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FINALS > GI AND LIVER > Flashcards

GI AND LIVER Flashcards

1
Q

what is achalasia?

A

-oesophageal aperistalsis and impaired relaxation of the lower oesophageal sphincter

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2
Q

what are the risk factors for developing achalasia?

A
  • Allgrove syndrome (achalasia, alacrima, adrenal insufficiency).
  • Viral infection.
  • Autoimmune disease such as multiple sclerosis and Sjogren’s syndrome.
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3
Q

what are the clinical features of achalasia?

A
  • Intermittent dysphagia for both solids and liquids from the onset.
  • Retrosternal chest pain due to oesophageal spasm.
  • Regurgitation of food.
  • Aspiration pneumonia.
  • Gradual weight loss.
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4
Q

what is the first line investigation for achalasia and what does it show?

A
  • upper GI endoscopy:
  • -Obscured mucosa
  • -Dilated oesophagus
  • -Food debris.
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5
Q

what is seen on barium swallow in achalasia?

A
  • Lack of peristalsis

- bird beak appearance of lower end of oesophagus.

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6
Q

which investigation is diagnostic of achalasia and what does it show?

A
  • manometry
  • Incomplete relaxation of the lower oesophageal sphincter
  • oesophageal peristalsis.
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7
Q

how is achalasia treated?

A
  • nifedipine or verapamil.
  • pneumatic dilatation or laparoscopic cariomyotomy
  • botox
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8
Q

what are the complications of acute pancreatitis?

A
  • haemorrhage
  • hyperglycaemia
  • hypocalcaemia
  • pancreatic pseudocyst
  • fistulas
  • pancreatic abscess
  • ARDS
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9
Q

what are the causes of acute pancreatitis in adults?

A
  • Idiopathic
  • Gallstones.
  • Ethanol.
  • Trauma.
  • Steroids.
  • Mumps.
  • Autoimmune.
  • Scorpion bites.
  • Hypertriglyceridaemia, hypercalcaemia, or hypothermia.
  • ERCP.
  • Drugs such as bendroflumethiazide, allopurinol, azathioprine and tetracyclines.
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10
Q

what are the causes of acute pancreatitis in children?

A
  • blunt abdominal trauma (RTA)
  • viral infection (mumps, Hep A, coxsackie B)
  • multisystem disease such as SLE, Kawasaki, HUS, IBD and hyperlipidaemia)
  • drugs and toxins (thiopurines, metronidazole, cytotoxic drugs)
  • pancreatic duct obstruction (e.g. cystic fibrosis, choledochal cysts or tumours)
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11
Q

what are the symptoms of acute pancreatitis?

A
  • Severe epigastric pain that radiates to the back. It is sudden onset, continuous, and worse with movement.
  • Nausea and vomiting.
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12
Q

what are the signs of acute pancreatitis?

A
  • Abdominal tenderness and distension.
  • Stony dull percussion due to pleural effusion.
  • Bluish discolouration around the Umbilicus (Cullen’s sign) or over both flanks (Grey Turner’s sign) due to haemorrhagic pancreatitis.
  • Facial spasm due to hypocalcaemia (Chvostek’s sign).
  • Tachycardia, hypotension, oliguria, sweating due to hypovolaemic shock.
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13
Q

what investigations should be performed for suspected acute pancreatitis and what is seen?

A
  • Amylase or lipase: 3x upper limit of normal
  • transabdominal USS: may see gallstones
  • FBC: neutrophils raised
  • CRP: raised
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14
Q

what three criteria should be met to diagnose acute pancreatitis?

A
  • Upper abdominal pain.
  • Serum lipase or amylase is greater than 3x the upper limit.
  • Radiological changes (USS, CT) consistent with pancreatitis.
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15
Q

what are the poor prognostic factors in pancreatitis?

A
  • PaO2 < 8.0 kPa
  • Age > 55 years.
  • Neutrophilia > 15 x 109/L
  • Calcium < 2 mmol/L
  • Renal Function: urea > 16 mmol/L
  • Enzymes: Serum LDH > 600 U/L
  • Albumin < 30 g/L
  • Sugar: Blood glucose > 10 mmol/L
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16
Q

how is acute pancreatitis managed?

A
  • fluid resus
  • supportive care e.g. analgesia, supplemental oxygen, antiemetic and calcium/magnesium replacement therapy
  • establish normal feeds when tolerable
  • ERCP for gallstones
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17
Q

how is pancreatic necrosis managed?

A
  • Administer intravenous antibiotics (imipenem).
  • Perform percutaneous catheter drainage.
  • Perform a necrosectomy if catheter drainage is unsuccessful.
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18
Q

what are the causes of chronic pancreatitis?

A
  • alcohol excess
  • hereditary pancreatitis
  • autoimmune pancreatitis
  • ductal adenocarcinoma
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19
Q

what are the complications of chronic pancreatitis?

A
  • pancreatic pseudocyst formation
  • pleural effusion
  • jaundice
  • fat necrosis
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20
Q

what are the symptoms of chronic pancreatitis?

A
  • An intermittent dull epigastric pain that radiates to the back, that is relieved by leaning forward, and worsened by eating.
  • Steatorrhoea.
  • Weight loss.
  • Malnutrition.
  • Bloating, abdominal cramps, excessive flatus.
  • Nausea and vomiting.
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21
Q

what are the signs of chronic pancreatitis?

A
  • Signs of chronic liver disease.
  • Epigastric tenderness.
  • Jaundice.
  • Abdominal distension due to a pseudocyst.
  • Skin nodules due to disseminated fat necrosis.
  • Shortness of breath due to a pleural effusion.
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22
Q

how is chronic pancreatitis managed?

A
  • lifestyle changes such as smoking and alcohol cessation, smaller, more frequent meals and minimising sugar intake.
  • analgesia (paracetamol) for pain relief.
  • pancreatin and fat soluble vitamins for exocrine insufficiency.
  • endoscopic drainage of pseudocysts if there is persistent pain or complications
  • biliary decompression if there is a two-fold elevation in ALP that persists for more than 1 month.
  • pancreatic ductal decompression for pain relief if other medications fail.
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23
Q

what is a mallory-weirs tear?

A

rupture of the oesophageal mucosa

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24
Q

what is Boerhaave syndrome?

A

perforation of the whole thickness of the oesophageal wall

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25
Q

what are the risk factors for the Mallory-weiss/Boerhaave syndrome?

A
  • Significant alcohol use.
  • History of food poisoning, gastroenteritis, gallstones, cholecystitis etc.
  • Chronic cough e.g. bronchiectasis, COPD, lung cancer.
  • Hiatus hernia.
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26
Q

what are the clinical features of Mallory-weiss/Boerhaave syndrome?

A
  • Haematemesis following second episode of vomiting, it may have a ‘coffee-ground’ appearance or bright-red bloody haematemesis.
  • Dizziness and postural hypotension.
  • Severe retrosternal pain (Boerhaave syndrome).
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27
Q

how should suspected mallory-weiss tear investigated and what does it show?

A
  • oesophagogastroduodenoscopy

- Red longitudinal defect.

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28
Q

how should boerhaave syndrome be investigated?

A

water double contrast enema (Gastrografin) to localise the lesion.

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29
Q

how is boerhaave syndrome managed?

A

-Early recognition and surgical management within 12 hours of rupture

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30
Q

what is mesenteric adenitis?

A

inflamed lymph glands in the abdomen

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31
Q

what are the clinical features of mesenteric adenitis?

A
  • abdominal pain
  • following a sore throat or cold
  • fever and generally unwell
  • nausea and diarrhoea
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32
Q

how is mesenteric adenitis diagnosed?

A
  • clinically

- by excluding other causes of abdominal pain

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33
Q

what are the clinical features of alpha-1-antitrypsin deficiency?

A
  • Productive cough.
  • Shortness of breath on exertion.
  • Wheezing.
  • Chest hyperinflation.
  • Jaundice.
  • Asterixis.
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34
Q

how is Alpha-1-Antitrypsin deficiency diagnosed?

A
  • Measure plasma AAT level: < 20 mmol/L.
  • Perform pulmonary function testing: Reduced FEV1, FVC and FEV/FVC; Increased TLC.
  • Perform CXR: Large lung volumes and emphysema.
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35
Q

how is Alpha-1-Antitrypsin deficiency managed?

A
  • lifestyle advice such as smoking cessation.
  • hepatitis A and B vaccination.
  • For pulmonary manifestations: Offer bronchodilators, inhaled steroids and antibiotics.
  • For hepatic manifestations: Offer diuretics for ascites, endoscopy to detect and manage varices, and liver transplantation in decompensated cirrhosis.
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36
Q

when does infant colic present?

A

first few months of life

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37
Q

what are the clinical features of infant colic?

A
  • Paroxysmal, inconsolable crying or screaming
  • accompanied by drawing up of the knees
  • passage of excessive flatus
  • takes place several times a day, particularly in the evening.
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38
Q

what are the symptoms of appendicitis?

A
  • Anorexia
  • Vomiting and nausea
  • Fever
  • Abdominal pain, initially central and colicky (appendicular midgut colic), but then localising to the right iliac fossa (from localised peritoneal inflammation)
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39
Q

what are the signs of appendicitis?

A
  • low-grade fever
  • Abdominal pain aggravated by movement
  • Persistent tenderness with guarding in the right iliac fossa (McBurney’s point).
  • Rovsing’s sign – palpation of the left lower quadrant increases pain in the right lower quadrant
  • Psoas sign – passive extension of the right thigh with the person in the left lateral position elicits pain in the RLQ, suggestive of a retrocaecal appendix
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40
Q

what is seen on FBC and CRP in appendicitis?

A
  • neutrophil dominant leucocytosis

- Elevated CRP

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41
Q

how is appendicitis managed?

A
  • supportive therapy - NBM, IV fluids and analgesia
  • Laparoscopic appendicectomy
  • postoperative antibiotics (e.g. amoxicillin + metronidazole) for complicated appendicitis where there is suspected perforation.
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42
Q

what is intussusception?

A

-invagination of proximal bowel into a distal segment.

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43
Q

what are the clinical features of intussusception?

A
  • Paroxysmal, severe colicky pain
  • pallor
  • May refuse feeds
  • may vomit, which may become bile-stained depending on the site of the intussusception
  • sausage shaped mass palpable in the abdomen
  • passage of redcurrant jelly stool
  • abdominal distention
  • shock
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44
Q

what is seen on ultrasound in intussusception?

A

target sign

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45
Q

how is intussusception managed?

A
  • Perform fluid resuscitation with 0.9% NaCl.
  • Give clindamycin and gentamicin if sepsis is suspected.
  • Perform pneumatic reduction (air insufflation) as first line management in patients who are clinically stable.
  • Perform surgical reduction if pneumatic reduction fails.
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46
Q

what is a volvulus?

A

a twist in the bowel that occludes its lumen.

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47
Q

what are the clinical features of volvulus?

A
  • Absolute constipation.
  • Crampy abdominal pain.
  • Bilious vomiting (caecal volvulus)
  • If ischaemia is present:
  • –Severe acute abdominal pain.
  • –Tachycardia.
  • –Tachypnoea.
  • –Acidosis.
  • –Guarding and rebound tenderness.
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48
Q

what is seen on AXR in volvulus?

A
  • Inverted U shaped loop in sigmoid volvulus

- Coffee bean share in caecal volvulus.

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49
Q

what is seen on upper GI contrast series in volvulus?

A
  • Bird-beak sign in sigmoid volvulus

- Corkscrew sign in caecal volvulus.

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50
Q

how is sigmoid volvulus managed?

A
  • Perform therapeutic flexible sigmoidoscopy with insertion of a rectal tube if there is no peritonitis or mucosal gangrene.
  • Perform surgical resection if there is peritonitis or mucosal gangrene.
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51
Q

how is caecal volvulus managed?

