Stewart-pemeriksaan Laboratorium Pada Gangguan Asam Basa.pdf

dr. Agustyas Tjiptaningrum, SpPK

GANGGUAN KESEIMBANGAN ASAM BASA, CAIRAN, DAN ELEKTROLIT

Acid Base Disorders

ACID-BASE REGULATION The body attempts to maintain a pH between 7.35 and 7.43 (hydrogen ion concentration between 35 and 45 nmol/L. This is achieved despite considerable variation in acid-base intake

Elimination of volatile acids Volatile hydrogen ion are eliminated by the lungs as CO2 based on: H+ + HCO3- ! H2CO3 ! CO2 + H2O

Sources of nonvolatile acids Diet, about 30 mEq of H ion is added to the body daily. (this can increase with a very high animal protein intake) Incomplete metabolism, about 30mEq/day (ketoacids,betahydroxybutyrate etc) Stool loss of Bicarbonate, around 20mEq bicarbonate is lost in stools daily.

Elimination of acid-base Lungs. The lungs eliminate a large amount of volatile acid as CO2.This can be greatly increased or modestly decreased if the lungs are normal. Kidneys. Acid excretion and alkali excretion Normally the kidneys are called on to excrete 70 to 100 mEq acid/day. This can be reduced to 0 or increased to fourfold. If faced with an alkaline load,the kidneys can excrete hundreds mEq of bicarbonate.

Abnormal States Lungs: Abnormalities can lead to reduced CO2 or too much CO2. Kidneys: Deficient or excess H ion excretion. Excess HCO3 regeneration or loss. Metabolic abnormalities: Diabetes, poor tissue perfusion, anaerobic metabolism. Gastrointestinal abnormalities: Vomiting, diarrhea.

Disturbances of Acid-base Balance

•  Buffer systems •  Respiration •  Renal function •  Maintain tight control within range 7.35 – 7.45

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The Central Role of the Carbonic AcidBicarbonate Buffer System in the Regulation of Plasma pH

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Figure 27.11a

The Central Role of the Carbonic AcidBicarbonate Buffer System in the Regulation of Plasma pH

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Figure 27.11b

Measurements and Calculations Hydrogen concentration (pH) Bicarbonate concentration (HCO3) pCO2 Anion Gap (AG).

The body’s buffer system. Carbonic acid – bicarbonate system Hemoglobin Protein

The Henderson – Hasselbalch equation Clinically, the carbonic acid – bicarbonate system is most important. By applying the law of mass action to the following reaction: CO2 + H2O ↔ H2CO3 ↔ H+ +HCO3one obtains the classic equation: pH = 6.1 + log [HCO3] / pCO2

The Henderson – Hasselbalch equation The classic equation: pH = 6.1 + log [HCO3] / pCO2 The practical equation: [H+] = 24 x pCO2 / [HCO3-] pH = 7.40 [HCO3-] = 24 mEq/L [H+] = 40 nmol/L pCO2 = 40 mmHg

Specific Disturbances Metabolic acidosis (a fall in pH and a decrease in HCO3-) Metabolic alkalosis (a rise in pH and an increase in HCO3-) Respiratory acidosis (a fall in pH resulting from a primary increase in pCO2) Respiratory alkalosis (a rise in pH from a decrease in pCO2)

Figure 27.6 The Basic Relationship between PCO2 and Plasma pH

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Figure 27.6

Acid-Base Disorders

•  Respiratory acid-base disorders •  Result when abnormal respiratory function causes rise or fall in CO2 in ECF •  Metabolic acid-base disorders •  Generation of organic or fixed acids •  Anything affecting concentration of bicarbonate ions in ECF

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Respiratory acid-base disorders •  Respiratory acidosis •  Results from excessive levels of CO2 in body fluids •  Respiratory alkalosis •  Relatively rare condition •  Associated with hyperventilation

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Compensation. Metabolic disorders: The pulmonary response will attempt to correct the pH. Respiratory correction occurs immediately. Respiratory disorders: The kidneys regulates bicarbonate levels It takes several hours to respond

Respiratory Acid-Base Regulation

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Figure 27.12a

Respiratory Acid-Base Regulation

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Figure 27.12b

Incomplete Compensation When compensation fails to occur, it is because of disease in that system. This is then termed a mixed or combined disorder

Anion Gap In the blood, when measured, cations seem to exceed anions in number. This is due to the plasma proteins, the difference amounts to about 10 – 12 mEq/L. Anion Gap = [Na+] – (Cl- + HCO3-)

Anion Gap An increased AG always means a metabolic acidosis is present. An increased AG implies that the cause of acidosis must be retention of some acid other than HCl.

