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PHASE 2 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Definition of cholelithiasis

A

Presence of solid concretions in the gallbladder

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2
Q

Definition of choledocholithiasis

A

Gallstones form in the gallbladder but may exit into bile ducts

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3
Q

Epidemiology of Cholelithiasis / Choleidocholethiasis and Biliary colic

A

10-15% of all adults in europe.
Asymptomatic in >80% of people. Once developed, 50% will go on to have recurrent pain while 3% develop complications. Asymptomatic 0.1-2% will experience a major complication each year.

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4
Q

Aetiology: Cholelithiasis / Choleidocholethiasis and Biliary colic

A

90% gallstones composed of cholesterol and form in the gallbladder

15% gallstones are black pigment stones consisting of polymerised calcium bilirubinate.

Brown pigment stones form in bile ducts as a result of stasis and infection. Consist of calcium bilirubinate (unconjugated bilirubin), calcium salts of long chain fatty acids and cholesterol. Usually develop from bacterial infection or partial biliary obstruction.

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5
Q

Risk Factors : Cholelithiasis / Choleidocholethiasis and Biliary colic

A

5F’s
Female
Fertile - pregnancy
Forty - Age
Family history
Fat - Obesity / Diabetes / Metabolic syndrome

Others:
Gene mutations
NAFLD
Rapid weight loss
Medications
Hispanic and Native-american ethnicity

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6
Q

Pathophysiology: Cholelithiasis / Choleidocholethiasis and Biliary colic

A

Occurs as a result of 3 defects: Bile supersaturated with cholesterol, Accelerated nucleation and gallbladder hypermobility.

Cholesterol supersaturation occurs when the liver excretes excessive amounts of cholesterol compared with its solubilising agents e.g. bile salts and lecithin.
Precipitation of cholesterol microcrystals then follows initiated by presence of nucleating agents (mucin). Impaired gallbladder contractility causes stagnation and retention in gallbladder, and microcrystals collect and grow into gallstones.

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7
Q

Key presentations: Cholelithiasis / Choleidocholethiasis and Biliary colic

A

RUQ or epigastric pain that typically increases in intensity and may last several hours. Can radiate to the upper back or right shoulder.
Postprandial pain - Onset of pain approx 1 hour after eating.
Pain also in sleep when lying down.

Signs - Response to analgesia and >15-20 mins but <8 hour increments.

Symptoms - Dyspepsia, heartburn, flatulence, bloating,

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8
Q

Investigations: Cholelithiasis / Choleidocholethiasis and Biliary colic

A

1st line
LFT’s
Choleliathiasis - Normal
Choledocholeliathiasis - elevated alkaline phosphatase and bilirubin, ALP
Brief biliary obstruction with stone passage = early transient elevation in Alanine aminotransferase ALT before alkaline phosphatase ALP rises.
FBC - Normal
Serum Lipase and Amylase - Normal

GOLD STANDARD: Abdominal Ultrasound - Stones in the gallbladder or bile duct with or without bile duct dilation.

Others:
MRCP - bile duct dilated in choledocholiathiasis
EUS - Stones present
Abdo CT - Stones. Refer if USS normal but having biliary pain

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9
Q

Management of Cholelithiasis / Choleidocholethiasis and Biliary colic

A

Biliary colic - NSAIDS - diclofenac or indomethacin. Paracetamol may be sufficient. With anti-spasmodic if needed (hyoscine).
Patients with symptomatic gallstones but no signs of cholecystitis then offer laparoscopic cholecystectomy.
Offer bile duct clearance of laparoscopic cholecystectomy to patients with bile duct stones. Clear bile duct either ERCP or surgically.
Advise patients to avoid triggering foods and symptoms to watch out for.

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10
Q

Complications of Cholelithiasis / Choleidocholethiasis and Biliary colic

A

Acute cholecystitis
ERCP associated pancreatitis
Acute cholangitis
Acute biliary pancreatitis
Mirizzi syndrome

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11
Q

Prognosis: Cholelithiasis / Choleidocholethiasis and Biliary colic

A

Recurrent bile duct stones occur in 5-20% people after endoscopic sphincterotomy.

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12
Q

DDx: Cholelithiasis / Choleidocholethiasis and Biliary colic

A

Acute Cholecystitis / Pancreatitis - Elevated WBC count, serum lipase and or amylase elevated >3 times.

Peptic ulcer disease - H pylori breath / stool antigen test positive. EGD - peptic ulcer

Gallbladder cancer - CT abdo shows intrahepatic mass lesion

Acalculous cholecystitis - No gallstones but murphy’s sign

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13
Q

Definition of acute cholangitis

A

Biliary obstruction with inflammation and bacterial seeding and growth in biliary tree.

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14
Q

Epidemiology acute cholangitis

A

1% of patients with cholelithiasis. Male to female ratio is equal.

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15
Q

Aetiology: acute cholangitis

A

Cholelithiasis
Choledocholelithiasis and biliary obstruction
Iatrogenic biliary duct injury
Sclerosing cholangitis

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16
Q

Risk Factors: acute cholangitis

A

Cholelithiasis
Choledocholelithiasis and biliary obstruction
Iatrogenic biliary duct injury
Sclerosing cholangitis

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17
Q

Pathophysiology acute cholangitis

A

Obstruction of the common bile duct results in bacterial seeding of biliary tree. Sludge forms, providing a growth medium for bacteria and as obstruction progresses, bile duct pressure increases.
This forms a pressure gradient causing extravasation of bacteria into the bloodstream and if not treated can lead to sepsis.

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18
Q

Clinical manifestations: acute cholangitis

A

Key Presentations
Presence of risk factors
RUQ pain or epigastric pain with abdominal tenderness
Jaundice
Pyrexia

Signs
Pale stools
Pruritus
Hypotension
Mental changes

Symptoms
Malaise, Fatigue, Nausea, Vomiting,

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19
Q

Investigations: acute cholangitis

A

1st Line
FBC - WCC >10x109 with low platelets
Raised serum urea and creatinine
ABG - raised lactate and low bicarbonate
LFTs - hyperbilirubinemia and raised serum transaminases and alkaline phosphatase.
CRP - raised
Serum potassium and magnesium - decreased
Transabdominal USS - dilated bile duct or common bile duct stones.

Gold Standard
ERCP - direct observation of obstruction and adequate clearance with therapy.

Others
MRCP - mass impinging on biliary tree, stricture
PTC - bile duct stone or other obstruction
EUS - Common Bile Duct stones, ampullary, pancreatic and or biliary masses.

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20
Q

Criteria: acute cholangitis

A

A Either fever or lab data of inc WCC
B Jaundice, Lab data of abnormal LFT (ALP, AST, ALT)
C Biliary dilation or evidence of aetiology on imaging

Diagnosis suspected : One in A and one in B or C
Definitive diagnosis : One in A, plus one in B, plus one in C

Grade III - Acute cholangitis with onset of dysfunctions from another organ / system e.g. Neurological or cardiovascular dysfunction.
Grade II - Any two of abnormal WCC, Fever, >75 years and hyperbilirubinemia or hypoalbuminemia.
Grade I - no criteria of grade II or III.

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21
Q

Management - acute cholangitis

A

TREAT SUSPECTED SEPSIS FIRST
Give broad spectrum IV antibiotics and IV hydration - Piperacillin or tazobactam. (Metronidazole in combination with gentamicin is an alternative to penicillin allergy.)
Correct electrolyte imbalances
Analgesia
ERCP or (PTC if contraindications)
Switch to specific antibiotic regimen once results back
Consider cholecystectomy and continue to monitor bloods.

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22
Q

Complications - acute cholangitis

A

Acute pancreatitis
Inadequate biliary drainage after procedure
Hepatic abscess

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23
Q

Prognosis of Acute cholangitis

A

Rapid clinical improvement once biliary drainage has occurred. Those who have severe underlying medical conditions and those whose decompression is delayed prognosis is poorer.

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24
Q

DDX of acute cholangitis

A

Acute cholecystitis - Positive murphy’s sign
Peptic ulcer disease - LFTs typically normal
Acute pancreatitis - Amylase and lipase greater elevation and CT shows stranding
Hepatic abscess - USS, CT or MRI
Acute Appendicitis - CT of abdo shows fat stranding around appendix.

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25
Q

Definition of Primary Biliary Cholangitis

A

Chronic disease of the small intrahepatic bile ducts that is characterised by excessive bile duct damage. Fibrosis develops as a consequence and toxic bile acids eventually lead to cirrhosis.

