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Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What is the step-wise progression on alcoholic liver disease?

A
  • Alcohol-related fatty liver-> temporary + reverses in 2 weeks if stop
  • Alcoholic hepatitis-> inflammation from binge drinking, mild usually reversible with permanent abstinence
  • Cirrhosis-> irreversible formation of scar tissue, stopping can prevent further damage
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2
Q

What is the weekly recommended limit of alcohol?

A

14 units a week spread over 3+ days and <5 units a day

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3
Q

What is the CAGE questionnaire and what are its components?

A

Assessment of harmful alcohol use

  • have you thought about Cutting down?
  • do you get Annoyed when people comment on your drinking?
  • do you feel Guilty about drinking?
  • ever had to have a drink in the morning to help with a hangover or nerves (Eye opener)?
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4
Q

What are the complications of harmful alcohol use?

A
  • Liver-> ALD, cirrhosis, hepatocellular cancer
  • Dependence and withdrawal
  • Wernicke-Korsakoff syndrome
  • Pancreatitis
  • Alcoholic cardiomyopathy
  • Increased risk of breast, mouth and throat cancers
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5
Q

What is the AUDIT tool?

A

Alcohol Use Disorders Identification Test-> 8/10 or more indicates harmful use

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6
Q

What are some clinical signs of liver disease?

A

Jaundice, hepatomegaly, spider naevi, palmar erythema, gynaecomastia, bruising easily, ascites, asterixis, caput medusae (engorged superficial epigastric veins)

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7
Q

Investigations for alcoholic liver disease?

A
  • Bloods-> FBC for macrocytic anaemia, deranged LFTs, high bilirubin in cirrhosis, high PTT, U+Es
  • US-> fatty change
  • Fibroscan-> elasticity + degree of cirrhosis
  • CT + MRI-> fatty liver, cancers, complicatins
  • Biopsy-> confirm diagnosis
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8
Q

Treatment for alcoholic liver disease?

A
  • Detox + abstinence
  • Thiamine
  • High protein diet
  • Steroids-> improve short term outcomes in severe
  • Liver transplant-> must abstain for 3+ months
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9
Q

How does alcohol withdrawal present?

A
  • 6-12 hours-> tremor, sweating, headache, cravings, anxiety
  • 12-24 hours-> hallucinations
  • 24-48 hours-> seizures
  • 24-72-> delirium tremens
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10
Q

How is alcohol withdrawal assessed?

A

Clinical Institute Withdrawal Assessment (CIWA-Ar)

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11
Q

How is alcohol withdrawal treated?

A
  • Chlordiazepoxide (benzo) oral reducing regime for 5-7 days
  • Pabrinex-> IV high dose vitami B
  • Thiamine-> low dose after pabrinex
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12
Q

What is delirium tremens?

A

Medical emergency associated with alcohol withdrawal

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13
Q

What is the pathophysiology of delirium tremens?

A
  • Alcohol stimulates GABA receptors + inhibits NMDA (glutamate) receptors-> inhibitory
  • Chronic use causes downregulation of GABA + upregulation of NMDA
  • Remove alcohol-> causes under + over function
  • Overall extreme excitability of the brain + excess adrenergic activity
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14
Q

What are the symptoms and signs of delirium tremens?

A
  • Confusion, agitiation, delusions, hallucinations

- Tremor, tachycardia, hypertension, hyperthermia, ataxia, arrhythmias

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15
Q

What is Wernicke-Korsakoff syndrome?

A

Disease due to alcohol excess-> thiamine (B1) deficiency due to poor diet + alcohol causing poor absorption

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16
Q

How does Wernicke-Korsakoff syndrome present?

A
  • Wernicke’s encephalopathy-> confusion + oculomotor disturbance + ataxia
  • Korsakoff’s syndrome-> irreversible memory impairment + behavioural change
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17
Q

How is Wernicke-Korsakoff syndrome treated?

A
  • Thiamine supplements

- Alcohol abstinence

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18
Q

What is the pathophysiology of liver cirrhosis?

A

Chronic inflammation-> damage-> replaced by scar tissue (fibrosis)-> nodules-> affect structure and blood flow-> increased resistance + portal hypertension

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19
Q

What are the causes of liver cirrhosis?

A

ALD, NAFLD, Hepatitis B or C, AI hepatitis, PBC, haemachromatosis, Wilson’s disease, CF, drugs (methotrexate, amiodarone, sodium valproate)

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20
Q

What are some investigations for liver cirrhosis?

