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Phase 2A Medicine > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

What 2 factors can increase the risk of intraluminal infections?

A

Less gastric acid

broad spectrum antibiotic

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2
Q

Which vitamin deficiency commonly occurs in biliary obstruction and why?

A

Vitamin K

Low intestinal concentration of bile salts results in poor absorption of vitamin K.

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3
Q

Describe the gross anatomy of the liver and biliary tree.

A

sinusoids allow mixing of oxygen (from hepatic artery) and nutrients portal vein) and are separated by plates of hepatocytes.
hepatocytes produce bile collected in canaliculi which empty into right and left hepatic ducts which join to form common hepatic duct.
common hepatic duct + cystic duct (from gall bladder) = common bile duct
CBD passes through neck of pancreas where the pancreatic duct connects to it at the ampulla of Vater. Their entry into the duodenum is controlled by the Sphincter of Oddi.

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4
Q

Describe liver biochemistry investigations.

A

LFTs: serum albumin, serum bilirubin, prothrombin time

Aminotransferases - transaminase enzymes released during hepatocellular damage.
AST- aspartate- non-specific as is raised is hepatic necrosis, MI, muscle injury and congestive cardiac failure.
ALT- alanine- more specific to liver damage as in viral hepatitis.

alkaline phosphatase- present in hepatic canalicular and sinusoidal membranes, bone, placenta, intestine. If yGT is also abnormal, assume it’s coming from the liver.

yGT- gamma glutamyl transpeptidase- induced by phenytoin, warfarin, rifampicin and alcohol. If ALP normal, yGT good guide for alcohol intake.

So… raised AST and ALT- hepatocellular damage
raised ALP and yGT- cholestasis

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5
Q

Biochemical tests and their results in Wilson’s disease.

A

Urinary copper raised
serum copper low
caeruloplasmin low

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6
Q

What does a high alpha-fetoprotein indicate?

A

produced by foetal liver so…
hepatocellular carcinoma in adults
neural tube defects in foetus

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7
Q

What can alpha-1 antitrypsin enzyme deficiency produce?

A

Cirrhosis

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8
Q

What is the predominant raised serum immunoglobulin in primary biliary cholangitis?

A

IgM

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9
Q

What is the predominant raised serum immunoglobulin in autoimmune hepatitis?

A

IgG

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10
Q

Why are raised serum immunoglobulins thought to indicate liver disease?

A

increased y-globulins are thought to result from reduced phagocytosis by sinusoidal and Kupffer cells of the gut-absorbed antigens so these antigens then stimulate antibody production in the spleen, lymph nodes, portal tract lymphoid and plasma cell infiltrates.

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11
Q

What are the symptoms of acute liver disease?

A

may be asymptomatic and anicteric (not accompanied by jaundice)

malaise
anorexia
fever

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12
Q

What are the symptoms of chronic liver disease?

A

non-specific symptoms: weakness, anorexia, fatigue

specific symptoms:
right hypochondrial pain due to liver distension
abdominal distension due to ascites
ankle swelling due to fluid retention
haematemesis and melaena from GI haemorrhage
pruritis due to cholestasis (early PBC symptom)
gynaecomastia, loss of libido and amenorrhoea due to endocrine dysfunction
confusion and drowsiness due to neuropsychiatric complications (portosystemic encephalopathy)

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13
Q

Where is jaundice best seen in the body?

A

sclerae and conjunctivae

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14
Q

What are the signs of compensated chronic liver disease?

A

Xanthelasma, parotid swelling, spider naevi, gynaecomastia, hepatomegaly, splenomegaly, palmar erythema, clubbing, Dupuytren’s contracture, xanthomas, scratch marks, testicular atrophy, purpura, pigmented ulcers.

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15
Q

What are the signs of decompensated chronic liver disease?

A

Neurological- disorientation, drowsy, coma, hepatic flap, foetor hepaticus.

loss of proximal muscle bulk
ascites
dilated veins on abdomen
oedema

skin- slate grey appearance in haemochromatosis

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16
Q

What is yellow fever?

A

Yellow fever is a viral infection carried by the mosquito Aedes aegypti and can cause acute hepatic necrosis.

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17
Q

How can you differentiate between infectious mononucleosis and toxoplasmosis?

A

Paul-Bunnell test:
IM- positive
toxo- negative

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18
Q

What abnormality of liver biochemistry is seen in hepatitis caused by herpes simplex virus?

A

aminotransferases are massively elevated

liver biopsy shows extensive necrosis

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19
Q

What would you use to treat hepatitis caused by herpes simplex virus?

A

Aciclovir

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20
Q

Which virus causes infectious mononucleosis? Which part of the liver does it affect in hepatitis?

A

Epstein-Barr virus

portal tracts and sinusoids are infiltrated with large mononuclear cells

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21
Q

What is acute hepatic failure?

