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Medicine Phase 2a > Hepatology > Flashcards

Hepatology Flashcards

1
Q

What are the normal Functions of the Liver?
What happens when they each go wrong?

A

Oestrogen Regulation - Gynaecomastia, Spider naevi, Palmer Erythema

Detoxification - Hepatic Encephalopathy

Metabolises Carbohydrates - Hypoglycaemia

Albumin production - Oedema, Ascites, Leukonychia

Clotting Factor production - Easy Bruising and Bleeding

Bilirubin Regulation - Pruritus, Jaundice +/- Stool and urine changes

Immunity - Complement factors + kupffer cells - Spontaneous Bacterial infection

Bile acid synthesis - Fat malabsorption + steatorrhoea

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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
Xanthelasma
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
Q

What is the management of gallstones present in the gall bladder?

A

Laparoscopic cholecystectomy
Bile acid dissolution therapy

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26
Q

What is the management of gallstones present in the Bile Duct?

A

ERCP w/ Sphincterotomy (opening of sphincter of Oddi)
Followed by removal of stones, crushing of stones and stent placement

Surgery - remove larger stones

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27
Q

What is a typical time frame for drug induced liver injury?

A

From 5 days after starting it
To 3-6 months whilst on it.

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28
Q

What accounts for 50% of the causes of drug induced acute liver failure?

A

Paracetamol overdose

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29
Q

What proportion of acute liver failure is drug induced?

A

> 65%

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30
Q

What are the different types of Drug induced Liver Injury?

A

Hepatocellular

Cholestatic

Mixed

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31
Q

What are the common drugs that are hepatotoxic? (2 mnemonics)

A

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

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32
Q

What is Liver Failure?

A

The liver loses its regenerative capacity due to hepatocyte death/necrosis causing decompensated liver injury and irreversible damage.

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33
Q

What are the different types of Liver Failure?

A

Acute Liver Failure
Fulminant Liver Failure
Acute-on-Chronic Liver Failure
Chronic Liver Failure

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34
Q

What is Acute Liver Failure?

A

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

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35
Q

What is Fulminant Liver Failure?
What are the different categories of Fulminant liver failure?

A

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??????????

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36
Q

What is the most common cause of Fulminant Liver Failure?

A

Paracetamol Overdose
50% of the cause in the UK

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37
Q

What is Acute-On-Chronic Liver Failure?

A

The acute and rapid decline of a Px with Chronic Liver failure Sx

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38
Q

What is Chronic Liver Failure?

A

Patient with progressive Hx of liver disease over 6+ months of constant liver injury

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39
Q

What is the Pathogenesis of Liver Failure?

A

Liver injury
Causes liver hepatitis
Chronic hepatitis leads to fibrotic liver
Leads to Liver cirrhosis
and then Decompensated Cirrhosis (End stage liver failure)

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40
Q

What are the main causes of acute liver failure?

A

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

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41
Q

What is Budd Chiari Syndrome?

A

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

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42
Q

What are the symptoms of acute liver failure?

A

Chronic pain
Abdominal pain - RUQ
Nausea and vomiting
Malaise

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43
Q

What are the clinical signs of Acute Liver Failure?

A

Jaundice
Coagulopathy
Hepatic Encephalopathy

+:
Confusion
Asterixis - sign of HE
Hepatomegaly
Ascites
Bruising

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44
Q

What are the diagnostic investigations of Acute Liver Failure?

A

Bloods:
LFTs - Inc bilirubin, Inc PT/INR, Dec Albumin
Serum AST/ALT Inc, NH3 Inc, Dec Glucose
FBC - Infection/Bleeds

U&Es - Hepatorenal Syndrome

Imaging:
1st - Abdo Ultrasound - Check for Budd Chiari
EEG - Grades HE (absent in Acute liver injury)
CT

Ascitic Tap + Microscopy and culture:
Blood culture, Urine culture, Ascitic tap - rule out infection

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45
Q

What is the treatment for acute Liver failure?

A

ICU,
ABCDE
Fluids
Analgesia

Tx underlying Cause and Tx complications

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46
Q

What is the treatment of paracetamol Overdose

A

<1 hour - Activated Charcoal + N-acetyl Cysteine

> 1 hour - N-acetyl Cysteine

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47
Q

What are some complications and their treatments of Acute Liver Failure?

A

Raised ICP - Mannitol

Hepatic Encephalopathy - Lactulose - increases NH3 excretion/ Rifaximin

Ascites - Diuretics (furosemide/spironolactone)/ paracentesis

Haemorrhage - Vitamin K

Hypoglycaemia - Dextrose

Sepsis - Sepsis 6

GI Bleeding - beta blockers

SBP - prophylactic Abx

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48
Q

What are the most common causes of Chronic Liver disease?

A

Alcoholic Liver Disease (ALD)
Non-Alcoholic Fatty Liver Disease (NAFLD)
Viral Hepatitis (B/C)

+ Metabolic, Autoimmune, PSC, PBC, Drugs, Budd Chiari

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49
Q

What is the main cause of Liver death in the UK?

A

Alcoholic Liver disease

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50
Q

What are the Major Risk factors for Chronic Liver failure?

A

Alcohol
Obesity
T2DM
Drugs
Inherited Metabolic Disease
Existing Autoimmunity

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51
Q

What is the Pathogenesis of Chronic Liver Failure?

A

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

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52
Q

What are the key clinical signs of Liver cirrhosis?

A

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

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53
Q

What are the stigmata of chronic liver disease?

A

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.

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54
Q

What are the major Complications of Decompensated Liver Cirrhosis?

A

Malnutrition
Hepatic Encephalopathy
Ascites
Coagulopathy
Portal Hypertension
SBP - spontaneous bacterial peritonitis
Hepatorenal Syndrome
Oesophageal Varices
Hepatocellular Carcinoma

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55
Q

How does liver cirrhosis lead to malnutrition?

A

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.

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56
Q

What is the management of Liver cirrhosis induced malnutrition?

A

Regular meals
Low sodium - minimise fluid retention
High protein and high calorie
Avoid alcohol

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57
Q

How does Liver cirrhosis lead to portal hypertension and subsequent varices?

A

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

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58
Q

What are the most common sites for varices to occur as a result of portal HTN?

A

Gastro-oesophageal junction (GOJ)
Ileo-caecal junction
Rectum
Anterior abdominal wall via umbilical vein (caput Medusae)

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59
Q

What is a treatment for stable varices (non bleeding)

A

Propranolol - reduce portal HTN
Elastic band ligation
Injection of sclerosant

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60
Q

How does Liver Cirrhosis lead to Ascites?

A

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

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61
Q

What is the management of Ascites?

A

Low sodium diet
Spironolactone
Paracentesis - ascitic tap/drain
Prophylactic Abx

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62
Q

What s SBP?

A

Spontaneous Bacterial Peritonitis that occurs secondary to ascites caused by cirrhosis.
This is an infection that develops in ascitic fluid without a clear cause

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63
Q

What is the presentation of SBP?

A

Can be ASx

Fever
Abdominal pain
Deranged bloods - Raised WBC, CRP, Creatinine
Ileus
Hypotension

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64
Q

What are the most common organisms in SBP?

A

E.coli
Klebsiella pneumoniae
Gram +tve cocci - Staphly/enterococci

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65
Q

What is the management of SBP?

A

Take an ascitic culture (paracentesis) prior to giving Abx

Often treated with IV Cephalosporin - Cefotaxime

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66
Q

How does Liver Cirrhosis lead to Hepato-Renal Syndrome?

A

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

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67
Q

What is hepatic encephalopathy?

A

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.

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68
Q

What is the pathophysiology of Hepatic Encephalopathy?

A

Decreased Liver function
Build up of toxic metabolites (NH3)
Astrocyte oncotic pressure increases causing Swelling of astrocytes
leads to cerebral oedema

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69
Q

What is the presentation of Hepatic Encephalopathy?

A

Liver Sx - jaundice, ascites, peripheral oedema

Mood disturbances - depression, confusion
Sleep disturbances - insomnia
Motor Disturbances - ataxia, bradykinesia, rigidity

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70
Q

How is hepatic encephalopathy Graded?

