W30 Clinical management of liver disease Flashcards

-Alcoholic liver disease (ALD) -Non-alcoholic fatty liver disease (NAFLD)

1
Q

Re-cap; function of the Liver:

A
  • Energy metabolism
  • Bile production & bilirubin metabolism
  • Fat-soluble vitamin storage and/or metabolism
  • Detoxification and clearance
  • Drug metabolism (Cyp P450)
  • Urea cycle (aa metabolism)
  • Ethanol
  • RBCs

Other Functions
* Thyroid hormone function - deiodination of T4 to T3
* Synthesis of nearly every plasma protein in the body, some examples include albumin, binding globulins, protein C, protein S, and all the clotting factors of the intrinsic and extrinsic
pathways besides factor VIII.

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2
Q

What can cause liver damage?

A
  • Most common risk factors for liver cirrhosis;
  • Alcohol misuse = alcoholic liver disease
  • Hepatitis B or C infection
  • Obesity or type 2 diabetes (with NAFLD) – if the patient doesn’t have NAFLD = not at
    immediate risk at developing cirrhosis
    (Note: not everyone with risk factors will develop cirrhosis)

Less common causes of cirrhosis include:
1. Autoimmune liver disease:
* autoimmune hepatitis
* primary biliary cholangitis
* primary sclerosing cholangitis

  1. Genetic conditions:
    * Haemochromatosis
    * Wilson’s disease
    * Cystic fibrosis
  • Medication use, usually over a long period of time e.g. methotrexate
  • Recognising risk factors early and managing them effectively may help prevent the development of cirrhosis, or slow its progression
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3
Q

Liver disease progression: What are the stages? (4)

A
  1. Healthy
  2. Fatty
  3. Fibrotic
  4. Cirrhotic
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4
Q

What is alcoholic liver disease?
How many stages?
What are they called?

A
  • Refers to liver damage that’s been caused by alcohol
  • 4- determine pt symptoms
    1. Alcoholic fatty liver disease
    2. Alcoholic hepatitis (inflammation- cell death)
    3. Fibrosis
    4. Cirrhosis
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5
Q

What is Alcoholic fatty liver disease? (stage 1 ALD)

A
  • Build up of fats in the liver usually due to drinking large amounts of alcohol, even if its
    just over a few day
  • Rarely causes any symptoms
  • Reversible if you abstain from drinking for a few months /years
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6
Q

What is Alcoholic hepatitis? (stage 2)
inflammation– cell death

A
  • Progresses as a result of alcohol misuse over a longer period of time
  • Mild cases - reversible if you stop drinking alcohol permanently
  • Severe cases – serious and life threatening illness
  • When this develops, usually the first time the patient is made aware they have liver damage
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7
Q

What is Fibrosis (stage 4 ALD)

A

Continuous inflammation of the liver results in scar tissue forming
* Liver becomes fibrous
* This is known as fibrosis

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8
Q

What are the 2 types of Cirrhosis? (Stage 4 ALD)
symptoms?

A

Compensated
* The liver can still function effectively
* No or very few noticeable clinical symptoms

Decompensated
* The liver can not effectively function
* Patients experience symptoms and complications of liver cirrhosis

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9
Q

Prognosis of cirrhosis:
What could the prognosis of cirrhosis influenced by?

A
  • Once cirrhosis has occurred, it is usually considered as irreversible
  • Patients with cirrhosis are generally well and have no clinical signs or symptoms for a period of time (compensated liver cirrhosis = liver is still able to function)
  • When the liver becomes damaged to the point its classified as decompensated, patients will start to develop symptoms and complications

The prognosis of cirrhosis is influenced by a number of factors,
* Underlying cause — successful treatment of the cause may prevent additional liver injury (for example antiviral treatment for hepatitis C)
* Lifestyle changes — obesity and alcohol use have prognostic relevance in people with cirrhosis, regardless of the underlying cause;
* Average survival in the compensated stage is more than 12 years
* Average survival in the decompensated stage it is around 2 years

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10
Q

Diagnosis of ALD (blood tests)

A

Assess liver function tests = maybe normal at many stages of liver disease

Liver function tests
* Elevated alanine transaminase (ALT)
* Elevated aspartate amino transferase (AST)
* Elevated ALT:AST ratio
* Elevated bilirubin
* Low albumin levels
* Raised Gamma GT = suggestive of alcohol misuse

Full blood count / clotting
* Low platelets
* Prolonged prothrombin time
* Elevated INR

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11
Q

Diagnosis of ALD- History taking:
What to ask?

A
  • Accurate history of alcohol intake
  • Identification of other risk factors;
    -Viral causes
    -Medication history
  • History of symptoms onset =early stage symptoms are non-specific
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12
Q

Diagnosis of ALD- Physical examination

A
  • Hepatomegaly = palpable left lobe of the liver
  • Splenomegaly (enlarged spleen)

Common symptoms in liver cirrhosis:
* Spider Navi
* Palma erytherma (red palms)
* White nails
* Clubbed fingers
* Muscle wasting

Signs and symptoms of decompensated liver disease:
* Ascites / oedema
* Jaundice
* Abnormal bruising
* Variceal bleeding
* Infections
* Encephalopathy

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13
Q

Diagnosis of ALD- Liver imagine / Biopsy

A
  • Ultrasound of the liver
  • CT / MRI scan
  • Liver biopsy = extent of liver scarring
  • Endoscopy = identify oesophageal varices
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14
Q

Liver disease symptoms
What are the Early symptoms? (fatty liver disease)

A
  • Bruise more easily
  • Feeling tired / unwell / excessive fatigue
  • Abdominal pain (right upper quadrant)
  • Loss of appetite
  • Weight loss and muscle wasting
  • Dark urine
  • Pale stools
  • Nausea and vomiting
  • Spider-like small blood capillaries on the skin above waist level (spider angiomas / spider navi)
  • Disturbed sleep patterns
  • Red palms
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15
Q

Liver disease symptoms:
What are the Later stage symptoms? = as the liver is struggling to function
(4 main symptoms)

A
  • Jaundice (yellowing of the skin and eyes) = intensely itchy skin
  • Ascites = Swelling of the abdomen
  • Coagulopathy = increased bleeding risk:
    -Frequent nose bleeds
    -Bleeding from the gums
    -Vomiting blood
  • Increased risk of infections;
    -Fever and rigors
  • Encephalopathy
  • Forgetfulness
  • Memory loss
  • Confusion
  • Drowsiness
  • Increased sensitivity to drugs, both medical and recreational
  • Increased sensitivity to alcohol
  • Clubbed fingers = ends of fingers become wider/thicker
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16
Q

Symptoms and complications of cirrhosis- Jaundice
What is Jaundice?
What causes it?
Why do cirrhosis pt have jaundice?

A

1) Jaundice
* Yellowing of the skin, eyes and mucus membrane as a result of an increase in bilirubin (yellow).
* Bilirubin is usually processed in the liver, mixed into bile and excreted via bile ducts into the gallbladder where its eventually released into the small intestine to help digest fats.
* In liver cirrhosis, bilirubin isn’t broken down and hence accumulates leading to jaundice
* Accumulation of bilirubin can also cause intense itchiness

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17
Q

Symptoms and complications of cirrhosis- Encephalopathy
What are the symptoms?
What are the 2 main types? and what do they have a deficiency of?

A

Hepatic encephalopathy is a dysfunction of the brain = liver insufficiency = results in build-up of nitrogen compounds in the blood (ammonia + glutamine) which INC permeability of BBB

Symptoms:
* Cognitive and behavioural changes (irritability, disorientation)
* Personality changes
* Sleep disturbance
* Motor problems
* Altered level on consciousness

  • Two main types that can present either together or in isolation:
    1. Wernicke’s encephalopathy; caused by an acute deficiency in thiamine (common in alcoholic patients)
    2. Hepatic encephalopathy; caused by excess build-up of toxins in the blood as the liver is unable to clear (e.g. medication)
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18
Q

Symptoms and complications of cirrhosis-
What is Coagulopathy?

A
  • Prolonged clotting time (^ bleeding risk)
  • Low platelets (help the blood clot)
  • Liver plays a role in hemostasis = synthesis of clotting factors, coagulation inhibitors and fibrinolytic proteins and produces Thrombopoietin which stimulates platelet production

In liver cirrhosis; patients tend to have:
* Low platelets (normal range 150 – 400 x 10 9 /L)
* Prolonged prothrombin time (PT) – blood test used to measure how long it takes your blood to clot (normal range: 10 – 13 seconds)

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19
Q

What is Portal Vein Hypertension?
Why does it occur?