A
  • Bloods-> LFTs, albumin (low), PTT (high), hyponatraemia, urea, creatinine
  • Alpha-fetoprotein-> hepatocellular marker checkec every 6 months in cirrhosis
  • Viral markers + auto-antibodies
  • Enhanced liver fibrosis (ELF) bloods-> for NAFLD + measured 3 markers (HA, PIIINP, TIMP-1)
  • US-> enlarged portal vein etc
  • Fibroscan-> every 2 years when high risk (for elasticity)
  • Endoscopy, CT, MRI, biopsy
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21
Q

What is the Child-Pugh scoring system?

A

Assessment of liver cirrhosis

  • 5 features-> bilirubin, albumin, INR, ascites, encephalopathy
  • Each scored out of 3-> 5 minimum + 15 maximum
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22
Q

What is the MELD scoring system?

A

Model for End-stage Liver Disease-> predicts mortality after liver transplant + other interventions

  • Looks at bilirubin, creatinine, INR, sodium and need for dialysis
  • Done every 6 months in cirrhosis
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23
Q

How is liver cirrhosis managed?

A
  • US + AFP + MELD score every 6 months
  • Endoscopy every 3 years
  • High protein low sodium diet
  • Transplant
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24
Q

What diet do people with liver cirrhosis need to follow and why?

A
  • Regular meals, low sodium, high protein, high calorie

- Due to increased use of muscle as fuel-> affects protein metabolism in liver + disrupts ability to store glucose

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25
Q

Why does portal hypertension and varices occur in liver cirrhosis?

A

Cirrhosis increases resistance of blood flow in the liver-> back pressure into portal venous system-> swollen + tortuous anasthamoses in systemic venous system (varices)

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26
Q

What does the portal system in the liver entail?

A

Superior mesenteric + splenic veins-> portal system-> blood to liver

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27
Q

Where do varices commonly occur in liver disease?

A

Gastro-oesophageal junction, ileocaecal junction, rectum, anterior abdominal wall (caput medusae)

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28
Q

How are stable varices in liver disease treated?

A
  • Propanolol
  • Elastic band ligation
  • Inject sclerosant
  • Transjugular intrahepatic portosystemic shunt (TIPS)-> stent from portal to hepatic vein to relieve pressure
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29
Q

How are bleeding varices treated in liver disease?

A
  • Terlipressin-> vasopressin analogue
  • Vitamin K + FFP for coagulopathies
  • Broad spectrum antibiotics
  • Urgent endoscopy + inject sclerosant
  • Ligation
  • Sengstaken-Blakemore tube
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30
Q

What is the pathophysiology behind ascites?

A
  • Increased pressure in portal venous system-> fluid leaks from capillaries in the liver + bowel-> into the peritoneal cavity
  • Circulatory volume drops-> reduced BP in kidneys-> RAAS activation-> sodium + fluid reabsorbed-> transudative (low protein) ascites
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31
Q

How is ascites managed?

A
  • Low sodium diet
  • Spironolactone (aldosterone antagonist)
  • Paracentesis
  • Prophylactic antibiotics for SPC (eg ciprafloxacin)
  • Transjugular intrahepatic portosystemic shunt (TIPS)
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32
Q

What is spontaenous bacterial peritonitis?

A

Infection in ascitic fluid + peritoneal lining

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33
Q

What organisms typically cause spontaneous bacterial peritonitis?

A

E.coli, Klebsiella pneumoniae, gram +ve cocci (eg staph)

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34
Q

What are the symptoms and signs of spontaneous bacterial peritonitis?

A

Asymptomatic, fever, abdominal pain + tenderness, deranged bloods, ileus, hypotension

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35
Q

What is the management for spontaneous bacterial peritonitis?

A
  • Ascitic culture

- IV cephalosporin-> eg cefotaxime

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36
Q

What is hepatorenal syndrome and what is its pathophysiology?

A

Hypertension in portal veins dilates blood vessels-> blood pools + causes loss of volume in kidneys-> RAAS activation-> renal vasoconstrction + low blood to kidney-> low function that can be fatal if not transplanted

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37
Q

What is hepatic encephalopathy and what is its pathophysiology?

A
  • Ammonia produced by intestinal bacterial when proteins broken down-> absorbed in gut
  • Ammonia builds up due to bypassing the liver (as metabolism impaired + collateral vessels formed_
  • Enters systemic circulation-> affects brain
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38
Q

How does hepatic encephalopathy present?

