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Phase 2a Gold Standard > Liver > Flashcards

Liver Flashcards

1
Q

What organs are retroperitoneal

A

SAD PUCKER
S - Suprarenal (adrenal) glands
A - Aorta
D - Duodenum

P - Pancreas
U - Ureter
C - Colon (descending, ascending)
K - Kidneys
E - Oesophagus (lower 2/3)
R - Rectum

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2
Q

Functions of the liver

A
  • Protein synthesis (albumin, clotting factors)
  • Glucose and fat metabolism
  • Defence against infection (reticuloendothelial system)
  • Detoxification and excretion (ammonia, bilirubin, drugs/hormones)
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3
Q

Describe the blood flow around the liver

A

Blood enters via hepatic artery (oxygenated blood) and portal vein (deoxygenated blood from intestine containing nutrients), which lie together in lobules with a bile duct. Blood flows into sinusoids, bathing liver cells, before exiting via central hepatic vein. Liver cells within lobule can be divided into zones 1 to 3, receiving progressively less oxygenated blood

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4
Q

End points of liver injury (in acute and chronic)

A

Acute
- Recovery
- Liver failure
- Progression to Chronic

Chronic
- Recovery
- Cirrhosis
- Liver failure
- Varices
- Hepatoma

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5
Q

What are cellular consequences of acute and chronic liver failure

A

Acute - damage to and loss of cells, causing necrosis or apoptosis

Chronic - Fibrosis (called cirrhosis when severe)

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6
Q

Define cholestasis

A

Any condition where bile flow is blocked

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7
Q

What tests are used to assess liver function? (7)

A
  • AST
  • ALT
  • ALP
  • GGT
  • Bilirubin
  • Albumin
  • Prothrombin time (and INR)
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8
Q

What do the LFTs help distinguish

A

AST, ALT, ALP, GGT differentiate hepatocellular damage (AST, ALT) and cholestasis (ALP, GGT)

Bilirubin, albumin, PT assess liver’s synthetic function

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9
Q

What does ALT stand for and show

A

alanine transaminase

Marker of hepatocellular damage; found in high concentrations within hepatocytes

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10
Q

What does ALP stand for and show

A

Alkaline phosphatase

Particularly concentrated in liver, bone and bile ducts. Shows liver pathology in response to cholestasis.

Also raised in bone pathology especially pagets and bone cancer

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11
Q

What does GGT stand for and show?

A

gamma glutamyl transferase

Raised GGT suggests biliary epithelial damage and bile flow obstruction. Can be used with ALP to suggest cholestasis.

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12
Q

How are ALT and ALP compared to find pathology

A

> 10x ALT, <3x ALP suggests predominantly hepatocellular injury

<10x ALT, >3x ALP suggests cholestasis

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13
Q

How is the AST/ALT Ratio used?

A

AST/ALT ratio
- ALT>AST - Chronic liver disease
- AST>ALT - Acute alcoholic hepatitis or cirrhosis

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14
Q

What blood test is a marker of pancreatitis

A

Serum amylase and lipase.

Lipase has a longer half life and is more specific, but takes longer to show as raised.

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15
Q

Define acute liver failure with 3 characteristic signs

A

Severe acute liver injury with impaired function and altered mental status in patient WITHOUT existing liver disease or cirrhosis

Jaundice
Coagulopathy (INR>1.5!!!!)
Hepatic encephalopathy

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16
Q

Causes of Acute Liver Failure

A

Drugs
- Paracetamol overdose
- Isonazid
- Alcohol

Infection
- Hepatitis A and B
- EBV
- CMV
- Herpes simplex virus

Vascular
- Veno-occlusive disease
- Budd-Chiari syndrome

  • Autoimmune hepatitis
  • Metabolic conditions (Wilson’s)
  • Cancer
  • Fatty liver of pregnancy
  • PBC/PSC
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17
Q

Pathophysiology of acute liver failure

A

Depends on underlying cause
- Massive hepatocyte necrosis/apoptosis.
- Causes jaundice, coagulopathy (INR>1.5), hepatic encephalopathy (ammonia builds up in blood, travels to brain, clearance causes cerebral oedema)
- HE usually within 8-28 days of noticing jaundice but can be up to 28

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18
Q

Grading system for Hepatic Encephalopathy

A

West Haven criteria
1 - Change in behaviour with minimal change in consciousness
2 - Gross disorientation, drowsiness, asterixis, inappropriate behaviour
3 - Marked confusion, speech problems, incoherent speech, rousable to verbal stimuli
4 - Comatose, no response to stimuli

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19
Q

Signs/symptoms of Acute liver failure

A
  • Jaundice
  • Coagulopathy
  • Hepatic Encephalopathy

Nausea, confusion, asterixis, abdominal pain

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20
Q

Investigations in Acute liver failure

A
  • Serum bilirubin (high), albumin (low), prothrombin time/INR (raised)
  • Serum transaminases (AST/ALT) suggest hepatocellular pathology

Others (to find cause)
- Abdominal US with dopper can be used to find vaso-occlusion
- ABG/paracetamol levels may indicate paracetamol overdose
- Blood culture to rule out infection
- EEG to grade HE
- Coagulation
- Lipase/amylase
- Serum ammonia

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21
Q

Management of acute liver failure

A

Raise head of bed, tracheal intubation and NG tube

Treat underlying cause/complications: - intracranial pressure - Mannitol IV
HE - Lactulose (NH3+ excretion)
Haemorrhage/bleeding (vit k)
Paracetamol overdose - N acetylcysteine

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22
Q

Complications of acute liver failure

A

Progression to chronic (Ascites, varices, oedema)
Bleeding
Hepatic Encephalopathy (confusion, coma, mood/behaviour change)

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23
Q

Pathophysiology of paracetamol overdose

A
  • Paracetamol usually metabolised by liver, but small amount metabolised by cytochrome P450 system
  • Toxic intermediate of p450 pathway (N-acetyl-p-benzoquinone imine (NAPQI)) is normally detoxified by conjugation with glutathione, when all glutathione used up, toxic intermediate remains and damages hepatocytes.
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24
Q

Treatment of paracetamol overdose

A
  • N-acetylcysteine (replenishes glutathione stores, which bind to NAPQI)

or
- Activated charcoal if patient presents within 1 hour of ingestion

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25
Q

Define chronic liver failure

A

Repeated liver insults over at least 6 months causing progressive liver dysfunction, resulting in inflammation, fibrosis and cirrhosis.

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26
Q

Causes of chronic liver failure

A
  • Alcohol (ALD)
  • Viral (Hepatitis B,C)
  • Inherited causes (A1 antitrypsin deficiency, Wilson’s, hereditary haemochromatosis)
  • Autoimmune hepatitis
  • PBC/PSC
  • Budd-Chiari syndrome
  • NAFLD
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27
Q

Pathophysiology of chronic liver disease

A

Repeat injury over time cause inflammation (hepatitis) -> fatty deposits (steatosis) -> scarring (fibrosis).

Normal liver replaced by fibrotic tissue and regenerative nodules.

Can be compensated (asymptomatic) or decompensated

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28
Q

Pathophysiology of chronic liver disease

A

Repeat injury over time cause inflammation (hepatitis) -> fatty deposits (steatosis) -> fibrosis/cirrhosis (normal hepatic tissue replaced by fibrotic tissue and regenerative nodules).

