Intestinal obstruction occurs when the normal progression of intestinal contents is obstructed. This can be due to mechanical obstruction from lesions inside or outside the bowel wall, or paralytic ileus where intestinal muscle function is impaired. Mechanical obstruction causes distension of the intestine above the obstruction from fluid and gas accumulation. This can lead to electrolyte imbalances and metabolic abnormalities. Strangulated obstruction involves impaired blood flow to the obstructed intestine, which can progress to tissue death if not resolved.
---------- Forwarded message ----------
From: UCD Graduate '09 None <ucdgrad09@gmail.com>
Date: 2009/2/12
Subject: Bambury tutorial Upper GI Surgery
To: ucdgrad09@gmail.com
She does not know that we have this so please don't print it and bring it to
the lecture
---------- Forwarded message ----------
From: UCD Graduate '09 None <ucdgrad09@gmail.com>
Date: 2009/2/12
Subject: Bambury tutorial Upper GI Surgery
To: ucdgrad09@gmail.com
She does not know that we have this so please don't print it and bring it to
the lecture
Strangulated intestinal obstruction is a relatively common type of acute abdomen and requires urgent surgical treatment. The causes of strangulated intestinal obstruction are many including primary volvulus, hernias, adhesions, bands, and intussusceptions.
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Anti ulcer drugs and their Advance pharmacology ||
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.
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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
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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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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2. • When there is pathological interference with the
normal progression of the intestinal luminal
contents distally, the condition is called intestinal
obstruction.
• Such obstruction may be due to mechanical
obstruction of the intestine when it is called
mechanical obstruction.
• It may also occur from paralysis of the intestinal
muscle so that the peristalsis of the intestine is
lost, so is the progression of the intestinal
contents.
• This is paralytic ileus.
3. AETIOLOGY
A. Mechanical Obstruction.— This includes :
1. OBSTRUCTION IN THE LUMEN may be caused by
• (i) Meconium,
• (ii) Bezoars which may be trichobezoar (hair) or
phytobezoar (fruit and vegetable fibres),
• (iii) gallstones,
• (iv) polypoid tumour of the bowel,
• (v) intussusception,
• (vi) impaction of barium or worms.
4.
5.
6.
7.
8.
9.
10.
11. • 2. LESIONS OF THE BOWEL WALL also cause intestinal
obstruction These can be classified into —
(a) Congenital.—This includes
• (i) Atresia and stenosis;
• (ii) Megacolon (Hirschsprung’s disease),
• (iii) Meckel’s diverticulum;
• (iv) Imperforate anus;
• (v) Diverticuli.
(b) Traumatic.
(c) Inflammatory.— (i) Crohn’s disease; (ii) Ulcerative
colitis (rare); (iii) Diverticulitis (rare).
(d) Neoplastic.— Various tumours of the small intestine
and large instestine also cause obstruction.
(e) Miscellaneous.— (i) Radiation therapy; (ii) Iatrogenic
stricture following intestinal anastomosis;
(iii) Potassium induced stricture.
16. • 3. LESIONS EXTRINSIC TO THE BOWEL are important
causes of intestinal obstruction.
• These are :
(a) Adhesive band constriction or angulation by
adhesion.— This is a leading cause of small intestinal
obstruction.
This may follow previous surgery or inflammation.
Adhesions may produce kinking or angulation of the
intestine or create bands of tissue that compress the
bowel.
(b) External hernia is the second common cause of
mechanical small intestinal obstruction. Inguinal,
femoral, umbilical and incisional hernia are important
causes of bowel obstruction.
17.
18.
19. (c) Volvulus.— This is a separate entity.
(d) Extrinsic masses e.g.
(i) Haematomas and abscess may press on the
bowel and cause obstruction (Neoplasms
outside the bowel can also press on it to cause
obstruction,
(iii) Annular pancreas,
(iv) Abnormal vessels may cause such
obstruction, which of course is extremely rare.