Metabolic Acidosis Metabolic acidosis results from three types of disorders: excess acid load decreased acid excretion by the kidney alkali (bicarbonate) loss

Metabolic acidosis Normal AG (hyperchloremic metabolic acidosis) A. Excess intake (HCl, NH4Cl) B. Bicarbonate loss 1. GI tract Diarrhea Fistulas 2. Proximal renal tubular acidosis C. Decreased renal acid secretion. (distal renal tubular acidosis)

Metabolic acidosis Increased AG A. Ketoacidosis 1. Diabetes mellitus 2. Alcohol B. Lactic acidosis (usually due to shock) C. Poisons D. Renal failure

Metabolic acid-base disorders •  Major causes of metabolic acidosis are: •  Depletion of bicarbonate reserve •  Inability to excrete hydrogen ions at kidneys •  Production of large numbers of fixed / organic acids •  Bicarbonate loss due to chronic diarrhea •  Metabolic alkalosis •  Occurs when HCO3- concentrations become elevated •  Caused by repeated vomiting Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

The Response to Metabolic Acidosis

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Figure 27.13

Workup of metabolic acidosis. low Bicarbonate 1. Measure pH high pH Respiratory alkalosis

low pH Metabolic acidosis 2. Determine AG

Increased Gap ketoacidosis lactic acidosis uremia

Normal Gap Renal tubular acidosis GI disease Acid intake

Workup of normal AG metabolic acidosis 1. Serum K

Decreased

2. Urinary pH

pH >5.5

Distal RTA

Increased or Normal : Early uraemic acidosis Obstructive nephropathy Mineralocorticoid deficiency Infusion / ingestion: HCl, NH4Cl

pH<5.5 Proximal RTA Acute Diarrhea

Metabolic Alkalosis

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Figure 27.14

Causes of metabolic alkalosis HCl loss a. Gastrointestinal b. Increased urine acidification Excess alkali intake a. Alkali abuse b. Treatment of acidosis Severe potassium depletion

Primary causes of alkalosis Vomiting/Diuretics Vomiting/Diuretics ↓HCl

↓ECV ↑Aldosterone

↑Bicarbonate Reabsorbtion

H+secretion

Alkalosis Alkalosis

↓KCl H+ Shift into cells

Secondary causes of alkalosis K Depletion

ECF Contraction

AKALOSIS Shift H+ Into cells

Proximal Tubule Bicarbonate Reabsorbtion Acid Urine

Exchange Na for H in Distal Tubule Exchange Na for K in Distal Tubule

Aldosterone

Workup of metabolic alkalosis elevated Bicarbonate 1. measure pH low pH Respiratory acidosis

high pH Metabolic alkalosis 2. Assess ECV a. history b. exam c. urine Na

ECV depletion a. GI losses b. Diuretics c. severe K depletion

ECV normal a. aldosteronism b. alkali intake c. severe K depletion

Respiratory disorders Respiratory Acidosis This disorder results from hypoventilation. Because chemical buffering is limited. Acute respiratory failure is associated with severe acidosis with little increase in plasma bicarbonate. Chronic respiratory failure causes increased renal generation of bicarbonate.

Causes of respiratory acidosis Depression of respiratory center Stroke, Tumors, Encephalitis, Drugs

Limitation of chest wall movement Neuromuscular disorders, Trauma, Surgery, Fixation of ribs

Pulmonary disease Chronic bronchitis, Chronic emphysema, Asthma, Pneumonia

Depression of respiratory center Strokes Tumors Encephalitis Drugs : narcotics sedatives tranquilizers

Limitation of chest wall movement Neuromuscular disorder : myasthenia gravis Guillain – Barré tetanus Trauma and surgery Fixation of ribs

Pulmonary disease Chronic bronchitis Chronic emphysema Asthma Pneumonia

Respiratory alkalosis This disorder results from hyperventilation due to a variety of causes. Acute hypocapnia causes release of H ions from tissue buffers, this tends to minimize the reduction of plasma bicarbonate. Chronic hypocapnia stimulates renal adaptation with reduced bicarbonate generation, thus lowering plasma bicarbonate concentration.

