Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pharmacy PH2506 > The Liver > Flashcards

The Liver Flashcards

1
Q

Assessing liver function

A
  • Drugs handled differently in the different liver conditions
  • Poor information on pharmacokinetics and pharmacodynamics of drugs in liver disease
  • Mix of tests, diagnosis and symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Child Pugh score meaning

A

-prognosis of liver disease
POINTS
-5-6: Class A; 1st year 100%; 2nd year survival 85%
-7-9: Class B; One year survival= 81%; 2nd year survival 57%
-10-15: Class C; 1st year 45%; 2nd year survival 35%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Child Pugh scoring system

A

1) Bilirubin: 1pt <34; 2pt= 34-50; 3pt >50
2) Serum albumin: 1pt>35; 2pt=28-35; 3 pt=<28
3) INR: 1pt=<1.7; 2pt=1.71-2.2; 3pt=>2.2
4) Ascites: 1pt=none; 2pt=Mild; 3pt= severe
5) Hepatic encephalopathy 1pt=None;2pt GradeI-II; 3pt= Grade–IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signs and symptoms

NON SPECIFIC

A
  • Malnutrition
  • Peripheral Oedema
  • Brusing and bleeding
  • Testicular atrophy
  • White nail
  • Splenomegaly (enlargement of the spleen)
  • Fatigue/Malaise
  • Abdominal or RUQ pain
  • Muscle cramp
  • Finger clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Liver Investigations

A
  • Ultra sound (pressure in system)
  • CT scan (cysts, masses and fluid in system)
  • MRI (structural info- surgery)
  • Liver biopsy (tissue sample- hallow needle)
  • Venography (pressure ballon in system)
  • Doppler (direction and speed in vessels, and identify collateral vessels)
  • Fibroscan (stiffness of liver, fibrosis)
  • Endoscopy (look for varcies and GI bleed)
  • Endoscopic Retrograde Cholangiopancreatography (ERCP- diagnose and treat- use endoscope into the stomach inwhich a dye can be injected, can treat gallstones)
  • Percutaneous transhepatic cholangiogramaphy (PTC- contrast medium is injected through needle through the skin, x ray image is used to identify obstructions in bilary tree)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diagnostic Terms

A
  • Acute (<6 months)
  • Chronic (>6 months)
  • Compensated (Still have synthetic function)
  • Decompensated (Lack of synthetic function)
  • Hepatitis (inflammation of the liver- drugs, alcohol, virus- when this is suspected a viral serology is required)
  • Fibrosis (Excessive accumulation of scar tissue)
  • Cirrhosis (Fibrosis and structural degradation )
  • Cholestasis (Reduced excretion of bile salts-INR may be raised due to lack of Vit K absorption, Bilary tree is effected so alkaline phosphate, bilirubin increase common sign is gallstone)
  • Mixed pictures are not uncommon especially as a condition progresses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Liver function tests (LFTs)

A
  • Markers of dysfunction rather than function
  • Used to monitor progression of liver disease
  • Only reflects status at time of test
  • Vary between male and female
  • Vary with time of day that samples taken
  • Do not just measure liver disease as not specific (Problems in other systems e.g. bone disease, haemolysis-high billirubin, ADRs to drugs e.g. penicillins, cholestatic jaundice)
  • No single test or combination in uniquely diagnostic
  • Only albumin and prothrombin show liver function
  • for liver enzymes 2x normal limit is still normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which tests Classed as liver function tests

A 
LIVER ENZYMES 
-Alkaline phosphatase 
-Aminotransferases:
-Aspartate aminotransferase (AST) 
-Alanine aminotransferase (ALT) 
-Gamma Glutamyl transferase 
SYNTHETIC FUNCTION 
-Bilirubin (urine and serum) 
-Plasma proteins: Albumin; Ig 
-Prothrombin time (Clotting studies) 
\+Suffering form liver disease 
\+harming themselfs through alcohol 
\+when starting or monitoring patients on drugs that will effect the liver (phenytoin, phenobarbitone, rifampicin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q 
Alkaline phosphatase (Alk Phos) 
-REF RANGE: 30-300 IU/L- higher in children
A

