TO3 PEMBAHASAN BATCH III PENYAKIT DALAM JUN-AGS 2013

PEMBAHASAN TO3 BATCH III
JUN-AGS 2013
dr. Ratna, dr. Yusuf, dr. Dini,
dr. Akhmad, dr. Carolina
ILMU PENYAKIT DALAM
Heberdens & Bouchards nodes
1. Arthritis
http://www.gentili.net/foot/ra.htm
1. Arthritis
Osteoarthritis:
space narrowing (white arrow),

osteophytes/spur (arrowhead),
subchondral cysts,
subchondral
sclerosis/eburnation (black
arrow).
Gout arthritis:
Acute gouty arthritis: soft tissue swelling.
Advanced gout: the erosion are slightly
removed from the joint space, have a

rounded or oval shape, & are
characterized by a hypertrophic calcified
"overhanging edge." The joint space may
be preserved or show osteoarthritic type
narrowing.
Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.

Harrisons principles of internal medicine. 18th ed. McGraw-Hill; 2011.
Ciri
Prevalens
Awitan
OA
RA
Arthritis
Gout
SA
Female>male, >50
thn, obesitas
Female>male
40-70 thn
Male>female, >30
thn, hiperurisemia
Male>female,
dekade 2-3
gradual
gradual
akut
Variabel
Inflamasi
Patologi
Degenerasi
Pannus
Mikrotophi
Enthesitis
Poli
Poli
Mono-poli
Oligo/poli
Tipe Sendi
Kecil/besar
Kecil
Kecil-besar
Besar
Predileksi
Pinggul, lutut,
punggung, 1st CMC,
DIP, PIP
MCP, PIP,
pergelangan
tangan/kaki, kaki
MTP, kaki,
pergelangan kaki &
tangan
Sacroiliac
Spine
Perifer besar
Bouchards nodes
Heberdens nodes
Ulnar dev, Swan

neck, Boutonniere
Kristal urat
En bloc spine
enthesopathy
Osteofit
Osteopenia
erosi
erosi
Erosi
ankilosis
Nodul SK,
pulmonari cardiac
splenomegaly
Tophi,
olecranon bursitis,
batu ginjal
Uveitis, IBD,
konjungtivitis, insuf
aorta, psoriasis
Normal
RF +, anti CCP
Asam urat
Jumlah Sendi
Temuan Sendi
Perubahan
tulang
Temuan
Extraartikular
Lab
2. Murmur & Heart Sounds
2. Murmur & Heart Sound
Lilly LS. Pathophysiology of heart disease.
2. Murmur & Heart Sound

The clinical presentation of MS depends largely on the degree of
reduction in valve area. The more severe the stenosis, the greater
the symptoms related to elevation of left atrial and pulmonary
venous pressures.
The earliest manifestations are those of dyspnea and reduced
exercise capacity. With advanced MS and pulmonary hypertension,
signs of right-sided heart failure ensue.
Murmurs caused by other valvular lesions are often found
concurrently in patients with MS. For example, mitral regurgitation
frequently coexists with MS. Additionally, rightsided heart failure
caused by severe MS may induce tricuspid regurgitation as a result
of right ventricular enlargement.
Lilly LS. Pathophysiology of heart disease.
3. Lung Disease
Diagnosis pneumonia:
Infiltrat baru/infiltrat progresif + 2 gejala:
1. Batuk progresif
2. Perubahan karakter dahak/purulen
3. Suhu aksila 38 oC/riw. Demam
4. Fisis: tanda konsolidasi, napas bronkial, ronkhi
5. Lab: Leukositosis 10.000/leukopenia 4.500
4. Food Poisoning
4. Food Poisoning
The foods typically implicated in C. Perfringens poisoning
include improperly cooked meat and meat products in
which residual spores germinate and proliferate during
slow cooling or insufficient reheating.
Illness results from the ingestion of food containing at least
108 viable vegetative cells, which sporulate in the alkaline
environment of the small intestine, producing C.
perfringens enterotoxin in the process.
The diarrhea that develops within 730 h of ingestion of

contaminated food is generally mild and self-limiting.
5. Arthritis
The management of acute
gout is to provide rapid & safe
pain relief.
NSAID,
Colchicine.
Corticosteroid if NSAID is
contraindicated.
Preventing further attacks by

uric acid lowering agent:
Allopurinol
Probenecid
Uric acid lowering agent

shouldnt be given on acute
attack, unless the patient has
consumed it since 2 weeks
before.
Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.
5. Arthritis
Colchicine given orally is a traditional and effective treatment if
used early in an attack. One useful regimen is one 0.6-mg tablet
given every 8 h with subsequent tapering.
The most effective NSAIDs for gout have a short half-life and include
indomethacin, 2550 mg tid; naproxen, 500 mg bid; ibuprofen, 800
mg tid; and diclofenac, 50 mg tid.
Glucocorticoids given IM or orally, for example, prednisone, 3050
mg/d as the initial dose and gradually tapered with the resolution
of the attack, can be effective in polyarticular gout. For a single joint
or a few involved joints intraarticular triamcinolone acetonide, 20
40 mg, or methylprednisolone, 2550 mg, have been effective and
well tolerated.
6. E.S. OAT Mayor

MAYOR
Kemungkinan Penyebab
HENTIKAN OBAT
Gatal & kemerahan
Semua jenis OAT
Antihistamin & evaluasi

ketat
Tuli
Streptomisin
Stop streptomisin
Vertigo & nistagmus (n.VIII) Streptomisin
Stop streptomisin
Ikterus
Sebagian besar OAT
Hentikan semua OAT s.d.

ikterik menghilang,
hepatoprotektor
Muntah & confusion
Sebagian besar OAT
Hentikan semua OAT & uji

fungsi hati
Gangguan penglihatan
Etambutol
Stop etambutol
Kelainan sistemik, syok &

purpura
Rifampisin
Stop rifampisin
6. E.S. OAT Minor

Minor
Kemungkinan Penyebab
Tata Laksana
Tidak nafsu makan, mual,

sakit perut
Rifampisin
OAT diminum malam

sebelum tidur
Nyeri sendi
Pyrazinamid
Aspirin/allopurinol
Kesemutan s.d. rasa

terbakar di kaki
INH
Vit B6 1 x 100 mg/hari
Urine kemerahan
Rifampisin
Beri penjelasan
7. TB Management
ISTC 10:
All patients should be monitored for response to therapy, best judged
in patients with pulmonary tuberculosis by follow-up sputum smear
microscopy (two specimens) at least at the time of completion of the
initial phase of treatment (two months), at five months, and at the
end of treatment.
Patients who have positive smears during the fifth month of treatment
should be considered as treatment failures and have therapy modifi ed
appropriately.
In patients with extrapulmonary tuberculosis and in children, the
response to treatment is best assessed clinically.
Follow-up radiographic examinations are usually unnecessary and may
be misleading.
International standards for tuberculosis care.
Untuk pemantauan pengobatan dilakukan pemeriksaan

spesimen sebanyak 2 kali (sewaktu, pagi). Bila salah
satu/keduanya (+), maka hasil dinyatakan BTA (+)
Tipe pasien TB
Pasien baru BTA (+),
OAT kategori 1
Waktu Periksa
Akhir tahap
intensif
Sebulan sebelum
akhir atau di akhir
pengobatan
Pasien baru BTA (-) &

Roentgen (+) OAT
kategori 1
Pasien baru BTA (+),
OAT kategori 2
Akhir intensif
Akhir intensif
Sebulan sebelum
akhir atau di akhir
pengobatan
Hasil BTA
Tindak Lanjut
(-)
Tahap lanjutan dimulai
(+)
OAT sisipan 1 bulan, jika masih (+) tahap

lanjutan tetap diberikan
(-)
Sembuh
(+)
Gagal, mulai OAT kategori 2
(-)
Berikan pengobatan tahap lanjutan s.d.

selesai, kemudian pasien dinyatakan
pengobatan lengkap
(+)
Ganti dengan kategori 2 mulai dari awal
(-)
Teruskan pengobatan dgn tahap lanjutan
(+)
OAT sisipan 1 bulan, jika masih (+) tahap

lanjutan tetap diberikan. Uji resistensi.
(-)
Sembuh
(+)
Belum ada obat, disebut kasus kronk. Rujuk.
Pelatihan DOTS. Departemen Pulmonologi & Ilmu Kedokteran Respirasi FKUI; 2008.
8. GERD
GERD
a pathologic condition of symptoms & injury to the
esophagus caused by percolation of gastric or
gastroduodenal contents into the esophagus
associated with ineffective clearance & defective
gastroesophageal barrier.
Symptoms:
Heartburn; midline retrosternal burning sensation
that radiates to the throat, occasionally to the
intrascapular region.
Others: regurgitation, dysphagia, waterbrash.
GI-Liver secrets
8. GERD
Management:
Aggressive lifestyle modification & pharmacologic therapy.
Surgery is encouraged for the fit patient who requires chronic
high doses of pharmacologic therapy to control GERD or who
dislikes taking medicines.
Endoscopic treatments for GERD are very promising, but
controlled long-term comparative trials with proton pump
inhibitors and/or surgery are lacking.
9. Heart Disease
9. Heart Disease
Clinical Manifestations:
Persistent bacteremia: fever, weight loss, anorexia,
night sweat, fatigue
Valvular/perivalvular infection: murmur, CHF,
conduction abnormality
Septic emboli
Immune complex phenomena: arthritis,
glomerulonephritis, ESR
9. Heart Disease
9. Heart Disease
10. Hematology
CLL
CML
ALL
AML
The bone marrow makes abnormal leukocyte dont die when they
should crowd out normal leukocytes, erythrocytes, & platelets.
This makes it hard for normal blood cells to do their work.
Prevalence
Over 55 y.o.
Mainly adults
Symptoms &
Signs
Grow slowly may

asymptomatic, the disease fund
during a routine test.
Common in
children
Adults &
children
Grow quickly feel sick & go to

their doctor.
Fever, swollen lymph nodes, frequent infection, weak,

bleeding/bruising easily, hepatomegaly/splenomegaly, weight loss,
bone pain.
Lab
Mature
lymphocyte
Mature
granulocyte
Therapy
Can be delayed if asymptomatic

CDC.gov
Lymphoblast
>20%
Myeloblast
>20%
Treated right away
10. Leukemia
Clinical Manifestation
More common in AML
Leukostasis (when blas count >50.000/uL): occluded microcirculation
headache, blurred vision, TIA, CVA, dyspnea, hypoxia
DIC (promyelocitic subtype)
Leukemic infiltration of skin, gingiva (monocytic subtype)
Chloroma: extramedullary tumor, virtually any location.
More common in ALL

Bone pain, lymphadenopathy, hepatosplenomegaly (also seen in
monocytic AML)
CNS involvement: cranial neuropathies, nausea, vomiting, headache,
anterior mediastinal mass (T-cell ALL)
Tumor lysis syndrome
Pocket medicine.
Diagnosis
Characteristic
Polycythemia
Vera
Persistent increased of hematocrite/Hb level caused by excessive

erythocytosis, as well as leukocytosis & thrombocytosis. Symptoms:
blood hyperviscosity impaired perfusion dizziness, visual
disturbance, stroke.
Leukemoid
reaction
The term "leukemoid reaction" is used to describe a condition where

peripheral white blood cells on a stained blood smear may have some
resemblance to leukemia cells. Quantatively, in a leukemoid reaction,
the neutrophil count may be as high as 50.000/uL with more immature
cells, particularly myelocytes, than are usually present in toxic left-shift
syndromes.
Myelodysplasia
Maturation defect of blood cell precursors in bone marrow caused by

mutation, results in normocytic normochrom anaemia and cells with
abnormal morphology (binucleated cell, etc), may be a predisposition
to leukemia.
Multiple myeloma Multiple myeloma: a malignant proliferation of plasma cells derived

from a single clone. The classic triad of myeloma: marrow
plasmacytosis (>10%), lytic bone lesions, serum and/or urine M
component.
11. Cara Pemberian Kina Parenteral

4 jam ke-1: Loading dose 20 mg/kgbb kina dilarutkan
dalam 500 mL dextrose 5% atau NaCl 0,9%.
4 jam ke-2: dextrose 5% atau NaCl 0,9% saja.
4 jam ke-3: maintenance dose 10 mg/kgbb dalam 500
mL dextrose 5% atau NaCl 0,9%.
4 jam ke-4: dextrose 5% atau NaCl 0,9% saja.
Lalu dosis maintenance sampai pasien sadar atau dapat
minum kina per oral (10 mg/kgbb/kali 3 kali/hari
hingga 7 hari terhitung dari kina perinfus).
12. Hematemesis
Cirrhosis
the development of fibrosis to the
point that there is architectural
distortion with the formation of
regenerative nodules.
This results in a decrease in
hepatocellular mass, and thus
function, & an alteration of blood
flow.
12. Hematemesis
Portal hypertension caused by:
intrahepatic resistance to the

passage of blood flow through
the liver due to cirrhosis &
regenerative nodules
splanchnic blood flow
secondary to vasodilation
within the splanchnic vascular
bed.
Portal hypertension cause

varices around the sites of
portosystemic anastomoses:
hemorrhoids at the anorectal
junction;
esophageal varices at the
gastroesophageal junction;
caput medusae at the
umbilicus.
13. Hemolytic Anemia

Heinz bodies can be
produced by the action on
red cells of a wide range of
aromatic nitro- and aminocompounds, as well as by
inorganic oxidizing agents.
They also occur when one or
other of the globin chains of
haemoglobin is unstable.
In man, the finding of Heinz
bodies is a sign of either
chemical poisoning, drug
intoxication, glucose-6phosphate dehydrogenase
(G6PD) deficiency, or the
presence of an unstable
haemoglobin (e.g., Hb Kln).

