Gastro

Question 1

Which LFTs suggest hepatocellular injury?

Answer 1

ALT/AST

Question 2

what are causes of hepatocullular injury ?

Answer 2

Hepatitis (viral, alcoholic, ischaemic)
Liver cirrhosis
Drug / toxin-induced liver injury (e.g. paracetamol overdose)
Malignancy (hepatocellular carcinoma)

Question 3

what in the ALT/AST suggest alcoholic liver disease

Answer 3

The AST:ALT ratio can help determine the aetiology of hepatocellular injury, with a >2:1 ratio classical of alcoholic liver disease.2

Question 4

where is ALP released from?

Answer 4

Serum alkaline phosphatase (ALP) is derived from biliary epithelial cells (cells lining the biliary tract) and bones.3 Raised ALP levels can therefore be caused by cholestasis or bone disease.

Question 5

Where is GGT released from?

Answer 5

Gamma-glutamyltransferase (GGT) is found in hepatocytes and also biliary epithelial cells.2 It is a non-specific but highly sensitive marker of liver damage and cholestasis.

Question 6

ALP with normal GGT

Answer 6

An ALP rise with normal GGT suggests bone disease (e.g. Paget’s disease, vitamin D deficiency, bony metastases)

Question 7

ALP with a rise GGT rise?

Answer 7

An ALP rise with associated GGT rise is more suggestive of cholestasis

Question 8

Isolated GGT

Answer 8

An isolated GGT rise is classically associated with alcohol excess.

Question 9

Bilirubin metabolism

Answer 9

When red blood cells are broken down, unconjugated (insoluble) bilirubin is created as a waste product and binds to albumin in the bloodstream
Hepatocytes take up unconjugated bilirubin and metabolise it to form conjugated (soluble) bilirubin
Hepatocytes excrete conjugated bilirubin into the biliary tract, where it flows into the bowel lumen as bile
Gut bacteria further metabolise bilirubin in bile to form urobilinogen, which is eventually excreted in the stools as stercobilinogen
A small amount of urobilinogen is reabsorbed from the intestine into the portal venous system, and as urobilinogen is water-soluble, the kidney is able to excrete some of this into the urine.

Question 10

Pre-hepatic jaundice?

Answer 10

Pre-hepatic jaundice occurs when increased red blood cell breakdown produces excess bilirubin. This can overwhelm metabolism/excretion pathways, leading to jaundice.

The most common cause of increased red blood cell breakdown is haemolysis. Bilirubin is unconjugated in the blood, as the hepatocytes have not yet metabolised it. The remainder of LFTs are generally normal, as the liver is otherwise working well.

Hint: In pre-hepatic jaundice, patients are often anaemic due to excess red blood cell breakdown. The diagnosis may be Gilbert’s syndrome if no anaemia is present.

Question 11

Gilbert’s syndrome?

Answer 11

Gilbert’s syndrome is a congenital disorder present in up to 5% of the population. It results from a deficiency of glucosyltransferase, the enzyme responsible for the conjugation of bilirubin within hepatocytes.

Gilbert’s syndrome classically presents following viral infection with raised bilirubin but normal LFTs/ full blood count. The disease is benign and requires no specific management.

Question 12

Hepatocellular jaundice

Answer 12

Hepatocellular jaundice occurs when hepatocytes are damaged and dysfunctional, leading to an inability to metabolise unconjugated bilirubin from the bloodstream. This leads to high levels of unconjugated bilirubin in the blood. There will generally also be very high ALT / AST levels, marking hepatocyte damage.

Hint: Common causes of hepatocellular injury are covered above (hepatitis, cirrhosis, malignancy, drug or toxin insult). When liver injury is severe, there are not enough functioning hepatocytes to metabolise bilirubin, and jaundice will develop.

Question 13

Cholestatic jaundice

Answer 13

Cholestasis is an interruption in bile flow from hepatocytes to the gut. When this interruption is severe, bilirubin levels will build up in the blood. The bilirubin has been metabolised in the liver, and thus the bilirubin in the blood is predominantly conjugated bilirubin. There will generally also be high ALP levels with associated high GGT, marking dysfunction of the biliary system.

Obstructive jaundice will classically lead to dark urine and pale stools. Bilirubin cannot enter the gastrointestinal tract due to cholestasis, leading to low stercobilinogen excretion in stools.

The bilirubin in the blood is conjugated and can be filtered by the kidneys. The presence of conjugated bilirubin gives the urine a very dark colour.

Hint: Stools may also be pale in hepatocellular jaundice, as there is decreased bilirubin metabolism/excretion, however as the bilirubin in the blood is unconjugated, it will not be able to pass into the urine. Therefore, the urine should remain a normal colour.

Question 14

causes of cholestasis??

Answer 14

Causes of intrahepatic obstruction (obstruction of the hepatic bile canaliculi):

Hepatitis
Cirrhosis
Malignancy
Drugs (e.g. antibiotics, oral contraceptive pills, anabolic steroids)
Pregnancy
Causes of extrahepatic obstruction (obstruction of hepatic ducts, or distal biliary tree):

Gallstones
Primary sclerosing cholangitis
Intraluminal malignancy: cholangiocarcinoma
Extraluminal malignancy causing duct compression: head of pancreas tumours

Question 15

comparing the pattern of ALT and ALP res

Answer 15

A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP suggests a predominantly hepatocellular injury
A less than 10-fold increase in ALT and a more than 3-fold increase in ALP suggests cholestasis
It is possible to have a mixed picture involving both hepatocellular injury and cholestasis
An isolated ALP rise without a GGT rise should raise your suspicion of bony pathology.

Question 16

Liver Screen

Answer 16

Hepatitis serology (A/B/C)
Epstein-Barr Virus (EBV)
Cytomegalovirus (CMV)
Anti-mitochondrial antibody (AMA)
Anti-smooth muscle antibody (ASMA)
Anti-liver/kidney microsomal antibodies (Anti-LKM)
Anti-nuclear antibody (ANA)
p-ANCA
Immunoglobulins – IgM/IgG
Alpha-1 Antitrypsin (to rule out alpha-1 antitrypsin deficiency)
Serum Copper (to rule out Wilson’s disease)
Ceruloplasmin (to rule out Wilson’s disease)
Ferritin (to rule out haemochromatosis)

Question 17

causes of acute liver failure?

Answer 17

paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy

Question 18

Clinical features of acute liver failure?

Answer 18

Features*
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)

*remember that ‘liver function tests’ do not always accurately reflect the synthetic function of the liver. This is best assessed by looking at the prothrombin time and albumin level.

Question 19

what is the definition of acute liver failure?

Answer 19

Acute liver failure (ALF) is a rare, life-threatening, potentially reversible condition with a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease

Question 20

How is liver failure classified?

Answer 20

ALF may be classified as hyperacute, acute, or subacute, depending on the interval from the onset of jaundice to the development of encephalopathy

Question 21

When should acute liver failure be discussed with transplant centre?

Answer 21

All cases of acute liver failure should be discussed with a transplant centre for consideration of transfer; however, robust supportive management prior to transfer is crucial.
For any acute liver injury with significant or worsening (liver-related) coagulopathy, rapid recognition and evaluation of severity should be followed by prompt discussion with a liver transplant centre, facilitating early provision of advice and transfer where appropriate.
.

Question 22

what is acute liver injury?

Answer 22

Acute liver injury (ALI) is defined as an acute derangement in liver function tests associated with liver-related coagulopathy, in the absence of underlying chronic liver disease (CLD)1. A subset progress to acute liver failure (ALF), a relatively rare syndrome characterised by altered consciousness due to hepatic encephalopathy (HE) in the setting of an ALI.

Question 23

what is acute on chronic liver failure?

Answer 23

cute-on-chronic liver failure (ACLF) is a distinct phenomenon, involving rapidly progressive organ failure in the context of established cirrhosis, triggered by superimposed liver injury or extrahepatic precipitants such as infection

Question 24

How is acute liver failure subcategorised?

Answer 24

ALF can be subcategorised by time elapsed between onset of jaundice and development of encephalopathy, into “hyperacute” (< 7 days), “acute” (7-28 days), and “subacute” (4-24 weeks) liver failure

Question 25

Assessment and initial investigations for acute liver failure?

Answer 25

Stabilise the patient through robust supportive care Determine aetiology Acquire baseline investigations and establish severity Exclude CLD and causes of secondary liver dysfunction (e.g. ischaemic hepatitis/malignant hepatic infiltration1) Ensure timely liaison with an LT centre.

