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Phase 2a Green Conditions > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is inflammatory bowel disease?

A
  • umbrella term for disease causing inflammation of the GI tract
  • associated with periods of remission and exacerbation
  • crohn’s and ulcerative colitis
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2
Q

Crohn’s vs UC: Crohn’s

A

NESTS

  • no blood or mucous (less common)
  • entire GI tract
  • skip lesions on endoscopy
  • terminal ileum most affected and transmural (full thickness) inflammation
  • smoking is a risk factor

also associated with weight loss, strictures and fistulas

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3
Q

Crohn’s vs UC: UC

A

CLOSEUP

  • continuous inflammation
  • limited to colon and rectum
  • only superficial mucosa affected
  • smoking is protective
  • excrete blood and mucus
  • use aminosalicyclates
  • primary sclerosing cholangitis
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4
Q

Presentation of inflammatory bowel disease

A
  • diarrhoea
  • abdominal pain
  • passing blood
  • weight loss
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5
Q

Testing for inflammatory bowel disease

A
  • routine bloods
  • CRP → inflammation and active disease
  • faecal calprotectin
  • DIAGNOSTIC = endoscopy (OGD/colonoscopy) with biopsy
  • imaging → complications
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6
Q

What is faecal calprotectin?

A
  • released by intestines when inflamed
  • >90% sensitive and specific to IBD in adults
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7
Q

What does management of IBD involve?

A
  • inducing remission
  • maintaining remission
  • surgery
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8
Q

Inducing remission in Crohn’s

A
  1. steroids → oral prednisolone, IV hydrocortisone
    - consider adding immunosuppressants
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9
Q

What immunosuppressants can be used in Crohn’s

A
  • mercaptopurine
  • azathioprinee
  • methotrexate
  • adalimumab
  • infliximab
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10
Q

Maintaining remission in Crohn’s

A

based on risks, side effects, nature of the disease, patient’s wishes

  1. azathioprine, mercaptopurine

alternatives = rest of the immunosuppressants

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11
Q

Surgery in Crohn’s

A
  • if only distal ileum affected → surgical resection of area to prevent further flare ups
  • treat stricture and fistulas
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12
Q

Inducing remission in UC

A

mild to moderate

  1. aminosalicylates eg mesalazine
  2. corticosteroids eg prednisolone

severe

  1. IV corticosteroids eg hydrocortisone
  2. IV ciclosporin
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13
Q

Maintaining remission in UC

A
  • aminosalicylates
  • azathioprine
  • mercaptopurine
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14
Q

Surgery in UC

A
  • removal of colon and rectum → panproctocolectomy
  • patient left with permanent ileostomy or ileo-anal anastomosis
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15
Q

What is IBS?

A
  • functional bowel disorder
  • no identifiable organic disease underlying symptoms
  • result of abnormal functioning of normal bowel
  • very common, more common if young/female
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16
Q

Symptoms of IBS

A

ABCDEF

  • abdominal pain
  • bloating
  • constipation
  • diarrhoea
  • eating makes it worse
  • fluctuating bowel habit
  • improved by opening bowels
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17
Q

Diagnostic criteria of IBS

A

diagnosis of exclusion

  • normal bloods
  • faecal calprotectin -ve
  • coeliac disease serology -ve
  • cancer not suspected/excluded
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18
Q

Management of IBS

A
  • general healthy diet and exercise advice
  1. loperamide for diarrhoea, linaclotide for constipation, antispasmodics for cramps
  2. tricyclic antidepressants
  3. SSRIs
    can also offer CBT
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19
Q

What is coeliac disease?

A
  • exposure to gluten = autoimmune reaction that causes inflammation in small bowel
  • usually develops in early childhood
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20
Q

Pathophysiology of coeliac disease

A
  1. auto-antibodies created in response to gluten
  2. target epithelial cells of the intestine → inflammation
  3. affects small bowel esp jejunum
  4. causes atrophy of intestinal villi and crypt hypertrophy
  5. malabsorption of nutrients → symptoms
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21
Q

Presentation of coeliac disease

A
  • often asymptomatic
  • failure to thrive in children
  • mouth ulcers
  • anaemia secondary to iron, B12, folate deficiency
  • dermatitis herpetiformis
  • neurological symptoms (rare)
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22
Q

What is dermatitis herpetiformis?

A

itchy blistering skin rash that typically appears on the abdomen

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23
Q

Diagnosis of coeliac

A
  1. raised anti-TTG
    - raised anti-EMA
    - total IgA levels → exclude IgA deficiency first
    - endoscopy and intestinal biopsy → crypt hypertrophy and villous atrophy
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24
Q

What conditions are associated with coeliac disease?

