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Year 3 > MedEd acute withdrawal > Flashcards

MedEd acute withdrawal Flashcards

1
Q

What is alcohol withdrawal?

A

Physiological and physical symptoms that arise when someone with alcohol dependancy stops or reduces alcohol intake within hours or days of presentation

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2
Q

What 2 receptors are involved in alcohol withdrawal? Which is excitatory and which is inhibitory?

A

NMDA receptors- excitatory

GABA (type A) receptors- inhibitory

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3
Q

Are NMDA receptors excitatory or inhibitory?

A

Excitatory

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4
Q

Are GABA type a receptors excitatory or inhibitory?

A

inhibitory

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5
Q

In chronic alcoholism what receptors are upregulated/ downregulated?

A

NMDA receptors are upregulated

GABA type a are downregulated

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6
Q

In acute alcohol what is the receptor balance?

A

GABA type a receptors are a lot higher than NMDA

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7
Q

In alcohol withdrawal what is the receptor balance?

A

NMDA receptors are a lot higher than GABA type a

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8
Q

What are RF for alcohol withdrawal?

A

Alcohol use disorder
Hx of alcohol withdrawal
Poor physical health

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9
Q

What are signs of chronic or decompensated liver disease? What molecules cause these

A

High ammonia- encephalopathy
Albumin- causes ascites and peripheral oedema
Bilirubin- causes jaundice
Reduced clotting factors- causes bruising

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10
Q

What is the triad for wernicke’s encephalopathy and what acronym is used to remember?

A

CAN:
confusion
ataxia
nystagmus

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11
Q

What is deficient in wernicke’s encephalopathy?

A

B1 and thiamine

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12
Q

What does thiamine and B1 deficiency cause?

A

Wernicke’s encpehalopathy

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13
Q

What are the 4 stages of alcohol withdrawal over time?

A

minor withdrawal symptoms
alcoholic hallucinations
withdrawal seizures
withdrawal delirium

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14
Q

As time from presentation progresses what stages of alcohol withdrawal are reached and when?

A

6-12 hrs= minor withdrawal symptoms
12-24hrs= alcoholic hallucinations
24-48 hrs= withdrawal seizures
48-72 hrs= withdrawal delirium

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15
Q

What are minor alcohol withdrawal symptoms?

A

Anxiety
Agitation
GI upset
Sweating/tremor

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16
Q

What type of withdrawal seizures occur in alcohol withdrawal?

A

Generalised tonic clonic seizures

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17
Q

What is seen in withdrawal delirium in alcohol withdrawal?

A

Delirium tremens
Severe tremor
Fever
High BP and HR

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18
Q

What are differentials for alcohol withdrawal?

A

Hypoglycaemia
Hepatic encephalopathy
Meningitis

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19
Q

How does hypoglycaemia present?

A 
Tremors
Palpitations
Anxiety
Seizures
Drowsiness
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20
Q

How does hepatic encephalopathy present?

A 
tremors
anxiety
palpitations
anxiety
seizures
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21
Q

What is the triad for meningitis and what is the limitation of this triad?

A

Fever
Altered mental status
Nuchal rigidity

not all patients present with nuchal rigidity

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22
Q

What scale is used to assess severity of alcohol withdrawal?

A

CIWA-AR scale

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23
Q

What ix might you do bedside for alcohol withdrawal and what will you see?

A

Screening- use CIWA-AR to assess severity
ECG- electrolyte abnormalities cause changes
VBG- resp alkalosis or metabolic acidosis or metabolic alkalosis with a high anion gap

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24
Q

What is seen on bloods for alcohol withdrawal?

A 
Glucose- hypoglycaemia
FBC- high MCV, thrombocytopenia 
UEs- electrolyte deficiency 
LFT- elevated AST, ALT, GGT
Coagulation studies- prolonged INR and PT
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25
Q

How is alcohol withdrawal managed?

A

Urgent= benzodiazepines, CT head, detect and treat co existing illness
Supportive treatments= rehydrate with IV fluids, pabrinex (vitamin B), glucose if hypoglycaemic, correct electrolyte imbalances

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26
Q

What is pabrinex and when is it given?

