GI Flashcards
Diarrhoea definition
the abnormal passage of loose or liquid stool more than 3 times daily
Acute diarrhoea definition
lasting less than 2 weeks
Chronic diarrhoea definition
lasting MORE THAN 2 weeks
Acute diarrhoea
- 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
Name an anti-diarrhoeal agent
Loperamide hydrochloride
Chronic diarrhoea
- 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)
Chronic diarrhoea - what can be used to differentiate between functional disorders and organic disease?
faecal markers of intestinal inflammation
Mechanisms of diarrhoea
- infective cause
- inflammatory cause
- steatorrhea (fat in stool)
- decreased stool consistency
- secretion of fluids and electrolytes
- functional (eg IBS)
- inflammatory discharge
mechanisms of diarrhoea - infective cause
- sudden onset bowel frequency
- crampy abdo pains
- fever
mechanisms of diarrhoea - inflammatory cause
- bowel frequency
- loose, BLOOD STAINED stools
mechanisms of diarrhoea - steatorrhea
- pale stools, offensive smell, increased gas
- floating, hard to flush stool
- loss of appetite and loss of weight
- giardiasis, coeliac can cause
mechanisms of diarrhoea - decreased stool consistency caused by water/ osmosis
- large quantities non absorbed hypertonic substances in bowel draw fluid into intestine
- diarrhoea stops when patient stops eating or malabsorptive state discontinued
mechanisms of diarrhoea - decreased stool consistency caused by water/ osmosis - CAUSES
- 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
mechanisms of diarrhoea - decreased stool consistency caused by water / SECRETORY (microscopic colitis)
- active intestinal secretion of fluid, electrolytes, also decreased absorption
- continues even when patient fasts !!!
mechanisms of diarrhoea - decreased stool consistency caused by water / SECRETORY (microscopic colitis) - CAUSES
- 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
mechanisms of diarrhoea - inflammatory discharge
- 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
INFECTIVE DIARRHOEA - epidemiology
- 2nd leading cause death children under 5 globally (after pneumonia)
- highest prevalence: south Asia, Africa
INFECTIVE DIARRHOEA - risk factors
- foreign travel
- PPI or H2 antagonist use
- crowded area
- poor hygiene
INFECTIVE DIARRHOEA- aetiology
- children: rotavirus (leading cause diarrhoea young children, affects nearly all children by age 4) - there is a vaccine now !
- adults: norovirus, campylobacter
what cause makes up the majority of diarrhoea illness?
viral causes
70% all infectious diarrhoea in paediatric age group world wide
INFECTIVE DIARRHOEA - viral causes
- rotavirus (most common children)
- norovirus ( most common adults, 10% child cases, associated w/ cruise ships, hospitals, restaurants (close proximity to others) )
- adenovirus
- astrovirus
INFECTIVE DIARRHOEA - bacterial causes
- campylobacter jejuni (MOST COMMON cause bacterial diarrhoea, poultry)
- E coli (more common children)
- Salmonella (more common children)
- Shigella spp. (more common children)
- antibiotic associated
INFECTIVE DIARRHOEA - bacterial causes - antibiotic associated - what is the rule of C’s?