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26
Q

Epidemiology Primary Biliary Cholangitis

A

35/100,000 with peak age 55-65 years. Patients in their 20s can also present more aggressive forms, less likely to respond to treatment.
More prevalent in European and western countries

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27
Q

Aetiology Primary Biliary Cholangitis

A

Coeliac Disease
Scleroderma
Other autoimmune diseases

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28
Q

Risk factors Primary Biliary Cholangitis

A

Main:
Female sex
Age between 45-65

Others:
Family history
Smoking
UTI

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29
Q

Pathophysiology Primary Biliary Cholangitis

A

Damage to and progressive destruction of biliary epithelial cells lining small intrahepatic ducts.
This can lead to bile duct loss causing cholestasis and bile acid retention, which can lead to fibrosis or eventually cirrhosis.

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30
Q

Clinical manifestations Primary Biliary Cholangitis

A

Key Presentations
Personal history of autoimmune disease or history of hypercholesterolaemia

Signs
Hepatomegaly

Symptoms
Dry eyes and mouth
fatigue
itch
sleep disturbance
Postural dizziness
Possible jaundice and ascites
Finger clubbing / cholesterol deposits
Xanthelasma

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31
Q

Investigations Primary Biliary Cholangitis

A

1st Line
LFT - ALT, AST, ALP and Gamma-GT all elevated
Serum Albumin - decreased
AMA and ANA - present
Abdominal ultrasound scan and magnetic resonance cholangiopancreatography - excludes obstructive lesion with visible bile ducts.

Gold Standard
Blood test AMA positive

Others
Liver biopsy - bile duct lesions
Prothrombin time - prolonged
Serum immunoglobulin - elevated IgM and IgG
Transient elastography - decreased liver elasticity.

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32
Q

Criteria Primary Biliary Cholangitis

A

Cholestatic liver biochemistry (elevated LFT)
Compatible serological tests (AMA and or PBC specific ANA)
Compatible liver histology

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33
Q

Management Primary Biliary Cholangitis

A

Early stage:
Bile acid analogue - ursodeoxycholic acid
If have significant inflammatory component then immunomodulatory therapy
With cholestatic pruritus - antipruritic therapy
With fatigue - lifestyle modification

For end stage liver disease - Liver transplantation.

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34
Q

Complications Primary Biliary Cholangitis

A

Hypercholesterolaemia
Osteoporosis
Portal hypertension secondary to cirrhosis
Hepatoma

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35
Q

Prognosis Primary Biliary Cholangitis

A

Slow progression
X2 risk of mortality with or without a liver disease
Impaired quality of life with side effects.

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36
Q

DDx Primary Biliary Cholangitis

A

Obstructive bile duct lesion - much more prominent pain and bacterial cholangitis much more likely

Small-duct primary sclerosing cholangitis - Associated with IBD and more common in younger males. PSC marker present.

Drug induced cholestasis - Antibody not associated and history of relevant drug exposure

Cholestasis of pregnancy

Infiltrative malignancy within the liver - liver biopsy.

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37
Q

Definition cholecystitis

A

Acute gallbladder inflammation. Complete cystic duct obstruction which leads to inflammation of the gallbladder wall.
In 5% cases, bile stasis can block the cystic duct, causing acalculous cholecystitis.

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38
Q

Epidemiology cholecystitis

A

Occurs in 10% of symptomatic patients. 3x more common in women than men up to the age of 50 years.

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39
Q

Aetiology cholecystitis

A

Gallstones
Starvation,
TPN,
narcotic analgesics
immobility
EBV

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40
Q

Risk factors cholecystitis

A

Main:
Cholelithiasis
Total parenteral nutrition (TPN)
Diabetes
Medications

Others:
Physical inactivity,
Low fibre,
Trauma,
Infections

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41
Q

Pathophysiology cholecystitis

A

Fixed obstruction or passage of gallstones into the gallbladder neck or cystic duct can cause acute inflammation of the gallbladder wall. The impacted gallstone causes bile to be trapped in the gallbladder, which causes irritation and increases pressure. This stimulates prostaglandin synthesis which mediates an inflammatory response and can result in secondary bacterial infection if untreated. It may resolve spontaneously 5-7 days after onset.

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42
Q

Clinical manifestations Cholecystitis

A

Key Presentations
Pain and tenderness in RUQ or epigastric area which can radiate to back
Fever
Palpable mass

Signs
Murphy’s sign, Pyrexia

Symptoms
Nausea, Malaise, Anorexia, vomiting

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43
Q

Investigations cholecystitis

A

1st Line
FBC - elevated WCC
CRP, Bilirubin, AST, ALT and Gamma-GT elevated
Serum lipase / amylase elevated
Abdo USS - distended and thickened gallbladder >3mm. With pericholecystic fluid
CT or MRI - irregular thickening of gallbladder wall, increased density of fatty tissue and gas in gallbladder wall or lumen.

Gold Standard
Ultrasonography - Ultrasound - murphy’s sign.

Others
MRCP
EUS

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44
Q

Management cholecystitis

A

Analgesia, fluid resuscitation and antibiotics
Laparoscopic cholecystectomy

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45
Q

Complications cholecystitis

A

Suppurative cholecystitis
Bile duct injury due to surgery
Gallstone ileus
Cholecystoenteric fistulas

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46
Q

Prognosis cholecystitis

A

If gallbladder perforates, mortality is 30%.
Untreated acute acalculous cholecystitis is associated with up to 50% mortality.

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47
Q

DDx cholecystitis

A

Cholangitis - Has jaundice whereas cholecystitis doesn’t
Chronic cholecystitis - persistent
Peptic ulcer disease - normal LFT
GORD - more heartburn and acid reflux than right pain.
Pancreatitis - amylase and lipase elevated more.

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48
Q

Definition Acute Pancreatitis

A

Disorder of the exocrine pancreas and is associated with acinar cell injury with local and systemic inflammatory responses.

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49
Q

Epidemiology Acute Pancreatitis

A

56/100,000 a year and is one of the most common GI diseases leading to hospital admission. Approx 50% caused by gallstones and 25% by alcohol.
More common in women >60 yo and more common in with patients with microlithiasis.

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50
Q

Aetiology Acute Pancreatitis

A

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune diseases
Scorpion
Hypercalcaemia
ERCP
Drugs
GET SMASHED

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51
Q

Risk factors Acute Pancreatitis

A

Main:
Middle aged women and young-middle aged men
Hypertriglyceridemia
Causative drugs
Trauma
ERCP

Others:
Hypercalcaemia
Coxsackievirus
Pancreatic cancer

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52
Q

Pathophysiology Acute Pancreatitis

A

Abnormal intracellular calcium accumulation causes an increase in calcium transients. This causes premature activation of zymogens leading to enzyme activation which destruct acinar cells, leading to an inflammatory response.
Ethanol-induced pancreatitis as ethanol has direct toxic result on acinar cell, causing inflammation and enzyme destruction.

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53
Q

Clinical manifestations Acute Pancreatitis

A

Key Presentations
Mid-epigastric or LUQ pain that radiates to the back. Sudden onset and constant and severe and is worse with movement. Tripoding relieves pain

Signs
Diminished bowel sounds if ileus has developed. Hypotension, oliguria, hyperhidrosis, Past medical history / risk factors. Grey turner / cullens sign

Symptoms
Nausea, Vomiting, Anorexia,

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54
Q

Investigations Acute Pancreatitis

A

1st Line
Serum Lipase and Amylase - >3 times normal (3-5 upper limit in diabetes)
FBC - WBC count >12x10 9 or <4 x 10 9. Elevated haematocrit >44% (pancreatic necrosis)
CRP >200mg/L = Pancreatic necrosis
Elevated urea and creatinine
LFT - high ALT >3 times limit signals gallstones as cause.

Gold Standard
Blood serum lipase and amylase

Others
Abdo ultrasound - confirms presence of gallstones

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55
Q

Classifications Acute Pancreatitis

A

Mild acute - no organ failure or local or systemic complications
Moderate acute - presence of transient organ failure (resolves in 48 hours) and or local complications or exacerbation of comorbidity
Severe - persistent organ failure >48 hours and local complications common. Peripancreatic fluid collections, pancreatic and peripancreatic necrosis, pseudocysts and walled off necrosis.

Radiological classification: Balthazar
A Normal
B Focal or diffuse gland enlargement with small intra-pancreatic fluid collection
C Peripancreatic inflammatory changes and <30% gland necrosis
D Any of above plus single extra-pancreatic fluid and 30-50% necrosis
E Extensive extra-pancreatic fluid, pancreatic abscess and >50% gland necrosis.

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56
Q

Management Acute Pancreatitis

A

Early-goal fluid resuscitation with crystalloid fluid plus analgesia
Establish oral feeding as soon as patient can tolerate it.

