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Phase 2a > GI > Flashcards

GI Flashcards

1
Q

Diarrhoea definition

A

the abnormal passage of loose or liquid stool more than 3 times daily

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2
Q

Acute diarrhoea definition

A

lasting less than 2 weeks

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3
Q

Chronic diarrhoea definition

A

lasting MORE THAN 2 weeks

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4
Q

Acute diarrhoea

A
  • usually due to infection eg travellers diarrh
  • flexible sigmoidoscopy with colonic biopsy performed if symptoms persist and no diagnosis
  • treat: symptomatic, maintain hydration w/ anti-diarrhoeal agents (short term relief) and antibiotics for specific indications
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5
Q

Name an anti-diarrhoeal agent

A

Loperamide hydrochloride

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6
Q

Chronic diarrhoea

A
  • organic causes (changes structure organ or tissue resulting in symptoms-increased stool weights)
  • functional causes (no physical cause for symptoms - freq passage low volume and weight stools eg IBS)
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7
Q

Chronic diarrhoea - what can be used to differentiate between functional disorders and organic disease?

A

faecal markers of intestinal inflammation

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8
Q

Mechanisms of diarrhoea

A
  • infective cause
  • inflammatory cause
  • steatorrhea (fat in stool)
  • decreased stool consistency
  • secretion of fluids and electrolytes
  • functional (eg IBS)
  • inflammatory discharge
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9
Q

mechanisms of diarrhoea - infective cause

A
  • sudden onset bowel frequency
  • crampy abdo pains
  • fever
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10
Q

mechanisms of diarrhoea - inflammatory cause

A
  • bowel frequency

- loose, BLOOD STAINED stools

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11
Q

mechanisms of diarrhoea - steatorrhea

A
  • pale stools, offensive smell, increased gas
  • floating, hard to flush stool
  • loss of appetite and loss of weight
  • giardiasis, coeliac can cause
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12
Q

mechanisms of diarrhoea - decreased stool consistency caused by water/ osmosis

A
  • large quantities non absorbed hypertonic substances in bowel draw fluid into intestine
  • diarrhoea stops when patient stops eating or malabsorptive state discontinued
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13
Q

mechanisms of diarrhoea - decreased stool consistency caused by water/ osmosis - CAUSES

A
  • ingestion non absorbable substances eg laxative eg magnesium sulphate
  • generalised malabsorption - high concs of solute eg glucose remain in lumen
  • specific malabsorptive defect eg disaccharide deficiency
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14
Q

mechanisms of diarrhoea - decreased stool consistency caused by water / SECRETORY (microscopic colitis)

A
  • active intestinal secretion of fluid, electrolytes, also decreased absorption
  • continues even when patient fasts !!!
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15
Q

mechanisms of diarrhoea - decreased stool consistency caused by water / SECRETORY (microscopic colitis) - CAUSES

A
  • enterotoxins eg E coli, cholera toxin
  • bile salts in colon following ileal disease, resection, or idiopathic bile acid malabsorption
  • fatty acids in colon following ileal resection
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16
Q

mechanisms of diarrhoea - inflammatory discharge

A
  • damage to intestinal mucosal cell leads to loss of fluid and blood and defective absorption of fluid and electrolytes
  • causes: INFETIVE or INFLAMMATORY
  • infective: shigella, salmonella
  • inflammatory: UC or Crohn’s
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17
Q

INFECTIVE DIARRHOEA - epidemiology

A
  • 2nd leading cause death children under 5 globally (after pneumonia)
  • highest prevalence: south Asia, Africa
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18
Q

INFECTIVE DIARRHOEA - risk factors

A
  • foreign travel
  • PPI or H2 antagonist use
  • crowded area
  • poor hygiene
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19
Q

INFECTIVE DIARRHOEA- aetiology

A
  • children: rotavirus (leading cause diarrhoea young children, affects nearly all children by age 4) - there is a vaccine now !
  • adults: norovirus, campylobacter
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20
Q

what cause makes up the majority of diarrhoea illness?

A

viral causes

70% all infectious diarrhoea in paediatric age group world wide

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21
Q

INFECTIVE DIARRHOEA - viral causes

A
  • rotavirus (most common children)
  • norovirus ( most common adults, 10% child cases, associated w/ cruise ships, hospitals, restaurants (close proximity to others) )
  • adenovirus
  • astrovirus
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22
Q

INFECTIVE DIARRHOEA - bacterial causes

A
  • campylobacter jejuni (MOST COMMON cause bacterial diarrhoea, poultry)
  • E coli (more common children)
  • Salmonella (more common children)
  • Shigella spp. (more common children)
  • antibiotic associated
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23
Q

INFECTIVE DIARRHOEA - bacterial causes - antibiotic associated - what is the rule of C’s?

