Acute and Trauma Flashcards

1
Q

Who is anaphylaxis most common in

A

0-4 YEARS

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2
Q

Most common anaphylaxis causes

A

Food
Drug
Toxins like venom etc

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3
Q

Risk factor for anaphylaxis

A

Atopy

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4
Q

Physiologically what happens in anaphylaxis

A

IgE mediated mast cell degranulation leading to bronchospasm, vasodilation and increased capillary permeability

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5
Q

ABCDE presentation of anaphlaxis

A
A- throat and tongue swelling, stridor
B- increased RR, reduced O2
C- shock, tachy 
D- reduced consciousness from hypoperfusion
E- skin rashes, flushing
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6
Q

Management of anaphylaxis 6 steps

A
  1. Call for help
  2. Remove trigger
  3. Lie flat and raise legs
  4. IM adrenaline 0.5mg 1/1000
  5. ABC
  6. IV hydrocortisone and chlorphenamine
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7
Q

Blood investigations findings in anaphylaxis

A

Raised tryptase and histamine

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8
Q

What is tryptase

A

Enzyme released by basal cells

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9
Q

Further management of anaphlaxis

A

Follow up with immunological clinic for IgE testing to determine allergy
Epipen and education
Alert bracelet

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10
Q

What are investigations for all suspected poisonings

A
ABCDE
ECG
FBC
U&Es
LFT, INR
Paracetamol, salicylate
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11
Q

Extreme poisoning management

A

Activated charcoal if less than 4 hours

Gastric lavage

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12
Q

Early presentation of aspirin OD

A

Tinnitus, deafness and vertigo
Tachypnoea
Nausea and vomitting
Sweating from hyperthermia

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13
Q

Later presentation of aspirin OD

A
Heart block
Seizures
Low GCS
Pulmonary oedema
Shock
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14
Q

ABG early finding aspirin OD

A

Resp alkalosis

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15
Q

ABG late finding aspirin OD

A

Metabolic acidosis with large anion gap

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16
Q

What causes resp alkalosis in early aspirin OD

A

Aspirin stimulates resp centre causing hyperventilation

17
Q

What causes metabolic acidosis in late aspirin OD

A

Leads to high levels of glucose metabolism that doesnt produce ATP ie glycolysis forming lactate. Ketogenesis is also stimulated

18
Q

Main blood test should do for suspected aspirin OD

A

Salicylate levels

19
Q

Management of aspirin OD

A

Urine alkalisation using IV sodium bicarbonate

Dialysis

20
Q

Pathophysiology of paracetamol OD

A

Glutathione gets used up so toxic NAPQI accumulates leading to hepatocyte damage

21
Q

Early presentation of paracetamol OD ( up to 24 hrs)

A

Nausea and vomiting

Lethargy

22
Q

Later presentation of paracetamol OD (24 hrs after OD)

A

RUQ pain
Hepatomegaly
Vomiting

23
Q

How long after paracetamol OD does acute liver failure start

A

After 72 hours

24
Q

Treatment for paracetamol OD

A

N-acetyl cysteine

Liver transplant may be needed

25
Q

Physiologically what happens with opiate OD

A

PNS activated

26
Q

What is presentation of opiate OD

A
Resp depression
Bradycardia
Shock
Pinpoint pupils
In later stages coma and seizures
27
Q

Management of opiate OD

A

IV naloxone

28
Q

What are some less common suicide attempt methods

A

Ethanol

Anti freeze