GI Flashcards
State some obstructive causes of dysphagia
Oesophageal carcinoma Peptic strictures Oesphageal web/ring Gastric carcinoma Pharyngeal carcinoma Extrinsic pressure from - lung carcinoma, restrosternal goitre
State some motility disorders which cause dysphagia
Achalasia Systemic sclerosis Stroke Myasthenia gravis Neurological disorders - Motor neurone isease, Parkinson's
Which GI ulcers are the most common?
Duodenal
4x times fore than gastric
When are the different GI ulcers relived after eating?
o Gastric - pain is worse SOON after eating
o Duodenal - pain is worse SEVERAL HOURS after eating
Identify appropriate investigations for peptic ulcer disease and gastritis
BLOODS o FBC (for anaemia) o Serum amylase (to exclude pancreatitis) o U&Es o Clotting screen o LFT o Cross-match if active bleeding o Secretin test (if Zollinger-Ellison syndrome suspected) - IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients)
ENDOSCOPY
o Biopsies of gastric ulcers can be taken to rule out malignancy
o Duodenal ulcers do NOT need to be biopsied
• Testing for H. pylori:
o C13-urea breath test :
• Radio-labelled urea is given by mouth
• C13 is detected in the expelled air o Serology:
• IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication
o Campylobacter-like organism (CLO) test:
• Gastric biopsy is placed with a substrate of urea and a pH indicator
• If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red
What is the Rockall score? And what does it indicate.
• Rockall Scoring:
o Scores the severity after a GI bleed
o Score < 3 carries good prognosis
o Score > 8 carries high risk of mortality
Generate a management plan for peptic ulcer disease and gastritis
ACUTE
o Fluid resuscitation needed if the ulcer is perforated or bleeding (IV colloids/crystalloids)
o Close monitoring of vital signs
o Endoscopy
o Surgical treatment
o NOTE: patients with upper GI bleeding should be treated with IV PPIs at presentation until the cause of bleeding is identified
• Endoscopy: o If the ulcer is bleeding, haemostasis can be achieved with: • Injection sclerotherapy • Laser coagulation • Electrocoagulation
• Surgery:
o Indicated if the ulcer has perforated or if the bleeding ulcer can’t be controlled
• Helicobacter pylori eradication:
o Triple therapy for 1-2 weeks
o Various combinations may be recommended M usually a combination of 2 antibiotics + PPI (e.g. clarithromycin + amoxicillin + omeprazole) **
• If peptic ulcer disease is NOT associated with H. pylori:
o Treat with PPIs or H2 antagonists
o Stop NSAID use
o Use misoprostol (prostoglandin E1 analogue) if NSAID use is necessary
Identify the possible complications of peptic ulcer disease and gastritis
• Rate of major complication = 1 % per year
• Major complications:
o Haemorrhage (haematemesis, melaena, iron-deficiency anaemia)
o Perforation
o Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)
Summarise the prognosis for patients with peptic ulcer disease and gastritis
- Overall lifetime risk = 10%
* Outlook is generally good because peptic ulcers associated with H. pylori can be cured by eradication
In triple therapy what AB can be used if the patient is allergic to penicillin?
Clarithromycin
Metronidazole
What’s the most common cause of duodenal ulcers?
H pylori (90%)
Whats the most appropriate investigation for a hiatal hernia?
Barium swollow
CXR - might show no abnormalities
What histological changes occur in barret’s?
The lower third of the oesophagus undergoes metaplasia of squamous cell to columnar
An adaptive mechanism in withstanding the erosive action of the stomach acid.
This metaplasia is described as premalignant state and increases the risk of adenocarcinoma of the oesophagus
IX - by OGD.
Which bacteria cause bloody diarrhoea?
Campylobacter
Salmonella
E Coli
Shigella
What is Budd-Chiari syndrome?
Hepatic vein outflow obstruction
Unkown cause in 50%
Triad:
- Acute abdominal pain
- Hepatomegaly
- Ascites
Can cause: liver failure, cirrhosis.
What is the most common cause of upper GI bleed?
Peptic Ulcers (35-50%) Mallory Weiss tears (15%)
oesophagitis gastritis and gastric erosions oesophageal varices drugs - NSAID's upper GI malignancy
Whats the prophylaxis for oesophageal varices?
Non-selective beta-blockers - reduces portal pressure and reduces risk of variceal bleeding
What is the most common cause of hepatitis?
Hep B & C
GI causes of ascites
Ascites secondary to venous hypertension: Cirrhosis, CHF, Constrictive pericarditis, Budd-Chiari syndrome, Portal vein thrombosis.
Ascites secondary to Hypoalbuminaemia: nephrotic syndrome, malnutrition
Ascites secondary to Malignant disease: 2’ mets of carcinomas of breast, ovary, colon.
Ascites secondary to Infections: TB
Ascites secondary to Others: pancreatic isease, ovarian disease, myxoedema.
Whats the pattern of inheritence of a1-antitrypsin deficiency?
Autosomal recessive
What is a1-antitrypsin a RF for?
Laz:
COPD
Liver cirrhosis (Portal hypertension)
500 SBA: Emphysema Chronic liver disease Hepatocellular carcinoma Asthma Pancreatitis Gallstones Wegener's granulomatosis
Most appropriate treatment for autoimmune hepatitis
Prednisolone
What kindo f cancer does PSC predispose you to
Cholangiocarcinoma
What are obstructive jaundice symptoms?
