Phase 2a GI Diseases Flashcards
List 3-5 infective causes of diarrhoea
Viruses
- Rota virus
- Norovirus
Bacteria
- E.coli
- V. cholerae
Antibiotics associated
- C.difficile
- S.aureus
Protozoal
- Cryptosporidium
- Giardia
Food poisoning
- Salmonella
- Campylobacter
- Bacillus Cereus
(Enteric fevers caused by Salmonella paratyphi and salmonella typhi)
Infective gastroenteritis
(treatment)
(RF)
Path
Symptoms
Investigations
Treatments
Acute inflammation of the lining of the stomach and intestines
RF (exposure to contaminated food or water sources, close contact with infected people, poor hygiene)
PATH
- Most common cause are viruses (Rotavirus, norovirus)
- Bacteria can also cause
+ Campylobacter (most common bacterial cause) - spread through raw/uncooked poultry, unpasteurised milk
+ E.coli (E.coli 0157 produces Shiga toxin - leads to symptoms) - spread through contact with infected faeces
+ Shigella - faecal oral route, contact with infected faeces (in food/water)
+ Salmonella - raw eggs/poultry
- Bacillus Cereus - spread through contaminated cooked food e.g. (fried rice that has been left at room temperature)
+ Giardia (parasite) - faecal oral transmission
SYMPTOMS
- Diarrhoea with mostly blood
- Nausea and VOMITING
- Increased frequency of defecation (lasting <14 days)
- ABDOMINAL CRAMPS/pain
- Fever
INVESTIGATIONS
- Stool sample for culture and microscopy
May identify: bacteria (campylobacter, salmonella, shigella, E.coli), protozoa and worm eggs
TREATMENT
1st line - Treat dehydration with oral rehydration or IV fluids
If patients at risk of complications and causative bacteria/organism has been confirmed THEN give antibiotics
Campylobacter - Clarithromycin
Salmonella and Shigella ONLY IN SEVERE CASES/IMMUNOCOMPROMISED - Ciprofloxacin (shigella can also give azithromycin) –> as they usually resolve on their own without antibiotics
Giardia - Metronidazole
Crohn’s disease
(RF)
Path
Symptoms
Investigations
Treatments
A chronic inflammatory autoimmune bowel disease characterised by TRANSMURAL inflammation of the GI tract which leads to fibrosis causing intestinal obstruction.
RF= White ancestry, Jewish, family history of CD, smoking
PATHOLOGY
- NOD 2 mutation (NOD 2 mediates pro inflammatory immune responses)
- Inflammation of the GI tract can appear anywhere from mouth to perianal area (but usually seen in the terminal ileum)
Initially –> Inflammatory infiltrate around intestinal crypts (due to autoimmune causes) –> causes ulceration of superficial mucosa –> inflammation progresses to deeper layers of intestinal wall forming non-caseating granulomas (non infectious causes = non caseating granulomas)
SYMPTOMS
- RLQ abdominal pain
- Prolonged diarrhoea (NOT BLOODY)
- Perianal lesions
- Bowel obstruction
(bloating, distension, vomiting)
(Possible malabsorption if SI is involved: B12,folate,iron deficiency - failure to thrive)
INVESTIGATIONS
- FBC - may be anaemic due to blood loss or malabsorption
FIRST LINE - Faecal calprotectin - raised suggestive of active inflammation
- Endoscopy - skip lesions, cobble stoning
- Tissue biopsy - transmural inflammation with non-caseating granulomas
- Immunologic tests - If pANCA negative and ASCA positive - likely Crohns (Anti-saccharomyces cerevisiae antibodies, perinuclear antineutrophil cytoplasmic antibodies)
TREATMENT
First line remission- Prednisolone (corticosteroid) and then azathioprine
(Possible TNF-alpha inhibitor - Infliximab)
Mesalazine - alternative if corticosteroids (prednisolone) is CI
(As it can span the entire GIT, surgery is not curative)
Complications (just take note)
- Bowel obstruction (due to fibrosis)
- Strictures
- Fistula (tunnel between end of bowel and opening of anus)
- Abscess formation
What are the differences between Crohn’s disease and Ulcerative colitis?
