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Pharmacy Yr3 Renal and hepatic diseases > Week 1- Liver disease Diagnosis & Monitoring & drug handling > Flashcards

Week 1- Liver disease Diagnosis & Monitoring & drug handling Flashcards

1
Q

how is liver disease diagnosed?

A 
 Medical history
 Blood tests
 Liver function tests (LFTs)
 Electrolytes
 Full blood count
 Viral screens
 blood clotting
 Imaging
 Ultrasound
 CT scan
 MRI
 Liver biopsy
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2
Q

what are the different types of LFTs serum enzyme found during a test?

A
  • Aspartate transaminase (AST)
  • Alanine transaminase (ALT)
  • Gamma glutamyl transferase (GGT)
  • Alkaline phosphatase (ALP)
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3
Q

what is Aspartate transaminase (AST)?

A

 Role in gluconeogenesis - catalyses reversible conversion of aspartate and alpha keto glutarate to oxaloacetate and glutamate
 Reference range – 5-40 IU/L (vary slightly between labs)
 Found in hepatocytes, but also in other tissues including heart, brain and skeletal muscle

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4
Q

what is Alanine transaminase (ALT)?

A

Also role in gluconeogenesis – catalyses reversible transfer of an amino group from L-alanine to alpha ketoglutarate resulting in pyruvate and L-glutamate
 Reference range – 5-30 IU/L
 More specific to liver

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5
Q

what kind of levels of ALT and AST will be found in the blood for hepatitis?

A

Very high levels in acute viral/toxic hepatitis

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6
Q

what kind of levels of ALT and AST will be found in the blood for cholestatic jaundice/cirrhosis?

A

 High levels in cholestatic jaundice/cirrhosis

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7
Q

how can the ratio of how much AST/ALT is present determine anything?

A

helps determine the type of liver disease
Ratio of AST/ALT useful in diagnosing different types of
liver disease eg AST/ALT>2 possibly alcohol injury,
whereas most other liver injuries AST/ALT <1

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8
Q

what is Gamma glutamyl transferase (GGT)?

A

 Catalyses transfer of gamma glutamyl moiety of glutathione to to
an amino acid, peptide or water (forming glutamate)
 Reference range – 5-45 IU/L (vary slightly between labs)
 Very high levels in biliary obstruction, lower increased levels in
chronic alcohol or drug toxicity, hepatitis, cirrhosis, or cholestasis
 Also in kidneys, pancreas, prostate

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9
Q

What is alkaline phosphatase (ALP)?

A

 Removes phosphate groups from nucleotides, proteins and alkaloids
 Reference range – 20-100 IU/L
 Very high levels in biliary obstruction
 Also in bone, intestinal wall, renal tubules, placenta

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10
Q

what are some other LFTs components that can be observed for?

A
  • Bilirubin
  • Plasma proteins and albumin
  • Prothrombin time (PT)
  • Urea and ammonia
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11
Q

what should be observed for when looking at bilirubin for liver disease?

A

 Reference range – 0-17mmol/L (vary slightly between labs)
 Jaundice occurs at >35mmol/L can lead to yellow/orange colour in skin
 Reflects depth of jaundice and useful for monitoring disease
progression
 Can measure conjugated/unconjugated can help differentiate what type of liver disease

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12
Q

what should be observed for when looking at plasma protein and albumin for liver disease?

A

 Reference ranges: 60-80g/dL total protein, 35-50g/dL albumin
 Albumin is synthesised solely by the liver
 t1/2 for plasma albumin is 20-26 days would show extended liver damage
 <20g/dl results in oedema

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13
Q

what should be observed for when looking at Prothrombin time (PT) for liver disease?

A

-how long it takes the blood to clot
 Reference range – 10-15 sec
 Increased PT when lack of clotting factors
 If hepatocellular damage – PT is unresponsive to vitamin K
 If cholestasis, increased PT due to deficiency in bile salts responsible for vitamin K absorption so responsive to vitamin K
10 mg i/v for 3 days

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14
Q

what should be observed for when looking at plasma protein and albumin for liver disease?