Question 26

Specific questions in history in a patient with acute liver failure?

Answer 26

Presentation - time from onset of jaundice to encephalopathy last time patient was clinically well PMH co-morbidities, previous abdominal surgery, performance status, exercise tolerance Drug history - paracetamol, over the counter, herbal remedies, recent abx SH - travel, smoking alcohol, drugs, high risk sexual behaviour mental health FH - Wilsons disease, IHD

Question 27

Investigations for ALF?

Answer 27

Bloods FBC, U&E's LFT including split bilirubin Coagulation screen group and save Ammonia ABG Non invasive liver screen - Viral, autoanibody screen, metabolic Paracetamol level Septic screen CT head, chest, abdominal, pelvis with triple phase liver imaging to assess vasculature Echo ECG

Question 28

Management of acute liver failure

Answer 28

ALF patients are usually intravascularly deplete, so hypotension mandates aggressive initial fluid resuscitation; where response is inadequate, inotropes (including Noradrenaline and Vasopressin) are utilised to maintain adequate mean arterial pressure (MAP)1. Endotracheal intubation to ensure airway protection is indicated in Grade 3-4 HE. Patients risk raised intracranial pressure from cerebral oedema driven by hyperammonaemia11. Neuroprotection is mandated (including nursing at 30º, Sodium control targeting 145-150mmol/L, high-volume CVVHF to lower ammonia levels, and avoidance of hypercapnia) ALF patients are vulnerable to bacterial and fungal infections, which can preclude LT or increase post-LT mortality11. Prophylactic broad spectrum antibiotics and anti-fungals are indicated. Prothrombin time/INR is a key marker of hepatic function, informing prognosis and guiding the need for LT3. Parenteral Vitamin K (10mg) should be administered, but coagulopathy should not be corrected without clear rationale (i.e. if bleeding)1,3, or following discussion with the LT centre. Hepatological: N-acetylcysteine is indicated for all ALF patients, irrespective of aetiology1,3,12. Enteral feeding with laxatives and enemea Monitor for AKI Patients are at risk of hypoglycaemia, and blood glucose should be checked hourly. Phosphate may fall rapidly, requiring aggressive replacement.

Question 29

Decompensated Cirrhosis care bundle?

Answer 29

Investigations Bloods, blood cultures, USS abdomen Ascitic tap irrespective of clotting parameters and send to lab If high alcohol intake - prescribe pabrinex and commence treatment for alcohol withdrawal if needed. Treat with abx SBP with abx and HAS Manage AKI and hyponatramia Suspend diuretics and nephrotoxic drugs Fluid resuscitation - HAS or NaCL Fluid balance Map > 80 Esceleta to higher care Manage GI bleeding Fluid resuscitation IV terlipressin Prophylactic abx PT prolonged - give IV VK, If > 20 seconds give FFP If pets < 50 give IV pets Transfer if Hb < 70 Lactulose 20-30mg TDS and phosphate enema

Question 30

How to differentiate ascites ?

Answer 30

SAAG can differentiate ascites resulting from portal hypertension and from other causes. It is more useful than the protein based exudate / transudate concept. Calculate SAAG by: SAAG = (serum albumin) – (ascites albumin) If SAAG >11g/L then ascites very likely the result of portal hypertension (97% accuracy).

Question 31

what would lead to SAAG < 11g/L

Answer 31

diffuse peritoneal mets TB peritonitis pancreatic ascites Nephrotic syndrome

Question 32

what would cause a SAAG > 11g/L

Answer 32

Cirrhosis alcohol hepatitis Cardiac ascites massive liver mets

Question 33

what should VTE prophylaxis be held in liver disease?

Answer 33

when Platelet count is < 50

Question 34

Differential diagnosis for abdominal pain?

Answer 34

Peptic ulcer appendicits pancreatitis Biliary colic acute cholecystitis diverticulitis AAA Intestinal obstruction Unusual causes : acute coronary syndrome diabetic ketoacidosis pneumonia acute intermittent porphyria lead poisoning

Question 35

Clinial features of acute upper GI bleeding?

Answer 35

Haematemesis Melena rise in urea

Question 36

Differentials for UGIB?

Answer 36

oesophageal varicose Oesophagitis Cancer Mallory weiss tear Gastric ulcer Diffuse erosive gastritis Dieulafor lesion (arteriovenous malformation) Aortic enteric fistula

Question 37

risk assessments in upper GI bleed?

