Liver Flashcards
1
Q
Where is the liver located?
A
Right upper qaudrant of the abdomen
2
Q
How many lobes are in the liver
A
2
3
Q
What are the lobes of the liver made up of?
A
Lobules
4
Q
Describe the lobules
A
centered on a branch of the hepatic vein
inerconnected by small ducts
5
Q
What is the portal triad?
A
at corners of adjacent lobules; branches of bile duct, portal vein, and hepatic artery
6
Q
What are hepatocytes separated by?
A
sinusoids
7
Q
What does the hepatic duct do?
A
transports bile produced by liver cells to the gallblader and duodenum
8
Q
What % of liver tissue needs to be destroyed before the body is unable to eliminate drugs and toxins?
A
~70%
9
Q
Can liver cells regenerate?
A
Yes
10
Q
what % of CO does the liver take?
A
~25%
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
12
Q
What does the venous flow from the portal vein do?
A
blood comes from small intestine directly to liver, pancreatic venous drainage
13
Q
What does the arterial flow from the hepatic artery do?
A
oxygenates the liver
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
15
Q
Major functions of the liver?
A
Excretion
Metbolism
Storage
Synthesis
16
Q
What does the gallbladder do?
A
stores and concentrates bile
17
Q
What does bile do?
A
emulsification of dietary fat, cholesterol, and vitamins
elimination of waste: excess cholesterol, xenobiotics, bilirubin
18
Q
What % of bile acids are reabsorbed due to enterohepatic recirculation?
A
95%
19
Q
How is bilirubin metabolized?
A
Glucuronidated in liver and excreted in bile
20
Q
What is indirect bilirubin?
A
bilirubin bound to albumin
21
Q
What is direct bilirubin?
A
bilirubin glucuronidated in liver
22
Q
What parameters are needed for the reversal of liver damage?
A
That there isnt destuction of the liver’s capacity to regenerate
23
Q
What is the pattern of hepatocellular injury?
A
necrosis –> degeneration -> inflammation –> regeneration or
necrosis –> degeneration -> inflammation –>fibrosis –> cirrhosis
24
Q
What can cause hepatic injury?
A
viruses
Drugs
Environmental toxins
Alcohol
25
What are the 2 main types of hepatic injury?
cholestasis
Hepatocellular
26
Define cholestasis
a failure of normal amounts of bile to reach the duodenum leading to accumulation of bile in liver cells and biliary passages.
27
What causes cholestasis?
Gall stones (cholelithiasis) - most common
tumor
viral hepatitis
alcohol-related liver disease
drugs
primary biliary cholangitis
primary sclerosing cholangitis
28
What is priamry biliary cholangitis?
slow, immune-mediated destruction of small bile ducts within the liver
29
What is the leading cause of liver transplant for women in Canada?
Primary biliary cholangitis
30
What is primary sclerosing cholangitis?
progressive inflammation and fibrosis affecting any part of the biliary tree
Leads to progressive destruction of bile ducts
Commonly associated with IBD
31
Cholestatic syndrome symptoms?
Pruritis
Jaundice
Dark Urine
Light coloured stools
Steatorrhea
Xanthoma and xanthelasma
Hepatomegaly
32
What is ursodiol used for?
Management of cholelithiasis
33
How does ursodiol work?
unknown MOA but, gradualy dissolves stones in 30-40% of pts
34
What drug can be used alternatively to ursodiol in PBC?
Obeticholic acid
35
Does ursodiol prevent progression of PSC?
Limited efficacy
36
Treatment of pruritis?
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
37
Describe hepatocellular damage.
Direct damage to hepatocytes, can be acute or chronic
38
Causes of hepatocellular damage?
Toxic agents: alcohol, drugs, toxins
Infections (hepatitis)
Longstanding cholestasis
Ischemic injury (thrombosis)
other diseases (autoimmune, iron overload)
39
what happens when hepatocytes are destroyed?
Contents of cell are released into the circulation, can compromise function of liver.
40
Liver enzyme increases that indicate cholestatic injury?
ALP and GGT
41
Liver enzyme increases that indicate hepatocellular injury?
