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PHASE 2A > Liver > Flashcards

Liver Flashcards

1
Q

Give 4 functions of the liver

A
  1. Glucose and fat metabolism
  2. Detoxification and excretion
  3. Protein synthesis (e.g. albumin, clotting factos)
  4. Bile production
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2
Q

Name 3 things that liver function tests measure

A
  1. Serum bilirubin
  2. Serum albumin
  3. Pro-thrombin time
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3
Q

Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease)

A

Alkaline phosphate

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4
Q

What enzymes increase in the serum in hepatocellular liver disease?

A

Transaminases - e.g. AST and ALT

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5
Q

What tests give no index of liver function and why?

A

Liver enzymes - alkaline phosphate, GGT, AST, ALT

Released by damaged cells

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6
Q

Define jaundice

A

Raised serum bilirubin

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7
Q

Name the 3 broad categories of jaundice

A
  1. Pre-hepatic
  2. Hepatic
  3. Post-hepatic
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8
Q

Give 2 causes of pre-hepatic jaundice

A

Excess bilirubin production

  1. Haemolytic anaemia
  2. Gilberts disease
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9
Q

Give 4 causes of hepatic jaundice

A
  1. Liver disease
  2. Hepatitis - viral, drug, immune, alcohol
  3. Ischaemia
  4. Neoplasm - HCC, mets
  5. Congestions - CCF
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10
Q

Give 3 causes of post-hepatic jaundice

A

Duct obstruction

  1. Gallstones
  2. Stricture - Malignancy, ischaemia, inflammatory
  3. Blocked stent
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11
Q

What colour is the urine and stools in pre-hepatic jaundice?

A

Both are normal

No itching and the LFTs are normal

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12
Q

What colour is the urine and stools in someone with cholestatic jaundice (hepatic and post hepatic)?

A

Dark urine
Pale stools
Ithching
LFTs are abnormal

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13
Q

What can cause raised unconjugated bilirubin?

A

A pre-hepatic problem (haemolysis, hypersplenism)

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14
Q

What can cause raised conjugated bilirubin?

A

Indicated cholestatic problem [liver disease (hepatic) or bile duct obstruction (post hepatic)]

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15
Q

Give 3 symptoms of jaundice

A
  1. Biliary pain
  2. Rigors - indicate an obstructive cause
  3. Abdomen swelling
  4. Weight loss
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16
Q

Why are liver patients vulnerable to infection?

A
  1. Impaired reticuloendothelial function
  2. Reduced opsonic activity
  3. Leucocyte function
  4. Permeable gut wall
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17
Q

Give 3 causes of Gallstones

A
  1. Obesity and rapid weight loss
  2. DM
  3. Contraceptive pill
  4. Liver cirrhosis
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18
Q

Give 4 risk factors for gallstones

A
  1. Female
  2. Fat
  3. Fertile
  4. Smoking
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19
Q

Name 2 types of gallstones

A
  1. Cholesterol (70%)

2. Pigment (30%)

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20
Q

Describe the pathophysiology of cholesterol gallstones

A

Excess cholesterol/lack of bile salts –> cholesterol crystals –> gallstone formation, precipitated by reduced gallbladder motility

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21
Q

Describe the pathophysiology of pigment gallstones

A

Excess bilirubin –> polymers and calcium bilirubinate –> stones

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22
Q

Give 4 symptoms of gallstones

A

Most are asymptomatic

  1. Biliary colic (sudden RUQ pain radiating to the back +/- nausea/vomiting)
  2. Acute cholecystitis (gallbladder distension –> inflammation, necrosis, ischaemia)
  3. Obstructive jaundice
  4. Cholangitis
  5. Pancreatitis
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23
Q

How can gallstones be removed from the gallbladder?

A

Laparoscopic cholecystectomy
ERCP with removal or destruction (mechanical lithotripsy) or stent placement
Bile acid dissolution therapy (for people not suitable for surgery)

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24
Q

What is liver failure?

A

When the liver has lost the ability to regenerate to repair, so that decompensation occurs

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25
Q

Name 3 types of liver failure

A
  1. Acute = sudden failure in previously healthy liver
  2. Chronic = liver failure on the background cirrhosis
  3. Fulminant = massive necrosis of liver cells –> severe liver function impairment
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26
Q

Give 5 causes of acute liver disease

A
  1. Viral hepatitis
  2. Drug induced hepatitis
  3. Alcohol induced hepatitis
  4. Vascular - Budd-CHiari
  5. Obstruction
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27
Q

Give 2 possible outcomes of acute liver disease

A
  1. Recovery

2. Liver failure

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28
Q

Give 5 causes of chronic liver disease

A
  1. Alcohol
  2. NAFLD
  3. Viral hepatitis (B,C,E)
  4. Autoimmune diseases
  5. Metabolic
  6. Vascular - Budd-Chairi
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29
Q

Give 2 possible outcomes of chronic liver disease

A
  1. Cirrhosis

2. Liver failure

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30
Q

Give 5 signs of acute liver failure

A
  1. Jaundice
  2. Fetor hepaticus (smells like pears)
  3. Coagulopathy
  4. Asterixis - liver flap
  5. Malaise
  6. Lethargy
  7. Encephalopathy
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31
Q

Give 5 signs of chronic liver disease

A
  1. Ascites
  2. Oedema
  3. Bruising
  4. Clubbing
  5. Depuytren’s contracture
  6. Palmar erythema
  7. Spider naevi
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32
Q

What investigations are conducted on someone on with liver failure?

