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Phase 2a > Hepatology+ > Flashcards

Hepatology+ Flashcards

1
Q

Define jaundice

A

Raised serum bilirubin causing yellowing of the skin, sclerae, and mucosae

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2
Q

Describe what happens to bilirubin, and the pathophysiology of jaundice

A

Bilirubin is produced from the breakdown of haemoglobin, 95% is unconjugated and circulates bound to albumin
In hepatocytes, the albumin is removed and bilirubin is converted to conjugated bilirubin by adding glucuronic acid (using glucuronosyltransferase enzyme), then excreted in bile
It is deconjugated by colonic bacteria into urobilinogen, which is oxidised into urobilin (then excreted in urine) and stercobilin (then excreted in the stools) or reabsorbed to the liver
Jaundice is caused by interference of the uptake, transport, conjugation, or excretion of bilirubin

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3
Q

What are the causes of jaundice?

A

Pre hepatic:
- haemolysis (haemolytic anaemias)
- Gilberts (impaired conjunction)
Intra hepatic:
- viral (hepatitis, EBV)
- drugs or alcohol
- autoimmune
- ischemia
- neoplasm
- congestion (CCF)
- primary biliary cholangitis
Post hepatic (obstructive):
- gallstones (bile duct)
- malignant
- ischemia
- inflammatory

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4
Q

What are the signs/symptoms of jaundice?

A

Dark urine (intra/post-hepatic cause)
Pale stools (post-hepatic cause)
Itching (intra/post hepatic cause)
Biliary pain
Abdominal swelling
Weight loss

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5
Q

What investigations are needed for jaundice?

A

LFTs
Conjugated bilirubin (high in pre-hepatic and sometimes intra-hepatic causes)
Unconjugated bilirubin (high in post-hepatic causes)
FBC: check for haemolysis
Blood cultures: check for viral infection
Imaging: ultrasound to detect hepatosplenomegaly and gall stones, CT/MRI if malignancy suspected

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6
Q

What type of bilirubin is elevated, and what happens to the urine/stools in each type of jaundice?

A

Pre-hepatic:
- elevated unconjugated bilirubin
- normal/pale urine
- dark stools
Hepatic:
- elevated conjugated and unconjugated bilirubin
- dark urine
- normal stools
Post-hepatic:
- elevated conjugated bilirubin
- dark urine
- pale stools

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7
Q

What is the treatment for jaundice?

A

Treat the cause
Ensure adequate hydration
Lifestyle advice
Monitor for ascites, encephalopathy

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8
Q

Define cirrhosis

A

Irreversible liver damage and the final stage of any chronic liver disease, characterised by fibrosis and the conversion of normal hepatic architecture into structurally abnormal nodules

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9
Q

What are the causes of cirrhosis?

A

Alcohol abuse (AFLD) - most common in developed countries
NAFLD
Hepatitis B and C
Metabolic liver disease
Autoimmune (PBC, PSC, hepatitis)
Hepatic vein events (Budd-Chiari)
Drugs (e.g. methotrexate, amiodarone)

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10
Q

What are the signs/symptoms of cirrhosis?

A

Often asymptomatic until complications
- oedema
- ascites
- easy bruising
- bleeding oesophageal varices
- spontaneous bacterial peritonitis
- jaundice
- pruritis
- spider naevi
- palmar erythema
- white nails
- clubbing
- dupuytren’s contracture
- hepatomegaly

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11
Q

What investigations are needed for cirrhosis?

A

LFTs: raised ALT
FBC: low platelets
Low albumin
Raised PT/INR
Imaging: ultrasound/MRI - show large liver with nodules
Liver biopsy: diagnostic

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12
Q

What are the treatments of cirrhosis?

A

Treat underlying cause
Manage complications
Ensure adequate nutrition
Alcohol abstinence
Prophylactic antibiotics
Liver transplant (for end-stage disease)

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13
Q

What are the complications or cirrhosis?

