Jaundice, or icterus, is caused by increased levels of bilirubin in the blood which deposits in tissues. It can be a sign of liver disease or hemolytic disorders. Bilirubin is produced from the breakdown of heme in red blood cells and transported to the liver where it is conjugated and excreted in bile or reabsorbed and excreted in urine. Defects in bilirubin production, uptake, conjugation or excretion by the liver can lead to jaundice. The document discusses the causes, signs, and differential diagnosis of jaundice.
Renal function test (RFT), also known as kidney function test is a group of tests used to assess the functions of kidney.
It is used screen for, detect, evaluate and monitor acute and chronic kidney diseases.
These are simple blood and urine tests that are used identify kidneys problems.
Tests of renal function have utility in-
Identifying the presence of renal disease
Monitoring the response of kidneys to treatment
Determining the progression of renal disease
RFT is ordered, if your doctor
thinks your kidneys may not be working properly which is known from signs and symptoms
and if you have other conditions that can harm the kidneys, such as diabetes or high blood pressure
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.
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.
Renal function test (RFT), also known as kidney function test is a group of tests used to assess the functions of kidney.
It is used screen for, detect, evaluate and monitor acute and chronic kidney diseases.
These are simple blood and urine tests that are used identify kidneys problems.
Tests of renal function have utility in-
Identifying the presence of renal disease
Monitoring the response of kidneys to treatment
Determining the progression of renal disease
RFT is ordered, if your doctor
thinks your kidneys may not be working properly which is known from signs and symptoms
and if you have other conditions that can harm the kidneys, such as diabetes or high blood pressure
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.
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.
Proteinuria – early indicator of renal disease
Increases the risk of renal impairment, hypertension & cardiovascular disease.
Proteinuria of 1+ or more persisting on 2 subsequent dipstick tests at weekly intervals – requires further investigations.
Causes of transient proteinuria to be excluded
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.
Proteinuria – early indicator of renal disease
Increases the risk of renal impairment, hypertension & cardiovascular disease.
Proteinuria of 1+ or more persisting on 2 subsequent dipstick tests at weekly intervals – requires further investigations.
Causes of transient proteinuria to be excluded
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.
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Jaundice - Etiology, pathogenesis, Clinical features, Investigation, Treatment and Outcome
1. Jaundice
Dr. M. N. Astagimath, M.D.
Associate Professor
Department of Biochemistry
KIMS, Hubli
2. Jaundice
• Jaundice, or icterus, is a yellowish
discoloration of tissue resulting from the
deposition of bilirubin.
• Tissue deposition of bilirubin occurs
only in the presence of serum
hyperbilirubinemia and is a sign of
either liver disease or, less often, a
hemolytic disorder.
3. Differential Diagnosis
• The differential diagnosis for yellowing of
the skin is limited. In addition to jaundice, it
includes carotenoderma, the use of the
drug quinacrine, and excessive exposure
to phenols.
4. Indicator of increased serum
hyperbilirubinemia
• The presence of scleral icterus indicates a
serum bilirubin of at least 3.0 mg/dl
• Underneath the tongue
• Darkening of the urine
• The skin will eventually become yellow
5. Sources of Bilirubin
• A tetrapyrrole pigment, is a breakdown
product of heme (ferroprotoporphyrin IX)
• 250 to 300 mg of bilirubin produced each
day
• 70 to 80% derived from the breakdown of
hemoglobin in senescent red blood cells
• Remainder comes from prematurely
destroyed erythroid cells and from the
turnover of hemoproteins
7. Formation of bilirubin
• Formation of bilirubin occurs in
reticuloendothelial cells.
• First reaction, catalyzed by the enzyme
heme oxygenase, oxidatively cleaves
the a bridge of the porphyrin group and
opens the heme ring.
• The end products of this reaction are
biliverdin, carbon monoxide, and iron.
8.
9. Formation of bilirubin
• The second reaction, catalyzed by the
cytosolic enzyme biliverdin reductase,
reduces the central methylene bridge of
biliverdin and converts it to bilirubin
10.
11. Transport to Liver
• Bilirubin is virtually insoluble in water
• Aqueous solubility 0.1-5 mg/dl
• Transport of unconjugated bilirubin in the
blood is accomplished by its reversible, non-
covalent binding to albumin
• Each molecule of albumin has
- one “high affinity binding site
(binds about 25mg/dl)
- one “low affinity” binding site
• The excess bilirubin is loosely bound and
thus easily detached, which diffuses into
tissues.
12. Uptake by Liver
• Bilirubin most likely enters the hepatocyte both by a facilitated
transport mechanism and by passive diffusion
• Unconjugated bilirubin bound to albumin, but not the albumin,
is taken up by hepatocytes
• Carrier-mediated facilitated membrane transport is the
predominant process
• Several putative bilirubin transporters have been identified
• Lateral extension of plasma membrane of liver cells facing
hepatic sinusoids has specific “receptor sites” for bilirubin
13. Intracellular Binding
• Having crossed the plasma membrane to
enter the cell, bilirubin partitions between
the lipid environment of intracellular
membranes
• In the aqueous cytosol, in which it is kept
in solution by binding as a nonsubstrate
ligand to several of the glutathione-s-
transferases, formerly called ligandins.
14. Conjugation
• When the carboxyl groups are esterified by
conjugation with glucuronic acid residues, the
internal hydrogen bonding is disrupted,
rendering the resulting mono- and
diglucuronide conjugates highly soluble in
aqueous solution
• Catalyzed by a specific UDP-
glucuronosyltransferase
17. UDP-glucuronosyltransferase
• Various first exons encode the specific
substrate-binding sites for each isoform, while
the shared exons encode common
glycosylation, UDP-glucuronic acid-binding,
transmembrane, and stop transfer domains.
• Encoded by the Exon A1 and the four common
exons, collectively designated the UGT1A1
gene.
• Mutation in one of the first exons will affect
only a single enzyme isoform. By contrast, a
mutation in exons 2 to 5 will alter all isoforms
encoded by the UGT1 gene complex.
18. Biliary Excretion
• Normal bile
-less than 5% unconjugated bilirubin
-7% bilirubin monoconjugates
- 90% bilirubin diconjugates.
• Bilirubin mono- and diglucuronides are
excreted across the canalicular plasma
membrane into the canaliculus by an ATP-
dependent transport process mediated by a
canalicular membrane protein called
multidrug resistance-associated protein 2
(MRP2).
19. BILIRUBIN IN PLASMA
• Indeed, when the direct-reacting fraction is
less than 15% of total bilirubin at virtually
any total bilirubin concentration, the
bilirubin in the sample can be considered
as essentially all unconjugated.
20. Bilirubin in the Gut
• An appreciable fraction is converted to
urobilinogen and related compounds by
bacterial metabolism within the ileum and
colon.
• Urobilinogen is reabsorbed from these sites,
reaches the liver via the portal circulation,
and is reexcreted into bile, undergoing an
enterohepatic circulation.
• Urobilinogen not taken up by the liver
reaches the systemic circulation, from which
some is cleared by the kidneys.
21. Renal Excretion of Bilirubin Conjugates
• Unconjugated bilirubin is not excreted in
urine no matter how high its plasma
concentration, since it is too tightly bound to
albumin for effective glomerular filtration
and there is no tubular mechanism for its
renal secretion.
• polar bilirubin conjugates are far less tightly
bound to albumin and are readily filtered at
the glomerulus
• bilirubinuria indicates the presence of
conjugated bilirubin in plasma and,
therefore, hepatobiliary dysfunction.
26. Over production
Hemolysis.
Icreased destruction of erythrocytes leads
to increased bilirubin turnover and
unconjugated hyperbilirubinemia.
Normal liver function.
Direct-reacting fraction as measured in a
typical clinical laboratory being 15% of
the total serum bilirubin.
27. Over production
Ineffective Erythropoiesis.
• Megaloblastic anemias, congenital
erythropoietic porphyria, lead poisoning,
and various dyserythropoietic anemias.
• Total bilirubin production derived from
ineffective erythropoiesis is increased,
reaching as much as 70% of the total, and
may be sufficient to produce modest
degrees of unconjugated
hyperbilirubinemia.
28. Uptake by Liver
• Decreased hepatic bilirubin uptake is
believed to contribute to the
unconjugated hyperbilirubinemia of
Gilbert's syndrome (GS).
• Drugs, including flavispidic acid,
novobiocin, and various
cholecystographic contrast agents,
have been reported to inhibit bilirubin
uptake.
29. Impaired Conjugation
• Physiologic neonatal jaundice birth. Peak
levels are typically less than 85 to 170
umol/l (5 to 10 mg/dl) and decline to normal
adult concentrations within 2 weeks.
• Prematurity - absolute levels in excess of
340 umol/l (20 mg/dl), puts the infant at risk
for bilirubin encephalopathy, or kernicterus,
in which bilirubin crosses an immature
blood-brain barrier and precipitates in the
basal ganglia and other areas of the brain.
30. HEREDITARY DEFECTS IN
BILIRUBIN CONJUGATION
Crigler-Najjar syndrome, type I (CN-I).
• Unconjugated hyperbilirubinemia (20 to 45
mg/dl) that appears in the neonatal period
and persists for life.
• Absent bilirubin-UDP-glucuronosyltransferase
enzymatic activity.
Crigler-Najjar syndrome, type II (CN-II).
• Lower bilirubin, characteristic increase in
monoglucuronides.
• UGT1A1 is usually present at reduced levels.
31. Gilbert's syndrome
• Mild unconjugated hyperbilirubinemia,
• Normal biochemical tests, and histology.
• UGT1A1 activity is typically reduced to 10
to 35% of normal,
• A characteristic increase in bilirubin
monoglucuronides.
• That hepatic bilirubin clearance is reduced
to an average of one-third of normal.
32. Acquired Conjugation Defects
• Advanced hepatitis or cirrhosis.
• However, conjugation is better preserved
than canalicular excretion.
• Various drugs, including pregnanediol,
novobiocin, chloramphenicol, and
gentamicin, may produce unconjugated
hyperbilirubinemia by inhibiting UGT1A1
activity.
• Breast milk jaundice - certain FAs and the
progestational steroid 3a,20b-pregnanediol.
• Lucey-Driscoll syndrome).
33. DEFECTS IN HEPATIC
EXCRETION
Dubin-Johnson syndrome
• Benign,low-grade (2 and 5 mg/dl),
predominantly conjugated
hyperbilirubinemia.
• A cardinal feature of Dubin-Johnson
syndrome is the accumulation in the
lysosomes of centrilobular hepatocytes of
dark, coarsely granular pigment. As a
result, the liver may be grossly black in
appearance.
34. Rotor Syndrome
• Liver in patients with rotor syndrome has
no increased pigmentation and appears
totally normal.
• The only abnormality in routine
laboratory tests is an elevation of
predominant total serum conjugated
bilirubin.
• No reflux of conjugated BSP back into
the circulation as seen in Dubin-Johnson
syndrome.
35. Benign Recurrent Intrahepatic
Cholestasis (BRIC)
• Recurrent attacks of pruritus and
jaundice.
• Begins with mild malaise and
elevations in serum aminotransferase
levels, followed rapidly by rises in
alkaline phosphatase and bilirubin
and onset of jaundice and itching.
36. Differential Diagnosis of Jaundice
Tests Pre
Hepatic Hepatic
Post
Hepatic
Conj. Bilirubin Absent
AST & ALT N N
ALP N Normal
Urine Bilirubin Absent Present Present
Urine
Urobilinogen
Present Present Absent
37. NORMAL BILIRUBIN
METABOLISM
Uptake of bilirubin by the liver is mediated by
a carrier protein (receptor)
Uptake may be competitively inhibited by
other organic anions
On the smooth ER, bilirubin is conjugated with
glucoronic acid, xylose, or ribose
Glucoronic acid is the major conjugate -
catalyzed by UDP glucuronyl tranferase
“Conjugated” bilirubin is water soluble and is
secreted by the hepatocytes into the biliary
canaliculi
Converted to stercobilinogen (urobilinogen)
(colorless) by bacteria in the gut
Oxidized to stercobilin which is colored
Excreted in feces
Some stercobilin may be re-adsorbed by the
gut and re-excreted by either the liver or
kidney
38. Prehepatic (hemolytic) jaundice
• Results from excess
production of bilirubin
(beyond the livers ability
to conjugate it) following
hemolysis
• Excess RBC lysis is
commonly the result of
autoimmune disease;
hemolytic disease of the
newborn (Rh- or ABO-
incompatibility);
structurally abnormal
RBCs (Sickle cell disease);
or breakdown of
extravasated blood
39. Intrahepatic jaundice
• Impaired uptake,
conjugation, or
secretion of bilirubin
• Reflects a generalized
liver (hepatocyte)
dysfunction
• In this case,
hyperbilirubinemia is
usually accompanied by
other abnormalities in
biochemical markers of
liver function
40. Posthepatic jaundice
• Caused by an obstruction
of the biliary tree
• Plasma bilirubin is
conjugated, and other
biliary metabolites, such
as bile acids accumulate in
the plasma
• Characterized by pale
colored stools (absence of
fecal bilirubin or urobilin),
and dark urine (increased
conjugated bilirubin)
• In a complete obstruction,