A
  • Portal vein hypertension is one of the earliest signs of liver cirrhosis

WHY DOES IT OCCUR?
* The portal vein carries blood from the digestive system and spleen to the liver
* The pressure in the portal vein can rise for two main reasons in liver cirrhosis:
1. There is a blockage = portal vein clot
2. Increased resistance in blood flow through the liver as a result of scarring

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20
Q

What can portal vein hypertension lead to?

A
  • Ascites
  • Spontaneous bacterial peritonitis
  • Variceal haemorrhage
  • Portal vein thrombus
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21
Q

What is Ascites?

A

Accumulation of fluid in the peritoneal cavity as a result of:
o splanchnic vasodilation
o sodium and water retention

Symptoms:
o Abdominal swelling
o Bloating
o Pain

  • Bodies way of reducing pressure in the portal vein = pushing fluid out of vein into abdominal space
22
Q

What is Spontaneous bacterial peritonitis (SBP)- caused by Ascites?
What are the symptoms?

A
  • Bacterial infection in the patients abdomen
  • Usually because of ascites
  • Ascitic fluid becomes infected

Symptoms:
* Fever / temperatures
* Rigors / chills
* Inc HR
* Worsening ascites
* Encephalopathy

23
Q

What are Oesophageal & abdominal varices?

A
  • Increase in portal vein pressure leads to the formation of varices
    =dilated veins in the oesophagus and around the abdomen
  • Bodies way of reducing blood pressure in the hepatic portal vein by bypassing the need for blood to flow through the liver:
    -Contributes to encephalopathy as blood by-passes the liver = toxins and drug / drug metabolites not metabolised
  • Can bust causing a haemorrhage:
    -Haematemesis (vomiting blood)
    -Malaena (blood in stools)
24
Q

Overview: Symptoms of liver cirrhosis

A
  1. Liver Failure
    -Jaundice
    -Encephalopathy
    -Coagulopathy
  2. Portal Vein Hypertension
    -Ascites
    –Spontaneous bacterial peritonitis
    -Variceal haemorrhage
    -Portal vein thrombus
  3. Hepatocellular Carcinoma (liver cancer)
25
Q

What are the symptoms of acute alcohol withdrawal?

A

Important to ensure patients alcohol withdrawal adequately managed = failure to do this can result in seizures, coma and sometimes death

Symptoms of withdrawal include:
* Hand tremors = “the shakes”
* Nausea & vomiting
* Elevated heart rate (pulse >100 bpm)
* Headaches
* Loss of appetite
* Depression
* Anxiety
* Irritability / restlessness
* Insomnia

  • NICE guidelines = CIWA-Ar protocol (Clinical Institute Withdrawal Assessment for alcohol scale)
    -Patients assessed based on withdrawal symptoms (10 symptoms looked at in total)
    -CIWA-Ar score of >11 suggests risk of severe alcohol withdrawal
    -Patients assessed every 1 – 2 hours
26
Q

What is the treatment that needs prescribing for acute alcohol withdrawal? (3)

A
  1. Diazepam 20mg PRN (PO)
    (to be given when CIWA-Ar score >11)
    * Class: benzodiazepine
    * Why: used to treat symptoms of alcohol withdrawal
  2. Diazepam 10mg PRN (PR)
    (to be given if the patient has a seizure)
    * Class: benzodiazepine
    * Why: used if the patient has a seizure
    as a result of alcohol withdrawal
  3. **Adrenaline 1:1000 (IM) **
    (to be given if the patient has anaphylaxis to pabrinex)
    * Class: Sympathomimetic
    * Why: used if the patient has anaphylactic reaction to pabrinex
27
Q

Encephalopathy: acute management
What is the aim of treatment?
What is the treatment? (1)

A

-Treat any underlying vitamin B deficiency

Drug: Pabrinex (IV or IM)
Dose:
-Treatment: 2 pairs TDS 5 days, then 1 pair OD
Contra-indications:
* Allergies to pabrinex

Side effects:
* Hypotension
* Injection site reaction

Practical points
- Ensure the patient isn’t on thiamine (oral) whilst on IV/IM pabrinex (threshold)

28
Q

Encephalopathy: prophylaxis
What is the aim of treament?
Thiamine
What is the dose?
Practical advice?