A

Grade I: irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

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71
Q

What are the investigations for Hepatic Encephalopathy?

A

FBC and Basal metabolic panel
Blood alcohol elevated
Blood ammonia raised

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72
Q

How is Hepatic Encephalopathy treated?

A

Laxatives (lactulose) - increase excretion of ammonia.

Abx (rifaximin) reduce bacterial production of ammonia

Nutritional support - potentially by NG tube

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73
Q

What is the Child Pugh Score?
What is involved?

A

Assess prognosis and Extent of required Tx for chronic liver failure:

Bilirubin
Ascites presence
Serum Albumin
PT/INR
HE

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74
Q

What is Decompensated Liver Cirrhosis a major risk factor for?

A

Hepatocellular Carcinoma

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75
Q

What is the Presentation of Chronic Liver Failure?

A

Jaundice
Ascites
HE
Portal HTN
Oesophageal Varices
Caput Medusae

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76
Q

What are the Diagnostic Investigations for Chronic Liver Disease?

A

Liver Biopsy - Gold standard - Determines Extent of CLD

LFTs,

Imaging - Ultrasound, CT for secondary findings

Ascitic Tap

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77
Q

What investigations are done in chronic liver disease (cirrhosis) to determine condition/cause?

A

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.

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78
Q

What is the Treatment of Chronic Liver Disease?

A

Tx underlying pathology
Prevent Progression - lifestyle modification
Consider Liver transplant - If decompensated liver
Manage complications

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79
Q

What is Alcoholic Liver Disease?

A

Progressive damage to the liver from long term excessive Alcohol Consumptions.

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80
Q

What is the Progression of Alcoholic Liver Disease?

A

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

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81
Q

What is the recommended alcohol intake per week?

A

14 units for men and women.

Taken over 3 or more days

No more than 5 units in one day

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82
Q

How do you calculate the number of units in an alcoholic drink?

A

Strength (ABV) x Vol/ml / 1000

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83
Q

What is 1 UNIT of alcohol?

A

8g OR 10ml

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84
Q

What are the symptoms of Alcoholic Liver disease?

A

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

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85
Q

What are the signs of ALD?

A

Jaundice
Tender hepatomegaly
Ascites
Asterixis: flapping tremor secondary to encephalopathy
Tremor: seen in alcohol withdrawal
Bruising (coagulopathy)
Stigmata of chronic liver disease

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86
Q

What tools are used to assess alcohol use?

A

Audit and CAGE:

CAGE:
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?

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87
Q

What investigations should be done for all patients with suspected Hepatitis?

A

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)

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88
Q

What are the Diagnostic investigations for ALD?

A

Bloods:
LFTs - Raised GGT, AST/ALT ratio >2

FBC - Macrocytic non-megaloblastic anaemia

Hx of Alcohol

Biopsy - confirm extent of hepatitis/cirrhosis

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89
Q

What Laboratory findings may be indicative of ALD?

A

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

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90
Q

What may be found in ALD on histology?

A

Mallory Cytoplasmic Inclusion Bodies

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91
Q

What are the treatments of ALD?

A

STOP ALCOHOL - Tx withdrawal if present
Detoxification regime if required

Healthy Diet / BMI
B1 & folate supplements

Steroids (prednisolone) short term management

Surgical - Consider Liver transplant in ESLF

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92
Q

What can be given to treat withdrawal Sx of ALD?

A

Chlordiazepoxide
Diazepam

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93
Q

To be eligible for a liver transplant, how long must you have abstained from alcohol for?

A

3+ months

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94
Q

What are the complications of Alcoholic Liver disease?

A

Pancreatitis
HE
Ascites
HCC
Mallory Weiss Tear
WERNICKE KORSAKOFF SYNDROME

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95
Q

What is Wernicke Korsakoff Syndrome?

A

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

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96
Q

What are the symptoms of Wernicke Encephalopathy and Korsakoff syndrome?

A

Wernicke Encephalopathy:
Confusion
Ophthalmoplegia
Ataxia

Korsakoff Syndrome:
Memory Impairment
Behavioural changes

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97
Q

How is Wernicke Korsakoff Syndrome treated?

A

IV Thiamine (Vit B1)
Pabrinex

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98
Q

What is NALFD?

A

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

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99
Q

What are the risk factors for NAFLD?

A

Obesity
HTN
Hyperlipidaemia
T2DM
FHx - PNPLA3
Endocrine disorders
DRUGS

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100
Q

What is the Epidemiology of NAFLD?

A

NAFL May affect 25% of the population

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.

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101
Q

What is Metabolic Syndrome?

A

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:

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102
Q

What are the factors of Metabolic Syndrome?

A

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

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103
Q

What drugs are RFs for NAFLD?

A

NSAIDS
Amiodarone

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104
Q

What is the pathogenesis of NAFLD?

A

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

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105
Q

How would a NAFLD Px present?

A

Often ASx
Any findings are incidental

If severe NAFLD then Sx/signs of Liver failure

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106
Q

What are the diagnostic tests for NAFLD?

A

Bloods:
Abnormal LFTs - Inc PT/INR, Dec Albumin, Inc Bilirubin
FBC - Thrombocytopenia, Hyperglycaemia

Imaging:
1st line - Abdominal Ultrasound - confirms diagnosis of hepatic steatosis

1st Line blood test - Enhanced Liver Fibrosis (EFL) if they have been diagnosed to determine degree of fibrosis
NAFLD fibrosis score
Fibroscan

Gold Standard - Biopsy is diagnostic

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107
Q

What investigation would be used to determine the cause of abnormal LFTs if the cause is unclear?

A

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

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108
Q

How is the risk of fibrosis assessed?

A

Using FIB-4 (fibrosis score)
Detects stiffness of the liver

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109
Q

What is the Tx for NAFLD?

A

Lose weight (lower BMI) - Exercise

Control RFs:
Statins - cholesterol
Metformin - diabetes
ACEi - BP
Vitamins

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110
Q

What are some complications of NAFLD?

A

HE
Ascites
HCC
Portal HTN
Oesophageal Varices

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111
Q

What is Autoimmune Hepatitis?

A

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

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112
Q

What are the risk factors for autoimmune hepatitis?

A

Female
Other autoimmune diseases - SLE
Viral hepatitis
HLA DR3/4

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113
Q

What are the types of Autoimmune Hepatitis?

A

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.

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114
Q

How may patients present with AIH?

A

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

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115
Q

What are the diagnostic investigations for AIH?

A

Serology - ANA/ASMA/anti-SLA/LP +/- ALC-1/ALKM1
LFTs - Hepatic (ALT/AST Raised)

Liver Biopsy

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116
Q

What may be seen on liver biopsy to aid the diagnosis of AIH?

A

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.

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117
Q

What are the antibodies associated with AIH?

A

Anti-nuclear (ANA) - Type 1
Anti-Smooth muscle (ASMA) - Type 1
Anti-soluble liver and pancreas (SLA/LP) - 75% of Type 1

Anti-liver/kidney Microsomes (ALKM1) - Type 2
Anti-Liver Cytosol Antigen (Anti-LC1) - Type 2

Anti-mitochondrial (AMA) - mainly for PBC

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118
Q

What Immunoglobulin is associated with AIH?

A

IgG are raised

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119
Q

How is AIH treated?

A

First Line: Prednisolone
GS: Prednisolone + Azathioprine

Hep B vaccination

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120
Q

What is a last resort Tx for AIH?

A

Transplant consideration (10-20% of Px may have this)

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121
Q

What is the process of RBC breakdown?

A

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

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122
Q

What is Jaundice?

A

Yellowing of the skin and eyes due to accumulation of conjugated/unconjugated bilirubin in the blood.

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123
Q

What are the different types of Jaundice?

A

Pre-hepatic - Haemolysis

Intra-hepatic - Liver dysfunction

Post hepatic - Obstruction

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124
Q

What are the causes of Pre-hepatic jaundice?

A

Haemolytic anaemias:
Sickle cell
Thalassaemia
G6PDH Def
Malaria

Ineffective Erythropoiesis

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125
Q

What is raised in Pre hepatic jaundice?

