1 TRUDY BAXTOR GIT#1 TRUDY BAXTOR GIT #1 1 Describe the nine regions and four quadrants of the abdominopelvic cav ity and lis t the organs they contain . 2 Describe the macroscopic anatomy of the pharynx and oesophagus. 3 Review the microscopic organization of GIT (from Year 1) and describe the histological structure of oesophagus in relation to its function. 4 Describe the mechanisms of swallowi ng, reflux and vomiting. 5 Describe the basic macroscopic anatomy of the stomach. Include blood suppl y, innervation and important immediate relations. 6 Describe the mechanism of pain from gastric pathology (including referred pain). 7 Describe briefly the development of the GIT and explain common developmental anomalies of the GIT. Include the development and organization of the peritoneal reflections and compartments of the abdominal cavity. 8 Describe the components of gastri c juice, the cell types responsible for secreting its components and indicate the i mp ortance of each component in stomach activity. 9 Describe the mechanisms of pr oduction of gastr ic acid by oxyntic cells in the gastric mucosa, in cluding the maj or ionic mecha nisms (especially the K+/H+ ATPase) 10 Describe the neur al and hormonal regulation of gastric acid secretion. 11 Describe the mechanisms of gastrointestinal motility. 12 Describe the neur al and hormonal regulation of gastri c emptying. 13 Describe the the maj or mechanisms that protect the stomach from self digestion and the leakage of gastric juice i nto the peritoneum. 14 Describe the role of Helicobacter pylori (H. pylori ), non -steroidal anti inflammatory drugs , and smoking in the formation of ul cers. 15 Describe the utility and limitations of imagi ng techniques, H. pylori tests, endoscopy and biopsy in the diagnosi s of oesophageal disease, peptic ulcer disease (PUD) and malignancy. 16 Outline the pr inciples of management of ulcers i ncluding antacids, H2 antagonists, acid pump inhibitors, H. pylori eradicatio n and surgical approaches (the last in only the most intractable cases). 17 Describe the pathology of diseas es of the oesophagus, i ncluding achalasia, varices, oesophagitis and tumours; and pathology o f diseases of the stomach, including gastritis, ulcer and gastric tumours. 18 Outline the indications for use and mechanism of action of antifungal dr ugs. 19 Review the concept of negligence and consider how it applies to thi s case in ter ms of: ythe conditions that create a "duty of care" ytypes of medical mistakes which may lead to an action in negligence yhow the Bolam Principle can be applied in a potential negligence case yprovisions in the Civil Liabil ity Act (Qld) 2003 that apply to cases of negligence ythe various elements of negligence that need to be satisfied for a successf ul action. 20 Demonstrate competence in exploring a patient's experience of i mportant gastrointesti nal presentations (abdominal pain, chang ed appetite, unintentional weight change, nausea, vomiting, heartburn, reflux, dyspepsia, dysphagia, odynophagia, ha ematemesis, melaena or rectal bleedi ng) [REVISION] including: the cardi nal characteristics of the symptom and its time course; relevant a ssociated symptoms; the patient's understanding of, and concerns about, what they are experiencing. 21 Demonstrate appropriate infection control manoeuvres prior to and after physical examination of a patient [REVISION]. 22 Prepare a patient appropriately for examination of the abdomen, in relation to appropr iate explanation, confir mation of conse nt and patient positioning. 23 Describe the anatomy of the abdomen and pelvis relevant to the performance o f abdominal examination. 24 Demonstrate competence in the physical examination of a patient for the assessment of pr esentations where abdominal si gns may occur, including inspection, palpation, percussion and auscultation of the abdomen, as well as the identification of organomegaly or abnormal masses, elicitation of tenderness and signs of peritonism, then discuss the significance of any abnormal findings.
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1 Describe the nine regions and four quadrants of the abdominopelvic cavity and list the organs they contain.
2 Describe the macroscopic anatomy of the pharynx and oesophagus.
3 Review the microscopic organization of GIT (from Year 1) and describe the histological structure of oesophagus in relation to its
function.
4 Describe the mechanisms of swallowing, reflux and vomiting.
5 Describe the basic macroscopic anatomy of the stomach. Include blood supply, innervation and important immediate relations.
6 Describe the mechanism of pain from gastric pathology (including referred pain).
7 Describe briefly the development of the GIT and explain common developmental anomalies of the GIT. Include the development andorganization of the peritoneal reflections and compartments of the abdominal cavity.
8 Describe the components of gastric juice, the cell types responsible for secreting its components and indicate the imp ortance of each
component in stomach activity.
9 Describe the mechanisms of production of gastric acid by oxyntic cells in the gastric mucosa, including the major ionic mecha nisms
(especially the K+/H+ ATPase)
10 Describe the neural and hormonal regulation of gastric acid secretion.
11 Describe the mechanisms of gastrointestinal motility.
12 Describe the neural and hormonal regulation of gastric emptying.
13 Describe the the major mechanisms that protect the stomach from self digestion and the leakage of gastric juice into the peritoneum.
14 Describe the role of Helicobacter pylori (H. pylori), non -steroidal anti inflammatory drugs, and smoking in the formation of ulcers.
15 Describe the utility and limitations of imaging techniques, H. pylori tests, endoscopy and biopsy in the diagnosis of oesophageal disease,
peptic ulcer disease (PUD) and malignancy.
16 Outline the principles of management of ulcers including antacids, H2 antagonists, acid pump inhibitors, H. pylori eradicatio n and
surgical approaches (the last in only the most intractable cases).
17 Describe the pathology of diseases of the oesophagus, including achalasia, varices, oesophagitis and tumours; and pathology o f diseases
of the stomach, including gastritis, ulcer and gastric tumours.
18 Outline the indications for use and mechanism of action of antifungal drugs.
19 Review the concept of negligence and consider how it applies to this case in terms of:
y the conditions that create a "duty of care"
y types of medical mistakes which may lead to an action in negligence
y how the Bolam Principle can be applied in a potential negligence case
y provisions in the Civil Liability Act (Qld) 2003 that apply to cases of negligence
y the various elements of negligence that need to be satisfied for a successf ul action.
20 Demonstrate competence in exploring a patient's experience of important gastrointestinal presentations (abdominal pain, chang ed
melaena or rectal bleeding) [REVISION] including: the cardinal characteristics of the symptom and its time course; relevant a ssociated
symptoms; the patient's understanding of, and concerns about, what they are experiencing.
21 Demonstrate appropriate infection control manoeuvres prior to and after physical examination of a patient [REVISION].
22 Prepare a patient appropriately for examination of the abdomen, in relation to appropriate explanation, confirmation of conse nt andpatient positioning.
23 Describe the anatomy of the abdomen and pelvis relevant to the performance of abdominal examination.
24 Demonstrate competence in the physical examination of a patient for the assessment of presentations where abdominal signs may
occur, including inspection, palpation, percussion and auscultation of the abdomen, as well as the identification of organomegaly or
abnormal masses, elicitation of tenderness and signs of peritonism, then discuss the significance of any abnormal findings.
Receptive relaxation - centrally mediated reflex, initiated by swallowing and resulting in inhibition of tonic contraction in the stomach
wall and consequent in intragastric volume. Receptive relaxation is a largely vagally mediated reflex. The transmitter released by
the inhibitory enteric neurons activated by the vagus is not known .
Peristalsis mediated by cells of Cajal which lie within and between the muscle layers and produce slow waves or BER (3/min for
stomach). Depolarizing starts at greater curvature by the inward flux of Ca2+
and the repolarizing efflux of K+. BER do not exceed
excitation threshold and so do not cause contraction themselves, merely set the maximum rate of contraction.
Local factors (stretch and ACh) cause spike potentials seen at the peak of depolarisation in BER and they cause initiation of
contraction. Adrenaline tends to inhibit spike potentials. Peristalsis moves bolus/chyme to pyloric antrum.
Intense Antral Peristaltic Contractions during Stomach Emptying = "Pyloric Pump."
Most of the time, stomach contractions are weak and f n
mainly to cause mixing of food
and gastric secretions.
20% of the time contractions become intense, beginning in midstomach and ending in
very tight ringlike constrictions that can cause stomach emptying.
Antral contractions are always stronger and cont ractions combined with a closed
pyloric sphincter
squeeze only 10% of
antral contents through
semi-contracted pyloric
sphincter sieve like.
Very strong antral
contractions disperselarge particles grinding.
As the stomach becomes progressively more and more empty, these
constrictions begin farther and farther up the body of the stomach,
gradually pinching off the food in the b ody of the stomach and adding
this food to the chyme in the antrum.
Stimuli mechanical (distention) and chemical (products of protein
digestion)
Pathways long (vaso-vagal) short (enteric)
Hormonal gastrin (response to...) Cholecystokinin (response to ...)
Small Intestine:
Peristalsis
Occur in all parts of intestine, faster in proximal and slower in distal. Moves and spreads the chyme. Weak and die after 3-5cm. Average
1cm/min 3-5hrs to complete journey. Stimulation via distention of wall intestinal wall, gastroenteric reflex (initiated by distention of stomach and via m yenteric plexus).
