1

PENUNJANG
PEMERIKSAAN
KLINIS
PRIHATINI
PK-FKUWKS –OSCE 2018
BUKU ACUAN 2

 Diana Nicoll et al,Pocket Guide Diagnostic Tests,McGraw

Hill 2001
 Desai ,Prait Cliinician’s Guide to laboratory
medicine,2000,lexi comp
 Fisbach,Dunning,A Manual of laboratory & Diagnostic test
2015,Wolter Kluwer
PENUNJANG 3

 Penyakit dalam
 Penyakit Paru
 Penyakit Jantung
 Penyakit anak
 4

Test /Range / Physiologic Basis Interpretation Comments

Collection
Alkaline Alkaline Increased in: Obstructive Alkaline phosph
phosphatase, phosphatases are hepatobiliary dis; bone performs well in
serum found in disease (physiologic bone measuring the extent
41–133 IU/L liver, bone, growth, Paget’s disease, of bone metastases
[0.7–2.2 μkat/L] intestine, and osteomalacia, in prostate cancer.
(method- and placenta osteogenic sarcoma, bone Normal:osteoporosis.
agedependent) metastases), Alkaline phosphatase
hyperparathyroidism, isoenzyme separation
rickets, benign familial by electrophoresis or
hyperphosphatasemia, differential heat
pregnancy inactivation is
(third trimester), GI unreliable. Use γ-
disease (perforated ulcer glutamyltranspeptidas
or bowel infarct), e(GGT), increases :
hepatotoxic drugs. hepatobiliary dis but
Decreased in: not in bone disease,
Test /Range / Collection Physiologic Basis Interpretation Comments 5
Bilirubin, serum Bilirubin, a product Increased in: Acute or Assay of total bilirubin
0.1–1.2 mg/dL of hemoglobin chronic hepatitis, includes conjugated
[2–21 μmol/L] metabolism, is cirrhosis, biliary tract (direct) & unconju-
Direct (conjugated to conjugated in the obstruction, toxic gated(indirect)
glucuronide) bilirubin: liver to mono- and hepatitis, neonatal bilirubin plus delta
0.1–0.4 mg/dL diglucuronides jaundice, congenital bilirubin(conjugated
[<7 μmol/L]; and excreted in bile. liver enzyme bilirubin bound to
Indirect Some conjugated abnormalities (Dubin- albumin).It is usually
unconjugated) bilirubin is bound to Johnson, Rotor’s, clinically unnecessary
bilirubin: serum albumin, so- Gilbert’s, Crigler- tofractionate total
0.2–0.7 mg/dL called D (delta) Najjar syndromes), bilirubin. The fractio-
[<12 μmol/L] bilirubin. fasting, hemolytic nation is unreliable by
Elevated serum disorders. the diazo reaction and
bilirubin occurs in Hepatotoxic drugs may underestimate
liver disease, biliary unconjugated bilirubin.
obstruction, Only conjugated
bilirubin appears in
the urine, and it is
indicative of liver
disease;hemolysis is
associated with
Test /Range / Physiologic Basis Interpretation Comments 6
Collection
Creatinine, serum Endogenous creatinine Increased in: Acute In alkaline picrate
(Cr) is excreted by or chronic renal method, substances
0.6–1.2 mg/dL filtration through the failure, urinary tract other than Cr (eg,
[50–100 μmol/L glomerulus and obstruction, acetoacetate,
by tubular secretion. nephrotoxic drugs, acetone, β- ydroxy-
Creatinine hypothyroidism. butyrate,α-keto-
clearance is an Decreased in: glutarate, pyruvate,
acceptable clinical Reduced muscle glucose) may give
measure of glomerular mass falsely high results.
filtration rate Therefore,patients with
(GFR), though it DKA
sometimes may have spuriously
overestimates elevated Cr.
GFR (eg, in cirrhosis). Cephalosporins may
For each 50% reduction spuriously
in GFR, serum increase or decrease
creatinine Cr measurement.
approximately doubles Increased bilirubin may
spuriously
decrease Cr.
Test /Range / Physiologic Basis Interpretation Comments
Collection
7
Creatinine Widely used test Increased in: High Serum Cr may, in
clearance, (GFR). Theoretically to the cardiac output, practice, be a more
(C1Cr) formula: exercise, reliable indicator of
Adults: 90–130 mL/ Clcr(mL/min)=UcrxV acromegaly, renal function than
min/1.73 m2 BSA Pcr diabetes mellitus), 24-hour C1Cr unless
$$ reliable,but often infections, urine collection
Collect carefully compromised by hypothyroidism is carefully
timed incomplete urine (early stage. monitored. An 8-hour
24-hour urine and collection.Crclearance is Decreased in: Acute collection provides
simultaneous calculated or chronic renal results similar to
serum/plasma From urine creatinine failure, decreased those obtained by a
creatinine (UCr [mg/dL]), renal blood flow 24-hour collection.
sample. Record plasma/serum (shock, C1Cr will over
patient’s weight creatinine (PCr [mg/dL]), & hemorrhage, estimate GFR to the
and urine dehydration, extent that Cr is
height. flow rate (V [mL/min]) CHF). Drugs: secreted by the renal
according to nephrotoxic drugs tubules (eg, in
Creatinine clearance is cirrhosis).
often “corrected” C1Cr can be
for body surface area estimated from the
(BSA[m2]) according serum
hipertensi 8

