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2a - SBCS > Liver > Flashcards

Liver Flashcards

1
Q

Functions of the Liver

A

storage
Protein synthesis (albumin)
Carb & lipid metabolism
Immunity
Detoxification and excretion

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2
Q

Causes of acute liver injury

A

Viral: hepatitis (A/B)
Drugs - paracetamol overdose , Ab
Vascular - budd chiari
Obstruction
congestion

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3
Q

Causes of chronic liver injury

A

Alcohol
Viral (B,C)
Metabolic - wilson’s
Autoimmune - sclerosing cholangitis

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4
Q

Presentation of acute liver injury

A

Malaise
Nausea
Anorexia
Jaundice

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5
Q

Presentation of chronic liver injury

A

Ascites
Oedema
Haematemesis
Anorexia
Easy bruising

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6
Q

Define liver failure

A

Where the liver loses its ability to repair and regenerate leading to decompensation

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7
Q

What are the 3 markers of liver function

A

Serum
* Bilirubin (high = damage)
* Albumin (low=damage)
* Prothrombin time (high=damage)

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8
Q

How are serum liver enzymes used in the investigation of liver function

A
  • They’re non specific to liver function but can show the likelihood of liver damage
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9
Q

Give examples of serum enzymes used in LFTs

A
  • Cholestatic: alkaline phosphatase, gamma-GT
  • Hepatocellular: transaminases - Aspartate transaminase (AST) and alanine transaminase (ALT)
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10
Q

What are the 3 types of jaundice and state whether they’re unconjugated or conjugated

A
  • Prehaptic (unconjugated)
  • Hepatic (conjugated)
  • Post-hepatic (conjugated)
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11
Q

Give 2 causes of prehepatic jaundice

A
  • Haemolytic anaemias
  • Gilbert’s syndrome
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12
Q

List 3 causes of hepatic jaundice

A
  • Hepatitis
  • Neoplasm
  • Ischaemia
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13
Q

Give 2 causes of post-hepatic jaundice

A
  • Gallstone
  • Stricture
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14
Q

Describe the urine and stool sample for conjugated jaundice

A
  • Dark urine
  • Pale stool
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15
Q

Which type of jaundice may experience itching

A

Conjugated

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16
Q

Signs and symptoms of acute liver failure

A
  • Jaundice
  • Coagulopathy
  • Hepatic encephalopathy - altered mood, dyspraxia etc
  • Renal failure
  • Hypoalbuminaemia
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17
Q

Describe the investigation of acute liver failure

A
  • LFTs - raised ALT/AST and PT/INR
  • USS
  • FBC - Leukocytosis. anaemia, thrombocytopenia
  • Microbiology to rule out infection - blood culture, peritoneal tap
  • ABG - metabolic acidosis
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18
Q

Describe the management of acute LF

A
  • Treat underlying cause and complications
  • ABCDE
  • Anaglesia
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19
Q

State complications of LD and how each would be treated

A
  • Encephalopathy - lactulose
  • Cerebral oedema - mannitol
  • Haemorrhage - Vit K
  • Ascites - diuretics
  • Sepsis - sepsis 6
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20
Q

Presentation of chronic liver disease

A
  • spider naevi - dilated blood vessel due to excess oestrogen
  • Splenomegaly
  • Palmar erythema - red palm
  • Jaundice
  • Abdo distension
  • Leukonychia (white nails)
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21
Q

Describe the investigation of CLD

A
  • GS: Liver Biopsy
  • Raised AST and ALT
  • FBC - low albumin, thrombocytopenia and prolonged INR
  • Abdo USS - nodularity, atrophy, signs of advanced cirrhosis
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22
Q

Management of CLD

A
  • Treat complications
  • Liver transplant
  • Lifestyle modifications
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23
Q

What is Gilbert’s syndrome

A
  • Auto Rec inheritance of UGT1A1
  • affects the liver’s ability to metabolise bilirubin
  • Raised unconjugated bilirubin
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24
Q

How does Gilbert’s syndrome typically present

A

Painless jaundice at a young age

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25
Q

What are ascites

A

Accumulated free fluid in the abdo cavity (peritoneal)

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26
Q

Causes of ascites

A
  • infection - TB
  • Neoplasia - ovary, pancreas
  • congestive HF, pericarditis - fluid leaks out
  • low albumin (nephrotic syndrome)
  • liver cirrhosis
  • Budd-Chiari syndrome
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27
Q

Signs and symptoms of ascites

A
  • Abdo distension
  • Shifting dullness (flanks)
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28
Q

Describe the investigation of ascites

A
  • Shifting dullness
    • CT/USS/MRI - diagnostic
  • Ascitic fluid tap - cytology (high WBC) and protein levels
  • Serum ascites albumin gradient:
  • Transudate: >11g/L, clear fluid (increased HP, portal HTN)
  • Exudate: <11g/L, cloudy fluid (inflammation mediated)
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29
Q