Glucose 6-phosphate dehydrogenase (G6PD) is a
housekeeping enzyme critical in the redox metabolism of
all aerobic cells.
In red cells its role is even more critical, because it is the
only source of NADPH that directly and via glutathione
(GSH) defends these cells against oxidative stress.
14. Bone Resorption Markers

Pyridinium Crosslinks (Pyridinoline & Deoxypyridinoline)
These collagen crosslinks are found in a unique ratio in the bone
(Pyr/Dpyr= 33.5 : 1), a fact that makes these substances ideal
candidates as markers for bone breakdown.
The clinical applications of measuring these substances include:
identification of individuals at risk for bone loss and fracture,

assessment of metabolic bone disease,
prediction of bone metastases,
subsequent skeletal complications, and even
outcome in cancer patients afflicted by solid tumors (prostate, breast,
and lung most commonly) and primary bone tumors,
management of antiresorptive therapy.
14. Bone Formation Markers

Alkaline Phosphatase
Bone alkaline phosphatase (ALP-B), an osteoblast membrane-bound enzyme.
Studies have shown that the amount of ALP-B activity in osteoblasts and in bone is
proportional to collagen formation; thus, it can provide an index of the rate of
bone formation.
Measurements of total serum ALP are useful to follow disease activity when the
amount of bone isoenzyme is exceptionally high, as in Pagets disease or
osteosarcoma.
Osteocalcin
Osteocalcin is the major noncollagenous protein of the bone matrix, and is
produced by osteoblasts, odontoblasts, and even chondrocytes.
During bone matrix synthesis, some osteocalcin is released into the circulation and
is rapidly cleared by the kidneys.
Osteocalcin is increased when there is high bone turnover, as occurs in
hyperparathyroidism, acromegaly, and Pagets disease.
15. Disorder of Calcium Balance

Hypoparathyroidism may
occur as a complication of
thyroidectomy
PTH released is inadequate
hypocalcemia.
Proximal tubular effect of
PTH to promote phosphate
excretion is lost
hyperphosphatemia
Low level of 1,25-(OH)2D
Less PTH is available to act
in the distal nephron
increase calcium excretion
Less PTH less Mg
reabsorption at ansa Henle.
McPhee SJ, et al. Pathophysiology of disease: an introduction
to clinical medicine. 5th ed. McGraw-Hill; 2006.
15. Disorder of Calcium Balance

Organ
Symptoms & Signs
Systemic
Confusion
Weakness
Neuromuscular
Paresthesias
Psychosis
Seizures
Carpopedal spasms
Chvostek's and Trousseau's signs
Depression
Muscle cramping
Parkinsonism
Irritability
Cardiac
Prolonged QT interval
T-wave changes
Congestive heart failure
Ocular
Cataracts
Dental
Enamel hypoplasia of teeth
Respiratory
Laryngospasm
Bronchospasm
Stridor
McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th ed. McGraw-Hill; 2006.
Carpal spasm
15. Electrolyte Disorder

Abnormalities of the plasma level of K, Ca, & Mg affect the ECG, though
changes in the plasma sodium level do not.
The only ECG book youll ever need.
16. Lung Infection

Severe Acute Respiratory Syndrome (SARS)
Etiology: coronavirus
Course:
incubation period 27 days
begins as a systemic illness marked by of fever accompanied by malaise,
headache, and myalgias
is followed in 12 days by a nonproductive cough and dyspnea.
Approximately 25% of patients have diarrhea.
Chest x-rays: infiltrates, including patchy areas of consolidationmost

frequently in peripheral and lower lung fieldsor interstitial infiltrates,
which can progress to diffuse involvement.
In severe cases, respiratory function may worsen during the second week
of illness and progress to frank adult respiratory distress syndrome
accompanied by multiorgan dysfunction.
Harrisons principles of internal medicine
16. Lung Infection

Avian Influenza
Influenza is an acute respiratory illness caused by infection
with influenza viruses.
In 1997, human cases of influenza caused by avian
influenza viruses (A/H5N1) were detected in Hong Kong
during an extensive outbreak of influenza in poultry.
The illness affects the upper and/or lower respiratory tract
and is often accompanied by systemic signs and symptoms
such as fever, headache, myalgia, and weakness.
The designation of influenza viruses as type A, B, or C is
based on antigenic characteristics of the nucleoprotein (NP)
& matrix (M) protein antigens.
17. Thyroid Disease

Hypothyroidism
Therapy: levothyroxine
17. Thyroid Disease
18. Penyakit Ginjal

Glomerular Disease:
hematuria, proteinuria, pyuria.
Sind. nefritik akut:

proteinuria 1-2 g/24 jam, hematuria dengan silinder eritrosit, pyuria,
hipertensi, retensi cairan, peningkatan kreatinin serum.
Jika kreatinin serum meningkat cepat dalam beberapa hari, kadang
nefritis akut disebut rapidly progressive glomerulonephritis (RPGN);
Sind. nefrotik:
proteinuria berat (>3.0 g/24 jam), hipoalbuminemia, hipertensi,
hiperkolesterolemia,, edema/anasarka, & hematuria mikroskopik.
Harrisons principles of internal medicine.

Pathophysiology of disease: an introduction to clinical medicine. 5th ed.
18. Renal Disorder

Diagnosis
Characteristic
Acute glomerulonephritis
an abrupt onset of hematuria & proteinuria with

reduced GFR & renal salt and water retention, followed
by full recovery of renal function.
Rapidly progressive
glomerulonephritis
recovery from the acute disorder does not occur.

Worsening renal function results in irreversible and
complete renal failure over weeks to months.
Chronic glomerulonephritis
renal impairment after acute glomerulonephritis

progresses slowly over a period of years & eventually
results in chronic renal failure.
Nephrotic syndrome
manifested as marked proteinuria, particularly

albuminuria (defined as 24-h urine protein excretion >
3.5 g), hypoalbuminemia, edema, hyperlipidemia, and
fat bodies in the urine.
Pathophysiology of disease: an introduction to clinical medicine. 5th ed.
19. Jaundice
The cardinal finding in
hepatitis is a rise in the
aminotransferases to
values greater than 200
IU/L and often to 500 or
even 1000 IU/L.
An exception to this
finding is seen in hepatitis
C, in which only modest
elevations of ALT (but not
AST) can occur.
The bilirubin is frequently
elevated and is composed
of both direct and indirect
types
19. Jaundice
Incubation periods for hepatitis A range from 1545 days (mean, 4 weeks), for
hepatitis B and D from 30180 days (mean, 812 weeks), for hepatitis C from 15
160 days (mean, 7 weeks), and for hepatitis E from 1460 days (mean, 56 weeks).
The prodromal symptoms

Constitutional symptoms of anorexia, nausea and vomiting, fatigue, malaise, arthralgias,
myalgias, headache, photophobia, pharyngitis, cough, and coryza may precede the onset of
jaundice by 12 weeks.
Dark urine and clay-colored stools may be noticed by the patient from 15 days before the
onset of clinical jaundice.
The clinical jaundice

The constitutional prodromal symptoms usually diminish.
The liver becomes enlarged and tender and may be associated with right upper quadrant pain
and discomfort. Spleen may enlarge.
During the recovery phase, constitutional symptoms disappear, but usually some
liver enlargement and abnormalities in liver biochemical tests are still evident.
20. Hepatitis A Prophylaxis

When administered before exposure or during the early incubation
period, IG is effective in preventing clinically apparent hepatitis A.
For postexposure prophylaxis of intimate contacts (household,
sexual, institutional) of persons with hepatitis A, the administration
of 0.02 mL/kg is recommended as early after exposure as possible;
it may be effective even when administered as late as 2 weeks after
exposure.
Prophylaxis is not necessary for:
those who have already received hepatitis A vaccine,

casual contacts (office, factory, school, or hospital),
most elderly persons, who are very likely to be immune, or
those known to have anti-HAV in their serum.
Harrisons principles of internal medicine. 18th eds.
20. Hepatitis B Prophylaxis

Three IM injections of hepatitis B vaccine are recommended at 0, 1, and 6
months for pre-exposure prophylaxis against hepatitis B in settings of
frequent exposure:
health workers exposed to blood;
hemodialysis patients and staff;
residents and staff of custodial institutions for the developmentally
handicapped;
injection drug users;
inmates of long-term correctional facilities;
persons with multiple sexual partners;
persons such as hemophiliacs who require long-term, high-volume
therapy with blood derivatives;
household and sexual contacts of HBsAg carriers;
persons living in or traveling extensively in endemic areas;
unvaccinated children under the age of 18;
Harrisons principles of internal medicine. 18th eds.
21. Lupus Nephritis

Lupus nephritis affects up to 50% of SLE patients. The principal mechanism
of injury is immune complex deposition in the glomeruli, tubular or
peritubular capillary basement membranes, or larger blood vessels.
21. Lupus Nephritis
23. Abdominal Pain
Gallstones are most often asymptomatic

surgery is not indicated
Of patients who do have symptoms:

nausea or abdominal discomfort after
eating fatty or fried foods to severe right
upper quadrant or midepigastric
abdominal pain & jaundice.
The typical patient with gallstones is
female, high dietary fat intake, has had
prior pregnancies, reflecting the role of
estrogens in gallstone pathogenesis, & is
in her 40s, reflecting the time necessary
for progression to symptomatic disease.
Surgery is indicated
Pathophysiology of disease. 2nd ed. Springer; 2006.
Lokasi Nyeri
Anamnesis
Pemeriksaan
Fisis
Nyeri epigastrik
Kembung
Membaik dgn
makan (ulkus
duodenum),
Memburuk dgn
makan (ulkus
gastrikum)
Tidak spesifik
Nyeri epigastrik
menjalar ke
punggung
Gejala: mual &

muntah, Demam
Penyebab: alkohol
(30%), batu
empedu (35%)
Nyeri tekan &

defans, perdarahan
retroperitoneal
(Cullen:
periumbilikal, Gray
Turner: pinggang),
Hipotensi
Ikterus,
Hepatomegali
Nyeri kanan atas/ Prodromal

epigastrium
(demam, malaise,
mual) kuning.
Nyeri kanan atas/ Risk: Female, Fat,
epigastrium
Fourty, Hamil
Prepitasi makanan
berlemak, Mual,
TIDAK Demam
Nyeri epigastrik/
Mual/muntah,
kanan atas
Demam
menjalar ke bahu/
punggung
Pemeriksaan
Penunjang
Diagnosis
Terapi
Urea breath test

(+): H. pylori
Endoskopi:
eritema (gastritis
akut)
atropi (gastritis
kronik)
luka sd submukosa
(ulkus)
Peningkatan enzim
amylase & lipase di
darah
Dispepsia
PPI:
ome/lansoprazol
H. pylori:
klaritromisin+amok
silin+PPI
Transaminase,
Serologi HAV,
HBSAg, Anti HBS
Nyeri tekan
USG: hiperekoik
abdomen
dgn acoustic
Berlangsung 30-180 window
menit
Murphy Sign
USG: penebalan
dinding kandung
empedu (double
rims)
Pankreatitis
Hepatitis Akut
Resusitasi cairan
Nutrisi enteral
Analgesik
Suportif
Kolelitiasis
Kolesistektomi
Asam
ursodeoksikolat
Kolesistitis
Resusitasi cairan
AB: sefalosporin
gen. 3 +
metronidazol
Kolesistektomi
23. PEA
PEA encompasses a
heterogeneous group of
organized electric rhythms that
are associated with either
absence of mechanical
ventricular activity or mechanical
ventricular activity that is
insufficient to generate a clinically
detectable pulse.
Drug Therapy for PEA/Asystole

A vasopressor can be given as soon
as feasible with the primary goal of
increasing myocardial and cerebral
blood flow during CPR and
achieving ROSC
Available evidence suggests that
the routine use of atropine during
PEA or asystole is unlikely to have a
therapeutic benefit.
24.Malaria
Clinical diagnosis
The WHO recommendations for clinical diagnosis/suspicion of
uncomplicated malaria in different epidemiological settings are as
follows:
in settings where the risk of malaria is low, clinical diagnosis of
uncomplicated malaria should be based on the possibility of exposure
to malaria and a history of fever in the previous three days with no
features of other severe diseases;
in settings where the risk of malaria is high, clinical diagnosis should
be based on a history of fever in the previous 24 h and/or the
presence of anaemia, for which pallor of the palms appears to be the
most reliable sign in young children.
In all settings, clinical suspicion of malaria should be confirmed

with a parasitological diagnosis.
Malaria Guidelines WHO 2011
24. Malaria
Parasitological diagnosis has the following
advantages:
improved patient care in parasite-positive patients;
identification of parasite-negative patients in whom
another diagnosis must be sought;
prevention of unnecessary use of antimalarials,
reducing frequency of adverse effects, especially in
those who do not need the medicines, and drug
pressure selecting for resistant parasites;
improved malaria case detection and reporting;
confirmation of treatment failures.
Thin blood films of P.

vivax
Thick blood
films of P. vivax
25. Acute Pulmonary Edema

Acute on chronic heart failure:
Profiles B & C are typical of patients with
acute pulmonary edema.
Physical examination of pulmonary edema:
Tachycardic
Tachypnea and coughing of frothy sputum
Rales are present initially at the bases & later
throughout the lung fields.
Braunwalds Heart Disease.