Causes of respiratory alkalosis Direct stimulation of respiratory center. Psychogenic, CNS disease, Sepsis, Hypermetabolic state, Exercise, Liver failure, Drugs

Reflex stimulation of respiratory center. Pneumonia, Pulmonary edema, Pulmonary fibrosis, Asthma, Cyanotic heart disease

Excessive mechanical ventilation

Direct stimulation of respiratory center Psychogenic CNS disease : stroke, encephalitis Sepsis Hypermetabolic state: fever, thyrotoxicosis. Exercise Liver faillure Drugs: salicylates, ammonia, progesterone

Reflex stimulation of respiratory center Pneumonia Pulmonary edema Pulmonary fibrosis Asthma Cyanotic heart disease

Detection of acidosis and alkalosis

•  Diagnostic blood tests •  Blood pH •  PCO2 •  Bicarbonate levels •  Distinguish between respiratory and metabolic

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A Diagnostic Chart for Acid-Base Disorders

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Figure 27.15

Aging and Fluid, Electrolyte, and Acid-base Balance •  Reduced total body water content •  Impaired ability to perform renal compensation •  Increased water demands •  Reduced ability to concentrate urine •  Reduced sensitivity to ADH/ aldosterone •  Net loss of minerals •  Inability to perform respiratory compensation •  Secondary conditions that affect fluid, electrolyte, acidbase balance

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TEORI STEWART UNTUK KESEIMBANGAN ASAM BASA dr. Agustyas Tjiptaningrum, SpPK

PENDAHULUAN •  Konsep asam basa tradisional

–  berdasarkan konsep Henderson-Hasselbalch serta Bronsted & Lowry pH = pKa + log10 ( [HCO3-] / PaCO2 ) •  Konsep tradisional tidak dapat menjelaskan beberapa keadaan gangguan keseimbangan asam basa seperti:

–  Asidosis hiperkloremik –  Asidosis dilusional •  Stewart menawarkan pendekatan baru: pendekatan fisika kimiawi / kuantitatif

PENDAHULUAN

Pendekatan teori Stewart: 1.  2.  3.  4. 

5. 

6. 

[H+] x [OH-] = K 'w (keseimbangan disosiasi air) [H+] x [A-] = KA x [HA] (asam lemah) [HA] + [A-] = [ATOT] (konservasi massa A) [H+] x [HCO3-] = KC x PCO2 (keseimbangan pembentukan ion bikarbonat) [H+] x [CO3=] = K3 x [HCO3-] (keseimbangan pembentukan ion karbonat) [SID] + [H+] - [HCO3-] - [A-] -[CO3=] - [OH-] = 0 (prinsip netralitas elektrik)

Grogono AW. Stewart’s strong ion difference [online]. 2006; Available from: URL: http://www.acidbase.com/strongion.php.

[H+] and [HCO3-] depend on concentrations of other ions Stewart’s Dependent Variables

Stewart’s Independent Variables

[H+]

[OH-]

PCO2

[HCO3-]

[CO3=]

[ATOT]

[HA]

[A-]

[HA] = weak acid [A-] = weak ions

[SID] [ATOT] = total non-volatile acids [SID] = net Strong Ion Difference

Grogono AW. Stewart’s strong ion difference [online]. 2006; Available from: URL: http://www.acid-base.com/ strongion.php.

FAKTOR YANG MEMPENGARUHI H+ DAN HCO3SID

pCO2

H+ / HCO3-

Asam lemah

Konstanta disosiasi air dan asam lemah Modifikasi dari: Slide 53 Story DA.. Crit Care. 2004;8:253-8.

