Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics > Exam 4 lecture 3 > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

AST (aspartate transaminase)
ALT (Alanine transaminase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Alk Phos
Bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does INR change in liver disease

A

INR increases with chronic liver disease, warfarin or malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does thrombocytopenia change with liver disease

A

Decreases with chronic liver disease, HIT or malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ELevated bilirubin can be a sign of

A

Acute or chronic liver issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do we assess severity of Acetaminophen DILI

A

AST, ALT and acetaminophen concentration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do we reverse toxic metabolite of acetaminophen DILI

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA of NAC (N-acetylcysteine)

A

Binds to NAPQI, decreasing hepatotoxic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

indication of NAC (N-acetylcysteine)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define Cirrhosis? MOrtality risk?

A

severe, chronic, irreversible fibrosis of liver

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

s/s of cirrhosis

A

fatigue, weightloss, pruritis

JAUNDICE

hepatomegaly or splenomegaly
Encephalopathy
Ascitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

complications of cirrhosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how to diagnose cirrhosis

A

s/s
markers of hepatic function
hepatic imaging
liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what tool assesses severity of cirrhosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define Ascites

A

Fluid accumulation in peritoneal space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

signs and symptoms of ascites

A

Abdominal pain
Abdominal distention
SOB
nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

goals of care of ascites

A

minimize fluid accumulation and symptoms

reduce need for paracentesis (invasive fluid removal)

Limit side effects from therapies

prevent complications from uncontrolled ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ascites non harm management

A

Sodium restriction (<2 g/day)
Assessment for liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

1st line tx of ascites

A

Aldosterone antagonist (spironolactone) + loop diuretic (furosemide) (if u could use only one, use aldosterone antagonist)

28
Q

2nd line tx for ascites

A

Paracentesis
TIPS

29
Q

what meds are contraindicated with cirrhosis

A

NSAIDs

30
Q

What is the recommended dosing ratio of spiro to furosemide in ascites? Max daily dose? Is combination superior or monotherapy in cirrhosis?

A

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
Q

side effects of aldosterone antagonist and loop diuretic

A

Aldosterone antagonist
-AKI
-increased potassium
- gynecomastia

Loop diuretic
- AKI
- decreased potassium

32
Q

monitoring in ascites

A

Accumulation of fluid, SCr, K+

33
Q

What is paracentesis? What is it indicated in?

A

2nd line for chronic management (can be used acutely in tense ascites)

Indicated in refractory/resistant ascites or in case of AKI

34
Q

WHat do we do if we give patient if we remove >5L via paracentesis? Why? How muc should we give?

A

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
Q

How is Esophageal varices (EV) caused?

A

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
Q

Risk factors for EV

A

Varices size (larger more likely to rupture)
CIrrhosis severity
Red color markings noted on endoscopy
Active alcohol use

37
Q

Variceal bleeding prophylaxis

A

Non selective BB

Endoscopic variceal ligation (EVL) showed decreased variceal and GI bleeding, but no mortality benefit

38
Q

What is primary prophylaxis for EV

A

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
Q

MOA of why NSBB are good for primary prophyaxis

A

NSBB block B1, decrease HR and decrease CO
B2 antagonist leads to vasoconstriction

40
Q

What are some NSBB? Side effects? Monitoring?

A

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
Q

What is EVL? What is it used for?

A

It is an endoscopic procedure which bands off varices

Used as primary prevention and management of acute variceal bleed

42
Q

Variceal bleeding clinical presentation? (EV and Variceal bleeding)

A

Esophageal varices is asymptomatic- visualized via endoscopy (EGD)

Variceal bleeding
-hematemesis
melena
fatigue
lightheaded/dizziness
Hypotension

43
Q

treatment of variceal bleeding immediately upon presentation

A

Blood transfusion
Octreotide (somatostatin analog, which is a vasoconstrictor)
Antibiotic prophylaxis

44
Q

What is the gold standard treatment of variceal bleeding?

A

EVL (endoscopic variceal ligation)

45
Q

What to do for variceal bleeding after EVL

A

secondary prophylaxis indefinitely until decompensated

46
Q

Are PPIs recommended for variceal bleeds

A

No,

47
Q

MOA of octreotide? indication? Duration?

A

-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
Q

Side effects/monitoring of octreotide

A

Side effects- N/V, HTN, bradycardia, hyperglycemia

Monitoring- S/s, BP, HR, BG

49
Q

Are EVL long term solutions for EV? How long within presentation should we do an EVL?

A

Goal is EVL within 12 hours upon presentation

not long term

50
Q

Indication for primary antibiotic prophylaxis in EV

A

Increased risk of infections with active variceal bleeding

51
Q

What are the antibiotics used in variceal bleeding? SIde effects? Monitoring? duration?

A

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
Q

therapies NOT recommended in pts with acute EV

A

Vitamin K (phytonadione), EVEN IF INR ELEVATED

53
Q

What are secondary prophylaxis for varices?

A

EVL: every 1-4 wks
NSBB indefinitely (until decompensated)

54
Q

Initial dosing for Nadolol and propranolol for EV

A

nadolol- 20-40 mg po daily
Propranolol- 20-40 mg PO BID

55
Q

What is SBP caused by? Who is at risk

A

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
Q

SBP clinical presentation

A

Fever
abdominal pain/tenderness
Leukocytosis
Encephalopathy
Asymptomatic

57
Q

How is SBP diagnosed? WHat is cutoff for diagnosis

A

Therapeurtic paracentesis and analyze for PMNs

Ascitic fluid >250 cells PMN = SBP

58
Q

SBP treatment? Monitoring? Duration?

A

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
Q

WHat is the likelihood that SBP will recur? What to do for secondary prophylaxis

A

Initiate prophylaxis with antibiotics and avoid PPIs (which increase risk of SBP)

60
Q

What agents to use for secondary prophylaxis of SBP? SIde effects? MOnitoring?

A

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
Q

What is the estimated incidence of DILI?

A

0.02%

62
Q

what are some classifications/mechanisms of liver injury?

A

Direct hepatotoxicity- acetaminophen
idiosyncratic hepatotoxicity- beta-lactams, fluoroquinolones, macrolides)
indirect- inducing metabolic abnormalities causing non-alcoholic fatty liver disease/steatotic liver disease

63
Q

What medications are at high risk for causing DILI

A
  1. acetaminophen
  2. anti- infectives
    - isoniazid
    - beta lactam antibiotics
    - fluoroquinolones
    - macrilides
64
Q

What is the dose of acetaminophen that could cause OD? What to do if suspected overdose?

A

> 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
Q
A

Therapeutics (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions