liver

Question 1

where is the liver located?

Answer 1

upper right abdomen under the ribs (right hypochondrium)

Question 2

what are the liver’s blood supplies?

Answer 2

portal vein (nutrient-rich) and hepatic artery (oxygenated)

Question 3

what are hepatocytes?

Answer 3

liver cells that perform most of its metabolic functions

Question 4

what are key liver functions?

Answer 4

protein, fat, carb metabolism

hormone and drug inactivation (regulates hormones: thyroid, cortisol, sex hormones, EPO; metabolises drugs via CYP enzymes)

bile and enzyme production

vitamin and ferritin (iron) storage

immune defence (Kupffer cells - destroy disease causing organisms)

Question 5

what is bile’s role?

Answer 5

emulsifies fats and removes waste (bilirubin), aids digestion

Question 6

what is acute liver disease?

Answer 6

sudden onset with rapid deterioration, e.g. from paracetamol OD

Question 7

what is chronic liver disease?

Answer 7

gradual liver damage over months/years, often asymptomatic

Question 8

what is cirrhosis?

Answer 8

irreversible scarring (fibrosis) and nodular changes in the liver

Question 9

what’s the difference between compensated and decompensated cirrhosis?

Answer 9

compensated = liver still functions., decompensated = liver fails, symptoms present

Question 10

what is cholestasis?

Answer 10

blocked or reduced bile flow from the liver

Question 11

what are major risk factors for liver disease?

Answer 11

alcohol, obesity, viral hepatitis, drug toxicity

Question 12

name 3 metabolic liver conditions

Answer 12

NAFLD/MASLD, Wilson’s disease, hereditary hemochromatosis

Question 13

what is Budd-Chiari syndrome?

Answer 13

liver blood outflow obstruction due to clotting

Question 14

outline the progression of liver disease

Answer 14

healthy liver → steatosis → hepatitis → fibrosis →cirrhosis → decompensation → HCC

Question 15

can liver disease be reversed?

Answer 15

yes, early-stage fibrosis can improve if cause is removed

Question 16

what is hepatocellular carcinoma (HCC)?

Answer 16

a primary liver cancer, often develops in cirrhotic livers

Question 17

name early symptoms of liver disease

Answer 17

fatigue, nausea, weight loss, upper-right quadrant pain

Question 18

what are signs of decompensated liver disease?

Answer 18

jaundice
ascites (due to portal HTN)
spider naevi (vascular lesions)
clubbing
gynaecomastia
variceal bleeding (veins in stomach area expand/swollen and can rupture due to portal HTN = fatal bleeding)
hepatic encephalopathy (due to build-up of neurotoxins like ammonia = confusion, crosses BBB),
spontaneous bacterial peritonitis (SBP - infection of ascitic fluid)
sepsis (at higher risk due to impaired immunity)
hepatorenal syndrome (kidney failure due to reduced blood flow - requires Tx such as terlipressin [vasoconstrictor] or liver transplant)

Question 19

what causes hepatic encephalopathy?

Answer 19

ammonia build-up due to liver dysfunction affecting brain function (crosses BBB)
triggers: infection, constipation, dehydration

Question 20

what is Wernicke’s?

Answer 20

Wernicke’s encephalopathy is an acute neurological condition which
develops due to thiamine deficiency and is reversible if treated early
Pt with a history of excessive alcohol intake will usually be
given intravenous B vitamins and then step down to oral thiamine (long term drinking reduces ability to absorb thiamine)

Question 21

what is ascites?

Answer 21

fluid accumulation in the abdomen from portal hypertension (arises from increased blood flow resistance in the liver = reduced blood flow = build-up of pressure) and low albumin (albumin helps to balance fluids in blood vessels)

Question 22

what do ALT/AST indicate?

Answer 22

hepatocyte injury; ALT > AST in most causes (AST > ALT in alcohol)

Question 23

what markers suggest cholestasis?

Answer 23

↑ bilirubin, ALP, GGT

Question 24

what does raised PT/INR indicate?

Answer 24

impaired liver synthetic function (e.g. reduced clotting factors)

Question 25

can LFTs be normal in cirrhosis?

Answer 25

yes - LFTs may appear normal even in advanced disease

Question 26

what’s the role of albumin in LFTs?

Answer 26

marker of chronic liver function; low in cirrhosis

Question 27

name 3 meds used for hepatic encephalopathy (HE)

Answer 27

lactulose, rifaximin, thiamine lactulose - draws ammonia from the blood into the colon where it's removed from the body rifaximin - non absorbable antibiotic, reduces production and absorption of ammonia thiamine - to prevent Wernicke's (severe brain disorder)

Question 28

which drug is safe in liver disease: paracetamol or NSAIDs?

Answer 28

paracetamol (at ≤3g/day); NSAIDs should be avoided

Question 29

what drug is used for SBP prophylaxis?

Answer 29

ciprofloxacin or co-trimoxazole

Question 30

what do NSBBs (non selective beta blockers) treat in liver disease?

Answer 30

portal HTN and variceal bleeding prevention (e.g. carvedilol)

Question 31

what drugs are commonly prescribed in liver disease?

Answer 31

NSBB diuretics - ascites - spironolactone = 1st line - anti-mineralocorticoid, (blocks aldosterone) and it helps address hyperaldosteronism, can be used in combo w furosemide (loop) vit D (colecalciferol) - deficiency is common in patients with liver cirrhosis as the liver is involved in vitamin D metabolism, converting it to its active from lactulose/rifaximin ciprofloxacin/co-trimoxazole - SBP prevention thiamine - alcohol excess - Wernicke's Tenofovir/entecavir - hep B analgesia - paracetamol but avoid NSAIDs (can cause AKI, increased risk of bleeds), low dose opioids can be started (titrated - risk of accumulating and = sedation) -> reduce paracetamol dose in decompensated liver failure LMWH - VTE prophylaxis fluids

Question 32

what should be considered for drug dosing in liver disease?

Answer 32

avoid hepatotoxic drugs reduce doses monitor for efficacy/toxicity use TDM where possible consider liver synthetic function ADME!

Question 33

why does paracetamol OD cause hepatic impairment?

Answer 33

metabolised by the liver via glucuronic acid conjugation, w small amounts metabolised by CYP450 enzymes --> NAPQI - usually, NAPQI is conjugated w glutathione, inactivated then eliminated in the urine - in overdose, the glucuronidation and sulfation pathways become saturated = ↑↑ paracetamol is metabolised by CYP450 = ↑ NAPQI formed - once glutathione stores are exhausted, NAPQI accumulates + has a direct hepatotoxic effect

Question 34

how can community pharmacists help prevent liver disease?

Answer 34

offer lifestyle advice, alcohol risk tools (e.g. Drinkaware), promote healthy behaviours

Question 35

what red flags should prompt referral?

Answer 35

jaundice vomiting blood confusion oedema weight loss

Question 36

how does the NHS Long Term Plan relate to pharmacy?

Answer 36

emphasises prevention, early detection, and minor illness management through community pharmacy