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APhase 3b flashcards > Liver et al > Flashcards

Liver et al Flashcards

1
Q

Main 4 points in acute liver failure

A

Hepatic encephalopahty
Jaundice
Coagulopathy
With no evidence of serious prior liver disease.

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2
Q

Time scale and classification of acute liver disease

A 
Hyperacute = within 7days 
Acute = 8-29 days
Subacute = 4 to 12 weeks

Also Fulminant = within 2 weeks and subfulminant within 2-12weeks.

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3
Q

Risk factors for acute liver failure

A

Chronic alcohol use
Poor nutrition
Older age (over 40)
Narcotic use

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4
Q

Causes of acute liver failure

A 
Paracetamol toxicity
Viral hepatitis - HBV and HAV
Budd-Chiari syndrome
CMV, EBV
Autoimmune liver disease
Wilson's disease
Alpha-1 antitrypsin deficiency.
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5
Q

S+S of acute liver failure

A

Jaundice
Symptoms of hepatic encephalopathy - altered mood, sleep disturbance, slurred speech, confused.
Abdo pain
Nausea and vomiting

O/E:
Signs of hepatic encephalopathy - apraxia, liver flap, stupor.
Jaundice
Hepatomegaly

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6
Q

How to test for apraxia

A

Copy a 5 point star

Show me how to brush your teeth, use a hammer, comb your hair etc etc

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7
Q

Ix for acute liver failure

A 
Laboratory:
FBC
U+E
LFT
Clotting and synthetic liver function
BM
Paracetamol levels
Viral hepatitis antibodies
Copper studies, alpha1-anti trypsin levels etc etc
Blood culture, urine culture, ascitic tap mc+s
Imaging:
Abdo USS
CT/MRI of liver
CT head
Doppler USS of liver and portal vein.
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8
Q

Management of acute liver failure

A

In ITU 🌈
A-E including urinary catheter, NG tube, frequent BMs.
Treat cause.

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9
Q

Treating complications of acute liver failure

1) Cerebal oedema
2) Ascites
3) Hypoglycaemia
4) Encephalopathy

A

1) 20% Mannitol IV
2) Fluid and salt restriction, diuretic e.g spironolactone.
3) 10% glucose IV
4) Lactulose + Rifaximin.

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10
Q

List 5 hepatotoxic drugs

A 
Pyrazinamide, Isoniazid (TB)
Paracetamol
Methotrexate
Azothioprine
Infliximab
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11
Q

Liver function test:
Which are markers of hepatocellular damage?
Which are markers of the liver’s synthetic function

A

Damage = ALT, AST, ALP, gamma-GT.

Synthetic liver function = PT, Albumin and bilirubin.

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12
Q

Interpreting ALT and ALP

A 
ALT = mostly found within hepatocytes so if serum levels high = injury to hepatocytes.
ALP = high concentrations in liver, bile duct and bone tissue, if serum levels high = cholestasis.

Therefore:
a >10X rise in ALT and a <3X rise in ALP = hepatocellular injury.
a >3X rise in ALP and a <10X rise in ALT = cholestasis.
And can have a mixed picture too.

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13
Q

List some functions of the liver

A

Bile production - stored in gallbladder.
Metabolise fat soluble vitamins e.g. vitamin D hydroxylation.
Drug metabolism using CYP450 enzymes.
Conjugation and elimination bilrubin
Synthesis of plasma proteins e.g. albumin
Synthesis of clotting factors
Gluconeogenesis

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14
Q

Pathophysiology of cirrhosis

A

Fibrosis and loss of normal liver architecture to abnormal, regenerative nodules.

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15
Q

Causes of cirrhosis

A 
Chronic HBV and HCV
Non-alcohol fatty liver diease
Chronic alcohol
Alpha1-antitrypsin deficiency
Wilson's disease
Budd-Chiari syndrome
Drugs = methotrexate
Primary biliary cholangitis
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16
Q

Presentation of liver cirrhosis

A 
Abdo distension
Jaundice
Itch
Easy bruising
Poor memory
Fatigue and weakness
Peripheral oedema

O/E: LOTS!!!
Hands = Leuconychia (white nails), clubbing, palmar erythema, spider naevi, Dupuyren’s contracture.
Face = telangiectasia, xanthelasma, yellowing of sclera in eyes (jaundice)
Abdo = gynaecomastia, hepatomegaly, visible collateral vessel sin the abdo wall. Ascites + shifting dullness and fluid thrill on percussion.
Other = muscle wasting, loss of pubic hair, testicular atrophy on men.

