1) Hemoglobin is broken down in red blood cells, producing bilirubin at a rate of approximately 250-350 mg per day.
2) Bilirubin binds to albumin and is transported to the liver, where it is conjugated and secreted into bile ducts.
3) Jaundice occurs when there is excessive bilirubin that cannot be processed by the liver, resulting in a buildup that discolors the skin and eyes. It can be caused by hemolytic anemia, liver disease, or bile duct obstruction.
Heme Catabolism and Degradation Pathway #Bilirubin metabolismAHLAD T.O
This video is about heme catabolism or heme degradation. Heme is degraded into bilirubin in a heme degradation pathway. Heme degradation pathway or heme degradation biochemistry is important for understanding different types of bilirubin being elevated in jaundice. Types of jaundice can be classified based on the type of bilirubin being elevated in the blood. Heme catabolism or heme degradation is important concept
Heme Catabolism (Heme Degradation Pathway)
heme catabolism
Bilirubin metabolism ( Heme catabolism)
Heme Catabolism and Degradation Pathway - Biochemistry Lesson
Bilirubin metabolism
Heme catabolism
Heme catabolism || Bilirubin metabolism || #Biochemistry
steps
Introduction
Bilirubin formation pathway
Transport of bilirubin to liver
Uptake of bilirubin in liver
Conjugation of bilirubin
Excretion of bilirubin in bile canaliculi
Fate of conjugated bilirubin in intestine
Entero-hepatic circulation of urobilinogen
Final excretion of UBG and SBG
As the channel name suggests, our channel will be a perfect lounge for the malayali medicos..we wil be covering videos which will be like lecture classes related to the subjects biochemistry and microbiology in which we are specialised.. It will be a better learning experience for the students especially for those who are not able to understand and follow the normal classes in college..we assure the students that you will get a basic idea regarding the topic and extra reading can be done from the reference textbooks...
If you like my video
#like
#comment
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Qualification
Ahlad.T.O
MSc MLT (Biochemistry)
Assistant Professor
Baby memorial college of allied Health science
Kozhikode
Our Partner Channel
Health & Voyage channel link - https://youtu.be/nzKqRVjlwc0
Heme catabolism
Heme degradation in macrophages
Bilirubin transport with albumin
Bilirubin metabolism
1. Uptake by hepatocytes by facilitated diffusion
2. Conjugation of unconjugated bilirubin
3. Secretion in to bile canaliculi by active transport through MRP 2
Congenital causes
UNCONJUGATED BILIRUBIN INCREASE
1. Crigler Najjar type 1
2. Crigler Najjar type 2
3. Gilbert syndrome
Conjugated bilirubin increase
1. Dubin Johnson syndrome
2. Rotor syndrome
#Mallu
#Microbiology
#Biochemistry
#MalluMedicosLounge
#HealthAndVoyage
#How to take online class
Heme Catabolism and Degradation Pathway #Bilirubin metabolismAHLAD T.O
This video is about heme catabolism or heme degradation. Heme is degraded into bilirubin in a heme degradation pathway. Heme degradation pathway or heme degradation biochemistry is important for understanding different types of bilirubin being elevated in jaundice. Types of jaundice can be classified based on the type of bilirubin being elevated in the blood. Heme catabolism or heme degradation is important concept
Heme Catabolism (Heme Degradation Pathway)
heme catabolism
Bilirubin metabolism ( Heme catabolism)
Heme Catabolism and Degradation Pathway - Biochemistry Lesson
Bilirubin metabolism
Heme catabolism
Heme catabolism || Bilirubin metabolism || #Biochemistry
steps
Introduction
Bilirubin formation pathway
Transport of bilirubin to liver
Uptake of bilirubin in liver
Conjugation of bilirubin
Excretion of bilirubin in bile canaliculi
Fate of conjugated bilirubin in intestine
Entero-hepatic circulation of urobilinogen
Final excretion of UBG and SBG
As the channel name suggests, our channel will be a perfect lounge for the malayali medicos..we wil be covering videos which will be like lecture classes related to the subjects biochemistry and microbiology in which we are specialised.. It will be a better learning experience for the students especially for those who are not able to understand and follow the normal classes in college..we assure the students that you will get a basic idea regarding the topic and extra reading can be done from the reference textbooks...
