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PHAR255 > Liver 1 > Flashcards

Liver 1 Flashcards

Hepatic injury, Labs, Cirrhosis

1
Q

Where is the liver located?

A

RUQ of abdomen
-2 lobes made up of thousands of lobules

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2
Q

Describe lobules.

A

centered on a branch of the hepatic vein
interconnected by small ducts
contain hepatocytes, separated by sinusoids
“portal triads” at the corners of adjacent lobules

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3
Q

What makes up a portal triad?

A

branches of the bile duct, portal vein, hepatic artery

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4
Q

What is the role of the hepatic duct?

A

transports bile produced by liver cells to the gallbladder and duodenum

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5
Q

What is the only organ in the body that is capable of regenerating its cells?

A

the liver
-70% of the liver tissue can be destroyed before the body is unable to eliminate drugs and toxins via the liver

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6
Q

How much of our cardiac output does the liver receive?

A

25%
-the liver has a dual blood supply

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7
Q

Describe blood supply to the liver.

A

venous flow in from the portal vein
-from small intestine, pancreatic venous drainage, spleen
arterial flow in from the hepatic artery
-liver oxygenation
venous flow out through the hepatic vein
-blood from both the portal vein and hepatic artery mix together in sinusoids and exits liver

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8
Q

What is the role of the gallbladder?

A

stores and concentrates bile

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9
Q

What are the major functions of the liver?

A

excretion (bile)
metabolism (bilirubin, drugs, nutrients, hormones)
storage (vitamins/minerals (B12, iron), CHO)
synthesis (plasma proteins like albumin)

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10
Q

What are the functions of bile?

A

emulsification: dietary fat, cholesterol, vitamins
elimination of wastes: excess cholesterol, xenobiotics, bilirubin

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11
Q

What is enterohepatic recirculation?

A

bile acids reabsorbed into bloodstream, taken up by hepatocytes, deconjugated and then re-secreted into bile
-95% of bile acids reabsorbed
-pool of bile acids largely remains the same

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12
Q

What is bilirubin?

A

end product of heme degradation
-from breakdown of RBC in spleen/liver

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13
Q

Differentiate between direct and indirect bilirubin.

A

indirect bilirubin=free bilirubin
-insoluble
-bound to albumin for transport to liver
direct bilirubin=conjugated bilirubin
-made by glucuronidation in liver
-excreted in bile

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14
Q

When does liver disease become irreversible?

A

when regeneration capacity is overcome
reversible: damage to the functional cells of the liver without destruction of the livers capacity for regeneration

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15
Q

What is fulminant liver failure?

A

insufficient residual hepatocytes to maintain minimal essential liver functions
-irreversible

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16
Q

Describe the pattern of hepatocellular injury.

A

necrosis–>degeneration–>inflammation
inflammation–>regeneration OR fibrosis
fibrosis–>cirrhosis

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17
Q

What are the etiologies of hepatic injury?

A

viruses
drugs
environmental toxins
alcohol

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18
Q

What are the two main types of hepatic injury?

A

cholestasis
hepatocellular

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19
Q

What is cholestasis?

A

failure of normal amounts of bile to reach the duodenum
leads to accumulation of bile in liver cells and biliary passages (intrahepatic or extrahepatic)

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20
Q

What are the causes of cholestasis?

A

cholelithiasis (gall stones)=most common
tumor, viral hepatitis, alcohol-related liver disease, drugs
PBC, PSC

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21
Q

What is PBC?

A

primary biliary cholangitis
-slow, immune-mediated destruction of small bile ducts within the liver=impaired excretion of bile

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22
Q

What is PSC?

A

primary sclerosing cholangitis
-progressive inflammation and fibrosis affecting any part of the biliary tree
-leads to progressive destruction of bile ducts

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23
Q

What are the symptoms of cholestasis?

A

pruritis
jaundice
dark urine
light coloured stools
xanthoma and xanthelasma
steatorrhea
hepatomegaly

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24
Q

What is the MOA of ursodiol?

A

MOA unclear: decrease cholesterol saturation
-gall stones are formed from supersaturation of cholesterol

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25
Q

What are the uses of ursodiol?

