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Phase 2a med mine > Liver > Flashcards

Liver Flashcards

1
Q

What are the main functions of the liver?

A

Oestrogen regulation
Detoxification
Carb metabolism
Albumin production
Clotting factor production
Bilirubin regulation
Immunity-Kupffer cells in reticuloendothelial system
Storage of vitamins/iron/copper/fat

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2
Q

What are the consequences of the liver being unable to regulate estrogen?

A

Gynecomastia
Spider naevi
Palmar erythema

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3
Q

What are the consequences of the liver being unable to detoxify substances?

A

Hepatic encephalopathy

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4
Q

Describe the pathophysiology of hepatic encephalopathy

A

Accumulation of NH3: normally detoxified and excreted via urea cycle
Crosses BBB and accumulates in CNS-causes confusion

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5
Q

What are the consequences of the liver being unable to metabolise carbohydrates?

A

Hypoglycaemia

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6
Q

Name a few conditions that affect the liver’s storage of things

A

Wilson’s: copper
Haemochromatosis: iron
A1AT deficiency:

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7
Q

What are the consequences of the liver being unable to produce albumin?

A

Oedema
Ascites
Leukonychia

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8
Q

What are the consequences of the liver being unable to produce clotting factors?

A

Easy bruising and bleeding

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9
Q

What are the consequences of impaired liver immunity function?

A

Increased susceptibility to infections

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10
Q

What are the consequences of the liver being unable to metabolise bilirubin?

A

Jaundice
Pruritus

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11
Q

Which blood tests directly relate to liver damage?

A

Bilirubin (mostly unconjugated)
Albumin
Prothrombin time

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12
Q

Would you expect bilirubin to be high or low in someone with liver damage?

A

High

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13
Q

Would you expect albumin to be high or low in liver damage?

A

Low

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14
Q

Would you expect PT/INR to be high or low in liver damage?

A

High

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15
Q

How are liver enzymes indicative of liver damage?

A

High levels suggest they have spilled out into the blood so likely liver damage

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16
Q

Where can you find AST and ALT?

A

Liver
Heart
Kidneys
Muscles

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17
Q

What is the normal ratio of AST:ALT?

A

1

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18
Q

When would you find high ALP levels?

A

Biliary tree specific damage and bone pathology

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19
Q

How is GGT helpful when looking at liver function?

A

High in acute liver damage
Also helps differentiate high ALP as a hepatic or bony cause

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20
Q

Define liver failure

A

Liver loses regeneration/repair ability and is irreversibly damaged. Decompensated

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21
Q

What is acute liver failure?

A

Live injury accompanied with hepatic encephalopathy, ascites, jaundice, and coagulopathy (>1.5 INR) in a patient with a previously healthy liver

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22
Q

What happens in fulminant liver failure?

A

Massive hepatocyte necrosis

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23
Q

What would you see histologically in someone with fulminant liver failure?

A

Multiacinar necrosis

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24
Q

What are the 3 categories of fulminant liver failure?

A

Hyperacute: HE within 7 days of jaundice
Acute: HE within 8-28 days of jaundice
Subacute: HE within 5-26 weeks of jaundice

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25
Q

What is the most common cause of chronic liver failure?

A

Paracetamol overdose

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26
Q

What is acute on chronic liver failure?

A

Abrupt decline in a patient with chronic liver symptoms

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27
Q

What is chronic liver failure?

A

Progressive liver disease >6 months due to repeated liver insults

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28
Q

Describe the progression of chronic liver failure

A

Hepatitis->fibrosis->compensated cirrhosis->decompensated cirrhosis

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29
Q

Name some causes of acute liver failure

A

Viral: Hep A, B, E, CMV, EBV
Autoimmune hepatitis
Drugs: paracetemol, alcohol, ecstasy
HCC
Metabolic: Wilson’s, haemochromatosis, A1ATD
Obstruction: Budd chiari, gallstones
Congestion: e.g. heart failure

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30
Q

Describe the signs and symptoms of acute liver failure

A

Jaundice, coagulopathy, HE
More seen in chronic:
Spider naevi
Fetor hepaticus(rotten egg+ garlic breath)
Caput medusae (distended abdominal blood vessels)
Dupuytren’s contracture(fingers bent towards hand)

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31
Q

What is the name of the criteria used to classify HE?

A

West Haven

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32
Q

Describe the West Haven criteria grades 1-4

A
  1. Altered mood, sleep issues
  2. Lethargy, mild confusion, asterixis
  3. marked confusion, quiet
  4. comatose
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33
Q

What is asterixis?

A

Liver flap-flap hands like a bird

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34
Q

What investigations could you use to diagnose acute liver failure?

A

Bloods: high AST/ALT, high NH3, low glucose, high bilirubin, low albumin, high PT/INR
Imaging: EEG to grade HE, abdominal US to check Budd chiari
Microbiology to rule out infections
Serology for Hep/high paracetamol levels

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35
Q

Describe the treatment for acute liver failure

A

Acutely: ABCDE, fluids, analgesia
Treat underlying cause and complications

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36
Q

What is the treatment for a paracetamol overdose?

A

Activated charcoal then N acetyl cysteine

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37
Q

How would you treat raised ICP?

A

IV mannitol

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38
Q

How would you treat HE?

A

Lactulose (increase NH3 excretion)

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39
Q

How would you treat ascites?

A

Diuretics, mostly spironolactone

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40
Q

How would you treat haemorrhage from acute kidney failure?

A

Vitamin K

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41
Q

What is the most common cause of chronic liver failure?

A

Alcoholic liver disease

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42
Q

Name some causes of chronic liver failure

A

Alcoholic liver disease
Non-alcoholic fatty liver disease
Viral: Hep B/C
Metabolic: Iron, copper
Budd Chiari
Autoimmune

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43
Q

What is Budd Chiari syndrome?

A

Obstruction of hepatic venous outflow

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44
Q

Name some risk factors for developing chronic liver disease

A

Alcohol
Obesity
T2DM
Drugs
Inherited metabolic disease
Existing AI diseases

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45
Q

Is fibrosis damage reversible or irreversible?

A

Reversible

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46
Q

Is cirrhosis damage reversible or irreversible?

A

Irreversible

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47
Q

What can cirrhosis lead to?

A

Compensated or decompensated(ed stage) liver failure

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48
Q

What is meant by compensated liver failure?

A

Some liver function is left

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49
Q

Name some signs of decompensated liver failure

A

Jaundice, HE, coagulopathy, ascites, portal HTN->oesophageal varices

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50
Q

What is a huge risk factor for developing HCC?

A

End-stage liver failure-decompensated cirrhosis

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51
Q

What is the Child pugh score used for?

A

Assessing prognosis and extent of chronic liver failure
Mostly for decompensated cirrhosis

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52
Q

What factors does the Child-Pugh score take into account?