LOCATION
Crohn’s - Can occur anywhere from mouth to anus
UC - Limited to the colon (Large intestine + rectum)
LAYERS IT AFFECTS
Crohn’s - Transmural
UC - Limited to the mucosa
PATTERN OF INFLAMMATION
Crohn’s - patchy (cobblestoning), skip lesions
UC - Continuous diffuse involvement
GRANULOMAS
Crohn’s - present (non caseating granulomas)
UC - Absent
ABDOMINAL PAIN
Crohn’s - LRQ abdominal pain
UC - LLQ abdominal pain
Crohn’s - Has no visual blood and mucous in stool
UC - Has visual blood and mucous in stool
ANTIBODY (but not fool proof as patients may not have the antibodies)
Crohn’s - ASCA
UC - pANCA
Ulcerative Colitis
- What drug to maintain remission?
(RF)
Path
Symptoms
Investigations
Treatments
A type of autoimmune inflammatory bowel disease which affects the rectum and extends towards the colon
RF - family history of IBD, infection, NSAIDS, HLA B27
PATH
- An autoimmune disease associated with HLA B27 that is initiated by an inflammatory response to colonic bacteria (pANCA)
- it arises in the rectum –> moves to sigmoid colon and so on in a continuous diffuse involvement manner, ONLY INVOLVING THE MUCOSA
SYMPTOMS
- Rectal bleeding, tenesmus (increased need to empty bowels)
- Has mucous in stool
- Bloody diarrhoea
- LLQ abdominal pain
- Primary sclerosing cholangitis (90% of UC patients have PSC)
INVESTIGATIONS
- Faecal calprotectin - raised suggestive of active inflammation
- Colonoscopy and biopsy
Colonoscopy - Continuous, diffuse involvement
Biopsy - Mucosal inflammation with crypt hyperplasia
- Immunologic test - pANCA positive and possible ASCA negative
(Can use Truelove and Witts critera to score severity of UC)
(GOBLET CELL DEPLETION)
TREATMENTS
First line (aminosalicylates) - Mesalazine (rectal)
If needed - add prednisolone (for severe exacerbation)
To maintain remission - azathioprine/infliximab
Definitive - Panproctocolectomy
- As UC typically only affects the large bowel and rectum, removing them via panproctocolectomy will remove the disease
Complication
- Toxic megacolon- complication of severe inflammation and colon is dilated. (high risk of bowel rupture)
Irritable Bowel Syndrome
- First line treatment
(RF)
Path
Symptoms
Investigations
Treatments
A chronic condition characterised by abdominal pain that is often relieved by defecation. (associated with bowel dysfunction)
PATHOLOGY
Multifactorial causes
- Stress + anxiety, abuse
- Bile malabsorption
- Bacterial overgrowth
- Inflammatory/immune system involvement
(most likely the case if patient has 6 months of GI symptoms with no underlying cause and everything has been ruled out + one of the symptoms mentioned)
IBS-C –> Mostly constipation
IBS-D –> Mostly diarrhoea
IBS-M –> Mostly mixed, (alternating between D and C)
Symptoms
- Abdominal pain and bloating relived by defecation. (or bloating relieved by passing of flatus)
- Alteration of bowel habits (diarrhoea/constipation/alternating)
INVESTIGATIONS
Diagnosis requires differentials to be excluded:
- Normal Serology to exclude coeliac
- Normal Faecal calprotectin to exclude IBD
- Normal ESR and CRP to exclude infections
MANAGEMENT
1st - Lifestyle and dietary modifications (no caffeine and exercise more)
Low FODMAP diet
For symptomatic - diarrhoea/constipation relief
Constipation - laxatives (senna)
Diarrhoea - anti motility drug (loperamide)
For severe cases where symptoms remain uncontrolled
- Amitriptyline (antidepressant)
- Consider cognitive behavioural therapy (CBT)
Coeliac disease
(KEY symptom)
(RF)
Path
Symptoms
Investigations
Treatments
An autoimmune condition triggered by eating gluten (wheat, rye, barley)
RF - Family history of coeliac disease, IgA deficiency, T1DM, autoimmune thyroid disease
PATHOLOGY
- Patients carry either HLA DQ2 or HLA DQ8 in order to develop coeliacs
- GLIADIN in wheat + other foods binds to HLA DQ2/8 and activates helper T cells –> leads to formation of Anti tissue transglutaminase antibodies and anti-endomysial antibodies (which are both IgA antibodies) –> they target epithelial cells resulting in inflammation of the small bowel –> leading to villous atrophy and crypt hyperplasia
Symptoms
- Diarrhoea
- Abdominal pain/discomfort
- Anaemia due to malabsorption (deficiency of iron, B12, folate)