Gallstone - arrange emergency endoscopic retrograde cholangiopancreatography ERCP within 24 hours

Alcohol related - alcohol abstinence programme

Do not request CECT in first 3-4 days as it cannot detect necrosis that early

Consider supplemental oxygen, antiemetic, IV antibiotics (if infection is confirmed) and nutritional support with severity assessment

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57
Q

Complications Acute Pancreatitis

A

Acute renal failure
Pancreatic abscess
Chronic pancreatitis
Sepsis
ARDS
Pancreatic effusion

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58
Q

Prognosis Acute Pancreatitis

A

80% recovery in 3-5 days. 25-30% in severe pancreatitis mortality.

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59
Q

DDx Acute Pancreatitis

A

Peptic ulcer disease - Normal or low lipase / amylase.
Intestinal obstruction - normal lipase and amylase
Cholangitis - normal lipase and amylase
Cholecystitis - normal or slightly elevated lipase and amylase with RUQ pain and thickened gallbladder wall on USS.

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60
Q

Definition Chronic Pancreatitis

A

Recurrent or persistent abdominal pain and progressive injury to the pancreas and surrounding structures - resulting in scarring and loss of function.

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61
Q

Epidemiology Chronic Pancreatitis

A

Hereditary - age 10-14 years
Juvenile idiopathic chronic pancreatitis - 19-23 years
Alcoholic acute pancreatitis - 36-44 years and senile at 56-62 years.
More prevalent in men over the age of 45 years.

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62
Q

Aetiology Chronic Pancreatitis

A

TIGAR-O
Toxins - alcohol, smoking, CKD, Hypercalcaemia/lipidaemia
Idiopathic
Genetic
Autoimmune
Recurrent and severe acute pancreatitis
Obstruction

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63
Q

Risk Factors Chronic Pancreatitis

A

Main:
Smoking
High fat / protein diet
Genetic predisposition
Coeliac

Others:
Psoriasis
Tropical geography
Coxsackievirus.

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64
Q

Pathophysiology Chronic Pancreatitis

A

Persistent cytokine secretion, pancreatic stellate cells secrete collagen stimulating fibrosis and chronic pancreatitis.

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65
Q

Clinical Manifestations Chronic Pancreatitis

A

Key Presentations
Presence of risk factors, Abdominal pain in LUQ and epigastric region and Steatorrhoea
Signs
Weight loss and malnutrition
Symptoms
Nausea, vomiting, Dyspnoea

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66
Q

Investigations Chronic Pancreatitis

A

1st Line
CT / MRI - pancreatic calcifications, focal or diffuse enlargement of pancreas and or vascular complications

Gold Standard
CT/MRI

Others
EUS - only used if diagnosis is still in question which will show ductal and parenchymal abnormalities
s-MRCP - abnormal exocrine function

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67
Q

Management Chronic Pancreatitis

A

Acute pain - smoking and alcohol cessation
Persistent pain - Alcohol and smoking cessation, analgesia, PPI and pancreatic enzymes.
Dietary modifications

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68
Q

Complications Chronic Pancreatitis

A

Pancreatic exocrine insufficiency
Diabetes mellitus
Pancreatic calcifications
Opioid addiction
Pancreatic duct obstruction

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69
Q

Prognosis Chronic Pancreatitis

A

Generally pain decreases or disappears overtime.
10 year survival is 20-30% lower than general population
Most common cause of death is pancreatic carcinoma.

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70
Q

DDx Chronic Pancreatitis

A

Pancreatic cancer - CT/MRI may show mass or lesion
Mesenteric ischaemia
Biliary colic
Peptic ulcer disease
Acute pancreatitis
Intestinal obstruction

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71
Q

Definition: Alcoholic Liver disease

A

Alcoholic liver disease has 3 stages of liver damage: Steatosis, Alcoholic hepatitis and alcoholic liver cirrhosis.

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72
Q

Epidemiology: Alcoholic Liver disease

A

3 millions deaths annually worldwide. Approx 40-80g/day in men and 20-40g/day in women for 10-12 years. There is approximately 14g in one shot of alcohol.
14.2 million people >18 years have alcohol use disorder and of these 9 million were men.

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73
Q

Aetiology: Alcoholic Liver disease

A

Chronic alcohol use and alcoholism.

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74
Q

Risk Factors: Alcoholic Liver disease

A

Main:
Obesity
Smoking - hepatocellular carcinoma

Others:
HCV
Female

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75
Q

Pathophysiology: Alcoholic Liver disease

A

Alcohol is metabolised by alcohol dehydrogenase and cytochrome P450 2E1.

Alcohol dehydrogenase converts alcohol to acetaldehyde which is then converted to acetate by acetaldehyde dehydrogenase.
This process converts NAD to NADH, which in excess inhibits gluconeogenesis and increases fatty acid oxidation.

When there is not enough acetaldehyde dehydrogenase, it binds to cellular proteins and produces acetaldehyde adducts which stimulate an immune response, causing inflammation and necrosis by neutrophils.

Cytochrome P450 2E1, increases production of free radicals through oxidation of NADPH to NADP. This creates more ROS. Improper metabolism of these ROS can stimulate hypoxia inducible factor 1 alpha - which increases TNF, and further intensifies immune response that leads to tissue injury.

Alcohol also damages intestinal mucosa, leading to endotoxemia, ending in hepatic inflammation.

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76
Q

Clinical manifestations: Alcoholic Liver disease

A

Key Presentations
Asymptomatic
RU abdominal discomfort with acute alcoholic hepatitis

Signs
Hepatomegaly, Ascites, malnutrition,
(Splenomegaly, jaundice, palmar erythema, asterixis)

Symptoms
Weight changes, anorexia, fatigue

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77
Q

Investigations: Alcoholic Liver disease

A

1st Line
Serum AST and ALT - men >30 units/l women >19 and ratio of AST/ALT >2. Can be decreased with excessive necrosis
Serum ALP and gamma GT - normal or elevated
Serum bilirubin - elevated
Serum albumin - low
FBC - anaemia, leukocytosis, thrombocytopenia, high MCV
U+E - high urea, low electrolytes.
Hepatic ultrasound

Gold Standard
LFT’s

Others
Viral hepatitis serology which will indicate absence of antigens.
CT abdo
Liver biopsy

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78
Q

Management: Alcoholic Liver disease

A

Alcohol abstinence and alcohol withdrawal management

Consider:
Weight reduction and smoking cessation
Nutritional supplementation
Immunisation - HAV and HBV
Liver Transplant - only if alcohol abstinent for >3 months
Corticosteroids - hepatic encephalopathy

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79
Q

Complications: Alcoholic Liver disease

A

Hepatic encephalopathy - buildup of harmful toxins - ammonia.
Portal hypertension - slowing of intrahepatic blood flow causing a backup of blood in portal vein
GI bleeding
Renal failure / hepatorenal syndrome - altered renal blood flow in response to altered blood flow in liver
Sepsis - bacterial infections high with cirrhosis

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80
Q

Prognosis: Alcoholic Liver disease

A

Alcoholic fatty liver returns to normal with alcohol abstinence.
5 year survival of those with cirrhosis if they stop drinking is 90% compared with 70% if they continue.
Glasgow alcoholic hepatitis score with a higher score indicating a worse prognosis.

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81
Q

DDx: Alcoholic Liver disease

A

Viral hepatitis - presence of antibodies
Cholecystitis - presence of gallstones and positive murphy’s sign.
Acute liver failure
Wilson’s disease - increased urinary copper

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82
Q

Definition NAFLD

A

NAFLD is the presence of hepatic steatosis without secondary causes of hepatic fat e.g. alcohol. Occurs when intrahepatic fat is >= 5% of liver weight.
NAFLD - presence of hepatic steatosis without evidence of hepatocellular injury in the form of hepatocyte ballooning
NASH - Non-alcoholic steatohepatitis - hepatic steatosis and ballooning, with or without fibrosis. This can lead to liver failure.

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83
Q

Epidemiology NAFLD

A

> 25% worldwide. Median age is 53 years but can occur at any age.

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84
Q

Aetiology NAFLD

A

HCV
Wilson’s disease
Starvation
Parenteral nutrition
Medications
Acute fatty liver of pregnancy
Metabolic disorders

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85
Q

Risk Factors NAFLD

A

Main:
Obesity - truncal / central
Insulin resistance or diabetes
Dyslipidaemia
Metabolic syndrome
Rapid weight loss
Medications
Total parenteral nutrition

Others:
HCV
Wilsons
Lipodystrophy

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86
Q

Pathophysiology NAFLD

A

Insulin resistance leading to accumulation of excessive triglyceride axxumulation in the liver and development of steatosis. Once developed, additional injury or oxidative injury can cause the necro-inflammatory component seen in steatohepatitis.
Antioxidant deficiency, hepatic iron, fat derived hormones (leptin and resistin) and intestinal bacteria have been linked to NASH development from NAFLD.

