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Phase 2a > Liver and Friends > Flashcards

Liver and Friends Flashcards

1
Q

What are the stages of alcoholic liver disease

A
  1. Alcoholic fatty liver - hepatic steatosis
  2. Alcoholic hepatitis
  3. Cirrhosis
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2
Q

Which process of alcoholic liver disease is irreversible

A

Cirrhosis - functional liver tissue is replaced with scar tissue

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3
Q

What is the alcoholic drinking recommendations

A

No more than 14 units per week

Across 3 days or more

No more than 5 units per day

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4
Q

What questions (2) can be used to screen for harmful alcohol use

A

CAGE questions

AUDIT questionnaire

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5
Q

Describe CAGE questions

A

Cut down?
Annoyed - commenting about drinking
Guilty
Eye opener - drink first thing in a morning

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6
Q

Name 3 risk factors for alcoholic liver disease

A

Prolonged and heavy alcohol consumption

Hepatitis C

Female sex

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7
Q

Name the clinical features of alcoholic liver disease

A

Ascites
Weight loss/gain
Malnutrition and wasting
Anorexia
Fatigue
Abdominal pain
Hepatomegaly

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8
Q

Name the investigations for alcoholic liver disease

A

GS- liver biopsy

Blood tests
Liver ultrasound
Transient elastography
Endoscopy
CT and MRI scans

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9
Q

What is the management of alcoholic liver disease

A

Stop drinking - alcohol withdrawal

Nutritional support - vitamins and high-protein diet

Treat complications of liver cirrhosis

Liver transplant

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10
Q

Define non-alcoholic liver disease

A

Characterised by excessive fat in the liver cells (specifically triglycerides)

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11
Q

Describe the pathophysiology of non-alcoholic fatty liver disease

A

Excessive fat interferes with normally functioning liver cells.

Can progress into hepatitis and cirrhosis

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12
Q

What are the stages of non-alcoholic fatty liver disease

A
  1. Non-alcoholic fatty liver disease.
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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13
Q

What are the risk factors for non-alcoholic fatty liver disease the same as

A

CVD

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14
Q

What is non-alcoholic fatty liver disease associated with

A

Metabolic syndrome = hypertension + obesity + diabetes

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15
Q

Describe the clinical features of non-alcoholic fatty liver disease

A

Early - asymptomatic

Late -
Nausea
Vomiting
Jaundice
Pruritis
Ascites
Memory impairment
Easy bleeding
Loss of appetite

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16
Q

Name 2 signs of non-alcoholic fatty liver disease

A

Jaundice

Spider angiograms

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17
Q

What are the investigations of non-alcoholic fatty liver disease

A

Raised alanine aminotransferase (ALT)

Liver ultrasound
Enhanced liver fibrosis blood test
Transient elastography
Liver biopsy

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18
Q

What tests can be used to score non-alcoholic fatty liver disease

A

NAFLD fibrosis score
Fibrosis 4

Both assess for liver fibrosis

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19
Q

What is the gold standard test for non-alcoholic fatty liver disease

A

Liver biopsy

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20
Q

What is the management for non-alcoholic fatty liver disease

A

Modifications
- Weight loss
- Healthy diet
- Avoid/limit alcohol intake
- stop smoking
- Control diabetes.

Refer patients for scoring
Specialist management

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21
Q

Which hepatitis are RNA viruses

A

A, D, E

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22
Q

Which hepatitis are DNA viruses

A

B, C

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23
Q

Which hepatitis route of transmission is Faeco-oral

A

A, E

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24
Q

Which hepatitis are blood/sexual transmission

A

B, C, D

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25
Q

What are the clinical features of hepatitis A infection

A

Cholestasis with:
- Pruritus
- Significant jaundice
- Dark urine
- Pale stools

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26
Q

Which hepatitis are a chronic infection

A

B, C, D

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27
Q

Describe the diagnosis of hepatitis A

A

IgM antibodies to hepatitis A

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28
Q

Describe the management of hepatitis A

A

Supportive - usually resolves without treatment

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29
Q

Describe the screening test for hepatitis B

A

Measure IgM and IgG versions of HBcAb

IgM - active infection
- high = acute
- low = chronic

IgG = past infection

HBsAg = active infection in acute phase (replicating)

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29
Q

Describe the management of hepatitis B

A

Supportive + antiviral (tenofovir, analogues)

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30
Q

Describe the serology of hepatitis C

A

HVC Ab = all patients

HCV RNA = chronic infection

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31
Q

Describe the investigations of hepatitis C

A

Hepatitis C antibody = screening test

Hepatitis C RNA testing - confirms diagnosis

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32
Q

What is the management of hepatitis C

A

Direct-acting antivirals

  • Pegylated interferon weekly injections

+ Ribavirin tablets

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33
Q

When can someone have hepatitis D

A

With a hepatitis B infection

Increases complications and disease severity of hepatitis B

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34
Q

What is the management of hepatitis D

A

pegylated interferon alpha

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35
Q

Which hepatitis currently have a vaccine

A

A, B

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36
Q

What is the prevention for hepatitis A and B

A

Pre and post exposure immunisation

B as well - behaviour modification

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37
Q

How is hepatitis C prevented

A

Blood donor screening

Behaviour modification

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38
Q

How is hepatitis D prevented

A

HBV immunisation

Behaviour modification

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39
Q

How is hepatitis E prevented

A

Clean drinking water

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40
Q

What is the treatment for hepatitis E

A

Supportive

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41
Q

Define liver cirrhosis

A

Due to chronic inflammation and damage to liver cells. Functional cells are replaced with scar tissue (fibrosis) - nodules of scar tissue

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42
Q

What are the 4 most common causes of liver cirrhosis

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C

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43
Q

What are the risk factors of liver cirrhosis

A

Alcohol misuse
IVDU
Unprotected intercourse
Obesity
Birth country

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44
Q

Name a complication of liver cirrhosis

A

Portal hypertension

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45
Q

Name the clinical features of liver cirrhosis

A

Cachexia
Jaundice
Hepatomegaly
Small nodular liver
Splenomegaly
Spider naevi
Palmar erythema

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46
Q

Describe the investigations of liver cirrhosis

A

GS-Gastroscopy

Blood tests
- LFTs
- Albumin
- Prothrombin time
- FBC

Non-invasive liver screening
Imaging

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47
Q

Name 2 tests for clinical diagnosis of liver cirrhosis

A

MELD score - model for end-stage liver disease

Child-Pugh Score

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48
Q

Describe MELD Score

A

Score every 6 months in patients with compensated cirrhosis

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49
Q

Describe the Child-Pugh score for liver cirrhosis

A

Used 5 factors (score 1,2,3) to assess the severity of cirrhosis and the prognosis

Max score 15

ABCDE
Albumin
Bilirubin
Clotting (INR)
Dilation (ascites)
Encephalopathy

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50
Q

What are the 4 principles of the management of liver cirrhosis

A
  1. Treat underlying condition
  2. Monitor for complications
  3. Manage complications
  4. Live transplant
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51
Q

When is liver transplant considered in liver cirrhosis

A

When features of decompensated liver disease

Features
Ascites
Hepatic encephalopathy
Oesophageal varices bleeding
Yellow (jaundice).