20.
21.
22. • B. Paralytic ileus.—
• The causes of paralytic ileus can be divided into two
categories;
• (a) Abdominal causes
• and
• (b) Systemic causes.
(a) Abdominal causes include
(i) intestinal distension,
(ii) peritonitis and
(iii) retroperitoneal lesions retroperitoneal haemorrhage,
retroperitoneal sarcoma, distension of the ureter etc.
(b) Systemic causes include
(i) electrolyte imbalance particularly hypokalaemia and
(ii) toxaemias.
23. CLASSIFICATION of intestinal obstruction can
also be made as follows :
• 1. Simple mechanical obstruction in which there is
obstruction but blood supply to the intestine
remains intact.
• 2. Strangulated obstruction, in which the
mesenteric vessels are occluded besides the usual
mechanical obstruction. This is a dangerous
condition and should be operated on without
delay.
• 3. Closed loop obstruction when both limbs of the
loop are obstructed so that there is neither
progression nor regurgitation.
24. Intestinal obstruction can be further
classified into:
(i) A cute obstruction
(i) Chronic obstruction
(ii) Acute-on-chronJc obstruction
25. (i) A cute obstruction
• Which is an obstruction to the small bowel
and is characterised by central abdominal
pain, early vomiting, central abdominal
destension constipation.
26. (ii) Chronic obstruction
• When obstruction is confined to the large
bowel and is characterised lower abdominal
colic, absolute constipation and later on
distension
27. (iii )Acute-on-chronJc obstruction
• Which starts in the large bowel but gradually
involves the small intestine.
• Early pain and constipation are the symptoms
to starts with but when the small intestine is
involved it is characterised by vomiting and
general abdominal distension.
28. PATHOLOGY
• BOWEL MOTILITY :-
• When the intestine is obstructed, the part of the
intestine above the obstruction shows vigorous
peristalsis to overcome the obstruction.
• This continues from 2 to 6 days.
• The more distal is the obstruction, the more vigorous is
the peristalsis and longer does it remain.
• If the obstruction is not relieved, increasing distension
of the intestine ensues and a time comes when
peristalsis ceases and the obstructed intestine remains
flaccid and paralysed.
29. PATHOLOGY
• For a few hours the intestine below the
obstruction shows normal peristalsis and
absorption.
• This will empty its contents and later on it
becomes immobile, contracted and pale.
30. PATHOLOGY
• DISTENSION :-
• In case of intestinal obstruction accumulation
of fluid and gas proximal to the obstruction
occurs.
• This produces distension of the intestine
proximal to the obstruction.
• Ingested fluid, digestive secretion and
intestinal gas play the major role to form this
distension.
31. PATHOLOGY
• Fluid and electrolyte imbalance :-
• Large volume of saliva, gastric secretion, bile and
pancreatic juice enter the gut daily.
• These are mainly absorbed in the small intestine.
• Distension increases intestinal secretion and
decreases absorption.
• This phenomenon results in increased fluid
accumulation in the bowel proximal to the
obstruction.
32. PATHOLOGY
• Besides ingestion of fluid, various digestive juices
comprise about 8000 ml/day.
• Saliva 1500 ml, gastric juice 2500 ml, bile and
pancreatic juice 1000 ml. and intestinal juice 3000 ml.
• Accumulation of such huge amount of fluid along with
repeated vomiting causes severe metabolic
disturbances.
• Particularly in proximal obstruction there is relatively
more vomiting and this leads to losses of water,
sodium, chloride, hydrogen and potassium ions
producing dehydration with hypochloraemia,
hypokalaemia and metabolic alkalosis.
33. PATHOLOGY
• Distal small bowel obstruction may cause loss of large
quantities of fluid, but the abnormalities of serum
electrolyte values are less dramatic, probably because
of hydrochloric acid losses are less.
• With dehydration the-e will be oliguria, haemo-
concentration and azotemia(high levels of nitrogen).