A

Acute liver failure is defined as acute liver injury with encephalopathy and deranged coagulation (INR>1.5) in a patient with a previously normal liver.

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22
Q

What is the typical presentation of a patient with drug-induced chronic hepatitis?

A

Female with jaundice and hepatomegaly.

Raised serum aminotransferases and globulin levels

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23
Q

What are the six main mechanisms by which drugs can cause liver damage?

A
  1. disruption of intracellular calcium homeostasis
  2. disruption of bile canalicular transport mechanisms
  3. formation of non-functioning adducts
  4. presentation of new immunogens on hepatic surface
  5. induction of apoptosis
  6. inhibition of mitochondrial function which prevents fatty acid metabolism and accumulation of lactate and ROS
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24
Q

How does a dose-dependent hepatotoxic drug cause liver damage?

A

When a small amount of the drug (e.g. paracetamol) is ingested, a large proportion of it undergoes conjugation with glucuronide and sulphate.

The remainder is metabolised by microsomal enzymes to produce toxic derivatives that are immediately detoxified by conjugation with glutathione.

If larger doses are ingested, the former pathway becomes saturated and the toxic derivative is produced at a faster rate. Once the hepatic glutathione is depleted, large amounts of the toxic metabolite accumulate and cause damage.

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25
Q

What effect does amiodarone have on the liver?

A

Leads to steatohepatitis and liver failure if not stopped in time.

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26
Q

What effect does paracetamol have on the liver?

A

liver cell necrosis

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27
Q

What effect do steroid compounds have on the liver?

A

cholestasis

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28
Q

What type of liver tumour is associated with oral contraceptives?

A

Hepatic adenomas.

Can present with abdo pain or intraperitoneal bleeding, resection required only in symptomatic patients. Discontinuation should shrink tumour.

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29
Q

What are the common origins for a secondary liver tumour?

A

gastrointestinal tract
bronchus
breast

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30
Q

Which abnormality in liver biochemistry is found in secondary liver tumours?

A

raised alkaline phosphatase

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31
Q

How would you first investigate a potential secondary liver tumour?

A

ultrasound

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32
Q

What type of malabsorption do lymphatic obstructions lead to?

A

Protein-losing enteropathy due to decreased protein uptake by intestinal lymphatics leading to abnormal protein loss from the digestive tract which results in low serum proteins.

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33
Q

Name the three characteristic features of coeliac disease seen in a duodenal or jejunal biopsy.

A
  1. villous atrophy
  2. crypt hyperplasia
  3. intraepithelial lymphocytosis
34
Q

The production of which intestinal hormones may be affected in severe coeliac disease?

A

pancreozymin, secretin and cholecystokinin which results in reduction of pancreatic secretion and bile flow

35
Q

What conditions are patients with coeliac disease at a higher risk of developing?

A
  1. chronic ulcerative jejunoileitis
  2. primary enteropathy associated T cell lymphoma (EATCL)
  3. adenocarcinoma of small bowel
36
Q

What is dermatitis herpetiformis?

A

This is an uncommon, blistering, subepidermal eruption of the skin associated with a gluten-sensitive enteropathy.

37
Q

How would you differentiate between coeliac disease and tropical sprue?

A

coeliac disease will show abnormalities in duodenal and jejunal biopsies; it spares the ileum.
Tropical sprue will show abnormalities in jejunal and ileal biopsies.
Tropical sprue is likely to have history of infection (E. coli, Enterobacter, Klebsiella) and will not improve on withdrawal of gluten from diet. Will respond to tetracycline and folate.

38
Q

How would you confirm if bacterial overgrowth is the cause of malabsorption?

A

Hydrogen breath test

39
Q

What are the implications of ileal resection?

A
  1. bile-salt-induced diarrhoea
  2. steatorrhoea and gall stone formation
  3. oxaluria and oxalate stones
  4. B12 deficiency
40
Q

What is stomatitis?

A

Inflammation of the mouth

angular stomatitis is inflammation of corners of the mouth

41
Q

What is dyspepsia?

A

a general term used to describe upper abdo symptoms of acidity, heartburn, pain or discomfort, nausea, wind, fullness or belching.

42
Q

What are the common alarm symptoms in GI?

A 
dysphagia 
weight loss
vomiting 
anorexia
haematemesis or melaena

especially above the age of 55

43
Q

What are the local GI causes of vomiting?

A

luminal toxins, inflammation, mechanical obstruction

44
Q

What are the central causes of vomiting?

A

raised intracranial pressure
vestibular disturbance e.g. motion sickness
migraine
toxins
drugs
metabolic disturbances- uraemia, hypercalcaemia

45
Q

What does faeculent vomiting suggest?

