perbedaan
TD >10 mmHg antara kedua lengan, bruit a. subklavia atau
aorta

Penyakit Jantung Reumatik

Sekuelae demam
reumatik akut yang
tidak di-tx adekuat
Manifestasi 10-30 th
pasca DRA
Penyakit jantung
katup
MS: fusi komisura
fish mouth
AI + MS
AS + AI + MS
Source: Valvular Heart Disease. Lilly LS. Pathophysiology of Heart Disease. 4th ed. 2007.
Sabatine MS. Pocket Medicine. 4th ed. 2011.

Endokarditis Infektif

Source: Sexton DJ. Diagnostic Approach to Infective Endocarditis. Available at:

Penyakit jantung reumatik Penyakit jantung katup (MS, AS, AI), riwayat
demam reumatik akut, tx tidak adekuat
Perikarditis

Nyeri dada tajam, menjalar ke m. Trapezius, dg

respirasi, dg duduk ke depan,
Pericardial friction rub +/-. Efusi perikardial +/EKG: ST elevasi difus, low QRS bila efusi
perikardial

Myokarditis

= perikarditis + Troponin
Tanda-tanda CHF

Penyakit Jantung Kongenital

PDA
PDA kecil: asimptomatik
PDA besar: simptomatik
ISPB berulang, takikardia,
poor feeding, slow growth
aliran ke paru

usia 2 3 bulan saat

tahanan vaskuler paru
turun
Pirau dari kiri ke kanan besar
beban volume LV & LA
dilatasi LA, LV left heart
failure
Hipertensi pulmonal
tahanan vaskuler paru tinggi
penyakit vaskuler paru
reversed shunting sianosis
(sindroma
Eisenmenger)
(s

BAYI PREMATUR
otot polos vaskuler paru belum
sempurna
tahanan vaskuler turun lebih cepat
gagal jantung lebih awal

Source: Congenital Heart Disease. Pathophysiology of Heart Disease. 2007.

Patent Ductus Arteriosus

PDA kecil
murmur kontinyu machinery murmur
pirau kiri - kanan saat fase sistolik dan diastolik

PDA besar PH
pulsus celler S2 (P2) keras
murmur kontinyu
pirau masih kiri - kanan
fase sistolik dan diastolik

murmur sistolik
pirau kiri - kanan hanya
fase sistolik

tidak terdengar murmur

murmur diastolik awal

Subklavia sinistra

aliran melewati katup mitral

Source: Roebiono P. Penyakit Jantung Bawaan: Lecture. 2009.

Claudicatio intermitten
Intermittent claudication akibat dari obstruksi
aliran darah oleh atheromas pada arteri sedang
dan besar
Pentoxifylline , a xanthine derivative, is thought
to act by reducing the viscosity of blood,
allowing it to flow more easily through partially
obstructed areas.
Cilostazol, a phosphodiesterase type 3 (PDE3)
inhibitor, is poorly understood, but may have
selective antiplatelet and vasodilating effects.

HeArt Failure

Gagal Jantung Kanan

Cor pulmonale: RV enlargement ec

primary lung disease RV hypertrophy
RV failure
Etiology:
Pulmonary interstitial disease: COPD,
asthma, interstitial lung disease
Pulmonary vascular disease: pulmonary
HT, PE
Mechanical ventilation: kiphoscoliosis,
obesity, OSA, neuromuscular

Signs & symptoms

Hypoxia tachycardia, cyanosis, clubbing

RHV RV lift
loud P2, right sided S4
RV failure backward failure
JVP, hepatomegaly (to cardiac
cirrhosis), ascites, pedal edema
tricuspid regurgitation RA dilation
right sided S4 gallop
Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Gagal Jantung Kanan

ECG: RVH
(RAD, R>S V1),
tachyarrythmia
Ro: RVH (bootshaped, apeks
terangkat)

Defibrilasi

Source: Jones SA. ECG Notes: Interpretation and Management Guide. 2005

Drugs for Heart Failure

Golongan

Sub Golongan

Sediaan

Inotropik

Glikosida jantung
Digitalis, Digoksin, Digitoksin
Agonis -adrenergik Dobutamin
Inhibitor
Amrinon, Milrinon
fosfodiesterase

Diuretik

Loop diuretik
Tiazid

Vasodilator

ACE inhibitor
Captopril, Enalapril, Fosinopril, Quinapril
Relaksasi otot polos Na nitropusid, Hidralasin, Isosorbid
Langsung
Minoksidil, Amlodipin, Felodipin

Furosemid
HCT
Bumetanid
Metolazon

Indikasi
Glikosida
Congestive heart failure
Depresi nodus AV (pada takikardi
supraventrikel paroksismal)

Digoksin
hati-hati pada GAGAL GINJAL
dosis diturunkan
Digitoksin
hati-hati pada GANGGUAN FUNGSI
HEPAR

KERACUNAN DIGITALIS
GEJALA
Ektopik ventrikel, disritmia ventrikel,
takikardi atrial paroksismal dengan
blok, blok jantung derajat 2 atau 3
(komplet)
Anoreksia, N/V, nyeri abdomen
Perubahan persepsi kuning-hijau,
halusinasi visual, psikosis

KEADAAN YANG MEMPERBERAT

Hipokalemia
Hiponatremia
Hipokalsemia
Hipomagnesia
Hipoksia
Hipotiroid
Cathecolamin

