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Sharon's Phase 2a Medicine Revision > Liver and friends > Flashcards

Liver and friends Flashcards

1
Q

What are the normal functions of the liver?

A
  • Oestrogen regulation
  • Detoxification
  • Metabolises carbohydrates
  • Albumin production
  • Clotting factor production
  • Bilirubin regulation
  • Immunity – Kupffer cells in reticuloendothelial system
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2
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with oestrogen regulation?

A

Gynecomastia in men (an increase of breast tissue)
Spider naevi
Palmar erythema (vasodilation in palms)

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3
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with detoxification?

A

Hepatic encephalopathy - changes in the brain that occur in patients with advanced, acute or chronic liver disease

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4
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with carb metabolism?

A

Hypoglycaemia

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5
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with albumin production?

A

Oedema
Ascites
Leukonychia (white nails)

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6
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with bilirubin regulation?

A

Jaundice – stool and urine changes
Pruritus

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7
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with clotting factor production?

A

Easy bruising
Easy bleeding

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8
Q

What symptoms/signs might a patient present with if there is liver dysfunction causing problems with immunity?

A

Spontaneous bacterial infection can occur

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9
Q

Define acute liver failure (ALF)

A

ALF is a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5, normal = <1.1), and hepatic encephalopathy in patients with no evidence of prior liver disease.

It is called acute-on-chronic liver failure if these symptoms occur in a patient with pre-existing liver disease.

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10
Q

What is the aetiology of ALF?

A
  • Paracetamol overdose (most in UK and US)
  • Acute hepatitis B
  • Acute hepatitis A
  • Autoimmune hepatitis
  • Ischaemic hepatitis
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11
Q

What signs and symptoms might a patient with ALF present with?

A

Symptoms

  • Abdominal pain
  • Nausea
  • Vomiting
  • Malaise

Signs

  • Jaundice (definitive)
  • Hepatic encephalopathy (definitive)
  • Signs of cerebral oedema
  • Right upper quadrant tenderness
  • Hepatomegaly
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12
Q

What investigations/tests are used to diagnose ALF?

A

Primary investigations:
Blood tests:

  • platelets low, PT/INR: INR > 1.5
  • LFTs - hyperbilirubinemia, typically raised ALT and AST
  • FBC - thrombocytopenia
  • Serum electrolytes: imbalance
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13
Q

What are the treatment options/management for ALF?

A

All patients:

  • Intensive care management + monitoring
  • Liver transplant assessment
  • Neurological status monitoring
  • Blood glucose & electrolytes monitoring
  • Treat underlying cause e.g. paracetamol overdose > N-acetylcisteine
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14
Q

Define liver cirrhosis (chronic liver failure higher yield than ALF)

A

Cirrhosis is a diffuse pathological process characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules.

  • Variety of causes
  • Final stage of any chronic liver disease
  • Considered irreversible in advanced stages but there can be significant recovery if the underlying cause is treated
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15
Q

What is the aetiology of liver cirrhosis?

A

Most common are:

  • Alcoholic liver disease
  • Non-alcoholic fatty liver disease
  • Chronic viral hepatitis
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16
Q

What signs and symptoms might a patient with liver cirrhosis present with?

A

Symptoms - non-specific:

  • Weight loss
  • Malaise
  • Fatigue
  • Easy bruising

Signs

  • Ascites/Oedema
  • Dupuytren’s contracture (fingers flex towards the palm)
  • Jaundice/Pruritus (itchy skin)
  • Palmar erythema
  • Spider Naevi/Caput Medusae (swollen veins in abdo)
  • Hepatosplenomegaly
  • Confusion and asterixis: hepatic encephalopathy
  • Haematemesis - variceal bleeding
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17
Q

What investigations and tests are used to diagnose liver cirrhosis?

A

Blood tests:

  • Platelets low, PT/INR high (INR > 1.5)
  • LFTs: deranged, AST > ALT in alcoholic liver disease
  • FBC - anaemia and thrombocytopenia
  • Serum bilirubin raised
  • Definitive diagnostic test - liver biopsy (for histology).
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18
Q

What are the treatments/management for liver cirrhosis?

A

Definitive treatment is liver transplant.

Options depend on the patient.

Conservative - fluids, analgesia, alcohol abstinence, good nutrition

Medical - treat complications of liver failure:

  • Ascites – diuretics (spironolactone) and restrict sodium.
  • Cerebral oedema - Mannitol as it decreases ICP
  • Bleeding – Vitamin K (more factors made) or give fresh frozen plasma if active bleeding
  • Encephalopathy - Lactulose (decreases ammonia), antibiotics and enemas – stops the flora making NH3
  • Hypoglycaemia - dextrose.
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19
Q

What are the possible complications of liver cirrhosis?

A

This is quite high yield!

  • Ascites
  • Portal hypertension
  • Varices
  • Hepatic encephalopathy
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20
Q

What are ascites?

A

Ascites is fluid accumulation in the peritoneal cavity.

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21
Q

What is the pathophysiology of ascites in cirrhosis?

A

Hypoalbuminaemia - reduced plasma oncotic pressure.

Portal hypertension - increased hydrostatic pressure

Results in accumulation of fluid in the extravascular space.

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22
Q

What causes ascites in cirrhosis?

A
  • Cirrhosis commonest cause - 50% of patients develop ascites in 10yrs.
  • 4 basic mechanisms
  • Peritonitis - leakier vessels
  • reduced plasma oncotic pressure as a result of hypoalbuminaemia
  • Increased capillary hydrostatic pressure as a result of portal hypertension
  • Peritoneal lymphatic draining
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23
Q

What is transudate ascites?

A

Transudate ascites = protein <25g/L

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24
Q

What are the causes of transudate ascites?

A
  • Portal hypertension due to liver cirrhosis most common
  • Liver failure (acute and chronic)
  • Alcoholic hepatitis
  • Heart failure.
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25
Q

What is exudate ascites?

A

protein >25g/L

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26
Q

What causes exudate ascites?

A
  • Peritonitis (inflammation of peritoneum lining organs)
  • Pancreatitis
  • Peritoneal malignancy
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27
Q

What are the signs and symptoms of ascites?

A
  • Shifting dullness (dull sounds on percussion)
  • Abdo distension
  • Signs of liver disease.
  • Respiratory distress (pleural effusion)
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28
Q

What investigations are used to diagnose ascites?

A

Diagnostic aspiration (albumin, neutrophil count) - biopsy of ascites fluid aka ascites tap

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29
Q

What is serum ascitic albumin gradient (SAAG)?

A

The serum ascitic albumin gradient (SAAG) indirectly measures portal pressure and can be used to determine if ascites is due to portal hypertension.

SAAG calculation

SAAG = (serum albumin) – (ascitic fluid albumin)

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30
Q

What does a high SAAG indicate?

A

A high SAAG (>1.1g/dL) suggests the ascitic fluid is a transudate.

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31
Q

What does a low SAAG indicate?

A

A low SAAG (<1.1g/dL) suggests the ascitic fluid is an exudate.

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32
Q

What is the treatment/management for ascites?

A

1st line - salt restriction.
Diuretics - furosemide/spironolactone.

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33
Q

What are the possible complications that can arise from ascites?

