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The Liver Pharmacology Flashcards

1
Q

Alcohol effects the GABA system. what does GABA stand for?

A

Gamma- Aminobutyric Acid

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2
Q

bilirubin is usually excreted via

A

excretion via bile ducts as a water-soluble conjugate

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3
Q

fibrosis and cirrhosis are characterised by

A

Inflammation + Fibrogenesis + Collagen deposition

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4
Q

high levels of ALT can be indicative of:

A

viral hepatitis, drugs, sepsis

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5
Q

How are Radicals produced in the liver?

A

When there’s higher alcohol intake, CYP450 2EI metabolises alcohol to unstable free radicals

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6
Q

list 5 signs of liver disease

A

Varices, Fatty Stools, Spider Naevi, Ascites and Jaundice

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7
Q

liver fibrosis can lead to

A

cirrhosis

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8
Q

name 3 other investigations done with LFTs

A

CT scan, liver Ultrasound, MRI

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9
Q

Name and explain an invasive treatment of Ascites

A

Paracentesis. is extracted from peritoneal cavity and colloids, albumin and terlipressin is exchanged

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10
Q

what is Steatohepatitis

A

Steatohepatitis is a type of fatty liver disease, characterized by inflammation of the liver with concurrent fat accumulation in liver. Mere deposition of fat in the liver is termed steatosis, and together these constitute fatty liver changes

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11
Q

normal albumin range?

A

35-50 g/dl

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12
Q

role of kupffer cells?

A

release macrophages to kill off bacteria and viruses in the liver

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13
Q

Treatment of SBP

A

3rd generation Cephalosporin, Co-Amoxiclav

Norfloxacin/Ciprofloxacin as prophylaxis

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14
Q

what are Ascites patients at risk of in terms of infection? where does it infect?

A

SBP - Spontaneous Bacterial Peritonitis. infects the peritoneal fluid

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15
Q

Long and short term consequences of alcohol

A

Short term:

  • Loss of consciousness
  • impotence
  • anxiety
  • acute poisoning
  • GI disturbances

Long term:

  • GI ulcer
  • Stroke
  • Increased BP
  • Obesity
  • Insomnia

(additionally generate free radicals, and affects GABA system)

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16
Q

what are the three main theories of Ascites

A
  1. underfill - reduction of circulating plasma volume
  2. overfill - increased plasma volume
  3. peripheral artery vasodilation
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17
Q

What are the two patterns of liver damage?

A

Cholestasis or Hepatocellular damage

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18
Q

what condition is Terlipressin used in? what is it?

A

Ascites and Variceal bleeding. It is a vasoactive drug used to raise blood pressure when norepinephrine doesn’t help.

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19
Q

what does ‘compensated liver disease’ mean

A

the small amount of viable liver you have left, works well.

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20
Q

what does ‘deompensated liver disease’ mean

A

the small amount of viable liver cells you have left doesn’t work well

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21
Q

normal range of bilirubin?

A

5-20 micromol/L

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22
Q

What is Varices, and what drug is used to treat it

A

Collateral vessels formed that enables blood to bypass the liver. Treat with Terlipressin

