Are most abundantly distributed organic compounds.
70 kg man= protein weight constitute 12 kg
Skeleton and connective tissue contains half
Body protein and other half is intracellular.
Glycolysis (from glycose, an older term for glucose + -lysis degradation) is the metabolic pathway that converts glucose C6H12O6, into pyruvate, CH3COCOO− + H+. The free energy released in this process is used to form the high-energy molecules ATP (adenosine triphosphate) and NADH (reduced nicotinamide adenine ...
Metabolism of amino acids (general metabolism)Ashok Katta
Metabolism of amino acids (general metabolism).
Part - I of amino acid metabolism.
This presentation covers Transamination, deamination, formation and Transport of Ammoniaand etc.
Are most abundantly distributed organic compounds.
70 kg man= protein weight constitute 12 kg
Skeleton and connective tissue contains half
Body protein and other half is intracellular.
Glycolysis (from glycose, an older term for glucose + -lysis degradation) is the metabolic pathway that converts glucose C6H12O6, into pyruvate, CH3COCOO− + H+. The free energy released in this process is used to form the high-energy molecules ATP (adenosine triphosphate) and NADH (reduced nicotinamide adenine ...
Metabolism of amino acids (general metabolism)Ashok Katta
Metabolism of amino acids (general metabolism).
Part - I of amino acid metabolism.
This presentation covers Transamination, deamination, formation and Transport of Ammoniaand etc.
designed for undergraduate level teaching of nitrogen metabolism in biochemistry. this is first in the series of three lectures. ideal for MBBS level teaching
In ureotelic organisms, the ammonia deposited in
the mitochondria of hepatocytes is converted to urea in
the urea cycle. This pathway was discovered in 1932 by
Hans Krebs (who later also discovered the citric acid cycle)
and a medical student associate, Kurt Henseleit.
Urea production occurs almost exclusively in the liver
and is the fate of most of the ammonia channeled there.
The urea passes into the bloodstream and thus to the
kidneys and is excreted into the urine. The production
of urea now becomes the focus of our discussion.
The urea cycle is the metabolic pathway that transforms nitrogen to urea for excretion from the body. Liver cells play a critical role in disposing of nitrogenous waste by forming urea hrough the action of the urea cycle.
Nitrogenous excretory products are then removed from the body through in the urine.
The urea excreted each day by a healthy adult (about 30 g) accounts for about 90% of the nitrogenous excretory products.
The cycle occurs mainly in the liver.
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
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
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
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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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.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
2. Presentation Overview
1) Introduction
2) History
3) Urea Cycle and It’s Reactions
4) Link between Urea Cycle and TCA Cycle
5) Regulation
6) Energetics
7) Disorder
8) Reference
3. Introduction
Urea is the major disposal form of amino groups derived from amino
acids pool and 90% of nitrogen containing component of urine
Urea cycle is a cyclic process
Urea formation takes place in the liver
Some reaction occur in mitochondria(1,2) and some In cytosol(3,4,5)
Synthesis of 1 molecule of urea need
• 3 Molecule of ATP
• 1 Molecule of ammonium ion
• 1 molecule of α-amino nitrogen of aspartate
5 enzyme catalyzed the numbered reaction
4. History
The urea cycle is the first metabolic
pathway to be elucidated.
Thecycleisknownas Krebs–Henseleit
Urea Cycle.
It was discovered five years before the
discovery of the TCA cycle.
It takes place primarily in the liver
and, to a lesser extent, in the kidneys.
5. Properties Of Urea
Non toxic
Water soluble
Combines two waste products into
one molecule:
• CO2
• NH3
6. Pros Of Urea Against Ammonia
Ammonia is an extremely toxic base and its
accumulation in our body would be quickly
fatal.
Liver contains a system of carrier molecules &
enzymes which coverts ammonia to urea.
7.
8. Blood Urea Nitrogen
Normal range: 7-18 mg/dL
Elevated in amino acid catabolism
Elevated in renal insufficiency
Decreased in hepatic failure
9.
10. 2 ATP 2 ADP
NH3 Pi
Step-1-Formation of Carbamoyl Phosphate
Reactionof bicarbonate with ATP forms carbonyl phosphate and ADP.
Ammonia then displaces ADP, forming carbamate and orthophosphate.
Phosphorylation of carbamate by the second ATP then forms carbamoyl phosphate.
11. This enzyme has no regulatory significance. The remainder of the urea cycle
steps take place in the cytosol. This requires the continuous export of
citrulline and the uptake of ornithine across the inner mitochondrial
membrane.
Step-2- Formation of Citrulline
The Carbamoyl group of Carbamoyl
phosphate is transferred to ornithine,forming
Citrulline and Ortho Phosphate
The reaction is catalyzed
by Ornithine
transcarbamoylase
Subsequent metabolism of Citrulline take
place in the cytosol.