PENGOBATAN KERACUNAN DIGITALIS

Stop glikosida & diuretika yang keluar K+
Rawat ICU
EKG kontinyu
Beri fenitoin, lidokain, prokainamid untuk
takiaritmia
Beri Kalium bila AV blok, kontraindikasi
Beri Ig antidigoksin
Hindari kardioversi elektrik

Anti Aritmia

Obat Antiaritmia
Golongan obat

Mekanisme Kerja & contoh obat

Kelas I

Obat-obat yang menurunkan respon membran melalui blokade

kanal Na, dikelompokkan sesuai efeknya pada repolarisasi:
A.Kuinidin, prokainamid, disopiramid
B.Lidokain, fenitoin, tokainid
C.Ekainid, flekainid

Kelas II

Obat-obat yang menghambat aktivitas simpatik melalui inhibitor

adrenergik:
A.Propanolol
B.Obat bloker sejenis

Kelas III

Obat-obat yang memperpanjang potensial aksi:

A.Amiodaron
B.Bretilium

Kelas IV

Obat-obat yang menghambat aliran masuk Ca yang lambat:

A.Verapamil
B.Obat bloker kanal Ca

Antiaritmia yang sering dipakai

Golongan

Preparat

Inhibitor kanal Na

Kuinidin, Prokainamid, Disopiramid, Aprindin

Lidokain, Meksilatin, Fenitoin, Tokainid

Inhibitor kanal Ca

Amiodaron
Verapamil, Diltiazem

Simpatoplegia

Propanolol, Bretilium

Indikasi
Kuinidin
Aritmia ventrikel & ektopik ventrikel
Flutter (Atrial Fibrilasi) sebelumnya
diberi digitalis atau bloker untuk
hindari vagolitik pada nodus AV
Kontraksi prematur atrial
Prokainamid (= kuinidin)

Disopiramid
Takikardi ventrikel
Kontraksi ektopik ventrikel

Lidokain
Disritmia ventrikel
Fenitoin
Disritmia ventrikel pada keracunan
digitalis

Bretelium
Aritmia ventrikel di ICU
Amiodaron
Disritmia atrial & ventrikular yang
resisten terhadap obat

Diabetes

Sulfonylurea

Sumber: Konsensus Pengendalian dan Pencegahan Diabetes Mellitus Tipe 2 di Indonesia. 2006.

Insulin

Sumber: Konsensus Pengendalian dan Pencegahan Diabetes Mellitus Tipe 2 di Indonesia. PERKENI 2006.

Koma HHS
Hyperosmolar Hyperglycaemic State
Hiperglikemia ekstrim (>600 mg/dL) +
hiperosmolaritas (>320 mOsm/L) + penurunan
kesadaran
Etiologi: defisiensi insulin relatif + asupan cairan
inadekuat
Hiperglikemia diuresis osmotik deplesi volume
azotemia prerenal hiperglikemia, dst.
Ketosis (-) masih belum sepenuhnya dimengerti
defisiensi insulin pada HHS < KAD
Ketosis (-) karena keberadaan beberapa insulin hambat hormone-sensitive
lipase (lipolysis).

Pencetus : infeksi, ~ KAD, dehidrasi, AKI

Riwayat polidipsi >>, intake cairan inadekuat
Osm = 2[Na] + glu/18

Sources: Diabetes Mellitus. Harrisons Principles of Internal Medicine. 17th Ed. 2008.
Sabatine MS. Pocket Medicine. 4th Ed. 2011.

KAD &
HHS
Source: Wolsdorf J., et al.
ISPAD Clinical Practice
Consensus Guidelines 20062007: Diabetic ketoacidosis.

Manajemen HHS
Rehidrasi agresif
1-3 L NS 0.9% ~2 jam
Jika Na+>150: larutan hipotonik NaCl
0.45%

Pasca hemodinamik stabil: mengganti

defisit cairan ~8-10 L dalam 1-2 hari
NaCl 0.45% lalu D5W
Infusion rates of 200300 mL/h of
hypotonic solution

Insulin (short acting)

Bolus 10 IU atau 0.15 IU/kgBB
Drip 0.1 IU/kgBB/jam
Sources: Diabetes Mellitus. Harrisons Principles of Internal Medicine. 17th Ed. 2008.
Petunjuk Praktis Terapi Insulin pada Pasien Diabetes Melitus. PERKENI 2007.

Dislipidemia

Hipertrigliseridemia
Manajemen Dislipidemia:
1. Tentukan sasaran LDL
2. Modifikasi gaya hidup ~6 minggu
3. Terapi farmakologis
1.
2.

3.

LDL
TG
jika > 200 pasca sasaran LDL tercapai, dosis
statin atau tambahkan asam nikotinat/fibrat
HiperTG s.d. >350 mg/dL: statin dpt
digunakan
HiperTG >400 mg/dL turunkan TG!
fibrat
HDL
If isolated low HDL in CHD equivalent: nicotinic
acid, fibrate
Sources: Petunjuk Praktis Penatalaksanaan Dislipidemia. PERKENI 2004.
National Cholesterol Education Program. Clinicians Pocket Reference. 2007.

Sources: Petunjuk Praktis Penatalaksanaan Dislipidemia. PERKENI 2004.

National Cholesterol Education Program. Clinicians Pocket Reference. 2007.