Liver cirrhosis can be compensated (asymptomatic, normal function) or decompensated (multiple complications/dysfunctions of liver)

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29
Q

Signs of decompensated liver disease

A
  • Coagulopathy
  • Jaundice
  • Encephalopathy
  • Ascites
  • GI bleeding
  • Varices
  • Easy bruising
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30
Q

Chronic liver disease signs and symptoms (8)

A
  • Spider naevi
  • Splenomegaly
  • Caput medusae (distended paraumbilical veins due to portal HTN)
  • Dupuytren’s contracture (thickening of palmar fascia, causing fixed flexion of MCP)
  • Ascites
  • Palmar erythema
  • Gynaecomastia and testicular atrophy
  • Asterixis (flapping tremor)
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31
Q

Investigations in chronic liver disease

A

Same as acute
- LFT AST ALT Raised (ALT>AST - Chronic liver disease)

  • Ultrasound
  • CT more detailed, good for secondary findings (MRI best, but most expensive)
  • Liver biopsy to check extent of CLD
  • Ascitic tap
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32
Q

Management of Chronic liver disease

A

Treat underlying pathology and complications

HE - Lactulose

Ascites - Aldosterone antagonist (Spironolactone)

GI bleed (beta blocker to reduce portal HTN, Endoscopic variceal band litigation)

SBP - Antibiotics

Prevent further disease by reducing risk factor

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33
Q

What are the 2 types of liver cirrhosis

A

Micronodular
- <3mm with uniform involvement of liver (alcohol or biliary disease cause)

Macronodular
- Varying sizes, normal acini, can be seen in larger nodules
- Caused by viral hepatitis

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34
Q

Define liver cirrhosis

A

Final stage of any liver disease. Normal liver architecture converted to regenerative nodules, separated by fibrous septa, with a loss of lobular architecture

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35
Q

Characteristic biopsy findings of cirrhotic liver

A

Regenerating nodules
Wide fibrous septa
Loss of lobular architecture

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36
Q

What is the cell behind liver cirrhosis and how does it do this?

A

Apoptosis/necrosis activates stellate cells, which release cytokines that attract neutrophils and macrophages, causing further inflammation and fibrosis. Stellate cells become myofibroblasts which lead to collagen deposition.

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37
Q

Signs/symptoms of liver cirrhosis (10)

A
  • Jaundice
  • Hepatomegaly
  • Splenomegaly
  • Spider naevi
  • Palmar erythema
  • Clubbing
  • Ascites
  • Leuconychia (hypoalbuminemia)
  • Xanthelasma (cholesterol deposits around eyes)
  • Caput medusae (cluster of swollen veins in abdomen)
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38
Q

What will ultrasound and MRI show in cirrhosis

A

US - Hepatomegaly, splenomegaly, ascites

MRI - Increased caudate lobe size, right posterior hepatic notch suggests alcoholic pathology

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39
Q

Treatment of pruritus

A

Colestyramine

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40
Q

Lifestyle advice in liver cirrhosis

A

Alcohol abstinence
Avoid NSAID
Good nutrition
Exercise

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41
Q

Complications of liver cirrhosis

A
  • Coagulopathy
  • Encephalopathy
  • Hypoalbuminaemia (Oedema/Ascites)
  • HCC!!!
  • AKI
  • SBP
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42
Q

What scoring systems are used in cirrhosis

A

Child-Pugh score (Encephalopathy, Ascites, Bilirubin/Albumin, INR) (severity of long term disease)
MELD score (model for end stage liver disease, indicator for transplant necessity)

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43
Q

Alcohol units calculation

A

(Alcohol by volume * vol(mL)) / 1000

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44
Q

Define alcoholic liver disease

A

3 stage liver disease caused by excessive alcohol drinking. Leads to steatosis, hepatitis and eventually cirrhosis.

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45
Q

Pathophysiology of Alcoholic liver disease

A

Alcohol is metabolised in the liver to acetaldehyde by 3 pathways (alcohol dehydrogenase, CYP2E1, Catalase). This causes an increase in NADH, whilst decreasing NAD+, so more fatty acid synthesis occurs, but less oxidation ∴ hepatic fatty acids accumulate (steatosis - reversible).

CYP2E1 pathway generates free radicals which can damage hepatic DNA and proteins.

Acetaldehyde binds to liver macromolecules, forming adducts. These are attacked by immune system causing inflammation and hepatomegaly (hepatitis - reversible). Mallory bodies and giant mitochondria are visible histologically.
Damaged liver leaks AST/ALT

As cells die, scarring occurs around central vein of liver (perivenular fibrosis). This causes irreversible cirrhosis

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46
Q

Signs/symptoms of Alcoholic liver disease

A

Early stages- little/no symptoms, worse as time goes on.

Chronic liver failure + alcohol dependency/withdrawal symptoms as time goes on.

  • Hepatomegaly
  • Abdominal pain
  • Dupuytren’s contracture
  • Asterixis
  • Palmar erythema
  • Clubbing
  • Spider naevi
  • Hepatic encephalopahty
  • Caput medusae
  • Easy bruising
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47
Q

Signs of liver failure on hands

A
  • Dupuytren’s contracture (fingers bend towards palm)
  • Clubbing
  • Palmar erythema
  • Asterixis
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48
Q

Name as many signs of liver failure as possible

A
  • Hepatomegaly
  • Abdominal pain
  • Dupuytren’s contracture
  • Asterixis
  • Palmar erythema
  • Clubbing
  • Spider naevi
  • Hepatic encephalopahty
  • Caput medusae
  • Bruising
  • Pruritus
  • Weight loss
  • Fever (cirrhosis)
  • Haematemesis
  • Splenomegaly
  • Jaundice
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49
Q

Investigations in alcoholic liver disease

A

AST/ALT - high due to leakage from damaged liver

Ultrasound or CT - fatty liver

Liver biopsy - Grade fibrosis. Would see mallory bodies, neutrophil infiltrates, giant macrophages, increased fat cells, necrosis etc.

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50
Q

Management of Alcoholic liver disease

A

1st - Stop alcohol intake. Join support groups, take Chlordiazepoxide (benzodiazepine) - aids alcohol withdrawal
- Give vitamin B1 (thiamine) IV. Prevent Wernicke’s Encephalopathy and Korsakoff’s syndrome. (confusion, oculomotor disturbance, memory impairment, behaviour change)

  • Short term steroids for hepatitis

Lifestyle advice
- Lose weight
- Stop smoking
- Increase vit K and B1
- High protein diet

  • Liver transplant if severe
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51
Q

Severe complication of alcohol withdrawal with treatment

A

Delirium Tremens (delusions, hallucinations, tremor, tachycardia, ataxia, arrhythmia). Lorazepam used to treat (rapid acting benzodiazepine)

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52
Q

What can long term alcohol usage cause. How is this caused and how is it treated

A

Thiamine (vit B1) is poorly absorbed in presence of alcohol. Can cause Wernicke’s Encephalopathy or Wernicke-Korsakoff syndrome

IV thiamine is therefore needed in patients with alcoholism

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53
Q

Complications of alcoholic liver disease

A

Pancreatitis
Ascites
HCC
Wernicke Korsakoff syndrome
Hepatic encephalopathy

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54
Q

Define Wernickes encephalopathy

A

Thiamine (vitamin b1) deficiency causing a neurological emergency

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55
Q

Pathophysiology of Wernickes encephalopathy

And what happens if brainstem, cerebellum, medulla affected

A

Alcohol abuse inhibits thiamine;
- Blocks phosphorylation of thiamine
- Reduces gene expression for thiamine transporter 1
- Fatty liver prevents thiamine storage.

Causes haemorrhage and necrosis of mammillary bodies of limbic system (memory)

Deficiency impairs glucose glucose metabolism.
- In brainstem, face/eyes affected
- In cerebellum, movement/ balance
- In medulla, heartrate/breathing

Wernicke’s is acute and reversible, but can progress to chronic, irreversible Wernicke-Korsakoff syndrome.

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56
Q

Signs/symptoms of Wernickes/Korsakoff syndromes

A

Wernicke’s - Ophthalmoplegia, nystagmus (rapid side to side eye movements), Ataxia/unsteady gait, confusion, apathy, arrhythmia

Korsakoff - Limbic system (memory) impairment
- Anterograde and retrograde amnesia
- Confabulation (stories to fill gaps in memory which they believe)
- Behavioural changes

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57
Q

Treatment and complications of Wernickes/Korsakoffs

A

Treatment - IV thiamine, given with glucose if hypoglycaemic. Thiamine first as without thiamine pyrophosphatase, glucose becomes lactic acid -> metabolic acidosis

Complications
- Metabolic acidosis
- Seizures
- Spastic paraparesis
- Coma
- Death

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58
Q

NAFLD Definition with causes

A

Non Alcoholic Fatty Liver disease. Deposition of fat in liver that cannot be attributed to alcohol or viral cause.