How are ascites treated

A
  • Treat underlying cause - e.g. Ab for bacterial infection
  • Diuretics to increase renal Na excretion (e.g. spironolactone)
  • Paracentesis - drain fluid
  • reduce dietary sodium
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30
Q

Describe the ascites percussion test

A
  • Percuss centrally to laterally until dull sound
  • Keep finger at dull spot and ask patient to lean to opposite side
  • If the dullness is fluid , it will have moved and the previously dull area will be resonant
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31
Q

Describe the progression of alcoholic liver disease

A

1) Alcohol related fatty liver - reversible
2) Alcoholic hepatitis - usually reversible
3) Cirrhosis - scar tissue

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32
Q

What is the recommended alcohol consumption per week

A

14 units
No more than 5 units per day

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33
Q

What questionnaires can be used to screen for alcohol dependency

A

1) CAGE (2<) - Cut down, Annoyed, Guilty, Eye opener
2) AUDIT - MCQ, 8/10 = harmful use

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34
Q

Describe the CAGE questionnaire

A
  • should Cut down
  • are people Annoyed by your drinking
  • feel Guilty about drinking
  • you drink in the morning (eye opener)
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35
Q

Signs and symptoms of ALD

A
  • Alcohol dependency
  • Jaundice
  • Spider naevi
  • Hepatomegaly
  • Palmar erythema - red palms
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36
Q

Describe the investigation of ALD

A
  • FBC - macrocytic non-megaloblastic anaemia
  • LFTs - ^ gamma-GT, ^ AST/ALT, low albumin
  • Elevated prothrombin time
  • Biopsy - inflammation, necrosis, mallory bodies
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37
Q

Describe the management of ALD

A
  • alcohol abstinence
  • Diet - vitamins and high protein
  • Treat complications of cirrhosis - ascites, portal HTN
  • Short term steroids
  • Liver transplant
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38
Q

What is delirium tremens

A

Medical emergency associated with alcohol withdrawal

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39
Q

Describe the presentation of delirium tremens

A
  • Ataxia - uncoordinated movements
  • Tremors
  • Severe agitation
  • Seizures
  • Delusions and hallucinations
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40
Q

Treatment for delirium tremens

A

Chlordiazepoxide
Diazepam (less common)

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41
Q

How can ALD cause Wernicke-Korsakoff Syndrome (WKS)

A
  • Excess alcohol leads to thiamine (Vit B1) deficiency
  • B1 is poorly absorbed in the presence of alcohol
  • 1st Wernicke’s encephalopathy then Korsakoff’s syndrome
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42
Q

Give 3 features of Wernicke encephalopathy

A
  • Confusions
  • Oculomotor disturbances
  • Ataxia
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43
Q

Give 2 features of Korsakoff’s syndrome

A
  • Memory impairment - unable to form new memories and unable to recall past memories
  • Behaviour changes
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44
Q

Give 3 RFs of ALD

A

Alcohol
Obesity
Smoking

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45
Q

Give 4 RFs of Non alcoholic fatty LD

A
  • Obesity
  • T2DM
  • HTN
  • Drugs - NSAIDS
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46
Q

Describe the stages of NAFLD

A
  1. NAFLD
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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47
Q

How does NAFLD typically present

A
  • Usually asymptomatic and found incidentally
  • Severe = signs of LF
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48
Q

Describe the investigation of NAFLD

A
  • Liver biopsy
  • Abnormal LFTs - particularly raised gamma GT
  • Abdo US - confirm fatty liver
  • Non-invasive liver screen
  • Enhanced liver fibrosis blood test
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49
Q

Describe the management of NAFLD

A
  • Weight loss
  • Control diabetes, HTN and cholesterol
  • exercise
  • Vit E
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50
Q

What is viral hepatitis

A

Inflammation of the liver as a result of viral replication within hepatocytes

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51
Q

What is the most common viral hepatitis

A

Hep A

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52
Q

What type of virus is Hep A

A

Acute RNA picornavirus

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53
Q

How is Hep A transmitted

A

Faeco-oral - usually contaminated water and food (uncooked shellfish)

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54
Q

Give 3 RFs of Hep A

A
  • Overcrowding
  • Shellfish
  • Travel
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55
Q

Describe the presentation of Hep A

A

Prodromal (1-2w):
* N+V, Fever, Malaise
Icteric (up to 3m):
* Jaundice, dark urine, pale stools

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56
Q

Describe the investigation of Hep A (HAV)

A
  • LFTs - ^ bilirubin
  • Serology - HAV IgM = acute infection, IgG anti-HAV
  • Bloods - raised ESR
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57
Q

How is Hep A treated

A
  • Self-limiting: usually clears up within 3 months
  • Travellers vaccine available
  • Rest, analgesia
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58
Q

What type of virus is Hep C (HCV)