A

Blood tests - FBCs, U+Es, LFTs, clotting factors, glucose
Imaging - EEG, USS, CXR, doppler USS
Microbiology - blood and urine culture and ascitic tap

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33
Q

What do the blood tests show in someone with liver failure?

A 
Raised bilirubin 
Low glucose 
High AST and ALT 
Low levels of coagulation factors 
Raised prothrombin time 
High ammonia levels
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34
Q

Describe the treatment for liver failure

A
  1. Nutrition
  2. Supplements
  3. Treat complications
    - Raised intracranial pressure = mannitol
    - PPI = reduce GI bleeds
    - Vit K, platelets, blood, FFP = coagulopthy
  4. Liver transplant
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35
Q

Give 4 complications of of liver failure

A
  1. Hepatic encephalopathy
  2. Abnormal bleeding
  3. Jaundice
  4. Ascites
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36
Q

What drugs should be avoided in liver failure?

A

Constipators
Oral hypoglycaemics
Warfarin has enhanced effects
Opiates

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37
Q

Describe the pathophysiology of paracetamol poisoning

A

Intermediate metabolite (NAPQI) causes cellular necrosis, builds up when conjugation pathway is saturated

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38
Q

What is the treatment for paracetamol poisoning?

A

N-acetyl cysteine (NAC) converts reactive intermediate to stable metabolite

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39
Q

What give someone a poor prognosis following a paracetamol overdose?

A
  1. Late presentation (NAC less effective >24hrs)
  2. Acidosis
  3. High prothrombin time
  4. High serum creatinine
    Liver transplant considered
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40
Q

What is cirrhosis?

A

Scarring of liver = irreversible
A chronic disease of the liver resulting from necrosis of liver cells followed by fibrosis (scarring)
The end result is impairment of hepatocyte function and distortion of liver architecture

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41
Q

Give 3 causes of cirrhosis

A
  1. Alcohol
  2. Chronic Hep B and V
  3. Non alcoholic fatty liver disease
  4. Genetic - Wilsons, A1ATD, HH, CF
  5. Autoimmune - AH, PBC, PSC
  6. Drugs - methotrexate, amiodarone, methyldopa
  7. Neoplasm
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42
Q

Give 4 signs of cirrhosis

A
  1. Hypoalbuminaemia
  2. Clubbing
  3. Terry’s nails
  4. Palmar erythema
  5. Spider naevi
  6. Hepatosplenomegaly
  7. Ankle oedema
  8. Loss of body hair
  9. Ascites
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43
Q

What investigations are done in someone with cirrhosis?

A
  1. FBC = decreased albumin, increased prothrombin time, low WCC and platelets
  2. LFTs = raised bilirubin, AST, ALT, ALP, GGT
  3. Imaging - USS, MRI = lesion, hepatomegaly, portal vein problems
  4. Ascitic tap = indicates SBP
  5. Liver biopsy = confirms clinical diagnosis
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44
Q

What is the treatment for liver cirrhosis?

A
  1. Good nutrition and alcohol abstinence
  2. Cholestryramine for pruritus
  3. Treat underlying cause
  4. Fluid and salt restriction for ascetics –> spironolactone, furosemide
  5. Consider for liver transplant
  6. Screen for HCC
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45
Q

Give 4 complications of cirrhosis

A
  1. Decompensation
  2. SBP
  3. Portal hypertension
  4. Increased risk of HCC
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46
Q

Approximately what percentage of blood flow to the liver is provided by the portal vein?

A

75%

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47
Q

Give 3 causes of portal hypertension

A
  1. Pre-hepatic = portal vein thrombosis
  2. Hepatic = cirrhosis, schistosomiasis, sarcoidosis
  3. Post-hepatic = Budd-Chiari, RHF, constrictive pericarditis
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48
Q

Give 3 signs of portal hypertension

A
  1. Ascites
  2. Splenomegaly
  3. Varices
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49
Q

Why can portal hypertension lead to varices?

A

Obstruction to portal blood flow

Blood is diverted into collaterals and so causes varices

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50
Q

What are the potential consequences of varices?

A

If they rupture –> haemorrhage

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51
Q

What is the primary treatment for varices?

A

Endoscopic therapy - banding

And Beta blocker

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52
Q

Describe the pathophysiology of hepatic encephalopathy

A

Ammonia accumulates and crosses the BBB causing cerebral oedema

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53
Q

Name 4 sequelae’s of hepatic encephalopathy

A

SAVE

  1. Splenomegaly
  2. Ascites
  3. Varices
  4. Encephalopathy
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54
Q

What is ascites?