KONSEP TRADISIONAL VERSUS STEWART

•  Tradisional: –  pH = pKa + log10 ( [HCO3-] / PaCO2 ) –  CO2 : komponen respiratorik –  HCO3-: komponen metabolik

•  Stewart: –  Tiga variabel yang independen: •  pCO2 •  Strong Ion Difference [SID] •  Total asam lemah nonvolatil [ATOT] Slide 54

ELEKTROLIT (ION KUAT) MENENTUKAN PH  

Ion kuat (strong ion) Disosiasi sempurna pada larutan air Misal: Na+, K+, Ca2+, Mg2+, dan Cl-

 

Ion lemah Terdapat dalam bentuk terdisosiasi (ion) dan bentuk tak terdisosiasi

 

SID: Perbedaan jumlah kation kuat dan anion kuat SID = [jumlah kation kuat] - [jumlah anion kuat] SID = [Na+] + [K+] + [Ca2+] + [Mg2+] - [Cl-] - [UA-] UA: konsentrasi anion kuat yang tak diukur (unmeasured strong anion) seperti asam keto, laktat, dan substansi endogen lain

Slide 55

pH RESPIRATORY

PCO2

METABOLIC

SID Na+, K+ Ca++, Mg++ ClLactate Ketoacids

ATOT Albumin Globulin Phosphat e

Sulfate

Constable PD. Review Article, Clinical Assessment of Acid-Base Status: Comparison of Henderson-Hasselbalch and Strong Ion Approaches. Veterinary Clinical Pathology, 29;4, 2000

SID

 

Perbedaan jumlah kation kuat dan anion kuat SID = [jumlah kation kuat] - [jumlah anion kuat] SID = [Na+] + [K+] + [Ca2+] + [Mg2+] - [Cl-] - [UA-] UA: konsentrasi anion kuat yang tak diukur (unmeasured strong anion) seperti asam keto, laktat, dan substansi endogen lain

 

Praktis:      

Slide 57

SIDa = (Na+ + K+ + Ca2+ + Mg2+) - (Cl- + Laktat -) SIDe = CO2 + ASIG = SIDa - SIDe

Prinsip elektronetralitas [jumlah kation] = [jumlah anion]

Slide 58

Kaplan LJ, Frangos S. Crit Care. 2005 Apr;9(2):198-203.

Prinsip fisika-kimiawi larutan biologik (2)  

Prinsip konservasi massa  

Jumlah substansi tetap konstan  

 

Penambahan ion kuat (contoh: NaCl)  

 

Bila tidak dihilangkan atau dipakai pada reaksi kimia: •  Menyebabkan perubahan elektronetralitas •  Ion H+ dan OH- dihasilkan atau dipakai untuk memelihara elektronetralitas.

Laktat    

Slide 59

Kecuali bila ditambahkan, diproduksi, dipindahkan atau dihilangkan

Di metabolisme tubuh Laktat dari cairan infus akan dimetabolisme sehingga kurang mempengaruhi SID tubuh

Total asam lemah (ATOT)  

Adalah variabel independen  

 

ATOT = AH + A-

 

A- bukan merupakan variabel independen  

   

Slide 60

juga menentukan konsentrasi H+ (prinsip konservasi massa A)

dipengaruhi oleh SID dan pCO2

Peningkatan ATOT : asidosis Penurunan ATOT : alkalosis

pCO2  

Ventilasi  

 

Eliminasi CO2 tidak mencukupi:    

 

 

Bukan karena HCO3 berfungsi sebagai buffer Karena fenomena fisika kimiawi guna mencapai chemical equilibrium

Kompensasi untuk peningkatan pCO2:  

Slide 61

Peningkatan pCO2 Peningkatan H+ dan HCO3-

Peningkatan HCO3 

 

Mempertahankan pCO2 arterial pada 35-45 mmHg

Regulasi SID oleh ginjal: ekskresi Cl-

APLIKASI TEORI STEWART

Aplikasi konsep tradisional versus Stewart  

 

Konsep tradisional hanya memperhatikan pCO2 dan HCO3Konsep Stewart lebih komprehensif karena memperhatikan peran lebih banyak faktor:      

Slide 63

CO2 Ion kuat seperti Na+, K+, Cl-, Ca2+, Mg+ Asam lemah seperti albumin, globulin dan fosfat

Constable PD. Vet Clin Pathol. 2000;29(4):115-28.