Category Systolic press mmHg Diastolic press mmHg

Optimal <120 <80
Normal <130 <85
High normal 130–139 85–89
Hypertension
Stage 1 (mild) 140–159 90–99
Stage 2 (moderate) 160–179 100–109
Stage 3 (severe) ≥180 ≥110
Isolated systolic
hypertension ≥140 ≥90
 BASIC TESTS FOR INITIAL EVALUATION hypertension
9
Always included
 a. Urine for protein, blood, and glucose
 b. Microscopic urinalysis
 c. Hematocrit
 d. Serum potassium
 e. Serum creatinine and/or blood urea nitrogen
 f. Fasting glucose
 g. Total cholesterol
BASIC TESTS FOR INITIAL EVALUATION 10
hypertension

2.Usually included, depending on cost and other

factors
 a. Thyroid-stimulating hormone
 b. White blood cell count
 c. HDL and LDL cholesterol and triglycerides
 d. Serum calcium and phosphate
 e. Chest x-ray; limited echocardiogram
SPECIAL STUDIES TO SCREEN FOR 11
SECONDARY HYPERTENSION

 1. Renovascular disease: angiotensin-converting enzyme

inhibitor radionuclide renal scan, renal duplex Doppler flow
studies, and MRI angiography
 2. Pheochromocytoma: 24-h urine assay for creatinine,
metanephrines, and catecholamines
 3. Cushing’s syndrome: overnight dexamethasone
suppression test or 24-h urine cortisol and creatinine
 4. Primary aldosteronism: plasma aldosterone: renin activity
ratio
12
DIABETES MELLITUS 13

Pemeriksaan dugaan:
 OGTT
 GDA
 GDA

Pemeriksaan rutin/berkala
 GDP
 GD2JPP
DIABETES MELLITUS 14

Pemeriksaan memantau komplikasi:

 HBA1c
 FG
 FH
Pemeriksaan klinis:
 Retinopati
 Neropati
 PJK /AMI
DM ,hiperglicemia, fosfate & 15
alkalifosfate

 Growth hormone & acromegali

 Bone growth : alkalifosfate meningkat
Early diagnosis of diabetic 16
nephropathy
 Table3.1 Albumin concentration in
the urine
 Normal range Less than 20 mg/l
 Microalbuminuria 20^200 mg/l
 Macroalbuminuria More than 200 mg/l
Hyperglikemia,BUN,asam urat,fosfor, 17
kolesterol ,alkalifosfat ,AST & LDH
meningkat
 TGT: berat dan tingkat DM
 Perlemakan hati: AST,LDH,ALKP &kdg bilirubin meningkat
 DKA: dehidrasi, protein, albumin & BUN meningkat
 Diabetic nefropati: kreatinin meningkat, dicek ketoasidosis
 Diabetik renal dis: menonjol kenaikan BUN, asam urat
,fosfor sedang albumin,protein menurun
Hyperglikemia, kolesterol, alkaliosfat 18
meningkat,
menurun: BUN ,protein albumin,&calcium

