LHD is an enzyme which is width sprid through the body tissue has an important role in the conversion of pyrovate into lactate within the tissue when ever there is hypoxia in the body
LHD is an enzyme which is width sprid through the body tissue has an important role in the conversion of pyrovate into lactate within the tissue when ever there is hypoxia in the body
Liver function tests and interpretation is a very important topic for students of medical and allied fields. It is essential for efficient practice of clinical and laboratory medicine.
The liver is the largest organ in the body
It is located below the diaphragm in the right upper quadrant of the abdominal cavity and extended approximately from the right 5th rib to the lower border of the rib cage.
AIP is an enzyme which is width sprid through the body tissue has an important role in alkaline medium for the conversion of phospate from one substance. to remove phosphate group.
Liver function tests and interpretation is a very important topic for students of medical and allied fields. It is essential for efficient practice of clinical and laboratory medicine.
The liver is the largest organ in the body
It is located below the diaphragm in the right upper quadrant of the abdominal cavity and extended approximately from the right 5th rib to the lower border of the rib cage.
AIP is an enzyme which is width sprid through the body tissue has an important role in alkaline medium for the conversion of phospate from one substance. to remove phosphate group.
It is characterized by a yellow appearance of the (1) Skin (2) Mucous membranes and (3) Sclera caused by bilirubin deposition. It is the most specific clinical manifestation of Hepatic dysfunction.
Jaundice is usually present clinically when the plasma bilirubin concentration reaches 2 to 3 mg/dl.
When bilirubin clearance from the Liver to the Intestinal tract is impaired (as in acute hepatitis and bile duct obstruction) it may be accompanied by alcoholic (Gray coloured) stools.Solubility increases in water , soluble conjugated bilirubin leads to Tea coloured urine.
Identifying and Treating Abdominal Lump in Children By Dr. Vivek Rege
This is part of the HELP Talk series at HELP,Health Education Library for People, the worlds largest free patient education library www.healthlibrary.com.
For info log on to www.healthlibrary.com.
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1.Detect presence of liver disease.
2.Distinguish among different types of liver diseases.
3.Estimate the extent of known liver damage.
4.Follow the response of treatment
This content is suitable for medical technologists/technicians/lab assistants/scientists writing the SMLTSA board exam. The content is also suitable for biomedical technology students and people also interested in learning about the liver. This chapter describes the liver and interpretation of the liver function tests. Please note that these notes are a collection I used to study for my board exam and train others who got distinctions using these.
Disclaimer: Credit goes to those who wrote the notes and the examiners of each exam question. Please use only as a reference guide and use your prescribed textbook for the latest and most accurate notes and ranges. The material here is not referenced as it is a collection of pieces of study notes from multiple people, and thus will not be held viable for any misinterpretations. Please use at your own discretion.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. AIM
• To discuss the normal physiological function of liver.
• To evaluate abnormal liver function tests findings in liver
disorders.
• Approach to various liver disorders.
3. Introduction
• The liver has a central and critical biochemical role in
metabolism
digestion
detoxification and
elimination of substance from the body
4. DEGRADATION OF HEME TO BILIRUBIN
85% is derived from RBCs
In normal adults this
results in a daily load of
250-300 mg of bilirubin
Normal plasma conc is
less than 1 mg/dL
Hydrophobic – transported
by albumin to the liver for
further metabolism prior to
its excretion
“unconjugated” bilirubin
6. Excretory function
• Bilirubin:
Orange-yellow pigment derived from heme, as a product of red blood
cell turnover.
250-350 mg of bilirubin produced daily, 85% from RBCs.
Transported across the hepatocyte membrane, conjugated with
glucuronic acid and excreted into bile by an energy dependent process.
7. Serum Bilirubin – Estimation
• Principle: When diazotised sulfanilic acid reacts with bilirubin, it
forms ‘azobilirubin’, a purple coloured product measured
colorimetrically. This reaction is known as Van den Bergh reaction.
Conjugated bilirubin
‘Direct positive’.
gives colour immediately (<1min)
Unconjugated bilirubin gives colour only after addition of
methanol ‘Indirect positive’(within 30 mins)
Both conjugated and unconjugated ‘Biphasic’(immediately
direct positive intensified by addition of alcohol indirect positive)
8. Fouchet’s Test
• Bilirubin in urine implies increased serum direct bilirubin and
excludes hemolysis as the cause
• Bile pigments adhere to the precipitate of barium sulphate.
