臨床數據的判讀-藥研所 2018

臨床檢驗數據的判讀
Interpretation of
Clinical Laboratory Tests
成大醫院腎臟科王明誠醫師
藥學系/臨床藥學與藥物科技研究所教授
1
數據的利用
 臨床數據的用途有二：
 幫助醫師確定疾病的種類
-- 可作為臨床診斷的依據。
 幫忙醫師了解疾病的進行情況
-- 可作為判定治療效果或預後的指標。
 數據能否發揮其用途，端賴醫師能否正確地判斷。
2
數據的正常值
 一般說來，實驗室檢查所得到的結果大致遵循著「常態
分佈」（Normal distribution），因此可用多次測定所得
到的「平均值」及「標準偏差」（Standard deviation）
來表達「數值的正常值」。
 在常態分布區線上，屬於「平均值  1 標準偏差」之間
的面積為68%，屬於「平均值  2 標準偏差」之間的面
積為95.4%。
 如果某一數值落於「 2 標準偏差」之區域外，它可能
不屬於「正常」，須加以注意。
 影響正常值的因素：年齡、性別、生活環境、飲食習慣、
檢驗方法。
3
正常值的分佈
正常值是根據多數健康者為對象施行測定所得到的數值
而求得的，並非都呈示均等的分佈，可呈現兩種型式：
左右對稱，「一般的常態分佈」例如 albumin、Na。
左右不對稱，「對數的常態分佈」
亦即將橫軸上的數值換為對數之後，就變為左右對稱型
的常態分佈了。例如 GOT、amylase。
4
檢驗數據的判讀
對於檢驗數據本身的判讀，必須根據：
（1）該項目之正常生化學性質、新陳代謝狀況及生理機能
（2）該項目在病態情況下可能發生的性質、代謝、機能之
變化情形及其與病變或病徵之關係
 第一個原則：時時將實驗室檢驗結果與病人呈現的臨床
病徵綜合在一齊考慮。
第二個原則：儘可能將數種檢驗數值綜合一齊考慮。
5
數據的性質
疾病
存在不存在
檢陽性 a b
驗陰性 c d
靈敏度 = a / ( a + c ) 特定度 = d / ( b + d )
偽陰性率 = c / ( a + c ) 偽陽性率 = b / ( b + d )
不正常數據的預測值 = a / ( a + b )
正常數據的預測值 = d / ( c + d )
6
冠狀動脈疾病
存在50% 不存在50% 臨床判斷
(500) (500)
不正常 a 400 b
運
輔動 130
助心 c d
檢電正常 100 370
驗圖
靈敏度80% 特定度74%
Positive predictive rate = 400 / (400+130) = 75%
正常數據的預測值 =d/(c+d)
Negative predictive rate = 370 / (370+100) = 79%
7
冠狀動脈疾病
(900) (100)
不正常 a 720 b
運
輔動 26
助心 c d
檢電正常 180 74
驗圖
8
冠狀動脈疾病
(900) (100)
不正常 a 720 b
運
輔動 26
助心 c d
檢電正常 180 74
驗圖
不正常數據的預測值 Positive predictive rate = 97%

正常數據的預測值 Negative predictive rate = 29%
醫師對於疾病存在的預估率很高時，檢驗數據的
正常與否對於該項疾病預估率的影響並不大 9
冠狀動脈疾病
(100) (900)
不正常 a 80 b
運
輔動 230
助心 c d
检電正常 20 670
驗圖
10
冠狀動脈疾病
(100) (900)
不正常 a 80 b
運
輔動 230
助心 c d
检電正常 20 670
驗圖
不正常數據的預測值 Positive predictive rate = 26%

正常數據的預測值 Negative predictive rate = 97%
醫師對於疾病存在的預估率很低時，檢驗數據的
正常與否對於該項疾病預估率的影響也不大 11
全身性紅斑性狼瘡症
Systemic lupus erythematosus
 用於評估可能罹患全身性紅斑性狼瘡症病人的
檢驗項目中:
ANA的靈敏度是 99% 而特定度為 80%，
狼瘡細胞檢查的靈敏度是 76% 而特定度為 80%，
Anti-nDNA抗體的靈敏度是 73% 而特定度為 99%，
Anti-Sm抗體的靈敏度是 30% 而特定度是 99%。
12
 由上述的各項檢驗的性質來看
 最初用以評估病人的檢驗最好是
抗核抗體 ANA (靈敏度是 99% 特定度為 80%)
此項檢查的目的是刪除可能性較低的疾病，
它的高靈敏度可以幫助醫師達到這個目的。
13
 如果抗核抗體ANA呈現陽性
 進一步應該施行的檢驗是
Anti- nDNA (靈敏度是 73% 特定度為 99%)
因為此時所需的檢查是能夠用以確定疾病
存在的高特定度檢查。
14
 Anti-Sm 的特定度雖然很高，但靈敏度
太低 (靈敏度是 30% 特定度是 99% )，一部分
病人可能無法用此項檢驗偵查出來，所以
不是十分理想的檢查。
 可用來輔助確認紅斑性狼瘡的診斷。
15
數據的單位
 The standardized system that has been adopted by many
countries throughout the world is the System International
(SI) units of measure.
 The SI is an outgrowth of the metric system.
 The basic underlying reasons for a change to SI units is that
biological substances react in vivo on a molar basis.
Test Current units Factor SI units

Creatinine 0.5-1.7 mg/dl 88.4 44-150 mol/L
Cholesterol < 200 mg/dl 0.0259 < 5.18 mmol/L
16
Clinical Laboratory Tests
 Chemistries
 Enzymatic activities
 Hormone values
 Urinary chemistries
 Hematologic values
 Immunology testing
 Therapeutic agents
 Antimicrobials
17
Total body water,
Plasma osmolality and sodium
 Water comprises about 60% of body weight in men and 50%
in women.
 The body water is distributed between 3 major compartments:
Intracellular fluid, ICF (2/3)
Extracellular fluid, ECF (1/3)
Intravascular and interstitial spaces ( 1:4 )
 Water and Na+ balance are regulated independently.
 Changes in [Na+] generally reflect disturbed water homeostasis
and ICF volume, whereas alterations in Na+ content are
manifested as ECF volume contraction or expansion and imply
Na+ balance.
18
總身體之體液容積
= 0.6  體重
( 42 liters in 70 kg 成年男性 )
細胞內液細胞外液
2/3 ( 28 liters ) 1/3 ( 14 liters )
血漿間質液
1/5 ( 3 liters ) 4/5 ( 11 liters )
水份於體內的分佈
19
體液的電解質成份
電解質血清間質液細胞內液 (肌肉)
mEq/L mEq/L mEq/kg H2O
陽離子
鈉 (Na+) 142 145 10+
鉀 (K+) 4 4 156
鈣 (Ca2+) 5 3.3
鎂 (Mg2+) 2 26
總陽離子 153 149 195
陰離子
氯 (Cl-) 102 114 2±
重碳酸鹽 (HCO3-) 26 31 8±
磷酸鹽 (HPO42-) 2 95
硫酸鹽 (SO42-) 1 20
有機酸 (Organic acid) 6
蛋白質 (Protein) 16 55
總陰離子 153 145 180+
Total body water,
Plasma osmolality and sodium
 Plasma sodium
Normal range: 135-145 mmol/L.
 Osmolality
 The solute or particle concentration of a fluid.
 Solutes that are restricted to the ECF (Na+ and accompanying
anions) or the ICF (K+ salts and organic phosphate esters)
determine the effective osmolality.
 Normal range of plasma osmolality: 275-300 mOsm/kg
[Glucose] BUN
 Calculated Posm  2  Plasma [Na+] + +
18 2.8
21
Hyponatremia (Na+ < 135 mmol/L)
Plasma osmolality
High Normal Low
*Hyperglycemia *Hyperproteinemia Maximal volume of

