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PM4B > Liver: managing patients with hepatic disease > Flashcards

Liver: managing patients with hepatic disease Flashcards

1
Q

Describe the structure of the liver

A

Hepatic vein- takes blood back to the heart

Right lobe

Left lobe

Common bile duct

Hepatic artery- brings blood from the heart

Portal vein- brings blood from the bowel

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2
Q

Describe each function of the liver

A

Metabolism- carbohydrate, fat, protein, steroid hormone, insulin, aldosterone, bilirubin, drugs, vitamin D

Synthesis- plasma proteins (albumin), clotting factors, cholesterol, glucose from fat and protein, urea from amino acids

Immunological- kupffer cells, filter antigens- infection

Secretion- bile and bile salts

Homeostasis- glucose (conversion to glycogen body heat)

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3
Q

What are the top 3 important treatment priorities regarding the liver

A

Alcoholic liver disease

Metabolic/ NAFLD or NASH

Viral hepatitis- Hepatitis C (HCV)

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4
Q

What is the process for chronic liver damage

A

Insult e.g. toxin or virus

hepatitis (inflammation) or steatosis (fatty) or steatohepatitis (mixed)

Reversible- liver regeneration

Insult not removed

Fibrosis- thickening and scarring of smooth muscle tissue

Cirrhosis- chronic liver disease

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5
Q

What are the complications of chronic liver damage

A 
Ascites
Varicose
Encephalopathy
Jaundice
Hepatocelluar Carcinoma
Death 
Anaemia
Sepsis
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6
Q

What does the term compensated mean in relation to the liver

A

Known as chronic liver damage but asymptomatic due to medication or enough healthy liver tissue to carry out normal function

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7
Q

What does decompensated mean in relation to the liver

A

When compensated liver disease becomes symptomatic

Ascites- fluid buildup in abdomen

Variceal bleed- When blood pressure increases in the portal vein system, veins in the esophagus, stomach, and rectum enlarge to accommodate blocked blood flow through the liver.

Encephalopathy- changed mental state that can have physical changes

Hepatorenal syndrome (HRS)- consists of rapid deterioration in kidney function

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8
Q

Describe how to grade cirrhosis levels

A

Child’s pugh
A= 5-6 points (compensated)
B = 7-9 points (moderate)
C= 10-15 points (advanced)

Scores:
Bilirubin
PT
Albumin 
Ascites
Encephalopathy
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9
Q

Describe acute liver failure grading in terms of hyperacute

A

Time from jaundice to encephalopathy- 6 to 7 days

Cerebral oedema- common

Renal failure- early

Ascites- rare

Coagulation disorder- marked

Prognosis- moderate

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10
Q

Describe acute liver failure grading in terms of acute

A

Time from jaundice to encephalopathy- 8 to 28 days

Cerebral oedema- common

Renal failure- late

Ascites- rare

Coagulation disorder- marked

Prognosis- poor

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11
Q

Describe acute liver failure grading in terms of subacute

A

Time from jaundice to encephalopathy- 29 to 84 days

Cerebral oedema- rare

Renal failure- late

Ascites- common

Coagulation disorder- modest

Prognosis- poor

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12
Q

What are causes of liver disease

A

Alcohol- acute HAV, HBV, HEV

Non alcoholic fatty liver disease (NAFLD)/ Non alcoholic steatohepatitis (NASH)- drugs like paracetamol, ecstasy

Metabolic e.g. haemochromatosis, wilsons, alpha-1 antitrypsin deficiency- infection, CMV malaria

Drugs- ischaemia

Malignancy- alcoholic hepatitis

Unknown- acute fatty liver of pregnancy

HCV and HBV (hepatitis B and C)

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13
Q

What are alcohol related complications

A

Acute alcohol withdrawal, seizures, Delirium Tremens (confusion)

Wernike’s encephalopathy- presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1).

Liver disease

Acute and chronic pancreatitis

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14
Q

Describe what is non-alcoholic fatty liver disease (NAFLD)

A

Spectrum of liver diseases ranging from simple fatty liver through to non alcoholic seato-hepatitis (NASH) to fibrosis and cirrhosis

More common if you are type 2 diabetic, metabolic syndrome

Rate of progression variable

Associated with excessive liver and cardiovascular morbidity/mortality + excess mortality from cancer

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15
Q

How do you assess and manage non-alcoholic fatty liver disease (NAFLD)

A

Weight loss- lifestyle, fish and veg

2-3 cups of coffee a day

Exercise- reduce fatty liver content

Lack of evidence with omega 3-FA

Reduce and stop alcohol and smoking

Statins- only stop if liver function tests double within 3 months of starting

Pioglitazone/vitamin E- if advanced fibrosis

Cardiovascular- antihypertensive

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16
Q

Describe how hepatitis C works, transmission, diagnosis and what to do if positive

