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Medicine block > Gastroenterology medicine block > Flashcards

Gastroenterology medicine block Flashcards

1
Q

How does someone present w IBD? Compare Crohn’s to UC

A

Px - change in bowel habits
Crohn’s - mouth to anus, skip lesions, full thickness, ulcers + fistulas, increased in smokers, non caseating granuloma
UC - rectum proximally, continuous, mucosal only, crypt abscess, decreased in smokers

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2
Q

What are the ix into IBD?

A
  • Bloods = FBC (ACD), CRP, U&E (derranged due to GI loss)
  • AXR if toxic megacolon
  • Stool culture or faecal calprotectin
  • CT, MRI rectum
  • Flexible sigmoidoscopy, colonscopy, capsule endoscopy
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3
Q

What is the treatment of acute IBD?

A
  • Any acute IBD presentation is at high risk of a VTE so need prophylactic heparin
  • Normally IV hydrocortisone if in hospital
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4
Q

What is IBD rescue therapy and when is it needed?

A

When a pt doesn’t improve w 3-5 days of IV hydrocortisone probs need escalation.
Rescue therapy - biologicals or surgery for UC + Crohn’s w the addition of ciclosporin for UC.

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5
Q

What steroids are used in IBD and how do u maintain remission?

A

Steroids - oral prednisolone or budesonide, IV hydrocortisone, enemas or suppositories.
UC - mesalazine for remission or azathioprine/biologicals if doesn’t work.
Crohn’s - azathioprine or mercaptopurine

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6
Q

What is the presentation of Coeliac’s disease?

A
  • Loose stools, bloating
  • Abdo cramps, flatulence
  • Weight loss
  • Dermatitis herpetiformis
  • No sx and found incidentally when ix iron def anaemia or if FH
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7
Q

What is dermatitis herpetiformis?

A

Blistering skin rash in Coeliac’s

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8
Q

What happens if Coeliac’s is left untreated?

A
  • Increase risk small bowel cancer and lymphoma
  • Osteoporosis
  • Gluten ataxia and neuropathy
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9
Q

What are the ix into Coeliac’s?

A
  • tTG - raised in most pt but not a diagnostic test in adults
  • OGD and duodenal biopsy = diagnostic = villous atrophy and intra epithelial lymphocytosis
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10
Q

What is the treatment of Coeliac’s?

A

Life long gluten free diet

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11
Q

How do you treat dyspepsia without red flag symptoms?

A

PPI +/- test for H. pylori

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12
Q

How do you manage dyspepsia w red flag sx? What are the red flag sx?

A

OGD needs to be considered.

Red flag - weight loss, older age, associated dysphagia

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13
Q

What do you need to establish in a dysphagia hx?

A
  • Is it difficulty swallowing or painful (odynophagia)
  • Prob w oro pharyngeal phase - problem moving food out of mouth
  • Prob w oesophageal dysphagia - moves food out of mouth but then it gets stuck
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14
Q

What are the causes of oesophageal dysphagia?

A
  • Neuromusc disorder - presbyoesophagus, achalasia, dysmotility
  • Physical obstruction - tumour, benign strictures, oesophagitis
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15
Q

Oesophageal dysphagia:

  • Ix
  • Treatment
A
  • Ix - OGD, barium swallow

- Treat - surgery to remove cancer or dilation of stricture

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16
Q

What are the causes of oropharyngeal dysphagia?

A

Problem w muscles that move food bolus to the back of the mouth eg. stroke

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17
Q

Oropharyngeal dysphagia:

  • Ix
  • Treatment
A

Ix - CN exam, speech therapy assessment, video fluroscopy

Treatment - alt consistencies of food and fluid, if doesn’t work may need enteral feeding tube

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18
Q

What are the important qs to ask in a hepatology history?

A
  • Blood transfusion prior to 1990 in the UK
  • IVDU
  • What meds do they take?
  • Any recent travel?
  • Sexual exposure
  • FH liver disease, DM, IBD
  • Alcohol
  • Obesity
  • Surgery/vaccine w poor procedure
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19
Q

What are the causes of acute vs chronic liver disease?

A

Acute - Hep A, E, drug induced liver disease, CMV, EBV

Chronic - Hep C, NASH, alcohol, autoimmune

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20
Q

What might you find on an exam if someone had liver disease?