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87
Q

Clinical manifestations NAFLD

A

Key Presentations
Presence of risk factors, absence of significant alcohol abuse, mild abnormality in LFT and truncal obesity

Signs
Hepatosplenomegaly

Symptoms
Fatigue, Malaise, RUQ abdominal discomfort

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88
Q

Investigations NAFLD

A

1st Line
LFT - AST, ALT, ALP, GGT, Bilirubin normal or slightly elevated
FBC - Anaemia and thrombocytopenia in cirrhosis and PHTN
Metabolic panel - abnormal and hyponatremia
Lipid panel - elevated total cholesterol, LDL, TGLY and low HDL.

Gold Standard
Liver Biopsy

Others
INR prothrombin - normal or elevated.
Serum albumin - normal or decreased.
Viral hepatitis - antibody negative
Liver ultrasound - abnormal echotexture.
Elastography - liver stiffness
Abdo MRI - increased liver fat content
Fasting insulin - elevated.

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89
Q

Management NAFLD

A

Weight loss with healthy diet and exercise
Pioglitazone - improves liver histological scores but be aware of side effects of potential weight gain
Vitamin E
Weight loss pharmacotherapy - Orlistat prevents absorption of fats
Gastric bypass - BMI >40 or >35 with at least one other obesity related comorbidity considered for bariatric surgery.

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90
Q

Complications NAFLD

A

Ascites
Variceal Haemorrhage
Hepatocellular carcinoma
Cirrhosis → liver failure
Death - advanced stage 3 or 4 fibrosis

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91
Q

Prognosis NAFLD

A

NASH associated with increased mortality over 14 years, usually as a result of CVD or other comorbidity rather than liver causes.
Recurrent NAFLD is 20-100% after liver transplantation.
Mortality increases as the fibrosis stage increases.

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92
Q

DDx NAFLD

A

ALD - AST/ALT ratio >2
Cryptogenic cirrhosis
Autoimmune hepatitis - antibody tests and hyperglobulinemia
Viral hepatitis - presence of antibodies
Haemochromatosis - elevated ferritin and iron saturation
Primary biliary cholangitis - significant elevation in ALP, GGT and IgM
Wilsons - elevated urinary copper and elevated hepatic copper.

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93
Q

Definition: chronic liver disease

A

Pathological end stage of any chronic liver disease, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules

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94
Q

Epidemiology: chronic liver disease

A

In Europe, cirrhosis related to either Viral infection or alcohol abuse were the main indications of a liver transplant. 1.5 billion people worldwide have chronic liver disease.

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95
Q

Aetiology: chronic liver disease

A

NAFLD
ALD
Viral hepatitis
Any chronic liver disease
Cryptogenic - idiopathic

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96
Q

Risk Factors: chronic liver disease

A

Main:
Alcohol misuse
IV drug misuse
Unprotected intercourse
Obesity
Country of birth - HBV and HCV.

Others:
Blood transfusions
Tattoos

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97
Q

Pathophysiology: chronic liver disease

A

Hepatic fibrosis occurs from hepatic stellate cells and leads to an accumulation of collagen I and III in hepatic parenchyma. With activation, stellate cells become contractile leading to increased portal resistance during liver fibrosis and cirrhosis. This leads to portal hypertension, development of ascites and gastro-oesophageal varices.

Compensated cirrhosis - Cirrhosis investigations present but liver synthetic function is preserved and generally no complications

Decompensated cirrhosis - Cirrhosis investigations present and liver synthetic function is decreased and development of complications such as PHTN, Variceal bleeding, hepatic encephalopathy and jaundice.

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98
Q

Clinical manifestations: chronic liver disease

A

Key Presentations
Ascites and abdominal distension
Jaundice and pruritus
Haematemesis (blood in vomit) and Melaena (black stool)

Signs
Palmar erythema, Spider naevi, leukonychia, hepatosplenomegaly, distension and collateral circulation, hepatic fetor, Peripheral oedema - salt retention.

Symptoms
Fatigue, weakness, weight loss,

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99
Q

Investigations: chronic liver disease

A

1st Line
LFTs - AST/ALT >=1 - cirrhosis. GGT elevated
Serum albumin and sodium - reduced
Serum potassium and prothrombin time - elevated
Platelet count - reduced

Depending upon aetiology - viral hepatitis antibodies may be positive.

Gold Standard
Liver Biopsy

Others
Abdo CT/MRI - liver surface nodularity with reduced liver size.
USS or EUS /\
Liver elastography

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100
Q

Management: chronic liver disease

A

Treatment of underlying chronic liver disease
Monitoring - USS, CT, EUS, MRI
Supportive and palliative care
Sodium restriction and diuretic therapy for ascites / oedema
Liver transplantation

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101
Q

Complications: chronic liver disease

A

Ascites
Gastro-oesophageal varices
Malnutrition and Sarcopenia
Hepatocellular carcinoma
Bleeding and thrombosis
Hepatorenal syndrome.

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102
Q

Prognosis: chronic liver disease

A

10 year survival with compensated cirrhosis is 90% with decompensated 50%
Mean survival time for decomp is 2 years
4 stages of cirrhosis:
No varices or ascites - 1% mortality per year
Varices with no bleeding, no ascites - 4%
With ascites with or without varices and no bleeding - 20%
GI bleeding due to PHTN with or without ascites - 57%

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103
Q

DDx: chronic liver disease

A

Budd-Chiari syndrome - Doppler ultrasound and CT - absence of hepatic vein filling
Portal vein thrombosis - MRI normal hepatic venous pressure but doppler and abdo CT show portal vein filling defect
Constrictive pericarditis
Idiopathic portal hypertension - Liver biopsy shows no evidence of cirrhosis

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104
Q

What is Portal Hypertension

A

PHTN - Portal hypertension is characterised by a pathologic increase in portal venous pressure that leads to the formation of an extensive network of portosystemic collaterals that divert a large fraction of portal blood to the systemic circulation, bypassing the liver. Blood backs up in nearby veins in the oesophagus and stomach, causing varices.

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105
Q

When do varices occur during liver disease

A

Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren’t designed to carry large volumes of blood.

106
Q

What is haematemesis

A

Vomiting fresh blood. This occurs as a result of bleeding occurring in any part of the upper gastrointestinal tract.

107
Q

Definition Hepatic Encephalopathy

A

Brain dysfunction caused by advanced liver insufficiency and or portosystemic shunt.

108
Q

Epidemiology Hepatic Encephalopathy

A

30-40% of patients with cirrhosis develop HE within their illness.
HE occurs in 55% of patients with a TIPS procedure within 2 years.

109
Q

Aetiology: Hepatic Encephalopathy

A

High ammonia levels
GI bleeding
Hypokalaemia
Metabolic encephalopathy
Brain atrophy
Brain oedema

110
Q

Risk Factors: Hepatic Encephalopathy

A

Cirrhosis
Acute hepatic failure
Portacaval shunt
Hypovolaemia,
GI bleeding
Excessive protein intake
Hypokalemia or hyponatremia
Hypoxia and metabolic alkalosis.

111
Q

Pathophysiology: Hepatic Encephalopathy

A

Impaired LFT leads to impaired ammonia clearance, which can alter cerebral concentration of amino acids and affect neurotransmitter synthesis and electrical activity. It can also lead to increased intracellular astrocyte osmolarity, inducing astrocyte swelling and can lead to raised ICP.

Patients with decompensated cirrhosis have altered intestinal microbiome and can lead to an overgrowth in potentially pathogenic bacteria, leading to pro-inflammatory cytokines such as IL1 and TNF. Systemic inflammation activates microglia in the brain producing neuroinflammation.

112
Q

Clinical Manifestations: Hepatic Encephalopathy

A

Key Presentations
Altered mental status, confusion, mood and motor disturbances

Signs
Ataxia, bradykinesia, hypokinesia, slow monotonous speech, coma, hyper-reflexia and nystagmus. Palmar erythema, jaundice, hepatomegaly, ascites

Symptoms
Euphoria, depression, insomnia or hypersomnia,

113
Q

Investigations Hepatic Encephalopathy

A

1st Line
LFT - abnormal
Serum electrolytes - normal or hyponatremia / kalcemia
FBC - normal or leukocytosis or thrombocytosis
Blood ammonia - Raised
CT scan - absence of other causes and presence of oedema

Gold Standard
Psychometric Hepatic Encephalopathy Score PHES.

Others
EEG - decrease in brain wave frequency and amplitude.

114
Q

Management: Hepatic Encephalopathy

A

Supportive care, reversal of precipitating factors and investigation of alternative causes
Lactulose - helps draw water from body into colon and soften stool. It also decreases intestinal production and absorption of ammonia.
Rifaximin - all those with symptoms persisting after lactulose or those contraindicated to lactulose.
Branches chain amino acids
Consider transplant or shunt.

115
Q

Complications: Hepatic Encephalopathy

A

Death
Falls
Neurological deficits
Re-admission

116
Q

Prognosis: Hepatic Encephalopathy

A

42% 1 year survival and 23% 3 year survival. When patient is at grade 4 (coma), mortality is at 80%.

