The document summarizes heme catabolism and bilirubin metabolism. Heme is broken down, with iron entering the iron pool, globin being reutilized, and the porphyrin ring being converted to bile pigments. Bilirubin is formed from heme in red blood cells and transported to the liver bound to albumin. In the liver, bilirubin is conjugated and excreted into bile. Clinical issues can arise if bilirubin conjugation or transport is impaired, leading to jaundice.
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.
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.
introduction for renal system
nephron
protein & urine
definition of microalbuminuria
causes
atherosclerosis role
DM role (micro¯ovascular changes due to atherosclerosis )
Hypertension role
possible sign and symptoms associated with microalbuminuria
enjoooooooooy ....... :)
Serum Protein and Albumin-Globulin RatioASHIKH SEETHY
For MBBS Biochemistry Practical. Explains various methods of protein estimation and estimation of AG ratio, conditions leading to alterations in AG ratio etc.
simple diagrammatic presentation of heme catabolism. highlighted the steps with explanation. Definition , causes, clinical features and biochemical investigation of various types of jaundice is explained in detail. congenital jaundice is included.
introduction for renal system
nephron
protein & urine
definition of microalbuminuria
causes
atherosclerosis role
DM role (micro¯ovascular changes due to atherosclerosis )
Hypertension role
possible sign and symptoms associated with microalbuminuria
enjoooooooooy ....... :)
Serum Protein and Albumin-Globulin RatioASHIKH SEETHY
For MBBS Biochemistry Practical. Explains various methods of protein estimation and estimation of AG ratio, conditions leading to alterations in AG ratio etc.
simple diagrammatic presentation of heme catabolism. highlighted the steps with explanation. Definition , causes, clinical features and biochemical investigation of various types of jaundice is explained in detail. congenital jaundice is included.
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
Details of integration of metabolism of three main food content - Carbs, fat and proteins in the form of flow chart - easy to understand and easy to remember.
This powerpoint contains details regarding detoxication reactions of xenobiotics. Examples of reactions of different phases of detoxication has been given.
A brief discussion on cytochrome P450 is also included.
A concise note for undergraduate students to learn the use of isotopes in research, analytical and treatment purpose in modern medicine. It also contains the basic of radioactivity and the health hazards associated with it.
A compele text of heme synthesis and the diseases associated with the process. Diseases have been discussed under the points of clinical featues, lab findings and treatment.
Quality control, or QC for short, is a process by which entities review the quality of all factors involved in the production. ISO 9000 defines quality control as "A part of quality management focused on fulfilling quality requirements"
This presentation gives a brief idea of Quality control and how to execute it.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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.
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.
2. Fate of Hb:
• Globin is reutilised or constituent amino acids are reutilised after
proteolysis
• Fe++ of haem enters “iron pool” for reutilisation or stored as “ferritin”
• Fe-free porphyrin portion of haem is degraded to bile pigments
Biliverdin and bilirubin, in RE cells
4. SOURCES OF BILIRUBIN
Mainly two –
(a) From ‘Haem’ of erythrocytes:
- 85% of bilirubin
Site: bone marrow, spleen and liver
(b) Other Sources of Bilirubin:
- 15% of newly synthesised bilirubin
• Haem formed from Hb - synthesis
• Destruction of immature erythrocytes
• Degradation of Hb, within erythrocyte precursors
• Breakdown of other haem pigments
5.
6. Formation of Bilirubin from Biliverdin:
• Occurs in RE cells
• Requires a specific enzyme bilirubin reductase
• NADH or NADPH act as hydrogen donor
Shunt Hyperbilirubinemia:
- Rare form of clinical jaundice
- Associated with ineffective erythropoiesis, hyperplastic bone marrow
- Unconjugated hyperbilirubinemia
7. Transport of Bilirubin
• Bilirubin formed in RE cells is in unconjugated form
• Highly lipid soluble
• Binding with albumin increases plasma solubility
• Normally in 100 ml of plasma, approx. 25 mg of bilirubin can be
tightly bound to albumin
8. Alterations of Albumin-Bilirubin Binding and its Biomedical
Significance
- Administration of anionic drugs like sulphonamides
- Increase in free fatty acids
- Asphyxia, hypoxia
All these promote Bilirubin encephalopathy
- Unconjugated bilirubin enters the neurons of the basal ganglia,
hippocampus, cerebellum, and medulla, causing necrosis of nerve cells
9. Transfer of Bilirubin from Plasma to Liver Cells
• Liver selectively remove unconjugated bilirubin
• Hepatic sinusoids have specific receptor
• Two non-albumin proteins help in intracellular binding of bilirubin
• They have been named as ligandins
11. Conjugated bilirubin:
• Water soluble and
• Smaller in molecular size
• Not bound to albumin
Glucuronyl Transferase Activity in Extrahepatic Tissues
• Skin, kidneys, adrenal glands, ovary, testes, intestinal mucosa and
synovial membrane.
