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CP1 > Hepato-biliary disease > Flashcards

Hepato-biliary disease Flashcards

1
Q

List the common infective causes of acute hepatitis and outline risk factors.

A

Can be cause by any of the hep viruses, A-E.
D and E are rare in the UK
ABC are usually asymptomatic except in IVDU who develop jaundice.
A commonly infects children (A+E exclusively acute)
Bacterial seeding from ascending infection, portal pyaemia and systemic septicaemia may cause hepatitis through abscess development.
Helminths
Protozoa

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2
Q

Describe the types of liver damage that may be caused by drug therapy.
This is a bit bollocks tbh

A

Paracetamol cause predictable, dose-dependent liver damage.
common drugs including: valproate, NSAIDs, amiodarone, diclofenac, methyldopa, isoniazid, minocycline, halothane and methotrexate. Other drugs may cause cholestasis: chlorpromazine, oestrogens (and other steroids), co- amoxiclav/flucloxacillin, chlorpropamide.

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3
Q

Describe the common causes of chronic hepatitis.

A

Most chronic disease is caused by Hep B and C.
B is less common in Uk and often transmitted from mother to child.
Hep C is mainly transmitted through blood, many who have it have a history of IV drug use.
Autoimmune hepatitis may also occur in response to infection.
Wilson’s disease, haemochromatosis and alpha-1 antitrypsin deficiency may lead to chronic liver disease.

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4
Q

Describe the morphology and pathological consequences of acute hepatitis

A

Hepatocytes undergo swelling and vacuolation before necrosis and rapid removal.
Necrosis is maximal in zone 3 as this receives the least supply of oxygenated blood.

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5
Q

Describe the morphology and pathological consequences of chronic hepatitis

A

Any hepatitis lasting more than 6 months, principle cause of chronic liver disease, cirrhosis and hepatocellular carcinoma.
Chronic inflammatory cell infiltrates are present in the portal tracts
Loss of portal limiting plate, confluent necrosis and fibrosis
Grading assesses the level of inflammation and staging assesses the extent of fibrosis/cirrhosis.

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6
Q

List common primary sites for metastatic tumour to the liver.

A 
Common, 40% of dead patients found with lung mets.
Common sites
GI tract
Bronchi
Breast
Ovary
Lymphoma
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7
Q

List risk factors for the development of primary hepatocellular carcinoma.

A 
Age
Male gender
Cirrhosis (80% of cases, caused by haemochromatosis, NAFLD, alcohol, alpha-1 anti-trypsin deficiency).
Aflatoxin produced by Aspergillus Flavus
Hep B and C
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8
Q

Define cirrhosis in pathological terms.

A

“a diffuse process characterised by fibrosis and conversion of the normal liver architecture into abnormal nodules surrounded by fibrotic scaffold (without portal triads).”
The end stage of many hepatic diseases.
Stellate cells are activated and transformed into myofibroblast like cells.

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9
Q

Discuss the initial investigation of a patient with suspected cirrhosis.

A

History, examination, liver function tests (incl albumin and clotting), ultrasound and biopsy.

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10
Q

Outline the pathophysiology underlying the clinical features of cirrhosis including hypoproteinaemia, abnormal clotting, secondary hyperaldosteronism and portal hypertension.

A

Hypoproteinaemia - Damage to hepatocytes causes reduction in albumin production.
Abnormal clotting - Reduction in production of vitamin K dependent clotting factors.
Secondary hyperaldosteronism - The liver usually metabolises steroids. However, during cirrhosis, these are not broken down and accumulate.
Portal hypertension - Blood flow through hepatocytes is compromised causing a backlog of pressure and portal hypertension.

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11
Q

Describe the clinical features of complications of cirrhosis and portal hypertension including oesophageal varices.

A

Varices may present with haematemesis and are responsible for 7% of upper GI bleeds.
They have a high mortality of 30%

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12
Q

Describe the clinical features of complications of cirrhosis and portal hypertension including ascites

A

75% of ascites is due to cirrhosis.
Patients present with abdominal distention and shifting dullness.
May be caused by portal hypertension and low albumin levels.

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13
Q

What are the clinical features of encephalopathy? 6

A 
Clinical features of encephalopathy: 
Drowsiness
Monotonous speech
Tremor
Incoordination
Extensor plantar response 
Decerebrate posture (everything extended)
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14
Q

What are the clinical features associated with chronic liver disease?

A 
Ascites
Jaundice
Haematemesis
Hypertension
Encephalopathy
Bruising
Anaemia
Pain 
Malaise
Tangelectasia (spider veins)
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15
Q

Describe portal venous anatomy

A

See diagram. Superior and inferior mesenteric arteries feed into hepatic portal vein. Spleen and pancreas drain via splenic vein into HPV, as well as gastric veins.

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16
Q

Define portal hypertension.

A

Portal hypertension refers to abnormally high pressure in the hepatic portal vein. Clinically significant portal hypertension is defined as an hepatic venous pressure gradient of 10 mm Hg or more.