A

Anaemia, thrombocytopaenia, coagulopathy
Oesophageal varices
Ascites
Spontaneous bacterial peritonitis
Hepatocellular carcinoma
Hepatic encephalopathy

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14
Q

Define fatty liver disease

A

The accumulation of fat in the liver (steatosis) which can progress and be associated with inflammation (steatohepatitis), divided into:
- alcoholic fatty liver disease (AFLD)
- non-alcoholic fatty liver disease (NAFLD) which can progress to non-alcoholic steatohepatitis (NASH)

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15
Q

Describe the pathophysiology of fatty liver disease

A

Defective fatty acid metabolism because of mitochondrial damage (from alcohol), insulin resistance, or impaired receptor or enzymes involved, leads to the accumulation of triglycerides and other lipids in the hepatocytes leads

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16
Q

Describe the progression of AFLD

A

90% of heavy drinkers will develop steatosis , which is reversible with abstinence from alcohol
If abstinence is not achieved, alcoholic steatohepatitis (fibrosis) will develop, which can lead to cirrhosis, and hepatocellular carcinoma
Some will develop alcoholic hepatitis, which can be resolved with abstinence, corticosteroids or liver transplant, but can lead back to cirrhosis

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17
Q

What are the risk factors for AFLD?

A

Female sex
Binge drinking pattern
High quantity of alcohol consumed
Obesity
Hepatitis C infection
Genetics

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18
Q

What are the associations of NAFLD?

A

Obesity (central)
Abnormal glucose tolerance (T2DM)
Dyslipidaemia
PCOS
Hypertension
Family history

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19
Q

What are the signs/symptoms of fatty liver disease?

A

The majority of patients with steatosis have no symptoms
Patients with steatohepatitis may have fatigue, malaise, or RUQ pain
Advanced disease: signs/symptoms or cirrhosis (jaundice, ascites, etc.)

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20
Q

What investigations are needed for fatty liver disease?

A

LFTs: abnormal (raised GGT if alcohol is cause)
FBC: low platelets in advanced liver fibrosis
Hepatitis viral serology
Auto-antibodies: check for autoimmune hepatitis (raised ANA and ASMA) or PBC (raised AMA)
Ultrasound: detects steatosis
Liver biopsy: diagnostic

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21
Q

What are the treatments of fatty liver disease?

A

AFLD: abstinence, adequate diet
Lifestyle changes (weight loss, regular exercise, healthy diet, avoid alcohol)
Control risk factors (hypertension, T2DM)
Drugs: for non-diabetic patients - vitamin E supplements (can improve histology), pioglitazone (increase insulin sensitivity)

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22
Q

Define liver failure

A

When the liver loses the ability to regenerate or repair:
- acute liver failure: occurs suddenly in a previously healthy liver (1-3 weeks)
- chronic liver failure: occurs with a background of cirrhosis (over 6 months)

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23
Q

What are the causes of acute and chronic liver disease?

A

Acute:
- viral (hepatitis A, B, EBV)
- drugs (antibiotics e.g. co-amoxiclav, paracetamol overdose)
- alcohol
- vascular (Budd-Chiari syndrome, veno-occlusive disease, ischemia)
- obstruction
- congestion (congestive cardiac failure)
Chronic:
- viral (hepatitis A, B, EBV)
- drugs (antibiotics and common)
- autoimmune (primary biliary cholangitis, primary sclerosing cholangitis)
- metabolic (iron or copper overload)
- neoplastic
- fatty liver disease (alcoholic and non-alcoholic)

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24
Q

What are the signs/symptoms of acute and chronic liver failure ?

A

Acute:
- may be asymptomatic
- generalised symptoms (malaise, nausea, anorexia)
- jaundice as disease progresses
- rare: confusion, bleeding, RUQ pain, hypoglycaemia
Chronic:
- ascites/oedema
- jaundice/pruritis
- bleeding (easy bruising, haematemesis)
- gynaecomastia
- spider naevi
- clubbing
- palmar erythema
- hepatosplenomegaly
- hepatic encephalopathy

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25
Q

What investigations are needed for liver failure?