A

Spontaneous bacterial peritonitis (SBP) (8%) - an infection of ascitic fluid.

The most common causes are E.coli then K.pneumoniae

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34
Q

What two veins form the portal vein?

A

Superior mesenteric vein (from the gut) and splenic vein (from the spleen) and transports blood into the liver through the porta hepatis (portal triad)

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35
Q

What is portal hypertension?

A

High blood pressure in the portal vein.

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36
Q

What are the causes of portal hypertension?

A

Causes:

  • Prehepatic - portal vein thrombosis
  • Intrahepatic - cirrhosis (most common)
  • Posthepatic - right-sided heart failure
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37
Q

What are the signs/symptoms of portal hypertension?

A

Usually asymptomatic

Sometimes there could be symptoms of complications:
- Ascites
- Bleeding varices

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38
Q

What are bleeding varices?

A

Varices = dilated (bulgy) veins

They can occur in the oesophagus or proximal stomach as a complication of cirrhosis

Most patients with cirrhosis develop varices, but only ⅓ bleed from them. Bleeding is often massive.

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39
Q

What is the 1st line/gold standard investigation for bleeding varices

A

Upper GI endoscopy

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40
Q

What signs/symptoms indicate bleeding varices/upper GI bleed?

A

Melaena
Haematemesis (coffee ground vomit)

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41
Q

What is the treatment/management for varices?

A

Active bleed :

  • ABCDE
  • Urgent gastroscopy/endoscopy
  • Fluid resuscitation - bleed can be massive
  • Terlipressin (ADH analogue)
  • Balloon tamponade - stops bleeding until definitive treatment
  • Gold standard/first-line - endoscopic variceal band ligation (EVL)

Prophylaxis as the risk of recurrence is high:

  • BB: Propranolol (secondary prevention)
  • Repeat band ligation (primary prevention)
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42
Q

Define alcoholic liver disease (ALD)

A

Alcoholic liver disease results from the effects of the long-term excessive consumption of alcohol on the liver.

3 stages: fatty liver (steatosis), alcoholic hepatitis (inflammation and necrosis), and alcoholic liver cirrhosis.

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43
Q

What is the cause of alcoholic liver disease?

A

Caused by chronic heavy alcohol ingestion.

About 40 to 80 g/day in men

20 to 40 g/day in women

Over 10 to 12 years can cause liver damage without other liver diseases.

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44
Q

What symptoms might a patient with ALD present with?

A

Non-specific:

Malaise
Weakness
Weight loss
Easy bruising

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45
Q

What are the signs of ALD?

A
  • Jaundice
  • Hepatomegaly
  • Spider Naevi
  • Palmar Erythema
  • Gynaecomastia
  • Bruising – due to abnormal clotting
  • Ascites
  • Caput Medusae – engorged superficial epigastric veins
  • Asterixis – “flapping tremor” in decompensated liver disease
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46
Q

What is the CAGE screening tool for alcohol use disorder?

A

CAGE: 4 questions

C: Have you ever felt you needed to CUT DOWN on your drinking?

A: Have people ANNOYED you by criticising your drinking?

G: Have you ever felt GUILTY about drinking?

E: Have you ever felt you needed a drink first thing in the morning (EYE-OPENER)?

A score of 2 or more indicates dependency

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47
Q

What investigations/tests are used to diagnose ALD?

A

Bloods - these are primary investigations

FBC – raised MCV

LFTs – AST:ALT (aspartate transaminase: alanine transaminase) ratio > 2

Clotting – elevated prothrombin time

U+Es may be deranged in hepatorenal syndrome.

Exclude secondary causes: e.g. viral hepatitis, autoimmune liver disease, HCC

Liver Biopsy - confirm the diagnosis of alcohol-related hepatitis or cirrhosis.

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48
Q

What are the treatments/management for alcoholic liver disease?

A

1st line: Stop drinking alcohol permanently

  • Benzodiazepines used to treat alcohol withdrawal
  • Weight loss + smoking cessation
  • Nutritional support with vitamins (particularly thiamine) and a high-protein diet
  • Steroids help in severe alcoholic hepatitis in the short-term
  • Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
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49
Q

What possible complications can arise from ALD?

A
  • Hepatic encephalopathy
  • Portal hypertension
  • GI bleeding
  • Coagulopathy
  • Renal failure (due to portal hypertension and increased RAAS activity)
  • Wernicke-Korsakoff Syndrome (WKS)
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50
Q

What is Wernicke-Korsakoff Syndrome (WKS)?

A

Wernicke-Korsakoff is a degenerative brain condition resulting from thiamine (vitamin B1) deficiency caused by excess alcohol.

Poor thiamine absorption + poor diet

Wernicke’s encephalopathy comes before Korsakoffs syndrome.

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51
Q

Define non-alcoholic fatty liver disease (NAFLD)

A

NAFLD is part of the metabolic syndrome group of conditions related to processing and storing energy.

Associated with obesity, dyslipidaemia, and type 2 diabetes mellitus.

NAFLD = intrahepatic fat is ≥5% of liver weight

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52
Q

What are the 4 stages of NAFLD?

A
  1. Non-alcoholic Fatty Liver Disease (steatosis - build-up of fat in liver)
  2. Non-Alcoholic Steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
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53
Q

What are the risk factors for developing NAFLD?

A

NAFLD shares the same risk factors as cardiovascular disease and diabetes.

Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
Middle age onwards
Smoking
High blood pressure

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54
Q

What signs and symptoms might a patient with NAFLD present with?

A

Many patients asymptomatic, only symptomatic when disease enters cirrhotic stage

Non- specific symptoms:

  • Malaise
  • Weakness
  • Weight loss
  • Easy bruising

Signs

  • Palmar erythema
  • Dupuytren’s contracture
  • Jaundice
  • Ascites
  • Spider naevi
  • Confusion and asterixis: hepatic encephalopathy
  • Haematemesis: variceal bleed
  • Hepatosplenomegaly
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55
Q

What tests do you carry out if a patient has mild abnormalities in LFTs? I.e. Elevated serum aspartate transaminase (AST) and alanine transaminase (ALT)

A

Liver sceens to assess for possible underlying causes of liver pathology:

  • Ultrasound Liver
  • Hepatitis B and C serology
  • Autoantibodies (autoimmune hepatitis)
  • Immunoglobulins (autoimmune hepatitis)
  • Caeruloplasmin (Wilsons disease)
  • Alpha 1 Anti-trypsin levels (alpha 1 antitrypsin deficiency)
  • Ferritin and Transferrin Saturation (hereditary haemochromatosis)
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56
Q

What investigations/tests are used to diagnose NAFLD?

A

Liver Ultrasound can confirm the diagnosis of hepatic steatosis (fatty liver).

1st line - Enhanced Liver Fibrosis (ELF) blood test. It measures three markers (HA, PIIINP and TIMP-1) and indicates the fibrosis of the liver:

< 7.7 - none to mild fibrosis
≥ 7.7 to 9.8 - moderate fibrosis
≥ 9.8 - severe fibrosis

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57
Q

What is the treatment/management for patients with NAFLD?

A

Conservative:

  • Weight loss
  • Exercise
  • Stop smoking
  • Avoid alcohol

Medical

  • Control of diabetes, blood pressure and cholesterol
  • Refer patients with liver fibrosis to a liver specialist, where they may treat with vitamin E or pioglitazone.