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17
Q

Investigating cirrhosis and expected results

A 
Laboratory:
LFT - raised liver enzymes.
Gamma-GT - raised.
Albumin - low
PT and INR - high
FBC 
Ascites tap mc+s
Find cause - viral hepatitis antibodies serology, ferritin, alpha1-antitrypsin levels.
Imaging:
Abdo US + duplex
Abdo CT/MRI
Liver biopsy
Transient elastography
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18
Q

What will you see in the histology of a liver biopsy in cirrhosis

A

Loss of hepatic architecture.
Bridging fibrosis.
Nodular regeneration.

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19
Q

Classification of liver cirrhosis

A

Child-Pugh-Turcotte Score.

Based on: (BAAIN mnemonic)
Bilirubin
Ascities
Albumin low
INR high
Encephalopathy

Class = level of cirrhosis and determines life expectancy.

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20
Q

End-stage liver disease score

A

Model of End-Stage Liver Disease score uses bilirubin, sodium, creatinine and INR/PT to assess liver disease.
Used in liver transplant list.

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21
Q

Management of cirrhosis

A

Lifestyle advice = avoid alcohol, exercise to avoid muscle wasting, good nutrition, avoid hepatotoxic drugs (NSAIDs).
Management of ascites = fluid restriction, low salt diet, spironolactone +/- furesomide, daily weight.
Liver transplant list appropriateness.

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22
Q

Fluid restriction level in ascites and target weight loss with spironolactone

A

Max 1.5L per day.

Aim for up to 0.5g/day of weight loss.

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23
Q

Complications of cirrhosis

A 
Hepaticellular carcinoma
Coagulopathy
Encephalopathy
Sepsis
Spontaneous bacterial peritonitis
Hypoglycaemia
Oesophageal varicies (and GI haemorrhage)
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24
Q

Spontaneous bacterial peritonitis

A

Ascites + sudden deterioration.
Commonly E.coli, Klebsiella
Rx = Cefotaxime or Tazosin
Can give prophylactic Ciprofloxacin.

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25
Q

Portal triad and another thing which helps bile flow

A

Portal vein
Hepatic artery
Bile duct
Found in a corner of each liver lobular.

Bile canaliculi.

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26
Q

Decompensated cirrhosis

A

Acute deterioration in a patient with chronic liver disease.
Precipitated by: infection (Spont bac peritonitis), high alcohol intake, drugs (NSAIDS, opiates), portal vein thrombus.
S+S: jaundice, increasing ascites, hepatic encephalopathy, AKI, oesophageal varices haemorrhage/GI bleed.
Ix: Vital signs, FBC, U+E, LFT, coagulation, blood glucose, blood cultures, ascitic tap MC+S, urine dipstick, CXR and AXR. Alcohol intake history.
Rx: A to E assessment, treat cause (ABx, FFP/transfusion, lactulose + Rifaxmin)

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27
Q

Grading of hepatic encephalopathy

A

West-Haven criteria

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28
Q

Compound involved in hepatic encephalopathy

A

Serum ammonia build up causing glutamine excess in brain which draws fluid in = cerebral oedema.

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29
Q

Name 3 metabolic liver diseases and how are they all inherited

A

Hereditary haemochromatosis, Chr 6
Wilson’s disease, Chr 13
Alpha-1 antitrypsin deficiency, Chr 14

All autosomal recessive 🧬

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30
Q

Pathophysiology of hereditary haemochromatosis

A

Autosomal recessive.
Inherited on chromosome 6, HFE gene.
Lack of hormone HEPCIDIN which regulates iron levels.
Increased iron absorption from intestine.
Deposits of iron in liver, heart, skin, joints and pancreas.
More common in males as females loose blood and hence iron during menses.

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31
Q

S+S of hereditary haemochromatosis

A

Early in life = asymptomatic, tiredness, arthralgia, low libido.
Mid-life = slate-grey tinged skin pigmentations, arthralgia, DM, fatigue and weakness, hepatomegaly, signs of cirrhosis and chronic liver disease, cardiac arrythmias.

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32
Q

Where is the arthralgia common in HH

A

2nd and 3rd metacarpophalangeal in hands.

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33
Q

Investigating hereditary haemochromatosis

A

Iron studies:
Serum transferrin saturation = >45% (specific marker).
Serum ferritin = raised.
Serim TIBC = low/normal

LFT
HFE gene testing.
MRI
Liver biopsy + Perl's stain = iron loading and fibrosis.
Liver FibroScan

Ix extra-hepatic manifestations: echocardiogram, BM/HbA1c/OGTT.

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34
Q

Management of hereditary haemochromatosis

A

Weekly venesection - target ferritin <50mcg/L.
Monitor for DM and arrhythmias.
Consider for transplant.