A

Bilirubin
Presence of ascites
Serum albumin
PT/INR
HE presence

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53
Q

Describe the staging of the Child-Pugh score

A

A: 100% 1-year survival
B: 80% 1 year survival
C: 45% 1 year survival

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54
Q

What is the Meld score used for?

A

Model for end-stage liver disease-stratifies severity of ESLD for transplant planning

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55
Q

Name some symptoms of chronic liver failure

A

Jaundice
ascites
HE
portal HTN and oesophageal varices
Caput medusae
Spider naevi
Palmar erhythema
Gynecomastia
Clubbing
Fetor hepaticus (breath)

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56
Q

What is the gold standard investigation for diagnosing chronic liver failure?

A

Liver biopsy

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57
Q

Why is a liver biopsy needed?

A

To determine extent of chronic liver disease: fibrosis vs cirrhosis

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58
Q

What investigations are used to diagnose chronic liver failure?

A

Biopsy-GS
LFT’s
Ultrasound
Ascitic tap culture

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59
Q

Describe the treatment of chronic liver disease

A

Prevent progression: lifestyle modifications
Consider liver transplant (if decompensated liver failure)
Manage complications

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60
Q

Name some complications and treatments for chronic liver disease

A

HE-lactulose
ascites-diuretics
Oesophageal varices ruptures
SBP (spontaneous bacterial peritonitis
HCC

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61
Q

What is the equation to calculate units of alcohol?

A

(Strength (ABV) x vol/mL ) / 1000

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62
Q

What is the maximum number of recommended units of alcohol a week

A

14 units

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63
Q

How many grams and mL are in 1 unit of alcohol?

A

8g
10mL

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64
Q

What are the risk factors for developing alcoholic liver disease?

A

Chronic alcohol use
obesity
smoking

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65
Q

Describe the progression of alcoholic liver disease

A

Steatosis (fatty undamaged liver)->alcoholic hepatitis (with mallory bodies)->alcoholic cirrhosis (micronodular)

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66
Q

Describe the early-stage symptoms of alcoholic liver disease

A

Might have none!

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67
Q

Describe the late stage symptoms of alcoholic liver disease

A

Jaundice, hepatomegaly, palmar erythema, ascites, HE, spider naevi, easy bruising etc
Also alcohol dependency!

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68
Q

What are the 2 main alcohol dependency questionnaires?

A

CAGE
AUDIT

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69
Q

Describe the CAGE questionnare

A

Should you Cut down?
Are people Annoyed by your drinking?
Do you feel Guilty about drinking?
Do you drink in the morning (Eye opener)
>2=dependent

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70
Q

Describe the AUDIT questionnare

A

10 questions, alcohol use disorder ID test

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71
Q

What investigations would you carry out to diagnose alcoholic liver disease?

A

Bloods
Biopsy

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72
Q

What would you expect to find in the liver function blood test results of a patient with alcoholic liver disease?

A

LFT’s: hgih bilirubin, low albumin
High PT
High GGT
AST: ALT>2

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73
Q

What would you expect to find in the FBC of a patient with alcoholic liver disease?

A

Macrocytic non-megaloblastic anaemia
Potentially low folate

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74
Q

Why is a biopsy needed and what would it show in a patient with alcoholic liver disease?

A

Needed to confirm extent of cirrhosis or if it’s just hepatitis
Inflammation, necrosis, mallory cytoplasmic inclusion bodies

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75
Q

What are the 3 approaches to treating alcoholic liver disease?

A

Conservative
Pharmacological
Surgical

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76
Q

Describe the conservative treatment for alcoholic liver disease

A

Stop alcohol intake, healthy diet, BMI

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77
Q

What is a potential serious complication of alcohol withdrawal?

A

Delirium tremens

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78
Q

How would you manage delirium tremens?

A

Give chlordiazepoxide or diazepam

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79
Q

Name some alcohol withdrawal symptoms

A

Tremors
Agitation
Ataxia
Disorientation

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80
Q

Describe the pharmacological treatment of alcoholic liver disease

A

Consider short term steroids
B1 and folate supplements

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81
Q

What discriminant value should you use when deciding wether to prescribe short term steroids to someone with alcoholic liver disease

A

Maddrey’s discriminant value >32
Assesses alcoholic liver disease severity and need for treatment

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82
Q

Describe the surgical management of alcoholic liver disease

A

Liver transplant for ESLF patients
Must abstain from alcohol for >3 months before consideration

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83
Q

Name some complications of alcoholic liver disease and how you would treat them

A

Pancreatitis (IgE and smashed)
HE (lactulose)
Ascites (diuretics)
HCC (chemo, surgery)
Mallory Weiss tear
Wernicke Korsakoff syndrome

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84
Q

What is a Mallory Weis tear?

A

Tearing of tissue in lower oesophagus

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85
Q

What is Wernicke’s encephalopathy?

A

Encephalopathy caused by lack of B1 due to alcohol abuse

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86
Q

What is Korsakoff syndrome?

A

Memory affected by lack of B1

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87
Q

What is Wernicke Korsakoff syndrome?

A

Combined B1 deficiency and alcohol withdrawal symptoms

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88
Q

Name some symptoms of Wernicke Korsakoff syndrome.

A

Ataxia
Nystagmus
Encephalopathy
‘Confabulational’ make up stories to fill up memory gaps-disproportionate memory loss compared to other symptoms

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89
Q

When else might you see ‘confabulation’?

A

Fronto-temporal lobe amnesia

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90
Q

What is non-alcoholic fatty liver disease?

A

Chronic liver disease not due to alcoholism

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91
Q

Name some risk factors for developing non-alcoholic fatty liver disease

A

Obesity, htn, hyperlipidaemia, T2DM
family hx, endocrine disroders, drugs

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92
Q

Which drugs are risk factors for developing non-alcoholic fatty liver disease

A

NSAID’S
Amiodarone

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93
Q

When should non-alcoholic fatty liver disease be suspected?

A

Anyone obese/with T2DM and deranged LFT’s

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94
Q

Describe the progression of non-alcoholic fatty liver disease

A

Hepatosteatosis(NAFLD)->non alcoholic steatohepatitis(NASH)->fibrosis->cirrhosis

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95
Q

Describe the symptoms of non-alcoholic fatty liver disease

A

Usually asymptomatic and incidental findings
If very severe: signs of liver failure

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96
Q

What investigations should be done to diagnose non-alcoholic fatty liver disease?

A

Bloods: deranges LFT’s (high PT/INR, low albumin, high bilirubin)
FBC: thrombocytopenia, hyperglycaemia
Imaging: US abdomen
Screen for other causes: metabolic, HbA1c, lipid profile, hep serology

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97
Q

Would you do a biopsy to look for NAFLD?

