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PHAR 255 > Liver > Flashcards

Liver Flashcards

1
Q

Where is the liver located?

A

Right upper qaudrant of the abdomen

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2
Q

How many lobes are in the liver

A

2

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3
Q

What are the lobes of the liver made up of?

A

Lobules

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4
Q

Describe the lobules

A

centered on a branch of the hepatic vein
inerconnected by small ducts

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5
Q

What is the portal triad?

A

at corners of adjacent lobules; branches of bile duct, portal vein, and hepatic artery

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6
Q

What are hepatocytes separated by?

A

sinusoids

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7
Q

What does the hepatic duct do?

A

transports bile produced by liver cells to the gallblader and duodenum

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8
Q

What % of liver tissue needs to be destroyed before the body is unable to eliminate drugs and toxins?

A

~70%

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9
Q

Can liver cells regenerate?

A

Yes

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10
Q

what % of CO does the liver take?

A

~25%

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11
Q

What kind of blood supply does the liver have?

A

a dual lood supply; venous flow in from portal vein, arterial flow in from hepatic artery

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12
Q

What does the venous flow from the portal vein do?

A

blood comes from small intestine directly to liver, pancreatic venous drainage

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13
Q

What does the arterial flow from the hepatic artery do?

A

oxygenates the liver

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14
Q

What does the venous flow out through the hepatic vein do?

A

mixes blood from portal vein and hepatic artery in sinusoids and exits liver

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15
Q

Major functions of the liver?

A

Excretion
Metbolism
Storage
Synthesis

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16
Q

What does the gallbladder do?

A

stores and concentrates bile

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17
Q

What does bile do?

A

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

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18
Q

What % of bile acids are reabsorbed due to enterohepatic recirculation?

A

95%

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19
Q

How is bilirubin metabolized?

A

Glucuronidated in liver and excreted in bile

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20
Q

What is indirect bilirubin?

A

bilirubin bound to albumin

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21
Q

What is direct bilirubin?

A

bilirubin glucuronidated in liver

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22
Q

What parameters are needed for the reversal of liver damage?

A

That there isnt destuction of the liver’s capacity to regenerate

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23
Q

What is the pattern of hepatocellular injury?

A

necrosis –> degeneration -> inflammation –> regeneration or
necrosis –> degeneration -> inflammation –>fibrosis –> cirrhosis

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24
Q

What can cause hepatic injury?

A

viruses
Drugs
Environmental toxins
Alcohol

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25
Q

What are the 2 main types of hepatic injury?

A

cholestasis
Hepatocellular

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26
Q

Define cholestasis

A

a failure of normal amounts of bile to reach the duodenum leading to accumulation of bile in liver cells and biliary passages.

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27
Q

What causes cholestasis?

A

Gall stones (cholelithiasis) - most common
tumor
viral hepatitis
alcohol-related liver disease
drugs
primary biliary cholangitis
primary sclerosing cholangitis

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28
Q

What is priamry biliary cholangitis?

A

slow, immune-mediated destruction of small bile ducts within the liver

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29
Q

What is the leading cause of liver transplant for women in Canada?

A

Primary biliary cholangitis

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30
Q

What is primary sclerosing cholangitis?

A

progressive inflammation and fibrosis affecting any part of the biliary tree
Leads to progressive destruction of bile ducts
Commonly associated with IBD

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31
Q

Cholestatic syndrome symptoms?

A

Pruritis
Jaundice
Dark Urine
Light coloured stools
Steatorrhea
Xanthoma and xanthelasma
Hepatomegaly

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32
Q

What is ursodiol used for?

A

Management of cholelithiasis

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33
Q

How does ursodiol work?

A

unknown MOA but, gradualy dissolves stones in 30-40% of pts

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34
Q

What drug can be used alternatively to ursodiol in PBC?

A

Obeticholic acid

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35
Q

Does ursodiol prevent progression of PSC?

A

Limited efficacy

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36
Q

Treatment of pruritis?

A

Cholestyramine (benefits seen in 90% of pts must be used as long as pruritis is present)
Antihistamines: hydroxyzine; no proven benefit but, their sedative propeties may help
Naltrexone, rifampin or sertraline: may be tried if refractory

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37
Q

Describe hepatocellular damage.

A

Direct damage to hepatocytes, can be acute or chronic

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38
Q

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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39
Q

what happens when hepatocytes are destroyed?