A

Chronic accumulation of fluid in the peritoneal cavity that leads to abdominal distension

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55
Q

Give 4 causes of ascites and an example for each

A
  1. Local inflammation - peritonitis
  2. Leaky vessels - imbalance between hydrostatic and oncotic pressures
  3. Low flow - cirrhosis, thrombosis, cardiac failure
  4. Low protein - hypoalbuminaemia
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56
Q

Describe the pathophysiology of ascites

A
  1. Increased intra-hepatic resistance leads to portal hypertension –> ascites
  2. Systemic vasodilation leads to secretion of RAAS, NAd and ADH –> fluid retention
  3. Low serum albumin also leads to ascites
    Transudate = blockage of venous drainage
    Exudate = inflammation
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57
Q

Give 3 signs of ascites

A
  1. Distension
  2. Dyspnoea
  3. Shifting dullness on percussion
  4. Signs of liver failure
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58
Q

What investigations might you do in someone who you suspect has ascites?

A
  1. USS

2 Ascitic tap

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59
Q

Describe the treatment for ascites

A
  1. Restrict sodium and fluids
  2. Diuretics - spirolactone
  3. Paracentesis
  4. Albumin replacement
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60
Q

Describe the effects of alcoholic liver disease

A
  1. Fatty liver –> hepatitis –> cirrhosis and fibrosis
  2. GIT –> gastritis, varices, peptic ulcers, pancreatitis , carcinoma
  3. CNS –> Degreased memory and cognition, wernicke’s encephalopathy
  4. Folate deficiency –> anaemia
  5. Reproduction –> testicular atrophy, reduced testosterone/progesterone
  6. Heart –> dilated cardiomyoapthy, arrhythmias
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61
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease?

A

Neutrophils and fat accumulation within hepatocytes

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62
Q

What type of anaemia do you associate with alcoholic liver disease?

A

Macrocytic anaemia

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63
Q

What blood test might show that someone has alcoholic liver disease?

A

Serum GGT will be elevated

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64
Q

What distinctive feature is often seen on biopsy in people suffering form alcoholic liver disease?

A

Mallory bodies

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65
Q

What are the CAGE questions?

A
  1. Cut down?
  2. Annoyed at criticism?
  3. Guilty about drinking?
  4. Eyeopener?
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66
Q

How do you treat alcoholic liver disease?

A 
Alcohol management 
1 = public health interventions 
2 = early alcohol use screening
3 = Pharmacoloigal - disulfiram, acamprosate calcium 
4 = Psychosocial - CBT, group support
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67
Q

How does alcoholic hepatitis present?

A 
Jaundice
Anorexia
Nausea
Fever
Encephalopathy 
Cirrhosis 
Hepatomegaly
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68
Q

How long does hepatitis persist for to be deemed chronic?

A

6 months

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69
Q

Give 4 types of hepatitis?

A
  1. Viral - A,B,C,D,E
  2. Drug induced
  3. Alcohol induced
  4. Autoimmune
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70
Q

Give 3 infective causes of acute hepatitis

A
  1. Hepatitis A-E infections
  2. EBV
  3. CMV
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71
Q

Give 3 non-infective causes of acute and chronic hepatitis

A
  1. Alcohol
  2. Drugs
  3. Toxins
  4. Autoimmune
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72
Q

Give 3 symptoms of acute hepatitis

A
  1. General malaise
  2. Myalgia
  3. GI upset
  4. Abdominal pain
  5. Raised AST, ALT
  6. +/- jaundice
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73
Q

What are the potential complications of chronic hepatitis?

A

Uncontrolled inflammation –> fibrosis –> cirrhosis –> HCC

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74
Q

If HAV a RNA or DNA virus?

A

RNA virus - PicoRNAvirus

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75
Q

How is HAV transmitted?

A

Faeco-oral transmission - contaminated food/water, shellfish

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76
Q

Who could be at risk of HAV infection?

A

Travellers and food handlers

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77
Q

Is HAV acute or chronic?

A

Acute

100% immunity after infection

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78
Q

How might you diagnose someone with HAV infection?

A

Viral serology - initially anti-HAV IgM and then anti-HAV IgG
AST and ALT rise 3-5 weeks after infection

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79
Q

Describe the management of HAV infection

A
  1. Supportive
  2. Monitor liver function to ensure no fulminant hepatic failure
  3. Manage close contacts
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80
Q

What is the primary prevention of HAV?

A

Vaccination

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81
Q

Is HBV a RNA or DNA virus?

A

DNA virus

Replicates in hepatocytes

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82
Q

How is HBV transmitted?