Answer 37

the Glasgow-Blatchford score at first assessment helps clinicians decide whether patients can be managed as outpatients or not the Rockall score is used after endoscopy provides a percentage risk of rebleeding and mortality includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

Question 38

What is the the Glasgow blatchford score?

Answer 38

Urea Hb BP HR Hepatic disease Cardiac failure syncope Melena

Question 39

how is UGIB managed?

Answer 39

Resuscitation - ABCDE, Wide bore IV access x 2 Platelet transfusion if pets < 50 FFP to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal prothrombin complex concentrate to patients who are taking warfarin and actively bleeding Endoscopy - immediately after resuscitation in patients with severe bleed, should be within 24 hours for all patients PPI if non-variceal bleeding If suspected variceal bleed then do not give PPI Variceal bleeding - terlipressing and prophylactic antibiotics Band ligations TIPS transjugular intrahepatic portosystemic shunts

Question 40

causes of pancreatitis?

Answer 40

Gallstones Ethanol Trauma Steroids Mumps (other viruses include Coxsackie B) Autoimmune (e.g. polyarteritis nodosa), Ascaris infection Scorpion venom Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia ERCP Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

Question 41

clinical features of pancreatitis?

Answer 41

- abdominal pain - N&V - Jaundice - shock - tachypnoea - temp may be low or normal initially but may develop persistent fever as the inflammatory responses progress - abdo tenderness with local guarding - Grey turners (flanks) and Cullen's signs (peri-umbilical) ARDS

Question 42

Investigations of pancreatitis?

Answer 42

amylase serum lipase (higher sensitivity and specificity) CT abdomen

Question 43

what can lead to an increase in amylase?

Answer 43

Upper gastrointestinal perforation Mesenteric or bowel ischaemia Renal failure Retroperitoneal haematoma Intra-abdominal ectopic pregnancy Inflammation or obstruction of the salivary glands

Question 44

management of pancreatitis?

Answer 44

Analgesia Anti-emetics NG tube on free drainage if vomiting is.a problem Nutrition as early as possible Fluid resuscitation (patients may need 10L of fluid in the first 24 hours) Monitor BMs

Question 45

complications of acute pancreatitis?

Answer 45

Peripanceatic fluid collection Pancreatic absces pancreatic necrosis Pseudocyst formation Ascites Retroperitoneal haemorrhage

Question 46

causes of C.diff?

Answer 46

C. difficile diarrhoea is primarily caused by the disruption of gut microbiota secondary to antibiotic use. Broad-spectrum antibiotics can lead to the depletion of protective bacteria, creating an environment conducive to C. difficile overgrowth. The most commonly implicated antibotics are: Cephalosporins Clindamycin Co-amoxiclav Risks - advanced age - prolonged hospitalisation - Immunosupression - recent GI surgery

Question 47

Clinical features of C.diff?

Answer 47

diarrhoea abdominal pain a raised white blood cell count is characteristic if severe toxic megacolon may develop

Question 48

Investigations for C.diff?

Answer 48

is made by detecting Clostridium difficile toxin (CDT) in the stool Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection

Question 49

Management of C.diff?

Answer 49

first-line therapy is oral vancomycin for 10 days second-line therapy: oral fidaxomicin third-line therapy: oral vancomycin +/- IV metronidazole

Question 50

Infectious causes of Diarrhoea?

Answer 50

Bacterial infections: Common organisms include Escherichia coli, Campylobacter jejuni, Salmonella and Shigella. These often present with acute onset diarrhoea, abdominal pain, fever and sometimes bloody stools. Viral infections: Notably Rotavirus, Norovirus, and Cytomegalovirus (CMV). Typically characterised by sudden onset watery diarrhoea, vomiting and low-grade fever. Parasitic infections: Such as Giardia lamblia, Cryptosporidium, and Entamoeba histolytica. These may cause chronic or intermittent diarrhoea with associated weight loss and malabsorption symptoms.

Question 51

Non-infectious causes of Diarrhoea?