Fluid or volume status assessment plays role:
In determining the need for diuretic therapy
In detecting sodium excesses or deficiencies.
At each visit, determine:

the degree of jugular venous distension,
the presence & severity of organ congestion
(pulmonary rales & hepatomegaly),
the magnitude of peripheral edema in the legs,
abdomen, presacral area, scrotum, ascites.
ACC-AHA. Heart Failure guideline.
Harrisons principles of internal medicine.
26. TB-HIV
TB is the most common cause of death in HIV &
increase progresivity of AIDS.
The problems in TB-HIV:
TB drugs & ARV have overlapping side effects
Drug interaction between TB drugs & ARV
Paradoxal therapy (immune reconstitution
inflammatory syndrome/IRIS): worsening symptoms
(fever, lymph node enlargement, infiltrate) after
receive TB drugs /ARV/both which are not caused by
therapeutic failure, but caused by reactivation of
immune system to TB antigen.
26. TB-HIV
Principles of medication:
TB medication is a priority
Do not give TB drugs & ARV simultaneously
because of drugs interaction, toxicity, & IRIS
In life threatening case (disseminated TB or CD4
<200/mm3), ARV & TB drugs can be given
concurrently with closed monitoring.
ARV that has been given is continued.
In situation where there is no threat to life, ARV
may be delayed to prevent IRIS & drug interaction.
26. TB-HIV
Management of tuberculosis & HIV coinfection. WHO.
ILMU BEDAH, ANESTESIOLOGI &

RADIOLOGI
27. Myiasis
Infestasi larva lalat di kulit. Penyebab terbanyak:
Dermatobia hominis & Cordylobia anthropophaga
2 bentuk myiasis kutaneus:
Furuncular myiasis: boil-like lesion, papul eritematosa,
nyeri, punktum sentral, ujung larva bisa muncul di ujung
punktum, limfadenopati
Wound myiasis: larva terdapat di luka yang supurasi dan
sudah terdekomposisi
Tata laksana:
Furuncular myiasis: bedah dgn anestesi lokal (lini
pertama), oklusi dengan wax, ivermectin
Wound myiasis: membersihkan luka dari larva
(debridement), bedah bila perlu
Grammatikopoulou E. Myiasis. http://emedicine.medscape.com/article/1491170-overview
Noutsis C. Myiasis. Dermatol Clin 1994; 12(4).
Furuncular myiasis
Wound myiasis
28-29. Triage
Triage Priorities
1. Red- highest priority patients

Need immediate care (usually
circulatory or respiratory)
2. Yellow- second highest priority
Able to wait longer before transport
(45 minutes)
*** mark triage priorities (tape, tag)
3. Green- walking
Able to wait several hours for

transport
4. Black- dead
Will die during emergency care
(have lethal injuries)
Triage Category: Red

Red (Highest) Priority:
Patients who need
immediate care and
transport as soon as
possible
Airway and breathing

difficulties
Uncontrolled or severe
bleeding
Decreased level of
consciousness
Severe medical problems
Shock (hypoperfusion)
Severe burns
Yellow
Yellow (Second) Priority:
Patients whose treatment
and transportation can be
temporarily delayed
Burns without airway
problems
Major or multiple bone or
joint injuries
Back injuries with or
without spinal cord damage
Green
Minor fractures
Minor soft-tissue
injuries
Green (Low) Priority:
Patients whose
treatment and
transportation can be
delayed until last
What is START?
START is an acronym for Simple Triage And Rapid
Treatment
It is a simple step-by-step triage and treatment
method to be used by the first rescuers responding
to a multi casualty incident. It allows these
rescuers to identify victims at greatest risk for
early death and to provide basic stabilization
maneuvers
Immediate
Patients
Delayed
Deceased
Your First Action

If you can walk, go stand over there!
All of Yall, go over there! (Texas version )
Mark green
Immediate
Patients
Delayed
Deceased
START Algorithm (Airway/Breathing)

RESPIRATIONS/VENTILATIONS
NONE
YES
REPOSITION AIRWAY
ASSESS RESPIRATIONS/VENTILATIONS
NONE
DECEASED
Immediate
Patients
Delayed
Deceased
YES
> 30/MINUTE
IMMEDIATE
IMMEDIATE
<30/MINUTE
ASSESS
PERFUSION
START Algorithm (Circulation)

PERFUSION
<2 SECONDS
ASSESS
MENTAL STATUS
> 2 SECONDS
CONTROL
BLEEDING
IMMEDIATE
Immediate
Patients
Delayed
Deceased
START Algorithm (Disability)

MENTAL STATUS
FOLLOWS
SIMPLE
COMMANDS
DELAYED
Immediate
Patients
Delayed
Deceased
FAILS TO FOLLOW
SIMPLE
COMMANDS
IMMEDIATE
http://emedicine.medscape.com/
30. Open Pneumothorax
Causes the lung to collapse due to increased

pressure in pleural cavity
Can be life threatening and can deteriorate
rapidly
Th/ :
ABCs with c-spine
control as indicated
High Flow oxygen
Listen for decreased
breath sounds on
affected side
Apply occlusive dressing
to wound
Notify Hospital and ALS
unit as soon as possible
http://www.cssolutions.biz
Occlusive dressing
31. Syok Anafilaktik
www.resus.org.uk/pages/reaction.pdf
2012.
Anaphylaxis flowchart
http://www.rch.org.au/clinicalguide/guideline_index/anaphylaxis/
32. Lidocain HCl

Maximum doses :
5 mg/kgBB (without epinephrine)
7 mg/kgBB (with epinephrine)
33. Dysphagia
Dysphagiadifficulty with swallowingis a
common condition, reported by 58% of the
general population aged over 50 years, and by
16% of the elderly.
Dysphagia, particularly oropharyngeal
dysphagia, is even more common in the
chronic-care setting; up to 60% of nursinghome occupants have feeding difficulties that
include dysphagia.
SWALLOWING
Mechanism is complex
Involves the actions of 26 muscles and 5 cranial nerves
CN V -- both sensory and motor fibers; important in
chewing
CN VII -- both sensory and motor fibers; important for
sensation of oropharynx & taste to anterior 2/3 of tongue
CN IX -- both sensory and motor fibers; important for taste
to posterior tongue, sensory and motor functions of the
pharynx
CN X -- both sensory and motor fibers; important for taste
to oropharynx, and sensation and motor function to larynx
and laryngopharynx; important for airway protection
CN XII -- motor fibers that primarily innervate the tongue
A normal adult swallows unconsciously 600 times in a 24-hour
period
Treatment
Remediate oropharyngeal dysphagia
Compensatory approaches
Restorative approaches according to causes
To maintain nutrition, dietary modifications and/or

alternative nutrition via a feeding tube
Nasogastric, gastrostomy, jejunostomy
Intravenous fluids and hospitalization may be
necessary for moderate to severe dehydration
Include ongoing assessment of clients response to

intervention, and adjust goals and approaches to fit
evolving needs
34. Gas gangrene

It is a rapidly progressive, potentially fatal
condition characterized by widespread
necrosis of the muscles and subsequent softtissue destruction.
This is a dreaded consequence of
inadequately treated missile wounds, crushing
injuries and high-voltage electrical injuries.
Causative agent
Closteridium species spore forming, Gram(+)
c.septicum
c.novyi
c. Perfringens
(mostly)
vegetative
cells multiply
Spores
germinate
Anaerobic
environment
Carbohydrates
Fermentation
PATHOGENESIS
Incubation period is
Gas production
In tissues
1-7 days
Toxemia and
death
Distension of
tissues
Interfering
Blood supply
Ischemia/
gangrene
Pathogenesis
- Bacteria
enters the
broken skin or
wound
- Spores
are
produced
- The toxins
(lecithinase)
and enzyme
are produced
- The
bacteria are
grow and ferment
the muscle
carbohydrate
- The bacteria
present in
circulation
system
the anaerobic
tissue present
Examples of enzyme:
colagenases, proteases
and lipases
- These enzymes will kill
other host cell and
extend the anaerobic
environment
- Produce gases (nitrogen,

hydrogen sulphide and
carbon dioxide)
- Crepitant tissue
( destroyed tissue)
Symptoms
High fever
Shock
Massive tissue destruction
Blackening of skin
Severe pain around a skin of wound
Blisters with gas bubbles form near the infected area,
The heartbeat and breathing become rapid
Presentation : Crepitation in tissues, sickly sweet odor

discharge, rapidly progressing necrosis, fever,
hemolysis, toxemia, shock, renal failure, and death
35. Forehand Fracture

Montegia Fracture Dislocation
It is a fracture of the
proximal 1/3rd of the Ulna
with dislocation of head of
radius anteriorly.
Posteriorly or laterally
Head of Radius dislocates
same direction as fracture
It requires ORIF or it will
redisplace
Lateral displacement
Colles Fracture
Most common fracture in Osteoporotic
bones
Extra-Articular : 1 inch of distal Radius
Results from a fall on dorsi flexed wrist
Typical deformity : Dinner Fork
Deformity is : Impaction, dorsal
displacement and angulation, radial
displacement and angulation and avulsion of
ulnar styloid process
Colles Fracture
optimized by optima
# distal 1 Impaction ,Dorsal

displacement and dorsal tilt
Galleazzi Fracture
It is a fracture of distal
Radius and dislocation of
inferior Radio- Ulnar joint
Like Monteggia fracture if
treated conservatively it
will redisplace
This fracture appeared in

acceptable position after
reduction and POP
Greenstick Fractures
Smith Fracture
Almost the opposite of Colles fracture

Much less common compared to colles
Results from a fall on palmer flexed wrist
Typical deformity : Garden Spade
Management is conservative : MUA and
Above Elbow POP
Smith Fracture
36. Thyroid Cancer

History
Symptoms
The most common presentation of a thyroid
nodule, benign or malignant, is a painless mass in
the region of the thyroid gland (Goldman, 1996).
Symptoms consistent with malignancy
Pain
Dysphagia
Stridor
Hemoptysis
Rapid enlargement
Hoarseness
Risk factors
Thyroid exposure to irradiation
Age and Sex
Benign nodules occur most frequently in women 20-40 years
(Campbell, 1989)
5%-10% of these are malignant (Campbell, 1989)
Men have a higher risk of a nodule being malignant
Family History
History of family member with medullary thyroid carcinoma
History of family member with other endocrine abnormalities
(parathyroid, adrenals)
History of familial polyposis (Gardners syndrome)
Evaluation of the thyroid Nodule

(Physical Exam)
Examination of the thyroid nodule:
consistency - hard vs. soft
size - < 4.0 cm
Multinodular vs. solitary nodule
multi nodular - 3% chance of
malignancy (Goldman, 1996)
solitary nodule - 5%-12%
chance of malignancy
(Goldman, 1996)
Mobility with swallowing
Mobility with respect to
surrounding tissues
Well circumscribed vs. ill defined
borders
Examine for ectopic thyroid

tissue
Indirect or fiberoptic
laryngoscopy
vocal cord mobility
evaluate airway
Systematic palpation of the
neck
Metastatic adenopathy
commonly found:
in the central
compartment (level VI)
along middle and lower
portion of the jugular vein
(regions III and IV) and
Evaluation of the Thyroid Nodule

Blood Tests
Radioactive iodine
Thyroid function tests

thyroxine (T4)
triiodothyronin (T3)
thyroid stimulating hormone (TSH)
Serum Calcium
Thyroglobulin (TG)
Calcitonin
USG :
90% accuracy in categorizing
nodules as solid, cystic, or mixed
(Rojeski, 1985)
Best method of determining the

volume of a nodule (Rojeski, 1985)
Can detect the presence of lymph
node enlargement and
calcifications
is trapped and organified

can determine functionality of a
thyroid nodule
17% of cold nodules, 13% of warm
or cool nodules, and 4% of hot
nodules to be malignant
FNAB : Currently considered to be the
best first-line diagnostic procedure in
the evaluation of the thyroid nodule
Classification of Malignant Thyroid

Neoplasms
Papillary carcinoma
Follicular variant
Tall cell
Diffuse sclerosing
Encapsulated
Follicular carcinoma
Overtly invasive
Minimally invasive
Hurthle cell carcinoma