A

generally, antibiotics beginning with C can give rise antibiotic induced Clostridium difficile diarrhoea

  • clindamycin
  • ciprofloxacin (quinolones)
  • co-amoxiclav (penicillins)
  • cephalosporins
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24
Q

Clostridium difficile

A
  • gram positive spore forming bacteria
  • 5% have C diff part of normal flora
  • pseudomembranous colitis when C diff replaces normal gut flora (normal gut flora die due to antibiotic use) causing dangerous diarrhoea
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25
Q

C diff risk factors

A
  • elderly
  • antibiotic use
  • long hospital admission
  • immunocompromised eg HIV
  • acid suppression can contribute: PPI or H2 receptor antagonist
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26
Q

C diff treatment

A
  • metronidazole
  • oral vancomycin
  • rifampicin/ rifaximin
  • stool transplant
  • stop C antibiotic
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27
Q

Infective diarrhoea - parasitic causes

A
  • Giardia lamblia - most common
  • Entamoeba histolytica
  • Cryptosporidium
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28
Q

Diarrhoea - clinical presentation

A
  • blood usually indicates bacterial infection: salmonella, shigella, E coli = bloody stools
  • vomiting
  • abdominal cramping
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29
Q

Diarrhoea clinical presentation - viral causes

A
  • fever, fatigue, headache, muscle pain

- general incubation period 12-72 hours post infection

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30
Q

Diarrhoea clinical presentation - differential diagnosis

A
  • appendicitis, volvulus, IBD, UTI, diabetes mellitus
  • pancreatic insufficiency, short bowel syndrome, coeliac disease
  • laxative abuse
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31
Q

Diarrhoea - diagnosis - bloods

A
  • low MCV and or Fe deficiency - coeliac, colon cancer
  • high MCV if alcohol abuse or decreased B12 absorption eg coeliac, Crohns
  • raised WBC if parasitic
  • raised ESR, CRP indicate infection, Crohns, cancer, UC
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32
Q

Diarrhoea - diagnosis - stool

A

-if suspected bacteria, parasites of C diff toxin

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33
Q

Diarrhoea diagnosis - 3 tests

A
  • bloods
  • stool
  • sigmoidoscopy with biopsy
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34
Q

Diarrhoea - treatment

A
  • treat causes
  • oral rehydration, avoid high sugar drinks in children (increases diarrhoea)
  • anti emetics treat vomiting eg metoclopramide
  • antibiotics
  • anti motility agents eg loperamide hydrochloride
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35
Q

General pharmacology - PPIs

A

lansoprazole, omeprazole, pantoprazole

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36
Q

general pharmacology PPI indications

A
  • first line prevention and treatment for peptic ulcer disease
  • symptomatic relief of dyspepsia, GORD
  • eradication H pylori with antibiotics
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37
Q

general pharmacology - mechanisms of PPIs

A
  • reduces gastric acid secretion by irreversibly inhibiting H+/K+ ATPase in gastric parietal cells (proton pump responsible H+ secretion, generating gastric acid)
  • suppresses gastric acid production significantly
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38
Q

general pharmacology - adverse effects/contraindications PPIs

A
  • GI disturbances/headaches common
  • increasing gastric pH may reduce body’s host defence against infection - slightly higher C diff risk
  • PPIs may disguise symptoms gastric cancer
  • increased fracture risk elderly (use with care if osteoporosis present)
  • can reduce antiplatelet effect of clopidogrel esp omeprazole so prescribe diff PPI
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39
Q

general pharmacology - H2 receptor antagonists

A

ranitidine

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40
Q

general pharmacology -H2 receptor antagonists indications

A

treatment, prevention gastric and duodenal ulcers, NSAID associated ulcers if PPIs are contraindicated

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41
Q

general pharmacology - H2 receptor antagonists - mechanisms

A
  • H+/K+ proton pump regulated by histamine which binds H2 receptors on parietal cells, activates pump
  • blocking receptor reduces activation of cell
  • does not completely suppress secretion (PP can be stimulated by other pathways) (PPIs produce more complete effect)
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42
Q

general pharmacology - H2 receptor antagonists - adverse effects/ contraindications

A
  • possible bowel disturbance, headache, dizziness
  • reduce dose in renal impairment
  • watch for symptoms gastric cancer - H2 antagonist can disguise these
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43
Q

general pharmacology - alginates/ antacids

A

gaviscon, peptac

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44
Q

general pharmacology - alginates/ antacids - indications

A
  • for GORD symptomatic relief heartburn

- short term relief indigestion, dyspepsia

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45
Q

general pharmacology - alginates / antacids - mechanisms

A
  • compound preparation alginate w/ one or more antacid eg calcium bicarbonate, magnesium, aluminium salts
  • alginates increase viscosity stomach contents - reduces reflux stomach acid into oesophagus
  • react with stomach acid, form floating raft separates gastric contents from G-O junction to prevent mucosal damage
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46
Q

general pharmacology - alginates/ antacids - adverse effects/ contraindications

A
  • Mg can cause diarrhoea
  • Al can cause constipation
  • Na, K containing compounds use with caution in fluid overload or hyperkalaemia ie in renal failure
  • antacids may reduce conc of ACEi, antibiotics, PPIs, bisphosphonates, digoxin so take dose at different times
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47
Q

general pharmacology - anti motility drugs

A

loperamide, codeine phosphate

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48
Q

general pharmacology - anti motility drugs - indications

A

-as symptomatic treatment of diarrhoea, usually for IBS, or GASTROENTERITIS

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49
Q

general pharmacology - anti motility drugs - mechanisms

A

loperamide = opioid but does not penetrate CNS so no analgesic effects, just an agonist of opioid receptors in GI tract- increases non propulsive contractions gut smooth muscle, reduces peristaltic contractions - transit of bowel content slowed, anal sphincter tone increased, more water absorbed from faeces as more time for this to occur so stools harden
-codeine same effect but also analgesic