A

Blood borne transmission - IVDU, needle-stick, sexual, vertical
Highly infectious

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83
Q

Describe the natural history of HBC in 4 phases

A
  1. Immune tolerance phase: unimpeded viral replication –> high HBV DNA levels.
  2. Immune clearance phase: the immune system ‘wakes up’ = liver inflammation and high ALT
  3. Inactive HBV carrier phase: HBV DNA levels are low = ALT levels are normal, no liver inflammation
  4. Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver –> fibrosis
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84
Q

What HBV protein triggers the initial immune response?

A

The core proteins

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85
Q

How might you diagnose someone with HBV?

A

Viral serology = HBV surface antigen can be detected from 6w-3m, anti-HBV core IgM after 3 months, AST elevation

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86
Q

Describe the management of HBV infection

A
  1. Supportive
  2. Monitor liver function
  3. Manage contacts
  4. Follow up at 6 months to see if HBV surface antigens has clears
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87
Q

How would you know if someone had acute or chronic HBV infection?

A

Follow up appointment at 6 months to see if HBV surface Ag has cleared
Still present = chronic hepatitis

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88
Q

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis
  2. HCC
  3. Decompensated cirrhosis
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89
Q

How can HBV infection be prevented?

A

Vaccination - injecting a small amount of inactivated HbsAg

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90
Q

Describe 2 treatment options for HBV infection

A
  1. Alpha interferon - boosts immune system

2. Antivirals - tenofovir, inhibits viral replications

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91
Q

Give 3 side effects of alpha interferon treatment for HBV

A
  1. Myalgia
  2. Malaise
  3. Lethargy
  4. Thyroiditis
  5. Mental health problems
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92
Q

Give 2 HBV specific symptoms

A

Arthralgia

Urticaria (hives)

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93
Q

If HCV a RNA or DNA virus?

A

RNA virus - flavivirus

94
Q

How is HCV transmitted?

A

Blood borne

95
Q

Give 4 risk factors for developing HBV/HCV infection

A
  1. IVDU
  2. People who have required blood products - blood transfusion
  3. Needle stick injuries
  4. Unprotected sex
  5. Vertical transmission
96
Q

How might you diagnose someone with current HCV infection?

A

Viral serology - HCV RNA tells you if the infection is still present

97
Q

Describe the treatment for HCV

A

Direct acting antivirals are currently in use

Weakly interferon injections

98
Q

What percentage of people with acute HCV infection will progress onto chronic infection?

A

Approximately 70%

99
Q

What percentage of people with acute HBV infection will progress onto chronic infection?

A

Approximately 5%

100
Q

How can HCV infection be prevented?

A
  1. Screen blood products
  2. Lifestyle modification
  3. Needle exchange
    No vaccination, and previous infection doesn’t confer immunity
101
Q

Is HDV a RNA or DNA virus?

A

Incomplete RNA virus

Needs Hep B for assembly

102
Q

How is HDV transmitted?

A

Blood borne transmission - particularly IVDU

103
Q

Is HEV a RNA or DNA virus?

A

Small RNA virus

104
Q

How is HEV transmitted?

A

Faeco-oral transmission

105
Q

Is HEV acute or chronic?

A

Usually acute but there is a risk of chronic disease in the immunocompromised

106
Q

How might you diagnose someone with HEV infection?

A

Viral serology - initially anti-HEV IgM and then anti HEV IgG

107
Q

Describe the primary prevention of HEV

A

Good food hygiene

Vaccine is in development

108
Q

What types of viral hepatitis are capable of causing choric infection?

A

Hepatitis B (+/- D), C and E in the immunosuppressed

109
Q

What is non alcoholic steatoheptitis (NASH)?

A

An advanced form of non-alcoholic fatty liver disease

110
Q

Give 3 causes of non-alcoholic fatty liver disease

A
  1. T2DM
  2. Obesity
  3. Hypertension
  4. Hyperlipidaemia
111
Q

How do you manage NAFLD?

A

Lose weight

Control HTN, DM and lipids

112
Q

What is Budd-Chiari syndrome?

A

Hepatic vein occlusion –> ischaemia and hepatocyte damage –> liver failure or insidious cirrhosis

113
Q

Name 3 metabolic disorders that can cause liver disease

A
  1. Haemochromatosis - iron overload
  2. Alpha 1 anti-trypsin deficiency
  3. Wilson’s disease - disorder of copper metabolism
114
Q

90% of people with haemochromatosis have a mutation in which gene?

A

HFE

115
Q

Haemochromatosis is a genetic disorder, how is it inherited?

A

Autosomal recessive inheritance

116
Q

Describe the pathophysiology of haemochromatosis

A

Uncontrolled intestinal iron absorption –> deposition of iron in liver, heart, pancreas, joins, skin –> fibrosis and functional organ failure

117
Q

Give 4 signs of haemochromatosis

A
  1. Hepatomegaly
  2. Cardiomegaly
  3. DM
  4. Hyperpigmentation of skin
  5. Lethargy
  6. Osteoporosis
118
Q

How might you diagnose someone with haemochromatosis?

A
  1. Raised ferritin
  2. HFE genotyping
  3. Liver biopsy
119
Q

What histological stain can be used for haemochromatosis?

