MED: Gastroenterology Flashcards
What are the subtypes of alcoholic liver disease?
Alcoholic fatty liver disease
Alcoholic hepatitis
Alcoholic cirrhosis
What are the early clinical features of ALD?
- Asymptomatic
- Fatigue
- Malaise
- Abdominal pain
- Anorexia
- Weakness
- Nausea and/or vomiting
What are the clinical features of alcoholic hepatitis?
- Jaundice
- Right upper quadrant pain
- Hepatomegaly - generally enlarged and smooth edge, rarely tender to palpation
- Palmar erythema
- Peripheral oedema
- Clubbing
- Dupuytren’s contracture
- Pruritis
- Xanthomas
- Spider angiomas - multiple are characteristic of CLD, while solitary angiomas are seen in other systemic disease
What are oestrogenic effects of ALD?
- Gynaecomastia and testicular atrophy (in males)
- Loss of body hair
- Amenorrhoea (in females)
- Loss of libido
What are the clinical features of portal hypertension?
- Ascites
- Dilated veins (e.g. caput medusae)
- Variceal bleeding and haemorrhage
- Splenomegaly
What are the investigations for ALD?
Bloods:
- Raised AST and ALT - ratio of AST : ALT > 2 - 3
- GGT raised
- ALP likely normal
- Conjugated bilirubin may be raised
- Low serum albumin
- Raised PT / INR
USS:
- Used to differentiate causes of abnormal liver function tests
Liver biopsy:
- Not usually necessary for ALD due to invasiveness of procedure
What are general measures used in the management of alcoholic liver disease?
- Alcohol abstinence
- Weight loss
- Vaccinations - in the absence of past / current infection, provide hep A and B immunisations
- Nutrition - high protein diet, consider feeding tube for enteral feeding if anorexia or altered mental status
What is the management of alcohol withdrawal?
Acute alcohol withdrawal = benzodiazepines (e.g. chlordiazepoxide / diazepam)
Lorazepam may be preferable in patients with hepatic failure
Alcohol withdrawal seizures = quick-acting benzodiazepine (e.g. lorazepam)
Delirium tremens = oral lorazepam
What is the management of acute alcoholic hepatitis?
Glucocorticoids (e.g. prednisolone)
- Pentoxifylline can be used as an alternative to glucocorticoids if they are contraindicated (e.g. hep B, TB, other serious infection)
Maddrey’s discriminant function (DF):
To identify patients with severe acute alcoholic hepatitis
- DF >32 predicts a high mortality within 90 days, and means a liver biopsy should be considered, with corticosteroid treatment initiation
What is the management of end stage ALD?
Liver transplantation can be considered
Usually must be alcohol free for >6 months
What is hepatic encephalopathy?
In severe cases of ALD, hepatic encephalopathy can occur as a result of significant toxin build-up (ammonia)
S/S:
- Confusion
- Drowsiness
- Hyperventilation
- Asterixis
- Fetor hepaticus
Management:
- Supportive care plus lactulose until laxative effect is achieved.
What is portal hypertension?
- Occurs once liver cirrhosis is established.
- Blood vessels in liver blocked due to severe fibrosis > high pressure develops in portal venous system > large varices within venous system in esophagus, stomach, rectum and umbilicus.
- This results in secondary complications such as variceal haemorrhage, ascites and splenomegaly.
- Ascites can be complicated by spontaneous bacterial peritonitis (suspect in patients with abdominal distention, pain +/- fever)
- This can be managed with a transjugular intrahepatic portal-systemic shunt (TIPSS) if there is acute bleeding, particularly if gastric varices are present
What is hepato-renal syndrome?
As a result of portal hypertension, there is widespread splanchnic vasodilation
This leads to a reduction in the effective circulating volume, which can reduce the blood flow to the kidneys, compromising the renal system and potentially leading to a life-threatening acute kidney failure
What is a worrying complication of liver cirrhosis?
Hepatocellular carcinoma
Hepatic ultrasound should be undertaken serially approximately every 6 months to yearly to screen for liver cancer development
Describe the classification of autoimmune hepatitis
Type 1:
- positive for ANA and/or SMA
- may also be associated with perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA).
- Accounts for the majority of cases.
Type 2:
- associated with either anti-liver kidney microsomal-1 (LKM-1) or anti-liver cytosolic-1 (LC-1) antibodies.
- generally more severe, patients are younger at diagnosis and the disease is usually more advanced at presentation
Type 3:
- associated with autoantibodies against soluble liver antigens (anti-SLA) or liver-pancreas antigen (anti-LP)
What are the clinical features of AIH?
- Can be asymptomatic
- Jaundice
- Non-specific symptoms e.g. fatigue, anorexia, weight loss, abdominal pain amenorrhoea.
- Features of cirrhosis e.g. ascites, variceal bleeding
- Pruritus
- Arthralgias.
- Maculopapular rash.
- Pyrexia of unknown origin.
- Raised transaminase levels and IgG
The classical picture of AIH is as a chronic disease with raised transaminase levels for at least three months. However, in about 40% of patients AIH may present acutely, sometimes preceded by a flu like illness
What other autoimmune diseases is AIH associated with?
- Most common - autoimmune thyroid disease
- Type 1 diabetes
- Rheumatoid arthritis
- Vitiligo
- Ulcerative colitis
- Coeliac
What are the investigations for AIH?
Lab tests:
- Raised ALT and AST
- Raised serum immunoglobulins, particularly IgG.
- Negative serum tests for viral hepatitis
- High titers of circulating autoantibodies - ANA and anti-SMA
- Serum ALP will be normal or only slightly raised
Liver biopsy required:
- Interface hepatitis - Inflammation of the hepatocytes at the junction of the portal tract and the hepatic parenchyma
- Periportal lymphocytic inflammation
- Hepatocyte swelling
- Necrosis
What is the management of autoimmune hepatitis?
**Patients with moderate to severe inflammation // symptomatic patients // younger patients more at risk of developing cirrhosis later in life should be offered treatment*
Moderate to severe inflammation suggested by:
- AST >5 times the normal serum level
- Immunoglobulins >2 times the normal serum level
- Liver biopsy showing necrosis
Prednisolone, sometimes in combination with azathioprine:
- In adjunct to this, patients should be vaccinated against hepatitis A and B infection, receive calcium and vitamin D supplementation, and have regular DEXA scans and screening for glaucoma and cataracts.
Liver transplantation:
- Indicated by either severe acute AIH resulting in liver failure, decompensated liver disease or hepatocellular carcinoma.
What are the complications of liver cirrhosis?
- Ascites
- Spontaneous bacterial peritonitis
- Haemorrhages (e.g. due to variceal bleeding)
- Hepatic encephalopathy
- Hepatocellular carcinoma
What are the extraintenstinal manifestations of coeliac disease?
- Dermatitis herpetiformis - intensely pruritic, vesicular rash, typically affecting the elbows, knees, and buttocks.
- Fatigue - due to malabsorption of essential nutrients or anaemia.
- Iron deficiency anaemia - common, may be the initial presenting feature in some
- Weight loss - result of malabsorption.
- Bone pain and fractures - due to osteoporosis or osteopenia, secondary to malabsorption of calcium and vitamin D
- Peripheral neuropathy - numbness, tingling, or burning sensations in the extremities
What are the investigations for coeliac disease?
Serological Testing:
- Anti-tTG antibodies
- Anti-EMA antibodies - used in cases with equivocal anti-tTG results or when confirmation of the diagnosis is needed.
- Total serum IgA levels - important to exclude selective IgA deficiency, which may lead to false-negative results in serological testing.
Duodenal Biopsy:
- gold standard for diagnosing coeliac disease
- Villous atrophy
- Crypt hyperplasia
- Increased intraepithelial lymphocytes
What is the management of coeliac disease?
- Strict gluten-free diet
- Supplementation with iron, folic acid, vitamin B12, calcium, and vitamin D may be necessary
- All patients offered pneumococcal vaccine
What are examples of foods containing gluten?
Wheat: bread, pasta, pastry
Barley: beer
Rye
Oats: some patients with coeliac disease appear able to tolerate oats
What malignancies are associated with coeliac disease?
Enteropathy-associated T-cell lymphoma (EATL):
- A rare and aggressive type of non-Hodgkin lymphoma arising from intraepithelial lymphocytes in the small intestine
- EATL has a poor prognosis and is often associated with refractory coeliac disease type II.
Small bowel adenocarcinoma:
- The risk of small bowel adenocarcinoma is also increased in coeliac disease, although the overall incidence remains low.
What are some extra intestinal manifestations of CD?
- Peripheral arthritis - large joints e.g. knees, ankles, and wrists, non-destructive, non-deforming
- Axial arthritis - ankylosing spondylitis and sacroiliitis, can cause low back pain and morning stiffness.
- Erythema nodosum - painful, raised, erythematous nodules on the lower extremities.
