Phase 2 - GI Flashcards
Infective causes of diarrhoea
Intraluminal infection
Systemic infection
Typically VIRAL:
1. Rotavirus (main in kids)
2. Norovirus (main in adults)
Also TRAVELLER’S diarrhoea (can be caused by a variety of things esp EHEC)
Non-infective causes of diarrhoea
Cancer
Radiation
Chemicals
- Poisoning
- sweeteners
- medications
Inflammatory bowel disease
IBS / malabsorption
Endocrine/hormonal eg Thyrotoxicosis
Anatomical e.g. post colesectomy
Evaluation for acute diarrhoea is warranted in individuals with which symptoms?
- persistent FEVER,
- BLOODY diarrhoea,
- severe ABDO PAIN,
- symptoms of VOLUME DEPLETION (eg, dark or scant urine, symptoms of orthostasis/postural hypotension),
- HISTORY of IBD,
- immunosuppression
Relevant history for diarrhoea
- ONSET/duration
- CHARACTERISTICS of stool
- Food/drink
- Travel
- IMMUNE status (immunocompromised can be affected by stuff normal immune people aren’t affected by)
- Unwell contacts
- Hobbies + FRESH WATER
- ANIMAL contact
- MEDS (recent - C. DIFF?)
What food is particularly related to which pathogen (+ inc. period + associated symptoms)
- Take-aways (lots of microbes/toxins)
- Warm rice
- BACILLUS CEREUS (1-6hr - toxin)
- PROFUSE VOmiting
- BACILLUS CEREUS (1-6hr - toxin)
- Meat/BBQ
- campylobacter spp, (24-72hr)
- PROFUSE DIARRHOEA + SEVERE abdo pain
- clostridium perfringens (12-24hr)
- Diarrhoea + COLICKY abdo pain
- campylobacter spp, (24-72hr)
- Poultry/eggs
- Salmonella spp (16-48hr)
- Diarrhoea + some abdo pain
- Salmonella spp (16-48hr)
- SHELLFISH
- NOROVIRUS,
- V. parahaemolyticus
- salmonella enterica serotype Typhi
- FINGER FOODS
- STAPH AUREUS (1-6hr - pre-formed toxin)
- SEVERE vomiting + FEVER
- STAPH AUREUS (1-6hr - pre-formed toxin)
Which mirobes are associated with fresh water/swimming
Cryptosporidium
Giardia
Aeromonas
Which animals are particularly associated with diarrhoea causing pathogens
Reptiles - salmonella
Puppies - campy
Characteristic symptoms of small bowel diarrhoea (esp proximally)
watery, large volume
- cramping, bloating, flatulence
Characteristic signs/symptoms colonic diarrhoea
frequent, small volume, painful
May contain blood, mucus
Oft associated fever
Can see RBCs + inflammatory cells in stool microscopy
Function of action of cholera toxin
Exports chloride into lumen - water follows
-> v. watery rice water stools
What does oral rehydration for diarrhoea consist of
1L water with 6 level teaspoons of sugar and 1/2 a level teaspoon of salt
- need sugar to give energy for active transport
Typical site of campy diarrhoea pain; what are it’s late onset complications
Periumbilical - mimics acute appendicitis
Complications - Guillan Barre Syndrome and reactive arthritis
Site of pain in yersinia spp diarrhoea and Complications.
RLQ pain
Yersinia septicaemia - in IMPAIRED IMMUNITY or IRON-OVERLOAD states
Which antibiotics in particular can predispose to C. difficile
CLINDAMYCIN
Co-amoxiclav (penicillins)
Ciprofloxacin (quinolones)
Cephalosporins:
- CEFUROXIME
- CEFTRIAXONE
- CEFALEXIN
Any BROAD SPECTRUM antibiotics
Virulence factors of C. diff
SPORE-forming
Toxin
Gram +ve
Anaerobic
When does C. diff infection typically start
During/up to 1 MONTH after antibiotics course
Natural history of C. diff infection
Asymptomatic carriage (or -> watery diarrhoea)
-> fulminant disease with severe colitis
-> toxic megacolon (potentially)
toxin producing C. diff can cause psudomembranous colitis - layer of dead cells creating a membrane-esq
Management of C. diff
- stop inciting antibiotic as soon as possible
Contact precautions/hand hygiene
(hand washing > alcohol - c. diff spores not killed by alcohol)
Antibiotics:
- METRONIDAZOLE
- VANCOMYCIN
Stool transplant
Investigations for diarrhoea
STOOL TESTS:
- microscopy (blood/pus)
- CULTURE
- Ova, cysts and parasites x3
- Toxin detection (C difficile)
PCR: Multi-pathogen molecular panels (use primers for specific pathogens - typically for viruses, C. diff, campy)
Blood tests:
- Culture
- Raised Inflammatory markers (ESR/CRP) - possible infection
- Alongside anaemia = IBD/cancer
- EOSINOPHILIA = PARASITES
- Alongside anaemia - think hookworm
- may test vomit
- Electrolytes + creatinine (won’t necessarily aid diagnosis but important)
Endoscopy/biopsy if necessary
Indications for testing for diarrhoea
Severe illness
Bloody diarrhoea/mucus
High risk (>70, immunocomp, IBD, pregnant)
Prolonged (>1 week)
Public health concerns
Diarrhoea red flags (may become severe, complications etc.)