Anaplastic carcinoma
Giant cell
Small cell
Medullary Carcinoma
Miscellaneous
Sarcoma
Lymphoma
Squamous cell carcinoma
Mucoepidermoid
carcinoma
Clear cell tumors
Pasma cell tumors
Metastatic
Direct extention
Kidney
Colon
Melanoma
Well-Differentiated Thyroid Carcinomas

(WDTC) - Papillary, Follicular, and Hurthle cell
Pathogenesis - unknown
Papillary has been associated with the RET protooncogene but no definitive link has been proven
(Geopfert, 1998)
Certain clinical factors increase the likelihood of

developing thyroid cancer
Irradiation - papillary carcinoma
Prolonged elevation of TSH (iodine deficiency) - follicular
carcinoma (Goldman, 1996)
relationship not seen with papillary carcinoma
mechanism is not known
WDTC - Papillary Carcinoma

60%-80% of all thyroid cancers
(Geopfert, 1998, Merino, 1991)
Histologic subtypes
Follicular variant
Tall cell
Columnar cell
Diffuse sclerosing
Encapsulated
Prognosis is 80% survival at 10
years (Goldman, 1996)
Females > Males
Mean age of 35 years
(Mazzaferri, 1994)
Lymph node involvement is

common
Major route of metastasis is
lymphatic
Clinically undetectable lymph
node involvement does not
worsen prognosis (Harwood,
1978)
WDTC - Follicular Carcinoma
20% of all thyroid malignancies

Women > Men (2:1 - 4:1) (Davis, 1992, De Souza, 1993)
Mean age of 39 years (Mazzaferri, 1994)
Prognosis - 60% survive to 10 years (Geopfert, 1994)
Metastasis
angioinvasion and hematogenous spread
15% present with distant metastases to bone and lung
Lymphatic involvement is seen in 13% (Goldman, 1996)
Medullary Thyroid Carcinoma

10% of all thyroid malignancies
1000 new cases in the U.S. each year
Arises from the parafollicular cell or C-cells of
the thyroid gland
derivatives of neural crest cells of the branchial arches
secrete calcitonin which plays a role in calcium metabolism
Medullary Thyroid Carcinoma

Diagnosis
Labs: 1) basal and pentagastrin stimulated serum
calcitonin levels (>300 pg/ml)
2) serum calcium
3) 24 hour urinary catecholamines
(metanephrines, VMA, nor-metanephrines)
4) carcinoembryonic antigen (CEA)
Fine-needle aspiration
Genetic testing of all first degree relatives
Anaplastic Carcinoma of the Thyroid
Highly lethal form of thyroid cancer

Median survival <8 months (Jereb, 1975, Junor, 1992)
1%-10% of all thyroid cancers (Leeper, 1985, LiVolsi, 1987)
Affects the elderly (30% of thyroid cancers in patients
>70 years) (Sou, 1996)
Mean age of 60 years (Junor, 1992)
53% have previous benign thyroid disease (Demeter, 1991)
47% have previous history of WDTC (Demeter, 1991)
Management
Surgery is the definitive management of thyroid cancer, excluding
most cases of ATC and lymphoma
Types of operations:
lobectomy with isthmusectomy
minimal operation required for a potentially malignant thyroid
nodule
total thyroidectomy
removal of all thyroid tissue
preservation of the contralateral parathyroid glands
subtotal thyroidectomy
anything less than a total thyroidectomy
37. Suturing
Suturing
http://www.jpatrick.net/MAHFiles/orient/woundcare_manual.html
Muscle
Fascia
Subcutis
Skin
38. Basilar skull fracture

is a fracture of the base of the skull, typically
involving the temporal bone, occipital bone,
sphenoid bone, and/or ethmoid bone.
Patients present with CSF otorrhea
Bruising over the mastoids, ie, Battle sign.
CSF rhinorrhea
Bruising around the eyes, ie, "raccoon eyes
emedicine.medscape.com/article/248108
Temporal Bone Trauma

Wide spectrum of
clinical findings
Knowledge of the
anatomy is vital to
proper diagnosis and
appropriate
management
Incidence and Epidemiology

Motorized Transportation
30-75% of blunt head trauma had associated temporal
bone trauma
Penetrating Trauma
More dismal prognosis
Barotrauma
Inner ear decompression sickness
The bends
Perilymphatic fistula
Blast Injuries
Physical Examination
Basilar Skull Fractures
Periorbital Ecchymosis
(Raccoons Eyes)
Mastoid Ecchymosis
(Battles Sign)
Hemotympanum
Longitudinal fractures
80% of Temporal Bone
Fractures
Lateral Forces along the
petrosquamous suture
line
15-20% Facial Nerve
involvement
EAC laceration
Transverse fractures
20% of Temporal
Bone Fractures
Forces in the
Antero-Posterior
direction
Inner ear injury
50% Facial Nerve
Involvement
EAC intact
CSF Otorrhea
Acquired
Postoperative (58%)
Trauma (32%)
Nontraumatic (11%)
Spontaneous
Bony defect theory
Arachnoid granulation theory
Temporal bone Fractures are the most common cause

of CSF Otorrhea
The halo sign is present when nasal/ear secretions on
bed linens or dressings form a halo
39. WHO Pain Management Stepladder
40. Urolithiasis
Urinary tract stone disease
Signs:
Flank pain
Irritative voiding symptom
Nausea
microscopic hematuria
Urinary crystals of calcium

oxalate, uric acid, or cystine
may occasionally be found
upon urinalysis
Diagnosis: IVP
optimized by optima
41. Trauma Uretra

Suspect that a patient
may have injured his
lower urinary tract if:
he has some injury
which makes this likely
(especially a fractured
pelvis)
cannot pass urine after
an accident
there is blood at the tip
of his urethra
Don't pass a diagnostic

catheter up the patient's
urethra because:
Retrograde
urethrography
The information it will give

will be unreliable.
May contaminate the
haematoma round the
injury.
May damage the slender
bridge of tissue that joins
the two halves of his
injured urethra
Posterior urethral rupture above the
intact urogenital diaphragm
following blunt trauma
http://ps.cnis.ca/wiki/index.php/68._Urinary
Primary imaging modality

for evaluating traumatic
injuries and inflammatory
and stricture diseases of
the male urethra
42. Intracranial Hemorrhage
Epidural hematoma:
Interval lucid decreased of
consciousness
Etiology: trauma rupture of a.
meningeal media
Subdural hematoma
Hemiparesis, decrease of
consciousness, cephalgia
Etiology: trauma rupture of bridging
vein in elderly or infant
Subarachnoid hemorrhage (stroke)

Thunderclap headache, meningeal
signs, decreased of consciousness
Etiology: aneurysma rupture e.c. heavy
exertion/sexual intercourse
Intracerebral hemorrhage (stroke)

Paresis, hypesthesia, ataxia, decreased
of consciousness
Etiology: Hypertension
Misulis KE, Head TC. Netters concise neurology. 1st ed. Saunders; 2007
43. Abdominal Colic
Blumberg Sign
http://www.nlm.nih.gov/medlineplus/ency/article
Differentials
Disorder
Clinical Feature
Pancreatitis
Chronic Abdominal pain, normal or mildly elevated pancreatic enzyme levels,

malabsorbsion (steatorrhea), diabetes mellitus (CHRONIC)
sudden in onset abdominal pain radiates the back, worse in supine
position,Profuse vomiting, fever(ACUTE)
Acute cholesistis Acute right upper quadrant pain and tenderness, radiates to back or below
the right shoulder blade,Fever and leukocytosis, Clay-colored stools, jaundice,
Nausea and vomiting,Palpable gallbladder/fullness of the RUQ ,Murphy sign
Other Signs
Puddle sign
Courvoisiers sign =
painless,
palpable/distended
gallbladder on exam
Turtles sign: If the fetal
shoulders remain in an
anterior-posterior
position during descent
or descend
simultaneously rather
than sequentially into the
pelvic inletleads to
shoulder dystocia
Dullness of abdominal
percussion in knee-chest
position: sign of
intraabdominal fluid
collection (e.g. Ascites)
http://en.wikipedia.org/wiki/Burn
44. Burn Injury
prick test (+)
Berat luka bakar:

Ringan: derajat 1 luas <
15% a/ derajat II < 2%
Sedang: derajat II 1015% a/ derajat III 510%
Berat: derajat II > 20%
atau derajat III > 10%
atau mengenai wajah,
tangan-kaki, kelamin,
persendian,
pernapasan
To estimate scattered burns: patient's

palm surface = 1% total body surface
area
Parkland formula = baxter formula

http://www.traumaburn.org/referring/fluid.shtml
Total Body
Surface Area
45. Osteosarcoma
X-rays of area of suspected infection would
not demonstrate darkened areas typical of
osteomyelitis.
Conventional features
Destruction of normal trabecular bone pattern
a mixture of radiodense and radiolucent areas
periosteal new bone formation
formation of Codman's triangle (triangular
elevation of periosteum)
No osteoblastic appearance,
fracture can be seen
Notice the osteoblasticosteolytic appearance
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.
The Canadian Journal of Diagnosis / May 2001
46. Epididymitis
Inflammation of
epididymis
If involving testicle
epididymoorchitis
STD is usually the cause
of epididymitis
Common sexually
transmitted pathogen,
Chlamydia
PRESENTATION
Scrotal pain radiating to groin &flank.

Scrotal swelling due to infl. Or hydrocele.
Symp. Of ureth.,cystitis,prostatitis.
O/E tendered red scrotal swelling.
Elevation of scrotum relieves pain phren
sign (+)
TREATMENT
ORAL ANTIBIOTIC.
SCROTAL ELEVATION, bed rest,&use of NSAID.
Admission & IV drugs used.
in STD treat partner.
in chronic pain do epididymectomy.
47. GIT Congenital Malformation

Disorder
Clinical Presentation
Hirschprung
Congenital aganglionic megacolon (Auerbach's Plexus)

Fails to pass meconium within 24-48 hours after birth,chronic constipation
since birth, bowel obstruction with bilious vomiting, abdominal distention,
poor feeding, and failure to thrive, Chronic Enterocolitis. RT : Explosive stools .
Criterion standardfull-thickness rectal biopsy.
Treatment remove the poorly functioning aganglionic bowel and create an
anastomosis to the distal rectum with the healthy innervated bowel (with or
without an initial diversion)
Anal Atresia
Anal opening (-), The anal opening in the wrong place,abdominal distention,
failed to pass meconium,meconium excretion from the fistula (perineum,
rectovagina, rectovesica, rectovestibuler).
Low lesionthe colon remains close to the skin stenosis anus, or the rectum
ending in a blind pouch. High lesionthe colon is higher up in the pelvis
fistula
Hypertrophic
Pyloric
Stenosis
Hypertrophy and hyperplasia of the muscular layers of the pylorus

functional gastric outlet obstruction
Projectile vomiting, visible peristalsis, and a palpable pyloric tumor(Olive
sign).Vomiting occur after every feeding,starts 3-4 weeks of age
Disorder
Clinical Presentation
Oesophagus
Atresia
Congenitally interrupted esophagus

Drools and has substantial mucus, with excessive oral secretions,.
Bluish coloration to the skin (cyanosis) with attempted feedings
Coughing, gagging, and choking, respiratory distress. Poor feeding
Intestine Atresia
Malformation where there is a narrowing or absence of a portion

of the intestine
Abdominal distension (inflation), fails to pass stools, Bilious
vomiting
http://en.wikipedia.org/wiki/
http://www.ncbi.nlm.nih.gov/pubmedhealth
aafp.org
http://www.aafp.org/afp/2000/0501/p2791.html
Hirschsprungs disease
Clinical symptoms
The disease can considered to be
incomplete intestinal obstruction
The lenght of the aganglionic segment is
variable
The symptoms are variable too
The symptoms appears in different ages
Symptoms in newborn age

Fail to pass meconium
(in 24 hours of life)
Abdominal distension,
but the abdomen is
palpable
Vomiting
The rectal tube cant be
put easily
After irrigation the signs
and symptoms return
again in a few days
Symptoms in newborn
age(enterocolitis)
Life-threatening condition
Diarrhea: it can be an
early sign
Toxic megacolon
Abdominal distension
Bile-stained vomiting
Fiver and signs of
dehydration
Rectal tube:explosive
expulsion of gas and foulsmelling stools
Symptoms in infants
Constipation
Meteorism
Palpable faecaloma
Sometimes
putrescent diarrhea
Ulceration, bleeding
Hypoproteinaemia,
anaemia
Electrolyt disorders
Symptoms in childhood
Gracile limbs
Dilated drumlike belly
Long history of constipation
Defecation in 7-10 days
Multiple fecal masses
The stimulus of defecation
is missing
Rectum is empty and
narrow
Darm kontur: visible shape of intestines on

the abdomen
Darm Steifung: visible peristaltic movement
on the abdomen
Rontgen :
Plain abdominal radiography
Dilated bowel
Air-fluid levels.
Empty rectum
Contrast enema
Transition zone
Abnormal, irregular contractions of
aganglionic segment
Delayed evacuation of barium
Biopsy :
absence of ganglion cells
hypertrophy and hyperplasia of nerve
fibers,
48. Buergers Disease (Thrombangiitis Obliterans)

