Pembahasan Seminar Part I No. 1-100

8/16/2019 Pembahasan Seminar Part I No. 1-100

1/189

Seminar Optima Preparation

Batch Mei 2015

Part I

No. 1-100

Office Address:

Jl Padang no 5, Manggarai, Setiabudi, JakartaSelatan(Belakang Pasaraya Manggarai)Phone Number : 021 8317064

Pin BB 2A8E2925WA 081380385694

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

www.optimaprep.com

dr. Widya, dr. Eno, dr. Yolina

dr. Cemara, dr. Yusuf

dr. Reza


2/189

ILMU PENYAKIT DALAM


3/189

1. Infeksi

Infection through themucosa or wounded skin

Proliferate in thebloodstream or

extracellularly within organ

Disseminatehematogenously 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 Harrison’s principles of internal medicine. 18th ed.


4/189

1. Infeksi•

Anicteric leptospirosis (90%),follows a biphasic course: – Initial phase (4 –7 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'sdisease (10%), monophasiccourse:

– Prominent features are renal andliver malfunction, hemorrhageand impaired consciousness,

– The combination of a directbilirubin < 20 mg/dL, a marked in CK, & ALT & AST


5/189

2 & 3.Infark Miokard


6/189


7/189

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 highrate of GI toxicity, a narrow window between toxic and anti-inflammatoryserum levels, and the inconvenience of multiple daily doses, aspirin’s 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the initial choice of drug therapy has largely been replaced by other NSAIDs• Glucocorticoid: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 withglucocorticoids, and then to taper these as the slower-acting DMARD begin towork.


8/189

4. Rheumatoid Arthritis• Medical management of RA involves five general approaches:

– The first is the use of NSAID & simple analgesics to control the symptoms andsigns 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 thedevelopment 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 agentsinclude 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 withT cell activation (abatacept).

– A fifth group of agents are the immunosuppressive &cytotoxic drugs, includingleflunomide, cyclosporine, azathioprine, and cyclophosphamide, amelioratethe disease process in some patients

Harrison’s principles of internal medicine. 18th ed.


9/189

5. GERD

•Barrett esophagus: – Komplikasi kronik GERD yang ditandai oleh metaplasia

intestinal di mukosa epitel gepeng esofagus.

Metaplasia Barrett dengan banyak

sel goblet


10/189

6. Endokrin

Thyroid Ophthalmopathy1. Vigouroux sign: eyelid fullness

2. Stellwag sign: incomplete and infrequent blinking

3. Grave sign: resistance to pulling down the retracted upper

lid4. 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


11/189

7. Endokrin


12/189

8. Anticoagulant Therapy


13/189


• ISI: international sensitivity index

– 1 is the best

• MNPT: mean normal PT laboratory


14/189

9. Unstable

Angina

• Recurrent

symptoms/ischemia,

• heart failure,

•serious arrhythmia.


15/189

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


16/189

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 > 220pg/ml

• Diagnosis – A1 + A2 + A3 establishes PV

– A1 + A2 + two of category B establishes PV


17/189

10. Polycythemia Vera

• Polycythemia vera (PV) develops slowly. The disease may not cause signs orsymptoms for years.

• When signs and symptoms are present, they're the result of the thick blood thatoccurs with PV. This thickness slows the flow of oxygen-rich blood to all parts ofyour 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 (anorgan 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 yourskin (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


18/189

11. Disentri

• Manifestasi klinis disentriamoeba: –

Awitan perlahan ataufulminan.

– Tenesmus terdapat pada50% pasien & selalu terkaitdengan keterlibatanrektosigmoid.

– Nyeri tekan abdomenbawah, biasanya di daerahcaecum, kolon transversumatau sigmoid.

• Trias disentri: demam, tenesmus, diare berdarah.


19/189

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. Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2012.


20/189

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


21/189

12. Angina

• Nifedipine side effects: hypotension, dizziness, flushing,

nausea, constipation, edema.


22/189

13. GI Tract Disease

Pancreatic cancer:

• Epidemiology: most common in 60 –79 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 (SisterMary Joseph's nodes).

• Diagnosis: – contrast-enhanced CT is the imaging modality of choice

– EUS-guided fine-needle aspiration is the technique of choice. If there’s anydoubt CT scan.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.


23/189

13. GI Tract DiseaseDiagnosis 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.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.


24/189

14. Penyakit Endokrin


25/189

14. Penyakit Endokrin

Limfosit tersensitisasi oleh antigen tiroid

Sekresi autoantibodi TgAb, TPOAb, TSH-Rab[block/inhibisi]

Infiltrasi limfosit folikel limfoid & germinal center

Destruksi parenkim tiroid tiroksin

TSH hipertrofi parenkim, destruksi tetap adastruma/tanpa struma end stage: atrofi

Eutiroid hipotiroid subklinis hipotiroid


26/189

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 mainfeature 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 alsoeffective if the uropathogen is known to be susceptible

Harrison’s principles of internal medicine. McGraw-Hill; 2011.


27/189

16. Angina Pektoris

• Nonpharmacology management:

– Oxygen (2 –4 L/min by mask or nasal prongs)should be administered to those who are

breathless or who have any features of heartfailure or shock.

– Bed rest, except for the patients who require theuse 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, 2909 –2945


28/189

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.


29/189

17. Anaemia MakrositikApakah terdapat hipersegmentasi netrofil atau

makroovalosit di GDT?