*Mannitol *Hyperlipidemia maximally dilute urine?
*Bladder irrigation
No Yes
ECF volume *Primary polydipsia

*Reset osmostat
22
Hyponatremia (Na+ < 135 mmol/L)
ECF volume
Increased Normal Decreased
*Heart failure *SIADH Urine Na+

*Hepatic cirrhosis *Exclude hypothyroidism concentration
*Nephrotic syndrome *Exclude adrenal insufficiency
*Renal insufficiency
< 10 mmol/L > 20 mmol/L
*Extrarenal Na+ loss *Na+-wasting nephropathy

*Remote diuretic use *Hypoaldosteronism
*Diuretic
*Remote vomiting
*Vomiting
23
• 25歲健康男性，於5天前發生無菌性腦膜炎併經常
嘔吐，理學檢查顯示病患呈缺水狀態。第5天，經
點滴補充後已恢復正常。
Day 2 Day 5
血漿
鈉 mmol/L 130 117
鉀 mmol/L 3.1 4.0
氯化物 mmol/L 87 83
重碳酸鹽 mmol/L 33 24
滲透壓 mosm/kg H2O 270 245
血糖 mg/dL 90 54
肌酸酉干 mg/dL 2.3 1.0
尿液
鈉 mmol/L 8 50
滲透壓 mosm/kg H2O 750 407 24
• 25歲健康男性，於5天前發生無菌性腦膜炎併經常
嘔吐，理學檢查顯示病患呈缺水狀態。第5天，經
點滴補充後已恢復正常。
Day 2 Day 5
血漿
鈉 mmol/L 130 117
鉀 mmol/L 3.1 4.0
重碳酸鹽 mmol/L 33 24
滲透壓 mosm/kg H2O 270 245
血糖 mg/dL 90 54
肌酸酉干 mg/dL 2.3 1.0
尿液
鈉 mmol/L 8 50
滲透壓 mosm/kg H2O 750 407 25
Potassium
 Within cells, K+ is the most abundant cation.
 About 2% of the body’s K+ is located in the extracellular
fluid (body K+ store = 50-55 mmol/kg).
 Normal range of plasma potassium: 3.5-5.0 mmol/L.
 Physiologic role of potassium:
 Cell growth
 DNA and protein synthesis
 Function of enzyme system
 Control of cell volume
 Maintenance of acid-base balance
 Maintenance of cell excitability and muscle contraction
(including heart)
26
Hypokalemia (K+ < 3.5 mmol/L)
Urinary K+ excretion
 15 mmol/d > 15 mmol/d
Acid-base status
Assess K+ secretion, TTKG
Metabolic acidosis Metabolic alkalosis

TTKG > 4 TTKG < 2
*Lower GI K+ loss *Remote diuretic use
*Remote vomiting *Na+-wasting
*K+ loss via sweat nephropathy
*Osmotic diuresis
Acid-base status *Diuretic
27
TTKG
 TTKG
Transtubular K+ concentration gradient
 A rapid and simple test designed to evaluate the
driving force for net K+ secretion
 TTKG
Urine K+ / Plasma K+
=
Urine osm / Plasma osm
28
Hypokalemia (K+ < 3.5 mmol/L)
TTKG > 4
Acid-base status
Metabolic acidosis Metabolic alkalosis
*Diabetic ketoacidosis Hypertension

*Proximal (type 2) RTA
*Distal (type 1) RTA No
Yes
*Amphotericin B
*Vomiting
*Mineralocorticoid excess
*Bartter’s syndrome
*Liddle’s syndrome
*Exclude diuretic abuse
*Hypomagnesemia
29
53-year-old woman presented with general weakness for 3 days.
Creatinine (mg/dl) 0.9

BUN (mg/dl) 12
Ca (mg/dl) 8.4
Na (mmol/L) 146
K (mmol/L) 2.1
Cl (mmol/L) 112
24-h urine K excretion (mmol) 47.6
TTKG 8.6
ABG
pH 7.291
HCO3 13.8
30
Calcium
 Calcium is essential for bone formation and neuromuscular
function.
 Approximately 99% of body calcium is in bone; most of the
remaining 1% is in the ECF.
 Nearly 50% of serum calcium is ionized (free), whereas the
remainder is complexed, primarily to albumin
 Normal range of plasma (total) calcium: 8.6-10.1 mg/dl.
 Correct calcium level for hypoalbuminemia
Corrected calcium = 0.8  [ 4.0 – Palbumin (g/dl)] + Pcalcium
31
Hypercalcemia
 Causes of hypercalcemia
 Primary hyperparathyroidism
>90%
 Malignancy
 Others
 Sarcoidosis, granulomatous diseases
 Vitamin D toxicity
 Hyperthyroidism
 Lithium use
 Milk-alkali syndrome
 Immobilization
 Thiazide diuretics
 Familial hypocalciuric hypercalcemia
32
Causes of Hypercalcemia
Uncommon Rare
Common
(< 1 %) (<0.01 %)
Primary Immobilization
Vitamin D excess
hyperparathyroidism
(99 % of outpatients) Vitamin D intoxication Familial hypocalciuric
Sarcoidosis hypercalcemia
Tuberculosis
Malignancy (calcium-sensing receptor
(~ 99% of ill patients) mutation , insensitive to
PTHrP Tertiary
negative feedback)
Solid tumors, (esp: lung, oral,
hyperparathyroidism
larynx, cervix, breast, renal Chronic renal failure  Medications
cell tumors) parathyroid hyperplasia Thiazide diuretics
T-cell lymphoma, myeloma Lithium (sti PTH secret)
Calcitriol : B-cell lymphoma Milk-alkali syndrome
Local osteolysis cytokines,TNF) (from calcium antacid)
Multiple myeloma Vitamin A intoxication
Breast cancer
Postgrad Med 2004;115(4):69:-73 Am Fam physician 2003;67:1959-66

Differential Diagnosis of Hypercalcemia
Serum Calcium
> 10.6 mg/dL
Determine whether hypercalcemia is real, measure ionized Ca

adjust for change in serum albumin level, careful drug history of Li, Vit D or A
Measure PTH
PTH high PTH - N or Low