- Weight loss/failure to thrive
- DERMATITIS HERPETIFORMIS - itchy, blistering skin rash on the abdomen (caused by deposition of IgA in the skin)
Investigations
1st line - Serology for anti-TTG IgA antibodies (above normal range)
- ALSO total IgA to EXCLUDE IgA deficiency (because if you have IgA deficiency, you will have a low anti-TTG leading to a false negative)
GS - Endoscopy and biopsy –> Showing crypt hyperplasia and villous atrophy (and epithelial lymphocyte infiltration)
TREATMENT
1st line - Gluten free diet (+ vitamins and mineral supplementation to replace for malabsorption)
(monitor for osteoporosis with DEXA scan - due to malabsorption of calcium and vit D)
Gastritis
(Causes)
(RF)
Path
Symptoms
Investigations
Treatments
Gastric mucosal inflammation
RF - H.pylori infection, NSAIDS, alcohol use, previous gastric surgery
PATHOLOGY
Commonly caused by
1) H.pylori - induces inflammatory response with gastric mucin degradation and increased mucosal permeability
2) NSAIDS - inhibit prostaglandin production, reducing mucosal protective factors (stomach is more susceptible to damage)
3) Alcohol - compromises integrity of mucosal barrier
Less common but possible
4) Autoimmune mediated atrophic gastritis with antiparietal cell antibodies. – antiparietal cell antibodies target parietal cells of the stomach lining which can lead to chronic inflammation and damage the stomach lining.
Symptoms
- Epigastric discomfort/pain
- N+V
(NO DIARRHOEA)
(dyspepsia)
Investigations
1st H.pylori urea breath test, faecal antigen test (positive in H pylori infection)
GS - Endoscopy and biopsy –> evidence of gastric erosions and/or atrophy
TREATMENT
For H.pylori - Triple therapy
- Omeprazole
- Clarithromycin
- Amoxicillin (or metronidazole if they are allergic to penicillin)
For erosive causes
- Stop NSAIDS and alcohol
Autoimmune
- IM Hydroxocobalamin
Complication - Gastroduodenal artery , obstruction, perforation
H.pylori
What kind of bacteria?
Pathology
What does it cause?
Investigations
Treatment
Gram negative bacilli that resides in the gastric antrum as a commensal.
1) It has urease which converts urea into carbon dioxide and ammonia –> ammonia neutralises the acidity of the stomach –> H pylori can move towards the stomach cells
2) Increases luminal gastric acid (H.pylori causes inflammation causing an increased production of gastrin)
3) It reduces bicarbonate secretion
(May reduce somatostatin secretion)
It can cause: Peptic ulcers, gastritis, gastric carcinoma
Investigations
H.pylori urea breath test
Stool antigen test - positive in H.pylori infection
Treatment
Triple therapy
- Omeprazole, clarithromycin, amoxicillin/metronidazole
Gastro-oesophageal reflux disease- investigations and treatment
(RF)
Path
Symptoms
Investigations
Treatments
Reflux of gastric contents into the oesophagus results in symptoms and/or complications
RF - family history of heartburn/GORD, older age, obesity, hiatus hernia (stomach enters oesophagus through hiatus of diaphragm, making it easier for reflux of contents from stomach to oesophagus)
Causes:
- Increased abdominal pressure - obesity, pregnancy
- Hiatus hernia
- Drugs (like anti muscarinics)
PATHOLOGY
Increased episodes of transient lower esophageal sphincter relaxation (result in reflux of gastric contents (and acid) into the oesophagus resulting in mucosal damage. (LOW LES PRESSURE)
SYMPTOMS
- Heartburn (retrosternal burning chest pain which is worse on lying down - as acid easier to reflux)
- Chronic and nocturnal cough
- Acid regurgitation (reflux of acid into the mouth)
- Dysphagia –> Bad sign, severe symptom
INVESTIGATIONS
If no red flags - straight to treatment (clinical/symptomatic diagnosis)
If red flags present (dysphagia, haematemesis, weight loss)
- Endoscopy –> may show oesophagitis or barrett’s oesophagus (stratified squamous to simple columnar)
Oesophageal manometry –> to measure LOS pressure and function
TREATMENT
1st - lifestyle modifications (stop smoking, avoid heavy meals before bed, lose weight, reduce coffee and alcohol)
2nd - PPI (H2 receptor antagonist if CI)
Last resort –>
Surgery - Nissen fundoplication (laparoscopic fundoplication) –> tightens the junction between the esophagus and stomach to prevent acid reflux.