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23
Q

what is acute liver failure

A

history of onset does not exceed 6 months

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24
Q

what is cholestasis

A

Disruption of bile flow. Can be intra out extra hepatic

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25
what is chronic liver failure
persists for more than 6 months, with permanent ***_structural_*** changes following standing cell damage
26
what is elevated bilirubin a clinical sign of
Haemolysis Hepatocellular damage Cholestasis
27
what is first line in alcohol withdrawal management plan and why? How to administer? **If the patient has cirrhosis what do we give?**
A Benzodiazepine: Chlordiazepoxide long half life sedative + anticonvulsant properties slower onset of action. Shorter acting than Oxazepam. Front loading - loading dose followed by repeat dose every 90 minutes **In cirrhosis, give lorazepam or oxazepam**
28
what is Hepatitis
Inflammation of the liver. can be caused by viruses
29
what is Hepatocellular disease caused by
- inflammation (Hepatitis) - Fatty infiltration (steatosis) - Injury to hepatocytes - necrosis
30
what is liver fibrosis.
in injury to liver, collagen develops haphazardly and scars replace liver cells. the hard tissue formed is non functioning
31
what is Sepsis
the body's own response to infection injures it's tissues and organs
32
what is Steatohepatitis
accumulation of fat plus hepatocellular injury
33
what is Steatosis?
**"Liver Enlargement".** There's a disruption of metabolic pathways (redox imbalance) in liver which cause accumulation large droplets lipid within hepatocyte.
34
what is the most important metabolite leading to liver disease?
Accumulation of Acetylaldehyde which is produced by oxidising ethanol (with alcohol dehydrogenase)
35
what unfortunate condition can occur several weeks after quitting alcohol? what can we give as first line?
Acute Alcoholic Hepatitis. Prednisone 40m OD to switch off the inflammatory process
36
what vitamin supplement do you recommend for alcohol management, and why do we need vitamins?
Panrinex. Patient is vitamin deficient due to poor diet. Pabinex contains a mixture of vitamins for supplementation e.g Thiamine and Ascorbic acid
37
What is this and what is the treatment for it?
Asterexis (a sign of liver diease) Lactulose, Phosphate enema - Metronidazole, Neomycin, Sodium benzoate - Rifaximin
38
what is jaundice? and what causes it?
Yellowing of the skin and whites of eyes. * It's caused by a build-up of bilirubin in the blood and tissues of the body. * Common signs of jaundice are: -yellowing of the skin, eyes and mucus membrane (the lining of the body's passageways and cavities, such as the mouth and nose * pale-coloured stools (faeces) -dark-coloured urine
39
40
What is Ascites?
Accumulation of fluid in the peritoneal cavity leading to swollen abdomen
41
Main theory of Ascites?
Most common cause **overflow** which begins from cirrhosis of the liver. There is a decreased effective intravascular volume which leads to renal sodium retention. This now **causes increased blood volume** resulting in acites as water moves out into peritonieal cavity
42
Treatment of Ascites
Diuretics: • Spironolactone • Amiloride • Furosemide • \*Fluid/Sodium restriction\* • Paracentesis for large volume. Need to maintain adequate circulating volume – colloids, albumin, Terlipressin • TIPS for more refractory ascites (along with paracentesis)
43
what does TIPS stand for?
Transjugular intrahepatic portosystemic shunting
44
Monitoring points in Ascites
Monitor: Daily U&Es – esp Na, K, Cr * Daily wt – aim for 0.5-1kg/day wt loss * Fluid chart – note fluid restriction, urine output * Avoid high Na contents preparation * Complications – dilutional hypoNa, HE, HRS, gynaecomastia, hyperK, muscle cramps, SBP
45
46
Terlipressin Indication, action and monitoring points. How to administer dose.
Indicated for vasiceal bleed. Has a Biphasic action: • Intact molecule has an immediate vasoconstricting effect * Followed by delayed effect caused by slow transformation of terlipressin in-vivo to lysine vasopressin * Administer in bolus doses 1-2mg every 4-6hours (continue until haemostasis achieved) Monitor - Blood pressure, sodium, potassium, fluid balance Side-effects include headaches, abdominal cramps, ischaemia
47
Secondary prophylaxis in variceal bleeds
* **Non-selective** beta-blocker e.g Propranolol * Splanchnic vasoconstriction (beta2 blockade) * **reduced Cardiac output** results in reduced portal pressures (beta1 blockade) * Beta-blockers: Prevent **re-bleeding and Increase survival**
48
What is this and what causes it?