A
  • Perform surgical resection as first line.
  • Offer supportive care including nasogastric tube, IV fluid resuscitation and prophylactic antibiotics.
  • If ischaemia is not present, gram positive cover is required e.g. cefazolin.
  • If ischaemia is present, gram negative cover is required e.g. cefoxitin.
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52
Q

what is meckel’s diverticulum?

A

blind-ended outpouching of the ileum on the antimesenteric border approximately 60 cm from the ileocaecal valve

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53
Q

what are the clinical features of Meckel’s diverticulum?

A
  • Haematochezia

- intractable constipation

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54
Q

how is Meckel’s diverticulum diagnosed?

A
  • Order a technetium-99m pertechnetate scan: Ectopic focus.

- Perform surgical exploration of the abdomen: Identify Meckel’s diverticulum.

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55
Q

how is Meckel’s diverticulum managed?

A
  • Perform a laparoscopic resection.
  • Give urgent blood transfusion if bleeding.
  • Remove any adhesive bands if obstruction.
  • Perform small bowel segmental resection and give cefotaxime and metronidazole if perforation and peritonitis.
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56
Q

what are the risk factors for developing gallstones?

A
  • Crohn’s disease.
  • Diabetes mellitus.
  • Diet high in triglycerides, refined carbohydrates, and low in fibre.
  • Female gender.
  • Hispanic and Native-American ethnicity.
  • Increasing age.
  • Octreotide, a somatostatin analogue, due to impaired gallbladder motility.
  • GLP-1 analogies.
  • Ceftriaxone, due to precipitation of bile.
  • Non-alcoholic fatty liver disease.
  • Obesity.
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57
Q

what are the clinical features of biliary colic?

A

-Severe epigastric and RUQ
pain

  • lasting several hours
  • associated with nausea and vomiting.
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58
Q

what is seen on abdominal ultrasound in biliary colic?

A
  • gallstones in gallbladder

- stones in the bile duct

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59
Q

what are the risk factors for acute cholecystitis?

A
  • Trauma.
  • Burns.
  • Immobility.
  • Starvation.
  • Sepsis.
  • Acute renal failure.
  • Diabetes mellitus.
  • Vascular disease.
  • Total parenteral nutrition.
  • Narcotic analgesics.
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60
Q

what are the clinical features of acute cholecystitis?

A
  • Sudden-onset, constant, severe pain in the upper right quadrant.
  • Referred pain in the shoulder or intrascapular region.
  • Tenderness in the upper right quadrant, with or without Murphy’s sign.
  • Nausea and vomiting.
  • Fever.
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61
Q

what is seen on serum LFTs in acute cholecystitis?

A
  • Raised aminotransferases

- raised ALP.

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62
Q

what is seen on abdominal ultrasound in acute cholecystitis?

A
  • Distended gallbladder

- Gallstones.

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63
Q

following ultrasound, which diagnostic investigations can be used?

A

MRCP and ERCP

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64
Q

how is acute cholecystitis managed?

A
  • Provide fluid resuscitation, analgesia and antibiotics to all patients.
  • Refer for laparoscopic cholecystectomy preferably within a week of onset.
  • Refer for percutaneous cholecystectomy to manage gallbladder empyema for patients unfit for general anaesthesia and surgery, and who do not improve after fluid resuscitation, analgesia, and antibiotics.
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65
Q

what are the risk factors for ascending cholangitis?

A
  • Above the age of 50.
  • History of cholelithiasis.
  • History of primary or secondary sclerosing cholangitis.
  • Surgical, endoscopic or radiological intervention of bile ducts.
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66
Q

what are the clinical features of ascending cholangitis?

A
  • Charcot’s triad: Fever, jaundice, right upper quadrant pain.
  • Reynold’s pentad: Charcot’s triad, in addition to hypotension and confusion, which are indicative or sepsis.
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67
Q

what is seen on serum LFTs in ascending cholangitis?

A
  • Raised ALT
  • raised ALP
  • hyperbilirubinaemia.
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68
Q

what are the diagnostic criteria for ascending cholangitis?

A
  • A: Systemic inflammation:
  • –Fever (>38 degrees celsius) and or shaking chills.
  • –Laboratory data: Raised WCC.
  • B: Cholestasis:
  • –Jaundice.
  • –Laboratory data: Abnormal LFTs.
  • C: Imaging:
  • –Biliary dilation.
  • –Evidence of aetiology: Stones.
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69
Q

how is ascending cholangitis managed?

A
  • Give intravenous antibiotics:
  • –Initially give piperacillin with tazobactam.
  • –Give metronidazole with ciprofloxacin as an alternative for patients with a penicillin allergy.
  • Perform biliary decompression:
  • –Perform ERCP with sphincterectomy, as first-line therapy.
  • –Perform percutaneous trans-hepatic cholangiography (PTC) for patients who are poor ERCP candidates.
  • –Perform laparoscopic choledochotomy with T tube
  • –Perform endoscopic lithotripsy for stones that are large or difficult to remove.

-Offer opioid analgesia (morphine, pethidine, fentanyl).

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70
Q

What are the risk factors for development of fulminant hepatic failure?

A
  • Chronic alcohol use
  • Poor nutritional status
  • Female sex
  • Age >40 years
  • Pregnancy
  • Chronic hepatitis B
  • Narcotics e.g. paracetamol
  • Hepatotoxic medication
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71
Q

what are the clinical features of fulminant hepatic failure?

A
  • jaundice
  • hepatomegaly
  • abdominal pain with RUQ tenderness
  • malaise
  • encephalopathy - drowsiness, confusion, coma
  • hypotension
  • hypoglycaemia
  • cerebral oedema
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72
Q

what is seen on LFTs and clotting in fulminant hepatic failure?

A
  • Hyperbilirubinaemia
  • Prolonged PT > 30 seconds
  • Elevated INR > 1.5.
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73
Q

how is paracetamol overdose managed?

A
  • Admit to ICU if blood paracetamol concentration is greater than > 700 mg/L, associated with coma and elevated lactate level.
  • Administer activated charcoal if the patient presents within 1 hour of ingestion.

-Additionally, administer intravenous acetylcysteine (140 mg/kg orally) within 8 hours for paracetamol toxicity.
o

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74
Q

in which cases should acetylcysteine be given immediately?

A
  • There is uncertainty about the time of overdose, but it is potentially toxic
  • The overdose was staggered over a time period longer than an hour
  • The plasma-paracetamol level is over the treatment line on the treatment graph
  • The overdose was taken 8-36 hours before presenting
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75
Q

how should an anaphylactoid reaction to acetylcysteine be managed?

A

-If anaphylactoid reaction to acetylcysteine occurs, stop the infusion, give nebulised salbutamol, then re-commence infusion at a lower rate.

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76
Q

what are the clinical features of alcoholic fatty liver?

A
  • often no symptoms or signs.
  • Vague abdominal symptoms of nausea, vomiting and diarrhoea are due to the more general effects of alcohol on the gastrointestinal tract.
  • Hepatomegaly, sometimes huge, can occur together with other features of chronic liver disease.
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77
Q

what are the clinical features of alcoholic hepatitis?

A
  • Right upper quadrant pain.
  • Hepatomegaly.
  • Jaundice.
  • Ascites
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78
Q

what are the clinical features of alcoholic cirrhosis?

A
  • Ascites.
  • Varices.
  • Hepatic encephalopathy.
  • Hepatocellular carcinoma.
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79
Q

what is seen on LFTs in alcoholic liver disease?

A
  • Raised AST and ALT
  • AST:ALT > 2
  • Elevated GGT.
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80
Q

how is alcoholic liver disease managed?

A
  • Recommend alcohol abstinence, weight reduction and smoking cessation.
  • Recommend bed rest with a diet high in protein and vitamin supplements.
  • Recommend the influenza and pneumococcal vaccine.
  • Offer prednisolone to patients with alcoholic hepatitis with a Maddrey’s Discriminant Function score of 32 or more.
  • Offer furosemide and spironolactone for patients with less severe ascites.
  • Consider liver transplantation in patients with end-stage disease.
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81
Q

what autoantibodies are present in type 1 autoimmune hepatitis?

A
  • Antinuclear antibody (ANA)
  • smooth muscle antibody (SMA)
  • soluble liver antibody (SLA) positive.
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82
Q

what autoantibodies are present in type 2 autoimmune hepatitis?

A

-Anti-liver/kidney microsomal-1 (ALKM1).

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83
Q

what are the clinical features of autoimmune hepatitis?

A
  • Fatigue.
  • Anorexia.
  • Abdominal discomfort.
  • Hepatomegaly.
  • Jaundice.
  • Pruritus.
  • Arthralgia.
  • Nausea.

Fever.

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84
Q

what is seen on LFTs in autoimmune hepatitis?

A
  • Raised AST and ALT
  • Mild elevation of ALP and GGT
  • Raised bilirubin
  • Low serum albumin.
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85
Q

what are the criteria for initiating management in autoimmune hepatitis?

A
  • Raised aminotransferase levels greater than 10-fold the upper list.
  • Raised gamma-globulin level at least twice the upper limit of normal.
  • Bridging necrosis on liver histology.
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86
Q

how is autoimmune hepatitis managed?

A
  • prednisolone and azathioprine
  • ursodeoxycholic acid in addition to initial management for patients with autoimmune hepatitis - primary biliary cholangitis overlap syndrome.
  • liver transplant
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87
Q

what are the clinical features of Budd-Chiari syndrome?

A
  • Right upper quadrant pain.
  • Tender hepatomegaly.
  • Ascites
  • Splenomegaly due to underlying myeloproliferative disease.
  • Leg oedema due to obstruction of the inferior vena cava.
  • Jaundice and hepatic encephalopathy with acute liver failure
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88
Q

what is seen on doppler ultrasonography in Budd-chiari syndrome?

A
  • Thrombosis

- stenosis.

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89
Q

how is budd-chiari syndrome treated?

A
  • Perform thrombolysis for symptomatic patients presenting within 72 hours.
  • Offer anticoagulation (enoxaparin or dalteparin) if the patient presents after 72 hours.
  • Perform hepatic angioplasty as the second line treatment.
  • Perform surgical shunting as the third line treatment.
  • Perform liver transplant as the fourth line treatment, or as an emergency procedure in patients with fulminant disease.
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90
Q

what is compensated cirrhosis?

A

the liver can still function effectively, and there are no or few clinical symptoms.

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91
Q

what is decompensated cirrhosis?

A

the liver is damaged to the point that it cannot function adequately and overt clinical complications.

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92
Q

what are the risk factors for the development of cirrhosis?

A
  • Alcohol misuse.
  • Hepatitis B and C (unprotected sex and intravenous drug use).
  • Obesity.
  • Autoimmune disease (autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis).
  • Genetic conditions (haemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency).
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93
Q

what are the clinical features of cirrhosis?

A
  • Presence of stigmata of chronic liver disease
  • Spider naevi.
  • Palmar erythema.
  • Leukonychia
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94
Q

what are the clinical features of variceal haemorrhage?

A
  • Haematemesis

- Melaena.

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95
Q

what are the clinical features of ascites?

A
  • Abdominal swelling.
  • Mild generalised abdominal pain.
  • Deterioration suggests spontaneous bacterial peritonitis.
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96
Q

what are the clinical features of hepatic encephalopathy?

A
  • Fetor hepaticus (sweet smell to breath).
  • Asterixis.
  • Decreased mental function.
  • Coma.
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97
Q

what is seen on LFT in cirrhosis?

A
  • Raised AST and ALT
  • Raised GGT
  • Prolonged PT (most sensitive and specific finding for liver cirrhosis).
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98
Q

how is ascites managed?

A
  • Initially give spironolactone.
  • Offer large volume paracentesis for symptomatic tense ascites or when diuretic therapy is insufficient to control accumulation of fluid.
  • Offer intravenous cefotaxime and human albumin solution for spontaneous bacterial peritonitis.
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99
Q

how are oesophageal varies managed?