A

Raised Unconjugated bilirubin due to increased RBC breakdown saturating conjugatory mechanisms

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126
Q

What are the causes of intra hepatic jaundice?

A

Parenchymal disease:
HCC
ALD/NAFLD
Hepatitis
Hepatotoxic drugs - Rifampicin
Gilberts syndrome
Crigler Najjar Syndrome

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127
Q

What is Raised in Intra hepatic jaundice?

A

Conjugated and unconjugated bilirubin
Can be mixed due to the failure of Hepatocytes to uptake, metabolise and or excrete bilirubin

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128
Q

What is Gilberts Syndrome?

A

Very common Autosomal recessive mutation of UGT1A1 gene

causes underactive UGT enzyme and therefore decreases CON bilirubin.

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129
Q

How may a Patient with Gilbert Syndrome present?

A

Young male
Painless jaundice that has sudden onset

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130
Q

What is Crigler Najjar Syndrome?

A

Autosomal recessive absence of UGT enzyme and therefore has an inability to conjugate bilirubin

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131
Q

What are the causes of Post hepatic Jaundice?

A

Biliary tree pathology
Choledocholithiasis - bile stone
Pancreatic cancer
cholangiocarcinoma
Mirizzi Syndrome
Autoimmune - PBC/PSC

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132
Q

What is Mirizzi Syndrome?

A

common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder

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133
Q

What is raised in Post hepatic jaundice?

A

Conjugated bilirubin is raised due to biliary obstruction.

This causes pale stools and Dark urine.

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134
Q

What is Courvoisier sign and what would it suggest?

A

Painless jaundice and palpable GB

Likely pancreatic cancer/cholangiocarcinoma

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135
Q

What is the Charcot Triad?

A

Fever
RUQ Pain
Jaundice

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136
Q

What combination of Charcot Triads symptoms suggest which conditions?

A

RUQ pain = Biliarycolic

Fever + RUQ pain = Cholecystitis

Fever + RUQ Pain + jaundice = Ascending cholangitis

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137
Q

What is Murphys Sign?

A

RUQ Tenderness
Ask Px to take a breath in whilst pressing on RUQ
Makes them wince

+tve for Cholecystitis

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138
Q

How can the type of Jaundice be diagnosed?

A

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

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139
Q

What is pancreatic cancer?

A

Adenocarcinoma of the exocrine pancreas
(99% of cases) of ductal origin.

Typically affects the head of the pancreas

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140
Q

who is typically affected by pancreatic cancer?

A

Males
60yrs +

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141
Q

What are the risk factors for pancreatic cancer?

A

Smoking
Males > 60
Alcohol
Diabetes Mellitus
FHx
Chronic pancreatitis
Genetics - PRSS-1 mutation

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142
Q

How would a patient with pancreatic cancer present/ what signs would they have?

A

Anorexia
Weight loss
Acute pancreatitis

Body and tail of pancreas:
Epigastric pain that radiates to back
Relieved by sitting forward

Head of pancreas:
Painless palpable gall bladder + jaundice (Courvoisier’s Sign)
Weight loss

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143
Q

What is the characteristic of the pain in a body/tail pancreatic cancer?

A

Epigastric pain
Radiates to the back
Relieved when sitting forward

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144
Q

What are the diagnostic investigations for pancreatic cancer?

A

1st line - abdominal ultrasound
GS - Pancreatic CT protocol then bile duct drainage

Ca19-9 tumour marker positive - monitors progression

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145
Q

What is the gold standard diagnostic investigation for pancreatic cancer?

A

Pancreatic CT
Diagnostic in 97% of cases

+ Biopsy confirmation

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146
Q

What marker indicates progression of pancreatic cancer?

A

Ca19-9 tumour marker

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147
Q

What is the Treatment of pancreatic cancer?

A

Very poor prognosis - 5yr survival - 3%

surgery (whipple) + post op chemo if no mets

Palliative care

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148
Q

What is Hepatocellular carcinoma (HCC)

A

arise from liver parenchyma
90% all primary liver cancers

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149
Q

What is the epidemiology of HCC?

A

One of the leading causes of cancer mortality
Highest risk in Asia due to increased burden of Viral Hepatitis

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150
Q

What are the major risk factors of HCC?

A

Chronic hepatitis - viral infection of Hep C and B

Cirrhosis of the liver - ALD/ NAFLD/ Haemochromatosis

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151
Q

What are some other risk factors for HCC (non major)?

A

Hepatitis D
Aflatoxin B1
Alcohol
Smoking
NAFLD
Metabolic Liver disease

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152
Q

Where do HCC metastases often travel to?
How do these travel?

A

Lymph nodes
Bones
Lungs

via haematogenous spread (hepatic/portal veins)

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153
Q

How would a patient with HCC present?

A

Sx of decompensated liver failure - HE, jaundice, ascites

Cancer signs - tATT, unexplained weight loss, Fatigue, N+V

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154
Q

What diagnostic investigations are done for HCC?

A

Imaging:
1st line - Abdo ultrasound
GS - CT (confirms diagnosis)

May also biopsy and Histology for diagnosis

Raised serum AFP (alpha fetoprotein)

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155
Q

What is the treatment of HCC?

A

Surgical Resection of the liver

Only cure is Liver transplantation if decompensated

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156
Q

What should be given to prevent HCC?

A

HBV Vaccination!!

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157
Q

What is a cholangiocarcinoma?

A

adenocarcinoma that arises from the biliary tree

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158
Q

What percentage of liver cancers are cholangiocarcinomas?

A

10%

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159
Q

What are the risk factors for cholangiocarcinoma?

A

Parasitic flukeworms
Biliary Cysts
Chronic Viral Hep B/C
IBD
PSC

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160
Q

How would a Px with cholangiocarcinoma present?

A

Signs of Cholestasis:
Courvoisier’s Sign - painless palpable gallbladder + jaundice
weight loss
pruritis
fever + fatigue
Late constellation Sx of tumour since it is slow growing

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161
Q

What diagnostic investigations would be used for a cholangiocarcinoma?

A

LFT - Inc Bilrubin, Inc Alkaline Phosphates

Inc Ca19-9

Imaging :
1st line - Abdo USS + CT
GS ERCP + Biopsy - imagine of biliary tree

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162
Q

What is the gold standard investigation for cholangiocarcinoma?

A

ERCP

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163
Q

What is the Tx of cholangiocarcinoma?

A

Chemo/radiotherapy possibly

ERCP - used to pace a stent in blocked bile duct to relieve Sx

Mostly inoperable due to late presentation of Px

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164
Q

What are some benign primary liver tumours?

A

Haemangioma
Hepatic Adenoma

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165
Q

What is more common, primary or secondary liver tumours?

A

Secondary are more common

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166
Q

Where can secondary Liver tumours come from?

A

GI tract
Lungs
Breast

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167
Q

How may a patient with a secondary liver tumour present?

A

Depends on the site of the primary cancer

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168
Q

What diagnostic investigations may show a secondary liver tumour?

A

Increased serum ALP(Alkaline Phosphatase)

Imaging:
1st line - Ultrasound
GS - CT/MRI for staging and primary tumour

169
Q

What is the Treatment of 2’ liver cancer?

A

Surgical resection if possible
Chemotherapy

170
Q

What are some different biliary tract diseases

A

Gallstones
Cholecystitis
Ascending Cholangitis

171
Q

What are the risk factors for biliary tract disease

A

5Fs
Fat
Female
Forty (40+)
Fertile
Fair

+ FHx, T2DM, NAFLD

172
Q

What are gallstones?

A

Small stones usually made of cholesterol that form in the gall bladder

173
Q

Define:
Cholelithiasis
Choledocholithiasis
Biliary Colic
Acute Cholecystitis
Acute Cholangitis

A

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 in the absence of inflammation

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.

174
Q

What is the epidemiology of gallstones

A

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

175
Q

What is the general composition of gallstones?

A

Phospholipids - lecithin

Bile pigments (broken down haemoglobin)

Cholesterol

176
Q

What are the 3 types of gallstones?

