pembahasan ukdi klinik 4

8/16/2019 Pembahasan Ukdi Klinik 4

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PEMBAHASAN

LATIHAN SOAL UKDI CLINIC 4

OPTIMAPREP

BATCH MEI 2015 Office Address:

Jl Padang no 5, Manggarai, Setiabudi, Jakarta Selatan(Belakang Pasaraya Manggarai)Phone Number : 021 8317064Pin BB 2A8E2925

WA 081380385694

Medan :Jl. Setiabudi No. 65 G, MedanPhone Number : 061 8229229Pin BB : 24BF7CD2

www.optimaprep.com

dr. Widya, dr. Eno, dr. Yolina

dr. Cemara, dr. Yusuf, dr. Reza


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ILMU PENYAKIT DALAM


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1. ACE-I + Diuretik

• Target 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.


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Drug Choices in HT with Compelling Indication

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


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2. Sulfonylurea

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


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3. Insulin

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


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4. Koma HHS

• Hiperglikemia ekstrim (>600 mg/dL) +hiperosmolaritas (>320 mOsm/L) + penurunankesadaran

• 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

• Pencetus : ~ KAD, dehidrasi, AKI• Rw polidipsi >>, intake cairan inadekuat

Osm = 2[Na] + glu/18

Sources: Diabetes Mellitus. Harrison’s Principles of Internal Medicine. 17th Ed. 2008.

Sabatine MS. Pocket Medicine. 4th Ed. 2011.


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KAD & HHS

Source: Wolsdorf J., et al. ISPAD Clinical

Practice Consensus Guidelines 2006-

2007: Diabetic ketoacidosis.


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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 200 –300 mL/h of hypotonicsolution

• Insulin (short acting) – Bolus 10 IU atau 0.15 IU/kgBB

– Drip 0.1 IU/kgBB/jam

Sources: Diabetes Mellitus. Harrison’s Principles of Internal Medicine. 17th Ed. 2008.Petunjuk Praktis Terapi Insulin pada Pasien Diabetes Melitus. PERKENI 2007.


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5. Hipertrigliseridemia

Manajemen Dislipidemia:

1. Tentukan sasaran LDL

2. Modifikasi gaya hidup ~6 minggu

3. Terapi farmakologis

1. LDL2. TG

jika > 200 pasca sasaran LDL tercapai, ↑ dosisstatin atau tambahkan asam nikotinat/fibrat

HiperTG s.d. >350 mg/dL: statin dpt digunakan

HiperTG >400 mg/dL turunkan TG! fibrat3. HDL

If isolated low HDL in CHD equivalent: nicotinicacid, fibrate

Sources: Petunjuk Praktis Penatalaksanaan Dislipidemia. PERKENI 2004.National Cholesterol Education Program. Clinician’s Pocket Reference. 2007.


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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 160

0-1 faktor risiko < 160 > 160 > 190

(160-189 obat

dipertimbangkan)

Sources: Petunjuk Praktis Penatalaksanaan Dislipidemia. PERKENI 2004.

National Cholesterol Education Program. Clinician’s Pocket Reference. 2007.


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Management of Dyslipidemia in Adults. Am Fam Physician. 1998

Hiper-LDL atau Hiper Kol-T ↓ asupan lemak total & lemak jenuh

Hiper-TG ↓ asupan karbohidrat, alkohol, lemak


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6. Grave’s Disease

• Autoimmune thyroid-stimulating Ig (TSI),antithyroglobulin, ANA

• Causes 60-80% ofthyrotoxicosis

• 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

– Plummer’s nail

Ophtalmology:

preorbital edema,

conjunctival

injection,

proptosis

Separated

fingernails from

nailbed

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


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Source: Thyroid Gland Disorders. Harrison’s Principles of Internal Medicine. 17th Ed. 2008.


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7. Kretinisme

• Hipotiroidisme kongenital,bayi, anak

• Etiologi: defisiensi iodine,

• Manifestasi klinis:

– Gangguan pertumbuhantulang short stature,coarse facial features, shortstature

– Gangguan perkembanganSSP retardasi mental t.u. In utero

– Coarse facial features

– Protruding tongue

Sources: Robbins & Cotran’s Pathologic Basis of Disease. 7th ed. 2005. Bate’s Guide to Clinical Examination.


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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)


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8. Creatinine Kinase

• Efek samping statin: miopati, peningkatan SGOT, SGPT

• Hati-hati pada penggunaan bersama fibrat (efeksamping serupa)

• Isoenzim CK:

– CK-MB (jantung, N


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9. Unstable Angina

• Angina saat aktivitas, stress emosional

• Hilang dengan istirahat ataunitrogliserinStable AP

• Angina new onset

• Angina at rest (or minimal activity)

• Angina crescendoUnstable AP

• Vasospasme fokal intermiten a.koroner

• Intensitas lebih berat dari anginabiasa, at rest

• EKG: ST elevation transien provokasi dengan asetilkolin

Prinzmetal’svariantangina

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

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


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Coronary Heart Disease

Source: Porth’s Essentials of Pathophysiology Concepts of Altered Health States


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10. Acute Coronary Syndromes

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


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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.


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11. Gagal Jantung Kanan

• Cor pulmonale: RV enlargement ec primarylung disease RV hypertrophy RVfailure

• 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 cardiaccirrhosis), ascites, pedal edema

tricuspid regurgitation RA dilation right sided S4 gallop

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


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Gagal Jantung Kanan

• ECG: RVH (RAD,R>S V1),

tachyarrythmia

• Ro: RVH (boot-shaped, apeks

terangkat)


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12. Defibrilasi


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VT

•Regular, wide QRS >0.12”

•Monomorph

VF

•Chaotic electrical activity (no Pwave, no PR segment, no QRS)

•No ventricular depolarization orcontraction

PEA

•Rhythm (+) but pulse (-)

•Rhythm may be SR, atrial,ventricular

asystole•No electrical activities

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

b l


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13. Emboli Paru ec DVT

• Temuan klasik – Takikardia

– Tanda2 disfungsi RV• Distensi vena

juguler

• Left parasternal lift

• S2 komponenpulmonal mengeras

• Murmur sistolik ygmeningkat pada

inspirasi


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14. Acute Limb Ischemia

• Penurunan perfusiekstremitas secaramendadak yang dapatmengancam viabilitas

jaringan

• Onset


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Chronic Limb

Ischemia

• Insufisiensi arteriperifer >2 minggu

• Klaudikasio

intermitten – Dipicu aktivitas

& elevasi tungkai

– Metabolismeanaerob asam

laktat musclecramping

– Nyeri atauburning padaplantar pedis

• Dx: ABI

Source: Vascular Disease of The Extremities. Harrison’s Principle of Internal Medicine. 17th ed. 2008.


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Tromboangitis

obliterans (Buerger’s

disease)

Rx inflamasi non-ateromatosa (vasospasme) pada arteri &

vena kecil ulkus atau gangren digiti

Laki-laki muda, perokok

Diabetic arteriopathy Makrovaskuler: CAD, PAD, CVAMikrovaskuler: 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 10 mmHg antara kedua lengan, bruit a. subklavia atau

aorta


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15. Penyakit Jantung Reumatik

• Sekuelae demamreumatik akut yangtidak 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.


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16. Endokarditis Infektif

Source: Sexton DJ. Diagnostic Approach to Infective Endocarditis. Available at: http://cmbi.bjmu.edu.cn

http://cmbi.bjmu.edu.cn/http://cmbi.bjmu.edu.cn/


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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 perikardialMyokarditis = perikarditis ↑ Troponin

Tanda-tanda CHF


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17. PJB

Congenital HeartDisease

Acyanotic

Left-to-right shunt

ASD VSD PDACongenita

l ASCoarctasi

on of

Aorta

Cyanoti

Right-to-left shunt

Tetralogy

of Fallot

Transposition of

GreatArteries


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17. PDA

• PDA kecil: asimptomatik

• PDA besar: simptomatik ISPB berulang, takikardia, poorfeeding, slow growth

– ↑ aliran ke paru

– usia 2 – 3 bulan saat tahananvaskuler paru turun

• Pirau dari kiri ke kanan besar beban volume LV & LA dilatasiLA, LV left heart failure

• Hipertensi pulmonal

- tahanan vaskuler paru tinggi penyakit vaskuler paru reversedshunting sianosis (sindromaEisenmenger)

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.


