Jaundice, or icterus, is a yellowish discoloration of the skin and eyes caused by high bilirubin levels. Bilirubin is produced from the breakdown of red blood cells and normally processed by the liver. Jaundice can be a sign of liver disease or hemolytic disease if bilirubin production exceeds the liver's ability to process it. The causes of jaundice include increased red blood cell breakdown, liver dysfunction that prevents bilirubin removal, and bile duct obstruction limiting bilirubin excretion. Physiological jaundice in newborns is also common as their liver matures after birth. Treatment depends on the underlying cause but may involve phototherapy to
Disorders of liver and kidney, Nitrogen metabolism.pdfshinycthomas
Disorders of liver and kidney – Jaundice, fatty liver, normal and abnormal functions of liver and kidney. Inulin and urea clearance.
Abnormalities of nitrogen metabolism
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.
Disorders of liver and kidney, Nitrogen metabolism.pdfshinycthomas
Disorders of liver and kidney – Jaundice, fatty liver, normal and abnormal functions of liver and kidney. Inulin and urea clearance.
Abnormalities of nitrogen metabolism
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.
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
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ASA GUIDELINE
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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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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
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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
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This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
2. What is Jaundice?
• Jaundice (french: Jaune-Yellow) or
icterus Is a yellowish discolouration of
tissue resulting from the deposition of
bilirubin .
• Equilibrium between bilirubin production &
clearance is disturbed .
• Serum bilirubin level greater than 2mg/dL
• Jaundice is NOT a disease, but rather a sign
of either liver disease or a hemolytic
disease.
3. Slight increase in serum
bilirubin are best detected
by examining the Sclera as
sclera is rich in elastin and
the bilirubin has high
affinity for the elastin .
How it is detected?
4. 1.Light-colored stools
2.Dark-colored urine
3.Itching of the skin.
4.Nausea and vomiting
5.Abdominal pain
6.Fever
7.Weakness
8.Loss of appetite
9.Headache
10.Confusion
11.Swelling of the legs and abdomen.
Signs and Symptoms of Jaundice
5. What is bilirubin?
•Bilirubin is a yellowish pigment found
in bile
•The breakdown product of Hb from
injured RBCs & other heme containing
proteins.
•Macrophages release the bilirubin into
circulation as free or unconjugated
bilirubin.
•Hepatocytes conjugate it and extrete
through bile channels into small
intestine.
8. What causes bilirubin?
1. Overproduction by
reticuloendothelial system
2. Failure of hepatocyte uptake
3. Failure to conjugate or excrete
4. Obstruction of biliary excretion into
intestine
9. Pathophysiology of Jaundice
• Both unconjugated (Indirect, free) bilirubin and
conjugated bilirubin (Direct, bilirubin glucuronides, combine with glucoronic acid)
may accumulate systemically.
• There are two important pathophysiologic
differences between the two forms of bilirubin:
1. Solubility in water &
2. Binding with Albumin
10. Unconjugated/Indirect/Free bilirubin
insoluble in water at physiologic pH and exists in
tight complexes with serum albumin. This form
cannot be excreted in the urine even when blood
levels are high.
.
Conjugated Bilirubin (Direct Bilirubin)
• Water-soluble, nontoxic, & only loosely bound to
albumin. Because of its solubility and weak
association with albumin, excess conjugated
bilirubin in plasma can be excreted in urine.
11.
12. Causes of Jaundice
Jaundice occurs when there is:
1. Increased destruction of RBCs,
with rapid release of bilirubin
into the blood.
2. A defect in the liver that
prevents bilirubin from being
removed from the blood, can
be caused due to a variety of
reasons.
3- Blockage of the bile ducts that
decreases the flow of bile and
bilirubin from the liver into the
intestines.
16. Mechanism
of Production
Excessive
breakdown of RBCs
producing
unconjugated
bilirubin in the
amounts more than
the healthy liver can
conjugate and
excrete.
Inability of liver to
conjugate &
transport bilirubin
into the bile due to
liver cell damage .
Obstruction of the bile
ducts so conjugated
bilirubin can’t flow
through the biliary
tract freely resulting in
increased serum
conjugated bilirubin.
Type of
serum
bilirubin
accumulated
Unconjugated
Both
unconjugated
& conjugated
bilirubin
Conjugated
HemolyticJaundice
(Prehepatic)
Hepatic
Jaundice
Obstructive
Jaundice
(Post hepatic)
17. Urine
urobilinogen Increases Decrease
s
Markedly
decreased/absent
(due to obstruction,
conjugated bilirubin is
not released into the
intestine thus no
urobilinogen is formed.