If you like my video
#like
#comment
#subscribe my channel
don't forget to subscribe my channel
Qualification
Ahlad.T.O
MSc MLT (Biochemistry)
Assistant Professor
Baby memorial college of allied Health science
Kozhikode
Our Partner Channel
Health & Voyage channel link - https://youtu.be/nzKqRVjlwc0
Heme catabolism
Heme degradation in macrophages
Bilirubin transport with albumin
Bilirubin metabolism
1. Uptake by hepatocytes by facilitated diffusion
2. Conjugation of unconjugated bilirubin
3. Secretion in to bile canaliculi by active transport through MRP 2
Congenital causes
UNCONJUGATED BILIRUBIN INCREASE
1. Crigler Najjar type 1
2. Crigler Najjar type 2
3. Gilbert syndrome
Conjugated bilirubin increase
1. Dubin Johnson syndrome
2. Rotor syndrome
#Mallu
#Microbiology
#Biochemistry
#MalluMedicosLounge
#HealthAndVoyage
#How to take online class
Inborn errors of amino acid metabolismRamesh Gupta
Inherited disorders of amino acid metabolism e.g. phenylketonuria, maple syrup urine disease, alkaptonuria, homocystinuria, Hartnup disease etc for medical, biochemistry and biology undergraduates
Catabolism of Heme | Jaundice | Hyperbilirubinemiakiransharma204
This PPT contain topics on Catabolism of heme; hyperbilirubinemia and jaundice
Books referred: https://www.amazon.in/Biochemistry-2019-Satyanarayana-Satyanarayana-Author/dp/B07WGHCTKZ/ref=sr_1_1?dchild=1&qid=1592209115&refinements=p_27%3AU+Satyanarayana&s=books&sr=1-1
Glucose tolerance test- Indications, contraindications, preparation of a patient, precautions, types of GTT, normal curve, diabetic curve, renal glycosuria, lag curve, Criteria for diagnosis of DM
Inborn errors of amino acid metabolismRamesh Gupta
Inherited disorders of amino acid metabolism e.g. phenylketonuria, maple syrup urine disease, alkaptonuria, homocystinuria, Hartnup disease etc for medical, biochemistry and biology undergraduates
Catabolism of Heme | Jaundice | Hyperbilirubinemiakiransharma204
This PPT contain topics on Catabolism of heme; hyperbilirubinemia and jaundice
Books referred: https://www.amazon.in/Biochemistry-2019-Satyanarayana-Satyanarayana-Author/dp/B07WGHCTKZ/ref=sr_1_1?dchild=1&qid=1592209115&refinements=p_27%3AU+Satyanarayana&s=books&sr=1-1
Glucose tolerance test- Indications, contraindications, preparation of a patient, precautions, types of GTT, normal curve, diabetic curve, renal glycosuria, lag curve, Criteria for diagnosis of DM
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 BY DR. PREMJEET KAUR, ASSISTANT PROFESSOR BIOCHEMISTRY Premjeet Kaur
BY THE END OF THIS PRESENTATION YOU WILL BE ABLE TO ANSWER WHAT, WHY, WHICH ABOUT LIVER FUNCTION TESTS , WHAT IS JAUNDICE , METABOLISM OF HEME , FORMATION OF BILE PIGMENTS FROM HEME , TRASFER OF LILIRUBIN FROM BLOOD TO BILE , DETERMINATION OF SERUM BILIRUBIN, RETENTION JAUNDICE , REGURGITATION JAUNDICE ,DETERMINATION OF AMMONIA IN BLOOD ,ANTIPYRINE TEST, SERUM ENZYMES IN LIVER DISEASE, ASSESING EXTENT OF LIVER DAMAGE , DIAGNOSIS OF SUBCLINICAL JAUNDICE , BCG TEST , PLASMA PROTEINS , DETOXIFICATION FUNCTION OF LIVER
This explains the complex carbohydrates and chemistry of heterpolysaccharides. composition, distribution and its function is explained for each GAGs. brief notes on blood group ag is available. difference between proteoglycan and glycoprotein is explained in a essay way to understand. clinical importance is also added.
rft is described in detail . function of kidney, objectives of doing the test. the various test available for assessing the renal function with clinical interpretation is available.
it describes transcription with simple diagram and animation. its steps and inhibitors are described for both eukaryotes and prokaryotes. it will be easily understood by UG students . post transcriptional modification of all the RNA are also described with diagrams.
describes the structure of hb, its variants in detail. Oxygen dissociation curve is explained with graph. Hemoglobinopathy is explained with diagram. myoglobin is also explained.
explains the breakdown of purine. source and excretion of purine is explained. hyperuricemia and hypouricemia is discussed. types of Gout, clinical features and treatment is included.
synthesis and degradation of glycine is discussed. specialized products formed from glycine is described in detail. disorders associated with metabolism of glycine is also explained.
synthesis and lipolysis is explained in detail. enzymes involved and their differences are tabulated. adipose tissue metabolism is also included. Fatty liver causes are explained in detail. obesity is briefly described.
describes the sources of lipids. enzymes and stages of digestion in detail. absorption form , transport form and disorders of digestion & absorption included.
explains the palmitate synthesis- which is most common FA stored in Adipose tissue , elongation system and Desaturation system, compares oxidation with synthesis.
