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Gastroenterology > Gastro Conditions > Flashcards

Gastro Conditions Flashcards

1
Q

List some clinical features of GORD

A
  • Burning chest pain after eating
  • Unpleasant taste in the mouth
  • Pain on swallowing
  • Cough, especially at night
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2
Q

What is Barrett’s oesophagus?

A

Metaplasia of squamous oesophageal epithelium into abnormal columnar epithelium caused by chronic gastric acid reflux and associated inflammation. Increased risk of oesophageal cancers with Barrett’s oesophagus.

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3
Q

Where does colorectal cancer commonly metastasise to?

A

Liver
Lungs
Peritoneal cavity
Bone

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4
Q

Is there a screening programme for bowel cancer?

A

Yes

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5
Q

What is the screening programme for bowel cancer?

A

FOB test (faecal occult blood) - Aims to detect microscopic amounts of blood in the faeces which may have originated from a bleeding polyps or adenocarcinoma

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6
Q

List some risk factors for developing colorectal cancer

A

Family history
Diet - low fibre, low vegetable, high red meat
Smoking
Alcohol
Other bowel disorders e.g. ulcerative colitis
Age > 65
Inactivity

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7
Q

Which part of the GI tract does ulcerative colitis involve? Which part of the GI tract does Crohn’s disease involve?

A

Ulcerative colitis = Colon and rectum only (maybe with extra-colonic features e.g. liver involvement)
Crohn’s = Entire GI tract, from mouth to rectum

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8
Q

Is unconjugated bilirubin soluble or insoluble?

A

INsoluble - it is a large molecule, bound to albumin

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9
Q

Which enzyme conjugates bilirubin?

A

Glucuronyl transferase

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10
Q

Which drugs may induce post-hepatic (cholestatic) jaundice?

A 
Antibiotics: Flucloxacillin, co-amoxiclav, fusidic acid, nitrofurantoin
Steroids: Anabolic, COCP
Sulfonylureas
Prochlorperazine
Chlorpromazine
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11
Q

Which drugs may induce hepatic jaundice?

A 
Paracetamol in overdose
TB drugs: isoniazid, rifampicin, pyrazinamide
MAO Inhibitors
Sodium valproate
Halothane
Statins
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12
Q

What type of jaundice is associated with pale stools and dark urine?

A

Cholestatic jaundice

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13
Q

List some clinical features of gut malabsorption

A 
Weight loss (without loss of appetite)
Diarrhoea
Steatorrhoea (fatty stool)
Bloating
Lethargy
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14
Q

What type of hernia is felt inferiorly and laterally to the pubic tubercle?

A

Femoral

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15
Q

What type of hernia is felt superiorly and medially to the pubic tubercle?

A

Inguinal

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16
Q

Give a definition of liver cirrhosis

A

Chronic liver disease characterised by fibrosis, formation or nodules, and loss of liver structure and function

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17
Q

Why might a patient with liver cirrhosis develop hepatic encephalopathy?

A

Portal hypertension may give rise to portal-systemic shunts where blood bypasses the filtration system in the liver and toxic products which are normally filtered e.g. ammonia, travel to the brain and cause encephalopathy

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18
Q

Which grading system assesses the severity of liver cirrhosis and predicts the risk of variceal bleeding?

A

Child-Pugh grading

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19
Q

What parameters are measured in the Child-Pugh score?

A 
Bilirubin
Albumin
Prothrombin time (in seconds > normal)
Presence of ascites
Presence of encephalopathy
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20
Q

What might you detect in the serum of a patient with acute Hep B infection?

A 
HBsAg +ve
HBeAg +ve
HBcAg +ve
HBcAb +ve
DNA ++
ALT raised
Antibody Type = IgM
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21
Q

What might you detect in the serum of a patient who has had previous exposure to Hep B virus?

A 
HBsAg -ve
HBsAg +ve
HBcAg -ve
HbeAg -ve
ALT normal
Antibody Type = IgG
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22
Q

What is autoimmune hepatitis?

A

Autoantibodies against the hepatocyte surface antigen, associated with suppressor T cell defects

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23
Q

What type of autoantibodies are seen in Type I autoimmune hepatitis?

A 
Anti-smooth muscle antibody (ASMA) in 80%
Antinuclear antibodies (ANA) in 10%
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24
Q

What type of autoantibodies are seen in Type II autoimmune hepatitis?