Steatosis > Steatohepatitis > Fibrosis > Cirrhosis

Caused by insulin resistance and Metabolic syndrome
- Diabetes
- HTN
- Obesity
- Hyperlipidaemia

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59
Q

NAFLD pathophysiology

A
  • Insulin resistance means receptors on hepatocytes become less responsive. Liver increases fat storage and decreases fatty acid oxidation. Fat droplets form in hepatocytes, swelling hepatocytes. Liver appears large, soft, yellow, fat, greasy (Steatosis)
  • Unsaturated fatty acids vulnerable to free radicals, causing fatty acid radical formation, which damage lipid membrane causing inflammation (Steatohepatitis)
  • Stellate cells lay down fibrous tissue (fibrosis), when architecture changes this becomes cirrhosis.
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60
Q

NAFLD signs/symptoms and investigations

A

Usually asymptomatic and found by accident. To be suspected in T2DM, obese, deranged LFT.

Signs of liver failure if severe.

LFT - Deranged LFT. (ALT>AST, high bilirubin)
FBC - anaemia, low platelets)
USS/MRI - show enlarged fatty liver.
Liver biopsy GOLD

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61
Q

Management of NAFLD

A

1st - Diet and exercise to reduce risk factor
Vitamin E supplements (Vit E clears free radicals)

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62
Q

How does Liver failure cause it’s signs

A
  • Coagulopathy (reducing clotting factor synthesis)
  • Jaundice (impaired breakdown of bilirubin)
  • Encephalopathy (poor detoxification of harmful substances)
  • Ascites (poor albumin synthesis and increased portal pressure due to scarring)
  • Gastrointestinal bleeding (increase portal pressure causing varices)
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63
Q

Hepatic encephalopathy definition and pathophysiology

A

Liver failure as a result of decompensated chronic liver disease.

Ammonia is a by product of gut bacteria, and is cleared by liver. Ammonia builds and goes to brain. Ammonia is neurotoxic. Astrocytes attempt to clear ammonia but cause a build up in glutamine, causing an osmotic shift of fluid into cells -> Oedema -> brain damage.

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64
Q

Signs/symptoms of hepatic encephalopathy

A

Mood - Euphoria, depression, anxiety, confusion
Sleep - Insomnia, hypersomnia
Motor disturbance - Asterixis, ataxia, bradykinesia, hypokinesia, tremor

Can lead to coma, hyperreflexia, nystagmus

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65
Q

Investigations and treatment of hepatic encephalopathy

A

EEG
Serum ammonia
Head CT or MRI
Other investigations to check liver disease/ rule out neuro pathology

Supportive (IV fluid)
Lactulose (remove ammonia)
Rifaxamin (antibiotic) - prophylaxis

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66
Q

Define jaundice with 3 types

A

Raised serum bilirubin causing yellowing of skin and eyes. AKA icterus.

Pre hepatic - Increased unconjugated bilirubin, usually due to increased haemolysis.
- Normal urine and stools

Hepatic - Uncon/conjugated bilirubin. Pathology of liver means hepatocytes cant take up, metabolise or excrete bilirubin.
- Dark/normal urine, normal stools

Post hepatic - Conjugated bilirubin. Due to obstruction in biliary system.
- Dark urine, pale stools.

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67
Q

Why is urine darkened and why are stools paled as more bilirubin becomes conjugated?

A

Conjugated bilirubin can be excreted in urine (water soluble), unconjugated can’t. Hence, dark urine in post hepatic (conjugated bilirubin) or intrahepatic (mixed), but normal in pre hepatic (unconjugated)

In an obstructive jaundice, less stercobilin (which normally gives it colour) goes into GI tract and stools, so they go pale.

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68
Q

Causes of pre hepatic jaundice

A

Due to increased haemolysis.

  • Sickle cell
  • G6PD deficiency
  • Hereditary spherocytosis
  • Thalassaemia
  • Malaria
  • Autoimmune haemolytic anaemia
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69
Q

Causes of hepatic jaundice

A

HCC
ALD/NAFLD
Hepatitis
Hepatotoxic drugs (rifampicin)
Gilbert syndrome

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70
Q

Causes of post hepatic jaundice

A

Biliary tree pathology/obstruction

  • Pancreatic cancer
  • Cholelithiasis
  • PBC/PSC
  • Cholangiocarcinoma
  • Drug induced cholestasis
  • Pancreatitis
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71
Q

What symptoms usually accompany jaundice?

A

Itching!

Dark urine/pale stools if obstructive
Abdominal pain
Fatigue

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72
Q

Investigations in jaundice

A

1st line imaging: Abdominal ultrasound.
- LFT
- Urine bilirubin (- normally, high in dark urine) and urobilinogen (normally +ve, high in haemolysis, low in intra/post hepatic causes)

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73
Q

What is neonatal jaundice? + Complication of it

A

Normal. Fetal RBCs break down easily, releasing lots of unconjugated bilirubin. Resolves in 10 days. If not, can cause Kernicterus (brain damage due to raised bilirubin)

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74
Q

Define Ascites

A

Accumulation of free fluid in peritoneal cavity. (Up to 20ml normal in women). Causes are transudative (raised portal pressure causing ultrafiltration of plasma) or exudative (normal portal pressure, usually inflammatory process causing leakage of whole plasma contents (proteins/cells))

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75
Q

Exudate vs Transudate

A

Exudate - Inflammatory fluid release, due to changes in capillary permeability

  • High protein
  • Coagulates
  • Contains inflammatory cells

Transudate - Non inflammatory (pressure gradients)

  • Low protein
  • Doesn’t coagulate
  • No inflammatory cells
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76
Q

Causes of ascites

A

Causes of portal HTN (transudate)
- Cirrhosis (MOST COMMON)
- Portal vein thrombosis
- Sarcoidosis
- Schistosomiasis
- Budd-Chiari syndrome
- Constrictive pericarditis
- Hypoalbuminaemia (low protein in blood, less fluid pulled into vessel)
- Nephrotic syndrome

Exudate
- Cancer
- Sepsis
- TB
- Nephrotic syndrome
- Bowel obstruction
- Pancreatitis
- Myxoedema

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77
Q

Signs/symptoms of ascites

A
  • Abdominal swelling
  • Distended abdomen
  • Shifting percussive dullness
  • Fullness/fluid in flanks
  • Respiratory distress
  • Peripheral oedema
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78
Q

Signs on examination of ascites

A

Abdominal distension, shifting percussive dullness, fluid in flanks

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79
Q

How is ascites examination done

A

Percuss centrally -> laterally until dull sound. Keep finger at dull spot and have patient turn. If the dullness is due to fluid, dullness will have moved.

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80
Q

Investigations of ascites

A

1) Percussion/examination
2) Serum ascites, albumin gradient
- High SAAG - Transudate (high portal pressure)
- Low SAAG - Exudate (low portal pressure)
3) Abdominal ultrasound GOLD
4) Paracentesis/Ascitic tap - Fluid aspiration to send for microbiology etc

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81
Q

Management and main complication of ascites

A

Treat underlying cause (cirrhosis, heart failure etc)
- Spironolactone (diuretic)
- Paracentesis (fluid drainage)

Low sodium diet.
Ciprofloxacin as prophylaxis for SBP

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82
Q

Main possible complication of ascites

A

Spontaneous Bacterial Peritonitis (SBP)
- Infection of ascitic fluid and peritoneal lining. This is why fluid sent to microbiology

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83
Q

The types of viral hepatitis, RNA or DNA

A

Hep A - RNA, no envelope, acute
Hep B - DNA, enveloped
Hep C - RNA, enveloped
Hep D - RNA enveloped
Hep E - RNA no envelope

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84
Q

What Hep viruses are acute and what are chronic

A

Hep A - Acute
Hep B, C, D- Acute and Chronic
Hep E - Mainly acute, but can progress to chronic in immunosuppression

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85
Q

Modes of transmission for Hep viruses

A

A - Faeco-oral
B - Body fluids and blood
C - Blood
D - Body fluids and blood (only in those with Hep B)
E - Faeco-oral

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86
Q

Define Hepatitis A with epidemiology

A

Infection of liver, by non-enveloped single-stranded RNA virus of Picornavirus (Picornaviridae) family.

It is a notifiable disease with faeco-oral transmission and is endemic in areas with poor sanitation. Travel history to Africa or South America is usually key,

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87
Q

Pathophysiology of HAV

A

Replicates in liver and then is excreted in bile and faeces for ~2 weeks before onset of symptoms. Incubation period of 2-6 weeks. 4 phases:
1. Incubation period 2-6 weeks (usually 28-30 days)
2. Prodromal phase: Early disease, mild symptoms
3. Icteric phase- JAUNDICE + more severe symptoms. Most infectious right before jaundice onset.
4. Covalescent: Self limiting recovery, resulting in 100% immunity.