Konsep Tradisional versus Stewart  

Peran Ginjal   Regulasi ekskresi H+ dan amonia

 

 

 

Slide 64

Regulasi ekskresi/ reabsorbsi elektrolit Terutama Cl- untuk keseimbangan asam basa NH4- sebagai konjugat Cl- supaya K+ atau Na+ tidak perlu diekskresi

Konsep Tradisional versus Stewart  

Peran saluran gastrointestinal   Lambung  

 

Ekskresi

 

H+

 

Cairan usus  

Lambung  

HCO3 

Pankreas    

 

 

Reabsorbsi ClSID cairan ≈ plasma

Usus besar    

Slide 65

Ekskresi Na+ Cairan pankreas •  SID tinggi

Usus halus  

 

Ekskresi ClCairan lambung •  SID rendah

Reabsorbsi Na+ Cairan usus besar •  SID tinggi

Diagnosis gangguan keseimbangan asam basa  

Gangguan respiratorik ≈ konsep tradisional

 

Kontribusi utama: gangguan metabolik

 

Pemeriksaan SID menuntut banyak parameter

 

Analisis anion gap (AG) masih bermanfaat Parameter

Perubahan

Status

SID

Meningkat

Alkalosis metabolik

SID

Menurun

Asidosis metabolik

ATOT

Meningkat

Asidosis metabolik

ATOT

Menurun

Alkalosis metabolik

Kellum JA. Crit Care. 2000;4(1):6-14. Slide 66

Anion gap: masih bermanfaat

Kaplan LJ, Frangos S. Crit Care. 2005 Apr;9(2):198-203. Slide 67

Gangguan metabolik  

Asidosis metabolik  

AG tinggi  

 

Ketosis, asidosis laktat, keracunan, gagal ginjal, sepsis

AG normal Asidosis tubuler ginjal: SID urin > 0

Nonrenal: SID urin < 0

Tipe I (distal): pH urin > 5,5

Gastrointestinal : diare Tipe II (proximal): pH urin < 5,5/ small bowel + serum K rendah drainase pankreas Tipe IV: defisiensi aldosteron: pH urin < 5,5 / serum K+ tinggi

Iatrogenik: nutrisi parenteral garam, anion exchange resins

SID urin = Na+ + K+ - ClKellum JA. Crit Care. 2000;4(1):6-14. Slide 68

Alkalosis metabolik (SID tinggi) Kehilangan klorida < kehilangan natrium Responsif klorida (konsentrasi Cl- urin <10 mmol/L) Kehilangan pada gastrointestinal: muntah, drainase gaster, chloride wasting diarrhea (villous adenoma) Postdiuretik Posthiperkapnia Resisten klorida (konsentrasi Cl- urin > 20 mmol/L) Kelebihan mineralokortikoid Penggunaan diuretik Beban natrium eksogen (> klorida) Pemberian garam natrium (asetat, sitrat): transfusi darah masif, nutrisi parenteral, expander volume plasma, natrium laktat (larutan Ringer) Penyebab lain Kellum JA. Crit Care. 2000;4(1):6-14. Slide 69

Defesiensi berat kation intraseluler: Mg2+, K+

Terapi cairan  

 

Terapi cairan dengan mempertimbangkan SID   Memperbaiki outcome Hindari asidosis metabolik Parameter

Konsentrasi cairan ekstrasel

Setelah dilusi dengan cairan NaCl

Setelah dilusi dengan air

[Na+] (mmol/L)

140

142,5

105

[Cl-] (mmol/L)

100

112,5

75

[A-] + [HCO3-]

40

30

30

SID

40

30

30

Cairan ekstrasel 3 L, NaCl 0,15 mol/L 1L, air 1L Morgan TJ. Crit Care. 2005;9(2):204-11. Slide 70

Kelemahan & Kelebihan Untung & Rugi

Kelemahan konsep tradisional  

Deskriptif kualitatif

 

Tidak bersifat mekanistik

 

 

Gangguan metabolik sukar dijelaskan

 

Skala pH kurang menggambarkan realitas [H+]

 

