Liver Flashcards

1
Q

Liver Functions

A
  • ELIMINATION OF BILIRUBIN
  • PRODUCTION OF BILE
  • FAT METABOLISM
  • VIT AND MINERAL STORAGE
  • PROTEIN METABOLISM
  • CARBOHYDRATE METABOLISM:
    GLUCOSE STORAGE, GLYCOGENOLYSIS,
    GLUCONEOGENESIS
  • BREAKDOWN OF HORMONES AND
    STEROIDS
  • SYNTHESIS OF COAGULATION FACTORS
  • DRUG/TOXIN METABOLISM
  • INFECTION CONTROL
  • HEAT PRODUCTION
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2
Q

Classifications of Liver Failure

A

Acute / Chronic Liver Failure

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3
Q

Stages of Acute liver failure timescales

A

Hyper Acute 8d
Acute 8-28 days
subacute 4-26 weeks

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4
Q

Causes of Liver Failure

A

Poisons/Chemicals/Drugs
infections
liver tumors

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5
Q

Stages of Alcohol liver disease

A

Fatty Liver > Liver Fibrosis > Cirrhosis

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6
Q

Fatty Liver stage of ALD is?

A

Deposits of fat causes liver enlargement. strict abstinence can lead to a full recovery

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7
Q

Fibrosis of the liver in ALD is ?

A

Scar tissue forms on the liver. Recovery is possible but scar tissue remains

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8
Q

Cirrhosis of the liver in ALD is ?

A

Growth of connective tissue destroys the liver cells. The damage is irreversible

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9
Q

Secondary causes of liver disease include

A

Ischaemia
liver tumours
acute on chronic
galactosaemia
reyes syndrome
wilsons disease
fatty liver in pregnancy

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10
Q

Clinical manifestations of liver disease

A

RESPIRATORY DYSFUNCTION
* CARDIOVASCULAR DYSFUNCTION
* ELECTROLYTE DISTURBANCES
* METABOLIC DISTURBANCES
* COAGULOPATHY/BLEEDING/DIC
* PORTAL HYPERTENSION
* RENAL DYSFUNCTION
* ASCITES
* JAUNDICE
* HEPATIC FOETER/PALMAR
ERYTHEMA/SPIDER
NAEVI/SPLENOMEGALY
* IMMUNOSUPPRESSION
* RARE COMPLICATIONS

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11
Q

Liver blood supply is from

A

Hepatic artery carrying oxygenated blood from the heart and the portal vein which delivers blood from organs such as stomach and intestines to your liver for processing.

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12
Q

The liver stores what

A

Glycogen, iron, copper, vit A, and many B-complex vitamins and vitamin D.

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13
Q

The liver produces what

A

albumin and other proteins, including clotting factors prothrombin and fibrinogen and anticoagulant heparin

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14
Q

what happens to amino acids in the liver

A

amino acids are deaminated (nitrogen removed)

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15
Q

What happens to nitrogen in the liver

A

it is used to produce new protein from carbohydrates or fat

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16
Q

The liver can make what from carbohydrates/proteins

A

It can make fat which is then stored and released as free fatty acids which can be utilised for energy

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17
Q

What can the liver do with cholesterol

A

Synthesizes cholesterol

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18
Q

In the liver, what is the purpose for phagocytes

A

To remove foreign substances and bacteria in the blood

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19
Q

What does the liver do to drugs

A

detoxifies drugs

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20
Q

what does the liver secrete

A

Cholesterol, bilirubin and enzymes

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21
Q

Liver generates what

A

Heat

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22
Q

What is Hepatitis?

A

Hepatitis: denotes any inflammation of the liver, usually due to acute viral infection. Lifelong immunity to the causative virus usually follows, but since several distinct viruses cause the disease, immunity to one type does not confer immunity to the others

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23
Q

Hepatitis A causes

A

Also known as infectious hepatitis, is transmitted by contaminated food or other objects taken into the mouth, or by unsterile hypodermic needle.

