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Exam 4 lecture 3 Flashcards

1
Q

What is the functionality of the liver

A

Bile production
drug/food/toxin metabolism
protein synthesis (including albumin and coagulation factors)
Storage/adjustment of vitamins/gluconeogenesis

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2
Q

What are some objective markers that increase with someone with acute liver injury

A

AST (aspartate transaminase)
ALT (Alanine transaminase)

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3
Q

Name an objective biomarker that increases with biliary tract injury from liver injury

A

Alk Phos
Bilirubin

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4
Q

What are some objective markers that decrease with chronic liver disease, malnutrition, CKD or acute inflammation

A

albumin

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5
Q

How does INR change in liver disease

A

INR increases with chronic liver disease, warfarin or malnutrition

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6
Q

How does thrombocytopenia change with liver disease

A

Decreases with chronic liver disease, HIT or malignancy

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7
Q

ELevated bilirubin can be a sign of

A

Acute or chronic liver issues

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8
Q

Chronic liver disease can decrease liver production, leading to changes in albumin, INR and billirubin. How are they changed

A

decreased albumin
Increased INR
Increased billirubin

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9
Q

What dose of acetaminophen leads to DILI? What does this lead to?

A

doses >8g of acetaminophen can result in toxic levels of N acetyl p benzoquinone imine (NAPQI), which causes direct hepatotoxicity

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10
Q

Signs and symptoms of acetaminophen DILI? What can happen if not managed?

A

symptoms- Abdominal pain, jaundice, N/V/D

If not managed can lead to irreversible liver damage

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11
Q

How do we assess severity of Acetaminophen DILI

A

AST, ALT and acetaminophen concentration.

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12
Q

How do we reverse toxic metabolite of acetaminophen DILI

A

Through use of N-acetylcysteine (NAC) +/- activated charcoal

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13
Q

MOA of NAC (N-acetylcysteine)

A

Binds to NAPQI, decreasing hepatotoxic effects

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14
Q

indication of NAC (N-acetylcysteine)

A

Based on concentration of acetaminophen (>4 hrs after ingestion)

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15
Q

dosing of NAC? Monitoring?

A

oral and IV equal efficacy.
If vomiting- use IV, if not use oral’

monitor- AST, ALT for 24 hrs. Assess s/s of overdose

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16
Q

Define Cirrhosis? MOrtality risk?

A

severe, chronic, irreversible fibrosis of liver

10%

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17
Q

Causative factors of cirrhosis

A

-chronic alcohol use (#1 in US)
-Viral hepatitis
-metabolic liver disease (hemochromatosis, nonalcoholic steatohepatitis)
-cholestatic liver disease (primary biliary cirrhosis)
- drugs (chronic use of amiodarone, methotrexate)

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18
Q

s/s of cirrhosis

A

fatigue, weightloss, pruritis

JAUNDICE

hepatomegaly or splenomegaly
Encephalopathy
Ascitis

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19
Q

complications of cirrhosis

A

Ascites
Esophageal varices (EV)
hepatic encephalopathy (HE)
Spontaneous bacterial peritonitis (SBP)

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20
Q

how to diagnose cirrhosis

A

s/s
markers of hepatic function
hepatic imaging
liver biopsy

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21
Q

what tool assesses severity of cirrhosis

A

Child-pugh score
MELD score (predicts 3 month mortality)