 Kehamilan:
 Plasenta alkap
 Sintesis hepatik:kolesterol meningkat
 BUN menurun: GFR meningkat
Gambaran di ginjal: 19

 Meningkat:BUN,asam urat,
fosfor,glukose,LDH,AST &ALKPosfat
 Menurun : protein,albumin & ,kalsium
 GAGAL GINJAL s kreatinin1/10 BUN
Hepatitis 20

 AST/SGOT & ALT/SGPT meningkat

 Alkalifosfatase & LDH meningkat
 bilirubin meningkat < 10 mg/dL
 Total protein meningkat (alb/glob ratio
menurun)
 Kolesterol menurun sedikit (menutupi
bilirubin,meningkat kolesterol 5 mg/dL
bilirubin
Test / Physiologic Basis Interpretation Comments
Range/Collection
Alanine intracellular Increased in: Acute ALT is the 21
aminotransferase, enzyme involved in viral hepatitis (ALT preferred
serum amino acid > AST), biliary tract enzyme for
(ALT, SGPT, GPT) metabolism. obstruction cholangitis, evaluation
0–35 U/L Present in large choledocholithiasis), of liver injury.
[0–0.58 μkat/L] concentrations in alcoholic hepatitis & Screening ALT
(laboratory- liver, kidney; cirrhosis (AST >ALT), in low-risk
specific) in smaller amounts, liver abscess, meta- populations
in skeletal muscle static or primary liver has a low
and heart. Released cancer; right heart (12%) positive
with tissue damage, failure, ischemia or predictive
particularly liver hypoxia, injury to value.
injury liver(“shock liver”),
extensive trauma.
Drugs that cause
cholestasis or
hepatotoxicity.
Decreased in:
Pyridoxine (vitamin B6)
deficiency.

Test /Range / Collection Physiologic Basis
Alanine aminotransferase, Pituitary ACTH (release
serum stimulated by
(ALT, SGPT, GPT) hypothalamic corticotropin-
0–35 U/L releasing factor) stimulates
[0–0.58 μkat/L] cortisol release from the
(laboratory-specific adrenal gland. There is
feedback regulation of the
system by cortisol.
ACTH is secreted
episodically and shows
circadian variation, with
highest levels at 6:00–8:00
AM; lowest levels at 9:00–
10:00 PM.
22
Interpretation
Increased in: Pituitary (40–
200 pg/mL) & ectopic (200–
71,000 pg/mL) Cushing’s
syndrome, primary adrenal
insufficiency(>250 pg/mL),
adrenogenital syndrome
with impaired cortisol
production.
Decreased in: Adrenal
Cushing’s syndrome
(<20 pg/mL), pituitary ACTH
(secondary adrenal)
insufficiency
(<50 pg/mL).
Collection
Albumin, Major component of plasma
serum proteins; influenced by
3.4–4.7 g/dL nutritional state,
[34–47 g/L] hepatic function, renal
function, and various
diseases. Major binding
protein.
While there are more than 50
different genetic variants
(alloalbumins), only
occasionally does a mutation
cause abnormal binding (eg,
in familial dysalbuminemic
hyperthyroxinemia).
Increased in: Serum albumin gives
Dehydration, shock, an indication of
Hemoconcentration.De severity in23chronic
creased in: Decreased liver disease. Useful
hepatic synthesis in nutritional assess-
(chronic liver disease, ment if there is no
malnutrition, impairment in
malabsorption, production or
malignancy, congenital increased loss of
analbuminemia [rare]). albumin and is an
Increased losses independent risk
(nephrotic syndrome, factor for all-cause
burns, trauma, mortality in the
emorrhage with fluid elderly (age >70).
replace-ment, fistulas, There is a 10%
nteropathy, acute or reduction in serum
chronic glomerulo- albumin level in late
nephritis).Hemo-dilution pregnancy
(pregnancy, CHF). (related to
Drugs: estrogens. hemodilution).
J Med Genet
1994;31:355. Proc Natl
Acad Sci U S A
1994;91:6476.JAMA
Test /Range / Physiologic Basis
Collection
Blood urea Urea, an end product of
nitrogen, protein metabolism,
serum is excreted by the kidney.
(BUN) BUN is directly related to
8–20 mg/dL protein intake &nitrogen
[2.9–7.1 mmol/L] metabolism and
inversely related to the rate
of excretion of urea.
Urea concen-tration in GFR
gloms the same as in
plasma, but its
tubular reabsorp-tion is
inversely related to the rate
of urine formation.
Thus, the BUN is a less
useful measure GFR
Than the serum creatinine
(Cr).
Interpretation Comments
24
Increased in: Renal Urease assay method
failure (acute /chronic) commonly used.
,urinary tract obstruct BUN/Cr ratio (normally
- tion, dehydration, 121–201) is Decreas -
shock, burns, CHF, GI ed in acute tubular
bleeding. Nephrotoxic necrosis, advanced
drugs (gentamicin). liver disease, low
Decreased in: protein intake, and
Hepatic failure, following hemo-
nephrotic syndrome, dialysis.
cachexia (low-protein BUN/Cr ratio is
and high-carbohydrate increased in
diets). dehydration,
GI bleeding, &
increased catabolism.
Nursing 1994;24:88.
Ann Emerg Med
1992;21:713.
HEPATO RENAL SYNDROME 25