Ya Tidak

Anemia megaloblastik ;

Periksa vitamin B12 dan folat

Defisiensi

vitamin B12

Tidak

defisiensi

Defisiensi

folat

Uji Schilling:

membaik

dgn faktor

intrinsik

Ya Tidak

Anemia

pernisiosa,

Reseksi

gaster

Peny. Ileal, pembedahan

Pertumbuhan berlebihan

bakteri usus halus

Cacing pita

Malabsorpsi karena obat

Peny. Sintesis

DNA herediter Obat yang

mengganggu

DNA

•Diet kurang

•Malabsorpsi dipicu obat

•Reseksi jejunum

•Tropical sprue, sensiivitas

thd gluten.

•Peningkatan kebutuhan:

kehamilan, hemolisis kronik

Anemia

nonmegaloblastik

Retikulosit

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


30/189

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 ControlSystem third edition


31/189

18. Cyanide Intoxication

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 patient’s vital signs and ECG

B. Specific drugs and antidotes

1. The cyanide antidote package consists of amyl & sodium nitrites,which produce cyanide-scavenging methemoglobinemia, & sodiumthiosulfate, which accelerates the conversion of cyanide tothiocyanate.

C. Prehospital.

Immediately administer activated charcoal if available. Do notinduce vomiting unless victim is more than 20 minutes from a

medical facility and charcoal is not available.


32/189

19. EKG


33/189

19. EKG

• RVH – R > S di V1

– R di V1 ≥ 7 mm,

– Rasio R/S di sepanjangprekordium

• LVH – S di V1 + R di V5 atau V6

≥ 35 mm

–

R di aVL + S di V3 > 28mm pada laki-laki atau >20 mm pada perempuan

– R di aVL ≥ 11 mm


34/189

19. EKG


35/189

20. Gagal Jantung

ACC/AHA 2005 Guideline Update for the Diagnosis and Managementof 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 ventrikelkiri, ukuran ventrikel kiri, ketebalan dinding jantung, & fungsi katup.

• Arteriografi koroner untuk pasien dengan angina atau iskemia,kecuali pasien tidak memenuhi syarat untuk revaskularisasi.


36/189

21. Toksisitas Statin

• Elevations of serum aminotransferase activity (up to three timesnormal) occur in some patients.

• Therapy may be continued in such patients in the absence ofsymptoms if aminotransferase levels are monitored and stable.

• Minor increases in creatine kinase (CK) activity in plasma areobserved in some patients receiving reductase inhibitors, frequentlyassociated with heavy physical activity.

•Rarely, patients may have marked elevations in CK activity, oftenaccompanied by generalized discomfort or weakness in skeletalmuscles. If the drug is not discontinued, rhabdomyolysis may causemyoglobinuria, leading to renal injury.


37/189

22. Leukemia Granulositik Kronik•

The marrow aspirate and biopsy are essential to the diagnosis of themyeloproliferative disorders.

• The marrow aspirate provides information as to individual cell morphology and thedistribution of cell types. It also provides essential information in diagnosis andmanagement of patients with CML as they become increasingly dysplastic andevolve to acute leukemia.

• Chromosomal studies of peripheral blood and marrow are important, primarily todistinguish CML from the other myeloproliferative disorders


38/189

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 andcentral nervous system, manifested by severe mental retardation,short stature, coarse facial features, a protruding tongue, andumbilical hernia

– Myxedema

• Developing in the older child or adult

• Symptoms: generalized fatigue, apathy, cold intolerant,overweight, constipation, decreased sweating, shortness ofbreath, & decreased exercise capacity.


39/189

23. Endokrin

• Jod-basedow effect

– Hipertiroidisme yang diinduksi oleh pemberian

iodin pada pasien dengan struma multinodular,

penyakit Grave laten.


40/189

24. Polyuria

• If polyuria is shown to be dilute, pathophysiologicmechanisms include:1. Hypothalamic or central diabetes insipidus with inability

to synthesize and secrete vasopressin;

2. Nephrogenic diabetes insipidus with an inadequate renalresponse to vasopressin;

3. Transient diabetes insipidus of pregnancy produced by

accelerated metabolism of vasopressin;

4. Primary polydipsia (psychogenic), in which the initiatingevent is ingestion of excess fluid and the subsequenthypotonic polyuria is an appropriate physiologic response.


41/189

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 themaximum 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 ofdesmopressin.

Harrison’s principles of internal medicine. 18th ed.

Greenspan’s clinical endocrinology.


42/189

25. Dyspepsia

• Epigastric pain described as a burning or gnawingdiscomfort can be present in both DU and GU.

• Duodenal ulcer: –

The typical pain pattern occurs 90 minutes to 3 hours after ameal and is frequently relieved by antacids or food.

– Pain that awakes the patient from sleep (between midnight and3 A.M.) is the most discriminating symptom, with two-thirds ofDU patients describing this complaint. Unfortunately, thissymptom 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.

Harrison’s principles of internal medicine


43/189

26. Hepatitis

• Incubation periods for hepatitis A range from 15 –45 days (mean, 4 weeks), forhepatitis B and D from 30 –180 days (mean, 8 –12 weeks), for hepatitis C from 15 –160 days (mean, 7 weeks), and for hepatitis E from 14 –60 days (mean, 5 –6 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 1 –2 weeks. – Dark urine and clay-colored stools may be noticed by the patient from 1 –5 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 someliver enlargement and abnormalities in liver biochemical tests are still evident.


44/189

27. Heart Failure

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


45/189

28. Osteoartritis


46/189

28. Osteoartritis

• Since OA is a mechanically driven disease, the mainstay oftreatment involves altering loading across the painful jointand improving the function of joint protectors, so they canbetter 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 thatbridge 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 duringweight bearing with a cane or a crutch.


47/189

29. Dengue Hemorrhagic Fever


48/189


49/189

30. Kardiologi

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


50/189


51/189

31 & 32. LeukemiaCLL 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 Common in

children

Adults &

children

Symptoms &

Signs

Grow slowly may asymptomatic,

the disease is found during a

routine test.