A

LOC, confusion, personality/memory/mood changes

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39
Q

What can precipitate hepatic encephalopathy?

A

Constipation, electrolyte disturbances, infection, high protein diet, medications (eg sedatives)

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40
Q

Management of hepatic encephalopathy?

A
  • Laxatives to promote excretion
  • Enemas
  • Antibiotics eg rifaximin-> reduce intestinal bacterial producing ammonia
  • Nutritional support
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41
Q

What is non-alcoholic fatty liver disease (NAFLD)?

A

Fat deposited in liver cells-> interfere with function-> can progress to hepatitis + cirrhosis

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42
Q

What are the 4 stages of non-alcoholic fatty liver disease (NAFLD)?

A
  • non-alcoholic fatty liver disease (NAFLD)
  • non-alcoholic steatohepatitis (NASH)
  • fibrosis
  • cirrhosis
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43
Q

What are the risk factors for non-alcoholic fatty liver disease (NAFLD)?

A

Same as diabetes + CVD

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44
Q

Investigations for non-alcoholic fatty liver disease (NAFLD)?

A

-When abnormal LFTs and no clear cause-> non-invasive liver screen
-Enhanced liver fibrosis (ELF) bloods-> 1st line
NAFLD fibrosis score-> age, BMI, liver enzymes, platelets, albumin, DM-> rule out fibrosis
-Fibroscan-> stiffness
-US liver-> can confirm
-Auto-antibodies for AI hep, PBC, PSC-> ANA, SMA, AMA, LMK-1
-Other-> hepatitis B/C serology, immunoglobulins (AI hep, PBC), ferritin + transferritin etc

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45
Q

Management for non-alcoholic fatty liver disease (NAFLD)?

A
  • Weight loss, control co-morbidities, avoid alcohol

- Liver specialist-> may give pioglitazone or vitamin E

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46
Q

What is hepatitis?

A

Inflammation of the liver-> acute, chronic, severe etc

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47
Q

What can cause hepatitis?

A

Alcohol, NAFLD, viral, AI, drug induced

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48
Q

How might hepatitis present (in general)?

A

Asymptomatic, abdominal pain, fatigue, pruritis, muscle + joint aches, N+V, jaundice, fever

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49
Q

What might blood tests look like in hepatitis?

A

Deranged LFTs-> high AST/ALT (inflammation) + proportionally small rise in ALP + high bilirubin

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50
Q

What is the most common type of hepatitis worldwide?

A

Hepatitis A

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51
Q

How is hepatitis A transmitted?

A

Faecal-oral route-> food/water

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52
Q

What type of virus is Hepatitis A?

A

RNA virus

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53
Q

How does Hepatitis A present?

A

N+V, anorexia, jaundice, cholestasis, dark urine, pale stoold, moderate hepatomegaly

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54
Q

How is Hepatitis A managed?

A
  • Often resolves spontaneously in 1-3 months
  • Analgesia
  • PHE notification
  • Prevention with vaccine
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55
Q

What type of virus is Hepatitis B?

A

DNA virus

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56
Q

How is Hepatitis B transmitted?

A
  • Blood + fluids-> sex, needles, toothbrushes, minor cuts

- Vertically-> mother to baby

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57
Q

What is the prognosis of Hepatitis B?

A
  • Most recover in 2 months

- 10% become carriers as viral DNA in own DNA continue to produce proteins

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58
Q

How is Hepatitis B tested for?

A
  • HBcAb-> core antibody, indicates previous infection when +ve
  • HBsAg-> surface antigen, indicates active infection when +ve
  • If these both positive then do others-> HBeAg, HBsAB, HBeAg, HBV DNA
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59
Q

What does a positive HBcAb test indicate when investigating Hepatitis B?

A

Core antibody-> previous infection

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60
Q

What does a positive HBsAg test indicate when investigating Hepatitis B?

A

Surface antigen-> active infection

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61
Q

What do the different tests for Hepatitis B mean?

A
  • HBcAb-> core antibody-> previous infection
  • HBsAg-> surface antigen-> active infection
  • HBeAg-> e antigen-> marks viral replication so high level means high infectivity
  • HBsAb-> surface antibody-> vaccination or past or current infection
  • HBV DNA-> direct viral load
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62
Q

How is Hepatitis B managed?