A

-Reduce the risk of patients developing encephalopathy in the future by treating;
- Vitamin B deficiencies
Dose: depends on the severity of the deficiency
* Mild: 50mg – 100mg daily (in divided doses)
* Severe: 200mg – 300mg daily (in divided doses)

  • Hold thiamine when a patient is being given IV pabrinex during acute episodes of encephalopathy (as it contains a high amount of b1 alr)
  • Dosing depends on severity of deficiency but you should also take the patients compliance into account when dividing the dose throughout the day (i.e. BD vs QDS dosing)
29
Q

Encephalopathy: prophylaxis
Lactulose:
What is the aim of treatment?

A

Reducing the amount of nitrogen circulating in the patients blood = prevent the patients BBB becoming more permeable

Dose: 30 – 50ml TDS
* Dose adjusted according to response
* Aim; 2 – 3 loose stools a day
Rationale of treatment
* By reducing the gut transit time = Dec time available for ammonia (NH3) to be reabsorbed
* Lactulose broken down by gut bacteria in lactic acid + acetic acid = acidic environment (OH-)
NH3 (easily absorbed) NH4+ (low absorption)

Contra-indications
* Risk of GI perforation (e.g. GI obstruction)
Side effects
* Abdominal pain
* Flatulence
* Diarrhoea
* N & V

Monitoring
* Stool chart = ensuring aim of treatment is being met

Counselling
* Educate patient on rational of treatment and importance of taking

30
Q

Rifaxamin:
What is it used in?

A

Encephalopathy prophylaxis:

Dose: 550mg BD

Rational:
- reduces the intestinal production and
absorption of ammonia
- Tends to be used to prevent recurrent hepatic encephalopathy – ie where lactulose alone isn’t effective

Contra-indications:
* Intestinal obstruction

Side effects:
* GI discomfort
* Ascites
* Constipation
* Nausea & vomiting
* Skin reactions

Cautioned:
* Use with caution in severe liver impairment increased risk of exposure and therefore s/e

Monitoring / counselling:
* Monitor for signs of constipation = want to avoid this in patients with liver cirrhosis

31
Q

Portal vein hypertension
What drugs are used?

A

By reducing the pressure in the portal vein = reduces risk of developing:
* Ascites, and therefore SBP
* Oesophageal and abdominal varices
* Portal vein thrombi

  1. Propanalol
  2. Carvedilol (unlicensed indication)
32
Q

Propranolol:
used for?
c/i?
dose?
SE?

A

Portal vein hypertension:
Dose:
* 40mg BD, increased as necessary
* Max dose 160mg BD

Contra-indications
* Asthma or Hx of bronchospasm
* Bradycardia (low HR)
* Severe peripheral arterial disease

Side effects
* Low HR
* Hypotension
* Dry eyes
* Sleep disorders = vivid dreams
* Cold extremities

Monitoring
* Blood pressure
* Heart rate
* Kidney function -risk of increased half life in poor renal function
* Lung function (if patient has a Hx of airway disease)

Counselling
* Avoid abrupt withdrawal – should be gradually reduced to stop
* Can cause vivid dreams and cold extremities

33
Q

Drug: Carvedilol (unlicensed indication)
What is the dose?
Side effects?

A

Dose:
* Starting dose: 6.25mg daily (usually in two divided doses)
* Increase as necessary if patient tolerated
Contra-indications
* Bradycardia
* Hypotension (systolic <95mmHg)
* Asthmatics

Side effects
* Low HR
* Hypotension
* Dry eyes
* Sleep disorders  vivid dreams
* Cold extremities
Monitoring
* Blood pressure
* Heart rate
* Kidney function  risk of increased half life in poor renal
function
* Lung function (if patient has a Hx of airway disease)
Counselling
* Avoid abrupt withdrawal – should be gradually reduced to stop
* Can cause vivid dreams and cold extremities

34
Q

Coagulopathy:
What drug is given?

A

Vitamin K

35
Q

Vitamin K

A

Dose:
* 10mg OD stat
* Duration will depend on how prothrombin time reacts
(max 5 days)
Route: PO or IV
Side effects
* Anaphylactic reactions (IV administration) 
important to give it slowly
Monitoring
* Prothrombin time (coagulation screen)
* Signs of bleeding
Practical points
* Hold anticoagulants (unless benefit outweighs risk)

36
Q

Ascites
What drug is given?