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17
Q

Classify the causes of portal hypertension.

A

Prehepatic causes:
Congenital Stenosis/atresia of HPV
External pressure
Thrombus (more common in children)

Hepatic causes
Cirrhosis
Acute liver disease
Schistomiasis
Congenital hepatic fibrosis
Sclerosis
Veno-occlusive disease
Drugs

Post hepatic causes
Budd-Chiari syndrome
LVF
Constrictive pericarditis

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18
Q

Describe the clinical manifestations of portal hypertension.

A 
Hepatosplenomegaly
Ascites
Hepatorenal syndrome (rapid deterioration of kidney funct as a result of cirrhosis) 
Varices
fetor hepaticus (breath of the dead)
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19
Q

List the common causes of splenomegaly.

A 
Infection:
Acute (endocrditis, sepsis), chronic (TB), parasitic (malaria)
Inflammation: 
rheumatoid arthritis, SLE, sarcoidosis
Portal hypertension:
Liver disease
Haematological: Myeloproliferative diseases, leukaemias, lymphomas, haemolytic anaemia.
Miscellaneous:
Storage disorders, amyloid, neoplasm
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20
Q

Classify the intrahepatic causes of cholestatic jaundice

A 
Caused by failure of bile secretion:
Viral or alcoholic hepatitis, 
cirrhosis, 
pregnancy, 
idiopathic 
congenital.
Bilirubin is unconjugated
21
Q

Classify the extrahepatic causes of cholestatic jaundice

A 
Extrahepatic jaundice is due to large duct obstruction distal to the canaliculi:
Common duct stones
Carcinoma
Biliary stricture 
Pancreatic pseudocyst
Sclerosing cholangitis
22
Q

What are the classical clinical features of obstructive jaundice?

A 
Jaundice of skin and sclera
Pruritis
Pale stools
Dark urine
Steatorrhoea
23
Q

Describe the laboratory and radiological investigation of a patient presenting with obstructive jaundice.

A

Serum bilirubin >2-3mg/dL (30-50umol/L)
LFTs will show obstructive pattern - ALT + AST increased, alk phosp + gamma GT (high levels of this suggests that it is not caused by hepatocellular damage) - Markedly increased
USS may be used to confirm the presence of gallstones or other pathology.
Urine bilirubin increased

24
Q

List the common types of gallstones and explain their formation.

A 
Cholesterol stones (80%)
Pigment stones-
Black stones (calcium bilirubinate and mucin glycoproteins)

yellow cholesterol stones

Brown stones (calcium bilirubinate and fatty acid calcium salts)

Formed from the crystallisation of bile salts

25
Q

Describe the symptoms and signs in a patient with biliary colic.

A

Crescendoing pain initially pain in epigastrium but radiates to RUQ and right shoulder.
May occur after eating fatty foods and at night.
Nausea and vomiting may accompany severe cases.

26
Q

Describe the symptoms and signs in a patient with acute cholecystitis.

A

Similar symptoms to biliary colic with the addition of:

Pyrexia, severe RUQ pain with guarding and tenderness

27
Q

List the common tests used in the diagnosis of calculus biliary tract disease.

A

Lab tests unaltered in biliary colic

LFTs may show obstructive pattern in acute cholecystitis, as well as moderate leukocytosis and raised inflammatory markers. Abdominal USS may be used for diagnosis.

28
Q

Describe the natural history of a young patient with asymptomatic gallstones.

A

Asymptomatic gallstones often picked up on incidental imaging. People with asymptomatic gall stones come across problems at a rate of 1-4% per year. Thus, prophylactic cholecystectomy is not favoured over a traditional “watch and wait” approach. However, a younger patient will have more time over which to encounter problems, and so treatment may be favoured. Small stones may be more dangerous.

29
Q

Describe the symptoms and signs of stones in the bile ducts.

A

Obstruction of the bile duct may lead to infection - ascending cholangitis:
Charcots triad: Swinging fever, rigors, RUQ pain and jaundice

Lodging of stones in the cystic duct may lead to acute cholecystitis.

30
Q

What is the management of stones in the bile ducts?

A

Immediate management = Fluids and analgesia and antibiotics if patient is septic.

Surgery is offered to those with recurrent attacks

If there is gas in the gallbladder or perforation/GI obstruction then emergency surgery may be performed.

31
Q

Define Murphy’s sign + what is it for?

A

Pain when examiners hand is placed on right costal margin MCL causing patient to stop breathing in.

Used for confirming cholecystitis.

32
Q

Define Courvoisier’s sign + what is it for?

A

This sign occurs when a palpable non-tender gallbladder is accompanied by painless jaundice.

This indicates that the pain is unlikely to be due to be due to gallstones and more likely to be caused by malignancy of the gallbladder or pancreas.

33
Q

What is a T tube used for?

A

A T tube may be inserted under the skin and placed into the bile duct to drain bile or insert contrast medium.

