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2a high tier > Liver and friends > Flashcards

Liver and friends Flashcards

1
Q

What is the aetiology of biliary colic?

A

Gall stones obstruct the cystic duct

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2
Q

What is the clinical presentation of biliary colic?

A

Right upper gastric pain ± jaundice

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3
Q

How is biliary colic diagnosed?

A

Abdominal USS to diagnose gall stone disease

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4
Q

How is biliary colic managed?

A
  • analgesia
  • rehydrate
  • remove gallbladder
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5
Q

What is the aetiology of acute cholecystitis?

A

Stone/ sludge impaction in the neck of the gallbladder

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6
Q

What is the pathophysiology of acute cholecystitis?

A

Fixed obstruction or passage of gallstones into the gallbladder neck or cystic duct causes acute inflammation of the gallbladder wall, causing irritation

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7
Q

What are the risk factors of acute cholecystitis?

A
  • gallstones
  • physical inactivity
  • low fibre intakes
  • severe illness
  • diabetes
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8
Q

What is the clinical presentation of acute cholecystitis?

A
  • continuous epigastric/ RUQ pain referred to right shoulder
  • vomiting
  • fever
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9
Q

What are the differential diagnoses of acute cholecystitis?

A
  • basal pneumonia
  • peptic ulcer disease
  • acute pancreatitis
  • intrahepatic abscess
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10
Q

How is acute cholecystitis diagnosed?

A
  • FBC (increased WCC and CRP)
  • raised bilirubin and alk phos
  • abdo USS (thick-walled, shrunken gallbladder, stones, pericholecystic fluid)
  • examination (RUQ tenderness and Murphy’s sign - pain of taking a deep breath when 2 fingers are placed on RUQ)
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11
Q

How is acute cholecystitis managed?

A
  • IV antibiotic infusion (e.g. cefuroxime)
  • remove gallbladder
  • open surgery if gallbladder is perforated
  • pure or near-pure cholesterol stones can be solubilised with oral ursodeoxycholic acid → stone dissolution
  • shock wave lithotripsy: shock wave directed at gallbladder stone to turn them into fragments to pass easily
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12
Q

What is the aetiology of chronic cholecystitis?

A

Chronic inflammation ± colic

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13
Q

What are the risk factors of chronic cholecystitis?

A
  • increasing age
  • female
  • FHx of gallstones
  • Hispanic and native-american ethnicity
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14
Q

What is the clinical presentation of chronic cholecystitis?

A
  • vague abdominal discomfort
  • flatulence
  • fat intolerance
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15
Q

What are the differential diagnoses of chronic cholecystitis?

A
  • peptic ulcer disease
  • gallbladder cancer
  • gallbladder polyps
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16
Q

How is chronic cholecystitis diagnosed?

A
  • FBC
  • serum LFT
  • serum lipase and amylase
  • abdominal USS
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17
Q

How is chronic cholecystitis managed?

A
  • no treatment if asymptomatic

- remove gallbladder

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18
Q

What is the aetiology of ascending cholangitis?

A
  • gallstones

- bile duct infection

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19
Q

What is the pathophysiology of ascending cholangitis?

A

Bile duct obstruction leads to bacterial seeding of the biliary tree and bacterial contamination

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20
Q

What are the risk factors of ascending cholangitis?

A
  • age >50y
  • benign stricture
  • malignant stricture
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21
Q

What is the clinical presentation of ascending cholangitis?

A
  • RUQ pain
  • biliary colic
  • jaundice → dark urine, pale stools, itchy skin
  • rigors
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22
Q

What are the differential diagnoses of ascending cholangitis?

A
  • acute cholecystitis
  • peptic ulcer disease
  • acute pancreatitis
  • hepatic abscess
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23
Q

How is ascending cholangitis diagnosed?

A
  • trans abdominal USS
  • magnetic resonance cholangiography
  • CT to exclude cancer
  • raised neutrophil, ESR, CRP, serum bilirubin, serum alk phos and aminotransferase
  • blood culture
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24
Q

How is ascending cholangitis managed?

A
  • antibiotics e.g. cefuroxime and metroniazole
  • urgent biliary drainage (removal of stones using basket or balloon, crushing of stones, stent placement)
  • surgery for large stones
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25
Q

What is the aetiology of acute pancreatitis?

A
  • gallstones
  • ethanol
  • trauma
  • steroids
  • mumps
  • autoimmune
  • hyperlipidaemia, calcaemia and hypothermia
  • drugs
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26
Q

What is the pathophysiology of acute pancreatitis?

