Lecture 11 - GIT Disorders Flashcards
What does a structural/neural abnormality of GIT involve?
Altered Chyme movement: Slowing, obstructing, acceletration
What does inflammatory/ulcerative conditions of GIT involve?
Changes in secretion, motility and absorption
Anorexia associated with?
Nausea, abdo pain, diarrhoea
Anorexia definition
Lack of desire to eat in presence of physiologiical stimuli, normally eliciting hunger
Vomiting reflex initiated by
- Duodenal presence of ipecac
- Severe pain
- Distension of stomach or duodenum
- Torsion or trauma of testes, ovaries, uterus, bladder or kidneys
Where is the ‘vomiting centre ‘?
‘Chemoreceptor trigger zone’ in postrema of medulla
Which neurotransmitters activate ‘chemoreceptor trigger zone’ of vomiting?
5-HT (Serotonin) - from intestinal enteroendocrine cells. (Also dopamine, acetylcholine, histamine and Substance P)
Which drugs are used as anti-emetics? (Antinausea)
Dopamine and serotonin receptor antagonists
Vomiting is preceded by?
Nausea and retching
What is retching?
Reverse peristalsis against closed upper oesophageal sphincter
What are sympathetic actions associated with vomiting?
tachycardia, tachypnoea, sweating
What are parasympathetic actions associated with vomiting?
Hypersalivation, Increased gastric motility, Relaxation of upper and lower oesophageal sphincters.
Mechanism of vomiting (Steps):
- Reverse peristalsis duodenum and pyloric antrum
- Oesophagus and gastric body reflex
- Contraction abdo muscles = force diaphragm up
- Stomach relax -> upper oesophagus contracts -> remaining chyme drops back into stomach
- repeat
Metabolic consequences of vomiting?
Disturbance of fluid, electrolyte and acid-base balance
Definition of constipation?
Decrease or infrequent defaecation (decrease in weekly bowel movements)
What causes constipation?
Personal habits, drugs, various disorders
Clinical manifestations of constipation?
Difficulties/change in bowel evacuation patterns. Smaller stool volume. Feeling of bowel fullness and discomfort.
Neurogenic constipation pathophysiology:
Defective neural pathways and altered mechanisms.
Slow transit time (Abdo muscles weakness and pain)
Personal Habit constipation pathophysiology:
Low residue diet -> Decreased volume and stools.
Sedentary lifestyle and lacking regular exercise.
Lack of access to toilet facilities and consistent suppression of urge to defaecate.
Systemic disease pathophysiology of constripation:
Hypothyroidism -> decreased bowel motility
Pathophy of drug caused constipation
Antacid use
Opiates inhibit bowel motility
Antidepressants (Anticholinergic)
Diagnosis of Constipation involves?
History: How long? sudden onset may indicate organic lesions.
Physical exam: palpation (colon distention, masses, tenderness).
Digital rectal exam (Sphincter tone and anal lesions)
Stool transit time
proctosigmoidoscopy
Barium Enema
Constipations treatment:
Bowel retraining Exercise More fluids Increased fibre intake Bilk supplements Stool softeners Laxative Infrequent enemas
Diarrhoea Definition
Increased frequency, fluidity, volume and weight of faeces
What influences stool volume and consistency?
Colonic H2O Content Presence of unabsorbed food Presence of unabsorbable material Intestinal secretions Adult stool volumes <200g a day
How much water is lost in stool per day?
150mL
Two forms of diarrhoea:
Large vol. Diarrhoea: (Increased volume of faeces due to:
Increased amounts H20, secretions or both.)
Small volume diarrhoea: Depending from intestinal motility (vol. not increased)
Mechanisms of osmotic diarrhoea?
Nonabsorbable substances draw H20 into lumen (Increased weight and vol. of stool).
- Mg, Sulphate, Phosphate (poorly absorbed)
- Deficiency (lactase, panreatic enzymes)
- ingestion synthetic, non-absorbable sugars
Mechanism of secretory diarrhoea?
Altered mucosal secretion and fluid electrolyes
- Bacterial enterotoxins, neoplasms. (Large vol. Diarrhoea)
- Inflammatory diseases such as Crohns and ulcerative colitis. Faecal impaction stimulates secretions to lubricate and move faeces. (Small vol. diarrhoea)
Mechanism of motility diarrhoea?
Inadequate food mixing and impaired digestion. Causes:
- Resection small intestine
- Surgical Bypass
- Fistula formation between loops intestine
- Hampered motility due to diabetic neuropathy
Clinical manifestations of chronic diarrhoea?
- Dehydration
- Electrolyte imbalance
- Acidosis
- Weight loss
Clinical manifestations of acute diarrhoea?
Fever with or without cramping pain with presence of diahhroea
Diagnosis of diarrhoea:
History: Onset and frq, travel? previous surgery? Iatrogenic?
Physical exam to identify systemic disease.
Abdominal X-ray, biopsies, stool culture, stool blood.
