Brainscape's Knowledge GenomeTM

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


See full index

GI/Hepatic Final > Alcohol withdrawal/Alcohol Liver Disease, NAFLD, and NASH > Flashcards

Alcohol withdrawal/Alcohol Liver Disease, NAFLD, and NASH Flashcards

1
Q

What is the CAGE questionnaire?

A

Tool for detecting individuals more likely to be abusing alcohol and therefor at a greater risk for alcohol withdrawal
>/= positive answers in an increased likelihood of alcohol abuse with a sensitivity of 71% and specificity of 90%

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

What does the C stand for in CAGE questionnaire?

A

Do you ever feel the need to Calm down on your alcohol use?

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

What does the A stand for in CAGE questionnaire?

A

Have you ever been Annoyed by others telling you that you drink too much?

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

What does the G stand for in CAGE questionnaire?

A

Have you ever felt Guilty about your drinking or something you did while were drinking?

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

What does the E stand for in CAGE questionnaire?

A

Do you ever have an Eye opened?

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

What are the different stages of alcohol poisoning with increasing doses?

A 
Sedation
Sleep
Unconsciousness
Coma
Surgical anesthesia
Fatal respiratory depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What neurotransmitters does alcohol affect?

A

Endogenous opiates, GABA, glutamine, DA and seotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is GABA

A

Major inhibitory neurotransmitter
Acute intoxication causes a release of GABA
Alcohol withdrawal can be considered a GABA deficient state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is glutamate?

A

Major excitatory neurotransmitter in the brain that is linked with memory formation and learning
Alcohol decreases the binding ability of glutamate to NMDA
Chronic users upregulate NMDA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is DA?

A

Reward system of the brain

Acute ingestion causes an increase in synaptic DA

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

What is serotonin?

A

Contributes to the nausea associated with alcohol

Might also affect the happiness that one feels while consuming alcohol

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

What are the s/sx of alcohol intoxication?

A

Sx - slurred speech, ataxia, sedated or unconcious

Signs - nystagmous, tachycardia, diaphoresis, or hyperthermia

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

How much ethanol is required to raise BAC?

A

14 grams of ethanol increases the BAC 0.02-0.025% in an average 70 kg male

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

What are the beverage equivalents in alcohol consumption?

A

14 grams of ethanol =
12 oz can of beer
4 oz glass of wine
1.5 oz shot of whiskey

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the diagnostic tests for alcohol consumption?

A

BAC
Full toxicologic screen to rule out other substances
CMP to evaluate electrolyte imbalances and deficiencies
CT on any patient w/focal neurologic findings, failure to improve, new onset seizures, or altered mental status is out of proportion to degree of intoxication

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

What are SE of BAC 0.02-0.09%?

A 
Euphoria
Loss of shyness
Feeling of well-being
Relaxation
Lower inhibition
Minor impairment of reasoning and memory
Slight impairment of balance
Speech
Vision
Reaction time and hearing
Judgement and self-control are reduced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the SE of BAC 0.10-0.24%?

A

Significant impairment of motor coordination and loss of good judgement
Speech can be slurred
Gross motor impairment
Lack of physical control
Euphoria is reduced and dysphoria is beginning to appear
Nausea begins to appear
The drinker is commonly referred to as a “sloppy drunk”

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

What are the SE of BAC 0.25-0.40%

A

Needs assistance in walking, total mental confusion, and loss of consciousness

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

What are the SE of BAC > 0.40%?

A

Onset of coma

Possible death caused by respiratory arrest

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

What is PK of alcohol?

A

Ethanol is absorbed w/in 5-10 minutes
Serum peak concentration are 30-90 minutes after consumption
On average the BAC is lowered by 15-22 mg/dl per hour in a non-tolerant individual
Ethanol follows zero order kinetics

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

How is alcohol metabolized?

A

90% metabolized by alcohol dehydrogenase in the liver to acetaldehyde which is further broken down to acetate by aldehyde dehydrogenase
Remaining 10% by catalase and 2E1
Acetaldehyde is a known toxin to the liver, pancreas, brain and GIT

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

What may be present after 2-3 days of withdrawal?

A 
Delirium tremens (DTs):
Hallucinations
Delirium
Fever
Tachycardia
- May lead to death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is tremulousness?

A

Tremors
Shaking
Quivering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the minor and major stages of alcohol withdrawal?

A

Minor: 1
Major: 2,3,4

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

What are the SE of stage 1 alcohol withdrawal?

A

Autonomic hyperactivity

Tremulousness (6-8h)

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

What are the SE of stage 2 alcohol withdrawal?

A

Hallucinations

Hallucinosis (10-30h)

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

What are the SE of stage 3 alcohol withdrawal?

A

Neuronal excitation

Seizures (6-48h)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the SE of stage 4 alcohol withdrawal?

A 
Delirium tremens
Delirium tremens (2-5 days)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the backbone of treatment for alcohol withdrawal?

A

Benzos (manage sx and avoid progression to the more serious stages of withdrawal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the MOA for benzos in alcohol withdrawal?

