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Liver diseases > Management of acute and chronic LD > Flashcards

Management of acute and chronic LD Flashcards

1
Q

What are some of the lifestyle modifications that are advised in early staged LD/Cirrhosis?

A

Avoid alcohol
Quit smoking
Lose weight if you’re overweight or obese
Do regular exercise to reduce muscle loss

Liver damage due to alcohol is reversible and therefore any patient presenting with some indicators of early stage fatty liver, should be advised to avoid alcohol. All recommendations can help to reduce chances of further complications and at any stage of liver disease.

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2
Q

Which liver diseases are curable?

A

Most aren’t however gallstones (which can be removed) and some viral infections can be. Therefore the main aim of management is to ease symptoms and reduce the risk of further complications.

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3
Q

Outline the main management strategies in cirrhosis and end stage LD.

A

Having a low protein diet due to the potential for waste products to build up causing hepatic encephalopathy.
Promoting a low Na+ diet and patients may be initiated on diuretics to reduce fluid retention
Patients may undergo ascites drainage by paracentesis
Surgery for the treatment of portal hypertension and to minimise the bleed risk
Introduction of medicines in the treatment of the disease and presence of complications
Potentially a liver transplant

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4
Q

At which time scale do each of the symptoms associated with acute alcohol withdrawal occur?

A

Minor symptoms resulting as a consequence of CNS hyperactivity, resolves within 24-48 hours

Depending on the extent of alcohol intake this can lead to:
Seizures which occur with 12-48 hours of the last drink in chronic alcoholics
If this is left untreated this will lead to delirium tremens which occur 48-96 hours after the last drink and if untreated can be fatal
Alcoholic hallucinations which resolve within 24-48 hours

Also results in fluid and electrolyte abnormalities

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5
Q

What are some of the symptoms you would expect to see in CNS hyperactivity?

A

Insomnia
GI upset
Mild anxiety
Tremulousness
Headache
Diaphoresis (excessive sweating)
Palpitations

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6
Q

What are some of the symptoms of Delirium tremens?

A

Hallucinations
Disorientation
Tachycardia
Hypertension
Hyperthermia
Agitation
Diaphoresis

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7
Q

What is the main treatment of acute alcohol withdrawal?

A

Symptom control by use of benzodiazepines which controls psychomotor agitation and prevent worsening.
Supportive care is also a key aspect of the management of acute alcohol withdrawal

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8
Q

What is the CIWA-Ar and when is it used?

A

It stands for Clinical Institute Withdrawal
Assessment – Alcohol, revised and is essentially is a questionnaire that helps professionals determine the severity of a patient’s alcohol withdrawal to help guide appropriate management and improve patient outcomes.
It consists of a number of symptoms which on patient assessment which can be scored based on severity, producing an overall total CIWA score.

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9
Q

What do the different CIWA scores mean?

A

7 or below: minimal to mild withdrawal
8-15: moderate withdrawal
16 or more: severe withdrawal (impending delirium tremens)

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10
Q

What is the SADQ and when is it used?

A

SADQ stands for the severity of alcohol dependency questionnaire it essentially a questionnaire a patient fills in with a number of questions with rated answers to calculate their overall alcohol dependency.

According to NNUH guidelines:
Never is rated 0
Sometimes 1
Often 3
Nearly always 4

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11
Q

What do the different SADQ scores mean?

A
  • Scores between 1-9 indicates low dependence
  • Scores between 10-19 indicates medium dependence and;
  • A score of 20 or more indicates high dependence
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12
Q

What are the two types of regimens that guide benzodiazepine dosing in acute alcohol withdrawal?

A

There is a fixed standard regime whereas dosing of benzodiazepines is gradually reduced over about 10 days according to the hospital policy.
However where specially trained staff are available to monitor the patient a symptom triggered regime may be used which involves frequent assessment of the clinical Institute Withdrawal Assessment of Alcohol Scale – CIWA-Ar of the severity of the patients withdrawal to guide dosing of benzodiazepines.

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13
Q

When is a symptom triggered approach favoured?

A

In hepatic impairment a symptom triggered regimen is more appropriate to encourage regular monitoring of signs of accumulation and titrating the dose accordingly. Or in other conditions where there is risk of accumulation.

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14
Q

What is a rough dosing regimen for Chlordiazepoxide?

A

Dosing is based on severity of withdrawal.
According to NNUH guidelines:
The dose should be estimated by initial assessment of predicted withdrawal intensity based on current level of use and previous experience of withdrawal; and will usually be in the range of 20-40 mg QDS.

PRN chlordiazepoxide (10-20mg QDS) should also be available.

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15
Q

What is a rough dosing regimen for Oxazepam?