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52
Q

Define jaundice

A

Yellow discolouration of the sclera and skin

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53
Q

Why does jaundice occur

A

Hyperbilirubinemia - occurs at > 51 micromol/L.

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54
Q

What is the normal range for total bilirubin

A

3.4-20 micromol/L

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55
Q

Describe the pathophysiology of jaundice

A

Bilirubin - conjugated within the liver = soluble.

Majority = ejested in the faeces as urobilinogen ad stercobilin

10% urobilinogen absorbed back into the blood stream and excreted by the kidneys

Jaundice occurs when this pathway is disrupted

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56
Q

Name the 3 types of jaundice

A
  1. Pre-hepatic
  2. Hepatocellular (intra-hepatic)
  3. Post-hepatic
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57
Q

Describe pre-hepatic jaundice

A

Excessive red cell breakdown - overwhelms the liver’s ability to make conjugated bilirubin

Causes - unconjugated hyperbilirubinemia

Unconjugated remains in the blood stream to cause the jaundice

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58
Q

Describe intra hepatic jaundice

A

Cirrhosis compresses the intra-hepatic proteins of the biliary tree to cause obstruction.

Leads to both conjugated and unconjugated bilirubin in the blood

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59
Q

Describe post hepatic jaundice

A

Obstruction of biliary drainage

Bilirubin is not excreted will have been conjugated by the liver

= conjugated hyperbilirubinemia

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60
Q

Name 3 causes pre-hepatic jaundice

A

Haemolytic anaemia
Gilbert’s syndrome
Criggler-Najiar syndrome

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61
Q

Describe the potential causes of intra-hepatic jaundice

A

Alcoholic liver disease
Viral hepatitis
Iatrogenic
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Hepatocellular carcinoma

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62
Q

Describe the potential causes of post-hepatic jaundice

A

Intra-luminal causes - gallstones

Mural causes
Extra-mural causes

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63
Q

Name the risk factors of jaundice

A

Drugs and alcohol
Social history
Autoimmune
Sexual history
Inflammation of the bile duct
Haemolytic anaemia
Obstruction of the bile duct

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64
Q

Pre-hepatic jaundice

Name
Urine
Stools
Itching
Liver tests

A

Normal
Normal
No
Normal

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65
Q

Describe intra/post-hepatic jaundice

Urine
Stools
Itching
Liver tests

A

Dark
May be pale
Maybe
Abnormal

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66
Q

Describe the investigations of jaundice

A

Liver enzymes
Biliary obstruction
Imaging

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67
Q

Describe the management of jaundice

A

Dependent on underlying cause

Obstructive
- removal of gallstones
- cholangiopancreatography or stenting of common bile duct

Symptomatic treatment - itching

Identify and manage any complications

Treatment of confusion

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68
Q

What is the treatment of confusion due to decompensating chronic liver disease

A

Laxatives +/- neomycin

Rifaximin

Attempts to reduce the number of ammonia-producing bacteria in the bowel

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69
Q

Define autoimmune hepatitis

A

Chronic inflammatory disease of the liver with unknown aetiology.

Characterised by the presence of circulating auto-antibodies with a high serum globulin concentration, inflammatory response changes on liver histology and favourable responses to immunosuppressive treatment.

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70
Q

What are the causes of autoimmune hepatitis

A

Occur due to combination of genetic and environmental factors

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71
Q

Name the different types of autoimmune hepatitis

A

Type 1 and 2

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72
Q

Describe type 1 autoimmune hepatitis

A

Affects women

Late 40-50s

Presents around or after menopause with fatigue and features of liver disease on examination

Less acute than type 2

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73
Q

Describe type 2 autoimmune hepatitis

A

Children or young people

More commonly girls

Acute hepatitis

Transaminases and jaundice

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74
Q

Name the risk factors of autoimmune hepatitis

A

Female sex
Genetic pre-disposition
Immune dysregulation

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75
Q

Name the investigations of autoimmune hepatitis

A

High transaminases
Minimal changes in ALP levels
Raised IgG

Liver biopsy

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76
Q

Describe the management of autoimmune hepatitis

A

Prednisolone + azathioprine (90%)

Liver transplant - autoimmune hepatitis can reoccur

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77
Q

Define Wernicke’s encephalopathy

A

Neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations

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78
Q

Define Korsakoff syndrome

A

Memory disorder that results from vitamin B1 deficency and is associated with alcoholism.

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79
Q

Describe the causes of Wernicke-Korsakoff syndrome

A

Acute or subacute deficiency of thiamine

Decreased intake - oral or parenteral

Increased demand, or malabsorption from the GI tract

Other causes:
- alcohol abuse
- dietary deficiency
- prolonged vomiting
- eating disorders
- effects of chemotherapy

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80
Q

Name the clinical features of Wernicke’s encephalopathy

A

Damage to the brain’s thalamus and hypothalamus

  • Neuropsychiatric manifestations
  • Confusion
  • Oculomotor disturbances
  • Ataxia
  • Gait and balance disorders
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81
Q

Describe the clinical features of Korsakoff syndrome

A

Memory impairment - retrograde or anterograde

Behavioural changes

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82
Q

Describe the investigations of Wernicke-Korsakoff syndrome

A

Therapeutic trial of parenteral thiamine

Other tests
- Finger-prick glucose
- Bloods

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83
Q

Describe the management of Wernicke-Korsakoff syndrome

A

Treated in emergency with thiamine replacement

Wernicke’s important to start thiamine replacement before beginning nutritional replenishment

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84
Q

What is the prevention of Wernicke-Korsakoff syndrome

A

Thiamine supplementation
Alcohol abstaining

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85
Q

Define hepatic encephalopathy

A

Brain dysfunction (neuropsychiatric syndrome) caused by acute or chronic advanced hepatic insufficiency and/or portosystemic shunt

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86
Q

Name the 3 pathophysiological mechanisms for hepatic encephalopathy

A

Ammonia absorbed into circulation through the portal venous system

Hyperammonaemia - affecting neurotransmitter synthesis

Increased activation of GABA

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87
Q

Describe the cause of hepatic encephalopathy

A

Combination of metabolic encephalopathy, brain atrophy and/or brain oedema

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88
Q

Name 4 symptoms of hepatic encephalopathy

A

Mood, sleep and motor disturbances

Advanced neurological deficits

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89
Q

Name 7 signs of hepatic encephalopathy

A

Asterixis
Palmar erythema
Spider angiomata
Peripheral oedema
Jaundice
Hepatomegaly
Ascites