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35
Q

Pathophysiology of Wilson’s disease

A

Autosomal recessive.
Mutation in chromosome 13.
Copper retention in liver and basal ganglia due to impaired excretion in the liver.

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36
Q

Presentation of Wilson’s disease

A

Early in life = Liver disease signs (hepatitis, cirrhosis).
Young adults = CNS signs (tremor, dysarthria, dystonia, dementia, ataxia).
Psych = depression, change in libido, personality change, poor memory.

O/E:
Kayser-Fleischer rings from copper in iris.
Blue nails
Hypermobile joints
Grey tinged skin
Hepatomegaly and signs of cirrhosis (spider naevi, jaundice, ascites, bruising).

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37
Q

Investigating Wilson’s disease

A

Copper studies:
24hr urinary copper excretion = high
Serum copper = low
Serum caeruloplasmin = low

LFT = raised enzymes.
Hepatic biopsy = high copper levels.
Slit-lamp exam = Kayser-Fleischer rings.
Head MRI = degeneration of basal ganglia.
Genetic testing for Wilson's disease
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38
Q

Management of Wilson’s disease

A

Lifestyle advice = avoid copper rich foods (chocolate, mushrooms, liver meat). Avoid alcohol and hepatotoxic drugs.
Chelation agent to bind to copper and excrete in urine = penicillamine (oral)
Prevent copper absorption = zinc compounds.
Liver transplantation appropriateness.
Screen family!

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39
Q

Drug for chelation of copper in Wilson’s disease

A

Penicillamine

S/Es = rash, nausea, anaemia, haematuria etc etc.

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40
Q

Pathophysiology of alpha1-antitrypsin deficiency

A

Autosome recessive.
Chromosome 14, SERPINA1 gene.
Loss of protease inhibitor involved in inflammatory cascade causing serpinopathy.
Loss of neutrophil elastase enzyme action.

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41
Q

S+S of alpha1-antitrypsin deficiency

A

Mostly males.
Symptoms fo COPD in under 40yrs e.g. productive cough, SOBOE, wheeze.
Symptoms of cirrhosis e.g. ascites, jaundice, confusion, hepatomegaly, cholestasis.

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42
Q

Investigating alpha1-antitrypsin deficiency

A

Serum alpha1-antitrypsin levels = low –> genetic testing/phenotyping.

Spirometry = obstructive pattern.
CXR

LFTs - raised enzymes.
Liver biopsy = diastase-resistant globules, +ve for Periodic acid Schiff

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43
Q

Management of alpha1-antitrypsin deficiency

A

Lifestyle advice - smoking cessation, annual influenza vaccine.
Treat as for COPD
Monitor LFT, screen for HCC.

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44
Q

Drug to help pruritus in liver disease

A

Colestyramine.

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45
Q

Pathophysiology behind autoimmune hepatitis

A

Autoantibodies against hepatocyte surface antigen cause inflammation and necrosis.
T-cell mediated attack.
Associated with HLA-DR3

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46
Q

Common patients with autoimmune hepatitis

A

Females. Not usually that old, under 40yrs.

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47
Q

Presentation of autoimmune hepatitis

A

Acute = 40% present acutely.
Fever, jaundice, abdo pain.
Subacute = gradual onset jaundice, pruritus, hepatomegaly, abdo discomfort, signs of cirrhosis (confusion, ascites)
CFx of other autoimmune diseases e.g. arthralgia, bowel dysfunction (UC).

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48
Q

Investigating autoimmune hepatitis

A

LFT - raised transaminases, ALT/AST >1.5X.
FBC - anaemia, low WCC, low platelets esp if splenic dysfunction too.

Criteria:
Serum protein electrophoresis for autoantibodies - ANA, ASMA, LKM1.
Hypergammaglobulinaemia esp IgG
Liver biopsy - mononuclear infiltrates of portal and periportal areas, piecemeal necrosis, fibrosis, cirrhosis.

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49
Q

What is seen in liver biopsy of autoimmune hepatitis

A

Mononuclear infiltrates in portal and periportal areas = interface hepatitis.
Piecemeal necrosis
Fibrosis.

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50
Q

Management of autoimmune hepatitis

A

1) Prednisolone - high dose then reduce after 1 month for maintenance.
2) If corticosteroids CI can use Azathioprine or if not responsive to mono therapy use in combo.

Liver transplant

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51
Q

Definition of portal hypertension

A

Increase in portal venous pressure due to increase in hepatic vascular resistance and hepatic blood flow. Commonly caused by chronic end-stage liver disease.
The raised pressure opens up venous collaterals to connect the portal and system circulation.

Clinically significant if pressure gradient is >10mmHg.