A
  • T1DM
  • thyroid disease
  • autoimmune hepatitis
  • PBC
  • PSC
  • Down’s syndrome
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25
Q

Complications of coeliac disease

A
  • vitamin deficiency
  • anaemia
  • osteoporosis
  • ulcerative jejunitis
  • non-hodgkin’s lymphoma
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26
Q

Treatment for coeliac diease

A

lifelong gluten free diet

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27
Q

What is GORD?

A
  • gastro-oesophageal reflux disease
  • acid from stomach refluxes through the lower oesophageal sphincter and irritates lining of oesophagus
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28
Q

Why is the oesophagus more sensitive to stomach acid?

A

the epithelial lining is squamous

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29
Q

Presentation of GORD

A
  • dyspepsia
  • heartburn
  • acid regurgitation
  • retrosternal/epigastric pain
  • bloating
  • nocturnal cough
  • hoarse voice
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30
Q

Diagnosis of GORD

A
  • clinical diagnosis
  • refer for endoscopy if red flags
31
Q

When would you refer for an endoscopy?

A
  • dysphagia
  • >55yrs
  • upper abdominal pain/reflux
  • treatment resistant dyspepsia
  • anaemia
  • raised platelets
32
Q

Management for GORD

A
  • lifestyle advice
  • acid neutralising medications → gaviscon, rennies
  • PPIs → reduce stomach acid eg omeprazole, lansoprazole
  • ranitidine = alternative to PPIs

surgery = laparascopic fundoplication → tie fundus of stomach around lower oesophagus → narrows lower oesophageal sphincter

33
Q

What lifestyle advice would you suggest for GI problems?

A
  • reduce tea, coffee, alcohol
  • weight loss
  • avoid smoking
  • smaller, lighter meals
  • avoid heavy meals before bed time
  • stay upright after meals
34
Q

What is a peptic ulcer?

A

ulceration of the mucosa of the stomach (gastric) or duodenum (duodenal)

duodenal are more common

35
Q

Risk factors of peptic ulcers

A
  • h.pylori
  • NSAIDs/SSRIs/steroids
  • smoking

gastric → stress
duodenal → alcohol

36
Q

Presentation of peptic ulcers

A

epigastric pain

  • gastric = worse on eating, relieved by antacids
  • duodenal = before meals and at night, relieved by eating/milk
  • N&V
  • dyspepsia
  • bleeding causing haematemesis, coffee ground vomiting, maelaena
  • iron deficiency anaemia
37
Q

Diagnosis of peptic ulcers

A
  • h.pylori test → urease breath test
  • endoscopy if red flags
38
Q

Treatment for peptic ulcers

A
  • lifestyle modification
  • treat cause
  • high dose PPIs
39
Q

Complications of peptic ulcer

A
  • haemorrhage
  • perforation
  • gastric outflow obstruction
  • malignancy
40
Q

What is appendicitis?

A
  • inflammation of the appendix
  • peak incidence = 10-20
  • less common in young children and adults over 50
41
Q

Pathophysiology of appendicitis

A
  1. pathogens can get trapped due to obstruction at the point where appendix meets bowel
  2. infection and inflammation
  3. may proceed to gangrene and rupture
  4. faecal contents and infective material are released into peritoneal cavity
  5. peritonitis → inflammation of peritoneal lining
42
Q

Signs and symptoms of appendicitis

A

KEY FEATURE = abdominal pain

  • loss of appetite
  • N&V
  • low-grade fever
  • Rovsing’s sign → palpation of LIF causes pain in RIF
  • guarding on palpation
  • rebound tenderness in RIF
  • percussion tenderness
43
Q

Describe abdominal pain in appendicitis

A
  • starts as central
  • moves down to RIF within first 24hrs
  • eventually becomes localised in RIF
  • on palpation → tenderness at McBurney’s point
44
Q

What is McBurney’s point

A

1/3 of the distance from the anterior superior iliac spine to the umbilicus

45
Q

Diagnosis of appendicitis

A
  • based on clinical presentation and raised inflammatory markers
  • GOLD STANDARD = CT → confirms diagnosis
  • US to exclude female pathology
46
Q

Differential diagnoses for appendicitis

A
  • ectopic pregnancy
  • ovarian cysts
  • Meckel’s diverticulum = malformation of distal ileum
  • mesenteric adenitis
47
Q

Management of appendicitis

A
  • appendicectomy
  • laparoscopic preferred → less risks and faster recovery
48
Q

Complications of appendidectomy

A
  • damage to other organs eg bowel, bladder
  • removal of normal appendix
49
Q

What is a diverticulum?