A
  • Screen high risk + other blood diseases
  • Refer to specialist + test for complications (eg US + fibroscan)
  • PHE notification + contact tracing
  • Antivirals-> reduce progression + transmission
  • Transplant
  • Vaccine
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63
Q

How does the Hepatitis B vaccine work?

A
  • Hep B surface antigen injected-> HBsAb tested to confirm

- 3 different doses in 6-in-1 vaccine at 8, 12 and 16 weeks

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64
Q

What type of virus is Hepatitis C?

A

RNA virus

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65
Q

How is Hepatitis C spread?

A

Blood + body fluids

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66
Q

What is the disease course of Hepatitis C?

A
  • 1/4 fight off the infection

- 3/4 get chronic infection

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67
Q

How is Hepatitis C investigated?

A
  • HepCAb-> screening

- HepC RNA-> confirm + calculate viral load

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68
Q

How is Hepatitis C managed?

A
  • Low screening threshold + for other diseases
  • Referral-> fibroscan + US
  • Direct acting antivirals-> tailored to genotype + cures 90%
  • PHE + education
  • May need transplant
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69
Q

What are the complications of Hepatitis C?

A

Cirrhosis and hepatocellular cancer

70
Q

What type of virus is Hepatitis D?

A

RNA virus

71
Q

When is the only time that it’s possible to get Hepatitis D?

A

With current Hepatitis B infection-> attached to HBsAg

72
Q

How is Hepatitis D managed?

A
  • PHE notification
  • No specific treatment
  • Looks for complications-> can increase severity of Hep B
73
Q

What type of virus is Hepatitis E?

A

RNA virus

74
Q

How is Hepatitis E spread?

A

Faecal-oral route

75
Q

How does Hepatitis E present and progress?

A
  • Mild illness + clears within a month

- Rare progression to chronic + liver failure when immunocompromised

76
Q

How is Hepatitis E treated?

A

None specific + needs PHE notification

77
Q

What causes autoimmune hepatitis?

A
  • Unknown

- Genetic + triggered by viral infection-> T cell response against liver cell

78
Q

What is type 1 autoimmune hepatitis and how does it present?

A
  • Mostly women in late 40s-50s
  • Around menopause with fatigue + liver disease
  • More chronic
79
Q

What is type 2 autoimmune hepatitis and how does it present?

A
  • In teens/early 20s
  • Acute hepatitis
  • Jaundice + high transaminases
80
Q

What investigations are done for autoimmune hepatitis?

A
  • Raised ALT, AST and IgG
  • Type 1 auto antibodies-> ANA, anti-actin, anti-SLA/LP
  • Type 2 auto antibodies-> anti-LKM1, anti-LC1
  • Liver biopsy-> confirms
81
Q

Treatment for autoimmune hepatitis?

A
  • High dose prednisolone tapered over time
  • Azathioprine immunosuppressant-> lifelong
  • Transplant
82
Q

What is haemachromatosis?

A

A genetic condition in which there are problems with iron storage leasing to excess total body iron + deposits in tissues

83
Q

What is the inheritance pattern and genetic mutation of haemachromatosis?

A
  • Autosomal recessive

- Human haemochromatosis protein (HFE) on chromosome 6-> regulates iton metabolism

84
Q

What are the symptoms of haemochromatosis?

A
  • Tired, joint pain, hair loss, erectile dysfunction, amenorrhoea, memory/mood problems
  • Pigmentation-> bronze + slate-grey discolouration
  • Usually symptomatic after age 40
  • Presents later in females as menstruation regularly eliminates iron from the body
85
Q

How is haemochromatosis diagnosed?

A
  • Serum ferritin-> acute phase reactant so use with transferrin sats to distinguish between other disease (both high)
  • Genetics-> if ferritin + transferrin high with no reason
  • Liver biopsy + Perl’s stain-> iron concentration in parenchymal cells
  • CT abdo-> high attenuation in liver
  • MRI-> detailed iron deposits in liver + heart
86
Q

What are the complications of haemochromatosis?

A
  • T1DM-> iron affects pancreas functioning
  • Deposits in pituitary and gonads-> endocrine + sexual dysfunction eg hypogonadism, impotence, amenorrhoea, infertility
  • Deposits in organs-> cardiomyopathy, hypothyroidism, pseudogout, arthritis
87
Q

Management of haemochromatosis?

A
  • Venesection-> weekly blood removal to decrease iron
  • Monitor ferritin
  • Avoid alcohol
  • Genetic counselling
  • Monitor and treat complications
88
Q

What is Wilson’s disease?

