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MedEd Tutorials > 15. Acute Medicine > Flashcards

15. Acute Medicine Flashcards

1
Q

What happens to the NDMA receptors and GABA receptors in acute and chronic alcohol consumption?

A

GABA, inhibitory receptors are increased and alcohol reduces NDMA receptor action.

In chronic, the body upregulates NDMA receptors (excitatory) and downregulates GABA.

Therefore, if you withdraw then the NMDA receptor increase is suddenly not dampened so the body goes into overdrive.

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2
Q

Risk factors for alcohol withdrawal?

A

Alcohol use disorder
History of alcohol withdrawal
Acute illness
Poor physical health (poor nutrition -> thiamine deficiency -> wernicke’s)

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3
Q

What are the signs of chronic or decompensated liver disease?

A 
Encephalopathy 
Ascites 
Peripheral oedema
Jaundice
Bruising

AABB - Ammonia, Albumin, Bilirubin, Blood factors

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4
Q

What are the signs of wernicke’s encephalopathy?

A 
Caused by thiamine - B1 deficiency
Triad of
Confusion
Ataxia
Nystagmus

CAN

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5
Q

How does alcohol withdrawal present?

A
  • 6hours after - minor withdrawal - anxiety, agitation, palpitations, GI upset, sweating/tremor
  • 12 hours - alcoholic hallucinosis
  • 24 hours - withdrawal generalised tonic-clonic seizures
  • 48 hours - withdrawal delirium - delirium tremens, severe tremor, fever, high BP and HR

spreading from the SNS, to mind, body and then systemic

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6
Q

How do we investigate alcohol withdrawal?

A 
Screen with CADE or AUDIT-C
ECG for arrhythmias
ABG for resp alkalosis or met acidosis
Glucose, FBC, U&E, LFTs, coagulation
CT head for falls
CXR - pneumonia or aspiration
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7
Q

Treatment for alcohol withdrawal?

A

Urgent!

  1. Benzos IV
  2. CT head urgent for seizures and head injury
  3. Detect and treat co-existing illnesses

Supportive.

  1. Rehydrate with IV fluid
  2. Pabrinex (vit B) for wernicke’s
  3. Glucose as often hypoglycaemic after thiamine!!
  4. Electrolytes imbalances

Always refer to alc management team

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8
Q

What are hives called in proper terms

A

Urticarial rash seen in anaphylaxis

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9
Q

What is angiodema?

A

Swelling around the face from anaphylaxis

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10
Q

How do we manage anaphylaxis?

A

Acute

  1. Call for help
  2. Remove the trigger e.g. IV antibiotics
  3. Lie the patient flat, legs elevated
  4. Adrenaline, 500 micrograms IM
  5. Reassess airway

Then,

  1. High-flow oxygen with 15L via non-rebreathe
  2. Monitor
  3. IV fluid challenge
  4. IM or slow IV chlorphenamine (the hives) and hydrocortisone
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11
Q

What do we do post-management for anaphylaxis?

A

Observe the patient
Safety netting with advice
Epipen on discharge with education
Refer to allergy service

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12
Q

What is anaphylaxis?

A

A sudden, life-threatening, systemic hypersensitive reaction characterised by sudden onset of airway and/or breathing and/or circulation problems after a trigger.

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13
Q

What does histamine cause to create anaphylaxis?

A
  1. Vessel dilation
  2. Leaky vessels
  3. Bronchospasm
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14
Q

What is different between asthma and anaphylaxis in bloods?

A

Anaphylaxis has tryptase

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15
Q

IV or IM adrenaline?

A

Always IM.

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16
Q

How does aspirin OD present?

A

Tinnitis, deafness, dizziness
Tachypnoea
Hyperthermia
N&V

Late -
Low BP and heart block
Pulmonary oedema
Low GCS and seizures

17
Q

How do we treat aspirin overdose?

A

No antidote, mainly supportive

Consider ICU

18
Q

How do we investigate aspirin OD?

A

ECG, ABG etc. for complications to assess

Plasma salicylate concentration!
Plasma paracetamol conc for mixed OD

19
Q

How might paracetamol OD present?

A 
Often asymptomatic
Mild N&V and lethargy
RUG pain
Hepatomegaly
Acute liver failure - jaundice
20
Q

How do we investigate paracetamol OD?

A 
ABG - lactic acidosis is a bad sign
Urinalysis for kidney failure
Serum paracetamol to stratifying liver injury
LFTs, PT, INR
Blood glucose
U&Es
FBC
21
Q

How do we manage paracetamol OD?

A

IV N-acetylcysteine

Liver transplant

22
Q

What are opiates vs opioids?

A

Opiate - naturally occuring e.g. codeine

Opioid - synthetic e.g. fentanyl

23
Q

How do opiate ODs present

A

Triad -
Reduced consciousness
Respiratory depression (bradypnoea)
Miosis

Coma

24
Q

How do we investigate opiate OD?

A

BM for low glucose differential
ABG for resp failure and acidosis
Plasma paracetamol for mixed OD
FBC, U&Es (renal impairment), LFTs, CT head for diff

25
Q

How do we treat opiate OD?

A

IV Naloxone

26
Q

Why might paracetamol concentration be low in an OD?

A

It drops quickly after oral intake and yet it’s still affected her liver etc.!
Important to check the lack of symptoms and then

MedEd Tutorials (32 decks)

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