Liver and Friends Flashcards

1
Q

What are the normal Functions of the Liver?

A

Protein Synthesis - albumin
Glucose and Fat metabolism
Detoxification and Excretion - drugs, hormones, bilirubin
Defense against infection - complement factors, clotting factors
Bile synthesis

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2
Q

What can chronic liver disease lead to?

A

Liver cirrhosis
Subsequent Liver failure

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3
Q

What does Acute Liver disease lead to?

A

Recovery - ability to regenerate
Acute Liver Failure

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4
Q

What is Acute Liver injury?

A

severe acute liver injury from a primary liver aetiology. It is characterised by liver damage (i.e. elevated transaminases) and impaired liver function (e.g. jaundice and coagulopathy with INR > 1.5). Hepatic encephalopathy is absent.

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5
Q

What are some causes of acute liver injury?

A

Viral A, B, EBV
Drugs - Paracetamol
Alcohol
Vascular – ischaemia (Budd Chiari Syndrome)
Obstruction – usually bile
Congestion – from heart failure

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6
Q

What are some causes of chronic liver disease?

A

Alcohol
Viral infection - Hepatitis (B/C)
Autoimmune liver disease
Metabolic dysfunction - iron/copper overload
NAFLD

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7
Q

What is a typical presentation of acute liver injury?

A

Non-specific signs:
Malaise
Nausea
Anorexia
Jaundice

GI Upset
Jaundice
Hepatomegaly

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8
Q

What are some common presentations of chronic liver disease?

A

Ascites
Oedema
Haematemesis (varices) – vomiting blood
Malaise
Anorexia
Wasting
Easy bruising
Itching
Erythema nodosum
Spider naevi
Hepatomegaly
Abnormal LFTs
Jaundice (rarer)
Confusion rarer)

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9
Q

What are the key liver function tests?

A

Serum Albumin - decreases in injury
Serum Bilirubin - increases in injury
Prothrombin time - increases in injury

Serum Liver Enzymes:
Hepatocellular - Transaminases (AST, ALT)
Cholestatic - Alkaline, Phosphatase Gamma GT

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10
Q

What LFT markers assess the livers synthetic function?
(what would happen to these markers in disease?)

A

Bilirubin (increase)
Albumin (decrease)
Prothrombin Time (increase)

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11
Q

What LFT markers would be raised in hepatocellular injury?

A

ALT
AST

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12
Q

What would the Ratio of AST/ALT suggest?

A

ALT>AST - chronic liver disease

AST>ALT - cirrhosis or acute alcoholic hepatitis

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13
Q

What LFT makers would be raised in cholestatic injury?

A

Alkaline Phosphatase (ALP/AP)
Gamma-glutamyltransferase (GGT)

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14
Q

What causes the yellow colour in jaundice?

A

The accumulation of bilirubin in the blood

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15
Q

What are the different classifications of jaundice?

A

Pre-hepatic - haemolysis, gilberts

Hepatic - liver damage/disease

Post hepatic - obstruction/biliary

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16
Q

What would be the colour/changes to urine and stools in pre hepatic jaundice?

A

Urine - Normal
Stools - Normal
Itching - None
Liver Tests - Normal

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17
Q

What would be the colour/changes to urine and stools in Intra hepatic/ Post Hepatic jaundice?

A

Urine - Dark
Stools - May be pale
Itching - Maybe
Liver Tests - Abnormal

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18
Q

What should be considered asking when a Px presents with Jaundice?

A
  1. Dark urine/ Pale stools, Itching
  2. Symptoms - Biliary pain, Rigors, abdo swelling, weight loss
  3. PHx - biliary disease, malignancy, HF, Autoimmune
  4. Drug Hx
  5. Social Hx - alcohol, Recent travel, IVDU
  6. FHx
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19
Q

What Tests would be wanted in a Px with Jaundice?

A

Liver enzymes - Very high AST/ALT suggests liver disease

Ultrasound - dilation of hepatic bile ducts in biliary obstruction

CT, MRCP, ERCP

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20
Q

What are MRCP/ERCPs?

A

Magnetic Resonance cholangiogram
Endoscopic Retrograde Cholangiogram

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21
Q

Where do Gallstones most commonly form?

A

In the gall bladder

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22
Q

What are the components of Gallstones?

A

70% cholesterol
30% pigment +/- Calcium

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23
Q

What are the risk factors for gallstones development?

A

4Fs
Female,
Fat
Fertile
Forty

(but can affect anyone)

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24
Q

What is the presentation of a Px with Gallstones?