A

Anti-liver/kidney microsomal (ALKM) type 1 antibodies

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25
Q

What type of autoantibodies are seen in Type III autoimmune hepatitis?

A

Anti-soluble liver antibody (SMA)

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26
Q

What type of autoimmune hepatitis is more commonly seen in children?

A

Type II

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27
Q

How would you define acute liver failure?

A

New, rapidly developing illness in a patient with no prior liver disease. Characterise by presence of coagulation disturbance (INR >1.5) and encephalopathy

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28
Q

What are the ALARM Symptoms in a patient presenting with dyspepsia?

A 
Anaemia (iron deficiency)
Loss of weight
Anorexia
Recent onset / progressive symptoms
Melaena / haematemesis
Swallowing difficulty
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29
Q

What would be the initial management of a 60 year old patient who presents with dyspepsia?

A

Referral for upper GI endoscopy

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30
Q

What would be the initial management of a 42 year old patient who presents with dyspepsia associated with difficulty swallowing?

A

Referral for upper GI endoscopy

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31
Q

What would be the initial management of a 42 year old patient who presents with dyspepsia and no other symptoms?

A
  • Stop drugs which might cause dyspepsia e.g. NSAIDs
  • Offer lifestyle advice
  • Recommend over-the-counter antacids
  • Review in 4 weeks
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32
Q

You are reviewing a 40 year old patient with dyspepsia. She came to see you 4 weeks ago and her symptoms have not improved. She has no other associated symptoms. What is the next step in her management?

A

H. pylori test

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33
Q

What is the treatment for eradication of H. pylori?

A

Omeprazole 20mg bd
Amoxicillin 1g bd
Clarithromycin 500mg bd

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34
Q

What is the treatment for a 40 year old patient with dyspepsia who has a negative test for H. pylori?

A

PPI e.g. omeprazole 20mg daily
or
H2 antagonist e.g. ranitidine 150mg bd
Treat for 4 weeks then review

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35
Q

List some risk factors for developing a duodenal ulcer

A 
H. pylori
Drugs (NSAIDs, steroids, SSRIs)
Increased gastric acid secretion
Increased gastric emptying
Blood group O
Smoking
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36
Q

How are haemorrhoids classified?

A

1st degree - remain in the rectum
2nd degree - protrude through the anus on defecation but spontaneously reduce
3rd degree - protrude through the anus on defecation and need digital reduction
4th degree - remain persistently prolapsed

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37
Q

What clinical features are associated with a presentation of haemorrhoids?

A 
Bright red blood - coating the stool, on wiping, or dripping into the pan
Usually not painful
Anaemia
Mucous discharge
Pruritis ani
38
Q

What 3 things is bile normally made up of?

A

Phospholipids
Bile pigments
Cholesterol

39
Q

Which type of gallstones are small, friable and irregular?

A

Pigment stones

40
Q

What causes pigment stones?

A

Haemolysis

41
Q

Where might pain from acute cholecystitis radiate to?

A

Shoulder

42
Q

What is Murphy’s sign?

A

Test for acute cholecystitis - Lay 2 fingers over RUQ and as patient to breath in. if they develop pain and stop breathing in, it’s a sign that there is an inflamed gallbladder moving beneath your fingers. Must compare with the LUQ To ensure the pain is not replicated here.

43
Q

How would you treat acute cholecystitis?

A
  • Nill by mouth
  • Pain relief
  • IV infusion
  • Antibiotics e.g. cefuroxime 1.5g/8hrs IV
  • Laparoscopic cholecystectomy
44
Q

What is primary biliary cirrhosis?

A

Autoimmune process causing damage to the bile ducts by a chronic granulomatous inflammation. Can lead to cirrhosis, fibrosis and portal hypertension.

45
Q

Which antibodies are associated with primary biliary cirrhosis?

A

Anti-mitochondrial antibodies (AMA)

46
Q

List some risk factors for development of primary biliary cirrhosis

A 
Family history
Recurrent UTIs
Past pregnancy
Use of nail polish / hair dye (as non-specific environmental pollutants may cause the disease)
Smoking
47
Q

What might liver enzymes show in a patient with primary biliary cirrhosis?