117
Q

DDx: Hepatic Encephalopathy

A

Brain tumours - MRI
Subdural haematoma - CT shows haemorrhage
Acute stroke - CT shows haemorrhage or infarct
Meningitis - Lumbar puncture shows cloudy CSF.

118
Q

Definition HAV

A

RNA virus with a faecal oral route of transmission. Most infections in adults and older children are symptomatic. Average incubation is 28 days. Not associated with chronic liver disease. 70% develop jaundice.

119
Q

Epidemiology HAV

A

In developed countries, outbreaks are associated with contaminated food and water. High prevalence in Africa, Asia and Latin america. Mainly occur in early childhood.
Vaccination to prevent this.

120
Q

Aetiology HAV

A

Close contact with an infected person
Contaminated food and or water

121
Q

Risk Factors: HAV

A

Main:
Living in or travelling to endemic region
Close personal contact with infected person
Homosexual men
Homelessness and illegal drug use.
Known foodborne outbreak

Others:
Occupational exposure - healthcare

122
Q

Pathophysiology: HAV

A

Virus transported to intestinal epithelium then through mesenteric veins to liver. Virus enters hepatocytes and replicates, is then excreted in bile and blood from infected hepatocytes.
Liver injury is when cytotoxic T cells lyse the infected hepatocytes.
Viral particles are then excreted in stools.

123
Q

Clinical Manifestations: HAV

A

Key Presentations
Travel
Fever
Malaise
Nausea and vomiting
Jaundice
RUQ pain

Signs
Hepatomegaly, clay coloured stools, Dark urine

Symptoms
Fatigue, Headache and pruritus

124
Q

Investigations: HAV

A

1st Line
LFT - ALT and AST, bilirubin elevated
U+E - elevated blood urea and serum creatinine
Prothrombin - slightly prolonged of 11-26 seconds

Gold Standard
IgM anti-hepatitis A test - positive - active infection
IgG anti-hepatitis A test - may be positive - will show recovery or recent infection

Others
Hepatitis A RNA detection - used if others inconclusive.

125
Q

Management: HAV

A

If known exposure <2weeks then immunisation if not already.
If confirmed Hep A - rest and recovery with supportive care.
If acute liver failure - liver transplant VERY RARE

126
Q

Complications: HAV

A

Acalculous cholecystitis
Pancreatitis

127
Q

Prognosis: HAV

A

85% full recovery within 3 months.
<1% patients have a fulminant course of illness and refer to liver transplant. 1 year expectancy with liver transplant for acute HAV is 69%.

128
Q

DDx: HAV

A

Other viral hepatitis - detected through serology of viral antibodies.
EBV - negative serology for all types of hepatitis and EBV IgG and IgM positive
Coxsackievirus - atypical lymphocytes but no viral hep serology
Autoimmune hepatitis - serum gamma-globulin more than 2x normal and sometimes have ANA antibodies.
Alcohol hepatitis - AST/ALT ratio of at least 2. FBC show anaemia, leukocytosis and or thrombocytopenia.

129
Q

Defintion HBV

A

DNA virus transmitted by percutaneous and permucosal routes.
Can be prevented with immunisation

130
Q

Epidemiology HBV

A

Most common liver infection globally. People from endemic areas (africa and asia) at increased risk.
350-400 million of the world population has chronic hepatitis B

131
Q

Aetiology HBV

A

Infected needles
Unprotected sex
Unsanitary conditions
Childbirth

132
Q

Risk factors HBV

A

Main:
Perinatal exposure to infant born with HBV positive mother
High risk sexual behaviours
IV drug use
Born in highly endemic region
Family history

Others:
Occupational workers
Infected with HIV
Possible haemodialysis

133
Q

Pathophysiology HBV

A

HBsAg - outer surface of virus (surface antigen)
HBcAg - Core of the virus (core antigen)
Viral DNA + E antigen (HBeAg) shows active replication and infection.

Causes an immune response and removal of HBV infected cells via CD8+ T lymphocytes.

At onset of virus, HBsAg and Viral DNA with HBeAg will be present. HBsAg for >6months indicates chronic infection

134
Q

Clinical manifestations of HBV

A

Key Presentations
Presence of risk factors and asymptomatic.

Signs
VERY RARE - Liver common symptoms and signs

135
Q

Investigations for HBV

A

1st Line
LFT - elevated AST, ALT and ALP with bilirubin. Decreased albumin
FBC - microcytic anaemia and or thrombocytopenia
U+E - hyponatremia and high urea

Gold Standard
Serum hepatitis B surface antigen or e antigen - Positive (in active onset or chronic)
Serum hepatitis B antibody to both surface and core antigen - positive in IgG and IgM
Others
Test for coinfections

136
Q

Management of HBV

A

Supportive care - 95% of immunocompetent will achieve antibodies
Antiviral therapy (entecavir) or liver transplant in those with acute liver failure
In pregnant women give tenofovir disoproxil

137
Q

Complications of HBV

A

Fulminant hepatic failure
Cirrhosis
Hepatocellular carcinoma
Hep B associated glomerulonephritis.

138
Q

Prognosis HBV

A

20% will develop chronic HBV. Children under 6 at increased risk as 50% to chronic HBV and % increases with decreasing age.

139
Q

DDX HBV

A

Other viral hepatitis
EBV - no viral antibodies
HSV - HSV IgM and HSV PCR positive
Acute alcoholic hepatitis - Negative for viral hepatitis
Autoimmune hepatitis - serum gamma-globulin more than 2x normal and sometimes have ANA antibodies.

140
Q

Definition HVC

A

Percutaneous exposure to infected blood.
Inflammation of the liver caused by hepatitis C virus.
Chronic infection causes liver inflammation and fibrosis - leading to development of cirrhosis, liver failure or liver cancer over 20-50 years.

141
Q

Epidemiology HVC

A

58 million people have hep C. European and eastern mediterranean regions have the highest prevalence rate. Genotype 1 is most prevalent worldwide.

142
Q

Aetiology HCV

A

Blood transmission
Injections
Sexual activity - homogenous
Haemodialysis and Perinatally

143
Q

Risk factors HCV

A

Main:
Unsafe medical practices
IV or intranasal drug use
Blood transfusions
Heavy alcohol use
HIV

Others:
Haemodialysis
Healthcare workers
Multiple sex partners
Tattoos or body piercings.

144
Q

Pathophysiology of HCV

A

Persistent infection appears due to weak CD4+ and CD8+ T cell responses during acute infection which fail to control viral replication. Liver damage is driven from local immune responses which triggers fibrogenesis.

145
Q

Clinical manifestations HCV

A

Key Presentations
Presence of risk factors
Asymptomatic

Signs
RARELY - Liver condition symptoms.

146
Q

Investigations HCV

A

1st Line
Hep C antibody-enzyme immunoassay - Positive indicates current or past infection
Serum aminotransferases - elevated.

Gold Standard
Hepatitis C RNA polymerase chain reaction - Indicates presence of active infection

Others
Liver biopsy - inflammation or fibrosis
Test for co-infection - Hep B

147
Q

Management HCV

A

Antiviral therapy e.g. glecaprevir
Treatment of cirrhosis or acute liver failure accordingly.

148
Q

Complications HCV

A

Cirrhosis
Hepatocellular carcinoma
Rheumatological conditions
Treatment related HBV reactivation

149
Q

Prognosis HCV

A

Europe - 5 year 91% survival and 10 year 79% with compensated cirrhosis
5 years 50% with decompensated survival .

150
Q

Ddx HCV

A

Chronic hep B
Alcoholic liver disease
Steatohepatitis - USS shows fatty liver and Hep C antibody test negative
Haemochromatosis - iron is abnormal

151
Q

Definition Autoimmune hepatitis

A

Chronic inflammatory disease of the liver of unknown aetiology.

152
Q

Epidemiology Autoimmune hepatitis

A

Female adults and children more commonly affected than males
AIH type 1 more common in women affecting age 10-60
Type 2 affects children.

153
Q

Aetiology Autoimmune hepatitis

A

Unknown

154
Q

Risk factors Autoimmune hepatitis

A

Main:
Genetic predisposition
Female

Others:
Other viral hepatitis
EBV
Drugs or herbal agents

155
Q

Pathophysiology Autoimmune hepatitis

A

Alteration in T-cell function and or B cell function.

Type 1 - ANA and smooth muscle antibody (SMA) positive
Type 2 - Anti-liver kidney microsomal-1 or anti liver cytosol specific positive.

156
Q

Clinical manifestations Autoimmune hepatitis

A

Key Presentations
Fatigue / Malaise/ anorexia and abdominal discomfort.

Signs
Hepatomegaly / Jaundice

Symptoms
Pruritus, nausea, fever, spider angioma, arthralgia.