A
  • RNA flavivirus
  • can be acute or chronic
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59
Q

How is HCV transmitted

A
  • Blood
  • Bodily fluids - sex
  • IV drug use
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60
Q

Describe the presentation of acute HCV

A
  • Usually Asymptomatic
  • May have flu like symptoms - N+V, fever, diarrhoea
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61
Q

How does chronic HCV present

A

Chronic liver signs and hepatosplenomegaly

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62
Q

Describe the diagnosis of HCV

A

Serology:
* HCV RNA - active infection
* HCV Ab +ve = active/ resolved

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63
Q

Describe the management of HCV

A
  • Direct acting antivirals (DAA) + Ribavirin
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64
Q

Give 2 complications of HCV

A
  • Liver cirrhosis
  • Hepatocellular carcinoma
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65
Q

What type of virus is Hep E (HEV)

A

Acute single stranded RNA

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66
Q

How is HEV transmitted

A

Faeco-oral spread
* Undercooked pork
* Contaminated water

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67
Q

Presentation of HEV

A

Mild illness usually asymptomatic

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68
Q

Describe the investigation of HEV

A

HEV IgM = acute infection
HEV RNA

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69
Q

How is HEV treated

A
  • Self limiting infection so usually clears up within a month
  • Supportive
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70
Q

Who is particularly susceptible to complications following HEV

A
  • Immunocompromised - chronic LF
  • Pregnancy - increased mortality
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71
Q

What type of virus is Hep B (HBV)

A
  • Double stranded DNA virus
  • Acute and chronic
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72
Q

How is HBV transmitted

A
  • Blood
  • Bodily fluids - sex
  • Needles - IVDU, tattoos
  • Vertical - mother to child
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73
Q

Give 3 RFs of HBV

A
  • Healthcare workers
  • Dialysis patients
  • IVDU
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74
Q

Describe the presentation of HBV

A
  • Prodromal (1-2w) - n+v, RUQ pain, fever
  • Icteric (up to 6m) - jaundice, dark urine, arthralgia, pale stool
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75
Q

Describe the HBV serology

A
  • Surface antigen (HBsAg) - active infection
  • Surface antibody (HBsAb) - past/current infection/ vaccine
  • Core Ab (HBcAb) - past/current infection
  • IgM = active/ recent + chronic
  • IgG = resolved/ chronic
  • E antigen (HBeAg) - marker of viral replication and implies high infectivity
  • HBeAb - chronic or been through active phase
  • HBV DNA - direct count of viral load
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76
Q

How does HBcIgM differ in acute and chronic infection

A

Acute = high titre
Chronic = low titre

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77
Q

Describe the management of HBV

A
  • Vaccination HBsAg - 3 doses
  • Anti-viral meds - Pegylated interferon alpha 2a
  • Entecavir (anti-viral)
  • Liver transplant
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78
Q

What type of virus is Hep D (HDV)

A

SSRNA virus

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79
Q

What is the only way HDV can survive

A

Only survive in patients who also have HBV

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80
Q

Describe the pathophysiology of HDV

A
  • It attaches itself to HBsAg (can’t survive without this)
  • HBV + HBD = greater chance of cirrhosis/ HCC
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81
Q

Describe the serology of HDV

A

Manifests as co-infection
* IgM HDV
* IgM HBV

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82
Q

What is autoimmune hepatitis

A

Possible genetic predisposition triggered by a viral infection that causes an autoimmune response against hepatocytes

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83
Q

What are the 2 types of autoimmune hepatitis

A

Type 1 (80%) - adult females (>45)
Type 2 - younger females

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84
Q

What autoantibodies are involved in type 1 autoimmune hepatitis

A
  • Anti-nuclear Ab (ANA)
  • Anti-smooth muscle Ab (ASMA)
  • Anti-soluble liver Ag (ASLA)
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85
Q

What autoantibodies are involved in type 2 autoimmune hepatitis

A
  • Anti-Liver Kidney Microsomes-1 (ALKM1)
  • Anti-Liver Cytosol Antigen Type 1 (ALC1)
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86
Q

Describe the presentation of autoimmune hepatitis

A
  • May be asymptomatic or have features of liver disease
  • Fatigue in type 1 following menopause
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87
Q

How is AIH investigated

A
  • Serology - autoantibodies
  • LFTs - elevated ALT and AST with normal/ mildly elevated ALP
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88
Q

Treatment for AIH

A
  • Steroids (prednisolone) + immunosuppressants (azathioprine)
  • Liver transplant
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89
Q

Describe the CAGE questionnaire

A
  • should Cut down
  • are people Annoyed by your drinking
  • feel Guilty about drinking
  • you drink in the morning (eye
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90
Q

What is biliary colic

A

Intermittent right upper quadrant pain caused by temporary obstruction of gallstones irritating the bile ducts

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91
Q

Describe the composition of gallstones

A
  • Form from concentrated bile in the bile duct
  • Most are made of cholesterol but can also be made out of pigment or mixed
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92
Q

Give 5 RFs for gallstones

A

5 Fs:
* Female
* Fat (overweight)
* Forty (or older)
* Fair (Caucasian)
* Fertile (pre-menopausal)

93
Q

What is acute cholecystitis

A

Acute inflammation of the gallbladder (95% involve gallstones)

94
Q

Describe the presentation of gallstones

A
  • Colicky RUQ pain
  • Worse after eating fatty meals
  • N+V
  • Episodes of pain for 30+ mins
95
Q

Describe the investigation of gallstones

A
  • 1st line: Ultrasound - stones, duct dilation
  • Raised alkaline phosphatase - non specific marker
96
Q

How are gallstones treated

A
  • NSAIDS for mild pain (diclofenac)
  • Cholecystectomy
  • ERCP - remove stones
  • Reduced fatty diet
97
Q

Describe the presentation of acute cholecystitis

A
  • RUQ pain which may radiate to right shoulder
  • Fever
  • +ve Murphy’s sign
98
Q

Describe a +ve murphy’s sign

A
  • Ask patient to breathe in and hold a deep breath while palpating the RUQ
  • Severe pain = +ve
99
Q

Describe the investigation of acute cholecystitis

A
  • Abdo ultrasound - Fluid around GB, stones/sludge in GB,
    thickened GB wall (>3mm)
  • LFT - normal
  • FBC - Leukocytosis and neutrophilia
  • Magnetic resonance cholangiopancreatography (MRCP) - if common bile duct stone is suspected but not seen in US
100
Q

Treatment for cholecystitis

A
  • Before surgery: IV fluids, analgesia, IV Ab if needed
  • Laproscopic cholecystectomy within 1 week (usually 72h)
101
Q

What is acute cholangitis

A

Inflammation of the bile ducts (85% due to gallstones)

102
Q

Explain how acute cholangitis increase the risk of sepsis

A
  • Prolonged bile duct blockage leads to bile stasis
  • Bacteria (typically E.coli) from the duodenum climbs up through the ampulla of Vater and causes biliary tree infection
103
Q

Describe the presentation of acute cholangitis

A
  • Charcot’s triad: fever, jaundice, RUQ pain
  • Obstructive: Reynolds pentad - Charcot’s triad + altered mental state and hypotension (sepsis)
104
Q

Investigations of acute cholangitis

A
  • FBC - leukocytosis
    LFTs - raised ALP and bilirubin
  • CRP raised
  • Endoscopic abdo ultrasound - common bile duct dilation and gallstones
  • endoscopic retrograde cholangiopancreatography
105
Q

Treatment of acute cholangitis

A
  • Treat sepsis - IV fluids + Abx
  • ERCP and stenting to clear blockage
  • Cholecystectomy
106
Q

What is primary biliary cholangitis (cirrhosis)

A

Condition where the immune system attacks the small bile ducts within the liver

107
Q

Explain the pathophysiology of PBC

A
  • Immune system attacks intralobar bile ducts (canals of Hering)
  • This causes obstruction of the outflow of bile (cholestasis)
  • Back-pressure of bile obstruction and overall disease process leads to fibrosis, cirrhosis and LF
108
Q

Give 3 RFs for PBC

A
  • 40-50 y/o women
  • Other autoimmune conditions (e.g. coeliac)
  • Rheumatoid conditions (e.g. sjogrens and arthritis)
109
Q

Describe the presentation of PBC

A
  • Pruritus - itchy skin (bile acids)
  • Fatigue
  • Jaundice (bilirubin)
  • Xanthelasma - cholesterol deposits in skin
  • Pale stools
  • GI disturbances and abdo pain (lack of bile acids)
  • Signs of cirrhosis and LF
110
Q

Dx of PBC

A
  • LFT - raised ALP, bilirubin
  • Serology: raised AMA (anti-mitochondrial Ab)
  • Liver biopsy - diagnose and stage disease
  • Raised IgM
111
Q

Describe the management of PBC

A
  • 1st: ursodeoxycholic acid - reduces intestinal absorption of cholesterol
  • Colestyramine - decreases bile acid reabsorption in SI helps with pruritus
  • Liver transplant in end stage
  • Immunosuppression - with steroids
112
Q

What is primary sclerosing cholangitis

A

Autoimmune chronic LD where the intrahepatic or extra-hepatic bile ducts become inflamed, strictured and fibrotic

113
Q

Give 4 RFs of PSC

A
  • Ulcerative colitis - strong link (70%)
  • Male
  • age 40-50
  • FHx
114
Q

Describe the presentation of PSC

A
  • Initially asymptomatic
  • Pruritus
  • Fatigue
  • Jaundice
  • Chronic RUQ pain
115
Q

How is PSC investigated

A
  • LFT - raised ALP, GGT
  • Autoantibodies: p-ANCA, antinuclear Ab
  • GS: MRCP
116
Q

Describe the management of PSC

A
  • Colestyramine for pruritus
  • ERCP can be used to dilate and stent strictures
  • Liver transplant
  • Fat soluble vitamin supplements
117
Q

Give 3 complications of PSC

A
  • Fat soluble deficiencies
  • Acute bacterial cholangitis
  • Cholangiocarcinoma
118
Q

What is liver cirrhosis

A
  • The result of chronic inflammation and damage to liver cells
  • When liver cells are damaged they’re replaced with fibrosis and nodules of scar tissue from within the liver
  • Irreversible
119
Q

Give 4 common causes of liver cirrhosis

A
  • ALD
  • NAFLD
  • Hep B
  • Hep C
120
Q

Give 3 metabolic conditions that cause liver cirrhosis

A
  • Haemochromatosis
  • Wilson’s disease
  • Alpha 1 antitrypsin deficiency
121
Q

Signs and symptoms of liver cirrhosis

A
  • Jaundice
  • Hepatomegaly
  • Splenomegaly
  • Spider naevi
  • Palmar erythema
  • Ascites
122
Q

Describe the investigation of cirrhosis

A
  • US and CT - splenomegaly, nodularity, enlarged portal vein
  • Biopsy - diagnostic
  • Bloods - low albumin, high INR
123
Q

Name and describe the score used to indicate the severity of cirrhosis

A

Child-Pugh score
* 5 factors: bilirubin, albumin, INR, ascites & encephalopathy
* Give score of 1/2/3

124
Q

Describe the management of cirrhosis

A
  • Liver transplant
  • Alcohol abstinence
  • Treat complications
  • Screen for hepatocellular carcinoma every 6m (marker=AFP)
125
Q

Give 5 complications of cirrhosis

A
  • Ascites and spontaneous bacterial peritonitis
  • Portal HTN
  • Varices/ variceal bleeding
  • Hepatocellular carcinoma
  • Malnutrition
126
Q

What is portal HTN

A

Elevated pressure in the portal venous system

127
Q

Give a prehepatic cause of portal HTN

A

Portal vein thrombosis

128
Q

Give 3 intrahepatic causes of portal HTN

A
  • Cirrhosis (mc)
  • Schistosomiasis (parasitic disease)
  • Budd Chiari syndrome
129
Q

Explain how cirrhosis causes portal HTN

A
  • Cirrhosis increases resistance of blood flow in liver
  • Results in increased back-pressure into portal system = portal HTN
130
Q

How does portal HTN typically present

A
  • Mostly asymptomatic
  • Can present with oesophageal varices rupture
131
Q

What are oesophageal varices

A
  • Dilated and tortuous collateral blood vessels
  • Direct consequence of portal HTN
132
Q

What is a DDx of oesophageal varices and how would they be distinguished

A

Mallory Weiss tear - acute Hx
Varices - long Hx of alcoholism/ cirrhosis

133
Q

What is the GS investigation for oesophageal varices

A

Upper GI endoscopy

134
Q

How are stable (non-bleeding) varices treated

A
  • Non-selective BB (e.g. propranolol + nitrates) - reduce portal HTN
  • Elastic band ligation
  • Injection of sclerosant
135
Q

How is a ruptured oesophageal varices treated

A
  • Resuscitation: ADH analogue (e.g IV terlipressin) - vasoconstriction = slow bleeding
  • Variceal banding
  • Sclerotherapy
  • Transjugular intra-hepatic portosystemic shunt (TIPS) - decrease portal pressure by diverting blood
136
Q

What are the signs of a ruptured oesophageal varices

A
  • Haematemesis (coffee ground)
  • Melena
137
Q

What is acute pancreatitis

A
  • Acute inflammation of the pancreas
138
Q

What are the 3 main RFs of acute pancreatitis

A
  • Gallstones
  • Alcohol
  • Post-ERCP
139
Q

Describe the pathophysiology of gallstones pancreatitis

A
  • Gallstones get trapped at the ampulla of vater which blocks the flow of bile and pancreatic juices into duodenum
  • Reflux of bile into pancreatic duct and prevention of pancreatic enzymes being secreted results in inflammation
  • Autodigestion of pancreas if host defences against pancreatic enzymes (trypsin) are overwhelmed
140
Q

How does alcohol cause pancreatitis

A

Alcohol is directly toxic to pancreatic cells
* mc in men and young ppl

141
Q

Causes of pancreatitis
I get smashed

A
  • Idiopathic
  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroid use
  • Mumps
  • Autoimmune
  • Scorpion stings
  • Hypercalcemia/ hyperlipidaemia
  • ERCP
  • Drugs
142
Q