A

Excess copper accumulation as removal in the liver impaired

89
Q

What is the inheritance pattern and gene mutation in Wilson’s disease?

A
  • Autosomal recessive

- Wilson disease protein on chromosome 13

90
Q

What organs are affected in Wilson disease and how can this present?

A
  • Liver-> hepatitis + cirrhosis
  • CNS/neuro-> dystonia, dysarthria, motor symptoms, Parkinsonism (basal ganglia), mild depression, psychosis
  • Eyes-> Kayser-Fleischer rings (copper in corneal membrane)
  • Blood-> haemolytic anaemia
  • Kidney-> renal tubular acidosis
  • Bones-> osteopaenia
91
Q

What can Kayser-Fleischer rings be a sign of?

A

Wilson disease

92
Q

How is Wilson disease diagnosed?

A
  • Liver biopsy-> gold standard
  • Serum caerulopasmin-> protein carrying copper in blood (will be low)
  • 24 hour urine assay-> raised
  • Serum copper (low)
  • MRI brain
93
Q

How is Wilson disease managed?

A

Copper chelation + penicillamine + trientene

94
Q

What is alpha-1 antitrypsin deficiency and what does it cause?

A
  • A genetic condition causing a deficiency in an enzyme that protects the liver and lungs against neutrophil elastase
  • Mutant protein causes trapping of proteins in liver-> cirrhosis + cancer
  • Excess protease attacks lung connective tissue-> bronchiectasis + emphysema
95
Q

What is the inheritance pattern for alpha-1 antitrypsin deficiency?

A

Autosomal recessive

96
Q

How is alpha-1 antitrypsin deficiency diagnosed?

A
  • Low serum A1AT
  • Liver biopsy + acid-Schiff-positive staiing globules
  • Genetic tests
  • High resolution CT of lungs
97
Q

How is alpha-1 antitrypsin deficiency managed?

A
  • Stop smoking to decelerate emphysems
  • Symptom control
  • Organ transplant
  • Monitor for HC cancer
98
Q

What is primary biliary sclerosis?

A

Autoimmune condition in which small bile ducts of the liver are blocked causing cholestasis and hence fibrosis + cirrhosis + liver failure

99
Q

What is the pathophysiology of primary biliary sclerosis?

A
  • 1st intralobal ducts ie small bile ducts of liver (Canals of Hering) attacked by immune system
  • Obstruction of bile flow-> cholestasis + back pressure-> fibrosis + cirrhosis + liver failure
  • Bile acids + bilirubin + cholesterol excretes from bile ducts to intestines-> obstruction + blood build up as not excreted
100
Q

How does primary biliary sclerosis present and why?

A
  • Fatigue
  • Pruritis-> bile acid
  • Jaundice-> bilirubin
  • GI disturbance (greasy stools + fat malabsorption)-> as bile acids help digest
  • Pale stools-> if lack bilirubin
  • Xanthelasma + xanthomas-> cholesterol deposits
  • Increased CVD risk-> hypercholesterolaemia
101
Q

What is primary biliary sclerosis associated with?

A
  • Middle aged women
  • Autoimmune disease
  • Rheumatoid (RA, SS)
102
Q

How is primary biliary sclerosis diagnosed?

A
  • ALP raised first then liver enzymes + bilirubin raised later
  • Anti-mitochondrial antibodies
  • Other-> ESR, IgM, liver biopsy
103
Q

How is primary biliary sclerosis treated?

A
  • Ursodeoxycholic acid-> reduced cholesterol absorption in intestine
  • Colestyramine-> binds to bile acids + prevent absorption in gut
  • Immunosuppression
  • Liver transplant
104
Q

How does primary biliary sclerosis progress?

A
  • May be asymptomatic for decades

- Can get advanced cirrhosis + portal HTN

105
Q

What are some of the complications of primary biliary sclerosis?

A

Pruritis, steatorrhoea (fatty stools), distal renal tubular acidosis, hypothyroidism, osteoporosis, HC cancer

106
Q

What is primary sclerosing cholangitis?

A
  • When the intrahepatic or extrahepatic ducts stricture and fibrose causing obstruction of bile outflow and imflammation
  • Can’t get out of liver to intestines-> hepatitis, fibrosis + necrosis
107
Q

What are the causes of primary sclerosing cholangitis?

A
  • Genetic or environmental
  • Associated with ulcerative colitis
  • Risk factors-> male, aged 30-40, UC, family history
108
Q

What are the symptoms of primary sclerosing cholangitis?

