Gastroenterology Flashcards

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1
Q

What is the pathophysiology and presentation of ulcerative colitis

A

Mucosal system exerts an inappropriate response to luminal antigens that enter epithelium.
Is restricted to the mucosa (different to Crohn’s), begins in the rectum and extends upwards.
The inflammation is continuous (whole area) - reddened and bleeds easily. In severe cases ulcers and pseudo-polyps form
Different classifications by area affected: just rectum (50%) - proctitis, rectum + left colon - left sided colitis, entire colon to ileocaecal valve - pancolitis/ extensive colitis. Never affects proximal to ileocaecal valve

Pain usually restricted to lower left quadrant, cramps
Episodic or chronic diarrhoea with blood and mucus
In acute: fever, tachycardia, tender/ distended. Blood diarrhoea (10-20 per day) associated with urgency and incontinence

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2
Q

Investigations for ulcerative colitis and Crohn’s

A

Colonoscopy and mucosal biopsy the gold standard, shows disease activity/ extent

Blood tests - white cell count and platelet count raised in moderate+. ESR and CRP raised, LFTs. Iron deficiency anaemia. pANC antibody may be positive - negative in Crohn’s

Stool samples - differentiate from infections
Faecal calprotectin (positive but not specific)

X ray for severe - exclude dilation and may be too severe for colonoscopy, US / CT for fistulas / abscesses / strictures

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3
Q

Management of ulcerative colitis

A

Sulfasalazine (aminosalicylate) reduces inflammation - oral or rectal
If severe glucocorticoid (oral prednisolone), ciclosporin / infliximab, surgery

Maintaining remission: mesalazine FL, azathioprine

Surgery - failure to respond to treatment, colon removed (panproctocolectomy) and rectum fused to ileum (remains continent, faeces stored in terminal ileum)
Whole colon and rectum removed, ileum out to stoma

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4
Q

Pathophysiology and presentation of Crohn’s

A

Inflammation is patchy (unlike UC)
Deep fissuring ulcers and granulomas form
Wall often thickens and lumen narrows

Inflammation causes: malabsorption, obstruction, perforation, fistula formation, cancer
Aetiology unknown but suspected that a bug causes

Diarrhoea with urgency, bleeding and pain. Can go 6+ times in an hour
Acute abdominal pain in right iliac fossa
Weight loss, malaise, anorexia, tenderness, perianal abscess, anal strictures

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5
Q

Management of Crohn’s

A

Oral prednisolone (reduce dose if symptoms resolve), severe - IV/ rectal hydrocortisone
Enteral nutrition - helps remission, treats nutritional deficiency, improves microbiome, removes inflammatory foods
If no improvement infliximab, azathioprine, methotrexate
Maintain remission - azathioprine, mercaptopurine
Surgery if failure to thrive: temporary ileostomy, resection (can result in short bowel syndrome and more diarrhoea and malabsorption)

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6
Q

What are the causes of malnutrition

A

Coeliac - villous atrophy and crypt hyperplasia (less absorptive area), T cell autoimmune in small bowel (immune response to gliadin in gluten)
Pancreatic insufficiency - lack of enzymes necessary to digest; alcohol abuse, cystic fibrosis
Defective bile secretion (can’t absorb fats) - biliary obstruction, ileal reaction (decreased uptake so can’t be reused)
Crohn’s/ surgery - less bowel available to absorb
Giardia lamblia - parasites coat villi blocking absorption
Rare: defective epithelial transport, lymphatic obstruction (lymphoma, tuberculosis)

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7
Q

Presentation, investigations and management of GORD

A

Heartburn, aggravated by bending/ stooping/ lying down/ hot drinks/ alcohol
Food/ water/ acid regurgitation (brash), painful swallowing
Nocturnal asthma, chronic cough, laryngitis, sinusitis

History alone if there are no red flag symptoms (weight loss, haematemesis, dysphagia)
If red flags present: endoscopy, barium swallowing (hiatus hernia), 24h oesophageal pH monitoring