Kelompok risiko

Sasaran
Kol LDL

Kadar LDL di
mana harus mulai
modifikasi gaya
hidup

Kadar Kol-LDL di mana

perlu dipertimbangkan
pemberian obat

PJK atau yang

disamakan PJK

< 100

100

> 130

> 2 faktor risiko

< 130

> 130

10 th risiko 10-20%: > 130

10 th risiko <10%: >160

0-1 faktor risiko

< 160

> 160

> 190
(160-189 obat
dipertimbangkan)

Hiper-LDL atau Hiper Kol-T

asupan lemak total & lemak

jenuh

Hiper-TG

asupan karbohidrat, alkohol, lemak

Management of Dyslipidemia in Adults. Am Fam Physician. 1998

Efek obat terhadap kadar lipid serum

(perkeni)
Obat

Kol-LDL

Kol-HDL

TG

Statin

18-55%

5-15%

7-30%

Resin

15-30%

3-5%

-/

Fibrat

5-25%

10-20%

20-50%

Asam nikotinat

5-25%

15-35%

20-50%

Penghambat
absorbsi kolesterol

17-18%

3-4%

Statins (HMG-CoA Reductase Inhibitors)

Common Features

Decrease LDL & VLDL

It is standard therapy to initiate
reductase inhibitor therapy immediately
after myocardial infarction, irrespective
of lipid levels
Hepatotoksik, rhabdomyolysis

Cholestyramine (Resin)
Treating patients having an isolated
increase in LDL

Fibrate
Hypertriglyceridemia dimana VLDL
predominan dan
dysbetalipoproteinemia.

Thyroid & Endocrine

lain

Graves Disease

Autoimmune thyroidstimulating Ig (TSI),

antithyroglobulin, ANA
Causes 60-80% of
thyrotoxicosis
Female:male = 5-10:1,
40-60 y
Clin. Manifestasion:
Diffuse, nontender
goiter. Thyroid bruit (+)
Palpitation, sweating,
anxiousness, fatigue,
weakness, weight loss,
diarrhea,
oligomenorrhea
Ophtalmology
Pretibial myxedema
Plummers nail

Ophtalmology:
preorbital
edema,
conjunctival
injection,
proptosis

Separated
fingernails from
nailbed

Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Source: Thyroid Gland Disorders. Harrisons Principles of Internal Medicine. 17th Ed. 2008.

Kretinisme
Hipotiroidisme kongenital,
bayi, anak
Etiologi: defisiensi iodine,
Manifestasi klinis:
Gangguan pertumbuhan
tulang short stature,
coarse facial features,
short stature
Gangguan perkembangan
SSP retardasi mental
t.u. In utero
Coarse facial features
Protruding tongue
Sources: Robbins & Cotrans Pathologic Basis of Disease. 7th ed. 2005.
Bates Guide to Clinical Examination.

Dwarfisme

Dwarfisme pituitari: short stature ec defisiensi growth hormone

Dwarfisme ec akondroplasia: short stature ec gangguan
pemanjangan tulang pada cakram epifisis

Gigantisme Hipersekresi growth hormone pada anak (sebelum penutupan

cakram epifisis)
Akromegali

Hipersekresi growth hormone setelah penutupan cakram epifisis

Mikrosefali

Ukuran kepala < -2 SD

Mixedema

Hipotiroidisme pada remaja atau dewasa

Ditandai dengan melambatnya aktivitas fisik dan mental, fatigue,
apatis, intoleran suhu dingin, overweight, sesak napas, edema,
broadening and coarsening of facial features, lidah membesar,
suara serak dan dalam (husky voice)

Creatinine Kinase
Isoenzim CK:
CK-MB (jantung, N <6%) pada AMI, miokarditis,
perikarditis dgn miokarditis, rhabdomiolisis, crush
injury
CK-MM (otot rangka, N = 94-100%) pada crush
injury, kejang, hipertermia maligna, injeksi IM
CK-BB (otak, N = 0%) pada cedera otak (CVA,
trauma), hipertermia maligna, infark kolon

Source: Gomella LG, Haist SA. Clinicians Pocket Reference. 11th ed. 2007.

Kasus Paru

Kasus Gagal Pengobatan

Jenis Kasus

Definisi

Kasus baru

Pasien yang tidak pernah mendapat terapi TB atau

pernah mendapat terapi <1 bulan

Kasus kambuh

Pasien yang pernah dinyatakan sembuh, timbul lagi

TB aktif

Kasus gagal (smear

positive failure)

Pasien yang sputum BTA tetap positif setelah

mendapat OAT> 5 bulan, atau
Pasien yang menghentikan pengobatannya setelah
mendapat OAT 1-5 bulan dan sputum BTA masih
positif

Kasus kronik

Pasien yang sputum BTA-nya tetap positif setelah

mendapat pengobatan ulang (retreatment) lengkap
yang disupervisi baik

MDR-TB

Resistensi terhadap rifampisin dan INH +/- OAT lain

Sumber: Tuberkulosis Pedoman Diagnosis & Penatalaksanaan di Indonesia. PDPI 2006.

Kategori OAT

Sumber: Tuberkulosis Pedoman Diagnosis & Penatalaksanaan di Indonesia. PDPI 2006.

Hepatitis Imbas Obat pada Terapi TB

Sumber: Tuberkulosis Pedoman Diagnosis & Penatalaksanaan di Indonesia. PDPI 2006.

Spirometri

PPOK: FEV1/FVC <70%

Derajat: FEV1

Source: Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. GOLD 2007.