A

Jaundice, chronic RUQ pain, pruritis, fatigue, hepatomegaly

109
Q

How is primary sclerosing cholangitis diagnosed?

A
  • MRCP-> gold standard
  • MRI of liver, bile ducts and pancreas-> strictures + lesions
  • LFTs-> cholestatic picture (ALP high + may be some ALT/AST derangement)
  • Autoantibodies> P-ANCA, ANA etc
110
Q

What are some of the associations/complications of primary sclerosing cholangitis?

A

Acute bacterial cholangitis, cholangiocarcinoma, colorectal cancer, cirrhosis, liver failure, fat soluble vitamin deficiency

111
Q

How is primary sclerosing cholangitis managed?

A
  • ERCP to dilate/stend strictures + improve flow
  • Colestyramine-> bind to bild acid + prevent absorption in gut
  • Liver transplant
  • Monitor complications
112
Q

What are the different types of liver cancer?

A
  • Hepatocellular (80% primaries)
  • Cholangiocarcinoma (20% of primary)
  • Secondary-> mets
113
Q

What are the risk factors for hepatocellular liver cancer?

A

Hepatocellular-> hepatitis B+C, alcohol, NAFLD, chronic liver disease

114
Q

What are the risk factors for Cholangiocarcinoma?

A
  • Primary biliary cholangitis

- Over 50’s

115
Q

How does liver cancer present?

A
  • Asymptomatic for long time + presents late

- Weight loss, abdominal pain, anorexia, N+V, jaundice, pruritis

116
Q

How does Cholangiocarcinoma present?

A
  • Painless jaundice

- Weight loss, N+V, pruritis etc

117
Q

What are the investigations for hepatocellular cancer?

A
  • Alpha-feto protein
  • Liver US
  • CT/MRI
118
Q

What are the investigations for Cholangiocarcinoma?

A
  • CA19-9
  • Liver US
  • CT/MRI
  • ERCP + biopsy/brushings
119
Q

How is hepatocellular cancer managed?

A
  • Resect or transplant in early disease can cure
  • Kinase inhibitors eg sorafenib-> inhibit cell proliferation
  • Usually resistant to chemo + radiotherapy
120
Q

How is Cholangiocarcinoma managed?

A
  • Can cure with early resection
  • ERCP-> stent + allow drainage
  • Resists chemo + radiotherapy
121
Q

What is a haemangioma?

A
  • Benign liver tumour + often incidental findings

- Usually no symptoms or treatment required

122
Q

What is focal nodular hyperplasia and what causes it?

A
  • Benign liver tumour of fibrotic tissue
  • Often oestrogen related eg OCP
  • Asymptomatic + no treatment usually needed
123
Q

What are the different types of liver transplant?

A
  • Orthotopic-> entire liver from deceased donor
  • Living donor-> portion
  • Split donation-> one liver to two donations
124
Q

What are the indications for liver transplant?

A
  • Acute failure-> viral hepatitis + paracetamol OD

- Chronic failure

125
Q

What are the contraindications to a liver transplant?

A
  • Severe CKD of HF
  • Excess weight loss or malnutrition
  • Active hepatitis B or C
  • End stage HIV
  • Active alcohol use-> needs 6 months abstinence
126
Q

What scar is typical of a liver transplant?

A

Rooftop or Mercedez-Benz scar

127
Q

What treatment/care is provided post-liver transplant?

A
  • Lifelong immunosuppression-> steroids, azathioprine, tacrolimus
  • Lifestyle-> avoid alcohol,
  • Monitor disease recurrence + cancer + rejection
128
Q

How might liver transplant rejection present?

A
  • Fever + jaundice + fatigue

- Abnormal LFTs

129
Q

What is the pathophysiology of gastro-oeseophageal reflex disease?

A
  • Stomach acid through the lower oesophageal sphincter-> irritates the lining
  • Squamous epithelial lining (more sensitive) turns to columnar epithelium in stomach (protective)
130
Q

How does gastro-oeseophageal reflex disease present?

A

Dyspepsia (indigestion), heartburn, acid regurgitation, retrosternal/epigastric pain, bloating, noctural cough, hoarse voice

131
Q

What symptoms alongside dyspepsia warrant a 2 week wait (urgent) endoscopy?

