LIVER Flashcards

1
Q

Describe Wernicke’s and korsakoff’s

A

common in alcoholic liver disease nystagmus - weird eye movements, confusion caused by thiamine deficiency - by alcohol

If WE left untreated - Korsakoff’s syndrome
- confabulation - make up events
- cannot remember previous memories
- and cannot form new memories

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2
Q

whats the livers function?

A

metabolism - carbs, proteins, fats, bilirubin, drugs

synthesis - proteins e.g. albumin, clotting factors, fibrinogen, gluconeogenesis

immune - kuppfer cells - macrophage system

storage - fat soluble vitamins

homeostasis - glucose

bile production

clearance - bilirubin, drugs, toxins

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3
Q

explain stages from fibrosis to cirrhosis

A

F0 - good blood flow, pink

f1 - f3 - active deposition of collagen, forming scar tissue, disruption of blood flow, fibrosis

f4 - cirrhosis, nodules form, erratic regenerating to compensate for lack of blood flow, constant damage

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3
Q

what is the classification of liver disease?

A

classified according to pattern of damage seen and time course over which damage occurs

cholestatic or hepatocellular - can lead to fibrosis and cirrhosis

cholestasis - disruption of bile flow - stagnation of bile in bile ducts, intrahepatic - affects bile ducts in liver, extrahepatic - affects bile ducts outside liver
- impaired biliary secretion - reduces absorption of fatty substances - leads to fatty stool - as its not absorbed but excreted
- accumulation of bile salts can damage hepatocyte

hepatocellular - damage to hepatocyte
- hep A, B, C, D, E
- fatty infiltration - accumulation of fat in hepatocyte, MACROVESICULAR - single large fat droplet + smaller fat droplets occupy cytoplasm of hepatocyte - push nucleus to periphery
MICROVESICULAR - cytoplasm filled with tiny lipid droplets, nucleus stays central
- inflammation - hepatits
- cell death - necrosis

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4
Q

interpret bilirubin

A

bilrubin - product of RBC breakdown
- normal range 5-20 micromol/L

transported to liver attached to albumin

liver transforms it into a conjugate - then excreted via bile into intestines

bilirubin increased due to:
- more RBC breakdown
- cholestasis - obstruction in bile duct - cannot be excreted via bile, goes into blood - high blood bilirubin
- liver disease - cannot conjugate bilirubin

clinical jaundice - bilirubin is >50 micromol/L

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5
Q

interpret LFTs - AST and ALT

A

transaminase enzymes

elevated in liver disease

AST:ALT ratio is typically 2:1 in alcohol liver disease

AST 0-40 iu/L normal range

ALT - 5-30 iu/L normal range

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6
Q

interpret LFTs ALP and GGT

A

ALP 30-120 iu/L

GGT 5-55 iu/L

if both levels increased - probably due to cholestasis

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7
Q

interpret albumin

A

albumin 35-50 g/dL

one of the proteins produced by liver

in chronic liver disease - decreased albumin
- liver cannot synthesise properly
- affects highly protein bound drugs
- more free drug available - more therapeutic effect - can become toxic

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8
Q

interpret INR

A

clotting factors produced by liver

INR measures how long it takes for blood to clot

in liver disease - INR will be raised - results in bleeding

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9
Q

what are the signs and symptoms of liver disease?

A

jaundice
ascites
unexplained bruising/bleeding
HE
abdominal pain
spider naevi
gynaecomastia
fatty stool
pale stools + dark urine

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10
Q

what is ascites and its management?

A

ascites - accumulation of fluid in the peritoneal cavity - swollen abdomen

portal hepatic vein transports nutrients to liver if obstruction - pressure builds up

portal HTN - renal sodium retention - increased blood vol - ascites

management:
- fluid/sodium restriction
- spironolactone - aldosterone antagonist
- furosemide - loop diuretic
- terlipressin

paracentesis - sterile needle into abdomen - drains fluid

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11
Q

what is spontaneous bacterial peritonitis and its management?

A

SBP - infection of ascitic fluid
- neutrophils >250 per mm3

management - 3rd gen cephalosporins, co-amoxiclav

ciprofloxacin as prophylaxis

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12
Q

what is hepatic encephalopathy and its management?

A

HE - brain dysfunction caused by liver insufficiency or portal systemic shunt - leads to neurological/psychiatric abnormalities

asterixis - flapping hand tremor - sign of HE

precipitating factors of HE
- increased protein load
- reduced ammonia secretion
- electrolyte imbalance
- dehydration
- infection

high levels of ammonia as liver cannot metabolise it properly into urea - crosses BBB and enters astrocytes in brain
- ammonia converted to glutamine in astrocytes - causes oedema

management:
- 1st line - lactulose - pee out ammonia
- rifaximin antibiotic
- other options - metronidazole

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13
Q

what is variceal bleeding and portal HTN and its management?

A

PHTN - due to increased resistance to flow
- collateral vessels form - enable blood to bypass liver

terlipressin and somatostatin analogues

infection is common in upper GI bleed in cirrhotic patients
- broad spectrum antibiotic prophylaxis
- 7 day antibiotic prophylaxis - broad spectrum tazocin
- ciprofloxacin in penicillin allergic patients

secondary prophylaxis to prevent re-bleeding
- non selective beta blockers
- propranolol and cardivelol

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14
Q

what is spider naevi

A

central red arteriole surrounded by capillaries - represents legs
- due to raised oestrogen

in liver disease - failure to metabolise oestrogen

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15
Q

management plan for acute alcoholic hepatitis (AAH)

A

1) Abstinence

2) manage withdrawal symptoms - including seizures

3) manage malnutrition and vitamin deficiency to prevent complications

4) use drugs to treat AAH - targeting inflammatory component

5) manage complications of liver disease - encephalopathy, coagulopathy, ascites

16
Q

symptoms of withdrawal and management

A

symptoms - tremor, restlessness, fever, rapid pulse, delusions

treatment - chloridiazepoxide + pabrinex
- benzos are sedating and anti-convulsants
- most form active metabolites which is good for increased therapeutic effect
- pabrinex - vitamins for thiamine deficiency

17
Q

signs and symptoms of AAH - drug treatment for it?

A

AAH - clinical syndrome of jaundice and liver failure
- fever, hepatomegaly, leukocytosis

corticosteroids - to turn of inlfammatory process
- prednisolone

pentoxyfylline - inhibits TNF-alpha
- other anti-TNF agents - infliximab

18
Q

what are the abstinence agents

A

chronic high levels of alcohol result in GABAergic and glutaminergic dysregulation

abstinence agents available:
- naltrexone
- disulfiram
- acamprosate