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22
Q

Define Ascites

A

Fluid accumulation in peritoneal space

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23
Q

signs and symptoms of ascites

A

Abdominal pain
Abdominal distention
SOB
nausea

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24
Q

pathophysiology of ascites

A

increased pressure with portal HTN drives fluid into peritoneal space

Compensatory mechanisms from portal HTN results in increased fluid retention

Hypoalbuminemia

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25
goals of care of ascites
minimize fluid accumulation and symptoms reduce need for paracentesis (invasive fluid removal) Limit side effects from therapies prevent complications from uncontrolled ascites
26
ascites non harm management
Sodium restriction (<2 g/day) Assessment for liver transplant
27
1st line tx of ascites
Aldosterone antagonist (spironolactone) + loop diuretic (furosemide) (if u could use only one, use aldosterone antagonist)
28
2nd line tx for ascites
Paracentesis TIPS
29
what meds are contraindicated with cirrhosis
NSAIDs
30
What is the recommended dosing ratio of spiro to furosemide in ascites? Max daily dose? Is combination superior or monotherapy in cirrhosis?
Recommended ratio is 100 spiro : 40 furo max dose is 400 mg spiro/ 160 mg furo combination is superior to monotherapy, if you need to use monotherapy, use spironolactone
31
side effects of aldosterone antagonist and loop diuretic
Aldosterone antagonist -AKI -increased potassium - gynecomastia Loop diuretic - AKI - decreased potassium
32
monitoring in ascites
Accumulation of fluid, SCr, K+
33
What is paracentesis? What is it indicated in?
2nd line for chronic management (can be used acutely in tense ascites) Indicated in refractory/resistant ascites or in case of AKI
34
WHat do we do if we give patient if we remove >5L via paracentesis? Why? How muc should we give?
We give albumin. It has been shown to decrease morbidity and decrease mortality If >5L replace with 6-8 g albumin/L Do not give 5% albumin as that has too much fluid for patient with ascites
35
How is Esophageal varices (EV) caused?
Portal hypertension causes hepatic/splanchnic vasodilation, resulting in decreased perfusion. compensatory "varices" form, dilation of EV occurs and results in variceal bleeding, which can be severe
36
Risk factors for EV
Varices size (larger more likely to rupture) CIrrhosis severity Red color markings noted on endoscopy Active alcohol use
37
Variceal bleeding prophylaxis
Non selective BB Endoscopic variceal ligation (EVL) showed decreased variceal and GI bleeding, but no mortality benefit
38
What is primary prophylaxis for EV
Before they have their actual bleeding. Non selective BB or EVL (NOT combination) NSBB indicated in window of moderate disease (not early or late disease)
39
MOA of why NSBB are good for primary prophyaxis
NSBB block B1, decrease HR and decrease CO B2 antagonist leads to vasoconstriction
40
What are some NSBB? Side effects? Monitoring?
Nadolol Propanolol Carvedilol Side effects- drowsiness or insomnia, bradycardia, hypotension Monitoring- HR goal 55-60 bpm BP: SBP > 90 mm hg s/s of VH (hemorrhage)
41
What is EVL? What is it used for?
It is an endoscopic procedure which bands off varices Used as primary prevention and management of acute variceal bleed
42
Variceal bleeding clinical presentation? (EV and Variceal bleeding)
Esophageal varices is asymptomatic- visualized via endoscopy (EGD) Variceal bleeding -hematemesis melena fatigue lightheaded/dizziness Hypotension
43
treatment of variceal bleeding immediately upon presentation
Blood transfusion Octreotide (somatostatin analog, which is a vasoconstrictor) Antibiotic prophylaxis
44
What is the gold standard treatment of variceal bleeding?
EVL (endoscopic variceal ligation)
45
What to do for variceal bleeding after EVL
secondary prophylaxis indefinitely until decompensated
46
Are PPIs recommended for variceal bleeds
No,
47
MOA of octreotide? indication? Duration?
-Inhibits release of vasodilatory peptides resulting in splanchnic vasoconstriction and decreased blood flow. Indicated in acute variceal bleed (not other types of bleeding) 2-5 day duration based on expert opinion, frequently stopped 24 hrs after
48
Side effects/monitoring of octreotide
Side effects- N/V, HTN, bradycardia, hyperglycemia Monitoring- S/s, BP, HR, BG
49
Are EVL long term solutions for EV? How long within presentation should we do an EVL?
Goal is EVL within 12 hours upon presentation not long term
50
Indication for primary antibiotic prophylaxis in EV
Increased risk of infections with active variceal bleeding
51
What are the antibiotics used in variceal bleeding? SIde effects? Monitoring? duration?
Cephalosporin (Ceftriaxone) Side effects- diarrhea Monitoring- S/s of infection, not renally cleared so do NOT monitor Scr Duration: Untl hemorrhage resolution (max 7 days)
52
therapies NOT recommended in pts with acute EV
Vitamin K (phytonadione), EVEN IF INR ELEVATED
53
What are secondary prophylaxis for varices?
EVL: every 1-4 wks NSBB indefinitely (until decompensated)
54
Initial dosing for Nadolol and propranolol for EV
nadolol- 20-40 mg po daily Propranolol- 20-40 mg PO BID
55
What is SBP caused by? Who is at risk
Spontaneous bacterial peritonitis is caused by bacterial translocation in which bacteria cross intestinal barrier annual risk of SBP in Cirrhosis and ascites is 10-30%
56
SBP clinical presentation
Fever abdominal pain/tenderness Leukocytosis Encephalopathy Asymptomatic
57
How is SBP diagnosed? WHat is cutoff for diagnosis
Therapeurtic paracentesis and analyze for PMNs Ascitic fluid >250 cells PMN = SBP
58
SBP treatment? Monitoring? Duration?
cephalosporin and albumin causes diarrhea Monitoring- s/s of infection (temp, EBC, cultures) Not renally cleared so do NOT monitor SCr duration- 5-7 days
59
WHat is the likelihood that SBP will recur? What to do for secondary prophylaxis
Initiate prophylaxis with antibiotics and avoid PPIs (which increase risk of SBP)
60
What agents to use for secondary prophylaxis of SBP? SIde effects? MOnitoring?
bactrim and cipro Side effects of bactrim - AKI, photosensitivity, hyperkalemia, hyponatremia, steven-johnson syndorme Monitor- SCr, electrolytes, CBC Side effects of Cipro- ANtibiotic resistance, muscoskeletal side effects, QTc prolongation, rash, altered mental status Monitor- Mental status, CBC, renal function Duration: Indefinite
61
What is the estimated incidence of DILI?
0.02%
62
what are some classifications/mechanisms of liver injury?
Direct hepatotoxicity- acetaminophen idiosyncratic hepatotoxicity- beta-lactams, fluoroquinolones, macrolides) indirect- inducing metabolic abnormalities causing non-alcoholic fatty liver disease/steatotic liver disease
63
What medications are at high risk for causing DILI
1. acetaminophen 2. anti- infectives - isoniazid - beta lactam antibiotics - fluoroquinolones - macrilides
64
What is the dose of acetaminophen that could cause OD? What to do if suspected overdose?
>8 g - activated charcoal only if ingested < 1 hour (prevents absorption). but not used if taken hours prior. NAC used if more than 1 hr. use oral NAC
65

Therapeutics (38 decks)

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