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GI P2a > Liver > Flashcards

Liver Flashcards

1
Q

What are examples of causes of metabolic liver disease?

A

haemochromatosis, Wilson’s disease, A1AT deficiency

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2
Q

what inheritance pattern is haemochromatosis?

A

autosomal recessive

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3
Q

what are symptoms of advanced haemochromatosis?

A

bronzing of skin, diabetes, hepatomegaly

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4
Q

What is total iron binding capacity in hemochromatosis?

A

decreased

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5
Q

What is a classic sign of Wilson’s disease, and how is it diagnosed?

A

Keiyser Fischer rings

Using a slit lamp analysis

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6
Q

What is the pathophysiology of Wilson’s disease?

A

Normally, copper is incorporated into caeruloplasmin. In Wilson’s, this is impaired, due to a mutation to the ATPase that acts to move Copper across intracellular membranes

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7
Q

What is the tx for Wilson’s?

A

prevention of copper absorption in the intestine via chelating agents such as zine

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8
Q

What are the three main pathological lesions associated with alcoholic liver disease? What are the symptoms associated with each stage? What damage is occurring at each stage?

A

Fatty liver -> asymptomatic. Possible hepatomegaly. Fatty droplets can lead to mitochondrial damage
Hepatitis -> rapid onset jaundice, nausea, anorexia, encephalopathy, fever, ascites. Ballooned hepatocytes, containing eosinophilic bodies (Mallory bodies), surrounded by neutrophils. Fibrosis and foamy degeneration
Cirrhosis -> may be asymptomatic. Can present with spider naevus, ascites, spontaneous bacterial peritonitis, portal HTN. Destruction and scarring of liver architecture and fibrosis

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9
Q

What are the LFT findings?

A

increased GGT, increased AST, elevated MVC

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10
Q

What are examples of aminotransferases and when are they released?

A

ALT: cystolic enzyme. specific to the liver.
AST: mitochondrial enzymes

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11
Q

What does high ALP indicate?

A

cell damage, but can locate where from. Released from damaged hepatic membranes. IF GGT also abnormal, from the liver

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12
Q

what is the most common acute cause of liver failure?

A

paracetamol OD

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13
Q

What is the normal aetiology of hepatocellular carcinoma?

A

Severe cirrhosis. Also haemochromatosis and hep B and C

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14
Q

What is the aetiology of cholangiocarcinoma

A

biliary cysts, flukes (flatworms), primary sclerosing cholangitis

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15
Q

What do bile salts do?

A

Form micelles around cholesterol/lipids. Allows action of lipase, so fat can be absorbed by the villi.

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16
Q

What are fat soluble vitamins?

A

A, B, E, K

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17
Q

What hormone causes gallbladder contraction

A

Cholecystekinin

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18
Q

What is secretin’s action

A

Stimulates biliary and pancreatic ductular cells to secrete bicarbonate and water in response to acid in the duodenum. Causes increased bile secretion

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19
Q

What is murphy’s sign? When is it seen?

A

Pain on inspiration when palpating the gallbladder. acute cholecystitis and cholangitis

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20
Q

What are the risk factors for gallstones?

A

3F’s: female, fat, forty

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21
Q

What is adimirand’s triad?

A

increased stone risk if decreased lethicin, decreased bile salts, increased cholesterol

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22
Q

How can sickle cell anaemia lead to gallstones?

A

Chronic haemolysis, in which bilirubin production is increased.

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23
Q

What bacteria is associated with CBD/ cystic duct obstruction?

A

E.coli. The stasis allows it to replicate

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24
Q

What is Charcot’s triad?

A

RUQ pain, fever, jaundice

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25
Q

What is primary sclerosing cholangitis?

A

chronic inflammation and fibrosis of the bile ducts. Presents with Charcot’s triad

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26
Q

How is each form of hepatitis spread?

A
  • Hep A: faecal-oral route. Also associated with shellfish
  • Hep B: verticle transmission or via blood products
  • Hep C: blood borne
27
Q

What is the most common UK hepatitis and the most common global hepatitis?

A
  • UK: Hep A

- worldwide: Hep B

28
Q

How do you diagnose hep A?

A
  • increased AST and ALT
  • IgM increased from day 25
  • IgG raised for life
29
Q

How do you diagnose Hep B?

A
  • HBsAg present 6 months after exposure

- HBcAg (anti HB core protein) = past infection

30
Q

why might hep B get to a chronic phase, and what is the difference?

A
  • acute: normally will be entirely cleared

- might persist due to immunocompetency or age of the patient

31
Q

What is the pathophysiology of verticle hep B?

A
  • chronic immune tolerance of HBV virus for 2 to 3 decades

- then immune clearance: hepatitis and cirrhosis

32
Q

What anti viral medication is used for Hep B?

A
  • interferon (immunostimulation)

- centecavir and tenofovir (anti viral replication)

33
Q

What is the treatment for Hep c?

A
  • anti virals: weekly peginterferon alfa-2a and daily oral ribavin. Eliminate HBV RNA to stop progress
34
Q

what is bruising/bleeding around the umbilicus indicative of?

A

Pancreatitis

35
Q

What is the pathophysiology of acute pancreatitis?

A

pancreas releases exocrine hormones that cause autodigestion of the organ.

36
Q

What is the final common pathway in acute pancreatitis?

A

increased intracellular calcium, activates intra cellular proteases and pancreatic enzymes released. Acinar cell injury leads to necrosis. Inflammatory response, organ failure

37
Q

What is the pathphysiology of chronic pancreatitis?

A

Inappropriate activation of enzymes in the pancreas. Leads to precipitation of protein plugs in the duct lumen. Leads to calcification, and ductal hypertension and pancreatic damage. Cytokine activation leads to inflammation and pancreatic fibrosis.

38
Q

What test is used to see if pancreatic exocrine function is damaged?

A

Secretin stimulation test

39
Q

What is budd-chiari syndrome?

A

obstruction of the hepatic vein via a tumour or thrombus. Leads to ischaemia and failure

40
Q

What are signs of liver failure:

A

asterixis (liver flap), Dupuytren’s constractures (finger changes), leukonchyia (white nails, spider naevus

41
Q

What is primary biliary cholangitis:

A

autoimmune condition that damages interlobular bile ducsts in the liver. Slow to present, often incidence finding due to raised ALP

42
Q

What is Wernicke’s encephalopathy:

A

lack of B1 or thiamine in the brain of chronic alcoholics

43
Q

What is the triad presentation of Wernicke’s encephalopathy?

A

eye paralysis, confusion, ataxia

44
Q

What is Gilbert syndrome?

A

inherited disorder. Impairs conjugation of bilirubin. OFten no symptoms except jaundice

45
Q

What is MALS?

A

Median arcuate ligament syndrome. compression can occur in liver disease. Coeliac artery is compressed

46
Q

What is jaundice due to?

A

Hyperbilirubinaemia –> bilirubin is the normal breakdown production from the catabolism of haem

47
Q

What is the normal pathology of bilirubin excretion?

A
  • conjugated in the liver, making it water soluble
  • excreted via the bile into the GI tract
  • egested in the faeces as urobilinogen and stercobilin
  • jaundice occurs when this pathway is disrupted
48
Q

What are the three types of jaundice?

A

pre hepatic, hepatic and post hepatic

49
Q

What occurs in prehepatic jaundice? What are the signs and the causes

A

Excess RBC breakdown. Overwhelm’s the liver’s ability to conjugate. There is normal urine, containing unconjugated bilirubin. normal AST + ALT and ALP

50
Q

What occurs in hepatic jaundice? What are the signs and the causes

A

Dysfunction of the hepatic cells. Liver loses the ability to conjugate bilirubin, and in cases where is also becomes cirrhotic, obstruction occurs. Leads to a mixed picture. There is dark urine due to conjugated bilirubin, normal stool. Very high AST and ALT, slight increase of ALP.

51
Q

What does ^^^ ALT and ^ ALP indicate

A

hepatocellular injury

52
Q

what does ^ATL and ^^^ALP indicate?

A

cholestasis

53
Q

What occurs in posthepatic jaundice? What are the signs and the causes

A

Obstruction of biliary drainage. Hyperconjugated bilirubinaemia. Dark urine, clay like stools. Slight increase in AST and ALT, but large increase in ALP.

54
Q

What are the functions of the liver (7)

A

oestrogen regulation, detoxification, metabolises carbohydrates, albumin production, clotting factor production, bilirubin regulatin, immunity

55
Q

What are the macrophages of the liver?

A

Kuppfer cells

56
Q

What is the difference between PBC and PBS?

A
  • women more affected by PBC
  • PBC: intralobular ducts affected
  • PSC: all ducts affected
57
Q

how is cerebral oedema treated

A

mannitol (reduces ICP)

58
Q

what are albumin levels like in liver disease?

A

low

59
Q

Which hepatitis can only infected in the presence of another?

A

D with B

60
Q

What is the difference between HB core Ab, HB surface Abm HB surface Ag?

A
  1. HBcAb: active immunity/ current disease
  2. HBSAb: immunity (active or passive)
  3. HBsAg: current infection
61
Q

What is the pathology of a paracetamol OD?

A

not enough glutathione stores in the liver so toxic NAPQI builds up and leads to liver damage

62
Q

What is wernicke-korsakoff encephalopathy and how is it treated?

A

lack of b1. via IV thiamine

63
Q

What does raised alpha fetoprotein indicate?

A

HCC

64
Q

PBC presenting features:

A
  • pruritus (most common), with or without jaundice
  • steatorrhoea
  • malabsorption of fat vitamins (A, D, E, K)
  • xanthelasma

GI P2a (12 decks)

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