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24
Q

Hepatitis B cause

A

Also known as serum hepatitis, recognised since WWII. Hep B is transmitted by contaminated injections/transfusions and by sexual contact.

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25
Q

Hepatitis C cause

A

‘non-A’ ‘non B’, transmitted in blood or body fluids and caused by a virus which has been cloned, is most common cause of post-transfusion hepatitis.

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26
Q

Hepatitis D cause

A

Hep D, Delta virus, cannot replicate on own needs hep B, has caused epidemics and may be chronic.

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27
Q

Hepatitis E cause

A

Hep E, is transmitted in contaminated drinking water and can cause epidemic form of hepatitis C

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28
Q

Hepatitis Symptoms

A

All begin with fever, usually followed by weakness, loss of appetite, digestive upsets, and muscle pains. The upper abdomen may be painful and tender. Jaundice appears gradually, reaching maximum intensity at two weeks.5% goes on to chronic form. Fatality rate from all types of hepatitis is about 1% but may be higher for Hep B.

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29
Q

What is Jaundice

A

(icterus) yellowing of the skin, conjunctivae and mucous membranes due to raised plasma bilirubin, which is formed from breakdown of haemoglobin.

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30
Q

How many types of Jaundice

A

Two. Unconjugated and conjugated

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31
Q

4 Causes of Jaundice

A

Haemolytic jaundice due to red blood-cell damage
Newborns can have hyperbilirubinemia due to temporary defect in synthesis of enzyme that breaks bile down
Heptocellular due to damaged liver cells either by virus or excessive alcohol.
Obstructive due to physical block of ducts, can be due to gallstones, tumour or inflamation

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32
Q

History taking with jaundice

A

Duration
Previous attacks
Pain
Chills, fevers, systematic symptons
Itching
Exposure to drugs (prescribed or illegal)
Biliary surgery
Anorexia, weight loss
Colour of urine and stool
Contact with other jaundiced people
History of injections or blood transfusions
Occupation

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33
Q

Examination of the Jaundiced patient should include

A

Depth of jaundice
Scratch marks
Signs of chronic liver disease; palmar erythema, clubbing, white nails, dupuytrens contracture, gynaecomastia
Liver; size, shape, surface
Enlarged gallbladder
Splenomegaly
Abdominal mass
Colour of urine and stools

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34
Q

Liver function tests are

A

A variety of blood tests that assess general state of liver and bilary system
True LFT’s serum albumin, prothrombin time.
Tests that are simply markers of liver or bilary tract disease, measuring activity of various enzymes
Specific liver tests e.g. viral serologic tests or autoimmune tests to determine specific cause of liver disease

35
Q

What are total serum protein levels

A

Concentration of total serum proteins outside normal range may occur in variety of circumstances
Increase in serum protein reflect increases in the levels of either of the two major serum proteins albumin and globulin, or increase in both. Generally, significantly increased total protein is seen if blood volume is reduced or in hypergammaglobulinaemia
A decrease in serum total protein reflects decreases in either albumin or globulin, or in both, and indicates a problem with liver function.

36
Q

What is Serum Albumin

A

Serum proteins are only produced in the liver.

Albumin levels are best test of medium to long-term hepatic function.

37
Q

Reduced levels of albumin are a useful indicator of

A

hepatic disease

38
Q

Albumin is made ?

A

Albumin is synthesised by the liver, making 10 to 14g daily to replace albumin degraded.

39
Q

Fluctuating albumin can be caused by

A

Albumin levels may fluctuate for many reasons,of which liver disease is one.
In liver disease, particularly more advanced cases, the amount of all liver proteins decreases and serum albumin levels drop to less than 35 g/l

40
Q

Half life of albumin

A

The half-life is 17 to 20 days, as a result impaired synthesis may take months to become apparent.

41
Q

Increased serum albumin is caused by

A

Increased serum albumin is not natural; Absolute increase may occur artificially by infusion of hyperoncotic albumin. Relative increase may occur if blood becomes concentrated.