End-stage liver disease:

  • Liver transplant
  • TIPS (Transjugular intrahepatic portosystemic shunt) - for patients with complications e.g. varices, PHTN
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58
Q

Define hepatitis

A

Hepatitis describes inflammation in the liver. This can vary from a chronic low level inflammation to acute and severe inflammation that leads to large areas of necrosis and liver failure.

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59
Q

What are the causes of hepatitis?

A
  • Alcoholic hepatitis
  • Non alcoholic fatty liver disease
  • Viral hepatitis
  • Autoimmune hepatitis
  • Drug induced hepatitis (e.g. paracetamol overdose)
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60
Q

What are the different types of viral hepatitis?

A

A, B, C, D, E

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61
Q

What is a good rhyme to remember hepatitis A - E?

A

A is Acquired by mouth from Anus, is Always cleared Acutely and only ever Appears once

B is Blood-Borne, and if not Beaten can be Bad

B and D is DastarDly

C is usually Chronic but Can be Cured - at a Cost. Caused by Crack (IVDU).

E is Even in England and can be Eaten (found in pigs), if not always beaten.

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62
Q

WHat type of virus causes hep A?

A

RNA virus

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63
Q

How is hep A transmitted?

A

Faecal-oral: contaminated food, fly vectors

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64
Q

What is the epidemiology of hep A?

A

Rare in the UK with < 1,000 cases in 2017, high prevalence in Africa, Asia, South America, Middle east.

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65
Q

What is the pathophysiology of hep A?

A

It can cause cholestasis (slowing of bile flow through the biliary system)

  • Dark urine (excess bilirubin excreted by kidneys)
  • Pale stools (indicate obstructive cause)
  • Hepatomegaly.

It resolves without treatment in around 1-3 months.

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66
Q

What signs and symptoms might a patient with hep A present with?

A

Non-specific symptoms:

  • Abdominal pain
  • Fatigue
  • Anorexia
  • Malaise
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and vomiting
  • Fever (viral hepatitis)

After 1-2 weeks liver symptoms/signs - jaundice (sign), hepatomegaly (sign), skin rash.

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67
Q

What investigations/tests are used to diagnose hepatitis A?

A

LFTs

  • Raised transaminases (AST / ALT) - enzymes released during inflammation
  • Raised bilirubin due to inflmmation
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68
Q

What investigations/tests are used to diagnose hepatitis A?

A

LFTs

  • Raised transaminases (AST / ALT) - enzymes released during inflammation
  • Raised bilirubin due to inflammation
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69
Q

What is the management for hep A?

A

A vaccine is available to reduce chance of developing hep A

Treatment is often not required, generally with analgesia

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70
Q

What is a complication that might arise from hep A?

A

Rare acute liver failure.

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71
Q

Is hepatitis A a notifiable disease?

A

Yes, public health need to be notified of all cases

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72
Q

What is a notifiable disease?

A

Registered medical professionals (doctors registered with GMC) have a legal duty to report a suspected/confirmed disease on the “notifiable disease list” to their “proper officer’ at their local council or local health protection team (HPT)

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73
Q

Are hep A - E notifiable diseases?

A

YES! Urgent - verbally within 24 hours via phone, encrypted email or secure fax

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74
Q

How soon does a doctor need to notify an infectious disease?

A

Send the form to the proper officer within 3 days, or notify them verbally within 24 hours if the case is urgent by phone, letter, encrypted email or secure fax machine.

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75
Q

What type of virus causes hep B?

A

DNA virus (only DNA one).

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76
Q

How is hep B transmitted?

A
  • Blood products (IVDU), sexually (particularly MSM).
  • Vertical transmission (mother to child) is most common transmission worldwide.
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77
Q

What is the epidemiology of hep B?

A

Present worldwide, prevalent in Africa, Middle and Far East.

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78
Q

What is the pathophysiology of hep B?

A

Acute infection infects hepatocytes. Cellular response usually clears it within two moths.

10% of patients become chronic help B carriers, because virus DNA has integrated into their own DNA, and so they will continue to produce the viral proteins

Depends on age/ immunocompetence. Inflammation can last 10 yrs -> cirrhosis.

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79
Q

What is the marker for chronic hep B?

A

Presence of HBsAg > 6 months post acute infection

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80
Q

What signs and symptoms might a patient with hep B present with?

A

Acute infection - usually asymptomatic but can present with malaise, fever, fatigue, right upper quadrant pain

If chronic, then signs of cirrhosis - jaundice, pruritus, ascites, Dupuytren’s contracture (fingers flex towards the palm), malaise, anorexia (loss of appetite) etc.

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81
Q

What investigations/tests are used to diagnose hep B?

A

LFTs and serology

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82
Q

What markers are present in hep B infection?

A

Antibodies are produced against pathogenic antigens.

Antigen

  • Surface antigen (HBsAg) – active infection
  • E antigen (HBeAg) – marker of viral replication and implies high infectivity.
  • Core antigen (HBcAg) - not useful as does not circulate in blood

Antibodies

  • Surface antibody (HBsAb) – implies vaccination or past or current infection.
  • E antibodies (HBeAb) - if postive but HBeAg negative, indicates previous active infection and immune response
  • Core antibodies (HBcAb) – implies past (high IgG) or current infection (high IgM

Viral load

  • Hepatitis B virus DNA (HBV DNA) is a direct count of the viral load.
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83
Q

What does the presence of HBcIgM indicate in relation to hep B?

A

IgM is an antibody made in response to acute help B infection, so presence of IgM suggest that the patient is currently infected with hep B

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84
Q

What does the presence of HBcIgG indicate in relation to help B?

A

IgG is made later on in hep B infection and can persist for months or years after the acute infection. The presence of IgG in absence of HBsAg indicates past or chronic hep B infection.

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85
Q

What markers are used when screening for hep B?

A
  • HBcAb - for previous infection
  • HBsAg - for active infection

If these are positive, then:

  • HBeAg - how infective? Viral replication levels?
  • HBV DNA - viral load
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86
Q

What is the management for hep B?

A
  • Antiviral medication - Tenofovir, pegylated interferon alpha 2a
  • Liver transplantation for end-stage liver disease
  • Vaccination for people at risk - med students got it in first year
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87
Q

Is hep B a notifiable disease?

A

YES!

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88
Q

What possible complications can arise from hep B infection?

A

If chronic, there is an increased risk of liver cirrhosis, hepatocellular carcinoma

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89
Q

What type of virus causes hep D?

A

RNA virus

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90
Q

How is hep D transmitted?

A

Bloodborne - sexually, IVDU

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91
Q

What is the pathophysiology of hep D?

A

Hep D is unable to replicate on its own and requires concurrent HBV infection. It attaches itself to the HBsAg to survive and cannot survive without this protein.

It makes Hep B infection more likely to progress to cirrhosis/hepatocellular carcinoma (HCC)

92
Q

How might a patient with hep D present?

A

Hep D is clinically indistinguishable from acute HBV infection

93
Q

What is the treatment/management for hep D?

A

It is the same as hep B

94
Q

What are the complications of hep D?

A

Cirrhosis and HCC

95
Q

What type of virus causes hep C?