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52
Q

Causes of portal HTN

A

Prehepatic - before portal vein in liver:

  • Congenital atresia
  • Portal venous thrombus
  • Extrinsic compression by tumour.

Hepatic:

  • Cirrhosis
  • Chronic hepatitis
  • Sarcoid granulomata.

Post-hepatic - block in hepatic vein:

  • Budd-Chiari syndrome
  • Constrictive pericarditis
  • Right heart failure
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53
Q

Sites for portal-systemic circulation collaterals

A

Gastro-oesophageal junction = oesophageal varices.
Anterior abdo wall = visible as caput medusae around umbilical area.
Ano-rectal junction
Retroperitoneal viscera.

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54
Q

Effects of portal HTN on systemic circulation

A 
Produce hyperdynamic circulation
Bounding pulse
Hypotension
Increases cardiac output
Salt and water retention = hypervolaemia and hypernatraemia.
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55
Q

Presentation of portal HTN

A

Presents as chronic liver disease mostly - jaundice, alcohol consumption, ascites, hepatomelgay, splenomegaly, hepatic encephalopathy, visible collaterals on abdo wall, spider naevi, gynaecomastia, liver flap, oesophageal varicies bleed.
Vital signs = bounding pulse, low BP but warm peripheries.

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56
Q

Investigating portal HTN

A 
Abdo USS.
Doppler US of portal vessels.
Spiral CT 
Endoscopy for oesophageal varices.
hepatic venous pressure gradient (>10mmHg)

Bloods:
LFT, U+E, FBC, clotting profile, PT.
Find cause - iron studies, copper studies, hepatitis serology etc etc

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57
Q

Management of portal HTN

A

Reduce BP = non-selective beta blockers (propranolol), nitrates.
Surgical = transjugular intrahepatic bypass shunt.
Treat or manage cause - diuretics, salt and fluid restriction,

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58
Q

Hepatopulmonary syndrome

A

Complication of portal HTN

Hepatic dysfunction, hyperaemia, extreme vasodilation.

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59
Q

Common cause of haemoperitoneum

A

Trauma + HCC

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60
Q

Common cancers in the liver

A

Most common are due to metastasis from breast, bronchus and GI tract.
Primary liver tumours = hepatocellullar carcinomas.

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61
Q

Risk factors/Causes for hepatocellular carcinoma

A 
MALE
Hepatitis B and C virus.
Heavy, chronic alcohol consumption.
Metabolic syndrome and obesity.
Non-alcohol fatty liver disease.
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62
Q

S+S of HCC

A 
Fatigue
Anorexia
RUQ pain
Loss of weight
Bruit over liver area on auscultation.

S+S of cirrhosis e.g.
Itch, bleeding oesophageal varices, ascites, jaundice, hepatomegaly,collateral veins on chest, liver flap.

63
Q

Ix for HCC

A

CT = DIAGNOSTIC, then MRI and BIOPSY.

Lab:
FBC, LFT, U+E, PT, viral hepatitis serology, alpha fetoprotein.

Screening via ultrasound scans.

64
Q

Management of HCC

A

Resection of tumour.
Ablation therapy
Liver transplant list.
Advanced/untreated = Lenvatinib or Sorafenib.

Not great prognosis, 6months from diagnosis.

65
Q

Prevention measures of HCC

A

High-risk group annual ultrasound scan screening and monitor AFP (HBV patients).
HBV vaccine programme.
Needle exchanges, safer sex education.

66
Q

Another name for Budd-Chiari Syndrome

A

Hepatic venous outflow obstruction - obstruction anywhere from inferior vena cava to small hepatic veins.

67
Q

Triad in Budd-Chiari

A

Abdo pain, ascites and hepatomegaly (quite rapid onset).

68
Q

Causes of hepatic venous outflow obstruction/ B-C syndrome

A

Vascular - right heart failure, constricitve pericarditis, protein C and protein D deficiency and other thrombophilic disoders.
Infective - syphilis, amoebic abscess
Trauma
Autoimmune - SLE, Sjogren’s, IBD
Iatrogenic - COCP
Neoplastic - HCC, Wilm’s tumour
Congenital - congenital anatomical abnormality in vena cava.

69
Q

Presentation of hepatic venous outflow obstruction

A

Sudden abdo pain
Ascites
Hepatomegaly
AKI

rare = jaundice.

70
Q

Ix and Mx of hepatic venous outflow obstruction

A

Doppler USS
Other = LFT, PT, ascitic fluid mc+s, CT or MRI of liver, US of hepatic vessels.
Liver biopsy.

Treat cause.