Bronkiektasis
Dilatasi bronkhi abnormal &
permanen pooling material
purulen
Inflamasi & destruksi saluran
napas uk. menengah fibrosis,
emfisema, bronkopneumonia,
ateletaksis
Etiologi:
Infeksi: P. aeruginosa, H.
influenza
Non-infeksi: gas ammonia, aspirasi
asam lambung

Manifestasi klinis: batuk purulen

berulang-persisten, hemoptisis
PF: rhonkhi, wheezing
Dx: ro, CT (gold standard)

Source: Bronchiectasis. Harrisons Principles of Internal Medicine. 17h ed. 2008.

TB with multiple nodules

Migratory bronchopneumonia
Multiple nodules heal with >>> calcified granulomas (TB
granulomas are usually 1 or 2 in number)
Histoplasmoma=target calcification=bulls-eye calcification in center
of nodule (Pathognomonic)
www.learningradiology.com

Asidosis Respiratorik
Disorder

Problem

Etiology

Physical findings

Metabolic
acidosis

Gain of H+ or
loss of HCO3-

Diarrhea, RTA, KAD,

lactic acidosis

Kussmaul respiratory,
dry mucous membrane,
specific physical finding
to its cause

Metabolic
alkalosis

Gain of HCO3or loss of H+

Loss of gastric secretion

(vomiting), thiazide/loop
diuretics

Tetany, Chvostek sign,

specific physical finding
to its cause

Respiratory
acidosis

Hypoventilatio
n (CO2
retention)

COPD, asthma, CNS

disease, OSA

Dyspnea, anxiety,
cyanosis, specific
physical finding to its
cause

Respiratory
alkalosis

Hiperventilatio
n (CO2 loss),
high altitude

Hypoxia tachypnea
pneumonia, pulm.
Edema, PE, restrictive
lung disease

Hyperventilation,
cardiac rhythm
disturbance

Penyakit Hepar

Ikterus Obstruktif

Kolesistitis Akut et causa Kolelithiasis

Ec obstruksi duktus sistikus

(biasanya pada Hartmanns pouch)
Manifestasi klinis:
Nyeri perut kuadran kanan atas,
intensitas & durasi > episode kolik
bilier sebelumnya
Demam, mual, muntah
Massa + nyeri tekan kuadran kanan
atas abdomen, bawah iga kanan
Defans muskuler
Murphys sign (SE = 65%, SP = 87%)

Dx: USG hepatobilier

Kolelithiasis: sensitif & spesifik

Kolesistitis: penebalan dinding >5 mm,
cairan perikolesistik, Murphy
sonografik

USG: posterior acoustic shadow

& Murphy USG

Source: Biliary system. Sabistons textbook of surgery: the biological basis of modern surgical practice. 18th ed. 2007.

NEJM 2008;358:2804.

Ensefalopati Hepatik
Kegagalan hati
memetabolisme NH3 +
substansi lain edema
serebri + false
neurotransmitter
Pemicu: ammonia (intake,
sirkulasi enterohepatik)
Clinical dx MS +
asterixis
Tx: protein, laktulosa,
rifaximin
Profilaksis 2o: laktulosa +
rifaximin
Source: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Pankreatitis Akut ec Kolelithiasis

Etiologi: batu empedu
(40%),alkoholisme (30%)
Manifestasi: nyeri
epigastrium menjalar ke
punggung, terusmenerus, dg bungkuk
Lab:

amilase, lipase
SGPT >3x menyokong
pankreatitis ec gallstone
ALP, bilirubin tidak
spesifik

Source: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Abses Hepar
Manifestasi klinis
Amoebiasis intestinal ulkus
bergaung (flask-shaped ulcer)
diare berdarah
Amoebiasis ekstraintestinal
menembus dinding colon sistemik
Amoebic liver disease (abses hepar)
demam menetap, nyeri epigastrium,
diare

Dx:
Disenteri amoeba: feses trofozoit
yang mengandung RBC di feses,
PCR, uji antigen feses
Amoebic liver disease USG,
serologi, mikroskopi sediaan
aspirasi

Tx:
Metronidazole 3 x 750 mg ~7-10 hari

Sources: Robbins & Cotrans Pathologic Basis of Disease. 7th ed. 2005.
Susanto, L. Parasitology lecture gastrointestinal module. Faculty of Medicine University of Indonesia.

Hepatitis Akut
Hepatitis A

Fecal-oral
No
chronicity
IgM:
acute
infection
IgG: past
infection

 Blood, sexual,
perinatal
Incubation 1-6 (23) mo
Acute infection:

Hepatitis B

70% subclinical
30% jaundice
1% fulminant
hepatitis

Chronicity
5% (adultacquired)
90% (perinatally
acquired)
Cirrhosis: 20-30%
of chronic hep B

Source: Sabatine MS. Pocket Medicine. 4th ed. 201

Acute Viral Hepatitis. Harrisons Principle of Internal Medicine. 17th ed. 200

Serologi & Virologi HBV

Petanda

Interpretasi

HBsAg

Infeksi aktif/sedang berlangsung. Muncul sebelum gejala2 muncul

HBeAg

Bukti replikasi virus dan infektivitas

IgM anti-HBc

Infeksi akut
Window period (HBsAg (-), anti-HBs not yet (+)

Anti-HBs

Resolusi penyakit aktif

Petanda imunitas (petanda tunggal pasca imunisasi)

IgG anti-HBc

Infeksi HBV lampau (HBsAg (-)) atau kronis (HBsAg (+))