A

RNA virus

96
Q

What is the epidemiology of hep C?

A

More common in the UK (118,000 in 2019), common in Africa

97
Q

What is the pathophysiology of hep C?

A

Transmission through percutaneous exposure - e.g. IVDU, unscreened blood products

Acute infection is often asymptomatic, allowing it to become chronic.

Chronic HCV infection causes slow progressive fibrosis over the years.

98
Q

What are signs and symptoms of hep C infection?

A

Acute = asymptomic

Later = signs of chronic liver disease e.g. jaundice, pruritis, ascites, hepatomegaly

99
Q

What proportion of patients with acute hep C infection becomes chronic carriers?

A

75% :( (3 in 4 people)

Only 1 in 4 fight off the infection

100
Q

What investigations/tests are used to diagnose hep C?

A
  • Screening test - Hepatitis C antibody
  • Hepatitis C RNA testing is used to confirm the diagnosis of hepatitis C , assess individual genotype and calculate viral load
101
Q

What is the treatment/management for hep C?

A

Direct acting antiviral agents (DAA) (Ribavirin) is curative

DAA treatment is tailored to the specific viral genotype.

They successfully cure the infection in over 90% of patients.

8 - 12 weeks treatment

102
Q

What complications are associated with hep C?

A

Chronic liver disease, hepatocellular carcinoma (HCC)

103
Q

What type of virus causes hep E?

A

RNA virus.

104
Q

How is hep E transmitted?

A

By the faecal-oral route

105
Q

What’s the epidemiology of hep E?

A

Becoming more common in the UK. Now the most common cause of short-term (acute) hepatitis in the UK.

Common in developing world, where there is poor sanitation

106
Q

How might a patient with hep E present?

A

95% of cases are asymptomatic, as it is usually self-limiting.

107
Q

What is the treatment for hep E?

A

Often not required, but supportive

108
Q

What possible complications can arise from hep E?

A

Complications are rare, but hep E can progress to chronic hepatitis and liver failure in immunocompromised patients

109
Q

What is autoimmune hepatitis?

A

Chronic hepatitis as a result of autoantibodies against hepatocytes

110
Q

What is the aetiology of autoimmune hepatitis?

A

Unknown, but thought to have an environmental trigger e.g. vira infection that causes a T cell-mediated response against hepatocytes

111
Q

What are the two types of autoimmune hepatitis?

A

They have different ages of onset and autoantibodies:

Type 1: occurs in adults
Type 2: occurs in children

112
Q

How might a patient with type 1 autoimmune hepatitis present?

A
  • Female
  • Late 40s - 50s
  • Around/after the menopause
  • Fatigue and features of liver disease on examination
113
Q

How might a patient with type 2 autoimmune hepatitis present?

A
  • Often in their teens/early twenties
  • Acute hepatitis with jaundice
114
Q

What investigations/tests are used to diagnose autoimmune hepatitis?

A
  • LFT - Raised transaminases (ALT and AST)
  • Raised IgG levels, and it is associated with many autoantibodies.
  • Diagnosis made using a liver biopsy
115
Q

What autoantibodies are associated with type 1 autoimmune hepatitis?

A
  • Anti-nuclear antibodies (ANA) - not specific
  • Anti-smooth muscle antibodies (anti-actin) - not specific
  • Anti-soluble liver antigens (anti-SLA) - highly specific to AIH
116
Q

What autoantibodies are associated with type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

117
Q

What is the treatment/management for autoimmune hepatitis?

A
  • High dose steroids (prednisolone)
  • Then taper introduce immunosuppressants e.g. azathioprine
  • Usually successful in inducing remission but required life-long.

End-stage liver disease - liver transplant but autoimmune hepatitis can occur in transplated liver

118
Q

Define jaundice

A

Jaundice = accumulation of bilirubin in the bloodstream and subsequent deposition in the skin, sclera, and mucous membranes.

Normal levels are 3.4 - 20 mmol/L

Jaundice may not be clinically evident until serum levels >51 mmol/L (3 mg/dL).

119
Q

Briefly, what are the causes of jaundice?

A

Jaundice might result from increased bilirubin production (prehepatic), diseases that impair hepatocyte function (hepatocellular), or obstruction of the biliary system (cholestatic).

120
Q

How is bilirubin normally processed in the body?

A

Haem from old RBC broken down into unconjugated bilirubin > travels to liver bound to albumin > conjugated bilirubin > water-soluble and excreted in bile > gut bacteria convert conjugated bilirubin into urobilinogen and stercobilinogen, which are excreted in the urine and stool.

121
Q

What is the pathophysiology of pre-hepatic jaundice?

A

Increased RBC destruction or dysfunction in bilirubin conjugation causes a rise in unconjugated (indirect) serum bilirubin

Referred to as prehepatic because the pathological process occurs before the liver metabolises the bilirubin.

122
Q

What is the pathophysiology of hepatocellular jaundice?

A

Damage to the structure and/or function of hepatocytes causes elevated conjugated (direct) bilirubin levels, which result in hepatocellular jaundice.

Conditions include infections, toxin, cancer, autoimmune conditions, and genetic conditions.

123
Q

What is the pathophysiology of cholestatic jaundice (post-hepatic jaundice)?

A

Obstruction of bile drainage causes elevated conjugated (direct) bilirubin levels.

Causes may be benign or malignant.

124
Q

What are some causes of pre-hepatic jaundice?

A

Haemolytic anaemia

Hereditary

  • Sickle cell anaemia
  • Thalassaemia

Acquired:

  • Cytomegalovirus, infectious mononucleosis (Epstein-Barr Virus), and toxoplasmosis infection

Autoimmune:

  • Rheumatic arthritis
  • Systemic lupus erythematosus
125
Q

What are the causes of hepatocellular jaundice?

A
  • Viral hepatitis A - E
  • HIV infection
  • ALD/NAFLD
  • Alcohol
  • HCC, lymphomas, liver mets
  • Gilbert’s syndrome
126
Q

What is Gibert’s syndrome?

A

Sometimes classified as pre-hepatic

An inherited condition caused by defect in the UGT1A1 gene > encodes hepatic conjugation enzyme uridine-diphosphoglucuronate glucuronosyltransferase (UGT enzyme) > underactive UGT enzyme

127
Q

What are the post-hepatic (cholestatic) causes of jaundice?

A
  • Choledocholithiasis (gallstones in common bile duct)
  • Postoperative stricture
  • Ascending cholangitis - an infection of the biliary tree, most commonly caused by obstruction
  • Pancreatic cancer
  • Metastases - liver mets can compress biliary tree
  • Lymphoma
128
Q

Define Wernicke-Kosarkoff syndrome

A

Two separate conditions that are closely associated.

They result from thiamine (B1) deficiency caused by excessive alcohol use

Wernicke’s encephalopathy comes before Kosarkoff’s syndrome (psychosis)

129
Q

What is Wernicke’s encephalopathy?

A

A neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations, typically involving mental status changes, gait and oculomotor dysfunction.

130
Q

What is Kosarkoff’s psychosis?

A

A late complication of Wernicke’s encephalopathy, characterised by anterograde and retrograde memory loss, disorientation and confabulation (false memories).