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88
Q

Signs/symptoms of HAV

A

Prodromal phase;
- Flu like. Fatigue, malaise, weakness, vomiting.

Icteric phase:
- Jaundice
- Rash
- Diarrhoea
- Dark urine/pale stools
- Hepatosplenomegaly

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89
Q

Investigations of HAV

A

ALT/AST high (ALT>AST)
Bilirubin high

Serology
- HAV IgM positive soon after symptoms develop and remains detectable for a few months. HAV IgG becomes positive 5-10 days after symptoms and is detectable lifelong.
- +IgM, +IgG = Acute Hep A
- -IgM, +IgG = Past infection or vaccination

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90
Q

Management of HAV

A

Disease management is supportive
All infectious hepatitis must be notified to UK Health Security Agency (UKHSA - Previously Public Health England)

Prophylactic Hep A vaccine if
- Travel to endemic area
- Chronic liver disease
- IV drug use
- Sexual MSM
Vaccine is inactivated viral vaccine.

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91
Q

Define Hepatitis B virus with mode of transmission and epidemiology

A

Enveloped dsDNA virus belonging to Hepadnaviridae family, can cause acute or chronic infection. Mode of transmission is through blood/bodily fluids;
- Unprotected sex
- Sharing needles/needlestick injury
- Perinatally
- Semen/saliva

Worldwide health problem

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92
Q

Hepatitis B protein products

A

HBsAg - Surface antigen on outer envelope. +ve in active infection. Takes up to 6 months to clear (carrier status until), and is replaced with HBsAb after.

HBeAg - Hep B ‘E’ Antigen secreted by infected cells. Marker of active replication and infection, increased E = Increased viral load/infectivity.

HbcAg - Hep B Core Antigen found on nucleocapsid in virus core. IgM antibodies of core antigen imply active infection. IgG imply past infection.

DNA polymerase and X protein also present

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93
Q

Hepatitis B antibodies

A

HBsAb - Surface antigen antibody. +ve in immunity (past infection or vaccination)

HBeAb - +ve, active disease phase over.

IgM HBcAb - Active acute infection (Decreases in chronic)

IgG HBcAb - +ve with +ve surface antigen = Active Chronic Infection
+ve with -ve surface antigen = Past infection

(Vaccination doesnt form defence against HbC)

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94
Q

Hep B pathophysiology

A

HBV enters hepatocytes, removes outer envelope and forms covalently closed circular DNA. cccDNA template for HBV proteins.

Usually (70%) subclinical with anicteric symptoms.
30% likely to go icteric.
Usually self limiting but can progress to chronic if HBsAg lingers >6 months (carrier status).

Chronic > Cirrhosis > HCC

  • Most cases in children go chronic. NEED TRANSPLANT
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95
Q

Extra hepatic manifestations of HBV

A

Polyarteritis nodosa, glomerulonephritis, papular acrodermatitis

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96
Q

Signs/symptoms of HBV

A

Acute
- Subclinical: Asymptomatic
- Anicteric - Malaise, anorexia, fever, nausea, vomiting, RUQ pain, rash, vomit
- Icteric - Same with athralgia, jaundice, urticaria

Chronic - May mimic acute
- Cirrhosis: hepatosplenomegaly, portal HTN
- Decompensated cirrhosis - ascites, encephalopathy, coagulopathy, GI bleed

97
Q

Serology of HBV
Acute infection
Chronic infection
Carrier
Cleared
Vaccinated
High/low viral load

A

Acute - HBsAg and IgM HBcAb
Chronic - HBsAg and IgG HBcAb
Carrier - HBsAg +/- and IgG HBcAb
Cleared - HBsAb and IgG HBcAb
Vaccinated - HBsAb (vaccination doesnt protect against HBcAb)
High/low viral load - Increased/low HBe

98
Q

Management of HBV

A

Acute - supportive; self limiting. Manage complications. HBV Ig

Chronic - Avoid alcohol. Manage cirrhosis, transplant may be needed.
- Antiviral: Nucleotide analogues
- PEGylated interferon (has side effects of haemolytic anaemia, anxiety)

HBV vaccination in 6 in 1 for babies.

99
Q

Complications of HBV

A

Fulminant liver failure
Cirrhosis
Decompensated cirrhosis/liver disease
HCC

100
Q

Define hepatitis C

A

HCV is an RNA virus of the Flavivirus family. Infection may be acute or chronic and is spread through blood to blood transmission.

101
Q

Properties of HCV

A

RNA flavivirus.
2 main types
1a and 1b
Mutate rapidly so difficult to make a vaccine, and previous infection does not confer immunity.

102
Q

Investigations of HCV

A

Serology
- HCV antibody
- HCV RNA PCR (GOLD) suggests active infection

103
Q

Management of HCV

A

Stop alcohol.
Only treat if viral load not falling

  • Triple therapy with NS5A (initiates viral replication) and NS5B (needed for viral replication) inhibitors.
    NS5A - End in ASVIR (ledipasvir)
    NS5B - End in BUVIR (sofosbuvir)
104
Q

HDV definition

A

Enveloped RNA virus with HBV surface antigen on outer envelope; Can only infect where HBsAg already positive.

Co infection - when both acquired together. Indistinguishable from B alone

Super infection - when D acquired in patient with current B infection. Usually more severe and 90% of cases go chronic.

105
Q

Pathophysiology of HDV

A

Acute
Coinfection - Similar to B usually full recovery
Superinfection - More severe hepatitis that can go fulminant. May present as exacerbated HBV or new in unknown HBsAg carrier

Chronic
Hep D suppresses Hep B so most damage from Hep D. Severe risk of fulminant failure, cirrhosis and HCC.

106
Q

Investigations for HDV

A
  • Anti-HDV antibodies (should be tested for if HBsAg is positive)
  • HDV RNA PCR GOLD
107
Q

Management of HDV

A

Antiviral therapy
Transplant if severe

108
Q

Hepatitis E definition with epidemiology

A

Small non enveloped RNA virus causing mainly acute hepatitis but can also lead to chronic in immunosuppressed patients. Has a faecooral spread. Is part of Hepeviridae family

Most common cause of acute hepatitis. Very dangerous in pregnancy (liver failure)

109
Q

Investigations and management of Hep E

A

Anti-HEV antibodies
- IgM Active
- IgG Past (No vaccine)

HEV RNA PCR GOLD

  • Mostly supportive, self limiting.
    Ribaviron if chronic
110
Q

Define autoimmune hepatitis

A

Chronic inflammatory condition of liver, characterised by high serum globulin (IgG), inflammatory changes to liver, favourable response to immunosuppression, and presence of circulating antibodies (ANA, Anti-SMA, Anti-SLA/LP, anti-LKM1, anti LC1)

111
Q

Risk factors for autoimmune hepatitis

A

Females
Other autoimmune disease
HLA-DR3/4
Viral hepatitis

112
Q

Genes involved in autoimmune hepatitis

A

HLA-DR3/DR4

113
Q

Antibodies in autoimmune hepatitis

A

Type 1 - Middle-aged women (ANA, ASMA, Anti SLA/LP)
Anti Nuclear Antibody
Anti Smooth Muscle Antibodies
Anti-soluble liver antigen/Liver-pancreas

Type 2 - Young children and early adulthood
Anti-LKM1 (liver kidney microsome 1)
Anti-LC1 (liver cytosol 1)

114
Q

Signs/symptoms of autoimmune hepatitis

A

Rash, anorexia, abdominal pain + chronic liver disease symptoms
- Jaundice
- Spider angioma
- Gynaecomastia
- Splenomegaly
- Variceal bleeding
- Encephalopathy

Fatigue, fever, malaise, urtcarial rash, weight loss, amenorrhoea

115
Q

Investigations in autoimmune hepatitis

A
  • Serum antibodies - present
  • Serum globulin - HIGH
  • High ALT/AST
  • Liver biopsy GOLD: Mononuclear infiltrates
116
Q

Management of autoimmune hepatitis

A

Immunosuppression

  • Prednisolone + Azathioprine

Liver transplant if REALLY REALLY bad

117
Q

What are the types of biliary tract disease and what are they usually caused by?