A

Raised ALP - often the patient is asymptomatic until this is discovered on routine LFT check
Raised GGT
Mildly raised AST and ALT

48
Q

What is the treatment for primary biliary cirrhosis?

A

Symptomatic: Cholestyramine for itching, codeine phosphate for diarrhoea
Prevent complications: Osteoporosis prevention
Specifics: Fat-soluble vitamins A, D, K…ursodeoxycholic acid
Liver transplantation

49
Q

What is primary sclerosing cholangitis?

A

Inflammation of the bile duct associated with stricture formation.

50
Q

Which antibodies are associated with primary sclerosing cholangitis?

A

p-ANCA

51
Q

There is an increased risk of which cancers in primary sclerosing cholangitis?

A

Bile duct, gallbladder, liver, colon

52
Q

What is Wilson’s disease?

A

Inherited (autosomal recessive) disorder of biliary copper excretion - causes high levels of copper in the liver and CNS

53
Q

What element accumulates in Wilson’s disease?

A

Copper

54
Q

What is the physiology of the accumulation of copper in Wilson’d disease?

A

Normally, copper is absorbed in the small intestine and incorporated into caeruloplasmin, a copper-carrying protein, in the liver. In Wilson’s disease the absorption process is normal but the incorporation into the carrier protein and subsequent excretion is abnormal.

55
Q

How might you treat Wilson’s disease?

A
  • Low copper diet i.e. avoid chocolate, liver, nuts, mushrooms, shellfish
  • Penicillamine (high dose for 1 year then maintenance) - s/e include nausea, rash, pancytopenia, haematuria, nephrosis, lupus
  • Liver transplantation
56
Q

What is erythema ab igne?

A

Mottled, dusky greyness affecting the abdomen - can be seen in chronic pancreatitis

57
Q

What is the main cause of chronic pancreatitis?

A

Alcohol

58
Q

A patient with cystic fibrosis is suffering from abdominal pain which bores through to the back. What is the likely diagnosis?

A

Chronic pancreatitis - can affect cystic fibrosis patients due to blockage of the ducts (they also get bronchiectasis and blocking of the vas deferens)

59
Q

True / False - Acute pancreatitis involves irreversible damage to the pancreas

A

False - the pancreas regains normal structure and function after resolution of an episode of acute pancreatitis. This is not the case in chronic pancreatitis, where persistent inflammation causes irreversible structural damage to the organ.

60
Q

How might a patient with acute pancreatitis present?

A

Sudden onset epigastric or abdominal pain, boring straight through to the back. Associated with nausea and vomiting.

61
Q

What is Cullen’s sign?

A

Periumbilical bruising (seen in acute pancreatitis)

62
Q

What is Grey Turner’s sign?

A

Bruising in the flank (seen in acute pancreatitis)

63
Q

Which blood markers are raised in acute pancreatitis?

A

Amylase

Lipase

64
Q

Which drugs can cause acute pancreatitis?

A

Steroids
5-ASAs e.g. sulfasalazine
DDI and other old HIV medication e.g. AZT
Azathioprine

65
Q

What are the causes of acute pancreatitis?

A

GET SMASHED

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia, hypothermia, hypercalcaemia
ERCP, Emboli
Drugs - sulfasalazine, azathioprine, DDI (and other older HIV medication e.g. AZT), steroids
…also pregnancy and neoplasms…or it may be idiopathic

66
Q

How would you treat acute pancreatitis?

A
  • Assess severity using Glasgow criteria
  • Nil by mouth, may need NG tube
  • IV infusion, 0.9% saline to replace that being lost from intravascular space - be guided by observations
  • Analgesia: Pethidine 75-100mg/4hrs IM or morphine
  • Hourly monitoring of: HR, BP, U/O
  • Daily monitoring of: FBC, U&E, CRP, ABG
  • If worsening, consider ITU admission, O2 if PaO2 declines, antibiotics in specific severe cases e.g. imipenem
  • ERCP and removal of gallstones
  • Repeat imaging to monitor severity
67
Q

Using the Glasgow criteria, how many positive findings would prompt a transfer of a patient with acute pancreatitis to ITU?

A

3 or more positive findings 48 hours after onset

68
Q

What are the 3 types of diarrhoea?

A

Osmotic
Secretory
Mucosal injury

69
Q

What is osmotic diarrhoea?