- Pyoderma gangrenosum - rapidly progressing, painful ulcers with undermined, violaceous borders, often involving the lower extremities or peristomal skin.
- Uveitis - eye pain, photophobia, and blurred vision.
- Episcleritis - eye redness and mild pain
- Scleritis - more painful and can lead to vision loss if untreated.
- Primary sclerosing cholangitis
- Cholelithiasis and fatty liver disease
- Anaemia, vitamin B12 and folate malabsorption.
- Increased risk for venous and arterial thromboembolic events, including DVT, PE, and stroke
What are the investigations for CD?
Blood tests:
- FBC, CRP, ESR, LFTs, serum albumin, and iron studies, vitamin B12 and folate levels
- Info about inflammation, anaemia, and nutritional status
Stool tests:
- Stool cultures, ova and parasite examination, and faecal calprotectin
- Can help differentiate between IBD and infectious or non-inflammatory causes of diarrhoea.
Colonoscopy and biopsy:
- Findings include aphthous ulcers, cobblestoning, non-caseating epithelioid cell granulomata, discontinuous/patchy inflammation with skip lesions
Capsule endoscopy:
- In cases where traditional endoscopy is inconclusive, video capsule endoscopy can be utilized to visualize the small bowel and detect areas of inflammation not reachable by colonoscopy or upper endoscopy.
CT/MRI:
- MRI preferred in CD due to its lack of ionizing radiation and superior soft tissue contrast.
Ultrasound:
- May be used as a non-invasive imaging modality, particularly for assessing disease activity, complications, or response to therapy.
Histology:
- Non-caseating granulomas, transmural inflammation, lymphoid aggregates, crypt architectural abnormalities, and cryptitis or crypt abscesses
What is the management of CD?
Conservative:
- Education on features and flare ups
- Support - www.crohnsandcolitis.org.uk
- Stop smoking
- Careful with NSAIDs and COCP (increased risk of relapse)
Inducing remission:
- First line = glucocorticoids e.g. pred (PO, topical or IV)
- Enteral feeding with an elemental diet may be used in addition / instead of other measures, particularly if concern regarding steroid SEs (e.g. young children)
- Second line = 5-ASA drugs (e.g. mesalazine)
- Azathioprine or mercaptopurine may be used as an add-on medication but not as monotherapy
- Methotrexate is an alternative to azathioprine
- Infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
- Metronidazole often used for isolated peri-anal disease
Maintaining remission:
- First line = azathioprine or mercaptopurine (cannot be given with TPMT mutation, cannot have live vaccines, must have pneumococcal and influenza vaccines)
- Second line = methotrexate
Surgery:
- For complications (obstruction, fistula, abscess, severe localised disease unresponsive to treatment)
What are the complications of CD?
- Strictures - managed with endoscopic balloon dilation, stricturoplasty, or bowel resection
- Fistulas - can cause abscess formation, recurrent infections, and malabsorption. Management includes medical therapy, endoscopic or surgical interventions
- Abscesses - managed with antibiotics and percutaneous or surgical drainage.
- Perianal disease - fissures, abscesses, and fistulas. Treatment may involve medical therapy, surgical intervention
- Malabsorption and nutritional deficiencies - iron, vitamin B12, and fat-soluble vitamins, resulting in anemia, osteoporosis, and other nutritional deficiencies.
- Colorectal cancer - regular surveillance colonoscopy with biopsies is recommended for early detection and management.
What are the investigations for GORD?
Whilst isolated symptoms do not require investigation, patients fitting any of the following criteria should be referred for oesophago-gastroduodenoscopy (OGD):
- Age >55 years
- Symptoms >4 weeks
- Dysphagia
- Persistent symptoms despite treatment
- Relapsing symptoms
- Weight loss
- Excessive vomiting
- GI bleeding
Other tests include:
- A barium swallow test should be performed to rule out hiatus hernia.
- A 24 hour oesophageal PH monitoring may be needed to distinguish GORD from other causes.
- Patients showing systemic symptoms, or who have lesions shown on OGD, should have a FBC to rule out anaemia.
What is the management of GORD?
Lifestyle changes:
- Reduce weight
- Stop smoking
- Decrease alcohol intake
- Raise head at night (sleep propped up)
- Avoid hot drinks, alcohol and eating within 3hrs of going to sleep
- Avoid nitrates, anticholinergics, tricyclic antidepressants, NSAIDs, K+ salts, alendronate
Drugs:
- Patient without any red flag symptoms should be given a 4 week full-does PPI therapy course.