A

Contents of cell are released into the circulation, can compromise function of liver.

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40
Q

Liver enzyme increases that indicate cholestatic injury?

A

ALP and GGT

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41
Q

Liver enzyme increases that indicate hepatocellular injury?

A

AST and ALT
LDH to LDH5 but very nonspecific

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42
Q

What happens to albumin level after a sustained assault on the liver?

A

Reduced

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43
Q

What tests the synthetic capability of the liver?

A

Albumin Levels

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44
Q

Bilirubin retention signs?

A

Yellow tinge to skin, dark urine, pale stools

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45
Q

What happens to prothrombin time if the liver is damaged?

A

Increases

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46
Q

Big 7 lab tests liver?

A

AST
ALT
ALP
GGT
Bilirubin
Albumin
INR/PTT

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47
Q

Cirrhosis?

A

Fibrosis and nodular formation of liver

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48
Q

What is ALD?

A

Alcohol-related liver disease

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49
Q

NAFLD?

A

non-alcoholic fatty liver disease

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50
Q

MASH?

A

metabolic dysfunction associated steatohepatitis

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51
Q

NASH?

A

non-alcoholic steatohepatitis

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52
Q

MASLD?

A

metabolic disfunction-assocaited steatotic liver disease

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53
Q

MeALD?

A

MASLD and increased alcohol intake

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54
Q

Alcohol recomendations (2023)

A

low risk: <= 2 drinks/week
Moderate risk: 3-6 drinks/week
High risk: > 6 drinks/week

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55
Q

Tests done to diagnose cirrhosis?

A

biochemical markers
AST to platlet ratio index
Abdominal ultrasound
elastography
Liver biopsy(rare)

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56
Q

Compensated cirrhosis characteristics?

A

body function well despite scaring
may be asymptomatic
anorexia, wt loss, wekaness, NV, GI upset, muscle wasting

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57
Q

Decompensated cirrhosis characteristics?

A

severe scarring and disrupted function
confusion, edema, fatigue, bleeding
Abnormal INR, albumin, bilirubin
Signs of portal HTN, ascites, varices, encephalopathy

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58
Q

what occurs if blood flow is obstructed in the liver?

A

portal HTN

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59
Q

Describe the portal system?

A

self-contained, low pressure venous system

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60
Q

What can cause portal HTN?

A

splanchnic dilation
increased NO
RAAS activation

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61
Q

what happens to the blood flow in portal HTN?

A

increased resistance to portal flow, increased portal venous inflow
backflow of blood widens the venous channels

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62
Q

portal HTN causing Splenomegaly? symptoms?

A

Enlargement of spleen, uncomfortable/painful
- increased sequestering and destruction of RBCs
- anemia (Very common in cirrhosis)
- thrombocytopenia

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63
Q

Consequences of protal to systemic shunting?

A

metabolites and toxins not processed by liver
increased sensitivity to noxious substances
malabsorption of fat in the stool
decreased bile flow
Contributes to complications like ascites, varices, hepatorenal syndrome

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64
Q

What is ascites?

A

collection of fluid in peritoneal cavity

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65
Q

How can ascites form?

A

hydrostatic pressure
hypoalbuminemia (reduced oncotic pressure)
RAAS activation –> salt and water retention

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66
Q

What should acites patients be evaluated for?

A

liver transplant b/c poor prognosis

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67
Q

what is SAAG?

A

serum-ascites albumin gradient

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68
Q

what does a SAAG of >11g/L indicate?

A

portal HTN

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69
Q

Is ascites responsive to diureses?

A

typically no

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70
Q

SAAG of >25g/L indication?

A

cardiac dysfunction

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71
Q

Treatment for ascites?

A

Salt restriction of 2g/day
Spironolactone + furosemide (usually)
Large volume paracentesis, TIPS, or transplant

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72
Q

what is sometimes given with paracentesis to help maintain oncotic pressure?

A

albumin

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73
Q

Risks of paracentesis?

A

abdominal perforation
INFECTION!!!!!!

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74
Q

What is TIPS?

A

transjugular intrahepatic portosystemic shunt;
stent to bypass liver to decrease portal pressure

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75
Q

When is fluid restriction recommended in ascites?

A

if Na is <120-125 mEq/L

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76
Q

Cure for ascites?