Hormones :
y Positive motility = gastrin, C CK, insulin, motilin, and serotonin.
y Negative motility = secretin and glucagon.
On reaching ileocecal valve the chyme is sometimes stopped here for hours until the person eats another meal. (gastroileal re flex)
Segmentation
Distention causes localised concentric contractions spaced @ intervals along intestine and lasting a fraction of a minute. Ma ximum
frequency is determined by BER (12 in duo 8-9 in ileum)
y Ulcers may be visualised as an irregular outline of the stomach or duodenal lining
y Carcinoma may be se en as a filling defect or an irregular ulcer with rolled edges.
y Less invasive.
Dis.
y Radiation exposure.
y Inability to confirm malignancy in gastric ulcers
H. pylori tests - Non Invasive methods13C Urea breath Test
y Breath in13
C Urea urease converts to13
CO2
y requires a mass spectrometer, but is very sensitive and specific.
y Can demonstrate eradication of the organism following treatment.
Serological Tests only good for detection
y Detect IgG Ab.
y Used in the diagnosis and epidemiological studies.
y IgG titres may take up to 1 year to fall by 50% after eradication therapy and are
therefore not useful for confirming eradic ation or the presence of a current
infection.
Stool Test
y Stool sample detect for H. Pylori proteins using engineered monoclonal
antibodies
H. pylori tests - Invasive techniques
Rapid Urease Test
y Gastric biopsies are added to a urea solution containing phe nol red. If H. pylori are present, the urease enzyme splits the urea torelease ammonia which raises the pH of the solution and causes a rapid colour change.
C ulture
y Biopsies obtained can be cultu red and sensitivities to antibiotics can be a scertained
H istology
y H. pylori can be detected histologically on routine Giemsa stained sections of gastric mucosa obtained at endoscopy.
Test Sensitivity/
Specificity
Advantages Disadvantages
Noninvasive Tests
Serum H.
pylori antibo
dies
90% to 97%
sensitivity
50% to 90%
specificity
Noninvasive test of choice when endoscopy
is not indicated and patient has not received
prior H. pylori eradication therapy.
Not affected by PPI, antibiotics, luminal
blood.
Does not confirm eradication because antibodies
to H. pylori can persist years after microbiologic
cure.
Not an option when the patient has received prior
antimicrobial therapy for H. pylori infection.
Urea breath
test
77.5% to 97%
sensitivity
90% to 99%
specificity
Simple.
Preferred for confirming cure of H.
pylori infection, but no sooner than 4 weeks
after completion of therapy.
Possibility of false-negative results s if testing is
done after Rx with PPIs, antibiotics, or bismuth
compounds.
Small radiation exposure with carbon-14 method.
Expensive.
Stool
antigen test
91% to 96%
sensitivity
89% to 95%
specificity
Can also be used to confirm cure of H. Pylori
infection.
With current tests, a positive result after 4
weeks is predictive of failed eradication.
Affected by intake of PPIs, antibiotics, and bismuth
compounds.
Older tests have shown lower accuracy in
predicting eradication.
Invasive Tests (Require Endoscopy)
Tissue
biopsy
93% to 100%
sensitivity; >95%
specificityGiemsa and Genta
stains have >95%
sensitivity and 99%
specificity
Direct confirmation of presence of H. pylori .
Can determine presence of neoplasm if
necessary.
When hematoxylin eosin stain is nondiagnostic, a
second staining method is required.
Results are dependent on the quality o f samplestaken.
16 . OUTLINE THE PRINCIPLES OF MANAGEMENT OF ULCERS INCLUDING ANTACIDS, H2 ANTAGONIST S, ACID PUMP
INHIBITORS, H. PYLORI ERADICATION AND SURGICAL APPROACHES (THE LAST IN ONLY THE MOST I NTRACTABLE
CASES) .
Drug Class Drug Mechanism of Action Adverse Effects Contraindication/
Caution
H2-receptor
antagonist
Cimetidine Reversibly competes with
H2 @ gastric H2 receptor
parietal cell
stimulation secretion
of HCl
Gynecomastia in male
patients, dizziness, headache,
fatigue; and confusion and
delirium (IV doses).
Cimetidine can interact with cytochrome
P450 enzymes (CYP1A2, CYP2C).
s bioavailability of of ketoconazole,
itraconazole, and ampicillin.
Pregnancy category B.
Ranitidine
Famotidine
Nizatidine
PPIs Omeprazole Irreversibly inactivates
the H+/K
+ATPase,
effectively reducing
gastric acid release into
the gastric lumen.
