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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
Sumber: Tuberkulosis Pedoman Diagnosis & Penatalaksanaan di Indonesia. PDPI 2006.
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19. Hepatitis Imbas Obat pada Terapi TB
Sumber: Tuberkulosis Pedoman Diagnosis & Penatalaksanaan di Indonesia. PDPI 2006.
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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)
Disorders Etiology Clinical
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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Disorders Etiology Clinical
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-
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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
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Site DistributionStaging
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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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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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Sumber: Ophthalmology. Lang. 2000.
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
Sumber: Ophthalmology. Lang. 2000.
• 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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Handbook of Neurocritical Care, 2005
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Handbook of Neurocritical Care, 2005
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