A

Biliary Pain
Obstructive jaundice

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25
What is the management of gallstones present in the gall bladder?
Laparoscopic cholecystectomy Bile acid dissolution therapy
26
What is the management of gallstones present in the Bile Duct?
ERCP w/ Sphincterotomy (opening of sphincter of Oddi) Followed by removal of stones, crushing of stones and stent placement Surgery - remove larger stones
27
What is a typical time frame for drug induced liver injury?
From 5 days after starting it To 3-6 months whilst on it.
28
What accounts for 50% of the causes of drug induced acute liver failure?
Paracetamol overdose
29
What proportion of acute liver failure is drug induced?
>65%
30
What are the different types of Drug induced Liver Injury?
Hepatocellular Cholestatic Mixed
31
What are the common drugs that are hepatotoxic? (2 mnemonics)
VAMPIRES: V - Valproate A - Amiodarone M - Methyldopa P - Pyrazinamide I - Isoniazid R - Rifampicin E - PhenYtoin S - Statins FAT PINK CARS: F - Fe salts A - Amiodarone T - Tetracyclines P - Pyrazinamide I - Isoniazid N - Nitrofurantoin K - Ketoconazole (and other antifungals) C - CCL4 A - Anaesthetic Agents (Halothane) R - Rifampicin S - Statins
32
What is Liver Failure?
The liver loses its regenerative capacity due to hepatocyte death/necrosis causing decompensated liver injury and irreversible damage.
33
What are the different types of Liver Failure?
Acute Liver Failure Fulminant Liver Failure Acute-on-Chronic Liver Failure Chronic Liver Failure
34
What is Acute Liver Failure?
Rapid decline of hepatic functions characterised by the development of hepatic encephalopathy and coagulopathy (>1.5 INR) in a patient who previously had a normal healthy liver
35
What is Fulminant Liver Failure? What are the different categories of Fulminant liver failure?
Rare syndrome of massive hepatocyte necrosis causing acute liver failure Hyperacute - HE (Hepatic Encephalopathy) within 7 days of jaundice Acute - HE within 8-21 days of Jaundice Subacute - HE within 5-26 weeks of Jaundice??????????
36
What is the most common cause of Fulminant Liver Failure?
Paracetamol Overdose 50% of the cause in the UK
37
What is Acute-On-Chronic Liver Failure?
The acute and rapid decline of a Px with Chronic Liver failure Sx
38
What is Chronic Liver Failure?
Patient with progressive Hx of liver disease over 6+ months of constant liver injury
39
What is the Pathogenesis of Liver Failure?
Liver injury Causes liver hepatitis Chronic hepatitis leads to fibrotic liver Leads to Liver cirrhosis and then Decompensated Cirrhosis (End stage liver failure)
40
What are the main causes of acute liver failure?
Viral infection - Hep A/E/B, EBV, CMV Autoimmune Hepatitis Drugs - Paracetamol OD, Alcohol, Ectasy, Isoniazid Metabolic Causes - Wilsons disease, A1AT, Haemachromotosis Budd-Chirai syndrome
41
What is Budd Chiari Syndrome?
Hepatic vein thrombosis usually seen in the context of other haematological disease This blocks the hepatic vein from draining leading to a backflow of blood into the liver causing liver damage
42
What are the symptoms of acute liver failure?
Chronic pain Abdominal pain - RUQ Nausea and vomiting Malaise
43
What are the clinical signs of Acute Liver Failure?
Jaundice Coagulopathy Hepatic Encephalopathy +: Confusion Asterixis - sign of HE Hepatomegaly Ascites Bruising
44
What are the diagnostic investigations of Acute Liver Failure?
Bloods: FBC - Infection/Bleeds LFTs - Inc bilirubin, Inc PT/INR, Dec Albumin Serum AST/ALT Inc, NH3 Inc, Dec Glucose U&Es - Hepatorenal Syndrome Imaging: EEG - Grades HE (absent in Acute liver injury) Abdo Ultrasound - Check for Budd Chiari CT Microbiology: Blood culture, Urine culture, Ascitic tap - rule out infection
45
What is the treatment for acute Liver failure?
ICU, ABCDE Fluids Analgesia Tx underlying Cause and Tx complications
46
What is the treatment of paracetamol Overdose
<1 hour - Activated Charcoal + N-acetyl Cysteine >1 hour - N-acetyl Cysteine
47
What are some complications and their treatments of Acute Liver Failure?
Raised ICP - Mannitol Hepatic Encephalopathy - Lactulose - increases NH3 excretion/ Rifaximin Ascites - Diuretics (furosemide/spironolactone)/ paracentesis Haemorrhage - Vitamin K Sepsis - Sepsis 6 GI Bleeding - beta blockers SBP - prophylactic Abx
48
What are the most common causes of Chronic Liver disease?
Alcoholic Liver Disease (ALD) Non-Alcoholic Fatty Liver Disease (NAFLD) Viral Hepatitis (B/C) + Metabolic, Autoimmune, PSC, PBC, Drugs, Budd Chiari
49
What is the main cause of Liver death in the UK?
Alcoholic Liver disease
50
What are the Major Risk factors for Chronic Liver failure?
Alcohol Obesity T2DM Drugs Inherited Metabolic Disease Existing Autoimmunity
51
What is the Pathogenesis of Chronic Liver Failure?
Hepatitis chronic inflammation leads to scarring Liver Fibrosis (reversible) Liver Cirrhosis (barely Reversible/irreversible) Compensated Liver cirrhosis - Some extent of liver function Decompensated Liver cirrhosis - End stage liver disease
52
What are the key clinical signs of Liver cirrhosis?
Stigmata of chronic liver disease Jaundice - Caused by raised bilirubin Hepatomegaly Splenomegaly - Caused by portal HTN Spider Naevi - telangiectasia with central arteriole and small vessels radiating away Palmer Erythema - Hyper dynamic circulation Gynaecomastia - endocrine dysfunction Bruising - abnormal clotting Ascites Dupytrens Contracture Caput Medusae - distended paraumbilical vein due to Portal HTN Asterixis - Flapping Tremor
53
What are the stigmata of chronic liver disease?
Caput medusa: distended and engorged superficial epigastric veins around the umbilicus. Splenomegaly: enlarged spleen. Palmar erythema: red discolouration on the palm of the hand, particularly over the hypothenar eminence. Dupuytren's contracture: thickening of the palmar fascia. Causes painless fixed flexion of fingers at the MCP joints (most commonly ring finger). Leuconychia: appearance of white lines or dots in the nails. Sign of hypoalbuminaemia. Gynaecomastia: development of breast tissue in males. Reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen. Spider naevi: type of dilated blood vessel (i.e. telangiectasia) with central red papule and fine red lines extending radially. Due to excess oestrogen. Usually found in the distribution of the superior vena cava.
54
What are the major Complications of Decompensated Liver Cirrhosis?
Malnutrition Hepatic Encephalopathy Ascites Coagulopathy Portal Hypertension SBP - spontaneous bacterial peritonitis Hepatorenal Syndrome Oesophageal Varices Hepatocellular Carcinoma
55
How does liver cirrhosis lead to malnutrition?
Increased use of muscle tissue as fuel and reduces amount of protein in the body. Cirrhosis affects liver metabolism of protein and disrupts glucose and glycogen storage/release leads to increased muscle used as fuel causing malnutrition.
56
What is the management of Liver cirrhosis induced malnutrition?
Regular meals Low sodium - minimise fluid retention High protein and high calorie Avoid alcohol
57
How does Liver cirrhosis lead to portal hypertension and subsequent varices?
Liver cirrhosis leads to increased resistance of blood flow in the liver. Increased pressure back into portal system Causes pressure at anastomoses with systemic venous system these swell and become tortuous causing varices
58
What are the most common sites for varices to occur as a result of portal HTN?
Gastro-oesophageal junction (GOJ) Ileo-caecal junction Rectum Anterior abdominal wall via umbilical vein (caput Medusae)
59
What is a treatment for stable varices (non bleeding)
Propranolol - reduce portal HTN Elastic band ligation Injection of sclerosant
60
How does Liver Cirrhosis lead to Ascites?
Increased pressure in portal system leads to portal HTN fluid leaks of of capillaries into the peritoneal cavity A drop in circulating volume reduces BP entering kidneys. This activates RAAS - can exacerbate issue. Lack of synthesis of albumin also lowers the oncotic pressure of the vasculature leading to fluid leakage
61
What is the management of Ascites?
Low sodium diet Spironolactone Paracentesis - ascitic tap/drain Prophylactic Abx
62
What s SBP?
Spontaneous Bacterial Peritonitis that occurs secondary to ascites caused by cirrhosis. This is an infection that develops in ascitic fluid without a clear cause
63
What is the presentation of SBP?
Can be ASx Fever Abdominal pain Deranged bloods - Raised WBC, CRP, Creatinine Ileus Hypotension
64
What are the most common organisms in SBP?
E.coli Klebsiella pneumoniae Gram +tve cocci - Staphly/enterococci
65
What is the management of SBP?
Take an ascitic culture (paracentesis) prior to giving Abx Often treated with IV Cephalosporin - Cefotaxime
66
How does Liver Cirrhosis lead to Hepato-Renal Syndrome?
Portal HTN decreases circulating volume in other areas such as kidneys. Activates RAAS Causes vasoconstriction (added to low blood supply to kidneys) starves kidneys of blood Rapid deterioration of kidney function - Hepatorenal syndrome
67
What is hepatic encephalopathy?
Cirrhosis leads to increased ammonia build up in the blood which can be transported to the brain. This can lead to reduced consciousness, confusion, personality changes, memory impairment and mood swings.
68
How is Hepatic Encephalopathy treated?
Laxatives (lactulose) - increase excretion of ammonia. Abx (rifaximin) reduce bacterial production of ammonia Nutritional support - potentially by NG tube
69
What is the Child Pugh Score? What is involved?
Assess prognosis and Extent of required Tx for chronic liver failure: Bilirubin Ascites presence Serum Albumin PT/INR HE
70
What is Decompensated Liver Cirrhosis a major risk factor for?
Hepatocellular Carcinoma
71
What is the Presentation of Chronic Liver Failure?
Jaundice Ascites HE Portal HTN Oesophageal Varices Caput Medusae
72
What are the Diagnostic Investigations for Chronic Liver Disease?