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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 hanyafase sistolik

tidak terdengar murmur murmur diastolik awal

aliran melewati katup mitral

Subklavia sinistra

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


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18. Kasus Gagal Pengobatan

Jenis Kasus Definisi

Kasus baru Pasien yang tidak pernah mendapat terapi TB atau

pernah mendapat terapi 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 setelahmendapat 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.


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Kategori OAT



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19. Hepatitis Imbas Obat pada Terapi TB



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20. Spirometri

• PPOK: FEV1/FVC


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21. Bronkiektasis

• Dilatasi bronkhi abnormal &permanen pooling materialpurulen

• Inflamasi & destruksi salurannapas 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. Harrison’s Principles of Internal Medicine. 17h ed. 2008.


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TB with multiple nodules

•Migratory bronchopneumonia

•Multiple nodules heal with >>> calcified granulomas

(TB granulomas are usually 1 or 2 in number)

•Histoplasmoma=target calcification=bull’s-eye

calcification in center of nodule (Pathognomonic)www.learningradiology.com

http://www.learningradiology.com/http://www.learningradiology.com/http://www.learningradiology.com/


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22. 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 HCO3-

or 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

(CO2 loss), high

altitude

Hypoxia tachypnea

pneumonia, pulm.

Edema, PE, restrictive lung

disease

Hyperventilation, cardiac

rhythm disturbance


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23. Ikterus Obstruktif


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24. Susp. Kolesistitis Akut ec Kolelithiasis

• Ec obstruksi duktus sistikus(biasanya pada Hartmann’s pouch)

• Manifestasi klinis: – Nyeri perut kuadran kanan atas,

intensitas & durasi > episode kolikbilier sebelumnya

– Demam, mual, muntah – Massa + nyeri tekan kuadran kanan

atas abdomen, bawah iga kanan – Defans muskuler – Murphy’s sign (SE = 65%, SP = 87%)

• Dx: USG hepatobilier – Kolelithiasis: sensitif & spesifik – Kolesistitis: penebalan dinding >5

mm, cairan perikolesistik, Murphysonografik

USG: posterior acoustic shadow &

Murphy USG

Source: Biliary system. Sabiston’s textbook of surgery: the biological basis of modern surgical practice. 18th ed. 2007.NEJM 2008;358:2804.


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25. Ensefalopati Hepatik

• Kegagalan hatimemetabolisme NH3 +substansi lain edemaserebri + falseneurotransmitter

• 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.


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26. Pankreatitis Akut ec Kolelithiasis

• Etiologi: batu empedu(40%),alkoholisme (30%)

• Manifestasi: nyeriepigastrium menjalar kepunggung, terus-menerus,

↓ dg bungkuk • Lab:

– ↑ amilase, lipase

– ↑ SGPT >3x menyokongpankreatitis ec gallstone

– ALP, bilirubin tidak spesifik

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


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ILMU BEDAH, ANESTESIOLOGI &RADIOLOGI

27 H d I j


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27. Head Injury


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28.Blunt trauma to abdomen

• History of blunttrauma to abdomen

• Pain during voidingand incompletebladder emptyingsensation

• Prolonged abdominalpain

Suspected

Bladder

Injury


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Bladder Injuries

• Causes: – Iatrogenic injury

• Transurethral resection of bladder tumour (TURBT)

• Cystoscopic bladder biopsy

• Transurethral resection of prostate (TURP)

• Cystolitholapaxy• Caesarean section, especially as an emergency

• Total hip replacement (very rare)

– Penetrating trauma to the lower abdomen or back

– Blunt pelvic trauma—in association with pelvic fracture or

‘minor’ trauma in the inebriated patient – Rapid deceleration injury—seat belt injury with full bladder inthe absence of a pelvic fracture

– Spontaneous rupture after bladder augmentation


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Types of Perforation

A-Intraperitonealperforationthe peritoneum overlying the bladder,

has been breached along with the

wall of the bladder, allowing urine to

escape into the peritoneal cavity.

B- Extraperitoneal perforation

the peritoneum is intact

and urine escapes into the space aroundthe bladder, but not into

the peritoneal cavity.

no peritonitis symptoms


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• Presentation: – Recognized

intraoperatively

– The classic triad of

symptoms and signs that

are suggestive of a

bladder rupture

• suprapubic pain and

tenderness, difficulty orinability in passing urine,

and haematuria

• Management: – Extraperitoneal

– catheter drainage alone, even in thepresence of extensive retroperitoneal orscrotal extravasation

– 87% of the ruptures were healed in 10

days, and virtually all were healed in 3weeks

– Obstruction of the catheter by clots ortissue debris must be prevented forhealing to occur

– Intra peritoneal :

• Open repair…why? – Unlikely to heal spontaneously.

– Usually large defects.

– Leakage causes peritonitis

– Associated other organ injury.European Association of Urology guidelines 2012

Bladder Injuries


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• Differing intraperitoneal/extraperitoneal

rupture→ important for course of treatment!

• Look for Signs of peritonitis:

– Muscle rigidity/ défense musculaire

– Rebound tenderness

– Absent bowel sound

– Pain during digital rectal examination

29 Burn Injuryhttp://en.wikipedia.org/wiki/Burn


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29. Burn Injury

prick test (+)


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• Berat luka bakar:• Ringan: derajat 1 luas <

15% a/ derajat II < 2%

• Sedang: derajat II 10-

15% a/ derajat III 5-10%

• Berat: derajat II > 20%

atau derajat III > 10%

atau mengenai wajah,tangan-kaki, kelamin,

persendian,

pernapasan

Total Body


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Total Body

Surface Area

To estimate scattered burns: patient's

palm surface = 1% total body surface

area

http://www.traumaburn.org/referring/fluid.shtml

Parkland formula = baxter formula


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30. Management of Trauma Patient

H po olemic Shock


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Hypovolemic Shock

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065003/


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Fluid Therapy


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Ringer Lactate vs Normal Saline

• 0.9% NS causes a normal anion gaphyperchloremic acidosis as well as moderatingcoagulation in models of hemorrhage

(elevated serum coagulation levels, decreasedfibrinogen, and increased blood loss)compared with LR and 5% Albumin solutions

• most studies suggest LR and Albumin have

better responses (in terms of MAP and BP)with less volume of solution administeredcompared to NS

Todd, S. Rob, Malinoski, Darren, et al. “Lactated Ringer’s is Superior to Normal Saline in Resuscitation of

Uncontrolled Hemorrhagic Shock.” J Trauma: 2007; 62: 636-639


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31. Blunt Abdominal Trauma

• Signs of intraperitonealinjury – Abdominal tenderness,

peritoneal irritation

– Distention -pneumoperitoneum, gastricdilation, or ileus

– Ecchymosis of flanks (gray-turner sign) or umbilicus(cullen's sign) -retroperitoneal hemorrhage

– Abdominal contusions – seatbelts sign

– ↓Bowel sounds suggestsintraperitoneal injuries

– DRE: blood or subcutaneousemphysema

http://regionstraumapro.com/post/663723636


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• Dullness in Traube's space – above the left midaxillary

costal margin – suggests an enlarged spleen,

and can occur on inspiration

• Kehr's sign

– the occurrence of acute painin the tip of the shoulder dueto the presence of blood orother irritants in theperitoneal cavity when aperson is lying down and thelegs are elevated

– Kehr's sign in the leftshoulder is considered aclassical symptom of aruptured spleen

• Injury to the membranousurethra occurs on traumaleading to fracture separationof the symphysis pubis orfracture of the pubic rami.

• The membranous urethra is

torn and the prostate is pulledupwards• During rectal examination the

prostate will found too high tobe examined by finger (highoverriding prostate)

http://www.sharinginhealth.ca/clinical_assessment/abdominal_exam.html


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• Organs

– Spleen (Traube’s space

dullness, Kehr’s sign)

– Intestine (free air,

sphincter tone

decreased)

– Urethra (high overriding

prostate)


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32. Urinary Tract Infection


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Acute Pyelonephritis

rapid onset (hours to a day)❏ lethargic and unwell,

fever, tachycardia,shaking, chills, nauseaand vomiting, myalgias

❏ marked CVA or flanktenderness; possibleabdominal pain on deeppalpation

❏ symptoms of lower UTImay be absent (urgency,frequency, dysuria)

33 Head Injury


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33. Head Injury

NICE clinical guideline 56


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Location of Lesions 34. The Breast


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34. The BreastTumors Onset Feature

Breast cancer 30-menopause Invasive Ductal Carcinoma , Paget’s disease (Ca Insitu),

Peau d’orange , hard, Painful, not clear border,infiltrative, discharge/blood, Retraction of the

nipple,Axillary mass

Fibroadenoma

mammae

< 30 years They are solid, round, rubbery lumps that move freely in

the breast when pushed upon and are usually painless.