A

Not unless absolutely necessary-US has 94% specificity for moderate-severe steatosis

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98
Q

Give an example of a non invasive scoring system used to assess the risk of fibrosis

A

Fibrosis 4 score
>2.67-advanced-refer to hepatology

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99
Q

Describe the treatment for NAFLD

A

Control risk factors:
Weight loss
Lipids: statins
Diabetes: metformin
Htn: ACE-i
Vitamin E: recommended by NICE-improves histological steatotic/fibrotic liver appearance)

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100
Q

Name some complications of NAFLD

A

HCC!
HE
Ascites
Portal htn and oesophageal varices

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101
Q

What is liver cirrhosis?

A

Diffuse pathological process characterised by fibrosis and presence of regenerative nodules.
Final stage of any chronic liver disease
Generally irreversible

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102
Q

Name some causes of liver cirrhosis

A

AFLD-most common in developed countries
Hep B/C
Fatty liver disease
HH
WD

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103
Q

How would you diagnose liver cirrhosis?

A

Deranged liver bloods: PT/IR high, albumin low, platelets low, thrombocytopenia etc
Liver biopsy gold standard

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104
Q

What is the definitive treatment for liver cirrhosis?

A

Liver transplant

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105
Q

What is the conservative treatment for liver cirrhosis?

A

Fluids, analgesia, alcohol abstinence, good nutrition

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106
Q

What is the medical treatment for liver cirrhosis?

A

Treat complications

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107
Q

Name some complications of liver cirrhosis

A

Ascites
Portal HTN
Varices
Also:
Jaundice
Coagulopathy
Hypoalbuminaemia(causing oedema)
Portosystemic encephalopathy
Hepatorenal and hepatopulmonary syndrome

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108
Q

What is viral hepatitis?

A

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

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109
Q

Which form of hepatitis is a notifiable disease to public health England?

A

Hep A

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110
Q

What type of virus is Hep A?

A

RNA

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111
Q

How is Hep A transmitted?

A

Faecal-oral, contaminated food, fly vectors

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112
Q

Describe the infection associated with Hep a

A

Acute-usually cleared by host immune system
100% immunity after infection

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113
Q

Describe the epidemiology of Hep A

A

Associated with travel history
High prevalence in Africa
Also Asia, south America, middle east

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114
Q

What are the risk factors for contracting Hep A?

A

Overcrowding
Poor sanitation
Shellfish
Travel

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115
Q

Describe the incubation and replication of Hep A

A

Incubation for 2 weeks
Replicates in liver, excreted in bile
Self limiting within 6 weeks

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116
Q

Describe the presentation of Hep A patients

A

Prodromal phase (1-2weeks): nausea, vomiting, malaise, fever, weight loss
After 1-2 weeks: liver symptoms: Jaundice, dark urine and pale stools, hepatosplenomegaly

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117
Q

What investigations can be done to diagnose Hep A?

A

Bloods: High ESR and leukopenia
LFT’S: raised ALT, raised bilirubin
HAV serology: HAV IgM if acutely infected

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118
Q

Describe the management of Hep A

A

Often not required, mostly supportive
Travellers vaccine available

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119
Q

Name a complication of Hep A

A

Fulminant liver failure

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120
Q

What kind of virus is Hep B?

A

DNA

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121
Q

Describe the infection caused by Hep B

A

Acute: infects hepatocytes, usually cleared
Chronic: If HBsAg>6 months, depends on age/immunocompetence. Inflammation can last 10 yrs->cirrhosis

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122
Q

Describe the transmission of Hep B

A

Blood products-needle sticks, IVDU, tattoos
Sexual
Vertical (mother to child)

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123
Q

In what bodily substances is Hep B found?

A

Semen
Saliva

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124
Q

Name some risk factors for contracting HBV

A

IVDU
MSM
Dialysis patients
Healthcare workers

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125
Q

Where in the world is HBV found?

A

Worldwide!
Especially Africa, Middle and far east

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126
Q

Describe HBV symptoms

A

1-2 weeks prodrome:
Then: deepening jaundice, dark urine, pale stools, hepatosplenomegaly urticaria, arthralgia

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127
Q

How long is the incubation period in HBV

A

1-6 months

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128
Q

How would you diagnose HBV?

A

HBVsAg: 1-6 months of infection
HBsAB: present after 6 months of infection
HbcAg: exposed to HBV at some point
HBcIgG: chronic infection/carrier
HBeAg: Marker of infectiousness(acutely infected)
HBeAB: All chronically infected patients or if they have cleared infection

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129
Q

What percentage of adult HBV cases progress to chronic liver failure and what does this increase the risk of?

A

5-10%
Increased HCC risk
HCC with HBV associated decompensation has worst prognosis

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130
Q

What percentage of HBV cases in children become chronic decompensation liver failure and how is this treated?

A

90%
Liver transplant

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131
Q

Describe the management of HBV

A

Vaccine available
Antivirals: Tenofovir, pegylated interferon alpha 2a

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132
Q

What are the main complications of HBV?

A

Increased risk of liver cirrhosis
HCC

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133
Q

What kind of virus is Hep C?

A

RNA

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134
Q

What kind of infections does Hep C cause?

A

Acute and chronic( causes slowly progressive fibrosis over years)

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135
Q

How is Hep C transmitted?

A

Blood borne
Especially IVDU
Also sexually but IVDU more

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136
Q

Describe the presentation of Hep C patients

A

Acute: often asymptomatic, occasionally flu-like symptoms
Present later with chronic liver signs and hepatosplenomagaly

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137
Q

How is Hep C diagnosed?

A

LFT’S
Serology:
HCVRNA: current infection/acte infection
HCVAb: within 4-6 weeks of infection

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138
Q

Describe the treatment for Hep C

A

Direct acting antivirals-ribavirin

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139
Q

What are the main complications of Hep C?

A

30% progress to chronic liver failure
cirrhosis and HCC risk

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140
Q

What kind of virus is Hep D?

A

RNA

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141
Q

How is Hep D transmitted?

A

Blood borne-sexually, IVDU

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142
Q

Describe the pathophysiology of Hep D

A

Unable to replicate on its own, requires concurrent HBV infection
Makes HBV more likely to progress to cirrhosis

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143
Q

How does Hep D manifest?

A

Same as co-infection
IgM HDV + IgM HBV

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144
Q

What kind of virus is Hep E?

A

RNA

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145
Q

Describe the transmission of Hep E

A

Faeco-oral-undercooked meat

146
Q

Describe the epidemiology of Hep E

A

Common in the UK

147
Q

Describe the presentation of Hep E

A

Mostly asymptomatic as virus is self-limiting

148
Q

How is Hep E diagnosed?