A

it is vitamin b and its given as supportive treatment eg alcohol withdrawal

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27
Q

When treating alcohol withdrawal what is it important to remember when giving glucose?

A

Only give it after thiamine but dont delay if hypoglycaemia is life threatening

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28
Q

What can you refer patients to for long term underlying alcohol dependance?

A

DALs, community services, therapy

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29
Q

How will someone with alcohol dependance present?- include the signs of which 2 conditions

A

Signs of chronic liver failure- jaundice, ascites/peripheral oedema, bruising
Signs of Wernicke’s encephalopathy- confusion, ataxia, nystagmus

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30
Q

What 3 molecules are associated with chronic liver failure and can help you remember what signs chronic liver failure causes?

A

Albumin
Bilirubin
Clotting factors

31
Q

What benzodiazepines might be used in alcohol withdrawal? Include what is used in emergenices and then long term

A

Lorazepam- use in emergencies

Chlordiazepoxide- use long term to wean patients off alcohol

32
Q

What benzodiazepine is used in emergency in alcohol withdrawal?

A

Lorazepam

33
Q

What benzodiazepine is used in long term in alcohol withdrawal?

A

Chlodiazepoxide

34
Q

If in A-E assessment breathing is an issue and o2 sats are low what should you do straight away?

A

15L oxygen via non rebreathe mask then reassess

35
Q

If in A-E assessment circulation is an issue and BP is low/ cap refill is prolonged/ signs of hypovolemia what should you do straight away?

A

Ask a nurse to put in 2 wide bore 18g cannulas in each arm

36
Q

What dose of adrenaline is given to adults and how is it administered?

A

500 microgram IM injection

37
Q

What 2 skin changes are seen on exposure of a patient in anaphylaxis?

A

Utricarial rash and angioedema

38
Q

How do you manage someone with anaphylaxis?

A

Call for help
Remove trigger eg IV abx
Lie the patient flat and raise their legs
Give 500 microgram IM adrenaline asap- do not delay
Reassess their airway and see if its patent
Then later on 15L/min via non rebreather mask o2, monitor obs, IV fluids and Im or slow steroids

39
Q

What is anaphylaxis?

A

A life threatening systemic hypersensitivity reaction characterised by sudden onset life threatening airway/ breathing/ circulation problems with or without skin changes after exposure to a trigger

40
Q

What are common triggers of anaphylaxis?

A

Food- nuts, shellfish, eggs
Drugs/chemicals- penicillin, NSAIDs, latex
Toxins- bee/wasp sting, venom

41
Q

What are RF for anaphylaxis?

A

hx of atopy

42
Q

Describe the pathophysiology behind and anaphylactic reaction

A 
b cells are sensitised by an antigen
they produce IgE antibodies 
IgE causes mast cell degranulation 
mast cell degranulation causes release of cytokines and histamines 
cytokines produce white cells 
there is vessel dilation
vessels become leaky 
there is bronchospasm
43
Q

What will be elevated on bloods in anaphylaxis?

A

Serum typtase and plasma histamine

44
Q

How will anaphylaxis present?

A

resp symptoms: SOB, stridor, wheeze
circulation symptoms: pale and clammy, hypotension
skin/mucosal symptoms: flushing, urticaria, angioedema

45
Q

What steroids might be given in anaphylaxis?

A

Chlorphenamine

Hydrocortisone

46
Q

What aftercare is done for someone post anaphylaxis?

A

Observe
Safety net
Give epipen
refer to allergy services

47
Q

How much aspirin needed for an OD? How is needed for severe OD?

A

> 150mg/kg

>500mg/kg is severe

48
Q

What are differentials for aspirin OD?

A

DKA

Paracetamol OD

49
Q

What do you need to get in a hx for aspirin OD?

A

What was the amount/ how was it prepped?
Was in intentional or accidental?
Was it isolated to mixed with something?