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50
Q

general pharmacology - anti motility drugs - adverse effects/ contraindications

A
  • most side effects are GI disturbances, mild
  • should be avoided in acute UC, where inhibition of peristalsis may result in megacolon and perforation, should also be avoided if risk of C diff or other bacterial infection
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51
Q

general pharmacology - bile acid

A

ursodeoxycholic acid

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52
Q

general pharmacology - bile acid - indications

A
  • used in primary biliary cirrhosis

- reduction in liver biochemistry, jaundice, ascites, itching

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53
Q

general pharmacology - bile acid - mechanisms

A
  • ursodeoxycholic acid reduces cholesterol absorption - used to dissolve cholesterol gallstones as alternative to surgery (but tend to recur so surgery still preferred)
  • normally in body helps regulate cholesterol by reducing rate at which intestine absorbs cholesterol molecules, while breaking up micelles containing cholesterol
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54
Q

general pharmacology - bile acid - adverse effects / contraindications

A
  • nausea, diarrhoea, very rarely gallstone calcification
  • contraindicated in gallbladder impairment, calcium gallstones, severe liver impairment
  • use with care in oral contraceptives, antacids, immunosuppressants, lipid regulating drugs as can decrease their effectiveness
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55
Q

gastro-oesophageal reflux disease - GORD - epidemiology

A
  • common
  • reflux stomach acid with/without bile causes troublesome symptoms (2 or more heartburn episodes a week) and/or complications
  • reflux gastric contents normal but when prolonged contact gastric contents with mucosa results in clinical symptoms
  • prolonged reflux may = oesophageal stricture, Barrett’s oesophagus
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56
Q

GORD - causes

A
  • lower oesophageal sphincter hypotension
  • hiatus hernia
  • loss oesophageal peristaltic function
  • abdominal obesity
  • gastric acid hypersecretion
  • slow gastric emptying
  • overeating
  • smoking, alcohol
  • pregnancy
  • fat, coffee, chocolate
  • drugs eg antimuscarinic, calcium channel blockers, nitrates
  • systemic sclerosis
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57
Q

GORD causes - hiatus hernia - sliding hiatus hernia

A
  • 80%
  • where G-O junction and part of stomach slides up into chest via the hiatus so that it lies above the diaphragm
  • acid reflux often happens as lower oesophageal sphincter becomes less competent in many cases
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58
Q

GORD causes - hiatus hernia - rolling or para oesophageal hiatus

A
  • 20%
  • G-O junction remains in abdomen but part of fundus of stomach prolapses through hiatus alongside oesophagus
  • as G-O junction remains in tact, reflux is uncommon
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59
Q

GORD - NORMAL physiology of stomach and oesophagus

A
  • between swallows, muscles of oesophagus relaxed EXCEPT muscles upper, lower oesophageal sphincters
  • LOS in distal oesophagus remains closed, unique property of muscle, relaxes when swallowing initiated
  • LOS relaxation part of normal physiology , some transient lower oesophageal relaxations are normal
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60
Q

GORD - pathophysiology

A
  • many more transient lower oesophageal sphincter (LOS) relaxations as LOS has reduced tone - allows gastric acid to flow back into oesophagus
  • clinical features appear when anti reflux mechanisms, thus prolonged contact acid gastric contents and LO mucosa
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61
Q

GORD - pathophysiology - contributing factors

A
  • LOS relaxes transiently, independently of a swallow, after meals
  • increased mucosal sensitivity to gastric acid and reduced oesophageal clearance acid contribute
  • delayed gastric emptying, prolonged post-eating and nocturnal reflex also contribute
  • hiatus hernia can impair anti reflux mechanisms (contributes)
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62
Q

GORD - clinical presentation - oesophageal symptoms

A

oesophageal :

  • heartburn (burning chest pain aggravated by bending, stooping, lying down (promote acid exposure) may be relieved by antacids. Worse with hot drinks or alcohol. Seldom radiates to arms.)
  • belching
  • food/acid brash(food/acid/bile regurgitation)
  • water brash (increased salivation)
  • odynophagia (painful swallowing)
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63
Q

GORD - clinical presentation - extra oesophageal symptoms

A
  • nocturnal asthma
  • chronic cough
  • laryngitis (hoarseness, throat clearing)
  • sinusitis
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64
Q

GORD - differential diagnosis

A
  • coronary artery disease (CAD)
  • biliary colic
  • peptic ulcer disease
  • malignancy
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65
Q

GORD - diagnosis

A
  • usually made without investigation provided no red flags eg weight loss, haematemesis, dysphagia
  • patients under age 45 can safely be treated initially without investigation
  • red flags need to investigate
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66
Q

GORD diagnosis - red flag investigations

A

endoscopy:
- symptoms for more than 4 weeks
- red flags - dysphagia, weight loss, haematemesis
- persistant vomiting
- GI bleeding
- palpable mass
- over 55
- symptoms despite treatment
- barium swallow may show hiatus hernia

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67
Q

GORD diagnosis - red flag investigations - aims of investigations

A
  • assess oesophagitis and hiatus hernia by endoscopy, if oesophagitis or Barret’s oesophagus then reflux is confirmed
  • document reflux by intraluminal monitoring - 24hr oesophageal pH monitoring helpful in diagnosing GORD when endoscopy normal or just prior to surgery to confirm reflux - also helpful if no response to PPIs
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68
Q

What is name of classification system used to classify GORD?