• On addition of Fouchet’s reagent, ferric chloride in the presence of
trichloroacetic acid oxidises yellow colour bilirubin to green colour
biliverdin and blue coloured cyanobilirubin forming pista green
colour.
9. Bile Salts
•
Source: cholesterol
• Primary bile acids: cholic and chenodeoxycholic acid.
• Metabolised by intestinal bacteria to secondary bile acids:
deoxycholic and lithocholic acid.
• Bile salts are Glycocholates and Taurocholates.
• Emulsification of Fatty acids
11. Synthetic Function
• Synthesis of Plasma proteins like Albumin, Transthyretin, Prothrombin
and Fibrinogen.
• Clotting factors except Von Willebrand factor and inhibitors of
coagulation, such as antithrombin.
• Post-translational carboxylation of (II, VII, IX and X) require vitamin
K, occurs within the hepatocyte
12. Synthetic Function
• Albumin:
Synthesized exclusively by liver.
Synthesis is inhibited by interleukin (IL)-6 in inflammatory
conditions.
Decreased concentrations in cirrhosis, autoimmune hepatitis and
alcoholic hepatitis.
Dye binding method (BCG) for estimation of albumin may give false
low values in patients with jaundice due to interference with bilirubin.
13. Synthetic Function
• Determination of total plasma proteins and A:G ratio.
• Severe or fulminant hepatic failure:
concentration of short lived hepatic proteins (transthyretin and
prothrombin) fall quickly.
minimal change in proteins with longer half lives.
• Decrease in fibrinogen levels <100 mg% seen in parenchymal liver
disease, acute hepatic necrosis.
14. Prothrombin Time
• It measures the activity of fibrinogen (I), Prothrombin (II) and factors
V, VII and X
• Prolonged PT indicates liver disease
• PT measures the time to clot after exposure of plasma to tissue factor.
• INR=[PT (patient)/PT (geometric mean of normal)]ISI
15. Prothrombin Time
• Prolonged due to lack of synthesis in hepatocellular disease or due to
lack of Vitamin-K absorption in obstruction
• Markedly prolonged PT indicates severe liver damage in hepatitis and
cirrhosis.
• Corrected within 24-48 hours by parenteral administration of vitamin
K (10mg/day for 3 days) in obstructive but not in hepatocellular
jaundice.
16. Carbohydrate metabolism
• Blood glucose levels maintained
During short fasts by hepatic glycogenolysis.
Prolonged fasts by hepatic gluconeogenesis
• Tests based on carbohydrate metabolism:
Galactose tolerance test
• Hypoglycemia is a common complication in liver diseases like Reye’s
syndrome, fulminant hepatic failure and advanced cirrhosis
17. Lipid Metabolism
• Metabolism of cholesterol, synthesis, esterification, oxidation and excretion.
• Cholesterol-Cholesteryl ester ratio:
• Normal level- 150 mg to 250 mg, 60-70% as ester.
• Cholesterol endogenously synthesized in liver.
• Acute hepatic necrosis marked reduction in esters.
• Cirrhosis- decrease in HDL.
• Alcohol induced liver injury increase in HDL levels.
18. Serum Enzymes
• Plasma activities of several cytosolic, mitochondrial, and membrane
associated enzymes are measured.
• Ability of liver enzymes to assist in diagnosis depends on
tissue specificity
subcellular distribution
relative activity of enzyme in liver and plasma
patterns of release
clearance from plasma.
19. AST( SGOT)
• Present in cytoplasm as well as mitochondria of hepatocytes.
• Mitochondrial isoenzyme represents a significant fraction of total AST within
hepatocytes, half lives of 87 hours.
• Require pyridoxal phosphate as cofactor.
• Plasma half lives of AST is 17 hours
• Upper reference range limits of 40 IU/L.
• Total cytoplasmic AST is present in highest activity in hepatocytes 7000 times higher
than plasma
20. ALT (SGPT)
• Plasma half life is 47 hours
• Liver specific activity in hepatocytes 3000 times higher than plasma
which is almost half of AST.