A

Cholesterol

Black Pigment

Mixed (brown pigment)

177
Q

What are the characteristics of cholesterol, Pigment and mixed stones?

A

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

178
Q

How are Cholesterol stones formed?

A

They occur due to crystallisation of cholesterol in bile (along with other compounds) due to supersaturation of cholesterol and crystillisation promoting factors

179
Q

How are pigment stones formed?

A

They occur in people with increased amounts of bilirubin in their bile - hyperbilirubinbilia. This occurs in patients with increased haemolysis

180
Q

How are Mixed Stones formed?

A

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.

181
Q

What is the cause of gallstones?

A

Lithogenic bile - Admirand’s triangle

Biliary sepsis

Altered composition of Bile

Gallbladder hypomotility:
- Pregnancy/oestrogen contraceptive pill
- Total parenteral nutrition/fasting

182
Q

What is Admirand’s triangle?

A

Low bile salts

Low lecithin

High cholesterol

183
Q

How are gallstones formed?

A

The 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

184
Q

What are the symptoms of gallstones?

A

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

185
Q

What investigations are done to confirm gallstones?

A

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

186
Q

What are the complications of gallstones in the gallbladder?

A

Biliary colic
Acute cholecystitis +- empyema
Chronic cholecystitis

Mucocele
Carcinoma
Mirrizi’s syndrome

187
Q

What are the complications of gallstones in the common bile duct?

A

Obstructive Jaundice
Pancreatitis
Cholangitis

188
Q

What are the symptoms of cholecystitis?

A

RUQ pain + Fever + Tender gall bladder

Reffered pain to top of right shoulder (phrenic)
Murphy Sign +tve

Vomiting

189
Q

What is Murphy Sign?

A

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.

190
Q

What is Reynold’s Pentad

A

Chartcot’s Triad + Altered Mental State + Hypotension

191
Q

What is the Diagnostic test for Gallstones

A

1st line = Abdo ultrasound

192
Q

What are the treatments for gallstones?

A

Pain management- NSAIDS (mild), Diclofenac (severe)
Lifestyle modifications - low fat in diet
Ursodeoxycholic acid – decreases cholesterol

Gallbladder stones:
Laparoscopic cholecystectomy
Bile acid dissolution therapy (<1/3 success)

Bile duct stones:
ERCP with sphincterotomy and:
removal (basket or balloon)

Surgery (large stones)

193
Q

What is Biliary Colic?

A

Where a patient has sudden onset cholicy pain due to a gallstone often in the gallbladder/temporary obstruction of biliary tree that occurs as the gallbladder contractions following the consumption of a large fatty meal

The gallstone has not yet caused inflammation and therefore the patient doesn’t present with a fever or jaundice. They will likely have RUQ pain (colicky) if Symptomatic

194
Q

What is the presentation of Biliary cholic?

A

ASx until eating large fatty meal.

As GB contracts - colicky pain in RUQ
may radiate to epigastrium/back

Nausea and Vomiting may also occur

195
Q

What are the investigations for Biliary Colic?

A

FBC + CRP - look for inflammatory response suggesting cholecystitis

LFTs - Raised ALP suggesting Biliary pathology

Amylase - Normal but excludes pancreatitis

GS Diagnostic - Abdo USS - duct dilation and obstruction

196
Q

What is the Treatment for Biliary Colic?

A

NSAIDs/Analgesia

Optional Cholecystectomy if reoccurrence

197
Q

What is acute cholecystitis?

A

gall bladder inflammation that develops over hours 95% of the time secondary to a gallstone blocking the bile outlet into the cystic duct

198
Q

What is the pathogenesis of acute cholecystitis?

A

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 may impede vascular supply.

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

199
Q

What are the causes of cholecystitis?

A

Gallstones
Tumour
Bile duct blockage
Infection
Blood vessel problems

200
Q

What is the presentation of Acute Cholecystitis?

A

RUQ pain - may radiate to shoulder (phrenic innervation)
Fever +fatigue
N+V

Positive Murphy’’s Sign
Tenderness and guarding

201
Q

What investigations are done for acute cholecystitis?

A

Urine tests - bilirubin and urobilinogen raised

FBC - Inc WCC

LFT - often normal

Imaging - abdominal USS
Shows stones, thick gallbladder walls (>3cm) and fluid around gallbladder

202
Q

What test is ordered if dilated bile ducts are found on ultrasound in suspected acute cholecystitis?

A

MRCP

203
Q

What are the differential diagnoses for acute cholecystitis?

A

Main:
Biliary Colic
Cholangitis

Others:
Peptic ulcer disease
Liver disease
IBD
GORD
Pancreatitis
Cardiac disease

204
Q

What is the management for Acute Cholecystitis?

A

Conservative: if ASx
Nil by mouth
Fluid resuscitation
Abx - Gentamicin
analgesia - Paracetamol/NSAIDS

If Symptomatic:
Laparoscopic cholecystectomy
Analgesia and fluids and Abx (gentamicin)

205
Q

What is Ascending Cholangitis?

A

Inflammation of the bile duct caused by bacteria ascending from the duodenum through the ampulla of Vater due to obstruction in the bile duct (85% due to Gallstones) causing stasis of bile flow.

206
Q

What is the pathophysiology of ascending cholangitis?

A

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

207
Q

What causes ascending cholangitis?

A

Gallstones

Iatrogenic - ERCP

Cholangiocarcinoma

Ascending infection from duodenum junction

208
Q

What are the risk factors of ascending cholangitis?

A

History of gallstones (5Fs)

Sclerosing cholangitis

HIV

Narrowing of common bile duct

209
Q

What is the Presentation of Ascending cholangitis?

A

Reynolds pentad:
RUQ pain
Fever
Jaundice

Altered mental state
Hypotension (shock)

210
Q

What are the investigations done for suspected or known ascending cholangitis?

A

FBC - WCC raised
CRP - Raised
LFT - Hyperbilirubinaemia, raised ALP

Blood Cultures/MC+S - guides Abx

Ultrasound +/- ERCP

211
Q

What imaging tests are ordered for ascending cholangitis?

A

1st: Abdo USS - CBD dilation and gallstones

GS: MRCP

212
Q

What is the management of ascending cholangitis

A

IV antibiotics e.g. co-amoxiclav
Fluids
ERCP (endoscopic retrograde cholangiopancreatography) to image/stent/remove stone
Shockwave lithotripsy

If this fails 🡪 laparoscopic/open cholecystectomy

213
Q

How can Sepsis occur in ascending cholangitis?

A

Biliary obstruction causes backflow of biliary sludge.
This causes stasis
CBD dilation and wides space to enable bacteria to enter blood from CBD
causing bacteraemia and sepsis

214
Q

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

A
  1. Biliary Colic
  2. Acute Cholecystitis
  3. Cholangitis
215
Q

What is Primary Biliary Cholangitis

A

A Granulomatous autoimmune condition against 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

216
Q

What is the pathophysiology of PBC?

A

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. Contents of bile ducts (bile and cholesterol) leak out into blood.

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.

217
Q

What autoantibodies are associated with PBC?

A

Anti-Mitochondrial (AMA) - 95% of patients.

Also ANA, Anti-gp210 and anti-sp100

218
Q

What ducts are affected in PBC?

A

Intralobar ducts
(Canals of Hering)

219
Q

What are the symptoms of PBC?

A

Fatigue
Pruritus
GI disturbance and abdominal pain
Signs of chronic liver disease

220
Q

Why do you get Xanthomas/Xanthelasmas and Pruritus in PBC?

A

Bile ducts are damaged leading to bile and cholesterol leaking out into the blood causing the deposition of these around the skin resulting in itching (bile) and Xanthomas (Cholesterol)

221
Q

What are the signs of PBC?

A

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)

222
Q

Who is PBC associated with?

A

Middle aged women >50 years (F:M = 9:1
Other autoimmune diseases (e.g. thyroid, coeliac)
Rheumatoid conditions

223
Q

What makes up 90% of patients with PBC?

A

Middle aged women 40-50yrs

224
Q

What is Xanthoma and Xanthelasma?