Name 3 drugs that can cause pancreatitis

A

Furosemide
mesalazine
Thiazide diuretic
Azathioprine

143
Q

Describe the presentation of acute pancreatitis

A
  • Severe epigastric pain that may radiate to the back
  • Tachycardia
  • Fever
  • N+V
  • Jaundice
  • Grey turner sign (flank bruising)
  • Cullen sign (Periumbilical bruising)
144
Q

Describe how acute pancreatitis is investigated

A
  • raised serum amylase
  • raised serum lipase (GS, more specific)
  • Raised CRP - level of inflammation
  • LFTs - raised ALP suggests gallstones as cause
  • US - assess for gallstones
145
Q

What are 2 scoring systems for acute pancreatitis

A
  • APACHE 2
  • Glasgow score
146
Q

Describe the glasgow score

A
  • Assess severity of pancreatitis
  • Gives numerical score for each factor
  • 3< = severe pancreatitis
    P – Pa02
    A – Age > 55
    N – Neutrophils
    C – Calcium
    R – uRea
    E – Enzymes
    A – Albumin
    S – Sugar
147
Q

Describe the treatment of acute pancreatitis

A
  • Nil by mouth
  • IV fluid
  • Analgesia - morphine
  • Treat GS - ERCP
  • Treat complications (eg drain large collections)
148
Q

Give 4 complications of acute pancreatitis

A
  • Necrosis
  • Chronic pancreatitis
  • Pseudocysts - same presentation
  • Acute peripancreatic fluid collections
149
Q

What is chronic pancreatitis

A
  • Chronic inflammation of the pancreas
  • 3m Hx of pancreatic deterioration
150
Q

Describe the pathophysiology of chronic pancreatitis

A
  • Persistent inflammation of the pancreas due to changes in pancreatic structure
  • Fibrosis and reduced function of pancreas
151
Q

Give 4 causes of chronic pancreatitis

A
  • Alcohol (mc)
  • CKD
  • genetics - CF and haemochromatosis
  • Recurrent acute pancreatitis
152
Q

Describe presentation of chronic pancreatitis

A
  • Epigastric pain radiation to back
  • Similar Sx to acute p but less intense and longer lasting
  • Sx worse after alcohol and better on leaning forward
  • Steatorrhea (fat in stool)
  • weight loss and malnutrition
153
Q

Describe the investigation of chronic pancreatitis

A
  • Serum amylase and lipase unlikely to be high in severe cases
  • MRI/CT abdo - pancreatic calcifications, ductal dilation
  • transabdo US - ductal/ parenchymal abnormalities, fibrosis
  • MRCP - used if CT is inconclusive, alternating dilation and stenosis of pancreatic ducts
  • ERCP - chain of lakes ( tortuous and dilated pancreatic duct)
154
Q

How is chronic pancreatitis treated

A
  • Alcohol cessation
  • pancreatic enzyme supplements - e.g. pancreatin with PPi (omeprazole) to increase absorption
  • Surgery
  • Simple analgesia
155
Q

How can chronic pancreatitis cause steatorrhea

A
  • Lack of pancreatic enzymes (lipase)
  • Malabsorption of fat
  • Steatorrhea
  • Deficiency in fat soluble vitamins
156
Q

What condition can develop as a result of loss of endocrine function in chronic pancreatitis

A

DM due to lack of insulin

157
Q

What is peritonitis

A

Inflamed peritoneal cavity

158
Q

What is spontaneous bacterial peritonitis

A

Infection in the ascitic fluid and peritoneal lining

159
Q

Give 3 bacteria that cause SBP

A
  • Gram -ve: E.coli, klebsiella pneumoniae
  • Gram +ve: Staph aureus (cocci)
160
Q

Describe the signs and symptoms of peritonitis

A
  • Sudden severe abdo pain
  • Guarding
  • May have ascites
  • Fever
161
Q

Describe the investigation of peritonitis

A
  • Ascitic tap - raised ascitic neutrophilia
  • Blood cultures - causative organism
  • FBC - anaemia, leukocytosis
162
Q

How is SBP treated

A
  • ABCDE
  • IV Abx (eg cefotaxime or vancomycin if sepsis)
  • Iv fluids/ albumin
  • Paracentesis - remove peritoneal fluid through needle
163
Q

What is a complication of SBP

A

septicaemia

164
Q

What is hepatic encephalopathy

A

Build up of toxins (ammonia) that affect the brain

165
Q

Why does hepatic encephalopathy occur in liver cirrhosis

A
  • Functional impairment of liver cells prevents ammonia being metabolised into harmless waste products
  • Collateral vessels between portal and systemic circulation mean that ammonia bypasses liver and enters systemic system directly
166
Q

Give 4 ways which hepatic encephalopathy presents

A
  • Reduced consciousness
  • Confusion
  • Memory problems
  • Mood/ personality changes
167
Q

Give 4 things that can trigger the onset of hepatic encephalopathy

A
  • Constipation
  • GI bleed
  • Electrolyte imbalance
  • Sedative meds
168
Q