Answer 51

-Infectious Causes Gastrointestinal disorders: Including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), coeliac disease, lactose intolerance. These conditions often present with chronic or recurrent diarrhoea. Associated symptoms like abdominal pain, bloating, weight loss or blood in stool can provide clues to the specific disorder. Malignancies: Colorectal cancer or lymphoma may present with changes in bowel habits including diarrhoea. There may be associated rectal bleeding, anaemia or unexplained weight loss. Medication induced: Numerous medications like antibiotics, laxatives, antacids containing magnesium can cause diarrhoea. The onset is usually related to the start of medication.

Question 52

Systemic disorders causing diarrhoea?

Answer 52

Endocrine disorders: Hyperthyroidism and Addison's disease can present with diarrhoea due to increased gut motility and malabsorption respectively. Liver and pancreatic diseases: Conditions like chronic pancreatitis or liver cirrhosis can lead to malabsorption causing fatty diarrhoea (steatorrhoea).

Question 53

Aetiology of UC?

Answer 53

Genetic susceptibility Immune dysregulation Environmental factors Gut microbiota

Question 54

Classification of ulcerative colitis?

Answer 54

Ulcerative proctitis: Inflammation is limited to the rectum. Proctosigmoiditis: Involves the rectum and sigmoid colon. Left-sided colitis: Extends from the rectum to the splenic flexure. Pancolitis: Affects the entire colon.

Question 55

Clinical features of UC?

Answer 55

Diarrhoea Bloods stools Mucus in stools Abdominal pain Tenesmus (a constant urge to defecare despite an empty colon can cause significant distress) Fever, fatigue, anorexia and weight loss s

Question 56

Extra-intestinal features of UC?

Answer 56

Arthralgia Uveitis Erythema nodosum Primary closing cholangitis

Question 57

Investigations for ulcerative colitis?

Answer 57

FBC, CRP and ESR Faecal calprotectin Sigmoidoscopy with colonoscopy MRI or CT

Question 58

Findings on colonoscopy and biopsy in patients with ulcerative colitis?

Answer 58

red, raw mucosa, bleeds easily no inflammation beyond submucosa (unless fulminant disease) widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps ('pseudopolyps') inflammatory cell infiltrate in lamina propria neutrophils migrate through the walls of glands to form crypt abscesses depletion of goblet cells and mucin from gland epithelium granulomas are infrequent Crypt Atrophy and Paneth Cell Metaplasia

Question 59

difference between UC and Crohn's on histology?

Answer 59

Crohns Inflammation in all layers from mucosa to serosa increased goblet cells granulomas UC No inflammation beyond submucosa (unless fulminant disease) - inflammatory cell infiltrate in lamina propria neutrophils migrate through the walls of glands to form crypt abscesses depletion of goblet cells and mucin from gland epithelium granulomas are infrequent

Question 60

Differences between UC and Crohn's on Radiology?

Answer 60

Crohns Small bowel enema high sensitivity and specificity for examination of the terminal ileum strictures: 'Kantor's string sign' proximal bowel dilation 'rose thorn' ulcers fistulae UC: Barium enema loss of haustrations superficial ulceration, 'pseudopolyps' long standing disease: colon is narrow and short -'drainpipe colon'

Question 61

Management of UC?

Answer 61

Aminosalicylates (mesalamine, sulfasalazine) are used first line Corticosteroids - prednisolone, hydrocortisone, budesonide Immunomodulators - Azathiorpine, 6-mercaptopurine, methotrexate Biologic therapies: Anti-tumor necrosis factor (anti-TNF) agents (infliximab, adalimumab, golimumab), anti-integrin agents (vedolizumab), and anti-interleukin-12/23 agents (ustekinumab) are used for patients with moderate-to-severe UC who are refractory to conventional treatments. Janus kinase (JAK) inhibitors: Tofacitinib is an oral JAK inhibitor approved for the treatment of moderate-to-severe UC in patients who do not respond to or are intolerant of other treatments. Surgery

Question 62

how is the severity of UC classified?

Answer 62

mild: < 4 stools/day, only a small amount of blood moderate: 4-6 stools/day, varying amounts of blood, no systemic upset severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

Question 63

How to induce remission in UC?

Answer 63

Mild-moderate Proctitis - topical aminosalicylate (rectal mesalazine). If remission not achieved within 4 weeks and an oral aminiosalicylate, if remission still not achieved - oral or topical steroids proctosigmoiditis and left-sided ulcerative colitis topical (rectal) aminosalicylate if remission is not achieved within 4 weeks, add a high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid if remission still not achieved stop topical treatments and offer an oral aminosalicylate and an oral corticosteroid xtensive disease topical (rectal) aminosalicylate and a high-dose oral aminosalicylate: if remission is not achieved within 4 weeks, stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid

Question 64

How is severe UC managed?