A

Xanthomas (deposition of cholesterol in the skin causing a nodule)
Xanthelasmas (deposition of cholesterol in the skin causing a papule or plaque)

225
Q

What are some complications of PBC?

A

Cirrhosis
Malabsorption of Fats + ADEK
steatorrhoea
osteomalacia

226
Q

How is the diagnosis for PBC made?

A

Diagnosis of PBC is based on the presence of cholestatic liver enzymes and positive anti-mitochondrial antibodies.

227
Q

What are the diagnostic tests for PBC?

A

LFTs:
Raised AP
Raised GGT
Raised Con Bilirubin
Dec Albumin

Antibodies:
AMA (anti mitochondrial) - specific to PBC (95%)
ANA (anti nuclear)

Liver Biopsy - portal tract infiltrate and fibrosis + 40% granulomatous

Imaging:
1st Line - Abdo USS to exclude extrahepatic cholestasis

Blood tests:
ESR Raised
IgM Raised

228
Q

What is the Treatment of PBC?

A

1st Line: Ursodeoxycholic acid - reduces intestinal absorption of cholesterol

Sx Treatment:
Colestyramine - for Pruritus
Rifampicin - Abx
SSRI (sertraline)
Vit ADEK Supplements

immunosuppression - steroids
Liver Transplant - in ESLF

229
Q

What is the most important disease progression of PBC?

A

Advanced liver cirrhosis
Portal Hypertension

230
Q

What is Primary Sclerosing Cholangitis?

A

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)

231
Q

What are the risk factors for PSC?

A

Male
Northern Europeans
Aged 30-40
Ulcerative colitis
FHx

232
Q

What is the aetiology of PSC?

A

Largely Unknown.
PSC is considered a progressive autoimmune disorder that is strongly associated with inflammatory bowel disease (IBD)

233
Q

How would PSC Present?

A

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

234
Q

What are the diagnostic tests for PSC?

A

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 (94%) /ANA (77%))

GS - MRCP imaging showing bile duct lesions/strictures

235
Q

What is the treatment of PSC

A

Conservative Sx management
Liver transplant is only effective Tx (curative)

Colestyramine - help pruritus
ERCP - for strictures and obstructions

NO Urosodeoxycholic acid

236
Q

How does Colestyramine help with pruritus?

A

Bile acids can bit itchy.
Colestyramine binds to bile acids and prevents their absorption (Bile acid Sequestration).

237
Q

What does PSC have a strong link to?

A

IBD - Ulcerative Colitis

238
Q

What are some complications of PSC?

A

Acute bacterial cholangitis
Cholangiocarcinoma
Colorectal cancer
Cirrhosis and liver failure

239
Q

What are some differential Diagnoses for PSC?

A

It is important to exclude secondary causes of sclerosing cholangitis before making the diagnosis.

Secondary causes of PSC include chronic bacterial cholangitis, cholangiocarcinoma, choledocholithiasis, recurrent pancreatitis, and surgical biliary trauma

240
Q

What is Acute Pancreatitis?

A

Acute inflammation of the pancreas

241
Q

What are the causes of Acute Pancreatitis?

A

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

242
Q

What drugs can cause Acute Pancreatitis?

A

thiazides.
ACEi
azathioprine.
NSAIDs
tetracyclines.
sodium valproate.
frusemide.
oestrogens.
corticosteroids.
sulphonamides.

243
Q

What is the pathogenesis of Acute pancreatitis?

A

Gallstones: trapped at end of biliary system. Block outflow of bile/pancreatic juices into duodenum. These reflux into pancreatic duct. zymogens become activated and can lead to autodigestion causing inflammation. leads to leakage of enzymes causing retroperitoneal haemorrhage.

Alcohol: Directly toxic to pancreatic cells causing inflammation. Leads to activation of zymogens and autodigestion causing further inflammation.

Retroperitoneal haemorrhage leads to greys/turners sign

Derange normal pancreatic enzymes - serum lipase, amylase leading to malabsorption. Loss of insulin causing hyperglycaemia

Oedema, fluid shift and vomiting leads to hypovolaemic shock

244
Q

What are the risk factors for acute pancreatitis?

A

Alcoholism

Smoking

Obesity

Family history

245
Q

What are the symptoms associated with acute pancreatitis?

A

Abdominal pain (may radiate to the back)
Nausea
Vomiting
Anorexia
Tachycardia
Haemodynamic Instability
Diarrhoea

246
Q

What are the signs of Acute pancreatitis?

A

Abdominal tenderness
Abdominal distention
Cullen’s Sign
Grey-Turner’s Sign

Signs of Shock:
Tachycardia
Tachypnea
Pyrexia

247
Q

What are the Eponymous signs for pancreatitis?

A

Cullen’s sign: peri-umbilical bruising (first described in ruptured ectopic pregnancy)

Grey-Turner’s sign: flank bruising

248
Q

What is a DDx of acute pancreatitis based on the pain experienced by Px?

A

AAA

249
Q

What diagnostic investigations would be performed in acute pancreatitis?

A

LFTs – inflammation of pancreas causes release of enzymes
GS - Raised serum amylase/serum lipase
Lipase to amylase >2 suggests alcoholic
CRP raised

Others to Consider for cause:
Erect AXR - exclude gastroduodenal artery perforation

Abdo USS - Diagnostic for gallstones

CT abdomen – (shows extent of damage) evidence inflammation, necrosis and pseudocyst

250
Q

What is the first line/Gold standard test for acute pancreatitis?

A

A serum amylase elevated 3 times above the reference range is considered diagnostic.

251
Q

What blood test is most specific for acute pancreatitis?

A

Serum Lipase as amylase levels can also rise in other conditions.

252
Q

What is required for Dx of Acute pancreatitis?

A

Px must have at least 2 of:
Characteristic Signs and Symptoms
Increased Amylase/Lipase
Radiological Evidence (USS)

253
Q

How is pancreatitis severity scored?

A

APACHE2 - Assess severity within 24 hrs

Glasgow Criteria - Assess the Severity of Pancreatitis based on number of key criteria present.

0-1 Mild
2 - moderate
3+ - severe

254
Q

What is the Glasgow criteria in assessing acute pancreatitis severity?

A

PANCREAS:
PaO2 < 8KPa
Age >55
Neutrophils - WBC >15
Ca2+ (low) <2
Renal Function - urea >16
Enzymes (LDH > 600)
Albumin <32
Sugar Glucose >10

255
Q

Why do patients with Acute Pancreatitis get hypocalcaemia?

A

Pancreatic inflammation
autodigestion
increased activity of digestive enzymes
Increased fat digestion (fat Necrosis)
Release of FFAs
React with serum calcium
Cause hypocalcaemia

256
Q

What is the Treatment of acute pancreatitis?

A

Emergency:

Nil By mouth w/ nutritional support (NG tube)
IV fluid + electrolytes
Analgesia - morphine
Catheterise
Abx prophylaxis

Tx Gallstones if present - ERCP/Cholecystectomy
Tx complications

257
Q

What is a major complication of acute pancreatitis?

A

SIRS (systemic Inflammatory Response Syndrome):
Tachycardia
Tachypnoea
Pyrexia
Increase WCC

Acute Respiratory Distress Syndrome – leading cause of death

Sepsis
Pancreatic pseudocyst
Hypovolaemic shock from ruptured vessels
DIC

258
Q

What are some complications of Acute pancreatitis and how are they managed?

A

ARDS - Give O2

Hyperglycaemia - Insulin

Shock - Hypovolaemic give fluids, Septic - Abx

259
Q

What are the 2 types of autoimmune pancreatitis?

A

Type 1 AIP: part of a systemic condition called IgG4-related diseases.

Type 2 AIP: a type of pancreatitis associated with inflammatory bowel disease but limited to the pancreas

260
Q

What Ig is Raised in a patient with Type 1 autoimmune chronic pancreatitis?

A

IgG4

261
Q

How is autoimmune Chronic pancreatitis treated?

A

With steroids

262
Q

What are the types of Hereditary Pancreatitis?