A
  • Offer a beta blocker for prophylaxis for variceal haemorrhage.
  • Offer terlipressin with suspected oesophageal variceal haemorrhage.
  • Perform endoscopic band ligation if bleeding does not stop following terlipressin.
  • Consider transjugular intrahepatic portosystemic shunt (TIPSS) if bleeding is not controlled by band ligation.
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100
Q

how is cirrhosis treated?

A

liver transplant

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101
Q

what are the risk factors for coeliac disease?

A
  • Family history of coeliac disease.
  • Type 1 diabetes.
  • Autoimmune thyroid disease.
  • Gluten exposure.
  • Down’s syndrome.
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102
Q

what are the clinical features of coeliac disease?

A
  • Diarrhoea.
  • Bloating.
  • Abdominal discomfort.
  • Anaemia.
  • Fatigue.
  • Weight loss.
  • Failure to thrive.
  • Depression and anxiety.
  • Peripheral neuropathy.
  • wasted buttocks
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103
Q

what is seen on coeliac serology?

A
  • Elevated titre of IgA-tissue Transglutaminase

- Elevated titre of IgG endomysial antibodies.

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104
Q

what is the gold standard investigation in coeliac disease and what does it show?

A
  • endoscopy

- subtotal villous atrophy and crypt hyperplasia

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105
Q

how is coeliac disease managed?

A
  • Advise long-term adherence to a gluten free diet. The usual cause for failure to respond to the diet is poor compliance.
  • Offer supplementation (iron, folic acid, calcium, vitamin D) if needed.
  • Offer pneumococcal vaccinations once every 5 years due to hyposplenism
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106
Q

how is coeliac crisis treated?

A
  • Rehydrate and correct electrolyte abnormalities.

- Offer a short course of glucocorticoid therapy (budesonide).

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107
Q

what is dermatitis herpetiformis?

A

uncommon blistering subepidermal eruption of the skin associated with a gluten-sensitive enteropathy

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108
Q

what are the clinical features of tropical sprue?

A
  • diarrhoea
  • anorexia
  • abdominal distension
  • weight loss.
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109
Q

how is tropical sprue diagnosed?

A
  • Acute infective causes of diarrhoea must be excluded, particularly Giardia
  • Malabsorption should be demonstrated, particularly of fat and B12.
  • The jejunal mucosa is abnormal, showing some villous atrophy (partial villous atrophy).
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110
Q

how is tropical sprue treated?

A
  • folic acid
  • tetracycline
  • Severely ill patients require resuscitation with fluids and electrolytes for dehydration, and nutritional deficiencies should be corrected.
  • Vitamin B12 (1000 μg) is also given to all acute cases.
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111
Q

what are the clinical features of gut bacteria overgrowth\?

A
  • diarrhoea and steatorrhoea
  • b12 deficiency
  • high folate
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112
Q

how is gut bacteria overgrowth diagnosed?

A

-hydrogen breath test

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113
Q

how is gut bacterial overgrowth treated?

A
  • correct underlying lesion

- rotating courses of antibiotics, such as metronidazole, a tetracycline or ciprofloxacin.

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114
Q

which factors predispose to adenocarcinoma of the small bowel?

A
  • coeliac disease

- Crohn’s

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115
Q

which factors predispose to lymphoma of the small bowel?

A
  • coeliac disease

- IPSID

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116
Q

how are small bowel adenocarcinomas treated?

A

-segmental resection

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117
Q

how is immunoproliferative small intestinal disease treated?

A
  • if there is no evidence of lymphoma, antibiotics, e.g. tetracycline, should be tried initially.
  • In the presence of lymphoma, combination chemotherapy is used
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118
Q

how is lymphoma of the small bowel treated?

A
  • surgery

- radiotherapy with chemotherapy

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119
Q

where do carcinoid tumours arise from?

A

enterochromaffin cells in the small intestine

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120
Q

what are the clinical features of carcinoid syndrome?

A
  • Diarrhoea.
  • Flushing.
  • Palpitations.
  • Abdominal cramps.
  • Telangiectasia.
  • Peripheral oedema.
  • Elevated JVP.
  • Cardiac murmurs.
  • Hepatomegaly.
  • Wheeze
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121
Q

how should suspected carcinoid syndrome be investigated?

A
  • Measure serum chromogranin A: Elevated.
  • Measure urinary 5-hydroxyindoleacetic acid: Elevated.
  • Perform an CT scan of the chest, abdomen and pelvis: Location of primary tumour and liver metastases.
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122
Q

how is carcinoid syndrome managed?

A
  • Perform surgical resection of localised disease with no evidence or lymph node involvement or distant metastases.
  • Give a somatostatin analogue (octreotide or lanreotide) which controls symptoms of flushing, diarrhoea, and wheeze.
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123
Q

what are the risk factors for developing colon cancer?

A
  • Increasing age.
  • A diet high in animal fat and red meat.
  • Obesity.
  • Smoking.
  • Hereditary non-polyposis colorectal cancer (HNPCC) (Lynch syndrome)
  • Familial adenomatous polyposis (FAP)
  • Peutz-Jeghers syndrome
  • IBD
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124
Q

what are the clinical features of colon cancer?

A
  • Rectal bleeding.
  • Looser and more frequent stools.
  • Tenesmus.
  • Symptoms of anaemia.
  • Rectal mass on DRE, and occasionally, a palpable abdominal mass on examination.
  • Weight loss and anorexia are associated with advanced disease.
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125
Q

what is seen on blood tests in colon cancer?

A
  • Perform a FBC: Anaemia suggestive of right sided colorectal cancer.
  • Measure LFTs: May be abnormal in liver metastases.
  • Measure U&Es: May be abnormal in renal metastases or diarrhoea.
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126
Q

which patients with suspected colon cancer should be referred on a 2 week wait?

A
  • Aged 40 and over with unexplained weight loss and abdominal pain.
  • Aged over 50 with unexplained rectal bleeding.
  • Over 60 with iron deficiency anaemia or change in bowel habit.
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127
Q

what is the diagnostic investigation for colon cancer?

A

colonoscopy with biopsy

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128
Q

which cancer antigen is measured in colon cancer?

A

serum carcinoembryonic antigen (CEA)

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129
Q

how is colon cancer managed?

A
  • surgery
  • chemotherapy
  • lifestyle advice (smoking cessation and reduced intake of red meat)
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130
Q

what are the risk factors for developing crohn’s disease?

A
  • Family history of Crohn’s disease.
  • Smoking.
  • Infectious gastroenteritis.
  • Appendicectomy.
  • Drugs such as NSAIDs.
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131
Q

what are the symptoms of Crohn’s disease?

A
  • Unexplained and persistent diarrhoea (frequent loose stools for more than 4 - 6 weeks), including nocturnal diarrhoea.
  • Abdominal pain or discomfort.
  • Perianal pain or tenderness.
  • Non-specific symptoms such as fatigue, malaise, anorexia, fever.
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132
Q

what are the signs of Crohn’s disease?

A
  • Pallor.
  • Clubbing.
  • Aphthous mouth ulcers.
  • Abdominal tenderness or mass, for example in the right lower quadrant.
  • Signs of malnutrition and malabsorption such as weight loss, faltering growth or delayed puberty.
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133
Q

what are the extra-intestinal manifestations of Crohn’s disease?

A
  • Pauci-articular or polyarticular arthritis.
  • Erythema nodosum usually on the anterior tibial area or extensor surfaces of the arms or legs.
  • Uveitis and episcleritis, both of which produce a red eye, but the formed is painful and is associated with blurred vision, photophobia, headache
  • Metabolic bone disorders such as osteoporosis, osteopenia, osteomalacia.
  • sacroiliitis causing buttock pain, or spondylitis causing back pain.
  • Pyoderma gangrenosum.
  • Psoriasis
  • Hepatobiliary conditions such as primary sclerosing cholangitis.
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134
Q

how do fistulas present in Crohn’s disease?

A
  • Recurrent urinary tract infections, passing gas or faeces through the urine or vagina.
  • Perianal discharge of mucus or pus.
  • Partial bowel obstruction presents as abdominal colicky pain and distension.
  • Complete bowel obstruction presents as severe abdominal pain, vomiting, no flatus, complete constipation.
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135
Q

what is seen on blood tests in crohn’s?

A
  • anaemia, either microcytic or normocytic
  • raised ESR and CRP
  • hypoalbuminaemia in severe disease
  • pANCA negative
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136
Q

what is seen on stool tests in Crohn’s?

A

-Faecal calprotectin and lactoferrin are raised in active colonic disease

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137
Q

what are the macroscopic changes on colonoscopy in Crohn’s disease?

A
  • skip lesions
  • cobblestone appearance
  • deep ulcers and fissures
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138
Q

what are the microscopic changes on colonoscopy in Crohn’s disease?

A
  • transmural inflammation

- non-caseating granulomas

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139
Q

how is remission induced in Crohn’s?

A
  • nutritional therapy in children
  • corticosteroids
  • aminosalicylate
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140
Q

how is remission maintained in Crohn’s?

A
  • thiopurine
  • methotrexate
  • TNFa inhibitor (infliximab or adalimumab) if no response to conventional therapy
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141
Q

how is a fistula treated in Crohn’s?

A
  • Offer colorectal surgery in patients with complicated perianal or internal fistulas or fistulas that fail to respond to optimal medical treatment.
  • Offer a thiopurine to maintain remission.
  • Offer 3-months post operative metronidazole to control infection.
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142
Q

what are the risk factors for developing UC?

A
  • Family history.
  • No appendicectomy.
  • Drugs such as NSAIDs.
  • Not smoking.
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143
Q

what are the symptoms of UC?

A
  • Bloody diarrhoea persisting for more than 6 weeks.
  • Rectal bleeding.
  • Faecal urgency and or incontinence.
  • Nocturnal defecation.
  • Tenesmus (persistent, painful urge to pass stool even when rectum is empty).
  • Abdominal pain, particularly in the left lower quadrant.
  • Pre-defecation pain that is relieved on passage of stool.
  • Non-specific symptoms such as fatigue, malaise, anorexia, or fever.
  • Weight loss, faltering growth, or delayed puberty
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144
Q

what are the signs of UC?

A
  • Pallor
  • Clubbing.
  • Abdominal distension, tenderness or mass, for example in the left lower quadrant.
  • Signs of malnutrition or malabsorption.
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145
Q

what is seen on blood tests in UC?

A
  • iron deficiency anaemia
  • raised WCC
  • raised platelets
  • Raised ESR and CRP
  • hypoalbuminaemia
  • positive pANCA
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146
Q

what is seen on colonoscopy in UC?

A
  • superficial inflammation that is continuous
  • the mucosa looks reddened, inflamed and bleeds easily (friability).
  • In severe disease there is extensive ulceration with the adjacent mucosa appearing as inflammatory (pseudo) polyps.
  • In ulcerative colitis, the mucosa shows a chronic inflammatory cell infiltrate in the lamina propria.
  • Crypt abscesses and goblet cell depletion are also seen.
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147
Q

how is mild-moderate UC treated to induce remission?

A
  • a topical aminosalicylate
  • oral aminosalicylate
  • corticosteroids
  • ciclosporin
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148
Q

how is remission maintained in UC?

A
  • thiopurine
  • methotrexate

intravenous TNF-alpha inhibitor (infliximab or adalimumab)

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149
Q

what are the risk factors for the development of diverticula?

A
  • Genetic factors.
  • Increasing age.
  • Low-fibre diet.
  • Smoking.
  • Obesity.
  • Drugs such as NSAIDs.
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150
Q

what are the clinical features of diverticular disease?

A
  • Intermittent abdominal pain in the left lower quadrant, which may be triggered by eating and relieved by the passage of stool or flatus.
  • Constipation, diarrhoea or occasional large rectal bleeds.
  • Bloating and passage of mucus rectally.
  • Tenderness in the left lower quadrant.
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151
Q

how should diverticular disease be investigated?