Dehydration
Electrolyte imbalance
- RENAL FAILURE
Immunocomp
Severe abdo pain
CANCER RISK FACTORS:
- >50 y/o
- chronic diarrhoea
- weight loss
- blood in stool
- family history
What is Zollinger Ellison syndrome
GASTRIN SECRETING TUMOUR - causes a triad
- pancreatic tumour
- gastric acid hypersecretion
- Widespread Peptic ulcers
GI red flags
Think ALARMS
Anaemia
Loss of weight
Anorexia (loss of appetite)
Recent onset of progressive symptoms (it’s always
low-level been there but it recently got worse)
MASSES/MELENA (or any other GI BLEEDING)
Swallowing difficulties (DYSPHAGIA)
and >55 y/o
- points to GI cancer
What causes enteric fever
Salmonella Enterica subtypes Typhi and Paratyphi
Presentation of enteric fever
Generalised RLQ pain,
FEVER, CHILLS
Headache, myalgia
Relative bradycardia
CONSTIPATION/green diarrhoea
(Rose spots (faint salmon-colored macules on the trunk and abdomen))
more common in kids/younger ppl
Diagnosis of enteric fever
2 large volumes of blood culture - before antibiotics
GOld standard - bone marrow aspirate
Complications of enteric fever
GI bleed
Perforation/peritonitis
Abscesses
Myocarditis
Oft need emergency surgery
(typically in week 2-3)
2-3% -> chronic carriers (asymp) - resides in gallbladder
Medical treatment for enteric fever
- azithromycin
- ciprofloxacin (quinolone)
- cephalosporins
- meropenem
What is the CLO test
Campylobacter-Like Organism test
it is a RAPID UREASE TEST - used for H. pylori detection
What is a Mallory Weiss tear
Longitudinal TEAR in tissue of LOWER OESOPHAGUS (typically only sub-/mucosa) due to SUDDEN INCREASES in INTRA-ABDOMINAL PRESSURE -> blood loss
- oft caused by violent COUGHING/VOMITING (alcoholism, bulimia); hiatus hernias; weight lifting
Common in 20-50 y/o males
Typically diagnosed and treated via ENDOSCOPY
- mainly LIFESTYLE CHANGES (maybe CBT/therapy for alcohol/bulimia)
Symptoms:
- Haematemesis (blood in VOMIT)
- Melena
- systemic: postural hypotension/dizziness (from blood loss)
*if severe - anaemia, fatigue, SOB, shock
Pathophysiology of Crohn’s
NOD2 mutation -> faulty GI epithelum
Enteric pathogens get into wall -> T cell mediated immune response (TNFa, IL1, IL6)
-> Granulomas + destruction of GI tissue
Causes TRANSMURAL ULCERS, in SKIP LESIONS through the whole gut but particularly in TERMINAL ILEUM AND PROXIMAL COLON. Also, FISSURES in lining.