A

In mild withdrawal:
20-10mg QDS reduced over about 7 days

In moderate withdrawal:
30-10mg QDS reduced over about 7 days

In severe withdrawal:
40-10mg QDS reduced over about 9-10 days

Additional when required Oxazepam 10-20mg QDS MUST also be prescribed

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16
Q

Which benzodiazepines are recommended for treatment of acute alcohol withdrawal?

A

Chlordiazepoxide and Oxazepam

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17
Q

Why are longer acting benzodiazepines used preferentially to short acting benzodiazepines for acute alcohol withdrawal?

A

The longer acting benzodiazepine has been shown to be more effective than short-acting ones in: preventing seizures and delirium, allowing smoother withdrawal with less rebound, and are less prone to abuse.

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18
Q

What is the first line benzodiazepine used?

A

Chlordiazepoxide is the first line benzodiazepine recommended for the management of acute alcohol withdrawal.
It has been shown to have a more gradual onset of psychotropic effects, is perhaps less toxic in overdose, and has less potential for misuse (compared with diazepam).

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19
Q

In which circumstances would Oxazepam be used preferentially?

A

Oxazepam has a shorter half life and therefore should be used in patients at risk of toxic accumulation of the benzodiazepine such as in the elderly or when there is significant liver damage.

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20
Q

What is a dosing consideration to make regarding benzodiazepines?

A

Lowest possible dose to relieve symptoms without causing sedation due to increased risk of hepatic encephalopathy.

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21
Q

Why aren’t patients normally sent home on the reducing dose of benzodiazepines?

A

Ideally the patient is not sent home still on the reducing dose of benzodiazepines due to the risk of causing respiratory depression (especially when taken with alcohol) as well as dependence.
The only times patients may be sent home is when there is support available in the local community for them to be able to do so safely.

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22
Q

What is the appropriate management of alcohol withdrawal seizures?

A

If alcohol withdrawal seizures occur, a fast-acting benzodiazepine (such as lorazepam [unlicensed indication]) should be prescribed to reduce the likelihood of further seizures.
If alcohol withdrawal seizures develop in a person during treatment for acute alcohol withdrawal, review their withdrawal drug regimen

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23
Q

What other supportive medications could be prescribed in acute alcohol withdrawal?

A

Nutritional supplements
IV fluids

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24
Q

What causes cholestatic pruritis?

A

Cholestatic pruritis is caused by deposition and accumulation of bile salts in tissues causing itching and discomfort. In patients with liver disease there are marked elevations in serum bile salts levels due to the inability of hepatocytes to remove bile acids from portal blood or due to portosystemic shunting by which the bile acids bypass hepatocyte and remain in circulation.

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25
Q

What type of LD is cholestatic pruritis associated with?

A

Cholestatic liver disease

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26
Q

What is the appropriate management of cholestatic pruritis?

A

Firstly identify and treat the underlying cause of the cholestasis.

First line Cholestyramine which is an ion exchange resin, binding to bile acids in the gut preventing their absorption, the dose:
4–8 g once daily

Non-sedating antihistamines may help such as Cetirizine and Loratadine

Calamine lotion or menthol in aqueous cream may also provide a cooling effect and relieve of irritation

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27
Q

Why are only non-sedating antihistamines recommended for cholestatic pruritis?

A

The sedating effect of some antihistamines such as chlorphenamine increase the risk of hepatic encephalopathy.

28
Q

How often does ascites occur?

A

Occurs in 50% of patients within 10 years of a diagnosis of liver disease.

29
Q

Briefly describe the pathophysiology of ascites.

A

In liver cirrhosis, changes in circulation such as portal hypertension, reduces perfusion through other organs such as the kidney.
When there is reduced renal perfusion, this activates RAAS, causing widespread vasoconstriction and aldosterone release which further exacerbates this effect, further increasing blood pressure. This results in secondary hyperaldosteronism. In addition, aldosterone relies on metabolism from the liver, when this has reduced function, there is an accumulation of aldosterone, exaggerating this effect.

There is also reduced albumin production in LD, reducing osmotic pressure within the plasma with both effects causing oedema and fluid accumulation within the peritoneal cavity (abdomen) specifically due to portal hypertension, known as ascites.

30
Q

Outline the main management plan of ascites.

A

Diuretics
Bed rest
Na+ and fluid restriction
Paracentesis

31
Q

Which diuretics are recommended for the treatment of ascites and why?

A

The first line diuretic that is recommended is Spironolactone which is a mineralocorticoid receptor antagonist, antagonising the effect of aldosterone, stopping the continuous RAAS activation cycle.

If the daily target weight loss is not achieved or peripheral oedema is also present, loop diuretics specifically Furosemide is used as add on therapy.

32
Q

State the therapeutic and toxic monitoring parameters for Spironolactone.