• If dehydration continues, there will be reduced cardiac
output, low central venous pressure, hypotension and
hypovolaemic shock.
• Distension of the abdomen will lead to elevation of the
diaphragm to impair proper ventilation.
34. PATHOLOGY
• Intestinal gas:-
• Much of the distension is caused by gas accumulation
in the intestine proximal to the obstruction.
This mainly consists of:
• (i) gas swallowed from the atmospheric air,
• (ii) diffusion from blood into the bowel lumen
(carbondioxide from neutralisation of bicarbonate) and
• (iii) organic gases (hydrogen sulphide, ammonia,
amines and hydrogen) from bacterial fermentation
(10%).
• Swallowed air is the most important source of gas in
causing intestinal distension.
• While the oxygen and carbon dioxide are absorbed,
nitrogen is not absorbed by intestinal mucosa.
35. PATHOLOGY
• BACTERIAL PROLIFERATION:-
• During intestinal obstruction there is rapid
proliferation of intestinal bacteria.
• Normally the small intestine contains very small
quantity of bacteria and may be considered as
almost sterile.
• Normal peristalsis with continued progression of
luminal content minimises small intestinal
bacterial flora.
• But during small intestinal obstruction, whatever
may be the cause, bacteria proliferate rapidly.
36. PATHOLOGY
• That is why, intestinal contents become
faeculent’ during obstruction.
• As the bacteria or bacterial toxins cannot cross
normal intestinal mucosa the bacteria in the
small intestine probably play no role in the ill
effects of simple mechanical small intestinal
obstruction.
37. PATHOLOGY
• Strangulated obstruction:-
• Strangulation develops when the circulation to the
obstructed intestine is impaired.
• This frequently occurs secondary to
• (i) Adhesive band obstruction,
• (ii) Hernia,
• (iii) Volvulus or
• (iv) Intussusception.
• If the obstructed distending bowel is held by unyielding
adhesive bands or hernial rings strangulation may occur.
• Similarly in volvulus or intussusception, the mesenteric
vessels are occluded by twisting of the mesentery.
• In strangulated obstruction the patient suffers from all the
ill effects of simple obstruction plus to the effects of
strangulation.
38. PATHOLOGY
• Distension:-
• Distension in case of strangulated obstruction is different from
simple obstruction.
• Unlike on-strangulated obstruction, early distension of the proximal
intestine is absent.
• In fact for a few minutes several hours the proximal intestine
contracts.
• After this, vigorous peristalsis occurs in the proximal segment
without any distension.
• When gangrene is imminent, retrograde thrombosis of the related
tributaries of the mesenteric vein will cause distension of both the
proximal and distal segments of the strangulated intestine.
• For a considerable time the strangulated segment alone distends.
• The greatest distension occurs when the venous return is
completely impaired and the arterial supply continues
uninterrupted.
39. PATHOLOGY
• The onset of gangrene:-
• Gangrene does not occur till the venous return
is completely occluded.
• At this time the colour of the intestine
changes from purple to black.
• Gradually the arterial supply is also impeded.
• Now the serous coat loses its glistening
appearance, the mucous membrane becomes
ulcerated and thus wet gangrene develops.
40. PATHOLOGY
• Loss of blood volume:-
• In addition to the accumulation of fluid and gas in the
obstructed loops, blockage of venous outflow from the
strangulated segment will cause extravasation of
bloody fluid into the bowel.
• So strangulation causes loss of blood and plasma.
• This loss of blood and plasma will cause shock
particularly the patient is already dehydrated.
• The amount of loss of blood volume will depend upon
the length of the strangulated segment.
• If strangulation produces gangrene, peritonitis with its
sequelae will occur.
• Rupture perforation of strangulated segment is
possible.
41. PATHOLOGY
• Transmigration of bacteria and toxin:-
• In addition to the loss of blood volume, another important
factor in strangulated obstruction is production of toxic
material in the strangulated bowel.