How is hepatic encephalopathy treated

A
  • Laxatives (i.e. lactulose) - promote excretion of ammonia
  • Ab (i.e. rifaximin) - reduce n.o intestinal bacteria
169
Q

What is haemochromatosis

A

Genetic disorder that causes the body to absorb and store excess iron

170
Q

What causes haemochromatosis

A

Autosomal recessive inheritance of mutated human haemochromatosis gene (HFE) on chrom 6

171
Q

Give 4 RFs of haemochromatosis

A
  • Middle age (40<)
  • Male
  • FHx
  • White ancestry
172
Q

Explain the pathophysiology of haemochromatosis

A

Excess iron is absorbed by the body and deposited in multiple organs

173
Q

Describe the presentation of haemochromatosis

A
  • Joint pain
  • Fatigue
  • Sexual problems (e.g. amenorrhoea) - hypogonadism
  • Bronze/ slate-grey discolouration
174
Q

Describe the investigation of haemochromatosis

A
  • Raised serum ferritin and transferrin
  • Liver biopsy (prior GS but no longer necessary due to genetic testing)
  • Genetic testing
175
Q

How is haemochromatosis treated

A
  • Venesection - weekly removing blood
  • Iron chelation (deferasirox)
  • Lifestyle: limit Vit C
176
Q

Complications haemochromatosis

A
  • T1DM - Fe affects function of pancreas
  • Liver cirrhosis
  • Hypogonadism
  • Hypothyroidism
  • HCC
177
Q

Give a contraindication to venesection

A

Anaemia

178
Q

What is Wilson’s disease

A

Excessive accumulation of copper in the body and tissues

179
Q

What causes wilson’s disease

A
  • Autosomal recessive mutation of ATP7B copper binding protein on chromosome 13
  • Results in reduced removal of Cu in liver
180
Q

Give 2 RFs of Wilson’s disease

A
  • Male
  • FHx
181
Q

Describe the hepatic presentation of Wilson’s disease

A

Hx of chronic hepatitis
cirrhosis - ascites (uncommon)
Jaundice (uncommon)

182
Q

Describe the neurological signs and Sx of wilson’s disease

A
  • Most Cu is deposited in basal ganglia
  • Tremor and chorea
  • Dysarthria - speech issues
  • behavioural problems
  • Incoordination - sloppy handwriting, walking, eating
183
Q

Give 2 psychiatric symptoms of Wilson’s disease

A
  • Mild depression
  • Psychosis
184
Q

What is parkinsonism

A

Umbrella term used to describe Sx of:
* Tremor
* Rigidity
* Bradykinesia (slowness of movement)

185
Q

What is an ophthalmological signs of Wilson’s disease

A

Kayser Fleischer rings
Cu deposits in cornea giving greenish brown appearance

186
Q

Describe the investigation of Wilson’s disease

A
  • Serum ceruloplasmin (protein that carriers copper) and CU - decreased levels
  • Liver biopsy
  • 24h urine Cu assay - elevated
  • Genetic analysis - ATP7B gene
  • Slit lamp exam - KF rings
187
Q

How is Wilson’s disease managed

A
  • Cu chelation - penicillamine or trientine hydrochloride
  • Avoid high Cu foods e.g. shellfish & mushrooms
  • Liver transplant as last resort
188
Q

Define alpha 1 antitrypsin (A1AT) deficiency and state the cause

A
  • Deficiency of alpha 1 antitrypsin enzyme
  • Autosomal codominant inheritance of protease inhibitor gene (serpine-1 gene)
189
Q

What chromosome is the gene for alpha 1 antitrypsin coded on

A

14

190
Q

Explain the pathophysiology of A1AT deficiency

A
  • Elastase is an enzyme secreted by neutrophils that digests CT
  • A1AT is produced in the liver and inhibits neutrophil elastase
  • Reduced A1AT affect 2 main organs:
  • Lungs
  • Liver
191
Q

How does A1AT deficiency affect the lungs

A
  • Excess breakdown of elastic fibres in lungs
  • Leads to emphysema and bronchiectasis
192
Q

How does A1AT deficiency affect the liver

A
  • Accumulation of abnormal A1AT causes liver damage
  • Progresses to cirrhosis
  • Can lead to HCC
193
Q

How does A1AT deficiency present

A
  • COPD like Sx: dyspnoea, chronic cough, sputum
  • Jaundice
194
Q

Describe the investigation of A1AT deficiency

A
  • Low serum A1AT
  • Genetic testing - A1AT gene mutation
  • CT thorax - emphysema
  • Pulm function - reduced FEV1, FVC etc
195
Q

How is A1AT deficiency treated

A
  • Smoking cessation
  • Liver transplant for end stage
    Symptomatic management e.g. inhalers for emphysema
196
Q