 MENINGKAT:
ALKALI FOSFAT,
KOLESTEROL,BILIRUBIN
 AST MENINGKAT SEDIKIT
 LDH NORMAL
OBSTRUKSI BILIER 26

 MENINGKAT:Alkalifosfatase,AST
,LDH & bilirubin
 Meningkat: asam urat
 Menurun: kolesterol, protein,
albumin,kalsium & BUN
 Pemeriksaan hepatitis diberbagai stadia
27
Peny/stadi HAV HBV HCV HDV HEV
a
Akut IgM;antiHAV IgManti-HBc, Anti-HCV HDAg IgM anti-HEV,
HBsAg

kronik tinjaHAV 1-2 2-10% >5 Th 85%Anti- 6% total Tidak

mg sbl gejala menjadi HCV anti-HDV diketahui
kronik
Penularan Tidak HBeAg,HBsA Anti-HCV total anti- Tidak
diketahui g,HBVDNA HDV diketahui

Penyem- Tidak Anti-Hbe Tidak Tidak Tidak

buhan diketahui ,anjti-HBs diketahui diketahui diketahui

Viral load HBV DNA HCV RNA

 Pemeriksaan hepatitis diberbagai stadia 28
Peny/stadia HAV HBV HCV HDV HEV
carrier Tidak HBsAg Tidak HBAg;anti- Tidak
diketahui diketahui HDV diketahui
Imuniti Total anti- HBsAg, Tidak Tidak Tidak
HAV Total anti- diketahui diketahui menentu
HBc
Pola virus IgM anti- HBsAg Anti-HCV
akut HAV Uji HIV
juga
Microalbuminuria is present at 29
the following values
 According to the time of urine collection:
 (a) Collection over a fixed time,
 e.g. overnight 20-200 lg/min
 (b) Collection over 24 hours 30-300 mg/24 h
 According to the rate of creatine excretion:
 For women 20-300 mg/g urinary creatine
 2.5-35 mg/mmol urinary creatine
 For men 20-200 mg/g urinary creatine
 2.5-25 mg/mmol urinary creatine
Microalbuminuria testing: when 30

and by whom?
 Therefore, to be sure that microalbuminuria truly
indicates the onset of diabetic nephropathy, the
test should be repeated after a gap of two to four
weeks
Who should be tested for 31
microalbinuria
 Patients withType 1diabetes:
 Children From puberty
 Adults From five years after diagnosis of diabetes
 Patients withType 2 diabetes:
 From the diagnosis of diabetes
 How to test urine for
microalbuminuria 32
Micral urine test strip