Answer 64

should be treated in hospital intravenous steroids are usually given first-line intravenous ciclosporin may be used if steroid are contraindicated if after 72 hours there has been no improvement, consider adding intravenous ciclosporin to intravenous corticosteroids or consider surgery

Question 65

Maintaining remission in UC?

Answer 65

Following a mild-to-moderate ulcerative colitis flare proctitis and proctosigmoiditis topical (rectal) aminosalicylate alone (daily or intermittent) or an oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent) or an oral aminosalicylate by itself: this may not be effective as the other two options left-sided and extensive ulcerative colitis low maintenance dose of an oral aminosalicylate Following a severe relapse or >=2 exacerbations in the past year oral azathioprine or oral mercaptopurine

Question 66

what levels should be checked prior to starting Azathioprine?

Answer 66

TPMT - thiopurine methytransferase Azathioprine is generally considered safe to use in pregnancy.

Question 67

complications of UC?

Answer 67

Bowel Ca

Question 68

clinical features of Crohn's disease?

Answer 68

Abdominal pain Diarrhoea Weight loss Perianal disease oral manifestations obstructive symptoms Extraintestinal manifestations Arthritis Skin manifestations Uveitis Primary sclerosing cholangitis Anaemia

Question 69

Investigations for Crohn's disease?

Answer 69

Colonoscopy (indings may include aphthous ulcers, cobblestoning, and skip lesions.) Capsule endoscopy Upper GI endoscopy

Question 70

Differentials for Crohn's disease?

Answer 70

UC IBS Intestinal TB - similar symptoms to Crohn's disease including abdominal pain, weight loss and diarrhoea. However, patients may also exhibit systemic signs such as fever and night sweats which are less common in Crohn's disease. Radiologically, intestinal tuberculosis tends to cause ileocaecal involvement mimicking that of Crohn’s disease. However, the presence of necrotic lymph nodes and asymmetric involvement of the intestine may suggest a diagnosis of intestinal tuberculosis over Crohn's disease.

Question 71

Management of Crohn's disease?

Answer 71

Inducing remission - Glucocorticoids - enteral feeding with an elemental diet - 5 ASA drugs - Azathioprine or mercaptourine (used as add ons but not as mono therapy) - Infliximab is useful in refactor disease and fistulating Crohn's - metronidazole is often used for isolated peri-anal disease Maintaining remission - azathioprine or mercaptopurine is used first-line to maintain remission - methotrexate is second line Surgery

Question 72

Complications of Crohn's ?

Answer 72

Strictures Fistulas Abscesses Perianal disease Malabsorption and nutritional deficiencies Colorectal cancer

Question 73

causes of viral gastroenteritis?

Answer 73

commonly - norovirus less common - adenovirus

Question 74

Clinical features of viral gastroenteritis?

Answer 74

Acute diarrhoea (duration of less than 7 days) Watery and non-bloody The presence of blood in the stool should raise suspicion of an alternative diagnosis, such as Shiga-toxin producing E-coli or Campylobacter infection. Vomiting Mild fever Abdominal pain

Question 75

causes of bacterial gastroenteritis?

Answer 75

The most common causative bacteria in the UK is Campylobacter jejuni, but other pathogens frequently associated include Salmonella species, E-coli and Shigella. Campylobacter typically contaminates undercooked meat (especially poultry), unpasteurised milk and untreated water. E-coli is usually harmless, but it is important to be aware that E-coli O157:H7 infection can progress to haemolytic uraemia syndrome. Typically E-coli is acquired from undercooked beef products (such as beef burgers) and can be transmitted from person to person by direct contact.

Question 76

bacteria causing food poisoning?

Answer 76

Staphylococcus aureus: from undercooked meats and cream products. Bacillus cereus: from reheated rice.

Question 77

differentials for viral gastroenteritis?

Answer 77

bacterial gastroenteritis food poisoning C.diff IBD IBS Coeliac disease

Question 78

when should a patient with viral gastroenteritis be admitted to hospital?

