Pembahasan Seminar Part I No. 1-100

Seminar Optima Preparation
Batch Mei 2015

Part I
No. 1-100
Office Address:
Jl Padang no 5, Manggarai, Setiabudi, Jakarta
Selatan
(Belakang Pasaraya Manggarai)
Phone Number : 021 8317064
Pin BB 2A8E2925
WA 081380385694
Medan :
Jl. Setiabudi No. 65 G, Medan
Phone Number : 061 8229229
Pin BB : 24BF7CD2
www.optimaprep.com
dr. Widya, dr. Eno, dr. Yolina

dr. Cemara, dr. Yusuf
dr. Reza
ILMU PENYAKIT DALAM
1. Infeksi
Infection through the
mucosa or wounded skin
Proliferate in the
bloodstream or
extracellularly within organ
Disseminate
hematogenously to all
organs
Multiplication can cause:

Hepatitis, jaundice, & hemorrhage in the liver
Uremia & bacteriuria in the kidney
Aseptic meningitis in CSF & conjunctival or scleral hemorrhage in the aqueous humor
Muscle tenderness in the muscles
Harrisons principles of internal medicine. 18th ed.
1. Infeksi
Anicteric leptospirosis (90%),
follows a biphasic course:
Initial phase (47 days):
sudden onset of fever,
severe general malaise,
muscular pain (esp calves),
conjunctival congestion,
leptospires can be isolated from
most tissues.
Two days without fever follow.

Second phase (up to 30 days):
leptospires are still detectable in
the urine.
Circulating antibodies emerge,
meningeal inflammation, uveitis &
rash develop.
Therapy:
Doxycycline (100 mg PO bid) or
Amoxicillin (500 mg PO tid) or
Ampicillin (500 mg PO tid)
Icteric leptospirosis or Weil's

disease (10%), monophasic
course:
Prominent features are renal and
liver malfunction, hemorrhage
and impaired consciousness,
The combination of a direct
bilirubin < 20 mg/dL, a marked
in CK, & ALT & AST <200 units is
suggestive of the diagnosis.
Hepatomegaly is found in 25% of
cases.
Therapy:
Penicillin (1.5 million units
IV or IM q6h) or
Ceftriaxone (1 g/d IV) or
Cefotaxime (1 g IV q6h)
2 & 3.
Infark Miokard
4. Rheumatoid Arthritis
NSAIDs:
Are important for symptomatic relief but play only a minor role, if any, in
altering the underlying disease process.
Aspirin is the oldest drug of the non-steroidal class, but because of its high
rate of GI toxicity, a narrow window between toxic and anti-inflammatory
serum levels, and the inconvenience of multiple daily doses, aspirins use as
the initial choice of drug therapy has largely been replaced by other NSAIDs
Glucocorticoid:
The paradigm ("bridge therapy") is to shut off inflammation rapidly with
glucocorticoids, and then to taper these as the slower-acting DMARD begin to
work.
4. Rheumatoid Arthritis
Medical management of RA involves five general approaches:

The first is the use of NSAID & simple analgesics to control the symptoms and
signs of the local inflammatory process.
An second line of therapy involves use of low-dose oral glucocorticoids
suppress signs and symptoms of inflammation, may also retard the
development and progression of bone erosions.
The third line of agents includes the disease modifying antirheumatoid drugs
(DMARD) decrease elevated levels of acute-phase reactants. These agents
include methotrexate, sulfasalazine, hydroxychloroquine.
A fourth group of agents are the biologics, which include TNG-neutralizing
agents (infliximab, etanercept, and adalimumab), IL-1-neutralizing agents
(anakinra), those that deplete B cells (rituximab), and those that interfere with
T cell activation (abatacept).
A fifth group of agents are the immunosuppressive &cytotoxic drugs, including

leflunomide, cyclosporine, azathioprine, and cyclophosphamide, ameliorate
the disease process in some patients
5. GERD
Barrett esophagus:
Komplikasi kronik GERD yang ditandai oleh metaplasia
intestinal di mukosa epitel gepeng esofagus.
Metaplasia Barrett dengan banyak
sel goblet
6. Endokrin
Thyroid Ophthalmopathy
1. Vigouroux sign: eyelid fullness
2. Stellwag sign: incomplete and infrequent blinking
3. Grave sign: resistance to pulling down the retracted upper
lid
4. Goffory sign: absent creases in the forehead on superior
gaze
5. Mobius sign: poor convergence
6. Ballet sign: restriction of one or more extraocular muscles
7. Lid signs: Lid lag and lid retraction
7. Endokrin
8. Anticoagulant Therapy
ISI: international sensitivity index

1 is the best
MNPT: mean normal PT laboratory
9. Unstable
Angina
Recurrent
symptoms/ischemia,
heart failure,
serious arrhythmia.
9. Unstable Angina
2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non
ST-Elevation Myocardial Infarction
10. Polycythemia Vera

Criteria PVSG (Polycythemia Vera Study Group)
A1 Raised red cell mass (RCM), male > 36 ml/kg, female > 32 ml/kg
A2 Normal arterial oxygen saturation > 92%
A3 Splenomegaly
B1 Platelet count > 400 x 109/l

B2 White blood cell count (WBC) > 12 x 109/l
B3 Leucocyte alkaline phosphatase > 100
B4 Serum B12 > 900 pg/ml or unbound B12 binding capacity > 220
pg/ml
Diagnosis
A1 + A2 + A3 establishes PV
A1 + A2 + two of category B establishes PV
10. Polycythemia Vera
Polycythemia vera (PV) develops slowly. The disease may not cause signs or
symptoms for years.
When signs and symptoms are present, they're the result of the thick blood that
occurs with PV. This thickness slows the flow of oxygen-rich blood to all parts of
your body. Without enough oxygen, many parts of your body won't work normally.
The signs and symptoms of PV include:
Headaches, dizziness, and weakness
Shortness of breath & problems breathing while lying down
Feelings of pressure or fullness on the left side of the abdomen due to an enlarged spleen (an
organ in the abdomen)
Double or blurred vision and blind spots
Itching all over (especially after a warm bath), reddened face, and a burning feeling on your
skin (especially your hands and feet)
Bleeding from your gums and heavy bleeding from small cuts
Unexplained weight loss
Fatigue (tiredness)
Excessive sweating
Very painful swelling in a single joint, usually the big toe (called gouty arthritis)
In rare cases, people who have PV may have pain in their bones.
http://www.nhlbi.nih.gov/health/health-topics/topics/poly/signs.html
11. Disentri
Trias disentri: demam, tenesmus, diare berdarah.
Manifestasi klinis disentri
amoeba:
Awitan perlahan atau
fulminan.
Tenesmus terdapat pada
50% pasien & selalu terkait
dengan keterlibatan
rektosigmoid.
Nyeri tekan abdomen
bawah, biasanya di daerah
caecum, kolon transversum
atau sigmoid.
11. Disentri
Diagnosis
Characteristic
Crohn disease
Diare; nyeri abdomen kuadran kanan bawah, sering timbul setelah

makanan; turun berat badan & terdapat nyeri tekan abdomen.
Diare biasanya tidak berdarah.
Colitis ulcerative
Diare, dengan atau tanpa darah. Jika inflamasi terdapat di rektum

(proktitis), darah dapat muncul di permukaan feses; gejala lain:
tenesmus, urgensi, nyeri rektum, keluar mukus tanpa diare.
Disentri
Diare akut dengan BAB berdarah, tenesmus, demam.
Shigellosis
Variasi dari diare cair yang ringan hingga disentri berat. Pada kasus
berat, awitan cepat, dengan tenesmus, demam, dan feses lendir
darah yang sering. Sering disertai demam, sakit kepala, & malaise.
IBS
Nyeri perut hilang dengan defekasi, hilang timbul, terkait stres,

tidak ada kelainan anatomis.
Fauci et al. Harrisons principles of internal medicine. 18th ed. McGraw-Hill; 2012.
12. Angina
Side effectsof organic nitrates: orthostatic hypotension, tachycardia,

& throbbing headache.
2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non
ST-Elevation Myocardial Infarction
12. Angina
Nifedipine side effects: hypotension, dizziness, flushing,

nausea, constipation, edema.
13. GI Tract Disease

Pancreatic cancer:
Epidemiology: most common in 6079 years.
Risk factors: smoking, chronic pancreatitis, DM.
Clinical presentation:
Obstructive jaundice painless jaundice
abdominal discomfort, pruritus, lethargy, & weight loss.
Physical sign:
Jaundice, cachexia, & scratch marks.
palpable gall bladder (Courvoisier's sign).
distant metastases hepatomegaly, ascites, left supraclavicular
lymphadenopathy (Virchow's node), & periumbilical lymphadenopathy (Sister
Mary Joseph's nodes).
Diagnosis:
contrast-enhanced CT is the imaging modality of choice
EUS-guided fine-needle aspiration is the technique of choice. If theres any
doubt CT scan.
Harrisons principles of internal medicine. 18th ed. McGraw-Hill; 2011.
13. GI Tract Disease

Diagnosis
Characteristic
Acute cholecystitis
epigastric or right upper quadrant abdominal pain lasting

longer than 3 hours, low grade fevers, vomiting. Murphy's
sign, an inspiratory pause during palpation of the right upper
quadrant, may be present.
Choledocolithiasis
Gallstone lodged in the common bile duct. Symptom: biliary

pain, right upper quadrant/epigastric pain, jaundice, pruritus,
nausea. Lab: Bilirubin . USG: seen in 50% of cases.
Acute pancreatitis
Mostly caused by gallstones & alcohol abuse. Symptom: acute

onset of epigastric abdominal pain that radiates into the back.
Lab: amylase and/or lipase rises threefold.
Chronic pancreatitis
Chronic alcohol abuse is the most common cause. Symptom:

epigastric, dull, constant, radiating to the back, improvement
with sitting or leaning forward, and worsening after meals,
nausea & vomiting. Serum pancreatic enzymes is not
diagnostic. Imaging (x-ray, transabdominal USG, CT) ensure
the diagnosis.
Harrisons principles of internal medicine. 18th ed. McGraw-Hill; 2011.
14. Penyakit Endokrin
14. Penyakit Endokrin

Limfosit tersensitisasi oleh antigen tiroid
Sekresi autoantibodi TgAb, TPOAb, TSHRab[block/inhibisi]

Infiltrasi limfosit folikel limfoid & germinal center
Destruksi parenkim tiroid tiroksin
TSH hipertrofi parenkim, destruksi tetap ada

struma/tanpa struma end stage: atrofi
Eutiroid hipotiroid subklinis hipotiroid
15. Infeksi Saluran Kemih

Mild pyelonephritis:
low-grade fever with or without lower-back/CVA pain.
Severe pyelonephritis:
high fever,
rigors,
nausea, vomiting, &
flank and/or loin pain.
Symptoms of cystitis may not be present. Fever is the main

feature distinguishing cystitis & pyelonephritis.
Lab: leukocytosispyuria, bacteriuria, hematuria, cillinder
Therapy:
DOC: 7-day course of ciprofloxacin
TMP-SMX (one double-strength tablet twice daily for 14 days) is also
effective if the uropathogen is known to be susceptible
Harrisons principles of internal medicine. McGraw-Hill; 2011.
16. Angina Pektoris

Nonpharmacology management:
Oxygen (24 L/min by mask or nasal prongs)
should be administered to those who are
breathless or who have any features of heart
failure or shock.
Bed rest, except for the patients who require the
use of a bedside commode, is mandatory during
the first 24 hour.
Diet: it generally has been recommended to avoid
extremes of hot and cold, have no caffeine.
Current diagnosis & treatment in cardiology.
European Heart Journal (2008) 29, 29092945
17. Anemia Makrositik

Vegetarian diet:
Consume less total protein than omnivores, but
meet the recommended dietary allowances.
ferritin levels are lower, but not depleted.
Serum vit B12 in vegans are generally lower
Calcium intake is lower
Vitamin D is less consumed
Modern Nutrition in Health & Disease.
17. Anaemia Makrositik