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

Lymphoblas

t >20%

Myeloblast

>20%, aeur rod

may (+)

Therapy Can be delayed if asymptomatic Treated right away

CDC.gov


52/189

33. Pharmacology

Acetaminophen intoxication• Acute ingestion of more than 150 –200 mg/kg in children or 6 –7 g in

adults is potentially hepatotoxic.

• High-risk patients include alcoholics and patients takinganticonvulsant medications or isoniazid.

• Clinical manifestations: – Early after acute acetaminophen overdose, there are usually no

symptoms other than anorexia, nausea, or vomiting. Rarely, a massiveoverdose may cause altered mental status and metabolic acidosis.

– After 24 –48 hours, when transaminase levels (AST and ALT) rise,hepatic necrosis becomes evident. If acute fulminant hepatic failureoccurs, encephalopathy and death may ensue.


53/189

33. Pharmacology

Management• N-acetylcysteine

– loading dose 140 mg/kg orally. The effectiveness of NAC depends onearly treatment, before the metabolite accumulates; it is of maximalbenefit if started within 8 –10 hours

– If vomiting interferes with oral acetylcysteine administration, give it bygastric tube and use high-dose metoclopramide (1 –2 mg/kgintravenously (IV); or ondansetron, or give the NAC intravenously ifnecessary.

• Decontamination

1. Prehospital. Administer activated charcoal, if available.2. Hospital. Administer activated charcoal. Gastric emptying is notnecessary if charcoal can be given promptly. Do not administer charcoal ifmore than 3 –4 hours have passed since ingestion, unless delayedabsorption is suspected.


54/189

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 ofdigitalis.

• Calcium ion facilitates the toxic actions of cardiac glycosides byaccelerating the overloading of intracellular calcium stores that appears tobe 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 inpatients with digitalis-induced arrhythmias.


55/189

35. Tuberkulosis

Roentgen

PF

Gejala KlinisGejala respiratori: batuk ≥2 minggu, batuk darah,sesak napas, nyeri dada. Gejala sistemik: demam,

malaise, keringat malam, turun berat badan

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

Lesi aktif: Bayangan berawan/nodular di apeks & posteriorlobus 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.


56/189

36. Infeksi Aliran Darah


57/189

37. DM Complications


58/189

38. Autoimmune Disease

Robbins & Cotran pathologic basis of diseases. 2010.


59/189


60/189

39. Diabetes

• Exercise increases the effectiveness of insulin.

• Regular daily moderate exercise improve utilizationof fats & carbohydrates in patients with diabetes.

• Strenuous exercise, however, can precipitatehypoglycemia in an unprepared patient, & patientswith diabetes must therefore be taught to reduce theirinsulin dosage or take supplemental carbohydrate inanticipation of strenuous activity.


61/189

40. Diabetes

41 Avian Influenza


62/189

41. Avian Influenza

(WHO case definition)

Suspected H5N1 case• A person presenting with unexplained acute lower respiratory illness with fever

(>38 ºC ) 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 environmentscontaminated by their faeces in an area where H5N1 infections in animals orhumans have been suspected or confirmed in the last month;

c. Consumption of raw or undercooked poultry products in an area where H5N1infections 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 alaboratory or other setting.

41 Avian Influenza


63/189

41. Avian Influenza


Probable H5N1 case• Probable definition 1:

A person meeting the criteria for a suspected case AND one of thefollowing additional criteria:

a. infiltrates or evidence of an acute pneumonia on chest radiograph

plus evidence of respiratory failure (hypoxemia, severe tachypnea)OR

b. positive laboratory confirmation of an influenza A infection butinsufficient laboratory evidence for H5N1 infection.

• Probable definition 2:

A person dying of an unexplained acute respiratory illness who isconsidered to be epidemiologically linked by time, place, andexposure to a probable or confirmed H5N1 case.

41 Avian Influenza


64/189

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 orinternational influenza laboratory whose H5N1 test results are acceptedby WHO as confirmatory:a. Isolation of an H5N1 virus;

b. Positive H5 PCR results from tests using two different PCR targets, e.g. primersspecific for influenza A and H5 HA;

c. A fourfold or greater rise in neutralization antibody titer for H5N1 based ontesting of an acute serum specimen (collected 7 days or less after symptomonset) and a convalescent serum specimen. The convalescent neutralizingantibody titer must also be 1:80 or higher;

d. A microneutralization antibody titer for H5N1 of 1:80 or greater in a singleserum specimen collected at day 14 or later after symptom onset and apositive result using a different serological assay, for example, a horse redblood cell haemagglutination inhibition titer of 1:160 or greater or an H5-specific western blot positive result.


65/189

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.


66/189

42. Pulmonologi

Current diagnosis & treatment in pulmonary medicine.


67/189

42. Pulmonologi

Murray & Nadel Textbook of pulmonary disease.


68/189

43. Penyakit Paru

Color atlas of pathophysiology. Thieme. 2003


69/189

43. Penyakit Paru

Peningkatan volume udara di paru

akibat obstruksi hipersonor


70/189

44. Tobacco Smoking

• Merokok meningkatkan risikoaterosklerosis & 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.


71/189

45. HIV


72/189

45. HIV

• Some treatment guidelines, particularly those in theUnited States, now recommend ART for all HIV-infectedpatients, 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 initiationguidelines is strongest for CD4 counts less than 200

cells/mm3 and weakens as the CD4 counts studiedincrease to greater than 500 cells/mm3.

Mandell Textbook of infectious disease. 2015.

46 Arthritis


73/189

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.

Swan neck deformity caused byHyperextension of the PIP joint with

fl i f th DIP j i t

Boutonnoere deformity caused byflexion of the PIP joint with

h t i f th DIP j i t


74/189

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.

flexion of the DIP joint .