AST and ALT
LDH to LDH5 but very nonspecific
42
What happens to albumin level after a sustained assault on the liver?
Reduced
43
What tests the synthetic capability of the liver?
Albumin Levels
44
Bilirubin retention signs?
Yellow tinge to skin, dark urine, pale stools
45
What happens to prothrombin time if the liver is damaged?
Increases
46
Big 7 lab tests liver?
AST
ALT
ALP
GGT
Bilirubin
Albumin
INR/PTT
47
Cirrhosis?
Fibrosis and nodular formation of liver
48
What is ALD?
Alcohol-related liver disease
49
NAFLD?
non-alcoholic fatty liver disease
50
MASH?
metabolic dysfunction associated steatohepatitis
51
NASH?
non-alcoholic steatohepatitis
52
MASLD?
metabolic disfunction-assocaited steatotic liver disease
53
MeALD?
MASLD and increased alcohol intake
54
Alcohol recomendations (2023)
low risk: <= 2 drinks/week
Moderate risk: 3-6 drinks/week
High risk: > 6 drinks/week
55
Tests done to diagnose cirrhosis?
biochemical markers
AST to platlet ratio index
Abdominal ultrasound
elastography
Liver biopsy(rare)
56
Compensated cirrhosis characteristics?
body function well despite scaring
may be asymptomatic
anorexia, wt loss, wekaness, NV, GI upset, muscle wasting
57
Decompensated cirrhosis characteristics?
severe scarring and disrupted function
confusion, edema, fatigue, bleeding
Abnormal INR, albumin, bilirubin
Signs of portal HTN, ascites, varices, encephalopathy
58
what occurs if blood flow is obstructed in the liver?
portal HTN
59
Describe the portal system?
self-contained, low pressure venous system
60
What can cause portal HTN?
splanchnic dilation
increased NO
RAAS activation
61
what happens to the blood flow in portal HTN?
increased resistance to portal flow, increased portal venous inflow
backflow of blood widens the venous channels
62
portal HTN causing Splenomegaly? symptoms?
Enlargement of spleen, uncomfortable/painful
- increased sequestering and destruction of RBCs
- anemia (Very common in cirrhosis)
- thrombocytopenia
63
Consequences of protal to systemic shunting?
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
64
What is ascites?
collection of fluid in peritoneal cavity
65
How can ascites form?
hydrostatic pressure
hypoalbuminemia (reduced oncotic pressure)
RAAS activation --> salt and water retention
66
What should acites patients be evaluated for?
liver transplant b/c poor prognosis
67
what is SAAG?
serum-ascites albumin gradient
68
what does a SAAG of >11g/L indicate?
portal HTN
69
Is ascites responsive to diureses?
typically no
70
SAAG of >25g/L indication?
cardiac dysfunction
71
Treatment for ascites?
Salt restriction of 2g/day
Spironolactone + furosemide (usually)
Large volume paracentesis, TIPS, or transplant
72
what is sometimes given with paracentesis to help maintain oncotic pressure?
albumin
73
Risks of paracentesis?
abdominal perforation
INFECTION!!!!!!
74
What is TIPS?
transjugular intrahepatic portosystemic shunt;
stent to bypass liver to decrease portal pressure
75
When is fluid restriction recommended in ascites?
if Na is <120-125 mEq/L
76
Cure for ascites?
transplant only
77
Spironolactone dosing and MOA? for ascites
100mg max 400mg
inhibition of aldosterone
Onset 3-5 days
78
Spironolactone monitoring?
hyperkalemia!!!!
dehydration (not common in monotherapy though)
Gynecomastia + other estrogen-like SE's
Can increase digoxin levels
79
Furosemide dosing and MOA? for ascites
40mg OD Max: 160mg
loop-diuretic
80
Cautions with furosemide use in ascites?
over diuresis
hypovolemia
81
Combo dosing titration of spironolactone and furosemide
100:40 to max of 400:160 mg
82
Major important monitoring for ascites diuretic therapy?