A
  • abnormal intracellular calcium accumulation can lead to premature enzyme activation
  • ehanol-induced = ethanol has a direct toxic effect on acinar cells, causing inflammation and membrane destruction
27
Q

What are the risk factors of acute pancreatitis?

A
  • middle-aged women
  • young/ middle aged men
  • gallstones
  • alcohol
  • hypertriglyceridaemia
28
Q

What is the clinical presentation of acute pancreatitis?

A
  • gradual/sudden severe epigastric or central abdo pain
  • vomiting
  • tachycardia
  • fever
  • jaundice
  • Grey-Turner’s sign (bilateral flank blue discolouration)
  • Cullen’s sign (peri-umbilical blue discolouration)
  • Chvostek’s sign (facial spasm when facial nerve is tapped)
29
Q

What are the differential diagnoses of acute pancreatitis?

A
  • peptic ulcer disease
  • oesophageal spasm
  • intestinal obstruction
  • AAA
  • cholangitis
  • hepatitis
30
Q

How is acute pancreatitis diagnosed?

A
  • raised serum amylase
  • serum lipase
  • ABG
  • abdo XR
  • CXR/ CT/ MRI
31
Q

How is acute pancreatitis managed?

A
  • usually self-limiting
  • nil-by-mouth, NG tube feeding
  • fluids
  • analgesia
  • hourly pulse, BP, urine output
  • daily FBC, U&E, ABG
  • antibiotics in severe cases
32
Q

What is the aetiology of chronic pancreatitis?

A
  • alcohol
  • cystic fibrosis
  • familial
  • haemochromatosis
  • pancreatic duct obstruction
33
Q

What is the pathophysiology of chronic pancreatitis?

A

Primary autoimmune of inflammatory response in pancreatic ducts

34
Q

What are the risk factors of chronic pancreatitis?

A
  • alcohol
  • smoking
  • family history
  • coeliac disease
35
Q

What is the clinical presentation of chronic pancreatitis?

A
  • epigastric pain that ‘bores’ to the back but relieved by sitting forward or hot water bottles
  • jaundice
  • weight loss
  • joint pain
36
Q

What are the differential diagnoses of chronic pancreatitis?

A
  • pancreatic cancer
  • acute pancreatitis
  • biliary colic
  • peptic ulcer disease
37
Q

How is chronic pancreatitis diagnosed?

A
  • USS and CT

- abdo XR

38
Q

How is chronic pancreatitis managed?

A

Medication:
- analgesia, fat-soluble vitamins, insulin if needed

Surgery:
- remove pancreas ± jejunum for unremitting pain, narcotic abuse or weight loss

39
Q

What is the aetiology of alcoholic liver disease?

A

Heavy alcohol ingestion

40
Q

What is the pathophysiology of alcoholic liver disease?

A

Chronic alcohol use upregulates cytochrome P450 (metabolic pathway) which generates free radicals and excessive NAHD which inhibits gluconeogenesis and promotes fatty infiltration in the liver

41
Q

What are the risk factors of alcoholic liver disease?

A
  • prolonged heavy alcohol consumption
  • Hep C
  • female
  • cigarette smoking
  • obesity
42
Q

What is the clinical presentation of alcoholic liver disease?

A
  • abdominal pain
  • hepatomegaly
  • ascites
  • weight loss or gain
  • jaundice
  • splenomegaly
  • hepatic mass
43
Q

What are the differential diagnoses of alcoholic liver disease?

A
  • Hep B, C and A
  • autoimmune hepatitis
  • cholecystitis
  • hepatic vein thrombosis
  • acute liver failure
  • biliary obstruction
44
Q

How is alcoholic liver disease diagnosed?

A
  • serum AST, ALT and alkaline phosphatase
  • serum bilirubin, albumin and GGT
  • FBC
  • hepatic USS
45
Q

How is alcoholic liver disease managed?

A

Lifestyle changes:

  • reduce/ cut out alcohol
  • weight loss
  • smoking cessation
  • nutritional supplementation

Corticosteroids

46
Q

What is the aetiology of cirrhosis?

A
  • chronic alcohol use
  • Hep B or C infection
  • biliary obstruction
  • drugs and toxins
  • autoimmune liver disease
47
Q

What is the pathophysiology of cirrhosis?

