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PHAR 255 > Liver > Flashcards

Liver Flashcards

1
Q

Explain liver blood supply

A

Venous flow in from the portal vein
Arterial flow in from the hepatic artery
Venous flow out through the hepatic vein
Connected to the GI tract via portal veins and bile ducts

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2
Q

Major functions of the liver

A

Excretion - bile
Metabolism - bilirubin, drugs, nutrients, hormones
Storage - vitamins/minerals, CHO
Synthesis

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3
Q

Where is bile stored?

A

Gallbladder

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4
Q

Functions of bile

A

Emulsification: dietary fat, cholesterol, vitamins
Elimination of waste: excess cholesterol, xenobiotics, bilirubin

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5
Q

What is enterohepatic recirculation?

A

95% of bile acids are reabsorbed
Some is lost in the feces

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6
Q

What is bilirubin?

A

End product of heme degradation (measured as indirect bilirubin)

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7
Q

Direct bilirubin is:

A

Glucuronidated in the liver
Conjugated bilirubin

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8
Q

Indirect bilirubin is:

A

Bound to albumin

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9
Q

What is the pattern(process) of hepatocellular injury?

A

Necrosis -> degeneration -> inflammation -> may regenerate OR -> fibrosis -> cirrhosis

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10
Q

Etiologies of hepatic injury

A

Viruses (hepatic)
Drugs
Environmental toxins
Alcohol*

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11
Q

What are the two main types of hepatic injury?

A

Cholestasis
Hepatocellular

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12
Q

What is cholestasis?

A

A failure of normal amounts of bile to reach the duodenum
- leads to accumulation of bile in liver cells and biliary passages

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13
Q

Causes of cholestasis

A

Cholelithiasis (gall stones) most common
Tumour
Viral hepatitis
Alcohol related liver disease
Drugs
PBC, PSC

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14
Q

What is PBC?

A

Primary biliary cholangitis
- caused by the slow, immune mediated destruction of small bile ducts within the liver

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15
Q

What is the leading cause of liver transplant in women?

A

PBC - primary biliary cholangitis

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16
Q

What is PSC?

A

Primary sclerosing cholangitis
- involves progressive inflammation and fibrosis affecting any part of the biliary tree -> progressive destruction of bile ducts

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17
Q

What is PSC commonly associated with?

A

Inflammatory bowel disease

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18
Q

What does cholestatic syndrome look like?

A

Pruritis
Jaundice
Dark urine
Light coloured stool
Steatorrhea
Xanthoma and xanthelasma (growths under skin)
Hepatomegaly

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19
Q

What is ursodeoxycholic acid (ursodiol) URSO?

A

Naturally occurring bile acid

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20
Q

What is ursodiol used for?

A

Cholelithiasis management
Also used in PBC or PSC (better for PBC)

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21
Q

What can be used for pruritis associated with cholestasis?

A

Cholestyramine
Antihistamines (for sedative properties)
Naltrexone, rifampin, sertraline (if refractory)

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22
Q

What is hepatocellular damage?

A

Direct damage to hepatocytes
May be acute or chronic

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23
Q

Causes of hepatocellular damage?

A

Toxic agents: alcohol, drugs
Infections: hepatitis
Longstanding cholestasis
Ischemic injury: thrombosis

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24
Q

What is hemochromatosis?

A

Excess iron absorption causing liver damage

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25
Q

How is liver function evaluated?

A

Liver enzyme measurement
Liver function tests (LFTs) - abc’s
- albumin, bilirubin, clotting

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26
Q

What are the liver enzyme measurement tests?

A

ALP
AST
ALT
GGT

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27
Q

What liver enzyme changes would indicate cholestatic injury?

A

Elevations in ALP & GGT

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28
Q

When might ALP also be elevated?

A

If there is high bone turnover

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29
Q

What does elevated GGT confirm?

A

Hepatic origin of ALP because it is a non-specific liver enzyme and is associated with all liver disorders

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30
Q

What liver enzyme changes would indicate hepatocellular injury?

A

Elevated AST and ALT (ALT is more specific then AST)
LDH (but very nonspecific)

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31
Q

What do LFTs test?

A

The synthetic capability of the liver

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32
Q

When are albumin levels reduced?

A

After sustained assault/injury (cirrhosis)

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33
Q

Symptoms of low albumin

A

Edema and ascites

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34
Q

What happens to bilirubin in liver disease?

A

It can be increased

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35
Q

Signs of elevated bilirubin

A

Dark urine
Pale stool
Yellow skin (jaundice)

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36
Q

Causes for elevated bilirubin

A

Obstruction: cholestasis
Impaired metabolism: hepatocellular
Excessive production - hemolytic anemia

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37
Q

What is unconjugated bilirubin?