A

 Reference range for urea: 2.5-7.8 mmol/L
 Reference range for ammonia: 16-60 (M), 11-51 (F) mmol/L
 Urea decreased in liver disease
 Ammonia increased in liver disease – hepatic encephalopathy

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15
Q

what LFT components do you look out for to decide if the liver is working?

A

 Albumin to see if its being produced

 Clotting factors to see if its being produced

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16
Q

what LFT components do you look out for to decide if the liver is damaged?

A 
-the different enzymes 
 ALT
 AST
 GGT
 ALT/AST ratio
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17
Q

what LFT components do you look out for to decide if the liver is damaged?

A

 Bilirubin conjugated/ unconjugated
 ALP
 GGT

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18
Q

what does liver disease result in effects on?

A

 on Drug clearance
 on Biotransformation
 on Pharmacokinetics

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19
Q

what factors are responsible alteration in the liver for liver disease?

A 
 Intestinal absorption
 Plasma protein binding
 Hepatic extraction ratio
 Liver blood flow
 Portal-systemic shunting
 Biliary excretion
 Enterohepatic circulation
 Renal clearance
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20
Q

what are the two stages of metabolism?

A

phase I

phase II

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21
Q

what is involved in phase I metabolism?

A

Oxidation eg azathioprine
Reduction eg halothane
Hydrolysis eg atropine, pethidine

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22
Q

What is involed in phase II metabolism

A

Glucuronidation eg paracetamol, morphine
Sulphonation eg steroids
Acetylation eg hydralazine, phenelzine
Methylation eg nicotine

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23
Q

what does the rate of extraction from the liver depend on?

A

blood flow through the liver

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24
Q

what is the extraction ratio?

A

-can be subdivided into 2 high and low

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25
Q

for the liver to have a high extraction ratio it depends on what?

A

clearance
depends on
hepatic blood flow
-drugs involved here undergo high first pass metabolism in the liver close to 1

26
Q

for the liver to have a low extraction ratio it depends on what?

A
  • clearance
  • depends on metabolising
  • capacity of liver close to 0
27
Q

what are the rules when modifying drug dosage in liver disease?

A

no rules so must monitor for clinical and toxic effects

28
Q

how does liver disease affect drug-metabolising enzyes?

A

 Inhibition and induction of drug-metabolising enzymes
are the most frequent and dangerous drug-drug
interactions
 Liver disease causes reduction in magnitude of
interactions due to enzyme inhibition & induction
 Monitor effects of drug and plasma concentrations

29
Q

what are the effects of enzyme inhibitors in the Cytochrome P450 system?

A

can potentially increase the level of drug

30
Q

what are the effects of enzyme inducers in the Cytochrome P450 system?

A

can potentially decrease the level of drug

31
Q

what LFT enzyme has raised levels in the serum when taking an enzyme inducer?

A

GGT

32
Q

what kind of drugs will people with liver disease have increased sensitivity for?

A

 affect clotting/bleeding
 affect CNS
 Diuretics
 constipation

33
Q

how many types of liver disease is there? no. ppl it effects

A

over 200 types and effects 2million ppl in UK and increasing

34
Q

what are the main causes for liver disease?

A

Alcohol
Obesity
Undiagnosed hepatitis infection
Drug or other chemical toxicity

35
Q

what are some of the types of liver disease?

A
  • Alcohol-related liver disease
  • Drug toxicity
  • Hepatitis (inflammation)
  • Non-alcoholic fatty liver disease (NAFLD)
  • Cirrhosis
  • Cancer
  • Gallstones stops biles salts from being secreted
  • Cholangitis
  • Hemochromatosis (iron overload, inherited)
  • Wilson’s disease (copper overload, inherited)
  • Gilbert’s disease (inability to metabolise bilirubin properly)
36
Q

what are the 2 types of liver disease?