A

Serology: HEV IgM-acute infection, HEV RNA

149
Q

Describe the treatment for Hep E

A

Supportive
Vaccine only in China

150
Q

Describe immunity after Hep E infection

A

100% immunity after infection

151
Q

Describe the complications of Hep E

A

Chronic disease in immunosuppressed
Can cause fulminant liver failure: normal mortality 1-2%, pregnancy 10-20%)

152
Q

How does hepatitis appear histologically?

A

Interface necrosis

153
Q

What is autoimmune hepatitis?

A

Adaptive immunity mounts autoimmune response against hepatocytes

154
Q

What is another name for AI hepatitis?

A

Lupoid hepatitis
Causes lupus-like rash

155
Q

Name some risk factors for developing AI hep

A

Female
Other AI diseases
Viral hepatitis
HLA DR3 or DR4

156
Q

What are the 2 types of AI hep?

A

Type 1: Adult females (80%): ANA, ASMA
Type 2: Young females: ALC1(anti liver cytosol)
ALKM1(anit liver kidney microsome)

157
Q

Describe the presentation of AI hep

A

25% asymptomatic
Many: jaundice, fever, hepatosplenomegaly

158
Q

Describe the diagnosis of AI hep

A

Serology
ANA
ASMA
ALC-1
ALKM1

159
Q

Describe the treatment for AI hep

A

Corticosteroids (prednisolone)
Azathioprine (immunosuppressant)
Hep A +B vaccination
Last resort: liver transplant

160
Q

Describe the process of RBC metabolism

A

In the spleen:
Hb->Haem and globin
Haem->Fe2+ and biliverdin
Biliverdin->unconjugated bilirubin, transported in blood bound to albumin
In the liver: Unconjugated bilirubin+glucuronic acid->conjugated bilirubin, travels in bile to duodenum
Conjugated bilirubin->urobilinogen
90%-stercobilin-faeces
5%-urobilin-urine
5%-enterohepatic recycling

161
Q

What is jaundice?

A

AKA icterus
Yellowing of the skin/eyes due to accumulation of conjugated/unconjugated bilirubin
Sign of liver dysfunction

162
Q

Describe the pathophysiology of pre-hepatic jaundice

A

Increased haemolysis (RBC breakdown) leads to increased unconjugated bilirubin as liver can’t conjugate it fast enough

163
Q

Name some causes of pre-hepatic jaundice

A

Haemolytic anaemias:
Sickle cell
G6PDH deficiency
AI haemolytic anaemia
Thalassaemia
Malaria

164
Q

Describe the pathophysiology of intra-hepatic jaundice

A

Liver damage leads to conjugated/unconjugated bilirubin in blood

165
Q

Name some causes of intra-hepatic jaundice

A

HCC
ALD/NAFLD
Hepatitis
Hepatotoxic drugs
Gilbert syndrome

166
Q

Describe the pathophysiology of post hepatic jaundice

A

Blockage of bile ducts leads to backflow of conjugated bilirubin into the blood

167
Q

Name some causes of post hepatic jaundice

A

Biliary tree pathology:
-Choledocholiathis(stone stuck in CBD)
-Pancreatic cancer
-Cholangiocarcinoma
-Mrizzi syndrome
-Drug induced cholestasis
Autoimmune: PBC + PSC

168
Q

What is Mirizzi syndrome?

A

Gallstones stuck in gallbladder neck and externally compress CBD and cause obstruction

169
Q

Give some examples of drugs that can cause drug-induced cholestasis

A

Ampicillin
COCP

170
Q

What is Gilbert’s syndrome?

A

Mutation of uGT1A1 gene->underactive uGT enzyme->low conjugated bilirubin

171
Q

Which kind of jaundice causes pale stool and dark urine?

A

Obstructive/post hepatic jaundice

172
Q

Explain the pathophysiology of pale stool and dark urine in obstructive jaundice?

A

Increased levels of conjugated bilirubin in blood and low levels in intestine
Less stercobilin->pale poo
Les urobilin->dark urine

173
Q

What is the inheritance pattern of Gilbert’s syndrome?

A

Autosomal recessive

174
Q

Describe the presentation of Gilbert’s syndrome

A

Typically young males
Painless jaundice, sudden onset

175
Q

What is Courvoisier sign?

A

Painless jaundice and palpable gallbladder

176
Q

What is Courvoisier’s sign indicative of?

A

Most likely pancreatic cancer or cholangiocarcinoma

177
Q

What is Charcot’s triad and what is it used to assess?

A

Fever, RUQ pain, jaundice
Biliary colic: RUQ pain
Cholecystitis: fever + RUQ pain
Ascendign cholangitis: all 3

178
Q

What is Reynold pentad and what is it indicative of?

A

Seen in ascending cholangitis
Fever, RUQ pain, jaundice, confusion, hypotension

179
Q

What is the Murphy sign and what is it indicative of?

A

RUQ tenderness, ask patient to breathe in while pressing RUQ. Patient will wince/stop inspiring normally
Cholecystitis

180
Q

What tests would you use to diagnose jaundice?

A

Bloods + LFT’s: bilirubin, albumin, PT/INR, AST, ALT, GGT, ALP
Urine bilirubin: Positive in dark urine, post and intra hepatic causes
Urobilinogen: Normally positive, high in haemolysis, low in intra/post hepatic causes
US 1st line

181
Q

Describe urine bilirubin and urobilinogen levels in a normal patient

A

Negative urine bilirubin
Positive urine urobilinogen

182
Q

Describe urine bilirubin and urobilinogen levels in a patient with a biliary obstruction

A

Positive urine bilirubin
Low urine urobilinogen

183
Q

Describe urine bilirubin and urobilinogen levels in a patient with hepatic disease

A

Positive urine bilirubin
Low urine urobilinogen

184
Q

Describe urine bilirubin and urobilinogen levels in a patient with haemolysis

A

Low urine bilirubin
High urine urobilinogen

185
Q

What is pancreatic cancer?

A

Adenocarcinoma of the exocrine pancreas(99% of cases) of cutal origin, typically affecting head

186
Q

Name some risk factors for developing pancreatic cancer

A

Smoking
Alcohol
diabetes
fhx
chronic pancreatitis
genetic predisposition
males, >60yrs

187
Q

Describe the common distribution of pancreatic cancer

A

Head: 60%
Body: 25%
Tail: 15%

188
Q

Describe the signs and symptoms of pancreatic cancer

A

Head: Courvoisier sign(painless jaundice +palpable gallbladder) with pale stool and dark urine
Body + tail: epigastric pain radiating to back, relieved when sitting forward
Maybe: trousseau sign of malignancy

189
Q

What is Trousseau’s sign of malignancy?

A

Non specific episodes of vessel inflammation and clots in different parts of the body: migratory thrombophlebitis

190
Q

Mutation in what gene makes you susceptible to pancreatic cancer?