34
Q

List the most common bacterial infections found in acute cholecystitis.

A

E.Coli.
C.Perfinigens
Klebsiella

These are gas producing organisms and may result in emphysematous cholecystitis (GB may perforate and may lead to gangrene and higher mortality rates.)

35
Q

In a patient with acute cholecystitis, demonstrate the right upper quadrant physical signs that support this diagnosis.

A

Tenderness and muscle guarding will be present. As well as Murphy’s sign.

36
Q

Classify pancreatitis on the basis of the severity of injury to the organ.

A

May be acute or chronic.

May be classified into mild or severe using: Modified Glasgow criteria, Ranson or APACHE II criteria.

37
Q

Describe the aetiology and pathology of pancreatitis.

A

Damage to acinar cells causes necrosis, haemorrhage and venous thrombosis.
Earlier, may result in perilobular necrosis but bay progress to panlobular necrosis and enzymes may leak out and digest perilobular and omental fat.

In gallstone disease, bile backtracks up pancreatic duct and causes inflammation.
in alcohol consumption. the ampulla spasms, ducts are plugged by viscous secretions and alcohol is directly toxic to acinar cells.

Chronic pancreatitis occurs in alcoholics after constant bouts of acute pancreatitis. Calcium may be deposited where the protein plugs are placed. Eventually resulting in fibrosis.

38
Q

What are the causes of acute pancreatitis?

A

I diopathic

G allstones
E thanol
T rauma

S teroids
M umps (infections)/malignancy
A utoimmune
S corpian stings
H yperlipidaemia/hypercalcaemia/hyperparathyroidism
E RCP
D rugs
39
Q

What are the potential early complications of acute pancreatitis?

A 
Retroperitoneal haemorrhage
Pancreatic necrosis
pseudo-cyst
Infection/abscess
Hypocalcaemia
ARDS/shock
DIC
MODS
40
Q

What is the Glasgow criteria for assessing the severity of pancreatitis?

A 
P - PaO2 <8kPa.
A - Age >55-years-old.
N - Neutrophilia: WCC >15x10(9)/L.
C - Calcium <2 mmol/L.
R - Renal function: Urea >16 mmol/L.
E - Enzymes: LDH >600iu/L; AST >200iu/L.
A - Albumin <32g/L (serum)
S - Sugar: blood glucose >10 mmol/L.
41
Q

Describe the clinical presentation of a patient with pancreatitis.

A

Severe epigastric pain which may radiate to the back.
Nausea and vomiting.
These symptoms may occur after a large meal or 6-12 hours following an alcoholic binge.

42
Q

What is Grey-Turner’s sign?

A

Bluish bruising and discolouration of the flanks from the last rib down to the hips.
Caused by a retroperitoneal bleed - may be present in severe acute pancreatitis.

43
Q

What is Cullen’s sign?

A

Cullen’s sign is superficial oedema and bruising in the subcutaneous fatty tissue around the umbilicus.
May be caused by acute pancreatitis, triple A or an ectopic pregnancy.

44
Q

Outline an appropriate diagnostic approach for a patient with suspected acute pancreatitis, emphasising the timing, interpretation and reliability of various studies.

A

History + examination.
Check serum amylase raised >x3 of normal, although this may normalise in first 24-48 hours. Urine amylase follows this trend but with a 2 day lag.
Serum ALT <3x is indicative of gallstones
USS is indicated early in diagnosis.
CT or USS may pick up signs of severe disease such as peripancreatic oedema and necrosis.
ERCP may also be useful? But may exacerbate the problem.

45
Q

What is the role of severity scoring systems in the treatment of acute pancreatitis?

A

Mild should be referred to hospital, given crystalloids, analgesia and NBM.
If severe, referral to ICU, monitoring for hypovolemic shock, maintaining fluids and urine output.
Surgical removal of gallstones and debridement of necrotic tissue should also occur, preferably within 48 hours.

46
Q

What is the clinical presentation of carcinoma of the pancreas?

A

Symptoms:
Cachexia, jaundice, thrombophlebitis migrans, GI bleed, acute pancreatitis.

Patients with a Ca in the head of the pancreas (2/3rds) may present with signs of obstructive jaundice (palpable GB, jaundice, pruritis, dark urine, pale stools.)

Signs:
Excoriations, lymohadenopathy, palpable GB, ascites, mass and late onset DM.

47
Q

Describe the morphology of pancreatic carcinoma.

A 
90% are ductal adenocarcinomas 
Others include:
Adenosquamous cell carcinomas
Giant cell carcinomas
Papillary cystadenocarcinomas
48
Q

Describe the symptoms and physical signs of pancreatic cancer on the basis of location of the tumour within the gland.

A

Cancers of the head are likely to cause symptoms of obstructive jaundice.
Cancers of the tail may present with metastasis, or malignant ascites.
Cancers in the body and tail may also obstruct the duodenem and present with obstructive symptoms as such (nausea, vomiting, anorexia, constipation.)

CP1 (10 decks)

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