71
Q

Pathophyisology behind ascites

A

Decreased oncotic pressure due to hypoalbuminaemia and increased hydrostatic pressure form portal hypertension

72
Q

3 stages of alcohol liver disease

A

Steatosis (fatty), mainly triglycerides.
Hepatitis (inflammation and necrosis)
Cirrhosis (regenerative nodules, fibrosis, loss of normal architecture)

73
Q

Investigating alcohol liver disease

A 
LFT
Bilirubin
Albumin
gamma-GT
PT
FBC, U+E.

Hepatic USS
Liver biopsy - depends on extent of disease on what you will see. Steatosis –>. hepatitis –> cirrhosis signs.

74
Q

Treatment of alcohol liver disease

A

Lifestyle = REDUCE alcohol consumption. Avoid smoking, reduce weight, nutritional advice.
Pharma = corticosteroids e.g prednisolone.
Assess appropriate for transplant?

75
Q

Other causes/RFx of non alcohol fatty liver disease

A 
Metabolic syndrome/Obesity
T2DM
PCOS
OSA
Hypothyroidism
Drugs e.g. methotrexate, corticosteroids
76
Q

Signs and symptoms of alcohol and non alcohol related fatty liver disease (steatosis/steatohepatitis)

A 
Asymptomatic
Fatigue
Right upper quadrant pain.
Hepatomegaly
Persistent elevation in LFTs!

S+S of cirrhosis:
Pruritus, jaundice, nausea, bruising, gynaecomastia, spider naevi, ascites etc etc

77
Q

LFT in steatosis

A

ALT x3 and are higher than AST levels.

Although AST:ALT ratio is <1

78
Q

LFT in acute alcohol hepatitis

A

AST:ALT ratio >2

79
Q

Management of non alcohol related fatty liver disease

A

LIFESTYLE: avoid alcohol, loose weight, control co-morbidities e.g. DM, HTN.
Secondary care Rx = vitamin E

80
Q

Causes of liver abscesses

A 
Pyogenic = bacteria e.g. E.coli, Klebsiella. Complications of appendicitis, cholangitis, biliary stones.
Amoebic = complication of amoebiasis - Entamoeba histolytica.

RFx = DM, immunocompromised, local malignancies, visit to amoebiasis area.

81
Q

S+S of liver abscess

A 
Fever
Fatigue
Nausea and vomiting
RUQ tenderness
Hepatomegaly
82
Q

Ix for liver abscess

A 
FBC
LFT
Synthetic function - albumin and PT
Blood cultures
CRP and ESR
Serology for E.histolytica.

Abdo USS –> CT.
Guided needle aspiration for mc+s

83
Q

Mx of liver abscess

A

Drainage

ABx - Tazosin

84
Q

Acute pancreatitis causes

A 
Causes:
Gall stones
Ethanol/alcohol
Trauma
Surgery
Malignancy
Autoimmune conditions e.g. SLE
Scorpion venom
Hyperlipidaemia, Hypercalcaemia
Post-endoscopic retrograde cholangiopancreatography.
EMV, mumps and other infections
Drugs e.g. thiazide diuretics
85
Q

Complications of acute pancreatitis

A

Haemorrhagic pancreatitis
Necrosis of pancreas and decline in pancreatic function and infected pancreatic necrosis.
Pseudocyst (disruption in pancreatic ducts lead to collections of pancreatic fluid).
Pancreatic abscess
Fistula e.g. to abdo cavity causing ascites, pericardial cavity causing effusions.

86
Q

Presentation of acute pancreatitis

A

Severe, sudden onset epigastric pain, radiating to back. (intensity and location of pain not correlate with severity)
Worse on movement and alleviated by fetal position.
Nausea and vomiting
Anorexia

O/E:
tachycardia
Hypotension
Abdo tenderness in upper right quadrant, rebound and guarding.
Abdo distension.
Cullen's sign
Grey-Turners sign
87
Q

Cullen’s sign
and
Grey-Turners sign

A

Present in haemorrhage pancreatitis.
Cullens = bluish discolouration around umbilicus.
Grey-Turner’s = bluish bruising-like discolouration on flanks.

88
Q

Ix and Mx for acute pancreatitis

A

Resusciation - oxygen, fluids, analgesia, assess feeding ability/NG tube, Abx e.g. Ciprofloxacin.

Ix to prioritise - Lipase, amylase, haematocrit (sign of necrosis), ABG. Transabdo USS in resus bay, CT of abdomen.

Analgesia - not morphine as can spasm Sphincter of Oddi, use buprenorphine ± intravenous (IV) benzodiazepines.

89
Q

Criteria for acute pancreatitis prognosis

A

Glasgow criteria
Uses info from first 48hrs of admission to predict prognosis. Score greater than 2 = severe pancreatitis likely.