A

Increase the frequency of the opening of the GABA chloride channel, allowing more GABA to enter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the MOA for phenobarbital in alcohol withdrawal?

A

Barbiturates allow the GABA chloride channel to stay open longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What medications may be used synergistically for alcohol withdrawal?

A

Benzos and phenobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the last line agent for pts refractory to phenobarbital or benzos?

A

Propofol - allows the opening of the GABA chloride channel to stay open without the presence of GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the treatment for sx-triggered alcohol withdrawal pts with sx?

A

Only when the patient is HAVING sx
Results in shorter treatment duration, potentially avoids, and allow for individualized treatment
Lorazepam 1-2 mg every hour as needed when a structured assessment scale indicates that the sx are moderate to severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the treatment for fixed schedule alcohol withdrawal patients?

A

Benzo given regularly at a fixed dose interval - has been used for years
Longer duration and higher doses
Lorazepam 1-2 mg IV/PO/IM every 8 hours decreasing the dose every 1-2 days as tolerated

36
Q

Do we treat seizures d/t alcohol withdrawal?

A

Typically no - seizures are of short duration and finish before treatment can be given
Yes in status epilepticus seizures

37
Q

How do we treat status epilepticus seizures in alcohol withdrawal?

A

Benzos w/phenobarb until etiology is confirmed

Then increase dose of benzo w/slow taper can be used during detox to prevent future seizure acitivty

38
Q

What are other treatments for pts with acute alcohol withdrawal?

A 
Thiamine 100mg IV/IM for max of 5 days
Folic acid 1mg QD x 3-5 days
IV fluids
Hyperactivity treatment: clonidine 0.05-0.03 mg/day as PO/transdermal patch
Antipsychotics
39
Q

What is thiamine used to prevent in acute alcohol withdrawal?

A

Wenicke-Korsakoff syndrome

40
Q

In what order is thiamine used for pts with acute alcohol withdrawal?

A

Before or with glucose, otherwise it worsens Wenicke-Korsakoff syndrome

41
Q

When are antipsychotics used in pts with acute alcohol withdrawal?

A

Agitation
Unresponsiveness to benzos
Hallucinations/delusions

42
Q

What medications are used for long term abstinence after detoxification?

A

Naltrexone
Acamprosate
Disulfiram

43
Q

Dosing of Naltrexone for long term abstinence?

A

PO: Day 1: 25 mg, Day 2 and on: 50mg
IM: 380 mg IM q4wk
For 6-12 weeks w/counseling

44
Q

What are the ADRs for Naltrexone?

A

Syncope
CNS
GI
Arthralgias

45
Q

What are the cautions for Naltrexone?

A

Hepatic dysfunction

46
Q

What is the dosing for acamprosate?

A

666mg PO TID (renal adjustment for CrCl <50)

47
Q

What is acamprosate MOA?

A

Decreased glutamate activity in the CNS

Decreased activity at the NMDA receptor

48
Q

What is the ADR for acamprosate?

A

Diarrhea

49
Q

What is disulfiram’s MOA?

A

Inhibits alcohol dehydrogenase

50
Q

What does disulfiram cause in patients who drink alcohol?

A 
Flushing
Throbbing HA
N/V
Sweating 
Hypotension
Confusion
51
Q

What are the DDIs for disulfiram?

A

Oral anticoagulants
Phenytoin
Isoniazid

52
Q

What is the most common phase of alcohol liver disease?

A

Fatty liver

53
Q

What is the common cause of fatty liver?

A

Binge/chronic drinkers

54
Q

What is the least common phase of alcohol liver disease

A

Chronic alcoholic progress

55
Q

What are the most important RFs for alcohol liver disease?

A

Quantity and duration

56
Q

What is a co-morbidity of alcohol liver disease that increase the risk of cirrhosis?

A

HCV

57
Q

How much alcohol does it take and for how many years for the development of alcohol liver disease?

A

Men: > 60-90 g/day for 10 years
Women: > 20-40 g/day for 10 years

58
Q

What is the presentation of Alcohol liver disease?

A 
RUQ pain
Nausea
Discomfort
Jaundice
Portal HTN
Ascites
Variceal bleeding (may be present)
59
Q

What are the labs seen in alcohol liver disease?

A

Modest elevations of AST/ALT/GGT in alcoholic steatosis
Elevated triglycerides, hypercholesterolemia, elevated bilirubin
In alcoholic hepatitis: AST/ALT are elevated 2-7 fold
AST/ALT > 2

60
Q

How do we diagnose alcohol liver disease?

A

Presentation
Lab features
Ultrasound
Liver biopsy

61
Q

What is the prognosis of alcohol liver disease?

A

Potentially reversible
Estimated with the MDF score (>32 is poor prognosis) or the MELF ( >18 is poor prognosis) and should be considered for treatment

62
Q

What is the preferred treatment for alcohol liver disease?