-Group of isoenzymes found in tissues around the body (Therefore is a non-specific indicators)
-Reference ranges larger for neonates and children-always use correct laboratory reference ranges
-High concentrations in biliary canaliculi, production increased if biliary damage
-Levels slightly raised in hepatocellular damage
-Levels greatly increased in biliary obstruction
-Other isoenzymes of Alk Phos in
+Osteoblasts- raised in pages disease, osteomalacia, bony metastases
+Kidney, intestine and placenta (Alk Phos also raised in hypoparathyroidism, pregnancy)
-Drug therapy- e.g. rifampicin, phenytoin, erythromycin, carbamazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alanine transaminases (AST and ALT)

A
  • AST= Aspartate Transaminase ref range 0-40 IU/L (non-specific but reliable)
  • ALT= Alanine Transaminase ref range 0-40 IU/L (greater specificity for liver)
  • Found in heart, liver, skeletal muscle, kidney, erythrocytes, pancreas, lung (ALT less so)
  • Levels may be raised following MI shock, haemolysis (cell lysing)
  • Patients with cirrhosis may have normal or only slightly raised enzyme levels
  • In chronic liver disease however, a rise may not occur due to reduced production
  • Raised ALT may indicate acute hepatitis (+++), Cirrhosis-only raised if continual inflammation (++/+) cholestatic jaundice (++) may also be raised in shock, highest levels in paracetamol toxicity
  • In hepitis C cells die by apoptosis, these cells must produce less enzymes so sensitivity is decreased
  • In alcohol injury AST levels are higher the ALT
  • Drugs e.g. rifampicin, erythromycin, isoniazid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Gamma glutamyl Transferase (GGT)- ref range 0-50 IU/L

A
  • Enzyme found in endoplasmic reticulum in hepatobiliary tract (Also in kidney, pancreas, intestine, prostate)
  • Released in all types of liver dysfunction
  • Synthesis increase in response to prolonged alcohol intake (Up to 20x)
  • Or may be raised by enzyme inducing drugs e.g. phenytoin, carbamazepine, rifampicin (2x-5x)
  • Levels also elevated in cholestasis, liver and pancreatic disease, MI and diabetes (fatty liver) (x3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bilirubin: range 2-20 mcmol/L

A
  • Jaundice (yellowing of skin caused by bilirubin)
  • Usually >50mcmol/L in adults (>80mcmol/L neonates)
  • Classification based on cause of raised bilirubin
  • Levels rise characteristically in cholestasis
  • May be raised in acute liver failure due to inability of hepatocytes to conjugate
  • In chronic decompensated cirrhotic patients bilirubin may be normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Classification of Jaundice- Pre hepatic

A
  • Usually caused by haemolysis- sickle cell
  • Levels rarely exceed 85-100 mcmol/L as unconjugated form
  • Excess production of unconjugated bilirubin
  • Not excretable in urine
  • Urine colour normal
  • Risk of gallstones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classification of Jaundice- Intra-hepatic jaundice

A 
\+Causes 
-Acute viral hepatitis 
-Drug induced liver injury 
-Alcoholic hepatitis 
-Primary biliary cirrhosis- autoimmune disease, destruction of bile ducts- increased bile= choleostasis 
-Pregnancy 
-Intrahepatic cholestasis 
-Acute fatty liver 
-Congenital hyperbilirubinaemia 
\+Accumulation of bilirubin in liver, mainly conjugated, water soluble 
\+Excreted in urine, causing darkening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Classification of Jaundice- Post hepatic Jaundice

A 
-Obstruction of extrahepatic bile ducts caused by:
\+Congenital biliary atresia 
\+Gallstone 
\+Structures (often biliary surgery)
\+Tumours (often head of pancreas) 
-Excess bilirubin is conjugated 
-Darkening of urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Albumin: ref range 35-50 g/L