A

RNA virus that spreads by infective hepatic cells then rapidly replicating- blood bourne virus

Can lead to development of cirrhosis

Transmission through:
Sharing same toothbrush 
Tattoos 
Shaving
blood transfusion
Piercings

Diagnosis:
Dry blood spot test or saliva- antibodies
Serum blood- antibodies or antigens

If positive:
blood viral RNA (virus present) and genotype
Fibroscan (nb other cofactors)
Refer for treatment with oral directly acting anti-virals (8 to 16 weeks)

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17
Q

Describe how hepatitis B (HBV) is transmitted and what it can progress to

A

Transmitted by blood and bodily fluids- childbirth, casual sex, close family members

5-10% infected can’t clear it and become carriers (in blood for 6 months or more) leading to chronic infection

Can progress to liver fibrosis or cirrhosis or Hepatocellular carcinoma (HCC)

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18
Q

Describe the use of liver function tests

A

Identifies patients suffering from liver or biliary tract disease

Not specific

Some LFTs reflect liver damage rather than function

In normal range despite underlying disease or abnormal in asymptomatic patients

Look for trends

Concern if 3 times the upper normal limit

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19
Q

What are the liver damages that liver function tests can identify

A

Acute Hepatoceullar Damage (paracetamol)

  • Rise in plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
  • Secondary rise in Bilirubin (unconjugated)
  • Prolonged PT
  • Normal albumin (long half life)

Chronic hepatocellular damage (cirrhosis)

  • Normal(ish) ALT and AST
  • Low albumin and prolonged prothrombin

Chloestatsis (blockage of bile duct)
- Rise in plasma Alkaline phosphatase (ALP) and bilirubin (conjugated)

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20
Q

What are the abnormal liver function tests that are investigated and what changes could indicate which liver disease

A

Clinical- alcohol or drugs

Other bloods- FBC, clotting, U and Es

USS liver (imaging technique) to exclude Common bile duct (CBD) dilatation and portal hypertension, hepatocellular carcinoma (HCC)
MRCP/CT scan then Endoscopic retrograde cholangiopancreatography (ERCP)

Liver screen if ruled out obstruction

  • Virus- hepatitis B or C if viral DNA present
  • Autoantibodies- positive in autoimmune primary biliary cholangitis (PBC), chronic hepatitis diseases
  • Immunoglobulins
  • Serum ferritin
  • Alpha antitripsen- deficiency= liver disease in infancy and cirrhosis in adults
  • Alpha fetaprotein- hepatoma
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21
Q

What are common diagnostic tests used

A

Biopsy

  • Cause vs assess damage
  • Bile duct leak, bleeding

Fibroscan

  • Measures liver stiffness
  • non invasive

Ultrasound

  • identify extra-hepatic duct dilatation
  • Other abnormalities- cysts, tumour

MRCP/ERCP
- Pancreatic/billary disease

Viral PCR
- HCV or HBV

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22
Q

How does drug indued liver injury occur and what does it increase in and what mechanisms does it involve

A

Caused by drugs including herbal remedies

Increases risk with age, female, genetics, alcohol, previous exposure, pre-existing liver disease, concomitant drugs, renal failure/diabetes, enzyme induction, pregnancy, poor nutrition, poly pharmacy

Several mechanisms- cytochrome p450, immune mediated damage to cells

Mimic almost every natural occurring liver disease- clinical features vary depending on damage

Leads to medications removed from market or black box warnings

ACUTE LIVER FAILURE (ALF)

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23
Q

Describe the two type of hepatotoxins

A

Intrinsics (TYPE A):
Predictable, dose dependent, reproducible
Short incubation period (hours or weeks)
Drug examples: paracetamol, tetracycline, salicylates, MTX, alcohol, iron, vitamin A, cyclophos, anabolics
Can occur at lower doses if you have pre-existing liver disease
Necrosis= type of injury
Direct toxicity

Idiosyncratic (type B)
Unpredictable, not dose related, injury variable, rare, more frequent in pre-existing liver disease
- Incubation typically weeks or months
- Any type of liver injury
- Due to hypersensitivity like methyldopa or metabolic abnormality (isoniazid)

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24
Q

Explain what direct insult leads to (steps)

A

Direct insult leads to drug induced hepatotoxicity, leads to
Cytotoxic cellular destruction
Mixed
Cholestatic- impaired bile flow