A

cholelithiasis management
-gradual dissolution of stones in 30-40%
chronic forms of cholelithiasis (PBC or PSC)
-improves serum biochemical tests
-limited efficacy in preventing disease progression in PSC

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26
Q

What is a con of ursodiol?

A

stones often recur after d/c

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27
Q

What is an alternative drug that can be used in PBC?

A

obeticholic acid

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28
Q

What is a symptom that is often associated with long standing cholestasis?

A

pruritis

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29
Q

What are the drugs we can use for pruritis due to cholestasis?

A

cholestyramine (best option)
-will benefit about 90% of pts, must be continued as long as pruritis is present
antihistamines (ex: hydroxyzine)
-no proven benefit, sedative properties may help
naltrexone, rifampin, sertraline
-may be tried if refractory

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30
Q

What is hepatocellular damage?

A

direct damage to hepatocytes

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31
Q

What are the causes of hepatocellular damage?

A

toxic agents: alcohol, drugs, toxins
infections: hepatitis
longstanding cholestasis
ischemic injury: thrombosis
other diseases (autoimmune, iron overload)

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32
Q

True or false: hepatocellular damage is chronic

A

false
can be acute or chronic

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33
Q

What does the course of hepatocellular injury depend on?

A

duration of assault
intensity of assault
-massive: fulminant hepatic failure
-mild to moderate: hepatitis

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34
Q

What occurs when hepatocytes are destroyed?

A

contents of cells are released into the circulation
functional ability of the liver may be compromised

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35
Q

What are some conditions which could lead to hepatocellular damage?

A

autoimmune hepatitis
-chronic inflammation of liver, genetic
hemochromatosis
-excessive absorption of iron

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36
Q

What are the two ways to measure liver function?

A

liver enzyme measurement
-testing for enzymes residing inside hepatocytes
liver function tests (ABC)
-evaluate synthetic capacity of liver
-albumin, bilirubin, clotting

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37
Q

Which liver enzymes are released into circulation after injury?

A

ALP
AST
ALT
GGT

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38
Q

How do liver enzymes help us distinguish the type of injury?

A

they are pretty specific to liver cells

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39
Q

Which liver enzymes are elevated with cholestatic injury?

A

ALP
GGT

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40
Q

Where is ALP found?

A

bile duct > hepatocytes
bone

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41
Q

When do we see elevations in GGT?

A

all liver disorders
-confirms hepatic origin of ALP (doesnt tell you much on its own)

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42
Q

Which liver enzymes are elevated with hepatocellular damage?

A

AST and ALT

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43
Q

Describe the aminotransferases.

A

ALT and ALT
-ALT more specific than AST (L for liver)
-poor correlation with severity, prognosis
-may be minimally elevated in cholestatic syndromes

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44
Q

Which liver enzyme is very non-specific and not used?

A

LDH

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45
Q

Describe albumin and the impacts liver diseases poses to normal levels.

A

most abundant plasma protein in the body
-decreases in liver disease
normal life span is ~ 20 days
-reduced levels after sustained assault
-sx: edema, ascites
-impacts on calcium, highly bound drugs

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46
Q

What is the advantage of using pre-albumin level rather than albumin levels?

A

more sensitive and provides more current information

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47
Q

What are the results of bilirubin retention?

A

deposits in skin and tissues
dark urine, pale stools, jaundice

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48
Q

Which coagulation factors are synthesized by the liver?

A

I, II, V, VII, IX, X
-clotting factors drop with liver disease (moderate to significant damage)

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49
Q

What happens to PT if liver is damaged?

A

increased (longer bleeding times)

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50
Q

What are the Big 7 for liver lab tests?

A

liver enzymes:
-AST (RBC, muscle, liver)
-ALT (liver)
cholestatic enzymes:
-ALP (liver, bone, placenta)
-GGT (liver)
liver function:
-albumin
-bilirubin
-INR/PTT

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51
Q

What is cirrhosis?

A

a chronic diffuse diseases characterized by fibrosis and nodular formation
result of continuous liver injury
-takes a long time to develop (unless its fulminant)
liver becomes hard, shrunken, and nodular
-loss of normal structure and function
-irreversible fibrosis

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52
Q

What are the causes of cirrhosis?