K, Na, SCr, wt, BP
83
What is refractory ascites?
unresponsive to Na restriction and high dose diuretics , reoccurence is rapid after paracentesis
84
Treatment of refractory ascites?
serial therapeutic paracentesis +/- albumin
TIPS
Transplant
85
What should be avoided in refractory ascites?
NSAIDs
86
What is the goal of a pts wt with ascites therapy?
gradual wt loss; ~05kg/d if no edema (higher with edema)
assumption is that 1 kg body wt = 1L of fluid
87
What to do if urinary Na is low? high?
Low: more diuresis
High: check for non-adherence to low Na diet
88
What other treatment should be consider w/ ascites?
SBP prophylaxis treatment
89
What is spontaneous bacterial peritonitis? cause?
infection in ascitic fluid without obvious cause
bacteria translocation from gut to blood stream
90
Symptoms of spontaneous bacterial peritonitis?
fever, chills, abdominal pain --> can be asymptomatic
91
3 most common pathogens for spontaneous bacterial peritonitis?
E. coli
Kleb pneumoniae
Strep pneumoniae
92
Diagnosis of spontaneous bacterial peritonitis?
daignostic paracentesis
93
Treatment of community acquired SBP?
Cefotaxime or ceftriaxone x 5 d
94
Treatment of nosocomial acquired SBP?
Piperacillin/tazobactam
meropenem +/- vancomycin
Albumin infusions if needed
95
when should a second ascitic fluid collection be done? why?
q48h after intitation of therapy
Decrease in PMN count by 25% to ensure clincal response
96
Prophylaxis drugs for SBP?
norfloxacin, septra, cipro
97
What is hepatorenal syndrome?
renal failure in pts with severe liver disease
98
Characterization of hepatorenal syndrome?
sever vasoconstriction of renal circulation
99
Is the identifiable pathological changes in the kidneys in hepatorenal syndrome?
No
100
When is hepatorenal system more often seen?
in pts with massive, tense ascites
101
What to do for hepatorenal syndrome?
STOP diuretics, nephrotoxic drugs
Transplant; usually see improvement with transplant
102
What occures for vaices to form?
high pressure in portal vein causing bypasses or shunts that causes small veins to become engorged with an excess of blood
103
Normal portal pressure? at what pressure do varices have a high risk of bleeding?
5-8 mmHg
12mmHg
104
Do we take portal pressure often?
No, very invasive
105
what % of advanced cirrhosis pts have esophageal varices?q
65%
106
What can happen with esophageal varices?
easily rupture and cause massive bleeding
107
Why are esophageal varice ruptures one of the most feared complications of cirrhosis?
hard to stop the bleeding
high risk of recurrent hemorrhage
108
Acute management of a variceal bleed?
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
Treatment strategies of variceal bleeds?
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
When should prophylaxis of variceal bleeding be given?
smal varice + increased risk of bleeding (child pugh C, alcohol use, portal pressure >12mmHg)
medium/ large varices
111
Why use propranolol and nadolol?
unopposed alpha constriction leading to arteriolar splanchnic vasoconstriction
reduces bleeding incidences by up to 50%
112
Precautions with non-selective beta blockers?
asthma
diabetes
refractory ascites (hypotension risk)
beta blocker SE's
113
Dosing of nadolol?
20mg OD max of 240mg/d or 120mg if ascites
titrate every 3-4 days
primarily renally eliminated
114
Dosing for propranolol?
20mg BID max of 320mg/d or 160mg/d with ascites
CYP 1A2 substrate
115
What do you base the titration of beta blockers on?
25% decrease in resting HR or a bpm of 55
116
What other beta-blocker can be used sometimes instead of nadolol and propranolol?
Carvadilol
117
Primary variceal bleeding prophylaxis treatment?
non-selective beta blocker
Endoscopic variceal ligation
118
Secondary varieal bleeding prophylaxis treatment?
non-selective beta blocker
Endoscopic variceal ligation
TIPS if re-bleeding w/ therapy
119
Primary treatment target of hepatic encephalopathy?