A

PRSS-1 mutation

191
Q

How would you diagnose pancreatic cancer?

A

1st line: abdominal US(less sensitive)
Pancreatic CT protocol then bile duct drainage

192
Q

What can be used to monitor pancreatic cancer progression?

A

Ca19-9 tumour marker

193
Q

What is the treatment for pancreatic cancer?

A

Poor prognosis: 5yr survival -3%
Surgery and post-op chemo if no mets
Palliative care if mets

194
Q

Describe the different types of liver cancers

A

Primary (less common): hepatocellular carcinoma, cholangiocarcinoma
Secondary: GI tract, breast, bronchial

195
Q

Where does HCC arise from?

A

Arise from liver parenchyma

196
Q

What percentage of primary liver cancers doe HCC make up?

A

90%

197
Q

Is HCC seen mostly in males or females

A

Males

198
Q

Name some risk factors for HCC

A

Chronic hep C/B virus
Cirrhosis from ALD/NAFLD/haemochromatosis

199
Q

Where does HCC metastasize to?

A

Lymph nodes
bones
lungs
Via hematogenous spread(hepatic/portal veins)

200
Q

Describe the symptoms of HCC

A

Signs of decompensated liver failure(jaundice, ascites HE etc)
Cancer signs: weight loss, night sweats etc
Might have irregular hepatomegaly

201
Q

How can HCC be diagnosed?

A

Might show high serum AFP
Imaging: US 1st line
CT confirmation

202
Q

Name 2 conditions that might show high AFP

A

HCC
Testicular cancer

203
Q

Why aren’t biopsies done to diagnose pancreatic cancer?

A

Prevents seeding of tumour elsewhere

204
Q

Describe the management of HCC

A

Surgical resection of tumor
Only real cure->liver transplant
Prevention: HBV vaccine

205
Q

Where does cholangiocarcinoma arise from?

A

Arises from biliary tree

206
Q

What kind of carcinoma is cholangiocarcinoma?

A

Typically adenocarcinomas

207
Q

Name some risk factors for cholangiocarcinoma

A

Parasitic flukeworms, biliary cysts, IBD, PSC

208
Q

Describe the symptoms of cholangiocarcinoma

A

Abdominal pain
jaundice
weight loss
pruritus
fevers
Also courvoiier’s sign-but more seen in pancreatic cancer

209
Q

How would you diagnose cholangiocarcinoma?

A

High CEA and high CA19-9
LFT: high bilirubin, high ALP
1st line imaging: abdominal US and CT
GS: ERCP(imaging of biliary tree)
Biopsy

210
Q

Name 2 advantages and one disadvantage of using ERCP to diagnose cholangiocarcinoma

A

Advantages: Can stent structures present in tree and can obtain sample for biopsy
Disadvantage: Invasive

211
Q

Describe the treatment for cholangiocarcinoma

A

Most cases are inoperable as patients present very late

212
Q

Name 2 benign liver primary tumours

A

Haemangioma: seen in infants as strawberry mark in skin within first weeks of life
Hepatic adenoma

213
Q

Are primary or secondary liver tumors more common?

A

Secondary tumours are more common

214
Q

Where do secondary liver tumours typically come from?

A

GI tract
lungs
breast

215
Q

How would you diagnose secondary liver tumours?

A

High serum ALP
Imaging: US, CT/MRI for staging

216
Q

Describe the treatment of secondary liver tumours

A

Surgical resection if possible of primary cancer and hepatic cancer
Chemo

217
Q

What are the 3 main biliary tract diseases?

A

Biliary colic(gallstones)
Cholecystitis
Ascending cholangitis

218
Q

What are gallstones made of?

A

Cholesterol-80%
Pigment
Mixed

219
Q

What are the risk factors for developing biliary tract diseases?

A

4F’s
Fat
Female
Forty +
Fertile (pregnancy/many children)
Also: FHx, T2DM, NAFLD, haemolytic conditions

220
Q

How is biliary colic different from typical colic?

A

Biliary colic: constant severe episodes of pain
Typical colic like renal colic: often comes and goes

221
Q

Describe the symptoms of gallstones

A

RUQ biliary colic (constant severe episodes of pain >30 minutes
Worse after eating a fatty meal
Referred shoulder pain
Nausea and vomiting

222
Q

Describe the symptoms of cholecystitis

A

RUQ pain: might be referred to shoulder by phrenic nerve
Fever
Tender gallbladder: Positive Murphy’s sign

223
Q

Describe the symptoms of ascending cholangitis

A

Charcot’s triad:
RUQ pain
Fever
Jaundice (obstructive-dark urine and pale stools)
Reynold’s pentad: Charcot’s triad + confusion + septic shock

224
Q

Describe the pathophysiology behind biliary colic

A

Temporary blockage of the cystic duct by gallstones

225
Q

Describe the pathophysiology of cholecystitis

A

Blockage of the cystic duct leads to the buildup of bile causing transmural inflammation of the gallbladder

226
Q

What is ascending cholangitis

A

Medical emergency characterized by bacteria(especially E.Coli) ascending through and colonising the biliary tree from the intestines leading to septicemia

227
Q

What does MRCP stand for?

A

Magnetic resonance cholangiopancreatography

228
Q

What does ERCP stand for?

A

Endoscopic retrograde cholangiopancreatography

229
Q

What investigations are done to diagnose a patient with biliary colic?

A

FBC, CRP, LFT’S
Abdominal US 1st line to ID gallstones

230
Q

Describe the treatment for gallstones

A

Analgesia: NSAID’s if mild, IM diclofenac if severe
Elective laparoscopic cholecystectomy if symptomatic
Lifestyle changes like low fat diets

231
Q

What investigations are done to diagnose cholecystitis?

A

FBC: leukocytosis+neutrophilia
CRP
LFT’s-should be normal
Abdominal US: >3mm thickened gallbladder wall

232
Q

Describe the treatment for cholecystitis

A

Early lap cholecystectomy(within 1 week) or have to wait 6 weeks
Supportive measures prior to surgery-fluids, analgesia, usually no antibiotics

233
Q

What investigations are done to diagnose ascending cholangitis?

A

FBC: leukocytosis + neutrophilia
LFT’s: high conjugated bilirubin
Amylase/lipase
CRP
US abdomen: CBD dilation and gallstones
MRCP: diagnostic and best pre-intervention management

234
Q

Describe the treatment of ascending cholangitis
eli sucks

A

Aggressive fluid resuscitation
IV abx: penicillins and aminoglycosides
ERCP for bile duct clearance first
Cholecystectomy once stable to prevent recurrence

235
Q

What is a major risk that must be considered when treat ascending cholangitis

A

Sepsis

236
Q

What is the difference between primary biliary cholangitis and primary biliary cirrhosis?

A

The is no difference!

