6.4 Disorders of the Lower Gastrointestinal Tract Flashcards
Are there villi or microvilli in the large intestine? What about circular folds?
- No villi/microvilli
- No circular folds
Outline the autoimmune mechanics of coeliac disease at a cellular level
- Specific MHC class II molecules that present gluten as a pathogen
- Picked up by autoreactive T cell
- Downstream immune activation and attacking of the small bowel
GI/extraintestinal symptoms of coeliac disease
GIT symptoms:
- Diarrhoea, flatulence, abdo pain, bloating
- Iron deficiency anaemia/other deficiencies
- Weight loss
- Fatigue
Extraintestinal:
- Skin blistering
- Other autoimmune diseases
- Osteoporosis
Coeliac disease Ix
- Gluten challenge diet (like a shitty viral video)
- Blood tests for antibodies
- Endoscopy/small intestine biopsy
Symptoms/signs of IBS
- Bloating
- Abdo pain
- Diarrhoea
- Constipation
What investigations/symptoms might we check for to determine if a patient has functional bowel disease like IBS?
Symptoms: weight loss, rectal bleeding, perianal symptoms, mouth ulcers
Investigations: Iron studies, CBC (?anaemia), CRP, faecal calprotectin, raised platelets, low albumin
What are the three broad characteristic principles of IBD pathogenesis?
- Defective host interactions with intestinal microflora (a war is being waged)
- Epithelial dysfunction (craters on the battlefield)
- Mucosal inflammatory response, driven by T cells
Extraintestinal symptoms of IBD
- Anterior uveitis
- Arthritis
- Osteopenia/porosis
- Thromboembolic event
Crohn’s Symptom
(Intermittent Attacks)
- Malabsorption
- Weight loss
- Perianal fissures
What macroscopic changes can Crohn’s make to the GI tract?
- Transmural inflammation
- Thickened/oedematous mesentery
- Strictures
- “Cobblestoning” fibrosis and ulceration
- Skip lesions
Crohn’s complications
- Bowel obstruction
- Ulcers
- Malabsorption
- Anaemia
- Carcinoma
What is the pattern of distribution of ulcerative colitis. How deep is the ulceration?
- Starts in rectum
- Spreads proximally
- Inflammation is more superficial than crohn’s
Ulcerative colitis symptoms
(Mostly intermittent attacks)
- Blood or pus in stool
- Diarrhoea
- Urgency
Describe acute severe ulcerative colitis
- > 6 bloody bowel motions/day
- One of: elevated HR, temp, CRP, or low Hb
- This is a medical emergency
Diverticulosis mechanism
- Increased intraluminal pressure from straining during defecation (due to deficiency in vegetable fibre)
- Causes mucosal “blowouts”, and circular muscle hypertrophy
- Plus, with age, tensile colonic strength decreases
- Causes diverticula to form
Diverticulitis mechanism
- Inspissated (thickened) stool gets trapped in diverticula
- Causes inflammation and localised ischaemia
- Bacteria may breach mucosa
Symptoms/investigations for acute diverticulitis
Symptoms: pain (usually left iliac fossa), fever, malaise, anorexia, change in bowel habirt, fever
Bloods: WCC elevated
Imaging: CT is best
How do we manage acute diverticulitis? What if there’s no initial improvement?
- Nil orally
- IV fluids
- IV antibiotics
- Analgesia
If no improvement: surgery
How does diverticular abscess differ from acute diverticulitis? How do we treat it?
- Walled off diverticulum
- Treated w/ IV antibiotics, radiological drainage, resection
(Smaller may go away on own; larger often need drainage and resection)
What are the two most common types of colonic fistula formed due to diverticulosis?
- Colovesical
- Colovaginal
What are some complications of diverticulitis?
- Fistula formation
- Bleeding
- Abscess occurrence
- Obstruction/stricture from recurrent
What must we always exclude if we’re considering diverticulosis? How?
Colorectal cancer (do a colonoscopy 6 weeks after event, to let mucosa calm down and reduce rupture risk)
Why is the appendix more likely to become gangrenous and perforate, as seen in appendicitis?
- End arterial supply
- More likely to become gangrenous and perforate
Mechanistically, what is the most likely cause of appendicitis?
Luminal obstruction
Why is it clinically relevant that the appendix can have multiple positions in different people?
Because this causes it to sit around different structures. Then, when inflamed affects those different structures to produce different symptoms.
Why does appendicitis pain classically shift to the RIF? What structure is irritated?
Irritation of parietal peritoneum.
Physical exam findings of appendicitis
- Tachycardia
- Fever
- RIF Tenderness
What are some possible mechanisms for Rovsing’s sign?
- Pressure on peritoneum
- Shifting small intestine
- Increased pressure
Appendicitis investigations (in a suspected case, accounting for other differentials)
- Bloods (raised WCC)
- Urinalysis (don’t assume UTI)
- Beta HCG in women
- Ultrasound for reproduce age females and children (radiation)
- CT scan for other people
Appendicitis management
- Nil orally
- IV fluids
- Analgesia
- If not getting better, appendectomy
What three different fates might happen to the appendix if appendicitis is not treated?
- Gangrene
- Suppuration
- Perforation
(GPS)