Parameters = PANCREAS
PaO2
Age (>55)
Neutrophils/WCC
Calcium
Renal function (urea)
Enzymes (Lactate dehydroengase)
Albumin
Sugar (blood glucose)
90
Q

Criteria for alcohol induced pancreatitis

A

Ranson score

91
Q

Causes of chronic pancreatitis

A 
ALCOHOL
Smoking
Autoimmune e.g. Sjogren's, primary biliary cirrhosis.
Drugs - oestrogen, thiazide diuretics.
Tropical
Idiopathic
92
Q

S+S of chronic pancreatitis

A

Recurrent, chronic upper epigastric pain. Can radiate to back. Described as deep, severe. Alleviated on sitting forward.
Nausea
Anorexia
Hx of alcohol misuse
Hx of recurrent acute pancreatitis.
Exocrine dysfunction = weight loss (malabsorption), statorrhoea.
Endocrine dysfunction = DM and impaired glucose regulation.

O/E:
Jaundice
Abdo distension

93
Q

2 pathological mechanisms in chronic pancreatitis

A

Endocrine dysfunction from islets of langerhans, failure to produce insulin.
Exocrine dysfunction from acini cells, failure to produce digestive enzymes.

94
Q

Ix chronic pancreatitis

A 
Lab:
FBC
Faecal elastase
U+E
Creatinine
Amylase
Calcium
HbA1c
LFT

Imaging:
Abdominal USS
CT scan

95
Q

Management of chronic pancreatitis

A

Lifestyle advice - avoid smoking and alcohol.
Diet advice - low fat, high protein, high calorie diet
Analgesia - paracetamol, ibuprofen.
Nutritional - replace pancreatic enzymes with Lipase, Creon. Supplement fat soluble vitamins.

Screen for DM
Screen for osteoporosis (malabsorption complication)

96
Q

Dietary and nutritional support in chronic pancreatitis

A

Low fat, high protein, high calorie diet.
Supplement fat soluble vitamins
Pancreatic enzyme supplements.

97
Q

Main complication of chronic pancreatitis

A

Diabetes mellitus.

98
Q

Functions of pancreas

A

Endocrine - Islets of Langerhans produce insulin
Exocrine - acinar cells produce pancreatic fluid
Pancreatic fluid = Lipase, amylase, proteases, bicarbonate and water etc etc

99
Q

Histology of pancreatic cancers

A

Most cancers are exocrine tumours - adenocarcinomas esp infiltrating ductal adenocarcinoma of head/neck/uncinate.

Endocrine cancers = pancreatic neuroendocrine tumours (PET).

100
Q

Risk factors for pancreatic exocrine tumours

A 
Smoking
FHx
Obesity
Chronic pancreatitis
Peutz-Jegher's syndrome
101
Q

Presentation of pancreatic exocrine tumours

A

Epigastric pain, radiating to back. Easing on sitting forward.
Back pain.
Painless, progressive, obstructive jaundice
Weight loss
Anorexia
Steatorrhoea and malabsorption

O/E:
Palpable gallbladder = Courvoisier’s sign.

102
Q

Courvoisier’s sign

A

Palpable gallbladder with painless jaundice.

Cause unlikely to be gallstones therefore Ix for neoplasm.

103
Q

Investigating pancreatic cancer

A

Lab:
FBC, LFT, glucose.
TUMOUR MARKER = CA19-9.

Imaging:
Pancreatic protocol CT scan or PET-CT
Endoscopic US with tissue sampling –> Biopsy histology and cytology.

104
Q

Management of pancreatic cancer

A

Nutritional support - pancreatin
Resection - Whipple’s procedure
Chemotherapy
Pallative care

105
Q

Example of a pancreatic neuroendocrine tumour

A

Insulinoma

Vipoma

106
Q

Biliary colic

A

Right upper quadrant pain, may radiate to intra-scapular region.
Impact of a stone in cystic duct or ampulla of water.

107
Q

Acute cholecystitis

A

RUQ pain + fever/raised WCC
Distension of the gallbladder causing ischaemia.
+ve Murphy’s sign.

108
Q

Ascending cholangitis

A

MEDICAL EMERGENCY!!
Stasis of bile due to obstruction leads to infection (E.coli, Klebsiella).
RUQ pain + fever/raised WCC + Jaundice = CHARCOT’S TRIAD

109
Q

What is Charcot’s triad and when does it occur

A

RUQ pain + fever/raised WCC + jaundice.

In ascending cholangitis (Infection of bile duct)

110
Q

Types of gallstones

A

Cholesterol stones (most common)
Pigment - black or brown.
Mixed

111
Q

What is in bile?