Spider Naevi. Caused by raised oestrogen level imbalance * pregnant women. Hormone replacement therapy, Oral Contraceptive Pill. (raised oestrogen) * Hepatic Disease – failure to metabolise oestrogen
49
50
What do Albumin and INR tell us about Drug Handling?
Generally: • Decreased Albumin and/or increased INR indicate reduced synthetic function • Significance will depend on the drug and is difficult to predict • Lower doses with close monitoring may be required Albumin * Decreased Albumin = **decreased** protein binding * Highly protein bound drugs - *increase* in “free” drug available to act and hence an increased clinical effect e.g. Phenytoin * Dose adjustment if PT \> 130% normal
51
52
Explain the Key liver function tests
1. *Albumin* * Hypoalbuminaemia = feature of advanced chronic liver disease (LD) 2. *Bilirubin* * An increase means a blockage in bile flow 3. *Aminotransferase (**AST** and **ALT**)* * An increase means hepatocellular damage 4. *Gamma-glutamyltransferase (****γ******GT**)* * Sensitive to drugs and alcohol 5. *Alkaline phosphatase (ALP)* * An increase means blockage of bile flow * yGT and ALP together indicate cholestatis -\> Partial or full blockage of bile ducts * If bile duct is inflamed/damaged, yGT and ALP spill out of liver into blood stream due to pressure.
53
what conditions cause a rise in yGT and ALP levels?
Scarring of the bile ducts Fatty liver (steatosis) Liver tumors Gall stones Alcoholic liver disease
54
what causes AST and ALT to rise
Viral hepatitis excess alcohol intake liver inflammation from medicines fatty liver autoimmune
55
normal range of: * AST * ALT * ALP * yGT * Albumin And what do they stand for?
AST (0-40 iu/L) Aspartate aminotransferase ALT (5-30 iu/L) Alanine aminotransferase ALP (30-120 iu/L) Alkaline Phospatase yGT-(5-55 iu/L) y-Glutamyltransferase Albumin (35-50 g/dL)
56
How do I interpret a LFT?
* LFTs are fairly non-specific * Generally if 2 x ULN considered abnormal * If Liver dysfunction – usually at least 2 will be deranged * Trends not isolation * Check reference ranges and units * Child's Pugh Scoring System takes into acount EABAI - Encephalopathy, Ascites, Bilirubin, Albumin and INR
57
what is hepatic encephalopathy
* Several theories including accumulation of toxins esp. ammonia, increased permeability of BBB, increased levels of neurotransmitters * Precipitating factors – increased protein load, reduced ammonia excretion, electrolyte disturbance, dehydration, drugs, infection * Occurs in 4 stages
58
what are the four stages of hepatic encephalopathy
**mental status** 1. Impaired attention, irritability, depression 2. Drowsiness and memory impairment 3. Confusion and amnesia 4. Stupor and coma **corresponding neuromuscular function** ​at stage 1: Tremor and incoordination at stage 2: Asterexis and slurred speech at stage 3: Hypoactive refleces at stage 4: dilated pupils
59
state invasive techniques to manage variceal bleeds
1. sclerotherapy (glue) 2. balloon taponade 3. band ligation
60
state 5 causes of liver disease
* Alcohol * viral infections * drugs * toxins * cancer * autoimmune
61
62
Outline the management plan for Alcoholic hepatitis
1. Manage withdrawal symptoms 2. Manage Vitamin deficiency 3. Treate acute alcoholic hepatits with anti-**inflammatory agent** 4. Manage any complications associated with liver disease e.g cirrhosis, coagulopathy, ascites
63
what are the presenting signs of alcohol withdrawal? What first line
delerium fever seizures rapid pulse tremor First line is to manage the symptom. Give **Chlordiazepoxide + Pabrinex**
64
65
If a patient is getting additional seizures from alcohol withdrawal, what do you reccommend?
Lorazepam or Haloperidol in sever psychosis
66
what markers are elevated in Acute Alcoholic Hepatits?
White Cell Count Neutrophil count Bilirubin INR Raised AST
67
How to treat alcoholic cirrhosis? How to manage Alcoholic Cirrhosis?
_Treatments_ * anti-TNF agents - Infliximab * Antioxidants * Vitamin E _Management_ * Diuretics for Ascites * Propanolol for Portal Hypertension * Vitamin K for * Coagulopathy * Antibiotics for SBP * Lactulose for HE
68
what causes alcohol dependence to begin with?
The release of **β-endorphins**, coupled with the release of dopamine, is thought to result in the pleasurable feelings associated with alcohol dependence. When alcohol is **withdrawn** the result is **_CNS Hyperactivity._** This explains the seizures
69
what agents can we give to help abstincence of alcholol
Disulfiram! - inhibits acetaldehyde degydeogenase. 800mg OD then reduce by 200mg each day. maintain at 100-200mg OD

GSS (10 decks)

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