A

Spironolactone

  • 100mg – 400mg OD
  • Dose adjusted according to dose
    Contra-indications
  • Hyperkalaemia (elevated K)
  • Addison’s disease
    Side effects
  • Hyperkalaemia (elevated K)
  • Acute kidney injury
  • Gynecomastia = swelling of breast tissue in males
  • Hypertrichosis = hair growth

Monitoring:
* Kidney function (Cr)
* Potassium
* Weight = indicator of fluid retention
* Fluid input and output
(Weekly when initiated/after dose change, monthly for first 3 months, 3 monthly for up to a year, Then every 6 months)

Counselling:
* Monitoring expectations

37
Q

Spontaneous bacterial peritonitis (SBP) – Treatment?

A

No penicillin allergy Tazocin (IV) 4.5g TDS
Non-severe penicillin
allergy
Cefotaxime (IV)
Metronidazole (IV)
2g TDS
500mg TDS
Severe Penicillin
allergy
Co-trimoxazole (IV)
Metronidazole (IV)
Gentamycin (IV)
960mg BD
500mg TDS
5mg/kg OD

38
Q

Oesophageal & abdominal varices
Non-pharmacological treatment?
What drug treatment?

A

Often treated via endoscopic intervention:
* Variceal band ligation = rubber bands used to prevent bleeding

Terlipressin:
Route: IV
Dose: 1mg – 2mg QDS (max. 72 hours)
Mechanism: vasopressin analogue = inc vasoconstriction

Cautions:
* Elderly patients
* Heart disease
* Hx of QT prolongation
* Arrhythmias
* Uncontrolled hypertension

Side effects:
* Abdominal cramps
* Arrhythmias
* Diarrhoea
* Headache
* Hypertension
* Vasoconstriction = chest pain

39
Q

Mr David Keene is a 56-year-old male patient who has been recently diagnosed with alcoholic liver disease and is still currently drinking approximately 60 – 80 units of alcohol per week. He has no known drug allergies and is not currently taking any regular medication. His urea and electrolyte blood results have also come back normal He has been admitted to his local medical admissions unit with the following symptoms:
* Acute alcohol withdrawal
* Increased confusion and changes to his behaviour
* Worsening ascites with spikes in temperature, Inc WCC, rigors

What medication would you expect the patient to be initiated on for his symptoms?

A

Diazepam 20mg PRN (PO)
Diazepam 10mg PRN (PR)
Adrenaline 1:1000 (IM)

Acute management encephalopathy
- Pabrinex (IV): 2 pairs TDS 5 days them 1 pair OD

Encephalopathy prophylaxis:
- Thiamine 50-300mg (div doses)
- Lactulose 30-50ml TDS

Ascites:
- Spironolactone 100-400mg OD

SBP:
- Tazocin 4.5g (IV) TDS

? Cause of ascites- portal vein hypertension
- Carvedilol/ propanalol

40
Q

During his admission, Mr Keene developed haematemesis (vomiting blood) and has been diagnosed with oesophageal varices. He is not yet stable enough for variceal band ligation.

  • What medication would you expect Mr Keene to be prescribed to acutely manage his bleeding oesophageal varices?
  • What is the mechanism of action?
A
  • Terlipressin IV 1-2mg QDS (max 72 hours)
  • Vasopressin analogue- vasoconstriction of bleeding blood vessel
41
Q

Medication to avoid in liver disease:
Encephalopathy? (2)

A
  1. Medications that can cause constipation = this will allow an increased absorption of ammonia compounds in the bowel due to increased gut transit time
    * Opioids (codeine, morphine)
    * Slow gut motility (loperamide)
  2. Medications that can cause sedation
    = any medication can has an affect on the
    CNS e.g.
    * Analgesics; opioids, gabapentinoids
    * Antipsychotics
    * Sedatives; benzodiazepines, sleeping tablets
42
Q

Medication to avoid in liver disease:
Coagulopathy/ Varices? (2)

A
  • Anticoagulants = this will further increase the patients bleeding risk
  • Risk vs benefit of anticoagulant treatment needs to be considered in patients with liver disease
  • Antiplatelet treatment = risk vs benefit of treatment needs to be carefully considered in patients with liver disease
  • E.g. NSAIDs, aspirin
43
Q

Medication to avoid in liver disease?
Symptom- Fluid overload (Ascites) - 3

A

Drugs that exacerbate fluid retention (risk of exaerbating oedema and ascites in patients with chronic liver disease e.g.
- Steroids
- NSAIDs
- CCBs

44
Q

Medication to avoid in liver disease
Symptom= Decreased Drug metabolism? (2)

A

One of the main function of the liver is its role in drug metabolism

  • Drugs that are metabolised by the liver = check BNF and SPC guidance for dose adjustments and when they should be avoided
  • Drugs that are secreted in the bile unchanged = some drugs are excreted in bile unchanged as part of their metabolism pathway. In cirrhosis, bile accumulates = accumulation of these drugs e.g. rifampicin, fuscidic acid
45
Q

Type of Medication to avoid in liver disease
Symptom= Decreased Protein Synthesis ?