generally, antibiotics beginning with C can give rise antibiotic induced Clostridium difficile diarrhoea
- clindamycin
- ciprofloxacin (quinolones)
- co-amoxiclav (penicillins)
- cephalosporins
Clostridium difficile
- 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
C diff risk factors
- elderly
- antibiotic use
- long hospital admission
- immunocompromised eg HIV
- acid suppression can contribute: PPI or H2 receptor antagonist
C diff treatment
- metronidazole
- oral vancomycin
- rifampicin/ rifaximin
- stool transplant
- stop C antibiotic
Infective diarrhoea - parasitic causes
- Giardia lamblia - most common
- Entamoeba histolytica
- Cryptosporidium
Diarrhoea - clinical presentation
- blood usually indicates bacterial infection: salmonella, shigella, E coli = bloody stools
- vomiting
- abdominal cramping
Diarrhoea clinical presentation - viral causes
- fever, fatigue, headache, muscle pain
- general incubation period 12-72 hours post infection
Diarrhoea clinical presentation - differential diagnosis
- appendicitis, volvulus, IBD, UTI, diabetes mellitus
- pancreatic insufficiency, short bowel syndrome, coeliac disease
- laxative abuse
Diarrhoea - diagnosis - bloods
- 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
Diarrhoea - diagnosis - stool
-if suspected bacteria, parasites of C diff toxin
Diarrhoea diagnosis - 3 tests
- bloods
- stool
- sigmoidoscopy with biopsy
Diarrhoea - treatment
- 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
General pharmacology - PPIs
lansoprazole, omeprazole, pantoprazole
general pharmacology PPI indications
- first line prevention and treatment for peptic ulcer disease
- symptomatic relief of dyspepsia, GORD
- eradication H pylori with antibiotics
general pharmacology - mechanisms of PPIs
- 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
general pharmacology - adverse effects/contraindications PPIs
- 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
general pharmacology - H2 receptor antagonists
ranitidine
general pharmacology -H2 receptor antagonists indications
treatment, prevention gastric and duodenal ulcers, NSAID associated ulcers if PPIs are contraindicated
general pharmacology - H2 receptor antagonists - mechanisms
- 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)
general pharmacology - H2 receptor antagonists - adverse effects/ contraindications
- possible bowel disturbance, headache, dizziness
- reduce dose in renal impairment
- watch for symptoms gastric cancer - H2 antagonist can disguise these
general pharmacology - alginates/ antacids
gaviscon, peptac
general pharmacology - alginates/ antacids - indications
- for GORD symptomatic relief heartburn
- short term relief indigestion, dyspepsia
general pharmacology - alginates / antacids - mechanisms
- 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
general pharmacology - alginates/ antacids - adverse effects/ contraindications
- 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
general pharmacology - anti motility drugs
loperamide, codeine phosphate
general pharmacology - anti motility drugs - indications
-as symptomatic treatment of diarrhoea, usually for IBS, or GASTROENTERITIS
general pharmacology - anti motility drugs - mechanisms
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
general pharmacology - anti motility drugs - adverse effects/ contraindications
- 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
general pharmacology - bile acid
ursodeoxycholic acid
general pharmacology - bile acid - indications
- used in primary biliary cirrhosis
- reduction in liver biochemistry, jaundice, ascites, itching
general pharmacology - bile acid - mechanisms
- 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
general pharmacology - bile acid - adverse effects / contraindications
- 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
gastro-oesophageal reflux disease - GORD - epidemiology
- 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
GORD - causes
- 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
GORD causes - hiatus hernia - sliding hiatus hernia
- 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
GORD causes - hiatus hernia - rolling or para oesophageal hiatus
- 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
GORD - NORMAL physiology of stomach and oesophagus
- 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
GORD - pathophysiology
- 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
GORD - pathophysiology - contributing factors
- 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)
GORD - clinical presentation - oesophageal symptoms
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)
GORD - clinical presentation - extra oesophageal symptoms
- nocturnal asthma
- chronic cough
- laryngitis (hoarseness, throat clearing)
- sinusitis
GORD - differential diagnosis
- coronary artery disease (CAD)
- biliary colic
- peptic ulcer disease
- malignancy
GORD - diagnosis
- 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
GORD diagnosis - red flag investigations
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
GORD diagnosis - red flag investigations - aims of investigations
- 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
What is name of classification system used to classify GORD?