A

The Los Angeles classification of GORD/oesophagitis - when doing endoscopy to gauge extent of damage

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69
Q

GORD - treatment - lifestyle changes

A
  • encourage weight loss
  • smoking cessation
  • small, regular meals
  • avoid hot drinks, alcohol, citrus fruits and eating less than 3 hours before bed
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70
Q

GORD - treatment - pharmacology

A
  • antacids (eg magnesium trisilicate mixture - forms gel/ foam raft with gastric contents to reduce reflux - diarrhoea side effect)
  • alginates (eg gaviscon - relives symptoms)
  • PPIs (lansoprazole to reduce gastric acid production)
  • H2 receptor antagonists (cimetidine - blocks histamine receptors on parietal cells, reducing acid release)
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71
Q

GORD treatment - surgery

A
  • Nissen fundoplication - aims to laparoscopically increase resting LOS pressure - only in severe GORD
  • use when not responding to therapy
  • complications include dysphagia, bloating
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72
Q

GORD complications - peptic stricture

A
  • oesophagitis resulting from gastric acid exposure causing narrowing thus stricture of oesophagus
  • usually occurs in 60+ age
  • presents as gradually worsening dysphagia
  • treat with endoscopic dilatation and long term PPI therapy
73
Q

GORD complications - Barret’s oesophagus

A
  • distal oesophageal epithelium undergoes metaplasia from squamous to columnar
  • always a hiatus hernia present
  • risk of progressing to oesophageal CANCER - its premalignant for adenocarcinoma of oesophagus
74
Q

Gastritis

A
  • inflammation that is associated with mucosal injury
  • gastropathy indicates epithelial cell damage and regeneration without inflammation - commonest cause is mucosal damage associated with NSAIDs/ Aspirin
75
Q

Gastritis - causes

A
  • Helicobacter pylori infection
  • Autoimmune gastritis
  • Viruses eg CMV, herpes simplex
  • Duodenogastric reflux - bile salts enter stomach, damage mucin protection = gastritis
  • Specific causes eg Crohns
  • Mucosal ischaemia (reduced blood supply to mucosal cells = less mucin produced)
  • Increased acid (overwhelms mucin, stress can increase acid production)
  • Aspirin and other NSAIDs eg naproxen
  • Alcohol
76
Q

Gastritis - pathophysiology - H pylori infection

A

Helicobacter pylori infection - most common cause - causes severe inflamm response
-gastric mucus degradation, increased mucosal permeability, directly cytotoxic to gastric epithelium (H pylori produces urease - converts urea to ammonia and CO2 which is toxic since ammonia and H+ form ammonium - toxic to gastric mucosa resulting in less mucus produced)

77
Q

Gastritis pathophysiology - autoimmune gastritis

A

-affects fundus and body of stomach leading to atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia (low RBC due to low B12)

78
Q

Gastritis pathophysiology - aspirin and other NSAIDs eg naproxen

A

-inhibit prostaglandins (which stimulate mucus production) via inhibition of cyclo-oxygenase = less mucus production thus gastritis

79
Q

Gastritis - clinical presentation

A
  • nausea or recurrent upset stomach
  • abdominal bloating
  • epigastric pain
  • vomiting
  • indigestion
  • haematemesis
80
Q

Gastritis - differential diagnosis

A
  • peptic ulcer disease (PUD)
  • GORD
  • non ulcer dyspepsia
  • gastric lymphoma
  • gastric carcinoma
81
Q

Gastritis - diagnosis

A
  • endoscopy - will be able to see gastritis
  • biopsy
  • H pylori urea breath test
  • H pylori stool antigen test
82
Q

Gastritis - treatment

A
  • remove causative agent eg alcohol
  • reduce stress
  • H pylori eradication (7-14 days) eradication confirmed by urea breath or faecal antigen test
83
Q

Gastritis - pharmacological treatment - ‘triple therapy’

A

TRIPLE THERAPY:
PPI for acid suppression eg lansoprazole
plus 2 from: metronidazole, clarithromycin, amoxicillin, tetracycline, bismuth
(quinolones eg ciprofloxacin, furozolidone, rifabutin used when standard regimes failed as ‘rescue therapy’
note: amoxicillin, tetracycline have low resisitance

84
Q

Gastritis - standard pharmacological treatment

A
  • H2 antagonists eg ranitidine, cimetidine
  • PPIs eg lansoprazole, omeprazole
  • antacids
85
Q

Gastritis - prevention

A

-Give PPIs alongside NSAIDs - also prevents bleeding from acute stress ulcers and gastritis which is often seen with ill patients - esp burns patients

86
Q

MALABSORPTION

A

the failure to fully absorb nutrients either because of destruction to epithelium or due to a problem in the lumen meaning food cannot be digested
! before malabsorption is diagnosed, insufficient intake must be ruled out !