Liver Biopsy - Gold standard - Determines Extent of CLD LFTs, Imaging - Ultrasound, CT for secondary findings Ascitic Tap
73
What investigations are done in chronic liver disease (cirrhosis) to determine condition/cause?
Non-invasive Liver Screening: Bloods: LFTs - Hepatocellular/cholestatic FBC - inflammation/infection Electrolytes - Hyponatraemia (Fluid retention) U&Es - hepatorenal syndrome (Urea + creatinine are deranged) viral markers/autoantibodies - virus/autoimmune cause Alpha-Fetoprotein - HCC Fibroscan - elasticity of the liver Ultrasound - Splenomegaly, Ascites, Enlarged portal veins Endoscopy - Oesophageal varices CT/MR - HCC, Hepatosplenomegaly, ascites Liver Biopsy - confirm cirrhosis.
74
What is the Treatment of Chronic Liver Disease?
Tx underlying pathology Prevent Progression - lifestyle modification Consider Liver transplant - If decompensated liver Manage complications
75
What is Alcoholic Liver Disease?
Progressive damage to the liver from long term excessive Alcohol Consumptions.
76
What is the Progression of Alcoholic Liver Disease?
Alcohol related Fatty liver (steatosis): Build up of fat in the liver (reversible in a few weeks) Alcoholic Hepatitis: Liver inflammation - Mallory Bodies Alcoholic Cirrhosis Liver becomes largely fibrotic - Micronodular
77
What is the recommended alcohol intake per week?
14 units
78
How do you calculate the number of units in an alcoholic drink?
Strength (ABV) x Vol/ml / 1000
79
What is 1 UNIT of alcohol?
8g OR 10ml
80
What are the symptoms of Alcoholic Liver disease?
Early stages may show little signs/Sx Jaundice Fever: important to rule out infection Anorexia Abdominal pain Abdominal distention (ascites) Muscle wasting Confusion: seen in encephalopathy and alcohol withdrawal
81
What are the signs of ALD?
Jaundice Tender hepatomegaly Ascites Asterixis: flapping tremor secondary to encephalopathy Tremor: seen in alcohol withdrawal Bruising (coagulopathy) Stigmata of chronic liver disease
82
What are the CAGE Questions?
C – CUT DOWN? Ever thought you should? A – ANNOYED? Do you get annoyed at others commenting on your drinking? G – GUILTY? Ever feel guilty about drinking? E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?
83
What investigations should be done for all patients with suspected Hepatitis?
Full blood count Urea & electrolytes Liver function tests Bone profile C-reactive protein Magnesium Coagulation (INR) Non-invasive liver screen Liver ultrasound +/- septic screen (e.g. blood cultures, urines, ascitic cultures, chest x-ray)
84
What are the Diagnostic investigations for ALD?
Bloods: LFTs - Raised GGT, AST/ALT ratio >2 FBC - Macrocytic non-megaloblastic anaemia Hx of Alcohol Biopsy - confirm extent of hepatitis/cirrhosis
85
What Laboratory findings may be indicative of ALD?
Moderately elevated transaminases (< 300 IU/L) AST/ALT ratio >2 (other liver diseases rarely cause this ratio) Elevated bilirubin (usually > 86 umol/L) Elevated gamma-glutamyl transferase (GGT) Elevated neutrophil count (typically < 20.0 x10^9/L) Elevated INR
86
What may be found in ALD on histology?
Mallory Cytoplasmic Inclusion Bodies
87
What are the treatments of ALD?
STOP ALCOHOL - Tx withdrawal if present Healthy Diet / BMI Pharmacological - Consider steroids short term B1 & folate supplements Surgical - Consider Liver transplant in ESLF
88
What can be given to treat withdrawal Sx of ALD?
Chlordiazepoxide Diazepam
89
To be eligible for a liver transplant, how long must you have abstained from alcohol for?
3+ months
90
What are the complications of Alcoholic Liver disease?
Pancreatitis HE Ascites HCC Mallory Weiss Tear WERNICKE KORSAKOFF SYNDROME
91
What is Wernicke Korsakoff Syndrome?
A memory disorder that results from Vitamin B1 (thiamine) deficiency caused by alcoholism as this is poorly absorbed in the presence of alcohol. Wernickes Encephalopathy comes before Korsakoffs syndrome
92
What are the symptoms of Wernicke Encephalopathy and Korsakoff syndrome?
Wernicke Encephalopathy: Confusion Nystagmus Ataxia Korsakoff Syndrome: Memory Impairment Behavioural changes
93
How is Wernicke Korsakoff Syndrome treated?
IV Thiamine (Vit B1)
94
What is NALFD?
Non-alcoholic fatty liver disease: excess fat with the liver, which is known as hepatic steatosis (i.e. fatty liver). A small amount of fat in the liver is normal, but when this is present in > 5% of hepatocytes we term it NAFLD
95
What are the risk factors for NAFLD?
Obesity HTN Hyperlipidaemia T2DM FHx - PNPLA3 Endocrine disorders DRUGS
96
What is the Epidemiology of NAFLD?
NAFLD is now the most common cause of abnormal liver blood tests within the UK and estimated to affect > 50% of patients with type 2 diabetes mellitus.
97
What is Metabolic Syndrome?
The metabolic syndrome refers to a group of risk factors that are associated with an increased risk of cardiovascular disease and stroke. These risk factors have also been associated with the development NAFLD and include:
98
What are the factors of Metabolic Syndrome?
Abdominal obesity: waist circumference > 94 cm men and > 80 cm women Hypertension: arterial blood pressure > 130/85 mmHg or treated for hypertension Impaired fasting glucose: fasting blood glucose > 5.6 mmol/L or treated for type 2 diabetes mellitus High triglycerides: serum level > 1.7 mmol/L Low HDL cholesterol <1mg/dl in Men and 1.3mg/dl in women
99
What drugs are RFs for NAFLD?
NSAIDS Amiodarone
100
What is the pathogenesis of NAFLD?
Accumulation of Fat within the liver promotes inflammatory changes. Hepatosteatosis (NAFLD) This can lead to liver injury promoting inflammation Non-alcoholic steatohepatitis (NASH) Excessive inflammation and hepatocellular death leads to fibrosis Fibrosis leading to Cirrhosis
101
How would a NAFLD Px present?
Often ASx Any findings are incidental If severe NAFLD then Sx/signs of Liver failure
102
What are the diagnostic tests for NAFLD?
Bloods: Abnormal LFTs - Inc PT/INR, Dec Albumin, Inc Bilirubin FBC - Thrombocytopenia, Hyperglycaemia Imaging: 1st line - Abdominal Ultrasound - confirms diagnosis of hepatic steatosis Enhanced Liver Fibrosis (EFL) NAFLD fibrosis score Fibroscan
103
What investigation would be used to determine the cause of abnormal LFTs if the cause is unclear?
Non-invasive Liver screen: FBC LFT U&E Ultrasound Hep B/C serology Autoantibodies - AIH, PBC,PSC Immunoglobulins - AIH, PBC Caeruoplasmin - wilsons disease Alpha 1 anti trypsin - A1AT Def Ferritin/Transferrin - HH
104
How is the risk of fibrosis assessed?
Using FIB-4 (fibrosis score) Detects stiffness of the liver
105
What is the Tx for NAFLD?
Lose weight (lower BMI) Control RFs: Statins - cholesterol Metformin - diabetes ACEi - BP Vitamins
106
What are some complications of NAFLD?
HE Ascites HCC Portal HTN Oesophageal Varices
107
What is Autoimmune Hepatitis?
Chronic liver inflammation (hepatitis) caused by autoimmune attack via T cells on the Liver. It has an unknown cause but likely genetics and then an environmental trigger
108
What are the risk factors for autoimmune hepatitis?
Female Other autoimmune diseases - SLE Viral hepatitis HLA DR3/4
109
What are the types of Autoimmune Hepatitis?
Type 1 - Adult females (80% of cases): ANA/ASMA Abs - Very specific for T1 AIH Type 2 - Young Females: ALC-1/ALKM1 Abs Seronegative AIH - 20% of AIH patients are autoantibody negative.
110
How may patients present with AIH?
25% ASx 40% with acute Hepatitis Sx: Anorexia Nausea Coryzal symptoms Jaundice Right upper quadrant pain Hepatomegaly 30% with Chronic Liver Disease Sx: Non-specific features Stigmata of chronic liver disease Complications of cirrhosis
111
What are the diagnostic investigations for AIH?
Serology - ANA/ASMA +/- ALC-1/ALKM1 LFTs - Hepatic (ALT/AST Raised) Liver Biopsy
112
What may be seen on liver biopsy to aid the diagnosis of AIH?
Interface hepatitis: inflammation and fibrosis at the lobular-portal interface Lymphoplasmacytic infiltrates: infiltration of lymphocytes and plasma cells Hepatocyte necrosis: specifically ‘bridging necrosis’. Hepatic Rosette formation: gland-like formations (Pseudoacini) that develop due to chronic inflammation.
113
What are the antibodies associated with AIH?
Anti-nuclear (ANA) - Type 1 Anti-Smooth muscle (ASMA) - Type 1 Anti-liver/kidney (ALKM1) - Type 2 Anti-mitochondrial (AMA) - mainly for PBC Anti-soluble liver and pancrease (SLA/LP) - 75% of Type 1
114
What Immunoglobulin is associated with AIH?
IgG are raised
115
How is AIH treated?
Immunosuppressants via Corticosteroids (Prednisolone) + Azathioprine Hep B vaccination
116
What is a last resort Tx for AIH?
Transplant consideration (10-20% of Px may have this)
117
What is the process of RBC breakdown?
RBC Hb is split into Haem and Globin Haem is split into Iron and Biliverdin (via Haemoxygenase). Globin into amino acids which is recycled for erythrocytes Biliverdin is converted to Unconjugated Bilirubin via biliverdin reductase UnC Bilirubin is bound to albumin and transported to the liver UDP GlucoronylTransferase (UGT) Conjugates Unc biliribin with Glucoronic acid to form Con Bilirubin. Con Bilirubin enters the small intestine via the CBD and enters at the A.o.V Con bilirubin is converted to urobilinogen via colonic flora. 5% - sent to kidneys to be oxidised and excreted as urobilin 5% - recycled via enterohepatic circulation 90% - Large intestine and reduced to stercobilin and excreted in faeces
118
What is Jaundice?
Yellowing of the skin and eyes due to accumulation of conjugated/unconjugated bilirubin in the blood.
119
What are the different types of Jaundice?
Pre-hepatic - Haemolysis Intra-hepatic - Liver dysfunction Post hepatic - Obstruction
120
What are the causes of Pre-hepatic jaundice?
Haemolytic anaemias: Sickle cell Thalassaemia G6PDH Def Malaria
121
What is raised in Pre hepatic jaundice?
Raised Unconjugated bilirubin due to increased RBC breakdown saturating conjugatory mechanisms
122
What are the causes of intra hepatic jaundice?