A

Activation of hepatic stellate cells leads to accumulation of collagen type I and III in the hepatic parenchyma

48
Q

What are the risk factors of cirrhosis?

A
  • alcohol misuse
  • IVDU
  • unprotected sex
  • obesity
49
Q

What is the clinical presentation of cirrhosis?

A
  • abdominal distension
  • jaundice
  • blood in vomit
  • black stool
50
Q

What are the differential diagnoses of cirrhosis?

A
  • constructive pericarditis
  • portal vein thrombosis
  • splenic vein thrombosis
  • IVC obstruction
  • schistosomiasis
51
Q

How is cirrhosis diagnosed?

A
  • liver function tests: increased AST, ALT and alk phos
  • GGT, serum albumin and sodium
  • decreased WCC, albumin and platelets
  • liver USS, duplex and MRI
  • ascitic tap to check for bacterial peritonitis
52
Q

How is cirrhosis managed?

A
  • good nutrition
  • no alcohol, NSAIDs, sedatives or opiates
  • treat underlying chronic liver disease (e.g. oral acting antivirals)
  • sodium restriction and diuretics for ascites
  • liver transplant in patients with complications
53
Q

What is a varices?

A

Dilated vein at risk of rupturing, resulting in haemorrhage and GI bleeding

54
Q

What is the aetiology of a varices?

A
  • alcoholism and viral cirrhosis = leading causes

- portal hypertension

55
Q

What is the pathophysiology of a varices?

A
  • contraction of activated myofibroblasts following liver injury and fibrogenesis contributes to increased resistance to blood flow
  • this leads to portal hypertension → splanchnic vasodilation → drop in BP → increased cardiac output to compensate → salt and water retention to compensate → hyperdynamic circulation/ increased portal flow → formation of collaterals between portal and systemic systems → gastro-oesophageal varices develop when portal pressure rises and they start to bleed
  • this can occur rapidly and result in major haemorrhage
56
Q

What are the risk factors of varices?

A
  • cirrhosis
  • portal hypertension
  • schistosomiasis infection
  • alcoholism
57
Q

What is the clinical presentation of varices?

A
  • signs of chronic liver damage (e.g. jaundice, increased bruising and ascites)
  • splenomegaly
  • ascites
  • hyponatraemia

If ruptured: haematemesis, abdo pain, shock (if major blood loss), fresh rectal bleeding, hypotension, tachycardia and pallor

58
Q

What are the differential diagnoses of varices?

A
  • peptic ulcer disease

- hiatal hernia

59
Q

How is varices diagnosed?

A

Endoscopy to find bleeding source

60
Q

How is varices managed?

A
  • eesuscitate until haemodynamically stable
  • if anaemic, then blood transfusion
  • correct clotting abnormalities – give vit K and platelet transfusion
  • vasopressin
  • prophylactic antibiotics
  • variceal banding (band put around varices using an endoscope)
  • balloon tamponade to reduce bleeding if banding fails
  • trans-jugular intrahepatic portocaval shunt if bleeding can’t be controlled

Prevention:

  • non-selective BB e.g. propranolol
  • variceal banding repeated to obliterate varices
  • liver transplant (best option if poor liver function)
61
Q

What is the aetiology of portal hypertension?

A

Pre-hepatic:
- portal vein thrombosis

Intra-hepatic:

  • cirrhosis (commonest cause in UK)
  • schistosomiasis (commonest cause worldwide)
  • sarcoidosis
  • congenital hepatic fibrosis

Post-hepatic:

  • IVC obstruction
  • right heart failure
  • constrictive pericarditis
62
Q

What is the pathophysiology of portal hypertension?

A
  • following liver injury and fibrogenesis (e.g. due to cirrhosis), the contraction of activated myofibroblasts contributes to increased resistance to blood flow
  • this leads to portal hypertension → splanchnic vasodilation → drop in BP → increased cardiac output to compensate → salt and water retention to compensate → hyperdynamic circulation/ increased portal flow → formation of collaterals between portal and systemic systems
  • microvasculature of he gut becomes congested and gives rise to portal hypertensive gastropathies and colonopathies
63
Q

What is the clinical presentation of portal hypertension?

A
  • patients are often asymptomatic
  • only clinical sign is splenomegaly which is unspecific
  • chronic liver disease features may present (haematemesis and melaena from ruptured varices. Clubbing, palmar erythema, Dupuytren’s contracture, spider naevi)

2a high tier (10 decks)

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