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90
Q

Name the investigations for hepatic encephalopathy

A

Blood
Urine culture
Urine toxin screen
Ultrasonography
Head CT or MRI

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91
Q

Name the primary objectives of the management of hepatic encephalopathy

A

Provide supportive care

Exclude other causes of altered mental state

Identify and correct precipitating factors

Reduce the nitrogenous load from the gut

Assess the need for long-term therapy

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92
Q

Describe the pathophysiology of pancreatic cancer

A

Tumour in the head of the pancreas grows large enough to compress the bile duct

Spread metastasis early

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93
Q

Name the risk factors for pancreatic cancer

A

Smoking
Family history

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94
Q

Name the clinical features of pancreatic cancer

A

Key = painless obstructive jaundice
- yellow skin and sclera
- pale stools
- dark urine
- generalised itching

Other vague presenting features

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95
Q

Name the clinical signs of pancreatic cancer

A

Courvoisier’s law
Trousseau’s sign of malignancy

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96
Q

Describe Courvoisier’s Law

A

Palpable gallbladder + jaundice = unlikely to be gallstones.

Usual cause - cholangiocarcinoma or pancreatic cancer

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97
Q

Describe Trousseau’s sign of malignancy

A

Migratory thrombophlebitis = sign of malignancy

Blood vessels become inflamed with associated thrombus in multiple different locations over time.

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98
Q

Describe the investigations of pancreatic cancer

A

Imaging

CA19-9 (carbohydrate antigen) = tumour marker.

Biopsy

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99
Q

How is a diagnosis of pancreatic cancer made.

A

Imaging (usually CT scan) + histology from biopsy

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100
Q

What are the NICE referral guidelines for pancreatic cancer

A

> 40 + jaundice = 2 week wait

> 60 + weight loss + one additional symptom = referred for a direct access CT abdomen

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101
Q

Describe the management of pancreatic cancer

A

Options

Surgery
Palliative treatment (if no surgery).

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102
Q

Define hepatocellular carcinoma

A

Main type of primary liver cancer = originates in the liver

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103
Q

Name the risk factors for hepatocellular carcinoma

A

Liver cirrhosis = main

Diabetes
Obesity
Family history

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104
Q

Describe the clinical features of hepatocellular carcinoma

A

Asymptomatic originally

Present late = poor prognosis
Non-specific features
- weight loss
- abdominal pain
- anorexia
- nausea and vomiting
- jaundice
- pruritus
- upper abdominal mass on palpitation

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105
Q

Describe the investigations for hepatocellular carcinoma

A

Alpha-fetoprotein
Liver ultrasound
CT/MRI scans
Biopsy

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106
Q

Describe the screening for hepatocellular carcinoma

A

Patients with cirrhosis screened every 6 months

Ultrasound
Alpha-fetoprotein

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107
Q

Describe the management of hepatocellular carcinoma

A

Surgery
Radiofrequency ablation
TACE
Radiotherapy
Targeted drugs

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108
Q

Describe cholangiocarcinoma

A

Cancer that originates in the bile duct

Majority = adenocarcinomas

Common site = perihilar region

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109
Q

What are the key risk factors of cholangiocarcinoma

A

Primary sclerosing cholangitis
Liver flukes (a parasitic infection)

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110
Q

What are the clinical features of cholangiocarcinoma

A

Key - obstructive jaundice
- Pale stools
- Dark urine
- Generalised itching

Non-specific symptoms

Courvoisier’s Law

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111
Q

Describe the investigations of cholangiocarcinoma

A

Imaging

CA19-9 tumour marker

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112
Q

What is the management of cholangiocarcinoma

A

Curative surgery
Palliative treatment

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113
Q

Name 6 types of hernias

A
  1. Inguinal
  2. Femoral
  3. Umbilical
  4. Incisional
  5. Epigastric
  6. Hiatal
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114
Q

Define the pathophysiology of a hernia

A

Occurs when there is a weak point in a cavity wall, usually affecting the muscle or fascia.

Weakness allows a body organ that would normally be contained within that cavity to pass through the cavity wall.

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115
Q

Describe an inguinal hernia

A

Soft lump in the inguinal region (in the groin)

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116
Q

What are the 2 types of inguinal hernia

A
  1. Indirect inguinal hernia
    - bowel herniates through the inguinal canal
  2. Direct inguinal hernia
    - Weakness in the abdominal wall at the Hesselbach’s triangle
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117
Q

Define a femoral hernia

A

Involves herniation of the abdominal contents through the femoral canal

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118
Q

Describe the pathophysiology of a femoral hernia

A

Occurs below the inguinal ligament

Opening between the peritoneal cavity and the femoral canal = femoral ring

Femoral ring leaves only a narrow opening for femoral hernias

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119
Q

What risks are femoral hernias associated with

A

Incarceration
Obstruction
Strangulation

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120
Q

Describe umbilical hernias

A

Occur around the umbilicus due to a defect in the muscle around the umbilicus

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121
Q

Describe an incisional hernia

A

Occur at the site of an incision from a previous surgery

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122
Q

Describe the pathophysiology of an incisional hernia

A

Due to weakness where the muscle and tissues where closed after a surgical incision

Bigger incision = higher risk

Difficult to repair = high recurrence rate

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123
Q

Define an epigastric hernia

A

Hernias in the epigastric area (upper abdomen)

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124
Q

Describe a hiatal hernia

A

Herniation of the stomach up through the diaphragm

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125
Q

Describe the pathophysiology of an hiatal hernia

A

Diaphragm opening should be at the level of the lower oesophageal sphincter and should be fixed in place.

Narrow opening helps to maintain the sphincter and stop acid and stomach contents refluxing.

When opening is wider - stomach can enter through the diaphragm and contents can reflux

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126
Q

Name the types of hiatal hernia

A

1 - Sliding - stomach slides up through the diaphragm

2 - Rolling - separate portion of the stomach folds around the entry of the diaphragm alongside the oesophagus

3 - Combination of sliding and rolling.

4 - Large opening with additional organs entering the thorax

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127
Q

Name the risk factors of inguinal hernias

A

Male sex
Older age
Family history
Prematurity
AAA

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128
Q

Name the risk factors of femoral hernias

A

Women
Increased age
Low BMI

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129
Q

Name the risk factors for hiatus hernias

A

Increasing age
Obesity
Pregnancy

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130
Q

Name the risk factors of umbilical hernias

A

Women
Down’s syndrome
Beckwith-Wiedemann syndrome
Raised intra-abdominal pressure

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131
Q

Name the risk factors of epigastric hernias

A

Men
Age 20-50
Central obesity

132
Q

What are the clinical features of an abdominal hernia

A

A soft lump protruding from the abdominal wall

Lump may be reducible or protrude with coughing

Aching, pulling or dragging sensation

133
Q

What are the clinical features of hiatus hernias

A

Present with dyspepsia
Heartburn
Acid reflux
Reflux of food
Burping
Bloating
Halitosis - bad breath

134
Q

What is the general management of abdominal wall hernias

A

Conservative management
Tension-free repair (surgery)
Tension repair (surgery)

135
Q

Define primary biliary cholangitis

A

Autoimmune condition which attacks the small bile ducts in the liver

Results in jaundice and liver disease

136
Q

Describe the pathophysiology of primary biliary cholangitis

A

Affects intrahepatic ducts (bile ducts)

Inflammation and damage to cholangiocytes.