A

colonoscopy

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152
Q

how is diverticular disease managed?

A

-Arrange urgent admission if the patient has significant rectal bleeding and is haemodynamically unstable (a pulse greater than 150 bpm, and a systolic blood pressure lower than 90 mmHg).

  • Offer lifestyle advice to patients who do not need admission:
  • –Recommend a healthy balanced diet contains whole grains, fruits, and vegetables.
  • –Recommend drinking an adequate fluid intake with a high-fibre diet.
  • Consider prescribing a bulk-forming laxative (Ispaghula husk) if a high fibre diet is insufficient, or if symptoms of constipation or diarrhoea persist.
  • Offer paracetamol for pain relief. Advise the patient to avoid NSAIDs and opiate analgesia.
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153
Q

what are the clinical features of uncomplicated diverticulitis?

A
  • Constant abdominal pain, usually severe and starting in the hypogastrium before localising in the left lower quadrant.
  • Fever.
  • Change in bowel habit.
  • Significant rectal bleeding.
  • Nausea, vomiting, dysuria, urinary frequency.
  • Tenderness in the left lower quadrant.
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154
Q

what are the clinical features of complicated diverticulitis?

A

-Abscess formation suggested by abdominal mass on examination.

-Perforation and peritonitis suggested by abdominal rigidity, guarding, and rebound
tenderness.

  • Sepsis suggested by skin discolouration, raised or lowered temperature, rigors, change in conscious level, confusion, rapid pulse, reduced urination.
  • Fistula formation: Faecaluria, pneumaturia.
  • Intestinal obstruction suggested by colicky abdominal pain, vomiting, inability to pass flatus, abdominal distension.
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155
Q

how is acute uncomplicated diverticulitis managed?

A
  • Offer paracetamol for pain relief.
  • Advise the patient to avoid NSAIDs and opiate analgesia.
  • Offer co-amoxiclav for patients who are systemically unwell, but do not meet the criteria for suspected complicated acute diverticulitis.
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156
Q

how is acute complicated diverticulitis managed?

A
  • Arrange urgent hospital admission if there is suspected acute diverticulitis:
  • –Offer intravenous antibiotics (co-amoxiclav or metronidazole + cefuroxime), fluid replacement, and analgesia.
  • Consider percutaneous drainage of an abscess that is greater than 3 cm.
  • Offer laparoscopic lavage or Hartmann’s procedure (sigmoid colectomy with formation of an end colostomy) for patients with faecal peritonitis or who fail to respond to antibiotic therapy.
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157
Q

what are the risk factors for the development of eosinophilic oesophagitis?

A
  • Family history of eosinophilic oesophagitis.
  • Male sex.
  • Atopic disease (asthma, atopic dermatitis, allergic rhinitis / sinusitis, food allergies).
  • Children and young adults.
  • White ancestry.
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158
Q

what are the clinical features of eosinophilic oesophagitis?

A
  • Dysphagia.
  • Food avoidance and modification behaviours.
  • Regurgitation.
  • Heartburn.
  • Oesophageal pain.
  • Nausea and vomiting.
  • Failure to thrive.
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159
Q

how is eosinophilic oesophagitis diagnoses

A
  • OGD

- Oesophageal biopsy

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160
Q

how is eosinophilic oesophagitis treated?

A
  • Offer a corticosteroid (budesonide or fluticasone) for 8 weeks.
  • Offer dietary elimination therapy for 6 weeks.
  • Offer endoscopic oesophageal dilation (wire-guided bougie) in patients with severe oesophageal narrowing.
  • Emerging therapy includes mepolizumab, a monoclonal antibody against IL-5.
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161
Q

what are the risk factors for squamous carcinoma of the oesophagus?

A
  • alcohol

- tobacco

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162
Q

what are the risk factors for adenocarcinoma of the oesophagus?

A
  • barrett’s oesophagus

- hiatus hernia

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163
Q

what are the clinical features of oesophageal cancer?

A
  • Progressive dysphagia for solids (meat and bread) and then liquids within weeks.
  • Odynophagia.
  • Weight loss.
  • Anorexia.
  • Lymphadenopathy.
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164
Q

how is oesophageal cancer diagnosed?

A

-OGD with biopsy

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165
Q

how is stage 0 and 1a oesophageal cancer managed?

A

-endoscopic resection.

166
Q

how is stage 1b and 2a oesophageal cancer managed?

A
  • oesophagectomy

- chemoradiotherapy

167
Q

how is stage 2b and 3 oesophageal cancer managed?

A

Perform oesophagectomy with preoperative chemoradiotherapy

168
Q

how is stage 4 oesophageal cancer managed?

A

Offer chemoradiotherapy (cisplatin, fluorouracil and radiotherapy) and offer endoscopic ablation and stenting for symptom relief

169
Q

what are the risk factors for developing gastric cancer?

A
  • Pernicious anaemia.
  • H.pylori.
  • N-nitroso compounds.
  • Smoking.
  • Family history.
  • Male sex.
  • Age 50 to 70 years.
170
Q

what are the symptoms of gastric cancer?

A
  • Epigastric pain.
  • Weight loss.
  • Vomiting.
  • Dysphagia.
171
Q

what are the signs of gastric cancer?

A
  • Anaemia from occult blood loss.
  • Virchow’s node.
  • Sister Mary Joseph’s nodule.
  • Acanthosis nigricans.
  • Dermatomyositis.
  • Thrombophlebitis.
172
Q

how is gastric cancer managed?

A
  • Perform surgical resection and perioperative chemotherapy (epirubicin + cisplatin + fluorouracil) in patients with early localised disease in a surgical candidate.
  • Offer chemoradiotherapy (fluorouracil + radiotherapy) in patients with early localised disease who are not surgical candidates.
  • For advanced and metastatic disease:
  • –Offer chemotherapy (ECF).
  • –Offer palliative gastrectomy.
173
Q

what are the risk factors for development of pancreatic cancer?

A
  • Cigarette smoking is the most important risk factor.
  • Type II diabetes mellitus.
  • Chronic pancreatitis.
  • Family history: Hereditary pancreatitis, Peutz-Jeghers syndrome, Lynch syndrome.
  • Increasing age.
  • Male gender.
174
Q

what are the clinical features of pancreatic cancer in the head of the pancreas?

A
  • Obstructive jaundice.
  • Characteristic stretch marks secondary to cholestasis.
  • Painless palpable gall-bladder.
  • Epigastric mass is a sign of advanced disease.
175
Q

what are the clinical features of pancreatic cancer in the body and tail of the pancreas?

A
  • Dull abdominal pain that radiates through the back, that is partially relieved by sitting forward.
  • Anorexia.
  • Weight loss.
  • Thromboembolic phenomena.
  • Polyarthritis.
  • Skin nodules.
176
Q

how is suspected pancreatic cancer investigated?

A
  • transabdominal ultrasound showing dilated bile ducts and pancreatic mass
  • CT scan
  • FDG-PET and ERCP if ambiguous CT
  • CA19-9 biomarker
177
Q

how is pancreatic cancer managed with resectable disease?

A
  • Pancreaticoduodenectomy (Whipple procedure).
  • Preoperative endoscopic stent insertion.
  • Neoadjuvant chemotherapy (5-fluorouracil).
178
Q

how is pancreatic cancer managed with unresectable disease?

A
  • Endoscopic stent insertion
  • Offer gemcitabine based combination chemotherapy or FOLFIRINOX.
  • Opioid analgesia or percutaneous neurolytic coeliac plexus block for pain relief.
179
Q

what are the risk factors for developing GORD?

A
  • Stress and anxiety.
  • Smoking and alcohol.
  • Trigger foods, such as coffee and alcohol.
  • Obesity, pregnancy, hiatus hernia.
  • Family history.
  • Drugs such as alpha blockers, anticholinergics, benzodiazepines, NSAIDs.
  • Children with cerebral palsy or other neurodevelopmental disorders
  • Preterm infants, particularly with coexistent bronchopulmonary dysplasia
180
Q

What are the clinical features of GORD?

A
  • Heartburn, which is aggravated by bending over or lying down, worsened after food, hot drinks, alcohol, and relieved by antacids.
  • Acid regurgitation mainly after meals.
  • Dysphagia is uncommon.
  • Posseting and poor feeding in children
181
Q

what lifestyle measures can improve symptoms of GORD?

A
  • Lose weight if the patient is overweight or obese.
  • Avoid trigger foods and eat smaller meals.
  • Stop smoking and reduce alcohol consumption.
  • Sleep with the head of the bed raised (bricks under head of bed if practical).
  • Relaxation strategies for stress and anxiety.
  • Stopping drugs that may exacerbate symptoms.
182
Q

How is GORD managed?

A

-PPI

183
Q

How is GORD managed in children?

A
  • thickening agents (carobel)
  • acid suppression (gaviscon or PPI)
  • Nissen fundoplication with complications
184
Q

what are the clinical features of Zollinger-Ellison syndrome?

A
  • Recurrent peptic ulcer disease.
  • Diarrhoea.
  • Epigastric abdominal pain.
  • Gastro-oesophageal reflux disease.
  • Steatorrhoea.
185
Q

how is Zollinger-Ellison syndrome diagnosed?

A
  • Measure fasting serum gastrin: Elevated.
  • Perform a secretin infusion test: Increase in fasting serum gastrin.
  • Measure serum calcium: Raised suggest MEN1 syndrome.
  • Consider a GI endoscopy: Prominent gastric folds.
186
Q

how is Zollinger-Ellison syndrome treated?

A
  • Offer a proton pump inhibitor (omeprazole 60 mg) to control gastric acid hypersecretion.
  • Offer surgery for localised disease if the primary site is causing symptoms.
  • Offer a somatostatin analogue (octreotide) and everolimus for liver metastases to limit tumour growth and symptoms.
  • Offer chemoradiotherapy for extrahepatic metastatic disease.
187
Q

what are the risk factors for hereditary haemochromatosis?

A
  • Middle age.
  • Male gender (the reduced incidence in women is probably explained by physiological blood loss and a smaller dietary intake of iron).
  • White ancestry.
  • Family history.
  • Supplemental iron.
188
Q

what are the clinical features of hereditary haemochromatosis?

A
  • Fatigue, weakness, lethargy.
  • Arthralgia.
  • Impotence and loss of libido.
  • Arrhythmia and heart failure (uncommon).
  • Bronze skin pigmentation due to excess melanin deposition.
  • Hepatomegaly.
189
Q

what is seen on iron profile in hereditary haemochromatosis?

A
  • Raised ferritin
  • raised serum transferrin
  • reduced total iron binding capacity
190
Q

how is hereditary haemochromatosis managed?

A
  • Perform venesection 500 mL twice weekly for 2 years.
  • Offer iron chelation therapy with desferrioxamine for patients who cannot tolerate venesection.
  • Patients should avoid iron and vitamin C containing supplements.
191
Q

what are the clinical features of Hirschprung’s disease?

A
  • Delay of passage of meconium.
  • Vomiting which can be bilious.
  • Abdominal distension.
  • Constipation.
  • Explosive passage of liquid and foul stools.
  • Fever and failure to thrive associated with enterocolitis.
192
Q

how should suspected Hirschprung’s disease be investigated?

A
  • Perform an AXR initially: Air-fluid levels present and dilated colon.
  • Perform a contrast enema which is the most useful diagnostic test: Contracted distal bowel and dilated proximal bowel.
  • Perform a rectal biopsy which allows for definitive diagnosis: Absence of ganglion cells.
193
Q

how is Hirschprung’s disease managed?

A
  • Perform bowel irrigation as the initial treatment prior to surgery. It allows evacuation of gas and liquid stool through the tube.
  • Perform a pull through procedure surgery (Swenson procedure) within the first week of life for segmental disease.
  • Administer intravenous metronidazole for enterocolitis.
  • Perform a total colectomy and ileostomy for total colon aganglionosis.
194
Q

what are the clinical features of ileus?