-> COBBLESTONE APPEARANCE
Risk factors for Crohn’s
Family history
(Jewish ethnicity)
SMOKING (2x risk)
NSAIDs
CHRONIC STRESS/DEPRESSION
Symptoms of Crohn’s
ABDO PAIN (usually) in RLQ
MALABSORPTION:
- B12, FOLATE, IRON deficiency (FATIGUE)
- Increased risk of kidney/gallstones (malabsorption of bile salts)
- WEIGHT LOSS, ANOREXIA
- CHANGES IN BOWEL HABIT
* watery diarrhoea/steatorrhoea, (melena)
Extra GI:
- CLUBBING
- APHTHOUS ULCERS
- episcleritis/uvitis
- erythema nodosum/ pyoderma gangernosum
- Ankylosing Spondylitis
Diagnosis of Crohn’s
pANCA -ve (perineuclear anti-neutrophil cytoplasmic antibodies);
may be ASCA +ve (antibodies to do with yeast)
increased FECAL CALPROTECTIN (non-specific - present in any type of IBD)
BIOPSY - transmural inflammation with non(?)-caseating granulomas
Treatment for Crohn’s
For FLARES:
- STEROIDS
* mild - PREDNISOLONE
* severe - HYDROCORTISONE
- and Mesalazine or Sulfasalazine (5-ASA - used for IBD in general)
- (or methotrexate as 2nd line)
For maintaining REMISSION - immunosuppression:
- AZATHIOPRINE (5-ASA)
- METHOTREXATE
Biologics:
- INFLIXIMAB (anti-TNFa)
- ustekenumab (IL 12 +23 inhib)
SURGERY NOT CURATIVE BUT VERY COMMON
Complications of Crohn’s
- PERFORATION
- Perianal ABSCESSES
- FISTULAS
- ADHESIONS
- Strictures
- Small bowel obstruction
Pathophys of Ulcerativ colitis
AUTOIMMUNE condition linked to HLA B27 GENE (also linked to other inflam diseases e.g. ARTHRITIS (esp ankylosing spondylitis))
CIRCUMFERENTIAL, CONTINUOUS inflammation extending proximally from the RECTUM to CEACUM (doesn’t affect ileum) .
MUCOSAL/SUBMUCOSAL ULCERS (muscularis if severe). Formation of CRYPT ABSCESSES + CRYPTITIS, GOBLET CELL DEPLETION.
Ulcerated areas become granulomatous - excess tissue can form PSEUDOPOLYPS
Destruction of mucosa/epithelium -> blood
Large intestine malabsorption -> diarrhoea
Risk factors for UC
Family history
(Jewish)
- NSAIDs
- CHRONIC STRESS/DEPRESSION
SMOKING IS PROTECTIVE
Symptoms of UC
ABDO PAIN (usually LLQ)
BLOODY, watery DIARRHOEA with MUCUS
TENESMUS (rectal pain on defecation)
Extra GI - A PIE SAC:
- ANKYLOSING SPONDYLITIS (also linked to HLA B27)
- Pyoderma gnagrenosum
- Iritis (ANTERIOR UVEITIS or Episcleritis)
- ERYTHEMA NODOSUM (nodules + arthralgia)
- SCLEROSING CHOLANGITIS
- Aphthous ulcers/amyloidosis
- CLUBBING
Diagnosis of UC
Bloods:
- CRP/ESR (inflam)
- WCC
- iron/vit B/folate ANAEMIAS (malabs)
IBD markers:
- pANCA +ve
- RAISED FECAL CALPROTECTIN (non-specific)
COLONOSCOPY + BIOPSY (if viable - risk of perforation - GOLD STANDARD):
- CONTINUOUS MUCOSAL INFLAM
- CRYPT ABSCESSES + distortion
- REDUCED GOBLET CELLS
‘lead pipe sign’ on x-ray
Treatment for UC
Flare:
- Mild:
* MESALAZINE or SULFASALAZINE (salysilic acid)
* PREDNISOLONE (steroid)
- Moderate/severe:
* Fluid resus if needed
* IV STEROID (HYDROCORTISONE)
* INFLIXIMAB
Remission:
AZATHIOPRINE
(METHOTREXATE - 2nd line)
Ciclosporin (calcineurin inhib - not as commonly used now)
Biologic:
INFLIXIMAB (TNFa inhib)
SURGERY IS CURATIVE (but less common in UC) - COLECTOMY is GOLD STANDARD
Complication of UC
TOXIC MEGACOLON
also INCREASED risk of COLON CANCER
UC vs Crohn’s
Crohn’s:
- entire GI
- transmural
- skip lesions
- fissures common
- granulomas present
- COBBLESTONE
- Strictures common (due to scarring)
- Thickened wall, narrow lumen
- ADHESIONS (inflammation/surgery)
- creeping fat around intestine
- raised cancer risk
UC:
- colon/rectum
- MUCOSAL/submucosal
- continuous
- fissures uncommon
- no granulomas
- PSEUDOPOLYPS