Exclusively associated with cigarette smoking
Occlusive lesions seen in muscular arteries, with a
predilection for tibial vessels
Presentation
rest pain
Gangrene
Ulceration
Recurrent superficial thrombophlebitis (phlebitis

migrans)
Young adults, heavy smokers, no other atherosclerotic
risk factors
Angiography - diffuse occlusion of distal extremity
vessels
Progression - distal to proximal
Clinical remission with smoking cessation
Disorder
Onset
Etiology
Buerger Disease
chronic
Segmental vascular Intermitten claudicatio,Smoking

inflammation
Polyarteritis nodosa
acute
immune complex
induced disease
Fever,Malaise,Fatigue,Anorexia,
weight loss,Myalgia,Arthralgia in large
joints,polyneuropathy, cerebral
ischemia, 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 burning sensation, 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
necrotizing
inflammatory lesions
small and mediumsized arteries
Clinical Feat.
49. Proximal Humerus Fracture

Proximal humerus fractures
comprise 4% to 5% of all
fractures
the most common humerus
fracture (45%).
The increased incidence in
the older population is
thought to be related to
osteoporosis.
2:1 female-to-male ratio
The axillary nerve courses

just anteroinferior to the
glenohumeral joint,
traversing the quadrangular
space.
It is at particular risk for
traction injury. it is
susceptible to injury during
anterior dislocation and
anterior fracturedislocation.
50. LUTS BPH
The size of prostate enlarged microscopically since the age

of 40.Half of all men over the age of 60 will develop an
enlarged prostate
By the time men reach their 70s and 80s, 80% will
experience urinary symptoms
But only 25% of men aged 80 will be receiving BPH treatment
What is Benign Prostatic Hyperplasia?
Peripheral zone
Transition zone
Urethra
BPH is part of the natural

aging process, like
getting gray hair or
wearing glasses
BPH cannot be
prevented
BPH can be treated
Peripheral zone
Transition zone
Urethra
Whats LUTS?
Voiding (obstructive)
symptoms
Hesitancy
Weak stream
Straining to pass urine
Prolonged micturition
Feeling of incomplete
bladder emptying
Urinary retention
Storage (irritative or
filling) symptoms
Urgency
Frequency
Nocturia
Urge incontinence
LUTS is not specific to BPH not everyone with

LUTS has BPH and not everyone with BPH has LUTS
Blaivas JG. Urol Clin North Am 1985;12:21524
Diagnosis of BPH
Symptom assessment
the International Prostate Symptom Score (IPSS) is recommended as it is used
worldwide
IPSS is based on a survey and questionnaire developed by the American Urological
Association (AUA). It contains:
seven questions about the severity of symptoms; total score 07 (mild), 819 (moderate), 20
35 (severe)
eighth standalone question on QoL
Digital rectal examination(DRE)

inaccurate for size but can detect shape and consistency
PV determination- ultrasonography
Urodynamic analysis
Qmax >15mL/second is usual in asymptomatic men from 25 to more than 60 years of
age
Measurement of prostate-specific antigen (PSA)
high correlation between PSA and PV, specifically TZV

men with larger prostates have higher PSA levels
PSA is a predictor of disease progression and screening tool for CaP
as PSA values tend to increase with increasing PV and increasing age, PSA may be
used as a prognostic marker for BPH
1
optimized by optima
Management
Lifestyle modification
Reduce fluid intake
Stop diuretics if poss
Avoid xs night time fluid intake/caffeine
/alcohol
Empty bladder before long trips/meetings
Management
Drug therapy
Alpha blockers
Improve bladder and
prostate smooth
muscle tone
More effective than 5
alpha reductase
inhibitors
All work equally well
Tamsulosin and
alfuzosin require no
dose titration
Drug therapy
5 alpha reductase inhibitors
Reduce prostate volume
Reduces risk of prostate cancer,
increases risk of high grade
disease
Combined therapy
Men with large prostate > 40g
or PSA >4 or moderate to severe
symptoms combined therapy
will prevent 2 episodes of
clinical progression per 100men
over 4yrs. Much less effective
for men with smaller prostates
http://www.medscape.org/viewarticle/541739_2
http://www.medscape.org/viewarticle/456664
PSAProstate Cancer
PSA >4.0 ng/mL mandatory biopsy
50% of all the cancers detected because of an
elevated PSA level are localized
these patients are candidates for potentially
curative therapy
51. Fluid Resuscitation

Crystalloids
Non-protein colloids
Are as effective as albumin in

post-operative patients
Are the initial resuscitation fluid
of choice for:
Hemorrhagic shock /
traumatic injury
Septic shock
Hepatic resection
Thermal injury
Cardiac surgery
Dialysis induced hypotension
Should be used as second-line

agents in patients who do not
respond to crystalloid
May be used in the presence of
capillary leak with pulmonary or
peripheral edema
Are favored over albumin due to
their lower cost
Fluid resuscitation
target:
Euvolemia
Improve perfusion
Improve oxygen
delivery
British Consensus Guidelines on

Intravenous Fluid Therapy for Adult
Surgical Patients 2011
52. Urine Incontinence
ILMU PENYAKIT MATA
53. Komplikasi DM
ANAMNESIS
MATA MERAH
VISUS NORMAL
Struktur yang
bervaskuler
sklera
konjungtiva
Tidak
menghalangi
media refraksi
Konjungtivitis
murni
Trakoma
mata kering,
xeroftalmia
Pterigium
Pinguekula
Episkleritis
skleritis
MATA TENANG
VISUS TURUN
MENDADAK
MATA MERAH
VISUS TURUN
Mengenai media
refraksi (kornea,
uvea, atau
seluruh mata)
Keratitis
Keratokonjungti
vitis
Ulkus Kornea
Uveitis
Glaukoma akut
Endoftalmitis
panoftalmitis
uveitis posterior
perdarahan vitreous
Ablasio retina
oklusi arteri atau
vena retinal
neuritis optik
neuropati optik akut
karena obat
(misalnya
etambutol),
migrain, tumor otak
MATA TENANG
VISUS TURUN
PERLAHAN
Katarak
Glaukoma
retinopati
penyakit
sistemik
retinitis
pigmentosa
kelainan
refraksi
Diabetic Retinopathy
DM ophthalmic complications :
Corneal abnormalities
Glaucoma
Iris neovascularization
Cataracts
Neuropathies
Diabetic retinopathy most
common and potentially most
blinding
Signs and Symptoms :
Seeing spots or floaters in the
field of vision
Blurred vision
Having a dark or empty spot in
the center of the vision
Difficulty seeing well at night
On funduscopic exam : cotton
wool spot, flame hemorrhages,
dot-blot hemorrhages, hard
exudates
Pemeriksaan :
Tajam penglihatan
Funduskopi dalam keadaan
pupil dilatasi : direk/indirek
Foto Fundus
USG bila ada perdarahan
vitreus
Tatalaksana :
Fotokoagulasi laser
http://www.ncbi.nlm.nih.gov/pubmedhealth/
54. Eyelids Disorders

Pathology
Feature
Chalazion
(meibomian gland
lipogranuloma)
Chronic inflamation of Zeis/Meibom gland; when acutely inflammed Painful,

warm, swollen, and firm eyelids, granulomatous reaction, lipogranuloma, usually on
the upper eyelid and inside the lid, painless nodules, Increased tearing, Sensitivity to
light
Hordeolum
Localized infection or inflammation of the eyelid margin involving hair follicles of the
eyelashes (external hordeolum) or meibomian glands (internal
hordeolum),Staphylococcal infection; painful, warm, swollen, and tender eyelids,
focal collection of PMN cells and necrotic tissue. erythematous, and
localized,Purulent material exudates
Chalazion
The result of obstruction of the duct of a meibomian gland, which is usually

idiopathic, with secondary lipogranulomatous inflammation
Epidemiology : higher incidence in seborrheoc dermatitis, rosacea, and DM
Clinical features : a pale, round, firm lesion of the lid.
Diagnosis : made clinically
Treatment : incision of the cyst and removed by curetting. Steroid injection can
initiate remission
Prognosis : ocaasionally recurrent
http://www.healblog.net/wp-content/uploads/Hordeolumand-Chalazion.jpg
55. Retinopati
Oklusi arteri
sentral retina
Penyumbataan arteri sentralis retina dapat disebabkan oleh radang arteri, thrombus dan emboli pada arteri, spsame
pembuluh darah, akibat terlambatnya pengaliran darah, giant cell arthritis, penyakit kolagen, kelainan hiperkoagulasi,
sifilis dan trauma. Secara oftalmoskopis, retina superficial mengalami pengeruhan kecuali di foveola yang
memperlihatkan bercak merah cherry(cherry red spot). Penglihatan kabur yang hilang timbul tanpa disertai rasa sakit
dan kemudian gelap menetap. Penurunan visus mendadak biasanya disebabkan oleh emboli
Oklusi vena
sentral retina
Penyumbatan vena sentralis retina mudah terjadi pada pasien dengan glaukoma, diabetes mellitus, hipertensi, kelainan
darah, arteriosklerosis, papil edema, retinopati radiasi, dan penyakit pembluh darah. Penurunan tajam penglihatan
sentral ataupun perifer mendadak yang dapat memburuk sampai hanya tertinggal persepsi cahaya. Tidak terdapat rasa
sakit dan biasanya mengenai satu mata. Gambaran klinis bervariasi dari perdarahan retina kecil-kecil teersebar dan
bercak cotton wool sampai gambaran perdarahan hebat dengan perdarahn rerina superficial dan dalam. Pada
funduskopi ditemukan : Papil udem, Tortositas vena meningkat, vena terlihat melebar dan berkelok-kelok, Flame shape
appearance.
Arteritis
temporal
inflammation and damage to blood vessels that supply the head area, particularly the large or medium arteries that
branch from the neck and supply the temporal area. Symptoms :Excessive sweating, Fever, General ill feeling, Jaw pain
that comes and goes or occurs when chewing, Loss of appetite, Muscle aches, Pain and stiffness in the neck, upper
arms, shoulder, and hips, Throbbing headache on one side of the head or the back of the head, Scalp sensitivity,
tenderness when touching the scalp, Vision difficulties, Blurred vision, Double vision, Reduced vision (blindness in one
or both eyes), Weakness, excessive tiredness, Weight loss (more than 5% of total body weight)
Amaurosis fugax
a transient monocular visual loss; appears as a "curtain coming down vertically into the field of vision in one eye,
dimming, fogging, or blurring
Ablatio retina
suatu keadaan lepasnya retina sensoris dari epitel pigmen retina (RIDE). Gejala:floaters, photopsia/light flashes,
penurunan tajam penglihatan, ada semacam tirai tipis berbentuk parabola yang naik perlahan-lahan dari mulai bagian
bawah hingga menutup
Inflammatory diseases
Ocular toxocariasis
Congenital toxoplasmosis
Congenital cytomegalovirus retinitis
Herpes simplex retinitis
Other types of fetal iridochoroiditis
Pseudo-uveitis
Endophthalmitis
Congenital malformations
Persistent Hyperplastic Fetal Vasculature (PHFV)
Posterior coloboma
Retinal fold
Myelinated nerve fibres
Morning Glory Syndrome
X-linked retinoschisis
Retinal dysplasia
Norries disease
Incontinentia pigmenti
Divers
Vitreous hemorrhage
Retinal detachment
Strabismus (Brckners phenomenon)
Stickler syndrome
Vascular diseases
Retinopathy of prematurity
Coats disease
Familial exudative vitreoretinopathy
Tumors
Retinoblastoma
Medulloepithelioma
Naevoxanthome juvenile
Glioneuroma
Leukemia
Choroidal hemangioma
Combined retinal hamartoma
Phakomatoses
Astrocytic hamartoma (Bournevilles tuberous
sclerosis)
Retinal capillary hemangioma (von HippelLindau)
Encephalotrigeminal syndrome (Sturge-Weber)
Neurofibromatosis (von Recklinhausen) (NF1
Trauma
Contusion of the globe
Intraocular foreign body
Shaken baby syndrome
56. Differential Diagnosis in