Hyperparathyroidism Malignancy- primary or metastasis
If cause remains unclear

measure Vit D
Consider others
Vit D high
*Hyperthyroidism
consider Sarcoidosis
*Milk-alkali syndrome
CXR *Familial hypocalciuric hypercalcemia
Syed Nasrat Imam, MD

Am Fam physician
2003;67:1959-66
Progressive deterioration of renal function developed in recent
2 years. Bilateral renal stones was diagnosed by sonography.
BUN 7-21 mg/dl 45

Creatinine 0.7-1.5 mg/dl 2.0
GOT/GPT 5-40 U/l 26/15
A/G 4.1/3.4
ALK-P 30-110 U/l 133
Na 135-145 mEq/l 136
K 3.5-5.5 mEq/l 5.1
Cl 95-105 mEq/l 110
Ca 8.1-10.1 mg/dl 13.0
P 2.5-5 mg/dl 2.9
Mg 1.7-2.2 mg/d 2.4
BUN 7-21 mg/dl 45
Creatinine 0.7-1.5 mg/dl 2.0
GOT/GPT 5-40 U/l 26/15
A/G 4.1/3.4
ALK-P 30-110 U/l 133
Na 135-145 mEq/l 136
K 3.5-5.5 mEq/l 5.1
Cl 95-105 mEq/l 108
Ca 8.1-10.1 mg/dl 13.0
P 2.5-5 mg/dl 2.8
Mg 1.7-2.2 mg/d 2.4
Bicarbonate 22-26 mmol/l 16
iPTH 8-74 pg/ml 849
Proteins
 Three major types of protein present in the plasma:

Albumin, globulin, and fibrinogen.
 The principal function of albumin is to provide colloid osmotic
pressure, which prevents plasma loss from the capillaries.
 The globulins perform a number of enzymatic functions in the
plasma, and they are principally responsible for both the natural
and acquired immunity.
 The fibrinogen polymerizes into long fibrin threads during
blood coagulation, thereby forming blood clots that help to
repair leaks in the circulatory system.
38
Proteins
 Essentially all the albumin and fibrinogen of the plasma
proteins, as well as 60 to 80% of the globulins, are formed
in the liver.
 The remainder of the globulins are formed in the lymphoid
tissues and other cells of the reticuloendothelial system.
These are mainly the gamma globulins that constitute the
antibodies.
 The rate of plasma protein formation by the liver can be as
great as 2 grams per hour or as much as 50 grams per day.
39
Albumin
 Normal range of plasma albumin: 3.5-5.0 g/dl.
 Plasma albumin
Increased in
 Dehydration (relative increase)
Decreased in
 Inadequate intake (e.g., malnutrition)
 Decreased absorption (e.g., malabsorption syndrome)
 Impaired synthesis (e.g., liver diseases, chronic infection)
 Increased breakdown (e.g., neoplasms, infection, trauma)
 Increased loss (e.g., burns, hemorrhage, nephrotic syndrome,
protein-losing enteropathy)
 Increased need (e.g., hyperthyroidism, pregnancy)
40
Blood urea nitrogen (BUN)
 The BUN measures the amount of urea nitrogen in the blood.
 Urea is formed in the liver as the end product of protein
metabolism and digestion.
 During ingestion, protein is broken down into amino acids.
In the liver these amino acids are catabolized and free ammonia is
formed. The ammonia molecules are combined to form urea,
which is then deposited in the blood and transported to the
kidneys for excretion.
 BUN is directly related to the metabolic function of the liver and
the excretory function of the kidney.
 Normal range of BUN: 7-21 mg/dl.
41
Blood urea nitrogen (BUN)
 Serum BUN
Increased in
 Pre-renal causes
 Hypovolemia
 Dehydration
 Congestive heart failure
 GI bleeding
 Excessive protein ingestion (alimentary tube feeding)
 Excessive protein catabolism
 Sepsis
 Renal (intrinsic) and post-renal diseases / renal failure
42
Creatinine
 Creatinine is a catabolic product of creatine phosphate, which
is used in skeletal muscle contraction.
 The daily production creatine, and subsequently creatinine,
depends on muscle mass, which fluctuates very little.
 Creatinine, as BUN, is excreted entirely by the kidneys and
therefore is directly proportional to renal excretory function.
 There are slight increases in creatinine levels after meals,
especially after ingestion of large quantities of meat.
 Normal range of creatinine:
Male: 0.7-1.5 (1.2) mg/dl
Female: 0.5-1.2 (0.9) mg/dl.
43
Creatinine
Serum creatinine
Increased in
 Impaired renal function
 Rhabdomyolysis
 Acromegaly
 Gigantism
Decreased in
 Debilitation
 Decreased muscle mass
(e.g., muscular dystrophy, myasthenia gravis)
44
急性腎臟衰竭原因的鑑別診斷？
Differential Diagnosis of Acute Renal Failure
Urine indices
Diagnostic index Prerenal Ischemic
azotemia intrinsic azotemia
FENa* (%) <1 >1
Urinary Na+ conc. (mEq/L) < 10 > 20
Urinary Cr / Plasma Cr ratio > 40 < 20
Urinary BUN / Plasma BUN ratio >8 <3
Urine specific gravity > 1.018 < 1.012
Urine osmolality (mOsm/kg H2O) > 500 < 250
Plasma BUN / Cr ratio > 20 < 10-15
Renal failure index*, UNa/UCr/PCr <1 >1
Urine sediment Hyaline casts Muddy brown
granular casts
單獨由 creatinine 推估腎功能的迷思
Male: 0.7-1.5 (1.2) mg/dl, Female: 0.5-1.2 (0.9) mg/dl
Medication >50 GFR 10-50 GFR <10 GFR

(ml/min) (ml/min) (ml/min)
Aminoglycosides
Amikacin 8-12 h 12 h >24 h
Gentamicin 8-12 h 12 h >24 h
Cephalosporins
Cefazolin 8h 12 h 24-48 h
Antiarrhythmics
Digoxin 24 h 36 h 48 h
46
單獨由 creatinine 推估腎功能的迷思
Male: 0.7-1.5 (1.2) mg/dl, Female: 0.5-1.2 (0.9) mg/dl
20-year-old man, body weight 100 kg, creatinine 2.5 mg/dL

24-h creatinine clearance  67 ml/min
70-year-old woman, body weight 30 kg, creatinine 1.2 mg/dL

20-year-old man, body weight 60 kg, creatinine 2.5 mg/dL

acute renal failure with anuria

47
Creatinine clearance (CrCl, Clcr, Ccr)
urine Cr (mg/dl)  urine volume (ml/day)
CrCl (24-hr) =
(ml/min)
1440  serum Cr (mg/dl)
Estimated CrCl (ml/min) ( Cockcroft and Gault formula)
( 140 – age (yr) )  LBW (kg)