The Los Angeles classification of GORD/oesophagitis - when doing endoscopy to gauge extent of damage
GORD - treatment - lifestyle changes
- encourage weight loss
- smoking cessation
- small, regular meals
- avoid hot drinks, alcohol, citrus fruits and eating less than 3 hours before bed
GORD - treatment - pharmacology
- 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)
GORD treatment - surgery
- Nissen fundoplication - aims to laparoscopically increase resting LOS pressure - only in severe GORD
- use when not responding to therapy
- complications include dysphagia, bloating
GORD complications - peptic stricture
- 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
GORD complications - Barret’s oesophagus
- 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
Gastritis
- 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
Gastritis - causes
- 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
Gastritis - pathophysiology - H pylori infection
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)
Gastritis pathophysiology - autoimmune gastritis
-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)
Gastritis pathophysiology - aspirin and other NSAIDs eg naproxen
-inhibit prostaglandins (which stimulate mucus production) via inhibition of cyclo-oxygenase = less mucus production thus gastritis
Gastritis - clinical presentation
- nausea or recurrent upset stomach
- abdominal bloating
- epigastric pain
- vomiting
- indigestion
- haematemesis
Gastritis - differential diagnosis
- peptic ulcer disease (PUD)
- GORD
- non ulcer dyspepsia
- gastric lymphoma
- gastric carcinoma
Gastritis - diagnosis
- endoscopy - will be able to see gastritis
- biopsy
- H pylori urea breath test
- H pylori stool antigen test
Gastritis - treatment
- remove causative agent eg alcohol
- reduce stress
- H pylori eradication (7-14 days) eradication confirmed by urea breath or faecal antigen test
Gastritis - pharmacological treatment - ‘triple therapy’
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
Gastritis - standard pharmacological treatment
- H2 antagonists eg ranitidine, cimetidine
- PPIs eg lansoprazole, omeprazole
- antacids
Gastritis - prevention
-Give PPIs alongside NSAIDs - also prevents bleeding from acute stress ulcers and gastritis which is often seen with ill patients - esp burns patients
MALABSORPTION
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 !
Malabsorption - disorders of the small intestine resulting in malabsorption
- coeliac disease
- Tropical Sprue
- Crohn’s
- Parasite infection
Malabsorption - 5 umbrella causes
- defective intraluminal digestion
- insufficient absorptive area
- lack of digestive enzymes
- defective epithelial transport
- lymphatic obstruction
Malabsorption causes - defective intraluminal digestion - 3 causes
- pancreatic insufficiency
- defective bile secretion (lack of fat solubilisation)
- bacterial overgrowth
Malabsorption causes - defective intraluminal digestion - pancreatic insufficiency
- 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
Malabsorption causes - defective intraluminal digestion - defective bile secretion (lack of fat solubilisation)
- 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
Malabsorption causes - insufficient absorptive area - 4 causes
Essentially anything that damages microvilli and villi thereby reducing absorptive surface area and thus absorption potential :
- Coeliac disease
- Crohn’s disease
- Giardia lamblia
- Surgery
Malabsorption causes - insufficient absorptive area - Coeliac disease
- gluten sensitive enteropathy
- villi are very short if present at all
- villous atrophy, crypt hyperplasia
- lots of lymphocytes in the epithelium
Malabsorption causes - insufficient absorptive area - Crohn’s disease
- causes inflammatory damage to the lining of the bowel
- results in cobblestone mucosa
- significant reduction absorptive surface
Malabsorption causes - insufficient absorptive area - Giardia lamblia
- Extensive surface parasitisation of the villi and microvilli
- parasites coat the surface of the villi thus food cannot be absorbed
Malabsorption causes - insufficient absorptive area - surgery
-small intestine resection or bypass in small bowel infarction
Malabsorption causes - lack of digestive enzymes
- 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
Malabsorption causes - defective epithelial transport
- Abetalipoproteinaemia - lack of transporter protein to transport lipoprotein across cell
- primary bile acid malabsorption - mutations in bile acid transporter protein
Malabsorption causes - lymphatic obstruction
- lymphoma
- tuberculosis
Coeliac disease / gluten sensitive enteropathy
-inflammation of mucosa of upper small bowel that improves when gluten is withdrawn from the diet or replases when gluten is reintroduced
Coeliac disease / gluten sensitive enteropathy
-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
Coeliac - when to suspect
in ALL diarrhoea, weight loss, anaemia (esp if iron, B12 deficient)
Coeliac - epidemiology
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
Coeliac - causes
GLUTEN found in wheat, barley, rye
Coeliac - risk factors
- 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
Coeliac - pathophysiology overview
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
Coeliac - specific pathophysiology
- 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
Coeliac - specific pathophysiology
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
Coeliac - clinical presentation
- 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
Coeliac - clinical presentation - OSTEOMALACIA
- 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)
Coeliac - clinical presentation - dermatitis hepetiformis
red raised patches often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks
Coeliac - diagnosis
! must maintain gluten ingestion for at least 6 weeks before testing to get true results !
