This document provides information about jaundice and hepatitis. It begins with an introduction to jaundice, defining it as a yellowish discoloration of the skin and eyes caused by elevated bilirubin levels. It then discusses the causes, signs, and types of jaundice, including hemolytic, hepatocellular, and obstructive jaundice. The document also covers hepatitis A-E, describing the viruses, transmission, prevention, and treatment of each type. It concludes with a discussion of liver anatomy and function, jaundice diagnosis and management, and nursing care for patients with jaundice or hepatitis.
Definition, Patterns/types and mechanisms of drug induced liver disorders, assessment of drug induced liver disorders and its treatment (pharmacotherapeutics-3)
Definition, Patterns/types and mechanisms of drug induced liver disorders, assessment of drug induced liver disorders and its treatment (pharmacotherapeutics-3)
It include the definition , signs and symptoms, types, diagnosis, medical management, Nursing management, preventive measures, complication, Post exposure prophylaxis of Hepatitis.
Jaundice otherwise called icterus, which may occurs due to high bilirubin level in blood. The slides here explains the epidemiology, metabolism of bilirubin, types of jaundice, their etiology, risk factors involved, symptoms diagnosis and treatment.
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Jaundice – a detailed view by Rxvichu :) :)RxVichuZ
Hello friends...............me ,Vishnu.......back to u all with a MEGA PPT..........................
This PPT, is terminalized by me as "MEGA" , coz It comprises DETAILED VERSIONS OF :
1. ADULT JAUNDICE
2. NEONATAL JAUNDICE
Surely will prove to be a great resource knowledge for anyone who go through this....................but mistakes and errors are humane.............so do share ur feedbacks and reviews..............
Will be back soon with a new ppt....
Keep studying well
#rxvichu-roar4more!!!
:)
It include the definition , signs and symptoms, types, diagnosis, medical management, Nursing management, preventive measures, complication, Post exposure prophylaxis of Hepatitis.
Jaundice otherwise called icterus, which may occurs due to high bilirubin level in blood. The slides here explains the epidemiology, metabolism of bilirubin, types of jaundice, their etiology, risk factors involved, symptoms diagnosis and treatment.
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Jaundice – a detailed view by Rxvichu :) :)RxVichuZ
Hello friends...............me ,Vishnu.......back to u all with a MEGA PPT..........................
This PPT, is terminalized by me as "MEGA" , coz It comprises DETAILED VERSIONS OF :
1. ADULT JAUNDICE
2. NEONATAL JAUNDICE
Surely will prove to be a great resource knowledge for anyone who go through this....................but mistakes and errors are humane.............so do share ur feedbacks and reviews..............
Will be back soon with a new ppt....
Keep studying well
#rxvichu-roar4more!!!
:)
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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
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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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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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
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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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2. INTRODUCTION
The term jaundice is derived from the
French word “jaune” which
means yellow.
Jaundice is not a disease, but rather a
visible sign of an underlying disease
process.
3. Jaundice in adults can be caused by a
variety of medical conditions, some of
which are serious and potentially life-
threatening.
Any adult who develops jaundice needs
to undergo a comprehensive medical
evaluation in order to determine its
cause.
4. DEFINITION
Jaundice is a yellowish discoloration of
the skin, mucous membranes and of
the white of the eyes caused by
elevated levels of the
chemical bilirubin in the blood
(hyperbilirubinemia).
5. EPIDEMIOLOGY
Jaundice typically present as a symptom
of a disease.
About 5% of the U.S population is
thought to have jaundice due to
hereditary causes.
About 10% American population has
jaundice due to cholelithiasis.
6. ANATOMY OF LIVER
The liver is a large,
highly vascular organ
located behind the ribs in
the upper right portion
of the abdominal cavity.
Weight=1200-1500g
8. PHYSIOLOGY OF LIVER
• Cleans the blood
• Regulates hormones
• Helps with blood clotting
• Produces bile
• Produces important enzymes
• Maintains blood sugar levels
9. Haemoglobin Metabolism
Bilirubin is a product of metabolism of
haemoglobin (80%) and other haem
containing proteins (e.g. Myoglobin,
cytochrome P450: 20%)
Degredation of haemoglobin into
bilirubin takes place in macrophages.
Bilirubin is then excreted into plasma
and binds with albumin
10. What is bilirubin?
The breakdown product of Hgb from
injured RBCs and other heme
containing proteins.
Produced by reticuloendothelial system
(macrophage system)
Released to plasma bound to albumin
Hepatocytes conjugate it and extrete
through bile channels into small intest.
