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PHAR 255 > Liver > Flashcards

Liver Flashcards

(95 cards)

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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
How is liver function evaluated?
Liver enzyme measurement Liver function tests (LFTs) - abc’s - albumin, bilirubin, clotting
26
What are the liver enzyme measurement tests?
ALP AST ALT GGT
27
What liver enzyme changes would indicate cholestatic injury?
Elevations in ALP & GGT
28
When might ALP also be elevated?
If there is high bone turnover
29
What does elevated GGT confirm?
Hepatic origin of ALP because it is a non-specific liver enzyme and is associated with all liver disorders
30
What liver enzyme changes would indicate hepatocellular injury?
Elevated AST and ALT (ALT is more specific then AST) LDH (but very nonspecific)
31
What do LFTs test?
The synthetic capability of the liver
32
When are albumin levels reduced?
After sustained assault/injury (cirrhosis)
33
Symptoms of low albumin
Edema and ascites
34
What happens to bilirubin in liver disease?
It can be increased
35
Signs of elevated bilirubin
Dark urine Pale stool Yellow skin (jaundice)
36
Causes for elevated bilirubin
Obstruction: cholestasis Impaired metabolism: hepatocellular Excessive production - hemolytic anemia
37
What is unconjugated bilirubin?
Bound to albumin Not soluble in water Measured as indirect
38
What is conjugated bilirubin?
Conjugated by the liver Soluble in water Measured as direct
39
What would happen to ‘clotting’ prothrombin time in liver damage?
We would expect it to be increased but its only seen after moderate to significant damage (longer bleeding time)
40
What does it mean if vitamin K is administered and we see improvement in INR?
Issue for low clotting (high clotting time) is not associated with the liver (due to vitamin K deficiency) - no response = problem with liver
41
Can liver enzyme tests tell us the magnitude of liver injury?
No. We would have to look at trends for the specific patient
42
What is cirrhosis?
Chronic diffuse disease characterized by fibrosis and nodular formation - result of continuous liver injury
43
What happens to the liver in cirrhosis?
Liver becomes hard, shrunken, and nodular - irreversible fibrosis (scarring)
44
Is there is cure for cirrhosis?
Liver transplant
45
What is ALD?
Alcohol-related liver disease
46
What is MASLD?
Metabolic dysfunction-associated steatotic liver disease - previously called non-alcoholic fatty liver disease (NAFLD)
47
What is MASH?
Metabolic dysfunction-associated steatohepatitis
48
What are the alcohol recommendations from previous Canadian liver foundation?
Women: limit alcohol to 2 drinks/day and 10/week Men: limit alcohol to 3 drinks/day and 15/week
49
What are the new recommendations from CCSA?
All levels of alcohol consumption are associated with some risk, so drinking less is better for everyone Low risk for /= 6 drinks/week
50
What are the standard drink equivalents?
12 oz of beer 12 oz of cider or cooler 5 oz of wine 1 1/2 oz of spirits
51
Diagnostic process for cirrhosis
Biochemical markers Scoring systems using biochemical markers Abdominal ultrasound Elastography Liver biopsy (rarely needed)
52
What does the Fibrosis-4 (FIB-4) score estimate?
The amount of scarring in the liver/risk of fibrosis using: - age - platelet count - AST - ALT
53
What is the AST to platelet ratio index (APRI) used to estimate?
Liver fibrosis specifically in patients with hepatitis C
54
What does an elastography determine?
Liver stiffness Stage 2-3 fibrosis = 7-11 kPa Stage 4 fibrosis (cirrhosis) >11-14 kPa
55
What is the prognosis for cirrhosis?
~5-15 years
56
Treatment for cirrhosis
Treat specific disease Treat complications Liver transplant
57
Presentation of compensated cirrhosis
Body functions fairly well May be asymptomatic Nonspecific: anorexia, weight loss, weakness, NV, GI upset, muscle wasting LETs may be abnormal
58
Presentation of decompensated cirrhosis
Severe scarring & disruption of function Confusion, edema, fatigue, bleeding Abnormal LFTs: INR, albumin, bilirubin Portal HTN, ascites, varices, encephalopathy
59
Potential findings on lab test with cirrhosis
Hypoalbuminemia Elevated prothrombin time (PT) Thrombocytopenia Elevated ALP, AST, ALT, GGT Elevated bilirubin
60
What causes portal HTN?
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