- If symptoms return, the dosage of PPI should be stepped down to the lowest level that still relieves symptoms.
- Offer H2RA therapy if there is inadequate response to a PPI
Consider referring anyone to a specialist who:
- Has unexplained GORD symptoms not responding to treatment.
- Is considering surgery.
Surgery:
- Laparoscopic fundoplication, also known as a Nissen fundoplication, is the surgical procedure of choice.
- It is indicated for patients who have a confirmed GORD diagnosis via endoscopy, respond to PPI therapy, but do not wish to continue it long term / cannot tolerate acid suppression therapy.
What are the complications of GORD?
- Oesophagitis
- Strictures
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
- Respiratory complications - chronic cough, asthma exacerbations, laryngitis, and recurrent pneumonia.
What is haemochromatosis?
An iron storage disorder in which iron depositions in multiple organs (such as the liver, skin, pituitary, heart and pancreas) leading to oxidative damage
What is the cause of haemochromatosis?
Primary (hereditary):
- Autosomal recessive mutations to the haemochromatosis (HFE) gene on chromosome 6.
Secondary (acquired):
- Frequent blood transfusions - each new transfusion introduces new iron which is recycled and stored
- Iron supplementation - over-supplementing, particularly with concurrent vitamin C.
- Diseases of erythropoiesis - ineffective erythropoiesis leads to iron accumulation
What are the clinical features of haemochromatosis?
- Asymptomatic
- Non-specific signs of iron overload (fatigue, arthralgias, impotence)
- Signs of organ damage, such as diabetes
- Joint symptoms are usually a non-inflammatory osteoarthritis presentation in the metacarpophalangeal and proximal interphalangeal joints, but may be present in larger joints such as the hip and shoulder.
- ‘classic triad’ of cirrhosis, diabetes mellitus and bronze pigmentation is rarely the initial presentation.
- Pigmentation will initially present as skin bronzing but if it has progressed then may be grey or brown.
- Pigmentation most commonly occurs on the face and neck, extensor surfaces of the forearms, dorsum of the hands, lower legs, genitals, and in old scars.
What are the investigations for haemochromatosis?
Bloods:
- Serum ferritin - raised
- Transferrin saturation - raised
- LFTs - AST and ALT raised
- FBC - normal
Molecular Testing:
- HFE gene mutation
Liver biopsy:
- If clinical evidence of liver involvement and/or serum ferritin >2247pmol/L
- To estimate hepatocyte iron content and assess extent of fibrosis or cirrhosis.
What is the management of haemochromatosis?
Patient advice:
- Avoid iron and iron-containing supplements
- Avoid vitamin C supplements (increases the bioavailability of iron for enteric absorption)
- Limit or avoid alcohol
- Consider hepatitis A and B vaccinations if no previous encounter.
Stage 0: Normal transferrin saturation and ferritin with no clinical symptoms:
- Monitoring iron labs and symptoms every 3 years
Stage 1: Transferrin saturation > 45%, normal ferritin, no clinical symptoms:
- Monitoring iron labs and symptoms every 1 year
Stage 2, 3, 4: Transferrin saturation > 45%, raised ferritin and/or clinical symptoms:
- Phlebotomy // venesection - blood removed to stimulate haematopoiesis, thereby utilising some of the excess iron for haem synthesis
- Iron chelation therapy - if phlebotomy contraindicated (e.g. anaemia, cardiac disease or venous access issues). Both oral agents (Deferasirox) and parenteral agents (Desferrioxamine) are available
Liver transplant:
- Patients with end-stage cirrhotic liver disease
What are the complications of haemochromatosis?
- Liver fibrosis / cirrhosis
- Hepatocellular carcinoma
- Diabetes
- Arrhythmia due to iron deposition in conduction pathway
- Cardiomyopathy: either dilated or dilated-restrictive
- Chronic congestive heart failure
- Hypogonadism
Describe the classification of IBS
- IBS with predominant constipation (IBS-C)
- IBS with predominant diarrhoea (IBS-D)
- IBS with mixed bowel habits (IBS-M)
- IBS unclassified (IBS-U)
What are the investigations for IBS?
Suggested primary care investigations are:
- full blood count
- ESR/CRP
- coeliac disease screen (tissue transglutaminase antibodies)
How is IBS diagnosed?
Rome IV criteria:
A patient must have recurrent abdominal pain for at least 1 day per week during the previous 3 months, and this pain should be associated with at least 2 of 3 three criteria:
- Pain related to defecation: The pain is either relieved or worsened by bowel movements.