Slide 72

Gagal membedakan variabel dependen dan independen

Akurasi menurun pada perubahan protein, suhu dan elektrolit

Kelebihan Teori Stewart  

Pendekatan sistematik

 

Beda variabel dependen dan independen

 

Penjelasan fisiologi dan patologi asam basa lebih baik      

 

Perbaiki upaya deteksi unmeasured ion  

 

Gunakan SIG

Strategi penatalaksanaan kelainan asam basa  

Slide 73

Peran amonia pada homeostasis asam basa Alkalosis metabolik pada penurunan albumin Asidosis hiperkloremik

Terapi cairan

Kelemahan  

Perhitungan SID: parameter banyak  

 

Analit dengan kadar rendah:  

   

 

Slide 74

Tidak praktis

Kesalahan relatif besar

Pengukuran ATOT tidak jelas Menolak pengaruh hemoglobin sebagai buffer plasma Data klinis masih kurang

Titik temu konsep Stewart dan tradisional

 

Peran CO2

 

Persamaan Henderson-Hasselbalch  

 

Kedua konsep dapat berguna dalam klinik?

 

Koreksi persamaan Hendersen-Hasselbalch  

Slide 75

Versi sederhana dari konsep Stewart yang berlaku lebih umum?

pH= 6,1 + log (SID-[ATOT]) / 0,03 x pCO2

Case illustration Liver cirrhosis, bleeding varices, male, 53 year. Alb. 13 g/L, K+. 5.2 mEq/L, Na+. 125 mEq/L, Cl-. 98 mEq/L, pH 7.4, [HCO3-] 24 mEq/L, PCO2 39 mmHg, Ca++ 3.2 mEq/L, Mg ++ 1 mEq/L, Pi (fosfat inorganik) = 1.55 mg/dL. Case analysis: [Alb-] = 13 x {0.123 x (7.4 – 0.631)} = 3.6296 mEq/L [Pi-] = (1.55 x 10/30.97) x 0.309 x (7.4 – 0.469) = 0.90968 mEq/L SIDe = 24 + 3.6296 + 0.90968 = 28.53928 mEq/L SIDa = (125 + 5.2 + 3.2 + 1) – 98 = 36.4 mEq/L Stong Ion Gap = 7.86072 (SIG > 5) mEq/L AG = 125 + 5.2 – (98 + 24) = 8.2 mEq/L AG corrected= AG + (0.25 x [44 – 13]) = 15,95 mEq/L BE = 0.9287 x (24 – 24.4) + 14.83 x (7.4 – 7.4) = - 0.37148 All traditional parameters are apparently normal. Metabolic acidosis, with water excess (low sodium) Fencl V. Jabor A. Kadza A. Figge J. Diagnosis of Metabolic Acid-Base Disturbances in Critically Ill Patients. Am J Respir Crit Care Med. 2000;162 (6): 2246 - 51

Case illustration Male, 41 year, multiple trauma. Alb.18 g/L, K+ 4.5 mEq/L, Na+ 143 mEq/L, Cl- 111 mEq/L, pH 7.4, [HCO3-] 25 mEq/L, PCO2 41 mmHg, Ca++ 4.0 mEq/L, Mg++1.6 mEq/L, Pi 2.05 mg/dL. Case analysis: [Alb-] = 18 x {0.123 x (7.4 – 0.631)} = 5.0256 mEq/L [Pi-] = (2.05 x 10/30.97) x 0.309 x (7.4 – 0.469) = 1.2031 mEq/L SIDe = 25 + 5.0256 + 1.2031 = 31.2287 mEq/L SIDa = (143 + 4.5 + 4.0 + 1.6) – 111 = 42.1 mEq/L SIG = 42.1 – 31.2287 = 10,8713 mEq/L AG = 143 + 4.5 – (25 + 111) = 11.5 mEq/L AG corrected= 11.5 + (0.25 x [44 – 18]) = 18 mEq/L BE = 0.9287 x (25 – 24.4) + 14.83 x (7.4 – 7.4) = 0.5572 Hyperchloremic acidosis matched by alkalosis of hypoalbuminemia. Traditional approach: no acid-base disturbance detected