Rheumatoid nodules &

olecranon bursitis.

hyperextension of the DIP joint.

Rheumatoid Arthritis


75/189



76/189


• The therapeutic range differs due to variation inthe laboratory methods used to determine aPTT.

•

The American College of Chest Physiciansconsensus conference has thereforerecommended dosage adjustments to atherapeutic range equivalent to heparin levels of

0.3 to 0.7 U per ml by anti –factor Xadeterminations, which correlates with aPTTvalues between 60 and 80 s.


77/189

48. TB-HIV

Management of tuberculosis & HIV coinfection. WHO.


78/189

49. Farmakologi

• Once-daily oseltamivir for 7 to 10 days is also effective forpostexposure prophylaxisin household contacts, including children,and when ill index cases receive concurrent treatment


79/189

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 setelahinhalasi bronkodilator (uji bronkodilator), atau setelah pemberianbronkodilator oral 10-14 hari, atau setelah pemberian kortikosteroid

(inhalasi/ oral) 2 minggu. – Menilai derajat berat asma

• Pemeriksaan arus puncak ekspirasi dengan spirometri atau peakexpiratory flow meter: – Reversibiliti, yaitu perbaikan nilai APE > 15% setelah inhalasi

bronkodilator (uji bronkodilator), atau bronkodilator oral 10-14 hari, ataurespons terapi kortikosteroid (inhalasi/oral) 2 minggu

– Variabilitas, menilai variasi diurnal APE yang dikenal dengan variabilitiAPE harian selama 1-2 minggu. Juga dapat digunakan menilai derajatasma.

PDPI. Asma: pedoman diagnosis & penatalaksanaan di Indonesia. 2004


80/189

ILMU PENYAKIT MATA

51. Tatalaksana Glaukoma Akut


81/189

•

Tujuan : merendahkan tekanan bola mata secepatnya kemudian bila tekanan normal danmata 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

T l k Gl k Ak


82/189

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 Asbury’s General Ophtalmology 17th ed. Ph iladephia: McGraw-Hill, 2007.

Tatalaksana Surgikal Glaukoma Akut


83/189

Tatalaksana Surgikal Glaukoma Akut

Sudut Tertutup

• Irodotomi: membuat lubang dengan laserpada 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, karenaserangan ulang bisa sewaktu-waktu terjadi

http://www.allaboutvision.com/conditions/glaucoma-surgery.htm

Tatalaksana surgikal glaukoma primer


84/189

Tatalaksana surgikal glaukoma primer

sudut terbuka

• Trabekuloplasti merupakan prosedur laseruntuk memodifikasi jaringan trabekula

sehingga meningkatkan aliran keluar aqueous

humour.

52 GLAUKOMA KONGENITAL


85/189

52. GLAUKOMA KONGENITAL

• 0,01% diantara 250.000penderita glaukoma

• 2/3 kasus pada Laki-laki dan2/3 kasus terjadi bilateral

•

50% manifestasi sejak lahir;70% terdiagnosis dlm 6 blnpertama; 80% terdiagnosisdalam 1 tahun pertama

• Klasifikasi menurut Schele:

– Glaukoma infantum: tampakwaktu lahir/ pd usia 1-3 thn

– Glaukoma juvenilis: terjadipada anak yang lebih besar

• Klasifikasi lainnya: – Glaukoma kongenital primer

anomali perkembangan yangmempengaruhi trabecularmeshwork.

–

Glaukoma kongenitalsekunder: kelainan kongenitalmata dan sistemik lainnya,kelainan sekunder akibattrauma, inflamasi, dan tumor.

Buku ilmu penyakit mata Nana Wijaya & Oftalmologi umum Vaugahn & Asbury

P t i


86/189

Patogenesis

Abnormalitas anatomi trabeluar meshwork penumpukancairan 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) korneamenipis sehingga kurvatura kornea berkurang

Ketika mata tidak dapat lagi meregang bisa terjadi

penggaungan dan atrofi papil saraf optik


G j l & Di i


87/189

Gejala & Diagnosis

• Tanda dini: fotofobia,epifora, dan blefarospasme

• Terjadi pengeruhan kornea

• Penambahan diameter

kornea (megalokornea;diameter ≥ 13 mm)

• Penambahan diameter bolamata (buphtalmos/ ox eye)

• Peningkatan tekanan

intraokuler

• Diagnosis glaukomakongenital tahap lanjutdengan mendapati:

– Megalokornea

– Robekan membran

descement – Pengeruhan difus kornea


T t l k


88/189

Tatalaksana

• Medikamentosa hinggaTIO normal

– Acetazolamide

– pilokarpin

• Operasi: – Goniotomi (memotong

jaringan yg menutup

trabekula atau memotong

iris yg berinsersi padatrabekula

– Goniopuncture: membuat

fistula antara bilik depan

dan jaringan

subkonjungtiva (dilakukanbila goniotomi tidak

berhasil)


53. Tatalaksana Glaukoma Akut


89/189

•

Tujuan : merendahkan tekanan bola mata secepatnya kemudian bila tekanan normal danmata 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)


T t l k Gl k Ak t


90/189

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 Asbury’s General Ophtalmology 17th ed. Ph iladephia: McGraw-Hill, 2007.

54. KONJUNGTIVITIS • Gejala & tanda:– Rasa gatal yang hebat dapat


91/189

VERNAL•

Nama lain: – spring catarrh

– seasonal conjunctivitis

– warm weather conjunctivitis

• Etiologi: reaksi hipersensitivitasbilateral (alergen sulit

diidentifikasi)• Epidemiologi:

– Dimulai pada masa prepubertal,bertahan selama 5-10 tahunsejak awitan

– Laki-laki > perempuan

–

Paling sering pada Afrika Sub-Sahara & Timur Tengah

– Temperate climate > warmclimate > cold climate (hampirtidak ada)

Vaughan & Asbury General Ophtalmology 17th

ed.