Men
( 140 – age (yr) )  LBW (kg)
Women  0.85
PS: Cockcroft-Gault formula overestimated GFR in patients with renal disease.
48
GFR之推算公式
Cockcroft-Gault 方程式
(140-age)  BW
x 1.73/BSA x ( 0.85 if female )
72  SCr
MDRD方程式
Equation without SUN or ALB
GFR (ml/min/1.73m2) =186  Scr-1.154  age-0.203  ( 0.742 if female )
Equation with SUN and ALB
GFR (ml/min/1.73m2)
=170  Scr-0.999  SUN-0.170  SAlb+0.318  age-0.176  ( 0.762 if female )
慢性腎臟疾病
Chronic Kidney Disease, CKD
定義
 腎臟結構或功能損壞  3個月
-- 無論GFR是否下降
-- 有病理、血液、尿液或影像上的變化
 GFR < 60 ml/1.73m  3個月，不論腎臟

2
是否有損害
慢性腎臟病之分期
期別說明腎絲球過濾率 GFR
2
( ml/min/1.73m )
1 腎臟受損但腎功能正常 ≥90
2 輕度腎衰竭 60~89
3 中度腎衰竭 30~59
4 重度腎衰竭 15~29
5 末期腎病 <15 或透析
Acute kidney injury, AKI
BioMed Research International 2016

Aspartate aminotransferase
(AST, SGOT)
Alanine aminotransferase
(ALT, SGPT)
53
ALT (SGPT) and AST (SGOT)
 AST and ALT activities are the most useful indicators of hepato-
cellular damage.
 The absolute levels of aminotransferases correlate poorly with
severity of liver injury or prognosis, and serial determinations are
usually most helpful.
 ALT is found predominantly in the liver; lesser quantities are found
in the kidney, heart, and skeletal muscle.
 Injury or disease affecting the liver parenchyma will cause a release
of this hepatocellular enzyme into the blood stream.
 In the hepatocyte, ALT is found exclusively in the cytosol.
54
ALT (SGPT) and AST (SGOT)
 AST is present in many tissues including heart, skeletal
muscle, kidney, and brain and is thus somewhat less
specific as an indicator of live function.
 Serum AST levels become elevated 8 hours after cell
injury, peak at 24 to 36 hours, and return to normal in 3 to
7 days. If the cellular injury is chronic, levels will be
persistently elevated.
 AST exists in mitochondria and the cytosol.
 Uremia may lead to spuriously low aminotransferase values.
55
AST (SGOT)
 Normal range of AST (SGOT): 5.0-40.0 U/L.
Increased in
 Heart diseases (e.g., myocardial infarction, myocarditis)
 Liver diseases (e.g., hepatitis, liver cirrhosis, drug-
induced liver injury, hepatic tumor, hepatic necrosis)
 Skeletal muscle diseases (e.g., skeletal muscle trauma,
severe burns, recent convulsion, myopathy, myositis)
 Other diseases
Acute hemolytic anemia
Acute pancreatitis
56
ALT (SGPT)
 Normal range of ALT (SGPT): ~ 55.0 U/L.
Increased in
 Hepatitis, hepatic necrosis, hepatic ischemia
 Hepatic tumor
 Liver cirrhosis
 Hepatotoxic drugs
 Cholestasis, obstructive jaundice, cholangitis
 Severe burns
 Trauma to striated muscle, myositis
 Myocardial infarction
 Pancreatitis
57
Bilirubin
 Bilirubin metabolism begins with the breakdown of RBCs in the
reticuloendothelial system (mostly the spleen).
 Hemoglobin is released from RBCs and broken down to heme
and globin molecules.
 Heme is then catabolized to form biliverdin, which is transformed
to bilirubin. This form of bilirubin is called unconjugated (indirect)
bilirubin.
 In the liver, indirect bilirubin is conjugated with a glucuronide
molecule, resulting in conjugated (direct) bilirubin. The
conjugated bilirubin is then excreted from the liver cells and into
the bowel through biliary system
58
59
Bilirubin
 Total bilirubin = Direct bilirubin + Indirect bilirubin
 Normally the indirect (unconjugated) bilirubin makes up 70% to
85% of the total bilirubin.
 In patients with jaundice, when more than 50% of the bilirubin is
direct (conjugated), it is considered a direct hyperbilirubinemia.
 Indirect hyperbilirubinemia is diagnosed when less than 15% to
20% of the total bilirubin is direct bilirubin.
 Direct bilirubin is water soluble and can be excreted into the urine.
Therefore bilirubin in urine suggests disease affecting bilirubin
metabolism after conjugation or defects in excretion (e.g., gall
stones).
60
Bilirubin
Normal range of bilirubin:
Direct (Bil-D): - 0.4 mg/dl; Total (Bil-T): 0.2-1.4 mg/dl.
Predominantly unconjugated hyperbilirubinemia

 Overproduction
 Hemolysis (intra- and extravascular)
 Ineffective erythropoiesis
 Decreased hepatic uptake
 Drugs (e.g., flavaspidic acid)
 Prolonged fasting (< 300 kcal/d)
 Sepsis
 Decreased bilirubin conjugation
 Neonatal hyperbilirubinemia
 Crigler-Najjar syndrome
 Gilbert syndrome
 Drug inhibition
 Acquired transferase deficiency (e.g., hepatocellular disease, sepsis)
61
Bilirubin
Predominantly conjugated hyperbilirubinemia
 Impaired hepatic excretion (intrahepatic defects)
 Familial or hereditary disorders
Dubin-Johnson syndrome; Rotor syndrome
Recurrent (benign) intrahepatic cholestasis
Cholestatic jaundice of pregnancy
 Acquired disorders
Hepatocellular diseases (e.g., viral or drug-induced hepatitis)
Drug-induced cholestasis (e.g., oral contraceptives, methyltestosterone)
Sepsis
 Extrahepatic biliary obstruction (mechanical obstruction,
e.g., stones, structure, tumor of bile duct)
62
Alkaline phosphatase (ALP, ALK-P)
 Although ALP is found in many tissues, the highest concentrations

are in the liver, biliary tract epithelium, and bone. The intestinal
mucosa and placenta also contain ALP.
 This phosphatase enzyme is called alkaline because its function is
increased in an alkaline (pH of 9 to 10) environment.
 Within the liver, ALP is present in Kupffer’s cells.
 New bone growth is associated with elevated ALP levels.
 Isoenzymes of ALP are also used to distinguish between liver and
bone diseases. The isoenzyme of liver origin (ALP1) is heat stable;
the isoenzyme of bone origin (ALP2) is inactivated by heat.
63
Alkaline phosphatase (ALP, ALK-P)
 Normal range of ALP: 30.0-110.0 U/L.
Increased in
 Primary biliary cirrhosis
 Intrahepatic or extrahepatic biliary obstruction
 Normal pregnancy (third trimester, early postpartum period)
 Normal bones of growing children
 Metastatic tumor to the bone
 Healing fracture
 Hyperparathyroidism
 Paget’s disease
 Intestinal ischemia or infarction
 Myocardial infarction
 Sarcoidosis
64
Abnormalities shown by tests of liver function
Type of liver disease