A

Perl’s stain

120
Q

What is the treatment for haemochromatosis?

A
  1. Iron removal - venesection
  2. Monitor DM
  3. Low iron diet
  4. Screening for HFE
121
Q

Give 2 complications of haemochromatosis?

A

Liver cirrhosis –> failure/cancer

DM due to pancreatic depositions

122
Q

How is alpha 1 anti-trypsin deficiency inherited?

A

Autosomal recessive mutation in serine protease inhibitor gene

123
Q

Describe the pathophysiology of alpha 1 anti-trypsin deficiency?

A

No protease inhibitor –> lung elastase/liver destruction (cirrhosis)

124
Q

How does Alpha 1 anti-trypsin deficiency present?

A

Liver disease in the young - cirrhosis, jaundice

Lung disease in the old (smokers) - emphysema

125
Q

How would you diagnose Alpha 1 anti-trypsin deficiency?

A

Bloods = decreased serum A1AT
LFT = obstructive disease pattern
Liver biopsy = periodic acid Schiff +ve

126
Q

What is the treatment for Alpha 1 anti-trypsin deficiency?

A

Smoking cessation

Liver/lung transplant

127
Q

What is Wilson’s disease?

A

An autosomal recessive disorder of copper metabolism

Excess deposition of copper in the liver

128
Q

Describe the pathophysiology of Wilson’s disease

A

Impaired incorporation of Cu into caeruloplasmin –> Cu accumulation in liver

129
Q

How does Wilson’s disease present?

A 
Children = liver disease - hepatitis, cirrhosis, fulminant liver failure 
Adults = CNS problems, mood changes, and Kayser-Fleischer rings
130
Q

What are Kayser-Fleischer rings?

A

Cu in iris and cornea –> bronze ring

131
Q

What CNS changes are seen in a patient with Wilson’s disease?

A 
Tremor
Dysarthria 
Dyskinesia 
Ataxia
Parkinsonism 
Dementia 
Depression
132
Q

What is the treatment for Wilson’s disease?

A

Lifetime treatment with penicillamine (chelating agent)
Low Cu diet - no liver, nuts, chocolate, mushrooms, shellfish
Liver transplant

133
Q

Describe the pathophysiology of autoimmune hepatitis

A

Abnormal T cell function and autoantibodies vs hepatocyte surface antigens

134
Q

What people are more likely to present with autoimmune hepatitis?

A

Young (10-30) and middle aged (>40) women

135
Q

How does autoimmune hepatitis present?

A 
Fatigue, fever, malaise 
Hepatitis 
Hepatosplenomegaly
Amenorrhoea 
Polyarthritis 
Pleurisy 
Lung infiltrates 
Glomuleronephritis
136
Q

What diseases are associated with autoimmune hepatitis?

A 
Autoimmune thyroiditis 
DM
Pernicious anaemia
PSC
UC
137
Q

What results would you see from the investigations of someone who you suspect has autoimmune hepatitis?

A

Raised LFTs - increased bilirubin, AST, ALT, ALP
Hypersplenism = low WCC and platelets
Autoantibodies = +ve anti-nuclear antibody
Liver biopsy = mononuclear infiltrate

138
Q

How is autoimmune hepatitis treated?

A

Prednisolone - immunosuppression

Liver transplant

139
Q

What is primary biliary cirrhosis?

A

An autoimmune disease where intra-hepatic bile ducts are destructed by chronic granulomatous inflammation –> cholestatis (bile in liver) –> cirrhosis, fibrosis, portal hypertension

140
Q

Describe 2 features of the epidemiology of primary biliary cirrhosis

A
  1. Females > males

2. Familial - 10 fold risk increase

141
Q

Give 3 disease associated with primary biliary cirrhosis

A
  1. Thyroiditis
  2. RA
  3. Coeliac disease
  4. Lung disease
    Other autoimmune diseases
142
Q

Give 3 symptoms of primary biliary cirrhosis

A
  1. Pruritis
  2. Fatigue
  3. Heptosplenomeglay
  4. Obstructive jaundice
  5. Cirrhosis and coagulopathy
143
Q

What would investigations show in someone with biliary cirrhosis?

A

Bloods = elevated LFTS (ALP), increased bilirubin, raised IgM decreased albumin and clotting factors
Positive anti-mitochondrial antibody = diagnostic
Liver biopsy = epithelial disruption and lymphocyte infiltration

144
Q

What is the treatment for primary biliary cirrhosis?

A

Ursodeoxycholic acid - improves bilirubin and aminotransferase levels
Cholestyramine - for pruritis
ADEK vitamins
Liver transplant

145
Q

What is Primary sclerosing cholangitis?