50
Q

What is seen on examination of someone with aspirin OD?

A 
Warm peripheries 
Bounding pulse 
Tachypnoea 
Hyperventilation
Cardiac arrhythmia 
Acute pulmonary oedema
51
Q

How does aspirin OD present? Describe the early and late symptoms?

A 
Early= tinnitus, hyperpnoea, hyperthermia and sweating, NV, diarrhoea 
Late= Low BP and heart block, pulmonary oedema, low GCS, seizures
52
Q

What bedside ix are done for aspirin OD and what would you see?

A

ECG- monitor arrhythmias

ABG- hyperventilation causes resp alkalosis wich progresses to high anion gap metabolic acidosis

53
Q

What clinical ix would you do for aspirin OD? Why are they done and what would you see?

A

Plasma salicylate conc- do at least 2 hrs after ingestion and then repeat every 2 hrs until peak conc is reached
Plasma paracetamol conc- to check if its a mixed OD
FBC- to exclude infectious aetiology
UEs- check for hyperkalemia as this is common
LFT- to see if theres hepatic dysfunction
Coagulation- check INR and PT

54
Q

What imaging might you do for aspirin OD and why?

A

CT head if theres altered mental status

55
Q

How is an aspirin OD classified? Give specific ranges

A

Mild toxicity= <300mg/L
Moderate toxicity= 300-700 mg/L
Severe toxicity= >700 mg/L

56
Q

How is aspirin OD managed?

A

There is no antidote
Mainly supportive management
Consider ITU admission if moderate or severe

57
Q

What dose is needed for paracetamol OD and what dose is fatal?

A

OD is >150mg/kg

12g can be fatal

58
Q

What are differentials for paracetamol OD?

A

Hep A/B

Ischaemic hepatitis

59
Q

How will someone with paracetamol OD present if within 24 hrs?

A

Usually asymptomatic

They may have mild NV and lethargy

60
Q

How will someone with paracetamol OD present within 24-72 hrs?

A

RUQ pain
Vomitting
Hepatomegaly

61
Q

How will someone with paracetamol OD present after 72 hrs?

A

Acute liver failure

There will be jaundice

62
Q

What will symptoms be in someone who has ODed on paracetamol over time?

A

Under 24hrs= mild NV, lethargy
24-72hrs= vomitting, hepatomegaly, RUQ pain
Over 72 hrs= acute liver failure with jaundice

63
Q

How will acid base balance progress in aspirin OD?

A

First hyperventilation will cause respiratory alkalosis

This will then progress to metabolic acidosis

64
Q

What bedside ix are done for paracetamol OD and what will you see?

A

ABG- lactic acidosis is a bad sign

Urinalysis- may show heamaturia or proteinuria which indicates kidney failure

65
Q

What lab ix are done for paracetamol OD? Why are they done and what would you see?

A

Serum paracetamol conc- to stratify risk of liver injury and see if acetylcysteine is needed
LFTs- check liver function, ALT would be high
Blood glucose- liver failure can cause hypoglycaemia
UE- high creatinine if there is acute kidney or liver injury
FBC- leukocytosis, anaemia, thrombocytopenia

66
Q

What happens to INR and PT in liver failure?

A

Both increase

67
Q

What happens to glucose levels in liver failure?

A

Hypoglycaemia

68
Q

How is paracetamol OD managed?

A

IV N-acetylcysteine

Liver transplant

69
Q

What is the difference between opiods and opiates?

A

Opiate- naturally occuring

Opioid- synthetically made

70
Q

Give examples of opiates

A

Morphine

Codeine

71
Q

Give examples of opioids

A

fentanyl

oxycodone

72
Q

What are some differentials for opiate OD?

A

Hypoglycaemia

Head injury

73
Q

What are early and late symptoms of opiate OD?

A 
early= reduced consciousness, respiratory depression, miosis, bardycardia, hypotension
late= low GCS, coma
74
Q

How do you remember what miosis is?

A

Miosis= mini= pupils get small/ constrict

Year 3 (104 decks)

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