Parenchymal disease: HCC ALD/NAFLD Hepatitis Hepatotoxic drugs - Rifampicin Gilberts syndrome Crigler Najjar Syndrome
123
What is Raised in Intra hepatic jaundice?
Conjugated and unconjugated bilirubin Can be mixed due to the failure of Hepatocytes to uptake, metabolise and or excrete bilirubin
124
What is Gilberts Syndrome?
Very common Autosomal recessive mutation of UGT1A1 gene causes underactive UGT enzyme and therefore decreases CON bilirubin.
125
How may a Patient with Gilbert Syndrome present?
Young male Painless jaundice that has sudden onset
126
What is Crigler Najjar Syndrome?
Autosomal recessive absence of UGT enzyme and therefore has an inability to conjugate bilirubin
127
What are the causes of Post hepatic Jaundice?
Biliary tree pathology Choledocholithiasis - bile stone Pancreatic cancer cholangiocarcinoma Mirizzi Syndrome Autoimmune - PBC/PSC
128
What is Mirizzi Syndrome?
common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder
129
What is raised in Post hepatic jaundice?
Conjugated bilirubin is raised due to biliary obstruction. This causes pale stools and Dark urine.
130
What is Courvoisier sign and what would it suggest?
Painless jaundice and palpable GB Likely pancreatic cancer/cholangiocarcinoma
131
What is the Charcot Triad?
Fever RUQ Pain Jaundice
132
What combination of Charcot Triads symptoms suggest which conditions?
RUQ pain = Biliarycolic Fever + RUQ pain = Cholecystitis Fever + RUQ Pain + jaundice = Ascending cholangitis
133
What is Murphys Sign?
RUQ Tenderness Ask Px to take a breath in whilst pressing on RUQ Makes them wince +tve for Cholecystitis
134
How can the type of Jaundice be diagnosed?
1st line = Abdominal Ultrasound Blood tests and LFTs Urine bilirubin: normally -tve +tve = Dark urine = post hepatic/intrahepatic -tve in haemolysis causes Urobilinogen: normally +tve Increased in haemolysis - Pre hepatic Decreased in Intra/post hepatic
135
What is pancreatic cancer?
Adenocarcinoma of the exocrine pancreas (99% of cases) of ductal origin. Typically affects the head of the pancreas
136
who is typically affected by pancreatic cancer?
Males 60yrs +
137
What are the risk factors for pancreatic cancer?
Smoking Alcohol Diabetes Mellitus FHx Chronic pancreatitis Genetics - PRSS-1 mutation
138
How would a patient with pancreatic cancer present/ what signs would they have?
Anorexia Weight loss Acute pancreatitis Body and tail of pancreas: Epigastric pain that radiates to back Relieved by sitting forward Head of pancreas: Painless jaundice (Courvoisier's Sign) Weight loss
139
What is the characteristic of the pain in a body/tail pancreatic cancer?
Epigastric pain Radiates to the back Relieved when sitting forward
140
What are the diagnostic investigations for pancreatic cancer?
1st line - abdominal ultrasound GS - Pancreatic CT protocol then bile duct drainage Ca19-9 tumour marker positive - monitors progression
141
What is the gold standard diagnostic investigation for pancreatic cancer?
Pancreatic CT Diagnostic in 97% of cases + Biopsy confirmation
142
What marker indicates progression of pancreatic cancer?
Ca19-9 tumour marker
143
What is the Treatment of pancreatic cancer?
Very poor prognosis - 5yr survival - 3% surgery + post op chemo if no mets Palliative care
144
What is Hepatocellular carcinoma (HCC)
arise from liver parenchyma 90% all primary liver cancers
145
What is the epidemiology of HCC?
One of the leading causes of cancer mortality Highest risk in Asia due to increased burden of Viral Hepatitis
146
What are the major risk factors of HCC?
Chronic hepatitis - viral infection of Hep C and B Cirrhosis of the liver - ALD/ NAFLD/ Haemochromatosis
147
What are some other risk factors for HCC (non major)?
Hepatitis D Aflatoxin B1 Alcohol Smoking NAFLD Metabolic Liver disease
148
Where do HCC metastases often travel to? How do these travel?
Lymph nodes Bones Lungs via haematogenous spread (hepatic/portal veins)
149
How would a patient with HCC present?
Sx of decompensated liver failure - HE, jaundice, ascites Cancer signs - tATT, unexplained weight loss
150
What diagnostic investigations are done for HCC?
Imaging: 1st line - Abdo ultrasound GS - CT (confirms diagnosis) May also biopsy and Histology for diagnosis Raised serum AFP (alpha fetoprotein)
151
What is the treatment of HCC?
Surgical Resection of the liver Only cure is Liver transplantation if decompensated
152
What should be given to prevent HCC?
HBV Vaccination!!
153
What isa cholangiocarcinoma?
adenocarcinoma that arises from the biliary tree
154
What percentage of liver cancers are cholangiocarcinomas?
10%
155
What are the risk factors for cholangiocarcinoma?
Parasitic flukeworms Biliary Cysts IBD PSC
156
How would a Px with cholangiocarcinoma present?
Abdo pain jaundice weight loss pruritis fever Late constellation Sx of tumour since it is slow growing
157
What diagnostic investigations would be used for a cholangiocarcinoma?
LFT - Inc Bilrubin, Inc Alkaline Phosphates Inc Ca19-9 Imaging : 1st line - Abdo USS + CT GS ERCP - imagine of biliary tree Biopsy
158
What is the gold standard investigation for cholangiocarcinoma?
ERCP
159
What is the Tx of cholangiocarcinoma?
Chemo/radiotherapy possibly Mostly inoperable due to late presentation of Px
160
What are some benign primary liver tumours?
Haemangioma Hepatic Adenoma
161
What is more common, primary or secondary liver tumours?
Secondary are more common
162
Where can secondary tumours come from?
GI tract Lungs Breast
163
How may a patient with a secondary liver tumour present?
Depends on the site of the primary cancer
164
What diagnostic investigations may show a secondary liver tumour?
Increased serum ALP(Alkaline Phosphatase) Imaging: 1st line - Ultrasound GS - CT/MRI for staging and primary tumour
165
What is the Treatment of 2' liver cancer?
Surgical resection if possible Chemotherapy
166
What are some different biliary tract diseases
Gallstones Cholecystitis Ascending Cholangitis
167
What are the risk factors for biliary tract disease
5Fs Fat Female Forty (40+) Fertile Fair + FHx, T2DM, NAFLD
168
What are gallstones?
Small stones usually made of cholesterol that form in the gall bladder
169
Define: Cholelithiasis Choledocholithiasis Biliary Colic Acute Cholecystitis Acute Cholangitis
Cholelithiasis: refers to gallstones - solid deposits that develop in the gallbladder. Choledocholithiasis: refers to gallstones within the biliary tree. Biliary colic: refers to a self-limiting pain in the RUQ/epigastrium associated with gallstones. Acute cholecystitis: refers to the acute inflammation of the gallbladder, most commonly caused by gallstones. Acute cholangitis: refers to infection of the biliary tree, commonly due to an obstructing stone in the common bile duct.
170
What is the epidemiology of gallstones
May be present at any age but unusual <30 Increasing prevalence with age More common in females More common in Scandinavians, S. Americans and Native North Americans Less common in Asian and African groups Most form in the GB Present in 10-20% of population
171
What is the general composition of gallstones?
Phospholipids - lecithin Bile pigments (broken down haemoglobin) Cholesterol
172
What are the 3 types of gallstones?
Cholesterol Black Pigment Mixed (brown pigment)
173
What are the characteristics of cholesterol, Pigment and mixed stones?
Cholesterol: Large often solitary Pigment: Small black and gritty, calcium bilirubinate Mixed: often have multiple Main component is cholesterol mixed with calcium bilirubinate and calcium salts
174
How are Cholesterol stones formed?
They occur due to crystallisation of cholesterol in bile (along with other compounds) due to supersaturation of cholesterol and crystillisation promoting factors
175
How are pigment stones formed?
They occur in people with increased amounts of bilirubin in their bile - hyperbilirubinbilia. This occurs in patients with increased haemolysis
176
How are Mixed Stones formed?
These stones are a mix of calcium bilirubinate and a calcium salts of fatty acids, accounting for around 5% of stones. They mostly occur in association with infection (bacterial or parasitic) and may develop de novo in the bile duct after cholecystectomy.
177
What is the cause of gallstones?
Lithogenic bile - Admirand's triangle Biliary sepsis Altered composition of Bile Gallbladder hypomotility: - Pregnancy/oestrogen contraceptive pill - Total parenteral nutrition/fasting
178
What is Admirand's triangle?
Low bile salts Low lecithin High cholesterol
179
How are gallstones formed?
Bile is secreted by hepatocytes into the biliary circulation. It is composed of bile acids (or salts), phospholipid, bilirubin, cholesterol and water. Imbalance in composition and stasis leads to stone formation.
180
What are the symptoms of gallstones?
Usually ASx but can cause cholic pain upon GB contraction RUQ biliary colic pain - constant severe pain for 30 mins Worse after a fatty meal as CCK induced gallbladder contraction against a stone Pain radiates to right shoulder Fever Jaundice - if stone obstructs duct nausea and vomiting
181
What investigations are done to confirm gallstones?
Murphy Sign Ultrasound scan LFTs - ALT raised due to backpressure. Bilirubin high if blockage. MRI - stones in bile duct CT - gallstone complications cholangiography - assess condition of the gallbladder
182
What are the complications of gallstones in the gallbladder?
Biliary colic Acute cholecystitis +- empyema Chronic cholecystitis Mucocele Carcinoma Mirrizi's syndrome
183
What are the complications of gallstones in the common bile duct?
Obstructive Jaundice Pancreatitis Cholangitis
184
What are the symptoms of cholecystitis?
RUQ pain + Fever + Tender gall bladder Reffered pain to top of right shoulder (phrenic) Murphy Sign +tve Vomiting
185
What is Murphy Sign?
patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner's hand, Murphy's sign is positive.
186
What is the treatment for Cholecystitis?
Abx, Analgesia and fluids Laparoscopic cholecystectomy
187
What are the symptoms of Ascending cholangitis?