3 Types of abdo pain causes?
Mechanical, inflammatory, ischaemic
Describe mechanical cause for abdo pain
Abdo organs sensitive to:
- Rapid stretch and distension
- traction on peritoneum
- Common bile duct distension
- Forceful peristalsis from intestinal obstruction.
Encapsulated organs:
- Contain pain afferent for stretch (gall bladder and liver)
Describe inflammatory causes of abdo pain?
Biochemical mediators: Histamine, bradykinin, serotonin stimulate visceral nerve endings
Oedema, vascular congestion -> Stretching: Seen with chemical, bacterial and viral inflammation
Describe ischaemic cause of abdo pain
Obstruction of blood flow from distension through bowel obstruction.
Mesenteric vessels thrombosis.
Increases tissue metabolites stimulates pain receptors.
Describe parietal abdo pain?
Parietal Peritoneum:
- Localised, intense
- Lateralised (innervated at any particular point, from only one side of nervous system)
Describe Visceral abdo pain?
Abdominal Organ:
- poorly localised, dull, diffuse, vague with radiating patten,
- nerve endings sparse (e.g. stomach pain manifests as sensation of fullness, cramping, gnawing at mid-epigastric
Describe refereed abdo pain?
Felt at distance from affected organ:
- Well-localised, felt in skin or deeper tissues that:
- -‘Share a general afferent pathway with organ’
- -e.g. gall-bladder pain starts as vague right epigastric pain, then referred to shoulder blades as sharp and localised.
Upper GIT Bleeding locations:
Oesophagus, stomach, duodenum
Causes of upper GIT bleeding?
- Oesophageal or gastric varices
- Peptic ulcers
- Mallory weiss tear at oesophageal-gastric junction from severe retching
Location of lower GIT bleeding?
jejunum, ileum, colon, rectum
Causes of lower GIT bleeding:
- polyps,
- inflammatory disease
- cancer
- haemorrhoids
Signs of gastrointestinal bleeding
- changes in blood pressure
- postural hypotension, lightheadedness, loss of vision,
- increased HR
- Blood in stool
Physiological response to GIT bleeding:
- Increased TPR to shunt blood to core.
Prolonged GIT bleeding leads to :
Hypovolaemic shock -> Decreased renal output -> Decreased urine output -> Tubular necrosis -> Renal failure -> Decreased cerebral and coronary blood flow -> Anoxia and death
Presentations of acute GIT Bleeding
Haematemesis
Melena
Haematochezia
Occult Bleeding
What is haematemesis?
Sign of acute GIT bleeding: Black vomitus: either fresh bright red or dark grainy digested blood
What is melena?
Sign of acute GIT bleeding: Black, sticky, tarry foul smelling stools caused y digestion of blood in GIT
What is Haematochezia?
Sign of acute GIT bleeding: Fresh bright red blood passed from rectum
What is occult bleeding
Trace amounts of blood in normal appearing stools or gastric secretions: Detectable only with a Guaiac Test
What does GERD stand for?
Gastrooesophageal reflex disease
What is GERD?
Regurgitation of stomach chyme through lower oesophageal sphincter into oesophagus.
What are complications of GERD?
Reflux Oesophagitis
Oesophageal ulcers,
Oesophageal scarring (Dysphagia)
What are the consequences of ssnk mucosa of oesophagus exposure to refluxed acid?
- Cell injury
- Accelerated desquamation
- Compensatory basal cell hyperplasia = Increased immature epithelium cells, elongated C.T papillae, low grade inflammatory response
Consequences of severe reflux
- Cell proliferation fails to keep pace with desquamation -> ulceration-> haemmorhage or perforation
- Haling occurs through fibrosis and epithelial regeneration
- Shrinkage of fibrous tissue = Stricture of oesophagus (narrowing of opening)
What occurs if epithelium of oesophages regenerates as columnar epithelium after reflux damage?
Barretts Oesophagus Disease
Causes of Reflux Oesophagitis?
- Inadequate resting tone of lower oesoph sphincter
- Increased intra-abdo pressure (vomiting, coughing, lifting, bending)
- Weak oesophageal peristalsis
- Delayed gastric emptying: (Increased chyme acidity, increased time-span for reflux) caused by gastric duodenal ulcers, pyloric strictures, hiatal hernia.
- gastric surgery.
What does the severity of oesophagitis depend on?
Composition of of gastric contents, duration of exposure to mucosa.
Clinical manifestations of reflux oesophagitis 1 hr after meal?
Within 1hr of meal:
- Heartburn
- Acid regurgitation
- Dysphagia
- chronic cough
- athsma
- upper abdo pain
How is reflux oesophagitis diagnosed?
- Manifestations
- Endoscopy (looking for erosions, oedema, dysplasia (Barrett’s), carcinoma
- pH monitoring
Baa++ swallow, associated with hiatal hernia, gastric ulcers
Aetiology of Barrett’s Oesophagus?
Epithelial substitution (Migration of cells from distal 2cm or from ducts of submucosal glands) Metaplasia (Differentiation from common stem cell - response to injury)
Clinical significance of Barrett’s Oesophagus?
- Premalignant condition
- Risk of cancer is 100x higher in these patients vs normal pop.