Fibrocysticmammae

20 to 40 years lumps in both breasts that. increase in size andtenderness just prior to menstrual bleeding. occasionally

have nipple discharge

Mastitis 18-50 years Localized breast erythema, warmth, and pain. May be

lactating and may have recently missed feedings.fever.

PhilloidesTumors 30-55 years intralobular stroma . “leaf -like”configuration.Firm,smooth-sided, bumpy (not spiky). Breast skin over the

tumor may become reddish and warm to the touch.

Grow fast.

Duct Papilloma 45-50 years occurs mainly in large ducts, present with a serous or

bloody nipple discharge , mass ussually small, not always

palpable


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Atheroma cyst (Sebacous cyst)

• A slow-growing, noncanceroustumor or swelling of the skin

• It is a small sac filled withmaterial from hair follicles, theskin, or an oily substanceknown as sebum.

• A sebaceous cyst can occurwhen a pilosebaceous unit ora sebaceous gland becomesblocked

• The color of the skin is usually

normal, and there is apunctum (comedo,blackhead) on the dome

35 Chest Traumahttp://emedicine.medscape.com/article/2047916

http://www.mdguidelines.com/tumor-benignhttp://www.mdguidelines.com/tumor-benignhttp://www.mdguidelines.com/tumor-benignhttp://www.mdguidelines.com/tumor-benignhttp://www.mdguidelines.com/tumor-benign


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35. Chest Trauma

Disorders Etiology Clinical

Hemothorax lacerated bloodvessel in thorax

Anxiety/Restlessness,Tachypnea,Signs ofShock,Tachycardia

Frothy, Bloody Sputum

Diminished Breath Sounds on Affected

Side,Flat Neck Veins, Dullness to percussion

Simple/Closed

Pneumothorax

Blunt trauma

spontaneous

Opening in lung tissue that leaks air into

chest cavity, Chest Pain,Dyspnea,Tachypnea

Decreased Breath Sounds on Affected Side,

Hipersonor

Open Pneumothorx Penetratingchest wound

Opening in chest cavity that allows air toenter pleural cavity, Dyspnea,Sudden sharp

pain,Subcutaneous Emphysema

Decreased lung sounds on affected side

Red Bubbles on Exhalation from wound

(Sucking chest wound)


Tension Penumothorax Anxiety/Restlessness Severe Poor Color


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Tension Penumothorax Anxiety/Restlessness, Severe ,Poor Color

Dyspnea,Tachypnea,Tachycardia

Absent Breath sounds on affected side, Accessory

Muscle Use, JV Distention

Narrowing Pulse Pressures,HypotensionTracheal Deviation, hypersonor

Flail Chest Trauma a segment of the rib cage breaks becomes

detached from the rest of the chest wall, 3 ribs

broken in 2 or more places,painful when

breathing,Paradoxical breathing

Pleural Efusion congestive heart

failure,

pneumonia,

malignancy, or

pulmonaryembolism

infection

Dyspnea, cough, chest pain, which results from

pleural irritation, Dullness to percussion,

decreased tactile fremitus, and asymmetrical

chest expansion, with diminished or delayed

expansion on the side of the effusion, decreasedtactile fremitus, and asymmetrical chest

expansion, diminished or delayed expansion on

the side of the effusion

Pneumonia Infection,

inflammation

Fever,dysnea,cough,rales in ausultation


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HYDROPNEUMOTHORAKS

• The accumulation of fluidand free air in the pleuralcavity

• Positive pressure in the

plaural cavity→collapsed lung

• Due to trauma → commonly blood →

hematopneumothorax• Air fluid level in thorax X-

ray

36 Compartment Syndrome


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36. Compartment Syndrome Diagnosis

• Pain out of proportion

• Palpably tense

compartment

• Pain with passive stretch• Paresthesia/hypoesthesia

• Paralysis

• Pulselessness/pallor

• “Pain and the aggravationof pain by passive

stretching of the muscles

in the compartment in

question are the mostsensitive (and generally

the only) clinical finding

before the onset of

ischemic dysfunction inthe nerves and muscles.”


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Clinical Evaluation

• Pain – most important. Especially pain out of

proportion to the injury (child becoming more and

more restless /needing more analgesia)

• Most reliable signs are pain on passive stretching

and pain on palpation of the involved

compartment

• Other features like pallor, pulselessness, paralysis,paraesthesia etc. appear very late and we should

not wait for these things.

Willis &Rorabeck OCNA 1990


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Surgical Treatment

• Fasciotomy• Casts and tight

bandages –remove or

loosen anyconstricting

bandages

All compartments !!!

h d


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37. Hemorrhoid

• Internal Hemorrhoids →

Internal hemorrhoidal plexus

– V. Rectus Inferior – V. Rectus Media

• External Hemorrhoids →

external hemrroidal plexus

–V. Rectus Inferior


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External Hemorrhoids Internal Hemorrhoids

Outside anal canal, around sphincter Inside anal canal

Symptoms due to thrombosis Symtomps due to bleeding and/or

irritation of mucosa

Can not be inserted to anal canal Can be inserted to anal canal up to grade

III

37 H l i Sh k


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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065003/

37. Hypovolemic Shock

Fl id Th


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Fluid Therapy

R i i


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Resuscitation

• Crystalloid solution rapidly equilibratesbetween the intravascular and interstitialcompartments

• Adequate restoration of hemostatic stabilitymay require large volumes of ringer's lactate.

• It has been empirically observed thatapproximately 300 cc of crystalloid is required

to compensate for each 100 cc of blood loss.(3:1 rule)

Res scitation


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European Resuscitation Council Guidelines for

Resuscitation 2010

Resuscitation

39 R d Ph


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39. Raynaud Phenomenon

• May appear as a component of other conditions.• Causes:

– connective tissue diseases (scleroderma & SLE)

– arterial occlusive disorders.

– carpal tunnel syndrome,

– thermal or vibration injury.

• In patients with connective tissue diseases/arterialocclusive disease: the digital vascular lumen is largely

obliterated by sclerosis or inflammation→ lowerintraluminal pressure & greater susceptibility tosympathetically mediated vasoconstriction

Raynaud’s Phenomenon vs Syndrome


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Raynaud s Phenomenon vs Syndrome

• Vasospastic disorder causingdiscoloration of the fingers, toes,

and occasionally other areas.

– Raynaud's disease ("Primary

Raynaud's phenomenon")→

idiopathic

– Raynaud's syndrome

(secondary Raynaud's),→

commonly connective tissue

disorders such as Systemic

lupus erythematosus

http://www.jaapa.com/the-patient-with-cold-hands-understanding-raynauds-disease/article/139839/

Disorder Onset Etiology Clinical Feat.

Buerger Disease chronic Segmental vascular Intermitten claudicatio,Smoking


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inflammation

Polyarteritis nodosa

necrotizinginflammatory lesions

small and medium-

sized arteries

acute immune complex –

induced disease

Fever,Malaise,Fatigue,Anorexia,

weight loss,Myalgia,Arthralgia in large

joints,polyneuropathy, cerebralischemia, rash, purpura, gangrene,

Abdominal pain, does not involve the

lungs

Vasculitis hypersensitif Acute/

chronic

Circulating immune

complexes→drugs,food,other

unknown cause

a small vessel vasculitis,usually affect

skin, but can also affect joints,gastrointestinal tract, and the

kidneys→itching, a burningsensation, or pain, purpura

Wegener

granulomatosis

chronic autoimmune tissue destruction of upper

respiratory tract (sinuses, nose, ears,and trachea *the “windpipe”+), the

lungs, and the kidneys

Takayasu arteritis chronic unknown of

inflammatory

proscess

systolic blood pressure difference

(>10 mm Hg) between arms,

pulselessness,bruit a.carotid

40 Sh ld di l ti


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40. Shoulder dislocation

Anterior Shoulder Subluxation/Dislocation


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Anterior Shoulder Subluxation/Dislocation

• Dislocation: – Complete separation of articular

surfaces

• Subluxation: – Abnormal translation of humeral

head on glenoid without

complete separation of articularsurfaces

• Humeral head can dislocateanteriorly, posteriorly orinferiorly

• Anterior dislocation mostcommon

• Mechanism:

– Forced extension, abduction,external rotation

– Direct blow to posterior orposterolateral shoulder

– Repeated episodes of overuse

(subluxation)

• Physical Exam:

– Intense pain

– Arm held in adduction & externalrotation

– Humeral head palpable anteriorly

– Unable to completely internallyrotate or abduct the shoulder

– Thorough neuro exam (closerelation of axillary nerve)

Anterior Shoulder


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Subluxation/Dislocation

• Radiographs:

True AP

Axillary View

Y view

41 O t liti


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41. Osteomyelitis

• Inflammation of the bone and bone marrowcaused by an infecting organism.