- Change in frequency of stool: The patient experiences an increase or decrease in the number of bowel movements per day.
- Change in form (appearance) of stool: The stool becomes harder or softer, or there is a change in its consistency.
These symptoms must be present for the last 3 months, with symptom onset at least 6 months before diagnosis.
What is the management of IBS?
First-line pharmacological treatment:
- pain: antispasmodic agents
- constipation: laxatives but avoid lactulose
- diarrhoea: loperamide
Second-line pharmacological treatment:
- low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg)
Psychological interventions:
- If symptoms do not respond to pharmacological treatments after 12 months and who develop a continuing symptom profile (refractory IBS), consider referring for CBT, hypnotherapy or psychological therapy
General dietary advice:
- have regular meals and take time to eat
- avoid missing meals or leaving long gaps between eating
- drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks such as herbal teas
- restrict tea and coffee to 3 cups per day
- reduce intake of alcohol and fizzy drinks
- consider limiting intake of high-fibre food
- reduce intake of ‘resistant starch’ often found in processed foods
- limit fresh fruit to 3 portions per day
- for diarrhoea, avoid sorbitol
- for wind and bloating consider increasing intake of oats and linseeds
What is ischaemic hepatitis?
An important cause of acute liver failure and occurs as a result of impaired blood flow to the hepatic parenchyma
What are the causes of ischaemic hepatitis?
Mostly no cause identified
Any condition resulting in a shock state may precipitate ischaemic hepatitis:
- Heart failure
- Septic shock
- Hypovolemic shock
- Respiratory failure
Other causes include:
- Portal vein thrombosis
- Budd-Chiari syndrome
- Sickle cell crisis
- Hepatic artery thrombosis
What are the clinical features of ischaemic hepatitis?
- Patients are generally older and often suffer from chronic cardiac, vascular, pulmonary, or hepatic comorbidities, which may be complicated by shock.
- The patient will present acutely unwell
- Symptoms are generally non specific and include abdominal pain, nausea, and vomiting.
- The clinical picture may be complicated by signs and symptoms of shock
What are the investigations for ischaemic hepatitis?
Liver enzymes:
- Transaminases in the thousands, rising to these levels within 24 hours, falling to half within 72 hours, and normalising within 2 weeks
- ALP will not typically show such a great increase, but may go up to twice the upper limit of normal
- LDH levels will also rise dramatically, often the ALT/LDH ratio will be less than 1
- Bilirubin levels start to rise as aminotransferase levels decline, and may go up to 4 times normal
Viral serology:
- To rule out acute viral hepatitis, typically hepatitis A, B or E
Toxicology:
- Toxin mediated hepatic damage is another cause of transaminases in the thousands, especially paracetamol overdose
Serum creatinine:
- Levels may be elevated as a result of hypotensive injury to the kidneys and may support a diagnosis of ischaemic hepatitis.
Other tests:
- Anti-smooth muscle antibody for autoimmune hepatitis
- Right upper quadrant USS with doppler to assess for portal vein thrombosis, Budd-Chiari syndrome, or congestive hepatomegaly
- If the diagnosis remains unclear, a liver biopsy may be performed
What is the management of ischaemic hepatitis?
The mainstay of management is resolution of the precipitant of the hepatic ischaemia.
Prompt resolution of any haemodynamic instability by providing fluid resuscitation, restoring cardiac output, and treating sepsis where appropriate is essential as delays in management are lethal.
Admission into an intensive treatment unit with close ongoing monitoring is often necessary.
Which conditions predispose to a Mallory-Weiss Tear?
- Alcoholism
- Hiatal hernia
- Bulimia nervosa
- Hyperemesis gravidarum
- GORD
What are precipitating factors for a MWT?
- Severe vomiting
- Coughing
- Blunt abdominal trauma
- Strained defecation
- Oesophageal instrumentation
What are the investigations for a MWT?
Initial laboratory investigation:
- FBC, including haematocrit to assess severity of initial bleeding episode
- Coagulation studies and platelet counts to detect coagulopathies and thrombocytopenias (routine platelet count, PT, and APTT) - typically normal
- LFTs to rule out liver disease
- Renal function, urea, creatinine, and electrolyte levels (to guide intravenous fluid therapy) - urea may be high in a patient with ongoing bleeding
- Cross-matching/ blood grouping and antibody screen (potential blood transfusion)
Other tests to consider:
- ECG, troponin, creatinine kinase (should be considered in patients with a history of CAD, symptoms of cardiac ischaemia, massive bleeding, or multiple comorbidities)
Diagnosis of aetiology:
- Upper endoscopy: It should be performed in all patients after stabilisation. It is the test of choice for diagnosis and treatment and should be done within 24 hours.