Apakah terdapat hipersegmentasi netrofil atau
makroovalosit di GDT?
Ya
Tidak
Anemia megaloblastik ;
Periksa vitamin B12 dan folat
Anemia
nonmegaloblastik
Retikulosit
Defisiensi
vitamin B12
Tidak
defisiensi
Uji Schilling:
membaik
dgn faktor
intrinsik
Peny. Sintesis
DNA herediter
Ya
Anemia
pernisiosa,
Reseksi
gaster
Obat yang
mengganggu
DNA
Tidak
Peny. Ileal, pembedahan
Pertumbuhan berlebihan
bakteri usus halus
Cacing pita
Malabsorpsi karena obat
Defisiensi
folat
Diet kurang
Malabsorpsi dipicu obat
Reseksi jejunum
Tropical sprue, sensiivitas
thd gluten.
Peningkatan kebutuhan:
kehamilan, hemolisis kronik
N/
Anemia hemolitik
Anemia hemoragik
Toksisitas alkohol
Hipotiroidisme
Penyakit hati
Bila bukan sebab
diatas: periksa
sumsum tulang
MDS
Aplasia eritrosit
Anemia sideroblastik didapat
Anemia diseritropoeitik herediter
tipe I, tipe III
18. Cyanide Intoxication

Source:
the vasodilator drug nitroprusside, natural sources are found in
cassava.
Mechanism of toxicity:
Cyanide binds to cellular cytochrome oxidase blocking the
aerobic utilization of oxygen metabolic acidosis.
Symptoms
headache, nausea, dyspnea, & confusion.
Syncope, seizures, coma, agonal respirations, & cardiovascular
collapse ensue rapidly after heavy exposure.
Poisoning & drug overdose by the faculty, staff and associates of the California Poison Control
System third edition

Treatment:
A. Emergency and supportive measures. Treat all cyanide exposures
as potentially lethal.
1. Maintain an open airway and assist ventilation if necessary.
2. Treat coma, hypotension, & seizures if they occur.
3. Start an IV line and monitor the patients vital signs and ECG
B. Specific drugs and antidotes
1. The cyanide antidote package consists of amyl & sodium nitrites,
which produce cyanide-scavenging methemoglobinemia, & sodium
thiosulfate, which accelerates the conversion of cyanide to
thiocyanate.
C. Prehospital.
Immediately administer activated charcoal if available. Do not
induce vomiting unless victim is more than 20 minutes from a
medical facility and charcoal is not available.
19. EKG
19. EKG
RVH
R > S di V1
R di V1 7 mm,
Rasio R/S di sepanjang
prekordium
LVH
S di V1 + R di V5 atau V6
35 mm
R di aVL + S di V3 > 28
mm pada laki-laki atau >
20 mm pada perempuan
R di aVL 11 mm
19. EKG
20. Gagal Jantung

ACC/AHA 2005 Guideline Update for the Diagnosis and Management
of Chronic Heart Failure in Adult
Evaluasi laboratorium: DPL, urinalisis, elektrolit (termasuk Ca &
Mg), ureum, kreatinin, GDP, profil lipid, tes fungsi hati, dan TSH.
EKG-12 lead & roentgen toraks (PA dan lateral) pada semua pasien.
Ekokardiografi dengan Doppler untuk menilai fraksi ejeksi ventrikel
kiri, ukuran ventrikel kiri, ketebalan dinding jantung, & fungsi katup.
Arteriografi koroner untuk pasien dengan angina atau iskemia,
kecuali pasien tidak memenuhi syarat untuk revaskularisasi.
21. Toksisitas Statin

Elevations of serum aminotransferase activity (up to three times
normal) occur in some patients.
Therapy may be continued in such patients in the absence of
symptoms if aminotransferase levels are monitored and stable.
Minor increases in creatine kinase (CK) activity in plasma are
observed in some patients receiving reductase inhibitors, frequently
associated with heavy physical activity.
Rarely, patients may have marked elevations in CK activity, often

accompanied by generalized discomfort or weakness in skeletal
muscles. If the drug is not discontinued, rhabdomyolysis may cause
myoglobinuria, leading to renal injury.
22. Leukemia Granulositik Kronik
The marrow aspirate and biopsy are essential to the diagnosis of the
myeloproliferative disorders.
The marrow aspirate provides information as to individual cell morphology and the
distribution of cell types. It also provides essential information in diagnosis and
management of patients with CML as they become increasingly dysplastic and
evolve to acute leukemia.
Chromosomal studies of peripheral blood and marrow are important, primarily to

distinguish CML from the other myeloproliferative disorders
23. Endokrin
Classic clinical manifestations of hypothyroidism include:
Cretinism
Hypothyroidism that develops in infancy or early childhood
Clinical features: impaired development of the skeletal system and
central nervous system, manifested by severe mental retardation,
short stature, coarse facial features, a protruding tongue, and
umbilical hernia
Myxedema
Developing in the older child or adult
Symptoms: generalized fatigue, apathy, cold intolerant,
overweight, constipation, decreased sweating, shortness of
breath, & decreased exercise capacity.
23. Endokrin
Jod-basedow effect
Hipertiroidisme yang diinduksi oleh pemberian
iodin pada pasien dengan struma multinodular,
penyakit Grave laten.
24. Polyuria
If polyuria is shown to be dilute, pathophysiologic
mechanisms include:
1. Hypothalamic or central diabetes insipidus with inability
to synthesize and secrete vasopressin;
2. Nephrogenic diabetes insipidus with an inadequate renal
response to vasopressin;
3. Transient diabetes insipidus of pregnancy produced by
accelerated metabolism of vasopressin;
4. Primary polydipsia (psychogenic), in which the initiating

event is ingestion of excess fluid and the subsequent
hypotonic polyuria is an appropriate physiologic response.
24. Polyuria
During the dehydration or water deprivation test:

primary polydipsia: able to concentrate
urine, blood not become hyperosmolar
diabetes insipidus: blood becomes
hyperosmolar without concentrating the
urine.
After the patient is given desmopressin:

Hypothalamic DI has minimal concentration
of the urine & an additional in urine
osmolality of at least 50%.
partial hypothalamic DI concentrate their
urine minimally with dehydration, but the
maximum urinary concentration is not
achieved, and there is an additional boost
with administered desmopressin
Nephrogenic DI do not concentrate their
urine & no further increase in urine
osmolality after the administration of
desmopressin.

Greenspans clinical endocrinology.
25. Dyspepsia
Epigastric pain described as a burning or gnawing
discomfort can be present in both DU and GU.
Duodenal ulcer:
The typical pain pattern occurs 90 minutes to 3 hours after a
meal and is frequently relieved by antacids or food.
Pain that awakes the patient from sleep (between midnight and
3 A.M.) is the most discriminating symptom, with two-thirds of
DU patients describing this complaint. Unfortunately, this
symptom is also present in one-third of patients with NUD.
Gastric ulcer:
Discomfort may actually be precipitated by food.
Nausea and weight loss occur more commonly in GU patients.
Harrisons principles of internal medicine
26. Hepatitis
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.
27. Heart Failure
Lilly LS. Pathophysiology of heart disease. 5th ed. LWW; 2011.
28. Osteoartritis
28. Osteoartritis
Since OA is a mechanically driven disease, the mainstay of
treatment involves altering loading across the painful joint
and improving the function of joint protectors, so they can
better distribute load across the joint.
Ways of lessening focal load across the joint include
(1) avoiding activities that overload the joint, as evidenced by
their causing pain;
(2) improving the strength and conditioning of muscles that
bridge the joint, so as to optimize their function; and
(3) unloading the joint, either by redistributing load within the
joint with a brace or a splint or by unloading the joint during
weight bearing with a cane or a crutch.
29. Dengue Hemorrhagic Fever
30. Kardiologi
Lilly LS. Pathophysiology of heart disease. 5th ed. LWW; 2011.
31 & 32. Leukemia

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 & Grow slowly may asymptomatic,

Signs
the disease is found 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,
smudge cells
Mature granulocyte,
dominant myelocyte
& segment
Therapy
Can be delayed if asymptomatic

CDC.gov
Lymphoblas Myeloblast
t >20%
>20%, aeur rod
may (+)
Treated right away
33. Pharmacology
Acetaminophen intoxication
Acute ingestion of more than 150200 mg/kg in children or 67 g in
adults is potentially hepatotoxic.
High-risk patients include alcoholics and patients taking
anticonvulsant medications or isoniazid.
Clinical manifestations:
Early after acute acetaminophen overdose, there are usually no
symptoms other than anorexia, nausea, or vomiting. Rarely, a massive
overdose may cause altered mental status and metabolic acidosis.
After 2448 hours, when transaminase levels (AST and ALT) rise,
hepatic necrosis becomes evident. If acute fulminant hepatic failure
occurs, encephalopathy and death may ensue.
33. Pharmacology
Management
N-acetylcysteine
loading dose 140 mg/kg orally. The effectiveness of NAC depends on
early treatment, before the metabolite accumulates; it is of maximal
benefit if started within 810 hours
If vomiting interferes with oral acetylcysteine administration, give it by
gastric tube and use high-dose metoclopramide (12 mg/kg
intravenously (IV); or ondansetron, or give the NAC intravenously if
necessary.
Decontamination
1. Prehospital. Administer activated charcoal, if available.
2. Hospital. Administer activated charcoal. Gastric emptying is not
necessary if charcoal can be given promptly. Do not administer charcoal if
more than 34 hours have passed since ingestion, unless delayed
absorption is suspected.
34. Farmakologi
Potassium & digitalis inhibit each other's binding to Na+/K+ ATPase.
Hyperkalemia reduces the enzyme-inhibiting actions of cardiac glycosides
abnormal cardiac automaticity is inhibited by hyperkalemia reduces the
(toxic) effects of digitalis.
Hypokalemia facilitates these actions increases the (toxic) effects of
digitalis.
Calcium ion facilitates the toxic actions of cardiac glycosides by

accelerating the overloading of intracellular calcium stores that appears to
be responsible for digitalis-induced abnormal automaticity.
Hypercalcemia therefore increases the risk of a digitalis-induced arrhythmia.
The effects of magnesium ion appear to be opposite to those of calcium.

These interactions mandate careful evaluation of serum electrolytes in
patients with digitalis-induced arrhythmias.
35. Tuberkulosis
Gejala Klinis
Gejala respiratori: batuk 2 minggu, batuk darah,

sesak napas, nyeri dada. Gejala sistemik: demam,
malaise, keringat malam, turun berat badan
PF
Kelainan paru di lobus superior (apeks & segmen posterior),

apeks lobus inferior: suara napas bronkial, amforik, suara
napas melemah, ronki basah, tanda penarikan paru,
diafragma, dan mediastinum
Roentgen
Lesi aktif: Bayangan berawan/nodular di apeks & posterior

lobus superior, segmen superior lobus inferior, Kavitas,
Bayangan bercak milier, efusi pleura. Lesi inaktif: fibrotik,
kalsifikasi, schwarte/penebalan pleura.
Tuberkulosis: pedoman diagnosis dan penatalaksanaan di Indonesia. PDPI: 2006.
36. Infeksi Aliran Darah
37. DM Complications
38. Autoimmune Disease
Robbins & Cotran pathologic basis of diseases. 2010.
39. Diabetes
Exercise increases the effectiveness of insulin.
Regular daily moderate exercise improve utilization
of fats & carbohydrates in patients with diabetes.
Strenuous exercise, however, can precipitate

hypoglycemia in an unprepared patient, & patients
with diabetes must therefore be taught to reduce their
insulin dosage or take supplemental carbohydrate in
anticipation of strenuous activity.
40. Diabetes
41. Avian Influenza