Hemolytic Jaundice
(Prehepatic)
Hepatic Jaundice Obstructive
Jaundice
(Post hepatic)
Urine
Bilirubin
Absent
(Acholuric Jaundice.)
Present
(choluric
jaundice)
Present
(Since conjugated
bilirubin is
filtered in urine)
18. Hemolytic
Jaundice
(Pre hepatic)
Hepatic
Jaundice
Obstructive
Jaundice
(Post hepatic)
Faecal
Fat level
normal
(as bile is present
in gut for normal
digestion of fat )
Increased
because of deficiency of bile
in the intestine, emulsi
fication and absorption of fat
is inadequate. This produces
bulky, pale, greasy and foul
smelling faeces called
steatorrhoea
Increased
Faecal
Stercobilinogen
markedly
Increased
stool dark brown
colour
Reduced
stools are pale in colour
Absent
stools:clay
coloured.
19. Physiological jaundice of new
born
A hyperbilirubinaemia producing jaundice
may be seen normally in the newborn.
Appears 2-5 days after birth &
disappears in 2 weeks
20. Mechanism of production of Physiological Jaundice
1.Excessive destruction of RBC occurs in first few days after
birth causing increase in serum bilirubin.
2.Hepatic immaturity in first few (7-10 ) days after birth also
contributes to increased serum bilirubin .
In the fetus bilirubin produced is cleared by the placenta
and eliminated by the maternal liver.
Immediately after birth, the neonatal liver as to take up this
work which takes 7–10 days to get mature for bilirubin clearance
and excretion.
21. TREATMENT.
PHOTOTHERAPY
Exposure of skin to
white light –
PHOTO-
ISOMERIZATION
of Bilirubin to water
soluble Lumirubin
which is excreted in
Bile without
conjugation
Editor's Notes
skin, sclera and mucous membranes
RESULTING from an increased bilirubin concentration or Hyperbilirubinemia
greenish-yellow pigment bilirubin, which is a major end product of hemoglobin degradation
Bilirubin exceedingly valuable tool for diagnosing both hemolytic blood diseases and various types of liver diseases
Macrophages releases unconjugated bil into circulation
the bilirubin is excreted from the hepatocytes by an active transport process into the bile canaliculi and then into the intestines.
Once in the intestine, about half of the “conjugated” bilirubin is converted by bacterial action into the substance urobilinogen, . Some of the urobilinogen is reabsorbed through the intestinal mucosa back into the blood, and most is re-excreted by the liver back into the gut, but about 5 percent is excreted by the kidneys into the urine
After exposure to air in the urine, the urobilinogen becomes oxidized to urobilin; alternatively, in the feces, it becomes altered and oxidized to form stercobilin
insoluble in water (due to intramolecular hydrogen bonding)
Deposition of excess bilirubin to brain mainly Basal Ganglia – Kernicterus.
hemolytic disease of the newborn (erythroblastosis fetalis) may lead to accumulation of unconjugated bilirubin in the brain, which can cause severe neurologic damage, referred to as kernicterus.
1. (for example, patients with hemolytic anemia have an abnormally rapid rate of destruction of their red blood cells that releases large amounts of bilirubin into the blood)
2.If the parenchymal cells of the liver are affected due to damages that arise as a result of infections or other conditions it can have a significant impact causing the reduction in the metabolism of the liver.
increased bilirubin concentration (hyperbilirubinaemia) in the body fluids
Affects rbc in which caused due to mutation of 5 genes , rbc will be sphere shaped rather biconcave
Hepatitis inflammation of liver caused by hepatitis virus
Cirrhosis: chronic liver damage from variety of causes
Childhood disease of liver in which one or more bile ducts are abnormally narrow, blocked or absent
1. unconjugated bilirubin is insoluble in water. It is transported in plasma in bound form with albumin. Since albumin is not filtered into urine, unconjugated bilirubin too is not filtered in urine. Because of this haemolytic jaundice is also called acholuric jaundice—no bile pigment in urine)
2. (Conjugated bilirubin is water soluble and is present in the plasma in dissolved form. It gets easily filtered in urine. Such a jaundice is also called choluric jaundice,)
3.liver is excreting lot of conjugated bilirubin in the intestine with the bile. So, more urobilinogen is formed. Part of it reabsorbed and goes to general circulation and thus urine urobilinogen is increased).
4. Damaged liver cells produce & excrete less of conjugated bilirubin so less urobilinogen is formed.)
Markedly increased (Because of more formation as described above).
Physiological jaundice of newborn is also called neonatal jaundice.