Fencl V. Jabor A. Kadza A. Figge J. Diagnosis of Metabolic Acid-Base

dr. Agustyas Tjiptaningrum, SpPK

AN IDEAL OF TUMOR MARKERS

•  SPECIFIC FOR A GIVEN TYPE OF CANCER (TUMOR SPECIFIC MARKERS) à NOT PRODUCE BY NORMAL CELLS OR BENIGN CELLS •  SENSITIVE TO DETECT SMALL TUMOR à FOR EARLY DIAGNOSIS OR SCREENING MOST ARE FOUND WITH DIFFERENT TUMOR OF THE SAME TISSUE TYPE (TUMOR ASSOCIATED MARKERS)

APPLICATION OF TUMOR MARKERS

• 

•  • 

NONE OF THE TUMOR MARKERS KNOWN TODAY MEETS THE REQUIREMENTS OF AN IDEAL MARKER à NONE HAS 100% SENSITIVITY 100% SPECIFICITY MOST OF THE TUMOR MARKERS ARE NOT DISEASE SPECIFIC NOT EVERY TUMOR OF THE SAME ORGAN EXPRESS THE SAME TUMOR MARKER

Aplikasi tumor marker yg ideal •  Mesti disekresikan ke darah atau cairan tubuh shg mudah dideteksi •  Memiliki half life yg panjang •  Memiliki spesifisitas dan sensitivitas yg tinggi

CLINICAL UTILITY OF TUMOR MARKERS

•  ADDITIONAL TOOL FOR DIAGNOSIS PROGNOSIS •  USEFUL FOR MONITORING COURSE OF DISEASE •  DETERMINE EFFECTIVENESS OF TREATMENT

•  Contoh alur diagnosis

CLINICAL UTILITY OF TUMOR MARKERS

•  MONITORING HIGH RISK GROUPS e.g AFP IN HBsAg CARRIERS LIVER CIRRHOSIS CALCITONIN IN FAMILIES SUSCEPTIBLE TO C CELL Ca •  DETERMINE PROGNOSIS à INCREASE VALUE CLOSELY LINKED TO PATIENT PROGNOSIS ALMOST ALL MARKERS SHOW HIGHER VALUE AT ADVANCED TUMOR STAGES

INDICATIONS FOR TUMOR MARKER DETERMINATION Marker

Screening

Diagnosis

Follow up

Prognosis

CEA

Risk group

C-cell Ca

Colon, breast, lung, C-cell

Colon

AFP

Risk group

Germ cell, HCC

Germ cell, HCC

Germ cell

Pancreas

Pancreas, billiary duct

--

CA19.9

--

CA125

--

--

Ovary

--

CA15.3

--

--

Breast

--

NSE

--

SCLC

SCLC, neurobl

--

SCC

--

--

Cervical, ENT, esophagus

--

Cyfra21.1

--

--

NSCLC

--

HCG

Risk group

Germ cell, trophobl tumor

Germ cell, trophobl tumor

Germ cell trophobl

PSA

Males>50

Prostate

Prostate

--

SCHEDULE OF TUMOR MARKERS

•  BEFORE TREATMENT •  BEFORE EACH CHANGE OF TREATMENT •  AFTER TREATMENT 1 – 2 year : MONTHLY AT FIRST UNTIL VALUE HAVE SHOWN MARKED DECREASE THEN EVERY 3 MONTHS 3 – 5 year : TWICE YEARLY > 6 year : YEARLY

SCHEDULE OF TUMOR MARKERS

• IF MARKER VALUE INCREASE FREQUENT MONITORING à 2 - 4 WEEKS •  IF RELAPSE OR METASTASIS IS SUSPECTED •  IF STAGING IS REPEATED

INTERPRETATION OF TUMOR MARKERS MARKER’S LEVEL SHOULD INCREASE WITH PROGRESSION DECREASE WITH REGRESSION

•  LINEAR INCREASE IN 3 CONSECUTIVE SPECIMEN WITH 3 MONTHS INTERVAL à RECURRANCE •  A DECREASE LEVEL OF 50% à PARTIAL REMISSION •  AN INCREASE LEVEL OF 25% FROM LAST LEVEL OR PROGRESSIVE INCREASE à RECURRANCE METASTASIS

CYFRA 21-1

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