Lifestyle: weight loss, smoking cessation, small regular meals, avoid exacerbating
Antacids - magnesium trisilicate mixture, neutralise the acid in stomach
Alginates - gaviscon, relieve symptoms (form foam raft in stomach)
Proton pump inhibitors - lansoprazole, reduce acid production
H2 receptor antagonists - cimetidine, block histamine receptors and reduce acid production

Surgery in severe, nissen fundoplication, increases resting LOS pressure

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8
Q

What is the presentation of colorectal cancer and indications for 2ww

A

Change in bowel habit, unexplained appetite change + weight loss, rectal bleeding, mass, iron deficiency, abdominal pain
May present acutely with obstruction: vomiting, abdominal pain, absolute constipation

2ww: 60+ bowel habit change / anaemia, 50+ unexplained rectal bleeding / abdominal pain / weight loss, 40+ abdominal pain + unexplained weight loss

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9
Q

Investigations and screening for colorectal cancer

A

Flexible colonoscopy GS, sigmoidoscopy, CT colonography. Staging: CT, MRI, PET-CT
Faecal immunochemical testing: human haemoglobin in stool; bowel cancer screening, 60-74, home FIT test every 2y - positive get colonoscopy
CEA tumour marker, only used for predicting relapse

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10
Q

Pathogenesis and presentation of appendicitis

A

Lumen of appendix obstructed by faecolith, lymphoid hyperplasia or filarial worms. Invasion of gut organisms to appendix wall. Inflammation leads to oedema, ischaemia, necrosis
If appendix ruptures then infected faecal matter will enter peritoneum

Pain in the umbilical region, migrates to right iliac fossa. More advanced will be localised at McBurney’s point (⅔ from umbilicus to ant superior iliac spine)
Anorexia, nausea and vomiting, constipation, fever
Tenderness (rebound / percussion = peritonitis) on examination maybe guarding, maybe mass

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11
Q

Diagnosis and management of appendicitis

A

Clinical diagnosis + bloods; CT gold standard to confirm or US
Blood - raised white cells, elevated ESR + CRP. bloods do not match symptoms - diagnostic laparoscopy

Emergency surgical removal - laparoscopically preferred, IV antibiotic preop
If mass present (omentum attached), IV fluids and antibiotics until mass disappears. Remove appendix later to prevent recurring

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12
Q

Causes of intestinal obstruction

A

Most common causes: adhesions (small), hernias (small), malignancy (large)
Intraluminal: tumours, diaphragm disease (multiple short circumferential lesions/ strictures cause narrowing, most often due NSAIDs), gallstone ileus (passes through fistula)
Intramural: Crohn’s (severe inflammation with fissuring ulcers), diverticulitis (mostly sigmoid, cave like pouches form, can rupture, probably low fibre and high pressure), some tumours, Hirschprung’s (lack of neural cells, becomes dilated and can’t contract)
Extramural: adhesions (abdominal strictures stick to each other/ bowel loops/ omentum, most common, often after surgery), volvulus (twist of bowel, sigmoid most common), peritoneal tumour

Functional - electrolyte imbalance, medication, recent surgery, neurological. Paralytic ileus

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13
Q

What is the pathophysiology of the complications of intestinal obstruction

A

Proximal dilation (increased secretions, decreased absorption, vessels compressed - oedema). Leads to ischaemia, necrosis, perforation
GI secretions cannot be reabsorbed in colon, fluid loss - hypovolaemia, the higher the obstruction the higher the fluid losses
Closed loop obstruction: unable to decompress, continual expansion - ischaemia and perforation

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14
Q

presentation of small and large bowel obstruction

A

Abdominal pain (diffuse), nausea + vomiting, absolute constipation, distension
Small: severe sudden onset, colicky pain, central pain, early vomiting (green bilious)
Large: chronic + slow onset, colicky vague pain, vomiting is delayed, constipation main