Ammonia
120
Grade 1 descriptions of encephalopathy?
changes in behaviour, mild confusion, slurred speech, disordered sleep, mild tremor, anxiety, impaired handwritting
121
Grade 2 descriptions of encephalopathy?
lethargy, moderate confusion, ataxia, asterixis (flapping hand tremor), personality change
122
Grade 3 descriptions of encephalopathy?
marked confusion, incoherent speech, sleeping but arousable, seizures, muscle twitching, delirium, bizarre behaviour
123
Grade 4 descriptions of encephalopathy?
Coma, unresponsive to pain
124
Potential factors of hepatic encephalopathy?
protein intake or GI bleeding
drugs
surgery
alcohol use
infection/sepsis
renal failure
metabolic alkalosis
125
Management of encephalopathy?
correct precipitant factor
restirct dietary protein
avoid CNS depressants
126
DOC for encephalopathy?
lactulose
127
how does lactulose work for encephalopathy?
reduces pH, reducing ammonia absorption and prodcution of urease-producing bacteria
128
Dosing of lactulose?
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
Tolerance issues w/ lactulose?
Very sweet
GI: gas, bloating, nausea, diarrhea
130
ALternative choices to lactulose for encephalopathy?
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
What is associated with long term use of metronidazole?
neuropathy
132
General approach to cirrhosis management?
D/c alcohol
dont use NSAIDs, ASA
avoid sedatives/narcotics
ADequate nutrition
133
What nutritional defeciencies are common in liver disease?
protein and micronutrients b/c of decreased dietary itnake, malabsorption and digestion
134
What deficiency do advanced alcohol related liver disease/ cholestatic disease often have?
Fat soluble vitamins (ADEK)
135
Prevention dose of Thiamine?
200mg/d orally
136
What can thiamine deficiency cause?
Wernicke's encephalopathy
137
suggested supplementation of Vit B6?
2mg od
138
Suggested supplementation of folate?
400 ug od
139
What is an overall suggestion to made about vitamins with a pt who has liver disease?
Consider a multivitamin to help reduce deficiencies
140
What is elevated in asymptomatic hepatitis?
AST and ALT
141
Hepatitis A virus type? transmission?
RNA virus
fecal-oral transmission --> more likely to occur in countries with poor hygiene and overcrowding
142
Hep A vaccines?
Harvix
Avaxim
Vaqta
Twinrex both A and B
143
Symptoms of Hep A?
fever, jaundice, sceral icterus, symptoms last approximately 3 months
144
Hep A Time from exposure to clinical manifestation?
30 days
145
Is hep A chronic?
no, fulminant very rare
146
Antivirals for Hep A?
None, no clear role of pharmacologics for treatment
147
Post-exposure prophylaxis timing?
within 14 days of exposure, Ig given ASAP if vaccine is not available
148
CI with Ig in Hep A?
under 1
149
What type of immunity does Ig give?
passive immunity
150
Idication of + total anti-HAV?
acute, resolved infection or immunity
151
Indication of + anti-HAV IgG?
immunity via previous exposure or vaccination
152
Indication of + anti-HAV IgM?
acute HAV infection
153
Hep B virus type?
DNA virus
154
Hep B transmission?
perinatal, sexual, blood
155
Vaccines for Hep B?
Engerix B
REcombivax HB
Twinrix (A and B)
156
When does revaccination need to reoccur in Hep B?
in hyperresponders, antibody resposne decreases with age in general so may need another booster in elderly
157
Symptoms of Hep B?
most pts subclincal or asymptomatic
jaundice dark urine, white stool, abdominal pain, fatigue, fever, chills, loss of appetite, and pruitus
158
Chance of Hep B being chronic?
90% in neonatal
25-50% in 1-5 years old
10% in adults
159
What other conditions can hep B cause?
fulminant Hep, cirrhosis, hepatic carcinoma
160
HBsAg indication?
+ indicates Hep B infection --> acute or chronic
161
Anti-HBs indication?
marker of immunity if HBsAg also present then Hep B infection persists
162
HBV-DNA indication?
marker of viral replication/infectiity --> used to assess and monitor treatment of chronic Hep B infection
163
Screening for Hep B?
at leas once for over 18
PWID
immunocompromised
incarceration
164
WHen is Hep B treated?
during immune active Hep B (increased Hep B DNA and ALT)
165
Treatment of Hep B?