Test Obstructive Parenchymal
AST and ALT(GOT&GPT)  
Alkaline phosphatase  
Albumin N 
Prothrombin time N 
Bilirubin N N
GGT  N
5'-Nucleotidase  N
65
72-year-old man presented with RUQ pain for 2 days.
Albumin (g/dl) 3.0

ALK-P (U/L) 300
Bilirubin-D (mg/dl) 14.4
Bilirubin-T (mg/dl) 15.7
GOT (U/L) 78
GPT (U/L) 65
BUN (mg/dl) 7
Creatinine (mg/dl) 0.8
Glucose
 Criteria for diagnosis of diabetes mellitus can be
established using any of the following criteria:
1. HbA1c  6.5%.
2. FPG  126 mg/dl after no caloric intake for  8 h.
3. 2-h plasma glucose  200 mg/dl during an oral glucose
tolerance test (eg. 75 g anhydrous glucose dissolved in water).
4. Classic symptoms of hyperglycemia or hyperglycemic crisis,
a random plasma glucose  200 mg/dl
* In the absence of unequivocal hyperglycemia, criteria 1–3 should be
confirmed by repeat testing.
FPG: fasting plasma glucose
Diabetes Care 2011;34 (Suppl 1):S62-S69 67
Glucose
 Impaired fasting glucose (IFG)
fasting plasma glucose 100 mg/dl to 125 mg/dl
 Impaired glucose tolerance (IGT)
2-h values in the oral glucose tolerance test (OGTT)
of 140 mg/dl to 199 mg/dl
Diabetes Care 2011;34 (Suppl 1):S62-S69

68
Cholesterol and Triglyceride
 Cholesterol is the main lipid associated with arteriosclerotic vascular

disease.
 Cholesterol is required for the production of steroids, sex hormones,
bile acids, and cellular membranes.
 Cholesterol is transported in the bloodstream by lipoprotien. Nearly
75% of the cholesterol is bound to low-density lipoproteins (LDL),
and 25% is bound to high-density lipoproteins (HDL).
 Triglycerides (TG) are a form of fat in the bloodstream. They are
transported by very-low-density lipoproteins (VLDL) and LDL.
 TGs are produced in the liver using glycerol and other fatty acids as
building blocks. TGs act as a storage source for energy.
69
Lipoprotein and Hyperlipidemia
 Lipoprotein analysis (lipid profiles): cholesterol, TG, LDL-C, HDL-C

LDL-C = Total cholesterol  HDL-C  ( Triglyceride/5 )
* this formula is not valid when TG greater than 400 mg/dl
 Hyperlipidemia increases the risk of developing CAD substantially in
patients with two or more risk factors and a total cholesterol level in
excess of 200 mg/dl, a LDL-C level greater than 130 mg/dl, or a HDL-
C level of less than 35 mg/dl.
 Treatment of hyperlipidemia can reduce the incidence of CAD by 25-
60% and the risk of death from CAD by up to 30%.
 Some data suggested that lowering TG and raising HDL may be
beneficial in patients with CAD and low HDL-C levels.
70
Cholesterol
 Serum cholesterol
Increased in
 Drugs (e.g., thiazide, -adrenergic antagonists, glucocorticoids,
oral contraceptives, cyclosporine)
 Hypothyroidism
 Uncontrolled diabetes mellitus
 Nephrotic syndrome
 Pregnancy
 High-cholesterol diet
 Xanthomatosis
 Biliary cirrhosis
 Familial hypercholesterolemia
 Familial hyperlipidemia 71
Triglyceride
 Serum triglyceride
Increased in
 Ingestion of fatty meals, alcohol
 High carbohydrate diet
 Pregnancy
 Drugs (e.g., cholestyramine, estrogen, oral contraceptives,
-adrenergic antagonists, thiazide diuretics)
 Hypothyroidism
 Poorly controlled diabetes
 Nephrotic syndrome
 Chronic renal failure
 Glycogen storage disease (von Gierke’s disease)
 Familial hypertriglyceridemia
72
Uric acid
 Uric acid is a nitrogenous compound that is the final

breakdown product of purine catabolism.
 75% of uric acid is excreted by the kidney and 25%
by the intestinal tract.
 Uric acid is made primarily by the liver. The blood level is
determined by the rate of synthesis by the liver and the
rate of excretion by the kidney.
 There is some variation of uric acid with age and sex.
(higher in male and old age)
73
74
Uric acid
 Normal range of uric acid:

Male: 4.0-7.0 mg/dl, Female: 3.0-6.0 mg/dl
Increased in
 Increased production of uric acid
 Increased ingestion of purines (e.g., liver, kidney, sweetbreads)
 Genetic inborn error in purine metabolism
 Malignancy (e.g., metastatic cancer, multiple myeloma, leukemia)
 Cancer chemotherapy
 Hemolysis
 Rhabdomyolysis
75
Uric acid
 Drugs  level of uric acid Decreased excretion of uric acid
 Alcohol  Idiopathic
 Ascorbic acid  Chronic renal disease
 Aspirin (low dose)  Acidosis (ketotic or lactic)
 Ethambutol
 Hypothyroidism
 Cisplatin
 Nicotinic acid  Toxemia of pregnancy
 Phenothiazines  Hyperlipoproteinemia
 Theophylline  Diuretics
 Levodopa  Shock or chronic blood volume
 Methyldopa depletion states
 Cyclosporin
76
休
息
一
下
！
77
Arterial blood gases (ABGs)
 Measurement of ABGs provides valuable information in

assessing and managing a patient’s respiratory (ventilation)
and metabolic (renal) acid-base and electrolyte homeostasis.
It is also used to assess the adequacy of oxygenation.
 ABGs are used to monitor patients on ventilators, monitor
critically ill nonventilator patients, establish preoperative
baseline parameters, and regulate electrolyte therapy.
78
Arterial Venous
pH 7.35-7.45 7.31-7.41
PCO2 (mm Hg) 35-45 40-50
HCO3- (mEq/L) 22-26 23-27
PO2 (mm Hg) 80-100 40-50
Base excess (mEq/L) 0±2
79
pH HCO3- PCO2
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
80
Metabolic and Respiratory
Acid-Base changes in Blood
pH PCO2 HCO3-
Acidosis
Acute metabolic D N D
Compensated metabolic N D D
Acute respiratory D I N
Compensated respiratory N I I
Alkalosis
Acute metabolic I N I
Chronic metabolic I I I
Acute respiratory I D N
Compensated respiratory N D D 81
Interpretation of ABG (1)
•先評估 O2 saturation
•再用Henderson-Hasselbalch equation 驗算
1. Evaluate the pH
If the pH is < 7.35, acidosis is present
If the pH is > 7.45, alkalosis is present
2. Next look at the PCO2
A. If the PCO2 is high in a patient who has been said to have acidosis, the
patient has respiratory acidosis
B. If the PCO2 is low in a patient who has been said to have acidosis, the
patient has metabolic acidosis and is compensating for that situation
by blowing off CO2
C. If the PCO2 is low in a patient who has been said to have alkalosis, the
patient has respiratory alkalosis
D. If the PCO2 is high in a patient who has been said to have alkalosis, the
patient has metabolic alkalosis and is compensating for that situation
by retaining CO2 82
Interpretation of ABG (2)
3. Next look at the bicarbonate ion (HCO3-)

 In patient A, HCO3- can be expected to be high in an attempt
to compensate for the respiratory acidosis
 In patient B, HCO3- can be expected to be low as a reflection
of the metabolic acidosis
 In patient C, HCO3- can be expected to be low to compensate
for the respiratory alkalosis
 In patient D, HCO3- can be expected to be high as a reflection
of the metabolic alkalosis
83
Renal and Respiratory Compensation
in Acid-Base Disorders
Metabolic acidosis
PCO2  1.2 mmHg per 1 mEq/L decrease in plasma [HCO3-]
Metabolic alkalosis
PCO2  0.6 mmHg per 1 mEq/L increase in plasma [HCO3-]
Respiratory acidosis
Acute: plasma [HCO3-]  1 mEq/L per 10 mmHg increase in PCO2
Chronic : plasma [HCO3-]  3.5 mEq/L per 10 mmHg increase in PCO2
Acute : plasma [HCO3-]  2 mEq/L per 10 mmHg decrease in PCO2
Chronic: plasma [HCO3-]  5 mEq/L per 10 mmHg decrease in PCO2
84
Acid-Base and Anion gap
[HCO3 -]
pH = 6.10 + log
0.03PCO2
PCO2
[H+] = 24 
[HCO3-]
Plasma anion gap = [Na+]  ( [Cl-] + [HCO3-] )
Urine anion gap = ( [Na+] + [K+] )  [Cl-]

85
Causes of metabolic acidosis (1)
High anion gap metabolic acidosis
A. Lactic acidosis: lactate
B. Ketoacidosis: -hydroxybutyrate
C. Renal failure: sulfate, phosphate, urate, hippurate
D. Ingestions
1. Salicylate: ketones, lactate, salicylate
2. Methanol or formaldehyde: formate
3. Ethylene glycol: glycolate, oxalate
4. Paraldehyde: organic anions
5. Toluene: hippurate
6. Sulfur: SO42-
E. Massive rhabdomyolysis 86
Causes of metabolic acidosis (2)
Normal anion gap (hyperchloremic) metabolic acidosis
A. Gastrointestinal loss of bicarbonate
Diarrhea
B. Renal bicarbonate loss
Type 2 (proximal) renal tubular acidosis
C. Renal dysfunction
1. Some cases of renal failure
2. Hypoaldosteronism (type 4 renal tubular acidosis)
3. Type 1 (distal) renal tubular acidosis
D. Ingestions
1. Ammonium chloride
2. Hyperalimentation fluid
E. Some cases of ketoacidosis, particularly during treatment
with insulin
Causes of metabolic alkalosis (1)
Loss of hydrogen
A. Gastrointestinal loss
1. Removal of gastric secretions - vomiting or nasogastric suction
2. Antacid therapy, particularly with cation-exchange resin
3. Chloride-losing diarrhea
B. Renal loss
1. Loop or thiazide-type diuretics
2. Mineralocorticoid excess
3. Postchronic hypercapnia
4. Low chloride intake
5. High-dose carbenicillin or other penicillin derivative
6. Hypercalcemia, including the milk-alkali syndrome
C. H+ movement into cells
1. Hypokalemia
2. Refeeding (?) 88
Causes of metabolic alkalosis (2)
Retention of bicarbonate
A. Massive blood transfusion
B. Administration of NaHCO3
C. Milk-alkali syndrome
Contraction alkalosis
A. Loop or thiazide-type diuretics
B. Gastric losses in patients with achlorhydria
C. Sweat losses in cystic fibrosis
89
Causes of respiratory acidosis
Acute
Due to decreased alveolar ventilation
 Pneumonia
 Pneumothorax
 Pulmonary edema
 Foreign body aspiration
 Laryngospasm, bronchospasm
 Mechanical ventilation
 General anesthesia
 Oversedation
90
Causes of respiratory acidosis
Chronic
Due to chronic obstructive or restrictive diseases
 Nerve diseases (e.g., poliomyelitis)
 Muscle diseases (e.g., myopathy)
 Central neurologic disorders (e.g., brain tumor)
 Restriction of thorax (e.g., musculoskeletal, scleroderma)
 Pulmonary diseases (e.g., prolonged pneumonia, COPD,
primary alveolar hypoventilation)
91
Causes of respiratory alkalosis
Due to hyperventilation
 CNS disorders (e.g., infection, tumor, trauma, CVA)
 Salicylate intoxication
 Fever
 Gram-negative bacteremia
 Liver disease
 Pulmonary diseases (e.g., pneumonia, pulmonary emboli, asthma)
 Mechanical overventilation
 Congestive heart failure
 Hypoxia (e.g., decreased barometric pressure, ventilation-perfusion
imbalance) 92
Arterial Blood Gas
Normal range Patient
pH 7.35-7.45 7.291
PO2 (mmHg) >80 110.5

HCO3 (mmol/l) 22-26 13.8
PCO2 (mmHg) 32-45 29.2
BE (mmol/L) ±2 -11.2
SO2 (%) >95 97.3
Antinuclear antibody (ANA)
 ANA is a group of protein antibodies that react against cellular
nuclear material.
 ANA is quite sensitive for detecting SLE. Positive results
occur in approximately 95% of patients with this disease.
 Many other rheumatic diseases are also associated with ANA;
therefore, ANA is not a specific test for SLE.
 Several different patterns of fluorescence for ANA are seen
under the ultraviolet microscope. When combined with the
specific subtype of ANA, the pattern can increase specificity
of the ANA subtypes for the various autoimmune diseases.
94
Common antinuclear antibodies and
diseases they cause
Common antinuclear antibodies Disease

Anti-ENA SLE, MCTD
Anti-Sm SLE
Anti-RNP MCTD, SLE, PSS
Anti-SSA (Ro) & Anti-SSB (La) Sjögren’s syndrome, SLE
Anti-scleroderma-70 PSS
Anti-Jo-1 Polymyositis, Dermatomyositis
Antihistone Drug-induced LE
Anticentromere CREST syndrome
95
Suggested pathway for the use of some available
antibody tests in patients suspected of having SLE (1)
Antinuclear antibody
 
SLE Test anti-ssDNA
Test Mixed connective tissue disease anti-Ro/SSA
anti-histone Other rheumatologic syndrome
Drug reactions Either Both
  
Malignancy
Probably Subacute bacterial endocarditis Possibly Probably
drug induced Elderly SLE not SLE
Antinuclear antibody titer > 1: 320
Probably: SLE
Mixed connective tissue disease
Other rheumatologic syndromes
96
Suggested pathway for the use of some available
antibody tests in patients suspected of having SLE (2)
Antinuclear antibody titer > 1: 320
Probably: SLE
Mixed connective tissue disease
Other rheumatologic syndromes
Test anti-Ro/SSA Test anti-ds DNA Test anti-Sm

anti-La/SSB anti-RNP
 
Be alert to associated May be useful in Anti- Anti-
Sjogren’s syndrome following SLE Sm  or low RNP  or low
disease activity  anti-RNP  anti-Sm
Probably Probably
SLE mixed connective
tissue disease
97
39 year-old woman presented with malar rash and arthritis.
ANA Speckled > 1:2560

Anti-dsDNA 1:10 (-)
Anti-Sm Ab Positive
Anti-RNP Ab Positive
Anti-SSA Ab Positive
Anti-SSB Ab Negative
C3 (mg/dl) 81.7
C4 (mg/dl) 21.8
98
Complete blood cell count
and Differential count
 The CBC and differential count are a series of tests of the peripheral blood
that provide a tremendous amount of information about the hematologic
system and many other organ systems.
 They are inexpensively, easily, and rapidly performed as a screening test
 The CBC and differential count include automated multimeasurement of the
following studies:
 Red blood cell count
 Hemoglobin
 Hematocrit
 Red blood cell indices
Mean corpuscular volume (MCV)
Mean corpuscular hemoglobin (MCH)
Mean corpuscular hemoglobin concentration (MCHC)
 White blood cell count and differential count
Neutrophils, lymphocytes, monocytes, eosinophils, basophils
 Platelet count
Normal range of complete blood cell
count and differential count -- Man
WBC k/cmm (103/l) 3.40-9.10
RBC M/cmm (106/l) 4.24-5.56
Hb g/dl 13.50-17.00
Hct % 39.10-48.90
MCV fl (m3) 82.60-97.40
MCH pg (pg/cell) 28.50-34.00
MCHC g/dl 33.80-35.60
RDW % 11.60-13.60
Pl k/cmm (103/l) 138.10-353.40
Seg % 43.00-64.00
Eos % - 6.00
Baso % - 1.00
Mono % 3.00-9.00
Lymph % 27.00-47.00100
Classification of anemia by cell size (1)
Microcytic anemia (MCV < 80 fL)

1. Insufficient iron reaching normoblasts for hemoglobin synthesis,
a. Total body iron content in reduced ( iron deficiency anemia )
b. Release of iron from mononuclear phagocytes is impaired despite an
adequate total body iron content ( anemia of chronic disease )
2. Hereditary genetic defect that diminish synthesis of one of the polypeptide
chains of globin ( thalassemic syndromes )
3. Uncommon disorders impairing the function of enzymes catalyzing heme
synthesis, as in
a. Steps in the synthesis of protoporphyrin are impeded ( Sideroblastic anemia )
b. Lead poisoning
c. Aluminum intoxication
101
Classification of anemias by cell size (2)
Macrocytic anemia (MCV >100 fL)

1. Macrocytic anemias with oval macrocytes and teardrop cells
a. Megaloblastic anemias
b. Myelofibrosis with extramedullary myeloid metaplasia
2. Macrocytic anemias with predominantly round macrocytes

a. Chronic liver disease
b. Patients treated with cytotoxic chemotherapeutic agents
c. Aplastic anemia and myelodysplastic refractory anemia (some patients)
d. Myxedema
e. Hemolytic anemia with marked reticulocytosis
102
Classification of anemias by cell size (3)
Normocytic anemia (MCV 80-100 fL)
1. Normocytic anemias without abnormally shaped RBCs (poikilocytes) or
polychromatophilic macrocytes
a. Chronic infectious and inflammatory states
b. Malignancies
c. Chronic renal disease
d. Endocrine hypofunction (hypopituitarism, hypothyroidism, hypogonadism)
e. Marrow suppression by drugs or toxins
2. Normocytic anemias with prominent poikilocytosis and occasional
polychromatophilic macrocytes
a. Leukemia
b. Myelofibrosis with extramedullary myeloid metaplasia
c. Meylodysplastic syndromes with refractory anemia
d. Carcinoma invading bone marrow
3. Normocytic anemia with numerous polychromatophilic macrocytes
Hemolysis 103
Reticulocyte and Anemia
Reticulocyte
 The new RBC remains a reticulocyte (possesses residual RNA)
for only 1.0 to 1.5 days, and blood normally contains about
one reticulocyte/100 RBCs (50,000 to 75,000 per L)
Reticulocyte Index ( RI )
Patient’s Hct
= Reticulocyte count (%)   Maturation factor
Normal Hct
 Maturation factor = 1 if Hct 45%
1.5 35%
2.5 25%
 RI < 2%, hematopoiesis
104
WBC (K/cmm) 7.7
RBC (M/cmm) 3.93
Hb (g/dl) 8.9
MCV (fl) 69.9
MCHC (g/dl) 32.4
Hct (%) 27.5/ 30.8
MCH (pg) 22.6
RDW (%) 18.5
Platelet (K/cmm) 285
Reticulocyte index (%) 3.2
Seg /Eos /Baso / Mono /Lymph (%) 78.7/ 1/ 0.3/ 6.1/ 13.9
Iron: 24 μg/dl; TIBC: 306 μg/dl; Ferritin: 5.2 ng/dl

105
Urinalysis
 Urinalysis is part of routine diagnostic and screening evaluations.

 It can reveal a significant amount of preliminary information about
the kidneys and other metabolic process.
 Urinalysis is routinely done in all patients admitted to the hospital,
pregnant women, and presurgical patients.
 It is done diagnostically in patients with abdominal or back pain,
dysuria, hematuria, or urinary frequency.
106
Urinalysis
 Appearance  Bilirubin
 Color  Urobilinogen
 Odor  Glucose
 pH  White blood cells (WBCs)
 Protein  Red blood cells (RBCs)
 Specific gravity  Epithelium
 Leukocyte esterase
 Crystals
 Nitrites
 Casts
 Ketones
Urine culture and sensitivity test
107
Urinalysis
SG 1.00-1.03
PH 4.50-8.00
LEU /L Negative
NIT Negative
PRO mg/dl
GLU mg/dl - 25.00
KET mg/dl Negative
UBG mg/dl
BIL mg/dl Negative
Ery /L Negative
WBC /HPF - 1.00
RBC /HPF - 5.00
Epith /HPF - 5.00
Cast /HPF - 2.00
Crystal /HPF
Bacteria 108
Urinalysis Normal Patient
SG 1.00-1.03 1.010
PH 4.50-8.00
LEU /L Negative (+)
NIT Negative (+)
PRO mg/dl 30
GLU mg/dl - 25.00 Negative
KET mg/dl Negative Negative
UBG mg/dl Negative
BIL mg/dl Negative Negative
Ery /L Negative 200
WBC /HPF - 1.00 50-60
RBC /HPF - 5.00 >100
Epith /HPF - 5.00 0-1
Cast /HPF - 2.00 Negative
Crystal/HPF Negative
Bacteria ++
臨床數據與檢驗的應用
110
Conn’s syndrome
(Primary aldosteronism)
Diagnosis of primary aldosteronism

1. Clinical features
2. Changes of related endocrine levels
3. Localization of the lesions
111
Conn’s syndrome
Clinical features
1. Hypokalemia
Weakness, tiredness, loss of stamina
2. Hypertension
112
Conn’s syndrome
Changes of related endocrine levels

1. Plasma renin activity 
2. Plasma aldosterone 
3. Urinary aldosterone 
113
Conn’s syndrome
Localization of the lesions

1. Adrenal sonography
2. CT scan
3. NP-59 adrenal scan
114
Conn’s syndrome
66-year-old woman
• Dizziness, weakness for 2 months
• Blood pressure: 160/100 – 180/110 mm Hg
• Serum potassium 2.6 mEq/L
• 24-hr urine potassium excretion: 55 mEq/L
• Plasma renin activity: 0.2 ng/ml/hr
Plasma aldosterone; 558 pg/mL
• Cortisol: 17.3 g/dL
115
CT scan: right adrenal adenoma
NP-59 adrenal scan (posterior view): right adrenal adenoma
Acute myocardial infarction (AMI)
Diagnosis of AMI
1. History of prolonged ischemic symptom
2. ECG changes consistent with AMI
3. Elevated cardiac enzymes
• CKMB
• Troponin
118
Thank You
for your attention !!
119
Phosphorus and phosphate
 Phosphorus is critical for bone formation and cellular energy

metabolism.
 Approximately 85% of body phosphorus is in bone and teeth, and
14% in soft tissues; only 1% is in the ECF.
 Phosphorus exists in the body as phosphate (PO43-).
[ phosphorus (mmol/L) = 0.323  phosphate (mg/dl) ]
 The phosphate content of the body amounts to approximately 1% of
body weight.
 Normal range of serum phosphate: 2.5-4.5 mg/dl.
120
Hypophosphatemia
 Causes of hypophosphatemia
 Pseudohypophosphatemia (e.g., acute leukemia, bilirubin>3 mg/dl)
 Decreased dietary intake
 Decreased intestinal absorption (e.g., vitamin D deficiency, phosphate
binding antacids, malabsorption, steatorrhea)
 Shift from serum into cells
Hormonal effects (e.g., insulin, glucagon, cortisol)
Nutrient effects (e.g., glucose, lactate, amino acids)
Cellular uptake syndromes (e.g., recovery from hypothermia, AML)
 Increased excretion into the urine
Hyperparathyroidism
Renal tubule defects 121
12-lead EKG
Time course of serum markers in acute MI
Test Onset Peak Duration
CK-total & MB 3-12 hrs 18-24 hrs 36-48 hrs
Troponins 3-12 hrs 18-24 hrs Up to 10 days
Myoglobin 1-4 hrs 6-7 hrs 24 hrs
LDH 6-12 hrs 24-48 hrs 6-8 days

Time of appearance and disappearance
of commonly used cardiac enzyme
Hours Days
Starts to Returns to
Enzyme Peaks
rise normal
Total CPK 4-6 24 3-4
CK-MB 4 18 2
AST 8 24-48 4
LDH 24 72 8-9
Troponin T 4-6 10-24 10
Troponin I 4-6 10-24 4
126
127

臨床數據的判讀-藥研所 2018

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臨床數據的判讀-藥研所 2018

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臨床檢驗數據的判讀

不正常數據的預測值 Positive predictive rate = 97%

不正常數據的預測值 Positive predictive rate = 26%

Test Current units Factor SI units

High Normal Low

*Hyperglycemia *Hyperproteinemia Maximal volume of

ECF volume *Primary polydipsia

Increased Normal Decreased

*Heart failure *SIADH Urine Na+

*Extrarenal Na+ loss *Na+-wasting nephropathy

 15 mmol/d > 15 mmol/d

Metabolic acidosis Metabolic alkalosis

Metabolic acidosis Metabolic alkalosis

*Diabetic ketoacidosis Hypertension

Creatinine (mg/dl) 0.9

Postgrad Med 2004;115(4):69:-73 Am Fam physician 2003;67:1959-66

Determine whether hypercalcemia is real, measure ionized Ca

PTH high PTH - N or Low

If cause remains unclear

Syed Nasrat Imam, MD

BUN 7-21 mg/dl 45

 Three major types of protein present in the plasma:

Medication >50 GFR 10-50 GFR <10 GFR

20-year-old man, body weight 100 kg, creatinine 2.5 mg/dL

70-year-old woman, body weight 30 kg, creatinine 1.2 mg/dL

20-year-old man, body weight 60 kg, creatinine 2.5 mg/dL

24-h creatinine clearance  0 ml/min

Estimated CrCl (ml/min) ( Cockcroft and Gault formula)

( 140 – age (yr) )  LBW (kg)

 GFR < 60 ml/1.73m  3個月，不論腎臟

BioMed Research International 2016

Predominantly unconjugated hyperbilirubinemia

 Although ALP is found in many tissues, the highest concentrations

Type of liver disease

Albumin (g/dl) 3.0

Diabetes Care 2011;34 (Suppl 1):S62-S69

 Cholesterol is the main lipid associated with arteriosclerotic vascular

 Lipoprotein analysis (lipid profiles): cholesterol, TG, LDL-C, HDL-C

 Uric acid is a nitrogenous compound that is the final

 Normal range of uric acid:

 Measurement of ABGs provides valuable information in

3. Next look at the bicarbonate ion (HCO3-)

Plasma anion gap = [Na+]  ( [Cl-] + [HCO3-] )

Urine anion gap = ( [Na+] + [K+] )  [Cl-]

PO2 (mmHg) >80 110.5

Common antinuclear antibodies Disease

Antinuclear antibody titer > 1: 320

Antinuclear antibody titer > 1: 320

Test anti-Ro/SSA Test anti-ds DNA Test anti-Sm

ANA Speckled > 1:2560

Microcytic anemia (MCV < 80 fL)

Macrocytic anemia (MCV >100 fL)

2. Macrocytic anemias with predominantly round macrocytes

Iron: 24 μg/dl; TIBC: 306 μg/dl; Ferritin: 5.2 ng/dl

 Urinalysis is part of routine diagnostic and screening evaluations.

Diagnosis of primary aldosteronism

2. Changes of related endocrine levels

3. Localization of the lesions

Changes of related endocrine levels

Localization of the lesions

 Phosphorus is critical for bone formation and cellular energy

Test Onset Peak Duration

CK-total & MB 3-12 hrs 18-24 hrs 36-48 hrs

Troponins 3-12 hrs 18-24 hrs Up to 10 days

Hyperglycemia Hyperproteinemia Maximal volume of

Heart failure SIADH Urine Na+

Extrarenal Na+ loss Na+-wasting nephropathy