GI Flashcards

1
Q

What is the aetiology of small-bowel obstruction?

A
  • Adhesions (60%): usually secondary to previous abdo surgery
  • Hernia
  • Malignancy
  • Crohn’s disease
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2
Q

What is the pathophysiology of small-bowel obstruction?

A
  • Mechanical obstruction is most common
  • Obstruction leads to bowel distension above the block with increased fluid secretion into the distended bowel
  • Also leads to proximal dilatation above the block (causes increased secretion and swallowed air in the SB)
  • More dilatation causes decreased absorption and mucosal wall oedema
  • Increased pressure with the intramural vessels becoming compressed, resulting in ischaemia and/or perforation
  • Untreated obstruction leads to ischaemia, necrosis and perforation
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3
Q

What is the presentation of small-bowel obstruction?

A
  • Pain – initially colicky then diffuse (higher in abdo than large bowel obstruction)
  • Profuse vomiting following pain (occurs earlier than in large bowel obstruction)
  • Less distension than large bowel obstruction
  • Nausea and anorexia
  • Tenderness suggests strangulation and urgent surgery is required
  • Constipation with no passage of wind occurs late
  • Increased bowel sounds
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4
Q

How is small-bowel obstruction investigated?

A
  • Abdominal x-ray: central gas shadows that completely cross the lumen, no gas in large bowel, distended loops of bowel proximal to obstruction, increased bowel sounds
  • Examination of hernia orifices and rectum
  • FBC essential
  • CT is gold standard to localise lesion accurately
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5
Q

How is small-bowel obstruction managed?

A
  • Aggressive fluid resuscitation
  • Bowel decompression
  • Analgesia and antiemetic
  • Antibiotics
  • Surgery to remove obstruction
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6
Q

What is the aetiology of large bowel obstruction?

A
  • 90% due to colorectal malignancy

- Volvulus is most common cause in African countries

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7
Q

What is the pathophysiology of large bowel obstruction?

A
  • Similar to SBO, but colon proximal to obstruction dilates
  • Increased colonic pressure and decreased mesenteric blood flow results in mucosal oedema
  • Can compromise arterial blood supply and cause mucosal ulceration
    In colonic volvulus:
  • 360o axis rotation results in a closed loop obstruction
  • Fluid and electrolytes shifts into the closed loop
  • Results in increased pressure and tension in the loop causing impaired colonic blood flow
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8
Q

What is the presentation of large bowel obstruction?

A
  • Abdominal pain is more constant than in SBO
  • Abdominal distension
  • Bowel sounds normal then increased then quiet later
  • Palpable mass e.g. hernia, distended bowel loop or caecum
  • Late vomiting which is more faecal like (suggestive of LBO)
  • Vomiting may be absent
  • Constipation
  • Fullness/ bloating/ nausea
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9
Q

How is large bowel obstruction investigated?

A
  • DRE (empty rectum, hard stools, blood)
  • FBC is essential (see low Hb if chronic occult blood loss)
  • Abdominal XR (peripheral blood shadows proximal to the blockage, caecum and ascending colon distended)
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10
Q

How is large bowel obstruction managed?

A
  • Aggressive fluid resuscitation
  • Bowel decompression
  • Analgesia and antiemetic
  • Antibiotics
  • Surgery to remove obstruction (if due to malignancy, then colorectal stents followed by elective surgery)
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11
Q

What is the aetiology of bowel pseudo-obstruction?

A
  • 80% is a complication of other conditions:
  • Intra-abdominal trauma, pelvic, spinal and femoral fractures
  • Postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic, neuro
  • Intra-abdominal sepsis
  • Pneumonia
  • Drugs e.g. opiates and antidepressants
  • Metabolic disorders e.g. electrolyte disturbances, malnutrition
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12
Q

What is the presentation of bow pseudo-obstruction?

A
  • Rapid and progressive abdominal distension with pain
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13
Q

How is bow pseudo-obstruction investigated?

A
  • XR shows gas-filled large bowel
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14
Q

How is bowel pseudo-obstruction managed?

A
  • Treat underlying problem e.g. withdrawal of opiate analgesia
  • IV neostigmine
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15
Q

What is the pathophysiology of diverticulitis?

A
  • Low fibre diet increases intestinal transit time and decreases stool volume resulting in increased intraluminal pressure and colonic segmentation, which predisposes to diverticular formation
  • Commonly form where vasa recti penetrate the colonic all, and food particle or faecal material may contribute to the development of infection
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16
Q

What are the risk factors of diverticulitis?

A
  • Low dietary fibre
  • Age >50
  • Western diet
  • Obesity (BMI>30)
  • Use of NSAIDs
17
Q

What is the presentation of diverticulitis?

A
  • Lower left quadrant pain
  • Leukocytosis
  • Fever
  • Rectal bleeding
  • Guarding and tenderness in lower left quadrant
  • Bloating
  • Constipation
18
Q

What are the differential diagnoses of diverticulitis?

A
  • Endometriosis
  • Colorectal cancer
  • Appendicitis
  • Ulcerative colitis
  • Crohn’s disease
  • UTI
  • Pyelonephritis
  • Ischaemic colitis
  • Pelvic inflammatory disease
  • IBS
19
Q

How is diverticulitis investigated?

A
  • FBC with differential (polymorphonuclear leukocytosis)
  • Abdominal x-ray (free air in bowel perforation)
  • Abdo CT (thickening of bowel wall, mass, abscess)
20
Q

How is diverticulitis managed? (Asymptomatic and symptomatic)

A
  • No treatment if asymptomatic

- Symptomatic then dietary modification and fibre supplementation + oral antibiotic therapy

21
Q

What is the aetiology of gastritis?

A
  • Most commonly due to H. Pylori infection
22
Q

What is the pathophysiology of gastritis?

A
  • H. Pylori infection induces a severe inflammatory response with gastric mucin degradation
  • NSAIDs and alcohol decrease gastric mucosal blood flow with loss of the mucosal protective barrier
23
Q

What are the risk factors of gastritis?

A
  • Helicobacter pylori infection
  • NSAID use
  • Alcohol use/ toxic ingestion
  • Previous gastric surgery
  • Critically ill patients
  • Autoimmune disease
  • Immunocompromised
24
Q

What is the presentation of gastritis?

A
  • Dyspepsia/epigastric discomfort
  • Nausea, vomiting and loss of appetite
  • Fever
  • Acute abdominal pain
  • Cognitive impairment
25
Q

What are the differential diagnoses of gastritis?

A
  • Peptic ulcer disease
  • GORD
  • Non-ulcer dyspepsia
  • Gastric lymphoma
  • Gastric carcinoma
26
Q

How is gastritis investigated?

A
  • H. Pylori urea breath test
  • H. Pylori faecal antigen test
  • FBC
  • Endoscopy
  • Serum vitamin B12
27
Q

How is gastritis managed?

A
  • H. Pylori eradicating therapy

- Anti-secretory agents