42
Q

Decreased level of albumin causes

A

In states of decreased synthesis due to malnutrition, malabsorption, liver disease
Increased loss due to nephrotic syndrome, many GIT conditions, thermal burns.
Increased catabolism due to thyroidtoxicosis, cancer chemotherapy.

43
Q

Serum Globulin is

A

Globulin is increased disproportionately to albumin in states characterised by chronic inflammation and B-lmphyocyte neoplasm.

44
Q

Decreased serum globulin is caused by

A

Decreased globulin may be seen in congenital or acquired hypogammaglobulinaemia

45
Q

Prothrombin time is

A

Defined as the time taken for a fibrin clot to form in plasma under standard conditions. Normal range is approx. 11-13 seconds,

46
Q

Prolonged prothrombin time is caused in which conditions

A

but this is prolonged when liver damage occurs, caused by; bile duct obstruction, cirrhosis, hepatitis, malabsorption of nutrients, vit k defiency, warfarin therapy.

47
Q

Prothrombin time is the best test of short term hepatic function, what factors are produced in the liver

A

factors 11, V11, 1X & X are produced in liver and have short half-lives.

48
Q

Prolonged PT can be caused by what

A

Prolonged PT can be caused by acute liver dysfunction or Vit K deficiency. Retesting 24 hrs after administration of Vit K can eliminate the latter.

49
Q

Gamma-glutamyltransforase (Gamma-GT) tests for

A

Very sensitive test for liver damage,

50
Q

Markedly increased GGT Levels indicate

A

Markedly increased in lesions which cause intrahepatic or extrahepatic obstruction of bile ducts.

51
Q

Slight increase in GGT indicate

A

Lesser elevations are seen in other liver disease and in infections, mononucleosis, hyperthyroidism, myotonic dystrophy
Drugs causing hepatocellular damage and cholestasis may also raise gamma-GT.
although unexpected, unexplained mild elevations are common. Alcohol is often the culprit.

52
Q

Increased Bilirubin levels are caused by

A

Infectious hepatitis
chemically induced damage from alcohol, hydrocarbons and other substances
drugs may damage liver or interrupt bile flow
neoplasm
biliary tract obstruction

53
Q

Decreased bilirubin levels indicate

A

Not usually of any clinical significance although has been observed in IDA

54
Q

Aminotransferase Enzymes types

A

Alanine aminotransferase(ALT)
and
aspartate aminotransferase(AST) are indicators of liver disease.

55
Q

Aminotransferase Enzymes location, cause of increase levels

A

ALT AST Both are located in liver cells and leak out into general circulation when cells damage

56
Q

Which aminotransferase enzyme is more liver specific

A

ALT is more specific to liver as AST may be elevated in heart or muscle disease

57
Q

Difference between acute and chronic ALT AST levels

A

in acute injury ALT & AST may be 100+ times normal, in chronic elevation may be minimal

58
Q

Mild / Moderate elevations of ALT AST causes

A

Mild or moderate elevations are nonspecific and may be caused by wide range of liver disease

ALT & AST are often used to monitor the course of chronic hepatitis and response to treatments, such as prednisolone and interferon

59
Q

Alkaline Phosphatase ((ALP)) increasing indications

A

Elevated in large number of disorders that affect the drainage of bile, gallstones, tumours, alcoholic or drug induced.

It is also found in other organs (bone, intestine) and for this reason GGT is utilized to ensure raised levels is due to liver. GGT will not be elevated in other organ disease.

60
Q

Imaging in acute/chronic liver disease

A

Plain radiography has limited role.
Chest may show subphrenic gas, abnormalities of diaphragmatic contour and related pulmonary disease, including metastes
Abdominal may be useful to show calcified or gas containing lesions (gallstones, chronic pancreatitis, liver abscesses)

61
Q

USS in acute/chronic liver disease is

A

First line imaging in patients with jaundice, right upper quadrant pain, or hepatomegaly.
Non-evasive, inexpensive and quick but requires experience in technique and interpretation.
Good identifying cysts, tumours, pancreatic masses and fluid collections. Visualisation of lower common bile duct and pancreas can be hindered by overlying bowel gas.