A
  • Decreased bowel sounds.
  • Nausea and vomiting.
  • Abdominal distension.
  • Constipation.
195
Q

what are the causes of ileus

A
  • GI surgery
  • electrolyte imbalances
  • release of inflammatory agents
  • dysregulation of sympathetic and parasympathetic input to GI tract
  • analgesia and anaesthesia
196
Q

how is ileus managed?

A
  • Patient should be nil by mouth.
  • Administer intravenous hydration with normal saline.
  • Reduce opioid analgesia.
197
Q

what is pyloric stenosis?

A

hypertrophy of the pyloric muscle

198
Q

what are the risk factors for pyloric stenosis?

A
  • 2 and 7 weeks of age
  • males
  • first born
  • family history on maternal side
199
Q

what are the clinical features of pyloric stenosis?

A
  • projectile, non-bilious vomiting
  • Hunger after vomiting until dehydration leads to loss of interest in feeding
  • Weight loss if presentation is delayed.
  • Tachycardia
  • Dry mucous membranes
  • Palpable pylorus
  • A hypochloraemic metabolic alkalosis with a low plasma sodium and potassium occurs as a result of vomiting stomach contents.
200
Q

how is pyloric stenosis diagnosed?

A

-Ultrasound examination is helpful if the diagnosis is in doubt, showing pyloric muscle thickness >4mm

201
Q

how is pyloric stenosis managed?

A
  • The initial priority is to correct any fluid and electrolyte disturbance with intravenous fluids (0.45% saline and 5% dextrose with potassium supplements).
  • pyloromyotomy
202
Q

what are the risk factors for developing IBS?

A
  • Psychosocial factors include stress, anxiety, depression.
  • Genetic factors.
  • Gastroenteritis.
  • Inflammatory bowel disease.
  • Dietary factors such as alcohol, caffeine, spicy and fatty foods.
  • Antibiotics.
203
Q

what are the clinical features of IBS?

A
  • Abdominal pain.
  • Bloating.
  • Change in bowel habits.
  • Lethargy.
  • Nausea.
  • Back pain.
  • Bladder symptoms such as nocturia.
204
Q

what are the Rome IV criteria for the diagnosis of IBS?

A
  • Recurrent abdominal pain, at least 1 day per week in the last 3 months:
  • Relieved by defecation.
  • Associated with a change in frequency of stool.
  • Associated with a change in appearance of stool.
205
Q

how is IBS managed?

A
  • Provide advice and reassurance.
  • Encourage stress management such as exercise or yoga.
  • Advise the patient to maintain a healthy, balanced diet:
  • Low FODMAP diet (low fermentable carbohydrate diet, avoiding fruits, artificial sweeteners, and some green vegetables).
  • Reduce intake of fibre if diarrhoea.
  • Fibre supplements or foods high in fibre if constipation.
  • Reducing caffeine, alcohol, spicy and fatty foods.
  • Adequate fluid intake.
  • Consider probiotics for a minimum of four weeks.
  • Offer loperamide for diarrhoea.
206
Q

how should constipation in IBS be managed?

A
  • Offer a bulk forming laxative (ispaghula husk).

- Offer linaclotide if constipation persists for over 12 months or if laxatives are poorly tolerated

207
Q

how should abdominal pain and spasm be managed in IBS?

A
  • Offer an antispasmodic agent (mebeverine hydrochloride).
  • Consider amitriptyline if abdominal pain persists.
  • Consider an SSRI (citalopram) if the patient is constipated, as TCAs can cause constipation, or where a TCA is ineffective, contra-indicated or not tolerated
208
Q

what are the risk factors for developing Hep A?

A
  • Travelling to countries where the virus is highly endemic.
  • Men who have sex with men, and people with risky sexual behaviours.
  • People with clotting factor disorders.
  • Intravenous drug use.
  • People at occupational risk such as laboratory workers, and sewage workers.
209
Q

what are the prodromal features of Hep A?

A
  • Flu-like symptoms, including fatigue, malaise, joint and muscle pain, low-grade fever.
  • Gastrointestinal symptoms, such as nausea, vomiting, anorexia, right upper quadrant discomfort.
  • Accompanying headache, cough, sore throat, or urticaria
210
Q

what are the icteric features of Hep A?

A
  • Pruritus.
  • Fatigue, anorexia, nausea, vomiting.
  • Hepatomegaly, splenomegaly, lymphadenopathy.
211
Q

what are the convalescent features of Hep A?

A
  • Malaise.
  • Anorexia
  • Muscle weakness.
  • Hepatic tenderness.
212
Q

what is seen on LFTs in Hep A?

A
  • Elevated ALT and AST (usually between 500 and 10,000 IU/L).
  • Low ALT in fulminant hepatitis
  • Elevated bilirubin
  • Prolonged PT.
213
Q

which serological result suggests acute Hep A infection?

A
  • Positive HAV-IgM

- positive HAV-IgG

214
Q

which serological result suggests past Hep A infection with immunity?

A
  • Negative HAV-IgM

- positive HAV-IgG

215
Q

which serological result suggests a false positive for Hep A?

A
  • Positive HAV-IgM

- negative HAV-IgG

216
Q

who should Hep A vaccination be given to?

A
  • People travelling to high-risk areas.
  • People with chronic liver disease.
  • People receiving plasma-derived clotting factors to treat haemophilia.
  • IV drug users.
  • Men who have sex with men with multiple sexual partners.
  • People at occupational risk.
217
Q

what supportive symptomatic treatment should be offered in Hep A?

A
  • Advise paracetamol or ibuprofen for pain relief.
  • Prescribe metoclopramide (for 5 days) or cyclizine for nausea.
  • Prescribe chlorphenamine for pruritus.
218
Q

what are the risk factors for the development of Hep B?

A
  • Sharing of drug injecting equipment.
  • Travelling to areas of high prevalence.
  • Receiving regular blood or blood products (such as people with haemophilia).
  • Occupational hazards including needle stick injuries or direct exposure of mucous membranes to infected blood.
  • Tattoos, body piercing, or acupuncture.
  • Sexual transmission via mucous membranes. Having sex unprotected sex or having multiple sexual partners produces the greatest risk.
  • Transmission during childbirth (perinatal transmission).
219
Q

what are the clinical features of acute Hep B?

A
  • Prodromal illness that includes fever, arthralgia or a rash.
  • Right upper quadrant abdominal pain.
  • Jaundice with dark urine or pale stools.
  • Extrahepatic manifestations, including glomerulonephritis, vasculitis, polyarteritis.
220
Q

what are the clinical features of chronic Hep B?

A
  • Spider naevi.
  • Finger clubbing.
  • Jaundice.
  • Hepatosplenomegaly.
  • In severe cases: thin skin, bruising, ascites, liver flap, encephalopathy.
221
Q

what is seen on LFTs in acute Hep B?

A
  • Elevated ALT and AST
  • Elevated ALP
  • Elevated bilirubin
  • Prolonged PT
222
Q

which hepatitis B serology result suggests acute infection?

A
  • A positive HBsAg and IgM

- negative IgG

223
Q

which hepatitis B serology result suggests chronic infection?

A
  • A positive HBsAg and IgG

- a negative IgM

224
Q

what symptomatic care should be given in acute Hep B infection?

A
  • paracetamol, ibuprofen, or a weak opioid for pain relief.
  • Metoclopramide for nausea.
  • Chlorphenamine for pruritus
225
Q

Which patients should be given antiviral therapy for Hep B?

A
  • Aged 30 years and older.
  • HBV DNA greater than 2000 IU/L and an ALT greater than 30 IU/L.
  • Evidence of necroinflammation or fibrosis on liver biopsy.
226
Q

which antiviral should be given for:

a) acute Hep B infection
b) chronic Hep B infection?

A

a) entecavir or tenofovir

b) peg-interferon alpha-2a

227
Q

what are the risk factors for developing Hep C?

A
  • Unsafe medical practices.
  • Intravenous drug use.
  • HIV.
  • Prisoners.
  • Multiple sexual partners, men who have sex with men.
  • Infected mother, especially if the mother is co-infected with HIV.
228
Q

what are the clinical features of Hep C?

A
  • Fatigue.
  • Myalgia.
  • Arthralgia.
  • Signs of advanced liver disease include ascites and signs of hepatic encephalopathy, including confusion, altered consciousness, and coma
229
Q

which patients with Hep C should be given direct acting anti-virals first line?

A
  • For patients with acute hepatitis in whom there is no spontaneous resolution (HCV RNA after 6 months).
  • For patients with chronic hepatitis.
230
Q

what are the clinical features of acute mesenteric colitis?

A
  • Peri-umbilical severe abdominal pain.

- Rapid forceful bowel evacuation.

231
Q

what are the clinical features of chronic mesenteric colitis?

A
  • Poorly localised abdominal pain after meals.
  • Sitophobia and associated weight loss.
  • Nausea and vomiting.
  • History of smoking.
232
Q

what are the clinical features of ischaemic colitis?

A
  • Peripheral severe abdominal pain and tenderness.

- Frequent bloody stools, characteristic maroon or red blood.

233
Q

what are the x-ray features of ischaemic colitis?

A

-thumbprint sign

234
Q

how is acute mesenteric ischaemia managed?

A
  • Offer adequate fluid resuscitation and oxygenation.
  • Offer empirical antibiotics (ceftriaxone and metronidazole).
  • Perform endovascular therapy.
  • Perform exploratory laparotomy if there is infarction, perforation or peritonitis.
235
Q

how is chronic mesenteric ischaemia managed?

A

-Consider endovascular treatment

236
Q

how is ischaemic colitis managed?

A
  • Most cases resolve spontaneously and only supportive care is needed.
  • Perform segmental colectomy for severe disease if there is generalised peritonitis or perforation.
237
Q

what are the causes of large bowel obstruction?

A
  • colorectal malignancy
  • Colonic volvulus (sigmoid or caecal).
  • Benign stricture (diverticulum).
  • Pelvic abscess.
  • Endometriosis.
238
Q

what are the clinical features of large bowel obstruction?

A
  • Colicky abdominal pain.
  • Tympanic abdomen.
  • Hard faeces.
  • Recent weight loss (suggests underlying malignancy).
  • Rectal bleeding (suggests underlying malignancy).
239
Q

what is seen on Abdominal X-ray in large bowel obstruction?

A
  • Gaseous distension of large bowel

- Coffee bean shape in volvulus

240
Q

what are the causes of small bowel obstruction?

A
  • adhesions from previous surgery
  • Appendicitis.
  • Intestinal malignancy.
  • Crohn’s disease.
  • Inguinal hernia.
241
Q

what are the clinical features of small bowel obstruction?

A
  • Cramping abdominal pain.
  • Nausea and vomiting.
  • Abdominal distension.
  • Constipation.
242
Q

how is small bowel obstruction managed?

A
  • Offer supportive care with fluid resuscitation and analgesia.
  • Perform nasogastric decompression for complete or complicated small bowel obstruction.
  • Declare the patient nil by mouth.
243
Q

what are the clinical features of liver abscess?

A
  • Fever.
  • Malaise
  • Right upper quadrant pain.
  • Anorexia.
  • Vomiting.
244
Q

what is seen on contrast-enhanced CT in liver abscess?

A

Hypo-dense liver lesion.

245
Q

how is a liver abscess treated?

A
  • Offer piperacillin with tazobactam and fluid resuscitation for haemodynamically unstable patients
  • Offer metronidazole and ciprofloxacin for patients who are haemodynamically stable.
  • Offer metronidazole in patients with suspected amoebic abscess.

-Perform ultrasound guided percutaneous drainage in all patients in addition to antibiotic
therapy.

-Offer anticandidal therapy (caspofungin) when liver abscess is diagnosed in an immunocompromised patient.

246
Q

what are the risk factors for non-alcoholic fatty liver disease?