Portal HTN results from:
Increase in resistance to portal flow and increase in portal venous inflow
62
What happens to the spleen and blood in portal HTN?
Enlarges 3-6x Increased destruction of RBCs
63
Consequences of portal-to-systemic shunting
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
What is ascites?
Collection of fluid in the peritoneal cavity Can cause massive distension
65
How is newly diagnosed ascites managed?
Aspiration of ascitic fluid and lab analysis
66
What does SAAG indicate for ascites?
>/= 11g/L is caused by portal HTN < 11g/L is likely other cause (infection or malignancy)
67
What does total protein concentration indicate for ascites?
>25g/L associated with SAAG >11g/L suggests cardiac dysfunction is the cause
68
Management of ascites
Salt restriction Spironolactone +/- furosemide Paracentesis - aspiration of peritoneal fluid with needle TIPS - transjugular intrahepatic portosystemic shunt Liver transplant
69
What is the dose of Spironolactone and furosemide for ascites?
100mg and 40mg OD (AM) Can titrate q3-5d using ration of 100:40 to max dose of 400mg and 160mg
70
DI of Spironolactone
Drugs affecting K+ May increase digoxin levels
71
What should be monitored in diuretic use for ascites?
SCr, Na, K Weight BP
72
What is spontaneous bacterial peritonitis?
Infection in ascitic fluid without obvious cause Thought to be from bacteria translocation
73
How is spontaneous bacterial peritonitis treated?
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
Who should receive prophylaxis treatment for spontaneous bacterial peritonitis?
Patients who survived an episode or high risk patients: - low ascitic fluid total protein ascites or varicella hemorrhage
75
Prophylaxis treatment of SBP
Norfloxacin Septra Ciprofloxacin
76
What is hepatorenal syndrome?
Renal failure in severe liver disease Characterized by severe vasoconstriction of the renal circulation
77
What should be done for hepatorenal syndrome?
Stop diuretics Avoid potential nephrotoxins
78
Autoimmune hepatitis can cause:
Hepatocellular injury
79
What is varices?
High pressure in portal vein Relatively small veins become engorged with an excess of blood
80
What are the principle sites for varices?
Veins in rectal area (hemorrhoids) Abdominal wall (umbilicus) Esophageal varices
81
What happens with esophageal varices?
Veins become enlarged and twisted Can easily rupture and cause massive bleeding - medical emergency if it starts to bleed
82
What are the treatment strategies for a variceal bleed?
Packed red blood cells Antibiotic prophylaxis of SBP Octreotide or somatostatin IV - to stop/slow bleeding Endoscopic therapies - band ligation, sclerotherapy
83
Who should receive prophylaxis for variceal bleeding
Patients with small varices + increased risk of bleeding Patients with medium/large varices
84
What is the prophylaxis treatment for varices?
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
Primary and secondary prophylaxis of variceal bleeding
Primary: non-selective BB OR EVL Secondary: non-selective BB + EVL
86
What is hepatic encephalopathy?
CNS dysfunction observed in late-stage cirrhosis
87
What is the cause of hepatic encephalopathy?
Accumulation in the bloodstream of neurotoxic substances that are normally removed by the liver - ammonia - tryptophan - GABA’ergic compounds
88
Presentation of encephalopathy
Drowsiness, personality changes, confusion, motor symptoms
89
Grade 1 symptoms of encephalopathy
Changes in behaviour, mild confusion, slurred speech, disordered sleep Mild tremor, anxiety, impaired hand writing
90
Grade 2 symptoms of encephalopathy
Lethargy, moderate confusion Ataxia, asterixis, personality changes
91
Grade 3 symptoms of encephalopathy
Marked confusion, incoherent speech, sleeping but arousable Seizures, muscle twitching, delirium, bizarre behaviour
92
Grade 4 symptoms of encephalopathy
Coma, unresponsive to pain
93
Therapies for encephalopathy
Aimed at lowering ammonia - Lactulose 15-45ml TID-QID (first line) - 15mL = 10g - antibiotics
94
What is the general approach to cirrhosis?
Discontinue alcohol Avoid ASA/NSAIDs Avoid sedatives/narcotics if possible Adequate nutritional intake Deficiencies are common
95
What nutrient deficiencies are associated with heavy alcohol use?
Thiamine (vitamin B1) Pyridoxine (vitamin B6) Folate

PHAR 255 (8 decks)

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