157
Q

Investigations Autoimmune hepatitis

A

1st Line
LFT - raised AST, ALP, Gamma GT and ALT and bilirubin
Serum globulin - increased
Serum albumin - decreased
Prothrombin time - Increased

Gold Standard
Liver biopsy - periportal lesion or interface hepatitis.

Others
ANA and SMA test - elevated in type 1
Anti LC1 - positive in type 2

158
Q

Management Autoimmune hepatitis

A

Acute severe - High dose corticosteroids - methylprednisolone sodium succinate or prednisolone.
AIH and primary biliary cirrhosis - Corticosteroid plus immunosuppressant and ursodeoxycholic acid.

159
Q

Complications Autoimmune hepatitis

A

Osteoporosis, Truncal obesity, DM or hypertension - due to corticosteroid therapy
Hepatocellular carcinoma
Infections - due to immunosuppressant
Liver failure.

160
Q

Prognosis Autoimmune hepatitis

A

Untreated 5 year survival 50% and 10 year 10%.
10 year survival with treated 90%
20 year with cirrhosis is 40% or 80% without.

161
Q

DDx Autoimmune Hepatitis

A

Primary biliary cirrhosis - ALP and Gamma glutamyl transferase raised more. AMA and ANA present. Liver biopsy shows bile duct lesion or periductal fibrosis.

Chronic Hepatitis - Presence of other viral hepatitis antibodies

Alpha 1 antitrypsin deficiency - low serum level

Wilsons - Serum copper decreased with excessive urinary copper excretion.

162
Q

Definition Infective Diarrhoea

A

Escherichia coli gram negative rod shaped bacterium that colonises the gastrointestinal tract. Ecoli becomes pathogenic by acquiring virulence factors or genetic mutations.
Infection of pathogenic strains through ingestion of contaminated food or water.

163
Q

Epidemiology Infective Diarrhoea

A

Older people, infants and people who are immunocompromised are more susceptible to infection and secondary complications.
Can also be associated with UTI and pneumonia.

164
Q

Aetiology Infective Diarrhoea

A

80% from enterohemorrhagic Ecoli (EHEC) infection
70% from enterotoxigenic E coli (ETEC) infection
30% from other types.

Norovirus
Rotovirus - most common cause

165
Q

Risk Factors Infective Diarrhoea

A

Main:
Ingestion of contaminated food
Travel
Poor hygiene
Infantile or advanced age

Others:
Immunocompromised state
Contact with infected animals

166
Q

Pathophysiology Infective Diarrhoea

A

Escherichia coli is a gram negative rod shaped bacteria that propels itself via flagella.
Diarrhoea is caused by a combination of intestinal inflammation, loss of absorptive surface and increased mucosal permeability and ion secretion.

167
Q

Clinical manifestations Infective Diarrhoea

A

Key Presentations
History of travel, contact with contaminated food or contact with infected people.
Diarrhoea - bloody or watery.

Signs
Volume depletion - dry mucous, reduced skin turgor and tachycardia or hypotension

Symptoms
Abdominal pain, fever, nausea, anorexia and lethargy.

168
Q

Investigations Infective Diarrhoea

A

1st Line
Stool cultures - positive for pathogenic E coli
FBC - elevated leukocyte count, low haemoglobin and or platelets
Renal function and electrolytes - raised urea and creatinine, Hypokalaemia

Gold Standard
/

Others
Blood cultures - positive for e coli
Abdominal x ray - bowel wall thickening
Abdo CT - mural thickening of colon.

169
Q

Complications Infective Diarrhoea

A

Haemolytic uraemic syndrome
Bacteraemia
IBS

170
Q

Prognosis Infective Diarrhoea

A

Most are asymptomatic and self limiting with average recovery 2-5 days.
Foodborne enterohemorrhagic E Coli - Fatality of up to 2% in industrialised countries with higher rates of older people and children.

Enterotoxigenic E coli - fatality of 0.1% in industrialised countries.

171
Q

Ddx Infective Diarrhoea

A

Viral gastroenteritis - shorter duration of 24-48 hours and no stool bacteria.

Alternative gastroenteritis / travellers diarrhoea - stool cultures will identify alternative pathogen e.g. salmonella, shigella

Amoebiasis - stool sample will show entamoeba

Crohns - more chronic history, slower onset and prolonged diarrhoea and weight loss.

172
Q

Management Infective Diarrhoea

A

Rehydration and supportive therapy - preferably glucose containing as glucose promotes absorption of sodium and water in intestinal lumen

Bismuth subsalicylate - reduce diarrhoea.

Antibiotic for moderate to severe cases - ciprofloxacin or rifamycin

173
Q

Definition Haemochromatosis

A

A group of autosomal recessive disorders of iron metabolism.

174
Q

Epidemiology Haemochromatosis

A

HFE related occurs primarily in norther european descent. 1 in 10 white people heterozygous for C282Y.
Clinical disease more common in men.
Typically age 30-50

175
Q

Aetiology Haemochromatosis

A

Mutations in the HFE gene - C282Y and H63D
Alcoholism
Dysmetabolic syndrome

176
Q

Risk factors Haemochromatosis

A

Middle age
Male sex
White ancestry
Family history
Supplemental iron

177
Q

Pathophysiology Haemochromatosis

A

C282Y - hepatic hepcidin gene expression is low and macrophages continually release iron from erythrophagocytosis. Leads to an elevation in serum iron and transferrin saturation.

Clinical manifestations are said to be caused by direct result of pro-oxidant effects iron has on organs - e.g. the liver where excess iron causes fibrosis.

178
Q

Classifications Haemochromatosis

A

Type 1: Hereditary HFE
Autosomal recessive mutation of HFE gene on chromosome 6
1A = mutation in C282Y. 1B = C282Y and H63D. 1C = HFE S65C

Type 2: Juvenile
A = mutation of the hemojuvelin gene 1p21
B = Hepcidin gene 19q13

Type 3: Transferrin receptor 2
Mutation in 7q22.

Type 4: Ferroportin
SLC40A1 gene 2q32.

179
Q

Clinical manifestations Haemochromatosis

A

Key Presentations
Mainly asymptomatic
Calcium pyrophosphate crystal deposition, with pseudogout and chronic arthropathy - 2nd and 3rd metacarpophalangeal joints and proximal interphalangeal joints.

Signs
Hepatomegaly, Hypogonadism, Diabetes

Symptoms
Fatigue, weakness, lethargy.

180
Q

Investigations Haemochromatosis

A

1st Line
Serum transferrin saturation >45%
Serum ferritin >674 picomoles in men and >449 in women

Gold Standard
HFE mutation analysis.
Others
HFE mutation analysis - C282Y homozygosity or C282Y/H63D heterozygosity etc.
Liver biopsy - raised iron content
LFT - aminotransferases above normal
Fasting blood sugar - raised
ECG and Echo - Dilated Cardiomyopathy and T wave flattening
Hormones - lowered

181
Q

Criteria Haemochromatosis

A

Stage 0 = C282Y homo with normal transferrin and ferritin with no clinical symptoms.

Stage 1 = C282Y homo and increased transferrin and normal ferritin with no symptoms.

Stage 2 = C282Y homo with both increased transferrin and serum ferritin but no symptoms

Stage 3 = C282Y homo both increased transferrin and ferritin with mild clinical symptoms affect life

Stage 4 = Same as stage 3 but with clinical symptoms manifesting organ damage.

182
Q

Management Haemochromatosis

A

Stage 0 = Patients monitored every 3 years with history, examination and BT

Stage 1 = Patients monitored once yearly.

Stage 2/3/4 = Phlebotomy every 1-4 weeks or 2-3 times yearly depending on stage by removing 7mL/kg blood per session to get levels in check.

Avoid Alcohol, Vit C and iron supplements.

183
Q

Complications Haemochromatosis

A

Cirrhosis
Diabetes Mellitus
Chronic congestive heart failure - fluid overload and arrhythmias.
HCC - hepatocellular carcinoma.
Hypogonadism
Bone loss

184
Q

Prognosis Haemochromatosis

A

Mean survival was 21 years and most will establish iron-overload related disease.
11% increase risk of dying from cancer.

185
Q

Ddx Haemochromatosis

A

Iron overload from chronic transfusion or anaemias - no HFE mutations
Hep B and Hep C - Positive hep serology without homozygous HFE mutations
Excessive iron supplementation - absence of homozygosity for HFE mutations.

186
Q

Definition Wilsons Disease

A

Autosomal recessive disease of copper accumulation and toxicity caused by a defect in the ATP7B causing a defect in the enzyme metal P type ATPase involved in the excretion of copper within hepatocytes.

187
Q

Epidemiology Wilsons Disease

A

Between 1 in every 30,000-50,000 people. All sexes and ethnic groups were affected equally. Appears around age 10-40.