237
Q

Describe the biliary tree

A

Common hepatic duct->Common bile duct
Cystic duct comes off common hepatic duct to gallbladder. Common bile duct->Ampula of Vater and pancreatic duct

238
Q

What is primary biliary cholangitis?

A

Progressive autoimmune destruction of the liver and biliary tree(intralobular bile ducts) leading to fibrosis and eventually cirrhosis

239
Q

What causes pruritus in PBC?

A

Excess conjugated bilirubin leaking out

240
Q

What are the risk factors for developing PBC?

A

Female
40-50yrs
Other AI diseases
Smoking

241
Q

Which is more common: PBC or PSC?

A

PBC more common

242
Q

Describe the pathophysiology of PBC

A

Autoantibodies cause intralobular bile duct damage->chronic AI granulomatous inflammation
Results in cholestasis->fibrosis, cirrhosis, portal htn and infections

243
Q

Describe the symptoms of PBC

A

Often asymptomatic/not specific symptoms at first
Fatigue
Pruritus
Advanced: jaundice, hepatomegaly, xanthelesma

244
Q

What complications can arise from PBC?

A

Cirrhosis
Malabsorption of fats and vitamins A,D,E,K->steatorrhoea
Osteomalacia
Coagulopathy

245
Q

What investigations are carried out to diagnose PBC?

A

LFT’s: high ALP and GGT, high conj. bilirubin, low albumin
Rule out acute hep: HeapBsAg, HCVAb
Serology: 95% have AMA antibodies
US: exclude extrahepatic cholestasis
Liver biopsy

246
Q

What would you see on a liver biopsy of a patient with PBC?

A

Portal tract infiltrate(lymphocyte and plasma cells)
40% granulomatous
Portal tract fibrosis

247
Q

Describe the treatment for PBC

A

Ursodeoxycholic acid: lifelong
For pruritus: colestyramine
Vitamin A,D,E,K supplements
Consider osteomalacia treatments
May ultimately need liver transplant

248
Q

What is ursodeoxycholic acid used for and how does it work?

A

PBC:
Bile acid analogue
Dampens immune response and reduces cholestasis

249
Q

What is primary sclerosing cholangitis?

A

Progressive sclerosis of the biliary tree leading to cholestasis and ESLD
AI destruction of intra and extra-lobular hepatic duct

250
Q

What are the risk factors foe developing PSC

A

Male
40-50
Strong link to IBD, especially UC

251
Q

Which affects more ducts: PBC or PSC?

A

PSC

252
Q

Describe the symptoms of PSC

A

Initially asymptomatic
Pruritus, fatigue, jaundice, Charcot’s triad (if CBD involved)
Hepatosplenomegaly
IBD relates symptoms

253
Q

What tests would you use to diagnose PSC?

A

LFT’s
Serology:
HBVsAg/HCVAb negative
ANA negative
Coeliac screen negative
pANCA often positive
GS: MRCP imaging

254
Q

What is acute pancreatitis?

A

Sudden inflammation of the pancreas leading to autodigestion of the gland-usually reversible

255
Q

Name the causes of acute pancreatitis

A

I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom/spider bite
Hypercalcaemia/hyperlipidaemia
ERCP
Drugs(NSAID’s, ACE-i’s, azathioprine0

256
Q

What is the most common cause of acute pancreatitis?

A

Gallstones

257
Q

What is the most common cause of chronic pancreatitis?

A

Ethanol

258
Q

Describe the pathophysiology of acute pancreatitis caused by gallstones

A

Gallstones obstruct pancreatic secretion, so digestive enzymes accumulate in the pancreas
Host defences soon overwhelmed
Autodigestion->inflammation and enzymes leak into blood

259
Q

Describe the symptoms of acute pancreatitis

A

Sudden severe epigastric pain radiating to the back
Jaundice
Pyrexia
Steatorrhea
Grey Turner sign (flank bleeding)
Cullen sign(periumbilical bleeding)

260
Q

How would you diagnose acute pancreatitis?

A

Bloods: High serum amylase/lipase, LFT’s, CRP
Erect CXR to exclude gastroduodenal perforation(can also increase amylase/lipase)
US: diagnostic for gallstones
CT/MRI: look at extent of damage

261
Q

Is serum amylase or lipase more specific for acute pancreatitis?

A

Lipase more specific but less routine

262
Q

For a diagnosis of acute pancreatitis to be made what criteria have to be met?

A

At least 2 of:
1. Characteristic symptoms/signs
2. High amylase/lipase
3. Radiological evidence

263
Q

What is a differential diagnosis for acute pancreatitis epigastric pain?

A

AAA

264
Q

Describe the acute pancreatitis scoring systems

A

APACHE 2: severity within 24 hours
Glasgow and Ranson score: prediciton of severe attack after 48 hours

265
Q

What is the treatment for acute pancreatitis?

A

Nil by mouth, TPN if required
Agressive fluid rescuscitation
Analgesia: usually morphine
Antibiotics if necrotising pancreatitis
Catheterise

266
Q

What complications can arise from acute pancreatitis?

A

SIRS
Pancreatic pseudocyst
Insulant dependent DM
ARDS and pleural effusion
DIC

267
Q

What is SIRS and how is it diagnosed?

A

Systemic inflammatory response syndrome-complication of acute pancreatitis
2 of:
Tachycardia
Tachypnoea
Pyrexia
High WCC

268
Q

What is chronic pancreatitis?

A

> 3-month history of pancreatic deterioration-irreversible pancreatic inflammation and fibrosis
Can be persistent pain and malabsorption or acute on chronic episodes

269
Q

Name some causes of chronic pancreatitis

A

Alcohol-most common
Cystic fibrosis
Cancer
AI
CKD
Traume
Recurrent acute pancreatitis

270
Q

Describe the symptoms of chronic pancreatitis and give a differential diagnosis for these symptoms

A

Epigastric pain boring to back, exacerbated by alcohol
Steatorrhoea
Weight loss-malabsorption
Insulin-dependent DM

DDx: pancreatic cancer

271
Q

How is chronic pancreatitis diagnosed?

A

Bloods: lipase and amylase: unlikely to be high in severe cases
Secretin stimulation test
Fecal elastase: typically high
US, CT-detects pancreatic calcification and dilated pancreatic duct

272
Q

Why are amylase and lipase unlikely to be high in severe chronic pancreatitis cases?

A

Such a deficiency that there’s none left to leak out

273
Q

Describe the management of chronic pancreatitis

A

Alcohol cessation
NSAID.s/opiates for pain
Pancreatic supplements like insulin and creon
ERCP or surgery if required

274
Q

What is portal hypertension?

A

Pathologically high BP in the portal vein

275
Q

Name the causes of portal hypertension

A

Pre hepatic: portal vein thrombosis
Intrahepatic: cirrhosis, schistosomiasis
Posthpeatic: Budd Chiari, RHS failure, constrictive pericarditis

276
Q

What is the normal and abnormal pressure in the portal vein?