A

Preferred: Prednisone 40 mg/kg/d for 4 weeks then taper
Alternate: Pentoxifylline 400mg po TID for 4 weeks (for pts who cannot tolerate corticosteroids)

63
Q

What is the Lille Model?

A

Determines if prednisone is effective (at day 3 and 7) or if it should be DCd

64
Q

What are the two types of non-alcoholic fatty liver disease?

A

NAFL

NASH (non-alcoholic steatophepatitis)

65
Q

What is NAFLD?

A

Hepatic steatosis with no evidence of secondary causes of fat accumulation in the liver

66
Q

What are the common causes of secondary hepatic steatosis?

A

Macrovascular steatosis

Microvascular steatosis

67
Q

What are the macrovascular steatosis causes?

A 
Excessive alcohol consumption
Hep C genotype 3
Wilson's disease
Lipodystrophy
Starvation
Parenteral nutrition
Abetalipoproteinemia
Medications (amiodarone, MTX, tamoxifen, corticosteroids)
68
Q

What are the microvascular steatosis causes?

A 
Reye's syndrome
Medications (valproate, anti-retroviral medicines)
Acute fatty liver of pregnancy
HELLP syndrome
Inborn errors of metabolism
69
Q

What is NAFLD strongly associated with

A

Insulin resistance (most important)
Obesity
Diabetes
Hyperlipidemia

70
Q

What are the RFs for NAFLD?

A

Obesity
T2DM
Dyslipidemia
Metabolic syndrome

71
Q

What are RFs that have emerging association with NAFLD?

A 
Polycystic ovarian syndrome
Hypothyroidism
Obstructive sleep apnea
Hypopituitarianism
Hypogonadism
Pancreato-duodenal resection
72
Q

What is a common deficiency in NAFLD?

A

Vit D - associated with the risk of NASH in patients with NALFD

73
Q

What are the s/sx of NAFLD?

A

Usually no sx

Only common sign is mildly elevated liver transaminases (2-3x ULN); AST/ALT ratio is usually less than 1

74
Q

How is NAFLD diagnosed?

A

Hepatic steatosis via imaging or histology
There is no significant alcohol consumption
There are not other competing etiologies for hepatic steatosis
There are no co-existing causes for chronic liver disease (hemochromatosis, autoimmune liver disease, chronic viral hepatitis, Wilson’s disease)

75
Q

How do we differentiate NAFL/NASH?

A

Presence of metabolism syndrome is a strong predictor for the presence of steatohepatitis
Biopsy is gold standard but is costly and risky
NOT IMAGING
Non-invasive methods being studied

76
Q

What are the non-invasive methods for differentiating NAFL/NASH?

A

Microbiota assessment from stool sample; 3 genera of bacteria are associated with NASH and fibrosis
NAFLD fibrosis score
Vibration Controlled Transient Elastography

77
Q

What does the NAFLD fibrosis score look at?

A

Utilizes age, BMI, hyperglycemia, plt count, albumin, AST/ALT ratio

78
Q

What is the vibration control transient elastography?

A

Point of care test
MRE with protein density fat fraction
Enhanced liver fibrosis scale (ELF)

79
Q

How do we manage NAFLD/NASH?

A

Lifestyle modifications
Insulin sensitizing agents
Hepatic oxidative stress reduction
Others

80
Q

What are insulin sensitizing agents?

A

Pioglitazone 30 mg QD - for biopsy proven NASH but long term safety and efficacy unknown

  • May improve or resolve NASH
  • No evidence to support use in NASH/NAFLD PLUS other chronic liver diseases (chronic HCV or primary biliary cirrhosis)
  • Rosiglitazone not effective
  • Metformin not recommended
81
Q

How do we treat hepatic oxidative stress reduction

A

Vitamin E 900 IU - improves histology
First line therapy for proven NASH in non-diabetic pts
Not currently recommended in NASH for diabetics, NAFLD w/o biopsy, NASH cirrhosis, cryptogenic cirrhosis

82
Q

What are other treatments for NASH/NAFLD?

A 
Ursodeoxycholic acid (UDCA) - not recommended
Omega-3 fatty acids - premature to recommend for treatment but may be considered first line agents to treat hypertriglyceridemia in patients with NAFLD
83
Q

What medication is in the pipeline for NASH/NAFLD?

A

Elafibranor
Agonist of the peroxisome proliferator-activated receptor alpha and gamma that play a role in fatty acid transport, oxidation, glucose homeostasis, and anti-inflammatory activities

84
Q

What are other recommendations for pts with NASH/NAFLD?

A

Bariatric surgery - premature to recommend for NALF/NASH
Alcohol use should be avoided
Statin use in both NAFL/NASH

85
Q

How do we treat NALFD in childhood?

A

Intensive lifestyle modification is first line
Vit E 800 IU/d offers histological benefit for biopsy proven NASH or borderline NASH but additional confirmatory studies are needed before it can be recommended for clinical practice

86
Q

What are the three phases of alcohol liver disease?

A

Fatty liver
Chronic Alcohol progress
Cirrhosis

GI/Hepatic Final (6 decks)

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