A

Bound to albumin
Not soluble in water
Measured as indirect

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38
Q

What is conjugated bilirubin?

A

Conjugated by the liver
Soluble in water
Measured as direct

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39
Q

What would happen to ‘clotting’ prothrombin time in liver damage?

A

We would expect it to be increased but its only seen after moderate to significant damage (longer bleeding time)

40
Q

What does it mean if vitamin K is administered and we see improvement in INR?

A

Issue for low clotting (high clotting time) is not associated with the liver (due to vitamin K deficiency)
- no response = problem with liver

41
Q

Can liver enzyme tests tell us the magnitude of liver injury?

A

No. We would have to look at trends for the specific patient

42
Q

What is cirrhosis?

A

Chronic diffuse disease characterized by fibrosis and nodular formation
- result of continuous liver injury

43
Q

What happens to the liver in cirrhosis?

A

Liver becomes hard, shrunken, and nodular
- irreversible fibrosis (scarring)

44
Q

Is there is cure for cirrhosis?

A

Liver transplant

45
Q

What is ALD?

A

Alcohol-related liver disease

46
Q

What is MASLD?

A

Metabolic dysfunction-associated steatotic liver disease
- previously called non-alcoholic fatty liver disease (NAFLD)

47
Q

What is MASH?

A

Metabolic dysfunction-associated steatohepatitis

48
Q

What are the alcohol recommendations from previous Canadian liver foundation?

A

Women: limit alcohol to 2 drinks/day and 10/week
Men: limit alcohol to 3 drinks/day and 15/week

49
Q

What are the new recommendations from CCSA?

A

All levels of alcohol consumption are associated with some risk, so drinking less is better for everyone
Low risk for </= 2 drinks/week
Moderate risk for 3-6 drinks/week
High risk for >/= 6 drinks/week

50
Q

What are the standard drink equivalents?

A

12 oz of beer
12 oz of cider or cooler
5 oz of wine
1 1/2 oz of spirits

51
Q

Diagnostic process for cirrhosis

A

Biochemical markers
Scoring systems using biochemical markers
Abdominal ultrasound
Elastography
Liver biopsy (rarely needed)

52
Q

What does the Fibrosis-4 (FIB-4) score estimate?

A

The amount of scarring in the liver/risk of fibrosis using:
- age
- platelet count
- AST
- ALT

53
Q

What is the AST to platelet ratio index (APRI) used to estimate?

A

Liver fibrosis specifically in patients with hepatitis C

54
Q

What does an elastography determine?

A

Liver stiffness
Stage 2-3 fibrosis = 7-11 kPa
Stage 4 fibrosis (cirrhosis) >11-14 kPa

55
Q

What is the prognosis for cirrhosis?

A

~5-15 years

56
Q

Treatment for cirrhosis

A

Treat specific disease
Treat complications
Liver transplant

57
Q

Presentation of compensated cirrhosis

A

Body functions fairly well
May be asymptomatic
Nonspecific: anorexia, weight loss, weakness, NV, GI upset, muscle wasting
LETs may be abnormal

58
Q

Presentation of decompensated cirrhosis

A

Severe scarring & disruption of function
Confusion, edema, fatigue, bleeding
Abnormal LFTs: INR, albumin, bilirubin
Portal HTN, ascites, varices, encephalopathy

59
Q

Potential findings on lab test with cirrhosis

A

Hypoalbuminemia
Elevated prothrombin time (PT)
Thrombocytopenia
Elevated ALP, AST, ALT, GGT
Elevated bilirubin

60
Q

What causes portal HTN?

A

Blood flow though liver is obstructed and pressure is increased
- portal blood bypasses the liver and directly enters systemic circulation (“portal-to-systemic shunting”)

61
Q

Portal HTN results from:

A

Increase in resistance to portal flow and increase in portal venous inflow

62
Q

What happens to the spleen and blood in portal HTN?

A

Enlarges 3-6x
Increased destruction of RBCs

63
Q

Consequences of portal-to-systemic shunting

A

Malabsorption of fat in the stool (decrease bile flow)
Unable to absorb fat soluble vitamins
Metabolites/toxins in the blood have not been processed by the liver first

64
Q

What is ascites?

A

Collection of fluid in the peritoneal cavity
Can cause massive distension

65
Q

How is newly diagnosed ascites managed?

A

Aspiration of ascitic fluid and lab analysis

66
Q

What does SAAG indicate for ascites?

A

> /= 11g/L is caused by portal HTN
< 11g/L is likely other cause (infection or malignancy)

67
Q

What does total protein concentration indicate for ascites?