A

Undigested food in the colon acts as an osmotic agent and draws water into the intestine

70
Q

Which cell is characteristic of Whipple’s disease?

A

PAS-positive macrophages

71
Q

What is the commonest bacterial cause of food poisoning in the Western world?

A

Campylobacter spp.

72
Q

What type of food is commonly infected with bacillus cereus?

A

Rice

73
Q

What type of food is commonly infected with S. aureus?

A

Milk products

74
Q

What is haemochromatosis?

A

An inherited disorder affecting iron metabolism, where there is increase absorption of iron in the intesting. This causes iron to be deposited in several areas in the body e.g. joints, liver, skin, heart, pancreas, pituitary, adrenals

75
Q

List some clinical features of haemochromatosis

A

Tiredness
Arthralgia - especially effecting 2nd and 3rd MCP joints, knee pseudo gout
Slate-grey skin pigmentation
Erectile dysfunction
Signs of chronic liver failure: hepatomegaly, cirrhosis
Cardiomyopathy
Endocrine disorders: Diabetes mellitus, hyporeninaemic hypoaldosteronism

76
Q

What is the treatment for haemochromatosis?

A

Venesection - regularly at first then maintenance
Low-iron diet
Monitor LFTs and glucose
Screening for 1st degree relatives

77
Q

What is the inheritance pattern for haemochromatosis?

A

Autosomal recessive

78
Q

What is the treatment for mild ulcerative colitis?

A

Induction and maintenance of remission: 5-ASAs e.g. sulfasalazine, mesalazine
Use steroids alongside to aid induction of remission e.g. prednisolone 20mg daily (reduce after 2 weeks if improvement)

79
Q

What is the treatment for moderate ulcerative colitis?

A

Prednisolone 40mg daily for 1 week, then 30mg daily for 1 week, then 20mg daily for 4 weeks, then wean off if improving

80
Q

What is the treatment for severe ulcerative colitis?

A

Admit for re-hydration and keep nil by mouth
IV hydrocortisone
Monitor for 48 for improvement - bowel motions should improve
Discuss surgery if no improvement e.g. subtotal colectomy
‘Rescue’ therapies e.g. cyclosporin, infliximab

81
Q

In which would you see ‘skip lesions’…ulcerative colitis or Crohn’s?

A

Crohn’s

82
Q

True / False: Smoking is protective against Crohn’s disease?

A

False

Smoking appears to have a protective effect in ulcerative colitis. It is a risk factor for Crohn’s disease.

83
Q

What are pale stools and dark urine a sign of?

A

Cholestatic jaundice

84
Q

What is Budd Chiari syndrome?

A

Hepatic vein obstruction caused by thrombus or tumour. This results in ischaemia and hepatocyte damage.

85
Q

What is Budd Chiari caused by?

A

Hyper-coagulable states (e.g. COCP, pregnancy, malignancy)
TB
Liver, renal, adrenal tumour

86
Q

What criteria is used to decide if a patient warrants a liver transplant?

A

King’s College Hospital criteria for liver transplantation

87
Q

What is the King’s College Hospital criteria for a liver transplant in a patient with paracetamol-induced liver failure?

A
  • Arterial pH 100s
  • Creatinine >300umol/L
  • Grade III or IV encephalopathy
88
Q

What is the King’s College Hospital criteria for a liver transplant in a patient with NON paracetamol liver failure?

A 
- Prothrombin time >100s
OR 3 out of 5 of the following:
- Drug induced liver failure
- Prothrombin time >50s
- Age 40 years old
- >1 week from 1st jaundice to encephalopathy
- Bilirubin >300umol/L
89
Q

What are the clinical features of irritable bowel syndrome?

A
  • Abdominal pain / discomfort relieved by defecating, or associated with change in stool form or bowel frequency
  • At least two of: urgency, incomplete evacuation, bloating / abdominal distension, mucous, worsening of pain after eating
  • Symptoms last > 6 months and are increased by stress, menstruation, gastroenteritis
90
Q

What is dysphagia?

A

Difficulty swallowing

91
Q

How is achalasia treated?

A

Nitrates or calcium channel blockers to relax the oesophageal sphincter
Botulinum toxin works for about 6 months
Endoscopic balloon dilatation
Surgical myotomy

Gastroenterology (3 decks)

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