All lead to:
Necrosis and/or steatosis (cell death or fatty degeneration)

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25
Q

Explain how acetaminophen (paracetamol) leads to a non toxic and toxic compound

A

Acetaminophen can conjugate into:
glucuronide- moiety (non toxic)
sulfate- moiety (non toxic)
N-acetyl-p-benzo-qunone mine NAPQI (toxic)

This NAPQI can be converted to cysteine and mercapturic acid conjugates that are non toxic via glutathione with NAC

26
Q

What could the pharmacist do if you think a drug could be the cause of induced liver injury

A

Review all potential medicines taken- herbal, OTC, P, POM, vitamins

Still taking which drugs
- Frequency, dose

Started, stopped
Drug reactions occur within first 3-6 months treatment (5-90 days from first dose, 15 days from last dose)

Presenting signs and symptoms

  • pattern of liver disease- pre-treatment
  • suspect drug if presents with jaundice until proven otherwise
  • some can cause jaundice, others none
27
Q

How does the liver handle and affect drugs

A

Main elimination route for many drugs
Can alter response to drugs in several ways

Drugs can affect metabolism of other drugs by induction and inhibition of cytochrome P450 (CYP450) enzymes in liver:

  • Inhibitors of erythromycin, amiodarone, ketoconazole, ciprofloxacin
  • Increased effect and toxicity of affect drug unless it is prodrug- warfarin

Inducers:
Barbiturates, carbamazepine, ethanol, phenytoin, rifampicin, St John Wort
- Increased hepatotoxic metabolites of other drugs
- Decreased pharmacological effect of affected drug

28
Q

What are the best prescribing tips for someone with liver problems

A

Most drugs are safe in stable liver disease

Use older and more established drugs

Consider patient factors

Avoid drugs in severe disease- especially if hepatotoxic

Consider renally excreted

Start with smaller doses and increase slowly or give PRN

Choose best option and monitor clinical response

29
Q

What is the analgesia of choice in chronic liver disease

A

Kept to minimum, smallest effective dose at greatest interval

Paracetamol- 500mg- 1g TDS
Overdose- severe liver damage
Common reason for liver transplant

Avoid NSAIDS and COX-2 inhibitors
Bleed, altered platelet function, GI irritation, ascites

Caution opioids
Sedation, hepatic encephalopathy
Tramadol then sevredol
Oramorph

Caution- soluble 10% ethanol

TCAs- low dose fine, nortriptyline

Gabapentin okay- neuropathic pain

30
Q

What is the anti-depressant of choice in chronic liver disease

A

TCAS- avoid- sedating- risk of hepatic encephalopathy

SSRI- confer to bleeding risk, hyponatraemia, use low dose or increased interval
Sertraline 25-50mg OM
Citalopram max 20mg
Mirtazepine 15mg ON- lowest bleeding risk but sedating

31
Q

Describe the use of statins in liver disease, is it okay to use?

A

All can cause elevations in transaminases (transient or persistent)

Monitor LFTs in all patents

No link between elevation in LFTs and developing toxicity

IF ALT > 3 x upper limit normal, asymptomatic repeat test

Avoid in acute liver and decompensated chronic liver disease

Can be used safely if no or mild synthetic dysfunction

Statins may be beneficial in NAFLD by improving transaminases

32
Q

What are signs of cirrhosis

A

Increased bilirubin, AST, ALP, GGT, PT

Decreased albumin and Hb

Jaundiced, weakness in legs, palmar erythema, haematoma, spider naevi

Ascites, muscle wasting

33
Q

What are the stages of alcoholic liver disease

A

Normal

Fatty liver or steatosis- reversible with abstinence, rarely symptomatic, occur after a few days

Steatohepatitis/ acute alcoholic hepatitis:
Accumulation of fat + hepatocellular injury, may or may not improve with abstinence, can occur several weeks after stopping drinking

Fibrosis or cirrhosis

34
Q

What are the short term effects of alcohol on the body

A 
Anxiety
Decrease respiratory rate
GI disturbance
Impaired judgement
Loss of consciousness 
Impotence
Acute poisoning
Unintentional injury
35
Q

What are the long term effects of alcohol on the body

A 
Liver disease
Cancer
Pancreatitis
GI ulceration
Osteoporosis
Infertility 
Heart disease
Stroke
Hypertension
Obesity
Dementia
36
Q

What are the withdrawal signs and symptoms from alcohol

A 
Minor withdrawals: 
Sweating
Shaking 
Depression
Anxiety
Irritability 
Nausea and vomiting
Restlessness
Poor concentration
Delirium tremens:
Severe agitation 
Delirium
Course tremor
Large increases in pulse, blood pressure, respiratory rate 
Auditory and visual hallucinations
Disorientation and reduced consciousness
Excessive sweating (diaphresis)
37
Q