Dip test strip in

the urine

Lie the test strip on

the glass
Compare the colour of the strip
with the calibration chart after
30 seconds
Hasil abnormal microalbumin 33

 DM
 Hipertensi
 CVD
 Nefropati perdarahan saluran kemih
 Hburia
 myoglobinuria
Positif palsu mikroalbuminuria 34

 ISK
 Darah
 Keadaan asam/basa
 oxytetracycline
35
Pemeriksaan fungsi paru indikasi: 36
 Menemukan peny paru/kardiogenik paru
 DD dyspnea
 Penilaian prabedah
 Menemukan kegagalan paru
 Memantau kemajuan peny bronkopulmonal
 Menafsir pekerja yang beresiko peny paru
 Untuk penggantian biaya pengobatan
 Memantau ssd pengobatan atau pembedahan
Pemeriksaan sputum 37

 Cat Gram
 BTA
 Kultur :
rasio epitel/netrofil =10/25
kultur spesifik Tbc
 Pola pneumonia spesifik
38
Tempat :
Macam pneumonia
 Multilobar
 Virus,legionellosis
 Upper lobes
 Klebsiella,mycoplasma
 Supra basilar lower lobe
 Aspirasi
 Aspirasi n segmen lobus
atas  Aspirasi

 Konsolidasi  Bakteri

 Kavitasi  Pseudomonas ,aspirasi

 Nodul  Staphylococcic

 Intertitial  Virus, mycoplasma

 efusi  Bakteri (khusus bila luas)

Pneumonia &sputum (+) 39

Gram +ve bakteri:

 Str pneumoniae,Str pyogenes,Stap aureus
Gram –ve bakteri:
 H.influenzae,K.pneumoniae; E.coli
Anaerobik bakteri:
 Bacterioges fusiform,
 Peptostreptococci ;
 microaerophilic Streptococci
Kontra indikasi torakosintesis 40

 Perdarahan ( diathesis)
 Antikoagulan
 Sedikit cairan pleura
 Ventilator mekanik
 Infeksi dikulit

 90
 Beda eksudat &transudat 41

Eksudat transudat

1.Terkumpul dirongga tubuh &jaringan 1.Terkumpul dirongga tubuh dari

akibat maligna /inflamasi kerusakan sirkulasi
2.Berkaitan proses inlamasi 2.Tak berkaitan proses inlamasi
3,kental, opaq/keruh smp purulen 3.Cairan banyak
4. Mengandung protein tinggi 4. Mengandung protein rendah(2,5-3
,sel,bahan padat dari sel g/dL) ,sel,bahan padat dari sel
5.Leukosit tinggi 5.Leukosit rendah
6gumpalan spontan (fibrinogen tinggi) 6.Tidak menggumpal
7.Mungkin ditemukan sel maligna sbg 7.Mungkin ditemukan sel maligna
bakteri
8.BJ > 1,016 8.BJ < 1,016
Pemeriksaan rutin cairan 42
pleura
 Protein
 Leukosit & diferensial
 Lactat dehydogenase(LDH)
 glukose
Glukose< 60 mg/dL 43

 Maligna
 Tbc
 rheumatoid arthritis
 Parapneumonia effusion /empyema
Leukosit diff.& penyebab 44

eksudat
 Tipe sel :  Etiologi:
 netrofilia  Inflamasi
 Pneumonia
 Emboli paru
 Abses subprenik
 Pankreatitis
 Awal tbc
Leukosit diff.& penyebab 45
eksudat
 Tipe sel :  Etiologi:

 eosinophilia  Udara
 Darah
 Infeksi parasit:ascariasis,
amebiasis,hydatis,paragonomiasis
 Reaksi pengobatan:
dantrolene,nitrofurantoin,bromocriptine
 Asbestosis
 Churg Strauss syndrome
Leukosit diff.& penyebab 46
eksudat
 Tipe:  Etiologi
 lymphocytosis sel  Maligna
 Tbc