A

Autosomal dominant: secondary to PRSS1 mutation. Encodes cationic trypsinogen

Autosomal recessive: associated with mutations in the CTFR gene (abnormal in cystic fibrosis) and SPINK1 gene known as pancreatic secretory trypsin inhibitor gene

263
Q

What is Chronic Pancreatitis?

A

3+ month history of pancreatic deterioration leading to irreversible pancreatic damage, inflammation and fibrosis.

264
Q

Give the pathophysiology of Chronic Pancreatitis

A

Progressive loss of lobular morphology and structure of pancreas due to persistent inflammation necrosis/apoptosis, duct obstruction

Deformation of the large ducts and severe changes in arrangement and composition of islets and lack of excretion of pancreatic enzymes

Causes autodigestion, inflammation and fibrosis.

Irreversible morphological and structure changes (calcium deposits) - impair exocrine and endocrine functions

265
Q

What are the causes of chronic pancreatitis?

A

AGITS:
Alcohol - Most common
Genetics - CF, Haemochromatosis
Immune
Triglycerides
Structural - Duct obstruction

CDK, Trauma, Recurrent acute Pancreatitis

266
Q

What are the risk factors for chronic pancreatitis?

A

Alcohol misuse (most common)

Smoking

Obesity

Recurrent acute pancreatitis

CKD

Gallstones

⍺1-antitrypsin deficiency

267
Q

How might a patient present with chronic pancreatitis?

A

Epigastric pain (often post prandial) - less intense but longer lasting than acute
Nausea
Vomiting
Anorexia

Exocrine Insufficiency:
Weight loss
Malabsorption
Bloating
Abdo discomfort
Loose stools (diarrhoea)
Steatorrhea (due to poor fat digestion)

Endocrine Insufficiency:
Polyuria
Polydipsia
Weight loss

268
Q

Why do Px with chronic pancreatitis develop malabsorption?

A

Damaged acinar cells due to pancreatic inflammation.
Failure to produce digestive enzymes
Malabsorption (weight loss, diarrhoea, steatorrhoea)

269
Q

What are the characteristics of pain in chronic pancreatitis?

A

Bores through the back

Relieved by sitting forward or hot water bottle

Exacerbated by fatty foods/alcohol

270
Q

What Diagnostic Investigations would be used for Chronic Pancreatitis?

A

Hx
Bloods:
Lipase + amylase
Faecal Elastase

(Diagnostic) Transabdominal Ultrasound + CT - detects pancreatic calcification + dilated pancreatic ducts

271
Q

What is the management of Chronic Pancreatitis?

A

Alcohol Cessation
Abdo Pain Sx - NSAIDs
Pancreatic Enzyme supplements

Surgical:
Endoscopic stenting (ERCP)
Whipple - Distal pancreatectomy

272
Q

What forms the Hepatic Portal Vein?

A

Union of the SMA and Splenic Veins

273
Q

What is Portal Hypertension?

A

Pathological high pressure in the portal vein commonly caused as a complication of other conditions such as liver cirrhosis and alcoholism

274
Q

What is the normal pressure range in the portal venous system and in portal HTN?

A

5-10 mmHg
When Pressure in portal vein is >10mmHg = Bad / >12mmHg = V.bad

275
Q

What is the pathophysiology of Portal Hypertension?

A
  • 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 gastroesophageal veins causing varices
276
Q

Where would varices tend to develop in portal HTN?

A

GOJ
Ileocecal Junction
Rectum
Peri-umbilical epigastric veins (caput Medusae)

277
Q

What are Varices?

A

A dilated vein that is at risk of rupture causing haemorrhage in the GI Tract

278
Q

How is Portal HTN Classified?

A

Site of the obstruction:
Pre-hepatic - blockage of PV before the liver (PV thrombosis)

Intrahepatic - Distortion of liver architecture (pre/post sinusoidal)

Post hepatic - Venous blockage outside the liver.

279
Q

What are some causes of Pre hepatic Portal HTN?

A

Portal Vein Thrombosis

280
Q

What are some causes of Intra hepatic portal HTN?

A

Cirrhosis - most common in UK
Schistosomiasis - Commonest world wide

281
Q

What are some causes of post hepatic portal HTN?

A

Budd Chiari (hepatic vein obstruction by tumour/thrombus)
RHF
Constrictive Pericarditis

282
Q

What are the Sx of Portal HTN?

A

Mostly ASx

Associated with LF and therefore Sx of LF may be present

Present when oesophageal varices rupture

283
Q

What investigations are required for portal HTN?

A

Abdominal Ultrasound - Dilated portal vein
Doppler US - slow PV velocity

Oesophagealgastroduodenoscopy (OGD) check for presence of oesophageal varices

284
Q

What are the complications of portal HTN?

A

Bleeding from gastric/oesophageal varices
Ascites
Pulmonary HTN
LF
Hepatopulmonary Syndrome
Hepatorenal Syndrome

285
Q

What is the Treatment of Portal HTN?

A

Tx underlying Cause
Salt reduction and Diuretics
Beta blockers/Nitrates to reduce BP.

286
Q

What causes oesophageal varices?

A

Portal HTN

287
Q

When are Gastro-oesophageal varices prone to rupture?

A

When portal pressure exceeds 12mmHg
Oesophageal veins are thin and not meant to support high pressures
This will lead to GI bleeding.

288
Q

What are the Sx of a patient who’s oesophageal varices have ruptured?

A

Haematemesis - coughing blood.
Abdo pain
Shock - if large blood loss
Hypotension and tachycardia
Ascites

289
Q

What are the investigations for Oesophageal Varices?

A

Upper GI Endoscopy

290
Q

What is the management of oesophageal varices?

A

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

291
Q

What is Ascites?

A

Accumulated free fluid in abdominal cavity commonly as a complication of Cirrhosis

292
Q

What is the epidemiology of Ascites?

A

10-20% survival 5-years from onset
Signifies other serious illness
Common post op

293
Q

What are the main causes of Ascites?

A

Local Inflammation - peritonitis, TB, Abdo cancer

Low protein - Nephrotic Syndrome, Hypoalbuminaemia (LF)

Flow Stasis - Liver cirrhosis, Budd Chiari, Congestive HF

294
Q

What is the pathophysiology of Ascites?

A

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

295
Q

What are the symptoms & signs of Ascites?

A

Abdominal Distension/swelling
Abdominal pain - severe suspect SBP
Shifting Dullness
Fluid in flanks
Fluid thrill

May have jaundice and Pruritus

296
Q

What are the risk factors for ascites?

A

High sodium diet

Hepatocellular carcinoma

Splanchnic vein thrombosis resulting in portal hypertension

297
Q

What investigations are done for Ascites?

A

Shifting Dullness Exam

Ultrasound

Ascitic Tap - Aspiration of ascitic fluid:
- Cytology
- WCC
- Protein Measurement (serum ascites albumin gradient (SAAG))
- Gram stain/Culture

298
Q

What would the different results of protein measurement suggest in an Ascitic tap?

A

Transudate:(raised portal pressure)
<30g/l
Low protein
Serum Albumin ascitic gradient (SAAG >1.1g/dl
Clear fluid - due to increased hydrostatic pressure

Exudate: (Normal portal pressure)
>30 g/L
High Protein
SAAG <1.1g/dL
cloudy fluid - due to inflammation mediated exudation

299
Q

What would a Transudate ascitic tap suggest the cause of Ascites is?

A

Portal HTN
ALF, cirrhosis
Budd Chiari
Constrictive pericarditis
Congestive HF
Nephrotic Syndrome

300
Q

What would an Exudate ascitic tap suggest the cause of Ascites is?

A

Malignancy
Peritonitis
Pancreatitis
Bowel Obstruction

301
Q

What is the management for ascites?

A

Tx underlying cause

Reduce Sodium - help live

Diuretics - increase Na excretion - Spironolactone

Paracentesis - fluid drain

Liver transplant

302
Q

What are some complications of ascites?

A

Spontaneous Bacterial Peritonitis

303
Q

What is Peritonitis?

A

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)

304
Q

What is peritonism?