- Strictures uncommon
- Thin wall, dilated lumen
- No adhesions
- normal fat
- EVEN HIGHER CANCER RISK
What is tropical sprue
CHRONIC bowel inflammation, acquired from TROPICS (SE asia, india, caribbean) - unknown cause
Signs/Symptoms of Tropical sprue
- DIARRHOEA, steatorrhoea
- ABDO PAIN
- WEIGHT LOSS (malabs)
- Dehydration
- Vit/folate/iron Anaemias - FATIGUE
Investigation for tropical sprue
JEJUNAL TISSUE BIOPSY (gold)
- shows INCOMPLETE VILLOUS ATROPHY
(* coeliac has COMPLETE villous atrophy)
Treatment for tropical sprue
Drink TREATED WATER
TETRACYCLINE for 6mths
Define Coeliac disease
Autoimmune condition where exposure to gluten (wheat, barley, rye) causes MUCOSAL INFLAMMATION of SMALL BOWEL and MALABSORPTION
Pathophys of Coeliac disease
TYPE 4 HYPERSENSITIVITY REACTION (T CELL MEDIATED - delayed)
Gluten braks down to Gliadin -> binds to IgA
- travels to lamina propria -> deaminated by tTG
- macrophages present it via MHC -> activates CD4+
-> inflammatory cytokines
-> B cells make AUTOANTIBODIES
* ANTI- TISSUE TRANSGLUTAMINASE (anti-tTG)
* ANTI-ENDOMYSIAL antibody (anti-EMA)
-> CD8 also activated
(mainly gliadin triggers immune response)
Targets EPITHELIAL cells of SMALL intestine
Causing:
-> COMPLETE VILLOUS ATROPHY
-> CRYPT HYPERPLASIA
-> INTRAEPITHELIAL LYMPHOCYTES
Risk factors for COELIAC
- GENETIC - HLA-DQ2 (or HLA-DQ8)
- FAMILIAL LINK (10% in 1st degree relatives)
- other AUTOIMMUNE conditions e.g. T1DM
- IgA Deficiency
Signs/symptoms of Coeliac disease
- DERMATITIS HERPETIFORMIS (papules on ELBOWS, KNEES, BUTTOCKS)
- Angular stomatitis
- Mouth ulcers
- STEATORRHOEA (pale, floating stools - fatty)
- DIARRHOEA
- BLOATING
- Weight loss
- ANAEMIA (2ndry to iron/b12/folate deficiency)
- Failure to thrive (children)
Diagnosis of Coeliac
Blood tests:
- RAISED ANTI-tTG (1st LINE)
- Raised anti-EMA (2nd)
ENDOSCOPY + DUODENAL biopsy (gold)
Management of Coeliac
LIFELONG GLUTEN-FREE diet
Define IBS
A chronic FUNCTIONAL bowel disorder characterised by ADBO PAIN + change in BOWEL HABITS
NO ORGANIC CAUSE
Aetiology of IBS
NO ORGANIC CAUSE
- Food hypersensitivity (to short chain carbs esp)
- Visceral hypersensitivity
- Gut MICROBIONE alteration (bacteria metabolise sugars -> gas + bloating)
Risk factors for IBS
FEMALE
YOUNGER (peak 20-30 y/o)
ANXIETY/DEPRESSION/STRESS
- eating disorders
Previous GI infection
Signs and symptoms of IBS
Think ABC
- ABDOMINAL PAIN (improves with defecation)
- BLOATING
- CHANGE in BOWEL HABITS
Symptoms worse after eating
Types of IBS
- IBS-C (constipation)
- IBS-D (diarrhoea)
- IBS- M (mixed - alternte constipation/diarrhoea)
- IBS unclassified (other)
Differentials for IBS
IBD
Coeliac disease
Lactose intolerence
Food allergies
GI infections
DIagnosis of IBS
Rule out diff:
- anti-tTG/anti-EMA (coeliac)
- faecal calprotectin (IBD)
- FBC, ESR/CRP (inflammation - IBS is NOT INFLAMMATORY)
- Colonoscopy (COLORECTAL CANCER)
Roman IV criteria:
- RECURRENT abdo pain at least 1 DAY/WEEK for the past 3 MONTHS
- BEGAN at least 6 MONTHS AGO and has 2/more of following:
* RELIEVED by DEFECATION
* change in bowel APPEARANCE
* change in bowel FREQUENCY
Management of IBS
Conservative:
- educate/reassure
- LOW FODMAP (short chain carbs) DIET
- AVOID CAFFINE/ALCOHOL
If constipated - increase fluid intake + avoid lactose (causes bloating)
Medical:
- LOPERAMIDE (antimotility - diarrhoea)
- LAXTIVES (constipation)
- Antispasmodics (BUSCOPAN - for cramps)
- Tricyclic antidepressants
- CBT
What are FODMAPs
Fermentable