188
Q

Aetiology Wilsons Disease

A

Genetic mutation in ATP7B gene

189
Q

Risk factors Wilsons Disease

A

History of hepatitis
Family history
ATP7B gene mutation

190
Q

Pathophysiology Wilsons Disease

A

ATP7B loads copper onto apoceruloplasmin to make ceruloplasmin and transports excess copper into bile. Loss of ATP7B function leads to lack of copper incorporation and it cannot be transported into bile and excreted into faeces. Copper accumulation exceeds liver capacity and is excreted into blood and accumulates in the tissues.
High levels of copper cause toxicity by oxidant damage which results in cell injury, inflammation and death.

191
Q

Classifications Wilsons Disease

A

H1 = Acute hepatic - acutely occurring jaundice, either due to hepatitis like illness or coombs negative haemolytic disease. May progress to liver failure

H2 = Chronic hepatic - any type of chronic liver disease with or without symptoms and may lead to or present as decompensated cirrhosis.

N1 = associated with symptomatic liver disease
N2 = not associated with
Nx = presence or absence of liver disease not investigated.

192
Q

Clinical manifestations Wilsons Disease

A

Key Presentations
Presence of kayser-fleischer rings

Signs
Acute liver failure, Tremor, Dysarthia, Dystonia, incoordination, poor handwriting

Symptoms
Behavioural abnormalities, depression, personality change

193
Q

Investigations Wilsons Disease

A

1st Line
LFT - elevated AST and ALT and bilirubin with low albumin.
INR - prolonged
24 hour urinary copper - >100mg
Slit-lamp exam - KF rings of gold-brown pigment representing copper deposition in the membrane of descemet of the cornea.
Serum ceruloplasmin - <200mg/L

Gold Standard
24 hour urinary copper - >100mg (>40 is suggestive)

Others
FBC - anaemia or low WBC/platelet count
Liver biopsy - liver copper >250mg/g
Non-ceruloplasmin bound copper concentrations (NCC) - elevated
DNA testing for ATP7B mutations

194
Q

Management Wilsons Disease

A

Liver transplantation in hepatic failure
In mild hepatic failure - Oral chelation therapy plus zinc and dietary restriction of copper. Zinc inhibits intestinal absorption of copper.
Penicillamine - oral chelator that promotes renal excretion of copper.

195
Q

Complications Wilsons Disease

A

Liver failure

196
Q

Prognosis Wilsons Disease

A

Normally if treatment started early, patients have a normal quality of life or in mild cases liver damage can recover.

197
Q

DDx Wilsons Disease

A

Hepatitis - hep antibody positive
Alpha 1 antitrypsin deficiency - Enzyme is deficient
Autoimmune hepatitis - positive AMA and ANA antibody
Steatohepatitis - fatty liver and inflammation on biopsy

198
Q

Defintion Alpha 1 Antitrypsin Deficiency

A

Autosomal codominant genetic disorder from allele mutations in the SERPINA1 gene at the protease inhibitor (PI) locus.

199
Q

Epidemiology Alpha 1 Antitrypsin Deficiency

A

Mean age that smokers with AAT deficiency present is 32-41 years.
Liver involvement present in neonates and is the second most common cause of liver transplantation in children.

200
Q

Aetiology Alpha 1 Antitrypsin Deficiency

A

PI allele

201
Q

Risk factors Alpha 1 Antitrypsin Deficiency

A

Family history of AAT deficiency
Male
Smoker aged 32-41

202
Q

Pathophysiology Alpha 1 Antitrypsin Deficiency

A

PI allele mutations in the rSERPINA1 gene that cause ineffective activity of specific protease inhibitor AAT, which is responsible for neutralising neutrophil elastase and preventing inflammatory tissue damage in the lungs.
Variants of the enzyme may also polymerise and accumulate in the liver, causing hepatic failure.

203
Q

Clinical manifestations Alpha 1 Antitrypsin Deficiency

A

Key Presentations
Productive cough
Dyspnoea on exertion
Current cigarette smoker
Signs
Hepatomegaly, Ascites, Chest hyperinflation
Symptoms
Wheezing

204
Q

Investigations Alpha 1 Antitrypsin Deficiency

A

1st Line
Plasma AAT level <20 micromol/L
Pulmonary function testing - signif reduce in FEV1, FVC, FEV1/FVC, increased TLC
Cxr - large lung volume and basilar predominant emphysema
Chest CT - panacinar emphysema and or bronchiectasis
LFT - elevated AST, ALT, ALP and bilirubin

Gold Standard
Plasma AAT level <20 micromol/L
Isoelectric focusing - AAT varients

Others
Genotyping - AAT alleles
Gene sequencing - SERPINA1 mutation
Exercise testing with ABG - reduced PaO2 and elevated A-a gradient

205
Q

Management Alpha 1 Antitrypsin Deficiency

A

Smoking cessation, Pollution avoidance, Hepatitis vaccination
With pulmonary manifestations - Standard COPD treatment and AAT augmentation therapy
Hepatic - Standard liver disease treatment and alcohol avoidance

206
Q

Complications Alpha 1 Antitrypsin Deficiency

A

HCC
Necrotising panniculitis

207
Q

Prognosis Alpha 1 Antitrypsin Deficiency

A

No cure but many have normal lifespans.
Between 50-72% deaths are caused by respiratory failure
Liver fibrosis occurs in 20-36% of asymptomatic adults with PI*ZZ AAT deficiency.
⅓ patients with advanced age and a homozygous phenotype will due to complications with PHTN and primary liver cancer.

208
Q

DDx Alpha 1 Antitrypsin Deficiency

A

COPD - long period of smoking and advanced age
Asthma - clinically indistinguishable, reversibility of obstruction is partial in AAT deficient emphysema but fully in asthma
Bronchiectasis - marked dilation of airways on CT
Viral hepatitis - viral serology markers
ALD - Altered Gamma GT, AST and ALT

209
Q

Definition Hepatic Cancer

A

Hepatocellular carcinoma (hepatoma) is a primary cancer arising from hepatocytes in a predominantly cirrhotic liver.

210
Q

Epidemiology Hepatic Cancer

A

6th most common cause of cancer worldwide and 2nd leading cause of cancer related death. 44% cases of HCC worldwide are from chronic HBV.
Mean age of diagnosis - 46 in africa, up to 60 in US and Europe.

211
Q

Aetiology Hepatic Cancer

A

Cirrhosis
HBV
HCV
Diabetes Mellitus

212
Q

Risk factors Hepatic Cancer

A

Cirrhosis
Heavy alcohol consumption
Viral hepatitis
Diabetes
Family history
Obesity

Cigarette smoking
AAT deficiency
Oral contraceptives
Haemochromatosis

213
Q

Pathophysiology Hepatic Cancer

A

Chronic HBV and HCV with metabolic conditions may lead to ROS from oxidative stress, that cause damage to DNA resulting in mutation of P53 gene.

HBV is a direct carcinogen and may cause methylation of the p16 gene which is known to cause hepatocellular carcinogenesis causing HCC.

214
Q

Clinical manifestations Hepatic Cancer

A

Key Presentations
All key symptoms of liver damage e.g. Ascites, Jaundice, RUQ pain, Hepatic encephalopathy
Signs
Weight loss, Splenomegaly, Palmar erythema, spider naevi, Oedema
Symptoms
Early satiety, Fatigue, Diarrhoea

215
Q

Investigations Hepatic Cancer

A

1st Line
FBC - anaemia and or thrombocytopenia
U+E - high urea and hyponatremia
LFT - Elevated ALT, AST, ALP, bilirubin and low albumin
INR - prolonged
AFP - elevated
USS - poorly defined margins and coarse, irregular internal echos

Gold Standard
Liver biopsy - poorly differentiated hepatocytes with large multinucleated giant cells having central necrosis

216
Q

Management Hepatic Cancer

A

Stage 0 / A or very early - consider resection, thermal ablation or transplant
Stage B - TACE or TARE or percutaneous ablation
Stage C - atezolizumab and bevacizumab
Stage D - Hospice care

217
Q

Complications Hepatic Cancer

A

Biliary obstruction
Cachexia
Hypoglycaemia
Hepatic failure

218
Q

Prognosis Hepatic Cancer

A

5 year survival is 20% in general or 0-10% if symptomatic
Non cirrhotic patients treated with surgical resection is 42% at 5 years
Those with a transplant - 75% 4 year survival rate
Stage D - 50% survival at <3 months

219
Q

DDx Hepatic Cancer

A

Cholangiocarcinoma - INR and transaminases mildly elevated or normal.
Hepatic adenoma - Doppler shows venous pattern instead of arterial hypervascularization of HCC
Haemangioma of liver - normal LFT and alpha fetoprotein

220
Q

Definition Ascites

A

Pathological collection of fluid in the peritoneal cavity.