A
  • Obesity, hypertension, type 2 diabetes and hyperlipidaemia
  • Hypertension
  • Medications including amiodarone, corticosteroids, diltiazem, methotrexate, tamoxifen
247
Q

what are the symptoms of non-alcoholic fatty liver disease?

A
  • Typically asymptomatic
  • Fatigue
  • Malaise
  • Pruritus
  • Hepatosplenomegaly
  • RUQ pain
248
Q

what is seen on LFTs in non-alcoholic fatty liver disease?

A
  • Elevated ALT and AST
  • Elevated ALP and GGT
  • Elevated bilirubin
  • Decreased serum albumin.
249
Q

what is seen on liver biopsy in non-alcoholic fatty liver disease?

A

-steatosis

250
Q

how is non-alcoholic fatty liver disease managed?

A
  • Offer lifestyle advice on gradual weight loss (rapid weight loss is a risk factor for NAFLD) through diet and exercise.
  • Offer metformin for patients with diabetes.
  • Offer a statin for patients with hyperlipidaemia.
  • For patients with advanced liver disease:
  • –Monitor for hepatocellular cancer using ultrasound scans and alpha-fetoprotein.
  • –Offer vitamin E or pioglitazone for advanced liver fibrosis.
  • –Refer for liver transplantation.
251
Q

what is gastritis?

A
  • inflammation associated with mucosal injury
252
Q

what is gastropathy?

A
  • epithelial cell damage and regeneration without inflammation.
253
Q

what are the clinical features of peptic ulcer disease?

A
  • Recurrent, burning epigastric pain which the patient can identify with a single finger.
  • Pain on hunger and at night suggests duodenal ulcer.
  • Pain worsened by eating suggests gastric ulcer.
  • Back pain suggests a penetrating duodenal ulcer into the pancreas.
  • Persistent vomiting suggests gastric outlet obstruction.
  • Haematemesis and melaena suggests haemorrhage.
  • Examination reveals epigastric tenderness on palpation.
254
Q

how is H.pylori diagnosed?

A
  • carbon-13 urea breath test

- stool antigen test

255
Q

which patients should be referred of OGD with suspected peptic ulcer disease?

A
  • older than 55

- have alarm symptoms such as dysphagia, weight loss, vomiting, anorexia, haematemesis or melaena.

256
Q

what lifestyle advice can improve the symptoms of peptic ulcer disease?

A
  • Lose weight if overweight or obese.
  • Avoid trigger food such as coffee, chocolate, tomatoes, fatty or spicy foods.
  • Eat smaller meals and avoid eating an evening meal 3 - 4 hours before bed.
  • Smoking cessation and reduced alcohol consumption.
  • Relaxation strategies if stress or anxiety.
  • Avoid NSAIDs, bisphosphonates, and corticosteroids.
257
Q

what regimes can be used for h.pylori eradication?

A
  • Offer omeprazole 20 mg twice daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily.
  • Offer metronidazole 400 mg twice daily in place of amoxicillin in patients who are allergic to penicillin.
  • Offer tetracycline hydrochloride 500 mg four times daily in place of clarithromycin in patients who have had previous exposure to clarithromycin.
258
Q

what are the risk factors for primary biliary cholangitis?

A
  • Female (F:M ratio of 10:1).
  • Increasing age (peak incidence between 45 and 60).
  • Family history of PBC or autoimmune disease.
  • Smoking.
  • Urinary tract infection.
259
Q

what are the clinical features of primary biliary cholangitis?

A
  • Pruritus.
  • Fatigue.
  • Dry eyes and mouth (associated Sjogren’s syndrome).
  • Sleep disturbance.
  • Postural dizziness.
  • Hepatomegaly.
260
Q

which antibodies are present in primary biliary cholangitis?

A
  • anti-mitochondrial antibody
  • ANA
  • anti-M2
261
Q

what are the diagnostic features of primary biliary cholangitis?

A
  • raised ALP

- presence of AMA.

262
Q

how is early stage primary biliary cholangitis treated?

A
  • Offer a bile acid analogue (ursodeoxycholic acid) to modify disease progression.
  • Offer cholestyramine for pruritus.
263
Q

how is end stage primary biliary cholangitis treated?

A

liver transplant

264
Q

what are the risk factors for primary sclerosing cholangitis?

A
  • Male sex.
  • Inflammatory bowel disease.
  • Genetic predisposition.
265
Q

what are the clinical features of primary sclerosing cholangitis?

A
  • Right upper quadrant pain.
  • Pruritus (excoriations on examination).
  • Fatigue.
  • Fever.
  • Jaundice
266
Q

which autoantibodies are present in primary sclerosing cholangitis?

A

-ANCA

267
Q

how is early stage primary sclerosing cholangitis treated?

A
  • Offer lifestyle advice such as maintaining a healthy diet and weight, and limiting alcohol consumption.
  • Offer cholestyramine for pruritus.
268
Q

how are acutely ill patients with primary sclerosing cholangitis treated?

A
  • Refer for ERCP and balloon dilatation of the structure.

- Offer percutaneous transhepatic cholangiogram if ERCP is unsuccessful

269
Q

what are the risk factors for hepatocellular carcinoma?

A
  • Cirrhosis.
  • Chronic hepatitis B infection.
  • Chronic hepatitis C infection.
  • Chronic heavy alcohol use.
  • Diabetes.
  • Obesity.
270
Q

what are the clinical features of hepatocellular carcinoma?

A
  • Weight loss.
  • Anorexia.
  • Fever.
  • Stigmata of chronic liver disease.
  • Clinical features of the complications of cirrhosis.
  • Examination reveals an enlarged, irregular tender liver.
271
Q

which tumour marker is raised in hepatocellular carcinoma?

A

serum alpha-fetoprotein

272
Q

how is hepatocellular carcinoma treated?

A
  • Offer liver transplantation for early disease (BCLC stage A).
  • Offer trans-arterial chemoembolisation (TACE) in intermediate disease (BCLC stage B).
  • Offer sorafenib or lenvatinib for advanced disease (BCLC stage C).
  • Offer hospice care for end-stage disease (BCLC stage D).
273
Q

what are the risk factors for cholangiocarcinoma?

A
  • Increasing age.
  • Choledocholithiasis.
  • Primary sclerosing cholangitis.
  • Ulcerative colitis.
274
Q

which serum tumour markers may be raised in cholangiocarcinoma?

A
  • serum CA19-9

- serum CEA

275
Q

how is resectable cholangiocarcinoma treated?

A
  • Perform partial liver resection for intrahepatic tumours.
  • Perform surgical excision of extrahepatic tumours.
  • Offer pre-operative portal vein embolisation.
276
Q

how is unresectable cholangiocarcinoma treated?

A
  • Offer liver transplant and chemoradiotherapy.

- Offer palliative care.

277
Q

what are the clinical features of Wilson’s disease?

A
  • Hepatitis.
  • Behavioural.
  • Tremor.
  • Dysarthria.
  • Dystonia.
  • Incoordination.
  • Sloppy or small handwriting.
  • Dysdiadochokinesia.
  • Abnormal extraocular movement.
  • Kayser-Fleischer ring, which appears as a greenish brown pigment at the corneoscleral junction.
  • neuropsychiatric features are more common in those presenting from second decade onwards
278
Q

how is Wilson’s disease treated?

A
  • Offer lifelong treatment with penicillamine.
  • Offer trientine or zinc if patient experiences severe adverse effects with penicillamine such as nephropathy, lupus like syndrome and bone marrow depression.
  • Offer liver transplantation for fulminant hepatic failure or decompensated cirrhosis.
279
Q

how is Wilson’s disease diagnosed?

A
  • > 100mcg urinary copper
  • Reduced blood caeruloplasmin
  • > 250mcg copper on liver biopsy
280
Q

how can constipation be self-managed?

A
  • increase fibre, fruits high ins orbital and veg
  • increase fluid intake
  • develop a toilet routine
281
Q

how should short duration constipation be managed?

A
  • manage secondary causes
  • increase fibre, fluid and activity
  • bulk-forming laxative (ispaghula)
  • osmotic laxative (macrogol or lactulose)
  • stimulant laxative
282
Q

how is chronic constipation managed?

A

increase fibre, fluid and activity

  • bulk-forming laxative (ispaghula)
  • osmotic laxative (macrogol or lactulose)
  • consider prucalopride
283
Q

how should faecal loading/impaction be managed?

A
  • with hard stool give macrogol
  • with soft stool give stimulant laxative
  • if laxative response is inadequate, give bisacodyl suppository or mini docusate/sodium citrate enema
  • if response is still inadequate, give sodium phosphate or arachis oil retention enema overnight before giving sodium phosphate or sodium citrate enema
  • regular laxatives
284
Q

how is constipation managed in children?

A
  • disimpaction regimen of stool softeners, initially with a macrogol osmotic laxative, e.g. polyethylene glycol + electrolytes (Movicol Paediatric Plain).
  • An escalating dose regimen is administered over 1–2 weeks or until impaction resolves.
  • If this proves unsuccessful, a stimulant laxative, e.g. senna, or sodium picosulphate, may also be required.
  • If the polyethylene glycol + electrolytes is not tolerated, an osmotic laxative can be substituted.
285
Q

what are the clinical features of travellers’ diarrhoea?

A
  • Abdominal pain
  • Cramps
  • Nausea
  • Vomiting
  • Dysentry
286
Q

when should a stool sample be sent with suspected gastroenteritis?

A
  • systemically unwell
  • blood or pus in the stool.
  • Persistent diarrhoea with suspected giardiasis.
  • Patient is immunocompromised.
287
Q

which antibiotic can be used in camplyobacter?

A

erythromycin

288
Q

how should salmonella be treated?

A

ciprofloxacin

289
Q

how should shigella be treated?

A

ciprofloxacin

290
Q

what are the clinical features of cholera?

A
  • incubation of few hours to 6 days.
  • profuse painless diarrhoea
  • vomiting
  • rice-water stools
  • hypovolaemic shock
  • muscle cramps
291
Q

how is cholera diagnosed?

A
  • clinical
  • rapid dipstick test
  • stool and rectal swabs for culture
292
Q

how is cholera treated?

A

-oral rehydration

293
Q

what are the clinical features of amoebiasis?

A
  • chronic, with mild intermittent diarrhoea and abdominal discomfort
  • may progress to bloody diarrhoea with mucus
294
Q

what are the features of Amoebic liver abscess?

A
  • Tender hepatomegaly
  • high swinging fever
  • profound malaise
295
Q

how is amoebiasis diagnosed?

A

-microscopic examination or colonic exudate obtained at sigmoidoscopy

296
Q

how is amoebiasis diagnosed?

A
  • metronidazole or tinidazole

- bowel should then be cleared of parasites with diloxanide furoate

297
Q

what are the clinical features of giardiasis?

A
  • diarrhoea, often watery
  • nausea
  • anorexia
  • abdominal discomfort
  • bloating
  • steatorrhoea
  • weight loss
298
Q

how is giardiasis diagnosed?

A
  • stool examination

- duodenal aspirate

299
Q

how is giardiasis treated?

A
  • metronidazole

- Alternative drugs include tinidazole, mepacrine and albendazole.

300
Q

what are the risk factors for C.diff?

A
  • Increasing age (more than 65 years old).
  • Antibiotic treatment.
  • Hospitalisation or residence in a nursing home.
  • History of C.difficile-associated disease.
  • Use of acid suppressing drugs.
  • Inflammatory bowel disease.
  • Solid organ or haematopoietic stem cell transplant recipients.
  • Chronic kidney disease.
  • HIV infection.
301
Q

what are the clinical features of C.diff?

A
  • Clinical features commence anything from 2 days to some months after antibiotics.
  • Mild diarrhoea to profusely, water, haemorrhagic diarrhoea.
  • Abdominal pain.
  • Fever.
  • Abdominal tenderness.
  • Hypotension (suggests life-threatening infection).
302
Q

how is c.diff diagnosed?