• As mentioned above, the bacteria proliferate and produce
toxic material within the strangulated segment.
• When the intestine mucous membrane is normal this toxic
material is not absorbed, but when the wall of the intestine
becomes partly devitalised, both bacterial toxin and the
products of tissue autolysis pass through the wall of
intestine into the peritoneal cavity, whence these are
absorbed into the circulation.
• So if the strangulation is external, it is far less dangerous
than intra peritoneal strangulation
42. PATHOLOGY
• Closed-loop obstruction:-
• When both afferent and efferent limbs of a loop of
bowel are obstructed, it is called closed-loop
obstruction.
• It is dangerous as this type of obstruction very rapidly
becomes strangulated even before the usual
manifestations of intestinal obstruction.
• Obstruction to blood supply occurs either from the
same mechanism which produces such obstruction or
by the twist of the bowel on the mesentery.
• Development of distension and onset of gangrene are
almost same as strangulated obstruction described
above
44. PATHOLOGY
• Colon obstruction:-
• In general, effects of colon obstruction is usually
much less dramatic than the effects of small bowel
obstruction.
• If the ileocaecal valve is competent colon obstruction
will lead to closed-loop obstruction.
• In this case pressure within the caecum becomes quite
high to compress blood vessels within its wall.
• Stercoral ulcers develop, followed by even perforation.
• If the ileocaecal valve is incompetent, signs of small
bowel distension may accompany colon obstruction.
45. PATHOLOGY
• Otherwise colon obstruction is less dangerous
as it produces less fluid and electrolyte
imbalance than small bowel obstruction.
• Further colon obstruction usually does not
strangulate except cases of volvulus.
46. CLINICAL FEATURES
The important symptoms of simple mechanical
intestinal obstruction are:
• (i) Abdominal pain,
• (ii) Vomiting,
• (iii) Failure to pass gas (flatus) or faeces per
rectum and
• (iv) abdominal distension.
47. (i) Abdominal Pain
• This is the first symptom and usually starts
suddenly.
• The pain is typically cramp like.
• This cramping pain is felt synchronously with
hyperperistalsis.
• The pain is represented by severe cramps with
intervals of 4 to 5 minutes in proximal intestinal
obstruction and with more intervals (15 to 20
minutes) in distal obstruction.
• In between attacks the patient is often free from
pain.
48. (i) Abdominal Pain
• The pain is diffuse, poorly localised and is felt
across the upper abdomen in high obstruction, at
the level of the umbilicus in low ileal obstruction,
in the lower abdomen in colon obstruction and in
the perineum in case of rectosigmoid
obstruction.
• When obstruction is not relieved the
characteristic abdominal colicky pain may stop by
itself and will be replaced steady generalised
abdominal discomfort.
49. (i) Abdominal Pain
• It must be remembered that continuous severe
pain without any quiescent period is usually
indicative of strangulation.
• In paralytic ileus there is no typical colicky pain
of mechanical obstruction, but there may be
steady generalised abdominal discomfort.
50. (ii) Vomiting
• There may be early vomiting which is ‘reflex’ and is
followed by a quiescent period of variable length
before ‘actual’ vomiting starts.
• This interval depends on the site of obstruction and is
short in high obstruction and long (every day or two) in
low small bowel obstruction.
• With high obstruction vomiting is more frequent and
copious and may cause some relief by decompressing
the obstructed bowel.
• With low small bowel obstruction vomiting is less
frequent and does not cause any relief.
• In this case vomiting may be ‘faeculent’ because of
large bacterial population of distal small bowel.
51. (ii) Vomiting
• In acute small intestinal obstruction, the
character of the vomitus alters.
• Initially it contains partly digested food next it
becomes yellow or green from regurgitation of
bowel and finally it becomes faeculent.
• In colon obstruction reflex vomiting is absent and
vomiting does not occur until due to incompetent
valve the small bowel is retro gradely involved.