Interferon (peginterferon alfa-2a) or
Nucleoside analogues ( lamivudine, tenofovir, entecavir, adefovir) suffix: ovir
166
goals of Hep B treatment?
permanent suppression/ elimination of virus
prevent cirrhosis, liver failure, and hepatocellular carcinoma
167
"cure of Hep B" in regards to HBsAg?
defined as HBsAg loss w/ or w/o appearance of antibodies to HBsAg
168
interferon therapy length and success rate?
16-48 weeks, 30% success
169
When is interferons used? advantages?
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
Disadvantages of interferon therapy?
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
Success rate with nucleoside analogues?
90% respond
10-15% develop immunity
40-50% seroconversion in 5yrs depending on agent
172
Advantages of nucleoside analogues?
Safer
fewer SEs
oral pill
173
Disadvantages of nucleoside analogues?
chronic therapy
can take years and may require therapy indefinetly
drug resistance possible
174
main use for lamivudine (heptovir)?
in pregnancy and for prophylaxis for those on immunosuppression
175
Use for adefovir (hepsera)?
less potent, used as add on in lamivudine resistance
176
SEs of adefovir?
nephrotoxicity
hypophosphatemia
177
what is the DOC for Hep B nucleoside analogues?
Tenofovir
- TDF
- TAF
178
Why is tenofovir the DOC? what kind of drug is it?
most potent and low chance of resistance
Both TDF and TAF are prodrugs (purine nucleotide reverse transcriptase)
179
What type of drug is entecavir (baraclude)?
selecive guanosine analogue
180
When should you NOT use entecavir?
to rescue lamivudine as it may confer resistance
181
When is a combo therapy used for Hep B w/ nucleoside analogues
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
Hep C virus type?
ssRNA
183
transmission of Hep C?
perinatal, sexual, blood
perinatal is seen the most
184
Prevalence of Hep C in canada?
0.8% in 2007
185
Symptoms of Hep C?
lots asymptomatic
jaundice, dark urine, white stool, abdominal pain, fatigue, fever, chills, loss of appetite, pruitus
186
what can hep C cause?
chronic hep C (75%)
cirrhosis
hepatocellular cancer
187
Genotypes of hep C?
1-6
188
Anti-HCV indication?
infection, acute or chronic
Remains positive for life despite clearance of infection
189
Why is an additional HCVRNA needed to confirm acute infection?
b/c anti-HCV can be negative within first 6 weeks after exposure
190
HCV RNA by PCR indication?
virus replication activity
191
How should pts be screened?
high risk anti-HCV but, if previously infected and cleared use HCV RNA test instead
192
Harvoni drugs? genotype treatment?
ledipasvir and sofosbuvir
g 1,4,5,6
193
SEs of harvoni?
fatigue, headache, insomnia, nausea
194
DI w/ harvoni?
PPI's
195
Drugs in zepatier? genotypes?
grazoprevir and elbasavir
g1,4
196
What needs to be added to zepatier if genotype 3?
sofosbuvir
197
What needs to be monitored with zepatier?
ALT, transient increase seen around week 8
198
drugs in epclusa?
sofosbuvir and velpatasvir
199
genotypes fro epclusa?
all, some activity against g3 but not always
200
Cure rate of epclusa?
99-100%
201
What might cirrhosis pts require with epclusa?
ribavirin
202
duration of therapy w/ sofosbuvir?
12-24 weeks
203
Disadvantage of sofosbuvir?
accumulation in renal disease, still not great results with g3
204
Maviret drugs?
glecaprevir and pibrentasvir
205
maviret genotype activity?
all 1-6
206
benefits of maviret?
can take w/ food
may be used in severe kidney disease
207
DI w/ epclusa?
acid suppressing drugs
208
Drugs in vosevi?
sofosbuvir, velpatasvir, and voxilaprevir
209
role for vosevi?
treatment failure
210
benefits of vosevi?
all genotypes
can take w/ food
211
when to avoid vosevi use?
in decompensated cirrhosis
212
Usual treatment length for Hep C? (epclusa and maviret used most now)
8-12 weeks
213
who to screen for Hep C?
people born between 1945-75
PWIDs
incarceration
remote blood transfusions
immigrants from endemic countries
214
Hep C screening test procedure?