- Findings include single and longitudinal tear that typically appears as a red longitudinal break in the mucosa.
Describe the immediate resuscitation of a patient with a MWT
- Establishment of a good central or peripheral IV access (usually 2 lines) along with fluid replacement.
- Packed RBCs infusion indicated if the Hb <8 gm/dl or if patient presents with signs of shock or severe bleeding.
- Nasogastric decompression using NG tube could be performed, especially in patients with ongoing bleeding or those suspected of having concomitant upper GI bleeding sources.
- Electrolyte imbalance correction
- Coagulation factors need to be optimised before proceeding with endoscopy.
Describe the management of a MWT
Pharmacological treatment:
- PPIs or H2 antagonists = first-line, given to all waiting for endoscopy / have clinically significant upper GI bleeding
- Anti-emetics: considered if N/V, which may be a cause / aggravating factor
- Somatostatin and its long-acting synthetic analogue octreotide: not routinely recommended for patients with non-variceal upper GI bleeding; however, they may be considered as an adjunct treatment to PPIs and endoscopy until more definitive diagnostic tests and therapeutic procedures are implemented
Endoscopic treatment:
- Oesophagogastroscopy is investigation of choice in all cases of upper GI bleeding. It is indicated after medical treatment is given in case of actively bleeding (spurting or oozing haemorrhage) MWT.
- Endoscopic band ligation (with or without epinephrine injection)
- Haemoclip placement is an effective method to control actively bleeding lesions.
- Thermocoagulation therapy
Surgery:
- Surgery usually reserved for situations where endoscopic haemostasis of bleeding has failed or transmural oesophageal perforation has occurred
What risk assessment / scoring systems are used in MWTs?
Glasgow-Blatchford bleeding score
Clinical Rockall score
> > Used to stratify patients as low or high risk. Patients are classified according to who should have an endoscopic evaluation, who may be discharged with minimal risk of complications, and who should be admitted to hospital for further observation.
What is microscopic colitis?
a chronic inflammatory condition of the gut
What are RFs for microscopic colitis?
smoking
drugs: NSAIDs, PPIs and SSRIs
What are the clinical features of microscopic colitis?
- Diarrhoea - chronic, watery, non-bloody diarrhoea that can persist for weeks to months or even years if left untreated
- Abdominal pain - intermittent abdominal pain or cramping that can be mild to moderate in intensity.
- Faecal urgency and incontinence
- Bloating and flatulence
- Weight loss - consequence of malabsorption or decreased oral intake due to fear of exacerbating diarrhoea.
- Nocturnal diarrhoea
Extraintestinal manifestations:
- Joint pain
- Erythema nodosum, pyoderma gangrenosum
- Increased prevalence of concomitant autoimmune disorders including celiac disease, thyroid dysfunction, rheumatoid arthritis, and type 1 diabetes mellitus
What are the investigations for microscopic colitis?
Initial investigations for chronic diarrhoea:
- Blood tests: FBC, CRP, TFTs and coeliac serology
- Stool samples: to exclude infective causes and for faecal calprotectin levels
- If malignancy is suspected then a 2-week wait referral should be considered
Colonoscopy and biopsy:
Only diagnosed by histology examination
- Lymphocytic colitis: increased number of intraepithelial and lamina propria lymphocytes (>20 per 100 cells)
- Collagenous colitis: as above, along with a thickened collagenous band in the subepithelial layer (>10μm)
What is the management of microscopic colitis?
Lifestyle factors:
- Stopping smoking
- Stopping medications such as NSAIDs, PPIs and SSRIs where possible
- Decreasing caffeine intake
- Decreasing dairy intake (in patients with lactose intolerance)
- Decreasing alcohol consumption
Pharmacological interventions:
Considered if lifestyle factors are unsuccessful in managing symptoms
- Mild cases = anti-diarrhoeal drugs such as loperamide may be effective in achieving symptomatic relief
- Budesonide = effective in the induction and maintenance of remission. A typical dosage is 9mg daily for 8 weeks and the medication then stopped to assess response. If symptoms recur, then re-initiation of budesonide may be necessary.
- No response to budesonide = immunomodulators (e.g. azathioprine) and biologics (e.g. anti-TNF-alpha drugs).
Describe the differences between the 2 oesophageal cancers