Overtime leads to obstruction through these ducts.

Reduced flow = cholestasis

Back pressure = liver fibrosis, cirrhosis and failure.

137
Q

What is the typical presentation of primary biliary cholangitis

A

White woman
Aged 40-60
Presenting with itching
Positive AMA
Raised alkaline phosphate

138
Q

What are the risk factors of primary biliary cholangitis

A

Women
Aged 40-60

139
Q

What are the clinical features of primary biliary cholangitis

A

Often asymptomatic

Fatigue
Puritus - itching
GI symptoms - pale, greasy stools.
Jaundice
Dark urine

140
Q

Describe the signs of primary biliary cholangitis

A

Xanthoma and xanthelasma

Excoriations

Hepatomegaly

Signs of liver cirrhosis and portal hypertension in end stage disease

141
Q

Describe the investigations of primary biliary cholangitis

A

LFTS
Autoantibodies
Raised IgM
Ultrasound
Liver biopsy

142
Q

Describe the management of primary biliary cholangitis

A

Ursodeoxycholic acid

Other treatments
- Obeticholic acid
- Cholestyramine
- Replacement of fat-soluble vitamins
- Immunosuppression

End stage - liver transplant

143
Q

Define primary sclerosing cholangitis

A

Condition where the intrahepatic and extrahepatic bile ducts become inflamed and damaged, developing strictures that obstruct the flow of bile out of the liver and into the intestines.

144
Q

Define sclerosis

A

Stiffening and hardening of the bile ducts

145
Q

Define cholangitis

A

Inflammation of the bile ducts

146
Q

What are the causes of primary sclerosing cholangitis

A

Unclear - genetics + environmental factors

Strong association with ulcerative colitis (70%).

147
Q

What are the risk factors of developing primary sclerosing cholangitis

A

Male
Aged 30-40
Ulcerative colitis
Family history

148
Q

Name the clinical features of primary sclerosing cholangitis

A

Pain and rigors
Jaundice
Abdominal pain in RUQ
Pruritus’ - itching
Hepatomegaly
Splenomegaly

149
Q

Describe the investigations of cholangitis

A

Liver function tests

Diagnosis - magnetic resonance cholangiopancreatography

Colonoscopy - for UC

Liver biopsy - used if diagnostic uncertainty

150
Q

Describe the management of primary sclerosing cholangitis

A

No treatments proven to be effective

Endoscopic retrograde cholangio-pancreatography

Liver transplant

Other
- Cholestyramine
- Replacement fat soluble vitamins
- Monitoring for complications

151
Q

What are some possible complications of primary sclerosing cholangitis

A

Biliary strictures
Acute bacterial cholangitis
Cholangiocarcinoma
Cirrhosis
Fat-soluble vitamin deficiency
Osteoporosis

152
Q

Define spontaneous bacterial peritonitis

A

An infection of the ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory or surgical correctable condition

153
Q

Describe the pathophysiology of spontaneous bacterial peritonitis

A

Bacterial translocation from the intestinal flora (sometimes not part of the intestinal flora) occurs by movement to the mesenteric lymph nodes from the bloodstream.

Cirrhosis predisposes to this colonisation and impairs the ability to resist infection.

After haematogenous spread of bacteria to the ascitic fluid, complement fluid cannot protect from infection due to many patients with cirrhosis have low ascites protein concentration.

154
Q

Describe the causes of spontaneous bacterial peritonitis

A

Microbial

Gram negative bacteria

Most common pathogens:
- E. coli
- Staph. aureus
- Step. pneumoniae.
- Kleb. penumoniae.
- Pseudomonas aeruginosa

155
Q

What are the risk factors of spontaneous bacterial peritonitis

A

Decompensated hepatic state (usually cirrhosis)

Low ascitic protein/complement.

GI bleeding.

Endoscopic sclerotherapy for oesophageal varices

156
Q

Describe the investigations of spontaneous bacterial peritonitis

A

Bloods
- FBC
- Serum creatinine
- Culture
- LFT
- PN/INR

Ascitic laboratory tests
- cell count
- culture
- appearance
- absolute neutrophil count

Urine testing

156
Q

Describe the clinical features of spontaneous bacterial peritonitis

A

Commonly minimally symptomatic, may be asymptomatic

Abdominal pain
Fever
Vomiting
Altered mental state
GI bleeding

157
Q

Describe the clinical diagnosis of spontaneous bacterial peritonitis

A

Ascitic fluid absolute neutrophil count > 250 cells/mm^3

158
Q

Describe the management of spontaneous bacterial peritonitis

A

Main = early administration of appropriate empirical antibiotics

Albumin

Continued antibiotics
- patients with ascitic fluid protein conc. < 15g/L
- Previous episode of SBP

159
Q

Define cholangitis

A

Infection and inflammation in the bile ducts

160
Q

What are the 2 main causes of cholangitis

A
  1. Obstruction in the bile ducts stopping bile flow
  2. Infection introduces in the common bile duct
161
Q

What are the risk factors of cholangitis

A

Age > 50 years
Cholelithiasis
Benign stricture
Malignant stricture
Post-procedure injury to bile ducts
History of scleorsing cholangitis

162
Q

Name the clinical features of cholangitis

A

Present with Charcot’s Triad
- RUQ pain
- Fever
- Jaundice - raised bilirubin

163
Q

Describe the investigations of cholangitis

A

Imaging - to diagnose bile duct stones and cholangitis

  • Abdominal ultrasound scan
  • CT scan
  • ERCP
  • Endoscopic ultrasound
164
Q

Describe the acute management of sepsis and acute abdomen

A

Nil by mouth
IV fluids
Blood cultures
IV antibiotics
Involvement of senior and potentially HDU, ICU.

165
Q

Describe the procedure options can be performed during an ERCP for cholangitis

A

Cholangio-pancreatography
Sphincterotomy
Stone removal
Balloon dilation
Biliary stenting
Biopsy
Percutaneous transhepatic cholangiogram

166
Q

Name 5 differential diagnosis for cholangitis

A

Acute cholecystitis
Peptic ulcer disease
Acute pancreatitis
Hepatic abscess
Acute pyelonephritis

167
Q

Define cholecystitis

A

Inflammation of the gallbladder

Causes blockage of the cystic duct preventing the gallbladder from emptying.