This topic covers the brief introduction of Ag and Ab in detail. Types and functions of Ig is explained in detail. Paraproteinemias is explained with simple pictures.
by Dr. N.Sivaranjani, MD
Describes the plasma membrane in detail, explains the each major component with its functions.
Transport mechanism across the cell is covered with detailed explanation with examples.
by Dr. N.Sivaranjani, MD
Enzyme inhibition is explained with its kinetics, animations showing mechanism of inhibitors action, examples of inhibitors are explained in detail with Enzyme inhibited.
by Dr. N. Sivaranjani, MD
Describes the structural organisation of proteins with example and its determination, interrelationship b/w structure and function of proteins, also biologically important peptides is covered.
by Dr. N. Sivaranjani, MD
2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
Acetabularia Information For Class 9 .docxvaibhavrinwa19
Acetabularia acetabulum is a single-celled green alga that in its vegetative state is morphologically differentiated into a basal rhizoid and an axially elongated stalk, which bears whorls of branching hairs. The single diploid nucleus resides in the rhizoid.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
Synthetic Fiber Construction in lab .pptxPavel ( NSTU)
Synthetic fiber production is a fascinating and complex field that blends chemistry, engineering, and environmental science. By understanding these aspects, students can gain a comprehensive view of synthetic fiber production, its impact on society and the environment, and the potential for future innovations. Synthetic fibers play a crucial role in modern society, impacting various aspects of daily life, industry, and the environment. ynthetic fibers are integral to modern life, offering a range of benefits from cost-effectiveness and versatility to innovative applications and performance characteristics. While they pose environmental challenges, ongoing research and development aim to create more sustainable and eco-friendly alternatives. Understanding the importance of synthetic fibers helps in appreciating their role in the economy, industry, and daily life, while also emphasizing the need for sustainable practices and innovation.
Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
2. Degradation of Hb
6g of Hb is broken per day
1g of Hb = 35 mg of bilirubin
Approx. 250-350 mg of bilirubin is formed per day
85% - old RBCs (120 days) degraded per day
15% - immature RBCs & other heme containing proteins.
dr. N. Sivaranjani 2
3. HemoglobinHeme globin
Amino acids
Reutilized
NADPH + H+
NADP+
Heme oxygenase
Fe3+
Hemoproteins
Hb - 80%
Myoglobin, Cytochromes – 20%
Reticuloendothelial cells- Liver,
Spleen, Bone marrow.
V
M
M M
V
M
PP
Fe++
CO
O2
P M
N
PM
N
VM
N
VM
N OO
IIVIIIII
I
IV
II
MICROSOMAL
Biliverdin
Linear Tetrapyrrole compoundH H H
Cleavage of the alpha
methenyl bridge b/w
pyrrole rings I and II.
dr. N. Sivaranjani 3
5. Unconj.BILIRUBIN - ALBUMIN
Endoplasmic reticulum
Conjugated Bilirubin
Unconj.Bilirubin
UDP-Glucuronate
UDP
UDP-glucuronyl transferase
Bilirubin monoglucuronide
UDP-Glucuronate
UDP
UDP-glucuronyl transferase
Bilirubin diglucuronide
UDP
PMVM
N N
OO
IIVIIIII
H H H
H2
H
NN
P M VM
Glucuronic acid Glucuronic acid
Active process - Rate limiting step
Uptake by LIVER
Conjugation is induced
by Phenobarbitone
dr. N. Sivaranjani 5
6. Albumin – 1 high affinity binding site and 1 low affinity
binding site for bilirubin
In 100 ml plasma- 25 mg of bilirubin bind to high affinity
binding site
Drugs – Aspirin, Sulpha antibiotic , Salicylates
Displace bilirubin from Albumin.