A

Cholelithiasis - Development of gallstones

  • Biliary colic - Acute, severe, self-limiting RUQ pain, caused by gallstones irritating bile ducts. (Stones fall back into gall bladder) RUQ pain
  • Cholecystitis - Inflammation of gall bladder, usually due to impacted gallstones (calculous) but can be acalculous. RUQ pain, fever
  • Ascending cholangitis - Infection of the biliary tree characteristically resulting in pain fevers and jaundice. RUQ pain, fever, jaundice
  • Gallstones can also cause Pancreatitis
118
Q

Risk factors for gallstone development

A

6Fs
Female
Fat (BMI>30)
Fertile (pregnant or oestrogen therapy)
Forties+
Fair (white)
Family history

  • Haemolytic conditions
  • Family history
  • Rapid weight loss/ prolonged fasting
  • High triglyceride/ cholesterol diet
  • Diabetes
119
Q

Factors leading to gallstone development

A
  • Biliary stasis - Bile flow slows when fasting, high oestrogen, oral contraceptive pill
  • Increased cholesterol - Obesity, diabetes
  • Decreased bile acids - Cirrhosis, crohn’s, ileal resection
120
Q

Gallstone composition

A
  • Cholesterol (80%)
  • Black pigment (calcium bilirubinate) - Patients with haemolysis
  • Brown pigment (calcium salts with bilirubin). Infection association
121
Q

Complications of gallstone development

A

Biliary colic
Acute cholecystitis
Acute (ascending) cholangitis
Acute pancreatitis
Obstructive jaundice

122
Q

Definition, signs/symptoms, and examination of biliary colic

A
  • Pain in RUQ/Epigastrum caused by gallstones irritating bile ducts. Episodes normally last 30 mins-6 hours
  • Pain can radiate to right shoulder or around to back. Accompanied by nausea/vomiting
  • Examination is normal.
123
Q

Investigations in biliary colic

A

Mostly normal. High bilirubin may suggest obstruction of bile ducts and amylase should be checked to exclude pancreatitis
- 1st: Abdominal ultrasound. Will show stones, thin GB wall, dilated cystic ducts (NORMAL bile ducts)
- GOLD: ERCP (endoscopic retrograde cholangiopancreatography) or MRCP (magnetic resonance cholangiopancreatography)

124
Q

Management of biliary colic

A

Analgesia (paracetamol or NSAID)
Low fat diet

ERCP allows for retrieval of stones, or cholecystectomy

125
Q

Gallstone pain radiates to shoulder. What nerve causes this?

A

Phrenic nerve

126
Q

Pathophysiology of cholecystitis

A

Inflammation of the gallbladder usually due to gallstones causing bile stasis.

  • Bile stasis irritates gallbladder wall causing mucosa to secrete mucus and inflammatory enzymes.
  • Bacteria can grow, (e.g. enterococci, e. coli, clostridium) and go through wall causing peritonitis.
  • If stone travels further down, it can cause obstruction of common bile duct causing bile to back up into liver, causing conjugated bilirubin to build up in blood (Jaundice!)

Severe systemic upset, surgery or trauma (sepsis, burn, cancer) can cause acalculous cholecystitis. Fasting and TPN (Total parenteral nutrition - basically IV) can also cause this!

127
Q

Signs/symptoms of cholecystitis

A
  • Epigastric pain/RUQ radiating to right shoulder/scapula and round to back
  • Fever
  • Malaise
  • Murphy’s sign positive! (palpate GB and ask patient to exhale then inhale, pain on inhalation)
  • Jaundice only present if stone travels to common bile duct, or if ascending cholangitis
128
Q

What is Murphys sign (in detail)

A

Tests for gallbladder inflammation!
- Hand is placed over RUQ and pressure applied
- Patient should exhale then take deep breath in
- On inhalation, gallbladder moves inferiorly and comes into contact with hand
- If inflamed, this will cause pain and patient will likely stop inhaling.

  • This should be negative on left side
129
Q

Investigations in cholecystitis

A

FBC - Neutrophils, CRP/ESR high
Serum amylase/lipase (Check pancreatitis) - normal

1st and GOLD - Abdominal ultrasound - stones in gallbladder, thickened gallbladder walls, distended gallbladder

2nd GOLD: MRCP, especially if suspecting CBD stone, or if LFTs are abnormal (ERCP can be used to extract

130
Q

Management of cholecystitis

A

NBM, IV fluids
IV Antibiotics (Coamoxiclav)
Urgent Laparoscopic cholecystectomy within 1 week of diagnosis

Percutaneous cholecystostomy if inappropriate (gangrene, sepsis, perforation)

131
Q

What kind of food aggravates an inflamed gallbladder

A

Fatty foods
Fat stimulates cholecystokinin which contracts gallbladder

132
Q

Define ascending (AKA Acute) cholangitis

A

Infection of biliary tree resulting in RUQ pain, jaundice and fever (charcot’s triad).

Infection secondary to biliary obstruction, promoting growth of usually gram negative bacteria. E. Coli most common

133
Q

Causes of ascending cholangitis

A
  • Gallstones causing blockage of bile ducts (choledocholithiasis)
  • Biliary strictures (narrowing), malignant or benign
  • Surgical injury of bile ducts
134
Q

Non cancer causes of biliary tract strictures

A

Chronic pancreatitis
ERCP
Blood clots
Radiotherapy/chemotherapy

135
Q

Signs/symptoms of Ascending Cholangitis

A

Charcot’s triad
RUQ Pain, fever, jaundice

  • Pruritus
  • Pyrexia
  • Scleral icterus
  • Tenderness/distension
136
Q

What can Charcot’s triad progress to?

A

Reynolds pentad suggests biliary sepsis/Obstructive ascending cholangitis

Charcots triad (RUQ pain, fever, jaundice) + Hypotension + confusion)

137
Q

Investigations of ascending cholangitis

A

FBC - Leukocytosis with neutrophilia
LFT - Obstructive jaundice with raised ALP>ALT (suggesting cholestasis) and bilirubin
Abdominal ultrasound - Common bile duct dilation and gallstones

First line imaging: Abdominal ultrasound
GOLD: MRCP (Magnetic resonance cholangiopancreatography)

138
Q

Management of ascending cholangitis

A

Sepsis 6 protocol if severe/Reynolds pentad
IV fluids and analgesia
IV antibiotics if needed (broad spectrum - Metronidazole, cefotaxime)

GOLD: Remove obstruction:
- ERCP (Endoscopic Retrograde Cholangiopancreatography)
- Shockwave lithotripsy (use sound to break stones)
- Stenting of stricture

139
Q

What is sepsis 6

A

Give 3 take 3

Administer oxygen
Give IV fluids
Give IV antibiotics (ceftriaxone)

Take blood culture
Check serum lactates
Measure urine output

140
Q

Red flags for sepsis 6

A

Confusion
Unresponsive
Hypotension
Tachycardia
High respiratory rate
Hypoxic
Not passing urine
High lactate
Recent chemotherapy

141
Q

Define Peritonitis with causes

A

Inflammation of peritonitis

Primary - Spontaneous Bacterial Peritonitis (Ecoli, Klebsiella (G-) or Staph aureus), or ascites
Secondary - Caused by other chemicals such as bile, intestinal perforation, ruptured appendix/ectopic pregnancy

Infection can spread directly or through blood

142
Q

Signs and symptoms of peritonitis

A
  • Sudden onset severe abdominal pain followed by general collapse and shock.
  • Pain begins poorly localised (visceral peritoneum) and becomes better localised (parietal peritoneum)
  • Tenderness and guarding of abdomen
  • Pain relieved by resting hands on abdomen (preventing movement of peritoneum)
  • Patients like to be still
  • Ascites
143
Q

Investigations in SBP

A
  1. Ascitic tap - High WCC (neutrophilia)
  2. Fluid/blood culture

Exclude others
CXR - air under diaphragm = Intestinal obstruction
Amylase/lipase - Pancreatitis
HCG (human chorionic gonadotrophin) - Check pregnancy as cause of pain

144
Q

Management of SBP

A

ABC
IV fluids
NG tube insertion
Broad spectrum antibiotic (Cephalosporin)

Surgery
- Laparotomy - Peritoneal lavage (full clean of peritoneal cavity)

145
Q

Complications of SBP

A
  • Toxaemia/septicaemia
  • Local abscess formation
  • Kidney failure
  • Paralytic ileus
146
Q

How does increased portal pressure cause varices

A

Portal vein carries blood from digestive tract, spleen and pancreas to liver.