A

Autoimmune inflammation and narrowing of intra and extra hepatic bile ducts

146
Q

Describe the pathophysiology of primary sclerosis cholangitis

A

Inflammation of the bile duct –> stricture and hardening –> progressive obliterating fibrosis of bile duct branches –> cirrhosis –> liver failure

147
Q

Give 3 causes of primary sclerosis cholangitis

A
  1. Primary = unknown causes
  2. Infection
  3. Thrombosis
  4. Iatrogenic trauma
148
Q

Give 3 symptoms of primary sclerosis cholangitis

A
  1. Pruritus
  2. Charcot’s triad = fever with chills, RUQ pain, obstructive jaundice
  3. Cirrhosis
  4. Liver failure
  5. Fatigue
149
Q

What would the investigations show in someone with primary sclerosis cholangitis?

A

Bloods = elevated ALP, bilirubin and Ig, AMA negative
Imaging = ERCP and MRCP
Liver biopsy = fibrous and obliterative cholangitis

150
Q

What is the treatment for primary sclerosis cholangitis?

A

Cholestyramine for pruritus
ADEK vitamins
Liver transplant

151
Q

What complications might occur due to primary sclerosis cholangitis?

A

Increased risk of bile duct, gallbladder, liver and colon cancer

152
Q

What is ascending cholangitis?

A

Obstruction of biliary tract causing bacterial infection

Regarded as a medical emergency

153
Q

Give 3 causes of ascending cholangitis?

A

Gallstone
Primary infection (Klebsiella, E. coli)
Strictures following surgery
Pancreases head malignancy

154
Q

Name the triad that describes the 3 common symptoms of ascending cholangitis

A

Charcot’s triad

  1. Fever
  2. RUQ pain
  3. Jaundice
155
Q

What other symptoms can present with Charcot’s triad with ascending cholangitis?

A

Reynolds pentad

  • Charcot’s triad
  • Hypotension
  • Confusion/altered mental state
156
Q

What investigations might you do in someone who you suspect might have ascending cholangitis?

A
  1. USS
  2. Blood tests - LFTS
  3. CT - excludes carcinoma
  4. ERCP - definitive investigation
157
Q

Describe the management of ascending cholangitis

A 
Fluid resuscitation 
Treat infection with broad spectrum antibiotics (cefotaxime, metronidazole)
ERCP to clear obstruction
Stenting 
Laparoscopic cholecystectomy
158
Q

What is the difference between ascending cholangitis and acute cholecystitis?

A

A patient with acute cholecystitis would not have signs of jaundice

159
Q

What is the main difference between biliary colic and acute cholecystitis?

A

Acute cholecystitis has an inflammatory component

160
Q

What complications can occur due to acute ascending cholangitis?

A 
Sepsis
Biliary colic
Acute cholecystitis
Empyema
Carcinoma 
Pancreatitis
161
Q

Are most liver cancers primary or secondary?

A

Secondary - metastasised to the liver

162
Q

Where have most secondary liver cancers arisen form?

A
  1. GI tract
  2. Breast
  3. Bronchus
  4. Uterus (women)
163
Q

Describe the aetiology of HCC

A
  1. Cirrhosis
  2. HBV/HCV
  3. Alcohol
  4. Haemochromatosis
164
Q

Give 5 symptoms of HCC

A
  1. Weight loss
  2. Anorexia
  3. Fever
  4. Malaise
  5. Ascites
  6. RUQ pain
165
Q

What investigations might you do on someone who you suspect has HCC?

A
  1. Blood - serum AFP may be raised
  2. US or CT to identify lesions
  3. MRI
  4. Biopsy = diagnostic
166
Q

Describe the treatment for HCC

A
  1. Surgical resection of solitary tumours
  2. Liver transplant
  3. Percutaneous ablation
  4. Prevention = Hep B vaccination
167
Q

What is cholangiocarcinoma?

A

Cancer of the biliary tree

168
Q

Give 3 causes of cholangiocarcinoma

A
  1. Flukes (parasitic worms)
  2. Primary sclerosing cholangitis
  3. HBV and HCV
  4. DM
169
Q

Give 4 symptoms of cholangiocarcinoma

A
  1. Fever
  2. Abdominal pain
  3. Ascites
  4. Early jaundice
  5. Malaise
  6. Fatigue
170
Q

What investigations might you do in someone who you think has cholangiocarcinoma?

A

Raised bilirubin and alkaline phosphate
Contrast MRI
ERCP for biopsy

171
Q

What is the management for cholangiocarcinoma?

A

Most are inoperable

Complete resection/stent = symptom relief

172
Q

What is peritonitis?

A

Inflammation of the peritoneal lining

173
Q

Name causes of peritonitis

A
  1. Primary = spontaneous bacterial peritonitis, ascites, immunocompromised
  2. Secondary = Bowel perforation, abdomen organ inflammation, TB, bowel ischaemia
174
Q

Give 3 symptoms of peritonitis

A
  1. Abdominal pain and tenderness
  2. Nausea
  3. Chills
  4. Rigors
  5. Fever
175
Q

Give 3 signs of peritonitis on an abdomen examination

A
  1. Guarding
  2. Rebound
  3. Rigidity
  4. Silent abdomen
176
Q

What investigations might you do in someone who you suspect could have peritonitis?