12. What causes bilirubin?
Overproduction by reticuloendothelial
system
Failure of hepatocyte uptake
Failure to conjugate or excrete
Obstruction of biliary excretion into
intestine
18. HEMOLYTIC JAUNDICE
Hemolytic jaundice is the result of an
increased destruction of the RBC, the
effect of which is to flood the plasma
with bilirubin so rapidly.
But the liver is functioning normally.
19. HEPATOCELLULAR JAUNDICE
Caused by the inability of damaged liver
cells to clear normal amount of bilirubin
from the blood.
Causes-
Hepatitis
Medications or chemical toxins(carbon
tetrachloride, chloroform, phosphorus)
alcohol
20. OBSTRUCTIVE JAUNDICE
Results from extrahepatic obstruction
may be caused by occlusion of bile duct
from a gallstone, an inflammatory
process, a tumor or pressure from an
enlarge organ
26. Clinical Features
Painless jaundice in older person with
epigastric mass & weight loss = biliary
obstruction from malignancy
Hepatomegaly with pedal edema, JVD,
and gallop = CHF
31. PREVENTION OF
JAUNDICE
Avoid high-risk behaviors such as -
unprotected intercourse
• intravenous drug use
implement universal precautions
when working with blood products and
needles. This can decrease your risk of
developing hepatitis B or hepatitis C.
32. vaccination against hepatitis A and
hepatitis B. There is currently no
available vaccine against hepatitis C.
Avoid potentially contaminated food
products or unsanitary water, as this
may decrease your risk of developing
hepatitis A.
33. When travelling to areas where malaria
is endemic, take the recommended
precautions and prophylactic
medications in order to prevent the
development of malaria.
Avoid alcohol and smoking, as it is a
risk factor for the development of
pancreatic cancer, as well as many
other malignancies.
35. 1. Pain management-
give analgesics
2. Antibiotics
3. IV fluids – to prevent dehydration
4. Blood Transfusion- in case of
anaemia and haemolysis
5. Anti-viral therapy
38. NURSING DIAGNOSIS
Acute pain related to disease condition
Imbalanced Nutrition Less Than Body
Requirements related to nausea and
vomiting
Impaired skin integrity related to
pruritis
39. HEALTH EDUCATION AND
DISCHARGE TEACHING
Encourage for healthy diet.
Advice for consumption of clean food
and water.
Hand hygiene
Safe intercourse
Adhere to medication
42. Etiology
Can have many causes
Drugs (Bromfenac,Troglitazone,Pemoline
etc)
toxins
alcohol
viral infections (A, B, C, D, E)
other infections (parasites, bacteria)
physical damage
43. PATHOPHYSIOLOGY
Due to etiology
Exposure to hepatitis virus
Infection and inflammation
of liver
Hepatocyte damage
Necrosis of the parts of liver,
alteration of liver function
44. Hepatitis Terms
Acute Hepatitis: Short-term
hepatitis.
Body’s immune system clears the virus
from the body within 6 months
Chronic Hepatitis: Long-term
hepatitis.
Infection lasts longer than 6 months
because the body’s immune system cannot
clear the virus from the body
48. Hepatitis A
TRANSMITION -
by consuming food or water
contaminated by feces from a
person infected with hepatitis A.
49. Hepatitis A
Prevention
Shot of immunoglobulin up to 2 weeks
after exposure
Good hand washing
Cook food well
Good diaper hygiene
Only drink clean water
VACCINation-
Children after 12 months
Adults 18 yrs or old (combo of hep A and
hep B, given in 3 shots-0,1,6 months)
50. Hepatitis B
What is it?
Hep B is a serious disease caused by a
Hep B virus that infects the liver
Can cause lifelong infection, cirrhosis
(liver scarring), liver cancer, liver
failure and death
51. Geographic Distribution of Chronic HBV
Infection
HBsAg Prevalence
8% - High
2-7% - Intermediate
<2% - Low
53. MODE OF TRANSMITION
Transmitted through puncture wounds
or contact with infectious body fluids,
such as blood, saliva, or semen.
Injection drug use
having sex with an infected partner
sharing razors of infected person
58. Hepatitis C
Shared injection equipment
Blood transfusion
Blood transfer ( tattoo, piercing)
Sex
Mother to child (<5%)
• How it is transmitted ?
60. Hepatitis C
PREVENTION-
Do not share injection equipment(it’s a
universal precaution).
Do not donate blood or plasma, organs or
sperm
Do not share toothbrushes, razors
Cover areas of open skin
Use of safer sex techniques
61. Hepatitis D
This is also called delta hepatitis.