Portal HTN causes splanchnic vasodilation, decreasing the overall BP. This causes increased cardiac output and salt and water retention as compensatory mechanisms. This causes hyperdynamic circulation and increased portal flow. Increased resistance from liver and increased flow causes blood to shunt into small gastroesophageal veins.

147
Q

Urine bilirubin and urobilinogen in haemolysis, hepatic disease and biliary obstruction

A

Haemolysis - B low, U high
Hepatic disease - B high, U negative/decreased
Biliary obstruction - B high, U high

148
Q

Treatment of oesophageal varices

A

Prevent bleeding
- Non selective Beta blocker (carvedilol or nadolol)
- Endoscopic variceal band litigation (repeated every 4 weeks till under control, monitored every year)

Active bleeding
- IV Terlipressin to stop bleeding. Broad spectrum antibiotics and blood transfusions to make patient stable if needed
- Urgent endoscopy when stable with Variceal banding

  • TIPS (Transjugular Intrahepatic Portosystemic Shunt) if ineffective or contraindicated
149
Q

Pre hepatic causes of portal HTN

A

Blockage of portal vein before liver

E.g. Thrombosis, atherosclerosis, embolism

150
Q

Intra hepatic causes of portal HTN

A

Distortion of liver architecture

  • Cirrhosis
  • Schistosomiasis - flatworms in liver
  • Sarcoidosis - Granulomas in liver
151
Q

Post hepatic causes of portal HTN

A

Venous blockage after liver, causing blood to back up into system

  • Right sided heart failure
  • Constrictive pericarditis
  • Budd-Chiari syndrome
  • IVC obstruction
152
Q

Where can varices develop due to portal HTN

A
  • Inferior part of oesophagus (oesophageal varices)
  • Rectum (superior portion of anal canal)
  • Anterior abdominal wall via umbilical vein (Caput medusae)
153
Q

Signs/symptoms of portal HTN

A

ABCDE
A - Ascites
B - Bleeding of varicose veins
C - Caput Medusae
D - Diminished liver function
E - Enlarged spleen

Haematemesis (vomiting blood) or malaena

154
Q

Gold standard investigation in portal HTN

A

Hepatic Venous Pressure Gradient Measurement (HVPGM)

155
Q

Define Primary Biliary Cholangitis and Primary Sclerosing Cholangitis

A

PBC - Autoimmune granulomatous destruction of small intrahepatic biliary ducts leading to subsequent leakage of bile into circulation

PSC - Chronic liver disease of intra or extra hepatic bile ducts characterised by inflammation, fibrosis and destruction.

156
Q

PBC vs PSC

A

PBC - Autoimmune, associated with other conditions (Sjogrens, Raynauds, Thyroid, RA, Systemic sclerosis), typical presentation is a woman with extreme itching.

PSC - Often asymptomatic, detected by accident, or symptoms of liver dysfunction. Male with history of IBD (mainly UC)

157
Q

Risk factors for PBC

A

Female
Autoimmune conditions
Family History
Past pregnancy
Excessive nail polish/hair dye use
Smoking

158
Q

Pathophysiology of PBC

A

Anti-Mitochondrial Antibodies (AMA) attack cells lining intrahepatic bile ducts. Causes leakage of bile into the blood. Damage causes inflammation which leads eventually to cirrhosis. ~50% have another associated autoimmune condition.

159
Q

Signs/symptoms of PBC

A

Key presentation is middle aged woman with severe itching!

  • Pruritus
  • Skin hyperpigmentation
  • Clubbing
  • Xanthelasma
  • Scleral icterus
  • Fatigue and weight loss
  • Hepatosplenomegaly
  • Deficiency of fat soluble vitamins (ADEK)

May have an associated autoimmune condition

160
Q

Investigations in PBC

A

LFT
- High ALT, ALP, GGT Conjugated Bilirubin
- Low albumin

Antibodies
- AMA antibodies

Abdominal Ultrasound - Extrahepatic cholestasis

MRCP may be needed

161
Q

Diagnostic criteria for PBC

A
  • High ALP or GGT
  • Presence of AMA
  • Liver biopsy showing granulomatous inflammation around intrahepatic bile ducts and cirrhosis
162
Q

Management of PBC

A
  1. Ursodeoxycholic acid (bile acid analogue) which dampens inflammatory response, acts an anti-apoptotic agent, improves cholestasis
  2. Fat soluble vitamin supplements
    Cholestyramine to relieve pruritus

Transplant in end stage liver failure

163
Q

Complications of PBC

A
  • Malabsorption of fat soluble vitamins due to cholestasis
  • Coagulopathy possible
  • Hypercholesterolaemia
  • Liver Cirrhosis
  • HCC
  • Metabolic bone disease
164
Q

Pathophysiology of PSC

A

An autoimmune trigger causes progressive intra and extrahepatic bile duct damage, causing bile duct inflammation, strictures and sclerosis. Strictures obstruct bile flow into intestines.

Between areas of fibrosis/stricturing, some areas are dilated (no fibrosis) giving “beaded” appearance on ERCP/MRCP

Damage leads to:
- Cholestasis
- Bile/toxin build up in liver
- Bile duct strictures
-> End stage liver failure

Too much fibrosis causes portal HTN -> hepatosplenomegaly

165
Q

Risk factors for PSC (3)

A
  • Male
  • Having IBD (UC especially)
  • Genetic predisposition/family history
166
Q

Signs/symptoms of PSC

A

Usually detected asymptomatic
- Jaundice
- Pruritus
- Fatigue
- RUQ/epigastric abdominal pain
- Symptoms of bowel disease (bloody stools etc)

167
Q

Investigations in PSC

A

LFT - ALP, GGT. Conjugated Bilirubin

Antibodies
- pANCA
- NO AMA (PBC only)

MRCP (Multiple biliary strictures showing a “beaded” appearance) (US first in PBC)

  • Urinary urobilinogen lowered

ERCP if biopsy needed
(if unclear)

168
Q

Management of PSC

A

Cholestyramine for pruritus
Lifestyle changes
Fat soluble vitamins

Liver transplant at end stage

169
Q

How is PSC monitored

A

Annual gallbladder ultrasound and colonoscopy - check for precancerous polyps (increased risk of cholangiocarcinoma)

170
Q

Complications of PSC

A
  • Ascending Cholangitis
  • Biliary strictures
  • Gallstones
  • Metabolic bone disease (Osteopenia/porosis) (lack of vit D)
  • End stage liver disease
  • Cholangiocarcinoma
  • HCC
  • Colorectal carcinoma
171
Q

What is secondary sclerosing/biliary cholangitis

A

No autoimmune involvement. Other cause possible such as gallstone, surgical complication, malignancy, trauma

172
Q

Define pancreatitis

A

Acute or chronic inflammatory damage to the pancreas. Most common causes are gallstones and alcohol. Recurrent bouts of acute can lead to chronic

173
Q

Causes of acute pancreatitis

A

IGETSMASHED
Iatrogenic
Gallstones
Ethanol
Trauma
Scorpion/spider bites
Mumps virus
Autoimmune (SLE, Sjogrens)
Steroids
Hypercalcaemia, lipidaemia
ERCP
Drugs (Azathioprine, thiazide diuretic, oestrogen, sitagliptin)

CYSTIC FIBROSIS!!

174
Q

General pancreatitis pathophysiology

A

Sudden inflammation causing leakage of enzymes leading to haemorrhaging of the pancreas by its own digestive enzymes (Autodigestion)

175
Q

General pancreatitis pathophysiology with normal function

A

Sudden inflammation and haemorrhaging of the pancreas by its own digestive enzymes (Autodigestion). This causes Liquefactive Haemorrhagic Necrosis of the pancreas, if fibrous tissue surrounds this it can become an abscess. Enzymes leak into blood.

