1. Liver lies in right hypochondrium and divided in to right and left lobes.
2. Microarchitecture : liver is divided into 1 to 2 mm hexagonal lobules.
3. There are four methods for liver biopsy.
4. Most hepatic infections are viral in origin.
5. In fulminant hepatitis hepatic insufficiency progresses from onset of symptoms to hepatic encephalopathy within2 to 3 weeks.
Hepatitis b virus (hbv) infection a silent epidemicAung Zayar Paing
Myanmar is one of the countries with high HBV prevalence. Compared to other diseases like TB, HIV and malaria, HBV received less attention than it should to be educated, tested, vaccinated and treated.
HCV- Hepatitis and Hepatitis C InfectionBishwashPdl
Hepatitis C Virus and Infection. History, Source and Mode of Infection, Types of infection, Factors promoting severity, Laboratory Diagnosis of Hepatitis C, ELISA, References.
Management Of Chronic Hepatitis B
by Dr S Khan
Courtesy Of Javed iqbal Farooqi
http://www.drkhanblogs.com/2015/05/management-of-chronic-hepatitis-b.html
Hepatitis b virus (hbv) infection a silent epidemicAung Zayar Paing
Myanmar is one of the countries with high HBV prevalence. Compared to other diseases like TB, HIV and malaria, HBV received less attention than it should to be educated, tested, vaccinated and treated.
HCV- Hepatitis and Hepatitis C InfectionBishwashPdl
Hepatitis C Virus and Infection. History, Source and Mode of Infection, Types of infection, Factors promoting severity, Laboratory Diagnosis of Hepatitis C, ELISA, References.
Management Of Chronic Hepatitis B
by Dr S Khan
Courtesy Of Javed iqbal Farooqi
http://www.drkhanblogs.com/2015/05/management-of-chronic-hepatitis-b.html
Viral hepatitis is a systemic disease primarily involving the liver.
Hepatotropic viruses : liver is the target organ and the main site of virus replication
Hepatitis A virus (HAV)
hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV, delta virus)
Hepatitis E virus (HEV).
Enterically:
virus is spread from person-to-person by putting something in the mouth that has been contaminated with the stool of a person with hepatitis E. This type of transmission is called "fecal-oral." For this reason, the virus is more easily spread in areas where there are poor sanitary conditions
Viral hepatitis is a systemic disease primarily involving the liver.
Hepatotropic viruses : liver is the target organ and the main site of virus replication
Hepatitis A virus (HAV)
hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV, delta virus)
Hepatitis E virus (HEV).
Enterically:
virus is spread from person-to-person by putting something in the mouth that has been contaminated with the stool of a person with hepatitis E. This type of transmission is called "fecal-oral." For this reason, the virus is more easily spread in areas where there are poor sanitary conditions
A serious liver infection caused by the hepatitis B virus that's easily preventable by a vaccine.
This disease is most commonly spread by exposure to infected bodily fluids.
Symptoms are variable and include yellowing of the eyes, abdominal pain and dark urine. Some people, particularly children, don't experience any symptoms. In chronic cases, liver failure, cancer or scarring can occur.
The condition often clears up on its own. Chronic cases require medication and possibly a liver transplant.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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.
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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.
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
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
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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
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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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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Liver 1
1. Title : Liver
Objectives: to
1. Describe anatomy and microarchitecture of liver.
2. Out line liver biopsy.
3. Study infectious disorders of liver .
4. Explain fulminant hepatitis.
2. Anatomy:
Liver lies in right hypochondrium.
Topographic division of liver into right, left, caudate,
and quadrate lobes.
Physiologicaly or functionaly: divided in to right and
left lobes.
Surgically: divided into eight segments.
3.
4. Adult liver weighs 1400 to 1600 gm,
representing 2.5% of body weight.
Incoming blood arrives portal vein and hepatic artery
through hilum of liver (porta hepatis).
Major bile ducts exit in porta hepatis.
Blood from all sources is collected into hepatic vein
which exits into inferior vena cava.
5. Microarchitecture:
Liver is divided into 1 to 2 mm hexagonal lobules.
In lobule, parenchyma is divided into three zones:
o zone 1 being closest to portal tract (periportal).
o zone 2 being intermediate ( midzone ).
o zone 3 abutting central vein (centrilobular ).
o This zonation is important since many hepatic disorders
exhibit a zonal distribution.
6.
7.
8. Liver Biopsy
There are four methods :
1. blind percutaneous needle biopsy.
2. peritoneoscopy .
3. open surgery .
4. transvenous (transjugular or less often transfemoral).
C T or U/S guided Fine Needle Aspiration (FNA) :
for diagnosing focal hepatic lesions.
9. Infectious Disorders:
Most hepatic infections are viral in origin.
Others include: miliary tuberculosis, malaria,
staph , salmonella , candida, and amebiasis.
VIRAL HEPATITIS : caused by:
(1) infectious mononucleosis (Epstein-Barr virus).
(2) cytomegalovirus: newborn or immunosuppression.
(3) yellow fever: tropical countries.
(4) rubella, adenovirus, herpesvirus, or enterovirus :
children and immunosuppression.
(5) Hepatotropic viruses (most important).
10. Viral hepatitis caused by Hepatotropic viruses
VIRUS TYPE INFECTION ROUTE DISEASE
Hepatitis A (HAV) RNA Fecal–oral Acute
Hepatitis B (HBV) DNA Parenteral Acute, chronic
Hepatitis C (HCV) RNA Parenteral Acute, chronic
Hepatitis D (HDV) RNA
Pathogenic when
combined with HBV
Acute, chronic
Hepatitis E (HEV) RNA Fecal–oral Acute
11. Acute viral Hepatitis
Pathology:
Parenchymal changes:
• Hepatocyte injury: swelling (ballooning degeneration).