87
Q

Malabsorption - disorders of the small intestine resulting in malabsorption

A
  • coeliac disease
  • Tropical Sprue
  • Crohn’s
  • Parasite infection
88
Q

Malabsorption - 5 umbrella causes

A
  • defective intraluminal digestion
  • insufficient absorptive area
  • lack of digestive enzymes
  • defective epithelial transport
  • lymphatic obstruction
89
Q

Malabsorption causes - defective intraluminal digestion - 3 causes

A
  • pancreatic insufficiency
  • defective bile secretion (lack of fat solubilisation)
  • bacterial overgrowth
90
Q

Malabsorption causes - defective intraluminal digestion - pancreatic insufficiency

A
  • pancreas produces majority of digestive enzymes eg amylase (starch)
  • Pancreatitis causes damage to most of glandular pancreas meaning less/ no enzymes released
  • Cystic fibrosis results in blockage of pancreatic duct due to excess mucus - enzymes fail to be released
91
Q

Malabsorption causes - defective intraluminal digestion - defective bile secretion (lack of fat solubilisation)

A
  • biliary obstruction eg gall stones

- ileal resection - we absorb bile salts in the terminal ileum so if removed then bile salt reuptake will be decreased

92
Q

Malabsorption causes - insufficient absorptive area - 4 causes

A

Essentially anything that damages microvilli and villi thereby reducing absorptive surface area and thus absorption potential :

  • Coeliac disease
  • Crohn’s disease
  • Giardia lamblia
  • Surgery
93
Q

Malabsorption causes - insufficient absorptive area - Coeliac disease

A
  • gluten sensitive enteropathy
  • villi are very short if present at all
  • villous atrophy, crypt hyperplasia
  • lots of lymphocytes in the epithelium
94
Q

Malabsorption causes - insufficient absorptive area - Crohn’s disease

A
  • causes inflammatory damage to the lining of the bowel
  • results in cobblestone mucosa
  • significant reduction absorptive surface
95
Q

Malabsorption causes - insufficient absorptive area - Giardia lamblia

A
  • Extensive surface parasitisation of the villi and microvilli
  • parasites coat the surface of the villi thus food cannot be absorbed
96
Q

Malabsorption causes - insufficient absorptive area - surgery

A

-small intestine resection or bypass in small bowel infarction

97
Q

Malabsorption causes - lack of digestive enzymes

A
  • Disaccharide deficiency (lactose intolerance) - cannot break lactose in milk down to glucose which can then be absorbed
  • undigested lactose passes into colon - then eaten up by bacteria and CO2 is released = wind and diarrhoea
  • bacterial overgrowth resulting in brush boarder damage
98
Q

Malabsorption causes - defective epithelial transport

A
  • Abetalipoproteinaemia - lack of transporter protein to transport lipoprotein across cell
  • primary bile acid malabsorption - mutations in bile acid transporter protein
99
Q

Malabsorption causes - lymphatic obstruction

A
  • lymphoma

- tuberculosis

100
Q

Coeliac disease / gluten sensitive enteropathy

A

-inflammation of mucosa of upper small bowel that improves when gluten is withdrawn from the diet or replases when gluten is reintroduced

101
Q

Coeliac disease / gluten sensitive enteropathy

A

-T cell mediated autoimmune disease of small bowel in which PROLAMIN (alcohol soluble proteins in wheat barley rye oats) intolerance causes villous atrophy and malabsorption
Prolamins= gliadin in wheat, hordeins in barley, secalins in rye
Prolamin is a component of gluten protein

102
Q

Coeliac - when to suspect

A

in ALL diarrhoea, weight loss, anaemia (esp if iron, B12 deficient)

103
Q

Coeliac - epidemiology

A

around 1% population affected
occurs any age,peaks in infancy and 50-60y
affects males and females equally
10% risk in 1st degree relatives, 30% risk in siblings

104
Q

Coeliac - causes

A

GLUTEN found in wheat, barley, rye

105
Q

Coeliac - risk factors

A
  • other autoimmune diseases (having one increases risk of others) eg type 1 diabetes, thyroid disease, Sjorgrens
  • IgA deficiency
  • breast feeding
  • age of introduction to gluten in diet
  • rotavirus infection in infancy increases risk
106
Q

Coeliac - pathophysiology overview

A

in wheat, in gluten the prolamin a-gliadin is toxic and resistant to digestion by pepsin and chymotrypsin due to their high glutamine and proline content and remain in intestinal lumen thereby triggering immune response

107
Q

Coeliac - specific pathophysiology

A
  • gliadin peptides pass through epithelium, are deaminated by tissue transglutaminase, increases their immunogenicity
  • gliadin peptides bind to antigen presenting cells which interact with CD4 T cells in the lamina propria via HLA class II molecules DQ2 or DQ8
  • HLA class II molecules activate the gluten sensitive T cells, which produce pro inflammatory cytokines, initiate an inflammatory cascade
108
Q

Coeliac - specific pathophysiology

A

inflmm cascade initiated by the T cells releases metaloproteinkinases and other mediators which contribute to villous atrophy, crypt hyperplasia, intraepithelial lymphocytes

