Acute medicine Flashcards

(30 cards)

1
Q

What is alcohol use disorder?

A

When a person continues to drink even though it is harmful and leads to physical health problems

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2
Q

What is alcohol dependence?

A

When a person has CRAVINGS for alcohol and has developed a TOLERANCE to it (needs more alcohol to have the same effect)

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3
Q

What is alcohol withdrawal?

A

Physical and psychological symptoms associated with sudden decrease in alcohol consumption

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4
Q

What is the pathophysiology of alcohol withdrawal?

A

GABA – inhibitory neurotransmitter
Glutamate – excitatory neurotransmitter

Alcohol is a GABA receptor agonist

Over time with chronic alcohol use:
- upregulation of glutamate receptors (compensatory mechanism)

So when you don’t take alcohol, there isn’t that CNS depressant effect to cancel out the upregulated CNS stimulatory effect →
excessive CNS stimulation → WITHDRAWAL SYMPTOMS

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5
Q

What is the presentation of alcohol withdrawal?

A

CNS overactivity → symptoms

Day 1:

MILD SYMPATHETIC AROUSAL
Minor withdrawal - approx. 6 hrs after you stop drinking:
- anxiety/agitation
- palpitations
- nausea & vomiting
- sweating + tremor

MIND BECOMES OVERACTIVE
Hallucinations - approx. 12 hrs:
- visual/tactile hallucinations
- normal mental status

Day 2:

BODY BECOMES OVERACTIVE
Seizures - approx. 36 hrs:
- short, generalised tonic-clonic seizures

Day 3:

SYSTEMIC OVERACTIVITY
Delirium tremens - 48-72 hours (FATAL):
- delirium 
- severe tremor
- fever
- high BP + HR
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6
Q

What are the differential diagnoses of delirium tremens?

A

Acute liver failure:
- ↑ Ammonia → ENCEPHALOPATHY
- ↓ Albumin → ascites and peripheral oedema
- ↑ Bilirubin → jaundice
- ↓ Blood factors → bruising
(encephalopathy can cause delirium tremens like symptoms)

Wernicke’s encephalopathy:

  • Confusion
  • Ataxia
  • Nystagmus
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7
Q

What would you include in the history and examination if you were suspecting alcohol withdrawal?

A

HISTORY:

Screen for alcohol-use disorder:

  • Brief CAGE questionnaire
  • Longer AUDIT questionnaire

Severity of withdrawal:
- CIWA-Ar scale (Clinical Institute Withdrawal Assessment from Alcohol Revised scale)

EXAMINATION (abdo):
- Signs of alcohol abuse (chronic liver disease)

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8
Q

What investigations would you do if you were suspecting alcohol withdrawal?

A

Bedside:
- Observations (tachycardia, temperature)

Bloods (to rule out differentials):

  • FBC
  • U&Es
  • LFTs, INR
  • Glucose

Differentials:

  • Hypoglycaemia
  • Electrolyte abnormalities
  • Hepatic encephalopathy
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9
Q

How would you manage alcohol withdrawal?

A
  1. Benzodiazepines (chlordiazepoxide, diazepam)
  2. Pabrinex (B vitamins - contains B1) to prevent Wernicke’s
  3. Glucose (if hypoglycaemic)
  4. Manage alcohol dependence:
    - drug and Alcohol Liaison Specialist (DALS)
    - community services (e.g alcoholics anonymous)
    - therapy
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10
Q

Define anaphylaxis

A

A life-threatening, systemic, hypersensitivity reaction

  • characterised by airway +/- breathing +/- circulation problems
  • usually associated with skin/mucosal changes
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11
Q

What is the epidemiology of anaphylaxis?

A

Most common in children 0-4 yrs

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12
Q

What is the aetiology and risk factors of anaphylaxis?

A

3 common triggers:

  • food (children) - e.g. nuts
  • drugs/chemicals (adults) - e.g. penicillin, NSAIDs, latex, contrast agent
  • toxins - e.g. bee/wasp sting, venom

Risk factor:
- history of atopy (hay fever, eczema, asthma)

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13
Q

What is the pathophysiology of anaphylaxis?