168
Q

What are the causes of cholecystitis

A

Gallstones (95%) - calculous cholecystitis

Small number of cases = dysfunction in the gallbladder emptying. Acalculous cholecystitis

169
Q

What are the risk factors of cholecystitis

A

Gallstones
Severe illness
Total parenteral nutrition
Diabetes

170
Q

What are the clinical features of cholecystitis

A

Main = Pain in RUQ - may radiate to R. shoulder

Tenderness RUQ
Signs and symptoms of inflammation
Palpable mass
Presence of risk factors
Murphy’s sign

171
Q

Describe Murphy’s sign

A

Place hand in RUQ and apply pressure.

Patient takes deep breath in.

Gallbladder will move downwards during
inspiration and encounter your hand.

Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration.

172
Q

Describe the investigations of cholecystitis

A

Imaging
- Abdominal ultrasound
- MRCP

173
Q

Describe the management of cholecystitis

A

Conservative management
- Nil by mouth
- IV fluids
- Antibiotics
- NG tube required if vomiting

ERCP

Cholecystectomy - removal of gallbladder

174
Q

Define gallbladder empyema

A

Infected tissue and pus collecting in the gallbladder

175
Q

Define acute pancreatitis

A

Presents with a rapid onset of inflammation and symptoms.

After an episode of acute pancreatitis, normally function usually returns.

176
Q

Define chronic pancreatitis

A

Involves long-term inflammation and symptoms with a progressive and permanent deterioration in pancreatic function

177
Q

What are the 3 main causes of pancreatitis

A
  1. Gallstones
  2. Alcohol (chronic)
  3. Post-ERCP
178
Q

What is the acronym to remember pancreatitis causes

A

I GET SMASHED

Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs - furosemide, thiazide diuretics, azathioprine

179
Q

Name the risk factors for acute pancreatitis

A

Middle-aged women
Gallstones
Alcohol
Hypertriglyceridemia
Use of causative drugs

180
Q

Name the risk factors for chronic pancreatitis

A

Alcohol
Smoking
Family history
Coeliac disease

181
Q

What are the general features of pancreatitis

A

Severe central pain going to the back
Nausea and vomiting
Fever
Oliguria
Cullens
Grey’s turners sign

182
Q

Describe the clinical features of acute pancreatitis

A

Severe epigastric pain
Radiating through to the back
Associated vomiting
Abdominal tenderness
Systemically unwell
- low grade fever
- tachycardia

183
Q

Describe the investigation seen in pancreatitis

A

Amylase
- Raised > 3x upper limit
- May not rise in chronic

Lipase

C-reactive protein - level of inflammation

Ultrasound - initial investigation choice for gallstones

CT abdomen - assess for complications

184
Q

What severity score is used in pancreatitis

A

MEWS

Good history
Response to resuscitation

Also - Glasgow Score

185
Q

Describe the Glasgow Score

A

Assess the severity of pancreatitis

Numerical based on how many of the criteria are present

186
Q

Describe the results of pancreatitis

A

PANCREAS

PaO2 < 8 kPa
Age > 55
Neutrophils (WBC > 15)
Calcium < 2
uRea > 16
Enzymes (LDH > 600 or AST/ALT > 200)
Albumin < 32
Sugar (glucose) > 10

187
Q

What is the treatment for acute pancreatitis

A

Admission for supportive management

Involves:
ABCDE approach - initial resuscitation
IV fluids
Nil by mouth
Analgesia
Careful monitoring
Treatment of gallstones (if needed)
Treatment of complications

Most patients will improve within 3-7 days

188
Q

Describe the management for chronic pancreatitis

A

Abstinence from alcohol and smoking

Analgesia

Replacement of pancreatic enzymes

Subcutaneous insulin regimes

ERCP with stenting

Surgery may be required

189
Q

Name some diagnosis differentials for pancreatitis

A

Peptic ulcer disease
Intestinal obstruction
AAA
Cholangitis
Cholecystitis

190
Q

Name some complications of acute pancreatitis

A

Necrosis of pancreas
Infection in a necrotic area
Abscess formation
Acute peripancreatic fluid collection
Pseudocysts
Chronic pancreatitis

191
Q

Name some complications of chronic pancreatitis

A

Chronic epigastric pain
Loss of exocrine/endocrine function
Damage and strictures to the duct system
Formation of pseudocysts or abscesses

192
Q

Define Gilbert’s Syndrome

A

Inherited (usually autosomal recessive) metabolic disorder characterised by a mild and intermittent elevation of unconjugated (indirect) bilirubin levels, due to defective conjugating enzymes in the liver

193
Q

Name the risk factors of Gilbert’s syndrome

A

Post-pubertal age
Weak
- Family history
- Type 1 DM

194
Q

Name the clinical features of Gilbert’s syndrome

A

Generally - asymptomatic

Symptoms (alterative diagnosis should be considered)

Abdominal pain
Itch
Pale stools
Dark urine

195
Q

Name the investigations for Gilbert’s syndrome

A

Unconjugated bilirubin
Liver aminotransferases
Gamma-glutamyl transpeptidase
Lactate dehydrogenase
FBC
Peripheral blood smear
Direct Coomb’s test

196
Q

What would be the findings of Gilbert’s syndrome

A

Mild unconjugated hyperbilirubinemia < 102 micromol/L

Liver function otherwise normal

197
Q

When would Gilbert’s syndrome suspected

A

Incidental finding of an increased serum bilirubin concentration + normal liver function test

Single episode (or intermittent) episode of mild jaundice with no clinical evidence of liver disease

198
Q

Describe the management of Gilbert’s syndrome

A

No treatment or regular monitoring required

Cannot progress or cause chronic liver disease

Any episodes of jaundice are self-limiting, should resolve within a few days

199
Q

Name 3 metabolic liver disease’s

A

Haemochromatosis

Wilson’s disease

Alpha 1 antitrypsin deficiency

200
Q

Define Wilson’s disease

A

Autosomal recessive genetic condition resulting in the excessive accumulation of copper in the body tissues, particularly in the liver

201
Q

Describe the pathophysiology of Wilson’s disease

A

Lack of protein leads to decreased copper excretion from the liver.

Copper overload in hepatocytes.

When hepatic storage capacity is exceeded, copper is released into the circulation and deposited in other organs

202
Q

What are the causes of Wilson’s disease

A

Mutations of Wilson’s protein on chromosome 13

Copper-transporting protein

Copper excreted into the bile

203
Q

What are the risk factors for Wilson’s disease

A

ATP7B gene mutation

Family history

204
Q

Name the clinical features of Wilson’s disease

A

1st - liver problems

Advanced stage
- Neurological symptoms
- Psychiatric symptoms
- Kayser-Fleischer in the cornea
- Haemolytic anaemia

205
Q

Describe Kayser-Fleischer in the cornea

A

Deposition of copper in Descemet’s membrane

Green-brown circles in surrounding iris of the eye

Usually seen with naked eye or silt lamp examination.