Oligosaccharides
Disaccharides
Monosaccharides
And
Polyols
just remember they are short-chain carbs - poorly absorbed
Define Gastritis
Inflammation of stomach mucosal lining
Causes of gastritis
Acute:
- HELICOBACTER PYLORI
- NSAIDs
- ALCOHOL abuse
- STRESS (critically ill, major surgery, life events)
- Ischaemia (cells stop producing mucin)
Chronic:
- H. PYLORI
- AUTOIMMUNE
Pathophys of NSAIDs causing gastritis
Inhibits COX-1 enzyme (cyclooxygenase)
-> INHIBITS PROSTAGLANDIN SYNTHESIS
-> REDUCED MUCUS secretion
mucosa -> inflamed by gastric acid
Pathophys of Autoimmune gastritis
PARIETAL cell and INTRINSIC FACTOR ANTIBODIES
-> REDUCED VIT B12 absorption in terminal ileum
-> PERNICIOUS ANAEMIA
Signs/symptoms of Gastritis
- DYSPEPSIA (indigestion)
- EPIGASTRIC PAIN
- anorexia (loss of appetite)
- nausea/vomiting (too acidic)
Diagnosis of gastritis
- H. pylori
- UREA BREATH TEST
- STOOL ANTIGEN TEST
NOTE: need to stop PPI at least 2 WEEKS before, and ANTIIBIOTICS at least 4 WEEKS before
ENDOSCOPY (+ biopsy)
- see INFLAMMATION/atrophy + MORE PROMINANT RUGAE
- Autoimmune (low B12, parietal cell antibodies, intrinsic factor antibodies - via bloods)
Differentials for gastritis
- peptic ulcer disease
- GORD
- gastric CARCINOMA
Management of gastritis
H. pylori:
- Triple therapy
* 1st LINE: CAP - Clarithromycin (500mg), Amoxicillin (1g), PPI (typically omeprazole)
* if penicillin allergy: ClaMP - Clarithromycin (500mg), Metronidazole (400mg), PPI
Stop ALCOHOL or NSAIDs if relevant
Autoimmune: IM VIT B12 (cyanocobalamine)
Complications of gastritis
PEPTIC ULCERS
- bleeding/anaemia
MALT lymphoma (mucosa-associated lymphoid tissue)
GASTRIC CANCER
Types of peptic ulcers
Gastric
Duodenal (more common)
Causes of peptic ulcer disease (PUD)
- Gastritis (-> peptic ulcer -> gastric adenocarcinoma)
- H. pylori infection
- NSAIDs (tho ENTERIC COATED NSAIDs don’t dissolve in stomach, only duodenum)
- Alcohol excess
- BILE REFLUX into stomach (mucin not designed for alkali)
Pathophys of H. pylori infection
Live in mucus layer overlying gastric mucosa (mucin)
- SYNTHESISE + secrete UREASE
-> converts urea to ammonia which reacts with H+ in lumen to form AMMONIUM (toxic to gastric mucosa)
-> DECREASED MUCUS
- Increased INFLAMMATION (H. pylori releases chemokines -> neutrophils)
-> INCREASED ACID production
(gastritis -> peptic ulcer)
Signs/symptoms of PUD
DYSPEPSIA
EPIGASTRIC PAIN
- Duodenal: BETTER after eating (for 1-5hrs)
- Gastric: WORSE after eating
HAEMATEMESIS/MELENA (perforation of artery)
Diagnosis of PUD
H. pylori tests
- urea breath test
- stool antigen test
ENDOSCOPY + BIOPSY (gold) - usually only if red flags present
- Histology + UREASE TEST to check for H. pylori
Treatment of PUD
Treat underlying:
- stop NSAIDs
- H. pylori triple therapy (CAP/ClaMP)
Reduce smokng/alcohol/stress
Description of Dyspepsia
Early satiation
- Anorexia
Severe epigastric pain
Acidic taste
Excessive bloating/belching after meals
Nausea
(these are the things to look for in questions about gastritis etc. i think)
Define GORD
Gastro-oesophageal reflux disorder
Reflux of gastric contents into the oesophagus due to LOWER oesophageal SPHINCTER (LOS) RELAXATION
Risk factors for GORD
- OBESITY
- Pregnancy
- HIATUS HERNIAS
- Smoking
- NSAIDs, alcohol, caffine (increased acid)
MALE (2x)
Signs/symptoms of GORD
- HEARTBURN
- REGURGITATION (worse when lying down)
- Epigastric pain
- Dysphagia
- DYSPEPSIA
- Bloating/belching
- Extra-GI:
- cough, asthma, DENTAL EROSION
- hoarse voice