  • mucosa of proximal small bowel predom effected, mucosal damage can mean B12, folate, iron cant be absorbed - anaemia
  • mucosal damage decreases in severity towards ileum - gluten is digested into small ‘non toxic’ fragments
109
Q

Coeliac - clinical presentation

A
  • 1/3rd are asymptomatic (detected routine bloods - raised MCV)
  • stinking stools/fatty stools (steatorrhea)
  • diarrhoea
  • abdominal pain
  • bloating
  • nausea and vomiting
  • angular stomatitis
  • weight loss
  • fatigue
  • anaemia
  • osteomomalacia
  • dermatitis hepetiformis
110
Q

Coeliac - clinical presentation - OSTEOMALACIA

A
  • softening of bones due to impaired bone metabolism due to LACK OF PHOSPHATE, CALCIUM and VITAMIN D
  • leads to osteoporosis (40-60% risk in untreated patients - fracture risk)
111
Q

Coeliac - clinical presentation - dermatitis hepetiformis

A

red raised patches often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks

112
Q

Coeliac - diagnosis

A

! must maintain gluten ingestion for at least 6 weeks before testing to get true results !

  • FBC
  • duodenal biopsy (gold standard)
  • serum antibody testing
113
Q

Coeliac diagnosis - blood tests

A

FBC :

  • low Hb
  • low B12
  • low ferritin
114
Q

Coeliac diagnosis - duodenal biopsy

A
  • gold standard for diagnosis
  • see villous atrophy, crypt hyperplasia, increased intraepithelial white cell count
  • all reverse on gluten free diet
115
Q

Coeliac diagnosis - serum antibody testing

A

-indications: persistant diarrhoea, folate or iron deficiency and family history of coeliac disease or associated autoimmune disease
-most sensitive test (95% sensitive unless patient IgA deficient)
-endomysial antibody (EMA)
-tissue transglutaminase antibody (tTG)
both are IgA antibodies, correlate with severity of mucosal damage -can be used for dietary monitoring

116
Q

Coeliac treatment

A
  • lifelong gluten free diet
  • correction mineral, vitamin deficiencies
  • DEXA scan
117
Q

Coeliac treatment - lifelong gluten free diet

A
  • no prolamins - use serum antibody testing for monitoring
  • eliminate wheat barley rye
  • poor compliance main reason for issues
  • oats usually tolerated unless contaminated with flour during production
  • meat dairy fruit veg all fine
118
Q

Coeliac treatment - correction of vitamin and mineral deficiencies

A

-B12, folate, iron, calcium, vitamin D

119
Q

Coeliac disease - complications

A
  • few patients do not improve on strict diet = non responsive coeliac disease
  • anaemia
  • secondary lactose intolerance
  • T cell lymphoma
  • increased risk of malignancy (gastric, oesophageal, bladder, breast, brain) due to increased cell turnover
  • OSTEOPOROSIS
120
Q

Tropical Sprue - epidemiology

A
  • reserved for severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition
  • residents or visitors to tropical areas where disease is endemic
  • most of Asia, some Caribbean islands, Puerto Rico, some South America
  • unknown cause, likely infective - occurs in epidemics, pts improve on antibiotics
121
Q

tropical sprue - pathophysiology

A
  • villous atrophy with malabsorption
  • acute onset, few days or many years after being in tropics
  • epidemics break out in villages, thousands affected at same time
122
Q

tropical sprue - clinical presentation

A
  • diarrhoea
  • anorexia
  • severe malabsorption
  • weight loss
  • abdominal distension
  • onset can be insidious - chronic diarrhoea, evidence nutritional deficiency
123
Q

tropical sprue - diagnosis

A
  • exclude acute infective causes of diarrhoea eg Giardia intestinalis - can produce similar syndrome
  • bloods
  • jejunal biopsy
124
Q

tropical sprue - diagnosis - bloods

A

-anaemia due to malabsorption B12, folate, iron

125
Q

tropical sprue - diagnosis - jejunal biopsy

A

-abnormal jejunal mucosa - partial villous atrophy (complete atrophy in coeliac)

126
Q

tropical sprue - treatment

A
  • leave area
  • daily FOLIC ACID
  • antibiotic eg tetracycline - ensure complete recovery - for up to 6 months
  • severe cases - resus with fluids, electrolytes, nutritional deficiencies corrected eg B12 given
  • excellent prognosis
  • mortality only associated water, electrolyte depletion esp in epidemics
127
Q

INFLAMMATORY BOWEL DISEASE (IBD)

A
  • two major forms - both CHRONIC AUTOIMMUNE CONDITIONS
  • ulcerative colitis
  • Crohn’s disease
128
Q

IBD - epidemiology

A
  • jewish people more prone to IBD than any other ethnic group
  • IBD occurs when mucosal immune system exerts an inappropriate response to luminal antigens eg bacteria which may enter mucosa via leaky epithelium
129
Q

IBD - UC

A
  • relapsing, remitting inflamm disorder colonic mucosa
  • may just affect rectum - proctitis (50%)
  • may affect rectum and left colon - left sided colitis - 30%
  • may affect entire colon - up to ileocaecal valve - pancolitis/extensive colitis (20%)
130
Q

IBD - UC - can UC affect bowel proximal to the ileocaecal valve?