• Although bone is normally resistant to bacterialcolonization, events such as trauma, surgery,

presence of foreign bodies, or prostheses maydisrupt bony integrity and lead to the onset ofbone infection

• Pathogenesis (Waldvogel, 1971) :

1. Hematogenous2. Contiguous focus of infection

3. Direct inoculation

S mptoms


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Symptoms

• Osteomyelitis is often diagnosed clinically with nonspecificsymptoms

– fever,

– chills,

– fatigue,

– lethargy,

– irritability.

• The classic signs of inflammation, including local pain,

swelling, or redness, may also occur and normally disappear

within 5-7 days

http://emedicine.medscape.com/article/1348767-overview#a0112


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Osteomyelitis


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Osteomyelitis

• S aureus is the most common pathogenic organism recovered frombone, followed by Pseudomonas and Enterobacteriaceae.

• Less-common organisms involved include anaerobe gram-negativebacilli.

• Intravenous drug users may acquire pseudomonal infections

• Acute hematogenous osteomyelitis has a predilection for the longbones of the body.

• The ends of the bone near the growth plate (the metaphysis) ismade of a maze like bone called cancellous bone.

• It is here in the rapidly growing metaphysis that osteomyelitis oftendevelops

http://www.hawaii.edu/medicine/pediatrics/pedtext/s19c04.html

42. Male Genital Disordershttp://en.wikipedia.org/wiki/http://emedicine.medscape.com/article/


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Testicular torsion Intra/extra-vaginal

torsion

Sudden onset of severe testicular pain followed by

inguinal and/or scrotal swelling. Gastrointestinalupset with nausea and vomiting.

Hidrocele Congenital anomaly,

blood blockage in the

spermatic cord

Inflammation orinjury

accumulation of fluids around a testicle, swollen

testicle,Transillumination +

Varicocoele Vein insufficiency Scrotal pain or heaviness, swelling. Varicocele is

often described as feeling like a bag of worms

Hernia skrotalis persistent patency of

the processus

vaginalis

Mass in scrotum when coughing or crying. Bowel

sound on scrotum. Strangulated→ nausea,

vomiting, fever, edematous, erythematous,

discolored

Radang testis

sinistra/Orchitis

Mumps virus Testicular pain and swelling, fatigue, fever, chills,

Testicular enlargement, induration of the testis,

Erythematous scrotal skin

Testicular torsion


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Testicular torsion

Signs and symptoms of testicular torsion include:• Sudden or severe pain in the scrotum — the

loose bag of skin under your penis that containsthe testicles

• Swelling of the scrotum

• Abdominal pain

• Nausea and vomiting

• A testicle that's positioned higher than normal orat an unusual angle


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43. Obstruction


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43. Obstruction

Accounts for 5% of all acute surgical admissionsPatients are often extremely ill requiring prompt

assessment, resuscitation and intensive monitoring

Obstruction A mechanical blockage arising from a

structural abnormality that presents aphysical barrier to the progression of gut

contents.

Ileus is a paralytic or functional variety ofobstruction

Obstruction is: Partial or complete

Simple or strangulated

Causes- Small Bowel


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Extraluminaluraluminal

Postoperative

adhesions

Congenital

adhesions

Hernia

Volvulus

Neoplasims

lipoma

polyps

leiyomayoma

hematoma

lymphoma

carcimoid

carinoma

secondary Tumors

Crohns

TB

Stricture

Intussusception

Congenital

F Body

Bezoars

Gall stone

Food Particles

A lumbricoides

1. History


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1. History

Colonic

• Preexisting change inbowel habit

•Colicky in the lower

abdomin

•Vomiting is late

•Distension prominent

•Cecum ? distended

Distal small bowel

•Pain: central and colicky

•Vomitus is feculunt

•Distension is severe

•Visible peristalsis

•May continue to pass

flatus and feacus beforeabsolute constipation

High

•Pain is rapid

•Vomiting copious and

contains bile jejunal content

•Abdominal distension is

limited or localized

•Rapid dehydration

The Universal FeaturesColicky abdominal pain, vomiting, constipation (absolute), abdominal

distension.

Complete HX ( PMH, PSH, ROS, Medication, FH, SH)

Persistent pain may be a sign of strangulation

Relative and absolute constipation

2. Examination


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2. Examination

• Darm kontur: visible shape of intestines on the abdomen

• Darm Steifung: visible peristaltic movement on the abdomen

Others

Systemic

examination

If deemed necessary.

•CNS•Vascular

•Gynaecological

•muscuoloskeltal

Abdominal

•Abdominal distension and it’s

pattern

•Hernial orifices

•Visible peristalsis•Cecal distension

•Tenderness, guarding and rebound

•Organomegaly

•Bowel sounds

–High pitched (metallic sound) –Absent

•Rectal examination

General

•Vital signs:

P, BP, RR, T, Sat

•dehydration

•Anaemia, jaundice, LN

•Assessment of vomitus

if possible

•Full lung and heart

examination


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Radiology: Flat and upright (or decubitus)abdominal X-Ray A. Sensitivity: 60% (up to 90%)B. Typical findings of Bowel Obstruction

1. Bowel distention proximal to obstruction2. Bowel collapsed distal to obstruction3. Upright or decubitus view: Air-fluid levels4. Supine view findings

a. Sharply angulated distended bowel loopsb. Step-ladder arrangement or parallel bowel

loops


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44 Osteosarcoma


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44. Osteosarcoma

• X-rays of area of suspected infection wouldnot demonstrate darkened areas typical ofosteomyelitis.

• Conventional features – Destruction of normal trabecular bone pattern

– a mixture of radiodense and radiolucent areas

– periosteal new bone formation

– formation of Codman's triangle (triangularelevation of periosteum)

No osteoblastic appearance, Notice the osteoblastic-


105/406

pp ,

fracture can be seen osteolytic appearance


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Codman triangles (white

arrow); and the large soft

tissue mass (black arrow)

Osteosarcoma of the distal femur,

demonstating dense tumor bone formation

and a sunburst pattern of periosteal reaction.

Periosteal reactions


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Periosteal reactions

onion-skin "sunburst" and "hair-on-end" periosteal reaction

Codman's triangle

• Radiographs of the primarytumor usually show a large,destructive, mixed lytic andblastic mass. The tumorfrequently breaks through thecortex and lifts the periosteum,

resulting in reactive periostealbone formation. The triangularshadow between the cortexand raised ends of periosteumis known radiographically asCodman triangle and is

characteristic, but notdiagnostic of this tumor.


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The Canadian Journal of Diagnosis / May 2001

45. Cardiac


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Arrest

• Indication forCPR

– No response

– Not breathing

– No pulse

• Check Pulse

→a.Carotis

http://circ.ahajournals.org/content/11

2/24_suppl/IV-156/F2.expansion.html

Identification Of Cardiac Arrest


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Identification Of Cardiac Arrest

• Healthcare Providers shouldcheck for a pulse before

performing chest

compressions on a

suspected victim of cardiacarrest.