• Mitochondrial isoenzyme has very low half life making it insignificant
in diagnosis
21. Patterns of release
• In most forms of acute hepatocellular injury AST is higher than ALT
initially, due to higher activity of AST in hepatocytes
• Within 24-48 hours, if ongoing damage occurs ALT will become higher
than AST due to its longer half life.
22. Patterns of release
• In Alcoholic liver disease studies suggest that alcohol induces
mitochondrial damage.
• This causes release of mitochondrial AST which besides predominant
AST in hepatocytes has significant longer half life than
extramitochondrial AST and ALT causing AST:ALT ratio (De Ritis
Ratio of 3-4:1)
23. Activity
• AST/ALT ratio >2 with ALT <300 U/L suggestive of alcoholic
hepatitis.
• ALT more specific for liver disease.
• Greater increase in AST than ALT favor viral hepatitis, post hepatic
jaundice.
24. Alkaline Phosphatase
• Present in number of liver tissues including liver, bone, kidney and
intestine.
• Liver isoenzyme has half life of 3 days
• Normal range: 20-130 IU/L.
• Increased in cholestasis, obstructive jaundice.
• ALP and GGT are membrane bound glycoprotein enzymes found at
the canalicular membrane of hepatocytes
25. ϒ-Glutamyl Transferase
• Regulates the transfer of amino acids across cell membranes.
• If ALP and GGT are both elevated source is likely to be hepatic.
• Levels increased in about 60-70% chronic alcoholics.
• Normal Range: 5-40 IU/L
26. Mechanism of release
• Bile acids, solubilize the release of GGT and ALP from plasma
membrane.
• Ethanol, Phenytoin and Carbamazepine induce microsomal enzyme
synthesis lead to increase in GGT and ALP
27. 5’- Nucleotidase
• Increased in cholestatic disorders.
• No increase in activity in patients with bone disease
• Confirms the increase in ALP from hepatic source.
28. Lactate Dehydrogenase
• Cytosolic glycolytic enzyme catalyses the reversible oxidation of
lactate to pyruvate.
• Normal upper limit: 150 U/L
• Liver isoenzymes have half life of 4-6 hours and low activity (about
500) times than plasma.
• Space occupying lesions of liver, metastatic carcinoma lead to increase
in LDH> 500 IU/L and ALP> 250 IU/L.
29. Rate of clearance
• The half life of ALT is 47 hrs, cytoplasmic AST is 17 hrs.
• Liver isoenzyme of ALP is 3 days.
• GGT –10 days
• The removal of enzymes takes place by receptor- mediated endocytosis by
liver macrophages.
• Conjugated bilirubin binds covalently to albumin and is stays longer in the
blood.
30. Biliprotein/ Delta Bilirubin
• Formed by covalent attachment of Bilirubin monoglucuronide
with lysine residues of albumin or other proteins postsynthetically.
• Increased levels are markers of hepatic dysfunction.
31. Cirrhosis
• Earliest laboratory abnormalities are:
fall in platelet count
increase in PT
decrease in albumin to globulin ratio <1
increase in AST/ALT > 1
• End stage cirrhosis- massive tissue destruction, decrease in AST and
ALT.
32. Model for End Stage Liver Disease(MELD)
• MELD is calculated as
= 3.8[Ln Serum bilirubin (mg/dL)]+11.2 [Ln INR]+9.6 [Ln Serum Creatinine
(mg/dL)]+ 6.4
• Identify patients with advanced cirrhosis, candidates for liver
transplantation.
• Superior to Child-Pugh scoring in predicting short term survival
• Risk of death over 3 months is Low if score <10, intermediate if 10-20 and
high if >20
33. Viral Hepatitis
• Acute viral hepatitis is defined by the sudden onset of significant
aminotransferase elevation as a consequence of diffuse necroinflammatory
liver injury.
• This condition may resolve or progress to fulminant failure or chronic
hepatitis
• Chronic viral hepatitis is defined as the presence of persistent (at least 6
months) necroinflammatory injury that can lead to cirrhosis.
• Histopathologic classification of chronic viral hepatitis is based on etiology,
grade, and stage.
34. Features of viral hepatitis
Feature
HAV
HBV
HCV
HDV
HEV
Incubation (days) 15–45, mean 30
30–180, mean 60– 15–160, mean 50
90
30–180, mean 60– 14–60, mean 40
90
Onset
Acute
Insidious or acute Insidious
Insidious or acute Acute
Clinical
Severity
Mild
Occasionally
severe
Moderate
Occasionally
severe
Mild
Fulminant
0.1%
0.1–1%
0.1%
5–20%
1–2%
None
Occasional (1–
10%) (90% of
neonates)
Common (85%)
Common
None
Carrier
None
0.1–30%
1.5–3.2%
Variable
None
Cancer
None
+
+
±
None
Prognosis
Excellent
Worse with age,
debility
Moderate
Acute, good
Chronic, poor
Good
Progression to
chronicity
36. Crigler-Najjar Syndrome
• Hereditary Glucuronyl Transferase Deficiency.
• Familial autosomal recessive disease (type I) and autosomal dominant
(type II)
• Indirect serum bilirubin is increased, appears first or second day of life
and persists for life.
• Type I complete enzyme deficiency, type II partial deficiency
37. Gilbert’s Syndrome
• Autosomal dominant
• Chronic, benign, intermittent, nonhemolytic and unconjugated
hyperbilirubinemia.
• Defective transport and conjugation of unconjugated bilirubin.
• Jaundice is accentuated by pregnancy, fever, exercise and various
drugs including alcohol.
38. Dubin-Johnson Syndrome
• Autosomal recessive disease.
• Conjugation of bilirubin-diglucuronide is normal
• Inability to transport bilirubin-glucuronide through hepatocytes into
canaliculi
• Symptoms: mild chronic recurrent jaundice and hepatomegaly
• Serum bilirubin (3-10 mg/dL rarely ≤ 30 md/dL), significant is direct.
39. Rotor’s Syndrome
• Autosomal recessive
• Asymptomatic, benign defective uptake and storage of conjugated
bilirubin, possibly in transfer of bilirubin from liver to bile.
• detected in adolescents or adults
• Jaundice accentuated by pregnancy, pills and alcohol
• Conjugated hyperbilirubinemia (<10 mg/dL)
40. Take Home Message
• Liver has central role in
metabolism, synthesis
and detoxification in
the body
• Interpretation of
liver function tests help in
early diagnosis of various
disorders.
41. References
• Tietze Textbook of clinical chemistry and molecular diagnostics-5th
Ed.
• Intepretation of Diagnostic Tests, Jacques Wallace-7th Ed.
• Textbook of Biochemistry with clinical correlations, Devlin-6th Ed
• Clinical Diagnosis and management by Lab methods- Henry 18th Ed
In Macrophages mainly in spleen, methemoglobin from red cells split to give free globin chains and heme. The porphyrin of heme is oxidized by the microsomal hemeoxygenase, producing the straight chain compound biliverdin and releasing iron. Biliverdin is reduced to bilirubin by NADPH dependent enzyme, biliverdinreductase. Bilirubin bound mainly to albumin transported to portal system to the liver where it enters the hepatocyte.
Organic componds of both endogenous and exogenous origin are extracted from the sinusoidal blood, biotransformed and excreted into the bile or urine.Bilirubin is transported from sites of production spleen, loosely bound to albumin, unconjugated form
provide surface active detergent molecule
Normal fibrinogen level 200-400 mg%. Patterns depend on the type, severity and duration of liver injury. In cirrhosis besides hepatocyte destruction, portal hypertension is the cause of diminished protein production by decreased delivery of amino acids to liver
ISI international sensitivity index
Galactose is a monosaccharide almost exclusively metabolized by the liver. Subject is given iv galactose about 300mg/day and blood is drawn at 10 minutes interval for the next 2 hours and galactose is estimated. Half life of galactose is 10-15 mins. markedly elevated in hepatocellular damage
Obstructive jaundice no change. Hepatocellular jaundice decreases. Acute hepatic necrosis marked reduction in esters.HDL levels increase by the expression of apolipoproteinapo A-I protein.
and ALT 47, ALT activity in hepatocytes is 300 times than plasma.
ALT is typically higher than AST because of slower clearance
Because of higher activity of AST in hepatocytes.
It catalyses the transfer of a glutamyl group from glutathione to a free amino acid