A

Stigmata of liver disease:

  • Spider nevi
  • Ascites
  • Palmar erythema
  • Clubbing
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21
Q

What are the grades of hepatic encephalopathy?

A

Grade 1 - reversed sleep pattern, psychomotor slowing, poor memory, apraxia
Grade 2 - agitation, lethargy, disorientation, liver flap
Grade 3 - drowsy
Grade 4 - coma

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22
Q

What are the blood tests for liver disease and what do they indicate?

A
  • ALT = damage to hepatocytes
  • ALP = damage to ducts
  • Bilirubin, albumin and PT = synthetic func tests, concerning if deranged in acute liver disease
  • AST:ALT 2:1 = alcoholic hepatitis
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23
Q

What are the causes of hepatitic liver disease >500 ALT?

A
  • Viral
  • Ischaemia
  • Toxic eg. paracetamol
  • Autoimmune
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24
Q

What are the causes of hepatitic liver disease 100-200 ALT?

A
  • NASH
  • Autoimmune hepatitis
  • Chronic viral hepatitis
  • Drug induced liver injury
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25
Q

What are the causes of cholestatic liver disease w dilated ducts?

A
  • Malignancy

- Gall stones

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26
Q

What are the causes of cholestatic liver disease w/o dilated ducts?

A
  • Alcoholic hepatitis
  • Cirrhosis
  • Drug induced liver injury
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27
Q

What is included in the liver screen?

A
  • Hep B+C serology
  • Fe
  • AutoAb
  • Caeuruloplasmin <30yo
  • Coeliac serology
  • TFT, lipids, glucose
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28
Q

What are the causes of chronic liver disease dependent on demographic?

A
  • Women > men = primary biliary cholangitis, autoimmune hepatitis
  • Men > women = haemachromatoma earlier, primary sclerosing cholangitis
  • Only in young adults = Wilson’s
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29
Q

How do you treat chronic liver disease?

A

Remove underlying cause eg. stop drinking, venesection, antivirals, lose weight to prevent further damage and progression to cirrhosis.

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30
Q

When should cirrhosis be suspected?

A
  • Thrombocytopenia
  • Varices seen on endoscopy
  • Stigmata of liver disease
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31
Q

What are the ix into cirrhosis?

A
  • Imaging but not very good
  • Fibro scan
  • If cirrhosis, DEXA as increased risk osteoporosis
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32
Q

What cancer does cirrhosis increase the risk of?

A

Hepatocellular carcinoma - screen all CLD/cirrhosis pt w a fetoprotein and USS every 6 months.

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33
Q

What is the treatment of ascites?

A
  • Spironolactone

- If tense - paracentesis

34
Q

What does every pt admitted to hospital w ascites need? What is being looked for?

A

Diagnostic tap - exclude spontaneous bacterial peritonitis

35
Q

What is involved in a nutritional assessment?

A
  • Hx - diet, appetite, changes in oral intake, changes in weight
  • Malnutrition universal screening tool (MUST) - BMI, % of weight loss, ill and >5 days no food
36
Q

What is involved in nutritional support?

A
  • Encourage high cal options and fortify food to help
  • Don’t interrupt meal times
  • Supplement - fortisips
  • Offer assistance w eating, correct teeth and cutlery
37
Q

Describe NG tube use and the risks

A
  • Is a short term solution, can provide all requirements or supplements on top of diet
  • Have to aspirate pH every time use to make sure tip in the stomach not the lungs, can be skewed by PPI use so need CXR to check
  • Stops pt aspirating food but can still aspirate saliva
  • Pt has to mobilise w a drip stand
38
Q

What are the tubes called that directly access the GI system? What are the risks of their use?

A

PEG and RIG - access stomach and PEGJ and RIGJ straight into small bowel.
Longer term use. Pt can still aspirate saliva though and have to puncture stomach.

39
Q

Describe parentral nutrition and the risks associated

A

Nutrition and fluid directly into a patients veins through PICC/Hickman line. Indicated when GI blocked or not working.
Risks - sepsis and liver dysfunction

40
Q

How do you assess GI bleeding?

A
  • Hx - need to establish what passing blood means = haemetemesis, malaena, fresh PR bleed, coffee ground vomit
  • Pt RF - use of NSAIDs, anticoag, anti platelet, CLD, varices, stigmata of CLD
  • ROCKALL score = chance of dying from GI bleed
  • Blatchford score = need for intervention and admission
41
Q

What are the ix into GI bleeding?