 Sel mesotelia
 Meningkat melawan
tbc
 Makrofag  Tak berarti
 Sel plasma  Multiple myeloma
Amylase meningkat 47

 Maligna
 Ruptur esofagus
 Penyakit pankreas
pH cairan pleura < 7,20 48

 Urinothorax
 Paragonomiasis
 Efusi/empyema
 Maligna pleura efussion
 SLE
 Asidosis sistemik
 Ruptur esofagus
 Rheumatoid artritis
Pemeriksaan lain cairan pleura 49

 Uji imunokimia
 Flow sitometri
 Adenosine deamnase(ADA)
 Pemeriksaan imunologi
 Pemeriksaan lemak
 Kultur mikrobiologi
 50

Pemeriksaan analisis
gas darah & elektrolit
Indikasi BGA 51

 Pemantauan pasien
 Mengetahui hasil terapi
 Keseimbangan elektrolit,blood gas
Pemeriksaan analisis gas 52
darah & elektrolit
 pH
 PCo2
 PO2
HCO3-
 Anion gap=(Na+ + K+)-(Cl- + HCO3 -)
BODY FLUID TESTS, HANDLING 53

, AND INTERPRETATION
. Body Fluid Commonly Specimen Tube Interpretation
Requested Tests and Guide
Handling
blood pH, PO2, PCO2 Glass syringe. acid-base
Evacuate air
bubbles; remove
needle;
position rubber
cap; place
sample on ice;
deliver
immediately.
Langkah Langkah 1,pH asam atau 54

alkalis?
 pH ditentukan ion H+ (pH
dewasa < 7,35 asam ; > 7,45
alkalis).
 Bila pH normal sedang analisis
gas darah abnormal ,perlu
analisis dilanjutkan
Langkah 2,penyebab abnormal 55

respirasi atau metabolik?

 2 komponen mempengaruhi keseimbangan
asam basa di tubuh CO2 dan
bikarbonat(HCO3)?
 Abnormal CO2 indikasi penyebab respirasi
dan abnormal HCO3 indikasi penyebab
metabolik.
 Peningkatan CO2 didarah terjadi asidosis
dan peningkatan HCO3 didarah
menyebabkan alkalosis.
Langkah ke3 apakah pH 56

terkompensasi,sebagian atau tidak

 Bila CO2 dan HCO3 kekuatan berlawanan

dalam keseimbangan asam basa,sistem
memperbaiki selama keadaan abnormal.
 Kompensasi pH keadaan normal terbatas
dengan keadaan kedua abnormal CO2 dan
atau HCO3
Asidosis respiratorik 57

 Terjadi karena penumpukan oksigen di tubuh

 Tekanan(depresi) SSP berkaitan kerusakan
kepala,
 Sedasi ( misal narkotik,sesudah operasi,
penenang, ,koma )
 Kerusakan dinding dada,dada yang
mengambang(flail)
 Sumbatan jalan napas/benda asing di tubuh
Alkalosis respiratorik 58

 Menurun CO2 ,terjadi hiperventilasi dan

CO2 dibuang menyebabkab alkalis
 Keadaan fisiologi: cemas, takut,nyeri
 Demam,
 sepsis,
 hamil,
 anemia berat
Asidosis metabolik & normal 59
Anion gap
Kehilangan bikarbonat & kenaikan
chlorid:
 Diare,drainage usus kecil atau
fistula,
Asidosis metabolik (bikarbonat rendah)& 60
normal Anion gap

 Ginjal:ATA(acute tubular
acidosis),acetazolamide
 Chloridetinggi:resorpsi Cl berubah,
hyperalimentasi par enteral,R/NaCl
&NH4CL
 Sekresi usus >: diare, fistula,suction,
fistula bilier
Anion gap rendah 61