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15
Q

Investigations and management of intestinal obstruction

A

CT gold standard; X ray, upper limits allowed: 3cm small, 6cm colon, 9cm caecum
FBC (low Hb sign of chronic occult blood loss), U+Es, venous blood gas (metabolic acidosis - vomiting), lactate (bowel ischaemia)

Fluid resuscitation, bowel decompression, analgesia, antibiotics, nil by mouth + NG with drainage
Surgery, remove obstruction laparoscopically. Also to fix volvulus, stents
Conservative appropriate if patient stable and obstruction secondary to adhesions or volvulus

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16
Q

Presentation, investigations and management of diverticulitis

A

Diverticular disease usually asymptomatic, if not - pain in left iliac fossae, constipation
Acute diverticulitis - severe pain in LIF, fever, constipation / diarrhoea, n+v, rectal bleeding

If symptomatic: bloods: FBC - increased polymorphonuclear leukocytes, increased ESR + CRP, CT colonography best. Sigmoidoscopy / colonoscopy not performed during acute attack

Uncomplicated: co-amoxiclav, analgesia, only clear liquids
Severe symptoms: hospital admission, nil by mouth, IV co amoxiclav / cefuroxime, IV fluids, analgesia, urgent CT - surgery
High fibre diet, antispasmodic (mebeverine)

17
Q

What are types and pathogenesis of bowel ischaemia

A

3 main types: acute mesenteric ischaemia, chronic mesenteric ischaemia, ischaemic colitis. Mesenteric = small bowel, colitis = large bowel

Blood supply from inferior + superior mesenteric arteries, watershed (vulnerable areas): splenic flexure + caecum
Superior mesenteric artery thrombosis (most common), SMA embolism due to AF, mesenteric vein thrombosis (hypercoagulability), non-occlusive disease (poor cardiac output)

18
Q

Presentation, investigations and management for ischaemic bowel

A

Mesenteric, classic triad: acute severe abdominal pain (constant central / right iliac fossa), no abdominal signs, rapid hypovolaemia resulting in shock
Chronic mesenteric: central colicky abdo pain after eating, weight loss (food avoidance), abdominal bruit
Ischemic colitis: sudden lower left abdominal pain, passage of bright red blood without diarrhoea, signs of shock

CT angiography, blood gas (metabolic acidosis and raised lactate), colonoscopy + biopsy after treatment

Fluid resuscitation, antibiotics, heparin (reduce clotting), surgery to remove dead bowel, remove / bypass thrombus
Intestinal angina: lifestyle, statins + antiplatelets, revascularisation

19
Q

Describe anal fissures, anal fistulas, pilonidal abscess

A

Abnormal connection between epithelial anal canal and skin, blocked anal glands leading to infection that does not heal correctly
Pain, blood / mucus discharge, itch, can become systemic abscess
Fistulotomy + excision, drain abscess

Painful tear in sensitive skin liner lower anal canal (distal to denate line)
Hard faeces, spasms can constrict inferior rectal artery resulting in ischaemia
Extreme pain especially on defecation, bleeding
Increase fibre and fluids, lidocaine + GTN ointment

Hair follicles get stuck under the skin in the bum crack, irritation + inflammation, small tracts that can become infected
Painful swelling, foul smell (pus filled abscess). 40% have recurrent

20
Q

Describe mallory-weiss tear

A

Linear mucosal tear occurring at oesophagogastric junction produced by a sudden increase in intra abdominal pressure
Often following coughing / retching - alcoholic dry heaves
Vomiting followed by haematemesis, retching
Usually heal within 24 hours

21
Q

What is the pathophysiology / causes of gastric ulcers

A

Helicobacter pylori colonise the mucin layer, destroy mucin layer (release urease → ammonia - damages), increases gastrin/ parietal cell mass so more acid is released
NSAIDs inhibit cyclooxygenase 1 and reduce prostaglandin (stimulator for mucous release)
Ischaemia of gastric cells (atherosclerosis, hypotension), less mucin produced
RF: stress, alcohol, caffeine, smoking, spicy food