A

transplant only

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77
Q

Spironolactone dosing and MOA? for ascites

A

100mg max 400mg
inhibition of aldosterone
Onset 3-5 days

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78
Q

Spironolactone monitoring?

A

hyperkalemia!!!!
dehydration (not common in monotherapy though)
Gynecomastia + other estrogen-like SE’s
Can increase digoxin levels

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79
Q

Furosemide dosing and MOA? for ascites

A

40mg OD Max: 160mg
loop-diuretic

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80
Q

Cautions with furosemide use in ascites?

A

over diuresis
hypovolemia

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81
Q

Combo dosing titration of spironolactone and furosemide

A

100:40 to max of 400:160 mg

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82
Q

Major important monitoring for ascites diuretic therapy?

A

K, Na, SCr, wt, BP

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83
Q

What is refractory ascites?

A

unresponsive to Na restriction and high dose diuretics , reoccurence is rapid after paracentesis

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84
Q

Treatment of refractory ascites?

A

serial therapeutic paracentesis +/- albumin
TIPS
Transplant

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85
Q

What should be avoided in refractory ascites?

A

NSAIDs

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86
Q

What is the goal of a pts wt with ascites therapy?

A

gradual wt loss; ~05kg/d if no edema (higher with edema)
assumption is that 1 kg body wt = 1L of fluid

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87
Q

What to do if urinary Na is low? high?

A

Low: more diuresis
High: check for non-adherence to low Na diet

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88
Q

What other treatment should be consider w/ ascites?

A

SBP prophylaxis treatment

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89
Q

What is spontaneous bacterial peritonitis? cause?

A

infection in ascitic fluid without obvious cause
bacteria translocation from gut to blood stream

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90
Q

Symptoms of spontaneous bacterial peritonitis?

A

fever, chills, abdominal pain –> can be asymptomatic

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91
Q

3 most common pathogens for spontaneous bacterial peritonitis?

A

E. coli
Kleb pneumoniae
Strep pneumoniae

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92
Q

Diagnosis of spontaneous bacterial peritonitis?

A

daignostic paracentesis

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93
Q

Treatment of community acquired SBP?

A

Cefotaxime or ceftriaxone x 5 d

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94
Q

Treatment of nosocomial acquired SBP?

A

Piperacillin/tazobactam
meropenem +/- vancomycin
Albumin infusions if needed

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95
Q

when should a second ascitic fluid collection be done? why?

A

q48h after intitation of therapy
Decrease in PMN count by 25% to ensure clincal response

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96
Q

Prophylaxis drugs for SBP?

A

norfloxacin, septra, cipro

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97
Q

What is hepatorenal syndrome?

A

renal failure in pts with severe liver disease

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98
Q

Characterization of hepatorenal syndrome?

A

sever vasoconstriction of renal circulation

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99
Q

Is the identifiable pathological changes in the kidneys in hepatorenal syndrome?

A

No

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100
Q

When is hepatorenal system more often seen?

A

in pts with massive, tense ascites

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101
Q

What to do for hepatorenal syndrome?

A

STOP diuretics, nephrotoxic drugs
Transplant; usually see improvement with transplant

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102
Q

What occures for vaices to form?

A

high pressure in portal vein causing bypasses or shunts that causes small veins to become engorged with an excess of blood

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103
Q

Normal portal pressure? at what pressure do varices have a high risk of bleeding?

A

5-8 mmHg
12mmHg

104
Q

Do we take portal pressure often?

A

No, very invasive

105
Q

what % of advanced cirrhosis pts have esophageal varices?q

A

65%

106
Q

What can happen with esophageal varices?

A

easily rupture and cause massive bleeding

107
Q

Why are esophageal varice ruptures one of the most feared complications of cirrhosis?

A

hard to stop the bleeding
high risk of recurrent hemorrhage

108
Q

Acute management of a variceal bleed?

A

packed RBCs: resuscitate blood volume : hgb target of 70-90 g/L
antibiotic prophylaxis of SBP: ceftriaxone, cirpo, septra, or norfloxacin
Octreotide or somatostatin IV: to slow/ stop bleeding, d/c once free of bleeding for q24h

109
Q

Treatment strategies of variceal bleeds?