What is a hernia

A

Protrusion of an organ (e.g. bowel) through a weak point in a cavity wall

197
Q

What is a reducible hernia

A

Lump may be pushed back into normal place

198
Q

What is an irreducible hernia

A

One that can’t be reduced back into it’s proper position
* Bowel trapped in herniated position (incarcerated)

199
Q

What can incarceration lead to

A
  • Obstruction - hernia causes a blockage in passage of faeces
  • Strangulated - hernia is non-reducible and the base of the hernia becomes so tight it cuts off the blood supply causing ischaemia
200
Q

What is an indirect inguinal hernia

A
  • Bowel herniates through inguinal ring
  • passes lateral to inferior epigastric artery
201
Q

What is a direct inguinal hernia

A
  • Hernia protrudes directly through abdominal wall (hesselbach’s triangle)
  • Passes medial to inferior epigastric artery
  • pressure over deep inguinal ring will not stop herniation
202
Q

What are the boundaries of Hesselbach’s triangle

A

RIP:
* Rectus abdominis - medial
* Inferior epigastric vessels - superior/lateral
* Poupart’s (inguinal) ligament - inferior

203
Q

What is a femoral hernia

A
  • Herniation of bowel through femoral canal
  • protrudes below inguinal ligament
  • High risk of strangulation due to rigid femoral canal borders
204
Q

What are hiatus hernias

A
  • Herniation of stomach up through the diaphragm
205
Q

What are the 2 main types of hiatal hernia

A
  • Sliding - stomach slides up through diaphragm
  • Rolling - separate portion (fundus) fold around and enters diaphragm
206
Q

How are hiatus hernias investigated

A
  • Barium swallow
  • CXR
207
Q

RFs of hiatal hernia

A
  • Pregnancy
  • Obesity
  • Over 50
208
Q

How are hernias treated

A

Surgery - tension free

209
Q

What is the most typical pancreatic cancer

A

Typically adenocarcinoma occurring in head of pancreas

210
Q

Give 4 RFs of pancreatic cancer

A
  • Smoking
  • Over 60
  • Chronic pancreatitis
  • T2DM
211
Q

Describe the presentation of pancreatic cancer

A
  • Painless obstructive jaundice: tumour blocks flow of bile - jaundice, pale stool, dark urine, itching
  • Courvoisier’s signs - palpable gallbladder and jaundice
  • Steatorrhoea
  • many present in non-specific way: anorexia, weight loss, epigastric pain
212
Q

Investigation of pancreatic cancer

A
  • GS: Pancreatic CT - mass
  • CA 19-9
  • abdo US - dilated bile and pancreatic ducts
  • Tumour marking - monitor progression
213
Q

How is pancreatic cancer managed

A

Poor prognosis as usually identified late tends to metastasise early to liver and lungs
* Surgery to remove tumour - pancreaticoduodenectomy (whipple procedure)
* Palliative - chemo/radiotherapy

214
Q

What type of liver cancer is most common

A

Secondary
MC a result of metastases

215
Q

Define hepatocellular carcinoma (HCC)

A

Primary hepatocyte neoplasia arising from liver parenchyma
* Accounts for 90% of all primary liver cancers

216
Q

4 causes of HCC

A
  • HBV - mc worldwide
  • HCV - mc Europe
  • Liver cirrhosis (RF)
  • Aflatoxin - poisonous carcinogens produced by moulds often in grains and seeds
217
Q

Where do HCC typically metastasise to

A

Via hepatic/portal veins
* Lymph nodes
* Bones
* Lungs

218
Q

Signs and symptoms of HCC

A
  • Jaundice
  • Ascites
  • Weight loss
219
Q

Investigations of HCC

A
  • 1ST: US - identify lesions
  • GS: CT - confirmation if lesion is large
  • Raised serum alpha-fetoprotein
220
Q

How is HCC treated

A
  • Liver transplant
  • Resection
221
Q

Which vaccine should be taken to prevent HCC

A

HBV vaccine

222
Q

Where are secondary liver tumours typical from

A
  • GIT
  • Breast
  • Lungs (bronchus)
223
Q

What is cholangiocarcinoma

A

Biliary tree cancer

224
Q

Causes/ RFs of cholangiocarcinoma

A
  • Infestation with parasitic worms (flukes)
  • PSC
  • HBV & HCV
  • IBD (RF)
225
Q

Signs and symptoms of cholangiocarcinoma

A
  • colicky Abdo pain
  • Weight loss
  • Palpable mass in RUQ
  • Fever
  • Jaundice and ascites
    Late onset of Sx as tumour is slow growing
226
Q

Investigation of cholangiocarcinoma

A
  • CT and US
  • GS: ERCP
  • Raised bilirubin and ALP
227
Q

Treated of cholangiocarcinoma

A
  • Surgery not possible in 70% of patients due to late presentation
  • ERCP - stenting
228
Q

3 Features of budd-chiari syndrome

A

Triad of:
*ascites
* abdo pain
* tender hepatomegaly

2a - SBCS (9 decks)

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