Normally, acinar cells secrete inactive enzymes (zymogens) in zymogen vesicles with protease inhibitors (proteases activate them)

Zymogens released into duodenum via pancreatic duct where they are activated by trypsin (which is activated from trypsinogen in the same granules as zymogens)

176
Q

How does alcohol cause pancreatitis

A

Alcohol increases zymogen secretion whilst decreasing fluid and bicarbonate secretion by ductal epithelial cells. Pancreatic juice becomes thick and viscous -> Obstruction of pancreatic duct. Fluids and so zymogens back up and zymogen granules fuse with lysosome granules. Lysosomes active trypsinogen into trypsin, which active the zymogens, auto digesting the pancreas.

177
Q

How do gallstones cause pancreatitis

A

Gallstones get lodged in sphincter of Oddi, blocking pancreatic secretion release, building up pressure and forcing mixing of granules. Similar mechanism to alcohol.

178
Q

Signs and symptoms of acute pancreatitis

A

Sudden severe epigastric pain which radiates to back “like being stabbed in back”. Worsens with movement

  • Nausea
  • Tachycardia
  • Cullens sign (bruising around umbilicus)
  • Grey-Turner’s sign (flank bruising)

(bruising caused by bleeding under skin)

History of gallstones or alcohol

179
Q

Diagnostic investigations in pancreatitis

A
  1. Serum amylase and lipase (3x upper limit)

USS to find gallstones
CT for complications (Necrosis, pseudocysts, abscesses, inflammation)

Modified Glasgow scoring

180
Q

What is the glasgow scoring criteria for pancreatitis

A

P - PO2 <8
A - Age>55
N - Neutrophils >15X10^9
C - Calcium <2
R - Renal function (urea>16)
E - Enzymes - High AST/LDH
A - Albumin <32
S - Sugar (glucose high)

3 or more in first 48 hours refer up

Ransons also used for mortality and APACHEII for severity but is non specific

181
Q

What to keep in mind when testing Amylase/ Lipase

A

Amylase - Rises and falls faster (within 24-48 hours). Non specific

Lipase - More specific for acute pancreatitis. Levels rise slower but have longer half life

182
Q

Management of pancreatitis

A

Admission to hospital.
- NBM
- Fluid resuscitation
- Treat gallstones
- Electrolyte replacement
- Oxygen if low

183
Q

Complications of pancreatitis

A
  • Pancreatic pseudocyst, abscess, necrotising pancreatitis
  • Progression to chronic
  • Bleeding

Systemic
- Systemic inflammatory response syndrome
- ARDS (acute respiratory distress syndrome)
- Pancreatic diabetes
- Paralytic ileus
- Hypocalcaemia
- Pleural effusions

184
Q

Define chronic pancreatitis with pathophysiology.

A

3+ month history pancreatic deterioration leading to irreversible inflammation, calcification, atrophy and fibrosis.

With repeat episodes, the ducts dilate, damaging pancreatic tissue. Stellate cells lay down fibrotic tissue, causing ductal stenosis, leading to acinar cell atrophy. Alcoholic pancreatitis causes calcium deposition.

Healthy pancreatic tissue replaced with
- Misshapen ducts
- Fibrosis
- Calcium deposits

185
Q

Signs of chronic pancreatitis

A

Acute signs +
- Steatorrhoea
- Weight loss
- Pancreatic Diabetes
- Skin nodules

186
Q

Investigations in Chronic Pancreatitis

A
  • Serum amylase/lipase - May be high or low, acinar cell destruction means they cant be produced
  • Transabdominal US first! - Atrophic, calcified or fibrotic pancreas
  • CT/MRI - Pancreatic calcifications, ductal dilation, atrophy
  • ERCP - GOLD - “Chain of lakes” pancreas
  • Histology - GOLD - Inflammation, fibrosis, loss of acini, calcification
  • Faecal elastase - low (enzyme produced by pancreas)
187
Q

Management of chronic pancreatitis

A

1 - abstain smoking + alcohol
- Analgesia for pain
- Replace digestive enzymes and fat soluble vitamins (ADEK)
- ERCP with stent to fix strictures
- Surgical duct drainage, abscess drainage, remove inflamed tissue

188
Q

Define Wilson’s disease with epidemiology

A

Autosomal-recessive disease of copper accumulation and toxicity caused by mutation in ATP7B gene, which codes for part of the biliary excretion pathway of copper.

Usually in ~20 year old male. Family history a risk factor

189
Q

Pathophysiology of Wilson’s Disease

A

Dysfunction of ATP mediated hepatocyte copper transport, causing increased copper absorption in SI and less hepatic copper excretion.

Copper accumulates in blood, eyes, basal ganglia, liver and kidneys causing
- Hepatic issues
- Neurological issues
- Psychiatric issues

190
Q

Signs/symptoms of Wilson’s Disease

A
  • Kayser Fleischer Rings (Copper deposits in eyes)
  • Hepatic (Jaundice, liver failure signs etc)
  • Neurological (Parkinsonism, dysarthria, dementia)
  • Kidney (renal tubular acidosis)
  • Blood (Haemolytic anaemia)
  • Blue nails, arthritis, grey skin, hypermobile joints.
191
Q

Investigations in Wilson’s

A
  • Ceruloplasmin REDUCED
  • 24 hour urinary copper INCREASED
  • Slit lamp exam (KF Rings in eyes)
  • Liver biopsy GOLD
  • Brain MRI - check for BG and cerebellar degeneration

Gene studies/family screening

192
Q

Treatment of Wilson’s disease

A

D-penicillamine (copper chelation)
Avoid dietary copper (shellfish, mushrooms)

Liver transplant last resort
(trientine hydrochloride can be used for copper chelation as second choice)

193
Q

Define haemochromatosis with epidemiology

A

Autosomal recessive mutation of HFE gene on chromosome 6, causing dysregulated iron absorption and increased release from macrophages.

European Male, 50ish years. (men present earlier than women as menstruation naturally removes iron)

194
Q

Other causes of iron overload (secondary haemochromatosis)

A

High intake of iron
Alcoholism
Frequent blood transfusions

195
Q

Pathophysiology of haemochromatosis

A
  • Missense mutation on HFE gene on chromosome 6
  • HFE protein interacts with transferrin receptor 1, and iron is absorbed way more than binding capacity of transferrin
  • Hepcidin also reduced, so less iron absorption homeostasis, facilitating iron overload.
  • Iron also creates free radicals through Fenton reaction
  • This causes damage to LIVER, skin, pancreas, heart, joints, pituitary gland/ gonads
196
Q

Signs/symptoms of haemochromatosis

A
  • Bronze skin (hyperpigmentation)
  • Arthritic joints
  • Testicular atrophy/amenorrhoea
  • Liver cirrhosis/HCC
  • Congestive heart failure
  • Osteoporosis and degenerative joint disease
  • T1DM and malabsorption if pancreas affected
197
Q

Investigations in haemochromatosis

A

Serum iron - high
Serum ferritin - high
Transferrin saturation - high

Total iron binding capacity - Low

Liver biopsy (GOLD) - Prussian blue (Perls) staining

198
Q

Secondary investigations in haemochromatosis

A

HbA1c
Joint X ray
CT abdomen
Liver biopsy
ECG
Family screening

199
Q

Management of haemochromatosis

A

Venesection - Drain blood to remove iron until serum ferritin 20-30 and transferrin saturation 50%
Then offer maintenance phlebotomy

Iron chelation - Desferrioxamine

200
Q

Complications of haemochromatosis

A

Liver
- Cirrhosis HCC

Endocrine
- DM, Hypogonadism, loss of libido

Cardiac
- Myopathy, Congestive heart failure

MSK
- Pseudogout, osteoporosis

201
Q

Define alpha 1 antitrypsin deficiency

A

Autosomal recessive disorder (Serpina-1 gene on chromosome 14) causing liver and pulmonary disease.

A1AT is a serine protease inhibitor. In it’s absence, neutrophil elastase destroys elastin in alveoli, causing early, non smoker COPD symptom onset.

In liver, A1AT proteins are misfolded causing them to get stuck in endoplasmic reticulum of hepatocytes, causing cell death, leading to hepatitis, jaundice, etc.

202
Q

Pathophysiology of A1 Antitrypsin deficiency

A

A1AT is a protease inhibitor made in liver that normally acts in lungs to protect alveoli from neutrophil elastase. Chromosome 14, Protease inhibitor (Pi) allele on SERINA-1 gene.

PiMM - normal A1AT levels
PiSS - 50% normal A1AT
PiZZ - 10% normal A1AT

PiZZ genotype increases risk of cirrhosis.