A

band ligation –> > control of hemorrhage and less risk of rebleeding, decreased AE’s chance
Sclerotherapy via injecting sclerosing agents
TIPS for pts unable to maintain hemostasis despite combined endoscopic and pharmacological therapy

110
Q

When should prophylaxis of variceal bleeding be given?

A

smal varice + increased risk of bleeding (child pugh C, alcohol use, portal pressure >12mmHg)
medium/ large varices

111
Q

Why use propranolol and nadolol?

A

unopposed alpha constriction leading to arteriolar splanchnic vasoconstriction
reduces bleeding incidences by up to 50%

112
Q

Precautions with non-selective beta blockers?

A

asthma
diabetes
refractory ascites (hypotension risk)
beta blocker SE’s

113
Q

Dosing of nadolol?

A

20mg OD max of 240mg/d or 120mg if ascites
titrate every 3-4 days
primarily renally eliminated

114
Q

Dosing for propranolol?

A

20mg BID max of 320mg/d or 160mg/d with ascites
CYP 1A2 substrate

115
Q

What do you base the titration of beta blockers on?

A

25% decrease in resting HR or a bpm of 55

116
Q

What other beta-blocker can be used sometimes instead of nadolol and propranolol?

A

Carvadilol

117
Q

Primary variceal bleeding prophylaxis treatment?

A

non-selective beta blocker
Endoscopic variceal ligation

118
Q

Secondary varieal bleeding prophylaxis treatment?

A

non-selective beta blocker
Endoscopic variceal ligation
TIPS if re-bleeding w/ therapy

119
Q

Primary treatment target of hepatic encephalopathy?

A

Ammonia

120
Q

Grade 1 descriptions of encephalopathy?

A

changes in behaviour, mild confusion, slurred speech, disordered sleep, mild tremor, anxiety, impaired handwritting

121
Q

Grade 2 descriptions of encephalopathy?

A

lethargy, moderate confusion, ataxia, asterixis (flapping hand tremor), personality change

122
Q

Grade 3 descriptions of encephalopathy?

A

marked confusion, incoherent speech, sleeping but arousable, seizures, muscle twitching, delirium, bizarre behaviour

123
Q

Grade 4 descriptions of encephalopathy?

A

Coma, unresponsive to pain

124
Q

Potential factors of hepatic encephalopathy?

A

protein intake or GI bleeding
drugs
surgery
alcohol use
infection/sepsis
renal failure
metabolic alkalosis

125
Q

Management of encephalopathy?

A

correct precipitant factor
restirct dietary protein
avoid CNS depressants

126
Q

DOC for encephalopathy?

A

lactulose

127
Q

how does lactulose work for encephalopathy?

A

reduces pH, reducing ammonia absorption and prodcution of urease-producing bacteria

128
Q

Dosing of lactulose?

A

15-45mL TID-QID
Onset of 12-48hrs
Maintenance dose based on mental state improvement and 2-3 soft stools/day
Can be d/c after improvement but usually on long term (prophylaxis)

129
Q

Tolerance issues w/ lactulose?

A

Very sweet
GI: gas, bloating, nausea, diarrhea

130
Q

ALternative choices to lactulose for encephalopathy?

A

Metronidazole: limited b/c AE’s
Rifaximin: costly but, EDS now in Sask but, second line and can be used in combo w/ lactulose

131
Q

What is associated with long term use of metronidazole?

A

neuropathy

132
Q

General approach to cirrhosis management?

A

D/c alcohol
dont use NSAIDs, ASA
avoid sedatives/narcotics
ADequate nutrition

133
Q

What nutritional defeciencies are common in liver disease?

A

protein and micronutrients b/c of decreased dietary itnake, malabsorption and digestion

134
Q

What deficiency do advanced alcohol related liver disease/ cholestatic disease often have?

A

Fat soluble vitamins (ADEK)

135
Q

Prevention dose of Thiamine?

A

200mg/d orally

136
Q

What can thiamine deficiency cause?

A

Wernicke’s encephalopathy

137
Q

suggested supplementation of Vit B6?

A

2mg od

138
Q

Suggested supplementation of folate?

A

400 ug od

139
Q

What is an overall suggestion to made about vitamins with a pt who has liver disease?

A

Consider a multivitamin to help reduce deficiencies

140
Q

What is elevated in asymptomatic hepatitis?

A

AST and ALT

141
Q

Hepatitis A virus type? transmission?