(WHO case definition)
Suspected H5N1 case
A person presenting with unexplained acute lower respiratory illness with fever
(>38 C ) and cough, shortness of breath or difficulty breathing.
AND 1/more of the following exposures in the 7 days prior to symptom onset:
a. Close contact (within 1 metre) with a person (e.g. caring for, speaking with, or
touching) who is a suspected, probable, or confirmed H5N1 case;
b. Exposure (e.g. handling, slaughtering, defeathering, butchering, preparation for
consumption) to poultry or wild birds or their remains or to environments
contaminated by their faeces in an area where H5N1 infections in animals or
humans have been suspected or confirmed in the last month;
c. Consumption of raw or undercooked poultry products in an area where H5N1
infections in animals or humans have been suspected or confirmed in the last
month;
d. Close contact with a confirmed H5N1 infected animal other than poultry or wild
birds (e.g. cat or pig);
e. Handling samples (animal or human) suspected of containing H5N1 virus in a
laboratory or other setting.
41. Avian Influenza

Probable H5N1 case
Probable definition 1:
A person meeting the criteria for a suspected case AND one of the
following additional criteria:
a.
b.
infiltrates or evidence of an acute pneumonia on chest radiograph

plus evidence of respiratory failure (hypoxemia, severe tachypnea)
OR
positive laboratory confirmation of an influenza A infection but
insufficient laboratory evidence for H5N1 infection.
Probable definition 2:
A person dying of an unexplained acute respiratory illness who is
considered to be epidemiologically linked by time, place, and
exposure to a probable or confirmed H5N1 case.
41. Avian Influenza

Confirmed H5N1 case (notify WHO)
A person meeting the criteria for a suspected or probable case AND one of
the following positive results conducted in a national, regional or
international influenza laboratory whose H5N1 test results are accepted
by WHO as confirmatory:
a. Isolation of an H5N1 virus;
b. Positive H5 PCR results from tests using two different PCR targets, e.g. primers
specific for influenza A and H5 HA;
c. A fourfold or greater rise in neutralization antibody titer for H5N1 based on
testing of an acute serum specimen (collected 7 days or less after symptom
onset) and a convalescent serum specimen. The convalescent neutralizing
antibody titer must also be 1:80 or higher;
d. A microneutralization antibody titer for H5N1 of 1:80 or greater in a single
serum specimen collected at day 14 or later after symptom onset and a
positive result using a different serological assay, for example, a horse red
blood cell haemagglutination inhibition titer of 1:160 or greater or an H5specific western blot positive result.
42. Pulmonologi
Obstruktif:
FEV1 is decreased out of proportion to the FVC, an obstructive pattern is
present.
The normal FEV1/FVC ratio is greater than 0.75 for those 60 years of age or
younger and greater than 0.70 for those older than 60 years.
A normal percent predicted FEV1 is between 80% and 120%.
Restriktif:
A reduction in all volumes and capacities.
The classic findings TLC or FRC < 75% of predicted, reduced RV and VC, and a
normal to high FEV1/FVC ratio.
42. Pulmonologi
Current diagnosis & treatment in pulmonary medicine.
42. Pulmonologi
Murray & Nadel Textbook of pulmonary disease.
43. Penyakit Paru
Color atlas of pathophysiology. Thieme. 2003
43. Penyakit Paru
Peningkatan volume udara di paru

akibat obstruksi hipersonor
44. Tobacco Smoking

Merokok meningkatkan risiko
aterosklerosis & penyakit jantung
iskemik.
Merokok dalam jumlah kecil sudah

meningkatkan risiko penyakit
jantung.
Bila tidak terdapat gejala angina,
dapat dilakukan tes stres EKG untuk
memeriksa adanya penyakit jantung
iskemik.
Murray & Nadel textbook of pulmonary disease. 2014.

Pathophysiology of heart disease.
45. HIV
45. HIV
Some treatment guidelines, particularly those in the
United States, now recommend ART for all HIV-infected
patients, regardless of CD4 count, whereas some other
(e.g., British) guidelines recommend ART for patients
with CD4 counts less than 350 cells/mm3.
The level of evidence to support therapy initiation
guidelines is strongest for CD4 counts less than 200
cells/mm3 and weakens as the CD4 counts studied
increase to greater than 500 cells/mm3.
Mandell Textbook of infectious disease. 2015.
46. Arthritis
Rheumatoid arthritis (RA)
Penyakit inflamasi kronik dengan penyebab yang belum
diketahui, ditandai oleh poliartritis perifer yang simetrik.
Skor 6/lebih: definite RA.
Faktor reumatoid merupakan autoantibodi yang
menyerang IgG lebih spesifik menandakan autoimunitas
daripada CRP yang merupakan penanda inflamasi.
Boutonnoere deformity caused by

flexion of the PIP joint with
hyperextension of the DIP joint.
Swan neck deformity caused by

Hyperextension of the PIP joint with
flexion of the DIP joint .
Rheumatoid Arthritis
Rheumatoid nodules &
olecranon bursitis.
Ulnar deviation of the fingers with wasting of the

small muscles of the hands and synovial swelling at
the wrists, the extensor tendon sheaths, MCP & PIP.

The therapeutic range differs due to variation in
the laboratory methods used to determine aPTT.
The American College of Chest Physicians

consensus conference has therefore
recommended dosage adjustments to a
therapeutic range equivalent to heparin levels of
0.3 to 0.7 U per ml by antifactor Xa
determinations, which correlates with aPTT
values between 60 and 80 s.
48. TB-HIV
Management of tuberculosis & HIV coinfection. WHO.
49. Farmakologi
Once-daily oseltamivir for 7 to 10 days is also effective for

postexposure prophylaxisin household contacts, including children,
and when ill index cases receive concurrent treatment
50. Asma
Pemeriksaan spirometri dalam diagnosis asma :
Obstruksi jalan napas diketahui dari nilai rasio VEP1/ KVP < 75% atau
VEP1 < 80% nilai prediksi.
Reversibilitas: perbaikan VEP1 15% secara spontan, atau setelah
inhalasi bronkodilator (uji bronkodilator), atau setelah pemberian
bronkodilator oral 10-14 hari, atau setelah pemberian kortikosteroid
(inhalasi/ oral) 2 minggu.
Menilai derajat berat asma
Pemeriksaan arus puncak ekspirasi dengan spirometri atau peak

expiratory flow meter:
Reversibiliti, yaitu perbaikan nilai APE > 15% setelah inhalasi
bronkodilator (uji bronkodilator), atau bronkodilator oral 10-14 hari, atau
respons terapi kortikosteroid (inhalasi/oral) 2 minggu
Variabilitas, menilai variasi diurnal APE yang dikenal dengan variabiliti
APE harian selama 1-2 minggu. Juga dapat digunakan menilai derajat
asma.
PDPI. Asma: pedoman diagnosis & penatalaksanaan di Indonesia. 2004
ILMU PENYAKIT MATA
51. Tatalaksana Glaukoma Akut
Tujuan : merendahkan tekanan bola mata secepatnya kemudian bila tekanan normal dan
mata tenang operasi
Supresi produksi aqueous humor
Beta bloker topikal: Timolol maleate 0.25% dan 0.5%, betaxolol 0.25% dan 0.5%,
levobunolol 0.25% dan 0.5%, metipranolol 0.3%, dan carteolol 1% dua kali sehari dan
timolol maleate 0.1%, 0.25%, dan 0.5% gel satu kali sehari (bekerja dalam 20 menit,
reduksi maksimum TIO 1-2 jam stlh diteteskan)
Pemberian timolol topikal tidak cukup efektif dalam menurunkan TIO glaukoma akut
sudut tertutup.
Apraclonidine: 0.5% tiga kali sehari
Brimonidine: 0.2% dua kali sehari
Inhibitor karbonat anhidrase:
Topikal: Dorzolamide hydrochloride 2% dan brinzolamide 1% (2-3 x/hari)
Sistemik: Acetazolamide 500 mg iv dan 4x125-250 mg oral (pada glaukoma akut
sudut tertutup harus segera diberikan, efek mulai bekerja 1 jam, puncak pada 4
jam)
Ilmu Penyakit Mata Ed 3. Jakarta: Balai Penerbit FKUI; 2006
Tatalaksana Glaukoma Akut
Fasilitasi aliran keluar aqueous humor

Analog prostaglandin: bimatoprost 0.003%, latanoprost 0.005%, dan travoprost 0.004%
(1x/hari), dan unoprostone 0.15% 2x/hari
Agen parasimpatomimetik: Pilocarpine
Epinefrin 0,25-2% 1-2x/hari
Pilokarpin 2% setiap menit selama 5 menit,lalu 1 jam selama 24 jam
Biasanya diberikan satu setengah jam pasca tatalaksana awal
Mata yang tidak dalam serangan juga diberikan miotik untuk mencegah serangan
Pengurangan volume vitreus
Agen hiperosmotik: Dapat juga diberikan Manitol 1.5-2MK/kgBB dalam larutan 20% atau urea
IV; Gliserol 1g/kgBB badan dalam larutan 50%
isosorbide oral, urea iv
Extraocular symptoms:
analgesics
antiemetics
Placing the patient in the supine position lens falls away from the iris decreasing pupillary
block
Pemakaian simpatomimetik yang melebarkan pupil berbahaya
Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asburys General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007.
Tatalaksana Surgikal Glaukoma Akut

Sudut Tertutup
Irodotomi: membuat lubang dengan laser
pada iris sehingga aliran aqueous humour
yang terhambat akibat pupillary block dari
COP bisa mengalir ke COA.
Laser pheripheral iridotomi dilakukan pada
glaukoma akut sudut tertutup walau TIO
telah diturunkan oleh obat-obatan, karena
serangan ulang bisa sewaktu-waktu terjadi
http://www.allaboutvision.com/conditions/glaucoma-surgery.htm
Tatalaksana surgikal glaukoma primer

sudut terbuka
Trabekuloplasti merupakan prosedur laser
untuk memodifikasi jaringan trabekula
sehingga meningkatkan aliran keluar aqueous
humour.
52. GLAUKOMA KONGENITAL

0,01% diantara 250.000
penderita glaukoma
2/3 kasus pada Laki-laki dan
2/3 kasus terjadi bilateral
50% manifestasi sejak lahir;
70% terdiagnosis dlm 6 bln
pertama; 80% terdiagnosis
dalam 1 tahun pertama
Klasifikasi menurut Schele:
Klasifikasi lainnya:
Glaukoma kongenital primer
anomali perkembangan yang
mempengaruhi trabecular
meshwork.
Glaukoma kongenital
sekunder: kelainan kongenital
mata dan sistemik lainnya,
kelainan sekunder akibat
trauma, inflamasi, dan tumor.
Glaukoma infantum: tampak

waktu lahir/ pd usia 1-3 thn
Glaukoma juvenilis: terjadi
pada anak yang lebih besar
Buku ilmu penyakit mata Nana Wijaya & Oftalmologi umum Vaugahn & Asbury
Patogenesis
Abnormalitas anatomi trabeluar meshwork penumpukan
cairan aqueous humor peninggian tekanan intraokuler
bisa terkompensasi krn jaringan mata anak masih lembek
sehingga seluruh mata membesar (panjang bisa 32 mm,
kornea bisa 16 mm buftalmos & megalokornea) kornea
menipis sehingga kurvatura kornea berkurang
Ketika mata tidak dapat lagi meregang bisa terjadi
penggaungan dan atrofi papil saraf optik
Gejala & Diagnosis