A

acute or chronic

37
Q

what does acute liver disease mean?

A
  • Usually self-limiting
  • Results in hepatocyte inflammation/damage
  • Occasionally severe resulting in liver failure
  • Generally caused by drugs or viruses
38
Q

what does chronic liver disease mean?

A

-Inflammation present > 6 months
- Results in permanent damage with structural changes
resulting in cirrhosis leading to loss of function
- Most common cause is alcohol abuse

39
Q

what are the different steps in liver disease progressing?

A
  • start off with normal liver then theres damage e.g. alcohol or viral infection or NAFLD
  • this leads to inflammation and may have a fatty liver
  • due to inflammation pro-inflammatory cytokines and immune cells causing activation of immune system
  • resulting in matrix deposition, parenchymal cell death hepaocytes die and angiogenesis
  • this leads to early fibrosis and this can be resolved to a normal liver by the removal of underlying cuase or anti-fibrotic drug
  • early fibrosis progresses to late fiborisi/cirrhosis where hepatocytes lose function, disruption to architecture
  • cirrhosis can lead to liver failure and portal hypertension and eventually needing a liver transplant or cancer process can take 5-50 years
40
Q

what kind of damage can occur that would lead to damage of the liver?

A
  • alcohol
  • viral infection
  • NAFLD
  • autoimmune disorder
  • cholestatic disorder
  • metabolic disease
41
Q

can cirrhosis go back to being a healthy liver?

A

no but there can be regression to early fibrosis

42
Q

what is a fatty liver due to?

A

obesity

-increase in triglycerides LFTS AND LIVER FAT.

43
Q

what type of cell is increased in appearance in a liver that has advanced fibrosis?

A
  • a lot of hepatic stellate cell
  • causing lots of extracellular matrix and fibrosis
  • inflitrating lymphocytes
  • kupffer cells are activated
  • sinsoid lumen with increased resistance to blood flow
44
Q

what virus can cause liver disease?

A

hepatitis

45
Q

what are the different types of hepatitis ?

A
  • Hepatitis A – fecal-oral route, acute inflammation that
    generally resolves spontaneously, vaccine available
  • Hepatitis B – body fluids, mother to baby, acute infection that
    progresses to chronic inflammation, cirrhosis and cancer,
    vaccine available
  • Hepatitis C – body fluids, chronic and may progress to
    cirrhosis and cancer, no vaccine
  • Hepatitis D – body fluids, requires concomitant infection with
    -Hepatitis B to survive
    Hepatitis E – contaminated food and water, usually self-limited
  • Hepatitis G – body fluids, chronic infection similar to HCV
46
Q

how do drugs cause liver disease?

A

-Hepatocytes become temporarily inflamed or
permanently damaged by drugs/medicines
- Some drugs require overdose to cause liver damage eg
paracetamol
- Others may cause damage even when appropriately
prescribed eg
Statins
Some common antibiotics eg amoxicillin, tetracycline
Methotrexate
- Some natural products can also cause liver damage
Herbal remedies eg kava kava
High doses of vitamin A
Some wild mushrooms

47
Q

how does alcohol cause liver disease?

A

-Most common cause of liver disease/cirrhosis
- Directly toxic to liver cells
- Alcohol causes inflammation which progresses to fatty
liver and eventually fibrosis
- Fibrosis alters structure and blood flow leading to portal
hypertension and eventual liver failure
- Damage occurs >40g/d in men and >20g/d in women
(1 unit = 9g)

48
Q

what are the uk alcohol guidelines?

A 
UK Alcohol guidelines:
• <14 units per week
• Don’t save them up
• Spread over at least 3 days
• No alcohol in pregnancy
49
Q

what is cholestatis? cause?

A

lack of bile
- Due to hepatocytes:
Failure of bile production and secretion
Causes include hepatitis from viruses, alcohol, drugs
Pregnancy
Due to bile duct:
Failure of outflow via bile ducts due to obstruction
Gallstones, carcinoma, cholangitis (progressive scarring of bile
ducts)

50
Q

what are some symptoms of acute liver disease?