206
Q

Describe the investigation of Wilson’s disease

A

Initial screening = serum caeruloplasmin

24-hour urine copper assay
Liver biopsy
Scoring systems

207
Q

Describe the management of Wilson’s disease

A

Depends on clinical presentation and treatment phase

Copper chelation

Other treatments
- Zinc salts
- Liver transplantation

208
Q

Describe the differential diagnosis for Wilson’s disease

A

Hepatitis B/C
Haemochromatosis
Alpha-1 antitrypsin deficiency
Autoimmune cirrhosis
Parkinson’s disease

209
Q

Describe the prognosis of Wilson’s disease

A

Neurological symptoms improve 5-6 months after start of treatment

Unless liver receives further insult should be normal life span

210
Q

Define alpha-1 antitrypsin deficiency

A

Genetic condition caused by low levels of alpha-1 antitrypsin

211
Q

What are the main 2 organs that alpha-1 antitrypsin deficiency affects

A

Lungs - COPD, bronchiectasis

Liver (depends on genotype) - dysfunction, fibrosis and cirrhosis

212
Q

Describe the pathophysiology of Alpha-1 antitrypsin deficiency

A

Disease severity depends on copies of the gene.

Alpha-1 antitrypsin = protease inhibitor.

Normal conditions

Protease enzyme = neutrophil elastase

Enzyme is secreted by neutrophils

Digests elastin - protein in connective tissue that keeps tissue flexible

Alpha-1 antitrypsin offers protection by inhibiting this action

213
Q

Describe alpha-1 antitrypsin deficiency pathophysiology in the liver

A

ATT produced in the liver.

Abnormal mutant version of protein gets trapped and builds up inside hepatocytes

Is toxic to them = inflammation

Overtime = fibrosis, cirrhosis and possible hepatocellular carcinoma

214
Q

What is the cause of alpha-1 antitrypsin deficiency

A

Decreased circulating plasma levels of AAT, due to inheritance of variant alleles of SEPRINA1 gene

215
Q

What are the clinical features of alpha-1 antitrypsin deficiency

A

Productive cough
SOB on exertion
Wheezing

216
Q

Describe the investigations of alpha-1 antitrypsin deficiency

A

Assess lung damage
- chest x-ray
- high resolution CT thorax
- pulmonary function test

Liver biopsy

Plasma AAT level

LFTs

217
Q

What is the clinical diagnosis of alpha-1 antitrypsin deficiency based upon

A

Low serum alpha-1 antitrypsin (screening test)

Genetic testing

218
Q

Describe the management of alpha-1 antitrypsin deficiency

A

Stop smoking

Symptomatic management e.g. COPD

Organ transplantation

Monitor complications - hepatocellular carcinoma

Screening of family members

Infusion of alpha-1 antitrypsin

219
Q

What are the differential diagnosis of alpha-1 antitrypsin deficiency

A

Asthma
COPD
Bronchiectasis
Viral hepatitis
Alcoholic liver disease

220
Q

What are the complications of alpha-1 antitrypsin deficiency

A

Hepatocellular carcinoma

Necrotising panniculitis

Granulomatosis with polyangiitis

221
Q

Describe the prognosis of alpha-1 antitrypsin deficiency

A

Non-smokers = normal

50-72% of deaths in AAT = respiratory failure

If people do not manifest pulmonary symptoms more likely to experience cirrhosis and liver failure

222
Q

Define haemochromatosis

A

Autosomal recessive genetic condition resulting in iron overload.

= iron storage disorder.

223
Q

Describe the pathophysiology of hemochromatosis

A

Majority of cases related to C282Y mutations in human hemochromatosis protein (chromosome 6).

Gene is important for regulating iron metabolism

224
Q

Describe the causes of haemochromatosis

A

4 different types

C28Y and H63D = most common mutations of the HFE gene

225
Q

Describe the clinical features of haemochromatosis

A

Chronic tiredness
Joint pain
Pigmentation - bronze skin
Testicular atrophy
Erectile dysfunction
Amenorrhoea
Cognitive symptoms
Hepatomegaly

226
Q

Define amenorrhoea

A

Absence of period in women

227
Q

Describe the investigations of haemochromatosis

A

Initial = serum ferritin

Other
- transferrin saturation
- genetic testing
- liver biopsy with Perl’s stain
- MRI

228
Q

Describe the management of haemochromatosis

A

Venesection - regularly removing blood to remove excess iron

Monitoring serum ferritin

Monitoring and treating complications

229
Q

Name the differential diagnosis of haemochromatosis

A

Iron overload
Hepatitis B/C
NAFLD
Excessive iron supplementation

230
Q

Name the complications of haemochromatosis

A

Secondary diabetes
Liver cirrhosis
Endocrine and sexual problems
Cardiomyopathy
Hepatocellular carcinoma
Hypothyroidism
Chondrocalcinosis

231
Q

Describe chondrocalcinosis

A

Calcium pyrophosphate deposits in the joints

Causes arthritis

232
Q

Define acute liver failure

A

Rare, life-threatening potentially reversible condition with rapid decline in hepatic function characterised by jaundice, coagulopathy (INR > 1.5) and hepatic encephalopathy in patients with no evidence of prior liver disease

233
Q

What are the classifications of liver failure

A

Hyperacute
Acute
Subacute

234
Q

Define chronic liver failure

A

Progressive deterioration of liver functions for more than 6 months, including synthesis of clotting factors, other proteins, detoxification of harmful products of metabolism and excretion of bile.

235
Q

Name the causes of chronic liver disease/failure

A

Alcohol
Non-alcoholic steatohepatitis
Viral hepatitis B, C
Immune
Metabolic
Vascular

236
Q

How is acute liver failure established by

A

History

Serological assays

Exclusion of alternative causes

237
Q

What are the causes of acute liver disease/failure

A

Most common - paracetamol overdose

Idiosyncratic drug-induced liver injury
Acute hepatitis A
Autoimmune hepatitis
Ischaemia hepatitis

238
Q

Name the risk factors of acute liver disease/failure

A

Chronic alcohol misuse
Poor nutritional status or feeding
Female sex
Pregnancy
Chronic hepatitis B
Chronic pain and narcotic use
Herbal and dietary supplement hepatotoxicity
Wilson’s disease

239
Q

Name 4 clinical features of acute liver disease/failure

A

Malaise
Nausea
Anorexia
Jaundice

240
Q

Describe the clinical features of chronic liver failure/disease

A

Ascites
Oedema
Haematemesis (varices)
Malaise
Anorexia
Wasting
Easily bruising
Itching
Hepatomegaly
Abnormal LFTs

241
Q

Describe the investigations of liver failure/disease

A

Liver function test

Viral serology

Immunology

Biochemistry

Radiological investigations

242
Q

Describe the management of acute liver disease/failure

A

ALF grade 2 or higher hepatic encephalopathy - admitted to ITUS.