A

low intestinal obstruction

presence of gastrocolic fistula

46
Q

What are the common five Fs causes of abdominal distension?

A

flatus, fat, foetus. fluid, faeces

47
Q

What is a succussion splash?

A

Succussion splash is a sloshing sound heard through the stethoscope during sudden movement of the patient on abdominal auscultation. It reflects the presence of gas and fluid in an obstructed organ, as in gastric outlet obstruction if the patient has not drunk for 2-3 hours.

48
Q

Describe the different types of stools as classified in the Bristol Stool Chart.

A

Type 1: separate hard lumps like nuts (hard to pass)
Type 2: sausage-shaped but lumpy
Type 3: Like a sausage but with cracks on its surface
Type 4: like a sausage or snake, smooth and soft
Type 5: soft blobs with clear-cut edges (passed easily)
Type 6: fluffy pieces with ragged edges, a mushy stool
Type 7: watery, no solid pieces, entirely liquid

49
Q

What are the risk factors for squamous cell carcinoma of the oesophagus?

A 
tobacco smoking
high alcohol intake
Plummer-Vinson syndrome (oesophageal web + iron def anaemia + glossitis + angular stomatitis)
achalasia 
corrosive strictures
coeliac disease
breast cancer treated with radiotherapy 
tylosis (rare autosomal dom condition with hyperkeratosis of palms and soles)
50
Q

What are the risk factors for adenocarcinoma of the oesophagus?

A 
longstanding heartburn
Barrett's oesophagus
tobacco smoking
obesity
breast cancer treated with radiotherapy
older age
51
Q

What staging system is used to classify gastric and oesophageal cancers?

A

TNM

52
Q

What set of criteria is used in the diagnosis of constipation?

A

The Rome criteria

53
Q

What is the most common cause of chronic liver disease?

A

Non-alcoholic fatty liver disease

54
Q

What are the risk factors for NAFLD?

A

obesity, hypertension, type 2 diabetes, hyperlipidaemia

55
Q

What histological changes are seen in NAFLD?

A

simple fatty change, fat and inflammation, fibrosis and cirrhosis

56
Q

Describe the pathogenesis of NAFLD.

A

Oxidative stress injury leads to lipid peroxidation in the presence of fatty infiltration and inflammation, enhanced by insulin resistance, leads to fibrosis which induces connective tissue growth factor.

57
Q

What investigations are used to diagnose NAFLD?

A

ultrasound- demonstrates steatosis in absence of other injurious causes lik alcohol
liver biopsy- allows staging of disease
elastography- evaluate degree of fibrosis

58
Q

What lifestyle advice would you give a person with NAFLD?

A

weight loss via calorie restriction
increase physical activity
attention to cardiovascular risk factors

59
Q

What drugs are used in the management of NAFLD?

A
  1. orlistat: enteric lipase inhibitor causes malabsorption of dietary fat (plus low fat diet to aid weight loss)
  2. Pioglitazone: aka vit E if whom lifestyle intervention has failed. improves steatohepatitis
    (bariatric surgery reduces steatohepatitis, steatosis and fibrosis)
60
Q

What are the causes of liver cirrhosis?

A

common- alcohol, hep B,C,D, NAFLD

others- primary and secondary biliary cholangitis, autoimmune hep, hereditary haemochromatosis, Budd-Chiari syndrome, Wilson’s disease, methotrexate, alpha-1 antitrypsin deficiency, cystic fibrosis.

61
Q

Describe the pathogenesis of liver cirrhosis.

A

chronic injury results in inflammation, matrix deposition, necrosis and angiogenesis.
Injury causes necrosis and apoptosis –> release of cell contents and ROS –> activation of hepatic stellate cells and tissue macrophages –> phagocytosis of necrotic and apoptotic cells –> release of pro-inflammatory mediators including transformation growth factor-beta –> transdifferentiation of stellate cells to myofibroblasts –> platelet-derived growth factor –> proliferation of myofibroblasts –> produce tissue inhibitors of metalloproteinases –> stops macrophages from degrade scar matrix –> matrix deposition and scar accumulation –> fibrosis.

62
Q

What is the only available treatment for liver failure?

A

liver transplantation

63
Q

What are the characteristic features of liver cirrhosis?

A

regenerating nodules separated by fibrous septa and loss of lobular architecture within the nodules.

64
Q

What usually causes macronodular cirrhosis?

A

chronic viral hepatitis

65
Q

What usually causes micronodular cirrhosis?

A

alcohol, biliary tract disease

66
Q

What investigations are used to assess the severity of liver disease?

A

LFT- serum albumin and prothrombin time
Liver BC- deranged in decompensated cirrhosis
serum electrolytes- low sodium indicates severe disease due to defect in free water clearance or excess diuretic therapy
serum creatinine- elevation is marker of poor prognosis
biomarkers- enhanced liver fibrosis test > 9.8 is severe
serum alpha-fetoprotein of >200 ng/mL suggests HCC

67
Q

What investigations are used to assess type of liver disease?