Tanda dini: fotofobia,
epifora, dan blefarospasme
Terjadi pengeruhan kornea
Penambahan diameter
kornea (megalokornea;
diameter 13 mm)
Penambahan diameter bola
mata (buphtalmos/ ox eye)
Peningkatan tekanan
intraokuler
Diagnosis glaukoma
kongenital tahap lanjut
dengan mendapati:
Megalokornea
Robekan membran
descement
Pengeruhan difus kornea
Tatalaksana
Medikamentosa hingga
TIO normal
Acetazolamide
pilokarpin
Operasi:
Goniotomi (memotong
jaringan yg menutup
trabekula atau memotong
iris yg berinsersi pada
trabekula
Goniopuncture: membuat
fistula antara bilik depan
dan jaringan
subkonjungtiva (dilakukan
bila goniotomi tidak
berhasil)
53. Tatalaksana Glaukoma Akut
Tujuan : merendahkan tekanan bola mata secepatnya kemudian bila tekanan normal dan
mata tenang operasi
Supresi produksi aqueous humor
Beta bloker topikal: Timolol maleate 0.25% dan 0.5%, betaxolol 0.25% dan 0.5%,
levobunolol 0.25% dan 0.5%, metipranolol 0.3%, dan carteolol 1% dua kali sehari dan
timolol maleate 0.1%, 0.25%, dan 0.5% gel satu kali sehari (bekerja dalam 20 menit,
reduksi maksimum TIO 1-2 jam stlh diteteskan)
Pemberian timolol topikal tidak cukup efektif dalam menurunkan TIO glaukoma akut
sudut tertutup.
Apraclonidine: 0.5% tiga kali sehari
Brimonidine: 0.2% dua kali sehari
Inhibitor karbonat anhidrase:
Topikal: Dorzolamide hydrochloride 2% dan brinzolamide 1% (2-3 x/hari)
Sistemik: Acetazolamide 500 mg iv dan 4x125-250 mg oral (pada glaukoma akut
sudut tertutup harus segera diberikan, efek mulai bekerja 1 jam, puncak pada 4
jam)
Tatalaksana Glaukoma Akut
Fasilitasi aliran keluar aqueous humor

Analog prostaglandin: bimatoprost 0.003%, latanoprost 0.005%, dan travoprost 0.004%
(1x/hari), dan unoprostone 0.15% 2x/hari
Agen parasimpatomimetik: Pilocarpine
Epinefrin 0,25-2% 1-2x/hari
Pilokarpin 2% setiap menit selama 5 menit,lalu 1 jam selama 24 jam
Biasanya diberikan satu setengah jam pasca tatalaksana awal
Mata yang tidak dalam serangan juga diberikan miotik untuk mencegah serangan
Pengurangan volume vitreus
Agen hiperosmotik: Dapat juga diberikan Manitol 1.5-2MK/kgBB dalam larutan 20% atau urea
IV; Gliserol 1g/kgBB badan dalam larutan 50%
isosorbide oral, urea iv
Extraocular symptoms:
analgesics
antiemetics
Placing the patient in the supine position lens falls away from the iris decreasing pupillary
block
Pemakaian simpatomimetik yang melebarkan pupil berbahaya
Sumber: Riordan-Eva P, Whitcher JP. Vaughan and Asburys General Ophtalmology 17th ed. Philadephia: McGraw-Hill, 2007.
54. KONJUNGTIVITIS
VERNAL
Nama lain:
spring catarrh
seasonal conjunctivitis
warm weather conjunctivitis
Etiologi: reaksi hipersensitivitas

bilateral (alergen sulit
diidentifikasi)
Epidemiologi:
Dimulai pada masa prepubertal,
bertahan selama 5-10 tahun
sejak awitan
Laki-laki > perempuan
Paling sering pada Afrika SubSahara & Timur Tengah
Temperate climate > warm
climate > cold climate (hampir
tidak ada)
Gejala & tanda:

Rasa gatal yang hebat, dapat
disertai fotofobia
Sekret ropy
Riwayat alergi pada RPD/RPK
Tampilan seperti susu pada
konjungtiva
Gambaran cobblestone
(papila raksasa berpermukaan
rata pada konjungtiva tarsal)
Tanda Maxwell-Lyons (sekret
menyerupai benang &
pseudomembran fibrinosa
halus pada tarsal atas, pada
pajanan thdp panas)
Bercak Horner Trantas
(bercak keputihan pada
limbus saat fase aktif
penyakit)
Dapat terjadi ulkus kornea
superfisial
Vaughan & Asbury General Ophtalmology 17th ed.
Tatalaksana
Self-limiting
Akut:
Steroid topikal (+sistemik
bila perlu), jangka
pendek mengurangi
gatal (waspada efek
samping: glaukoma,
katarak, dll.)
Vasokonstriktor topikal
Kompres dingin & ice
pack
Jangka panjang & prevensi

sekunder:
Antihistamin topikal
Stabilisator sel mast Sodium
kromolin 4%: sebagai
pengganti steroid bila gejala
sudah dapat dikontrol
Tidur di ruangan yang sejuk
dengan AC
Siklosporin 2% topikal (kasus
berat & tidak responsif)
Desensitisasi thdp antigen

(belum menunjukkan hasil
baik)
Vaughan & Asbury General Ophtalmology 17th ed.
Table. Major Differentiating Factors Between VKC and AKC

Characteristics
VKC
AKC
Age at onset
Generally presents at a younger age

than AKC
over 30 years
Sex
Males are affected preferentially.
No sex predilection
Seasonal variation
Typically occurs during spring months Generally perennial
Discharge
Thick mucoid discharge
Watery and clear discharge
Conjunctival
scarring
Higher incidence of
conjunctival scarring
Horner-Trantas
dots
Horner-Trantas dots and shield ulcers Presence of Horner-Trantas

are commonly seen.
dots is rare.
Conjunctiva
Cobblestone appearance
papillae
Corneal
neovascularization
Not present
Deep corneal
neovascularization tends to
develop
Presence of
eosinophils in
conjunctival
scraping
Conjunctival scraping reveals

eosinophils to a greater degree in
VKC than in AKC
Presence of eosinophils is
less likely
55. Diabetic Eye Disease

DM ophthalmic complications :
Corneal abnormalities
Glaucoma
Iris neovascularization
Cataracts
Neuropathies
Diabetic retinopathy
most common and
potentially most blinding
Retinopathy and other

microvascular complications of
diabetes are multifactorial,
attributed to chronic
hyperglycemia, vascular
damage and leakage, edema,
capillary basement membrane
thickening, neovascularization,
hemorrhage, and ischemia.
It is an ocular manifestation of
systemic disease which affects
up to 80% of all patients who
have had diabetes for 10 years
or more.
RETINOPATI DIABETIK - KLASIFIKASI
RETINOPATI DIABETIK
NONPROLIFERATIF
ditandai dengan kebocoran
darah dan serum pada
pembuluh darah kapiler
menyebabkan edema jaringan
retina dan terbentuknya
deposit lipoprotein (hard
exudates)
Tidak menyebabkan gangguan
penglihatan mengenai
makula
Edema makula penebalan
daerah makula sebagai akibat
kebocoran kapiler perifoveal
RETINOPATI DIABETIK
PROLIFERATIF
ditandai dengan adanya

proliferasi jaringan fibrovaskular
atau neovaskularisasi pada
permukaan retina & papil saraf
optik serta vitreus
Proliferasi respon dari oklusi
luas pembuluh darah kapiler
retina yang menyebabkan iskemia
retina
menyebabkan gangguan
penglihatan sampai kebutaan
melalui mekanisme;
Perdarahan vitreus
Tractional retinal detachment
Glaukoma neovaskular
RETINOPATI DIABETIK
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
Bedah vitrektomi
56. Sildenafil
Used in the treatment of erectile dysfunction.
Ocular side-effects include a bluish tinge to the
visual field, hypersensitivity to light, and hazy
vision.
These effects are reversible and may last only a
few minutes or hours.
It has been reported that only 3% of patients
have visual side-effects with the standard 50
milligram dose.
With increased dosage, the ocular side-effect
incidence rate significantly increases.
57. ASTIGMATISME - DEFINISI

Ketika cahaya yang
masuk ke dalam
mata secara paralel
tidak membentuk
satu titik fokus di
retina.
Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry
http://www.mastereyeassociates.com/Portals/60407/images//astig
matism-Cross_Section_of_Astigmatic_Eye.jpg
Tipe-tipe astigmatisma
Astigmatisma hipermetropikus
simpleks, satu meridian utamanya
emetropik, meridian yang lainnya
hipermetropik.
Astigmatisma miopikus simpleks,
satu meridian utamanya emetropik,
meridian lainnya miopi
kompositus, kedua meridian utama
hipermetropik dengan derajat
berbeda.
Astigmatisma miopikus kompositus,
kedua meridian utamanya miopik
dengan derajat berbeda
Astigmatisma mikstus, satu
meridian utamanya hipermetropik,
meridian yang lain miopik.
Penentuan Jenis Astigmatisme

1.
2.
3.
4.
5.
Sferis (-) silinder (-) pasti

miop kompositus
Sferis (+) silinder (+) pasti
hipermetrop kompositus
Sferis (tidak ada) silinder (-)
pasti miop simpleks
Sferis (tidak ada) silinder (+)
pasti hipermetrop
simpleks
Untuk sferis dan silinder
yang saling berbeda
tandanya, mohon lihat
pembahasan TO2
58. KATARAK-SENILIS
Katarak senilis adalah kekeruhan lensa yang

terdapat pada usia lanjut, yaitu usia di atas 50
tahun
Epidemiologi : 90% dari semua jenis katarak
Etiologi :belum diketahui secara
pastimultifaktorial:
Faktor biologi, yaitu karena usia tua dan
pengaruh genetik
Faktor fungsional, yaitu akibat akomodasi
yang sangat kuat mempunyai efek buruk
terhadap serabu-serabut lensa.
Faktor imunologik
Gangguan yang bersifat lokal pada lensa,
seperti gangguan nutrisi, gangguan
permeabilitas kapsul lensa, efek radiasi
cahaya matahari.
Gangguan metabolisme umum
4 stadium: insipien, imatur (In some patients, at

this stage, lens may become swollen due to
continued hydration intumescent cataract),
matur, hipermatur
Gejala : distorsi penglihatan, penglihatan
kabur/seperti berkabut/berasap, mata tenang
Penyulit : Glaukoma, uveitis
Tatalaksana : operasi (ICCE/ECCE)
59. GERAK BOLA MATA
72. Gerak Bola Mata
GERAK BOLA MATA
60. Uveitis
Anterior
Intermediate
Posterior
Panuveitis
Fuchs
heterochromic
uveitis
Sarcoidosis
Toxoplasmosis
Tuberculosis
Posner
Schlossman
syndrome
Tuberculosis
Acute retinal
necrosis
Sarcoidosis
Infective uveitis
Lymes disease
Arthritis
associated
uveitis
Behcets disease
Vogt-KoyanagiHarada
Deepankur Mahajan, Pradeep Venkatesh, S.P. Garg ; Uveitis and glaucoma: a critical review : Journal of Current
Glaucoma Practise, September December 2011; 5(3): 14-30
Behcets Disease
Chronic, relapsing, occlusive systemic vasculitis

Etiology unknown
Affects both anterior & posterior segment
Type:
Neuro BD
Ocular BD
Intestinal BD
Vascular BD
Behet disease
Oral or genital sores
Uveitis
Uveitis Anterior/Media/Posterior (Panuvetis)

HLA-B51+
Skin lesions
Criteria for Behet's disease:

Mouth sores (oral ulcers) at least 3 times in 12 months
Any 2 of the following:
Recurring genital sores/ulcers
Uveitis
Skin: Pustules or erythema nodosum
Positive pathergy (skin prick test)
Vogt-Koyanagi-Harada Syndrome
Uncommon multisystem disease of Autoimmune etiology

Chronic, bilateral, diffuse, granulamatous pan-uveitis
Associated with Integumentary, Neurologic, Auditory involvement
Commonly affects darkly pigmented ethnic groups
History of the disease:
1. Prodromos flu-like-syndrome
2. Acute fase:
Neurologic symptoms: meningismus, tinnitus, pleocytosis in CFS

Uveitis
3. Convalescent phase: poliosis, skin/uveal discoloration,

poliosis, Sigiura sign (perilimbic discoloration), vitiligo,
alopecia areata
4. Chronic recurrent phase: recurrent anterior uveitis
Vogt Koyanagi Harada syndrome

1. Prodromus
2. Neurologic symptoms+ Bilateral

uveitis
3. Late cutaneous symptoms
Posterior uveitis with serous detachments

Granulomatous bilateral uveitis
Late: poliosis, Sigiura sign, sunset-glow fundus
Posner- Schlossman syndrome