62
Q

Computed Tomography in acute/chronic liver disease is

A

Complementary to ultrasongraphy, provides information on liver texture, gallbladder disease, bile duct dilation, and pancreatic disease.

Particularly valuable for detecting small lesions in the liver and pancreas.

63
Q

Liver biopsy is useful when

A

Provides information regarding hepatic lobular architecture and is most helpful in patients with undiagnosed persistent jaundice

64
Q

Bilirubin > 100mol/l =

A

= urgent referral to hospital (Primary care)

65
Q

Bilirubin < 100mol/l + ALP + GGT ^ =

A

obstruction

66
Q

Bilirubin < 100mol/l + ALT^ =

A

hepatitis

67
Q

Hepatitis A IgM + =

A

treat for Hep A

68
Q

Cirrhosis features

A

Focal or diffuse inflammation and liver cell necrosis that causes severe changes in the structure and function of liver cells

Inflamed liver cells compress the liver lobule and cause increased resistance to blood flow and portal hypertension

Liver tissue is regenerated, but not in the normal fashion

Fibrotic changes are irreversible causing liver dysfunction; same clinical S & S of liver failure

69
Q

Causes of Liver Cirrhosis

A

Alcoholic: results from long-term alcohol abuse; (most common)

Biliary: caused by a decrease in bile flow; commonly caused by long-term obstruction of bile ducts

Cardiac: caused by long-term right-sided CHF

Postnecrotic: result from hepatoxins, chemicals, or infection with hepatitis B or C

70
Q

Portal HTN features

A

Fibrosis of the liver structures causes an increase resistance to blood flow within the liver, therefore an elevation in the portal venous pressure
This increase in pressure can cause
varices
ascites
splenomegaly

71
Q

Varices features/ causes

A

Increased pressure in the portal vein is transmitted back to veins which supply it
Most commonly affected are those from the oesophagus and rectum
Increased pressure in these vessels causes varicosities
Varices may rupture causing massive bleeding, exacerbated by disordered clotting

72
Q

Ascities is

A

Accumulation of fluid in the peritoneal cavity

73
Q

Ascities mechanisms include

A

Mechanisms include:
an increase in portal venous pressures
sodium and water retention
decreased blood osmotic pressure due to decreased production of albumin

74
Q

Splenomegaly mechanism

A

Increased portal pressure is transmitted to splenic vein causing enlargement
Increased transit time of blood through enlarged spleen causes increased destruction of all types of blood cell

75
Q

Hepatic failure mechanism

A

Occurs when the liver is unable to perform its many functions

May happen acutely or as result of progressive degeneration

Most often caused by viral hepatitis or cirrhosis

76
Q

Features of Hepatic Failure

A

Hepatomegaly at first and then atrophy of liver

77
Q

Cause of paleness/lethargy in hepatic failure

A

Anaemia due to decreased production or increased haemolysis

78
Q

Cause of Bruising/Haematuria/ GI Bleeds in hepatic failure

A

Clotting disorders due to thrombocytopenia, decrease in clotting factor production and vitamin K absorption

79
Q

Cause of Amenorrhoea, gynaecomastia
Fluid retention in hepatic failure

A
  • Endocrine disorders due to abnormal metabolism of sex hormones and aldosterone
80
Q

Features of hepatic failure : skin disorders include

A

Spider naevi, palmar erythema
Jaundice

81
Q

Features of hepatic failure :Kidney disorders include

A

renal failure

82
Q

Features of hepatic failure :neurological disorders include

A

Hepatic encephalopathy due to failure to convert ammonia
Tremor
Deterioration of mental function leading eventually to coma

83
Q

Features of hepatic failure :portal hypertension complications/ disorders include

A

varices, ascities