What drug treatments should be started

A

Chlordiazepoxide PRN
Pabrinex IV HP 1 pair OD (3 days)
Then multivitamin 1 OD, thiamine 100mg BD

Spironolactone 100mg OD

Furosemide 40mg OD

Lactulose 30mL TDS

Chlorphenamine and aqueous cream and menthol

Dalteparin 5000 units OD

38
Q

What should the acute alcohol withdrawal policy include

A

Benzodiazepine
- Chlordiazepoxide, lorazepam, diazepam

Thiamine (IV pabrinex and/or oral)

Multi-vitamins

Nutrition

Fluid and electrolyte replacement

Document history of alcohol intake- AUDIT or CAGE questionnaire

Referral to community support where possible

39
Q

Describe the fixed dose regimen of chlordiazepoxide

A 
Day 1: 
30mg QDS, 10mg (max 200mg/24 hours) PRN
Day 2: 
20mg QDS, 10mg (max 200mg/24 hours) PRN
Day 3: 
20mg TDS
Day 4: 
20mg BD
Day 5: 
10mg BD
Day 6: STOP
  • Appropriate if previous delirium tremens, seizures or moderate alcohol withdrawal syndrome (AWS)
  • Anxiolytic and anticonvulsant
  • Review daily
  • Individual titration
  • Monitor for over sedation, respiratory depression, hypotension
  • Can fit as dose is tailed off
  • Risk of chest infection
  • Reassess reducing dose if >3 prn doses are needed in 24 hours
  • Maximum 10mg BD for 24 hours on discharge
40
Q

Describe the symptom triggered flexible regimen

A

Tailored to individual requirements based on severity of withdrawal

Benzodiazepine dosed and administered via validated assessment tool: clinical institute withdrawal assessment scale for alcohol (CIWA-Ar)

  • calculate every 2-4 hours- severity linked to frequency of assessment
  • 10 item assessment to quantify severity and monitor and medicate appropriately
  • Score 8+ an accepted trigger for PRN dosing

Several studies show lower total dose and shorter hospitalisation periods vs fixed dose regimen

41
Q

Describe what you should do when oral route is unavailable or inadequate for instance delirium tremens (DT) occurs?

A

IV diazepam 5-10mg into large vein every 15-30 minutes until patient is calm

Parenteral diazepam repeated after 5 minutes

Lorazepam IV 1-4mg 15-60 minutes

Patients may need high doses

42
Q

Describe seizures in complications of withdrawal

A

Complication of withdrawal, can occur if benzodiazepine is tailed off too quickly

Options:
IV lorazepam or PR diazepam

Status epilepticus:
IV diazepam
Pabrinex
Chlordiazepoxide

Increase dose of oral benzodiazepine (BDZ) to reduce further seizure risk

Phenytoin not appropriate

43
Q

What antipsychotics be used in Delirium tremens

A

Unlicensed in UK

Adjunctive to benzodiazepine

Not as mono therapy- do not treat alcohol withdrawal since can lower seizure threshold

Exclude Wernike’s encephalopathy and hepatic encephalopathy before starting

Use of haloperidol or olanzepine

44
Q

What other considerations do you consider in patients with liver disease

A

Nutrition:
Poor intake, chronic pancreatitis, chronic liver disease, poor absorption
Consider NG feeding (caution varicose)
Risk of re-feeding syndrome- electrolytes

Thiamine: 
Prevent polyneuritis and wernike's encephalopathy (confusion, ataxia, memory loss, opthlmoplegia and subsequent Korsakoffs psychosis) 
IVI pabrinex
PO thiamine
Other multivitamins
45
Q

What do you give a patient when they are discharged

A

Maximum 24 hour benzodiazepines

Oral B vitamins

Referral to drug and alcohol support services

Needle exchange

46
Q

How do you encourage abstinence from alcohol in a patient

A

Psychological support- local drug and alcohol services

Drugs given: 
Disulfiram
Acamprosate 
Naltrexone
Nalamefene

Be aware of alcohol containing drugs, toiletries, mouthwashes

47
Q

Describe acute alcoholic hepatitis: markings and characterisation

A

Presented with marked inflammation of the liver presented with jaundice

Occur on background of a normal liver or complicate cirrhosis

Occur several weeks after stopping drinking

Reversible with abstinence but often underlying cirrhosis

Characterised by fever, hepatomegaly, leucocytosis, signs of liver failure e.g. ascites, raised ALT