A

5-8mmHg
>10: bad
>12: very bad

277
Q

Explain the pathophysiology behind portal hypertension

A

Cirrhosis: increased resistance to blood flow->splanchnic dilation and compensatory increase in CO->fluid overload in the portal vein

278
Q

How does portal hypertension lead to oesophageal varices?

A

Fluid overload in portal vein->collateral blood shunting to gastroesophageal veins(typically small)->oesophageal varices

279
Q

Where are oesophageal varices most commonly found?

A

Cardia and lower oesophagus

280
Q

Describe the symptoms of portal hypertension

A

Mostly asymptomatic
Ascites
Bleeding varices

281
Q

When do patients with portal hypertension most commonly present?

A

When oesophageal varices rupture

282
Q

What is a differential diagnosis for oesophageal varices and how can you differentiate between them?

A

Mallory Weiss tear: very acute history, high abdominal pressure(retching, alcoholic heaves)
Varices: History of alcoholism/liver cirrhosis

283
Q

What is the main concern of ruptured oesophageal varices

A

Haemorrhage, patients with haematemesis

284
Q

How do you diagnose oesophageal varices?

A

Oesophagogastroduodenoscopy

285
Q

Describe the management of haemorrhaging oesophageal varcise

A

Acutey: resus until haemodynamically stable
Consider blood transfusion (Hb<70g/L)

Stop bleed:
1. IV Terlipressin
2. Variceal banding
3. TIPPS: transjugular;ar intrahepatic portasystemic shunt-decrease portal pressure by diverting blood to other larger veins

Prevent bleed:
Beta blocker-propanolol and nitrates
Repeat variceal banding
Last resort: liver transplant

286
Q

What is ascites?

A

Free fluid in the peritoneal cavity

287
Q

Name the causes of ascites

A

Local inflammation: peritonitis, TB, abdominal cancer
Low protein: hypoalbuminemia(liver failure), nephrotic syndrome
Flow stasis: build-up causes leakage: cirrhosis, Budd Chiari, congestive heart failure, constrictive pericarditis

288
Q

What are the symptoms of ascites?

A

Abdominal distention
May have jaundice and pruritus
Shifting dullness and fullness in flanks

289
Q

How do you diagnose ascites?

A

Shifting dullness on exam
Ascitic tap (periocentesis of 10-20ml fluid)
Cytology: WCC, albumin etc
Protein measurement

290
Q

Explain transudate measurement and causes for ascites

A

<30g/L protein (low), <11gL SAAG
Clear fluid
Fluid due to high hydrostatic pressure
Portal hypertension, budd chiari, constrictive pericarditis, CJF, nephrotic syndrome

291
Q

Explain exudate protein measurement and causes for ascites

A

> 30g/L protein, SAAG >11g/L
Cloudy fluid
Fluid due to inflammation, mediated exudation or low oncotic pressure
Malignancy, peritonitis, pancreatitis

292
Q

What is SAAG?

A

Serum albumin-ascitic gradient
Serum albumin-albumin in ascitic fluid

293
Q

How do you treat ascites?

A

Treat underlying cause
Diuretic to increase Na+ excretion so more fluid is pushed out-spironolactone
Paracentesis
Liver transplant

294
Q

What is peritonitis?

A

Inflammation of the peritoneal cavity

295
Q

What are the different sensations in the abdomen related to peritonitis?

A

T5-9: epigastric: greater splanchnic, foregut(up to duodenum)
T10-11: umbilical: lesser splanchnic, midgut (2/3 transverse colon)
T12: hypogastric: least splanchnic, hindgut (up to rectum)

296
Q

What is the difference between primary and secondary peritonitis?

A

Primary: ascites, SBP
Secondary: underlying cause e.g. bile, malignancy

297
Q

What is the most common cause of peritonitis?

A

SBP (infection)

298
Q

Describe the bacterial causes of peritonitis

A

Gram negative: E.Coli+Kliebsiella (colliform rods)
Gram positive: Staph aureus (cocci)

299
Q

Name some chemical causes of peritonitis

A

Bile
Old clotted blood
Ruptured ectopic pregnancy
Intestinal perforation
Ultimately get infected

300
Q

Describe the symptoms of peritonitis

A

Sudden onset severe abdominal pain, then collapse, fever, septic shock
Rigidity helps pain: guarding, hands on abdo to stop it moving and avoid speedbumps when driving
Poorly localised
Ascites

301
Q

What is a differential diagnosis for rigidity helping pain from peritonitis

A

Renal colic

302
Q

How is peritonitis diagnosed

A

Ascitic tap: neutrophilia
Cultures: causative organism
High ESR and CRP
Exclude pregnancy and bowel obstruction as cause
Erect CXR: under diaphragm-indicates perforated colon

303
Q

How is peritonitis treated?

A

ABCDE
Treat underlying cause
IV fluids, antibiotics (cefotaxime, metronidazole)
Surgery: peritoneal lavage

304
Q

Name some causes of peritonitis

A

Scepticaemia
Subphrenic/pelvic abscesses
Paralytic ileus

305
Q

What are the 3 main metabolic liver diseases?

A

Haemochromatosis
Wilson’s disease
Alpha 1 antitrypsin deficiency

306
Q

What is hemochromatosis?

A

Autosomal recessive mutation of HFE gene that leads to dysregulated iron absorption and increased iron release from macrophages

307
Q

Why is hemochromatosis unlikely in women?

A

Iron loss in menstruation

308
Q

Name some risk factors for hemochromatosis

A

Male
50 years
FHx

309
Q

Describe the pathophysiology of hemochromatosis

A

Excess Fe uptake by transferrin 1 and low hepcidin synthesis->accumulation of iron which accumulates and causes fibrosis o organs: liver, joints, pancreas, heart, skin, gonads

310
Q

What does hepcidin do?

A

Protein that regulates iron homestasis

311
Q

How much iron is usually in the body and how much is there in hemochromatosis?

A

Usually: 3-4g
hemochromatosis: 20-30g

312
Q

Describe the symptoms of hemochromatosis

A

Fatigue
joint pain
hypogonadism
slate grey->bronze skin
liver cirrhosis symptoms
osteoporosis
heart failure

313
Q

What is the gross Fe overlad triad?

A

Bronze statue skin
Hepatomegaly
T2DM

314
Q

What can cause secondary iron overload?

A

Multiple transfusion

315
Q

How is hemochromatosis diagnosed?

A

Fe studies: High serum Fe, high ferritin, high transferrin index, low TIBC
Genetic test
Liver biopsy-assess degree of liver stain with prussian blue stain

316
Q

Describe the treatment of hemochromatosis

A

Venesection: regularly removing blood
Iron chelation 2nd line: desfernoxamine
Lifestyle changes, low iron, avoid fruits
Definitive: liver transplant

317
Q

What is Wilson’s disease?