Pediatric Leukocoria
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704541/
Retinoblastoma
Retinoblastoma (Rb) is a rapidly

developing cancer that develops in
the cells of retina, the light-detecting
tissue of the eye.
Caused by a mutation in a gene
controlling cell division, causing cells
to grow out of control and become
cancerous.
Signs and Symptoms :
The pupil of the eye appears white instead
of red when light shines into it (known as
"cat's eye reflex" or "white eye"). This may
be seen in flash photographs of the
patient.
The eyes appear to be looking in different
directions (crossed eyes).
Pain or redness in the eye.
An enlarged or dilated pupil
Blurred vision or poor vision
Different colored irises
Treatment : The priority is to

preserve the life of the child, then to
preserve vision, and then to minimize
complications or side effects of
treatment.
Treatment options :chemotherapy,
cryotherapy, radioactive plaques,
laser therapy, external beam
radiotherapy and surgical removal of
the eyeball (enucleation)
Katarak
kongenital
Perubahan pada kebeningan struktur lensa mata yang muncul pada saat kelahiran
bayi atau segera setelah bayi lahir, dapat terjadi di kedua mata bayi (bilateral)
maupun sebelah mata bayi (unilateral). Keruh/buram di lensa terlihat sebagai bintik
putih jika dibandingkan dengan pupil hitam yang normal dan dapat dilihat dengan
mata telanjang. Etiologi: keturunan (genetik), infeksi, masalah metabolism, diabetes,
trauma (benturan), inflamasi atau reaksi obat, anti biotik tetracycline, ibu bayi
menderita infeksi seperti campak atau rubella (penyebab paling lazim), rubeola,
chicken pox, cytomegalovirus, herpes simplex, herpes zoster, poliomyelitis,
influensza, virus Epstein-Barr, sifilis, dan toxoplasmosis.
Macula kornea
distrofi
an autosomal recessive condition, which is the least common but the most severe of
the 3 major stromal corneal dystrophies. It is characterized by multiple, gray-white
opacities that are present in the corneal stroma and that extend out into the
peripheral cornea.
Visible in the cornea during the first decade of life. Over time,
vision decreases, and patients develop photosensitivity, eye pain from recurrent
corneal erosions.
Korpus alienum
Benda asing pada mata. Riwayat trauma.
Strabismus/
squint
a condition in which the eyes are not properly aligned with each other
57. Keratitis
Keratitis : inflammation of the cornea
Type
Etiology
History
Sign and Symptom
Bacterial
Staphylococcus aureus,
Contact lens wearer,
Staphylococcus
disease of the
epidermidis, Streptococcus corneal surface
pneumoniae, Pseudomonas
aeruginosa, Moraxella.
Corneal ulcer, hypopion,

corneal infiltrate,
reduce vision
Viral
Herpes simpleks, herpes

zooster
Elderly,
immunosuppressed
person
Dendritic keratitis
Fungal
Aspergillus fusarium
After ocular trauma

due to introduction
of plant material
Satellite lesions,
hypopion
Fungal Keratitis
Etiology :after ocular trauma due to the introduction of plant
materials into the eye, usually Aspergillus fusarium and
Cephalosporium species.
Epidemiology :rare
Clinical features :resembles bacterial keratitis. A gray-white
infiltrate with fine outliers in the stroma (satellite lesions).
Hypopion. Condition worsens when steroid is given.
Diagnosis :the history. No response to antibiotics fungal should
be considered.Scrapings from the margin to examined histologically.
Corneal sensitivity decreased
Treatment : local natamycin eye ointment. Mydriatics if there is
anterior chamber irritation. Systemic treatment with ketoconazole.
Prognosis :show healing process
Opthalmology; Color Atlas of Ophthalmology
Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006
58. BLEPHARITIS VIRUS

Etiologi
Epidemiologi
Gejala
Pengobatan
Herpes
Zoster
Usia lanjut. Infeksi

pada ganglion giseri
saraf trigeminus. Bila
terkena ganglion
cabang oftalmik
gejala pada mata dan
kelopak mata atas
Gejala tidak akan melampaui

garis median kepala. Nyeri
pada daerah tsb. Demam.
Vesikel pada cabang oftalmik
saraf trigeminus superfisial
Penglihatan berkurang. Mata
merah. Keratitis vesikular
Simptomatik
Dapat diberi acyclovir
5x800 mg
Steroid superfisial
mengurangi radang
Herpes
Simpleks
Vesikel kecil dikelilingi

Simptomatik
eritema pada kelopak dan
Bila ada infeksi
juga pada bibir. Blefaritis
sekunder antibiotik
simpleks: radang tepi kelopak
sesuai sistemik atau
mata ringan terbentuk krusta
topikal
kuning basah pada tepi bulu
Kortikosterod
mata kedua kelopak
kontraindikasi
lengket
menularkan
Asiklovir : pada infeksi
dini
Vaughn DG, Oftalmologi Umum, ed.14
59. Glaukoma
Glaukoma adalah penyakit saraf mata yang berhubungan dengan peningkatan
tekanan bola mata (TIO Normal : 10-24mmHg)
Ditandai : meningkatnya tekanan intraokuler yang disertai oleh pencekungan
diskus optikus dan pengecilan lapangan pandang
Jenis Glaukoma :
Primer yaitu timbul pada mata yang mempunyai bakat bawaan, biasanya bilateral
dan diturunkan.
Sekunder yang merupakan penyulit penyakit mata lainnya (ada penyebabnya)
biasanya Unilateral
Mekanisme : Gangguan aliran keluar humor akueus akibat kelainan sitem

drainase sudut kamera anterior (sudut terbuka) atau gangguan akses humor
akueus ke sistem drainase (sudut tertutup)
Pemeriksaan :
Tonometri : mengukur tekanan Intraokuler (TIO)
Penilaian diskus optikus : pembesaran cekungan diskus optikus dan pemucatan
diskus
Lapang pandang
Gonioskopi : menilai sudut kamera anterior sudut terbuka atau sudut tertutup
Pengobatan : menurunkan TIO obat-obatan, terapi bedah atau laser
Tatalaksana Glaukoma Akut

Tujuan : merendahkan tekanan bola mata secepatnya
kemudian bila tekanan normal dan mata tenang operasi
Pada serangan akut :
Pilokarpin 2% setiap menit selama 5 menit,lalu 1 jam selama 24 jam
Asetazolamide 500mg IV,lalu 250mg tab setiap 4 jam
Dapat juga diberikan Manitol 1.5-2MK/kgBB dalam larutan 20% atau
urea IV
Gliserol 1g/kgBB badan dalam larutan 50%
Mata yang tidak dalam serangan juga diberikan miotik untuk
mencegah serangan
Pemakaian simpatomimetik yang melebarkan pupil berbahaya
60. Defek Lapang Pandang
http://medical-dictionary.thefreedictionary.com/homonymous+hemianopia
61. Konjungtivitis Vernal

Akibat reaksi hipersensitivitis
yang mengenai kedua mata
dan rekuren
Terutama pada musim panas
Pasien usia muda
Tanda :
Papil besar dengan permukaan
rata pada konjungtiva tarsal
(coble stone)
Rasa gatal berat
Sekret gelatin
Benjolan di daerah limbus
dengan bercak Horner Trantas
Terapi :
Steroid topikal (tetes dan
salep)
Antihistamin
Desensitisasi
Kompres dingin
62. Defek Kornea

ANAMNESIS
MATA MERAH
VISUS NORMAL
Struktur yang
bervaskuler
sklera
konjungtiva
Tidak
menghalangi
media refraksi
Konjungtivitis
murni
Trakoma
mata kering,
xeroftalmia
Pterigium
Pinguekula
Episkleritis
skleritis
MATA TENANG
VISUS TURUN
MENDADAK
MATA MERAH
VISUS TURUN
Mengenai media
refraksi (kornea,
uvea, atau
seluruh mata)
Keratitis
Keratokonjungti
vitis
Ulkus Kornea
Uveitis
Glaukoma akut
Endoftalmitis
panoftalmitis
uveitis posterior
perdarahan vitreous
Ablasio retina
oklusi arteri atau
vena retinal
neuritis optik
neuropati optik akut
karena obat
(misalnya
etambutol),
migrain, tumor otak
MATA TENANG
VISUS TURUN
PERLAHAN
Katarak
Glaukoma
retinopati
penyakit
sistemik
retinitis
pigmentosa
kelainan
refraksi
Keratitis
Keratitis : inflammation of the cornea
Etiology
Microorganism
Characteristic
Sign and symptoms
Bacterial
Staphylococcus aureus,
Contact lens wearer,
Staphylococcus
disease of the
epidermidis, Streptococcus corneal surface
pneumoniae, Pseudomonas
aeruginosa, Moraxella.
Corneal ulcer, hypopion,

corneal infiltrate,
reduce vision
Viral
Herpes simpleks, herpes

zooster
Elderly,
immunosuppressed
person
Dendritic keratitis
Fungal
Aspergillus fusarium
After ocular trauma

due to introduction
of plant material
Satellite lesions,
hypopion
Keratitis
Peradangan pada kornea
Etiologi : bakteri, virus, fungal
Gejala : nyeri moderat sampai intens, penglihatan
menurun, biasanya dengan riwayat trauma/abrasi
Gambaran klinis : lesi kornea berupa
kekeruhan/infiltrat
Tes Fluoresin: (+) defek epitel/infiltrat
Terapi : berdasarkan etiologi
http://paramedik.blox.ua/2012/10/Asthenopia-eye-fatigue.html
63. ASTHENOPIA
Eye strain : an ophthalmological condition that manifests itself through nonspecific

symptoms such as fatigue, pain in or around the eyes, blurred vision, headache and
occasional double vision
Symptoms :
blurred vision,
ghosting and blurring of the image,
distortion of the shape and size of the observed objects,
inflammation of the eyes,
lacrimation,
eye fatigue, increase in temperature,
feeling of discomfort, pain, or burning rubber.
a headache, and irritability
Causes :
After using computer, regardless of the type of monitor.

Prolonged driving, especially at dusk and at night.
The work requires constant visual attention.
Prolonged reading.
Daily television viewing.
Incorrect glasses.
Wrong to illuminate in the living room and in the workplace.
ASTHENOPIA
Varieties :
Accommodative asthenopia : the most common form of eye fatigue. It can be due to
presbyopia, weakened as a result of accommodation of common diseases, spasm of
accommodation.
Muscular asthenopia can be caused by overexertion convergence. Unpleasant effects
disappear if close one eye, that is, off convergence. Exotropia may occur.
Mixed asthenopia, usually characterized combined picture and the accommodative
muscle of eye fatigue.
Neurogenic asthenopia often seen as a manifestation of the general neurasthenia and
hysteria.
Symptomatic asthenopia seen as a symptom that accompanies some inflammatory
diseases of the eye and nose
Treatment :
Possible early use corrective glasses for hyperopia, presbyopia and astigmatism.
http://emedicine.medscape.com/article/1206081
64. Buphthalmos
Characterized by eye enlargement that results from elevated
IOP, which is often caused by primary congenital glaucoma
Rarely present at birth
The differential diagnosis of large corneas in a child :
glaucoma, primary megalocornea, and keratoglobus
Primary congenital glaucoma
the result of abnormal formation of anterior chamber angle (site of
draining the eye fluid), causing obstruction of the fluid outflow and
elevated eye pressures
Develops within months after birth
Treatment : surgery
Classic triad
Photophobia
Tearing
blepharospasm in bright light
www.medscape.com
http://en.wikipedia.org
Congenital Glaucoma
Disorders
Feature
Ambliopia
Decrease of vision; disuse/inadequate foveal/peripheral retinal

stimulation and/or abnormal binocular interaction that cause different
visual input
Congenital
glaucoma
abnormal eye development, congenital infection

present at birth, epiphora, photophobia, and blepharospasm,
buphtalmus (>12 mm)
Sindrom Marfan
a genetic disorder of the connective tissue. A diagnosis of Marfan

syndrome is based on family history and a combination of major and
minor indicators of the disorder, rare in the general population, that
occur in one individual for example: four skeletal signs with one or
more signs in another body system such as ocular and cardiovascular in
one individual.
Katarak
congenital
clouding of the lens of the eye that is present at birth, Leukocoria or

white reflex, nfant doesn't seem to be able to see,nystagmus
Peters anomaly
anterior segment dysgenesis , may have an inherited pattern, Central,

paracentral, or complete corneal opacity,no vascularization of this
opacity occurs
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002582/
NEUROLOGI
http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/baseskull.htm
65. Fraktur Basis Kranii

Basal skull fractures are most frequently diagnosed by clinical findings
Findings :
Anterior Fossa Fracture - anosmia, epistaxis, rhinorrhea, subconjunctival
hemorrhage, periorbital hemorrage (raccoon eyes, visual disturbances, altered
eye movement, ptosis, loss of sensation to forehead, cornea and nare
Middle Fossa Fracture - loss of sensation to lower face, ottorrhea, deafness,
tinnitus, facial palsy, hemotympanium
Posterior Fossa Fracture - echymosis behind the ear (battle sign), impaired gag
reflex
Catastrophic injuries can occur if there is a major disruption of the carotid

artery (blood supply to middle and anterior cerebral cortex) or vertebral
artery (blood supply to brainstem and posterior cerebral cortex), or if the
brain stem is disrupted.
Fraktur Basis Kranii
66. Epilepsi
A seizure is defined by release of excessive
and uncontrolled electrical activity in the
brain. Seizures themselves are not a disease,
they are an event.
Epilepsy (seizure disorder) is a neurological
condition, that in different times produce brief
disturbances in the electrical functions of the
brain. Seizures are a symptom of epilepsy.
PPM Dept. Neurologi
Status Epileptikus
Suatu keadaan kejang atau serangan epilepsi yang
terus-menerus disertai kesadaran menurun selama >
30 menit; atau kejang beruntun tanpa disertai
pemulihan kesadaran yang sempurna
Merupakan keadaan gawat darurat menyebabkan
kematian dan kecacatan permanen
Tatalaksana : Perbaiki jalan nafas, pasang jalur IV,
diazepam 0,3mg/kgBB IV sampai maksimum 20 mg,
dapat diulang jika masih kejang stlh 5 menit, bila
kejang teratasi lanjutkan dengan fenitoin IV
18mg/kgBB
PPM Dept. Neurologi
67. Gangguan Kesadaran