A

Therapeutic:
Weight loss of 0.5-0.75kg per day
Symptom improvement, visible in fluid accumulation

Toxic:
Weight loss either greater or less than 1-1.5 kg daily.
U & Es – hyperkalaemia, hyponatremia
Renal function
Blood pressure, hypotension
Symptoms of hepatic encephalopathy (neurological disturbances)

33
Q

State the therapeutic and toxic monitoring parameters for Furosemide.

A

Therapeutic:
Weight loss of 0.5-0.75kg per day
Symptom improvement, visible in fluid accumulation

Toxic:
Weight loss either greater or less than 1-1.5 kg daily.
Renal function
Blood pressure – hypotension
Hyperglycaemia (less common than thiazides)
U & Es – hypokalaemia, hyponatremia, hypomagnesaemia, hypocalcaemia
IV rate not greater than 4mg/min due to risk of ototoxicity
Symptoms of hepatic encephalopathy (neurological disturbances)

34
Q

When may a greater daily weight loss be indicated for diuretic use?

A

If peripheral oedema is also present alongside ascites a daily target weight loss of 1-1.5kg/day is recommended.

35
Q

What is the risk of achieving too rapid weight loss?

A

Too rapid, weight loss as a results of diuretic use leads to:
Hypovolemia
Hyponatremia
Hypokalaemia

All of which increase the risk of hepatic encephalopathy

Therefore monitoring closely and titrate dose accordingly.

36
Q

If diuretic use and Na+/fluid restriction does not improve ascites what is the next line management?

A

Paracentesis which is the physical drainage of fluid within the peritoneal cavity.

37
Q

Briefly describe what causes Wernicke-Korsakoff syndrome.

A

It is a neurological disorder as a consequence of thiamine (Vitamin B1) deficiency associated with alcohol malnutrition. Alcohol inhibits the absorption of some nutrients including B vitamins.

38
Q

Are Wernicke and Korsakoff the same condition?

A

Wernicke-Korsakoff syndrome includes Wernicke encephalopathy and Korsakoff amnesic syndrome which are not different conditions but different stages of the same disease (Wernicke-Korsakoff syndrome). Wernicke’s encephalopathy represents the “acute” phase of the disorder and Korsakoff’s amnesic syndrome represents the disorder progressing to a “chronic” or long-lasting stage.

39
Q

What happens if Wernicke-Korsakoff syndrome is left untreated?

A

Can result in permanent brain damage

40
Q

What are some of the symptoms of B1 deficiency?

A

Due to the effects on the thalamus and hypothalamus, symptoms may include:
Mental confusion
Vision problems
Coma
Hypothermia
Low blood pressure
Lack of muscle coordination (ataxia)

41
Q

What are some of the symptoms of Korsakoff syndrome?

A

Amnesia
Tremor
Coma
Disorientation
Vision problems

42
Q

What is the management of Wernicke-Korsakoff syndrome?

A

IV Pabrinex which is a mix of Vitamin B and C
Due to the incompatibility of the two vitamins 2 pairs of ampules are mixed together immediately before treatment.
The overall dosing regimen is 2 pairs of ampoules three times a day for 3-5 days.

43
Q

What is an important consideration of Pabrinex use?

A

Can cause severe allergic reactions and therefore anaphylaxis treatment should be available nearby.
May also cause injection site reactions.

Monitor the patient closely during the infusion especially the first one.

44
Q

What is the long-term treatment and prophylaxis of Vitamin B deficiency?

A

Thiamine 100mg TDS PO (although regimens can vary)
It is usually administered at the same time as the IV infusion and then continued for 3-6 months after abstinence/indefinitely if heavy drinking occurs sometimes at a lower dose.

45
Q

What causes hepatic encephalopathy?

A

It is the accumulation of ammonia and nitrogenous waste products within the brain resulting in neurological disturbances. Usually these products are metabolised in the liver and are cleared from the blood by hepatobiliary clearance however in LD the reduced ability of the liver to perform this metabolism results in increased serum levels. At increased serum levels these products become permeable to the blood brain which they are able to cross.

46
Q

What is the first line management of hepatic encephalopathy and why?

A

High dose Lactulose is the first line agent for the treatment of hepatic encephalopathy attributed to three main mechanisms due to the disaccharide reducing the intestinal pH from 7 to 5 resulting in:
Ionisation of nitrous agents, making them completely impermeable to the BBB
Causing alteration of the intestinal flora, reducing the ammonia producing microflora
As an osmotic laxative it also reduces the gut transit time, hence reducing intestinal absorption of ammonia

47
Q

What is the dosing regimen for Lactulose in the treatment of hepatic encephalopathy?

A

30-50mL three times a day

48
Q

State the therapeutic and toxic monitoring parameters of Lactulose.