- FBC
- duodenal biopsy (gold standard)
- serum antibody testing
Coeliac diagnosis - blood tests
FBC :
- low Hb
- low B12
- low ferritin
Coeliac diagnosis - duodenal biopsy
- gold standard for diagnosis
- see villous atrophy, crypt hyperplasia, increased intraepithelial white cell count
- all reverse on gluten free diet
Coeliac diagnosis - serum antibody testing
-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
Coeliac treatment
- lifelong gluten free diet
- correction mineral, vitamin deficiencies
- DEXA scan
Coeliac treatment - lifelong gluten free diet
- 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
Coeliac treatment - correction of vitamin and mineral deficiencies
-B12, folate, iron, calcium, vitamin D
Coeliac disease - complications
- 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
Tropical Sprue - epidemiology
- 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
tropical sprue - pathophysiology
- 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
tropical sprue - clinical presentation
- diarrhoea
- anorexia
- severe malabsorption
- weight loss
- abdominal distension
- onset can be insidious - chronic diarrhoea, evidence nutritional deficiency
tropical sprue - diagnosis
- exclude acute infective causes of diarrhoea eg Giardia intestinalis - can produce similar syndrome
- bloods
- jejunal biopsy
tropical sprue - diagnosis - bloods
-anaemia due to malabsorption B12, folate, iron
tropical sprue - diagnosis - jejunal biopsy
-abnormal jejunal mucosa - partial villous atrophy (complete atrophy in coeliac)
tropical sprue - treatment
- 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
INFLAMMATORY BOWEL DISEASE (IBD)
- two major forms - both CHRONIC AUTOIMMUNE CONDITIONS
- ulcerative colitis
- Crohn’s disease
IBD - epidemiology
- 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
IBD - UC
- 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%)
IBD - UC - can UC affect bowel proximal to the ileocaecal valve?
No - NEVER
UC only affects colon - large bowel
IBD - UC epidemiology
- 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
IBD - UC epidemiology - an appendicectomy
- 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
IBD - UC risk factors
- family history
- NSAIDs - associated w onset IBD, flares
- chronic stress, depression triggers flares
IBD - UC pathophysiology
Restricted mucosal disease differentiates it from crohns
- macroscopic
- microscopic
IBD - UC pathophysiology macroscopic
- 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
IBD - UC pathophysiology microscopic
- mucosal inflammation - does not go deeper, not transmural
- no granulomata (rare)
- depleted goblet cells
- increased crypt abscesses
IBD - UC clinical presentation
- 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
IBD - acute UC/ acute attack clinical presentation
- 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
IBD - UC clinical presentation - extra intestinal signs
- clubbing
- aphthous oral ulcers
- erythema nodusum (red round lumps below skin surface)
- amyloidosis
IBD - UC complications
- liver
- colon
- joints
- skin
- eyes
IBD - UC complications - liver
- fatty change
- chronic pericholangitis
- sclerosing cholangitis
IBD - UC complications - colon
- blood loss
- perforation
- toxic dilatation
- colorectal cancer
IBD - UC complications - skin
- erythema nodusum (red round lumps below skin surface)
- pyoderma gangrenosum (painful ulcers on skin)
IBD - UC complications - joints
- ankylosing spondylitis
- arthritis
IBD - UC complications - eyes
- iritis (iris inflammation)
- uveitis (inflammation middle layer of eye -uvea)
- episcleritis
IBD - UC differential diagnosis
-alternative causes of diarrhoea should be excluded eg Salmonella spp, Giardia intestinalis, Rotavirus
IBD - UC diagnosis
- blood tests
- stool samples
- faecal calprotectin
- colonoscopy w/ mucosal biopsy
- abdominal X ray
IBD - UC diagnosis - blood tests
- 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
IBD - UC diagnosis - stool sample
to exclude C diff and Campylobacter
IBD - UC diagnosis - faecal calprotectin
indicates IBD but not specific