Gastric Peptic Ulcer
(RF)
Path
Symptoms
Investigations
Treatments
A break and ulceration in the mucosal lining of the stomach more than 5mm in diameter (with depth to the submucosa)
RF - H.pylori, NSAIDS, smoking, old age
PATHOLOGY
Mainly caused by H.pylori and NSAIDS.
More uncommon causes - Gastric ischemia and Zollinger-ellison syndrome (gastrin secreting tumour - pancreatic or rarely intestinal tumour –> hyper secretion of gastric acid –> widespread peptic ulcers)
SYMPTOMS
- Epigastric pain that is worse on eating (often nocturnal)
(Pain better between meals)
- Weight loss (patients with gastric ulcers tend to lose weight due to fear of pain on eating)
INVESTIGATIONS
If no melaena, haematemesis, dysphagia (otherwise may need urgent endoscopy)
1st line - H.pylori urea breath test/stool antigen test (It is non invasive that’s why first line
(THEY MUST BE OFF PPI FOR at least 2 weeks otherwise possible false negative)
GS - Endoscopy (detects peptic ulcer) + biopsy (to check for malignancy)
Treatment
TREATMENT
- STOP NSAIDS
AND
For H.pylori –> Triple therapy with (CAP)
Clarithromycin/metronidazole + amoxicillin + omeprazole (PPI)
No H.pylori –> PPI (or H2 receptor antagonist if CI)
(Perform endoscopy 6-8 weeks later to ensure ulcer healing)
(Complication - upper GI bleeding as ulcer may erode into wall of left gastric artery)
Duodenal Peptic Ulcers (more common than gastric ulcers)
- What would you see on biopsy?
- What is a complication of duodenal peptic ulcer?
(RF)
Path
Symptoms
Investigations
Treatments
Complication
A break or ulcer in the mucosal lining of the duodenum more than 5cm in diameter (with depth to the mucosa)
PATHOLOGY
- Mostly due to H.pylori (inflammation + inhibition of secretion of somatostatin leads to increased gastrin release)
- More uncommon - NSAIDS, Zollinger-ellison syndrome.
SYMPTOMS
- Epigastric pain that is worse 2-3 hours after food (pain between meals) –> PAIN IS BETTER WITH FOOD
(NO WEIGHT LOSS LIKE GASTRIC ULCERS)
INVESTIGATIONS
- If no red flags (haematemesis, melaena, dysphagia)
DO NON INVASIVE TESTING
- H.pylori Urea breath test/stool antigen test
Patient must be off PPI for 2 weeks otherwise possible false negative
If red flags/GS
- Endoscopy (detects peptic ulcer) + biopsy (Brunner’s gland hyperplasia - increased mucin production to protect duodenal mucosal lining)
TREATMENT
- STOP NSAIDS
For H.pylori –> Triple therapy with (CAP)
Clarithromycin/metronidazole + amoxicillin + omeprazole (PPI)
No H.pylori –> PPI (or H2 receptor antagonist if CI)
(Perform endoscopy 6-8 weeks later to ensure ulcer healing)
COMPLICATION - Gastroduodenal bleeding - most common
Appendicitis
-What antibiotic?
- First line investigation?