A

alcohol
viral
autoimmune
inherited
drugs/toxins
NAFLD

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53
Q

What is MASLD and MASH?

A

metabolic dysfunction-associated steatotic liver disease
-previously known as NAFLD
metabolic dysfunction associated steatohepatitis
-previously known as NASH
fat deposited in liver but not related to alcohol intake, related to insulin resistance and metabolic syndrome

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54
Q

What are the 2023 alcohol recommendations?

A

all lvls of alcohol consumption are associated with some risk
among healthy individuals, there is a continuum of risk:
-negligible/low: < 2 standard drinks/week
-moderate: 3-6 standard drinks/week
-high: > 6 standard drinks/week

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55
Q

Which population has potential for greater health risks from alcohol?

A

women

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56
Q

What are the recommendations for alcohol and pregnancy/breastfeeding?

A

pregnancy: dont drink (pre-conception period as well)
breastfeeding: safest not to drink

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57
Q

How much alcohol is needed to cause cirrhosis?

A

depends:
-how much
-how often
-how long
-pattern of drinking
-body composition, age, drinking experiences, genetics, social factors

58
Q

What are the ways that cirrhosis can be diagnosed?

A

biochemical markers
-for screening
abdominal ultrasound
-first imaging modality recommended
elastography
-new, non-invasive
liver biopsy
-rarely needed now for diagnosis

59
Q

What does cirrhosis result in?

A

decreased functioning liver tissue
-impaired function and diminished reserve
-portal HTN
pts will die ~5-15 years after diagnosis

60
Q

What is a general overview of the treatment for cirrhosis?

A

tx of the specific disease
tx of the complications
liver transplant

61
Q

Differentiate compensated and decompensated cirrhosis.

A

compensated:
-body functions fairly well despite scarring of liver
-may be asymptomatic or non-specific symptoms
-liver enzymes may be abnormal
decompensated:
-severe scarring & disruption of function
-sx: confusion, edema, fatigue, bleeding
-abnormal LFTs
-abnormal exam

62
Q

What are the potential laboratory findings of cirrhosis?

A

hypoalbuminemia
elevated PT
thrombocytopenia
elevated ALP
elevated AST, ALT, GGT
elevated bilirubin

63
Q

What are the potential signs and symptoms of cirrhosis?

A

asymptomatic
splenomegaly
jaundice, palmar erythema, spider nevi
ascites and edema
malaise, anorexia, weight loss
encephalopathy
testicular atrophy, loss of body hair, amenorrhea, gynecomastia

64
Q

What are the complications of cirrhosis?

A

portal HTN
ascites
SBP
hepatorenal syndrome
varices
hepatic encephalopathy

65
Q

True or false: normally the portal system is a high pressure venous system

A

false
normally a low pressure venous system

66
Q

What occurs if blood flow through the liver is obstructed?

A

pressure is increased (portal HTN)
-opens “detours” between the portal and systemic circulation
-blood is diverted around the liver rather than filtered through the liver
-portal blood bypasses liver and directly enters systemic circulation (portal-to-systemic shunting)

67
Q

What is portal HTN the result of?

A

increase in resistance to portal flow and increase in portal venous inflow
-splanchnic dilation
-increase in NO leading to vasodilated state
-RAAS
end up with “back flow” of blood and widening of the venous channels that connect the portal and systemic circulation

68
Q

What can portal HTN cause?

A

splenomegaly
-uncomfortable/painful to the patient
-sequestration and destruction of RBCs (anemia and thrombocytopenia)

69
Q

What are the consequences of portal-to-systemic shunting?

A

portal blood bypassing the liver:
-metabolites/toxins in the blood have not been processed by the liver
-increased sensitivity to noxious substances absorbed from GI tract (encephalopathy)
-malabsorption of fat in the stool
-contributes to other complications (ascites, SBP, varices, hepatorenal syndrome)

70
Q

What are ascites?

A

collection of fluid (up to 20L) in the peritoneal cavity
-can cause massive distention

71
Q

What is the pathogenesis of ascites?