A
  1. Blood tests: raised WCC, platelets, CRP, amylase, reduced blood count
  2. CXR: look for air under the diaphragm
  3. Abdominal x-ray: look for bowel obstruction
  4. CT: can show inflammation, ischaemia or cancer
  5. ECG: epigastric pain could be related to the heart
  6. B-HCG: a hormone secreted by pregnant ladies
177
Q

What is the management for peritonitis?

A
  1. ABC
  2. Treat the underlying cause
  3. Surgical repair of abdomen
  4. Anti-inflammatories
178
Q

Give 5 potential complications of peritonitis

A
  1. Hypovolaemia
  2. Kidney failure
  3. Systemic sepsis
  4. Paralytic ileus
  5. Pulmonary atelectasis (lung collapse)
  6. Portal pyaemia (pus in portal vein)
179
Q

What is the commonest serious infection in those with cirrhosis?

A

Spontaneous bacterial peritonitis

180
Q

Name a bacteria that can cause spontaneous bacterial peritonitis

A
  1. E. coli

2. S. pneumoniae

181
Q

How can spontaneous bacterial peritonitis be diagnosed

A

By looking for the presence of neutrophils in ascitic fluid

182
Q

Describe the treatment for spontaneous bacterial peritonitis

A

Cefotaxime and metronidazole

183
Q

What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important

A

Ascitic tap to rule out spontaneous bacterial peritonitis

184
Q

You do an ascitic in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?

A

Spontaneous bacterial peritonitis

185
Q

What is acute pancreatitis?

A

An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase)

186
Q

Describe the pathophysiology of acute pancreatitis

A

Self-perpetuating exocrine enzyme mediated auto-digestion of organ
Acinar cell injury –> inflammatory response –> multiple organ damage
Oedema + fluid shift –> hypovolaemia –> EC fluid is stuck in gut/peritoneum

187
Q

Give 5 causes of pancreatitis

A 
I GET SMASHED – remember 
Idiopathic
Gallstones (60%)
Ethanol = alcohol (30%)
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia/hypothermia/high Ca
ERCP (endoscopic retrograde cholangiopancreatography) 
Drugs (furosemide, corticosteroid, NSAIDs, ACEi)
188
Q

Give 4 symptoms of acute pancreatitis

A
  1. Severe epigastric pain that radiates to the back
  2. Anorexia
  3. Nausea, vomiting
  4. Signs of septic shock - fever, dehydration, hypotension, tachycardia
  5. Necrotising - umbilical (Cullens sign) vs flank (Grey Turners sign)
189
Q

What investigations are done on someone you think has acute pancreatitis?

A

Raised serum amylase and lipase
Erect CXR
Contrast CT
MRI

190
Q

Name a scoring system that can be used as a prognostic tool in acute pancreatitis

A

Glasgow and ranson

191
Q

What 8 points make up the Glasgow and ranson scoring system?

A
  1. Hypoxia = PaO2 < 8kPa
  2. Age > 55 years
  3. Neutrophilia > 15x10^9
  4. Hypocalaemia < 2mmol/L
  5. Hyperuricaemia > 15mmol/L
  6. Elevated enzymes
  7. Hypoalbuminaemia < 32g/L
  8. Hyperglycaemia - serum glucose > 15mmol/L
192
Q

Describe the treatment for acute pancreatitis

A
  1. Analgesia
  2. Catheterise and ABC approach for shock patients
  3. Drainage of oedematous fluid collections
  4. Antibiotics
  5. Nutrition - NJ tube feeding
193
Q

Give 2 potential complications of acute pancreatitis

A
  1. Systemic inflammatory response syndrome
  2. Multiple organ dysfunction
  3. Pancreatic necrosis
194
Q

Why is morphine contraindicated in acute pancreatitis?

A

Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis

195
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage
- Progressive loss of exocrine pancreatic tissue which is replaced by fibrosis

196
Q

Describe the pathogenesis of chronic pancreatitis

A

Pancreatic duct obstruction leads to activation of pancreatic enzymes –> necrosis –> fibrosis

197
Q

Name 3 causes of chronic pacnreatitis

A
  1. Excess alcohol
  2. CKD
  3. Idiopathic
  4. Recurrent acute pancreatitis
  5. Genetic - CF, HH, Hereditary pancreatitis
198
Q

Describe how alcohol can cause chronic pancreatitis

A

Alcohol –> proteins precipitate in the ductal structure of the pancreas (obstruction) –> pancreatic fibrosis

199
Q

Give 5 symptoms of chronic pancreatitis

A
  1. Severe epigastric pain that radiate through to the back
  2. Weight loss
  3. Nausea, vomiting
  4. Steatorrhea (lack of lipase)
  5. Exocrine/endocrine dysfunction
200
Q

A sign of chronic pancreatitis is exocrine dysfunction, what can be consequence of this?