A

FBC: check for signs of infection
Viral serology
LFTs: transaminases = high, alkaline phosphate = high/normal
Clotting: raised PT and INR (coagulopathy)
Doppler ultrasound: check hepatic vein, look for neoplasms and ascites
Imaging of head, EEG: check for cerebral oedema, check level of encephalopathy

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26
Q

What is the treatment for liver failure?

A

Treat cause if known
Monitor for infection, hypoglycaemia, bleeds
Haemofiltration/haemodialysis if AKI develops
Liver transplant

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27
Q

What are the complications of liver failure?

A

Prone to infection (spontaneous peritonitis, opportunistic)
Portal hypertension
Cerebral oedema (intracranial hypertension, death)
Haemorrhage (e.g. from oesophageal varices)

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28
Q

Define ascites

A

Abnormal collection of fluid in the peritoneal cavity, can be mild (only detectable on US) to severe (clearly visible from examination)

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29
Q

What are the causes of ascites?

A

Cirrhosis (most common)
Malignancies (mostly gynaecological)
Heart failure
Pancreatitis
Nephrotic syndrome
Malnutrition
Portal hypertension

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30
Q

Describe the pathophysiology of ascites

A

Portal hypertension - increased hydrostatic pressure
Hypoalbuminaemia - reduced plasma oncotic pressure
Renal fluid and sodium retention - due to secretion of renin, angiotensin, vasopressin, causing peripheral arterial vasodilation

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31
Q

What are the signs/symptoms of ascites?

A

Abdominal distension
Weight gain
Shifting dullness on percussion
Fluid thrill/wave
Signs of liver disease (e.g. jaundice)
Signs of respiratory distress (pleural effusion)

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32
Q

What are the investigations needed for ascites?

A

Aspiration (diagnostic)
Imaging: ultrasound to assess degree of ascites, and may show cause
Bloods: FBC, renal function, LFTs, clotting screen, albumin (show underlying cause)

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33
Q

What is the treatment for ascites?

A

Treat underlying cause (e.g. alcohol abstinence)
Fluid and salt restriction
Diuretics (spironolactone +/- furosemide)
Large-volume paracentesis (drains fluid) + albumin replacement
Indwelling drain: home paracentesis, smaller volumes
Surgical: transjugular intrahepatic portosystemic shunt (TIPS)

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34
Q

Define hepatic encephalopathy

A

Cerebral oedema and neuropsychiatric abnormalities caused by the build up of ammonia due to liver failure leading to the passage of neurotoxins to the brain

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35
Q

What are the causes of hepatic encephalopathy?

A

AKI
Electrolyte imbalance
GI bleed
Infection
Constipation
Sedative drugs
Diuretics

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36
Q

What are the signs/symptoms of hepatic encephalopathy?

A

Mild: confusion, forgetfulness, mood changes, sleep disturbance, dyspraxia
Severe: lethargy, severe personality changes, seizures, severe disorientation and confusion, incompressible speech
Very severe: coma

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37
Q

What investigations are needed for hepatic encephalopathy?

A

Psychometric tests: draw a 5-pointed star, count in 7s
Ammonia: raised
MRI/CT: exclude other causes of altered mental function

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38
Q

What are the treatments for hepatic encephalopathy?

A

Antibiotics (e.g. rifaximin)
Lactulose - increases use of ammonia
Liver transplant (for recurrent cases)

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39
Q

What are the causes of portal hypertension?

A

Cirrhosis (80%)
Fibrosis
Thrombosis (portal or splenic vein)
Schistosomiasis (parasitic worm infection)
Budd-Chiari syndrome (blocked/narrowed hepatic veins)
Right-sided heart failure

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40
Q

Describe the pathophysiology of portal hypertension

A

Increased hepatic resistance and/or increased splanchnic blood flow causing the blood pressure in the portal system to rise, leading to varices (oesophageal, gastric) and splenomegaly

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41
Q

What are the signs/symptoms of portal hypertension?