Neurological status monitored

Liver transplantation

243
Q

Describe the general management of the complications of liver disease/failure

A

Malnutrition - naso-gastric feeding

Variceal bleeding - endoscopic banding, propranolol, terlipressin

Encephalopathy - lactulose

Ascites/oedema - salt/fluid restriction, diuretics, paracentesis

Infection - antibiotics

244
Q

Name the differential diagnosis of liver disease/failure

A

Viral (A, B, C, CMV, EBV)

Drug-induced

Autoimmune

Alcoholic

245
Q

What medications may be prescribed in liver disease/failure

A

Analgesia

Sedation - short acting benzodiazepines

Diuretics

Antihypertensives

AVOID
- aminoglycosides
- ACE inhibitors

246
Q

What are the clinical features of a paracetamol overdose

A

Often asymptomatic

Mild GI symptoms

Untreated - vary liver injury 2-4 days after

Severe overdose
- coma
- severe metabolic acidosis

247
Q

Describe the time course of drug-induced liver injury

A

Onset
- usually 1-12 weeks after starting
- earlier is unusual unless re-challenged

Resolution
- 3 months after stopping
- 5-10% prolonged

Inadvertent re-challenge
- Seen in 6% - 2% are fatal

248
Q

Describe the investigations of drug induced liver injury

A

Serum paracetamol conc.
LFTs
Prothrombin time and INR
Blood glucose
U&E, creatinine
Venous or arterial blood gas
FBC

249
Q

Describe the risk factors of drug induced liver-injury

A

History of:
- self harm
- frequent or repeated use of medications for pain relief

Glutathione deficiency

Drugs that induce liver enzymes

Low body weight < 50kg

250
Q

What is the management of a paracetamol overdose

A

N acetyl cysteine

Supportive to correct
- coagulation defects
- fluid electrolyte and acid base balance
- renal failure
- hypoglycaemia
- encephalopathy

251
Q

Describe the complications of poor prognosis of paracetamol overdose

A

80% mortality if below

Late presentation

Acidosis pH < 7.3

PT > 70 seconds

Serum creatinine > (or equal to) 300 umol/L

Consider emergency liver transplant

252
Q

Define ascites

A

Pathological collection of fluid in the peritoneal cavity

253
Q

Describe the pathophysiology of ascites in cirrhosis

A

Splanchnic arterial vasodilation leads to increased lymph formation = activation of RAAS system and SNS and release ADH

Causes renal sodium (major contributor) and water retention

Increased resistance to portal flow results in portal hypertension, collateral vein formation and shunting of blood in the systemic circulation

254
Q

Describe the classification of ascites

A

Stage 1 - detectable only after careful examination/ultrasound scan

Stage 2 - easily detectable but of relatively small volume

Stage 3 - obvious, not tense ascites (moderate)

Stage 4 - tense ascites (large)

255
Q

What are the causes of ascites

A

Most common = cirrhosis

Chronic liver disease

Neoplasia

Pancreatitis, cardiac causes

256
Q

What are the risk factors of ascites

A

Liver disease
- heavy alcohol consumption
- Viral hepatitis
- IVDU
- blood transfusion pre 90s
- Tattoos
- Residence of birth

Non-alcoholic steatohepatitis
- DM type 2
- Obesity
- Hypercholesterolemia

Cancer
Cardiac
Renal-nephrotic syndrome
Malnutrition

257
Q

Describe the clinical features of ascites

A

Abdominal distention
Shifting dullness
Nausea
Loss of appetite
Constipation
Cachexia
Weight loss
Pain/discomfort
- present - malignant
- absent - non malignant

258
Q

What are the signs of ascites

A

Jaundice
Abdominal distention - up to 1.5-2L
Puddle sign 150mL
Shifting dullness 500mL
Flanks fullness 1500+ mL
Fluid thrill

259
Q

Name the investigations of ascites

A

Imaging - confirms diagnosis

Blood test - LFTs
Abdominal diagnostic paracentesis
Microscopy and culture
Analysis of ascitic fluid
Biochemistry

260
Q

Describe the management of ascites

A

Treat underlying cause

Hypertension
Shunts

261
Q

What are the complications of ascites

A

Infections
Electrolyte imbalance
Bowel perforation
Bleeding
Leak of fluid through abdominal wall
Injury to the kidneys

262
Q

Describe the management of ascites caused by hypertension

A

Fluid and salt restriction

Diuretics
- spironolactone
- +/- furosemide
- others - amiloride, metolazone, mannitol

Large-volume paracentesis + albumin

263
Q

Name the causes of portal hypertension

A

Cirrhosis
Fibrosis
Portal vein thrombosis

264
Q

Describe the pathology of portal hypertension

A

Increased hepatic resistance

Increased splanchnic blood flow

265
Q

Define portal hypertension

A

Increased resistance and pressure in the portal system

266
Q

Describe the pathophysiology of portal hypertension

A

Fibrosis affects the structure and blood flow through the liver

Increases the resistance in the vessel leading to the liver

267
Q

Define oesophageal varices

A

Dilated collateral blood vessels that develops as a complication of portal hypertension, usually in the setting of cirrhosis

268
Q

Describe the pathophysiology of oesophageal varices

A

Cirrhosis develops

Increases hepatic vein pressure gradient and deteriorating liver function may result in the formation of oesophageal varices

269
Q

Name the cause of oesophageal varices

A

US + Europe - alcoholic liver disease

Worldwide - hepatitis B, C

270
Q

Name the risk factors of oesophageal varices

A

Portal hypertension
Large varices
Red wale marks
Decompensated cirrhosis

271
Q

Name the clinical features of oesophageal varices

A

Asymptomatic

Brisk haematemesis

272
Q

Describe the investigations of oesophageal varices

A

Gastroscopy

Bloods

Coagulation profile

Blood typing/cross-matching

Hepatitis B surface antigen

Anti-hepatitis C virus IgG

273
Q

Describe the management of oesophageal varices

A

Prevent development of variceal bleeding
- Non-selective beta-blockers
- endoscopic ligation

Additional management
- Prophylactic antibiotics

274
Q

Define the differential diagnosis of oesophageal varices

A

Hiatal hernia
Gastric varices
Mallory-Weiss tear
Peptic ulcer disease

275
Q

Define biliary colic

A

Crystalised bile causing sudden painful spasm of the gallbladder wall triggered by a gallstone