A
  • a pouch/pocket in the bowel wall
  • 0.5-1cm
  • diverticulosis = diverticula without inflammation or infection
  • diverticular disease = if patients have symptoms
  • diverticulitis = inflammation and infection of diverticula
50
Q

Pathophysiology of diverticula

A
  • wall of LI contains a layer of circular muscle
  • weaker in areas penetrated by blood vessels
  • increased pressure can cause a gap to form
  • mucus herniates through muscle layer and forms diveritcula

do not form in the rectum

51
Q

Diverticulosis

A
  • wear and tear of bowel
  • most commonly in sigmoid colon
  • diagnosis = colonoscopy or CT
  • treatment not needed if asymptomatic
  • high fibre diet, bulk-forming laxatives
52
Q

Presentation of diverticulitis

A
  • pain and tenderness in LIF
  • fever
  • D,N&V
  • rectal bleeding
  • palpable abdominal mass
  • rasied inflammatory markers
53
Q

Management of diverticulitis

A
  • oral co-amoxiclav (5 days)
  • analgesia (not NSAIDs or opiates)
  • clear liquids until symptoms improve

severe
- manage like acute abdomen/sepsis

54
Q

Complications of diverticulitis

A
  • perforation
  • peritonitis
  • peridiverticular disease
  • large haemorrhage
  • fistula
55
Q

What is acute gastritis?

A

acute inflammation of the stomach mucosa due to imbalance between mucus defence and acid

56
Q

Pathophysiology of acute gastritis

A
  • stomach usually lined by HCO3, prostaglandins and mucus barrier → protects against stomach acid
  • acid damage → superficial inflammation and can given erosions
  • loss of superficial layer
  • progression to ulcer
  • loss of mucosal layer
57
Q

Risk factors for acute gastritis

A
  • alcohol
  • drugs → NSAIDs, steroids
  • hiatus hernia
58
Q

Symptoms of acute gastritis

A
  • epigastric pain/discomfort
  • vomiting
  • heartburn
59
Q

Management of acute gastritis

A
  • PPIs/H2 blockers
  • decrease alcohol and tobacco
60
Q

What is chronic infective gastritis?

A
  • most common form of gastritis
  • caused by H.pylori → makes a urease enzyme
  • breaks down mucus defence
  • destroys protective layer
  • leads to chronic inflammation
61
Q

What can chronic inflammation lead to in gastritis?

A

increases risk of

  • gastric adenocarcinoma
  • MALT lymphoma
62
Q

Symptoms of chronic infective gastritis

A
  • epigastric pain
  • peptic ulcer disease
63
Q

Tests for chronic infective gastritis

A
  1. breath test
  • stool antigen, serology
  • histology from biopsy, CLO test → pH
64
Q

Management for chronic infective gastritis

A

tripe therapy to kill H.pylori

  • PPI → lansoprazole
  • amoxicillin
  • clarithromycin
65
Q

What is chronic autoimmune gastritis?

A
  • occurs due to autoimmune destruction of gastric parietal cells
  • T cells make antibodies against parietal cells and/or IFs → stomach atrophy

main problem = lack of IF → B12 deficiency

66
Q

Symptoms of chronic autoimmune gastritis

A
  • megaloblastic/pernicious anaemia (lack of IF)
  • mild jaundice
  • diarrhoea
  • sore tongue
67
Q

Management of chronic autoimmune gastritis

A
  • B12 injections
  • folic acid supplements
68
Q

What is Barrett’s oesophagus?

A
  • metaplasia of lower oesophagus mucosa
  • stratified squamous to columnar epithelium with goblet cells
69
Q

Risk factors for Barrett’s oesophagus

A
  • GORD
  • male
  • caucasian
  • family history
  • hiatus hernia
  • obesity
  • smoking
  • alcohol
70
Q

Presentation of Barrett’s oesophagus

A

classic history = middle aged caucasian male with long history GORD and dysphagia

71
Q

Investigations for Barrett’s oesophagus

A
  • oesophago-gastro-duodenoscopy
  • biopsy
72
Q

Management of Barrett’s oesophagus

A
  • lifestyle changes
  • endoscopic surveillance with biopsies
  • high dose PPIs
  • dysplasia → endoscopic mucosal resection, radiofrequency ablation
  • severe = oesophagectomy
73
Q

What lifestyle changes are needed in Barrett’s oesophagus?

A
  • weight loss
  • smoking cessation
  • reduce alcohol
  • small regular meals
  • avoid hot drinks/alcohol/eating <3hrs before bed
  • avoid nitrates, anticholinergics, TCAs, NSAIDs, K+ salts, alendronate

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