A
  • Major protein synthesised in the liver
  • Marker of synthetic capacity of liver
  • Long half life (20 days)- Indicator of chronic disease
  • Hypoalbuminaemia leads to peripheral oedema and ascites due to loss of oncotic pressure (osmotic pressure exerted by proteins)
  • Fluid retention may lower albumin concentration
  • Affects transport of protein bound drugs and Ca, this means there effects can go on for longer
  • Malnutrition, Malabsorption and nephrotic syndrome also reduce serum albumin
  • Albumin synthesis depressed in inflammatory states- increased protein demand (burns, trauma, sepsis)
  • Normal albumin levels lower in pregnancy
17
Q

Clotting factors INR range (0.9-1.2)

A
  • Liver synthesis Vit K dependant clotting factors II,V, VII, IX and X
  • Prothrombin time (PT- time taken for clot to form) becomes abnormal when 80% of liver synthesising capacity is lost
  • May be due to reduced absorption Vit K or reduced liver synthesis of clotting factors
  • Clotting factors have short life, sensitive marker of loss of liver function
  • Failure to absorb Vit K absorption (Chronic cholestasis, fat malabsorption) supplementation
  • Caution with NSAID
18
Q

Drug induced Liver injury

A
  • Acute reactions and from long term use
  • 2% of jaundice patients
  • 50% of acute Liver Injury Patients
  • Hepatocellular, cholestatic, mixed presentations
  • Direct hepatotoxicity e.g. paracetamol or idiosyncratic drug reactions
  • Steatosis (Abnormal retention of fat)
  • Oral contraceptives
  • Risk factors: age, other medications, poor renal function, previous liver injury
19
Q

Drug handling in liver failure

A

-Issues of drug absorption
+Cholestasis- reduce absorption of fat soluble drugs
+Ascites
-Issues of altered distribution
+Ascites- changes water soluble drugs
+Lack of albumin- protein bound drugs phenytoin
-Metabolism
+Lack of function- increased half-lives
-Elimination
- Reduction of first pass metabolism (Varacies, portal HTN)- propanolol and morphine

20
Q

Side effects to consider in Liver disease

A
  • Hepatotoxicity-
  • Biliary effects-
  • Bleeding risk - no NSAIDs
  • GI- SSRI and NSAID cause bleeding (liver disease random clotting factor release)
  • Neurological- mask encepthalopgy
  • Electrolyte disturbances- bad in ascites due to shift of fluid
  • Fluid accumulation
  • Renal- more susceptably to kidney decline
21
Q

Prescribing in liver failure

A
  • Keep number of medicines to a minimum
  • Small doses
  • Avoid modified release preparations
  • Short half life
  • Plan to monitor for side effects of drugs and consider side effects when choosing an agent
  • NO NSAID (fluid retention, bleeding and increased kidney injury)
  • Check SPCs- Bioavailability, protein binding etc
22
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

JAUNDICE

A
  • Jaundice
  • high levels of bilirubin occur in acute hepatitis or cirrhosis
  • this is not an indication of liver function gilberts syndrome is a begin condition and LF is not effected
  • In people with dark skin, it can still be seen to sclera of eye and gums
23
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

PALE AND DARK STOOLS

A
  • Pale stool and dark urine
  • sign of obstructive jaudince water soluble conjugated bilirubin cannot be excreted through faeces so increases renal elimination through urine
24
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

steatorrhoea

A

Steatorrhoea

  • fat in poo, bile salt defficiency which means less fat is absorbed from the gut
  • Orlistat causes this
  • Reduction is fat soluble vitamins including K
25
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

SPIDER NAEVI

A

-Spider Naevi

(vascular changes and long term liver disease)

26
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

HEPATIC ENCEPHALOPATHY

A

-Hepatic Encephalopathy -Severe, caused by toxic substances
e,g, ammonia, fatty acids and nitrogen based comounds
act as false neurotransmitter
-This increases when liver cannot clear them OR if the circulation bypass liver
-Symptoms: aggression; confusion; poor concentration; coma
-This is graded in terms of severity- this can be tested by asking them to hold there arms out straight. If they have the disorder the arms will flap
+It is termed liver flap