– Rasa gatal yang hebat, dapatdisertai fotofobia

– Sekret ropy

– Riwayat alergi pada RPD/RPK

– Tampilan seperti susu padakonjungtiva

– Gambaran cobblestone(papila raksasa berpermukaanrata pada konjungtiva tarsal)

– Tanda Maxwell-Lyons (sekretmenyerupai benang &pseudomembran fibrinosahalus pada tarsal atas, padapajanan thdp panas)

– Bercak Horner Trantas(bercak keputihan pada

limbus saat fase aktifpenyakit)

– Dapat terjadi ulkus korneasuperfisial

Tatalaksana


92/189

Tatalaksana

• Self-limiting

• Akut:

• Steroid topikal (+sistemik

bila perlu), jangka

pendek mengurangigatal (waspada efek

samping: glaukoma,

katarak, dll.)

• Vasokonstriktor topikal• Kompres dingin & ice

pack

• Jangka panjang & prevensisekunder:

• Antihistamin topikal

• Stabilisator sel mast Sodiumkromolin 4%: sebagaipengganti steroid bila gejala

sudah dapat dikontrol

• Tidur di ruangan yang sejukdengan AC

• Siklosporin 2% topikal (kasusberat & tidak responsif)

• Desensitisasi thdp antigen(belum menunjukkan hasilbaik)

Vaughan & Asbury General Ophtalmology 17th

ed.

Table. Major Differentiating Factors Between VKC and AKC


93/189

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

are commonly seen.

Presence of Horner-Trantas

dots is rare.

Conjunctiva Cobblestone appearance papillae

Corneal

neovascularization

Not present Deep corneal

neovascularization tends todevelop

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


94/189

55. Diabetic Eye Disease

DM ophthalmic complications :

• Corneal abnormalities

• Glaucoma

•

Iris neovascularization• Cataracts

• Neuropathies

• Diabetic retinopathy→

most common andpotentially most blinding

•

Retinopathy and othermicrovascular complications ofdiabetes are multifactorial,attributed to chronichyperglycemia, vasculardamage and leakage, edema,capillary basement membranethickening, neovascularization,hemorrhage, and ischemia.

• It is an ocular manifestation ofsystemic disease which affectsup to 80% of all patients whohave had diabetes for 10 yearsor more.

RETINOPATI DIABETIK KLASIFIKASI


95/189

RETINOPATI DIABETIK - KLASIFIKASI

RETINOPATI DIABETIKNONPROLIFERATIF

• ditandai dengan kebocorandarah dan serum padapembuluh darah kapiler

• menyebabkan edema jaringanretina dan terbentuknyadeposit lipoprotein (hardexudates)

• Tidak menyebabkan gangguanpenglihatan mengenai

makula• Edema makula penebalan

daerah makula sebagai akibatkebocoran kapiler perifoveal

RETINOPATI DIABETIKPROLIFERATIF

• ditandai dengan adanyaproliferasi jaringan fibrovaskularatau neovaskularisasi padapermukaan retina & papil saraf

optik serta vitreus• Proliferasi respon dari oklusi

luas pembuluh darah kapilerretina yang menyebabkan iskemiaretina

• menyebabkan gangguan

penglihatan sampai kebutaanmelalui mekanisme; – Perdarahan vitreus

– Tractional retinal detachment

– Glaukoma neovaskular

RETINOPATI DIABETIK


96/189

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, flamehemorrhages, dot-blot

hemorrhages, hard exudates

Pemeriksaan :

• Tajam penglihatan

• Funduskopi dalam keadaanpupil dilatasi : direk/indirek

•Foto Fundus

• USG bila ada perdarahanvitreus

Tatalaksana :• Fotokoagulasi laser

• Bedah vitrektomi

56 Sildenafil


97/189

56. Sildenafil

• Used in the treatment of erectile dysfunction.• Ocular side-effects include a bluish tinge to the

visual field, hypersensitivity to light, and hazyvision.

• These effects are reversible and may last only afew minutes or hours.

• It has been reported that only 3% of patientshave visual side-effects with the standard 50

milligram dose.• With increased dosage, the ocular side-effect

incidence rate significantly increases.

57 ASTIGMATISME DEFINISI


98/189

57. ASTIGMATISME - DEFINISI

• Ketika cahaya yangmasuk ke dalam

mata secara paralel

tidak membentuk

satu titik fokus diretina.

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 Penentuan Jenis Astigmatisme


99/189

p p g

• Astigmatisma hipermetropikussimpleks, satu meridian utamanya

emetropik, meridian yang lainnyahipermetropik.

• Astigmatisma miopikus simpleks,satu meridian utamanya emetropik,meridian lainnya miopi

• Astigmatisma hipermetropikus

kompositus, kedua meridian utamahipermetropik dengan derajatberbeda.

• Astigmatisma miopikus kompositus,kedua meridian utamanya miopikdengan derajat berbeda

• Astigmatisma mikstus, satu

meridian utamanya hipermetropik,meridian yang lain miopik.

g

1. Sferis (-) silinder (-) pasti

miop kompositus2. Sferis (+) silinder (+) pasti

hipermetrop kompositus

3. Sferis (tidak ada) silinder (-)

pasti miop simpleks

4. Sferis (tidak ada) silinder (+)

pasti hipermetrop

simpleks

5. Untuk sferis dan silinder

yang saling berbedatandanya, mohon lihat

pembahasan TO2

58 KATARAK SENILIS



100/189

58. KATARAK-SENILIS

•

Katarak senilis adalah kekeruhan lensa yangterdapat 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 radiasicahaya matahari.