• Cholestasis (canalicular bile plugs).
• Hepatocyte necrosis: isolated cells or cell clusters.
• Cytolysis (rupture), or apoptosis (shrinkage) with
acidophil bodies (Councilman bodies) formation.
12. • If severe: bridging necrosis ( portal-portal,
central-central, portal-central ).
• Lobular disarray: loss of normal architecture.
Regenerative changes:
• Hepatocyte proliferation.
Sinusoidal cell reactive changes:
• phagocytosed cellular debris in Kupffer cells.
• Influx of mononuclear cells into sinusoids.
Portal tracts:
• Inflammation: predominantly mononuclear.
• Inflammatory spillover into adjacent parenchyma.
13.
14. Chronic Hepatitis:
Symptomatic, biochemical, or serologic
evidence of continuing or relapsing
hepatic disease for more than 6 months, with
histologically documented inflammation and necrosis.
Hepatitis viruses (HBV, HCV, and HBV+HDV)
are responsible for most cases.
Other causes include :
o chronic alcoholism.
o Wilson disease.
o α1-antitrypsin deficiency.
o drugs ( isoniazid, α-methyldopa, methotrexate ).
o autoimmunity.
15. Chronic viral Hepatitis:
Pathology:
Changes shared with acute hepatitis:
• Hepatocyte injury, necrosis, and regeneration.
• Sinusoidal cell reactive changes.
Portal tracts:
• Inflammation:
Confined to portal tracts.
Spill over into adjacent parenchyma, with necrosis of
hepatocytes (interface hepatitis originally termed
piecemeal necrosis).
Bridging inflammation and necrosis.
16. Fibrosis:
Portal deposition.
Portal and periportal deposition.
Formation of bridging fibrous septa.
HBV :
ground-glass hepatocytes ( accumulations of viral
antigen in endoplasmic reticulum ).
sanded nuclei ( nuclear viral inclusions ).
HCV :
bile duct epithelial cell proliferation.
lymphoid aggregate formation .
Cirrhosis : The end-stage outcome.
18. Lymphoid follicles in portal tract of patient
with chronic hepatitis C.
Sanded nuclei (nuclear inclusions) are
seen in HBV-replicative hepatocytes.
19. Serologic Diagnosis in viral hepatitis
HAV: Incubation period
(2–6 wks).
IgM: appears in blood
at onset of symptoms,
constituting a reliable
Marker of acute infection .
Fecal shedding of virus ends
as IgM titer rises.
IgM begins to decline in few
months and is followed by
appearance of
IgG which persists for years,
perhaps for life, providing
Protective immunity against
Reinfection by all strains of
HAV, Hence HAV vaccine is
effective.
20. HBV: ( incubation period 6 to 8 wks)
HBsAg : appears before onset of
symptoms, peaks during overt
disease, declines in 3 to 6 months.
HBeAg: appear soon after HBsAg, and signify
active viral replication.
IgM anti-HBc : shortly before onset of
symptoms, concurrent with onset of elevation
of serum aminotransferases. Over months,
IgM antibody is replaced by IgG anti-HBc.
Anti-HBe : shortly after disappearance of
HBeAg
IgG anti-HBs : after disappearance of HBsAg.
and may persist for life, conferring protection.
The carrier state is defined by presence of
HBsAg in serum for 6 months or longer after
initial detection.
The persistence of circulating HBsAg, HBeAg ,
usually with anti-HBc and occasionally
anti-HBs indicate progressive liver
damage.
21. HCV : incubation period 6 and 12 wks .
HCV is detectable in blood for 1 to 3
weeks, coincident with elevations in
Serum transaminases (ALT) .
anti-HCV antibodies emerge after 3 to 6
weeks.
In chronic HCV infection, circulating HCV
persists in many patients despite
presence of neutralizing antibodies,
Hence, in patients with symptoms of
chronic hepatitis, HCV testing must be
performed to confirm diagnosis of
HCV infection.
A clinical feature that is quite
characteristic of chronic HCV infection
is episodic elevations in serum
aminotransferases, with intervening
normal or near-normal periods.
22. Fulminant hepatitis and hepatic failure:
Hepatic insufficiency progresses from onset
of symptoms to hepatic encephalopathy within
2 to 3 weeks.
Causes :
o HAV or HBV.
o Drug and chemical toxicity : acetaminophen , isoniazid ,
halothane, and methyldopa.
o Miscellaneous : mycotoxins of mushroom.
o Unknown : 18% of cases
23. Clinical features:
Jaundice , encephalopathy, and fetor hepaticus.
Mortality rate ranges from 25% to 90% in absence
of liver transplantation.
Morphology :
Grossly: necrotic areas have a muddy red appearance .
Microscopically : complete destruction of hepatocytes
in contiguous lobules leaves only a collapsed reticulin
framework and preserved portal tracts.
there may be surprisingly little inflammation.
25. Summary:
1. Liver lies in right hypochondrium and
divided in to right and left lobes.
2. Microarchitecture : liver is divided into
1 to 2 mm hexagonal lobules.
3. There are four methods for liver biopsy.
4. Most hepatic infections are viral in origin.
5. In fulminant hepatitis hepatic insufficiency
progresses from onset of symptoms to hepatic
encephalopathy within2 to 3 weeks.
26. Questions:
1. What are the pathological changes in chronic
viral hepatitis?
2. Draw a table for hepatotropic viruses including their
types, infectious routes, and diseases they cause?
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