A

No - NEVER

UC only affects colon - large bowel

131
Q

IBD - UC epidemiology

A
  • highest incidence, prevalence Northern Europe, UK, North America
  • higher incidence than Crohns per year
  • affects males and females equally
  • present mostly 15-30y
  • 3 times more common non/ex smokers-symptoms may relapse on stop of smoking
  • unknown cause
  • 1 in 6 have first degree relative with UC
132
Q

IBD - UC epidemiology - an appendicectomy

A
  • an appendicectomy appears to be PROTECTIVE against development of UC - esp if performed for appendicitis before 20y
  • also leads lower incidence colectomy, reduced need for immunosuppressants
133
Q

IBD - UC risk factors

A
  • family history
  • NSAIDs - associated w onset IBD, flares
  • chronic stress, depression triggers flares
134
Q

IBD - UC pathophysiology

A

Restricted mucosal disease differentiates it from crohns

  • macroscopic
  • microscopic
135
Q

IBD - UC pathophysiology macroscopic

A
  • affects only colon to ileocaecal valve
  • begins in rectum - extends
  • CIRCUMFERENTIAL and CONTINUOUS INFLAMMATION - no skip lesions
  • mucosa red, infalmmed, bleeds easily
  • ulcers, pseudo-polyps (regenerating mucosa) in severe disease
136
Q

IBD - UC pathophysiology microscopic

A
  • mucosal inflammation - does not go deeper, not transmural
  • no granulomata (rare)
  • depleted goblet cells
  • increased crypt abscesses
137
Q

IBD - UC clinical presentation

A
  • runs course of remissions & exacerbations
  • restricted pain - usual lower left quadrant
  • episodic or chronic diarrhoea w/ blood and mucus
  • cramps
  • bowel frequency linked to severity
138
Q

IBD - acute UC/ acute attack clinical presentation

A
  • acute UC may be fever, tachycardia, tender distended abdomen
  • acute attack - bloody diarrhoea (10-20 liquid stools per day), diarrhoea at night w/ urgency, incontinence= severely disabling
139
Q

IBD - UC clinical presentation - extra intestinal signs

A
  • clubbing
  • aphthous oral ulcers
  • erythema nodusum (red round lumps below skin surface)
  • amyloidosis
140
Q

IBD - UC complications

A
  • liver
  • colon
  • joints
  • skin
  • eyes
141
Q

IBD - UC complications - liver

A
  • fatty change
  • chronic pericholangitis
  • sclerosing cholangitis
142
Q

IBD - UC complications - colon

A
  • blood loss
  • perforation
  • toxic dilatation
  • colorectal cancer
143
Q

IBD - UC complications - skin

A
  • erythema nodusum (red round lumps below skin surface)

- pyoderma gangrenosum (painful ulcers on skin)

144
Q

IBD - UC complications - joints

A
  • ankylosing spondylitis

- arthritis

145
Q

IBD - UC complications - eyes

A
  • iritis (iris inflammation)
  • uveitis (inflammation middle layer of eye -uvea)
  • episcleritis
146
Q

IBD - UC differential diagnosis

A

-alternative causes of diarrhoea should be excluded eg Salmonella spp, Giardia intestinalis, Rotavirus

147
Q

IBD - UC diagnosis

A
  • blood tests
  • stool samples
  • faecal calprotectin
  • colonoscopy w/ mucosal biopsy
  • abdominal X ray
148
Q

IBD - UC diagnosis - blood tests

A
  • WBC/ platelets raised in moderate/severe attacks
  • iron deficiency anaemia
  • ESR and CRP raised
  • liver biochemistry may be abnormal
  • hypoalbuminaemia in severe disease
  • pANCA (anti neutrophilic cytoplasmic antibody) may be positive - in crohns this is negative
149
Q

IBD - UC diagnosis - stool sample

A

to exclude C diff and Campylobacter

150
Q

IBD - UC diagnosis - faecal calprotectin

A

indicates IBD but not specific

151
Q

IBD - UC diagnosis - colonoscopy with mucosal biopsy

A
  • GOLD STANDARD for diagnosis
  • allows assessment disease activity and extent
  • can see inflamm infiltrate, goblet cell depletion, crypt abscesses, mucosal ulcers
152
Q

IBD - UC diagnosis - abdominal X ray

A
  • in all patients suffering severe acute attacks to exclude colonic dilatation
  • useful when UC too severe for colonoscopy
153
Q

IBD - UC treatment

A
  • aim to induce remission
  • aminosalicylate acts topically in colon lumen
  • active component is 5-aminosalicylic acid (5-ASA) which is absorbed in small intestine
  • preparations designed to deliver active 5-ASA to colon by binding something else
  • Sulfasalazine, Mesalazine, Olsalazine
154
Q

IBD - UC treatment of mild / moderate

A
  • oral 5-ASA - first line for left sided/extensive
  • rectal 5-ASA - for proctitis
  • glucocorticoid eg oral prednisolone if do not respond to 5-ASA
155
Q

IBD - UC treatment of severe

A

glucocorticoid eg oral prednisolone

156
Q

IBD - UC treatment of severe with systemic features eg liver, skin, eye involvement