Reynolds pentad: RUQ pain Fever Jaundice Altered mental state Hypotension
188
What is Reynold's Pentad
Chartcot's Triad + Altered Mental State + Hypotension
189
What is the Diagnostic test for Gallstones
1st line = Abdo ultrasound
190
What are the investigations for Ascending Cholangitis?
Ultrasound abdomen FBC Raised WBCs Raised ESR and CRP Raised serum bilirubin (very high if bile duct obstruction) and serum alkaline phosphatase ERCP MRCP to locate stone LFTs CT
191
What is the treatment for Ascending Cholangitis?
IV antibiotics e.g. co-amoxiclav Fluids ERCP (endoscopic retrograde cholangiopancreatography) to image/stent/remove stone Shockwave lithotripsy If this fails 🡪 laparoscopic/open cholecystectomy
192
What are the treatments for gallstones?
Elective laparoscopic cholecystectomy if Sx Until then pain management- NSAIDS (mild), Diclofenac (severe) Lifestyle modifications - low fat in diet
193
What is Biliary Colic?
Where a patient has cholic pain due to a gallstone often in the gallbladder that has not yet caused inflammation and therefore the patient doesn't present with aa fever or jaundice. They will likely have RUQ pain (colicky) if Symptomatic
194
What is acute cholecystitis?
gall bladder inflammation that develops over hours
195
What is the pathogenesis of acute cholecystitis?
Large fatty meals stimulate CCK which signals bile release from GB When the GB has a gallstone in it, the squeezing of the GB can get it lodged in the cystic duct Bile stasis becomes a chemical irritant stimulates mucosa in wall to release mucus and inflammatory enzymes 🡪 inflammation, distension and pressure build up Bacteria can start to grow e.g. E. coli and invade into gallbladder wall 🡪 Cholecystitis If they penetrate the GB wall then this can lead to peritonitis
196
What are the causes of cholecystitis?
Gallstones Tumour Bile duct blockage Infection Blood vessel problems
197
What investigations are done for acute cholecystitis?
Urine tests - bilirubin and urobilinogen raised FBC - Inc WCC Imaging - abdominal USS
198
What test is ordered if dilated bile ducts are found on ultrasound in suspected acute cholecystitis?
MRCP
199
What are the differential diagnoses for acute cholecystitis?
Main: Biliary Colic Cholangitis Others: Peptic ulcer disease Liver disease Pancreatitis Cardiac disease
200
What is the management for Acute Cholecystitis?
Conservative: if ASx Nil by mouth Fluid resuscitation Abx - Gentamicin analgesia - Paracetamol/NSAIDS If Symptomatic: Laparoscopic cholecystectomy Analgesia and fluids and Abx (gentamicin)
201
What is Ascending Cholangitis?
Inflammation of the bile duct caused by bacteria ascending from the duodenum through the ampulla of Vater
202
What is the pathophysiology of ascending cholangitis?
Normally, bacteria can’t go up CBD as bile and pancreatic juices travel down and flush bacteria out Obstruction of common bile duct 🡪 stasis of bile 🡪 invasion of bacteria from duodenum High pressure on the CBD (due to the obstruction) can cause spaces between the cells do widen which allows the bacteria and the bile access to the blood stream 🡪 bacteraemia and jaundice Can be obstructed by stone, cancer, stricture, parasite (ascaris). Also, infection can be introduced through intervention e.g. ERCP
203
What causes ascending cholangitis?
Gallstones Iatrogenic - ERCP Cholangiocarcinoma Ascending infection from duodenum junction
204
What are the risk factors of ascending cholangitis?
History of gallstones (5Fs) Sclerosing cholangitis HIV Narrowing of common bile duct
205
What are the blood tests done for suspected or known ascending cholangitis?
FBC - WCC raised CRP - Raised LFT - Hyperbilirubinaemia
206
What imaging tests are ordered for ascending cholangitis?
Transabdominal ultrasound
207
What is the management of ascending cholangitis
Antibiotics ERCP - bile duct clearance
208
How can Sepsis occur in ascending cholangitis?
Biliary obstruction causes backflow of biliary sludge. This causes stasis Bacteria from the intestines can enter the biliary duct and colonise the biliary tree
209
What are the differential diagnoses for a patient who has: 1. RUQ pain, No fever , No jaundice. 2. RUQ pain, Fever, no jaundice 3. RUQ pain, Fever and Jaundice
1. Biliary Colic 2. Acute Cholecystitis 3. Cholangitis
210
What is Primary Biliary Cholangitis
Autoimmune system attacks the small bile ducts in the liver. This causes obstruction of the outflow of the bile (cholestasis) The back pressure of bile obstruction can lead to fibrosis and liver disease
211
What is the pathophysiology of PBC?
PBC is characterised by T-cell mediated attack to small bile ducts within the liver. Autoreactive T cells seem to target the E2 subunit of the pyruvate dehydrogenase complex, which is expressed on the luminal surface of bile duct epithelial cells in PBC. Chronic inflammation leads to bile duct destruction and loss. This leads to cholestasis (poor bile flow), which causes the build-up of potentially toxic substances at high concentrations, such as bile acids, that can lead to damage to hepatocytes. Over time, this leads to chronic liver disease.
212
What autoantibodies are associated with PBC?
Anti-Mitochondrial (AMA) - 95% of patients. Also ANA, Anti-gp210 and anti-sp100
213
What ducts are affected in PBC?
Intralobar ducts (Canals of Hering)
214
What are the symptoms of PBC?
Fatigue Pruritus GI disturbance and abdominal pain Signs of chronic liver disease
215
What are the signs of PBC?
Hepatomegaly Excoriation marks Xanthomas (deposition of cholesterol in the skin causing a nodule) Xanthelasmas (deposition of cholesterol in the skin causing a papule or plaque) Xerosis (dry skin) Hyperpigmentation of skin: due to melanin deposition but reason unknown Jaundice: more common as disease advances Features or chronic liver disease (advanced disease)
216
What is PBC associated with?
Middle aged women >50 years Other autoimmune diseases (e.g. thyroid, coeliac) Rheumatoid conditions
217
What is Xanthoma and Xanthelasma?
Xanthomas (deposition of cholesterol in the skin causing a nodule) Xanthelasmas (deposition of cholesterol in the skin causing a papule or plaque)
218
What are some complications of PBC?
Cirrhosis Malabsorption of Fats + ADEK steatorrhoea osteomalacia
219
How is the diagnosis for PBC made?
Diagnosis of PBC is based on the presence of cholestatic liver enzymes and positive anti-mitochondrial antibodies.
220
What are the diagnostic tests for PBC?
LFTs: Raised AP Raised Con Bilirubin Dec Albumin Antibodies: AMA (anti mitochondrial) - specific to PBC (95%) ANA (anti nuclear) Liver Biopsy Imaging: 1st Line - Abdo USS to exclude extrahepatic cholestasis Blood tests: ESR Raised IgM Raised
221
What is the Treatment of PBC?
Ursodeoxycholic acid - reduces intestinal absorption of cholesterol Sx Treatment: Colestyramine - for Pruritus Rifampicin - Abx SSRI (sertraline) Vit ADEK Supplements Liver Transplant - in ESLF
222
What is the most important disease progression of PBC?
Advanced liver cirrhosis Portal Hypertension
223
What is Primary Sclerosing Cholangitis?
Autoimmune attack on the intrahepatic and/or extrahepatic ducts causing them to become strictured and fibrotic. This causes an obstruction to bile outflow from the liver eventually resulting in cholangitis, hepatitis and Liver cirrhosis (Same pathology as PBC)
224
What are the risk factors for PSC?
Male Northern Europeans Aged 30-40 Ulcerative colitis FHx
225
What is the aetiology of PSC?
Largely Unknown. PSC is considered a progressive autoimmune disorder that is strongly associated with inflammatory bowel disease (IBD)
226
How would PSC Present?
Early stages may be ASx Sx: Fatigue Pruritus Features of cholangitis - Fever, malaise, night sweats, RUQ pain, Rigors Signs: Hepatomegaly Splenomegaly Excoriations Stigmata of chronic liver disease
227
What are the diagnostic tests for PSC?
LFTs: Cholestatic - ALP and GGT is raised Then later bilirubin may become raised later in disease Antibodies are not sensitive or specific for PSC (sometimes pANCA) GS - MRCP imaging showing bile duct lesions/strictures
228
What is the treatment of PSC
Conservative Sx management Liver transplant is only effective Tx (curative) Colestyramine - help pruritus
229
How does Colestyramine help with pruritus?
Bile acids can bit itchy. Colestyramine binds to bile acids and prevents their absorption (Bile acid Sequestration).
230
What does PSC have a strong link to?
IBD - Ulcerative Colitis
231
What are some complications of PSC?
Acute bacterial cholangitis Cholangiocarcinoma Colorectal cancer Cirrhosis and liver failure
232
What are some differential Diagnoses for PSC?
It is important to exclude secondary causes of sclerosing cholangitis before making the diagnosis. Causes of Sclerosing Cholangitis: Inflammatory: IgG4-sclerosing cholangitis, pancreatitis Malignancy: cholangiocarcinoma, hilar lymphadenopathy, head of pancreas tumour Infection: recurrent pyogenic cholangitis, biliary infestation (e.g. flukes) Stones: choledocholithiasis Other: drugs, papillary stenosis
233
What is Acute Pancreatitis?
Acute inflammation of the pancreas
234
What are the causes of Acute Pancreatitis?
I GET SMASHED: Idiopathic Gallstones - 50% of all acute causes Ethanol - 80% of chronic causes Trauma Steroids Mumps Autoimmune Scorpion Sting/Spider Bite Hypercalcaeima/Hyperlipidaemia ERCP Drugs - Azathioprine, NSAIDs, ACEi
235
What drugs can cause Acute Pancreatitis?
Azathioprine NSAIDs ACEi
236
What is the pathogenesis of Acute pancreatitis?
Obstruction of pancreatic secretions/damage to pancreas causes accumulation of digestive enzymes in the pancreas Zymogens become activated within the pancreas Leads to autodigestion of the pancreas creating inflammation and enzymes leak into the blood. Can lead to retroperitoneal haemorrhage Oedema, fluid shift and vomiting leads to hypovolaemic shock
237
What are the risk factors for acute pancreatitis?
Alcoholism Smoking Obesity Family history
238