A

Asymptomatic
Symptoms of complications: ascites, bleeding varices (gastro-oesophageal)

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42
Q

What is the treatment for portal hypertension?

A

Endoscopic banding (oesophageal) or sclerotherapy (gastric) of varices
Fluid resuscitation if large bleed
Beta-blocker (e.g. propranolol)

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43
Q

Define ascending cholangitis

A

Bacterial infection (Klebsiella spp., E. coli, Enterobacter spp.) of the biliary system (often common bile duct) due to partial or complete obstruction of ducts

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44
Q

What are the causes of ascending cholangitis

A

Gallstones
ERCP
Tumours
Bile duct stricture or stenosis
Parasitic infection

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45
Q

What are the signs/symptoms of ascending cholangitis?

A

Charcot’s triad:
- jaundice
- fever
- right upper quadrant pain (colicky)
Additional features (Reynold’s pentad):
- hypotension (septic shock)
- mental confusion

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46
Q

What investigations are needed for ascending cholangitis?

A

FBC: raised WBC
ESR, CRP: may be raised
LFTs: raised ALP, show obstructive jaundice
U&E: associated renal dysfunction
Blood culture (and culture of bile if available)
Imaging: ultrasound (shows obstruction), ERCP

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47
Q

What is the treatment needed for ascending cholangitis?

A

Fluid resuscitation
Antibiotics e.g. piperacillin/tazobactam
ERCP (treat obstruction)

48
Q

Define biliary colic

A

Gallstones causing obstruction of the cystic or common bile duct, resulting in pain (but no fever or inflammation)

49
Q

What are the signs/symptoms of biliary colic?

A

Pain:
- RUQ or epigastric
- may radiate to back
- intermittent
Rare: may have jaundice if stone is passed into common bile duct

50
Q

What are the investigations needed for biliary colic?

A

FBC: normal
Ultrasound
ERCP

51
Q

What are the treatments for biliary colic?

A

Analgesia
Surgical removal (ERCP)

52
Q

Define cholecystitis

A

Gallstone obstruction causing distention of the gall bladder, with subsequent inflammation and necrosis of the mucosal wall

53
Q

What are the risk factors for cholecystitis?

A

Female
Forty
Fat (obesity)
Fertile (had more than 1 child, increase oestrogen)
Family history
Fair (Caucasian)

54
Q

What are the signs/symptoms of cholecystitis?

A

Pain:
- RUQ or epigastric
- continuous
- referred to shoulder tip or around side
- worse on inspiration
Murphy’s sign: pressing on RUQ while breathing in causes pain + arrest of inspiration, but no pain on left
Fever
Vomiting
Jaundice (if stone moves to common bile duct)

55
Q

What are the investigations needed for cholecystitis?

A

FBC: raised WBC
Ultrasound: shows thick-walled, shrunken gall bladder + stones

56
Q

What are the treatments for cholecystitis?

A

Analgesia
Antibiotics
Surgical removal or drain

57
Q

Define primary biliary cirrhosis/cholangitis

A

Progressive autoimmune destruction of the small bile ducts of the liver, with granulomatous inflammation leading to fibrosis and eventually cirrhosis

58
Q

What are the causes of primary biliary cholangitis?

A

Autoimmune
Thought to be environmentally triggered in genetically predisposed individuals

59
Q

What are the risk factors for primary biliary cholangitis?

A

Female
Family history
Smoking
Other autoimmune conditions (e.g. thyroid disease, RA)
Hepatocellular carcinoma

60
Q

What are the signs/symptoms of primary biliary cholangitis?