A

hydrostatic pressure
hypoalbuminemia (reduced oncotic pressure)
-hypovolemia–>aldosterone secretion
renal retention of Na+ and water

72
Q

What should patients with ascites be evaluated for and why?

A

liver transplant
-poor prognosis

73
Q

What is an essential step in the management of patients with newly diagnosed ascites?

A

aspiration of ascitic fluid
laboratory analysis: WBC, total protein [ ], albumin

74
Q

What is SAAG?

A

serum-ascites albumin gradient
=serum albumin - ascitic fluid albumin
if > 11g/L: indicates portal HTN
-likely responsive to diuretics
if < 11g/L likely other causes
-not typically responsive to diuretics

75
Q

What does an elevated total protein concentration tell us in the context of ascites?

A

> 25g/L associated with a SAAG of > 11g/L
-suggest cardiac dysfunction as etiology of ascites

76
Q

What are the goals of treating ascites?

A

remove abdominal fluid
prevent symptoms and maintain reasonable QoL

77
Q

What is the management of ascites?

A

mainly focused on symptom management
salt restriction
diuresis
paracentesis
TIPS
liver transplant

78
Q

What should be the salt restriction of a patient with ascites?

A

< 2g/day
10-25% will respond

79
Q

Which diuretics are used for ascites?

A

spironolactone (of choice) & furosemide

80
Q

What is paracentesis?

A

aspiration of peritoneal fluid with a needle
-may help decrease discomfort
-fastest for relief

81
Q

What can occur with a large volume aspiration via paracentesis?

A

fluid steal from the vascular space

82
Q

What is the risk with paracentesis?

A

abdominal perforation and infection

83
Q

What is TIPS?

A

transjugular intrahepatic portosystemic shunt

84
Q

What is the only available cure for ascites?

A

liver transplant

85
Q

Which guidelines are no longer recommended for ascites?

A

bed rest no longer recommended
fluid restriction no longer recommended unless Na+ < 120-125mEq/L

86
Q

What is the MOA of spironolactone?

A

inhibits the effects of aldosterone
-weak diuretic and anti-HTN unless aldosterone levels are high

87
Q

What is the onset of spironolactone?

A

3-5 days

88
Q

What are the safety concerns for spironolactone?

A

hyperkalemia
dehydration (uncommon if monotherapy)
estrogen-like AEs
DI: drugs affecting K+, may increase digoxin lvl

89
Q

What are the safety concerns for furosemide?

A

over-diuresis
hypovolemia (potent diuretic)

90
Q

What is the dosing regimen of diuretics for ascites?

A

spironolactone 100mg
furosemide 40mg
AM dose (OD)

91
Q

What is the dosing titration of diuretics for ascites?

A

100mg:40mg q3-5d
-max 400mg of spironolactone & 160mg furosemide
or start with spironolactone and add on furosemide

92
Q

What are the other diuretics that might be considered for ascites?

A

metolazone
-refractory ascites to spironolactone and furosemide
amiloride
-intolerant to spironolactone

93
Q

What are the monitoring parameters for diuretics for ascites?

A

SCr, Na, K
weights and bp

94
Q

What is refractory ascites?

A

unresponsive to Na-restricted diet and high dose diuretic treatment (400mg spiro and 160mg furosemide)
-recurs rapidly after a therapeutic paracentesis & high-dose diuretics
-poor prognosis

95
Q

Which drugs should be avoided in ascites/cirrhosis in general?

A

NSAIDs

96
Q

What is the treatment for refractory ascites?

A

serial therapeutic paracentesis
TIPS
or liver transplant

97
Q

What are the principles of therapy for ascites?

A

patients should monitor daily weights
-gradual weight loss is the goal
-< 0.5kg/d if no edema, more if edema
-assumes 1kg body weight=1L of fluid
if no response, check urinary sodium
-if low: more diuretic
-if high: non-adherence to low Na diet (counsel)
monitor SCr, Na, K
consider SBP treatment/prophylaxis

98
Q

What is SBP?

A

spontaneous bacterial peritonitis
-infection in ascitic fluid without obvious cause
-thought to be from bacteria translocation

99
Q

What are the symptoms of SBP?