85% of patients with untreated WE develop Kosarkoff’s psychosis

131
Q

What are the signs and symptoms of Wernicke’s encephalopathy?

A
  • Confusion
  • Oculomotor disturbances (disturbances of eye movements)
  • Ataxia (difficulties with coordinated movements)
132
Q

What investigations/tests are used to diagnose Wernicke’s encephalopathy?

A
  • Evidence of long-term alcohol abuse: e.g. macrocytic anaemia, deranged LFTs and clotting
  • Therapeutic trial of parenteral thiamine - clinical response to treatment
  • Finger-prick glucose - normal
  • FBC - normal
  • Serum electrolytes - normal but may be abnormal if not treated or in late-presenting disease
133
Q

What is the treatment for Wernicke’s encephalopathy?

A

Acute:

  • Stabilisation/resuscitation
  • Thiamine
  • Magnesium
  • Multivitamins
  • Folic acid (B9)

For patients with chronic alcoholism and poor dietary intake - dietary thiamine supplement

134
Q

Define hepatic encephalopathy

A

A brain dysfunction caused by advanced liver dysfunction and portosystemic shunt (abnormal connection between the portal vascular system and systemic circulation, bypasses liver).

Liver dysfunction and portosystemic shunt cause a build-up of toxins (especially ammonia) in the blood.

135
Q

What is the pathophysiology of hepatic encephalopathy?

A

Ammonia is produced by intestinal bacteria when they break down proteins and is absorbed in the gut.

  1. Functional impairment of the liver cells in cirrhosis prevents the metabolism of ammonia into harmless waste products
  2. Collateral vessels between the portal and systemic circulation allow ammonia bypasses the liver altogether and enters the systemic system directly.
136
Q

What signs and symptoms might a patient with hepatic encephalopathy present with?

A

Acutely, it presents with reduced consciousness and confusion. It can present chronically with changes to personality, memory and mood.

137
Q

What are the precipitating factors that can lead to hepatic encephalopathy?

A

Precipitating Factors - factors that trigger the current problem and maintain the problem once established

  • Constipation
  • Electrolyte disturbance - particularly hypokalaemia
  • Infection
  • GI bleed
  • High protein diet
  • Medications (particularly sedative medications)
138
Q

What investigations/tests are used to diagnose hepatic encephalopathy?

A
  • LFTs- abnormal
  • Serum glucose - normal to rule out hyper-and hypoglycemia
  • Coagulation profile - increased prothrombin time
  • Serum electrolytes - hyponatremia and hypokalemia (which can precipitate HE)
139
Q

What is the treatment/management for hepatic encephalopathy?

A
  • Laxatives (i.e. lactulose) promote the excretion of ammonia before its absorbed by the gut. They may require enemas initially.
  • Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia.
  • Nutritional support. They may need nasogastric feeding.
140
Q

Define biliary colic

A

Intermittent right upper quadrant pain caused by gallstones irritating bile ducts

141
Q

Define cholestasis

A

Cholestasis: blockage to the flow of bile

142
Q

Define cholelithiasis

A

Cholelithiasis: presence of gallstone(s)

Gallstone disease (cholelithiasis) is highly prevalent, but most cases are asymptomatic

143
Q

Define choledocholithiasis

A

Choledocholithiasis: gallstone(s) in the common bile duct

144
Q

Define cholecystitis

A

Cholecystitis: inflammation of the gallbladder

145
Q

Define cholangitis

A

Cholangitis: inflammation of the bile ducts

146
Q

Define cholecystectomy

A

Cholecystectomy: surgical removal of the gallbladder

147
Q

Define cholecystostomy

A

Cholecystostomy: inserting a drain into the gallbladder

148
Q

What signs and symptoms might a patient with cholelithiasis present with?

A

Most cases are asymptomatic but can cause symptoms if a stone obstructs the cystic, bile, or pancreatic duct, preventing gallbladder drainage.

Typical symptom = biliary colic

Other symptoms include:

  • Severe, colicky epigastric or right upper quadrant pain
  • Pain triggered by meals (particularly high-fat meals)
  • Lasting between 30 minutes and 8 hours
  • Nausea and vomiting
149
Q

What complications can arise from cholelithiasis

A
  • Acute cholecystitis (inflammation of the gallbladder caused by stones blocking the cystic duct)
  • Acute cholangitis (inflammation of the bile duct caused by stones blocking bile drainage)
  • Obstructive jaundice - resulting from the stones blocking the ducts
  • Pancreatitis
150
Q

Why can fatty meals cause biliary colic in cholelithiasis (exam fodder!)?

A

Fat entering the digestive system causes cholecystokinin (CCK) secretion from the duodenum.

CCK triggers contraction of the gallbladder, which leads to biliary colic in the presence of gallstones

Patients with gallstones and biliary colic are advised to avoid fatty foods to prevent CCK release and gallbladder contraction.

151
Q

What signs and symptoms might a patient with acute cholecystitis present with?

A

Symptoms

  • RUQ pain
  • Nausea
  • Right shoulder pain

Signs

  • RUQ tenderness with or w/o Murphy’s sign (inspiratory arrest upon applying pressure to the RUQ)
  • Signs and symptoms of inflammation (fever, elevated WBC, ESR, CRP)
  • Palpable mass - distended, tender gallbladder
152
Q

What investigations/tests are used to diagnose acute cholecystitis?

A
  • 1st line: abdominal ultrasound - if the patient is not septic, confirms diagnosis
  • CT or MRI of the abdomen - if the patient septic
  • FBC - elevated WBC due to inflammation
  • CRP - elevated due to inflammation
  • Bilirubin - elevated
  • LFTs - elevated alkaline phosphatase (ALP), Alanine transaminase (ALT) and aspartate transaminase (AST)
153
Q

What investigation is used if the ultrasound scan does not detect stones in the cystic duct, but there is bile duct dilatation or raised bilirubin suggestive of obstruction?

A

Magnetic resonance cholangiopancreatography (MRCP) - MRI scan hat produces a detailed image of the biliary system.

It is very sensitive and specific for biliary tree diseases, such as stones in the bile duct and malignancy.

154
Q

What is the treatment/management for acute cholecystitis?

A

Severe acute cholecystitis:

  • ICU management, analgesia + fluid resuscitation
  • Antibiotics therapy
  • Percutaneous cholecystostomy for patients unsuitable for surgery (draining of fluid from the gallbladder)

Mild/moderate:

  • Analgesia
  • Fluid resuscitation
  • Antibiotic therapy (if patients are at risk of infection and sepsis)
  • Early laparoscopic cholecystectomy (i.e. keyhole surgery or percutaneous cholecystostomy
155
Q

What are some complications that can arise from acute cholecystitis and surgery?

A

Bile duct injury during surgery

Cholecystoenteric fistulas - can lead to small bowel obstruction if gallstone falls through into GI tract

156
Q

Define acute (ascending) cholangitis

A

Acute cholangitis, previously known as ascending cholangitis, is an infection of the biliary tree, most commonly caused by obstruction.

157
Q

What is the aetiology of acute cholangitis?

A

Most common:

  • Cholelithiasis leading to choledocholithiasis and biliary obstruction.
  • Iatrogenic biliary duct injury - via surgical injury during cholecystectomy > benign strictures > obstruction
158
Q

What is the pathophysiology of acute cholangitis?