A

Very non-specific:
Itching
Fatigue
Dry eyes
Joint pains
Hepatosplenomegaly
Jaundice
Liver failure in advanced disease: ascites, spider naevi, portal hypertension

61
Q

What are the investigations needed for primary biliary cholangitis?

A

FBC: often normal
LFTs: abnormal
Raised IgM
Antimitochondrial antibodies in 98%
Imaging: ultrasound/CT to exclude obstruction

62
Q

What is the treatment for primary biliary cholangitis?

A

Treat symptoms
Ursodeoxycholic acid (reduces inflammation, delays damage)
Liver transplant (can recur in transplanted liver)

63
Q

Define primary sclerosing cholangitis

A

Progressive inflammation and fibrosis of the biliary tree, resulting in strictures (narrowing due to scarring)

64
Q

What are the risk factors of primary sclerosing cholangitis?

A

Male
IBD (present in 80%, mostly UC)
Cholangiocarcinoma
Colorectal cancer

65
Q

What are the signs/symptoms of primary sclerosing cholangitis?

A

Mostly asymptomatic
Non-specific: pruritis, fatigue
Advanced: ascending cholangitis, cirrhosis, liver failure

66
Q

What are the investigations for primary sclerosing cholangitis?

A

LFTs: abnormal
IgM/G may be raised
p-ANCA antibodies
Cholangiopancreatography: visualise intra and extrahepatic bile ducts

67
Q

What are the treatments for primary sclerosing cholangitis?

A

Treat symptoms
Ursodeoxycholic acid (can improve LFTs, but no survival benefit)
Liver transplant

68
Q

Define haemochromatosis

A

A genetic disorder (autosomal recessive inheritance) causing iron overload

69
Q

Describe the pathophysiology of haemochromatosis

A

Defects in the HFE gene cause uncontrolled intestinal iron absorption with deposition in the liver, heart, and pancreas

70
Q

What are the signs/symptoms of haemochromatosis?

A

Initial: non-specific, fatigue, weakness, arthropathy, abdominal problems
Advanced disease: diabetes, cirrhosis, hepatomegaly, bronzing of skin, arrhythmias, cardiac myopathy, hypogonadism

71
Q

What are the investigations needed for haemochromatosis?

A

LFTs: raised
Ferritin: raised
Transferrin saturation: raised
HFE genetic testing

72
Q

What are the treatments for haemochromatosis?

A

Phlebotomy
Liver transplant (for end-stage disease)

73
Q

Define Wilson’s disease

A

A genetic disorder (autosomal recessive disorder) causing deposition of copper in the liver and CNS

74
Q

What are the signs/symptoms of Wilson’s disease?

A

Hepatic features: liver failure, cirrhosis, hepatomegaly
Psychiatric features: depression, behavioural problems, poor memory, slow problem solving
Neurological features: tremor, difficulty speaking and swallowing, ataxia, clumsiness
Ophthalmological features: Kayser-Fleisher ring - brown/green ring on cornea

75
Q

What are the investigations needed for Wilson’s disease?

A

Serum caeruloplasmin: low
24-hr urine excretion of copper: high
Liver biopsy

76
Q

What are the treatments of Wilson’s disease?

A

Avoid high-copper foods (liver, chocolate, nuts, shellfish)
Penicillamine (copper chelation)
Liver transplant (if in liver failure, or end-stage disease)

77
Q

Define alpha-1 antitrypsin deficiency

A

An inherited disorder affecting the lungs and liver, caused by a genetic misfolding in the SERPINA1 gene, meaning that a1AT can’t be transported out of the liver:
- accumulating in the liver causes inflammation and cell destruction (cirrhosis)
- lack of a1AT in the lungs allows the destruction of elastin in the alveolar walls (emphysema)

78
Q

What are the signs/symptoms of alpha-1 antitrypsin deficiency?