In lungs, neutrophil elastase normally destroy harmful causes of infection and inflammation, but also destroy elastin in alveoli, causing panacinar emphysema.

203
Q

How do smoking and A1AT affect acini differently?

A

Smoking - Centriacinar destruction and emphysema, primarily upper lobes affected

A1AT - Panacinar destruction/emphysema, most severe in lower lobes

204
Q

What is an acinus

A

Functional lung unit, consisting of a bronchiole and its alveoli

205
Q

Signs/symptoms of A1 antitrypsin deficiency

A

Respiratory
- Early onset dyspnoea, productive cough
- Prolonged expiratory phase and wheeze
- Pursed lip breathing
- Barrel chest due to hyperexpanded lungs

Liver
- Only in PiZZ genotype, symptoms of cirrhosis (jaundice, hepatomegaly, ascites, coagulopathy, hepatic encephalopathy, portal HTN)

Young, non smoking history

206
Q

Investigations of A1AT

A
  • Serum A1AT - Reduced
  • FEV1/FVC <0.7 (Obstructive pattern)
  • LFT deranged
  • Liver biopsy with staining. Periodic acid schiff and diastase used (diastase should destroy A1AT). If A1AT deformed, it will stain +ve but be diastase resistant.
  • CT chest - panacinar emphysema
  • Genetic testing - PiSS, or PiZZ
207
Q

Management/complications of A1AT

A

Respiratory
- Smoking cessation
- COPD treatment (bronchodilators and inhaled corticosteroids)
- IV A1AT

Liver
- Avoid alcohol
Liver transplant in end stage

  • Respiratory failure and cirrhosis/HCC
  • Cholestasis in children
208
Q

Hernia classifications

A

Reducible - Can be manually pushed back
Irreducible - Cant be manually pushed back
Obstructed - e.g. bowel contents not being able to pass due to intestinal hernia obstruction
Strangulated - Ischaemia due to blood supply of sac being cut off EMERGENCY
Incarcerated - Contents of hernial sac stuck due to adhesions

209
Q

Define inguinal hernia with risk factors

A

Protrusion of abdominal contents through inguinal canal. Most common type of hernia. Usually due to excessive straining/abdominal pressure.

  • Male
  • Chronic cough
  • Constipation
  • Heavy lifting
  • Urinary obstruction
  • Ascites
  • Past abdominal surgery
210
Q

Types of inguinal hernia

A

Indirect (80%)
- Hernia protrudes into inguinal canal through deep inguinal ring
- Lateral to inferior epigastric artery so can strangulate

Direct (20%)
- Hernia protrudes into inguinal canal through posterior wall (Hesselbach’s triangle)
- These hernias rarely strangulate and are reducible

211
Q

Signs/symptoms of inguinal hernia

A
  • Swelling in groin (painful if obstruction/strangulation)
  • Swelling bulges/expands with coughing or straining
212
Q

What are the surgical treatment options for hernias

A

Herniotomy - Contents reduced and sac removed
Herniorrhaphy - Remove sac and repair damaged wall
Hernioplasty - Sac removal and mesh to reinforce weak wall

213
Q

Define hiatal hernia

A

Stomach pushes up into lower chest due to diaphragm weakness

214
Q

Types of hiatal hernia and main signs

A

Sliding hiatus hernia - Gastrooesophageal junction slides up into chest. This can cause acid reflux as lower oesophageal sphincter becomes less competent

Paraoesophageal (rolling) hernia - GO junction remains in abdomen but bulge of stomach herniates into chest alongside oesophagus. GORD less common

Small hernias are asymptomatic but large hernias can cause symptoms of GORD and dysphagia

215
Q

Investigations for Hiatal hernia

A

Upper GI Endoscopy, CXR
Barium Swallow GOLD

216
Q

Management of hiatal hernia

A

Weight loss
GORD treatment
Surgical treatment if risk of strangulation

217
Q

Define Umbilical hernia

A

Paediatric hernia of intestines through opening in abdominal muscles near navel. Common, harmless, usually self resolve.

218
Q

Define epigastric hernia

A

Hernia in midline between belly button and sternum.

219
Q

Define incisional hernia

A

Tissue protrudes through weak surgical scar. Usually due to emergency surgery, wound infection, persistent coughing/heavy lifting post op, and poor healing.

220
Q

Define femoral hernia

A

Bowel enters femoral canal (mass in upper medial thigh). Occur more in middle aged females.

Irreducible and strangulation likely!

221
Q

Sum up Gilbert’s syndrome (red)

A

Hereditary cause of jaundice. Autosomal recessive. Unconjugated bilirubin.
Mostly harmless

Painless jaundice at young age.
If pain or other symptoms, crigler najjar possible (so phototherapy needed to break down bilirubin)

222
Q

What is the main cause of liver cancer

A

Metastasis from other cancers (90%)

e.g. Stomach, lung, colon, breast, uterus, pancreas, leukaemia

223
Q

What is the most common primary liver cancer

A

Hepatocellular carcinoma (90%)

224
Q

Causes and metastases of HCC

A

HBV and HCV!
Autoimmune hepatitis
Cirrhosis
NAFLD
Anabolic steroids
Alcohol
Alfatoxin

Metastasises to lymph, bones, lungs by haematogenous spread

225
Q

Investigations in HCC

A

Serum AFP (alpha fetoprotein) (also high in testicular cancer)
Imaging - Ultrasound (1st)
CT can confirm (hard if small lesion)

Biopsy avoided as may causes seeding along biopsy track

226
Q

Management, prevention and monitoring of HCC

A

Resect solitary tumours
Percutaneous tumour ablation
Transplant

Prevention
- HBV vaccination
- Reduce alfatoxin exposure

Monitor AFP and do regular ultrasounds (6 months)

227
Q

Define cholangiocarcinoma with risk factors

A

Biliary tree cancer, usually adenocarcinoma

  • Parasitic worms
  • PSC
  • Biliary cysts
  • HBV/HCV
  • DM
228
Q

Investigations in liver cancers

A

CT/Ultrasound - identify lesions
MRI - Check benign or malignant
ERCP
AFP, clotting, FBC, LFT, Bilirubin etc to check liver function

229
Q

Management and prognosis of cholangiocarcinoma

A

Surgery (not possible in 70% of patients at presentation, as cancer is slow growing)
Liver transplant

  • Prognosis poor 5 yr survival - 30%
230
Q

Signs of liver cancer

A

Enlarged, irregular, tender liver
Signs of chronic liver disease with decompensation
Weight loss, chronic fatigue
RUQ pain

231
Q

Define pancreatic cancer with risk factors

A

Adenocarcinoma of exocrine pancreas ducts. Typically affects head of pancreas.
Extremely poor prognosis

  • Male
  • Family history
  • Obesity
  • Alcohol
  • Smoking
  • Diabetes
  • Chronic pancreatitis
  • Multiple Endocrine Neoplasia
232
Q

Signs/symptoms of pancreatic cancer

A
  • Courvoisier’s sign. Painless obstructive jaundice (pale stool, dark urine) + Palpable gallbladder
  • Trousseau sign of malignancy - migratory thrombophlebitis (inflammation of veins)
  • Weight loss
  • Fatigue
  • Epigastric pain radiating to back, relieved by sitting forward
233
Q

Investigations in pancreatic cancer

A

CT abdomen, chest, pelvis 1st/GOLD
- CA19-9 non specific but raised, and shows disease progression
- PET CT if CT inconclusive

234
Q

Management of pancreatic cancer

A

Localised: Surgical resection
- Whipples resection (pancreaticoduodenectomy)

Non localised
- Chemo/radiotherapy
- ERCP to clear obstruction with stenting to provide relief

235
Q

Monitoring of pancreatic cancer

A

CA19-9 - non diagnostic but can monitor progression

236
Q

What is the main sign of malignancy

A

Trousseau sign - Episodes of migratory thrombophlebitis (inflammation of veins) in different parts of body

237
Q

Alcoholism screening

A

CAGE
Cut down (do they feel they should)
Annoyed (by critiques of their habits)
Guilt (do they feel guilty about their habits)
Eye opener (do they drink first thing)

2+ = significant problems

238
Q

What triad of symptoms is associated with Budd-Chiari syndrome

A
  • Abdominal Pain
  • Ascites
  • Hepatomegaly

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