A

Obstruction of the common bile duct causes inflammation, bacterial accumulation, and growth in the biliary tree, which initially leads to a less severe form of acute cholangitis.

Over time, as the obstruction progresses, the pressure in the bile duct continues to increase. This can cause the extravasation of bacteria into the bloodstream.

If untreated, then it can lead to sepsis - this is known as toxic cholangitis or cholangitis with sepsis - LIFE-THREATENING!

159
Q

What signs and symptoms might patients with acute cholangitis present with?

A
  • Charcot’s triad: fever (most common), RUQ abdominal pain, Jaundice
  • If more severe - Reynold’s pentad = Charcot’s triad with confusion and hypotension (evidence of sepsis)
160
Q

What are the investigations/tests to diagnose acute cholangitis?

A

First line: transabdominal ultrasound detects common bile duct dilatation and the presence of gallstones.

FBC: leukocytosis with neutrophilia

LFTs: obstructive jaundice with raised ALP > ALT, and bilirubin

U&Es: pre-renal acute kidney injury in sepsis

CRP raised

BLood culture - check for sepsis

161
Q

What is the treatment/management for acute cholangitis?

A
  • 1st line: ERCP (Endoscopic retrograde cholangiopancreatography) to help see where to insert stent + drainage stent
  • Aggressive fluid resuscitation
  • IV Abx → penicillins and aminoglycosides
  • Analgesia: opioids + paracetamol
  • Cholecystectomy when better
162
Q

Define primary biliary cholangitis

A

Progressive autoimmune destruction of the liver and biliary tree leading to fibrosis and eventually cirrhosis

163
Q

What is the aetiology of primary biliary cholangitis?

A

An autoimmune disease, autoantibodies against mitochondrial antigens (antimitochondrial antibodies - present in 95% of patients)

Mainly directed against pyruvate dehydrogenase complex E2 subunit (PDC-E2)

164
Q

What is the pathophysiology of primary biliary cholangitis?

A

Autoantibodies cause inflammation and the progressive destruction of the epithelial cells lining the small intrahepatic bile ducts

Progressive damage > liver fibrosis > eventually cirrhosis

End-stage disease = complete loss of small intrahepatic bile ducts.

165
Q

What are the risk factors for primary biliary cholangitis?

A
  • Female sex (F:M = 10:1)
  • Age between 45-60 years
  • Family history of PBC/autoimmune disease
  • Smoking
166
Q

What signs and symptoms might a patient with primary biliary cholangitis present with?

A

Classic presentation: middle-aged female with a significant itch, might have hx of hypercholesterolemia and fx
of autoimmune disease

Symptoms

  • Pruritus
  • Fatigue and weight loss
  • Dry eyes and dry mouth: Sjögren’s syndrome
  • Obstructive jaundice (late sign) - Pale stool and dark urine

Signs

  • Clubbing
  • Skin hyperpigmentation: due to increased melanin
  • Mild hepatosplenomegaly
  • Xanthelasma (yellow fat deposits under skin, commonly eyelid) (late sign)
  • Scleral icterus (late sign)
167
Q

What investigations/tests are used to diagnose primary biliary cholangitis?

A

Primary investigations:

  • Antimitochondrial antibodies (AMA): 95% of patients (highly specific)
  • Antinuclear antibodies (ANA): 50% of patients
  • LFTs: obstructive picture = raised ALP, gamma-glutamyl transferase (GGT) and bilirubin. AST and ALT may be mildly deranged
  • Coagulation profile: assess the synthetic function of the liver. Deranged in advanced disease
  • Transabdominal ultrasound: excludes other causes of cholestasis e.g. gallstones.
168
Q

What is the treatment/management for primary biliary cholangitis?

A

Early-stage disease:

First-line - Bile acid therapy using ursodeoxycholic acid to reduce cholestasis

Fat-soluble vitamin supplements - ADEK

Cholestyramine: bile acid sequestrant for symptomatic relief of pruritus

End-disease disease: liver transplant

169
Q

What are the possible complications that can arise from primary biliary cholangitis?

A
  • Hypercholesterolaemia
  • Osteoporosis
  • Portal hypertension secondary to cirrhosis
    long term
  • Hepatoma (or hepatocellular carcinoma)
170
Q

Define primary sclerosing cholangitis.

A

A condition where the intrahepatic or extrahepatic ducts become strictured (narrowed) and fibrotic (hardened).

This obstructs bile flow from the liver and into the intestines.

Sclerosis = stiffening and hardening of the bile ducts

Cholangitis = inflammation of the bile ducts

Chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis and cirrhosis (end-stage liver disease)

171
Q

What is the aetiology of primary sclerosing cholangitis?

A

Aetiology is not established yet, thought to be a combination between genetic, autoimmune, intestinal microbiome and environmental factors.

There is an established association with ulcerative colitis - around 70% patients with primary sclerosing cholangitis have UC

172
Q

What are the risk factors for primary sclerosing cholangitis?

A
  • Male
  • Aged 30-40
  • Ulcerative Colitis
  • Family History
173
Q

What signs and symptoms might a patient with primary sclerosing cholangitis present with?

A
  • Jaundice
  • Chronic right upper quadrant pain
  • Pruritus
  • Fatigue
  • Hepatomegaly
174
Q

What investigations/tests are used to diagnose primary sclerosing cholangitis?

A

GOLD STANDARD and diagnostic = magnetic resonance cholangiopancreatography (MRCP)

  • MRI scan of the liver, bile ducts and pancreas. > shows bile duct lesions or strictures (beaded appearance)

Autoantibodies - elevated:

  • Antineutrophil cytoplasmic antibody (p-ANCA) (~94%)
  • Antinuclear antibodies (ANA) (~77%)

LFTs - cholestatic picture (slowing of flow through bile ducts) - Alkaline phosphatase - deranged

Bilirubin levels - elevated

175
Q

Which group of patients screened for primary sclerosing cholangitis?

A

Patients with inflammatory bowel disorders

Heavily associated with ulcerative colitis - 70% patients with PSC has UC.

176
Q

What is the treatment/management plan for primary sclerosing cholangitis?

A

Liver transplant (around 80% survival at five years).

ERCP (Endoscopic Retrograde Cholangio-Pancreatography) can be used to dilate and stent any strictures

Cholestyramine - helps with pruritus

177
Q

What is Endoscopic Retrograde Cholangio-Pancreatography (ERCP)?

A

ERCP - a camera is inserted through the patient’s oesophagus to the duodenum (sphincter of Oddi and into the ampulla of Vater) > bile ducts

X-rays and injected contrasts can then identify any strictures and doctors can treat them

178
Q

What monitoring is carried out for patients with primary sclerosing cholangitis?

A

Patients are monitored for complications such as cholangiocarcinoma, cirrhosis and oesophageal varices

179
Q

What conditions are patients with primary sclerosing cholangitis predisposed to develop?

A

Predisposed to developing hepatocellular carcinoma, cholangiocarcinoma and colorectal cancer, fat-soluble vitamin deficency

180
Q

Define pancreatitis

A

Pancreatitis = inflammation of the pancreas

Two types:
Acute pancreatitis- after an episode, normal function usually returns.

