Liver and friends Flashcards
1
Q
What is the aetiology of biliary colic?
A
Gall stones obstruct the cystic duct
2
Q
What is the clinical presentation of biliary colic?
A
Right upper gastric pain ± jaundice
3
Q
How is biliary colic diagnosed?
A
Abdominal USS to diagnose gall stone disease
4
Q
How is biliary colic managed?
A
- analgesia
- rehydrate
- remove gallbladder
5
Q
What is the aetiology of acute cholecystitis?
A
Stone/ sludge impaction in the neck of the gallbladder
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
7
Q
What are the risk factors of acute cholecystitis?
A
- gallstones
- physical inactivity
- low fibre intakes
- severe illness
- diabetes
8
Q
What is the clinical presentation of acute cholecystitis?
A
- continuous epigastric/ RUQ pain referred to right shoulder
- vomiting
- fever
9
Q
What are the differential diagnoses of acute cholecystitis?
A
- basal pneumonia
- peptic ulcer disease
- acute pancreatitis
- intrahepatic abscess
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)
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
12
Q
What is the aetiology of chronic cholecystitis?
A
Chronic inflammation ± colic
13
Q
What are the risk factors of chronic cholecystitis?
A
- increasing age
- female
- FHx of gallstones
- Hispanic and native-american ethnicity
14
Q
What is the clinical presentation of chronic cholecystitis?
A
- vague abdominal discomfort
- flatulence
- fat intolerance
15
Q
What are the differential diagnoses of chronic cholecystitis?
A
- peptic ulcer disease
- gallbladder cancer
- gallbladder polyps
16
Q
How is chronic cholecystitis diagnosed?
A
- FBC
- serum LFT
- serum lipase and amylase
- abdominal USS
17
Q
How is chronic cholecystitis managed?
A
- no treatment if asymptomatic
- remove gallbladder
18
Q
What is the aetiology of ascending cholangitis?
A
- gallstones
- bile duct infection
19
Q
What is the pathophysiology of ascending cholangitis?
A
Bile duct obstruction leads to bacterial seeding of the biliary tree and bacterial contamination
20
Q
What are the risk factors of ascending cholangitis?
A
- age >50y
- benign stricture
- malignant stricture
21
Q
What is the clinical presentation of ascending cholangitis?
A
- RUQ pain
- biliary colic
- jaundice → dark urine, pale stools, itchy skin
- rigors
22
Q
What are the differential diagnoses of ascending cholangitis?
A
- acute cholecystitis
- peptic ulcer disease
- acute pancreatitis
- hepatic abscess
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
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
25
What is the aetiology of acute pancreatitis?
- gallstones
- ethanol
- trauma
- steroids
- mumps
- autoimmune
- hyperlipidaemia, calcaemia and hypothermia
- drugs
26
What is the pathophysiology of acute pancreatitis?
- 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
What are the risk factors of acute pancreatitis?
- middle-aged women
- young/ middle aged men
- gallstones
- alcohol
- hypertriglyceridaemia
28
What is the clinical presentation of acute pancreatitis?
- 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
What are the differential diagnoses of acute pancreatitis?
- peptic ulcer disease
- oesophageal spasm
- intestinal obstruction
- AAA
- cholangitis
- hepatitis
30
How is acute pancreatitis diagnosed?
- raised serum amylase
- serum lipase
- ABG
- abdo XR
- CXR/ CT/ MRI
31
How is acute pancreatitis managed?
- 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
What is the aetiology of chronic pancreatitis?
- alcohol
- cystic fibrosis
- familial
- haemochromatosis
- pancreatic duct obstruction
33
What is the pathophysiology of chronic pancreatitis?
Primary autoimmune of inflammatory response in pancreatic ducts
34
What are the risk factors of chronic pancreatitis?
- alcohol
- smoking
- family history
- coeliac disease
35
What is the clinical presentation of chronic pancreatitis?
- epigastric pain that 'bores' to the back but relieved by sitting forward or hot water bottles
- jaundice
- weight loss
- joint pain
36
What are the differential diagnoses of chronic pancreatitis?
- pancreatic cancer
- acute pancreatitis
- biliary colic
- peptic ulcer disease
37
How is chronic pancreatitis diagnosed?
- USS and CT
| - abdo XR
38
How is chronic pancreatitis managed?
Medication:
- analgesia, fat-soluble vitamins, insulin if needed
Surgery:
- remove pancreas ± jejunum for unremitting pain, narcotic abuse or weight loss
39
What is the aetiology of alcoholic liver disease?
Heavy alcohol ingestion
40
What is the pathophysiology of alcoholic liver disease?
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
What are the risk factors of alcoholic liver disease?
- prolonged heavy alcohol consumption
- Hep C
- female
- cigarette smoking
- obesity
42
What is the clinical presentation of alcoholic liver disease?
- abdominal pain
- hepatomegaly
- ascites
- weight loss or gain
- jaundice
- splenomegaly
- hepatic mass
43
What are the differential diagnoses of alcoholic liver disease?
- Hep B, C and A
- autoimmune hepatitis
- cholecystitis
- hepatic vein thrombosis
- acute liver failure
- biliary obstruction
44
How is alcoholic liver disease diagnosed?
- serum AST, ALT and alkaline phosphatase
- serum bilirubin, albumin and GGT
- FBC
- hepatic USS
45
How is alcoholic liver disease managed?
Lifestyle changes:
- reduce/ cut out alcohol
- weight loss
- smoking cessation
- nutritional supplementation
Corticosteroids
46
What is the aetiology of cirrhosis?
- chronic alcohol use
- Hep B or C infection
- biliary obstruction
- drugs and toxins
- autoimmune liver disease
47
What is the pathophysiology of cirrhosis?
Activation of hepatic stellate cells leads to accumulation of collagen type I and III in the hepatic parenchyma
48
What are the risk factors of cirrhosis?
- alcohol misuse
- IVDU
- unprotected sex
- obesity
49
What is the clinical presentation of cirrhosis?
- abdominal distension
- jaundice
- blood in vomit
- black stool
50
What are the differential diagnoses of cirrhosis?
- constructive pericarditis
- portal vein thrombosis
- splenic vein thrombosis
- IVC obstruction
- schistosomiasis
51
How is cirrhosis diagnosed?
- 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
How is cirrhosis managed?
- 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
What is a varices?
Dilated vein at risk of rupturing, resulting in haemorrhage and GI bleeding
54
What is the aetiology of a varices?
- alcoholism and viral cirrhosis = leading causes
| - portal hypertension
55
What is the pathophysiology of a varices?
- 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
What are the risk factors of varices?
- cirrhosis
- portal hypertension
- schistosomiasis infection
- alcoholism
57
What is the clinical presentation of varices?
- 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
What are the differential diagnoses of varices?
- peptic ulcer disease
| - hiatal hernia
59
How is varices diagnosed?
Endoscopy to find bleeding source
60
How is varices managed?
- 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
What is the aetiology of portal hypertension?
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
What is the pathophysiology of portal hypertension?
- 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
What is the clinical presentation of portal hypertension?
- 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)