Glaucomatocyclitic crisis
Mild anterior uveitis with very
high IOP
Discomfort, blurring of vision,
haloes, No pain, No redness
PG level in aqueous
unilateral recurrent episodes of
mild cyclitis and heterochromia.
Its pathogenesis still remains
unknown, with suggested
possible associations including an
immunogenetic factor involving
HLA-Bw54, viral infections (HSV
and CMV)
CLINICAL FEATURES:
mild ciliary flush
a dilated or sluggishly reactive
pupil
corneal epithelial edema
open angles (No shallow AC)
The IOP is in the range of 40 70
mmHg during an acute attack
Minimal flare
Few cells
Few Keratic precipitate
No pheripheral anterior
synechiae and posterior
synechiae
Reiter syndrome/Reactive arthritis

Urethritis /gastroenteritis
1-5weeks before:
Ocular
yellowish serous papules at
soles and palms
HLAB27+
Infectious
agents: Chlamydiae, Salmonella, Shi
gella, Yersinia, Campylobacter
yellowish serous papules at soles
and palms even nails, scrotum,
scalp and trunk.
Keratoconjunctivitis+urethritis +arthritis
Previously: urethritis ( can be seen as genital
ulcer too) /gastroenteritis
61& 62. ASTIGMATISME DEFINISI

Ketika cahaya yang
masuk ke dalam
mata secara paralel
tiudak membentuk
satu titik fokus di
retina.
Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometry
http://www.mastereyeassociates.com/Portals/60407/images//astig
matism-Cross_Section_of_Astigmatic_Eye.jpg
Tipe-tipe astigmatisma
simpleks, satu meridian
utamanya emetropik, meridian
yang lainnya hipermetropik.
Astigmatisma miopikus simpleks,
satu meridian utamanya
emetropik, meridian lainnya
miopi
kompositus, kedua meridian
utama hipermetropik dengan
derajat berbeda.
Astigmatisma miopikus
kompositus, kedua meridian
utamanya miopik dengan derajat
berbeda
Astigmatisma mikstus, satu
meridian utamanya
hipermetropik, meridian yang lain
miopik.
Penentuan Jenis Astigmatisme

1.
2.
3.
4.
5.
sferis (-) silinder (-) pasti

miop kompositus
Sferis (+) silinder (+) pasti
hipermetrop kompositus
Sferis (tidak ada) silinder (-)
pasti miop simpleks
Sferis (tidak ada) silinder (+)
pasti hipermetrop
simpleks
Untuk sferis dan silinder
yang saling berbeda
tandanya, mohon lihat
pembahasan TO2
Pada soal dikatakan setelah dilakukan pemeriksaan

didapatkan VODS 20/30 setelah dikoreksi menjadi
20/20 dengan S -0,75 C-0,50 Axis 180.
Seharusnya kelainan yang diderita pasien adalah
astigmatisme miopia kompositus, dimana bayangan
jatuh di dua titik yang berbeda di depan retina. Hal ini
disebabkan karena kelengkungan kornea yang berbeda
tapi tidak ada di pilihan jawaban
Astigmatisme miopia kompositus kedua titik jatuh di
depan, sehingga memiliki sifat miopi o.k jawaban
yang paling mendekati adalah aksial bola mata yang
panjang
63. Klasifikasi Trakoma Menurut

MacCallan
Stadium
Nama
Stadium I
Trakoma insipien (insipient

trachoma)
Stadium II
Trakoma (established
trachoma)
Gejala
Folikel imatur, hipertrofi papilar
minimal
Folikel matur pada dataran tarsal
atas
Stadium IIA
Dengan Hipertrofi folikular yang

menonjol
Keratitis, Folikel limbal
Stadium IIB
Dengan Hipertrofi papilar yang

menonjol
Aktivitas kuat dengan folikel matur

tertimbun dibawah hipertrofi
papilar yang hebat
Stadium III
Trakoma memarut (sikatrik)
Parut pada konjungtiva tarsal atas,

permulaan trikiasis, entropion
Stadium IV
Trakoma sembuh
Tak aktif, tak ada hipertrofi papilar

atau folikular, parut dalam
bermacam derajat variasi
64. Aspirin & Occular Complications
Ocular side-effects associated

with aspirin use are rare.
However, this drug is secreted
in tears so transient blurred
vision can occur along with
aggravation of dry eyes and
keratitis.
These symptoms can be
idiosyncratic or hypersensitive.
Journal of the American

Medical Association (JAMA) in
2013 Research conducted
among 2,400 middle-aged and
elderly people for 15 years:
Regular aspirin use was
significantly associated with an
increased incidence of
neovascular [wet] age-related
macular degeneration (AMD)
The 'wet' form is less common
but progresses more rapidly
and is more likely to lead to
vision loss than the 'dry' form.
Ibuprofen & Occular Complications

The most common side-effect associated with this
medication is transient blurred vision.
In a drug re-challenge test, there were also documented
reports of refractive error changes, diplopia, photophobia,
dry eyes, visual field changes, and altered color vision.
If they occur, vision changes usually resolve after 1-3
months, but color vision problems can take up to 8 months
to resolve.
Corneal vortex keratopathy, which generally resolves within
3 weeks, has been documented, and reversible toxic
amblyopia is rare but a real side-effect.
There are also a few reports of a rare, idiosyncratic,
unilateral or bilateral optic nerve response that can reduce
acuity to between 20/80 and 20/200.
Steroid & Occular Complication

Cataracts occur most
commonly as a sequela of
continuous systemic steroid
use
Glaucoma is more often
associated with topical ocular
or periocular steroids than
with systemic steroids
Ocular rebound inflammation
may develop secondary to
rapid tapering or abrupt
discontinuation of topical
ocular steroid use and is best
prevented with gradual
tapering.
Opportunistic infections of the

eye include bacterial, viral, and
fungal infections and are most
often associated with the use
of topical ocular steroids.
Ophthalmologic evaluation is
indicated promptly if patients
treated with ocular steroids
develop ocular discharge, pain,
photophobia, or redness.
65. UVEITIS
Radang uvea:
mengenai bagian
depan atau
selaput pelangi
(iris) iritis
mengenai bagian
tengah (badan
silier) siklitis
mengenai
selaput hitam
bagian belakang
mata koroiditis
Biasanya iritis
disertai dengan
siklitis = uveitis
anterior/iridosikl
itis
UVEITIS
Dibedakan dalam bentuk
granulomatosa akut-kronis dan
non-granulomatosa akut- kronis
Bersifat idiopatik, ataupun terkait
penyakit autoimun, atau terkait
penyakit sistemik
Biasanya berjalan 6-8 minggu
Dapat kambuh dan atau menjadi
menahun
Gejala akut:
mata sakit
Merah
Fotofobia
penglihatan turun ringan
mata berair
Tanda :
pupil kecil akibat rangsangan
proses radang pada otot
sfingter pupil
edema iris
Terdapat flare atau efek tindal
di dalam bilik mata depan
Bila sangat akut dapat terlihat
hifema atau hipopion
Presipitat halus pada kornea
Radang iris dan badan siliar menyebabkan rusaknya Blood Aqueous Barrier sehingga terjadi
peningkatan protein, fibrin, dan sel-sel radang dalam humor akuos. Pada pemeriksaan biomikroskop
(slit lamp) hal ini tampak sebagai flare, yaitu partikel-partikel kecil dengan gerak Brown (efek tyndall).
UVEITIS
Tatalaksana :
Steroid topikal dan sistemik
Siklopegik
Pengobatan spesifik bila
diketahui kuman penyebab
Penyulit: Glaukoma
sekunder karena adanya
sinekia posterior yang
menyebabkan iris
bombans peningkatan
TIO
66. Glaukoma Simpleks

Merupakan suatu glaukoma primer (idiopatik) yang
ditandai dengan sudut bilik mata terbuka
Paling sering di usia > 40 tahun, namun dapat pula
mengenai usia muda
Diturunkan secara dominan atau resesif pada 50%
kasus
Diagnosis :
TIO sehari hari tinggi atau > 20 mmHg
Mata tidak merah atau tidak terdapat keluhan baik pada
anatomis atau fisiologis yg disadari oleh penderita
(keluhan sedikit dan progresifitas berjalan lambat)
Penatalaksanaan :
Bila diagnosis telah ditegakkan penderita harus
memakai obat seumur hidup untuk mencegah
kebutaan
Tujuan pengobatan memperlancar pengeluaran
dan mengurangi produksi aqueous humor
Bila TIO di atas 21 mmHg dan terdapat kelainan
lapang pandang dan papil, maka diberikan
Pilokarpin 1-4% 3x/hari
Bila tidak ada perbaikan tambah timolol 0,25-0,5%,
asetazolamide 3 x 250 mg atau epinefrin 1-2%
Bila pengobatan tidak berhasil trabekulotomi laser
Sidarta Ilyas. Ilmu Penyakit Mata. FKUI
67. Trauma Mekanik Bola Mata

Cedera langsung berupa ruda
paksa yang mengenai jaringan
mata.
Beratnya kerusakan jaringan
bergantung dari jenis trauma
serta jaringan yang terkena
Gejala : penurunan tajam
penglihatan; tanda-tanda
trauma pada bola mata
Komplikasi :
Endoftalmitis
Uveitis
Perdarahan vitreous
Hifema
Retinal detachment
Glaukoma
Oftalmia simpatetik
Panduan Tatalaksana Klinik RSCM Kirana, 2012
Pemeriksaan Rutin :
Visus : dgn kartu Snellen/chart
projector + pinhole
TIO : dgn tonometer
aplanasi/schiotz/palpasi
Slit lamp : utk melihat segmen
anterior
USG : utk melihat segmen
posterior (jika memungkinkan)
Ro orbita : jika curiga fraktur
dinding orbita/benda asing
Tatalaksana :
Bergantung pada berat trauma,
mulai dari hanya pemberian
antibiotik sistemik dan atau
topikal, perban tekan, hingga
operasi repair
HIFEMA
Definisi:
Perdarahan pada bilik mata
depan
Tampak seperti warna
merah atau genangan
darah pada dasar iris atau
pada kornea
Halangan pandang parsial

/ komplet
Etiologi: pembedahan
intraokular, trauma
tumpul, trauma laserasi
Tujuan terapi:
Mencegah rebleeding
(biasanya dalam 5 hari
pertama)
Mencegah noda darah
pada kornea
Mencegah atrofi saraf
optik
Komplikasi:
Perdarahan ulang
Sinekiae anterior perifer
Atrofi saraf optik
Glaukoma
68. Trauma Basa atau Alkali

Pada trauma alkali akan terbentuk kolagenase merusak
kolagen kornea
Klasifikasi Thoft :
Derajat 1 : hiperemi konjungtiva disertai keratitis pungtata
Derajat 2 : hiperemi konjungtiva disertai hilang epitel kornea
Derajat 3 : hiperemi konjungtiva disertai nekrosis konjungtiva
dan lepasnya epitel kornea
Derajat 4 : konjungtiva perilimbal mengalami nekrosis sebanyak
50%
Untuk menilai defek pada epitel kornea digunakan uji

fluorescein
Kertas fluorescein dibasahi dengan garam fisiologis lalu dilekkan
pada sakus konjungtiva inferior bila kornea kehijauan dengan
sinar biru defek kornea
69. Astenopia (Computer Vision