Hepatitis D is a serious liver disease
caused by the hepatitis D virus (HDV).
62. MODE OF TRANSMITION
Transmitted through puncture wounds
or contact with infected blood.
Hepatitis D is a rare form of hepatitis
that occurs in conjunction with hepatitis
B infection
63. Hepatitis E
Hepatitis E is a waterborne disease
caused by the hepatitis E virus (HEV).
Hepatitis E is mainly found in areas with
poor sanitation and is typically caused
by ingesting contaminated food and
water.
64. COMMON SIGNS AND
SYMPTOMS
fatigue
flu-like symptoms
dark urine
pale stool
abdominal pain
loss of appetite
unexplained weight loss
yellow skin and eyes, which may be
signs of jaundice
65. Signs and Symptoms of
Hepatitis
There are three phases of Hepatitis –
Preicteric
Icteric
Posticteric.
66. Preicteric phase
nausea / vomiting
decreased appetite / weight loss
Fever
Fatigue
headache and joint pain
rt upper quadrant abdominal pain
enlarged spleen/liver/lymph nodes
rash and itching of the skin (urticaria).
67. Icteric phase
These symptoms include the symptoms
of preicteric phase
jaundice (yellowing of the skin)
pruritus (intense / persistent itch)
clay or light-colored stools and dark
urine
70. DIAGNOSTICS TEST
Complete history of patient
Physical examination
Serum bilirubin
Liver function test
Ultrasound
Liver biopsy
Viral Antibody Testing
72. HEPATITIS A
Hepatitis A isn’t usually treated.
Bed rest may be recommended if
symptoms cause a great deal of
discomfort.
For vomiting or diarrhoea give high
fluid and caloric diet to prevent
malnutrition or dehydration.
73. HEPATITIS B
Acute hepatitis B doesn’t require specific
treatment. Chronic hepatitis B is treated
with antiviral medications.
ANTIVIRAL THERAPY-
Lamivudine
adefovir
74. Hepatitis C
Antiviral medications are used to treat
both acute and chronic forms of
hepatitis C
Treatment
Interferon A and Ribavirin (suggest 40%
“cure” rate)
76. Hepatitis E
There are currently no specific medical
therapies to treat hepatitis E
It typically resolves on its own. People
with this type of infection are often
advised to get adequate rest, drink
plenty of fluids, get enough nutrients,
and avoid alcohol.
78. Nursing Diagnosis:
1. Acute Pain related to swelling of
the liver
2. Breathing Pattern related to intra-
abdominal fluid collections ascites
decreased lung expansion and
accumulation of secretions
3. Imbalanced Nutrition Less Than
Body Requirements related to
nausea and vomiting
79. NURSING INTERVENTION
1. Acute pain related to swelling of
the liver
Monitor and record vital signs.
assess the severity,frequency, and
characteristic of pain.
Provide divertional activities such as
reading newspapers.
administer medication as ordered.
80. 2.Imbalanced Nutrition Less Than
Body Requirements related to
nausea and vomiting
Monitor the inclusion of diet / calories.
Give a little meal in the frequency often.
Provide oral care before meals.
Encourage intake of orange juice,
beverage and candy carbonate heavy
throughout the day.
Keep an eye on blood glucose.
81. 3.Impaired skin integrity related to
pruritis
Assess for pruritis.
Nails of the patient should be cut short
to prevent skin injury.
Apply emollient, don’t leave the skin
dry.
Apply antibiotic ointment if any injury is
present
82. HEALTH EDUCATION AND
DISCHARGE TEACHING
Get regular medical care
Get needed rest
No alcohol, no over the counter drug use
Avoid chemical fumes and other
environmental toxins
Get vaccinated.
83.
84. CONCLUSION
HEPATITIS A B C D E
Mode of
transmission
Faeco -
oral
Body fluid Body fluid Body fluid Faeco - oral
Immunization available available Not
available
Not
available
Not
available
Severity More sever
85. CONCLUTION
Liver is chemical factory of human
body.
Hepatitis is a viral infection which
causes inflammation of liver.
Its timely management is important to
prevent complications.
88. 2) All patients with jaundice should be
admitted to the hospital for further workup.
A. True
B. False
Ans- (b)
89. 3) A marker of acute hepatocyte injury
&/or hepatocyte death is:
A. PT
B. ALT
C. Albumin
D. Direct bilirubin
E. Ammonia
Ans- (b)
90. 4) In which of the following phase clay
coloured stool is present?
A) pre-icterus phase
B) icterus phase
C) post-icterus phase
D) all phase
Ans- b)