A

> 25g/L associated with SAAG >11g/L suggests cardiac dysfunction is the cause

68
Q

Management of ascites

A

Salt restriction
Spironolactone +/- furosemide
Paracentesis - aspiration of peritoneal fluid with needle
TIPS - transjugular intrahepatic portosystemic shunt
Liver transplant

69
Q

What is the dose of Spironolactone and furosemide for ascites?

A

100mg and 40mg OD (AM)
Can titrate q3-5d using ration of 100:40 to max dose of 400mg and 160mg

70
Q

DI of Spironolactone

A

Drugs affecting K+
May increase digoxin levels

71
Q

What should be monitored in diuretic use for ascites?

A

SCr, Na, K
Weight
BP

72
Q

What is spontaneous bacterial peritonitis?

A

Infection in ascitic fluid without obvious cause
Thought to be from bacteria translocation

73
Q

How is spontaneous bacterial peritonitis treated?

A

Empirically treated with positive culture
Broad spectrum empiric therapy
- community acquired: cefotaxime or ceftriaxone x 5d
- nosocomial acquired: piperacillin/tazobactam or meropenem +/- vancomycin
Albumin infusions may be added as well

74
Q

Who should receive prophylaxis treatment for spontaneous bacterial peritonitis?

A

Patients who survived an episode or high risk patients:
- low ascitic fluid total protein ascites or varicella hemorrhage

75
Q

Prophylaxis treatment of SBP

A

Norfloxacin
Septra
Ciprofloxacin

76
Q

What is hepatorenal syndrome?

A

Renal failure in severe liver disease
Characterized by severe vasoconstriction of the renal circulation

77
Q

What should be done for hepatorenal syndrome?

A

Stop diuretics
Avoid potential nephrotoxins

78
Q

Autoimmune hepatitis can cause:

A

Hepatocellular injury

79
Q

What is varices?

A

High pressure in portal vein
Relatively small veins become engorged with an excess of blood

80
Q

What are the principle sites for varices?

A

Veins in rectal area (hemorrhoids)
Abdominal wall (umbilicus)
Esophageal varices

81
Q

What happens with esophageal varices?

A

Veins become enlarged and twisted
Can easily rupture and cause massive bleeding
- medical emergency if it starts to bleed

82
Q

What are the treatment strategies for a variceal bleed?

A

Packed red blood cells
Antibiotic prophylaxis of SBP
Octreotide or somatostatin IV - to stop/slow bleeding
Endoscopic therapies - band ligation, sclerotherapy

83
Q

Who should receive prophylaxis for variceal bleeding

A

Patients with small varices + increased risk of bleeding
Patients with medium/large varices

84
Q

What is the prophylaxis treatment for varices?

A

Propranolol 20mg BID initial -> max: 320mg/day(160mg with ascites)
Nadolol 20mg OD initial -> max: 240mg/day (120mg with ascites)
(Non-selective BBs)
- carvedilol can be used if no response to these

85
Q

Primary and secondary prophylaxis of variceal bleeding

A

Primary: non-selective BB OR
EVL
Secondary: non-selective BB + EVL

86
Q

What is hepatic encephalopathy?

A

CNS dysfunction observed in late-stage cirrhosis

87
Q

What is the cause of hepatic encephalopathy?

A

Accumulation in the bloodstream of neurotoxic substances that are normally removed by the liver
- ammonia
- tryptophan
- GABA’ergic compounds

88
Q

Presentation of encephalopathy

A

Drowsiness, personality changes, confusion, motor symptoms

89
Q

Grade 1 symptoms of encephalopathy

A

Changes in behaviour, mild confusion, slurred speech, disordered sleep
Mild tremor, anxiety, impaired hand writing

90
Q

Grade 2 symptoms of encephalopathy

A

Lethargy, moderate confusion
Ataxia, asterixis, personality changes

91
Q

Grade 3 symptoms of encephalopathy

A

Marked confusion, incoherent speech, sleeping but arousable
Seizures, muscle twitching, delirium, bizarre behaviour

92
Q

Grade 4 symptoms of encephalopathy

A

Coma, unresponsive to pain

93
Q

Therapies for encephalopathy

A

Aimed at lowering ammonia
- Lactulose 15-45ml TID-QID (first line) - 15mL = 10g
- antibiotics

94
Q

What is the general approach to cirrhosis?

A

Discontinue alcohol
Avoid ASA/NSAIDs
Avoid sedatives/narcotics if possible
Adequate nutritional intake
Deficiencies are common

95
Q

What nutrient deficiencies are associated with heavy alcohol use?

A

Thiamine (vitamin B1)
Pyridoxine (vitamin B6)
Folate

PHAR 255 (8 decks)

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