IgG anti-HBe

Replikasi virus <<, infektivitas <<

HBV DNA

Replikasi aktif virus di hepar

Source: Sabatine MS. Pocket Medicine. 4th ed. 201

Hepatitis C

90%
transfusion,
50% IDU
Little evidence
of sexual or
perinatal
transmission
Incubation 1-5
(2) mo
Acute infection:

75%
subclinical
25% jaundice

Chronicity

50%

20%
Source: Sabatine Cirrhosis:
MS. Pocket Medicine.
4th ed. 201
ofInternal
chronic
Acute Viral Hepatitis. Harrisons Principle of
Medicine. 17th ed. 200

Barium Enema Ca Kolorektal

IBD: risiko
Gejala:
Kolon distal: perubahan pola
defekasi, obstruksi, kolik abdomen,
hematochezia
Kolon proksimal: anemia def. Besi,
nyeri dull, feses cair

Tumor marker: CA 19-9

Screening:
Barium enema Se 50-90%
Kolonoskopi gold standard utk
screening Se 90%
CT kolonografi

Dx: Biopsi kolonoskopi

Barium enema double

contrast: karsinoma anular
konstriktif: apple core
lesion

Sources: Lieberman DA. Screening for colorectal cancer. NEJM 2009;361:1179.

www.learningradiology.com

Systemic Lupus Erythematosus

Reaksi Hipersensitivitas
Prototype
Disorder

Immune Mechanisms

Pathologic Lesions

Tipe I Immediate

Anaphylaxis;
allergies; bronchial
asthma (atopic
forms)

Production of IgE antibody immediate

release of vasoactive amines and other
mediators from mast cells; recruitment of
inflammatory cells (late-phase reaction)

Vascular dilation,
edema, smooth muscle
contraction, mucus
production, inflammation

Tipe AntibodyII
mediated

Production of IgG, IgM binds to antigen

Autoimmune
on target cell or tissue phagocytosis or
hemolytic anemia;
lysis of target cell by activated
Cell lysis; inflammation
Goodpasture
complement or Fc receptors; recruitment
syndrome
of leukocytes

Immune
Tipe
complex
III
mediated

Systemic lupus
erythematosus;
some forms of
glomerulonephritis;
serum sickness;
Arthus reaction

CellTipe
mediated
IV
(delayed)

Contact dermatitis;
multiple sclerosis;
Activated T lymphocytes i) release of
type I, diabetes;
cytokines and macrophage activation; ii)
transplant
T cell-mediated cytotoxicity
rejection;
tuberculosis

Type

Deposition of antigen-antibody complexes

complement activation recruitment of Necrotizing vasculitis
leukocytes by complement products and (fibrinoid necrosis);
Fc receptors release of enzymes and inflammation
other toxic molecules

Perivascular cellular
infiltrates; edema; cell
destruction; granuloma
formation

Rematologi

Diagnosis Banding Arthritis

OA

RA

Gout

Patologi

degeneratif

Pannus

Deposisi kristal urat

(mikrotophi)

Onset

gradual

Gradual

Akut

Inflamasi

(-)

(+)

(+)

Lokasi

Panggul, lutut,
vertebra

MCP, PIP, wrist,

ankle, kaki

MTP, kaki, ankle,

Keterlibatan sendi

Poli

Poli, simetris

Mono

Temuan khas

Nodus Bouchard,
Heberden

Deviasi ulnar, swan

neck, boutonniere

Kristal urat

Ekstraartikuler

Nodul subkutan,
pulmoner, kardiak,
splenomegali

Tophi
Batu ginjal
Bursitis olekranon

Lab

dbn

RF (+), anti-CCP (+)

as . Urat

Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Gout

Chronic Gout
Manifestation: tophi, nephrolithiasis, bursitis, chronic
tophaceous gout
Chronic treatment:
urate production (low purine diet)
(-) dehydration & drugs (thiazid, loop diuretic,
pyrazinamide)
Prophylaxis frequent attack & when starting
antihyperuricemic therapy (NSAID, colchicine)
Antihyperuricemic goal UA <6 mg/dL

If: tophi (+), nephrolithiasis (+), or frequent attack (min. 2

attacks), uric acid >9 mg/dL
Xanthine oxidase inhibitor (allopurinol)
Uricosuric (probenecid)
Do not start w/o prophylaxis & until 2-4 wk after acute attack
Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.
Gout and Other Crystal Arthropathies. Harrisons Principles of Internal Medicine. 17th ed. 2008.

Rheumatoid Arthritis
Signs: chronic,
symmetric polyarthritis
Pathology: Inflammatory,
proliferative synovial
tissue (pannus)
formation), idiopathic,
genetic
Pain, swelling, morning
stiffness >1 h
PIP, MCP, wrists, knees,
ankles, MTPs, cervical
spine
Joint deformities
Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Source: Aletaha et al. 2010 Rheumatoid arthritis classification criteria. Arth Rheum. 2010
September;76:256981.