A

Cholesterol, bile pigments (broken down Hb), phospholipids.

112
Q

Cholelithiasis

A

Presence of solid stones in gallbladder

113
Q

Presentation of gallstones

A

Most are asymptomatic.
Biliary colic (most common presentation) - post-prandial, nausea.
Acute cholecystitis
Ascending cholangitis = jaundice.

114
Q

Who gets gallstones // Risk factors

A

Family history, fat, around 40, females.

Obesity, DM,

115
Q

Investigating gallstones

A

FBC, LFT, lipase and amylase.
Abdominal USS shows thickened gallbladder wall, dilated CBD.
ERCP
MRCP (magnetic resonance cholangiopancreatography).

116
Q

Managing gallstones

A

Watch and wait.
Analgesia - pethidine
Laparoscopic cholecystectomy +/- bile duct clearance.

117
Q

Murphy’s sign - what is it and when is it seen?

A

2 fingers over RUQ and patient inspires = pain and pt will stop breathing in. Repeat in left upper quad and no pain.

Seen in acute cholecystitis.

118
Q

Ix, Mx and complications for ascending cholangitis

A

ABC (if all there make diagnosis if only A+ B or C suspected it)
A = systemic inflammation (fever, elevated WCC or CRP)
B = Cholestasis (Jaundice abnormal LFTs)
C = Imaging KUB XR/USS or CT or MRCP (biliary dilation, evidence of gallstones)

Other Ix = U+E, amylase, blood cultures.

Mx = Resuscitation. Broad spec ABx (metronidazole + ceftriaxone), emergency biliary drainage.

Cx = sepsis/septic shock, AKI, liver abscess, liver failure.

119
Q

What conditions are associated with primary sclerosis cholangitis

A

Inflammatory bowel disease (UC and Crohn’s)
Hepato-biliary malignancies e.g. HCC
Colorectal cancer.

120
Q

Pathophysiology behind primary sclerosis cholangitis

A

Chronic, cholestatic liver disease due to inflammation and fibrosis of intrahepatic and extra hepatic bile ducts.
Leads to bile duct stricture formation.
Progressive disorder which can cause development of cirrhosis, portal hypertension and hepatic decompensation.

121
Q

Presentation of primary sclerosis cholangitis

A

Hx of IBD
RUQ pain
Jaundice
Weight loss, fatigue.

O/E:
Hepatomegaly
Jaundice (yellowing of sclera)

122
Q

Ix for primary sclerosis cholangitis

A 
LFT - high ALP, ALT. 
Immunoglobulins - high IgG
Autoantibodies e.g. p-ANCA
Imaging: Liver USS, MRCP - shows multifocal strictures and dilations of bile ducts.
Biopsy to stage.
123
Q

Mx of primary sclerosis cholangitis

A

Lifestyle advice = avoid alcohol.
Supplementation for fat soluble vitamins
Pruritus = Colestyramine.
Bile acid analogue = Ursodeoxycholic acid, improve LFT not life expectancy.
Annual colonoscopy for colorectal cancer.
Liver transplant

124
Q

Another name for primary biliary cirrhosis

A

Primary biliary cholangitis

125
Q

Pathophysiology behind biliary cholangitis

A

Chronic autoimmune granulomatous inflammation damages interlobular bile ducts (canals of Hering) leading to cholestasis, fibrosis, cirrhosis and portal hypertension.

126
Q

Which autoantibody is most highly associated with primary biliary cholangitis

A

Antimitochondrial antibodies (AMA)

127
Q

Sterotypical patient presenting with primary biliary cholangitis

A

50yr old woman who’s sister has got similar symptoms.

128
Q

S+S of primary biliary cholangitis

A

Fatigue
Pruritus
RUQ pain

O/E:
jaundice
Xanthelasma
hepatomegaly

129
Q

Most common autoimmune conditions associated with primary biliary cholangitis

A

Sjorgren’s syndrome - dry eyes, dry mouth.

Thyroid disease

130
Q

Criteria to diagnose primary biliary cholangitis

A

Biochemical evidence fo cholestasis (raised ALP).
AMA +ve
Biopsy shows evidence of interlobular bile duct destruction.

131
Q

Ix for primary biliary cholangitis

A 
Biochemical:
LFT - raised ALP, raised gamma-GT
Autoantibodies - AMA +
Thyroid function test
Immunoglobulins - raised IgM
Cholesterol raised
In later disease - raised bilirubin

Imaging
USS to exclude other causes of cholestasis. MRCP/cholangiography.
Biopsy

132
Q

Mx for primary biliary cholangitis

A

Pruritus = cholestyramine
Bile acid analogue = Ursodeoxycholic acid
Immunosuppression = Prednisolone

Curative = transplant

133
Q

Differences between primary sclerosis cholangitis and primary biliary cholangitis

A

PSC = male, sclerosis, intrahepatic and extrahepatic ducts, associated with p-ANCA autoantibodies, common in UC and colorectal cancer patients.