Syndrome)
Astenopia, Eye Strain, Visual
Discomfort dan Ocular fatigue
atau disebut juga mata lelah
Kondisi oftalmologis yang
bermanifestasi lewat gejala
nonspesifik seperti lelah dan
nyeri sekitar atau pada mata,
penglihatan buram, sakit kepala
dan kadang diplopia. Biasanya
timbul setelah membaca, lama
melihat komputer atau aktivitas
mata yang terus-menerus.
Terjadi akibat:
1. Cahaya masuk ke mata dari benda
yang dilihat tidak cukup.
2. Pemusatan cahaya pada retina mata
tidak sempurna.
3. Mekanisme penggabungan bayangan
(fusi) oleh sistem penglihatan yang
lebih sentral (otak) dan upaya untuk
mempertahankannya tidak memadai.
Gejala:
Pandangan kabur
Distorsi bentuk dan ukuran objek
Inflamasi mata
lakrimasi
Mata lelah, terasa panas
Rasa tidak nyaman di mata
Nyeri kepala
Klasifikasi
Refraktif Astenopia
Astenopia yang terjadi akibat kelainan refraksi dan
berkurang dengan penggunaan kacamata
Muscular Astenopia
Terkait dengan kelainan akomodasi dan
ketidakcukupan konvergensi, gejala akan
berkurang dengan latihan konvergensi dan
akomodasi
70. Presbiopia
Koreksilensa positif
untuk menambah
kekuatan lensa yang
berkurang sesuai usia
Kekuatan lensa yang

biasa digunakan:
+ 1.0 D usia 40 tahun
http://www.ivo.gr/files/items/1/145/51044.jpg
http://emedicine.medscape.com/article/1206147
71. Jenis Glaukoma
Causes
Etiology
Clinical
Acute Glaucoma
Pupilllary block
Acute onset of ocular pain, nausea, headache, vomitting, blurred

vision, haloes (+), palpable increased of IOP(>21 mm Hg),
conjunctival injection, corneal epithelial edema, mid-dilated
nonreactive pupil, elderly, suffer from hyperopia, and have no
history of glaucoma
Open-angle
(chronic)
glaucoma
Unknown
History of eye pain or redness, Multicolored halos, Headache,

IOP steadily increase, Gonioscopy Open anterior chamber
angles, Progressive visual field loss
Congenital
glaucoma
abnormal eye
development,
congenital infection
present at birth, epiphora, photophobia, and blepharospasm,

buphtalmus (>12 mm)
Secondary
glaucoma
Drugs
(corticosteroids)
Eye diseases (uveitis,
cataract)
Systemic diseases
Trauma
Sign and symptoms like the primary one. Loss of vision
Absolute
glaucoma
end stage of all types of glaucoma, no vision, absence of

pupillary light reflex and pupillary response, stony appearance.
Severe eye pain. The treatment destructive procedure like
cyclocryoapplication, cyclophotocoagulation,injection of 100%
alcohol
72. ARMD (Age Related Macular Degeneration)

Degenerasi progresif makula retina yg dpt memberikan
gangguan pd penglihatan sentral
Biasanya tjd pd usia di atas 60 thn
Gejala klinis gradual loss of visual acuity. Where macular
edema is present, patients complain of image distortion
(metamorphopsia),macropsia, or micropsia
Drussen deposit lipofiuscin di lapisan pigmen epitel retina yg

berwarna kekuningan
Sumber: Ophthalmology. Lang. 2000.
73. DAKRIOSISTITIS
Partial or complete obstruction of the nasolacrimal duct
with inflammation due to infection (Staphylococcus aureus
or Streptococcus B-hemolyticus), tumor, foreign bodies,
after trauma or due to granulomatous diseases.
Clinical features : epiphora, acute, unilateral, painful
inflammation of lacrimal sac, pus from lacrimal punctum,
fever, general malaise, pain radiates to forehead and teeth
Diagnosis : Anel test(+) :not dacryocystitis, probably skin
abcess; (-) or regurgitation (+) : dacryocystitis. Swab and
culture
Treatment : Systemic and topical antibiotic, irrigation of
lacrimal sac, Dacryocystorhinotomy
Evaluasi Sistem Lakrimal-Drainase Lakrimal :

Uji Anel : Dengan melakukan uji anel, dapat diketahui apakah fungsi
dari bagian eksresi baik atau tidak.
Cara melakukan uji anel :
Lebarkan pungtum lakrimal dengan dilator pungtum
Isi spuit dengan larutan garam fisiologis. Gunakan jarum lurus atau
bengkok tetapi tidak tajam
Masukkan jarum ke dalam pungtum lakrimal dan suntikkan cairan
melalui pungtum lakrimal ke dalam saluran eksresi , ke rongga hidung
Uji anel (+): terasa asin di tenggorok atau ada cairan yang masuk
hidung. Uji anel (-) jika tidak terasa asinberarti ada kelainan di
dalam saluran eksresi.
Jika cairan keluar dari pungtum lakrimal superior, berarti ada
obstruksi di duktus nasolakrimalis. Jika cairan keluar lagi melalui
pungtum lakrimal inferior berarti obstruksi terdapat di ujung nasal
kanalikuli lakrimal inferior, maka coba lakukan uji anel pungtum
lakrimal superior.
74. Penatalaksanaan Astigmatisme

Terapi astigmatisme meliputi penggunaan
kacamata, lensa kontak atau pembedahan
refraktif
Peresepan kacamata untuk astigmatisme, bila
didapatkan rumus S 0.75 C- 0.5 axis 180 :
Lensa spheris yang dibutuhkan untuk mengoreksi
myopia adalah 0,75
Koreksi total untuk silindris yang dibutuhkan
adalah (-0,75 + -0,5 - 1,25 )
75. Komplikasi Uveitis

Anterior uveitis iritis, iridocyclitis
Bentuk uveitis terbanyak
Gejala klinis : nyeri, fotofobia, mata merah, blurred vision
Injeksi siliar, injeksi kornea, keratic precipitates (sel-sel radang di
permukaan endotel, ukuran besar disebut mutton fat), flare (protein
di bilik mata depan)
Penyulit : sinekia posterior dan sinekia anterior perifer glaukoma
sekunder
Uveitis intermediate (cyclitis, peripheral uveitis, pars planitis)

Vitreous major site of inflammation
Gejala klinis : floaters, blurred vision, nyeri, fotofobia, mata merah
Pd pemeriksaan: vitritis snowballs, snowbanking
Posterior uveitis meliputi retinitis, choroiditis, retinal vasculitis,

papillitis
Gejala klinis : floaters, scotoma, decreased vision
Sumber: General opthalmology. Vaughan, et al. 17th ed
Keratic Presipitates
76. Pemeriksaan ketajaman

penglihatan
6/60 penderita hanya bisa membaca dari jarak
6 meter sedangkan orang normal dapat membaca
dari jarak 60 m
Pemeriksaan dengan kartu snellen gagal
membaca huruf terbesar sampai terkecil hitung
jari1/60
Lambaian tangan1/300
Sinar senter1/tak terhingga
Bila tidak dapat melihat sinar maka dikatakan
tajam penglihatan 0
77. Klasifikasi MIOPIA

Miopia secara klinis :
Simpleks: kelainan fundus ringan, < -6D
Patologis: Disebut juga sebagai miopia degeneratif, miopia maligna atau
miopia progresif, adanya progresifitas kelainan fundus yang khas pada
pemeriksaan oftalmoskopik, > -6D
Miopia berdasarkan ukuran dioptri lensa :

Ringan (levior): lensa koreksinya 0,25 s/d 3,00 Dioptri
Sedang (moderate) : lensa koreksinya 3,25 s/d 6,00 Dioptri.
Berat (gravior): lensa koreksinya > 6,00 Dioptri.
Miopia berdasarkan umur :
Kongenital : sejak lahir dan menetap pada masa anak-anak.

Miopia onset anak-anak : di bawah umur 20 tahun.
Miopia onset awal dewasa : di antara umur 20 sampai 40 thn.
Miopia onset dewasa : di atas umur 40 tahun (> 40 tahun).
78. Entropion
Merupakan pelipatan palpebra ke arah dalam
Penyebab: infeksi (ditandai dengan adanya jaringan
parut), faktor usia, kongenital
Enteropion involusional
yang paling sering dan terjadi akibat proses penuaan
Mengenai palpebra inferior, karena kelemahan otot
palpebra
Enteropion sikatrikal
Mengenai palpebral inferior/ superior
Akibat jaringan parut tarsal
Biasanya akibat peradangan kronik seperti trakoma
Pada enteropion bisa disertai dengan trikiasis
ILMU KESEHATAN ANAK
79. Tatalaksana Demam Tifoid
Tatalaksana Demam Tifoid
80.
Derajat
Serangan
Asma
Alur
Penatalaksanaan
Serangan Asma
81. Diarrheagenic Escherichia coli

Noninflammatory Diarrheas
Enterotoxigenic E. coli (ETEC)
Rapid onset of watery, nonbloody diarrhea of considerable

volume, accompanied by little or no fever. Diarrhea and
other symptoms cease spontaneously after 24 to 72 hours
Inflammatory Diarrheas
Enteroinvasive E. coli (EIEC)
Present most commonly as watery diarrhea. Minority of

patients experience a dysentery syndrome, with fever,
systemic toxicity, crampy abdominal pain, tenesmus, and
urgency
Enteropathogenic E. coli (EPEC)
Profuse watery, nonbloody diarrhea with mucus, vomiting

and low-grade fever. Chronic diarrhea and malnutrition can
occur. Usually at < 2 y.o, esp <6 mo (at weaning period)
Shigatoxin-producing E. coli
(STEC)/EHEC
Symptoms ranging from mild diarrhea to severe

hemorrhagic colitis and hemolytic-uremic syndrome in all
ages
Enteroaggregative E. coli (EAggEC)
Watery, mucoid, secretory diarrhea with low-grade fever

and little or no vomiting. One third of patients have grossly
bloody stools. The watery diarrhea usually persist 14 days
Diarrheagenic Escherichia coli
Diarrheagenic Escherichia coli

E. coli species are members of the Enterobacteriaceae
family.
Characteristic: oxidase-positive, facultatively anaerobic,
gram-negative bacilli. Fermentation of lactose(+).
Pada soal, pasien berusia 1 tahun dengan keluhan BAB
tanpa darah kemungkinan ETEC atau EPEC
ETEC dan EPEC sama-sama menyebabkan infantile diarrhea,
ETEC pada anak >1 tahun, EPEC pada anak < 2 tahun
(terutama usia 6 bulan)
ETEC banyak pada daerah yang endemis terutama di
daerah tropis
Oleh karena itu, penyebab diare pada soal lebih condong
pada ETEC
Behrman: Nelson Textbook of Pediatrics, 17th ed
82-83. Gagal Ginjal Akut

Gagal ginjal akut (GGA) ialah penurunan fungsi ginjal mendadak
yang mengakibatkan hilangnya kemampuan ginjal untuk
mempertahankan homeostasis
Terdapat peningkatan kadar kreatinin darah secara progresif 0,5
mg/dL per hari dan peningkatan ureum sekitar 10-20 mg/dL per
hari.
GGA dapat bersifat oligurik dan non-oligurik.
Oliguria ialah produksi urin <1 ml/kgBB/ jam untuk neonatus dan <0,8
ml/kgBB/jam untuk bayi dan anak.
Jenis GGA
GGA prarenal: dehidrasi, syok, perdarahan, gagal jantung, sepsis
GGA renal: pielonefritis, glomerulonefritis, nefrotoksisitas karena obat
atau kemoterapi, lupus nefritis, nekrosis tubular akut, SHU, HSP
GGA pascarenal: keracunan jengkol, batu saluran kemih, obstruksi
saluran kemih, sindrom tumor lisis, buli-buli neurogenik
Tatalaksana Medikamentosa GGA

Terapi sesuai penyakit primer
Bila terdapat infeksi, dosis
antibiotik disesuaikan dengan
beratnya penurunan fungsi
ginjal
Pemberian cairan disesuaikan
dengan keadaan hidrasi
Koreksi gangguan
ketidakseimbangan cairan
elektrolit
Natrium bikarbonat untuk
mengatasi asidosis metabolik
sebanyak 1-2 mEq/kgBB/ hari
sesuai dengan beratnya
asidosis
Pemberian diuretik pada GGA

renal dengan furosemid 1-2
mg/kgBB dua kali sehari dan
dapat dinaikkan secara
bertahap sampai maksimum
10 mg/kgBB/kali. (pastikan
kecukupan sirkulasi dan bukan
merupakan GGA pascarenal).
Bila gagal dengan
medikamentosa, maka
dilakukan dialisis peritoneal
atau hemodialisis.
Pada soal, pasien mengalami
GGA prerenal, sehingga
pemberian furosemide
tidaklah tepat. Pilihan jawaban
jatuh pada hemodialisa
84. Urinalisis
Makroskopik
Kimia urin
Kekeruhan: clear, slightly cloudy, cloudy,

or turbid
Warna & konsentrasi: tidak berwarna,
kuning, kuning gelap, merah
Mikroskopik
Eritrosit
Leukosit
Epitel
Bakteri
Silinder
Kristal
Specific gravity (1.002-1.035)

pH
Protein (N: negatif)
Glucose (N: negatif)
Ketones (N: Negatif)
Blood/ hemoglobin
Leukocyte esterase: enzim yang
terdapat di dalam leukosit,
biasanya tidak terdeteksi. Jika
terdeteksi terdapat kemungkinan
ISK
Nitrite: bakteri mengubah nitrat
menjadi nitrit. Jadi, hasil positif
mengindikasikan ISK
Bilirubin (N: negatif)
Urobilinogen
85. Antibiotika untuk ISK pada Anak
86. Pemeriksaan Penunjang ISK