Penatalaksanaan RA

Reverse pyramid
approach now is
favored DMARDs
are initiated quickly to
slow disease
progression as early
as possible
Considerations:
Joint damage begins
early in the disease
DMARDs have
significant benefits
when used early
Benefits of DMARDs
may be enhanced
when the drugs are
used in combination

Rindfleisch JA, Muller D. Diagnosis and management of rheumatoid arthritis. Am Fam Physician.2005 Sep 15;72(6):1037-

Osteoartritis

Hematologi

Anemia

Anemia Aplastik

Hiposelularitas sumsum tulang

Pansitopenia
Anemia
Leukopenia infeksi berulang
Trombositopenia petechiae, purpura

Bimodal peak remaja & lansia

Etiologi:
Idiopatik
Destruksi sel punca: radiasi, kemo, kimia
(benzen)
Rx obat idiosinkratik: kloramfenikol,
NSAID, sulfa, prep. Emas, karbamazepin
Virus: HHV-6, HIV, EBV, parvo-B19,
posthepatitis (non A, B, C)

Sumsum hipoproliferatif, digantikan

oleh jaringan lemak

Dx:
Pansitopenia dg RI <2%
Biopsi sumsum tulang
Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Anemia Megaloblastik
ANEMIA MAKROSITIK
Anemia megaloblastik
gangguan sintesis DNA
Defisiensi asam folat
Malnutrisi (alkoholik, vegan)
Ggn metabolisme folat (pirimetamin,
trimetoprim)
demand (hamil, dialisis)

Defisiensi B12 neuropati

(perifer, kolumna lateralis &
posterior traktus spinothalamikus,
korteks serebri) baal, parestesi,
sensasi posisi & vibrasi, demensia,
ataksia
Malnutrisi (alkoholik, vegan)
Anemia pernisiosa
Gastrektomi ,Crohns, sprue

Ukuran eritrosit > limfosit, oval (makroovalosit)

Anemia non-megaloblastik: liver

disease, alkoholisme
Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Multiple myeloma
Malignansi sel B Ab monoklonal IgM
Gejala:
Proliferasi sel plasma di sumsum tulang anemia
Lesi litik tulang nyeri tulang, fraktur kompresi,
hiperCa2+
Infeksi berulang ec hipogammaglobulinemia
Ginjal protein light chain toksik thd ginjal gagal
ginjal, sindroma nefrotik

Elektroforesis Hb: Bence-Jones protein (light chain)

Hapus darah tepi: rouleaux
Biopsi sumsum tulang: plasmasitosis >10%
Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Multiple punch-out lesions

Source: www.learningradiology.com

Osteopenia
Fraktur kompresi

Manifestasi
Fraktur
kompresi
Osteodistrofi
ginjal

Retensi fosfat
hiperfosfatemia
hipokalsemia hiperPTH
sekunder

Osteopenia - osteoporosis

Strain lumbal

Nyeri ec regangan pada

otot

Nyeri berubah dengan pergerakan

Osteomielitis

Infeksi tulang

Tanda-tanda inflamasi, demam, lesi litik

tulang osteopenia, hiperkalsemia

Sources: The Pediatric Orthopaedic Society of North America.

2012.

Idiopathic Thrombocytopenic Purpura (ITP)

Trombositopenia <100,000/mm3
10% ITP + anemia hemolitik autoimun Evans syndrome
Etiologi

Primer: dx eksklusi
Sekunder: virus (HIV, HCV, HBV, EBV), H. Pylori, ANA
Anak: akut pasca infeksi
Dewasa: kronik

Manifestasi klinis: perdarahan mukokutan, petechiae,

purpura. Perdarahan spontan bila Tr <20,000/mm3
Pemeriksaan lab
BT, CT
Hapus darah tepi: megakariosit
Biopsi sumsum tulang: megakariosit

Diatesis Perdarahan Lain

Hemolytic Uremic
Syndrome

Thrombotic
Thrombocytopenic
Purpura

Definisi

Kelainan oklusif vaskuler

ec agregasi platelet
intrarenal

Kelainan oklusif vaskuler ec

agregasi platelet sistemik

Etiologi

Shiga toxin

aktivitas protease --> vWF

di endotel agregasi
platelet

Epidemiolog Anak, didahului diare

i
berdarah ec EHEC

Dewasa

Manifestasi
Klinis

Pentad TTP
(trombositopenia + anemia
hemolitik mikroangiopatik +
MS + gagal ginjal +
demam)

Trias HUS
(trombositopenia +
anemia hemolitik
mikroangiopatik + gagal
ginjal

Patologi

Manifestasi

Anemia
hemolitik
autoimun

Autoimun
(Idiopatik, SLE, obat (sulfa,
rifampisin, quinidin, NSAID,
dll))

Anemia

Anemia
aplastik

Hipoproliferasi sumsum tulang Pansitopenia

Limfoma

Malignansisel-sel limfoid di
jaringan limfoid

Limfadenopati,
demam, keringat
malam

Leukemia

Myeloproliferasi

Leukositosis +
bisitopenia

Malaria

Malaria
Berat

Source: Guidelines for the treatment of malaria. 2nd ed. WHO 2010

Tatalaksana Malaria Berat

Artemisinin IV/IM
Artesunat IV atau IM 2.4 mg/kgBB (dibagi 2 dosis)
pada 0, 12, 24 jam, selanjutnya 1.2 mg/kgBB qd s.d.
pasien dapat minum obat (~hari 4-5)
atau
Artemeter IM 3.2 mg/kgBB (dibagi 2 dosis),
selanjutnya 1.6 mg/kgBB qd s.d. Pasien dapat
minum obat oral
ACT lanjutan (PO)
Artemisinin + amodiakuin ~3 hari
atau
Kuinin + tetrasiklin/doksisiklin/klindamisin ~7 hari

Sources: Guidelines for the treatment of malaria. 2nd ed. WHO 2010
Malaria Berat. Sudoyo AW, dkk. Buku Ajar Ilmu Penyakit Dalam. Edisi IV. 2006