A
  • Anaemia (iron deficiency) or low Hb
  • Loss of weight
  • Anorexia
  • Recent onset of progressive symptoms
  • Melaena/haematemesis
  • Swallowing difficulty (dysphagia)
  • Aged 55 or over
132
Q

How is gastro-oeseophageal reflex disease managed?

A
  • Lifestyle-> reduce caffeine + alcohol, weight loss, avoid smoking, smaller meals + avoid food before bed, stay upright after meals
  • Acid-neutralising medications-> gaviscon + rennies
  • PPIs-> omeprazole/lansoprazole to reduce acid secretion
  • H2 receptor antagonists-> ranitidine
  • Laparoscopic fundoplication-> fundus of stomach around lower oesophagus to narrow lower sphincter
133
Q

What is the pathophysiology of H.pylori infection?

A
  • Gram negative bacteria living in stomach
  • Damages epithelial lining cells via chemicals produced
  • Avoids acid by forcing way into gastric mucosa + breaks it creates exposes epithelial cells under to acid
  • Produces ammonia which neutralises acids-> ammonia directly damaged cells
  • Causes gastritis, ulcers, increased stomach cancer risk
134
Q

How is H.pylori infection investigated?

A
  • Offered to anyone with dyspepsia-> have to e off PPIs for 2 weeks
  • Urea breath test-> radiolabelled carbon 13
  • Stool antigen test
  • Rapid urease test ie campylobacter-like organism test-> biopsy during endoscopy and add urea-> converts to ammonia so alkaline pH test
135
Q

How is H.pylori treated?

A
  • Triple therapy with PPI + 2 antibiotics (eg amoxicillin + clarithromycin) for 7 days
  • Urea breath test-> can use to see if eradicated
136
Q

What is Barrett’s oesophagus?

A
  • Metaplasia from squamous to columnar epithelium due to constant acid in lower oesophagus
  • Premalignant-> risk factor for adenocarcinoma of the oesophagus
137
Q

What can Barrett’s oesophagus put you more at risk of?

A

Adenocarcinoma of the oesophagus

138
Q

How does Barrett’s oesophagus present?

A

Reflux symptoms then improvement

139
Q

How does Barrett’s oesophagus transition to malignancy?

A

Barrett’s-> low grade dysplasia-> high grade-> adenocarcinoma

140
Q

How is Barrett’s oesophagus treated?

A
  • PPIs

- Ablation-> photodynamic, laser, cryotherapy to destroy epithelium + replace with normal cells

141
Q

What is the pathophysiology behind peptic ulcers?

A
  • Stomach/duodenum mucosa prone to breakdown of protective layer and increased stomach acid (eg stress, alcohol, caffiene, smoking, spicy food)
  • Mucous and bicarb secreted from mucosa-> broken down by meds (steroids + NSAIDs) or H.pylori
142
Q

What can increase the amount of stomach acid?

A

stress, alcohol, caffiene, smoking, spicy food

143
Q

How do peptic ulcers present?

A
  • Epigastric pain/discomfort, N+V, dyspepsia, iron deficiency anaemia, haematemesis, melaena
  • Eating-> worsens pain (gastric) or improves (duodenal)
144
Q

What type of peptic ulcer is most common?

A

Duodenal

145
Q

What type of peptic ulcer is worsened by eating?

A

Gastric

146
Q

What type of peptic ulcer is improved upon eating?

A

Duodenal

147
Q

How are peptic ulcers managed?

A
  • Endoscopy, rapid urease test (for H.pylori) + biopsy (malignancy)
  • Treatment-> high dose PPI
  • Monitoring-> endoscopy to ensure healing
148
Q

What are the complications of peptic ulcers?

A
  • Bleeding
  • Perforation-> acute abdomen + peritonitis
  • Pyloric stenosis due to scarring + stricture of muscles-> hard to empty contents
149
Q

How does pyloric stenosis present and when can it occur in adults?

A
  • Difficulty emptying contents-> abdo pain, distention, N+V after eating
  • Can be a complication of peptic ulcers
150
Q

What are the features of Chron’s disease?

A

Crows NESTS

  • No blood or mucous (less common)
  • Entire GI tract
  • Skip lesions on endoscopy
  • Terminal ileum (most affected) + transmural (full thickness inflammation)
  • Smoking is a risk factor
  • Others-> weight loss, strictures, fistulas, diarrhoea, abdominal pain
151
Q

What are the features of ulcerative colitis?