A

Main mechanism (type 1 hypersenstivity):

1) Sensitisation
→ immune system recognises substance (e.g. peanut)
→ triggers IgE production (abnormal)
→ IgE becomes bound to the surface of mast cells and basophils

2) Repeat exposure
→ IgE already bound the mast cells and basophils bind to the antigen (i.e. from the peanut)
→ degranulation and release of histamine into the bloodstream
→ systemic effects - ANAPHYLAXIS

Main effects of histamine:
- vasodilation
- increased capillary permeability 
- bronchoconstriction
(responsible for presentation)
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14
Q

What is the presentation of anaphylaxis?

A

ABC + skin/mucosal

Airway:

  • throat/tongue swelling
  • stridor

Breathing:

  • SOB
  • increased RR
  • decreased O2

Circulation:
- SHOCK → low BP, high HR, decreased consciousness

Skin/Mucosal:

  • urticaria and angioedema
  • flushing
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15
Q

What investigations would you do if you suspect anaphylaxis and what would you expect to see?

A

If diagnosis in uncertain, you can do blood tests:

  • ↑ serum tryptase
  • ↑ plasma histamine
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16
Q

How would you manage anaphylaxis?

A

1) Call for help
2) Remove trigger (allergen)
3) Lie patient flat and raise legs
4) IM adrenaline 0.5mg 1:1000
5) Manage airways, breathing, circulation
6) IV chlorphenamine + IV hydrocortisone

Follow up:

  • Refer to allergy/immunology clinic
  • RAST specific IgE testing to determine allergies
  • Provide Epipen and education re anaphylaxis
  • Medic Alert bracelet
17
Q

What is poisoning?

A

Administration of excess pharmaceutical agent

18
Q

What is the epidemiology of poisoning?

A

Accidental poisoning in children < 10yrs

Deliberate poisoning > 10yrs, usually 15-35yrs, often associated with alcohol use

19
Q

What investigations would you do if you suspected poisoning?

A
  • ABCDE assessment
  • ECG
  • FBC, U&E, LFT, INR, glucose
  • Paracetamol and Salicylate levels
  • ABG
20
Q

How would you manage poisoning?

A

TOXBASE provides information on dealing with various poisons

National Poisons Information Service (NPIS) helpline

Consider activated charcoal if <4h
(reduces absorption of drug)

Consider gastric lavage (rare)

21
Q

What is aspirin overdose defined as?

A

Overdose if > 150mg/kg

Severe if >500mg/kg

22
Q

What is the presentation of aspirin overdose?

A

Early presentation:

  • tinnitus, deafness, dizziness (aspiringing)
  • hyperpnoea (raspirin)
  • hyperthermia, sweating (perspirin)
  • N&V, diarrhoea

Late/severe presentation:

  • low BP and heart block
  • pulmonary oedema
  • low GCS + seizures
23
Q

What are the laboratory findings of aspirin overdose?

A

Early:
respiratory alkalosis

Intermediate:
mixed respiratory alkalosis and metabolic acidosis

Late:
high anion gap metabolic acidosis

24
Q

What is the management of aspirin overdose?

A

Urine alkalinisation with IV sodium bicarbonate

Dialysis

25
What is paracetamol overdose defined as?
Overdose if 150mg/kg 12g can be fatal
26
What is the pathophysiology of paracetamol overdose?
Paracetamol converted to NAPQI which is an electrophile → this allows it to conjugate with glutathione Overdose → paracetamol still being converted into NAPQI but there is not enough glutathione to conjugate with all the NAPQI → NAPQI accumulation – electrophile so extremely reactive → starts reacting with proteins in the liver → damage to liver tissue (hepatocyte necrosis)
27
What is the presentation of paracetamol overdose?
Often asymptomatic < 24 hrs: mild N&V, lethargy 24-72 hrs: RUQ pain, vomiting, hepatomegaly > 72hrs: acute liver failure
28
What is the management of paracetamol overdose?
IV N-acetyl cysteine if below treatment line Liver transplant
29
What is the presentation of opiate overdose?
CNS depression (PNS effects): - respiratory depression - bradycardia, Hypotension - pinpoint pupils - late/severe: low GCS/coma
30
What is the management of opiate overdose?
IV naloxone