• Probably monoglucuronide is formed
12. SECRETION OF BILIRUBIN IN THE BILE
• Active transport process
• Require MRP-2 (multi drug resistance protein 2) also called
“multispecific organic anion transporter” (MOAT)
• Located in the plasma membrane of the bile canalicular
membrane
14. Clinical aspect:
A. Inhibition of Glucuronyl Transferase Activity:
- Drugs and steroidal derivative inhibits the exzyme
- Basis of breast milk jaundice
- Pregnane –3 α-20β-diol is present in breast milk
- It inhibits the enzyme
- Unconjugated hyperbilirubinemia
- Stopping breast milk feeding, jaundice disappears
15. B. Transient Neonatal “Physiological” Jaundice
- Accelerated haemolysis, immature hepatic system for uptake,
conjugation and secretion of bilirubin
- Also reduced synthesis of substrate
- Kernicterus
Treatment:
- Administration of phenobarbital
- Exposure to visible light (phototherapy)
16. c. Crigler-Najar Syndrome
- Type -1: autosomal recessive disorder
- Inherited absence of glucuronyl transferase activity
- Mutations in the gene encoding bilirubin-UGT in Ch 2
- Nonhaemolytic unconjugated hyperbilirubinaemia,
kernicterus
- T/t – Phototherapy
- Type – 2: Milder defect with benign course
- Some activity of the enzyme is retained
- No risk of kernicterus
17. d. Gilbert’s syndrome:
- Multifactorial
- low grade chronic unconjugated hyperbilirubinaemia and jaundice
- Bilirubin level <3 mg/dl
- Mild icterus of sclera of eye
- Patient usually complaints of fatigue, weakness, and abdominal pain
- Symptomatic management
18. e. Dubin johnson syndrome
- Autosomal recessive
- Mutations in the gene encoding MRP-2
- Conjugated hyperbilirubinaemia
f. Rotor syndrome
- Autosomal recessive
- Mutations in the gene encoding MOAT
- Conjugated hyperbilirubinaemia
19. Jaundice
- Yellowish discolouration of scle, skin and mucosa due to increased
deposition of bilirubin
- Clinical jaundice – bilirubin > 2mg/dL
Etiological classification of Jaundice
1. Hemolytic (Prehepatic)
2. Hepatocellular
3. Obstructive (Post hepatic)
20. Causes –
Hemolytic:
• Excessive RBC breakdown
a. Live failure
b. Renal disorder
c. Hypersplenism
d. Burns
e. Infections
f. Hemoglobinopathies
g. Drug induced hemolysis
h. Autoimmune diseases
21. Hepatocellular
• Infective or toxic damage to liver
a. Infective hepatitis
b. Alcoholic hepatitis
c. Cirrhosis of liver
d. Toxic chemicals
Obstructive
• Obstruction to bile overflow
a. Gall stones
b. Cancer of biliary system or pancreas
22. a. Intrahepatic cholestasis:
i. Chronic active hepatitis
ii. Biliary cirrhosis
iii. Lymphomas
iv. Primary hepatoma
v. Obstructive stage of viral hepatitis.
b. Extrahepatic obstruction:
i. Stones in the gallbladder or biliary tract
ii. Carcinoma of head of pancreas
iii. Enlarged lymph glands in the porta hepatis
23. FEATURES HEMOLYTIC
HEPATO
CELLULAR
OBSTRUCTIVE
TOTAL SEUM
BILIRUBIN
RAISED RAISED RAISED
CONJUGATED NORMAL ELEVATED ELEVETED
UNCONJUGATED ELEVETED ELEVETED NORMAL
UROBILINOGEN INCREASED DECREASED ABSENT
URINE NORMAL DEEP YELLOW DEEP YELLOW
STOOL DARK BROWN PALE
CLAY
COLOURED
STERCOLIBINOGEN INCREASED REDUCED ABSENT
Editor's Notes
One gram of Hb yields approx. 35 mg bilirubin
Each molecule of albumin appears to have:
• One “high-affinity” site
• One “low-affinity” site for bilirubin.
designated as ‘Y’ and ‘Z’
isolated from liver cytoplasm and account for most
of
The enzyme catalyses the transfer of Glucuronic acid from UDP-GA to various phenolic, carboxylic and amine receptors. The process is called conjugation reaction and it is carried out in the smooth endoplasmic reticulum of liver cells.
Glucuronic acid is attached through“ester-linkage” to the propionic acid carboxyl group of bilirubin
conjugated bilirubin can pass through glomerular filter and can appear in urine (bilirubinuria).
Unconjugated bilirubin cannot pass through glomerular filter and does not appear in urine.
Maleimide fragments, and Geometric isomers, which are excreted in bile
compensated haemolysis associated with unconjugated hyperbilirubinaemia
Due to a defect in hepatic clearance of bilirubin, possibly due to defect in uptake of bilirubin by liver cells
Due to reduced glucuronyl transferase activity
Due to mutations in the gene encoding bilirubin UGT
Hemolytic disease of newborns
Hemolytic disease of adults - G6PD deficiency