27
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

DUPUYTENS CONTRACTURE

A
  • Dupuytens contracture
  • fixed forward contracture of a finger, with a fibrous link-
  • starts as nodules and they join together to form cords of tissue
  • If this cord shortens the finger contracts
28
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

PRUITUS

A
  • Pruritus
  • High conc of bile salt in the skin, this is when bilirubin is above 50
  • This causes a central itch
  • opiate antagonists , antihistamines are both treatments
29
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

LEUCONYCHIA TOTALIS

A
  • Leuconychia totalis
  • white nail, is from a lack of albumin and is not just shown in liver dysfunction e.g. congenital disorders where there is poor protein absorption or renal
  • Sulphonamides also can cause this
30
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

HEPATOMGEALY

A
  • Abdominal signs
  • Hepatomegaly
  • enlargement of the liver may disappear as hepatocytes are destroyed and replaced with fibrous tissue
31
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

Palmar erythema

A
  • Reding of palms, hands and soles of feet

- Can occur in pregnancy, RA and other conditions

32
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

ASCITES

A
  • This is excess fluid in the peritoneal cavity
  • Large amounts can be uncomfortable and effects breathing
  • This comes from increased portal pressure, lack of albumin and over activity of RAAS
  • Liver failure leads to salt and water retention, this decreases renal blood flow and GFR,
  • Excess reabsorbtion of sodium and water leads to increase in renin and aldosterone
  • This is then exacerbated by the liver which cannot metabolised aldosterone or vasopressin
  • Hypoalbumaemia lowers the collidal osmotic pressure and encourages oedema formation and contributes to poor renal blood flow
33
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

GYNAECOMASTIA

A
  • Increase in male breast tissue
  • This occurs from reduce oestrogen metabolism
  • This can be an indication that drug metabolism is also impaired
  • Spironolactone can also cause this as a side effect
34
Q

Signs and symptoms- specific vs non-specific: SPECIFIC

OESOPHAGEAL AND GASTRIC VARICES

A
  • Portal HTN is an increase in BP in the portal venous system
  • Vessels from stomach, spleen and pancreas merge into this system
  • This then branches through the liver
  • The hepatic venous pressure gradient approx the gradient pressure between the portal vein and the inferior vena cava
  • This quantifies the degree of portal HTN
  • A normal value is between 1-5mmHg
  • Portal HTN is stated to be present when this value is above 6
  • Above a value of 10, this is now clinically significant and oesophageal varies may develop
  • At above 12 the patient may be at risk of varieal bleeding and the development of ascites
  • This increase in pressure can increase for a number of reasons: pressure on the portal vein because of a tumor; disorganised blood flow through the liver due to cirrhosis: thrombosis of hepatic vein (due Budd-chari syndrome)
  • Portal HTN can be pre-hepatic; intra-hepatic or post-hepatic
  • Oesophageal and gastric varices can burst due to portal HTN, these are abnormally dilated collateral vessels
  • The porto-systemic collateral circulation in stomach or oesophagus rises due to increase HTN this allows blood to bypass vessels
  • Higher mortality 30% die;
  • Reduction is 1st pass metabolism so drugs can have a greater effect on the body- dont use these drugs
35
Q

Splenomegaly

A
  • Patients with portal HTN may have an enlarged spleen

- This is because it may get congested due to increase iun pressure

36
Q

Back to structure

A
  • Hepatocytes can regenerate if injured and life span is around 5 months
  • Will always be liver enzymes released from cells
  • Most drug injury occurs in area 3 of the acinus- where ALT and AST release
  • Alkaline phosphate occurs in cells around bile ducts, so we would except an increase in bilirubin to indicate problem with bilary tree rather than hepatic problem

Clinical Pharmacy PH2506 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions