Liver Function Tests and Enzymes
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Transcript of Liver Function Tests and Enzymes
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Normal liver functionsA. Metabolic Functions:
glucose homeostasis
Protein synthesis
Lipid synthesis
tected by liver enzymes
B. Synthetic Functions:
AlbuminPT & APTT
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D. Catabolic Functions:
including hormones and serum proteins, are
catabolized by the liver.Ammonia (NH4)
E.
Excretory Functions:The principal excretory product of the liver is bile
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Liver function tests
Noninvasive method of screening for thepresence of liver dysfunction
Allows recognition of general type of disorder
To assess the severity and occasionallyallow prediction of outcome
To follow the course of the disease, evaluate
response to treatment, and adjust treatmentwhen necessary
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General categories of tests
Tests of the capacity of the liver to
transport organic anions and metabolize
drugsEg. S bilirubin, s bile acids, BSP (Brosulphalein) etc
Measures ability of the liver to clear endogenous or exogenous
substances from the circulation
Tests to detect injury to hepatocytesAll the enzyme tests
Most commonly done and most useful are
aminotransferases and alkaline phosphatase
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Tests of the biosynthetic capacity of the liver
Tests to detect fibrosis in the liver
Tests for chronic inflammation or altered
immunoregulation
Eg. S albumin, prothrombin time
Eg. Type 4 collagen, Fibrotest etc
Immunoglobulins and specific antibodies
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Common serum liver chemistry tests
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Normal values
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Case study 1
A woman, 35 years of age, complained of abdominal pain and dark urine. She was
clinically mildly jaundiced. Her liverfunction tests were as follows:
Albumin 36 g/L (3448)
Protein 83 g/L (6585)
Total bilirubin 45 mol/L (224)
GGT 439 U/L (
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Case study 2
A man, 39 years of age, had the following results as part of an insurance medical:
Albumin 37 g/L (3448)
Protein 72 g/L (6585)
Total bilirubin 13 mol/L (224)
GGT 46 U/L (
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Case study 3A man, 66 years of age, presented with weight loss and fatigue. He had a normocytic
anaemia. His LFTs were as follows:
Albumin 22 g/L (3448)
Protein 59 g/L (6585)
Total bilirubin 12 mol/L (224)
GGT 926 U/L (
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Initial approach to the evaluation of
abnormal liver enzyme tests
Asymtomatic or symptomatic
History and physical
Alcohol consumption
Risk factors for viral hepatitis - IV drug abuse, sexual promiscuity,
homosexual relations, tattoos, nonsterile body piercing, blood and blood
products, medications, herbal or alternative med., occupational exposure to
toxins
Diabetes, obesity, hyperlipidemia
Family history - Wilsons dis, hemochromatosis, autoimmune diseases
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Evaluation of abnormalities of ALT
(SGPT) and AST (SGOT) levels
AST and ALT are markers of hepatocellularinjury
Participate in gluconeogenesis, transfer of amino
groups from aspartate or alanine to ketoglutaricacid to form oxaloacetete or pyruvate.
AST present in cytosol and mitochondria in liver,cardiac muscle, skeletal muscle, kidney, brain,pancreas, lungs, WBC and RBC.
ALT a cytosolic enzyme, highest concentration inthe liver
ALT considered a liver specific enzyme
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Useful paradigm to categorize
increased levels of AST, ALT
Mild AST, ALT elevation (less than 5
times ULN) - ALT predominant or AST
predominantAST, ALT greater then 15 times normal
Elevations in the intermediate range -
less useful for limiting the DD, caused bydiseases from both above categories
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Acute Liver Disease
Reliable history
Ratio of SGOT(AST) to SGPT(ALT) is atleast 2:1
Reflects low level of activity of SGPT
SGOT rarely exceeds 300 IU
Higher values - seek additional cause of liver
injury A GGT (gammaglutamyl transferase) twice
normal and AST/ALT ratio of 2:1 or more,highly suggestive of alcohol abuse
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NAFLD
Hepatic steatosis (fatty liver) and NASH
Asymptomatic increase in transaminases
Raised BMI, Type 2 DM and hyperlipidemia
No evidence of clinically relevant alcohol use Probably commonest cause of mild
transaminase increases
AST/ALT ratio usually < 1:1 in the absence of
cirrhosis Values < 250 IU usually
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DD of moderately elevated
aminotransferases (5 to 15 times ULN)
Wide range of liver diseases
ALT, AST less useful in determining
cause Entire spectrum of liver diseases causing
mild or severe aminotransferase
elevation
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DD of severe elevations of ALT,
AST (> 15 times ULN)
Relatively limited
Indicate marked hepatocellular injury or
necrosis Drug induced - acetaminophen
Occupational/environmental toxins -CCl4
Ischemic hepatitis
Viral hepatitis - A, B, D, E, Herpes
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Suggested algorithm for evaluating raised transaminases
PMJ 2003
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Other enzyme tests for hepatocellular
necrosis
Glutamate dehydrogenase
Isocitrate dehydrogenase
Lactate dehydrogenase
Sorbitol dehydrogenase
More useful as marker for
Hemolysis,
Myocardial infarction
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Enzymes for the detection of cholestasis
Alkaline phosphatase
Present in nearly all tissues - isoenzymes
Localised in the microvilli of the bile canalicus in the liver
Also present in bone, intestine, placenta, kidney and wbcElevation may be physiological or pathological
Physiological
In tissues undergoing metabolic stimulationThird trimester of pregnancy
Adolescence
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Normal adult serum AP is from liver andbone
Intestine contributes about 15%
Several procedures used to measure activity- differs in substrates used, end productsmeasured, etc
Isoenzymes differ in reactions in variousassay systems
Hence different units such as IU, KA,Bodansky
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Elevation of s. alkaline
phosphatase
Isolated
Associated with hyperbilirubinemia
(cholestatic disorders) May be sole abnormality in many
cholestatic or infiltrative diseases
To be interpreted in the clinical setting ofhistory and physical examination if soleabnormality
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When SAP elevation is detected
Repeat the test
Confirm the hepatic origin
If medications suspected, discontinue them and repeat test
Persistently elevated SAP - evaluate for
Serum gammaglutamyl transferase
5-Nucleotidase
AP isoenzymes
Cholestatic liver disease
Infiltrative liver disease
Biliary obstruction
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AP elevation upto 3 times ULN
> 3 times ULN
Nonspecific
Occurs in all types of liver disorders
Viral hepatitis
Cirrhosis
Infiltrative diseases of the liver
CHF etc
Cholestatic disorders Extrahepatic
Intrahepatic
Infiltrative disorders
Mets
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Suggested algorithm for evaluating a
raised s.alkaline phosphatase
PMJ 2003
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Gammaglutamyl transferase
(-glutamyl transpeptidase)
Found in hepatocytes and biliary epithelial cells
Sensitive for hepatobiliary disease but limited by lackof specificity
With other enzyme abnormalities, raised GGT wouldsupport a hepatobiliary cause
Can confirm hepatic source for a raised AP
Raised GGT and raised transaminases with ratio ofAST to ALT 2:1 or more suggestive of ALD
Medications can cause mild rise
Normal range 0 to 30 IU/L
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Causes of raised serum
gammaglutamyl transferase (SGGT)
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5-Nucleotidase
Normal 0.3 to 3.2 Bodansky units
Spectrum of abnormality similar to that of
Serum AP Specificity for hepatobiliary disease
May be used to confirm hepatic origin of
elevated Serum AP
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A 63-year old man presented with haematemesis. He had lost 12
kg of weight over the preceding 6 months. Gastroscopy showed
a carcinoma of the stomach. The following results .
urea 5.0 mmol/l (1.7-6.7) creatinine 66 mol/l (60-115) total protein 55 g/l
(60-80) albumin 23 g/l (35-50) calcium 1.86 mmol/l (2.1-2.6) total bilirubin
15 mol/l (
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RE cell plasma hepatocyte
HEME UCB UCB
+
albumin
UCB+ligandin
BMG
BDG
bile
urobilinogen stercobilinogen
Bilirubin
UDP-glucoronyltransferase
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Isolated unconjugatedhyperbilirubinemia
IDB fraction > 85% of total bilirubin
1. Increased production
hemolysis
ineffective erythropoiesis : folate, IDA drugs : rifampicin resolution of hematoma
2. Defects in hepatic uptake/conjugation Gilberts syndrome Crigler-Najjar syndrome
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DB > 50% of total bilirubin
cant differentiate obstruction and
parenchymal disease Delta fraction
Conjugated bilirubin tightly bound to albumin
tendency of hyperbilirubinemia to resolvemore slowly than other biochemical tests
Conjugated hyperbilirubinemia
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The following results were obtained from a patient who presented with mild
jaundice:
Albumin 45g/l (35-50), total bilirubin 43mol/l (
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A medical student recovering from a bout of 'flu noticed he was
slightly jaundiced. These results were found:
total bilirubin 60 mol/l (
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A 14-year-old boy has the sudden onset of severe abdominal
and back pain. On physical examination his abdomen is
diffusely tender. He has scleral icterus. Laboratory studies
include a hemoglobin electrophoresis that reveals 98% Hgb S,
1% Hgb A2, and 1% Hgb F. Which of the following serum
analytes is likely to be increased the most in this boy?
A Creatine kinase (CK)
B Amylase
C Alkaline phosphataseD Lactate dehydrogenase (LDH)
E Alanine aminotransferase (ALT)
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A 30-year-old woman has developed nausea and vomiting over
the past week. On physical examination she has mild scleral
icterus. A hepatitis panel reveals a positive HAV IgM, negative
HBsAg, positive HBsAb, and negative HBcAb. Which of the
following laboratory tests is most likely to be abnormallyelevated in this woman?
A Creatine kinase (CK)
B Amylase
C Alkaline phosphataseD Lactate dehydrogenase (LDH)
E Alanine aminotransferase (ALT)
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A 42-year-old woman has had intense pruritus for the past 3
months. She is becoming increasingly jaundiced. On physical
examination she has scleral and skin icterus. A liver biopsy is
performed and on microscopic examination shows destructionof intrahepatic bile ducts leading to marked portal fibrosis.
Which of the following laboratory test findings is she most
likely to have?
A Markedly decreased serum immunoglobulin A
B Decreased serum ceruloplasmin
C Increased serum alpha-fetoprotein
D Decreased serum alpha-1-antitrypsin
E Positive serum anti-mitochondrial antibody
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Increased unconjugated plasma bilirubin is mostly seen in
A. Sickle cell anemia
B. Drug induced cholestasis
C. Liver cirrhosis
D. Carcinoma of the liver
E. Hepatitis C infection
Excess urobilinogen in urine is seen in
A.. Hemolytic anemia
B. Obstructive jaundiceC. Primary biliary cirrhosis
D. New- born babies
E. Acquired immunodeficiency patients
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The carrier protein for bilirubin is
A .Pre albumin
B.Transferrin
C. AlbuminD. Haptoglobulin
E. Alpha- globulin
BILE ACID ( BILE SALT) METABOLISM
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BILE ACID (= BILE SALT) METABOLISM
From cholesterol metabolism are chenodeoxycholic acid and cholic acid, by 7--
hydroxylation
Conjugated to glycine or taurine (this increases their solubility).
In the GIT, bacterial enzymes deconjugate and dehydroxylate the primary bile
acids and convert them to the secondary bile acids lithocholic acid and deoxycholic
acid.
Most of the bile acids in the GIT are reabsorbed into the portal circulation (75%in the ileum and 10% in the colon), taken up by the liver again and re-excreted
(enterohepatic circulation). Re-uptake of bile acids by the liver is highly efficient,
but sensitive to liver damage
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A 50-year-old man with a history of alcohol abuse is
found down with a decreased level of
consciousness. On examination he has palmarerythema, spider angiomata of the skin of his upper
extremities, fetor hepaticus, and asterixis. Which of
the following blood analytes is most likely to be
elevated in this man?
A Ammonia
B Cholesterol
C CreatinineD Creatine kinase BB
E Glucose
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Albumin
depends on nutrition, hormonal factors,vascular integrity, catabolism, loss in stooland urine
not specific for liver disease T1/2 = 19-21 days
Not a reliable indicator of acute liver disease Levels fall in progressive disease, reflects synthetic
function
Correlates with prognosis in Chronic Liver Disease
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A 44-year-old man has become increasingly lethargic over the
past month. On physical examination his liver span is increasedand there is an abdominal fluid wave. Laboratory studies show a
serum AST of 240 and an ALT of 155 U/L. The total serum
bilirubin is 2.4 mg/dL with direct bilirubin of 1.6 mg/dL. His
serum alkaline phosphatase is 55 U/L. The serum albumin is 2.6
g/dL with total serum protein of 4.9 g/dL. The serum amylase is
72 U/L. Which of the following is the most likely diagnosis?
A Chronic pancreatitis
B Gilbert syndrome
C Chronic alcoholismD Acute viral hepatitis
E Autoimmune hemolytic anemia
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Prothrombin timeprolonged :
vitamin K deficiency (malnutrition,malabsorption, antibiotics)
massive transfusion congenital disease liver disease warfarin DIC
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Prothrombin time
in vit K deficiency, vit K 10 mg SC decreasesprolonged PT >30% within 24 hrs
INR (international normalised ratio)
More often tested now
Standardising reports of PT
Avoids interlab variabilityINR = [Patient PT/mean control PT] ISI
ISI - international sensitivity index
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Prothrombin time
The liver synthesizes coagulation factors except
FVIII
Most present in excess, clotting abnormality
occurs only when substantial impairment in
ability of liver to synthesise the CF
PT : FI, II, V, VII, IX and X
T1/2 FVII 6 hrs. (shortest) prognosis : acute, chronic hepatocellular
disease
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Modified Child-Turcotte-Pugh score for gradingseverity of liver disease
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Take home message
initial evaluation : assess in clinicalcontext
classified in 3 groups
1. synthetic function : albumin, clotting
time2. cholestasis : bilirubin, ALP, GGT
3. hepatocyteinjury : AST, ALT
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misnomer
Does not effectively assess actual function
not always specific for the liver limited information regarding presence or
severity of complication
Liver Function Tests
Liver Chemistry Tests
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When to refer for a specialist opinion?
Unexplained liver abnormalities > 1.5 times
normal on 2 occasions, a minimum of 6
months apart
Unexplained liver disease with evidence of
liver dysfunction (hypoalbuminemia,
hyperbilirubinemia, prolonged PT or INR)
Known liver disease where treatment beyondwithdrawal of the implicating agent is
required Limdi et al, Postgrad Med J 2003
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What tests to do before referral?
Consider the following;
Screen for viral hepatitis
Antinuclear antibodies
Ceruloplasmin in pts < 40 yrs
Iron studies - S ferritin, transferrin saturation
US of the hepatobiliary system
IgM anti HAV
HBsAgAnti HCV
PMJ 2003
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Enzymes
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Nomenclature
First were given emperical name eg
pepsin
Then using name of substrate + suffixase .eg
Urease :hydrlyzing urea
Amylase: hydrolze amylum(Starch)Phosphatase:Hydrolyzing phosphat
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Normal plasma enzyme
Its level reflects the balance between therate of synthesis & release into plasma duringcell turnover, and the rate of clearance from thecirculation.
(S+E ES P(reaction product +E(Free enzyme)
Its level depends on:
rate of release fr damaged cells rate of damage is occuring
extent of cell damage
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In absenceof cell damagerate ofrelease depends : Rate of cell proliferation
Degree of induction of enzymesynthesis
All these factors are balanced by the rate
of enzyme clearance fr the circ.
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Localization of Damage How do we make specific diagnosis?
Diagnosticprecision is improved by:
1. Estimate > than 1 enzyme
2. isoenzyme determinationexist inmore than 1 form, may be separated by theirdifferent physical or chemical properties
3. serial enzyme estimationpersistently
raised activity suggests chronic/impairedclearance
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Causes ofNon-specific raisedplasma enzymes activities change in plasma enzyme activity is
pointing towards a specific disease, wemust exclude nonspecific causes.
e.g. Elevated AST can be due to MI,moderate exercise, muscle exercise orlarge IM injection.
So, we can do a few discriminating testssuch as CK-MB, troponin, CK
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Causes of Markedincrease in CK Shock & Circulatory collapse
MI
Muscular dystrophies &Rhabdomyolysis(breakdown of skeletal muscle)
Plasma CK is increased in all types of muscular
dystrophy.
Not in neurogenic muscle disorder e.g.poliomyelitis, myastenia gravis, parkinson.
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Moderate increase in CK Muscle injury
Post-op ( 1 week)
Physical exertion only after moderate exercise,muscle cramp or after an epileptic fit
After IM injection
Hypothyroidism (thyroxine catabolism of enzyme)
Alcoholism (alcoholic myositis) CVA & Head injury cases
Those predispose to Malignant Hyperpyrexia
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Isoenzymes of CK CK consist of 2 protein subunit M & B
When combined can form 3 isoenzyme :CK BB, CKMB & CK MM(CK-1 , CK-2 & CK-3)
CK MM is the predominant CK in skeletal & cardiacmuscle.
In Cardiac muscle : CK MB 35% of
total CK activity
In Skeletal muscle : CK MB
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IsoenzymeCK CK BB is present in high conc. In brain &
in smooth muscle of GIT & Genitaltracts.
Can be raised during parturition
Also has been reported, that after braindamage & in association with malignant
tumours e.g. bronchus, prostate &breast, there is a raised CK BB.
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A 55-year-old man with unstable angina presents
with a history of chest pain that has been
worsening over the past eight hours. The pain
radiates down his left arm. On physical
examination he is now diaphoretic, with pulse of
104/minute and an irregular cardiac rhythm.
Which of the following is the most appropriatelaboratory test to order on this man?
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A) CK-MB
B) Total CK
C) ASTD) Total LDH
E) LDH-1
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A 51-year-old man with a history of
diabetes mellitus suddenly collapses. On
physical examination he is afebrile but
his heart rate is 90/minute and irregular.
Laboratory studies show total creatine
kinase (CK) 495 U/L with an MB
isoenzyme fraction of 10%. Which of thefollowing is the most likely diagnosis?
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A Blunt force injury to the abdomen
B Acute myocardial infarction
C Cerebral infarction D Trichinosis
E Prostatic adenocarcinoma
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Amylase Is a hydrolase that breaks down glycogen &
starch
Present in high conc. in saliva & pancreatic
juice and can be extracted from tissues likegonads, fallopian tubes, skeletal muscle &adipose tissue
Can be excreted in urine due to lowmolecular weight.
Plasma amylase activity help diagnoseacute pancreatitis and other intra & extraabdominal conditions which cause similarpain.
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Causes of Raised Amylase Marked Increase (5-10 times UARL)
Acute pancreatitis
Severe glomerular impairment
Severe DKAPerforated peptic ulcer ( esp. in lesser sac)
Moderate Increase ( up to 5 times UARL)
Other acute abdominal dis.:
perforated PUacute choleycystitis
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ContModerate increaseof AmylaseIntestinal obstruction
Abdominal trauma
Ruptured ectopic pregnancy
Salivary gland disorder
mumps
salivary calculi
Sjogren syndrome
post injection of contrast medium into salivary gland
for sialography Others morphine administration,( spasm of s.
oddi), MI, DKA, severe glomerular dys(fx), acutealcoholic intoxication & macroamylasaemia
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Macroamylasaemia In some pts, a high plasma amylase activity
is due to low renal excretion of the enzymedespite normal glomerular f(x).
Symptomless Thought that either the enzyme is bound to a
high molecular wt plasma component e.g.protein
Or amylase molecules form large polymersthat cant pass through glomerularmembrane
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Pancreatic Pseudocyst If plasma amylase activity does not fall after
an attack of acute pancreatitis, there may bea leakage of pancreatic fluid into lesser sac.
Urinary amylase are high, so this is anindication to do a urine amylase activitywhich is inappropriately low relative to theplasma activity if got macroamylaseamia or
glomerular impairment. So, this differentiates it from
macroamylaseamia
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Isoenzymes of Amylase It is rarely necessary to identify the isoezymes.
Can be distinguished by electrophoresis / by usinginhibitor derived from wheat germ
30-40% of total plasma amylase activity is due topancreatic (p) isoenzyme & remainder is of salivary.
Specific estimation of p-isoenzyme is of no
additional diagnostic value to differentiate acutepancreatitis from non-pancreatic abdominal
emergencies.(due to leaked pancreatic amylase intoperitoneal area gets into bldstream)
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A 40-year-old man with HIV infection is
receiving highly active antiretroviral
therapy (HAART) that includes protease
inhibitors. He has developed acute
abdominal pain over the past day, along
with nausea and vomiting. On physical
examination he has peripheral fatwasting but a prominent dorsocervical fat
pad. Laboratory studies show a serum
triglyceride of 1440 mg/dL and serum
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Which of the following is the most likely
diagnosis?
A) HepatitisB)Appendicitis
C) Cholecystitis
D) PancreatitisE) Pyelonephritis
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