Nausea, diarrhea, dizziness Decreases bioavailability of ketoconazole,
itraconazole, and ampicillin.
Cytochrome P450 interactions: exercise
caution when used with warfarin,
phenytoin, and diazepam.
Pregnancy category B; pregnancy
category C (omeprazole).
Esomeprazole
Lansoprazole
Pantoprazole
Rabeprazole
Polysaccharide Sucralfate Undergoes
polymerization in acid
environment, binding to
proteins and coating
mucosal defects.
Constipation Caution in patients with renal
insufficiency, may develop aluminum
toxicity.
Pregnancy category B.
Bismuth
compound
Bismuth
subcitrate
Binds to ulcer base,
promoting bicarbonate
and mucin production.
Has intrinsic
antimicrobial effects.
Few systemic effects.
Converted by intestinal
bacteria to bismuth sulfide,
leading to black stools that
may be confused with melena.
Bismuth subsalicylate is contraindicated
in children younger than 12 years.
Use with caution in patients with renal
insufficiency.
Pregnancy category C/D
Anticholinergic
agents
Telenzepine Act as antagonists to
muscarinic receptors,
decreasing acid
secretion.
Dry mouth, blurred vision,
constipation.
Enhanced effect when used with other
drugs with antimuscarinic properties and
with monoamine oxidase inhibitors.
Antagonistic effect with
parasympathomimetics.
Pirenzipine
Antacids Al(OH)3+Mg(OH)
2
Alkali, neutralizes gastric
acid.
Belching, abdominal
distention, constipation
(aluminum- containing
compounds), d intestinal
motility (magnesium-containing compounds).
Contraindicated in patients with renal
failure.
Prostaglandin
analogue
Misoprostol Synthetic prostaglandin,
stimulates mucin and
bicarbonate production.
Abdominal pain, diarrhea,
nausea, vomiting.
Contraindicated in pregnancy; potent
abortifacient.
Pregnancy category X.
H. Pylori Eradication
All pts with gastric and duodenal ulcers have eradication therapy regardless of whether t his is an incidental finding. Standard eradication
therapies are successful in 90%. Reinfection uncommon (1%) in developed countries, more so in developed countries.
y good compliance is essential
y there is a high incidence of resistance to metronidazole, particularly in some populations
y oral metronidazole has frequent side-effects
y bismuth chelate is unpleasant to take, even as tablets.
Metronidazole, clarithromycin, amoxicillin, tetracycline and bismuth are the most widely used agents. Resistance to amoxicill in (12%) and
tetracycline (< 1%) is low. Quinolones such as ciprofloxacin, furazolidone and rifabutin are also used when standard regimens have failed(rescue therapy). Bismuth suppresses H. pylori effectively. None of these drugs is effective alone; eradication regimens th erefore usually
comprise two antibiotics given with powerful acid suppression in the form of a PPI, all given for 7 days.
Example regimes are:
y omeprazole 20 mg + clarithromycin 500 mg and amoxicillin 1 g all twice daily
y omeprazole 20 mg + metronidazole 400 mg and clarithromycin 500 mg all twice daily.
Surgery
y Hardly ever done - 90% of all ulcer operations are interventions for hemorrhage, perforation, or obstruction
y Endoscopic therapy remains the procedure of choice for the majority of patients with rebleeding. However, emergency surgery i s
preferred among patients with hypotension and with a large ulcer siz e (> 2 cm diameter).
REFLUX, DYSPEPSIA, DYSPHAGIA, ODYNOPHAGIA, HAEMATEMESIS, MELAENA OR RECTAL BLEEDING) [REVISION] INCLUDING: THE
CARDINAL CHARACTERISTICS OF THE SYMPTOM AND ITS TIME COURSE; RELEVANT ASSOCIATED SYMPTOMS; THE PATIENT'S
UNDERSTANDING OF, AND CONCERNS ABOUT, WHAT THEY ARE EXPERIENCING.
21. DEMONSTRATE APPROPRIATE INFECTION CONTROL MANOEUVRES PRIOR TO AND AFTER PHYSICAL EXAMINATION
OF A PATIENT [REVISION].
22 . PREPARE A PATIENT APPROPR IATELY FOR EXAMINATION OF THE ABDOM EN, IN RELATION TO APPROPRIATEEXPLANATION, CONFIRMATION OF CONSENT AND P ATIENT POSITIONING.
23 . DESCRIBE THE ANATOMY OF THE ABDOMEN AND PELVIS RELEVANT TO THE PERFOR MANCE OF ABDOMINAL