276
Q

What are the types of biliary colic

A

Cholesterol

Pigment stones
- bile acid
- phosphate
- magnesium

Mixed stones

277
Q

What are the risk factors of biliary colic

A

5 Fs

Forty
Fat
Female
Fertile
Fair

278
Q

What are the clinical features of biliary colic

A

Post prandial colicky pain

Nausea and vomiting

Should not be that tender to touch

279
Q

What are the investigations of biliary colic

A

1st - ultrasound

Other investigations
- Bloods
- MRCP vs ERCP

280
Q

Describe MRCP

A

Image of the gallbladder and ducts

Similar to CT

Sees end of bile duct sits in the C with the 2nd part of the duodenum - lots of gas here so ultrasound will not be able to see

281
Q

Why is CT not used as an image technique in gallstones

A

Some gallstones are opaque so will not show

282
Q

Describe the management of biliary colic

A

Analgesia - NSAID with PPI cover

ERCP

Cholecystectomy

Bile duct exploration/reconstruction

283
Q

Describe the blood results in alcoholic liver disease

A

Increase
- bilirubin
- PT
- GGT

Decrease
- albumin

AST:ALT > 2

FBC - macrocytic anaemia

284
Q

What anaemia is seen in alcoholic liver disease

A

Macrocytic liver disease

285
Q

Describe GGT marker

A

Increased in cholestasis - blockage of intra-/extrahepatic ducts

Increased in alcoholic liver disease

286
Q

What is 1st pass metabolism completed by

A

Liver

287
Q

What is the major blood supply to the liver

A

Portal vein

288
Q

Describe AST and ALT

A

Enzyme made in hepatocytes

Marker for hepatic inflammation.

Injury of liver cells increases these

289
Q

Describe AST

A

Low specificity for the liver

290
Q

Describe ALT

A

High specificity for the liver

Think L

291
Q

What type of injury will AST and ALT be raised in

A

Acute (recent injury)

Increase in all forms of liver injury does not tell about liver function

Think smoke with fire - there may be no smoke due to nothing left to burn (no hepatocytes) or the fire has been extinguished

292
Q

What is a marker of long term injury of the liver

A

Albumin - has approx 20 day half life

293
Q

Describe albumin

A

Protein made in the liver

Chronic hepatocellular damage

In acute it stays up

294
Q

What is the key LFT for alcoholic liver disease

A

AST: ALT > 2

295
Q

Describe PT/INR as a marker of liver disease

A

In acute and chronic liver damage

Measures clotting time - requires many enzymes made in the liver

Very sensitive

Shows how bad the liver is

296
Q

What may affect PT/INR that is not liver damage

A

Warfarin

1972, or 1,5 factor deficiency

297
Q

What are the key investigations in liver failure

A

LFTS

Increased - AST, ALT, PT

298
Q

What are other investigations (than the main one) in alcoholic liver disease

A

Increased - bilirubin, PT, GGT

Decreased - albumin

299
Q

What are the key investigations in non-alcoholic liver disease

A

LFTS

Increased - PT, INR, bilirubin

Decreased - albumin

300
Q

Describe other investigations (than LFTs) in non-alcoholic liver disease

A

Ultrasound - hepatitic stenosis

Thrombocytopenia

Hyperglycaemia

301
Q

What would a liver biopsy of primary biliary cholangitis show

A

Inflamed bile ducts with intraepithelial lymphocytes, epithelioid, granuloma + fibrosis

302
Q

Describe LFTs and FBCs in primary biliary cholangitis

A

Increased - GGT, ALT, bilirubin

FBC - increased AMA

303
Q

What is the GS investigation for primary sclerosing cholangitis

A

MRCP

304
Q

What would be seen on blood tests of primary sclerosing cholangitis

A

Increased ALP

pANCA

305
Q

What is the GS investigation for acute pancreatitis

A

Lipase and amylase

306
Q

What is GS investigation for chronic pancreatitis

A

Abdominal USS + CT

307
Q

How do you differentiate on tests between acute and chronic pancreatitis

A

Acute = raised lipase and amylase

Chronic = not raised

308
Q

What would be raised in chronic pancreatitis

A

Faecal elastase

309
Q

What is the mnemonic to remember the causes of acute pancreatitis

A

I GET SMASHED

310
Q

Breakdown I GET SMASHED

A

Idiopathic
Gallstones
Ethanol
Trauma
Scorpion stings
Mumps
Autoimmune
Steroids
Hypercalcaemia/hypertriglyceridemia
Endoscopic retrograde cholangiopancreatography
Drugs/medications

311
Q

Define ERCP

A

Endoscopic retrograde cholangiopancreatography

Combines endoscopy + xray to examine and treat conditions of bile duct and pancreas ducts

312
Q

Name some drugs that cause acute pancreatitis

A

Tetracyclines
Aminosalicylate e.g. sulfasalazine
Diuretics

313
Q

What is the most common cause of acute pancreatitis

A

Gallstones

314
Q

What is the most common cause of chronic pancreatitis

A

Ethanol (alcohol)

315
Q

Name the 3 most common causes of acute pancreatitis

A

The GET in I GET SMASHED

Gallstones
Ethanol (alcohol)
Trauma

316
Q

Name the symptoms of acute pancreatitis

A

Severe epigastric pain radiating to the back
Fever
N&V
Steatorrhea

317
Q

Name the signs of acute pancreatitis

A

Grey tuners sign
Cullens sign

318
Q

Define grey turners sign

A

For acute pancreatitis

Flank bleeding

319
Q

Define cullen sign

A

For acute pancreatitis

Periumbilical bleeding

320
Q

What scoring system is used in acute pancreatitis

A

Glasgow + Ranson’s score

APPACHE II - severity in 24 hours

321
Q

Describe the treatment of acute pancreatitis

A

Emergency hospital admission

IV fluids
Oxygen
Analgesia
IV antibiotics
Nil by mouth
NG tube for feeding

322
Q

Describe systemic inflammatory response as a complication of acute pancreatitis

A

Tachycardia
Tachypnoea
Pyrexia
Increased WBC

323
Q

Name the localised complications of acute pancreatitis

A

Pancreatic necrosis
Pseudocyst
Pancreatic abscess

324
Q

Name the systemic complications of acute pancreatitis

A

Multi organ failure
Sepsis
AKI
ARDs
DIC

325
Q

Define chronic pancreatitis

A

Chronic, irreversible inflammation and/or fibrosis of pancreas often characterised by severe pain + progressive endocrine and exocrine insufficiency for > 3 months.

326
Q

What is the main symptom of chronic pancreatitis

A

Epigastric pain radiating to back - exacerbated by alcohol

327
Q

Describe the management of chronic pancreatitis

A

Lifestyle modification – alcohol cessation

Pain management – NSAIDs

Pancreatic enzyme replacement therapy e.g. lipase, amylase, protease

Phase 2a (15 decks)

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