 MM
 Hiponatremia(serum kental)
 Bromide ingestion(hyperchloremia)
Asidosis metabolik & Anion 62

gap meningkat
 Meningkat anion gap=menurun HCO3
-

 Penyakit kronik tgt renal clearance

 Asidosis metabolik & Anion gap 63
meningkat
Potasium tinggi:  Potasium rendah:
 Bahan asam  Diare
 Kekurangan mineral
 Uretral sigmoidoskopi&
kortikoid
malfungsi ileostomi
 Penyakit ginjal SLE
 Intertitial nefritis  Renal tubulus asidosis
 Amyloidosis hydronefrosis (proksimal &distal)
 Sickle sel nefropati
 Gagal ginjal tak spesifik
 Alkalosis metabolik & Anion gap 64
Saline respon,Ekskresi Cl<10
meq/hari:
 Alkalosis renalis: Saline
pengobatan diuretik
unrespon,Ekskresi
resorsbsi anion jelek
 Alkalosis gastrointestinal:
Cl<10 meq/hari,
Gastrik alkalosis  Alkalosis renalis:
Intestinal alkalosis(diare) hipoparatirodi
 Alkali eksogen:
 Baking soda  Hipertensi: endogen
 Sodium sitrat,laktat mineralokortikoid
 Transfusi
 Primer aldosteron
 antasid
 Base excess interpretasi
pCO2
mmol/L
mmHg 65
pH Asidosis repiratorik
primer dgn
positif
Tinggi kompensasi ginjal
>0,45
normal
Asidosis repiratorik
primer
asidemia negatif
Normal
0,35-0,45 Gabungan asidosis
respiratorik &
negatif
metabolik

Asidosis metabolik
primer
rendah
<0,35
negatif Asidosis metabolik
primer dgn kompensasi
respiratorik
 Base excess interpretasi
pCO2
mmol/L
mmHg 66
Alkalosis metabolik
pH primer dgn kompensasi
respiratorik
positif
Tinggi
>0,45
alkalosis metabolik
alkaliemia primer
normal
Normal
0,35-0,45 Gabungan alkalosis
respiratorik &
positif metabolik

Alkalosis
normal
respiratorik primer
rendah
<0,35
negatif Alkalosis respiratorik
primer dgn kompensasi
ginjal
67
Kasus 1 68

 Laki-laki 56 tahun berat badan menurun selama 6

bulan terakhir,badan terasa lemah ,akhir-akhir ini
sering kencing,terutama malam ; pemeriksaan
terakhir Tensi 180/110 mmHg.hasil pemeriksaan:
urine protein positif tapi reduksi negatif.
1. Pemeriksaan yang dilakukan di laboratorium apa
saja?
2. Dugaan diagnosis?
3. Penyebab anemia ?
Jawab kasus 1 69

1. Pemeriksaan darah lengkap

2. Pemeriksaan glukose darah acak
3. Pemeriksaan urine lengkap
Hasil pemeriksaan lab : 70

 Pemeriksaan darah lengkap:

 Hb 9,1 g/dL
 Lekosit 8000/uL
 glukose darah acak:125 mg/dL
 Urinalisis:Lekosit 5-10 plp,
 sedimen: silinder lekosit 1-5/plp,eritrosit
2-5 sel/plp
Dugaan diagnosis? 71

 Gagal ginjal?
 Perlu pemeriksaan tambahan apa
saja
Hasil lab selanjutnya sbb 72

 Sodium 130mmol/L(135-140 mmol/L )

 Potasium 5,2 mmol/L(3,6-5,0mmol/L)
 Bicarbonate 16 mmol/L(22-30 mmol/L)
 Urea 43 mmol/L(3,3,-6,7 mmol/L)
 Kreatinin 640µmol/L(60-110µmol/ L)
 Glukose 115 mg/dl(<100 mg/L)
 Kalsium1,92 mmol/L(2,2-4,6mmol/L)
 Fosfat 2,42 mmol/L(0,8-1,4mmol/L)
 Alkalifosfat 205 iu/L(4-11 iu/L)
Diagnosis pasien 73

 Hipertensi
 Anemia
 Alkalifosfatemia tinggi osteodystrofi
 Mengalami gagal ginjal kronik
Kasus 2 74

 Wanita 50 tahun hidup sendirian, dikirim ke RSUD

ditemukan anaknya tak sadar dirumah ,penderita
rajin kontrol kesehatan ,Napas normal
 Pemeriksaan laboratorium yang diminta dokter
IRD?
 Selanjutnya pemeriksaan MRS
Pemeriksaan laboratorium 75

yang diminta dokter IRD?