A

viral markers
serum autoantibodies
serum immunoglobulins
iron indices and ferritin- to exclude hereditary haemachromatosis
copper and caeruloplasmin- especially in young people for Wilson’s
alpha1-antitrypsin
genetic markers

68
Q

What imaging techniques are used to investigate liver disease?

A

ultrasound- change in size and shape of liver, distortion of arterial vasculature, patency of portal and hepatic veins, detection of HCC
transient elastography (to avoid liver biopsy)- limited use in ascites or morbid obesity
CT scan- hepatomegaly, contrast enhancement to detect HCC
Endoscopy- detection and treatment of varices and portal hypertensive gastropathy, colonoscopy for colopathy
MRI scanning- diagnosis of malignant and benign tumours. MR angiography- vascular anatomy, MR cholangiography- biliary tree

69
Q

What is the gold standard investigation to assess type and severity of liver disease?

A

liver biopsy

70
Q

What are the poor prognostic indicators of cirrhosis?

A 
low serum albumin
low serum sodium
prolonged prothrombin time
raised creatinine
persistent jaundice 
failure to respond to therapy
ascites
haemorrhage from varices
encephalopathy 
small liver
persistent hypotension
continued drinking if alcoholic cirrhosis
71
Q

What does the management of liver cirrhosis involve?

A
  1. manage complications in decompensated cirrhosis
  2. six-monthly ultrasound to screen for HCC
  3. Hep A and B vaccinations for those at risk
  4. reduce salt intake
  5. avoid alcohol and NSAIDs
72
Q

What scoring systems are used as prognostic predictors in liver cirrhosis?

A

Modified Child-Pugh classification and Model of End-Stage Liver Disease (MELD)- they look at bilirubin, creatinine and INR

73
Q

What is acute-on-chronic liver failure and how does it differ from decompensated cirrhosis?

A

ACLF refers to the condition of patients hospitalised for acute complications of cirrhosis accompanied by organ failure.
Different due to involvement of organ failure, high mortality rate, younger age, alcohol aetiology, higher level of systemic circulation and higher prevalence of precipitating factors like bacterial infections or active alcohol excess.

74
Q

What is the gut-liver axis?

A

The connection between intestinal microbiota and the liver. In advanced liver disease, gut immune defences are low due to reduced motility and increased permeability so bacteria enter portal circulation where Toll-like receptors in the liver produce an inflammatory response which leads to complications of cirrhosis.

75
Q

What is the only established treatment for liver disease?

A

Liver transplant

76
Q

What is the indication for liver transplant in acute liver disease?

A

acute hepatic failure of any cause

77
Q

What is the indication for liver transplant in chronic liver disease?

A

complications of cirrhosis that are no longer responsive to therapy

78
Q

What are the absolute contraindications to liver transplant?

A
  • active sepsis outside hepatobiliary tree
  • malignancy outside the liver
  • liver metastases (except neuroendocrine)
  • lack of psychological commitment on the side of the patient
79
Q

What are the various forms of rejection to liver transplants?

A
  1. acute or cellular rejection- 5-10 days post transplant, asymptomatic or fever. Biopsy shows pleomorphic portal infiltrate with prominent eosinophils, bile duct damage and endothelialitis of blood vessels. Responds well to immunosuppression.
  2. Chronic ductopenic rejection- 6 wks to 9 months post transplant- vanishing bile duct syndrome + arteriopathy with narrowing and occlusion of arteries. mostly requires retransplantation
  3. graft-versus-host disease - very rare
80
Q

What is portosystemic encephalopathy?

A

PSE is a chronic neuropsychiatric syndrome that is secondary to cirrhosis. It is caused by blood bypassing the liver due to shunts of collaterals in portal hypertension and hence allowing toxic metabolites to passed directly to the brain.

81
Q

Give examples of precipitating factors for portosystemic encephalopathy.

A
  • high dietary protein
  • GI haemorrhage
  • constipation
  • infection (incl spontaneous bacterial peritonitis)
  • fluid and electrolyte disturbance due to diuretic therapy or paracentesis
  • drugs (CNS depressant)
  • portosystemic shunt operations, TIPS
  • any surgical procedure
  • progressive liver damage
  • development of HCC
82
Q

What are the clinical features of portosystemic encephalopathy?

A

acute- drowsiness and comatose state
chronic- alterations in personality, mood and intellect with a reversal of normal sleep rhythm. Irritable, confused, disorientated and has slow, slurred speech. Nausea, vomiting, weakness, hyper-reflexia and increased tone.

Phase 2A Medicine (16 decks)

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