A

-Measure stool PCR or ELISA which is diagnostic: Toxin A or B present

303
Q

how is c.diff managed?

A
  • oral metronidazole for 10 days for mild/moderate infection
  • oral vancomycin for severe infection
304
Q

what is failure to thrive?

A

sub-optimal weight gain in infants and toddlers.

305
Q

what are the non-organic causes of inadequate intake failure to thrive?

A
  • feeding problems
  • insufficient or unsuitable foods
  • lack of regular feeding
  • infant difficult to feed
  • conflict over feeding
  • intolerance of normal feeding behaviour
  • problems with finances
  • low socioeconomic status
  • poor maternal-infant interaction
  • maternal depression
  • poor maternal education
  • neglect or child abuse
306
Q

what are the organic causes of inadequate intake failure to thrive?

A
  • oromotor dysfunction
  • neurological disorder
  • cleft palate
307
Q

what are the inadequate retention causes of failure to thrive?

A
  • vomiting

- severer GORD

308
Q

what are the malabsorption causes of failure to thrive?

A
  • coeliac
  • CF
  • cow’s milk protein allergy
  • cholestatic liver disease
  • short gut syndrome
  • post-NEC
309
Q

what are the failure to utilise nutrients causes of failure to thrive?

A
  • syndromes
  • chromosomal disorders
  • IUGR
  • extreme prematurity
  • congenital infection
  • metabolic disorders
310
Q

what are the increased requirement causes of failure to thrive?

A
  • thyrotoxicosis
  • CF
  • malignancy
  • chronic infection
  • CHD
  • chronic renal failure
311
Q

what are the thresholds for concern in faltering growth?

A
  • a fall across 1 or more weight centile spaces, if birth weight was below the 9th centile.
  • a fall across 2 or more weight centile spaces, if birth weight was between the 9th and 91st centiles.
  • a fall across 3 or more weight centile spaces, if birth weight was above the 91st centile.
  • when current weight is below the 2nd centile for age, whatever the birth weight.
312
Q

when is enteral nutrition used?

A

-when the digestive tract is functioning

313
Q

what are the clinical features of marasmus?

A
  • weight for height more than -3 standard deviations from the median
  • wasted, wizened appearance
  • withdrawn and apathetic
314
Q

what are the clinical features of kwashiorkor ?

A
  • a ‘flaky-paint’ skin rash with hyperkeratosis (thickened skin) and desquamation
  • a distended abdomen and enlarged liver (usually due to fatty infiltration)
  • angular stomatitis
  • hair which is sparse and depigmented
  • diarrhoea, hypothermia, bradycardia and hypotension
  • low plasma albumin, potassium, glucose and magnesium.
315
Q

how is severe acute malnutrition managed in children?

A
  • Hypoglycaemia–common; correct urgently, particularly if coma or severely ill.
  • Hypothermia–wrap, especially at night.
  • Dehydration–correct, but avoid being overzealous with intravenous fluids, as may lead to heart failure.
  • Electrolytes–correct deficiencies, especially potassium.
  • Infection–give antibiotics; fever and other signs may be absent. Treat oral candida if present.
  • Micronutrients–give vitamin A and other vitamins
  • Initiate feeding–small volumes, frequently, including through the night.
316
Q

what are the causes of rickets?

A
  • northern latitudes
  • dark skin
  • decreased exposure to sunlight
  • poor diet
  • intestinal malabsorption
317
Q

what are the clinical features of rickets?

A
  • misery
  • failure to thrive
  • frontal bossing of skull
  • craniotabes
  • delayed closure of anterior fontanelle
  • delayed dentition
  • rickety rosary
  • harrison sulcus
  • expansion of metaphases
  • bowing of legs
  • hypotonia
  • seizures
318
Q

how is rickets diagnosed?

A
  • dietary history
  • low serum calcium
  • low phosphorus
  • plasma alkaline phosphatase
  • low 25-hydroxyvitamin D
  • elevated PTH
319
Q

how is rickets managed?

A
  • advice about a balanced diet
  • correction of predisposing risk factors
  • daily administration of vitamin D3 (cholecalciferol).
320
Q

what are the clinical features of vitamin A deficiency?

A
  • blindness
  • xerophthalmia
  • increased susceptibility to measles
321
Q

what are the causes of vomiting in infants?

A
  • GORD
  • Feeding problems
  • infection
  • dietary protein intolerance
  • intestinal obstruction
  • inborn errors of metabolism
  • congenital adrenal hyperplasia
  • renal failure
322
Q

what are the causes of vomiting in pre-school children?

A
  • gastroenteritis
  • infection
  • appendicitis
  • intestinal obstruction
  • raised ICP
  • coeliac
  • renal failure
  • inborn errors of metabolism
  • testicular torsion
323
Q

what are the causes of vomiting in school aged and adolescents?

A
  • gastroenteritis
  • infection
  • peptic ulceration and H.pylori
  • appendicitis
  • migraine
  • raised ICP
  • coeliac
  • renal failure
  • DKA
  • alcohol and drug use
  • cyclical vomiting syndrome
  • Eating disorder
  • pregnancy
  • testicular torsion
324
Q

what are the clinical features of gingivitis?

A
  • Reddening and swelling of the gum margins

- Bleeding of gums with toothbrushing, flossing, gentle probing or eating hard foods such as an apple

325
Q

what are the clinical features of periodontitis?

A
  • Halitosis
  • Foul taste in the mouth
  • Drifting/loosening of teeth causing difficulty in eating
  • Periodontal abscess which may cause pain
  • Bleeding, pus and debris expressible from gingival pockets
  • Loosening or drifting of teeth
  • Periodontal abscess
326
Q

what are the clinical features of acute necrotising ulcerative gingivitis?

A
  • Intensely painful gums, particularly when brushing teeth
  • Bleeding gums with no or minimal trauma
  • Severe halitosis
  • Anorexia
  • Malaise or fever
  • Punched out gingival ulcers covered with a white, yellowish or grey pseudomembrane
  • Cervical lymphadenopathy
327
Q

how is gingivitis and periodontitis managed?

A
  • Advise routine regular review by a dentist
  • Give advice on oral hygiene
  • Smoking cessation
328
Q

how is acute necrotizing ulcerative gingivitis managed?

A
  • Urgently see a dentist
  • Give metronidazole 400mg three times daily for 3 days in adults, or 200-250mg 3 times daily for 12-18 year olds
  • Give amoxicillin 500mg three times daily for 3 days if metronidazole inappropriate
  • Paracetamol or ibuprofen for pain relief
  • Chlorhexidine or hydrogen peroxide
  • Regular review by a dentist
  • Give advice on oral hygiene
329
Q

what are the clinical features of IgE-mediated food allergy?

A
  • urticaria
  • facial swelling
  • anaphylaxis
  • usually occurring 10–15 min after ingestion of a food.
330
Q

what are the clinical features of non-IgE-mediated food allergy?

A
  • diarrhoea
  • vomiting
  • abdominal pain
  • failure to thrive
  • colic
  • eczema
331
Q

how is IgE mediated food allergy diagnosed?

A
  • skin prick tests

- RAST

332
Q

what are the clinical features of rotavirus?

A
  • vomiting
  • fever
  • diarrhoea
  • metabolic consequences of water and electrolyte loss.
333
Q

how is rotavirus diagnosed?

A
  • PCR for genome detection

- ELISA for antigen detection in faeces

334
Q

what are the clinical features of yellow fever?

A
  • 3-6 day incubation period
  • high fever
  • headache
  • Retrobulbar pain
  • myalgia
  • arthralgia
  • flushed face
  • suffused conjunctivae
  • epigastric pain
  • vomiting
  • relative bradycardia
  • jaundice
  • hepatomegaly
  • ecchymosis, bleeding from the gums, haematemesis and melaena
  • coma
335
Q

what is seen on liver histology in yellow fever?

A
  • mid-zone necrosis

- eosinophilic degeneration of hepatocytes (Councilman bodies)

336
Q

how is yellow fever diagnosed?

A

-serology

337
Q

what are the clinical features of scarlet fever?

A
  • regional lymphadenopathy
  • fever
  • rigors
  • headache
  • vomiting
  • blanching rash, which initially occurs on the neck but rapidly becomes punctate, erythematous and generalised
  • typically rash is absent from the face, palms and soles
  • circumoral pallor
  • strawberry tongue
  • raspberry tongue
338
Q

how is scarlet fever treated?

A

penicillin V

  • amoxicillin
  • clarithromycin
  • for 10 days.
339
Q

what is seen on blood tests in haemolytic jaundice?

A
  • raised urinary urobilinogen
  • raised bilirubin
  • normal serum ALP, AST, ALT and albumin
340
Q

what are the clinical features of Gilbert’s syndrome?

A
  • asymptomatic

- raised bilirubin

341
Q

how are Dubin-johnson and rotor syndromes inherited?

A

autosomal recessive

342
Q

how does the liver appear in dubin-johnson syndrome?

A

-black due to melanin deposition

343
Q

what are the clinical features of biliary atresia?

A
  • jaundice
  • pale stools and dark urine
  • hepatomegaly
344
Q

what is seen on investigation of suspected biliary atresia?

A
  • fasting abdominal USS shows contracted or absent gallbladder
  • Radioisotope scan with iminiodiacetic acid derivatives shows good uptake but no excretion into the bowel
345
Q

how is biliary atresia treated?

A
  • surgical bypass of the fibrotic ducts
  • hepatoportoenterostomy (Kasai procedure), in which a loop of jejunum is anastomosed to the cut surface of the porta hepatis, facilitating drainage of bile from any remaining patent ductules.
346
Q

how do choledochal cysts present?

A
  • abdominal pain
  • a palpable mass
  • jaundice
  • cholangitis.
347
Q

how are choledochal cysts diagnosed?

A

ultrasound or radionuclide scanning

348
Q

how are choledochal cysts managed?

A

surgical excision of the cyst with the formation of a Roux-en-Y anastomosis to the biliary duct

349
Q

what are the clinical features of galactosaemia?

A
  • poor feeding
  • vomiting
  • jaundice
  • hepatomegaly when fed milk.
  • Liver failure, cataracts and developmental delay are inevitable if galactosaemia is untreated.
  • A rapidly fatal course with shock, haemorrhage and disseminated intravascular coagulation, often due to Gram-negative sepsis, may occur.
350
Q

how is galactosaemia diagnosed?

A
  • prolonged (persistent) jaundice, by detecting galactose, a reducing substance, in the urine.
  • measuring the enzyme galactose-1-phosphate-uridyl transferase in red cells.
351
Q

how is galactosaemia treated?

A

galactose-free diet

352
Q

what are the features of vitamin E deficiency?

A
  • peripheral neuropathy
  • haemolysis
  • ataxia
353
Q

how can pruritus associated with liver disease in children be treated?

A
  • Loose cotton clothing, avoiding overheating
  • Emollients or evening primrose oil
  • Phenobarbital to stimulate bile flow
  • cholestyramine
  • ursodeoxycholic acid
354
Q

what are the indications for liver transplant in children?

A
  • Severe malnutrition unresponsive to intensive nutritional therapy
  • Recurrent complications (bleeding varices, resistant ascites)
  • Failure of growth and development
  • Poor quality of life.
355
Q

what liver disease is seen in cystic fibrosis?

A
  • hepatic steatosis is the most common

- cirrhosis and portal hypertension develop in some

356
Q

what are the clinical features of portal hypertension?

A
  • Haematemesis or melaena from rupture of gastro-oesophageal varices or portal hypertensive gastropathy
  • Ascites
  • Breathlessness due to pulmonary hypertension or hepatopulmonary syndrome
  • splenomegaly
  • haemorrhoids
  • caput medusae
357
Q

what are the causes of haemorrhoids?

A
  • Constipation with prolonged straining is a key factor
  • Diarrhoea
  • Effects of gravity due to posture
  • Congestion from a pelvic tumour, pregnancy, portal hypertension
  • Anal intercourse
358
Q

how are haemorrhoids classified?