A
  1. Malabsorption
  2. Weight loss
  3. Diarrhoea
  4. Steatorrhoea
201
Q

A sign of chronic pancreatitis is endocrine dysfunction, what can be consequence of this?

A

DM

202
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

A

IgG4

203
Q

How is autoimmune chronic pancreatitis treated?

A

Steroids

204
Q

What is the treatment for chronic pancreatitis?

A

Alcohol cessation
Analgesia (NSAIDs, tramadol)
Pancreatic enzyme (creon) and vitamin replacement
If DM = insulin
Surgery - local resection, for unremitting pain

205
Q

Why can pancreatitis cause malabsorption?

A

Pancreatitis result in pancreatic insufficiency and so lack of pancreatic digestive enzymes
Defective intra-luminal digestion leads to malabsorption

206
Q

What 2 enzymes, if raised, suggest pancreatitis?

A

LDH (lactate dehydrogenase) and AST

207
Q

Give 3 complications of chronic pancreatitis

A
  1. Diabetes
  2. Pseudocyst
  3. Biliary obstruction –> obstructive jaundice, cancer
208
Q

Name a drug that can cause drug induced liver injury

A
  1. Co-amoxiclav
  2. Flucloxacillin
  3. Erythromycin
  4. TB drugs
209
Q

Give 5 causes of diarrhoea infection

A
  1. Traveller’s diarrhoea
  2. Viral - (rotavirus/norovirus)
  3. Bacterial (E. coli)
  4. parasites (helminths, protozoa)
  5. Nosocomial (C. diff)
210
Q

Give 5 causes of non-diarrhoeal infection

A
  1. Gastritis/peptic ulcer disease (H. pylori)
  2. Acute cholecystitis
  3. Peritonitis
  4. Thyphois/paratyphoid
  5. Amoebic liver abscess
211
Q

Give 3 ways in which diarrhoea can be prevented

A
  1. Access to clean water
  2. Good sanitation
  3. Hand hygiene
212
Q

What is the diagnostic criteria for travellers diarrhoea?

A

> 3 unformed stools per dat and a least one of:
- abdominal pain
- cramps
- nausea
- vomiting
Occurs within 2 weeks (usually 3 days) of arrival in a new country

213
Q

Give 3 casues of traveller’s diarrhoea

A
  1. Enterotoxigenic E. coli
  2. Norovirus
  3. Giardia
214
Q

Describe the pathophysiology of traveller’s diarrhoea

A

Heat labile ETEC modifies Gs and it is in a permanent ‘locked on’ state
Adenylate cyclase is activated and there is increased production of cAMP
Leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient –> diarrhoea

215
Q

Which type of E. coli can cause bloody diarrhoea and has a shiga like toxin?

A

Enterohaemorrhagic E.coli (EHEC)

216
Q

What does EIEC stand for?

A

Enteroinvasive E. coli

217
Q

What type of E. coli is responsible for causing large volumes of watery diarrhoea?

A

Enteropathogenic E.coli (EPEC)

218
Q

What does EAEC stand for?

A

Enteroaggregative E. coli –> infantile diarrhoea

219
Q

What does DAEC stand for?

A

Diffusely adherent E. coli

220
Q

What is the leading cause of diarrhoea illness in young children?

A

Rotavirus

There is a vaccine = rotary

221
Q

Name a helminth responsible for diarrhoea infection?

A

Schistosomiasis

Strongyloides

222
Q

Give 5 symptoms of helminth infection

A
  1. Fever
  2. Eosinophilia
  3. Diarrhoea
  4. Cough
  5. Wheeze
223
Q

Why is c. diff infectious?

A

Spore forming bacteria (gram positive)

224
Q

Give 5 risk factors for c.diff infection

A
  1. Increasing age
  2. Comordities
  3. Antibiotic use
  4. PPI
  5. Long hospital admission
  6. NG tube feeding and GI surgery
  7. Immunocompromised - HIV, anti-caner drugs
225
Q

Name 5 antibiotics that can cause c. diff infection

A
  1. Ciprofloxacin (quinolones)
  2. Co-amoxiclav (penicillins)
  3. Clindamycin
  4. Cephlosporins
  5. Carbapenems
    RULE OF C’s
226
Q

Describe the treatment for c. diff infection

A

Metronidazole and vancomycin (PO)
Rifampicin/rifaximin
Stool transplant

227
Q

What can helicobacter pylori infections cause?

A

H. pylori produces urease –> ammonia –> damage to gastric mucosa –> neutrophil recruitment and inflammation
Causing gastritis, peptic ulcer disease, gastric cancer

228
Q

Describe H. pylori

A

A gram negative bacilli with a flagellum

229
Q

Describe the treatment for H. pylori infection

A

Triple therapy = 2 antibiotics and 1 PPI

Omeprazole, clarithomyocine and amoxicillin

230
Q

Define biliary colic

A

Pain associated with the temporary obstruction of the cystic or common bile duct

PHASE 2A (16 decks)

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