Hep C antibody
if + Hep C antigen
if + Hep C RNA PCR
215
Suffix of the NS3/4A protease inhibitors?
previr
216
suffix of the NS5B inhibitors?
buvir
217
suffis of the NS5A inhibitors?
asvir
218
Hep D virus type?
RNA virus
219
what does Hep D occur with?
HBV
220
What vaccine covers Hep D?
Hep B vaccines
221
what can Hep D cause?
chronic infection
hepatic carcinoma
cirrhosis
222
Treatment of Hep D?
Peg interferons at standard dosing for minimum 12 months
223
Hep E virus type?
RNA
224
Hep E transmission?
fecal-oral
225
who has a high mortalilty rate w/ Hep E?
pregnant women
226
who is more affected by drug-induced hepatotoxicity?
women
227
Hepatocellular DILI characteristics?
Increased AST and ALT
usually occurs within 1 year of starting drug
Ex: aluperinol
228
What can result from a hepatocellula DILI?
fulminant hepatitis
229
Steatonecrosis DILI characteristics?
increased FA synthesis, hepatocytes become engorged and burst open causing inflammation
Ex: alcohol, tetracycline
230
Fibrosis DILI characteristics?
mild, chronic hepatitis leads to fibrosis which can lead to cirrhosis if drug not d/c
Ex: methotrexate
231
Cholestatic DILI characteristics?
PRevents proper elimination of bile by liver leading to accumulation
increase in ALP
Ex: carbamazepine, erythomycin
232
Clinically significant ALT increase?
> 3x upper limit of normal
233
Clinically significance of bilirubin?
> 2x upper limit of normal
234
R value equation?
(ALT / upper limit normal ALT) /
(ALP / upper limit normal ALP)
235
R value of > 5?
hepatocellular injury
236
R value between 2 and 5?
mixed
237
R value of < 2?
cholestatic injury
238
Intrinsic DILI mechanism?
predictable, direct hepatotoxin where a drug has ability to induce injury in all individuals --> dose dependant or time dependant and reproducable
239
Idiosyncratic DILI mechanism?
unpredictable, variable, further classified into allergic and non-allergic
240
Most common intrinsic DILI drug?
general AST/ALT levels?
Acetaminophen
>3500 5x upper limit usually
241
Acetaminophen liver metabolism?
90% glucuronidated or sulfated
2% CYP450
242
How does acetaminophen toxicity occur?
glucuronidated or sulfated pathway saturated
CYP elimination produces toxic metabolite that is detoxified by glutathione but glutathione becomes quickly depeleted
243
Toxic Acetaminphen produt?
NAPQI
244
4 stages of acetaminophen toxicity?
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
Acetaminophen toxic doses?
ADults: > 7.5g
children: >150mg/kg
246
What does the rumack-mathew nomogram predict?
likelihood of AST/ALT > 1000
247
Gut decontamination options?
Syrup of Ipecac
Activated Charcoal
248
Antidote for acet toxicity?
Acetylcysteine
249
How does acetylcysteine work?
enhances glutathione stores
250
What is the likely cause of non-allergic DILI?
likely caused by toxic metabolites
onset is 1 week- 1 year
Reoccurence can take days to weeks possibly accumulation lag time?
251
Allergic DILI drug examples?
phenytoin, phenobarb, carbamazepine
allopurinol
dapsone, minocycline, propythiourocil
sulfa antibiotics
252
non-allergic DILI examples?
isoniazid
valproic acid
ketoconazole
methyldopa
253
Approach to suspected DILI?
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
Steps to manage suspected DILI?
d/c all potential hepatotoxic drugs
provide supportive care
monitor liver enzymes to ensure the return to normal
255
How does the severity of the child pugh rank?
A least, C worst
256
Is there a risk increase for DILI in pts w/ liver disease?
No, but likelihood for recovery is lower