• For Adults and Children, a

pulse should be assessed in

the carotid artery for 5 to

10 seconds

• No pulsecardiac arrest

http://www.cardiopulmonaryresuscitation.net/

46 Lymphedema


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46. Lymphedema

Definition

• The progressive swelling of a body part, usually an extremity,following developmental (primary lymphoedema) or acquired(secondary lymphoedema) disruption of the lymphatic systemresulting in lymph (a protein-rich fluid) accumulating in theinterstitial space

• The extremities are most commonly involved, followed by thegenitalia

• Secondary lymphoedema – usually unilateral

• Primary lymphoedema

– frequently bilateral – Defined by swelling that begins distally and progresses proximally

Lymphatic Filariasis


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Lymphatic Filariasis

• Caused by three species of

filaria: Wucheria bancrofti,Brugia malayi, B. timori

• Adult worms (macrofilariae)live in the lymphatic vesselsand lymph nodes of the

lower body half• Progessive chronic disease

can lead to wide spreadfibrosis and damage oflymphatic vessels, which

can result in rupture anddischarge of lymph into theurinary system (chyluria) orthe scrotum


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47. Osteoporosis


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47. Osteoporosis

A systemic skeletal disease characterizedby low bone mass and micro architecturaldeterioration of bone tissue lead to bonefragility and susceptibility to fracture

Prevalence of osteoporosis


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Prevalence of osteoporosis

Osteopenia Osteoporosis

Female

Age > 50 year

37-50% 13-18%

Male

Age > 50 year

28-47% 3-6%

Incidence of osteoporotic Fx


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Incidence of osteoporotic Fx

Vertebral

FractureForearm

Fracture

HipFracture

Osteoporosis


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Osteoporosis

48. Derajat Parrish (Gigitan Ular)


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48. Derajat Parrish (Gigitan Ular)

• Derajat 0 – Tidak ada gejala sistemik

setelah 12 jam

– Pembengkakan minimaldiameter 1 cm

• Derajat 1

– Bekas gigitan 2 taring

– Bengkak dengan diameter1-5 cm

– Tidak ada tanda-tandasistemik sampai 12 jam

• Derajat 2 – Sama dengan derajat 1

– Ptechiae, echimosis

– Nyeri hebat dalam 12 jampertama

• Derajat 3

– Sama dengan derajat 2

– Syok dan distresspernafasan/ptechiae,

echimosis seluruh tubuh• Derajat 4

– Sangat cepat memburuk


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Venomous Snakebites in the United States: Management

Review and Update at

http://www.aafp.org/afp/2002/0401/p1367.html

49. Acute Achilles Tendon Rupture


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49. Acute Achilles Tendon Rupture

• Adults 40-50 y.o.primarily affected (M>F)

• Athletic activities,

usually with suddenstarting or stopping

• “Snap” in heel with pain,

which may subsidequickly

Diagnosis


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Diagnosis

• Weakness in plantarflexion

• Gap in tendon

• Palpable swelling

• Positive Thompson test

Differential Diagnosis


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Differential Diagnosis

50. Colonic Carcinoma


123/406

Site DistributionStaging


124/406

Staging


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http://www.radiologyassistant.nl/en/p4b8ea8973928a/rectal-cancer-mr-imaging.html

51. Fiksasi Fraktur


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Bidai /Splint adalah alat yang digunakan untuk mengimobilisasibagian tubuh, alat tersebut dapat bersifat lunak ataupun kaku

(rigid)

• Plaster slab adalah lempengan gips untuk imobilisasi sendi atau

daerah cidera sehingga terjadi penyembuhan. Sebagian besarfraktur dislab untuk 24-48 pertama untuk mengakomodasi

pembengkakan, sebelum dipasang gips sirkuler.

• Lempengan Gips/CAST → Dapat Digunakan Pada

– Imobilisasi Fraktur – Imobilisasi pada penyakit tulang dan sendi

– Pencegahan deformitas muskuloskeletal

* Aryadi K, Syaiful AH. Penggunaan Gips Paris. In: Petunjuk pemasangan gips paris pada kasus orthopaedi, Divisi Orthopaedi dan

traumatologi, 2006. hal 2-6

51. Tibia-fibula Shaft Fracture


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• Tscherne Classification

– 0-3

– Based on degree of

displacement and

comminution• C0→simple fracture configuration with

little or no soft tissue injury

• C1 → superficial abrasion, mild tomoderately severe fracture

configuration

• C2 → deep contamination with localskin or muscle contusion, moderately

severe fracture configuration

• C3 → extensive contusion or crushingof skin or destruction of muscle, severe

fracture

Treatment


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Nonoperative• Fracture reduction followed byapplication of a long leg cast withprogressive weight bearing canbe used for isolated, closed, low-energy fractures with minimal

displacement and comminution.• Cast above knee, with the knee in

0 to 5 degrees of flexion

• After 4 to 6 weeks, the long legcast may be exchanged for a

patella-bearing cast or fracturebrace.

• Union rates as high as 97%

https://www2.aofoundation.org

Kenneth J.; Zuckerman, Joseph D. Handbook of Fractures,

3rd Edition

Lippincott Williams & Wilkins 2006


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Operative fracture management• Operative treatment of displaced unstable

tibia shaft fractures is the treatment of choice

if it can be performed in facilities with thenecessary equipment and skills

• Surgical treatment is necessary for open

fractures (wound debridement), compartmentsyndromes, and repair of arterial injuries

52. Extrication


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• To move victim(s) fromthe scene to safer

location or where

treatment will be

possible (e.g. hospital)

• Always consider spinal

injury in traffic

accidents until provenotherwise

• Keep spinal collumstraight

• Easier transport with

more personnel


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132/406

ILMU PENYAKIT MATA

KELAINAN MATA


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Mata merah

Visus normal

Mata tenangTrauma

Tidak kotor

• Pterigium

• Pinguekula

• Episkleritis

• Skleritis

• Perdarahan sub-

konjungtiva

Kotor

• Konjungtivitis

• Trakoma

• Dry eye

• Defisiensi vit A

• Keratitis

• Ulkus kornea• Glaukoma akut

• Uveitis

• Endoftalmitis

• Panoftalmitis

Visus perlahan

• Katarak

• Glaukoma simpleks

• Retinopati• ARMD (Age Related

Macula

Degenerative)

• Retinitis Pigmentosa

Visus mendadak

• Neuritis optik

• Ablasio retina

• Oklusi arteri retinasentral

• Oklusi vena retina

sentral

• Perdarahan /

kekeruhan vitreus

• Uveitis posterior

• CSR• Trombosis arteri

interna

• Malingering

Visus ↓

53. Tes Fluoresensi


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• Tes fluoresensi utkmelihat adanya defekepitel kornea

• Tonometri utkmengukur tekanancairan intraokuler

Tonometri applanasi

Tonometri Schiotz


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• Tes konfrontasi utkmemeriksa lapang

pandang

• Funduskopi utk

memeriksa fundus,

menggunakanoftalmoskop

Oftamoskopi langsung Oftamoskopi tak langsung


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• Refraktometri utk mengukur kesalahanrefraksi mata

54. Presbiopia


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• Merupakan keadaan berkurangnya daya akomodasi pdusia lanjut

• Penyebab: – Kelemahan otot akomodasi

– Lensa mata tdk kenyal / berkurang elastisitasnya akibatsklerosis lensa

• Diperlukan kacamata baca atau adisi : – + 1.0 D : 40 thn

– + 1.5 D : 45 thn

– + 2.0 D : 50 thn – + 2.5 D : 55 thn

– + 3 .0 D : 60 thn

Sumber: Ilmu Penyakit Mata. Sidarta Ilyas. 2000.

55. Konjungtivitis Vernal


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Sumber: General opthalmology. Vaughan, et al. 17th edition

• Konjungtivitis alergi / hipersensitivitas:– Konjungtivitis vernal bilateral sangat gatal


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Konjungtivitis vernal bilateral, sangat gatal,bertahi mata berserat-serat, papil raksasa pd

konjungtiva tarsal superior (cobblestone) – Konjungtivitis atopik sensasi terbakar, bertahi mataberlendir, merah, fotofobia, papila halus yg lbh seringterdapat di tarsus inferior

– Konjungtivitis fliktenularis respon hipersensitivitas

lambat thd protein mikroba, plg srg protein basiltuberkel

Konjungtivitis vernal

56. Katarak HipermaturInsipien Imatur Matur Hipermatur


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Insipien

(kortikal)

Imatur Matur Hipermatur

Kekeruhan Ringan Sebagian Seluruh Masif

Cairan lensa Normal Bertambah (air

masuk)

Normal Berkurang

(air+masa lensa

keluar)

Bilik mata

depan

Normal Dangkal Normal Dalam

Sudut bilik

mata

Normal Sempit Normal Terbuka

Shadow test Negatif Positif Negatif Pseudopositif

Penyulit - Glaukoma - Uveitis+Glaukoma

Sumber: Ilmu Penyakit Mata. Sidarta Ilyas. 2000.