A
  • FBC - reduced Hb and platelets (need replacing, reduced in CLD)
  • U&E - increased urea = bleed
  • G&S in case need transfusion
  • Clot - need to correct if abnormal
  • Venous blood gas - quickest way to find out Hb
42
Q

What is the presentation of variceal bleeding? How is it managed?

A

Haemetemesis and malaena.

  • IV access, fluid resus if haemodynamically compromised and then blood
  • IV terlipressin and IV abx, need upper GI endoscopy
  • Oesophageal banding, TIPPS
43
Q

What are the causes of non variceal bleeding?

A

Peptic ulcer disease and angiodysplasia

44
Q

What is the treatment of non variceal bleeding?

A
  • IV access, fluid resus then blood
  • Need to be haemodynamically stable before endoscopy
  • Can stop bleeding in endoscopy, by embolisation or surgery
  • PPI after endoscopy to treat ulcer
45
Q

Give differentials for haemetemesis

A
  • Mallory Weiss tear
  • Oesophageal varices rupture
  • Peptic ulcer eroding blood vessel
  • Gastric malignancy
  • Oesophagitis
46
Q

Give differentials for melaena

A
  • Upper GI bleed - gastric ulcer
  • Variceal bleed
  • Upper GI malignancy if ulcerating
  • Gastritis/oesophagitis
  • Mallory Weiss tear, less common
47
Q

Give differentials for jaundice

A
  • CLD, ALD, hepatitis
  • Biliary colic, cholangitis, cholecystitis, pancreatitis.
  • HPB cancer
  • Haemolytic anaemia
  • Haemachromatosis
48
Q

Give differentials for diarrhoea

A
  • IBD, IBS, Coeliac’s disease
  • Gastroenteritis, viral or bacterial
  • Acute appendicitis
  • Colorectal cancer
  • Drugs
49
Q

Give differentials for N+V

A
  • Gastritis, peptic ulcer disease, acute gastroentertitis, GORD
  • Post op and chemo induced
  • Gastro paresis
  • DKA
  • IBD
50
Q

What are the clinical features of a paracetamol overdose?

A
  • Asymptomatic
  • N+V
  • Loin pain/RUQ pain
  • Haematuria, proteinuria
  • Jaundice
  • Coma and severe met acidosis
51
Q

What is the pathophysiology of a paracetamol overdose?

A

Metabolism of paracetemol = NAPQI, normally inactivated by glutathione but stores decrease in overdose so NAPQI builds up - causes liver and kidney damage.

52
Q

What is the management of a paracetamol overdose?

A
  • <1 hour = activated charcoal
  • Staggered overdose or >15 hours ago = N-acetylcysteine
  • <4 hours ago wait for 4 hours then start N-acetylcysteine based one level
53
Q

What patients are at increased risk of toxicity after a paracetamol overdose?

A
  • Pt on long term enzyme inducers
  • Reg alcohol excess
  • Pre existing liver disease
  • Glutathione depleted = eating disorder, malnutrition, HIV
54
Q

What are the common causes of viral hepatitis?

A
  • Hep B
  • Hep C
  • CMV
  • EBV
55
Q

What are the clinical features of viral hepatitis?

A
  • Malaise and fatigue
  • N+V
  • RUQ pain
  • Diarrhoea - pale stools and dark urine, jaundice
  • Hepatomegaly, splenomegaly, lymphadenopathy
56
Q

Hep B:

  • Transmission
  • Clinical features
  • Management
A

Transmission - intercourse, transfusion, vertical
Features - most children develop chronic disease, lower risk in adults
Management - only if HbsAg +ve, compensated liver disease or pregnant will have treatment

57
Q

What is the serology of Hep B?

A
  • HBsAg - acute/chronic infection
  • HBeAg - highly infectious
  • HBsAb - previous vaccination/infection
58
Q

Hep C:

  • Transmission
  • Features
A

Transmission - IVDU, blood transfusion, haemodialysis, sex, needlestick injuries
Features - most pt asymptomatic and will become chronic -> cirrhosis, high LFTs, hepatocellular carcinoma, liver fail

59
Q

What are the ix into Hep C?

A
  • Anti HCV serology - 90% +ve 3 months after infection

- HCV RNA - positive for more than 2 months = need treatment

60
Q

What is the management of Hep C?