- After diagnosis, regular colonoscopies check for dysplasia
Barrett’s Oesophagus:
3 types of columnar mucosa and their function.
- Junctional type: normal gastric cardia
- Atrophic fundal type: scanty specialised secretory cells
- ‘Specialised mucosa’: epithelium undergoing further metaplastic changes towards intestinal type with acquired goblet cells.
What is peptic ulcer disease?
Ulceration of mucosal lining of (oesophagus, stomach, duodenum)
Difference between an erosion and a true ulcer in peptic ulcer disease?
Erosions: superficial, do not penetrate muscularis mucosae.
True Ulers: Penetrate muscularis mucosae and blood vessel damage
Peptic ulcer risk factors:
smoking, advanced age, habitual NSAID use, EtOH, chronic diseases (emphysema, Rheumatoid arthritis, cirrhosis, diabetes). Helicobacter pylori infection of gastric duodenal mucosa., stress
Duodenal ulcers occur most in (population)..
Men, younger people, type O blood.
Pathophysiology of Duodenal ulcers:
i. NSAIDS inhibit prostaglandins = Decreased HCO-3 and mucus production
ii. H.pylori urease -> formation of cytotoxic ammonia.
iii. H.pylori phospholipases and other enzymes from micoorg -> damage to mucosa
iv. H.pylori -> Increased gastrin production -> HCl secretion -> ulcer formation
v. rapid gastric emptying exceeds buffer capacity of HCO-3 righ panc. juice
vi. Increase secretion form parietal cells
vii. Smoking
Viii. Decreased mucosal HCO3 secretion
Clinical manifestations of duodenal ulcers:
- Epigastric pain (chronic intermittent) :2-3 hours post-grandial, relieved by food consumption or antacids
- haemorrhage: with history of asprin or anticoag use, most common in elderly
- perforation: if all wall layers destroyed, sudden severe epigastric pain
- obstruction of duodenum: oedema from inflammation or scarring.
- haematemesis or melena
Diagnosis of duodenal ulcers:
- X-ray with barium contrast meal
- flexible endoscope
- radioimmune assays of gastrin levels
- detection of helicobacter pylori
Prevention of duodenal ulcers
high vit A and fibre diet
Gastric ulcers epidemiology
Equal in males and females
55-65 yrs
25% less common than duodenal ulcers
Clinical manifestations of gastric ulcers:
similar to duodenal
- pain-food relief
- pain may occur post-prandial
- tends to be chronic
- anorexia, vomiting, weight loss
Gastric ulcer pathophys:
- Increased mucosa permeability to H+ ions
- Gastric secretions decreased (chronic gastritis)
- Chronic gastritis -> ulcer,
- duodenal reflux
- ulcerogenic drugs
- Increased bile salt = electrical potential disruption -> H+ diffuse back into mucosa.
- Histamine from damaged mucosa -> increased blood flow pepsinogen and acid production and capillary permeability
What is ulcerative colitis?
Chronic inflammation of rectum an sigmoid colon
UC most common in… (population)
- Genetically susceptible (20-40yrs), Jewish descent, white
Causes of UC?
- infection
- genetics
- immunological: humoral factors (anticolon antibodies in sera), activated macrophages, cytotoxic T cells attack colonocytes, often accompanied by other immune disorders
Pathophysiology of UC?
Primary lesion at base of colonic crypts. Hyperaemic mucosa. SMall erosions merge into ulcers.
- Abscess formation (necrosis, ragged mucosal ulceration)
- Oedema and thickening of m.mucosa > narrow lumen
- mucosal destruction
- Bleeding, cramping pain, urge to defaecate, purulent mucus = decreasing colonic transit time = large volumes of watery diarrhoea
Clinical manifestations of mild UC?
Intermittent periods of remission and exacerbation. (less mucosa)
- increased frequency of BMs, bleeding, pain.
Clinical manifestations of severe UC?
(entire colon)
- fever, increased pulse rate
- frequent diarrhoea (10-20/day)= dehydration
- urgency
- bloody stool
- continuous bloody stools = anaemia
- continuous crampy pain
- weight loss
- increased colon cancer risk
Diagnosis of UC?
Medical history and clinical manifestations.
Differential diagnosis with Crohn’s disease
- Sigmoidoscopy
- X-rays with barium enema
- Stool culture rules out infection
Where does crohns occur?
Large and small intestine but seldom rectum.
Crohns disease immune system effects:
Decreased suppressor T cells IgA production Macrophage activation luminal flora antigens
Pathophysiology of Crohns:
Begins in intstinal submucosa
- tissue injury from activated neutrophils and macrophages
- ascending and transverse colon and small intestine (skip lesions)
- may be unilateral
- fissures that penetrate lymphoid tissue
- granuloma is typical lesion
- fistulae between intestinal loops in perineal area or into bladder
Crohns vs UC
Crohns: Focal or patchy mucosal involvement. Fissure ulcers. Aggregated transmural chronic inflammatory cell infiltrate.
UC: Horizontal undermining ulcers. Diffuse mucosal Inflammation