57. Katarak Senilis Matur


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Insipien

(kortikal)

Imatur Matur Hipermatur

Kekeruhan Ringan Sebagian Seluruh Masif

Cairan lensa Normal Bertambah (air

masuk)

Normal Berkurang

(air+masa lensa

keluar)Bilik mata

depan

Normal Dangkal Normal Dalam

Sudut bilik

mata

Normal Sempit Normal Terbuka

Shadow test Negatif Positif Negatif Pseudopositif

Penyulit - Glaukoma - Uveitis+Glaukoma

• Pembagian katarak berdasarkan usia:


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– Katarak kongenital usia < 1 thn

– Katarak juvenil

sesudah usia 1 thn – Katarak senilis > 50 thn

• Katarak komplikata akibat penyakit mata lain, mis:radang, glaukoma, tumor, dll. Dpt jg disebabkan olehpeny.sistemik endokrin (mis: DM) dan keracunan obat

(mis: steroid lokal lama)• Katarak traumatik akibat trauma, plg sering

disebabkan oleh cedera benda asing atau traumatumpul bola mata

• Katarak sekunder tjd sesudah operasi katarak atausesudah suatu trauma yg memecah lensa

Sumber: - Ilmu Penyakit Mata. Sidarta Ilyas. 2000.

- General opthalmology. Vaughan, et al. 17th edition

58. Funduskopi


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• Funduskopi pemeriksaan utk melihatbagian dalam mata atau fundus okuli,

menggunakan oftalmoskop

• Kampus visi memeriksa lapang pandang• Fluoresensi menilai defek pd kornea

• Tonometri mengukur tekanan cairan

intraokuler

59. Blepharitis


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• Merupakan radang pd kelopak mata• Dapat disebabkan infeksi dan alergi

• Gejala umum kelopak mata merah, bengkak,

sakit, eksudat lengket, dan epifora

• Srg disertai dgn konjungtivitis dan keratitis

• Blepharoptosis posisi satu atau kedua


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palpebra superior yg terlalu rendah

• Blepharospasm kedipan kelopak mata ygkeras, tdk disadari, dpt berlangsung bbrp detik

smp bbrp jam

• Blepharochalasis idiopatik; kulit palpebratampak tipis, berkerut, menggelambir

Blepharochalasis

60. Atrofi Difus


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• Glaukoma ditandai oleh

meningkatnya TIO yg disertai oleh

pencekungan diskus optikus dan

pengecilan lapang pandang

• Glaukoma tekanan-normal kelainan

glaukomatosa pd diskus optikus atau

lapang pandang dgn TIO tetap di bwh 22

mmHg

• Penilaian diskus optikus pd glaukoma

CD ratio ↑ (>0,5); atrofi lapisan serat

saraf

• TIO normal : 10-24 mmHg – Hsl sekali pembacaan tdk

menyingkirkan kemungkinan

glaukomaOptic Nerve Cupping

Sumber: General opthalmology. Vaughan, et al. 17th

ed

61. Konjungtivitis Viral


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62. Konjungtivitis GO Tetes Mata Gentamisin


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• Terapi konjungtivitis neonatal :

• Toxic conjunctivitis (Credé’s method of prophylaxis) regularlyflushed & the eyelids cleaned, symptoms will abate


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spontaneously within one or two days

• GO conjungtivitis Topical administration of broad-spectrumantibiotics (gentamicin eyedrops every hour) & systemicpenicillin (penicillin G IV 2 mill. IU daily) or cephalosporin in thepresence of penicillinase-producing strains

• Chlamydial conjunctivitis Systemic erythromycin and topical

erythromycin eyedrops five times daily. There is a risk ofrecurrence where the dosage or duration of treatment isinsufficient. It is essential to examine the parents and includethem in therapy

• Herpes simplex conjunctivitis application of acyclovir

ointment. Systemic acyclovir therapy is only required in severecases

Sumber: Ophthalmology. Lang. 2000.


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63. Trauma kimia• Secara umum trauma kimia ada 2 jenis yaitu trauma kimia


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Secara umum trauma kimia ada 2 jenis yaitu trauma kimia

asam dan truma kimia basa

• Secara umum trauma kimia asam lebih kurang berbahaya

dibanding trauma kimia basa

• Trauma kimia basa

– Nekrosis liquefactive alkali akan menembus cepat dgn

menghidrolisis protein dan sel

• Trauma kimia asam

– Nekrosis koagulasi kerusakan terbatas dan lokal krn sel yg

mengalami koagulasi bertindak sbg barier thd kerusakan &

penetrasi lbh dlm

– Bbrp asam dgn konsentrasi tinggi dpt bereaksi spt trauma basa

dan menyebabkan cedera berat, misal: asam sulfat, asam nitrat


• Tatalaksana trauma kimia:

– Lakukan irigasi segera denganl t b ff t il (RL NS) t


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larutan buffer steril (RL, NS) atau jika tdk ada dpt dgn air biasa, min.

15-30 mnt smp pH netral – Tetes mata steroid (dexamethasone

0.1 %, prednisolon 0.1%) utkmengontrol inflamasi

– Antibiotik topikal

– Analgetik oral, siklopegik (SA 1%) utk mengontrol nyeri

– Turunkan TIO jika >30mmHg

– Bantu proses penyembuhan dengan

air mata buatan, Vit C, pemasanganlensa kontak sampai terjadiregenerasi epitel

64. Pemeriksaan Snellen


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• Pemeriksaan tajam penglihatan merupakanpemeriksaan dasar mata yg hrs dilakukan pd setiap

pasien


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NEUROLOGI

65. HEAD INJURY


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Disorders of the Nervous System, Reeves&Swenson

66. TRAUMA


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Handbook of Neurocritical Care, 2005


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67. Glasgow Coma Scale


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• The Glasgow Coma Scale is a neurological scale to give areliable, objective way of recording the conscious state of aperson, for initial as well as continuing assessment

• A patient is assessed against the criteria and the resultingpoints give the Glasgow Coma Score

Generally, comas are classified as:1. Severe, with GCS ≤ 82. Moderate, GCS 9 - 123. Minor, GCS ≥ 13.• Highest score is 15/15.the person in this case is alert and

oriented to person, place and time

• Lowest score is 3/15 there’s no 0.The patient is in deep comaand is considered brain dead if he can’t breath without a

ventilator

Neurology and Neurosurgery Illustrated

Glasgow Coma Scale Eye opening Motor Response Verbal Response


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Spontaneously

=4 Points

Obeys Commands

=6 Points

Oriented when speaking to

person, place and time)

=5 Points

To speech and

commands

=3 Points

Unconscious but can localize

pain

=5 Points

Confused Disoriented to

person, place and time)

=4 Points

To pain

=2 Points Withdrawal Response to pain

(but can

t localize pain)

= 4 Points

Words only unconscious but

responds to painful stimuli by

words)=3 Points

No Response

= 1 Point Decortication(spastic flexion

of the upper limbs and

extension of the lower

limbs)+Rigidiy

= 3 Points

Sounds Only

=2 Points

Decerebration(extension and

outwards turning of the arms

and legs)+ Rigidity

= 2 Points

No Response

=1 Point

No Response

=1 Point

68. HEADACHE


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MIGRAINE


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69. CARPAL TUNNEL SYNDROME


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• Carpal tunnel syndrome, the mostcommon focal peripheralneuropathy, results fromcompression of the median nerveat the wrist.

• Clinical Features: Pain

Numbness

Tingling

Symptoms are usually worse at night

and can awaken patients from sleep. To relieve the symptoms, patients

often “flick” their wrist as if shakingdown a thermometer (flick sign).

Physical examination


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• Phalen’s maneuver (Penderita melakukan fleksi tangan secara maksimal. Bila dalam

waktu 60 detik timbul gejala → CTS +)• Tinel’s sign (timbul parestesia atau nyeri pada daerah distribusi nervus medianus kalau

dilakukan perkusi pada terowongan karpal dengan posisi tangan sedikit dorsofleksi)

• Luthy's sign/bottle's sign (Penderita diminta melingkarkan ibu jari dan jari telunjuknya

pada botol atau gelas. Bila kulit tangan penderita tidak dapat menyentuh dindingnya

dengan rapat→

CTS +)

• Pemeriksaan sensibilitas/two-point discrimination (Bila penderita tidak dapat

membedakan dua titik pada jarak lebih dari 6 mm di daerah nervus medianus CTS +)

Phalen’s maneuver

Tinel’s sign

Treatment


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• CONSERVATIVE TREATMENTS – GENERAL MEASURES (resting the arm)

– WRIST SPLINTS

– ORAL MEDICATIONS (Vit. B6, NSAIDs)

– LOCAL INJECTION

– ULTRASOUND THERAPY (physiotherapy)

• SURGERY

70. VERTIGOCommon Causes:


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• the illusion that the environment is

spinning

• a subtype of dizziness, where there is a

feeling of motion when one is

stationery

• Classification :

Peripheral

Central

o o auses1.Peripheral

• Physiological (motion sickness)• Benign paroxysmal positionalvertigo (BPPV) most common

• Vestibular neuronitis• Labyrinthitis• Meniére disease• Perilymph fistula

2.Central• Brainstem TIA/infarct• Posterior fossa tumors• Multiple sclerosis• Syringobulbia• Arnold - Chiari deformity• Temporal lobe epilepsy

• Basilar migraine3.Other

• Cardiac, GI, psycogen, toxins,medications, anemia,hypotension

Vertigo


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• Peripheral vertigo : caused

by problems within theinner ear/vestibularsystem; also called otologicor vestibular vertigo.