A

RNA virus
fecal-oral transmission –> more likely to occur in countries with poor hygiene and overcrowding

142
Q

Hep A vaccines?

A

Harvix
Avaxim
Vaqta
Twinrex both A and B

143
Q

Symptoms of Hep A?

A

fever, jaundice, sceral icterus, symptoms last approximately 3 months

144
Q

Hep A Time from exposure to clinical manifestation?

A

30 days

145
Q

Is hep A chronic?

A

no, fulminant very rare

146
Q

Antivirals for Hep A?

A

None, no clear role of pharmacologics for treatment

147
Q

Post-exposure prophylaxis timing?

A

within 14 days of exposure, Ig given ASAP if vaccine is not available

148
Q

CI with Ig in Hep A?

A

under 1

149
Q

What type of immunity does Ig give?

A

passive immunity

150
Q

Idication of + total anti-HAV?

A

acute, resolved infection or immunity

151
Q

Indication of + anti-HAV IgG?

A

immunity via previous exposure or vaccination

152
Q

Indication of + anti-HAV IgM?

A

acute HAV infection

153
Q

Hep B virus type?

A

DNA virus

154
Q

Hep B transmission?

A

perinatal, sexual, blood

155
Q

Vaccines for Hep B?

A

Engerix B
REcombivax HB
Twinrix (A and B)

156
Q

When does revaccination need to reoccur in Hep B?

A

in hyperresponders, antibody resposne decreases with age in general so may need another booster in elderly

157
Q

Symptoms of Hep B?

A

most pts subclincal or asymptomatic
jaundice dark urine, white stool, abdominal pain, fatigue, fever, chills, loss of appetite, and pruitus

158
Q

Chance of Hep B being chronic?

A

90% in neonatal
25-50% in 1-5 years old
10% in adults

159
Q

What other conditions can hep B cause?

A

fulminant Hep, cirrhosis, hepatic carcinoma

160
Q

HBsAg indication?

A

+ indicates Hep B infection –> acute or chronic

161
Q

Anti-HBs indication?

A

marker of immunity if HBsAg also present then Hep B infection persists

162
Q

HBV-DNA indication?

A

marker of viral replication/infectiity –> used to assess and monitor treatment of chronic Hep B infection

163
Q

Screening for Hep B?

A

at leas once for over 18
PWID
immunocompromised
incarceration

164
Q

WHen is Hep B treated?

A

during immune active Hep B (increased Hep B DNA and ALT)

165
Q

Treatment of Hep B?

A

Interferon (peginterferon alfa-2a) or
Nucleoside analogues ( lamivudine, tenofovir, entecavir, adefovir) suffix: ovir

166
Q

goals of Hep B treatment?

A

permanent suppression/ elimination of virus
prevent cirrhosis, liver failure, and hepatocellular carcinoma

167
Q

“cure of Hep B” in regards to HBsAg?

A

defined as HBsAg loss w/ or w/o appearance of antibodies to HBsAg

168
Q

interferon therapy length and success rate?

A

16-48 weeks, 30% success

169
Q

When is interferons used? advantages?

A

in pts w/ lower HBV DNA levels an elevated serum aminotransferase values
Advantages:
- shorter course of therapy
- absence of resistance
- a chance at full seroconversion

170
Q

Disadvantages of interferon therapy?

A

Lots of SEs
contraindicated in decompensated cirrhosis
increased risk of life-threatening infection and possible worsening of hepatic decompensation
SQ injection
influenza like illness, emotional liability, myleosuppressive effects, hyper/hypothyroidism

171
Q

Success rate with nucleoside analogues?

A

90% respond
10-15% develop immunity
40-50% seroconversion in 5yrs depending on agent

172
Q

Advantages of nucleoside analogues?

A

Safer
fewer SEs
oral pill

173
Q

Disadvantages of nucleoside analogues?

A

chronic therapy
can take years and may require therapy indefinetly
drug resistance possible

174
Q

main use for lamivudine (heptovir)?

A

in pregnancy and for prophylaxis for those on immunosuppression

175
Q

Use for adefovir (hepsera)?

A

less potent, used as add on in lamivudine resistance

176
Q

SEs of adefovir?

A

nephrotoxicity
hypophosphatemia

177
Q

what is the DOC for Hep B nucleoside analogues?

