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Medical Studies 2B > 6.4 Disorders of the Lower Gastrointestinal Tract > Flashcards

6.4 Disorders of the Lower Gastrointestinal Tract Flashcards

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USMLE® Step 1 flashcards
1
Q

Are there villi or microvilli in the large intestine? What about circular folds?

A
  • No villi/microvilli
  • No circular folds
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2
Q

Outline the autoimmune mechanics of coeliac disease at a cellular level

A
  • 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
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3
Q

GI/extraintestinal symptoms of coeliac disease

A

GIT symptoms:
- Diarrhoea, flatulence, abdo pain, bloating
- Iron deficiency anaemia/other deficiencies
- Weight loss
- Fatigue

Extraintestinal:
- Skin blistering
- Other autoimmune diseases
- Osteoporosis

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4
Q

Coeliac disease Ix

A
  1. Gluten challenge diet (like a shitty viral video)
  2. Blood tests for antibodies
  3. Endoscopy/small intestine biopsy
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5
Q

Symptoms/signs of IBS

A
  • Bloating
  • Abdo pain
  • Diarrhoea
  • Constipation/diarrhoea
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6
Q

What investigations/symptoms might we check for to determine if a patient has functional bowel disease like IBS?

A

Symptoms: weight loss, rectal bleeding, perianal symptoms, mouth ulcers

Investigations: Iron studies, CBC (?anaemia), CRP, faecal calprotectin, raised platelets, low albumin

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7
Q

What are the three broad characteristic principles of IBD pathogenesis?

A
  • Defective host interactions with intestinal microflora (a war is being waged)
  • Epithelial dysfunction (craters on the battlefield)
  • Mucosal inflammatory response, driven by T cells
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8
Q

Extraintestinal symptoms of IBD

A
  • Anterior uveitis
  • Arthritis
  • Osteopenia/porosis
  • Thromboembolic event
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9
Q

Crohn’s Symptom

A

(Intermittent Attacks)
- Malabsorption
- Weight loss
- Perianal fissures

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10
Q

What macroscopic changes can Crohn’s make to the GI tract?

A
  • Transmural inflammation
  • Thickened/oedematous mesentery
  • Strictures
  • “Cobblestoning” fibrosis and ulceration
  • Skip lesions
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11
Q

Crohn’s complications

A
  • Bowel obstruction
  • Ulcers
  • Malabsorption
  • Anaemia
  • Carcinoma
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12
Q

What is the pattern of distribution of ulcerative colitis. How deep is the ulceration?

A
  • Starts in rectum
  • Spreads proximally
  • Inflammation is more superficial than crohn’s
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13
Q

Ulcerative colitis symptoms

A

(Mostly intermittent attacks)
- Blood or pus in stool
- Diarrhoea
- Urgency

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14
Q

Describe acute severe ulcerative colitis

A
  • > 6 bloody bowel motions/day
  • One of: elevated HR, temp, CRP, or low Hb
  • This is a medical emergency
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15
Q

Diverticulosis mechanism

A
  • 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
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16
Q

Diverticulitis mechanism

A
  • Inspissated (thickened) stool gets trapped in diverticula
  • Causes inflammation and localised ischaemia
  • Bacteria may breach mucosa
17
Q

Symptoms/investigations for acute diverticulitis

A

Symptoms: pain (usually left iliac fossa), fever, malaise, anorexia, change in bowel habirt, fever

Bloods: WCC elevated
Imaging: CT is best

18
Q

How do we manage acute diverticulitis? What if there’s no initial improvement?

A
  • Nil orally
  • IV fluids
  • IV antibiotics
  • Analgesia

If no improvement: surgery

19
Q

How does diverticular abscess differ from acute diverticulitis? How do we treat it?

A
  • Walled off diverticulum
  • Treated w/ IV antibiotics, radiological drainage, resection
20
Q

What are the two most common types of colonic fistula formed due to diverticulosis?

A
  • Colovesical
  • Colovaginal
21
Q

What are some complications of diverticulitis?

A
  • Fistula formation
  • Bleeding
  • Obstruction/stricture from recurrent
22
Q

What must we always exclude if we’re considering diverticulosis? How?

A

Colorectal cancer (do a colonoscopy 6 weeks after event, to let mucosa calm down and reduce rupture risk)

23
Q

Why is the appendix more likely to become gangrenous and perforate, as seen in appendicitis?

A
  • End arterial supply
  • More likely to become gangrenous and perforate
24
Q

Mechanistically, what is the most likely cause of appendicitis?

A

Luminal obstruction

25
Q

Why is it clinically relevant that the appendix can have multiple positions in different people?

A

Because this causes it to sit around different structures. Then, when inflamed affects those different structures to produce different symptoms.

26
Q

Why does appendicitis pain classically shift to the RIF? What structure is irritated?

A

Irritation of parietal peritoneum.

27
Q

Physical exam findings of appendicitis

A
  • Tachycardia
  • Fever
  • RIF Tenderness
28
Q

What are some possible mechanisms for Rovsing’s sign?

A
  • Pressure on peritoneum
  • Shifting small intestine
  • Increased pressure
29
Q

Appendicitis investigations

A
  • 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
30
Q

Appendicitis management

A
  • Nil orally
  • IV fluids
  • Analgesia
  • If not getting better, appendectomy
31
Q

What might happen to the appendix if appendicitis is not treated?

A
  • Gangrene
  • Suppuration
  • Perforation

Medical Studies 2B (57 decks)

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