Suatu keadaan terganggunya
pengintegrasian impuls eferen
(input) dan aferen (output).
Derajat penurunan kesadaran
dapat ringan sampai berat
(somnolen/letragi/obtudansisopor/stupor-koma ringan-koma)
Dibagi atas :
Akibat proses pada susunan saraf
pusat
Akibat proses metabolik
sekunder/penyakit sistemik organ
lain selain SSP dan akibat toksik
metabolik lainnya
Akibat adanya gangguan SSP :

Gangguan supratentorial diensefalik
(seperti meningitis, ensefalitis, trauma
kepala, lesi vaskuler, hematoma,
neoplasma)
Gangguan infratentorial diensefalik
(lesi vaskuler batang otak, trauma
kepala, neoplasma, granuloma,
perdarahan serebelum)
Akibat adanya gangguan bihemisferik

difus :
Ensefalopati metabolik primer (seperti
peny.Alzheimer, Korea Huntington)
Ensefalopati metabolik sekunder
(hipoksia, hipoglikemia, hiperglikemia,
peny.organik di luar SSP seperti gagal
hati, gagal ginjal, intoksikasi, gangguan
elektrolit dan air)
68. Gerak Bola Mata
69. Kejang
A seizure is an event in which there is a temporary change in behavior resulting from a sudden,
abnormal burst of electrical activity in the brain
Generalized Seizure :
www.doe.virginia.gov/support/health_medical/seizure_management.pdf
Kejang
Partial Seizure :
Kejang
70. Brachial Plexus
71. Back Pain

Hernia Nucleus
Pulposus
A condition in which part or all of the soft, gelatinous central portion of an

intervertebral disk is forced through a weakened part of the disk, resulting in back pain
and nerve root irritation
Osteoarthritis
Degenerative arthritis or degenerative joint disease or osteoarthrosis, is a group of

mechanical abnormalities involving degradation of joints,including articular cartilage and
subchondral bone. Symptoms may include joint pain, tenderness, stiffness, locking, and
sometimes an effusion.
Ankilosing
Spondilitis
A chronic inflammatory disease of the axial skeleton with variable involvement of

peripheral joints and nonarticular structures. Initial symptoms are typically chronic pain
and stiffness in the middle part of the spine or the entire spine, often with pain referred
to one or other buttock or the back of thigh from the sacroiliac joint.
Spondylolisthesis
The anterior or posterior displacement of a vertebra or the vertebral column in relation

to the vertebrae below. General stiffening of the back and a tightening of the
hamstrings, with a resulting change in both posture and gait.
Rheumatoid
Arthritis
An autoimmune disease that results in a chronic, systemic inflammatory disorder that

may affect many tissues and organs, but principally attacks flexible (synovial) joints. It
can be a disabling and painful condition
Herniated Nucleus Pulposus

Clinical Features
Injury : history of falling, or lifting

heavy weights
Leg pain : Root irritation or
compression produces pain in the
distribution of the affected root.
Coughing, sneezing or straining
aggravates the leg pan which is more
severe than backache
Parasthesia : Numbness or tingling
occurs in the distributing of affected
root
Muscle weakness or fatigue in the
buttocks, legs and feet
Soreness or stiffness
Neurology and Neurosurgery Illustrated
Neurologic Examination
Straight leg raising (SLR) test
L5 & S1 comrpresion causes

limitation to less than 60o from
horizontal and produces pain down
the back of leg.
Dorsoflexion of the foot while the
leg is elevated aggravates the pain.
Elevation of the good leg may
produce pain in the other leg.
Femoral strech test

Test for irritation of higher nerve roots ( L4 and above)
Other Investigation :
X- Ray Lumbosacral :
limited benefit, excluding
other pathology e.q
matastatic carcinoma
CT scan :
MRI :
best choice
Radiculography
Management :
Nonoperative Care
Initial bed rest
Nonsteroidal anti-inflammatory
(NSAID) medication
Physical therapy
Exercise/walking
Steroid injections
Operative Care
Reccurent attacks of leg pain
Severe unremitting leg pain
The development of
neurological deficit
Neurology and Neurosurgery Illustrated
72. Stroke
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
Manifestasi Klinis :
Kelumpuhan wajah atau anggota
badan (biasanya hemiparese),
timbul mendadak
Gangguan hemisensorik
Perubahan mendadak status
mental
Afasia; disartria
Gangguan penglihatan atau
diplopia
Ataksia
Vertigo, mual, muntah, nyeri
kepala
Kapita Selekta Neurologi
Faktor Resiko :
Usia
Riw. TIA atau stroke
Peny. Jantung koroner
Hipertensi
DM
Merokok
Dislipidemia
Perdarahan
epidural
Perdarahan yang terletak antara durameter dan tulang, biasanya sumber

pendarahannya adalah robeknya Arteri meningica media (paling sering). Gejala
klinis yang khas adalah : Lucid Interval (adanya fase sadar diantara 2 fase tidak
sadar karena bertambahnya volume darah)
Perdarahan
subdural
Perdarahan yang terletak diantara lapisan duramater dan arhacnoid dengan

sumber perdarahan dapat berasal dari vena jembatan atau bridging vein
(paling sering). Gejala yang timbul segera hingga berjam - jam setelah trauma
sampai dengan hari ke tiga.
Perdarahan
intraserebral
Perdarahan yang terjadi pada jaringan otak biasanya akibat robekan pembuluh
darah yang ada dalam jaringan otak. Secara klinis ditandai dengan adanya
penurunan kesadaran yang kadang-kadang disertai lateralisasi pada
pemeriksaan CT Scan didapatkan adanya daerah hiperdens yang indikasi
dilakukan operasi jika Single, diameter lebih dari 3 CM, Perifer, Adanya
pergeseran garis tengah.
Perdarahan
subarakhnoid
Perdarahan didalam ruang subarakhnoid akibat perdarahan non-traumatik,

biasanya berasal dari ruptur aneurisme berry atau arteriovenous malformation
(AVM). Gejala : sering didahului nyeri kepala hebat, kaku kuduk, kernig sign +
Perdarahan
Perdarahan di dalam rongga cairan otak
73. Sistem Muskulus Paha
http://en.wikipedia.org/wiki/Table_of_muscles_of_the_human_body:_Lower_limb
74. Gangguan Kognitif
Cognitive impairment affects our ability to concentrate, think, comprehend,

formulate ideas, reason, remember, and judge or evaluate our actions
MMSE : a screening tool for cognitive impairment, a low score (< 23) indicates
both the likelihood of cognitive impairment and the need for further
evaluation
Used to classify the severity of cognitive impairment in patients with dementia
and/or other medical conditions
Low MMSE scores should not be used to make a diagnosis of dementia or to
discriminate between various forms of dementia or other disorders
Cutoff :
normal cognitive function = 27-30
mild cognitive impairment = 21-26
moderate cognitive impairment = 11-20
severe cognitive impairment = 0-10
75. Head Injury
CME, Penatalaksanaan Kedaruratan Cedera Kranioserebral, Lyna Soertidewi
Tatalaksana
CKR :
Dilakukan PF, perawatan luka,
foto kepala, isitirahat baring
dengan mobilisasi bertahap
sesuai kondisi pasien disertai
terapi simptomatis.
Observasi 24 jam di RS untuk
menilai kemungkinan hematoma
intrakranial, misalnya riwayat
lucid interval, nyeri kepala,
muntah-muntah, kesadaran
menurun, gejala lateralisasi (pupil
anisokor, refleks patologis positif)
Tidak perlu dirawat jika:
Orientasi (waktu dan tempat baik)

Gejala fokal neurologik (-)
Muntah/sakit kepala (-)
Fraktur tulang kepala (-)
Tempat tinggal dalam kota
Ada yang bisa mengawasi dengan
baik di rumah, dan bila dicurigai ada
perubahan kesadaran dibawa
kembali ke RS
Tatalaksana
CKS :
Bisa mengalami gangguan

kardiopulmoner
Periksa dan atasi gangguan jalan
napas (ABC)
Periksa singkat tingkat kesadaran,
pupil, tanda fokal serebral, cedera
organ lain. Jika curiga adanya fraktur,
lakukan fiksasi pada tulang tersebut.
Foto kepala, bila perlu foto bagian
tubuh lainnya
CT scan otak bila curiga hematoma
intrakranial
Observasi fungsi vital, kesadaran,
pupil, dan defisit fokal serebral
lainnya
CKB :
Biasanya disertai cedera multipel

Bila didapatkan fraktur servikal,
segera pasang kerah fiksasi leher,
bila ada luka terbuka dan ada
perdarahn, dihentikan dengan
balut tekan untuk pertolongan
pertama.
Tindakan sama dengan CKS
dengan pengawasan lebih ketat
dan dirawat di ICU
Sering berada dalam keadaan
hipoksi, hipotensi, dan hiperkapni
akibat gangguan kardiopulmoner
76. PARKINSON DISEASE

Parkinson Disease : a degenerative disorder of
the central nervous system.
The motor symptoms of Parkinson's disease
result from the death of dopamine-generating
cells in the substantia nigra, a region of the
midbrain; the cause of this cell death is
unknown. A synucleinopathy due to an abnormal
accumulation of alpha-synuclein protein in the A Lewy body (stained brown) in a
brain cell of the substantia nigra
brain in the form of Lewy bodys
in Parkinson's disease. The brown
colour is positive
3 main symptoms:
immunohistochemistry staining for
Tremors
Rigidity
Slowed motion (Bradykinesia)
Other symptoms include:

Dementia, sleep disturbances,
depression, etc.
alpha-synuclein.
Parkinson Disease
No definitive tests for PD. PET scans can aid to determine levels of
dopamine.
Medical history and neurological tests are conducted to diagnose.
Usually, if two of the cardinal symptoms are present
Treatment can be divided into two stages.
Early and Later stages
Early stage
Onset of symptoms, treated with physical therapy and medications
(Levodopa, dopamine agonists, etc)
Later stage
Usually after having received 5+ years of levodopa treatment.
Wearing-off and On/Off effect develops, other medication in
conjunction levodopa is commenced.
MAO-B and COMT inhibitors.
230
www.aafp.org
ILMU PSIKIATRI
77. Acute Psychotic

Diagnosis
Karakteristik
Psikotik akut
Onset < 2 minggu, gejala beraneka ragam & berubah cepat atau
schizophrenia like, adanya stres akut yang berkaitan.
Psikotik akut
lir skizofrenia
Onset < 2 minggu, terdapat gejala skizofrenia untuk sebagian besar

waktu, tidak memenuhi kriteria psikosis polimorfik akut.
Polimorfik
psikotik akut
tanpa gejala
skizofrenia
1) Onset < 2 minggu, 2) ada beberapa jenis halusinasi/waham yang

jenis & intensitasnya berubah-ubah, 3) terdapat keadaan emosional
yang beragam, 4) walau gejala beragam tapi tidak satupun dari gejala
itu konsisten memenuhi kriteria skizofrenia/manik/depresi
Polimorfik
psikotik akut
dengan gejala
skizofrenia
Onset < 2 minggu, ada beberapa jenis halusinasi/waham yang jenis &
intensitasnya berubah-ubah, memenuhi poin 1-3 psikotik polimorfik
akut disertai gejala yang memenuhi skizofrenia. Jika lebih dari 1
bulan maka diagnosis menjadi skizofrenia
77. Acute Psychosis

Acute schizophrenia is typically associated with severe
agitation, which can result from such symptoms as
frightening delusions, hallucinations, or suspiciousness, or
from other causes, including stimulant abuse.
Antipsychotics and benzodiazepines can result in relatively
rapid calming of patients.
With highly agitated patients, intramuscular administration
of antipsychotics produces a more rapid effect.
Haloperidol IM or IV, initially 2-10 mg.
Then every 4-8 hours, according to the response.
The total maximum dose is 18 mg.
78. Gangguan Afektif

Mania
Mood harus meningkat, ekspansif, atau iritabel, dan abnormal
untuk individu yang bersangkutan. Perubahan mood minimal
berlangsung 1 minggu.
Gejala:
1) peningkatan aktivitas,
2) banyak bicara,
3) flight of idea,
4) hilangnya inhibisi dari norma sosial,
5) berkurangnya kebutuhan tidur,
6) harga diri atau ide-ide kebesaran yang berlebihan,
7) distraktibillitas atau perubahan aktivitas atau rencana yang konstan,
8) perilaku berisiko atau ceroboh tanpa menyadari akibatnya,
9) peningkatan energi seksual.
78. Gangguan Afektif

Pada gangguan afektif dengan ciri psikotik, waham
bersifat mood-congruent (konsisten dengan
depresi/manik)
Depresi: waham tentang dosa, kemiskinan,
malapetaka, & pasien merasa bertanggung jawab.
Manik: waham tentang kekuasaan, uang, utusan
Tuhan.
Diagnosis
Gejala Psikotik
Gangguan Afektif
Skizofrenia
Ada
Durasi singkat
Skizoafektif
Ada, dengan atau tanpa

gangguan afektif
Hanya ada bila gejala

psikotik (+)
Gangguan afektif dengan

ciri psikotik
Hanya ada selama

gangguan afektif (+)
Ada, walau tanpa gejala

psikotik
79. Skizofrenia
Skizofrenia
Gangguan isi pikir, waham, halusinasi, minimal