A

Therapeutic:
Production of 2-3 soft stools daily
Absence of symptoms of hepatic encephalopathy (confusion, personality changes, seizures etc)

Toxic:
Patient reported GI symptoms- Abdominal pain, Flatulence, Nausea and Vomiting
Diarrhoea, dehydration or haemorrhage lead to hypovolemia potentially worsening the encephalopathy in addition to the below
U&Es- Hypokalaemia

49
Q

When is Rifaximin added on?

A

When optimised Lactulose isn’t working

50
Q

How does Rifaximin work?

A

It is a semi-synthetic derivative of the antibiotic Rifamycin and works by decreasing the production and absorption of intestinal ammonia.

51
Q

Aside from Lactulose and Rifaximin how else can encephalopathy be managed?

A

Phosphate enemas if the oral route isn’t an option.
Also avoiding precipitating factors:
Dehydration
Hypokalaemia
GI haemorrhage (and anything increases the risk)
CNS drugs
Constipation (anything as a side effect)
High dietary protein

52
Q

How does portal hypertension occur?

A

Liver cirrhosis (hardening of the liver) causing a backlog within the portal vein resulting in hypertension known as portal hypertension. There is also reduced onward perfusion to other organs.

53
Q

What is the key aim of management of portal hypertension?

A

Reducing portal hypertension, crucial in reducing the risk of bleeding associated with collateral circulation. In addition to reducing the resting heart rate by 25%.

54
Q

What are the first line drug used in the management of portal hypertension?

A

First line: low dose Propranolol followed by the slow up titration due to the drug undergoing extensive first pass metabolism.

Add in drugs are usually nitrates if optimised Propranolol is not effective.

55
Q

What are the therapeutic and toxic monitoring parameters for Propranolol?

A

Therapeutic:
Reduced portal hypertension - bp
Reduction in resting heart rate by 25%
Absence of complications such as bleeding oesophageal varices

Toxic:
Blood pressure – hypotension
Pulse- bradycardia
Respiratory rate/PEFR (peak expiratory flow rate) – Bronchospasm
Glucose levels- hypoglycaemia and masked symptoms of hypos (DM1 esp.)
Patient reported side effects – GI side effects, numbness of fingers and toes

56
Q

How do bleeding oesophageal varices occur?

A

Oesophageal varices are dilated submucosal distal esophageal veins connecting the portal and systemic circulations. This happens due to portal hypertension (most commonly a result of cirrhosis. It is the most common fatal complication of cirrhosis and the severity of liver disease correlates with the presence of varices and risk of bleeding.
Veins of the oesophagus and stomach are particular prone to bleeding as they are very narrow and therefore not able to withstand high volume and pressure of blood within them.

57
Q

What is the mortality rate associated with a first oesophageal bleed?

A

50% and then 30% with subsequent bleed

58
Q

What is the first line management of oesophageal haemorrhage?

A

Resuscitation and correction of hypovolemia which involves IV fluids and blood transfusions.

Injection of vasoactive therapy such as Vasopressin, Terlipressin and Octreotide which causes vasoconstriction of the collateral blood vessels and reduce portal bp. They are initiated when haemorrhage is suspected.

59
Q

After resuscitation what investigations occur?

A

Endoscopy to identify exactly where the bleeding is, this then leads to:

Sclerotherapy - injection of ethanolamine to quarterise or stop the bleeding
Other techniques to stop the bleeding include:
Ligation/banding
Balloon tamponade
TIPS

60
Q

How many LD patient demonstrate clotting abnormalities?

A

75%

61
Q

What are the signs and symptoms of clotting abnormalities?

A

Presenting as anaemic on blood tests
Increased bleeding and bruising

62
Q

What causes clotting abnormalities in LD patients?

A

Hepatocytes are responsible for the synthesis of most blood coagulation factors, such as fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII, as well as protein C and S, and antithrombin. Liver cirrhosis reduces the ability of the liver to produce these clotting factors therefore leading to an increased risk of bleeding.

63
Q

What is the prothrombin time in LD patients?

A

Greater than 18 seconds

64
Q

What is used in the treatment of increased PT?

A

IV Phytomenadione which is Vitamin K

65
Q

When will / won’t Phytomenadione work?

A

In severe liver disease hepatocytes become completely unresponsive to Vitamin K which is involved in the production of these clotting factors.
However in bile acid insuffiency or cholestasis hepatocytes do respond leading to a reduced prothrombin time back to normal as Phytomenadione replaces the Vitamin K that is not absorbed due to lack of bile acids.

66
Q

State the therapeutic and toxic monitoring parameters for Phytomenadione.

A

Therapeutic:
PT returns to baseline (ref. 9-13 seconds)

Toxic:
Adult formulation Konakion® MM should not be administered by intramuscular injection
PT below baseline due to increased thrombosis risk*
Reduce dose in the elderly

67
Q

Which medications should be avoided in patients with clotting abnormalities?

A

Aspirin, NSAIDs, Warfarin due to increased risk of bleeding.

Liver diseases (6 decks)

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