A

Autosomal recessive mutation of ATP78 gene on chromosome 13-> excess body copper

318
Q

Describe a typical patient with Wilson’s disease

A

Young-20yrs
Family history

319
Q

Describe the pathophysiology of Wilson’s disease

A

Impaired copper biliary excretion and normal transport-> copper accumulation in liver , basal ganglia and cornea

320
Q

Describe the symptoms of Wilson’s disease

A

Hepatic: liver disease, jaundice etc
Neurological: Parkinsonian, depression, memory problems
Opthalmological: Kayser Fleischer rings(green-brown rings)

321
Q

How is Wilson’s disease diagnosed?

A

24 hr urine copper and blood caeruloplasmin(low)
Liver biopsy: definitive
MRI brain: cerebellar and BG degeneration

322
Q

Describe the treatment for Wilson’s disease

A

D-Penicillinamine (copper chelation-lifelong)
Diet changes-avoid high copper foods like mushrooms and shellfish
Last resort: liver transplant

323
Q

What is A1AT deficiency?

A

Deficiency of alpha 1 antitrypsin enzyme due to autosomal recessive mutation of protease inhibitor gene(‘SERPINA-1 gene) on chromosome 14

324
Q

Describe the pathophysiology of A1AT deficiency

A

A1AT normally inhibits neutrophil elastase(degrades elastic tissue)
Insufficient A1AT->high NE
Lungs: degrades elastic tissue causing alveolar duct collapse, air trapping and panacinar emphysema
liver: unprotected, soon become fibrotis-cirrhosis and HCC risk

325
Q

How does liver fibrosis make A1AT synthetic function even worse?

A

A1AT made by liver

326
Q

Describe the presentation of a patient with A1AT deficiency

A

Young/middle-aged male with no/little smoking history but symptoms of COPD
Dyspnoea, chronic cough, sputum production, barrel chest
Liver symptoms like jaundice

327
Q

How is A1AT diagnosed?

A

Serum A1AT (low: <20mmol/L)
Barrel chest on exam, CXR: hyperinflated lungs
CT: panacinar emphysema
LFT: Spirometry shows obstruction (FEV:FVC<0.7)
Genetic test: positive PI mutation

328
Q

Describe the management for A1AT deficiency

A

No curative treatment
Smoking cessation
Manage emphysema: inhalers, SABA’s/LABA’s
Consider hepatic decompensation patients for liver transplants

329
Q

What does of paracetamol is classed as an overdose?

A

> 75mg/kg

330
Q

Describe teh sympotms of a paracetamol overdose

A

Acute severe RUQ pain, severe nausea and vomiting

331
Q

Describe normal paracetemol metabolism

A

90%: glucuronidation/sulfation->excreted
10%: Phase 1 conjugation (CYP450)->NAPQ1->phase 2 glutathione->excreted

332
Q

What happens to paracetamol metabolism in an overdose?

A

Glucuronidation and sulfation pathways saturated, more metabolised by P450->depleted glutathione->increases NAPQ1 production which is toxic and accumulates in the liver

333
Q

What is the treatment for a paracetamol overdose?

A

Activated charcoal (within 1 hour of ingestion) and N-acetyl-cysteine

334
Q

What does N acetyl cysteine do?

A

Increases availability of glutathione to get rid of excess NAPQ1

335
Q

What is Gilbert’s syndrome?

A

Most common cause of hereditary jaundice
Autosomal recessive
Liver unable to conjugate bilirubin

336
Q

Name some risk factors for Gilbert’s syndrome

A

Male
T1DM
fhX

337
Q

Describe the pathophysiology of Gilbert’s syndrome

A

Deficient or abnormal uGT-> increased unconjugated bilirubin

338
Q

Describe the symptoms of Gilbert’s syndrome

A

30% asymptomatic
May present with just painless jaundice at a young age
Criggler Najjor: more severe: jaundice with nausea and vomiting and lethargy

339
Q

Describe the management of Gilbert’s syndrome

A

Usually fine without treatment

340
Q

What is Crigler Najjar syndrome and why is it dangerous?

A

More severe porgression
Can die from kernicterus (accumulation of bilirubin in basal ganglia->neurological deficits) in childhood

341
Q

What is the treatment for Crigler Najjar syndrome?

A

Phototherapy: breaks down unconjugated bilirubin

342
Q

What are hernias?

A

Protrusion of an organ through defect in containing cavity, typically bowerl

343
Q

What is a hiatal hernia?

A

Stomach hernia through diaphragm aperture

344
Q

What are the 2 types of hiatal hernia?

A

Rolling(20%): LES stays in abdomen, part of fundus rolls into thorax
Sliding (80%): LES slides into abdomen

345
Q

Name some symptoms of hiatal hernia

A

GORD
Dysphagia

346
Q

How are hiatal hernias diagnosed?

A

CXR
Barium swallow
OGD

347
Q

Name some risk factors for developing a hiatal hernia

A

Obese
Female
>50

348
Q

How can hernias be classed?

A

Reducible->pushed back into place
Irreducible:
Obstructed-intestinal obstruction
Strangulated-intestinal ischaemia->gangrene, infarction
Incarcerated-contents are fixed in sac due to size/adhesion

349
Q

What is a femoral hernia?

A

Bowel through femoral canal
Very likely to strangulate due to rigid femoral canal borders

350
Q

Name some risk factors for developing a femoral hernia

A

Female
Mid-old age

351
Q

Name some symptoms of a femoral hernia

A

Swelling in upper thigh pointing down

352
Q

How would you diagnose a femoral hernia?

A

US abdo/pelvis if unsure, but usually can be diagnosed clinically

353
Q

What is an inguinal hernia?

A

Spermatic cord herniates through inguinal canal
Direct(20%): In Hesselbachs triangle, medial to inferior epigastrics
Indirect(80%): Lateral to inferior epigastric, not in triangle

354
Q

Name some risk factors for developing an inguinal hernia

A

Male
Hx of heavy lifting/abdominal pressure

355
Q

Name some symptoms s of an inguinal hernia

A

Painful swelling in groin
Points along groin margin

356
Q

How are inguinal hernias diagnosed?

A

Usually clinical
If unsure: AUSS/CT/MRI

357
Q

What is the curative treatment for hernias?

A

Surgery

358
Q

What is an umbilical hernia?

A

Intestine pushes through umbilical ring
Common in children
May get worse when laughing/sneezing

359
Q

What is an incisional hernia?

A

Protrusion of tissue at the site of a healing surgical scar

360
Q

Where is an epigastric hernia found?

A

Between sternum and belly button

Phase 2a med mine (11 decks)

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