A

Tenofovir
- TDF
- TAF

178
Q

Why is tenofovir the DOC? what kind of drug is it?

A

most potent and low chance of resistance
Both TDF and TAF are prodrugs (purine nucleotide reverse transcriptase)

179
Q

What type of drug is entecavir (baraclude)?

A

selecive guanosine analogue

180
Q

When should you NOT use entecavir?

A

to rescue lamivudine as it may confer resistance

181
Q

When is a combo therapy used for Hep B w/ nucleoside analogues

A

ppl w/ cirrhosis and who have resistance and could have fatal flares
generally add on such as:
- lamivudine and tenofovir or tenofovir and entecavir

182
Q

Hep C virus type?

A

ssRNA

183
Q

transmission of Hep C?

A

perinatal, sexual, blood
perinatal is seen the most

184
Q

Prevalence of Hep C in canada?

A

0.8% in 2007

185
Q

Symptoms of Hep C?

A

lots asymptomatic
jaundice, dark urine, white stool, abdominal pain, fatigue, fever, chills, loss of appetite, pruitus

186
Q

what can hep C cause?

A

chronic hep C (75%)
cirrhosis
hepatocellular cancer

187
Q

Genotypes of hep C?

A

1-6

188
Q

Anti-HCV indication?

A

infection, acute or chronic
Remains positive for life despite clearance of infection

189
Q

Why is an additional HCVRNA needed to confirm acute infection?

A

b/c anti-HCV can be negative within first 6 weeks after exposure

190
Q

HCV RNA by PCR indication?

A

virus replication activity

191
Q

How should pts be screened?

A

high risk anti-HCV but, if previously infected and cleared use HCV RNA test instead

192
Q

Harvoni drugs? genotype treatment?

A

ledipasvir and sofosbuvir
g 1,4,5,6

193
Q

SEs of harvoni?

A

fatigue, headache, insomnia, nausea

194
Q

DI w/ harvoni?

A

PPI’s

195
Q

Drugs in zepatier? genotypes?

A

grazoprevir and elbasavir
g1,4

196
Q

What needs to be added to zepatier if genotype 3?

A

sofosbuvir

197
Q

What needs to be monitored with zepatier?

A

ALT, transient increase seen around week 8

198
Q

drugs in epclusa?

A

sofosbuvir and velpatasvir

199
Q

genotypes fro epclusa?

A

all, some activity against g3 but not always

200
Q

Cure rate of epclusa?

A

99-100%

201
Q

What might cirrhosis pts require with epclusa?

A

ribavirin

202
Q

duration of therapy w/ sofosbuvir?

A

12-24 weeks

203
Q

Disadvantage of sofosbuvir?

A

accumulation in renal disease, still not great results with g3

204
Q

Maviret drugs?

A

glecaprevir and pibrentasvir

205
Q

maviret genotype activity?

A

all 1-6

206
Q

benefits of maviret?

A

can take w/ food
may be used in severe kidney disease

207
Q

DI w/ epclusa?

A

acid suppressing drugs

208
Q

Drugs in vosevi?

A

sofosbuvir, velpatasvir, and voxilaprevir

209
Q

role for vosevi?

A

treatment failure

210
Q

benefits of vosevi?

A

all genotypes
can take w/ food

211
Q

when to avoid vosevi use?

A

in decompensated cirrhosis

212
Q

Usual treatment length for Hep C? (epclusa and maviret used most now)

A

8-12 weeks

213
Q

who to screen for Hep C?

A

people born between 1945-75
PWIDs
incarceration
remote blood transfusions
immigrants from endemic countries

214
Q

Hep C screening test procedure?

A

Hep C antibody
if + Hep C antigen
if + Hep C RNA PCR

215
Q

Suffix of the NS3/4A protease inhibitors?

A

previr

216
Q

suffix of the NS5B inhibitors?

A

buvir

217
Q

suffis of the NS5A inhibitors?

A

asvir

218
Q

Hep D virus type?

A

RNA virus

219
Q

what does Hep D occur with?

A

HBV

220
Q

What vaccine covers Hep D?

A

Hep B vaccines

221
Q

what can Hep D cause?

A

chronic infection
hepatic carcinoma
cirrhosis

222
Q

Treatment of Hep D?

A

Peg interferons at standard dosing for minimum 12 months

223
Q

Hep E virus type?