Gangguan metabolisme umum

•

4 stadium: insipien, imatur (In some patients, atthis stage, lens may become swollen due tocontinued hydration ‘intumescent cataract’),matur, hipermatur

• Gejala : distorsi penglihatan, penglihatankabur/seperti berkabut/berasap, mata tenang

• Penyulit : Glaukoma, uveitis

• Tatalaksana : operasi (ICCE/ECCE)

59 GERAK BOLA MATA


101/189

59. GERAK BOLA MATA

GERAK BOLA MATA


102/189

GERAK BOLA MATA

60 Uveitis


103/189

60. Uveitis

Anterior Intermediate Posterior Panuveitis

Fuchs’

heterochromic

uveitis

Sarcoidosis Toxoplasmosis Tuberculosis

PosnerSchlossman

syndrome

Tuberculosis Acute retinalnecrosis

Sarcoidosis

Infective uveitis Lyme’s disease Behcet’s disease

Arthritis

associated

uveitis

Vogt-Koyanagi-

Harada

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


104/189

Behcet’s Disease

• Chronic, relapsing, occlusive systemic vasculitis

• Etiology unknown

• Affects both anterior & posterior segment

• Type:

– Neuro BD

– Ocular BD

– Intestinal BD

– Vascular BD

Behçet disease


105/189

ç

• Uveitis Anterior/Media/Posterior (Panuveítis)

• HLA-B51+

Oral or genital sores

UveitisSkin lesions

Criteria for Behçet'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)


106/189

Vogt-Koyanagi-Harada Syndrome


107/189

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-syndrome2. 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


108/189

• Posterior uveitis with serous detachments

• Granulomatous bilateral uveitis

• Late: poliosis, Sigiura sign, sunset-glow fundus

1. Prodromus

2. Neurologic symptoms+ Bilateraluveitis

3. Late cutaneous symptoms


109/189

Posner- Schlossman syndrome


110/189

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 ofmild cyclitis and heterochromia.

• Its pathogenesis still remainsunknown, with suggestedpossible associations including animmunogenetic factor involving

HLA-Bw54, viral infections (HSVand CMV)

CLINICAL FEATURES:• mild ciliary flush

• a dilated or sluggishly reactivepupil

• corneal epithelial edema

• open angles (No shallow AC)

• The IOP is in the range of 40 – 70mmHg during an acute attack

• Minimal flare

• Few cells

• Few Keratic precipitate

•No pheripheral anteriorsynechiae and posteriorsynechiae

Reiter syndrome/Reactive arthritis


111/189

• Keratoconjunctivitis+urethritis +arthritis

• Previously: urethritis ( can be seen as genital

ulcer too) /gastroenteritis

Urethritis /gastroenteritis

1-5weeks before:

Ocularyellowish serous papules atsoles and palms

HLAB27+

Infectious

agents: Chlamydiae, Salmonella, Shi

gella, Yersinia, Campylobacter

yellowish serous papules at soles

and palms even nails, scrotum,scalp and trunk.

61& 62. ASTIGMATISME -


112/189

DEFINISI

• Ketika cahaya yangmasuk ke dalam

mata secara paralel

tiudak membentuk

satu titik fokus diretina.

Astigmatism, Walter Huang, OD. Yuanpei University: Department of Optometryhttp://www.mastereyeassociates.com/Portals/60407/images//astig

matism-Cross_Section_of_Astigmatic_Eye.jpg

Tipe-tipe astigmatisma Penentuan Jenis Astigmatisme


113/189

• Astigmatisma hipermetropikussimpleks, satu meridian

utamanya emetropik, meridianyang lainnya hipermetropik.

• Astigmatisma miopikus simpleks,satu meridian utamanyaemetropik, meridian lainnyamiopi

• Astigmatisma hipermetropikuskompositus, kedua meridianutama hipermetropik denganderajat berbeda.

• Astigmatisma miopikuskompositus, kedua meridian

utamanya miopik dengan derajatberbeda

• Astigmatisma mikstus, satumeridian utamanyahipermetropik, meridian yang lainmiopik.

1. sferis (-) silinder (-) pasti

miop kompositus2. Sferis (+) silinder (+) pasti

hipermetrop kompositus

3. Sferis (tidak ada) silinder (-)

pasti miop simpleks

4. Sferis (tidak ada) silinder (+)

pasti hipermetrop

simpleks

5. Untuk sferis dan silinder

yang saling berbedatandanya, mohon lihat

pembahasan TO2


114/189

•Pada soal dikatakan setelah dilakukan pemeriksaandidapatkan VODS 20/30 setelah dikoreksi menjadi20/20 dengan S -0,75 C-0,50 Axis 180.

• Seharusnya kelainan yang diderita pasien adalahastigmatisme miopia kompositus, dimana bayangan

jatuh di dua titik yang berbeda di depan retina. Hal inidisebabkan 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 jawabanyang paling mendekati adalah aksial bola mata yangpanjang

63. Klasifikasi Trakoma Menurut


115/189

MacCallanStadium Nama Gejala

Stadium I Trakoma insipien (insipienttrachoma)

Folikel imatur, hipertrofi papilar

minimal

Stadium II Trakoma (establishedtrachoma)

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


116/189

64. Aspirin & Occular Complications

• Ocular side-effects associatedwith aspirin use are rare.

• However, this drug is secretedin tears so transient blurredvision can occur along with

aggravation of dry eyes andkeratitis.

• These symptoms can beidiosyncratic or hypersensitive.

