Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
An intestinal obstruction occurs when your small or large intestine is blocked. The blockage can be partial or total, and it prevents passage of fluids and digested food. If intestinal obstruction happens, food, fluids, gastric acids, and gas build up behind the site of the blockage.
Bowel obstruction, also known as intestinal obstruction, is a mechanical or functional obstruction of the intestines which prevents the normal movement of the products of digestion. Either the small bowel or large bowel may be affected. Signs and symptoms include abdominal pain, vomiting, bloating and not passing gas.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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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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.
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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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.
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
3. CLASSIFICATION
There are different types of classification of
intestinal obstruction.
According to the pathological nature.
According to the level of the obstruction.
According to the onset and the course of
the obstruction.
4. According to the pathological nature.
1. Mechanical obstruction: is
caused by an organic block.
2. Paralytic ileus (Adynamic): is
due to loss of propulsive peristalsis
leading to functional obstruction.
5. According to the level of the obstruction.
1. High small bowel obstruction.
2. Low small bowel obstruction.
3. Large bowel obstruction.
6. ACCORDING TO THE ONSET
1. Acute .
2. Chronic: e.g., colon cancer, the symptoms are
insidious and slowly progressive. The patient has
constipation and distension.
3. Acute on chronic: A chronic obstruction may
develop acute symptoms as the obstruction suddenly
becomes complete when a narrowed lumen becomes
totally occluded.
8. AETIOLOGY
1. In the lumen, e.g., faecal impaction, gallstone and
parasitic infestation.
2. In the wall, e.g., congenital atresia, tumours, Crohn's
disease, chronic diverticulitis and mesenteric vascular
occlusion.
3. Outside the wall, e.g., adhesions (commonly post-
operative), strangulated hernia, and volvulus.
9. PATHOLOGY
Distal to the obstruction the intestine empties and becomes
collapsed.
Proximally the intestine becomes distended by gas and fluids.
Gaseous distension is due to swallowed air, diffusion from
congested vessels and bacterial fermentation.
GI secretions (8 litres per day) accumulate above the site of
obstruction.
As intraluminal pressure rises, absorption ceases.
10. The stretched smooth muscles undergo hyperperistalsis
in an attempt to overcome the obstruction.
Distension impairs blood supply, and may end in
ulceration and perforation.
This is evident in cases of colon obstruction with a
competent ileocaecal valve (closed loop obstruction).
The rising pressure in the closed proximal colon causes
perforation of the caecum.
11. SYMPTOMS
1. Pain is usually the first symptom. It is colicky and is caused by the
hyperperistalsis.
2. Distension: is marked in large bowel obstruction (mainly in the
flanks). It is less marked and is central in small bowel obstruction.
3. Constipation: is an early symptom in large bowel obstruction but
late in small bowel obstruction.
4. Vomiting occurs early in small bowel obstruction but it is late or
even absent when the large bowel is obstructed.
12. SIGNS
On General examination: Evidence of dehydration as tachycardia,
oliguria, dry tongue, or even hypotension may be present.
On Abdominal inspection: Distension, visible peristalsis.
Scars of previous abdominal surgery may denote intraabdominal adhesions.
On Abdominal palpation: A mass may be felt (tumour or intussusception).
On Auscultation: Accentuated intestinal sounds.
Rectal examination reveals an empty rectum, or the finding of a hard
faecal mass, especially in elderly bed-ridden patient causing faecal
impaction.
13. Strangulation is suspected with:
Fever.
Evidence of blood loss as pallor, tachycardia,
and hypotension.
Pain that is not relieved by naso-gastric suction.
Marked tenderness, rebound tenderness, and
rigidity.
14. INVESTIGATIONS
Aimed to :-
Confirm the diagnosis
Define its level.
Define the aetiology.
Estimate the severity of water and electrolyte
imbalance.
15. Plain abdominal X-Ray: Multiple gas-fluid levels on an erect film
confirm the case as intestinal obstruction.
On a supine film the level of obstruction is known by the gas pattern of
the distended proximal intestine.
Distended jejunal loops show the characteristic circular mucosal folds
crossing from one side of the lumen to the other.
Distended ileal loops appear as featureless tubes with no mucosal
pattern.
A colon full of gas shows haustrations that do not appear to reach
the other side of the lumen.
16.
17.
18.
19. CBC
Blood urea and electrolytes.
Ultrasound examination can reveal distended
bowel loops. A mass of intussusception can also
be demonstrated.
CT scan with contrast has a sensitivity of 80-90%
for the diagnosis of bowel obstruction.
21. PREOPERATIVE PREPERATION
Intravenous replacement of fluid and electrolytes
together with blood and plasma if the patient is
shocked. Ringer's lactate solution is needed.
Gastric aspiration by a nasogastric tube to decompress
the bowel and to reduce the risk of aspiration during
induction of anaesthesia.
Antibiotics are given if there is a possibility of
strangulation.
A Foley catheter is inserted to check the urine output.
22. THE OPERATION
A longitudinal exploratory incision. In the the case of strangulated
hernia the incision is placed directly over it.
Look at the caecum.
If it is collapsed, this denotes small gut obstruction. If it is distended,
this means large bowel obstruction.
Determine the level of obstruction which is the junction of dilated
and collapsed bowe loops.
Relief of obstruction is attained by division of adhesive bands,
reduction and repair ofa hernia, or untwisting of volvulus.
Assess bowel viability.
23. Non-viable bowel is known by
Loss of peristalsis,
Loss of normal lustre.
Colour change to greenish or black bowel.
Loss of pulsations in the mesentery.
Resect the Non-viable intestine.
Anastomosis.
24. CONSERVATIVE
may be successful in certains situations provided thatthere is no clinical
evidence of ischaemia.
Adhesive intestinal obstruction may be relieved by IV drip and nasogastric
suction.
lleocaecal intussusception may be reduced by the hydrostatic effect of a
barium enema.
Sigmoid volvulus. Untwisting may be attempted using a rectal tube passed
through a sigmoidoscope.
Faecal impaction is treated by enema to dissolve the obstructing hard
faecal mass.
* Failure of conservative treatment and the suspicion of strangulation are
indications for surgery.
25. PARALYTIC ILEUS
is a form of adynamic obstruction in
which there is failure of the peristaltic
waves of the intestine due to failure of the
neuromuscular mechanism.
Paralytic ileus is most common after major
abdominal surgery.
26. AETIOLOGY
Reflex inhibition of intestinal motility following abdominal
operations retroperitoneal haemorrhage.
Metabolic abnormalities as hypokalaemia, uraemia,
and diabetic ketoacidosis.
Peritonitis induces paralytic ileus due the direct toxic
effect on the nerve plexuses of the intestine.
Drugs as anticholenergics, and tricyclic antidepressants
may produce paralytic ileus if taken in large doses.
27. CLINICAL FEATURES
Symptoms: Abdominal distension, absolute
constipation, and projectile vomiting . no colicky
abdominal pain but there is only a sense of fullness and
discomfort.
Signs: Abdominal distension and inaudible intestinal
sounds (silent abdomen) .
There may be evidence of localized or generalized
peritonitis.
28. PREVENTION
Prevention and correction of electrolyte
disturbances guided by serum level estimation.
Gentle handling of the intestine during surgery.
For major abdominal surgery, a naso-gastric
tube is used to decompress the bowel
postoperatively.
29. MANAGEMENT
Intravenous replacement of the lost fluids and
electrolytes.
Naso-gastric suction.
Correct underlying metabolic abnormalities
Occasionally in resistant cases a
parasympathomimetic, e.g., prostgimine, may
be useful.