1 bulan
Paranoid
merasa terancam/dikendalikan
Hebefrenik
15-25 tahun, afek tidak wajar, tidak dapat

diramalkan, senyum sendiri
Katatonik
stupor, rigid, gaduh, fleksibilitas cerea
Skizotipal
perilaku/penampilan aneh, kepercayaan aneh,

bersifat magik, pikiran obsesif berulang
Waham menetap hanya waham

Psikotik akut
gejala psikotik <2 minggu.
Skizoafektif
gejala skizofrenia & afektif bersamaan

PPDGJ
80. Antidepressan
A review of the use of antidepressants (Anderson, 01):
There is little difference in efficacy among most new (post1980) and older TCAs & monoamine oxidase inhibitor
(MAOI) antidepressants;
The serotonin (5-HT) and norepinephrine (NE) reuptake
inhibitors (SNRIs), including venlafaxine, and the TCAs are
superior in efficacy to the selective serotonin reuptake
inhibitors (SSRIs);
Fluoxetine has a slower onset of therapeutic action than
the other SSRIs;
The different antidepressant class adverse effect profiles
make the SSRIs more tolerable than the TCAs. (Case files:
SSRI is commonly used as first line drug for major
depression)
81. Ansietas
Diagnosis
Karakteristik
Fobia
Rasa takut yang kuat dan persisten terhadap suatu objek atau
situasi, antara lain: hewan, bencana, ketinggian, penyakit,
cedera, dan kematian.
Gangguan
penyesuaian
Gejala emosional (ansietas/afek depresif ) atau perilaku

dalam waktu <3 bulan dari awitan stresor. Tidak
berhubungan dengan duka cita akibat kematian orang lain.
Reaksi stres akut
Gangguan yang muncul segera setelah stresor luar biasa.

Klinis: depresi, ansietas, marah, overaktif, penarikan diri.
Gangguan panik
Serangan ansietas yang intens & akut disertai perasaan akan

datangnya kejadian menakutkan. Tanda utama: serangan
panik yang tidak diduga tanpa adanya stimulus.
Gangguan cemas
menyeluruh
Ansietas berlebih terus menerus disertai ketegangan motorik

(gemetar, sulit berdiam diri, dan sakit kepala), hiperaktivitas
otonomik (sesak napas, berkeringat, palpitasi, & gangguan
gastrointestinal), kewaspadaan mental (iritabilita).
82. Drug Abuse

Zat
Intoksikasi
Withdrawal
Alkohol
Cadel, inkoordinasi, unsteady gait, nistagmus,

gangguan memori/perhatian, stupor/koma
Hiperaktivitas otonom, tremor, insomnia,

mual/muntah, halusinasi, agitasi,
ansietas, kejang.
Heroin
Euforia, analgesia, ngantuk, mual, muntah,

napas pendek, konstipasi, midriasis, gangguan
jiwa
Miosis/midriasis, mengantuk/koma,
cadel, gangguan perhatian/memori
Kanabis/ganja
/marijuana
Injeksi konjungtiva, peningkatan nafsu makan,

mulut kering, takikardia
Kokain
Taki/bradikardia, dilatasi pupil,

peningkatan/penurunan TD,
perspirasi/menggigil, mual/muntah, turun BB,
agitasi/retardasi psikomotor, kelemahan otot.
Depresi napas, nyeri dada, aritmia, bingung,
kejang, distonia, koma
Disforik mood, fatigue, mimpi buruk,

insomnia/hipersomnia, peningkatan
nafsu makan, agitasi/retardasi psikomotor
Amfetamin
Taki/bradikardia, dilatasi pupil,

peningkatan/penurunan TD,
perspirasi/menggigil, mual/muntah, turun BB,
agitasi/retardasi psikomotor, kelemahan otot.
Depresi napas, nyeri dada, aritmia
Disforik mood, fatigue, mimpi buruk,

insomnia/hipersomnia, peningkatan
nafsu makan, agitasi/retardasi psikomotor
Benzodiazepin
Cadel, inkoordinasi, gangguan berjalan,

nistagmus, gangguan perhatian/memori,
stupor/koma.
Hiperaktivitas otonom, tremor, insomnia,

mual/muntah, halusinasi
visual/taktil/auditorik, agitasi psikomotor,
ansietas, bangkitan grand mal.
82. Drug Abuse

Alcohol withdrawal:
Minor withdrawal symptoms: insomnia, tremulousness, mildanxiety,
gastrointestinal upset, headache, diaphoresis, palpitations, anorexia
6 to 12 hours:
Alcoholic hallucinosis: visual, auditory, or tactile hallucinations
12 to 24 hours:
Withdrawal seizures: generalized tonic-clonic seizures
24 to 48 hours:
Alcohol withdrawal delirium (delirium tremens): hallucinations (predominately

visual), disorientation, tachycardia, hypertension, low-grade fever, agitation,
diaphoresis
83. Gangguan Kepribadian

Diagnosis
Ciri
Paranoid
curiga, sensitif, dendam.
Skizoid
tidak peduli, afek datar, tidak ingin berteman.
Dissosial
tidak peduli perasaan, tidak bertanggung jawab, tidak

merasa bersalah, tidak mampu memelihara hubungan
Histrionik
teatrikal, labil, terlalu peduli fisik.
Anankastik
perfeksionis, kaku, memaksa orang lain.
Cemas menghindar
tegang, peka kritik & penolakan, menghindari aktivitas

sosial
Dependen
bergantung pada orang lain
84. Sleep Disorder

DSM-IV-TR divides primary sleep disorders
into:
Dyssomnias: disorders of quantity or timing of
sleep
Insomnia
Hypersomnia
Parasomnias: abnormal behaviors during sleep or

the transition between sleep and wakefulness.
Sleep walking , night terror, nightmare
Kaplan & Sadock synopsis of psychiatry
84. Insomnia
According to severity:
Mild: almost every night,
minimum impairment of
quality of life (QoL)
Moderate: every night,
moderate impairment
QoL with symptoms
(irritability, anxiety,
fatigue)
Severe: every night,
moderate impairment
QoL with more severe
symptoms of irritability,
anxiety, fatigue
According to form of
presentation:
Sleep onset/early
insomnia (difficulty
falling asleep)
Sleep
maintenance/middle
insomnia (waking
frequently)
End of sleep/late
insomnia (waking too
early)
84. Sleep Disorder

Insomnia is difficulty initiating or maintaining sleep. It is the
most common sleep complaint and may be transient or
persistent.
Primary insomnia is commonly treated with benzodiazepines.
Kaplan & Sadock synopsis of psychiatry
85. Pharmacotherapy
Atypical antipsychotic side effects:

All of these drugs cause sedation to a greater or lesser degree.
Antipsychotic drugs can cause the neuroleptic malignant syndrome.
This is characterized by fever, anorexia, rigidity, lowered level of consciousness,
and autonomic disturbances (tachycardia, hyperthermia), and can be fatal.
85. Pharmacotherapy
Extrapyramidal (antidopaminergic) adverse effects are
common.
Acute dystonias can develop after only a few doses.

Akathisia tends to develop if large initial dosages are used.
Parkinsonian symptoms develop gradually.
Tardive dyskinesia is most commonly associated with prolonged
use, but can occur after short-term treatment. This is
characterized by involuntary dyskinetic movement of the jaw,
lips, and trunk.
The antidopaminergic actions can also cause prolactin release,
leading to galactorrhoea, gynaecomastia, and menstrual
disturbances.
The anticholinergic actions can cause dry mouth, blurred

vision, and urinary retention.
86. Psychomotor Disturbance

Diagnosis
Karakteristik
Coprolalia
Involuntary use of vulgar or obscene language. Observed in some

cases of schizophrenia and in Tourette's syndrome.
Echolalia
Psychopathological repeating of words or phrases of one person by

another; tends to be repetitive and persistent. Seen in certain kinds
of schizophrenia, particularly the catatonic types.
Echopraxia
Imitation of another person behavior. Seen sometimes in

schizophrenia & Tourette syndrome.
Cataplexy
Temporary sudden loss of muscle tone, causing weakness and

immobilization; can be precipitated by a variety of emotional states
and is often followed by sleep. Commonly seen in narcolepsy.
Palilalia
Increasingly rapid repetition of the same word or phrase, usually at

the end of sentence.
Kaplan & Sadock synopsis of psychiatry.
87. Gangguan Neurotik

Untuk menegakan diagnosis pasti, gejala
obsesif atau tindakan kompulsif, atau keduaduanya, harus ada hampir setiap hari selama
sedikitnya 2 minggu berturut-turut.
Merupakan sumber penderitaan atau
mengganggu aktivitas penderita

Gejala-gejala obsesif :
1. Harus disadari sebagai pikiran atau impuls diri
sendiri;
2. Sedikitnya ada 1 pikiran/tindakan yang tidak
berhasil dilawan;
3. Pikiran untuk melakukan tindakan tsb bukan hal
yang memberi kepuasan atau kesenangan
4. Gagasan, pikiran, atau impuls tsb harus
merupakan pengulangan yang tidak
menyenangkan

Predominan Tindakan Kompulsif (Obsessional Rituals)
Tindakan kompulsif umumnya berkaitan dengan :
kebersihan (mencuci tangan), memeriksa berulang untuk
meyakinkan bahwa suatu situasi yang dianggap berpotensi
bahaya tidak terjadi, atau masalah kerapian & keteraturan.
Dilatarbelakangi perasaan takut terhadap bahaya yang

mengancam dirinya atau bersumber dari dirinya
88. Sexual Disorder

Diagnosis
Karakteristik
Fetishism
Sexually arousing fantasies, sexual urges, or behaviors involving the

use of nonliving objects (e.g., female undergarments).
Frotteurism
Sexually arousing fantasies, sexual urges, or behaviors involving

touching and rubbing against a nonconsenting person.
Masochism

act (real, not simulated) of being humiliated, beaten, bound, or
otherwise made to suffer.
Sadism
Sexually arousing fantasies, sexual urges, or behaviors involving acts

(real, not simulated) in which the psychological or physical suffering
(including humiliation) of the victim is sexually exciting to the person.
Voyeurism

act of observing an unsuspecting person who is naked, in the process
of disrobing, or engaging in sexual activity.
Necrophilia
Necrophilia is an obsession with obtaining sexual gratification from

cadavers.
Kaplan & Sadock synopsis of psychiatry.

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PEMBAHASAN TO3 BATCH III

ILMU PENYAKIT DALAM

Heberdens & Bouchards nodes

space narrowing (white arrow),

removed from the joint space, have a

Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.

Ulnar dev, Swan

2. Murmur & Heart Sounds

2. Murmur & Heart Sound

Lilly LS. Pathophysiology of heart disease.

2. Murmur & Heart Sound

Lilly LS. Pathophysiology of heart disease.

The diarrhea that develops within 730 h of ingestion of

Harrisons principles of internal medicine. 18th ed. McGraw-Hill; 2011.

Preventing further attacks by

Uric acid lowering agent

Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.

Harrisons principles of internal medicine. 18th ed. McGraw-Hill; 2011.

6. E.S. OAT Mayor

Gatal & kemerahan

Semua jenis OAT

Antihistamin & evaluasi

Vertigo & nistagmus (n.VIII) Streptomisin

Sebagian besar OAT

Hentikan semua OAT s.d.

Muntah & confusion

Sebagian besar OAT

Hentikan semua OAT & uji

Kelainan sistemik, syok &

6. E.S. OAT Minor

Tidak nafsu makan, mual,

OAT diminum malam

Kesemutan s.d. rasa

Vit B6 1 x 100 mg/hari

Untuk pemantauan pengobatan dilakukan pemeriksaan

Pasien baru BTA (-) &

Tahap lanjutan dimulai

OAT sisipan 1 bulan, jika masih (+) tahap

Gagal, mulai OAT kategori 2

Berikan pengobatan tahap lanjutan s.d.

Ganti dengan kategori 2 mulai dari awal

Teruskan pengobatan dgn tahap lanjutan

OAT sisipan 1 bulan, jika masih (+) tahap

Belum ada obat, disebut kasus kronk. Rujuk.

Grow slowly may

Grow quickly feel sick & go to

Fever, swollen lymph nodes, frequent infection, weak,

Can be delayed if asymptomatic

Treated right away

More common in ALL

Persistent increased of hematocrite/Hb level caused by excessive

The term "leukemoid reaction" is used to describe a condition where

Maturation defect of blood cell precursors in bone marrow caused by

Multiple myeloma Multiple myeloma: a malignant proliferation of plasma cells derived

11. Cara Pemberian Kina Parenteral

intrahepatic resistance to the

Portal hypertension cause

13. Hemolytic Anemia

13. Hemolytic Anemia

13. Hemolytic Anemia

14. Bone Resorption Markers

identification of individuals at risk for bone loss and fracture,

14. Bone Formation Markers