A

Lung disease: similar to COPD, early-onset (30-40 y/o) emphysema:
- dyspnoea
- wheezing
- cough
Liver disease: doesn’t occur in all cases, usually presents in children:
- neonatal jaundice and hepatitis
- older children my develop hepatitis, cirrhosis, liver failure

79
Q

What are the investigations needed for alpha-1 antitrypsin deficiency?

A

Serum levels of a1AT
CXR and lung function testing (reduced FEV1 with obstructive pattern)
LFTs and liver biopsy
Phenotyping

80
Q

What are the treatments of alpha-1 antitrypsin deficiency?

A

Lung disease:
- smoking cessation
- bronchodilators
- lung volume reduction or transplant
- vaccination against lung infection
Liver disease:
- monitor liver function
- screen for hepatocellular carcinoma
- liver transplant for liver failure
a1AT replacement: not yet recommended by NICE

81
Q

Define hepatitis

A

Inflammation of the liver
Acute = 1st 6 months
Chronic = any inflammation after 6 months

82
Q

What are the signs/symptoms of acute hepatitis?

A

None or non-specific (malaise, lethargy, myalgia)
GI upset
Abdominal pain
Jaundice + pale stools/dark urine
Tender hepatomegaly
Sings of acute liver failure (bleeding, ascites, encephalopathy)

83
Q

What are the causes of acute hepatitis?

A

Viral infection:
- hepatitis A, B +/- D, C, E
- herpes viruses (VZV, EBV)
- influenza
- SARS-CoV-2
Non-viral infection:
- spirochaetes (leptospirosis)
- mycobacteria (M. tuberculosis)
- bacteria
- parasites
Non-infection:
- drugs, alcohol
- toxins/poisoning
- NAFLD
- pregnancy
- autoimmune
- hereditary metabolic causes

84
Q

What are the signs/symptoms of chronic hepatitis?

A

Can be asymptomatic or have non-specific symptoms only
Clubbing
Palmar erythema
Spider naevi
Coagulopathy
Jaundice
Ascites
Encephalopathy
Portal hypertension (varices, bleeding)

85
Q

What are the causes of chronic hepatitis?

A

Infection:
- hepatitis B +/- D, C, E
Non-infection:
- drugs, alcohol
- toxins/poisoning
- NAFLD
- autoimmune
- hereditary metabolic causes

86
Q

Describe the causes, clinical course, testing, and management for Hepatitis A

A

Causes: faeco-oral transmission, contaminated food and water
Clinical course: usually symptomatic, acute liver failure is rare, self-limiting - no chronic disease , 100% immunity after infection
Testing: anti-HAV IgM is high in acute phase, high anti-HAV IgG detectable after 5-10 days and persist, HAV RNA in immunocompromised patients
Management: supportive treatments, monitor liver function, treat close contacts, vaccination (for high risk, and contacts)

87
Q

Describe the causes, clinical course, testing, and management for Hepatitis E

A

Cause: faeco-oral transmission, contaminated food and water, undercooked meat
Clinical course: usually symptomatic and self-limiting, extra-hepatic manifestations, risk of chronic infection in immunosuppressed patients, high mortality in pregnancy
Testing: anti-HEV IgM is high in acute phase, high anti-HEV IgG will persist after acute infection
Management: supportive treatments, monitor liver function, reverse immunosuppression in chronic infection, treat with ribavirin if persistent HEV RNA

88
Q

Describe the natural history of hepatitis B in an immunocompetent adult or neonates/infants

A
  • 95% of immunocompetent adults but 10% of neonates/infants will be symptomatic, and have spontaneous resolution, but with risk of reactivation is immunosuppressed
  • 5% of immunocompetent adults but 90% of neonates/infants will be asymptomatic and have chronic infection, increasing the risk of cirrhosis and hepatocellular carcinoma
89
Q