•

Journal of the AmericanMedical Association (JAMA) in2013 Research conductedamong 2,400 middle-aged andelderly people for 15 years:Regular aspirin use was

significantly associated with anincreased incidence ofneovascular [wet] age-relatedmacular degeneration (AMD)

• The 'wet' form is less commonbut progresses more rapidly

and is more likely to lead tovision loss than the 'dry' form.

Ibuprofen & Occular Complications


117/189

Ibuprofen & Occular Complications

•The most common side-effect associated with thismedication is transient blurred vision.

• In a drug re-challenge test, there were also documentedreports of refractive error changes, diplopia, photophobia,dry eyes, visual field changes, and altered color vision.

• If they occur, vision changes usually resolve after 1-3months, but color vision problems can take up to 8 monthsto resolve.

• Corneal vortex keratopathy, which generally resolves within3 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 reduceacuity to between 20/80 and 20/200.

Steroid & Occular Complication


118/189

Steroid & Occular Complication

•

Cataracts occur mostcommonly as a sequela ofcontinuous systemic steroiduse

• Glaucoma is more oftenassociated with topical ocular

or periocular steroids thanwith systemic steroids

• Ocular rebound inflammationmay develop secondary torapid tapering or abruptdiscontinuation of topical

ocular steroid use and is bestprevented with gradualtapering.

•

Opportunistic infections of theeye include bacterial, viral, andfungal infections and are mostoften associated with the useof topical ocular steroids.

• Ophthalmologic evaluation is

indicated promptly if patientstreated with ocular steroidsdevelop ocular discharge, pain,photophobia, or redness.

65. UVEITIS


119/189

Radang uvea:• mengenai bagian

depan atauselaput pelangi(iris)iritis

• mengenai bagiantengah (badansilier)siklitis

• mengenaiselaput hitambagian belakangmatakoroiditis

• Biasanya iritis

disertai dengansiklitis = uveitisanterior/iridosiklitis

UVEITIS


120/189

• Dibedakan dalam bentukgranulomatosa akut-kronis dan

non-granulomatosa akut- kronis• Bersifat idiopatik, ataupun terkait

penyakit autoimun, atau terkaitpenyakit 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 rangsanganproses radang pada ototsfingter pupil

– edema iris

– Terdapat flare atau efek tindaldi dalam bilik mata depan

–Bila sangat akut dapat terlihathifema 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


121/189

UVEITIS

• Tatalaksana : – Steroid topikal dan sistemik

– Siklopegik

– Pengobatan spesifik bila

diketahui kuman penyebab

• Penyulit: Glaukoma

sekunder karena adanya

sinekia posterior yangmenyebabkan iris

bombans peningkatan

TIO

66. Glaukoma SimpleksB


122/189

66. Glaukoma Simpleks

• Merupakan suatu glaukoma primer (idiopatik) yangditandai dengan sudut bilik mata terbuka

• Paling sering di usia > 40 tahun, namun dapat pulamengenai 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 padaanatomis atau fisiologis yg disadari oleh penderita(keluhan sedikit dan progresifitas berjalan lambat)


123/189

Sidarta Ilyas. Ilmu Penyakit Mata. FKUI

• Penatalaksanaan :

–

Bila diagnosis telah ditegakkan penderita harusmemakai obat seumur hidup untuk mencegahkebutaan

– 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

67. Trauma Mekanik Bola MataA


124/189

• Cedera langsung berupa rudapaksa yang mengenai jaringan

mata.• Beratnya kerusakan jaringan

bergantung dari jenis traumaserta jaringan yang terkena

• Gejala : penurunan tajampenglihatan; tanda-tandatrauma pada bola mata

• Komplikasi : Endoftalmitis

Uveitis

Perdarahan vitreous

Hifema Retinal detachment

Glaukoma

Oftalmia simpatetik

• Pemeriksaan Rutin : Visus : dgn kartu Snellen/chart

projector + pinhole TIO : dgn tonometer

aplanasi/schiotz/palpasi

Slit lamp : utk melihat segmenanterior

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 atautopikal, perban tekan, hinggaoperasi repair

Panduan Tatalaksana Klinik RSCM Kirana, 2012

HIFEMA


125/189

•

Definisi: – Perdarahan pada bilik mata

depan

– Tampak seperti warnamerah atau genangandarah pada dasar iris ataupada kornea

• Halangan pandang parsial/ komplet

• Etiologi: pembedahan

intraokular, traumatumpul, trauma laserasi

• Tujuan terapi: – Mencegah rebleeding

(biasanya dalam 5 haripertama)

– Mencegah noda darahpada kornea

– Mencegah atrofi sarafoptik

• Komplikasi: – Perdarahan ulang

– Sinekiae anterior perifer

– Atrofi saraf optik

– Glaukoma

68. Trauma Basa atau AlkaliB


126/189

•

Pada trauma alkali akan terbentuk kolagenase merusakkolagen kornea

• Klasifikasi Thoft : – Derajat 1 : hiperemi konjungtiva disertai keratitis pungtata

– Derajat 2 : hiperemi konjungtiva disertai hilang epitel kornea

– Derajat 3 : hiperemi konjungtiva disertai nekrosis konjungtivadan lepasnya epitel kornea

– Derajat 4 : konjungtiva perilimbal mengalami nekrosis sebanyak50%

• Untuk menilai defek pada epitel kornea digunakan ujifluorescein – Kertas fluorescein dibasahi dengan garam fisiologis lalu dilekkan

pada sakus konjungtiva inferior bila kornea kehijauan dengansinar birudefek kornea

69. Astenopia (Computer Vision

S ndrome)

C


127/189

Syndrome)•

Astenopia, Eye Strain, VisualDiscomfort dan Ocular fatigue

atau disebut juga mata lelah

• Kondisi oftalmologis yang

bermanifestasi lewat gejala

nonspesifik seperti lelah dannyeri 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 bendayang dilihat tidak cukup.