• When the ileocaecal valve is competent vomiting
is absent in colon obstruction
52. (iii) Constipation
• Failure to pass gas (flatus) or faeces through
the rectum is an important symptom of
intestinal obstruction.
• But it must be remembered that it becomes
evident only after the bowel distal to the
obstruction has been evacuated.
• So there may be one or two natural actions of
bowel after the onset of attack before
constipation develops.
53. (iii) Constipation
• It should be remembered that in a few
conditions of intestinal obstruction there may
not be constipation e.g. Richter’s hemia,
mesenteric vascular occlusion and intestinal
obstruction with pelvic abscess.
54. (iv) Distension
• In early case of small intestinal obstruction there may
not be any abdominal distension.
• Distension is much less in high small bowel
obstruction.
• In low small bowel obstruction centrally placed
distension becomes evident but late.
• Visible peristalsis may be present, if the abdomen is
inspected very carefully.
• This is evident in the proximal loops.
• Borborygmi may be quite loud and may not require a
stethoscope to hear it.
• In auscultation, sound of hyperperistalsis coinciding
with attack of colic is definite evidence of intestinal
obstruction.
55. PHYSICAL EXAMINATION
Tachycardia and hypotension indicate severe
dehydration and/or peritonitis.
The degree of dehydration is estimated by
examination of the skin turgor and moisture of
the mucous membrane.
Fever suggests strangulation.
In strangulated obstruction patient appears very
ill during this early period.
56. INSPECTION
• In early stage visible peristalsis may be the
only sign present particularly in these
individuals with long standing obstruction.
• One must look for surgical scars, indicative of
previous surgery (which indicates adhesion or
cancer).
57. INSPECTION
• Abdominal distension is a late sign of
intestinal obstruction.
• But one must exclude distension due to
ascites.
• In the latter case there will be fluid thrill,
shifting dullness and fullness in the flanks.
• All hernial orifices must be inspected.
• This will diagnose many obscure hernias (even
strangulated) to be the cause of intestinal
obstruction.
58. PALPATION
• During colic there may be muscle guarding.
• Slight tenderness may be present between attacks of
pain.
• Tenderness and rigidity at the site of obstruction
usually indicate strangulation.
• Rebound tenderness suggests peritonitis and likelihood
of strangulation.
• Abdomen should be thoroughly palpated to exclude
presence of mass (lump) which may be present in
intussusception, neoplasms and abscesses.
• Again all the hernial orifices should be palpated to
exclude presence of hernia (impulse on coughing
should be tried)
60. AUSCULTATION
• It is of great value.
• In simple mechanical obstruction — during
attacks of colic the bowel sounds become
loud, high-pitched and metallic.
• In paralytic ileus occasional isolated bowel
sound may be heard.
• In presence of strangulation, bowel sound is
completely absent at that region.
61. RECTAL EXAMINATION
• Rectal Examination should be performed in all cases of
intestinal obstruction.
• Presence of mass on rectal examination within or
outside the lumen will give a clue to the diagnosis.
• Most of rectal cancers are within the reach of the rectal
examination finger.
• It should be noted presence or absence of faeces in the
rectum.
• Absence of faeces means the obstruction is higher up.
• If present, it should be studied for presence of occult
blood, which indicates mucosal lesion e.g. cancer,
intussusception or infarction.
63. SPECIAL INVESTIGATIONS
• 1. BLOOD EXAMINATION
• 2. RADIOLOGICAL EXAMINATIONS
• BARIUM ENEMA
• Intravenous urography may be indicated to
exclude presence of ureteric calculi (which
has not been visualised straight X-ray), which
may cause marked paralytic ileus.
64. MANAGEMENT
• Principle of treatment of intestinal
obstruction includes :
• (a) fluid and electrolyte therapy,
• (b) decompression of the bowel and
• (c) timed surgical intervention to relieve the
obstruction.