(RF)
Path
Symptoms
Investigations
Treatments
Inflammation of the appendix
RF - smoking, (improved personal hygiene?)
PATHOLOGY
Mainly caused by OBSTRUCTION OF THE LUMEN OF THE APPENDIX by:
- FAECOLITH - hard mass of faecal matter
- Lymphoid hyperplasia (As a reaction to infections)
This obstruction results in the lumen filling with mucus –> allowing resident bacteria to multiply (E.coli, Bacteroides fragilis) –> As pressure in the appendix builds up –> it can rupture, releaseing faecal contents and infective material into the peritoneal cavity, causing peritonitis - SBP
SYMPTOMS
- Umbilical pain that localises at the right iliac fossa later (1-12 hours later)
- Tenderness at Mc Burney’s point on palpation
- Anorexia, N+V
- Rebound tenderness and abdominal guarding
SIGNS
1) Rovsing’s sign - palpation of the left iliac fossa causes pain in the right iliac fossa
INVESTIGATIONS
FBC - Leukocytosis
CRP - elevated
GS - (usually ultrasound first line?) CT scan
Also do pregnancy test to rule out ectopic pregnancy (Serum HCG) FIRST before CT (for women of childbearing age)
MANAGEMENT
Antibiotics (co-amoxiclav) and then appendectomy (laparoscopic surgery less invasive than open surgery)
(If abscess is present - drain it, OTHERWISE INTERFERES WITH ANTIBIOTICS)
Complications of appendectomy
Bleeding, infection, damage to surrounding organs, venous thromboembolism
What is
Diverticulum
Diverticulosis
Diverticular disease
Diverticulitis
Meckel’s diverticulum
Diverticulum (diverticula) - a pouch in the bowel wall
Diverticulosis - presence of an asymptomatic diverticula
Diverticular disease - presence of a symptomatic diverticula
Diverticulitis - When patients experience inflammation and infection as a result
Meckel’s diverticulum - a paediatric disorder where there is failure of obliteration of the vitelline duct
Diverticulosis (and diverticulitis)
Treatment of diverticulitis
(RF)
Path
Symptoms
Investigations
Treatments
A pouch in the bowel wall (that can be asymptomatic or symptomatic)
RF - >50 years, MARFAN and EHLERS-DANLOS, obesity, low dietary fibre, NSAIDS, sedentary lifestyle
PATHOLOGY
Most common site - sigmoid colon
Due to different causes + risk factors, there is increased pressure in the colon –> pushing on the mucosa and submucosa till they push through at weak spots (where blood vessel penetrates muscle layer) forming an out pouch –> bacteria and undigested food may get stuck in the out pouches and cause infection - DIVERTICULITIS
SYMPTOMS
Diverticulosis is typically asymptomatic till the diverticula becomes inflamed –> diverticulitis
Triad: LLQ pain, constipation, rectal bleeding (haematochezia)
(possible fever)
INVESTIGATION
FBC - leukocytosis
CRP - elevated
GS - Contrast CT scan of abdomen
(consider colonoscopy)
MANAGEMENT
Diverticulosis - Watch and wait (asymptomatic)
Diverticular disease
- BULK FORMING LAXATIVES (ispaghula husk)
(if significant symptoms - surgery to remove the affected area)
Diverticulitis
Oral Co amoxiclav
paracetamol + a liquid diet (Anitbiotics + analgesia)
- IV fluids
(if significant symptoms - surgery)
Complications - abscess formation, fistula (when abscess formation ruptures into adjacent organs), strictures/obstruction due to inflammation.
Meckel’s diverticulum (investigation)
(RF)
Path
Symptoms
Investigations
Treatments
A congenital malformation of the small bowel where a diverticulum forms due to failure of the vitelline duct to obliterate –> leads to a blind end pouch
Mostly seen in children <2 years (but meckel’s diverticulitis occurs more in adults)
Symptoms: haematochezia, constipation, abdominal pain/tenderness/cramps
Investigations
- Technetium 99m (pertechnetate) scan (Meckel’s scan)
- CT scan
TREATMENT
Asymptomatic - no treatment needed
Symptomatic - Surgical excision of diverticulum