Penyulit Malaria
Black water
fever

Acute intravascular hemolysis classically occuring after

the re-introduction of quinine in long-term residents in
Plasmodium falciparum endemic areas and repeatedly
using the product. 1
CLINICAL PROFILE: The symptomatology appears
brutally with emission of porto-colored urine, icterus,
pallor, nausea, fever and acute renal failure.1

Algid Malaria

A rare complication of tropical malaria and it occurs in

0.37% of cases. Algid malaria is characterized by
hemodynamic disorders as shock with pronounced
metabolic changes and hypothermia.2
A syndromic diagnosis of varying etiology (dehydration,
bacterial infection, bleeding and/or adrenal insufficiency).3

Source: 1) Bruneel F, et al. Black water fever. Presse Med. 2002 Sep 7;31(28):1329-34.
2) Popov AF. Algid malaria. Med Parasito (Mosk). 2005 Jan-Mar;(1):10-2.
3) Lacerda MV. Algid malaria: a syndromic diagnosis. Rev Soc Bras Med Trop. 2009 JanFeb;42(1):79-81.

Malaria tertiana (vivax)

Perjalanan Penyakit Malaria

Istilah

Definisi

Serangan primer

Periode mulai dari akhir masa inkubasi hingga mulai

terjadi serangan paroksismal (trias dingin, menggigil,
demam & berkeringat)

Periode laten

Periode asimptomatik tanpa parasitemia, antara dua

keadaan paroksismal

Rekurensi

Berulangnya parasitemia aseksual setelah pengobatan.

Dapat disebabkan oleh rekrudensi, relaps (P. vivax dan P.
ovale), atau infeksi baru

Rekrudensi

Berulangnya parasitemia aseksual (dengan infeksi yang

sama) pasca pengobatan. Akibat klirens parasitemia
inkomplit karena pengobatan yang tidak adekuat.

Relapse/rechute

Berulangnya parasitemia aseksual pada malaria P. vivax

dan P. ovale yang dorman (hipnozoit) di hati.
Dapat terjadi dalam interval minggu-bulan.
Sources: Guidelines for the treatment of malaria. 2nd ed. WHO 2010.

Tifoid

Demam Tifoid
Incubation
period
Asymtomatic

Invasive phase

Toxic phase Convalescence

Continuous fever
period

Intermitent fever
Headache
Fatique
Abdominal discomfort
Constipation
Diarrhoea

Bradycardia
Hepatomegaly
Splenomegaly
Constipation
Diarrhoea
Rose spot

Complications
400C

37 C
0

Day -15

Day 0

Day 7

Day 21

Blood culture
Fecal culture
Sources: Hadinegoro SRS. Fever in Children: Lecture. FMUI.2010

 Dx methods: culture of blood, stool, urine, duodenal (bile) aspirate, BM

aspirate specimen
Blood culture: mainstay for dx Se after day-7
Gold standard: BM aspirate
Widal:
Peningkatan >4x lipat setelah 1 minggu menegakkan dx
Uji tunggal dengan titer O 1/320 atau H 1/640 + klinis menyokong dx
Sources: Background document:The diagnosis, treatment and prevention of typhoid fever. WHO 2003.
Panduan Pelayanan Medik. PAPDI 2009.

Dengue

Demam Dengue

Amoebic Liver Disease

Manifestasi klinis
Amoebiasis intestinal ulkus
bergaung (flask-shaped ulcer)
diare berdarah
Amoebiasis ekstraintestinal
menembus dinding colon sistemik
Amoebic liver disease (abses hepar)
demam menetap, nyeri epigastrium,
diare

Dx:
Disenteri amoeba: feses trofozoit
yang mengandung RBC di feses,
PCR, uji antigen feses
Amoebic liver disease USG,
serologi, mikroskopi sediaan
aspirasi

Tx:
Metronidazole 3x750 mg ~7-10 hari

Entamoeba histolytica
Trofozoit (Vegetatif)

Ektoplasma kaki semu

(rhizopod/pseudopod)
Endoplasma granuler
Nukleus tunggal
Mengandung eritrosit

Entamoeba histolytica
Bentuk Kista

Nuklei (panah hitam)

Badan kromatin (panah
merah)
Mengandung beberapa
nuklei (kista matur: 4
nuklei)
Endoplasma granuler

CDC. Laboratory identification of parasites of public health concern. Available at

http://dpd.cdc.gov/dpdx/Default.htm

Helminthologi

Trichuriasis
Manifestasi klinis:
Anak lebih berat daripada
dewasa
Infeksi berat: nyeri
abdomen, diare (berdarah
& lendir), tenesmus,
prolapsus rekti

Dx: mikroskopi feses

telur
Tx:

Telur Trichuris trichiura: bentuk elips,

dinding tebal, tempayan, dua kutub

Albendazole 400 mg
(single dose)
Mebendazole 2 x 100 mg
~3 hari

Susanto, L. Parasitology lecture gastrointestinal module. Faculty of Medicine University of Indonesia. 2007
CDC. Laboratory identification of parasites of public health concern. Available a

Fasciolosis
Liver fluke disease (F. hepatica > F. gigantica)
Infeksi saluran empedu dan hepar
Fase akut: migrasi parasit dari ileum ke
hepar
Mual, muntah, nyeri tekan abdomen, demam,
ruam, sesak

Fase kronik: parasit menetap di saluran

empedu
Inflamasi (sumbatan) duktus empedu intermiten,
hepatitis, kolesistitis, pankreatitis
CDC. Fasciolosis. Available at: www.dpd.cdc.gov/dpdx/html/fascioliasis.htm