PBC = female, interlobular hepatic bile duct involvement, associated with AMA autoantibodies, common in Sjorgren’s and thyroid disease patients.

134
Q

Name a cancer of the biliary tree 🌲 and list some facts about it.

A

Cholangiocarcinoma / Klatskin’s tumour:

  • Ductal adenocarcinomas
  • Associated with liver flukes so more common in SE Asia.
  • Jaundice, RUQ pain, pruritus, hepatomegaly, weight loss, cholestasis (raised ALP).
  • CA19-9 and CEA raised.
  • Rx = resection.
135
Q

Where is bile made and where is stored

A

Made in liver, stored and concetrated in gall bladder.

136
Q

What is the poo and wee like in cholestasis?

A

Dark urine, pale stools - conjugated hyperbilirubinaemia.

Conjugated bilirubin can’t be excreted in faeces so reflexed back into systemic circulation and excreted in urine.

137
Q

Blood test results in cholestasis

A 
Raised ALP (x3)
Raised serum bilirubin
138
Q

Main symptoms of cholestasis and their treatment

A

Jaundice
Dark urine, pale stools
Pruritus - cholestyramine

139
Q

2 types of causes for jaundice

A

Unconjugated hyperbilirubinaemia - unconjugated bilirubin is water insoluble. Caused by: over production from haemolysis, poor hepatic uptake from ischaemic hepatitis, Gilbert’s syndrome.

Conjugated hyperbilirubinaemia - conjugated bilirubin is soluble so dark urine. Caused by: hepatocellular dysfunction from cirrhosis, haemachromatosis, hepatitis, Budd-Chiari and cholestasis from PBC, PSC, pancreatic cancer.

140
Q

What type of bilirubin is found in urine and faeces

A 
Urine = urobilinogen
Faeces = stercobilinogen.
141
Q

Describe hepatorenal syndrome

A
  • Renal failure with severe liver disease.
  • Poor prognosis.
  • Renal vasoconstriction, portal hypertension.
  • Diagnosis must exclude cause of renal failure.
  • Mx = terlipression, dialysis, TIPS
142
Q

Causes of ascites

A

Cirrhosis and liver disease
Heart failure
Nephrotic syndrome
Ovarian malignancy

143
Q

2 signs O/E for ascites

A

Fluid thrill

Shifting dullness

144
Q

Complications of ascites

A

Spontaneous bacterial peritonitis

Hepatorenal syndrome

145
Q

Why would someone with chronic liver disease get prophylactic ABx

A

For spontaneous bacterial peritonitis - which has a high mortality rate.

146
Q

CFx, common organisms and Mx for SBP

A

CFx = abdo pain, fever, vomiting. O/E: guarding, rebound tenderness, pain on palpation diffusely over abdo.
Ix = paracentesis (cloudy appearance, high neutrophils, gram-staining and culture..
Mx = ABx e.g. ceftriaxone
Common organisms = E.coli, S.aureus, Klebsiella.

147
Q

Ix for Budd-Chiari

A

Doppler USS

148
Q

Biopsy of steatohepatitis

A

Fat inclusions and cells are swollen

if alcohol related = mallory bodies

149
Q

Complications of HBV

A 
Chronic = HCC, Cirrhosis.
Acute = Fulminant hepatic necrosis - increasing INR, need transplant!
150
Q

Autoimmune hepatitis and associated antibodies

A

Type 1 = most common. ANA (antinuclear antibody) +ve, ASM (anti smooth muscle) +ve.
Type 2 = anti-LKM1, rapidly progressive.
Type 3 = anti-SLA

151
Q

Differentials for acute pancreatitis

A 
Abdo aorta aneurysm
PUD
Intestinal obstruction
Cholangitis
Mesenteric ischaemia
152
Q

What is TIPS

A

Transjugular intrahepatic portosystemic shunt.

Shunt form hepatic to portal vein to relieve pressure.

153
Q

Surgical/endoscopic interventions for a variceal upper GI bleed

A

band ligation
balloon tamponade
sclerotherapy
injection with adhesives/glue

154
Q

Criteria for HCC and components of score

A

CLIP (Cancer of the liver Italian programme)

Scores for Child-Pugh stage, Tumour morphology, Extent/presence of portal vein thrombosis, Serum alpha fetoprotein.

APhase 3b flashcards (16 decks)

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