• The most common cause :BPPV (32%)

• Central vertigo : arisesfrom injury to the balancecenters of the CNS; lessprominent movementillusion and nausea.

• Has accompanyingneurologic deficits (e.g.slurred speech and doublevision), and pathologicnystagmus (pure vertical/torsional)

Meniere’s disease An inner ear disorder that causes one to experience

periods of vertigo, dizziness, nausea, ear pressure,

sensitivity to light and tinnitus, hearing loss. Usually

affects only one ear


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affects only one ear.

Vestibular Neuritis A paroxysmal, single attack of vertigo, a series of attacks,

or a persistent condition that diminishes over three to six

weeks. It is a type of unilateral vestibular dysfunction and

may be associated with nausea, vomiting, eye

nystagmus, and previous upper respiratory tract

infections. Has no auditory symptoms.

Labyrinthitis An ailment of the inner ear and a form of unilateralvestibular dysfunction. Can cause balance disorders,

vertigo, hearing loss and tinnitus. Often follows an upper

respiratory infection.

Sensorineural hearing loss a type of hearing loss in which the cause lies in the

vestibulocochlear nerve (cranial nerve VIII), the inner ear,

or central processing centers of the brain

BPPV A clinical syndrome characterized by brief recurrent

episodes of vertigo triggered by changes in head position

with respect to gravity. Dix-Hallpike test (+)

71. POLYNEUROPATHY


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• a neurological disorder that occurs when many nerves throughout the

body malfunction simultaneously.

• It may be acute and appear without warning, or chronic and develop

gradually over a longer period of time.

• Many polyneuropathies have both motor and sensory involvement; some

also involve dysfunction of the autonomic nervous system.• These disorders are often symmetric and frequently affect the feet and

hands, causing weakness, loss of sensation, pins-and-needle sensations or

burning pain.

• Damage may occur to axon, myelin sheath, cell body, supporting

connective tissue and nutrient blood supply to nerves. 3 basic pathologicalprocess occurs : wallerian degeneration, segmental demyelination, distal

axon degeneration

Guillaine Barre Syndrome


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• Acute immune-mediated polyneuropathies

• Peripheral nerve myelin is target of an immune attack

• Starts at level of nerve root → conduction blocks → muscle

weakness. Eventually get widespread patchy demyelination →

increased paralysis

• Usually postinfection• Immune-mediated: infectious agents thought to induce Ab

production against specific gangliosides/glycolipids

• Lymphocytic infiltration of spinal roots/peripheral nerves & thenmacrophage-mediated, multifocal stripping of myelin

•Result: defects in the propagation of electrical nerve impulses, witheventual conduction block and flaccid paralysis

GBS


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Clinical Feature :Progressive, fairly symmetric muscle

weakness, typically starts in proximal

legs, weakness in face arm, severe

respiratory muscle weakness

Absent or depressed DTROften prominent severe pain in lower

back

Common to have paresthesias in

hands and feet

Dysautonomia is very common:tachycardia, urinary retention,

hypertenison alternating w/

hypotension, ileus

Diagnosis :• CSF : protein elevated

• Nerve conduction studies: findings of

multifocal demyelination with

slowing of motor conduction,

conduction block, prolonged distalmotor latencies

Treatment:

Supportive, with management of the

paralyzed patient and with elective

ventilation for impending respiratory

failure

Neurology Illustrated

St k D fi it N l i

72. STROKE


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Stroke : Defisit Neurologis

Menurut Penyebab, Stroke dibagi :

1. Stroke Hemoragik

a. Intra cerebral hemoragik (ICH)

OK : Hypertensi, Aneurysma dan arterioveneus Malformasi (AVM)

b. Sub Arachnoid Hemoragik (SAH)

→ diagnosis medis : CT brain scan

2. Stroke Non Hemoragik (Iskemik)

OK : Arteriosklerosis & sering dikaitkan dengan : DM,

Hypercolesterolemia, Asam urat, hyperagregasi trombosit

3. Emboli → Sumber dari tronkus di arteria carotis communis di jantung → Lepas → trombus embolus → otak.

Stroke


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Manifestasi Klinis :• Kelumpuhan wajah atau anggota

badan (biasanya hemiparese),timbul mendadak

• Gangguan hemisensorik

• Perubahan mendadak statusmental

• Afasia; disartria

• Gangguan penglihatan ataudiplopia

• Ataksia• Vertigo, mual, muntah, nyeri

kepala

Faktor Resiko :• Usia

• Riw. TIA atau stroke

• Peny. Jantung koroner

• Hipertensi

• DM

• Merokok

• Dislipidemia

Kapita Selekta Neurologi


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73. SPINAL INJURY


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http://www.merckmanuals.com/home/brai n_spinal_cord_and_ne

rve_disorders/spinal_cord_disorders/overview_of_spinal_cord_dis

orders.html

SPINAL INJURY


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74. MENINGITIS


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• Meningitis: radang pada selaput otak yang melapisi otak dansumsum tulang belakang

• Manifestasi klinis : nyeri kepala, dapat menjalar ke tengkukdan punggung, kaku kuduk, kernig (+), brudzinsky (+)

• Klasifikasi (berdasarkan perubahan pada cairan otak) :

Meningitis serosa : cairan otak jernih, paling sering disebabkan olehMycobacterium tuberculosa, penyebab lain: virus, toxoplasma gondhii,ricketsia

Meningitis purulenta : cairan mengandung pus, penyebabnya antaralain diplococcus pneumoniae, neisseria meningitidis, streptococcus

haemolyticus, staphylococcus aureus, haemophilus influenza,pseudomonas aeruginosa

Kapita Selekta

Meningitis Bakterial


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• Infeksi akut/subakut leptomeningen disertai perubahan sel(predominan PMN) dan kimia CSF (menjadi keruh krn

mengandung pus)

• Etiologi : penyebaran infeksi dari tempat lain melalui darah

(meningokok, pneumokok, hemofilus influenza), atau

penjalaran radang langsung dari infeksi THT (OMP, mastoiditis,

sinusitis), infeksi gigi (gangren pulpa), dan luka terbuka pada

kepala

• Gejala : demam, nyeri kepala, muntah, kesadaran menurun,

kejang, kaku kuduk, laseque


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Meningitis TB Kuman

Tuberkulosis;

riw.penderita TB

+ + +

Meningitis Kriptokok Kriptokokus;

sering pada AIDS

+ + +

Encephalitis

Toxoplasma

Toxoplasma;

sering pada AIDS

- - +

Meningoencephalitis

virus

Virus + + +

PPM Dept.Neurologi, 2007


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• A seizure is defined by release ofexcessive and uncontrolled electricalactivity in the brain. Seizures themselvesare not a disease, they are an event .

• Epilepsy (seizure disorder ) is aneurological condition, that in differenttimes produce brief disturbances in the

electrical functions of the brain. Seizuresare a symptom of epilepsy.

Epilepsy - Classification


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• Focal seizures – account for 80%of adult epilepsies

- Simple partial seizures

- Complex partial seizures

- Partial seizures secondarilly generalised

• Generalised seizures

• Unclassified seizures

Partial Seizure


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Simple• Seizure activity in the brain

causing:• Rhythmic movements -

isolated twitching of arms, face,legs

• Sensory symptoms -tingling, weakness, sounds,smells, tastes, feeling of upsetstomach, visual distortions

• Psychic symptoms -déjà vu, hallucinations, feelings of

fear or anxiety• Usually last less than one minute

• May precede a generalizedseizure

Complex Characterized by altered

awareness

Confusion, inability to

respond

Automatic, purposeless

behaviors such as picking at

clothes, chewing or

mumbling.