Fasciola hepatica
Cacing pipih
(trematoda)
Dx:
Mikroskopi telur di
feses telur
dikeluarkan di
feses beberapa
bulan pasca infeksi
akut
Bentuk elipsoidal
lebar, memiliki
operkulum
Antibodi
CDC. Fasciolosis. Available at: www.dpd.cdc.gov/dpdx/html/fascioliasis.htm

Schistosoma japonicum
Telur: lateral knob
(tonjolan di satu sisi)
Dewasa: betina
selalu menempel
pada jantan pada
kanalis ginekoporis
Habitat: vena
mesenterika ileus

Susanto, L. Parasitology lecture gastrointestinal module. Faculty of Medicine University of Indonesia. 2007
CDC. Laboratory identification of parasites of public health concern. Available a

Schistosomiasis
Transmisi: host siput
serkaria penetrasi kulit
manusia
Manifestasi klinis
Akut: demam, flu-like
syndrome
Kronik: disfungsi saluran
cerna & hepatik, nyeri
abdomen, diare berdarah

Dx:
Mikroskopi: telur
Serologi

Tx: prazikuantel 40-60

mg/kg satu atau dua dosis

Susanto, L. Parasitology lecture gastrointestinal module. Faculty of Medicine University of Indonesia. 2007
CDC. Laboratory identification of parasites of public health concern. Available a

HIV/AIDS
Infeksi primer
Replikasi virus >>> + rapid activation of
CD4 exhaustion CD4 depletion
Asimptomatik/simptomatik
Acute retroviral syndrome 3-6 mg
pasca infeksi ~1-2 mg
mononucleosis-like illness
Konstitusional: demam, flu-like sy,
limfadenopati generalisata
Neurologis (ensefalitis, meningitis,
neuropati perifer)
Dermatologis: ruam makulolapular
eritematosa, ulkus mukokutan
Window period : 6-12 minggu sebelum
Ab (+)
Fase laten
Asimptomatik, CD4
AIDS: HIV + CD4 <200 atau IO

Chronic Kidney Disease

48. Acute Kidney Injury

Cr 50% from
baseline, or
absolute by 0.5-1.0
mg/dL
Oliguria
(UO <400 mL/24 h
<0.5 mL/kg ~6 h)
Anuria (UO <100 mL/24
h)

Prerenal: BUN/Cr ratio >20

Nephrotic syndrome

Nephrotic Syndrome

Proteinuria >3.5 g/24 h

Hypoalbuminemia <3.0 g/L
Edema
Hyperlipidemia
Lipiduria

Complication: hypercoagulable state,

infection, drug toxicities ec decreased
protein binding

Sistitis

Source: Bremnor JD, Sadovsky R. Evaluation of Dysuria in Adults. Am Fam

Sistitis

Asidosis Laktat
Disorder

Problem

Etiology

Physical findings

Metabolic
acidosis

Gain of H+ or
loss of HCO3-

Diarrhea, RTA, KAD,

lactic acidosis

Kussmaul respiratory,
dry mucous membrane,
specific physical finding
to its cause

Metabolic
alkalosis

Gain of HCO3or loss of H+

Loss of gastric secretion

(vomiting), thiazide/loop
diuretics

Tetany, Chvostek sign,

specific physical finding
to its cause

Respiratory
acidosis

Hypoventilation
(CO2 retention)

COPD, asthma, CNS

disease, OSA

Dyspnea, anxiety,
cyanosis, specific
physical finding to its
cause

Respiratory
alkalosis

Hiperventilation Hypoxia tachypnea

(CO2 loss), high pneumonia, pulm.
altitude
Edema, PE, restrictive
lung disease

Hyperventilation,
cardiac rhythm
disturbance

Krisis Tiroid

Sources: Thyroid Gland Disorders. Harrisons Principles of Internal Medicine. 17th Ed. 2008.

Hipokalemia
Etiology:
Transcellular shifting: alkalemia,
insulin
GI loss: diarrhea, laxative
abuse
Renal loss: DKA, RTA, loop
diuretics, hyperaldosteronism

Clin. Manifestation: nausea,

vomiting, ileus, weakness,
muscle cramp, arrythmia,
ECG: flattening of T wave T
inversion, U wave

Sources: Sabatine MS. Pocket Medicine. 4th ed. 2011.

Hyperkalemia

Weakness, flaccid paralysis, nausea, paresthesia,

palpitation
ECG: tall T

Hyponatremia

Usualluy with Na <125 mEq/L: nausea, vomiting,

confusion, lethargy, disorientation
Severe (<120 mEq/L) or abrupt: seizure, coma, death

Hypernatremia

Confusion, irritability, lethargy, stupor, coma, muscle

twitching, seizure

Hypocalcemia

Hyperactive deep tendon reflex, carpopedal spasm,

Chvostek sign, seizure, tetany, laryngospasm
ECG: prolonged QT interval

Hypercalcemia

HT, hyporeflexia, MS
ECG: shortening of QT interval

Hypomagnesemia

Tachycardia, tremor, muscle twitching, hyperactive reflex,

tetany, seizure

Hypermagnesemia Nausea, vomiting, hypotension, hyporeflexia, weakness,

quadraparesis, bradycardia, resp. Distress, coma
Iron deficiency

Pale, tachycardia, loss of tongue papillae

Source: Gomella LG. Clinicians Pocket Reference. 11th ed. 2007.