Describe the causes, clinical course, testing, and management for Hepatitis B

A

Causes: blood-borne (needles, blood transfusions/products, sexual transmission, vertical transmission)
Clinical course: if symptomatic - self-limiting, chronic infection - asymptomatic, can cause cirrhosis and hepatocellular carcinoma
Testing: HB surface antigen (will persist in chronic infection), anti-HB IgM, anti-HB IgG, anti-HB surface antibody (shows recovery and immunity after vaccination)
Management: supportive treatment of symptoms, pegylated interferon-alpha 2a, or nucleotide analogues (e.g. tenofovir), vaccination (at risk groups and contacts)

90
Q

Describe the causes, clinical course, testing, and management for Hepatitis D

A

Causes: blood borne, acquired simultaneously with, or after HBV infection
Clinical course: worse outcomes than HBV alone
Testing: HDV antibody, the HDV RNA
Management: pegylated interferon-a (limited success), liver transplant may be needed

91
Q

Describe the causes, clinical course, testing, and management for Hepatitis C

A

Cause: blood borne (needles, blood transfusions/products, sexual transmission, vertical transmission)
Clinical course: 30% spontaneously clear the infection but can be reinfected, 70% develop chronic infection leading to complications (cirrhosis, hepatocellular carcinoma)
Testing: HCV antibody, then RNA, then genotype
Management: directly-acting antiviral therapy, no vaccine

92
Q

Define autoimmune hepatitis

A

An inflammatory liver disease of unknown cause, characterised by abnormal cell function and autoantibodies directed against hepatocyte surface antigens

93
Q

What are the associations of autoimmune hepatitis?

A

Female (most commonly affecting young or middle aged)
Other autoimmune conditions: UC, T1DM, pernicious anaemia, autoimmune thyroiditis

94
Q

What are the signs/symptoms of autoimmune hepatitis?

A

40% present with acute hepatitis and signs of autoimmune disease:
- fatigue, myalgia
- pruritis
- nausea
- upper abdominal discomfort
- anorexia, diarrhoea
- skin rashes
- hepatosplenomegaly
- jaundice
Others present with…
- gradual jaundice
- signs of chronic liver disease
- no symptoms

95
Q

What investigations are needed for autoimmune hepatitis?

A

LFTs: raised
Positive autoantibodies (ASMA and ANA)
Raised IgG
FBC: anaemia, low WBC, low platelets
Exclusion of viral, drug-induced, and metabolic liver disease
Liver biopsy

96
Q

What are the treatments for autoimmune hepatitis?

A

Immunosuppressant steroid therapy (prednisolone), followed by azathioprine to maintain remission
Liver transplant (for terminal phases, may recur in transplanted liver)

97
Q

Define acute pancreatitis

A

Sudden inflammation of the pancreas, releasing exocrine enzymes that cause autodigestion of the gland, which can sometimes be reversed

98
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps, malignancy
Autoimmune
Scorpion venom
Hyperlipidaemia, hypercalcaemia
ERCP and emboli
Drugs (tobacco, thiazides)

99
Q

What are the signs/symptoms of acute pancreatitis?

A

Severe central abdominal pain (sudden onset radiates to back, sitting forwards may relieve)
Vomiting
Jaundice (if caused by gallstones)
Mild fever
Absent bowel sounds in later stages
Bruising around umbilicus (Cullen’s sign), or flanks (Grey Turner’s sign)

100
Q

What investigations are needed for acute pancreatitis?

A

Serum amylase and lipase: raised (lipase is more specific for pancreatitis)
ABG: low O2
Calcium: low
Abdominal X-ray: exclude other causes (intestinal obstruction, perforation)
Ultrasound: shows gallstones
CT: shows severity of disease

101
Q

What are the treatments of acute pancreatitis?

A

Analgesia (very strong)
Antiemetics
IV fluids
Nil by mouth - bowel rest
Prophylactic antibiotics (if necrosis)
ERCP for gallstone removal

102
Q

What are the complications of acute pancreatitis?