What are the symptoms associated with acute pancreatitis?
Abdominal pain (may radiate to the back) Nausea Vomiting Anorexia Diarrhoea
239
What are the signs of Acute pancreatitis?
Abdominal tenderness Abdominal distention Cullen's Sign Grey-Turner's Sign Signs of Shock: Tachycardia Tachypnea Pyrexia
240
What are the Eponymous signs for pancreatitis?
Cullen’s sign: peri-umbilical bruising (first described in ruptured ectopic pregnancy) Grey-Turner’s sign: flank bruising
241
What is a DDx of acute pancreatitis based on the pain experienced by Px?
AAA
242
What diagnostic investigations would be performed in acute pancreatitis?
FBC: High WCC GS - Liver enzymes: Serum Amylase and Lipase High LFTs: Cholestatic - High AST, LDH High Conc bilirubin Low Urobilinogen Imaging; CXR - Exclude duodenal ulcer USS Gallstones
243
What is the first line/Gold standard test for acute pancreatitis?
A serum amylase elevated 3 times above the reference range is considered diagnostic.
244
What is required for Dx of Acute pancreatitis?
Px must have at least 2 of: Characteristic Signs and Symptoms Increased Amylase/Lipase Radiological Evidence (USS)
245
How is pancreatitis severity scored?
APACHE 2 - assess severity in 24hrs Glasgow Criteria - Prediction of severe attack (only after 48hrs)
246
What is the Glasgow criteria in assessing acute pancreatitis severity?
PANCREAS: PaO2 Age Neutrophils Ca2+ Renal Function Enzymes Albumin Sugar
247
What is the Treatment of acute pancreatitis?
Emergency: Nil By mouth IV fluid Analgesia - morphine Catheterise Abx prophylaxis
248
What is a major complication of acute pancreatitis?
SIRS (systemic Inflammatory Response Syndrome) Tachycardia Tachypnoea Pyrexia Increase WCC
249
What are some complications of Acute pancreatitis and how are they managed?
ARDS - Give O2 Hyperglycaemia - Insulin Shock - Hypovolaemic give fluids, Septic - Abx
250
What Ig is Raised in a patient with autoimmune chronic pancreatitis?
IgG4
251
How is autoimmune Chronic pancreatitis treated?
With steroids
252
What is Chronic Pancreatitis?
3+ month history of pancreatic deterioration leading to irreversible pancreatic damage, inflammation and fibrosis.
253
Give the pathophysiology of Chronic Pancreatitis
Progressive loss of lobular morphology and structure of pancreas due to necrosis/apoptosis, inflammation and/or duct obstruction Deformation of the large ducts and severe changes in arrangement and composition of islets Irreversible morphological and structure changes - impair exocrine and endocrine functions
254
What are the causes of chronic pancreatitis?
AGITS: Alcohol - Most common Genetics - CF, Haemochromatosis Immune Triglycerides Structural - Duct obstruction CDK, Trauma, Recurrent acute Pancreatitis
255
What are the risk factors for chronic pancreatitis?
Male sex Alcohol misuse Smoking Obesity Recurrent acute pancreatitis CKD Gallstones ⍺1-antitrypsin deficiency
256
How might a patient present with chronic pancreatitis?
Epigastric pain Steatorrhoea (increased levels of fat in stool) and weight loss Endocrine Dysfunction - Diabetes mellitus - polyuria, polydipsia Epigastric mass - pseudocyst
257
What are the characteristics of pain in chronic pancreatitis?
Bores through the back Relieved by sitting forward or hot water bottle Exacerbated by fatty foods/alcohol
258
What Diagnostic Investigations would be used for Chronic Pancreatitis?
Hx Bloods: Lipase + amylase Faecal Elastase Transabdominal Ultrasound + CT - detects pancreatic calcification + dilated pancreatic ducts
259
What is the management of Chronic Pancreatitis?
Alcohol Cessation Abdo Pain Sx - NSAIDs Pancreatic Enzyme supplements Surgical: Endoscopic stenting Whipple - Distal pancreatectomy
260
What forms the Hepatic Portal Vein?
Union of the SMA and Splenic Veins
261
What is Portal Hypertension?
Pathological high pressure in the portal vein commonly caused as a complication of other conditions such as liver cirrhosis and alcoholism
262
What is the normal pressure range in the portal venous system and in portal HTN?
5-10 mmHg When Pressure in portal vein is >10mmHg = Bad / >12mmHg = V.bad
263
What is the pathophysiology of Portal Hypertension?
Increased vascular resistance in portal venous system Causes splanchnic dilations and compensatory Increase in CO Results in fluid overload in portal vein This opens venous collaterals - connecting portal and systemic venous systems. Venous collaterals shunt blood to gastroeosophageal veins causing varices
264
Where would varices tend to develop in portal HTN?
Lower oesophagus and gastric cardia
265
What are Varices?
A dilated vein that is at risk of rupture causing haemorrhage in the GI Tract
266
How is Portal HTN Classified?
Site of the obstruction: Pre-hepatic - blockage of PV before the liver Intrahepatic - Distortion of liver architecture (pre/post sinusoidal) Post hepatic - Venous blockage outside the liver.
267
What are some causes of Pre hepatic Portal HTN?
Portal Vein Thrombosis
268
What are some causes of Intra hepatic portal HTN?
Cirrhosis - most common in UK Schistosomiasis - Commonest world wide
269
What are some causes of post hepatic portal HTN?
Budd Chiari (hepatic vein obstruction by tumour/thrombus) RHF Constrictive Pericarditis
270
What are the Sx of Portal HTN?
Mostly ASx Associated with LF and therefore Sx of LF may be present Present when oesophageal varices rupture
271
What investigations are required for portal HTN?
Abdominal Ultrasound - Dilated portal vein Doppler US - slow PV velocity Oesophagealgastroduodenoscopy (OGD) check for presence of oesophageal varices
272
What are the complications of portal HTN?
Bleeding from gastric/oesophageal varices Ascites Pulmonary HTN LF Hepatopulmonary Syndrome
273
What is the Treatment of Portal HTN?
Tx underlying Cause Salt reduction and Diuretics Beta blockers/Nitrates to reduce BP.
274
What causes oesophageal varices?
Portal HTN
275
When are Gastro-oesophageal varices prone to rupture?
When portal pressure exceeds 12mmHg This will lead to GI bleeding.
276
What are the Sx of a patient who's oesophageal varices have ruptured?
Haematemesis - coughing blood. Abdo pain Shock - if large blood loss Hypotension and tachycardia Ascites
277
What is the management of oesophageal varices?
Resus until haemodynamically stable Consider blood transfusion - get Hb to 80g/L Stop the bleed: IV Terlipressin (give IV Somatostatin if CI in IHD) - causes vasoconstriction Variceal banding TiPPS - Transjugular intrahepatic portosystemic shunt Prevent Bleed: Propranolol and Nitrates Prophylactic Abx
278
What is Ascites?
Accumulated free fluid in abdominal cavity commonly as a complication of Cirrhosis
279
What is the epidemiology of Ascites?
10-20% survival 5-years from onset Signifies other serious illness Common post op
280
What are the main causes of Ascites?
Local Inflammation - peritonitis, TB, Abdo cancer Low protein - Nephrotic Syndrome, Hypoalbuminaemia (LF) Flow Stasis - Liver cirrhosis, Budd Chiari, Congestive HF
281
What is the pathophysiology of Ascites?
Local inflammation - Fluid accumulation Low protein - Lower osmotic potential of intravascular space Low flow - Fluid cannot move forwards (i.e. due to clot) - Raises pressures in vessels
282
What are the symptoms & signs of Ascites?
Abdominal Distension/swelling Abdominal pain - severe suspect SBP Shifting Dullness Fluid in flanks Fluid thrill May have jaundice and Pruritus
283
What are the risk factors for ascites?
High sodium diet Hepatocellular carcinoma Splanchnic vein thrombosis resulting in portal hypertension
284
What investigations are done for Ascites?
Shifting Dullness Exam Ascitic Tap - Aspiration of ascitic fluid: - Cytology - WCC - Protein Measurement (serum ascites albumin gradient (SAAG))
285
What would the different results of protein measurement suggest in an Ascitic tap?
Transudate:(raised portal pressure) <30g/l Low protein Serum Albumin ascitic gradient (SAAG) ,11g/l Clear fluid - due to increased hydrostatic pressure Exudate: (Normal portal pressure) >30 g/L High Protein SAAG >11g/L cloudy fluid - due to inflammation mediated exudation
286
What would a Transudate ascitic tap suggest the cause of Ascites is?
Portal HTN ALF, cirrhosis Budd Chiari Constrictive pericarditis Congestive HF Nephrotic Syndrome
287
What would an Exudate ascitic tap suggest the cause of Ascites is?
Malignancy Peritonitis Pancreatitis Bowel Obstruction
288
What is the management for ascites?
Tx underlying cause Reduce Sodium - help live Diuretics - increase Na excretion - Spironolactone Paracentesis - fluid drain Liver transplant
289
What are some complications of ascites?
Spontaneous Bacterial Peritonitis
290
What is Peritonitis?
Inflammation of peritoneum Can be primary (inflammation on its own i.e. bacterial infection/ascites) Can be secondary (i.e. bile - treat underlying cause to manage peritonitis)
291
What is peritonism?
Tensing of muscles to prevent movement of peritoneum
292
What are the causes of peritonitis?
AEIOU: A – Appendicitis – umbilicus to RIF pain E – Ectopic pregnancy – low abdominal pain, sudden onset, tachycardia, low BP I – Infection with TB Bacterial – most common Gram-negative e.g. E. Coli and Klebsiella Gram-positive staphylococcus e.g. S. Aureus O – Obstruction – colicky pain, history of abdominal surgery U – Ulcer – epigastric pain radiating to shoulder Peritoneal dialysis
293
What are the different pathways of infection for peritonitis?
GI perforation Transmural translocation - from pancreatitis etc Exogenous contamination - drains, surgery etc, UTI Haematogenous spread - septicaemia
294
What are the Sx of Periotonitis?
Sudden onset severe abdominal pain General collapse fever malaise Nausea and vomiting + Ascites / Septic Shock
295
What are the characteristics of the abdominal pain in peritonitis?
Rigidity helps pain - Pain relieved by resting hands on abdomen - stops abdominal movement Localised guarding and rebound tenderness Well localised - more inflamed as it has reached parietal layer and overlying dermatome Poorly localised - less inflammation pressing only on visceral nerves