Chronic pancreatitis - longer-term inflammation and symptoms with a progressive and permanent deterioration in pancreatic function.

181
Q

What are the causes of acute pancreatitis?

A

Most common causes:

  • Gallstones
  • Alcohol
  • Idiopathic

I GET SMASHED:

I – Idiopathic (~20%)
G – Gallstones (~40%)
E – Ethanol (alcohol consumption) (~30%)
T – Trauma
S – Steroids
M – Mumps
A – Autoimmune
S – Scorpion sting (the one everyone remembers)
H – Hyperlipidaemia
E – ERCP
D – Drugs (furosemide, thiazide diuretics and azathioprine)

182
Q

What are the causes of chronic pancreatitis?

A

Most common:

  • Excess alcohol ~70 - 80% cases
  • Idiopathic
183
Q

How can alcohol cause pancreatitis?

A

Alcohol is directly toxic to pancreatic cells, resulting in inflammation. Alcohol-induced pancreatitis is more common in men and younger patients.

184
Q

How can gallstones cause pancreatitis?

A
  • Pancreatitis can occur when gallstones become trapped at the ampulla of Vater (biliary-duodenal junction), blocking the flow of bile and pancreatic juice into the duodenum and causing reflux of bile into the pancreatic duct > inflammation of the pancreas
  • More common in women and older patients.
185
Q

What signs and symptoms might a patient with acute pancreatitis present with?

A

Symptoms

  • Severe epigastric pain - classically radiating through to the back
  • Associated vomiting
  • Systemically unwell (e.g., low-grade fever and tachycardia)
  • Poor urinary output

Signs

  • Abdominal tenderness
  • Abdominal distension
  • Tachycardic and/or hypotensive: patients may be in shock
186
Q

What signs and symptoms might a patient with chronic pancreatitis present with?

A
  • Severe epigastric pain (dull, radiating to back, 15-30 mins after eating, improves by leaning forward)
  • Steatorrhoea (increased fat in stool)
  • Weight loss and malnutrition
  • Symptoms of DMTII e.g. polydipsia, polyuria
  • Nausea + vomitting

Signs

  • Epigastric tenderness
  • Signs of liver disease (e.g. jaundice and ascites)
  • Diabetes mellitus/glucose intolerance
187
Q

What is the Glasgow Score?

A

The Glasgow Score is used to assess the severity of pancreatitis.

Each criterion below adds 1 point

P - PAO2 on room air <8 kPa
A -age >55 years
N - neutrophils, WCC >15 x 10⁹/L
C - calcium < 2mmol/L
R - renal, urea > 16.1 mmol/L
E - enzymes, lactate dehydrogenase
A - albumin <32 g/L
S - sugar, blood glucose >10.0 mmol/L

188
Q

Glasgow score: what scores indicate mild, moderate and severe pancreatitis?

A

0 or 1 – mild pancreatitis
2 – moderate pancreatitis
3 or more – severe pancreatitis

> 3 point = ITU

189
Q

What investigations are used to diagnose acute pancreatitis?

A

2 out of 3 can diagnose acute pancreatitis:

  • Amylase (x3 normal) or lipase elevated - more sensitive and specific than amylase (first line)
  • Clinical features are consistent with pancreatitis (e.g. epigastric pain radiating to back)
  • CT abdomen shows signs of acute pancreatitis (e.g. inflammation), not needed for diagnosis

Tests for the Glasgow score:

  • FBC (for white cell count)
  • U&E (for urea)
  • LFT (for transaminases and albumin)
  • Calcium
  • ABG (for PaO2 and blood glucose)
190
Q

What investigations are used to diagnose chronic pancreatitis?

A

CT or MRI abdomen is recommended first-line for the diagnosis - demonstrate pancreatic calcification and enlargement

191
Q

What is the management plan for acute pancreatitis?

A

Patients can rapidly deteriorate so immediate supportive management is needed

Moderate/severe cases = ITU/HDU

  • First-line: Initial resuscitation (ABCDE approach + IV fluids) - to combat insensible fluid loss, third-spacing
  • Nil by mouth (pancreas rest)
  • Analgesia with opates
  • Early nutritional support - e.g. oral/enteral feeding
  • Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)
  • Treatment of complications (e.g., endoscopic or percutaneous drainage of large collections)

Most patients will improve within 3-7 days.

192
Q

What is the management plan for chronic pancreatitis?

A
  • Pancreatic enzymes replacement (Creon) plus PPI
  • Alcohol and smoking cessation
  • Analgesia - OTC and weak opioid e.g. tramadol
  • Low-fat diet - 5 -6 small meals a day

A lack of enzymes leads to fat malabsorption, greasy stools (steatorrhoea), and deficiency in fat-soluble vitamins.

193
Q

What would happen if pancreatic enzyme replacements were not given to patients with chronic pancreatitis?

A

If untreated, a lack of pancreatic enzymes leads to fat malabsorption, greasy stools (steatorrhoea), and deficiency in fat-soluble vitamins.

194
Q

What complications can arise from acute pancreatitis?

A
  • Necrosis of the pancreas
  • Infection in a necrotic area
  • Abscess formation
  • Pseudocysts (collections of pancreatic juice)
  • Chronic pancreatitis
195
Q

What are the main complications that can arise from chronic pancreatitis?

A
  • Chronic epigastric pain
  • Loss of exocrine function > a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract
  • Loss of endocrine function > lack of insulin > diabetes
  • Damage and strictures to the duct system > obstructs the excretion of pancreatic juice and bile into the duodenum
  • Formation of pseudocysts or abscesses
196
Q

Define peritonitis

A

Inflammation of the peritoneal cavity

197
Q

What are the causes of peritonitis?

A

Primary:

  • Spontaneous bacterial peritonitis (SBP)
  • Ascites (secondary to liver cirrhosis)

Secondary - underlying case

  • Malignancy
  • Ruptured ectopic pregnancy
  • Perforated bowel
198
Q

Define spontaneous bacterial peritonitis

A

10% patient with ascites secondary to liver cirrhosis

When a bacterial infection develops in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).

199
Q

What bacteria most commonly causes SBP?

A

Gram-negative: Escherichia coli, Klebsiella pnuemoniae

Gram-positive cocci: staphylococcus and enterococcus

200
Q

What signs and symptoms might a patient with SBP present with?

A

Symptoms

  • Can be asymptomatic
  • Fever
  • Abdominal pain

Signs

  • Ileus (failure of peristalsis in GI tract)
  • Hypotension
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
201
Q

What is the investigation/tests are used to diagnose SBP?

A

Ascitic tap - extracting ascitic fluid for culture showing causative microorganism

Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)

Rule out as cause:

  • Pregnancy (hGH (human chorionic gonadotropin) test)
  • Bowel perforation (Abdo XR)
202
Q

What is the management plan for SBP?

A
  • IV resuscitation + ABCDE
  • IV Abx e.g. metronidazole, cefotaxime)
  • Surgery - peritoneal lavage which is surgical clean-out of the peritoneum
203
Q

What possible complications can arise from SBP?

A
  • Septicemia if not treated early
  • Pelvic abscesses
  • Ileus (lack of bowel contraction)
204
Q

Define haemochromatosis

A

Haemochromatosis is an autosomal recessive disorder where there is iron storage dysfunction that results in excessive total body iron and the deposition of iron in tissues.