A

Shock
Acute respiratory distress syndrome
Renal failure
Sepsis
Pancreatic necrosis and pseudocyst
Abscesses
Bleeding
Thrombosis
Hypocalcaemia (breakdown of peri-pancreatic fat by enzymes, releasing free fatty acids which react with calcium)

103
Q

Define chronic pancreatitis

A

Long-standing inflammation causing irreversible damage to the pancreas

104
Q

What are the causes of chronic pancreatitis?

A

Alcohol
Smoking
Autoimmune
Familial
Cystic fibrosis

105
Q

What are the signs/symptoms of chronic pancreatitis?

A

Abdominal (epigastric, radiating to back)
Nausea and vomiting
Decreased appetite
Exocrine dysfunction (malabsorption with weight loss, diarrhoea, steatorrhoea)
Endocrine dysfunction (diabetes mellitus)

106
Q

What investigations are needed for chronic pancreatitis?

A

Secretin stimulation test
Ultrasound/CT: detects calcification

107
Q

What are the treatments for chronic pancreatitis?

A

Management of pain and malabsorption (replacement of pancreatic enzymes with Creon, vitamins ADEK)
Lifestyle advice (smoking, alcohol intake)
ERCP (remove pancreatic duct stones) or surgical resection

108
Q

What are the complications of chronic pancreatitis?

A

Diabetes mellitus
Pericardial, peritoneal, or pleural effusions
Pseudocysts
GI haemorrhage
Pancreatic carcinoma
Malabsorption

109
Q

What causes gallstone formation?

A

Cholesterol supersaturation (diet/weight loss, hormonal influence)
Genetics (gallbladder motility)
Increased haemoglobin turnover (haemolytic anaemia, cirrhosis, sickle cell)

110
Q

Define peritonitis

A

Inflammation of the peritoneum (visceral and/or parietal), which can be classified as acute or chronic, primary or secondary, generalised or localised, and by cause

111
Q

What are the causes of peritonitis?

A

Bacterial (most common)
Chemical (e.g. bile, barium)
Traumatic (e.g. operative handling)
Ischemia (e.g. strangulated bowel, vascular occlusion)
Miscellaneous (e.g. familial Mediterranean peritonitis)

112
Q

Describe the pathways to peritoneal infection

A

GI perforation (e.g. perforated ulcer, appendix, diverticulum)
Transmural translocation (e.g. pancreatitis, ischemic bowel, primary/spontaneous bacterial peritonitis)
Exogenous contamination (e.g. drains, open surgery, trauma, peritoneal dialysis)
Female genital tract infection (e.g. pelvic inflammatory disease)
Haematogenous spread (e.g. septicaemia)

113
Q

What are the signs/symptoms of peritonitis?

A

Localised:
- signs/symptoms of the underlying condition
- pain (localised or generalised guarding, rebound tenderness, referred shoulder tip pain)
- nausea and vomiting
- fever
- tachycardia
- tender rectal/vaginal examination if pelvic peritonitis
- infrequent/absent bowel sounds (in generalised peritonitis)
- circulatory failure and loss of consciousness in late presentation of generalised peritonitis

114
Q

What are the investigations needed for peritonitis?

A

Urine dipstick: for UTI
ECG: rule out cardiac causes of abdominal pain
U&Es
FBC: high WBC
Serum amylase: shows acute pancreatitis/perforated duodenal ulcer
Imaging: erect CXR (shows free air under diaphragm), CT (shows cause), US (limited use)
Aspiration: shows high neutrophils in spontaneous bacterial peritonitis

115
Q

What are the treatments of peritonitis?

A

Correction of fluid loss
Urinary catheter
Abdominal decompression (NG tube)
Antibiotics (broad-spectrum e.g. piperacillin + tazobactam)
Analgesia (allows early mobilisation to prevent DVT)
Surgical treatment of cause

116
Q

Define spontaneous bacterial peritonitis

A

Also called primary bacterial peritonitis
Acute bacterial infection of ascitic fluid
Diagnosed by aspiration (showing high neutrohpils)

Phase 2a (14 decks)

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