Urinalisis: ditemukan proteinuria, leukosituria
(>5/LPB), hematuria (>5/LPB)
Diagnosis pasti: ditemukannya bakteriuria
bermakna pada kultur urin, yang jumlahnya
tergantung dari metode pengambilan sampel
urin.
Fungsi ginjal ureum & kreatinin
Pemeriksaan penunjang lainnya:
USG, foto polos abdomen, miksio-sisto-ureterogram,
dan pielografi intravena
Interpretasi Hasil Biakan Urin
87. Tetralogi Fallot

Sianotik: R-L
shunt
Pulmonary
stenosis, VSD,
overriding
aorta, RVH.
Boot like heart
pada radiografi
Cyanotic spell/
tets spell
(serangan
sianosis yg
dikompensasi
dengan
berjongkok
lutut ditekuk)
Tet Spell/ Hypercyanotic Spell

Serangan biru yang terjadi
secara mendadak
Anak tampak lebih biru,
pernapasan cepat, gelisah,
kesadaran menurun, kadangkadang disertai kejang.
Biasanya muncul usia 6-12
bulan, tapi bisa muncul usia 24 bulan
Tingkat sianosis dan terjadinya
tet spell ditentukan dari
systemic vascular resistance
dan derajat keparahan
komponen stenosis pulmonal.
PPM IDAI Jilid I
Tatalaksana
Knee chest position/ squatting

Diharapkan aliran darah paru
bertambah karena peningkatan
resistensi vaskular sistemik dan
afterload aorta akibat penekukan
arteri femoralis
Morfin sulfat 0,1-0,2 mg/kgBB SC,

IM, atau IV untuk menekan pusat
pernapasan dan mengatasi
takipnea
Natrium bikarbonat 1 mEq/kgBB
IV untuk mengatasi asidosis.
Dosis yang sama dapat diulang
dalam 10-15 menit.
Pelepasan
katekolamine
takikardia
increased
myocardial
contractility +
infundibular
stenosis.
VICIOUS
CYCLE
menangis, BAB, demam,

aktivitas yg meningkat
aliran balik vena sistemik meningkat shg resistensi

vaskular pulmonal meningkat (afterload pulmonal
meningkat) + resistensi vaskular sistemik rendah
KEMATIAN
Right-to-left shunt meningkat
aliran darah ke
paru berkurang
secara tiba-tiba
TET SPELL
HYPERCYANOTIC SPELL
sianosis progresif
penurunan PO2 dan
peningkatan PCO2 arteri
penurunan pH darah
Stimulasi pusat pernapasan di

reseptor karotis + nucleus
batang otak
hiperpnoea
88. Hepatitis Viral Akut
Hepatitis viral: Suatu proses

peradangan pada hati atau
kerusakan dan nekrosis sel
hepatosit akibat virus hepatotropik.
Dapat akut/kronik. Kronik jika
berlangsung lebih dari 6 bulan
Perjalanan klasik hepatitis virus
akut
Stadium prodromal: flu like
syndrome,
Stadium ikterik: gejala-gejala pada
stadium prodromal berkurang
disertai munculnya ikterus, urin
kuning tua
Anamnesis Hepatitis A :
Manifestasi hepatitis A: Anak
dicurigai menderita hepatitis A jika
ada gejala sistemik yang
berhubungan dengan saluran cerna
(malaise, nausea, emesis, anorexia,
rasa tidak nyaman pada perut) dan
ditemukan faktor risiko misalnya
pada keadaan adanya outbreak atau
diketahui sumber penularan.
Hepatitis A
Virus RNA (Picornavirus)
ukuran 27 nm
Kebanyakan kasus pada usia
<5 tahun asimtomatik atau
gejala nonspesifik
Rute penyebaran: fekal oral;
transmisi dari orang-orang
dengan memakan makanan
atau minumanterkontaminasi,
kontak langsung.
Inkubasi: 2-6 minggu (rata-rata
28 hari)
Pedoman Pelayanan Medis IDAI
Behrman RE. Nelsons textbook of pediatrics, 19th ed. McGraw-Hill; 2011.
Serologi
Hepatitis
Depending on its form, cyanide may

cause toxicity through parenteral
administration, inhalation, ingestion,
or dermal absorption
Source:
the vasodilator drug nitroprusside,
natural sources are found in pits,
seeds, bark, and leaves of apricots,
plums, peaches, cherries, almonds,
and apples (containing amygdalin, a
cyanide-producing glycoside, is
hydrolyzed to hydrocyanic acid by
chewing)
cassava (Manihot esculenta)
Mechanism of toxicity:
Cyanide binds to cellular cytochrome
oxidase blocking the aerobic
utilization of oxygen.
Symptoms arise within 15 30

minutes:
Disruption of cellular respiration:
Respiratory depression, coma, death.
Bitter almond smell to breath.
Toxic effects respond to Cyanide
Antidote Kit.
headache, nausea, dyspnea, &
confusion.
Syncope, seizures, coma, agonal
respirations, & cardiovascular
collapse ensue rapidly after heavy
exposure.
Cherry-red skin color

Poisoning & drug overdose by the faculty, staff and associates of the California Poison Control System third edition
Cyanide Intoxication: Treatment

A. Emergency and supportive measures. Treat all cyanide
exposures as potentially lethal.
1.
2.
3.
Maintain an open airway and assist ventilation if necessary.

Treat coma, hypotension, & seizures if they occur.
Start an IV line and monitor the patients vital signs and ECG
B. Specific drugs and antidotes

Hydroxocobalamin: Combines with cyanide to form cyanocobalamin (vitamin B-12),
which is renally cleared
Sodium nitrites: Induce cyanide-scavenging methemoglobinemia in red blood cells,
(combines with cyanide, thus releasing cytochrome oxidase enzyme)
Sodium thiosulfate: Enhances the conversion of cyanide to thiocyanate , which is renally
excreted
Administer sodium bicarbonate in severe poisoning because of marked lactic acidosis
C. Prehospital
Immediately administer activated charcoal if available. Do not induce vomiting unless
victim is more than 20 minutes from a medical facility and charcoal is not available.
90. Cerebral Palsy
Cerebral palsy (CP) describes a group of

permanent disorders of the development of
movement and posture, causing activity
limitation, that are attributed to non-progressive
disturbances that occurred in the developing
fetal or infant brain.
The motor disorders of cerebral palsy are often
accompanied by disturbances of sensation,
perception, cognition, communication, and
behaviour, by epilepsy, and by secondary
musculoskeletal problems. (Rosenbaum et al,
2007 )
91. Infeksi Hepatitis Perinatal

Pada ibu dengan pengidap
hepatitis B, hanya 5-10% bayi
yang bermanifestasi sebagai
hepatitis akut.
Penularan hepatitis B perinatal
umumnya di negara endemik
dan sangat terkait dengan ibu
yang memiliki HBeAg yang
positif.
Antigen dapat melintasi
plasenta barrier, tetapi hampir
semua infeksi perinatal terjadi
saat persalinan.
Risiko infeksi kronik dari ibu

HBeAg positif terhadap
bayinya sebesar 85% hingga
90%, sebaliknya pada ibu
dengan HBeAg negatif hanya
5% hingga 31%.6
Kombinasi imunisasi aktif dan
pasif, yaitu 1 dosis HBIg
(sebelum usia 24 jam)
dilanjutkan dengan 3-4 dosis
vaksin, memberikan efektifitas
95% pada bayi-bayi risiko
tinggi.
Perjalanan Infeksi Hepatitis B
Vaksin HepB pada Bayi Baru lahir
92. Diabetic Ketoacidosis

Diagnostic criteria*
Blood glucose: > 250 mg per dL
(13.9 mmol per L)
pH: <7.3
Serum bicarbonate: < 15 mEq/L
Urinary ketone: 3+
Serum ketone: positive at 1:2
dilutions
Serum osmolality: variable
Typical deficits
Water: 6 L, or 100 mL per kg
body weight
Sodium: 7 to 10 mEq per kg body
weight
Potassium: 3 to 5 mEq per kg
body weight
Phosphate: ~1.0 mmol per kg
body weight
*Not all patients will meet all diagnostic criteria,

depending on hydration status, previous
administration of diabetes treatment and other
factors.
Adapted with permission from Ennis ED, Stahl EJ, Kreisberg RA. Diabetic
ketoacidosis. In: Porte D Jr, Sherwin RS, eds. Ellenberg and Rifkin's Diabetes
mellitus. 5th ed. Stamford, Conn.: Appleton & Lange, 1997;82744.
CLASSIC TRIAD OF DKA
IV Fluid Key Points

Start IV fluids: 10-20 ml/kg of 0.9%NS over the first hour
In a severely dehydrated patient, this may need to be repeated
Fluids should not exceed 50 ml/kg over first 4 hours of therapy
Clinical assessment of dehydration to determine fluid volume
Children with DKA have a fluid deficit in the range of 5-10%
Mild DKA 3-4% dehydration
Moderate DKA 5-7% dehydration
Severe DKA 10% dehydration
Shock is rare in pediatric DKA

Replace fluid deficit evenly over 48 hours
ALL PATIENTS WITH DKA REQUIRE SUPPLEMENTAL FLUIDS

50
until SQ insulin
initiated
the ph >7.30 and/or the HCO3 >15 mEq/L an

serum ketones have cleared
Insulin Administration
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American Diabetes Association. Hyperglycemic crises in
diabetes.treatment
Diabetes Care. 2004;27(Suppl.
1):S94-S102
Insulin
is begun
after the initial fluid resuscitation
INSULIN
IV insulin infusion
regular insulin
0.1 units/kg/hr
Continue until acidosis

clears
(pH >7.30, HC03 >15 mEq/L)
Insulin therapy
Turns off the production of ketones
Decreases blood glucose
Low-dose insulin infusion

Decreases risk of hypoglycemia or
hypokalemia
Goal is to decrease blood glucose by
100mg/dL/hour
Insulin Key Points
Do not reduce or discontinue the insulin infusion

based solely upon the blood glucose
Prior to insulin administration, reassess vital signs, blood glucose
Decrease to
Thestatus
insulin infusion should be continued until
and neurological
0.05 units/kg/hr
the ph >7.30 and/or the HCO3 >15 mEq/L and the
until SQ insulin
serum ketones have cleared
initiated
Insulin is administered as a continuous intravenous infusion of

regular insulin at a rate of 0.1 units/kg per hour (prepared
by
51
pharmacy)
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American Diabetes Association. Hyperglycemic crises in
diabetes. Diabetes Care. 2004;27(Suppl. 1):S94-S102
Do not give insulin as a bolus
Potassium Administration
initial serum potassium is <2.5 mmol/L (hypokalemia)
Administer 0.5-1 mEq/kg of potassium chloride in IV
Start potassium replacement early, even before starting insulin therapy
Initial serum potassium is 2.5 - 3.5 mmol/L

Administer potassium 40 mEq/L in
IV solution until serum potassium > 3.5 mmol/L
Monitor serum potassium hourly
Administer potassium 30 40 mEq/L in IV solution to maintain serum potassium
at 3.5 5.0 mmol/L
initial serum potassium is 3.5 - 5.0 mmol/L