Short term mortality among patients

48
Q

What does the glasgow alcoholic hepatitis score look at

A 
Age
White cell count
Urea 
Prothrombin ratio
bilirubin
49
Q

What can spironolactone and furosemide be used for in liver disease patients

A

Ascites and peripheral oedema

Causes:
low albumin, impaired aldosterone metabolism, reduced renal blood flow, portal hypertension, increased hepatic lymph production

Avoid drugs that can exacerbate:
NSAIDs, saline, high salt, fluid restriction

Natural history in chronic liver disease
- Diuretic sensitive than resistant, associate with HRS and hyponatraemia
50% mortality over 2 years

50
Q

How do you treat and monitor ascites

A 
Treatment: 
Fluid and salt restriction- bed rest
Spironolactone- Aldosterone antagonist
Furosemide- add cautiously for peripheral oedema 
Paracentesis (+ albumin)
TIPSS
Peritonea-Venous shunt
Monitoring: 
Weight loss
Urine output/renal function
Yes (Na, K, Cr)
BP and encephalopathy
Diagnostic ascitic tap 
SBP- temp and WCC
51
Q

What is lactulose used for

A

Hepatic encephalopathy

52
Q

Define encephalopathy and what are the neuropsychiatric changes

A

Reversible changes in mental state secondary to failure of liver to metabolise digestive products or toxins; toxins bypass liver to brain

Neuropsychiatric changes- four reversible stages:
Stage 1: forgetfulness, confusion, agitation (day night muddle)
Stage 4: coma, unresponsive to painful stimulus

53
Q

How do you treat encephalopathy

A

Remove and avoid precipitants
Reduce protein intake
Decrease bacterial ammonia product and enhance elimination

Lactulose:
Prevents constipation and inhibits colonic bacteria to convert NH3 to NH4

Phosphate enemas

Rifaximin- poorly absorbed antibiotic that eliminates colonic bacteria

54
Q

Describe what chlorphenamine and aqueous cream with menthol is used for

A

Pruritus: due to bile acids within skin, up regulation of endogenous opioids, serotonergic pathways

Generally less severe than with pure chloestasis

Other options:
Colestyramine
Ursodeoxycholic acid 
Rifampicin
Sertraline
Ondansertron 
Naltrexone
55
Q

Describe what dalteparin is used for and in terms of liver disease too

A

VTE prophylaxis

Liver- synthesis of clotting factors

Used as an indicator for prothrombin time

Acute and chronic liver disease elevated

Increase prolongation of clotting time if clotting factor deficient

Avoid intramuscular injections- haematoma

Usually used in more advanced cirrhosis with low albumin levels

56
Q

What is the aetiology of a vatical haemorrhage

A

Decreased blood flow through liver
Portal hypertension >12mmHg
Collateral vessels
Varices (stomach, oesophagus, rectum)

57
Q

What is the acute treatment of bleeding varicies that include oesophageal varies and gastric varices

A

Resuscitate
Terlipressin- until haemostasis for five days
Prophylactic antibiotics

Oesophageal varices
Banding
Consider transjugular intrahepatic portosystemic shunts (TIPSS) if bleeding not controlled by banding

Gastric varices
Endoscopic injection of N-butyl-2-cyanoacrylate
Uses TIPS if not controlled by injection

58
Q

In prophylactic treatment, what are the complications post bleeding

A

Bacterial sepsis- must use ceftriaxone 2g for 2 days of the week

Ascites- tx once BP is stable

Ulceration around scope site- oral PPI

alcohol withdrawal syndrome- pabrinex + benzodiazepine

59
Q

In prophylactic treatment, how do you prevent rebleed

A

Weekly endoscopies until varicies are eradicated then every 2 years

Carvedilol or propranolol reduces portal pressure

Laxatives- POST TIPS

TIPS/Transplant

60
Q

How do you help adherence

A

Keep medication to minimum and review regularly

Once daily timings

Stop drinking- support groups

Help with prescription costs

Counsel on indications and importance of medication prescribed

Medication charts (MDS)

District nurses support e.g. enemas for hepatic encephalopathy

Advise on OTC, herbals, illicit (no NSAIDS)

61
Q

What is the role of the pharmacist in liver disease

A

Communicate with and offer evidence on based prescribing advice to multi-drug therapy

Check drug dosing in liver disease and potential induced liver disease

Drug history reviews

Check for cytochrome p450 interactions for hepatitis C

patient and carer medication education

Specifying drug regimens- adherence, pill burden

Contribute to production of guidelines- local and national

Monitor drug expenditure- HCV expensive

Audit- against local and national prescribing guidelines

PM4B (13 decks)

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