A
  • 1st - Remain in rectum
  • 2nd - Prolapse through the anus on defecation but spontaneously reduce
  • 3rd - Prolapse but can be reduced manually
  • 4th - Remain persistently prolapsed
  • external haemorrhoids originate the dentate line
359
Q

how do haemorrhoids present?

A
  • Bright red rectal bleeding (since blood from capillaries) that often coats stools, seen on tissue or drips into toilet
  • Mucus discharge and pruritus ani (itchy bottom)
  • Severe anaemia may occur
  • Weight loss and change in bowel habit should prompt thoughts of pathology
360
Q

how are haemorrhoids diagnosed?

A

-Abdominal examination to rule out other disease

  • PR (per rectum) exam:
  • –Prolapsing piles are obvious
  • –Internal haemorrhoids are not palpable
  • Proctoscopy (rectal scope) to see internal haemorrhoids
  • Sigmoidoscopy to see rectal pathology higher up
361
Q

how are first degree haemorrhoids treated?

A
  • Increase fluid and fibre

- Topical analgesic and stool softener

362
Q

how are second and third degree haemorrhoids treated?

A
  • Rubber band ligation: Cheap, produces an ulcer to anchor the mucosa (side effects are bleeding, infection and pain)
  • Infra-red coagulation: Locally coagulates vessels and tethers mucosa to subcutaneous tissue
363
Q

how are fourth degree haemorrhoids treated?

A
  • Excisional haemorrhoidectomy - excision of piles

- Stapled haemorrhoidopexy

364
Q

how are prolapsed or thromboses piles treated?

A
  • analgesia
  • ice packs
  • stool softeners
365
Q

what is an anal fistula?

A

• An abnormal connection between the epithelised surface of the anal canal and skin

366
Q

what are the causes of an anal fistula?

A
  • Perianal sepsis
  • Abscesses
  • Crohn’s
  • TB
  • Diverticular disease
  • Rectal carcinoma
367
Q

what are the clinical features of anal fistulas?

A
  • Pain
  • Discharge (bloody or mucus)
  • Pruritus ani (itchy bottom)
  • Systemic abscess if it becomes infected
368
Q

how are anal fistulas diagnosed?

A
  • MRI: To exclude sepsis and to detect associated conditions e.g. Crohn’s or TB
  • Endoanal ultrasound: To determine tracks location and underlying causes
369
Q

how are anal fistulas treated?

A
  • Surgical
  • Fistulotomy and excision
  • Drain abscess with antibiotics if infected
370
Q

what are the causes of anal fissures?

A
  • Hard faeces
  • Spasm may constrict the inferior rectal artery resulting in ischaemia which makes healing difficult and perpetuates the problem
  • Syphilis
  • Herpes
  • Trauma
  • Crohn’s
  • Anal cancer
371
Q

how do anal fissures present?

A
  • Extreme pain especially on defecation
  • Bleeding
  • Anal spasm and a tearing sensation on passing stool
372
Q

how are anal fissures treated?

A
  • Increase dietary fibre and fluids to make stools softer
  • Advise that sitting in a shallow warm bath several times a day may help relieve pain
  • lidocaine ointment for extreme pain on defecation
  • GTN ointment for those with symptoms for 1 week without improvement
  • If anal fissure is unhealed after 6-8 weeks, prescribe topical diltiazem ointment
  • Surgery if medication fails
373
Q

what are the clinical features of perianal abscess?

A
  • Painful swellings
  • Tender
  • Discharge
374
Q

how are peri-anal abscesses diagnosed?

A
  • MRI

- Endoanal ultrasound

375
Q

how are perianal abscesses treated?

A
  • drainage

- antibiotics

376
Q

what are the risk factors for developing pilonodal sinus?

A
  • Obese caucasians and those from Asia, Middle East and Mediterranean are at increased risk
  • Large amount of body hair
  • Sedentary job
  • Occupation involving sitting or driving
  • Family history
377
Q

how do pilonodal sinuses present?

A
  • Painful swelling over days
  • Pus filled with foul smell from abscess
  • Systemic signs of infection
378
Q

how are acute pilonodal sinuses treated?

A
  • Arrange for urgent same day incision and drainage
  • Offer paracetamol for pain
  • Following I and D, advise meticulous hygiene and buttock hair removal
379
Q

what are the adverse effects of alginates and antacids?

A
  • Magnesium salts cause diarrhoea

- Aluminium salts cause constipation.

380
Q

with which drugs do alginates and antacids interact with?

A
  • Reduce serum concentration of –ACE inhibitors
  • -antibiotics
  • -bisphosphonate
  • -digoxin
  • -levothyroxine
  • -proton pump inhibitors.
381
Q

what are the adverse effects of PPIs?

A
  • GI disturbances
  • Headache
  • Hypomagnesaemia leading to tetany and ventricular arrhythmias
382
Q

in which patients should PPIs be used with caution?

A
  • Caution in patients presenting with ‘red-flag features’ of gastric cancer as PPIs can disguise symptom
  • Caution in patients at risk of osteoporosis due to increased risk of fractures
383
Q

with which drugs do PPIs interact?

A
  • Increases anticoagulant effect of warfarin

- Decreases anti-platelet effect of clopidogrel.

384
Q

what are the adverse effects prostaglandin analogues such as misoprostol?

A
  • Nausea and vomiting
  • Diarrhoea
  • Abdominal cramps
  • Uterine constrictions.
385
Q

what are the adverse effects of bismuth chelate?

A
  • Black tongue and faeces

- Nausea and vomiting.

386
Q

in which patients should bismuth chelate be avoided?

A
  • Avoid in children due to risk of Reye’s syndrome

- Caution in clotting disorders and gout.

387
Q

what are the indications for macrolide antibiotics?

A
  • Eradication of H.pylori in peptic ulcer disease
  • Respiratory and skin infections when penicillin is contraindicated by allergy
  • Severe pneumonia added to penicillin to cover Legionella pneumophilia and Mycoplasma pneumoniae.
388
Q

what are the adverse effects of macrolide antibiotics?

A
  • Nausea and vomiting and less frequently antibiotic-associated colitis
  • cholestatic jaundice
  • prolongation of QT syndrome
  • ototoxicity.
389
Q

with which drugs do macrolide antibiotics interact?

A
  • Increased risk of bleeding with warfarin
  • increased risk of myopathy with statins
  • increased risk of prolonging QT interval with amiodarone, antipsychotics, SSRIs.
390
Q

what are the indications for broad spectrum penicillins?

A
  • Eradication of H.pylori in peptic ulcer disease
  • Pneumonia caused by gram positive (S.pneumonia) or gram negative (H.influenza)
  • urinary tract infections (mostly E.coli)
  • combination treatment for hospital acquired infection or sepsis
  • combination treatment for peptic ulcers (H.pylori).
391
Q

what are the adverse effects of broad spectrum penicillins?

A
  • Nausea and diarrhoea and less frequently antibiotic-associated colitis
  • penicillin allergy presenting as a IgG-mediated skin rash or less commonly IgE mediated anaphylactic reaction
  • cholestatic jaundice with co-amoxiclav.
392
Q

with which drugs do broad spectrum penicillins interact?

A
  • Reduced renal excretion of methotrexate, increasing risk of toxicity
  • Enhance anticoagulant effect of warfarin by killing gut flora that synthesise vitamin K.
393
Q

what are the indications for D2 antagonist anti-emetics?

A
  • Prophylaxis and treatment of nausea and vomiting due to reduced gut motility
  • GORD in patients who do not respond to proton pump inhibitors and H2-receptor antagonists.
394
Q

what are the adverse effects of D2 antagonist anti-emetics?

A
  • Diarrhoea
  • Acute dystonias (metoclopramide)
  • QT prolongation (domperidone).
395
Q

in which patients should D2 antagonist anti-emetics be avoided?

A
  • Avoid with GI obstruction, perforation, haemorrhage or recent surgery
  • Avoid domperidone with long QT syndrome
  • Caution with metoclopramide in patients under 20 and epilepsy.
396
Q

with which drugs do D2 antagonist anti-emetics interact?

A
  • Dopaminergic agents
  • Antipsychotics
  • Drugs that prolong the QT interval (e.g. clarithromycin, fluconazole, diltiazem).
397
Q

what are the adverse effects of H1 antagonist antiemetics?

A
  • Drowsiness due to H1 antagonism

- Dry mouth, blurred vision, urinary retention and constipation due to antimuscarinic effects.

398
Q

in which patients should H1 antagonist antiemetics be avoided?

A
  • patients with prostatic hypertrophy and hepatic encephalopathy
  • in neonates.
399
Q

what are the indications for antimuscarinics such as hyoscine?

A
  • Irritable Bowel Syndrome
  • Bradycardia
  • Reducing respiratory secretions.
400
Q

what are the adverse effects of anti-muscarinics?

A
  • dry mouth
  • tachycardia
  • urinary retention
  • blurred vision
  • drowsiness
  • confusion.
401
Q

in which patients should anti-muscarinics be avoided?

A
  • Caution in angle-closure glaucoma

- Caution with arrhythmias.

402
Q

what are the adverse effects of aminosalicylates?

A
  • GI disturbances
  • Headache
  • Leucopenia and thrombocytopenia
  • Renal impairment
  • Oligospermia
  • Hypersensitivity reactions.
403
Q

with which drugs do aminosalicylates interact?

A
  • Reduced efficacy with drugs that alter gut pH (PPIs in stomach, lactulose in gut)
  • Increased risk of leucopenia with azathioprine, mercaptopurine.
404
Q

what is a direct inguinal hernia?

A

pierces the posterior abdominal wall and the abdominal contents are forced through a defect in the inguinal canal.

405
Q

what is an indirect inguinal hernia?

A

does not pierce the posterior abdominal wall and the abdominal contents pass through the deep inguinal ring.

406
Q

what are the risk factors for developing inguinal hernias?

A
  • Male sex.
  • Old age.
  • Smoking.
  • Family history.
  • Abdominal aortic aneurysm.
  • Marfan’s syndrome or Ehlers-Danlos syndrome.
407
Q

what are the clinical features of inguinal hernias?

A
  • Groin discomfort or pain with bulge.
  • Groin mass.
  • Abdominal discomfort and pain is uncommon.
  • Acute abdomen and an irreducible abdomen suggests strangulation.
408
Q

how is an inguinal hernia managed?

A
  • Refer for urgent surgical repair if the hernia is irreducible which suggests a strangulated hernia.
  • Refer urgently to a paediatric surgeon (preferably to be seen within 2 weeks) if an infant or young boy presents with a hernia.
  • Refer all others for routine surgical repair unless:
  • –They have minimally symptomatic hernias.
  • –They have significant comorbidity.
  • –They do not wish to have surgery.

-Cefazolin prophylaxis for repair

409
Q

what are the clinical features of angiodysplasia?

A
  • Chronic, painless, low-grade, intermittent bleeding

- Symptoms of anaemia

410
Q

what is seen on OGD and colonoscopy in angiodysplasia?

A
  • Abnormal epithelium
  • small lesions with irregular edges
  • a draining vein
411
Q

how are haemodynamically unstable patients with angiodysplasia managed?

A
  • Upper GI endoscopy employing electrocautery, photocoagulation, clips and adrenaline to treat a lesion
  • If upper GI endoscopy is negative, mesenteric angiogram with or without embolisation, and supportive care
  • If angiography unavailable, perform colonoscopy employing electrocautery, photocoagulation, clips and adrenaline, or subtotal hemicolectomy if large bleed
412
Q

how are haemodynamically stable patients with angiodysplasia managed?

A
  • Perform interventional endoscopy, angiography with embolisation or wireless capsule enteroscopy as needed
  • Surgery may be required if the above techniques are unavailable
  • If the patient is not a surgical candidate, consider octreotide, conjugated oestrogens or thalidomide.

FINALS (18 decks)

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