205
Q

What is the aietology of haemochromatosis?

A

Haemochromatosis is most commonly caused by mutations in the human haemochromatosis protein (HFE) gene located on chromosome 6.

Genetic mutations are autosomal recessive.

This gene is essential in regulating iron metabolism.

206
Q

What are the risk factors for developing hemochromatosis?

A
  • Middle age
  • Male sex (presents later in females as menstrual cycle removes iron each month)
  • White ancestry
  • Family history
207
Q

What are the risk factors for developing haemochromatosis?

A
  • Middle age
  • Male sex (presents later in females as mensural cycle removes iron each month)
  • White ancestry
  • Family history
208
Q

What is the pathophysiology of haemochromatosis?

A

Low levels of iron regulatory hormone, hepcidin leads to unregulated duodenal absorption of iron > iron overload

209
Q

What signs and symptoms might a patient with haemochromatosis present with?

A

Usually presents after 40 when iron overload becomes symptomatic, presents later in women because menstruation removes iron:

  • Chronic tiredness
  • Joint pain
  • Skin hyperpigmentation (bronze/slate-grey discolouration)
  • Hair loss
  • Erectile dysfunction
  • Amenorrhoea (absence of menstruation)
  • Cognitive symptoms (memory and mood disturbance)
210
Q

What investigations/tests are used to diagnose haemochromatosis

A

First-line

  • Serum transferrin saturation (>50% male, 40% female)
  • Ferritin > 300 mg/L (male) or > 200 mg/L (female)
  • Serum iron raised
211
Q

What is the management plan for haemochromatosis?

A
  • Venesection (a weekly protocol of removing blood to decrease total iron)
  • Monitoring serum ferritin
  • Avoid alcohol
  • Genetic counselling
  • Monitoring and treatment of complications
212
Q

What are some complications that can arise from hemochromatosis?

A
  • Type 1 Diabetes (iron affects the functioning of the pancreas)
  • Liver Cirrhosis
  • Iron deposits in the pituitary and gonads lead to endocrine and sexual problems
    (hypogonadism, impotence, amenorrhea, infertility)
  • Cardiomyopathy (iron deposits in the heart)
  • Hepatocellular Carcinoma
  • Hypothyroidism (iron deposits in the thyroid)
  • Chondrocalcinosis/pseudogout (calcium deposits in joints) causing arthritis
213
Q

Define Wilson’s disease

A

Wilson’s disease is a rare, autosomal recessive disorder of copper accumulation and toxicity.

214
Q

What is the aetiology of Wilson’s disease?

A

It is caused by mutations in the ATP7B gene on chromosome 13, resulting in dysfunction in ATP-mediated hepatocyte copper transport.

215
Q

What is the pathophysioogy of WIlson’s disease?

A

The mutation in the ATP7B gene causes dysfunction in ATP-mediated hepatocyte copper transport.

Copper is not transported into bile and
combined with ceruloplasmin (copper carrier protein) > reduced biliary excretion

Therefore, copper accumulation in hepatocytes and leakage into the serum

Increased free serum copper > toxic accumulation tissues including basal ganglia, kidney, and cornea, causing oxidative damage.

216
Q

What signs and symptoms might a patient with Wilson’s disease present with?

A

Patients are usually young and will present with a range of neuropsychiatric and liver disease signs and symptoms:

Neurological

  • Behavioural and psychiatric issues: such as depression and delusions, often the first presentation
  • Parkinsonism: half of patients present with a tremor
  • Asterixis (abnormal movement)

Hepatic

  • Hepatosplenomegaly
  • Hepatitis and cirrhosis
  • Jaundice
  • Ascites
  • Asterixis and encephalopathy

Also, Kayser-Fleischer rings present in the cornea - a a hallmark of Wilson’s disease

217
Q

What investigations/tests are used to diagnose Wilson’s disease?

A

Usually diagnosed from clinical presentation.

1st line

Copper studies:

  • Reduced ceruloplasmin levels AND Increased 24-hour urinary copper excretion highly suggestive of WD
  • Increased free serum copper but reduced total serum copper.
  • LFTs: deranged with increased AST and ALT due to hepatitis
218
Q

What is the management plan for Wilson’s disease?

A

1st line: copper chelation, chelators bind copper and facilitate renal excretion. E.g. D-penicillamine

Lifestyle advice: high copper-content foods such as shellfish should be avoided.

Liver transplantation: indicated in acute liver failure or decompensated cirrhosis

219
Q

What are some complications that can arise from Wilson’s disease?

A

Liver failure - may need transplantation.

Renal failure: often due to D-penicillamine therapy rather than the disease itself

220
Q

Define alpha-1 antitrypsin deficiency

A

Alpha-1-antitrypsin (A1AT) deficiency is a condition caused by an abnormality in the gene for a protease inhibitor called alpha-1-antitrypsin.

221
Q

What is the aetiology of A1AT deficiency?

A

A1AT is coded for on chromosome 14. In A1AT deficiency, there is an autosomal recessive mutation in the gene for A1AT.

A1AT is produced by the liver and is a protease inhibitor of elastase. Elastase is an enzyme that digests connective tissue, secreted by neutrophils.

A lack of A1AT = elastase-mediated damage, particularly in the lungs

222
Q

What is the pathophysiology of A1AT deficiency?

A

The liver and the lungs are mainly affected by A1AT deficiency.

Liver:

  • Normal A1AT made in the liver
  • In A1AT deficiency, mutated version produced and accumulates in the liver > liver damage > cirrhosis after 50 > can lead to HCC

Lungs:

Absence of functioning alpha-1-antitrypsin protein > an excess of elastase that attacks connective tissue in the lungs > bronchiectasis (bronchial widening causing excess mucus accumulation) and emphysema after 30 years old

223
Q

What signs and symptoms might a patient with A1AT deficiency present with?

A

COPD-like symptoms:

  • Chronic productive cough (productive of spetum)
  • Shortness of breath on exertion
  • Current cigarette smoker (common for smokers aged 32 -41 to present with symptoms)
  • Wheezing
  • Chest hyperinflation
224
Q

What are the investigations/tests used to diagnose A1AT deficiency?

A
  • Gold standard: serum-alpha 1-antitrypsin levels - low
  • Liver biopsy - cirrhosis and staining shows mutant A1AT proteins in hepatocytes
  • Genetic testing for the A1AT gene
  • High-resolution CT thorax diagnoses bronchiectasis and emphysema.
225
Q

What is the management plan for A1AT deficiency?

A

Not curable

  • Stop smoking (smoking dramatically accelerates emphysema)
  • Treat COPD with short and long-acting bronchodilators, and inhaled corticosteroids
  • Patients with very low A1AT levels and respiratory disease start on IV A1AT therapy
  • Organ transplant for end-stage liver or lung disease
  • Monitoring for complications (e.g. hepatocellular carcinoma)
226
Q

Describe ALT/AST ratios and what they mean.

A

The AST/ALT ratio can be used to determine the likely cause of LFT derangement:

ALT > AST is associated with chronic liver disease

AST > ALT is associated with cirrhosis and acute alcoholic hepatitis

Sharon's Phase 2a Medicine Revision (10 decks)

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