IBD - UC diagnosis - colonoscopy with mucosal biopsy
- GOLD STANDARD for diagnosis
- allows assessment disease activity and extent
- can see inflamm infiltrate, goblet cell depletion, crypt abscesses, mucosal ulcers
IBD - UC diagnosis - abdominal X ray
- in all patients suffering severe acute attacks to exclude colonic dilatation
- useful when UC too severe for colonoscopy
IBD - UC treatment
- 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
IBD - UC treatment of mild / moderate
- 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
IBD - UC treatment of severe
glucocorticoid eg oral prednisolone
IBD - UC treatment of severe with systemic features eg liver, skin, eye involvement
- hydrocortisone
- ciclosporin
- infliximab
IBD - UC treatment to maintain remission
- 5-ASA - most patients require maintenance treatment
- azathioprine - patients who relapse despite 5-ASA treatment / ASA intolerant
IBD - UC treatment - surgery
- 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
INTESTINAL OBSTRUCTION
Arrest/ blockage of onward propulsion of intestinal contents
Intestinal obstruction - classification of obstruction
- According to site
- Extent of luminal obstruction
- According to mechanism
Intestinal obstruction classification - according to site
large bowel, small bowel, gastric
intestinal obstruction classification - extent of luminal obstruction
- partial
- complete - volvulus can result in this, resulting in overflow and sickness
intestinal obstruction classification - according to mechanism
- mechanical
- true (intraluminal / extraluminal)
- functional (paralytic ileus - adynamic bowel due to absence of normal peristaltic contractions, caused by abdo surgery or acute pancreatitis)
intestinal obstruction classification - according to pathology
- simple
- closed loop
- strangulation
- intussusception (one hollow structure into its distal hollow structure, usually seen in children as bowel is softer)
intestinal obstruction - pathology
- obstruction of lumen
- disease in wall of bowel causing obstruction
- outside bowel which causes obstruction
intestinal obstruction pathology - obstruction of lumen
- tumors: carcinoma, lymphoma
- diaphragm disease
- meconium ileus (neonates sticky bowel contents causes blockage)
- gallstone ileus (gallstone within lumen small bowel)
intestinal obstruction pathology - disease in wall of bowel causing obstruction
- INFLAMMATORY eg crohns, diverticulitis
- TUMORS
- NEURAL (Hirschprungs)
intestinal obstruction pathology - disease in wall of bowel causing obstruction - DIVERTICULITIS (OUTPOUCHING)
- 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
intestinal obstruction pathology - disease in wall of bowel causing obstruction - NEURAL - HIRSCHPRUNG’S DISEASE
- 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
intestinal obstruction pathology - something outside the bowel which causes obstruction
- adhesions
- volvulus
- tumor (peritoneal tumor seen in ovarian carcinoma)
intestinal obstruction pathology - something outside the bowel which causes obstruction - ADHESIONS
- 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
what is the MOST COMMON CAUSE OF OBSTRUCTION IN ADULTS?
ADHESIONS - (80% caused by adhesions)
intestinal obstruction pathology - something outside the bowel which causes obstruction - VOLVULUS
- 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’
Intestinal obstruction - general facts
- most due to mechanical block
- one of most common causes hospital admis
- tinkling bowel sounds, tympanic percussion typical of obstruction
SMALL BOWEL OBSTRUCTION - epidemiology
- 60-75% intestinal obstruction
- majority caused by previous surgery
- Crohns disease significant cause
SMALL BOWEL OBSTRUCTION - main causes
- 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
SMALL BOWEL OBSTRUCTION - pathophysiology
- 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
small bowel obstruction pathophysiology - proximal dilatation above block leads to ?
- increased secretions and swallowed air in small bowel
- decreased absorption, mucosal wall oedema
- increased pressure with intramural vessels becoming compressed = ischaemia and or perforation