So bilirubin cross BBB , enter brain & cause injury – drugs
are avoided in New born.
dr. N. Sivaranjani 6
7. Uptake of bilirubin by Liver -Ligandin
Conjugation of bilirubin – disrupts the internal H
bonding which limits the aqueous solubility of
bilirubin.C1 of Glucuronic acid condenses with carboxyl gr of
Propionic acid.
Secretion of conj. bilirubin into bile –
Active process - RATE LIMING STEP
MOAT – Multispecific Organic Anion Transport.
3 process
dr. N. Sivaranjani 7
9. Reduced form of Bilirubin
– Colorless tetrapyrroles
Urobilinogen
Mesobilinogen
Stercobilinogen
Oxidized form
of Bilirubin
UROBILIN
STERCOBILIN
MESOBILIN
On exposure to atmospheric air, these are oxidized to colored product.
dr. N. Sivaranjani 9
10. Jaundice is a symptom of underlying
disease , NOT a disease itself.
• Jaundice is yellowish discoloration of the Sclera, Skin and mucous
membranes due to hyper-bilirubinemia and deposition of bile
pigments.
11. Bilirubin
• The normal conc. of serum bilirubin is
Total bilirubin - 0.1 to 1.0 mg/dl
Conjugated (direct) - 0.1 to 0.4 mg/dl
Unconjugated (indirect) - 0.2 to 0.7 mg/dl
1-2 mg/dl – Subclinical JAUNDICE
>3 mg/dl – ICTERUS – Clinical JAUNDICE.
dr. N. Sivaranjani 11
12. JAUNDICE
Failure of disease
LIVER to excrete
bilirubin produced in
NORMAL amounts
Production of more
bilirubin than LIVER
can conjugate -
Increased haemolysis
Mechanical obstruction
of BILE DUCT –bilirubin
cannot enter intestine
dr. N. Sivaranjani 12
14. • Main Clinical features of hemolytic jaundice
Icterus
Anemia
Splenomegaly
Other investigations :
Hb – dec.
Reticulocytes – inc.
Bone marrow – Hyperplasia
dr. N. Sivaranjani 14
16. • Hepatic jaundice
Caused by impaired uptake of bilirubin by LIVER
Drugs – Rifampicin – dec uptake of bilirubin
- Novobiocin ,Primaquine – affects conjugation
Hepatotoxic drugs – Tetracycline, Paracetamol , Alcohol
Congenital – Gilberts ,Crigler Najjar synd.
Caused by infective hepatitis – varying degree of liver necrosis
Damaged liver – uptake & conjugation affected- unconj. Bilirubin inc.
Intrahepatic cholestasis –due to block of bile canaliculi by swelling
of liver cell or bile thrombi – regurgitate of conj. Bilirubin to blood-
conj. Bilirubin inc.
dr. N. Sivaranjani 16
17. • Clinical presentation of viral hepatitis
4-10 days
Bilirubin starts to rise
Nausea, vomiting,
Anorexia, Abdominal
discomfort, Arthalgia
1-4 days
Jaundice appears
Hepatomegaly,
Occasionally
splenomegaly,
Sr. Bilirubin dec &
returns to normal
Pre icteric phase
dr. N. Sivaranjani 17
18. Infection
Obstruction
Tumour
Cholecystitis
Biliary cirrhosis
Gall stones
Bile duct obstruction / biliary atresia
Post infective strictures
Ca head of pancreas
Ca gallbladder
Ca of CBD
Obstruction in Bile duct - Prevents the
passage of bile into the intestine
dr. N. Sivaranjani 18
19. • Cholestatic jaundice / Surgical jaundice clinical features
Icterus
Pruritis – retention of Bile salts
Hepatomegaly
Purpura – Impaired Vit.K absorption
Extrahepatic cholestasis –
Gall stones in CBD
Tumor of bile duct
Atresia of main bile duct
Bile duct stricture
Ca head of pancreas
Intrahepatic cholestasis –
Congenital – D-J synd., Rotor synd.
Primary biliary cirrhosis
Intra hepatic atresia
Sclerosing cholangitis
Bile duct ca
dr. N. Sivaranjani 19
20. Van den Bergh test - Bilirubin reacts with diazo reagent (diazotized
sulphanilic acid) to produce colored azo pigment - Purple color
Bilirubin Van den Bergh test
Conjugated bilirubin Colour develops immediately ,response
is direct positive.
Unconjugated
bilirubin
Colour obtained only when alcohol is
added, this response is indirect
positive.
Both unconjugated
and conjugated
bilirubin
Colour develops immediately and it gets
intensified on adding alcohol, response
is Biphasic.