A

RNA

224
Q

Hep E transmission?

A

fecal-oral

225
Q

who has a high mortalilty rate w/ Hep E?

A

pregnant women

226
Q

who is more affected by drug-induced hepatotoxicity?

A

women

227
Q

Hepatocellular DILI characteristics?

A

Increased AST and ALT
usually occurs within 1 year of starting drug
Ex: aluperinol

228
Q

What can result from a hepatocellula DILI?

A

fulminant hepatitis

229
Q

Steatonecrosis DILI characteristics?

A

increased FA synthesis, hepatocytes become engorged and burst open causing inflammation
Ex: alcohol, tetracycline

230
Q

Fibrosis DILI characteristics?

A

mild, chronic hepatitis leads to fibrosis which can lead to cirrhosis if drug not d/c
Ex: methotrexate

231
Q

Cholestatic DILI characteristics?

A

PRevents proper elimination of bile by liver leading to accumulation
increase in ALP
Ex: carbamazepine, erythomycin

232
Q

Clinically significant ALT increase?

A

> 3x upper limit of normal

233
Q

Clinically significance of bilirubin?

A

> 2x upper limit of normal

234
Q

R value equation?

A

(ALT / upper limit normal ALT) /
(ALP / upper limit normal ALP)

235
Q

R value of > 5?

A

hepatocellular injury

236
Q

R value between 2 and 5?

A

mixed

237
Q

R value of < 2?

A

cholestatic injury

238
Q

Intrinsic DILI mechanism?

A

predictable, direct hepatotoxin where a drug has ability to induce injury in all individuals –> dose dependant or time dependant and reproducable

239
Q

Idiosyncratic DILI mechanism?

A

unpredictable, variable, further classified into allergic and non-allergic

240
Q

Most common intrinsic DILI drug?
general AST/ALT levels?

A

Acetaminophen
>3500 5x upper limit usually

241
Q

Acetaminophen liver metabolism?

A

90% glucuronidated or sulfated
2% CYP450

242
Q

How does acetaminophen toxicity occur?

A

glucuronidated or sulfated pathway saturated
CYP elimination produces toxic metabolite that is detoxified by glutathione but glutathione becomes quickly depeleted

243
Q

Toxic Acetaminphen produt?

A

NAPQI

244
Q

4 stages of acetaminophen toxicity?

A

stage 1: GI symptoms within 24hrs
stage 2: 24-72 hrs, resolution of stage 1 symptoms, onset of RUQ pain, increased bilirubin PT and transaminases
stage 3: 72-96hrs, asymptomatic to fulminant hepatic failure, AST and ALT peak (100x normal), death if it occurs at 3-5 days after ingestion
stage 4: recovery stage, symptoms subside, and levels normalize. no chronic hepatic dysfunction in survivors

245
Q

Acetaminophen toxic doses?

A

ADults: > 7.5g
children: >150mg/kg

246
Q

What does the rumack-mathew nomogram predict?

A

likelihood of AST/ALT > 1000

247
Q

Gut decontamination options?

A

Syrup of Ipecac
Activated Charcoal

248
Q

Antidote for acet toxicity?

A

Acetylcysteine

249
Q

How does acetylcysteine work?

A

enhances glutathione stores

250
Q

What is the likely cause of non-allergic DILI?

A

likely caused by toxic metabolites
onset is 1 week- 1 year
Reoccurence can take days to weeks possibly accumulation lag time?

251
Q

Allergic DILI drug examples?

A

phenytoin, phenobarb, carbamazepine
allopurinol
dapsone, minocycline, propythiourocil
sulfa antibiotics

252
Q

non-allergic DILI examples?

A

isoniazid
valproic acid
ketoconazole
methyldopa

253
Q

Approach to suspected DILI?

A

take med history
examin labs and identify type of liver injury
symptoms presented?
assess if alternate cause
consider onset and drug timing
Se’s go away after rug d/c

254
Q

Steps to manage suspected DILI?

A

d/c all potential hepatotoxic drugs
provide supportive care
monitor liver enzymes to ensure the return to normal

255
Q

How does the severity of the child pugh rank?

A

A least, C worst

256
Q

Is there a risk increase for DILI in pts w/ liver disease?

A

No, but likelihood for recovery is lower

PHAR 255 (14 decks)

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