Emotional outbursts

May be confused with:

Drunkenness or drug use

Willful belligerence,aggressiveness

GENERALIZED SEIZURES

INVOLVE WIDE AREAS OF THE BRAIN AND LOSS


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INVOLVE WIDE AREAS OF THE BRAIN AND LOSSOF CONSCIOUSNESS

• PETIT MAL : CONSCIOUSNESS IS TRANSIENTLY LOSTAND THE EEG DISPLAYS SPIKE AND WAVE ACTIVITY

• GRAND MAL : CONSCIOUSNESS LOST FOR A LONGERPERIOD AND THE INDIVIDUAL WILL FALL IFSTANDING WHEN SEIZURE STARTS.

• TONIC PHASE: GENERALIZED INCREASED MUSCLETONE.

• CLONIC PHASE: SERIES OF JERKY MOVEMENTS.BOWEL AND BLADDER MAY EVACUATE.

Epilepsi-Klasifikasi (etiologi)


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• Idiopatik epilepsi : biasanya berupa epilepsi dengan serangan

kejang umum, penyebabnya tidak diketahui. Pasien denganidiopatik epilepsi mempunyai inteligensi normal dan hasilpemeriksaan juga normal dan umumnya predisposisi genetik.

• Kriptogenik epilepsi : Dianggap simptomatik tapi penyebabnyabelum diketahui. Kebanyakan lokasi yang berhubungan denganepilepsi tanpa disertai lesi yang mendasari atau lesi di otak tidakdiketahui. Termasuk disini adalah sindroma West, Sindroma LennoxGastaut dan epilepsi mioklonik. Gambaran klinis berupaensefalopati difus.

• Simptomatik epilepsi : Pada simptomatik terdapat lesi struktural diotak yang mendasari, contohnya oleh karena sekunder dari trauma

kepala, infeksi susunan saraf pusat, kelainan kongenital, prosesdesak ruang di otak, gangguan pembuluh darah diotak, toksik(alkohol, obat), gangguan metabolik dan kelainan neurodegeneratif.

Diagnosis Epilepsi Lengkap-Perdossi

76. TRIGEMINAL NEURALGIA


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•Characterised by paroxysmal attacks of severe, short, sharp,stabbing pain→ affecting one or more divisions of the

trigeminal nerve

• The pain can be precipitated by : chewing, speaking, washing

the face, tooth-brushing, cold winds, or touching a specific

“trigger spot” (e.g. Upper lip or gum)

• Etiology :

Many remains unexplained

Compression of the nerve root

by tumors of the cerebellopontine angle

Demyelination

Trigeminal Neuralgia


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Investigation :• CT/MRI to exclude a cerebello-pontine angle lesion

Management :

• Carbamazepine (600-1600mg/day)

• Nerve block

• Trigeminal ganglion/root injection with alcohol/phenol

• Microvascular decompression

• Radiofrequency thermocoagulation


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ILMU PSIKIATRI

77.Gangguan waham menetap


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• Waham merupakan satu-satunya ciri khasklinis atau gejala yang paling mencolok.Waham tersebut (baik tunggal maupunsebagai suatu sistem waham ) harus sudah

ada sedikitnya 3 bulan lamanya, dan harusbersifat khas pribadi (personal) dan bukanbudaya setempat

• Tidak ada gejala skizofrenia• Tidak ada halusinasi auditorik

78. Skizofrenia katatonik


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Subtipe SKIZOFRENIA menurut DSM-IV TR1. Tipe katatonik

terdapat 2 jenis atau lebih gejala berikut:

A. Imobilitas motorik

B. Aktivitas motorik yang berlebihan, tetapi tidak memiliki tujuan dan tidakdipengaruhi oleh stimuli eksternal

C. Negativisme yang ekstrim, mutisme

D. Gerakan volunter yang aneh, seperti posturing, gerakan stereotipik, maneisme ataugrimacing (seringai) yanng menonjol

E. Ekolalia atau ekopraksia

2. Tipe Disorganisasi (Herbrefenik)

A. Menonjolnya disorganisasi bicara dan perilaku, afek datar atau afek tidak sesuaiB. Kriteria skizofrenia tipe katatonik tidak terpenuhi

3. Tipe paranoidA. Preokupasi dengan waham atau halusinasi yang menonjol

B. Kriteria skizofrenia tipe disorganisasi tidak terpenuhi


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4. Tipe tidak tergolongkan (Undifferentiated type)Tidak memenuhi kriteria untuk tipe paranoid, disorganisasi, ataupun tipe katatonik

5. Tipe Residual

A. Waham -, halusinasi-, disorganisasi bicara -, perilaku katatonik-,disorganisasi perilaku-

B. Terdapat terus menrus gangguan yang ditunjukan oleh adanyagejal negatif atau lebih dari kriteria DSMIV TR dari skizofrenia dalambentuk yang lebih ringan (keyakinan yang aneh, pengalamanpersepsi tidak lazim)

79. Bipolar episode manik

Gangguan Bipolar :


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Gangguan Bipolar :Episode berulang (minimal dua episode) dimana

afek dan tingkat aktivitasnya terganggu :

– Satu waktu terjadi peningkatan afek danpenambahan energi (mania )

– Diwaktu yang lain terjadi penurunan afek dankehilangan energi (depresi)

Biasanya ada penyembuhan

sempurna antar episode

80. Terapi Desensitisasi


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F40. GGN ANSIETAS FOBIK

•Agorafobia:

–Ansietas dicetuskan oleh adanya situasi berupa banyak orang/keramaian,

tempat umum, bepergian keluar rumah dan bepergian sendiri, yg sbnrnya

pada saat kejadian ini tidak membahayakan

–Pasien menghindari situasi fobik (house bound)•Fobia Sosial:

–Ansietas harus mendominasi atau terbatas pada situasi sosial tertentu

(outside the family circle)

•Fobia Khas:

–Ansietas terbatas pada adanya objek atau situasi fobik tertentu

•Klaustrofobia (tempat sempit), xenofobia (orang/sesuatu yg asing), akrofobia

(tempat tinggi)

Terapi Fobia


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–Desensitisasi sistematik (serial), ketika kliensecara progresif dipajankan pada objek yang

mengancam, di lingkungan yang aman, sampai

ansietas berkurang

–Flooding, bentuk desensitisasi cepat yang

dilakukan oleh terapis, ketika individu

dihadapkan dengan objek fobia sampai objek

tsb tidak menimbulkan ansietas

81.Gangguan obsesif kompulsif


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• Gejala :o Harus disadari sebagai pikiran atau impuls diri sendiri

o Sedikitnya ada satu pikiran yang tidak bisa dilawan

o Pikiran untuk melakukan tindakan tsb bukan merupakan hal yang

memberi kepuasan

o Pikiran tsb merupakan pengulangan yang tidak menyenangkan

• Obsesif : bayangan pikiran yang mengganggu

• Kompulsif : tindakan berkaitan dengan kebersihan diri, memeriksa

berulang, atau masalah kerapihan dan keteraturan

• Harus ada hampir setiap hari sedikitnya 2 minggu berturut-turut

82. Antidepresan• SSRI

S li P i Fl i (1 20 ) Ci l


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SSRI

• Sertraline, Paroxetine, Fluoxetine (1x20mg), Citalopram,

Fluvoxamine

• Trisiklik• Amitriptilin (2-3x25mg) , imipramine, clomipramine,

Opipramol

• Tetrasiklik• Maprotiline, Amoxapine

• MAO Inhibitor

• Moclobemide

• Antidepresan atipikal

• Tiazodone, Mirtazapine

83. Gangguan Cemas MenyeluruhF41. GGN ANSIETAS LAINNYA


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•Ggn. Cemas menyeluruh

–Ansietas sbg gejala primer, berlangsung hampir setiap hari utkbbrp mgg sampai bulan, tidak terbatas pada keadaan situasi khusus.

–Gejala mencakup: kecemasan, ketegangan motorik, overaktivitasotonomik

•Ggn. Panik –Ggn. Panik baru ditegakkan bila tdk ditemukan adanya ggn.Ansietas fobik

–Terdapat bbrp kali serangan ansietas berat dalam masa kira-kirasatu bulan

•Pada keadaan yg secara objektif tdk ada bah

pembahasan ukdi klinik 4

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