221
Q

Aetiology Ascites

A

Portal hypertension
Cirrhosis
Chronic liver disease
Congestive heart failure
Hypoalbuminemia
Fulminant hepatitis

222
Q

Clinical manifestations Ascites

A

Key Presentations
Abdominal distension and tenderness.
Signs
Fluid on physical exam with shifting dullness
Symptoms
Early satiety, SOB,

223
Q

Investigations Ascites

A

1st Line
USS, CT or MRI

224
Q

Management Ascites

A

Abdominal paracentesis

225
Q

Complications Ascites

A

Spontaneous bacterial peritonitis

226
Q

Prognosis Ascites

A

If SBP 10-28% mortality rate.

227
Q

Ddx Ascites

A

HCV
ALD
Congestive heart failure

227
Q

Definition Pancreatic Cancer

A

Primary pancreatic ductal adenocarcinoma. Goes from pre-invasive pancreatic intraepithelial neoplastic lesions to invasive ductal adenocarcinoma.

228
Q

Aetiology Pancreatic Cancer

A

Cigarette smoking
Hereditary pancreatitis
Family history

229
Q

Risk Factors Pancreatic Cancer

A

Smoking
Family history pancreatic cancer
Family history of other hereditary cancers

230
Q

Epidemiology Pancreatic Cancer

A

Most common at age 65-75 years and generally presents late. Median age was 70 and median age of death was 72.

231
Q

Pathophysiology Pancreatic Cancer

A

65% in the head, 15% body and 10% tail of pancreas. Progression from normal epithelium to invasive carcinoma follows a linear progression. Early genetic alterations include telomere shortening and mutations in the KRAS2 oncogene followed by inactivation of the p16 tumour suppressor gene.

232
Q

Clinical manifestations Pancreatic Cancer

A

Key Presentations
Jaundice, Non specific upper abdominal pain, weight loss and anorexia and back pain.
Signs
Hepatomegaly
Symptoms
Nausea, vomiting, early satiety, Polyuria, thirst, Steatorrhoea,

233
Q

Investigations Pancreatic Cancer

A

1st Line
Pancreatic CT - mass in pancreas
Abdo USS - pancreatic mass, dilated bile ducts or liver metastases
LFT - bilirubin, ALP and Gamma GT raised in obstructive jaundice.

Gold Standard
Biopsy - EUS.
Others
PT - prolonged
FBC - low platelets and anaemia in GI bleeds
Cancer antigen - elevated

234
Q

Management Pancreatic Cancer

A

Stage I or II = Surgical resection with pancreatic enzyme replacement, followed by adjuvant chemotherapy
Stage III or IV = Endoscopic stent insertion or palliative surgery with chemotherapy and pain management and pancreatic enzyme replacement

235
Q

Complications Pancreatic Cancer

A

Surgical complications of pancreatic leaks or fistula, and early delayed gastric emptying
Cholangitis
DVT and pulmonary embolism

236
Q

Prognosis Pancreatic Cancer

A

Average 5 year survival is 10.8% with a mean survival of 4.6 months.

Stage I and II 10% of patients- 5 year survival is 20% with average of 15-18 months

50-55% patients present with metastatic disease with a survival of 3-6 months.

237
Q

DDx Pancreatic Cancer

A

Chronic pancreatitis - histological features not present
Bile duct stones - ERCP will rule out stricture (seen in pancreatic cancer) and confirm presence of bile duct stones
Cholangiocarcinoma - CT/MRI show absence of pancreatic mass and thickening of bile duct

238
Q

Definition Hernias

A

Protrusion of a viscous out of a containing cavity.

239
Q

Epidemiology Hernias

A

Inguinal - more common in men
Femoral - more common in women
More than 20 million hernias repaired every year around the world

240
Q

Aetiology Hernias

A

A combination of pressure and an opening or weakness of muscle or fascia

241
Q

Risk Factors Hernias

A

Main:
Male
Older
Chronic coughing - smokers
Obesity

Others:
Pregnancy
Family history

242
Q

Pathophysiology Hernias

A

Contents of the abdominal cavity have herniated through the abdominal wall. Umbilicus, Inguinal canal, femoral region and at previous sites of surgery (incisional). Hiatus hernia, stomach passes up into chest cavity through diaphragm.

Bowel that passes into a hernia can become stuck and ischaemic, called a strangulated hernia and is an emergency.

Inguinal - Indirect - through deep inguinal ring and direct come into inguinal canal through defect in posterior wall of the canal.

Femoral – irreducible and strangulated. Go down femoral canal and are usually found below and lateral to inguinal ligament.

Umbilical - Omentum or bowel can herniate through them

Epigastric - pass through linea alba above umbilicus

Inscisional - appear along lines of previous incision during surgery

243
Q

Clinical manifestations Hernias

A

Key Presentations
pain, swelling or fullness at the site of occurrence that can change with position or Valsalva. Most common asymptomatic and appear as a bulge when cough or strain.

244
Q

Investigations Hernias

A

1st Line
Physical exam or Abdo CT, MRI or USS to confirm presence.

245
Q

Management Hernias

A

Reducing the hernia if possible
Repair - mesh technique and surgery. Patients are advised to lose weight and stop smoking before op. Patients can return to work after 2 weeks or 4 weeks for geriatric.

246
Q

Complications Hernias

A

Constipation
Strangulation
Intestinal obstruction

247
Q

Prognosis Hernias

A

1% chance that any given hernia can become strangulated.

248
Q

DDX Hernias

A

Diastasis recti,
Abscess,
Muscle strain
Soft tissue malignancy

249
Q

Definition Paracetamol Overdose

A

Excessive ingestion of paracetamol leading to toxic effects.

250
Q

Epidemiology Paracetamol Overdose

A

In UK, paracetamol is the most common drug taken in overdose, with 48% of poisoning hospital admissions.

251
Q

Classifications of Paracetamol Overdose

A

> 150mg/kg can cause serious effects and >12g is potentially fatal.
Acute - <75mg / kg is unlikely to cause toxicity unless staggered. If a patient has ingested more or is in need of an urgent psychiatric assessment hospital admission is warranted.
Staggered - excessive ingestion over period longer than an hour. >150mg/kg in any 24 hour period.

252
Q

Risk factors Paracetamol Overdose

A

History of self harm
History of frequent or repeated use of medications for pain relief
Iatrogenic paracetamol poisoning following IV administration

253
Q

Pathophysiology Paracetamol Overdose

A

Paracetamol is primarily metabolised in the liver. This occurs via conjugation with the addition of glucuronide to form a water soluble metabolite that can be excreted in the urine. When there is excess paracetamol, such as with overdose, conjugation become saturated and paracetamol is converted into the metabolite N-acetyl-p-benzoquinoneimine (NAPQI).
NAPQI has a short half-life and is usually conjugated by the addition of glutathione, which is then renally excreted. When glutathione stores are depleted, excess NAPQI binds to hepatocellular proteins and results in oxidative damage, mitochondrial dysfunction and ultimately hepatocellular injury.

254
Q

Clinical manifestations Paracetamol Overdose

A

Key Presentations
Asymptomatic and mild GI symptoms. History and abdo pain.
Signs
scars - previous evidence of self harm, bruising, jaundice, tachycardia or coma
Symptoms
nausea and vomiting, anorexia, malaise, altered mental status

255
Q

Risk assessment Paracetamol Overdose

A

Date, Time, Period since ingestion and Amount
Weight
Pregnancy
Current suicidal risk

256
Q

Investigations Paracetamol Overdose

A

1st Line
LFT - raised ALT
INR and prothrombin - raised and prolonged
BG - <3.3mmol/L
Creatinine - acutely elevated
FBC - leukocytosis, anaemia or thrombocytopenia

Gold Standard
Serum paracetamol conc >700mg/L
Others
Urinalysis - haematuria or proteinuria
Urine drug screen - positive

257
Q

Management Paracetamol Overdose

A

N-acetylcysteine for 21 hour regimen. Done over 3 infusions between 1 and 16 hours. After bloods are retaken to see any hepatic impairment. However, be aware of anaphylactoid reactions which occur in 30% of patients.

Acute ingestion and <8 hours - Activated charcoal, look for abnormal bloods and treatment not normally required if asymptomatic.

4 hours post ingestion do paracetamol levels and blood and assess nomogram for if NAC is required.

Treatment can be stopped when INR <1.31 and ALT within normal or raised range but not more than 2x limit.

258
Q

Complications Paracetamol Overdose

A

DILI
ALF - acute liver failure

259
Q

Prognosis Paracetamol Overdose

A

If treated it has a 0.1% mortality

260
Q

DDx Paracetamol Overdose

A

DILI or alternative toxicity
Hepatitis
Wilson disease

PHASE 2 (7 decks)

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