A

fever, chills, abdominal pain, etc
-typical symptoms may be absent

100
Q

What should be done as soon as a patient with ascites and cirrhosis is hospitalized and why?

A

diagnostic paracentesis for SBP
-mortality rates are high and presentation is variable

101
Q

What are the most common pathogens to cause SBP?

A

E coli
Klebsiella pneumoniae
Streptococcus pneumoniae

102
Q

When do we empirically treat for SBP?

A

culture +
PMN > 250/uL
high degree of suspicion (dont wait for culture if unavailable)

103
Q

What is the treatment for SBP?

A

community acquired:
-cefotaxime or ceftriaxone x 5d
nosocomial acquired:
-piperacillin/tazobactam
-meropenem +/- vancomycin

104
Q

When should a second ascitic fluid collection be performed for someone with SBP?

A

48h after initiation of treatment
-clinical response: decrease in PMN by 25%

105
Q

When do we consider prophylaxis for SBP?

A

pts having survived an episode of SBP (secondary prophylaxis)
those at high risk (primary prophylaxis)
-high risk: low ascitic fluid total protein ascites or variceal hemorrhage

106
Q

Which antibiotics are used for SBP prophylaxis?

A

norfloxacin
ciprofloxacin
septra

107
Q

What should occur for the patient after experiencing SBP?

A

referral for liver transplant

108
Q

What is hepatorenal syndrome?

A

renal failure in patients with severe liver disease
-characterized by severe vasoconstriction of renal circulation
-no pathologic changes identifiable in kidney

109
Q

Which patients tend to experience hepatorenal syndrome?

A

patients with massive, tense ascites
-may be precipitated by aggressive diuresis or SBP

110
Q

What is the management of hepatorenal syndrome?

A

stop diuretics
avoid nephrotoxins (ex: NSAIDs, aminoglycosides)

111
Q

What are varices?

A

high pressure in portal vein
-creates bypasses/shunts
relatively small veins become engorged with excess blood

112
Q

What are the principles sites of varices?

A

rectal area
abdominal wall
esophageal

113
Q

What is the poor outcome that can occur with esophageal varices?

A

rupture causing massive bleeding
-complicated by clotting disorders
-causes massive hematemesis
-very difficult to stop the bleeding
-high risk of recurrent hemorrhage

114
Q

Which type of varices are most common in cirrhosis?

A

esophageal

115
Q

What are the treatment goals for the acute management of variceal bleed?

A

adequate blood volume resuscitation
protection of airway from aspiration of blood
prophylaxis against SBP and other infections
control of bleeding
prevention of re-bleeding
preservation of liver function/prevention of hepatic encephalopathy
prevention of AKI

116
Q

What are the treatment strategies for acute variceal bleed?

A

packed RBCs
-resuscitates blood volume
-goal: HgB 70-90g/L
antibiotic prophylaxis for SBP
-all pts with liver disease with GI bleed should receive
-greater chance of infection with bleed
octreotide or somatostatin IV
-vasoconstrictors which decrease splanchnic blood flow
-stops/slow bleeding
-d/c when free of bleed x 24 hrs
endoscopic therapies
-band ligation or sclerotherapy
TIPS
-if failure despite combined endoscopic and pharmacologic therapy

117
Q

Which patients should receive prophylaxis for variceal bleeding?

A

patients with small varices + increased risk of bleeding
patients with medium/large varicies

118
Q

Which drugs are used for prophylaxis of variceal bleeding?

A

nadolol and propranolol

119
Q

What is the MOA of nadolol and propranolol for prevention of variceal bleeding?

A

decreased portal venous pressure via:
-decreased CO
-alpha vasoconstriction

120
Q

What is the effectiveness of propranolol and nadolol for prevention of variceal bleeding?

A

reduces bleeding incidence by up to 50%

121
Q

Differentiate nadolol and propranolol.