Entry of ornithine into mitochondria and exit
of citrulline from mitochondria involves
mitochondrial inner membrane transport
systems
12. Production of arginino-succinate is an energetically expensive process, since the ATP is split
to AMP and pyrophosphate.
The pyrophosphate is then cleaved to inorganic phosphate using pyrophosphatase , so
the overall reaction costs two equivalents of high energy phosphate per mole.
The reaction requires ATP and involves intermediate formation of citruIlyl-AMP.
Subsequent displacement of AMP by aspartate then forms Argininosuccinate.
Step-3- Formation Of Arginosuccinate
13. Step-4- Cleavage Of Arginosuccinate
Cleavage of argininosuccinate catalyzed by argininosuccinate lyase
(ASL), proceeds with retention of nitrogen in arginine and release of
the aspartate skeleton as fumarate.
Addition of water to fumarate forms L-malate, and subsequent NAD+-
dependent oxidation of malate forms oxaloacetate.
Transamination of oxaloacetate by glutamate aminotransferase then
reforms aspartate. carbon skeleton of aspartate-fumarate thus acts as a
carrier of the nitrogen of glutamate into a precursor of urea
14. In each case fumarate is formed as a by-product. Fumarate is not
transported by mitochondria, so this requires the presence of
cytosolic fumarase to form malate.
Fumarate Malate
Fumarase MDH
Oxaloacetate Aspartate
Aminotransferase
NAD+ NADH+H+
15. Step-5- Cleavage of Arginine
Hydrolytic cleavage of the guanidino group of
arginine,catalyzed by liver arginase (ARGl)
releases urea, the other product,Ornithine,
reenters liver mitochondria for addition a l
rounds of urea synthesis.
Ornithine and lysine a repotent inhibitors of
arginase,competitive with arginine.
Arginase is activated by Co2+ & Mn2+
Ornithine & lysine compete with arginine
(competitive inhibition).
16. Link Between Citric Acid
Cycle And Urea Cycle
The fumarate produced in the urea cycle is an intermediate in
citric acid cycle
Aspartate formed in mitochondria by transamination between
oxaloacetate and glutamate which is transported to the cytosol.
Where it serves as nitrogen donor in the urea cycle.
These reactions , making up the aspartate-arginosuccinate shunt,
provide metabolic link between these two pathways.
17.
18. Regulations Of Urea Cycle
Coarse regulation
• Enzyme level changes with protein content of diet
• Starvation, urea cycle elevated to meet increase rate of
protein catabolism
Fine regulation (allosterically)
• Majorly via CPS-1, through positive effector is N-acetyl
glutamate (NAG)
• Arginine activate NAG synthase
19.
20. Energetics Of Urea Cycle
The overall reaction may be summarized as:
NH3 + CO2 + aspartate → urea + fumarate
2 ATP are used in 1st reaction
Another ATP is converted to AMP + ppi in the 3rd step which is equivalent to
two ATPs
The urea cycle consumes 4 high energy PHOSPHATE BONDS.
Fumarate formed in the 4th step may be converted to malate
Malate when oxidised to oxaloacetate produces 1 NADH equivalent to 2.5 ATP.
• So net energy expenditure is only 1.5 high energy phosphates.
• The urea cycle & TCA cycle are interlinked & it is called as "urea bicycle".
21. The main function of Urea cycle is to remove toxic ammonia from
blood as urea.
Defects in the metabolism of conversion of ammonia to urea, i.e.,
Urea cycle leads to Hyperammonaemia or NH3 intoxication.
Disorders of Urea Cycle
22. Inherited disorders of urea
cycleenzymes- familial
hyperammonaemia.
Acquired disorders- Liver
Disease, severe Renal
disease -Acquired
hyperammonaemia.
Hyperammonaemia
23. Increased levels of ammonia crosses BBB, formation of glutamate.
More utilization of α-ketoglutarate.
Decreased levels of α- Ketoglutarate in Brain.
α-KG is a key intermediate in TCA cycle.
Decreased levels impairs TCA cycle.
Decreased ATP production.
Glutamate
NADPH + H+ NADP+
GDH
α- Ketoglutarate + NH3
Ammonia Toxicity
24. In diseases of the liver, hepatic failure can finally lead to hepatic coma &
death.
Hyperammonemia is the characteristic feature of liver failure.
The condition is also known as portal systemic encephalopathy.
Normally the ammonia & other toxic compounds produced by
intestinal bacterial metabolism are transported to liver by portal
circulation & detoxified by the liver.
But when there is portal systemic shunting of blood, the toxins bypass
the liver & their concentration in systemic circulation rises.
Hepatic Coma (Acquired
Hyperammonemia)