A
  • Symptomatic early on
  • Antivirals benefit all pt irrespctive of amount of cirrhosis eg. sofobuvir = undetectable viral loads
  • Manage underlying cirrhosis
61
Q

What is hereditary haemochromatosis?

A

Disordered Fe met = too much Fe in body and deposited in liver, heart, joints, pit, pancreas, skin

62
Q

What are the clinical features of hereditary haemochromatosis?

A
  • Bronze skin
  • T2DM
  • Fatigue, joint pain
  • Liver cirrhosis
  • Adrenal insufficiency
63
Q

What are the Ix into hereditary haemochromatosis?

A
  • Bloods - derranged LFTs, raised serum ferritin and transferrin
  • Genetic testing
  • MRI brain and heart = Fe deposition
  • Liver biopsy = increased Fe
64
Q

What is the management of hereditary haemochromatosis?

A
  • Therapeutic venesection

- Desforrioxamine = iron chelating agent

65
Q

What is the pathophysiology of alcoholic liver disease?

A

Hepatic ethanol breakdown = increased triglyceride synthesis in the liver and chronic inflam = steatohepatitis which causes fibrosis and sclerosis = portal hypertension and cirrhosis.

66
Q

What are the clinical features/stages of ALD?

A
  • Alcoholic fatty liver = asymptomatic, hepatomegaly, regresses after alcohol stopped
  • Alcoholic hepatitis = reversible if mild, get nausea, loss of appetite, weight loss, low grade fever, hepatomegaly, jaundice, splenomegaly, ascites, variceal bleeding
  • Alcohol related cirrhosis = final stage ALD
67
Q

How do you diagnose ALD?

A
  • Lab tests = increased AST, ALT, ALP, GGT, bilirubin, PT time, reduced albumin, anaemia
  • Imaging = alcoholic fatty liver/cirrhosis, hepatomegaly
  • Confirm cirrhosis on biopsy
68
Q

How do you treat ALD?

A
  • Immediate cessation of alcohol

- Glucocorticoids eg. prednisolone in severe disease

69
Q

What is acute liver failure?

A

Rapid decrease in hepatic func:

  • Jaundice
  • Coagulopathy
  • Hepatic encephalopathy
70
Q

What are the signs of hepatic encephalopathy?

A

Nervous system problems:

  • Confusion
  • Memory loss
  • Change in personality+behaviour
  • Inappropriate action
  • Irritable and uninterested
71
Q

What are the symptoms of acute liver failure?

A
  • Pain in RUQ
  • Ascites
  • N+V, malaise
  • Disorientation+drowsy
  • Breath = musty/sweet smell
72
Q

What are the causes of acute liver failure?

A
  • Paracetamol overdose and other drugs eg. Abx, NSAIDs, anticonvulsants
  • Hepatitis, autoimmune diseae
  • Clot in hepatic venous system
  • Metabolic disease eg. Wilson’s
  • Malignancy
  • Sepsis
  • Heat stroke
73
Q

How do you manage acute liver failure?

A
  • Treat underlying cause
  • IV fluid resus
  • May need ICU and airway management
74
Q

What is NAFLD and NASH?

A

Non alcoholic fatty liver disease and non alcoholic steatohepatitis = fatty and inflammation.

75
Q

What are the RF of NAFLD?

A
  • Obesity and metabolic syndrome

- T2DM

76
Q

What is the treatment of NAFLD?

A

Weight loss = reduces fat, inflam and fibrosis. Healthy diet also helps.

77
Q

List some RF for GI bleed

A
  • Drugs = NSAIDs, anticoag, antiplatelet, SSRIs
  • Alcohol and smoking
  • Peptic ulcer disease, H.pylori infection
  • CLD and varices
  • Chronic vom
78
Q

Decompensated vs compensated liver disease

A

Compensated cirrhosis - no varices or ascites

Decompensated cirrhosis - varices and bleeding, ascites, encephalopathy

79
Q

What are the criteria for liver transplant in paracetamol overdose? What is it called?

A

King’s college criteria:
pH <7.3 24 hours after overdose
or all of the following three: prothrombin time >100 secs or INR >6.5, grade 3 or 4 hepatic encephalopathy, creatinine >300

80
Q

How do you treat hepatic encephalopathy and what causes it?

A

Caused by build up of ammonia secondary to liver cirrhosis.
1st line - lactulose, inhibits ammonia production
2nd line - rifaximin, liver transplant

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