A

nadolol:
-initiate 20mg OD, max 240mg/day (120mg with ascites)
-titrate q3-4 days
-minimal CNS effects
-renally excreted
propranolol:
-initial 20mg BID, max 320mg/day (160mg with ascites)
-titrate q3-4 days
-1A2 substrate
titrate both to 25% decrease in resting HR or pulse 55bpm

122
Q

Differentiate therapy for primary prophylaxis and secondary prophylaxis of variceal bleeding.

A

primary prophylaxis:
-NSBB
-EVL (if high risk of bleed, refractory ascites, SBP)
secondary prophylaxis:
-NSBB + EVL
-TIPS for re-bleeding

123
Q

What is hepatic encephalopathy?

A

CNS dysfunction observed in late-stage cirrhosis

124
Q

What is the cause of hepatic encephalopathy?

A

not entirely clear MOA:
-accumulation in the bloodstream of neurotoxic substances that are normally removed by the liver
-substances implicated: ammonia, tryptophan, GABA

125
Q

What is the presentation of hepatic encephalopathy?

A

presentation is variable
-drowsiness, personality changes, confusion
-many sx are reversible with appropriate therapy

126
Q

What are the different severities of hepatic encephalopathy?

A

grade 1:
-changes in behaviour, mild confusion, slurred speech, disordered sleep
-mild tremor, anxiety, impaired hand writing
grade 2:
-lethargy, moderate confusion
-ataxia, asterixis, personality changes
grade 3:
-marked confusion, incoherent speech, sleeping but arousable
-seizures, muscle twitching, delirium, bizarre behavior
grade 4:
-coma, unresponsive to pain

127
Q

What are the precipitating factors for hepatic encephalopathy?

A

protein intake or GI bleeding
drugs (diuretics, sedatives/CNS depressants)
surgery
continued alcohol use
constipation
infection/sepsis
renal failure
hypokalemia and/or metabolic acidosis

128
Q

When should treatment for hepatic encephalopathy begin?

A

ASAP if symptoms appear

129
Q

What is the management of hepatic encephalopathy?

A

identify and correct precipitant
restrict dietary protein
avoid CNS depressants
therapies aimed at lowering blood ammonia
-lactulose, antibiotics

130
Q

True or false: lactulose is absorbed by the gut

A

false

131
Q

What is the MOA of lactulose?

A

degraded by colonic bacteria to formic, acetic, and lactic acids
reduces pH–>reducing ammonia absorption, decreases production of urease-producing bacteria
reduces GI transit time

132
Q

What is the first line therapy for hepatic encephalopathy?

A

lactulose

133
Q

What is the dosage of lactulose for hepatic encephalopathy?

A

15-45ml TID-QID
-MD: 2-3 soft formed stools/day
-can decrease dose once mental state improves, often dc within days to weeks

134
Q

What is the onset of lactulose?

A

12-48 hours

135
Q

What are the adverse effects of lactulose?

A

nausea, gas, bloating, diarrhea

136
Q

What are the alternatives to lactulose for hepatic encephalopathy?

A

metronidazole
-sterilizes GIT & inhibits activity of urease-producing bacteria, decreasing ammonia production
-limited use due to adverse effects
rifaximin
-non absorbable derivative of rifampin
-at least as effective as lactluose
-costly

137
Q

Describe the general approach to care for cirrhosis.

A

discontinue alcohol
avoid ASA/NSAIDs
avoid sedatives/narcotics
adequate nutritional intake (deficiences are common)

138
Q

Which deficiencies are common in liver disease?

A

protein and micronutrients
-multifactorial: decreased intake, malabsorption/digestion
pts with advanced alcoholic-liver disease or cholestatic disease often have deficiencies in fat-soluble vits (ADEK)

139
Q

Describe thiamine (B1) deficiency due to heavy alcohol use.

A

ppl with alcohol-related liver disease at risk because:
-inadequate intake, impaired absorption/utilization, increased requirements
deficiency–>Wernickes Encephalopathy
prevention: 200mg/day

140
Q

Describe pyridoxine (B6) and folate deficiency due to heavy alcohol use.

A

pyridoxine:
-deficiency in 50% of people with AUD
-2mg OD supplementation is suggested
folate:
-deficiency in 2/3 of binge drinkers
-400ug OD supplementation recommended

PHAR255 (24 decks)

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