A

Drugs with high-protein binding potential
* Re-cap; drugs are in their active form when unbound
* In liver disease, dec albumin production = any drugs that are highly protein bound = increased risk of toxicity
* E.g. phenytoin, prednisolone

46
Q

Medication to avoid in liver disease:
Hepatotoxic drugs
Examples? (6)

A
  • Patients with liver disease will likely experience toxicity at lower doses and more frequently vs patients with a normal liver function
  • These drugs should be avoided or used carefully in patients with liver disease e.g.
  • Methotrexate
  • Sodium valproate
  • Amiodarone
  • Trimethoprim / co-trimoxazole
  • TB medication; isoniazid
  • Tamoxifen
47
Q

Two main types of non-alcoholic fatty liver disease (NAFLD);

A
  1. Primary NAFLD
    * Excessive fat (triglyceride) accumulation in the liver
    * Specifically where triglycerides are present in >5% of hepatocytes
    * Not the result of excessive alcohol consumption or secondary causes
  2. Secondary NAFLD
    * Liver damage as a result of another cause e.g.
    * Drug treatments; amiodarone, tamoxifen
    * Viral infection; hepatitis C
    * Endocrine conditions; polycystic ovarian syndrome

NAFLD is usually asymptomatic, but may occasionally cause non-specific symptoms;
* Fatigue
* general malaise
* abdominal discomfort

48
Q

Risk factors for NAFLD?

A

Metabolic risk factors for non-alcoholic fatty liver disease (NAFLD) include;
* Features of the metabolic syndrome that indicate increased cardiovascular risk
* Central obesity = 91% of people with BMI
>30 kg/m2 or increased waist circumference (greater than 94 cm in men or 80 cm in women) have been found to have NAFLD
* Impaired glucose regulation
* Type 2 diabetes mellitus (T2DM). Global prevalence of NAFLD among people with T2DM is 55%
* Hypertension
* Hyperlipidaemia
* Other possible risk factors for NAFLD include
* Obstructive sleep apnoea syndrome
* Endocrine disorders for example, Polycystic Ovary
syndrome
* Hypothyroidism
* A family history of NAFLD.
* Ethnicity — higher risk in Hispanic and Asian people
and lower risk in black people.
* Nutritional factors:
* Patients who have TPN / refeeding syndrome
* Rapid weight loss
* Drugs
* NSAIDS
* Amiodarone
* Corticosteroids
* Diltiazem
* Methotrexate
* Tamoxifen.
*Other liver conditions
* hepatitis C
* Wilson’s disease

49
Q

What causes NAFLD? (3)

A
  • The exact cause of NAFLD is unknown = closely linked to insulin resistance, obesity and metabolic syndrome
  • Environmental factors and genetic factors play a role in NAFLD development
    -Genetic link
    -More common in patients of European and latino decent?
50
Q

Symptoms / complications of NAFLD:

A

Liver symptoms / complications
* Portal hypertension.
* Variceal haemorrhage.
* Liver failure.
* Hepatocellular carcinoma (HCC).
* Sepsis
These complications are rare even in untreated NAFLD.

Metabolic complications:
* ^ risk of hypertension
* ^ risk of CKD
* ^ risk of impaired glucose regulation
* ^ risk of Type 2 diabetes
* In patients with Type 2 diabetes with NAFLD (Approx. 55%)
* ^ risk for AF
* ^ risk for MI
* ^ risk of stroke
* ^ risk of death from CVD

Mortality from cardiovascular or liver disease:
* Cardiovascular disease (MI, stroke, HF) is the most common cause of death in patients with NAFLD

51
Q

Treatment for NAFLD?
non-pharmacological?
pharmacological? (2)

A

1) Lifestyle advice
- weight loss advice
- increasing physical activity
- alcohol recommended limits
- do not offer omega 3 fatty acids
- continue taking statins

2) Pharmacological
- Pioglitazone 15-30mg OD
- Vitamin E 400-1000 units OD