EHRLICH'S test – UROBLINOGEN
dr. N. Sivaranjani 20
21. Types of jaundice Pre hepatic Hepatic Post hepatic
Type of bilirubin
elevated
unconjugated
bilirubin
Both conjugated &
unconjugated bilirubin
conjugated
bilirubin
Serum bilirubin -
Van den Bergh test
Indirect positive Biphasic Direct positive
Urine
Conj.Bilirubin
Urobilinogen
Bile salt
Absent
+++
Absent
++
+ early, obst.-dec.
+
+++
Absent
++
Urine color Normal-Acholuric Dark – Choluric Dark – Choluric
Stool color Dark brown colour N /decreased Clay colored stools
AST & ALT Normal Very high inc.
ALP Levels Normal 2-3 times increased 10-12 times inc.dr. N. Sivaranjani 21
22. Unconj. Bilirubin inc in serum
UBG inc. in urine
Urine normal color
Dark color stool
Unconj. & Conj. Bilirubin inc.
UBG is slightly inc & dec in case
of obstructive phase in urine
Urine dark color
Normal color stool
Conj. Bilirubin inc in serum
UBG dec. in urine
Urine dark color
Clay color stooldr. N. Sivaranjani 22
23. Neonatal Physiological jaundice
• Most common and harmless
• it presents 2nd days of birth & disappears by 2 weeks (appro.10 day)
Reason for inc.unconjugated bilirubin (not more than 5 mg/dl) :-
Liver is immature for uptake, conjugation (low E) & secretion of
bilirubin
Shorter life span of fetal RBCs of 80 - 90 days – inc. Hemolysis
Low conversion of bilirubin to Urobilinogen by the intestinal flora.
dr. N. Sivaranjani 23
24. Pathological Jaundice – appears in the first 24 hours of life.
>19 mg/dl – unconjugated hyperbilirubinemia.
Causes :- blood incompatibilities, blood diseases, genetic syndromes,
hepatitis, cirrhosis, bile duct blockage, other liver diseases, infections,
or medications. in addition, it applies to newborns with jaundice
exaggerated by dehydration, prematurity.
Breast milk jaundice
Occurs in breast fed infants
Usually appears at 1st week of life
High level of Estrogen derivative in maternal blood, which is
excreted through the milk- Inhibits UDP GT enzyme
Harmless and resolves spontaneously
dr. N. Sivaranjani 24
25. BILIRUBIN is – NEUROTOXIC - Inc. Bilirubin
(>20 mg/dl) cross BBB – deposits in Basal ganglia,
Cerebellum etc.
PREMATURE infants are at RISK.
Cause IRREVERSIBLE brain damage
Leads to KERNICTERUS - FATAL
Permanent Neurological deficit
POOR FEEDING
LETHARGY
FITS
SPASTICITY
MENTAL RETARDATION
dr. N. Sivaranjani 25
26. Rx
• Phototherapy : uses Blue light
(420-470 nm).
Bilirubin absorbs blue light maximally.
Photoisomerization – Unconjugated bilirubin converted into a
non-toxic isomer lumirubin, which is excreted.
• Phenobarbital - induce UDP GT enzymes
• Blood transfusion – to prevents brain damage.
dr. N. Sivaranjani 26
27. Crigler-Najjar
syndrome
• AR
• Type I- total
absence of UDP
glucuronyl transf.
• Type II– partial
def. of UDP GT.
• Unconj. Bilirubin
>20mg/dl
• Kernicterus
• Death – 1yr of life
Gilbert’s
syndrome
• AD inheritance
• Males
• defective uptake
of bilirubin by
the liver
• Unconj. Bilirubin -
3 mg/dl
• harmless , no Rx
Dubin –Johnson
syndrome
• AR
• Defective
excretion of conj.
Bilirubin into
BILE
• Mutation in gene
encoding MOAT
protein
• Black liver
jaundice
Rotor
syndrome
• AR
• Exact
cause??
• Abnormal
excretion
• Harmless,
No Rx
Congenital hyperbilirubinemias:
Due to abnormal uptake/ abnormal conjugation /abnormal excretion of
bilirubin.
dr. N. Sivaranjani 27
29. Deconjugated
& reduced to
Stercobilinogen
excreted in
feces
• Bilirubin –
Albumin
complex
Conjugation
of bilirubin
Secretion of
conj. Bilirubin
into bile
Excreted as
Urobilinogen
in urine
dr. N. Sivaranjani 29