296
What are the signs of Peritonitis?
Pain relieved by resting hands on abdomen – stops movement of peritoneum and therefore pain Guarding/rebound tenderness Absence of bowel sounds Rigid abdomen Pain worse on coughing or moving Patient wants to lie still Sepsis/septic shock – hypotension, tachycardia, oliguria, fever
297
What region of the abdomen is innervated by which nerves?
T5-9 = Epigastric (greater splanchnic - foregut to 2nd part of duodenum) T10-11= Umbilical (lesser splanchnic - 2nd part of duodenum to 2/3 transverse colon) T12 = Hypogastric (least splanchnic - 2/3 transverse colon to upper rectum)
298
How is peritonitis diagnosed?
Ascitic Tap shows Neutrophilia Blood test and culture Increased ESR/CRP Urine dipstick for UTIs Bloods: U&Es FBC Serum amylase - rule out acute pancreatitis Erect CXR - rule out perforated colon if no free air under diaphragm CT Scan AXR - bowel obstruction hCG - rule out pregnancy
299
What is the Treatment of Peritonitis?
ABCDE Tx underlying cause Analgesia + urinary catheterisation +/- GI decompression IV fluids + Electrolytes (fluid resus) IV Abx - Cefotaxime, Metronidazole Surgery - Remove/divert cause of peritonitis - Peritoneal Lavage (cleaning of peritoneum)
300
What are the main complications of peritonitis?
Septicaemic if not Tx early (suspect if BP is low) Local Abscess formation Kidney Failure
301
What are the differential diagnoses for peritonitis?
Bowel Obstruction
302
Give 3 causes of iron overload.
1. Genetic disorders e.g. haemochromatosis. 2. Multiple blood transfusions. 3. Haemolysis. 4. Alcoholic liver disease.
303
What is Hereditary Haemochromatosis?
Autosomal recessive mutation of the HFE gene on chromosome 6 that results in excess Iron uptake by transferrin 1 leading to increased iron storage and deposition of iron in tissues.
304
Who is typically affected by Haemochromatosis?
Males 50yrs old +
305
Why are women less likely to be affected by haemochromatosis?
They will lose iron in blood during menstruation
306
What is the pathophysiology of Hereditary Haemochromatosis?
Excess iron uptake by transferrin 1 and decreased Hepcidin synthesis (loss of iron homeostasis regulatory protein) Iron accumulation into the liver Causes fibrosis of Liver and can lead to iron deposition in other organs
307
What organs can iron be deposited in in haemochromatosis?
Pancreas Kidney Heart Skin Ant. Pituitary
308
What are the risk factors for hereditary haemochromatosis?
Genetic Alcohol
309
What are the Sx of Haemochromatosis?
Males in 40-50s (women often present later) Chronic tenderness Joint pain Pigmentation - Slate grey statue Hair loss Erectile dysfunction Amenorrhoea Cognitive Sx - memory/mood
310
What is the Gross iron overload triad?
Bronze statue skin Hepatomegaly T2DM
311
What are the diagnostic investigations for Haemochromatosis?
Iron studies: Inc serum Fe Inc Ferritin Inc Transferrin sat Dec TIBC Genetic test - HFE gene mutation Liver biopsy to quantify Fe and assess degree of damage
312
What are some complications of hereditary haemochromatosis?
T1DM - iron affects pancreatic function Liver cirrhosis Endocrine issues - Iron deposits in pit. Cardiomyopathy - iron in heart HCC Hypothyroidism - Iron in thyroid Arthritis
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What is the management of Haemochromatosis?
1st Line - Venesection - remove blood to reduce iron Use Deferoxamine (chelation therapy) if CI Low iron diet.
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90% of people with haemochromatosis have a mutation in which gene?
HFE.
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What protein is responsible for controlling iron absorption?
Hepcidin. Levels of this protein are decreased in haemochromatosis.
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Name 3 metabolic disorders that can cause liver disease.
1. Haemochromatosis - iron overload. 2. Alpha 1 anti-trypsin deficiency. 3. Wilson's disease - disorder of copper metabolism.
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What is Wilsons Disease?
Autosomal Recessive mutation of ATP7B gene on chromosome 13 leading to excess body copper accumulation
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Who is typically affected by Wilsons Disease?
Young patient 20 yrs FHx Has RF
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What is the pathophysiology of Wilsons Disease?
Mutation of copper transporting ATPase Impairs ability of hepatocyte to incorporate copper into caeruloplasmin and excrete into bile Copper accumulates in liver and later on in other organs (CNS)
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What are the clinical features of Wilsons Disease?
CLANKAH: Cornea - Kayser Fleischer Rings - Cu deposits in cornea) Liver disease - Jaundice etc Arthritis Neurological - Parkinsonism, Memory issues Kidney - Fanconi's Syndrome Abortions Haemolytic Anaemia
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What are Kayser Fleischer rings?
Copper deposits in the cornea of the eyes that are symptomatic in Wilsons Disease
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What investigations are required for Wilsons Disease?
Blood tests: Low serum Copper - copper is deposited in tissues so not in blood Low Caeruloplasmin - protein thta carries copper Liver Biopsy - high Hepatic Copper MRI - Basal ganglia degeneration
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What is the management of Wilsons Disease?
1st Line - D-Penicillamine (copper chelation) Trientene Diet - avoid high copper foods
324
What are the side effects of Penicilamine?
Skin rashes Fall in WCC, Hb and Platelets haematuria Renal Damage
325
What is ⍺-1 antitrypsin deficiency?
Inherited autosomal recessive condition where there is a deficiency of alpha 1 anti-trypsin enzyme due to a mutation in the SERPINA-1 gene on chromosome 14
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What is the pathophysiology of Alpha 1 anti-trypsin?
alpha 1 anti-trypsin normally inhibits neutrophil elastase (an enzyme that degrades elastic tissue) Therefore in Deficiency there is increased Neutrophil Elastase that targets: Lungs - degrades Elastic tissue causing alveolar duct collapse and panacinar emphysema Liver - Unprotected elastic degeneration leads to liver becoming fibrotic and at increased risk of cirrhosis and HCC
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Where is Alpha 1 anti-trypsin synthesised?
In the liver and therefore A1AT deficiency causing damage to the liver is made worse due to a loss of synthetic function.
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What are the symptoms of a patient with A1AT deficiency?
Young/middle aged male Often present COPD like symptoms with no smoking Hx: Dyspnoea, chronic cough, sputum production Potentially Liver Sx too
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What is the Diagnostic investigations for A1AT deficiency?
Serum A1AT is low <20mm/dl Barrel chest exam - CXR shows hyperinflated lungs - pulmonary emphysema Liver Biopsy CT - panacinar Emphysema Genetic testing +tve SERPINA mutation
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What would be found on liver biopsy in A1AT Deficiency?
Acid schiff positive staining globules in hepatocytes Break down produces due to the action of proteases
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What is the management of A1AT deficiency?
No definitive Tx Stop smoking manage emphysema - inhales (SABAs, LABAs) Consider liver transplantation in hepatic decompensation
332
What amount of paracetamol is ingested for overdose?
75mg/Kg
333
What is paracetamol overdose responsible for in the UK?
50% of all fulminant liver failures
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What are the Sx of paracetamol overdose?
Acute severe RUQ pain Severe Nausea and Vomiting
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What is the normal metabolism of paracetamol?
Metabolised by the liver: 90% by phase 2 metabolism - glucoronidation to then be excreted 10% by phase 1 CYP 450 to create NAPQI (toxic metabolite) which is then conjugated with glutathione before being excreted.
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What happens to paracetamol metabolism in overdose?
Phase 2 pathway becomes saturated and therefore there is increased shunting down phase 1 metabolism. This increases NAPQI (toxic) production. Over time glutathione is depleted leading to accumulation of NAPQI in the liver. NAPQI is hepatoxic and will cause liver damage and fulminant liver failure
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How is Paracetamol overdose treated?
Activated charcoal if within 1hr of ingestion + N-acetylcysteine N-acetylcysteine if >1hr after ingestion.
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What is the purpose of Treating paracetamol overdose with N-acetylcysteine?
Increases availability of glutathione to remove NAPQI
339
What is Gilberts Syndrome? + crigler Najjar
Most common cause of hereditary jaundice where you are deficient or produce abnormal UGT. Gilberts - Deficiency CN - Absence Therefore you cannot conjugate bilirubin and this leads to increased unconjugated hyperbilirubinaemia
340
What is the Treatment of Gilberts/Crigler Najjar syndrome?
Gilberts - should be ok w/out Tx CN - Phototherapy to break down unconjugated bilirubin.
341
What is a hernia?
Protrusion of a viscus/part of viscus through a defect in the wall of its containing cavity into an abnormal position
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What is a reducible hernia?
Can be pushed back into abdominal cavity with manual manoeuvring
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What is an irreducible hernia?
Cannot be pushed back into place
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What is an obstructed hernia?