A

Tensing of muscles to prevent movement of peritoneum

305
Q

What are the causes of peritonitis?

A

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

306
Q

What are the different pathways of infection for peritonitis?

A

GI perforation
Transmural translocation - from pancreatitis etc
Exogenous contamination - drains, surgery etc,
UTI
Haematogenous spread - septicaemia

307
Q

What are the Sx of Periotonitis?

A

Sudden onset severe abdominal pain
General collapse
fever
malaise
Nausea and vomiting

+ Ascites / Septic Shock

308
Q

What are the characteristics of the abdominal pain in peritonitis?

A

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

309
Q

What are the signs of Peritonitis?

A

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

310
Q

What region of the abdomen is innervated by which nerves?

A

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)

311
Q

How is peritonitis diagnosed?

A

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

312
Q

What is the Treatment of Peritonitis?

A

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)

313
Q

What are the main complications of peritonitis?

A

Septicaemic if not Tx early (suspect if BP is low)

Local Abscess formation

Kidney Failure

314
Q

What are the differential diagnoses for peritonitis?

A

Bowel Obstruction
Ectopic pregnancy
Pancreatitis

315
Q

Give 3 causes of iron overload.

A
  1. Genetic disorders e.g. haemochromatosis.
  2. Multiple blood transfusions.
  3. Haemolysis.
  4. Alcoholic liver disease.
316
Q

What is Hereditary Haemochromatosis?

A

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.

317
Q

Who is typically affected by Haemochromatosis?

A

Males
50yrs old +

318
Q

Why are women less likely to be affected by haemochromatosis?

A

They will lose iron in blood during menstruation

319
Q

What is the pathophysiology of Hereditary Haemochromatosis?

A

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

320
Q

What organs can iron be deposited in in haemochromatosis?

A

LIVER
Pancreas
Kidney
Heart
Skin
Ant. Pituitary

321
Q

What are the risk factors for hereditary haemochromatosis?

A

Genetic

Alcohol

322
Q

What are the Sx of Haemochromatosis?

A

Males in 40-50s (women often present later)
Chronic tenderness
Abdo pain
Fatigue and weakness
Joint pain
Pigmentation - Slate grey statue
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive Sx - memory/mood

323
Q

What is the Gross iron overload triad?

A

Slate grey statue skin
Hepatomegaly
T2DM

324
Q

What are the diagnostic investigations for Haemochromatosis?

A

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

325
Q

What are some complications of hereditary haemochromatosis?

A

Diabetes Mellitus - iron affects pancreatic function
Liver cirrhosis
Hypopituitarism
Cardiomyopathy
HCC
Hypothyroidism - Iron in thyroid
Arthropathy

326
Q

What is the management of Haemochromatosis?

A

1st Line - Venesection - remove blood to reduce iron

2nd Line - Use Desferoxamine (chelation therapy) if CI

Low iron diet.

327
Q

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

A

HFE.

328
Q

What protein is responsible for controlling iron absorption?

A

Hepcidin.
Levels of this protein are decreased in haemochromatosis.

329
Q

Name 3 metabolic disorders that can cause liver disease.

A
  1. Haemochromatosis - iron overload.
  2. Alpha 1 anti-trypsin deficiency.
  3. Wilson’s disease - disorder of copper metabolism.
330
Q

What is Wilsons Disease?

A

Autosomal Recessive mutation of ATP7B gene on chromosome 13 leading to excess body copper accumulation

331
Q

Who is typically affected by Wilsons Disease?

A

Young patient
20 yrs
FHx
Has RF

332
Q

What is the pathophysiology of Wilsons Disease?

A

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)

333
Q

What are the clinical features of Wilsons Disease?

A

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

334
Q

What are Kayser Fleischer rings?

A

Copper deposits in the iris of the eyes that are symptomatic in Wilsons Disease

335
Q

What investigations are required for Wilsons Disease?

A

Blood tests:
Low serum Copper - copper is deposited in tissues so not in blood
Low Caeruloplasmin - protein that carries copper

24h Urine Cu Assay - Elevated

Liver Biopsy (GS) - high Hepatic Copper

MRI - Basal ganglia degeneration

336
Q

What is the management of Wilsons Disease?

A

1st Line - D-Penicillamine (copper chelation)

Trientene

Diet - avoid high copper foods

Liver Transplant if severe

337
Q

What are the side effects of Penicilamine?

A

Skin rashes
Fall in WCC, Hb and Platelets
haematuria
Renal Damage

338
Q

What is ⍺-1 antitrypsin deficiency?

A

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

339
Q

What is the pathophysiology of Alpha 1 anti-trypsin Deficiency?

A

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

340
Q

Where is Alpha 1 anti-trypsin synthesised?

A

In the liver and therefore A1AT deficiency causing damage to the liver is made worse due to a loss of synthetic function.

341
Q

What are the symptoms of a patient with A1AT deficiency?

A

Young/middle aged male
Often present COPD like symptoms with no smoking Hx:

Dyspnoea, chronic cough, sputum production (COPD)

Potentially Liver Sx too (jaundice)

342
Q

What is the Diagnostic investigations for A1AT deficiency?

A

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

343
Q

What would be found on liver biopsy in A1AT Deficiency?

A

Acid schiff positive staining globules in hepatocytes

Break down produces due to the action of proteases

344
Q

What is the management of A1AT deficiency?

A

No definitive Tx
Stop smoking
manage emphysema - inhales (SABAs, LABAs)
Consider liver transplantation in hepatic decompensation

345
Q

What amount of paracetamol is ingested for overdose?

A

75mg/Kg

346
Q

What is paracetamol overdose responsible for in the UK?

A

50% of all fulminant liver failures

347
Q

What are the Sx of paracetamol overdose?

A

Acute severe RUQ pain
Severe Nausea and Vomiting

Jaundice
Confusion
Anorexia

348
Q

What is the normal metabolism of paracetamol?

A

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.

349
Q

What happens to paracetamol metabolism in overdose?

A

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

350
Q

How is Paracetamol overdose treated?

A

Activated charcoal if within 1hr of ingestion + N-acetylcysteine

N-acetylcysteine if >1hr after ingestion.

351
Q

What is the purpose of Treating paracetamol overdose with N-acetylcysteine?

A

Increases availability of glutathione to remove NAPQI

352
Q

What is Gilberts Syndrome?
+ crigler Najjar

A

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

353
Q

What is the Treatment of Gilberts/Crigler Najjar syndrome?

A

Gilberts - should be ok w/out Tx

CN - Phototherapy to break down unconjugated bilirubin.

354
Q

What is a hernia?

A

Protrusion of a viscus/part of viscus through a defect in the wall of its containing cavity into an abnormal position

355
Q

What is a reducible hernia?

A

Can be pushed back into abdominal cavity with manual manoeuvring

356
Q

What is an irreducible hernia?

A

Cannot be pushed back into place

357
Q

What is an obstructed hernia?

A

I.e. intestine

Intestine obstructed due to pressure from edges of hernia, but blood flow is maintained

358
Q

What is an incarcerated hernia?

A

Contents of the hernial sac are stuck inside by adhesions

359
Q

What is a strangulated hernia?

A

Blood supply is cut off

Ischaemia +- gangrene/perforation of the hernial contents

Patient becomes toxic and requires urgent surgery

360
Q

What is an inguinal hernia?

A

Protrusion of abdo contents through inguinal canal

361
Q

What is a femoral hernia?

A

Bowel moves through the femoral canal below the inguinal ligament

362
Q

What is an incisional hernia?

A

Through weak surgical scar

363
Q

What is a sliding hiatus hernia?

A

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

364
Q

What is the pathophysiology of inguinal hernias?

A

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

365
Q

What is the pathophysiology of femoral hernias?

A

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

366
Q

What are some risk factors for hernias?

A

Male - inguinal
Heavy lifting
Coughing
Surgery

367
Q

What are some symptoms of a hiatal hernia?

A

Gastro oesophageal reflux
Dysphagia

368
Q

What are some symptoms of a femoral hernia?

A

Swelling in upper thigh pointing down

369
Q

What are some symptoms of an inguinal hernia?