Yellow Sclera
Pale stools
Dark Urine
Pruritus
State some benign liver tumors
Hemangioma (most common) Adenoma Cyst Focal nodular hyperplasia Fibromas Leiomyomas
State some causes/risk factors of UC
Family History
pANCA
PSC
Summarise the epidemiology of ulcerative colitis
• Higher prevalence in: o Ashkenazi jews o Caucasians • Uncommon before the age of 10 yrs • Peak onset: 20J40 yrs • Equal sex ratio up to the age of 40 yrs (higher in males from then on)
Recognise the presenting symptoms of ulcerative colitis
- Bloody or mucous diarrhoea (stool frequency depends on severity of disease)
- Tenesmus and urgency
- Crampy abdominal pain before passing stool
- Weight loss
- Fever
- Extra-GI manifestations (e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum)
Recognise the signs of ulcerative colitis on physical examination
• Signs of iron deficiency anaemia (e.g. conjunctival pallor) • Dehydration • Clubbing • Abdominal tenderness • Tachycardia • Blood, mucus and tenderness on PR examination • Extra-GI manifestations
List some extra-GI manifestations of UC
Uveitis
Scleritis
Erythema nodosum
Pyoderma gangrenosum
Identify appropriate investigations for ulcerative colitis
BLOODS o FBC: • Low Hb • High WCC o High ESR or CRP o Low albumin o NOTE: X-match if there is severe blood loss
STOOL
o Infectious colitis is a differential diagnosis so a stool culture maybe useful
o Faecal calprotectin* allows differentiation of IBS from IBD (raised in IBD not raised in IBS)
AXR
o Rule out toxic megacolon
FLEX SIG AND COLONOSCOPY
o Determines severity
o Histological confirmation
o Detection of dysplasia
BARIUM ENEMA
o Shows mucosal ulceration with granular appearance and filling defects (due to pseudopolyps)
o Narrowed colon
o Loss of haustral pattern - leadpipe* appearance (right)
o Colonoscopy and barium enema may be DANGEROUS
during an acute exacerbation - risk of perforation
Markers of disease activity in UC
o Decreased Hb
o Decreased albumin
o Increased ESR and CRP
o Diarrhoea frequency:
• < 4 = mild
• 4M6 = moderate
• 6+ = severe
o Bleeding
o Fever
What is the management of an Acute Exacerbation of UC
o IV rehydration o IV corticosteroids o Antibiotics o Bowel rest o Parenteral feeding may be necessary o DVT prophylaxis o If toxic megacolon - the patient is likely to need a proctocolectomy because toxic megacolon has a high mortality
• Management of Mild Disease of UC
o Oral or rectal 5-ASA derivatices (e.g. mesalazine, olsalazine, sulphasalazine)
o And/or rectal steroids
• Management of Moderate to Severe Disease of UC
o Oral steroids
o Oral 5-ASA
o Immunosuppression (with azathioprine*, cyclosporine, 6-mercaptopurine or infliximab (anti-TNF monoclonal antibody))
What is the surgical managment of UC and the advice fiven to patients.
• Advice
o Patient education and support
o Treat complications
o Regular colonoscopic surveillance
• Surgical
o If medical treatment fails, presence of complications or to prevent colonic carcinoma
o Procedures:
• Proctocolectomy with ileostomy
• Ileo-anal pouch formation (J pouch)
Which part of the GI is mostly affected in Crohn’s and which deficiency is associated with this?
Terminal ileum
B12 deficiency
Define coeliac disease
• An inflammatory disease caused by intolerance to GLUTEN, causing chronic intestinal
malabsorption.
• It leads to subtotal villous atrophy and crypt hyperplasia
Explain the aetiology/risk factors of coeliac disease
- Due to sensitivity to the GLIADIN* component of gluten
- Exposure to gliadin triggers and immunological reaction in the small intestine leading to mucosal damage and loss of villi
What are the genetic associations in coeliac disease?
- 10% risk of first-degree relatives being affected
* Clear genetic susceptibility associated with HLA-B8, HLA-DR3 and HLA-DQW2 haplotypes
Recognise the presenting symptoms of coeliac disease
Diarrhoea and abdominal bloating/distention/discomfort.
- May be asymptomatic
- Abdominal discomfort, pain and distention
- Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away)
- Diarrhoea
- Tiredness, malaise, weight loss (despite normal diet)
- Failure to ‘thrive’ in children
- Amenorrhoea in young adults
Recognise the signs of coeliac disease on physical examination
• Signs of anaemia: pallor
• Signs of malnutrition: o Short stature o Abdominal distension o Wasted buttocks in children o Triceps skinfold thickness gives indication of fat stores
- Signs of vitamin/mineral deficiencies: osteomalacia, easy bruising
- Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)
Identify appropriate investigations for coeliac disease
• Blood: o FBC (low Hb, iron and folate) o U&E o Albumin o Calcium o Phosphate
• Serology: **
o IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic
o NOTE: IgA deficiency is quite COMMON (1/50 with coeliac) so Ig levels should be measured to avoid false negatives
- Stool: culture to exclude infection, faecal fat tests for steatorrhoea
- D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption
• Endoscopy: allows direct visualisation of villous atrophy in the small intestine (mucosa appears flat and smooth)
o Biopsy will show villous atrophy and crypt
hyperplasia in the duodenum
o The epithelium adopts a cuboidal appearance
- there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria
Generate a management plan for coeliac disease
- Advice: avoid gluten (wheat, rye and barley products)
* Medical: vitamin and mineral supplements. Oral corticosteroids if disease does not subside with avoidance of gluten
Identify the possible complications of coeliac disease
- Iron, folate and B12 deficiency**
- Osteomalacia
- Ulcerative jejunoileitis
- GI lymphoma (particularly T cell)
- Bacterial overgrowth
- Cerebellar ataxia (rarely)
Summarise the prognosis for patients with coeliac disease
- FULL RECOVERY in most patients who strictly adhere to a gluten-free diet
- Symptoms usually resolve within weeks though histological changes may take longer
- Gluten-free diet must be followed for life