2. Pemusatan cahaya pada retina matatidak sempurna.

3. Mekanisme penggabungan bayangan(fusi) oleh sistem penglihatan yanglebih sentral (otak) dan upaya untukmempertahankannya 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


128/189

• 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. PresbiopiaB


129/189

p

• Koreksi→lensa positifuntuk menambah

kekuatan lensa yang

berkurang sesuai usia

• Kekuatan lensa yangbiasa digunakan:

+ 1.0 D → usia 40 tahun


+ 2.0 D → usia 50 tahun+ 2.5 D → usia 55 tahun


https://reader015.{domain}/reader015/html5/0714/5b48dfee5fb12/5b48e03a7efcb.jpg

71. Jenis GlaukomaCauses Etiology Clinical

http://emedicine.medscape.com/article/1206147

B


130/189

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


131/189

72. ARMD (Age Related Macular Degeneration) A


132/189

• Degenerasi progresif makula retina yg dpt memberikan

gangguan pd penglihatan sentral

• Biasanya tjd pd usia di atas 60 thn

• Gejala klinisgradual 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


133/189

73. DAKRIOSISTITISB


134/189

•

Partial or complete obstruction of the nasolacrimal ductwith inflammation due to infection (Staphylococcus aureusor 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 skinabcess; (-) or regurgitation (+) : dacryocystitis. Swab andculture

•Treatment : Systemic and topical antibiotic, irrigation oflacrimal sac, Dacryocystorhinotomy

• Evaluasi Sistem Lakrimal-Drainase Lakrimal :


135/189

Evaluasi Sistem Lakrimal Drainase Lakrimal :

• Uji Anel : Dengan melakukan uji anel, dapat diketahui apakah fungsidari bagian eksresi baik atau tidak.

• Cara melakukan uji anel :

– Lebarkan pungtum lakrimal dengan dilator pungtum

– Isi spuit dengan larutan garam fisiologis. Gunakan jarum lurus ataubengkok 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 didalam saluran eksresi.

• Jika cairan keluar dari pungtum lakrimal superior, berarti adaobstruksi di duktus nasolakrimalis. Jika cairan keluar lagi melaluipungtum lakrimal inferior berarti obstruksi terdapat di ujung nasalkanalikuli lakrimal inferior, maka coba lakukan uji anel pungtumlakrimal superior.

74. Penatalaksanaan AstigmatismeD


136/189

• Terapi astigmatisme meliputi penggunaankacamata, lensa kontak atau pembedahan

refraktif

• Peresepan kacamata untuk astigmatisme, biladidapatkan 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

B


137/189

, y

– 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


138/189

Keratic Presipitates

76. Pemeriksaan ketajaman

penglihatan

B


139/189

penglihatan

•

6/60 penderita hanya bisa membaca dari jarak6 meter sedangkan orang normal dapat membacadari 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 dikatakantajam penglihatan 0

77. Klasifikasi MIOPIAC


140/189

• 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. EntropionD


141/189

•

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 ototpalpebra

• Enteropion sikatrikal – Mengenai palpebral inferior/ superior

– Akibat jaringan parut tarsal – Biasanya akibat peradangan kronik seperti trakoma

• Pada enteropion bisa disertai dengan trikiasis


142/189


143/189

ILMU KESEHATAN ANAK

79. Tatalaksana Demam Tifoid


144/189


145/189

80.

Derajat


146/189

Derajat

SeranganAsma


147/189

Alur

Penatalaksanaan

Serangan Asma

81. Diarrheagenic Escherichia coli


148/189

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


149/189

Diarrheagenic Escherichia coli


150/189

•

E. coli species are members of the Enterobacteriaceaefamily.

• 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


151/189

• Gagal ginjal akut (GGA) ialah penurunan fungsi ginjal mendadakyang mengakibatkan hilangnya kemampuan ginjal untukmempertahankan homeostasis

• Terdapat peningkatan kadar kreatinin darah secara progresif 0,5mg/dL per hari dan peningkatan ureum sekitar 10-20 mg/dL perhari.

• GGA dapat bersifat oligurik dan non-oligurik. – Oliguria ialah produksi urin


152/189

• Terapi sesuai penyakit primer

• Bila terdapat infeksi, dosisantibiotik disesuaikan denganberatnya penurunan fungsiginjal

• Pemberian cairan disesuaikan

dengan keadaan hidrasi• Koreksi gangguan

ketidakseimbangan cairanelektrolit

• Natrium bikarbonat untukmengatasi asidosis metaboliksebanyak 1-2 mEq/kgBB/ harisesuai dengan beratnyaasidosis

• Pemberian diuretik pada GGArenal dengan furosemid 1-2mg/kgBB dua kali sehari dandapat dinaikkan secarabertahap sampai maksimum10 mg/kgBB/kali. (pastikankecukupan sirkulasi dan bukanmerupakan GGA pascarenal).

• Bila gagal denganmedikamentosa, makadilakukan dialisis peritonealatau hemodialisis.

• Pada soal, pasien mengalamiGGA prerenal, sehinggapemberian furosemidetidaklah tepat. Pilihan jawaban jatuh pada hemodialisa

84. Urinalisis


153/189

Makroskopik• Kekeruhan: clear, slightly cloudy, cloudy,

or turbid

• Warna & konsentrasi: tidak berwarna,kuning, kuning gelap, merah

Kimia urin• Specific gravity (1.002-1.035)

• pH

• Protein (N: negatif)

• Glucose (N: negatif)

• Ketones (N: Negatif)• Blood/ hemoglobi

Documents

Pembahasan Seminar Part I No. 1-100