A
  • hydrocortisone
  • ciclosporin
  • infliximab
157
Q

IBD - UC treatment to maintain remission

A
  • 5-ASA - most patients require maintenance treatment

- azathioprine - patients who relapse despite 5-ASA treatment / ASA intolerant

158
Q

IBD - UC treatment - surgery

A
  • indicated for severe colitis that fails to respond to treatment
  • colectomy w/ ileoanal anastamosis (terminal ileum used to form reservoir pouch to store faeces - pt remains continent)
  • Panproctocolectomy with ileostomy - whole colon and rectum removed, ileum brought out onto abdominal wall as a stoma
159
Q

INTESTINAL OBSTRUCTION

A

Arrest/ blockage of onward propulsion of intestinal contents

160
Q

Intestinal obstruction - classification of obstruction

A
  • According to site
  • Extent of luminal obstruction
  • According to mechanism
161
Q

Intestinal obstruction classification - according to site

A

large bowel, small bowel, gastric

162
Q

intestinal obstruction classification - extent of luminal obstruction

A
  • partial

- complete - volvulus can result in this, resulting in overflow and sickness

163
Q

intestinal obstruction classification - according to mechanism

A
  • mechanical
  • true (intraluminal / extraluminal)
  • functional (paralytic ileus - adynamic bowel due to absence of normal peristaltic contractions, caused by abdo surgery or acute pancreatitis)
164
Q

intestinal obstruction classification - according to pathology

A
  • simple
  • closed loop
  • strangulation
  • intussusception (one hollow structure into its distal hollow structure, usually seen in children as bowel is softer)
165
Q

intestinal obstruction - pathology

A
  • obstruction of lumen
  • disease in wall of bowel causing obstruction
  • outside bowel which causes obstruction
166
Q

intestinal obstruction pathology - obstruction of lumen

A
  • tumors: carcinoma, lymphoma
  • diaphragm disease
  • meconium ileus (neonates sticky bowel contents causes blockage)
  • gallstone ileus (gallstone within lumen small bowel)
167
Q

intestinal obstruction pathology - disease in wall of bowel causing obstruction

A
  • INFLAMMATORY eg crohns, diverticulitis
  • TUMORS
  • NEURAL (Hirschprungs)
168
Q

intestinal obstruction pathology - disease in wall of bowel causing obstruction - DIVERTICULITIS (OUTPOUCHING)

A
  • usually in sigmoid colon
  • diviticular forms at gaps in wall of gut where blood vessels penetrate
  • low fibre diet-colon must push harder to move things along-pressure increases- which pushes mucosa through gaps
  • outpouching can get inflamed/burst = acute peritonitis, possible death
169
Q

intestinal obstruction pathology - disease in wall of bowel causing obstruction - NEURAL - HIRSCHPRUNG’S DISEASE

A
  • neonates born without complete innervation of colon to rectum
  • gut dilatation, filling of faeces which remains-no ganglion cells to cause peristalsis/ movement of contents
170
Q

intestinal obstruction pathology - something outside the bowel which causes obstruction

A
  • adhesions
  • volvulus
  • tumor (peritoneal tumor seen in ovarian carcinoma)
171
Q

intestinal obstruction pathology - something outside the bowel which causes obstruction - ADHESIONS

A
  • abdominal structures sticking to each other, bowel loops, omentum, other solid organs or abdominal wall by fibrous tissue
  • common post surgery
  • intestines no longer able to move around freely, at site of adhesion-intestine can twist on itself-obstruction of blood supply/ normal movement of contents
  • in particular small intestines
172
Q

what is the MOST COMMON CAUSE OF OBSTRUCTION IN ADULTS?

A

ADHESIONS - (80% caused by adhesions)

173
Q

intestinal obstruction pathology - something outside the bowel which causes obstruction - VOLVULUS

A
  • twist/rotation of segment of bowel eg sigmoid which is on a long mesentery can twist on itself causing obstruction
  • ALWAYS at part of bowel w/ mesentery
  • ‘closed loop bowel obstruction’
174
Q

Intestinal obstruction - general facts

A
  • most due to mechanical block
  • one of most common causes hospital admis
  • tinkling bowel sounds, tympanic percussion typical of obstruction
175
Q

SMALL BOWEL OBSTRUCTION - epidemiology

A
  • 60-75% intestinal obstruction
  • majority caused by previous surgery
  • Crohns disease significant cause
176
Q

SMALL BOWEL OBSTRUCTION - main causes

A
  • Adhesions (60%) (usually 2ndry to prev abdo surgery - esp pelvic, gynae, colorectal surgery)
  • Hernia (abnormal protrusion of organ/tissue out of body cavity in which normally lies, developing world, untreated can cause strangulation)
  • Malignancy
  • Crohn’s disease
177
Q

SMALL BOWEL OBSTRUCTION - pathophysiology

A
  • mechanical obstruction most common eg adhesions, hernia, crohns
  • obstruction, bowel distension above block, increased secretion of fluid into distended bowel
  • also proximal dilatation above block
178
Q

small bowel obstruction pathophysiology - proximal dilatation above block leads to ?

A
  • increased secretions and swallowed air in small bowel
  • decreased absorption, mucosal wall oedema
  • increased pressure with intramural vessels becoming compressed = ischaemia and or perforation

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