 GDA
 DL
 UL
Hasil laboratorium 76

 GDA= 800 mg/dL

 DL Hb=12,3 g/dL
 Ul=protein+++; Keton=+
Hasil laboratorium lain 77

 Sodium 149mmol/L(135-145mmol/L)
 Potasium 4,7 mmol/L(3,6-5,0mmol/L)
 Bicarbonate 18 mmol/L(22-30 mmol/L)
 Urea 35 mmol/L(3,3,-6,7 mmol/L)
 Kreatinin 180µmol/L(60-110µmol/ L)
 Total protein 90g /L (60-80 g /L)
 Osmolality 370 mmol/kg(280-295 mmol/kg)
Hasil abnormal: 78

 Osmolality tinggi:
diuresis,dehidrasi,GFR turun
 BUN,creatinin retensi dan protein
tinggi sehngg cairan dari serum
menurun
 Bikarbonat rendah , H+
 Na+ tinggi diuresis osmotik
 Nonketotik hiperglikemia
Diagnosis pasien 79

 Nonketotik hiperglikemia
 Perlu pengobatan insulin mencegah
lipolisis
 Memantaupasien:glukose darah,
keseimbangan cairan
 Bila
keadaan akut terlampaui pasien
dapat diberi OHO
Kasus 3 80

 26 tahun wanita pegawai bank 3 bulan nafsu

makan meningkat,Berat badan menurun akhir ini
sukar menulis Merasa kedinginan ,dokter
mengamati matanya agak menonjol dan kelenjar
tiroid agak membesar.Pemeriksaan fisik :
sadar,Tensi120/80 mmHg, Nadi80/menit ;
Respirasi 24/menit
 Pemeriksaan laboratorium yang dilakukan ?
 Pemantauan apa yang dilakukan?
Hasil laboratorium 81

 T4 > 200 mmol/L

 T3 8 nmol/L
 Free FT4 40 pmol/L
diagnosis 82

gejala:
 BB menurun
 Tangan gemetar
 Palpitasi
 Mata menonjol
 Kel tiroid>(goitre)

 Gejala + laboratorium tirotoksikosis

Kasus 4 83

 40 tahun perempuan ke poli penyakit dalam

denganikterus(jaundice) Riwayat kontak hepatitis
waktu bepergian ,mendapat transfuse .Pasien tak
minum alcohol mengalami gatal seluruh tubuh
sebelumnya .
1. Pemeriksan laboratorium yang diminta?
2. Pemeriksaan khusus apa saja untuk gejala
pasien?
Jawab Kasus 4 84

1. Pemeriksan laboratorium yang diminta?\

 DL
 UL
2. Pemeriksaan khusus apa saja untuk gejala pasien?
 LFT
 Serologi hepatitis
Hasil pemeriksaan Kasus 4 85

 Serum:
 Total protein 85 g/dL( 60-80 g /L)
 Albumin 28 g/L(35-50 g/L)
 Bilirubin 340 µmol/L(3-20µmol/L)
 Alkalifosfatasi 522 iµ/L(30-90 iµ/L)
 AST 98 iu /L()
 Ÿglutamyl transpeptidase 242 iu/L(<60 iu/L)
Hasil pemeriksaan Kasus 4 86

 ALFost >> cholestatic jaundice

 Albumin rendah kronik peny Hati
 Gatal  garam empedu
 Serum globulin 57g/L auto imun liver dis
Diagnosis /DD Kasus 4 87

 Kronikliver diseases
 Diagnosis pasti biopsy
 Primary biliary cirrhosis
88