I.e. intestine Intestine obstructed due to pressure from edges of hernia, but blood flow is maintained
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What is an incarcerated hernia?
Contents of the hernial sac are stuck inside by adhesions
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What is a strangulated hernia?
Blood supply is cut off Ischaemia +- gangrene/perforation of the hernial contents Patient becomes toxic and requires urgent surgery
347
What is an inguinal hernia?
Protrusion of abdo contents through inguinal canal
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What is a femoral hernia?
Bowel moves through the femoral canal below the inguinal ligament
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What is an incisional hernia?
Through weak surgical scar
350
What is a sliding hiatus hernia?
Gastro-oesophageal junction and part of stomach roll ups into the chest via the hiatus so it lies above the diaphragm Normally leads to gastric reflux
351
What is the pathophysiology of inguinal hernias?
The inguinal canal is a short passage that extends medially and inferiorly, through the inferior part of the abdominal wall From deep inguinal ring to superficial ring Pathway through which structures can pass from abdominal wall to external genitalia Common site for herniation - potential site of weakness
352
What is the pathophysiology of femoral hernias?
Bowel enters femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament (points down the leg) Likely to be irreducible and to strangulate (canal's borders rigid) Neck of the hernia is felt inferior and lateral to the pubic tubercle
353
What are some risk factors for hernias?
Male - inguinal Heavy lifting Coughing Surgery
354
What are some symptoms of a hiatal hernia?
Gastro oesophageal reflux Dysphagia
355
What are some symptoms of a femoral hernia?
Swelling in upper thigh pointing down
356
What are some symptoms of an inguinal hernia?
Painful swelling in groin Points along groin margin.
357
What diagnostic tests can be done to investigate: Hiatus hernias Inguinal Hernias Femoral Hernias
Hiatus Hernias - CXR, Barium swallow (diagnostic) Inguinal Hernias - usually clinical but potentially USS Femoral Hernias - Usually clinical but potentially USS
358
What is the curative treatment for hernias?
Surgery.
359
What are the 5 viruses that cause hepatitis?
Hepatitis A (HAV) - RNA Hepatitis B (HBV) - DNA Hepatitis C (HCV) - RNA Hepatitis D (HDV) - RNA Hepatitis E (HEV) - RNA
360
How are hepatitis A and E transmitted?
Via Faecal-oral transmission
361
How are hepatitis B,C and D transmitted?
Blood to blood transmission
362
What is acute hepatitis? What Hepatitis viruses cause acute hepatitis?
A sudden illnesss with a mild to severe course followed by complete resolution All hepatitis Viruses
363
What is chronic hepatitis What Hepatitis viruses cause acute hepatitis?
A prolonged course of active disease or silent asymptomatic infection. HBV, HCV, HDV
364
Outline Acute hepatitis
**Variable incubation period** -Systemic symptoms first: -**Fatigue, low-grade fever, muscle/joint aches, cough, runny nose, and pharyngitis. ** **Jaundice** (1-2 weeks after infection) LFTs (rise through hepatocyte death from virus) **ALT and AST to elevate to very high ** levels, while **GGT, ALP, and bilirubin are only mildly elevated**
365
Outline Chronic Hepatitis
More difficult to Diagnose Patient is often asymptomatic Clinical manifestations are the same regardless of virus causing hepatitis.
366
Describe the transmission of hepatitis A
Ingesting contaminated drinking water or food (shellfish) Associated with Recent Travel Hx - Africa Close person to person contact Often infects young children
367
What is the pathogenesis of HAV?
-Initial immune response consists IgM antibody; important in the laboratory diagnosis of hepatitis A. -1 to 3 weeks later IgG antibody is produced→ lifelong protection
368
What are the clinical findings of HAV?
Incubation of 2-4 weeks Usually symptomatic in adults - constitutional Sx + abdo pain. Rarely causes fulminant hepatitis
369
What Ix are required for HAV diagnosis?
Serology - Detection of anti-HAV IgM confirms the diagnosis and remails for 3-6 months. Also: LFTs: High AST and ALT. Bilirubin and ALP usually only mild. Bloods - Inc ESR, Leukopenia
370
What is the treatment for HAV infection?
Self limiting - no chronic disease Supportive therapy Primary prevention - travellers vaccine 100% immunity after infection
371
What is Hepatitis B virus?
DNA virus that lives in all human body fluids in an infected individual. Semen, urine, saliva, blood, breast milk
372
What are HBV markers?
HBsAg - surface antigen - active infection HBsAg Ab - implies vaccination or past/current infection HBV DNA - direct count of viral load HBeAg - viral replication marker - high infectivity HBcAg - Core antigen - implies past or current infection
373
How can HBV be transmitted and give examples?
Blood to blood transmission - parenteral transmission. Needle sharing, accidental medical exposures, sexual contact Blood transfusions
374
Where is HBV prevalent
ASIA
375
How does HBV present?
3 clinical states: Acute hepatitis Fulminant hepatitis - severe acute hepatitis with rapid destruction of the liver Chronic Hepatitis
376
How do you diagnose HBV infection?
HBsAg antigen means there is LIVE virus and infection. Anti - HBsAg antibodies - patient is protected and immune HBcAg - exposure to HBV at some point. HBcAg IgG - chronic fection/carrier
377
How is HBV infection prevented?
Antenatal screening - HBsAg of pregnant mothers Universal childhood vaccination PrEP - tenofovir + emtricitabine
378
What are the complications of HBV infection?
HDV co-infection Hepatocellular carcinoma End-stage liver disease/cirrhosis
379
How is HBV infection managed?
Pegylated Interferon 2A Oral nucleoside analogues - Tenofovir, entecavir (better tolerated than PEG IFN)
380
What is Hepatitis C virus
RNA virus Incubation period 6-12 weeks
381
What is the clinical signs of HCV infection?
Acute infection is usually asymptomatic - some patients will present with classic acute hepatitis symptoms Up to 85% of patients of HCV will develop chronic hepatitis HCV strongly predisposes HCC.
382
Outline HCV transmission
Blood-to-blood contact via blood transfusions, injecting drug use, nosocomial (needle sticks, dialysis, inadequate sterilisation of colonoscopes
383
What is the most common indication for liver transplantation?
Liver cirrhosis resulting from chronic HCV infection
384
What comorbidities arise with HCV infection?
HCV infection can lead to significant autoimmune reactions: vasculitis, arthralgias, purpura, membranoproliferative glomerulonephritis
385
How is HCV diagnosed?
Testing for antiHCV antibodies (detectable within 6-8 weeks after exposure and remain positive thereafter) Measure HCV viral RNA An ELISA antibody test for detectable viral RNA is positive for at least 6 months. HCV Genotype - Genotype governs Tx
386
What is the treatment for HCV infection
Direct acting Anti-virals (DAAs) No vaccine currently exists. Liver Transplantation for End stage liver disease
387
What are the different targets of DAAs?
NSE3/4A Protease inhibitors (suffix = previr) NS5A Inhibitors (Suffix = Asvir) NS5B Inhibitors (Suffix = buvir)
388
Give some examples of DAA combination therapy?
Glecaprevir/Pibrentasvir Sofosbuvir/Velpatasvir Triple Therapy: Sofosbuvir/Velpatasvir/Voxilaprevir
389
Can HCV be cured?
Yes however that does not confer immunity and there is still a risk of re-infection
390
What is Hepatitis D virus?
An RNA virus It is a defetive virus an it cannot replicate itself due to not having the genes to envelop protein. HDV can only be replicated in cells co-infected with HBV. HDV uses HBsAg to evelope its protein.
391
Outline the transmission of HDV?
Transmitted in the same way as HBV Coinfection of HBV and HDV is more severe than those infected with HBV alone.
392
What is the presentation of a HDV infection?
Can range from asymptomatic to fulminant liver failure Simultaneous co-infection with HBV/HDV - causes acute hepatitis. HDV superinfection of a carrier of HBV can cause liver flare.
393
What diagnostic tests are required for HDV infection?
Detecting delta antigen or IgM antibody against delta antigen in the patient's serum.
394
What is the treatment for HDV infection?
PegINF alpha can mitigate chronic effects but does not eradicate the carrier state. no vaccine against HDV but a person immunized against HBV will not get HDV infection.
395
What is Hepatitis E infection?
RNA virus similar to HAV.
396
How is HEV transmitted?
Via the faecal oral route Waterborne transmission is most common.
397
What is the clinical presentation of HEV infection?
Clinically similar to HAV infection. Often Asymptomatic (95% cases) - usually self limiting Chronic infection can be caused in immunocompromised individuals.
398
How is HEV diagnosed?
Detecting IgM antibodies to HEV.
399
What is the treatment to HEV infection?
Self limiting No antiviral drug available for acute infection in immunocompetent patients. (consider ribavirin if really ill) Treatment is supportive.
400
What are some complications of hereditary haemochromatosis?
T1DM - iron affects pancreatic function Liver cirrhosis Endocrine issues - Iron deposits in pit. Cardiomyopathy - iron in heart HCC Hypothyroidism - Iron in thyroid Arthritis
401
How are gallstones formed?
he formation of cholesterol crystals and gallstones in lithogenic bile is promoted by factors that favour nucleation such as mucus and calcium Gallstone formation further promoted by reduced GB motility and stasis
402
What is SBP?
Spontaneous bacterial peritonitis: infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition. It is one of the most frequently encountered bacterial infections in patients with cirrhosis.
403
How is SBP diagnosed?
Ascitic tap and analysis via paracentesis. Asses fluid appearance, cell count and culture. Also FBC, LFT, blood cultures