A
  • Possibly asymptomatic
  • Generalised malaise
  • Anorexia
  • Fever-due to inflammation
  • Possibly jaundice (later) yellow colour
51
Q

what are the symptoms of chronic liver disease?

A
  • Fatigue and weakness
  • Loss of weight
  • Nausea/vomiting
  • Loss of appetite
  • Cachexia – wasting of muscle in arms and legs
  • Abdominal swelling
  • Right upper quadrant abdominal pain and tenderness
  • Jaundice
  • Bleeding from gums/nose and easy bruising
52
Q

what are the symptoms of chronic disease?

A

Could be specific depending on type of disease eg
gallstones upper abdominal pain and vomiting after greasy meal

Individuals with cirrhosis develop progressive
symptoms as liver fails
- Inability to metabolise waste as liver fails
- Failure to produce proteins required for body function eg
clotting
- Symptoms include easy bruising, gynecomastia,
impotence, confusion, ascites, portal hypertension,
oesophageal varices

53
Q

what are some signs and complications of liver disease?

A 
Jaundice
 Ascites
 Portal hypertension and oesophageal varices
 Hepatic encephalopathy
 Hematological changes
 Circulatory changes
 Skin changes
 Endocrine abnormalities
 Renal failure – due to reduced renal blood flow
54
Q

what is jaundice? cause?

A

Yellow discolouration of skin & mucous membranes
(sclera)
Causes: bilirubin build up
-Haemolysis (haemolytic jaundice) RBC are breaking down liver not getting rid of haem so build up of bilirubin
Hepatocellular damage (hepatic jaundice) hepatocyte build up
- Cholestasis (obstructive jaundice) bile from liver being made but not being moved due to obstruction in bile duct

55
Q

what is portal hypertension? cause

A

-where there’s a back pressure because of resistance of blood flow due to cirrhosis, because of fibrosis that’s happening so there resistance of blood flow in the liver leading to back pressure in portal vein
-high blood pressure pushes blood into the surrounding blood vessles including thin walled veins in oesophagus close to the surface.
-If pressure too high, they can
rupture and bleed –
uncontrolled bleeding leads to
shock and death

56
Q

what is ascites? cause

A 
Abnormal accumulation of fluid in
the peritoneal cavity due to
pressure imbalance between
inside the circulation (high) and
outside, in this case the
peritoneal cavity (low)
 Causes:
 Portal hypertension
 Low plasma albumin
 Salt and water retention by
kidneys eg secondary
hyperaldosteronism
57
Q

whats Hepatic encephaloathy?

A
  • Neurological abnormality caused by build up of substances (mainly
    ammonia) normally metabolised by liver in the blood and crosses
    blood brain barrier
  • Can be associated with cirrhosis, or acute liver failure or portal-systemic bypass of liver
  • Results in altered mental state, fetor hepaticus,
    asterixis, drowsiness, confusion, coma
    Due to ammonia & nitrogenous substances from gut
    by-passing liver & crossing BBB
    Precipitated by:
    Dehydration, hypovolaemia, GI bleed, CNS drugs,
    alcohol, ↑ dietary protein, constipation
58
Q

what is Wernicke encephalopathy?

A

due to deficiency of
thiamine, with decreased mental function. Occurs in
chronic alcohol abuse

59
Q

what are some hematogical changes during liver disease?

A 
Anaemia
 Effects on iron homeostasis
 Splenomegaly from portal hypertension
 Alcohol toxic to bone marrow etc
 Reduction in clotting factor synthesis
 Bleeding and bruising
 Reduction in clotting factor synthesis
60
Q

what are some circulatory and skin changes during liver disease?

A 
Circulatory:
 Palmar erythema
 Spider naevi
 Finger clubbing
 Skin:
 Pruritis

Pharmacy Yr3 Renal and hepatic diseases (5 decks)

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