Answer 78

If they are unable to to maintain oral intake due to vomiting Some elderly individuals >60 years old, who are more at risk of severe dehydration Abdominal tenderness Diarrhoea lasting 10 days or more

Question 79

Campylobacter infection symptoms?

Answer 79

Diarrhoea - may be blood and may have mucus abdominal pain N&V Fever muscle aches

Question 80

complications of campylobacter infection?

Answer 80

Bacteremia: This is rare but more likely in immunocompromised patients or those with underlying conditions such as liver disease or malignancy. Pancreatitis, cholecystitis, or appendicitis-like syndrome: These can occur when the infection spreads beyond the gastrointestinal tract. Post-infectious complications: These include reactive arthritis, Guillain-Barré syndrome, and irritable bowel syndrome. The risk of these complications is low but they can result in significant morbidity. GBS Miller Fisher syndrome Milker's nodule

Question 81

Management of campylobacter?

Answer 81

usually self-limiting the BNF advises treatment if severe or the patient is immunocompromised. Clinical Knowledge summaries also recommend antibiotics if severe symptoms (high fever, bloody diarrhoea, or more than eight stools per day) or symptoms have last more than one week the first-line antibiotic is clarithromycin ciprofloxacin is an alternative although the BNF states that 'Strains with decreased sensitivity to ciprofloxacin isolated frequently'

Question 82

Symptoms of HUS?

Answer 82

The symptoms of HUS can include bloody diarrhoea, abdominal pain, vomiting, and decreased urine output

Question 82

what is Haemolytic Uraemia syndrome?

Answer 82

Haemolytic uraemic syndrome (HUS) is a rare but serious condition that can lead to renal failure, anaemia and thrombocytopenia. It is most commonly caused by an infection with certain strains of E. coli bacteria, particularly in children under the age of five. HUS can also be caused by other infections, medications, or genetic factors.

Question 83

Treatment of HUS

Answer 83

Treatment for HUS involves supportive care, such as fluid and electrolyte management, blood transfusions, and dialysis if necessary. Antibiotics are not recommended unless there is evidence of an active bacterial infection.

Question 84

genetic pre-disposition to Coeliac disease?

Answer 84

HLA-DQ2 or HLA-DQ8

Question 85

Clinical features of Coeliac ?

Answer 85

diarrhoea, abdominal pain, and malabsorption to extraintestinal manifestations such as dermatitis herpetiformis, fatigue, anaemia, and neurological complications. Coeliac disease is associated with an increased risk of complications, including malignancies, osteoporosis, and other autoimmune disord

Question 86

Investigations for coeliac disease?

Answer 86

Anti-tissue transglutaminase (False negative results may occur in patients with selective IgA deficiency) Anti-endomysial antibodies (EMA) Total serum IgA levels Duodenal Biopsy (Villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes)

Question 87

Differentials for coeliac?

Answer 87

IBS IBD Non-coeliac gluten sensitivity (NCGS) - unlike coeliac disease, there is no damage to the small intestine in NCGS. NCGS does not have the same genetic associations as coeliac disease. HLA-DQ2 and HLA-DQ8 are present in nearly all patients with coeliac disease but are not commonly found in those with NCGS.

Question 88

complications of coeliac disease?

Answer 88

Malabsorption Lactose intolerance Refectory coeliac disease (symptoms despite strict adherence to gluten free diet) Malignancies - Enteropathy associated T cell lymphoma Small bowel adenocarcinoma Osteoporosis and osteopenia Dermatitis herpetiformis Infertility and adverse pregnancy outcomes

Question 89

what are the different classifications of peritonitis?

Answer 89

Primary Peritonitis - (AKA SBP, typically occurs when there is no identifiable source of infection within the abdomen. It is often associated with conditions leading to ascites such as cirrhosis or nephrotic syndrome.) Secondary peritonitis - a result of contamination from an intra-abdominal source. Common causes include perforation of a gastrointestinal organ, postoperative complications, trauma or ischemia. Tertiary peritonitis - refers to persistent or recurrent infection after adequate treatment for primary or secondary peritonitis. It is often seen in immunocompromised patients and those in intensive care units.

Question 90

Features of peritonitis ?

Answer 90

Abdo pain GI symptoms (N&V, bowel disturbance) Systemic symptoms - fever, tachycardia, hypotension Abdominal distension Peritoneal signs - tenderness, guarding, rigidity, indicative of peritoneal inflammation, percussion tenderness may also be present