Administer potassium 30 40 mEq/L in IV solution to maintain serum potassium
at 3.5 5.0 mmol/L
Monitor serum potassium hourly
Dextrose Administration
Dextrose
Add to IV fluids when the blood glucose

concentration reaches 250 mg/dL
Change to 5% dextrose with 0.45 NaCl at a

rate to complete rehydration in 48 hr
Check glucose hourly and electrolytes every

2-4 hr until stable
After resolution of DKA, initiate SQ insulin

0.5 1.0 units/kg/day (or according to insulin
dosing guidelines per institution or physician
policy)
Maintain glucose between

150 to 250 mg/dL to
prevent hypoglycemia
Check glucose hourly until
stable
Check electrolytes every 24 hrs until stable
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American
Diabetes Association. Hyperglycemic crises in diabetes.
Diabetes Care. 2004;27(Suppl. 1):S94-S102
61
Bicarbonate
Bicarbonate therapy is generally
contraindicated in Pediatric DKA due to
increased risk of cerebral edema.
Bicarbonate therapy should only be
considered in cases of:
Severe acidemia
Life-threatening hyperkalemia
Pediatric Hyperglycemia and Diabetic Ketoacidosis (DKA). EMSC Illinois
93. Trauma Lahir Ekstrakranial:

Hematom Sefal
Perdarahan sub periosteal akibat
ruptur pembuluh darah antara
tengkorak dan periosteum
Benturan kepala janin dengan pelvis
Paling umum terlihat di parietal
tetapi kadang-kadang terjadi pada
tulang oksipital
Ukurannya bertambah sejalan
dengan bertambahnya waktu
5-18% berhubungan dengan fraktur
tengkorak (foto kepala)
Umumnya menghilang dalam waktu 2 8

minggu
Komplikasi: ikterus, anemia
Kalsifikasi mungkin bertahan selama > 1
tahun.
Tatalaksana:
Observasi pada kasus tanpa komplikasi
Transfusi jika ada indikasi
Fototerapi (tergantung dari kadar
bilirubin total)
94. Kelainan Radiologis pada Paru

Pneumonia lobaris
Characteristically, there is homogenous opacification in a lobar pattern. The

opacification can be sharply defined at the fissures, although more
commonly there is segmental consolidation. The non-opacified bronchus
within a consolidated lobe will result in the appearance of air
bronchograms.
Pneumonia
lobularis/
bronkopneumonia
associated with suppurative peribronchiolar inflammation and subsequent

patchy consolidation of one or more secondary lobules of a lung in
response to a bacterial pneumonia: multiple small nodular or
reticulonodular opacities which tend to be patchy and/or confluent.
Asthma
pulmonary hyperinflation Increased Bronchial wall markings (most

characteristic) Associated with thicker Bronchial wall, inflammation
Flattening of diaphragm (Associated with chronic inflammation or
Associated with accessory muscle use)
Hyperinflation (variably present)
Patchy infiltrates (variably present) from Atelectasis
bronkiolitis
Hyperexpansion (showed by diaphragm flattening), hyperluscent,

Peribronchial thickening, hilar prominence
Variable infiltrates or Viral Pneumonia
Acute bronchitis
Interstitial shadowing, signs of hyperinflation, hila prominence with hazy

outlines, hazy peribronchial markings
95-96. KLASIFIKASI DBD

Derajat (WHO 1997):
Derajat I : Demam dengan test rumple leed
positif.
Derajat II : Derajat I disertai dengan perdarahan
spontan dikulit atau perdarahan lain.
Derajat III : Ditemukan kegagalan sirkulasi, yaitu
nadi cepat dan lemah, tekanan nadi menurun/
hipotensi disertai dengan kulit dingin lembab dan
pasien menjadi gelisah.
Derajat IV : Syock berat dengan nadi yang tidak
teraba dan tekanan darah tidak dapat diukur.
WHO. SEARO. Guidelines for treatment of dengue fever/dengue hemorrhagic fever in

small hospitals. 1999.
97-99. Difteri
Penyebab : toksin Corynebacterium diphteriae
Organisme:
Basil batang gram positif
Pembesaran ireguler pada salah satu ujung (club shaped)
Setelah pembelahan sel, membentuk formasi seperti huruf cina
atau palisade
Gejala:
Gejala awal nyeri tenggorok
Bull-neck (bengkak pada leher)
Pseudomembran purulen berwarna putih keabuan di faring,
tonsil, uvula, palatum. Pseudomembran sulit dilepaskan. Jaringan
sekitarnya edema.
Edema dapat menyebabkan stridor dan penyumbatan sal.napas
Todar K. Diphtheria. http://textbookofbacteriology.net/diphtheria.html
Demirci CS. Pediatric diphtheria. http://emedicine.medscape.com/article/963334-overview
http://4.bp.blogspot.com/
Pemeriksaan : Pemeriksaan Gram & Kultur; sediaan berasal dari

swab tenggorok, jika bisa diambil dibawah selaput pseudomembran
Obat:
Antitoksin: 40.000 Unit ADS IM/IV, skin test
Anbiotik: Penisillin prokain 50.000 Unit/kgBB IM per hari selama 7 hari
atau eritromisin 25-50 kgBB dibagi 3 dosis selama 14 hari
Hindari oksigen kecuali jika terjadi obstruksi saluran repirasi
(Pemberian oksigen dengan nasal prongs dapat membuat anak tidak
nyaman dan mencetuskan obstruksi)
oksigen harus diberikan, jika mulai terjadi obstruksi saluran
respiratorik dan perlu dipertimbangkan tindakan trakeostomi.
Jika anak demam ( 390 C) beri parasetamol.
Jika sulit menelan, beri makanan melalui pipa nasogastrik.
Indikasi krikotirotomi/ trakeostomi/intubasi : Terdapat tanda tarikan
dinding dada bagian bawah ke dalam yang berat
Belum terdapat persamaan pendapat mengenai kegunaan obat ini
pada difteria.
Dianjurkan korikosteroid diberikan kepada kasus difteria yang disertai dengan
gejala obstruksi saluran nafas bagian atas (dapat disertai atau tidak bullneck)
dan bila terdapat penyulit miokarditis.
Pemberian kortikosteroid untuk mencegah miokarditis ternyata tidak terbukti.
Dosis : Prednison 1,0-1,5 mg/kgBB/hari, p.o. tiap 6-8 jam pada kasus berat
selama 14 hari.
Pelayanan Kesehatan Anak di Rumah Sakit. WHO.
100. Poliomyelitis
Poliomyelitis is an enteroviral
infection
Poliovirus is an RNA virus that is
transmitted through the oralfecal route or by ingestion of
contaminated water
The viral replicate in the
nasopharynx and GI tract
invade lymphoid tissues
hematologic spread viremia
neurotropic and produces
destruction of the motor neurons
in the anterior horn
Poliomyelitis:
90-95% of all infection remain
asymptomatic
5-10% abortive type:
Fever
Headache, sore throat
Limb pain, lethargy
GI disturbance
1-2% major poliomyelitis:
Meningitis syndrome
Flaccid paresis with asymmetrical
proximal weakness & areflexia,
mainly in lower limbs
Paresthesia without sensory loss or
autonomic dysfunction
Muscle atrophy
Pemeriksaan penunjang
Darah:
Leukosit normal/sedikit meningkat

Serum antibodi akut dan konvalesens
Peningkatan titer IgG 4x lipat atau titer anti-IgM (+) pada stadium akut
PCR
LCS:
20-300 sel, predominan limfosit (lymphocytic pleocytosis), glukosa normal,
protein normal/sedikit meningkat
PCR
Kultur:
Dilakukan pemeriksaan kultur virus dari fese dan apus tenggorok, pada pasien
tersangka infeksi poliomyelitis (pasien AFP)
Histologi:
Ag spesifik enterovirus dilakukan imumofluresens dan pemeriksaan RNA
melalui PCR
Tata Laksana
Tidak ada antivirus untuk terapi infeksi oleh virus polio
Suportif
Pemberian antipiretik/analgetik bila terdapat keluhan demam, nyeri kepala,
atau nyeri otot
Ventilasi mekanik seringkali diperlukan pada pasien paralisis bulbar
Trakeostomi dilakukan pada pasien yang membutuhkan dukungan ventilasi
mekanik jangka panjang
Rehabilitasi medis diperlukan pada kondisi paralisis untuk mencegah
terjadinya dekubitus, pneumonia akibat berbaring lama, serta latihan aktif
serta pasif untuk mencegah kontraktur
Konstipasi diatasi dengan pemberian laksatif dan pemasangan kateter urin
Terapi hipertensi bila terjadi ensefalopati hipertensif
Bedah : Diperlukan bantuan bedah ortopedi bila terjadi sekuele yang

mengakibatkan displasia atau kontraktur
Diet
Keseimbangan cairan dan elektrolit sangat diperlukan, bilamana
memungkinkan diet tinggi serat untuk mencegah konstipasi
Hindari terjadinya aspirasi
Pencegahan: Vaksin Polio yaitu inactivated poliovirus vaccine (IPV) dan

oral attenuated poliovirus vaccine (OPV).

Pembahasan Seminar Part I No. 1-100

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Seminar Optima Preparation

Batch Mei 2015

dr. Widya, dr. Eno, dr. Yolina

ILMU PENYAKIT DALAM

Multiplication can cause:

Two days without fever follow.

Icteric leptospirosis or Weil's

Medical management of RA involves five general approaches:

A fifth group of agents are the immunosuppressive &cytotoxic drugs, including

ISI: international sensitivity index

MNPT: mean normal PT laboratory

10. Polycythemia Vera

B1 Platelet count > 400 x 109/l

10. Polycythemia Vera

Diare; nyeri abdomen kuadran kanan bawah, sering timbul setelah

Diare, dengan atau tanpa darah. Jika inflamasi terdapat di rektum

Diare akut dengan BAB berdarah, tenesmus, demam.

Nyeri perut hilang dengan defekasi, hilang timbul, terkait stres,

Side effectsof organic nitrates: orthostatic hypotension, tachycardia,

Nifedipine side effects: hypotension, dizziness, flushing,

13. GI Tract Disease

13. GI Tract Disease

epigastric or right upper quadrant abdominal pain lasting

Gallstone lodged in the common bile duct. Symptom: biliary

Mostly caused by gallstones & alcohol abuse. Symptom: acute

Chronic alcohol abuse is the most common cause. Symptom:

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

14. Penyakit Endokrin

14. Penyakit Endokrin

Sekresi autoantibodi TgAb, TPOAb, TSHRab[block/inhibisi]

Destruksi parenkim tiroid tiroksin

TSH hipertrofi parenkim, destruksi tetap ada

Eutiroid hipotiroid subklinis hipotiroid

15. Infeksi Saluran Kemih

Symptoms of cystitis may not be present. Fever is the main

16. Angina Pektoris

17. Anemia Makrositik

Modern Nutrition in Health & Disease.

17. Anaemia Makrositik

18. Cyanide Intoxication

18. Cyanide Intoxication

20. Gagal Jantung

21. Toksisitas Statin

Rarely, patients may have marked elevations in CK activity, often

22. Leukemia Granulositik Kronik

Chromosomal studies of peripheral blood and marrow are important, primarily to

4. Primary polydipsia (psychogenic), in which the initiating

During the dehydration or water deprivation test:

After the patient is given desmopressin:

Harrisons principles of internal medicine. 18th ed.

The prodromal symptoms

The clinical jaundice

27. Heart Failure

Lilly LS. Pathophysiology of heart disease. 5th ed. LWW; 2011.

29. Dengue Hemorrhagic Fever

Lilly LS. Pathophysiology of heart disease. 5th ed. LWW; 2011.

31 & 32. Leukemia

Symptoms & Grow slowly may asymptomatic,

Grow quickly feel sick & go to

Fever, swollen lymph nodes, frequent infection, weak,

Can be delayed if asymptomatic

Calcium ion facilitates the toxic actions of cardiac glycosides by

The effects of magnesium ion appear to be opposite to those of calcium.

Gejala respiratori: batuk 2 minggu, batuk darah,