A

Painful swelling in groin
Points along groin margin.

370
Q

What diagnostic tests can be done to investigate:
Hiatus hernias
Inguinal Hernias
Femoral Hernias

A

Hiatus Hernias - CXR, Barium swallow (diagnostic)

Inguinal Hernias - usually clinical but potentially USS

Femoral Hernias - Usually clinical but potentially USS

371
Q

What is the curative treatment for hernias?

A

Surgery.

372
Q

What are the 5 viruses that cause hepatitis?

A

Hepatitis A (HAV) - RNA
Hepatitis B (HBV) - DNA
Hepatitis C (HCV) - RNA
Hepatitis D (HDV) - RNA
Hepatitis E (HEV) - RNA

373
Q

How are hepatitis A and E transmitted?

A

Via Faecal-oral transmission

374
Q

How are hepatitis B,C and D transmitted?

A

Blood to blood transmission

375
Q

What is acute hepatitis?
What Hepatitis viruses cause acute hepatitis?

A

A sudden illnesss with a mild to severe course followed by complete resolution

All hepatitis Viruses

376
Q

What is chronic hepatitis
What Hepatitis viruses cause chronic hepatitis?

A

A prolonged course of active disease or silent asymptomatic infection.

HBV, HCV, HBV +/-HDV, HEV (immunocompromised)

377
Q

Outline Acute Viral hepatitis

A

Variable incubation period

Prodromal Phase:

  • Systemic symptoms first:
  • **Fatigue, low-grade fever, muscle/joint aches, cough, runny nose, and
    pharyngitis. **

Icteric Phase:

  • 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

378
Q

Outline Chronic Hepatitis

A

More difficult to Diagnose
Patient is often asymptomatic
Clinical manifestations are the same regardless of virus causing hepatitis.

379
Q

Describe the transmission of hepatitis A

A

Ingesting contaminated drinking water or food (shellfish)

Associated with Recent Travel Hx - Africa

Close person to person contact

Often infects young children

380
Q

What is the pathogenesis of HAV?

A

Prodromal phase 1-2 weeks
N+v, fever, malaise, RUQ pain

Icteric phase -3 months
Jaundice, pruritus

-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

381
Q

What are the clinical findings of HAV?

A

Incubation of 2-4 weeks
Usually symptomatic in adults - constitutional Sx + abdo pain.

Rarely causes fulminant hepatitis

382
Q

What Ix are required for HAV diagnosis?

A

Serology - Detection of anti-HAV IgM confirms the diagnosis and remains for 3-6 months.

Also:
LFTs: High AST and ALT.
Bilirubin and ALP usually only mild.

Bloods - Inc ESR, Leukopenia

383
Q

What is the treatment for HAV infection?

A

Self limiting - no chronic disease

Supportive therapy

Primary prevention - travellers vaccine

100% immunity after infection

384
Q

What is Hepatitis B virus?

A

DNA virus that lives in all human body fluids in an infected individual.

Semen, urine, saliva, blood, breast milk

385
Q

What are HBV markers?

A

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

386
Q

How can HBV be transmitted and give examples?

A

Blood to blood transmission - parenteral transmission.

Needle sharing,
accidental medical exposures,
sexual contact
Blood transfusions

387
Q

Where is HBV prevalent

A

ASIA

388
Q

How does HBV present?

A

3 clinical states:
Acute hepatitis

Fulminant hepatitis - severe acute hepatitis with rapid destruction of the liver

Chronic Hepatitis

389
Q

What proportion of patients have spontaneous resolution following HBV infection and what proportion go on to develop Chronic HBV infection?

In Adults?
In Neonates/Infants?

A

Adults:
Spontaneous resolution - >95%
Develop chronic Infection - <5%

Neonates/Infants:
Spontaneous Resolution - 10%
Develop Chronic Infection - 90%

390
Q

How do you diagnose HBV infection?

A

HBsAg antigen means there is LIVE virus and infection.

Anti - HBsAg antibodies - patient is protected and immune

HBeAg - Infected and viral replication

Anti- HBeAg - Low activity and infectivity

HBcAg - exposure to HBV at some point.

HBcAg IgM/G - Recent infection or chronic infection/carrier

391
Q

How is HBV infection prevented?

A

Antenatal screening - HBsAg of pregnant mothers

Universal childhood vaccination

PrEP - tenofovir + emtricitabine

392
Q

What are the complications of HBV infection?

A

HDV co-infection

Hepatocellular carcinoma
End-stage liver disease/cirrhosis

393
Q

How is HBV infection managed?

A

Pegylated Interferon 2A

Oral nucleoside analogues - Tenofovir, entecavir (better tolerated than PEG IFN)

394
Q

What is Hepatitis C virus

A

RNA virus
Incubation period 6-12 weeks

395
Q

What is the clinical signs of HCV infection?

A

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.

396
Q

Outline HCV transmission

A

Blood-to-blood contact via blood transfusions, injecting drug use, nosocomial (needle sticks, dialysis, inadequate sterilisation of colonoscopes

397
Q

What is the most common indication for liver transplantation?

A

Liver cirrhosis resulting from chronic HCV infection

398
Q

What comorbidities arise with HCV infection?

A

HCV infection can lead to significant autoimmune reactions:
vasculitis, arthralgias, purpura, membranoproliferative glomerulonephritis

399
Q

How is HCV diagnosed?

A

Testing for anti-HCV 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.

Hc RNA -tve = No infection / Hc RNA +tve = Active infection
Anti Hc Ab +tve = Previous and resolved infection

400
Q

What is the treatment for HCV infection

A

Direct acting Anti-virals (DAAs) + Ribavirin
No vaccine currently exists.

Liver Transplantation for End stage liver disease

401
Q

What are the different targets of DAAs?

A

NSE3/4A Protease inhibitors (suffix = previr)

NS5A Inhibitors (Suffix = Asvir)

NS5B Inhibitors (Suffix = buvir)

402
Q

Give some examples of DAA combination therapy?

A

Glecaprevir/Pibrentasvir

Sofosbuvir/Velpatasvir

Triple Therapy:
Sofosbuvir/Velpatasvir/Voxilaprevir

403
Q

Can HCV be cured?

A

Yes
however that does not confer immunity and there is still a risk of re-infection

404
Q

What is Hepatitis D virus?

A

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.

405
Q

Outline the transmission of HDV?

A

Transmitted in the same way as HBV
Coinfection of HBV and HDV is more severe than those infected with HBV alone.

406
Q

What is the presentation of a HDV infection?

A

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.

407
Q

What diagnostic tests are required for HDV infection?

A

Detecting delta antigen or IgM antibody against delta antigen in the patient’s serum.

408
Q

What is the treatment for HDV infection?

A

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.

409
Q

What is Hepatitis E infection?

A

RNA virus similar to HAV.

410
Q

How is HEV transmitted?

A

Via the faecal oral route
Waterborne transmission is most common.

411
Q

What is the clinical presentation of HEV infection?

A

Clinically similar to HAV infection.

Often Asymptomatic (95% cases) - usually self limiting

Chronic infection can be caused in immunocompromised individuals.

412
Q

How is HEV diagnosed?

A

Detecting IgM antibodies to HEV.

413
Q

What is the treatment to HEV infection?

A

Self limiting

No antiviral drug available for acute infection in immunocompetent patients. (consider ribavirin if really ill)

Treatment is supportive.

414
Q

What are some complications of hereditary haemochromatosis?

A

T1DM - iron affects pancreatic function
Liver cirrhosis
Endocrine issues - Iron deposits in pit.
Cardiomyopathy - iron in heart
HCC
Hypothyroidism - Iron in thyroid
Arthritis

415
Q

How are gallstones formed?

A

The 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

416
Q

What is SBP?

A

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.

417
Q

How is SBP diagnosed?

A

Ascitic tap and analysis via paracentesis.
Asses fluid appearance, cell count and culture.

Also FBC, LFT, blood cultures

418
Q

What are the investigations for Hepatic Encephalopathy?

A

FBC and Basal metabolic panel
Blood alcohol elevated
Blood ammonia raised

Medicine Phase 2a (20 decks)

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