A

CLOSEUP

  • Continuous inflammation
  • Limited to colon + rectum
  • Only superficial mucosa affected
  • Smoking is protective
  • Excrete blood + mucus
  • Use amino-salicylates
  • Primary sclerosing cholangitis
  • Others-> diarrhoea, abdominal pain, passing blood, weight loss
152
Q

How is inflammatory bowel disease investigated?

A
  • Bloods-> FBC (anaemia + infection), TFTs, U+Es, LFTs, CRP (raised when active)
  • Faecal calprotectin-> released when intestines inflamed
  • Endoscopy-> OGD + colonoscopy (diagnostic)
  • Imaging-> US, CT, MRI etc for complications
153
Q

How is Chron’s managed (to induce remission)?

A
  • 1st line-> steroids ie oral prednisolone of IV hydrocortisone
  • 2nd line (ie doesn’t work)-> azathioprine, methotrexate, infliximab etc
154
Q

How is Chron’s managed (to maintain remission)?

A
  • Azathioprine or mercaptopurine
  • Some others can be used if doesn’t work
  • Surgery-> resect distal ileum if only disease there, for strictures + fistulas if present etc
155
Q

How is ulcerative colitis managed in a mild to moderate flare?

A
  • 1st line-> aminosalicylates eg mesalazine

- 2nd line-> prednisolone

156
Q

How is ulcerative colitis managed in a severe flare?

A
  • 1st line-> IV hydrocortisone

- 2nd line-> IV ciclosporin

157
Q

How is ulcerative colitis managed (maintaining remission)?

A
  • Mesalazine, azathioprine or mercaptopurine

- Panproctocolectomy-> remove rectum + colon, ileostomy or J-pouch created

158
Q

What is a J pouch?

A

Ileo-anal anastamosis-> ileum folded into rectum like structure

159
Q

What is irritable bowel syndrome?

A

Abnormal bowel dysfunction with no organic cause

160
Q

Who is IBS most common in?

A
  • Women

- Young adults

161
Q

What are the symptoms of IBS?

A
  • Diarrhoea, constipation, fluctuating bowel habit, abdominal pain, bloating
  • Symptoms worse after eating + improved after opening bowels
162
Q

What is the diagnostic criteria for IBS?

A
  • 2+ of abnormal stools, bloating, worsens after eating, PR mucous
  • Abdominal pain relieved when open bowels

Exclude other pathology

  • Bloods-> FBC, ESR, CRP
  • Faecal calprotectin-> IBD
  • Anti-TTG antibodies-> coeliac
  • Cancer
163
Q

How is IBS managed?

A
  • Reassurance
  • Healthy diet + exercise (eg FODMAP)
  • Probiotic trial for 4 weeks
  • Loperamine for diarrhoea
  • Laxatives
  • Antispasmodics-> Buscopan
  • Tricyclic antidepressants or SSRIs
  • CBT-> coping + distress
164
Q

What is coeliac disease?

A

Inflammatory bowel caused by gluten

165
Q

What is the pathophysiology of coeliac disease?

A
  • Anti-tissue transglutaminase (anti-TTG) + anti-endomysial (anti-EMA) autoantibodies-> more active in active disease
  • Target epithelial cells of intenstine
  • Atrophy of intestinal villi + crypt hypertrophy (mainly in jejunum)-> malabsorption of nutrients + cause symptoms
166
Q

What are the symptoms of coeliac disease?

A
  • May be asymptomatic
  • FTT, diarrhoea, fatigue, weight loss, mouth ulcers
  • Anaemia-> iron, B12, folate deficiencies
  • Dermatitis herpetiformis-> itchy blistering rash on abdomen
  • Often linked with T1DM
  • Rare neuro symptoms-> peripheral neuropathy, cerebellar ataxia, epilepsy
167
Q

How is coeliac disease diagnosed?

A

-Should stay on gluten diet during investigation to detect antibodies
-Raised anti-TTG + anti-EMA
-Total IgA-> exclude deficiency
-

168
Q

What conditions are associated with coeliac disease?

A

T1DM, thyroid disease, AI hepatitis, PBC, PSC

169
Q

What are the complications of untreated coeliac disease?

A

Vitamin deficiencies, anaemia, osteoporosis, ulcerative jejunitis
-Cancers-> Non-Hodgkins lymphoma, enteropathy-associated T-cell lymphoma (EATL) of intestine, small bowel cancer

170
Q

How is coeliac disease managed?

A
  • Lifelong gluten free diet

- Check antibodies (monitoring)

Medicine (13 decks)

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