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5th Year > ACT Emergency > Flashcards

ACT Emergency Flashcards

1
Q

Description of anaphylaxis

A

Anaphylaxis is a life threatening Type 1 hypersensitivity reaction. There is IgE mediated release of histamine from mast cells in response to a presensitised allergen. The cascade release of inflammatory cytokines increases capillary permeability causing oedema.

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2
Q

Aetiology of anaphylaxis

A

Exposure to an allergen such as a food or drug, presensitises individuals. When there is subsequent exposure, IgE activation of mast cells causes a type 1 hypersensitivity reaction.

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3
Q

Complications of anaphylaxis

A

The resulting swelling can occlude the patients airway.

Fluid shift out of the intravascular space can cause a distributive shock.

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4
Q

Assessment of suspected anaphylaxis

A

A to E approach - Full set of Observations
Dx- Acute onset, Life threatening ABC problem and/or skin changes
Check drug chart
Ask ward staff for recent medications

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5
Q

Immediate management of anaphylaxis

A 
Stop allergen exposure 
Call for Help 
Lie flat + Legs up
Adrenaline 1:1000 500micrograms IM
Establish airway + 15L non-rebreathe 
IV access  - Mast cell tryptase, FBC, U&Es
\+/- Fluid challenge 
Chlorphenamine 10mg slow IV
Hydrocortisone 200mg slow IV
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6
Q

Investigations for anaphylaxis

A

Bloods: FBC, U&Es
Serum Mast cell tryptase x 3: up to 1 hr, at 3hr and 24 hrs
Diagnosis will show a peak then return to normal by 24hrs

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7
Q

Explanation of anaphylaxis to patient

A

Anaphylaxis is a type of severe allergic reaction which occurs when the body comes into contact with something the immune system has become sensitive to.
It can be caused by many things including foods such as nuts and shellfish or drugs such as antibiotics
Symptoms can include a rash with itching and tingling, swelling of the lips and tongue and difficulty breathing.

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8
Q

Long term management of anaphylaxis

A

Follow up appointment with immunologist for:
Patient education
Rx of Epipen and training

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9
Q

Differential diagnosis for anaphylaxis

A

Carcinoid syndrome - paraneoplastic release of serotonin

Phaeochromocytoma - neuroendocrine tumour of adrenal medulla secreting catecholamines

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10
Q

Description of septic shock

A

Sepsis with hypotension and a lactate > 2mmol/L despite adequate fluid resuscitation.
The patient needs vasopressors to maintain a mean arterial pressure of 65mmHg

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11
Q

Aetiology of septic shock

A

There is loss of vascular tone following a systemic inflammatory response to pathogenic toxins.
Fluid shift out of the intravascular space causes a drop in blood pressure.

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12
Q

Complications of shock

A

Hypo-perfusion of end organs can lead to schema and dysfunction. If prolonged can lead to multiple organ failure and death

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13
Q

Management of septic shock

A

A to E - BUFALO
Call for senior help
Requires ICU Early Goal Directed Therapy
Vasopressors to maintain mean arterial pressure >65mmHg

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14
Q

Description of cardiogenic shock

A

A state of end-organ hypoperfusion due to cardiac failure and the inability of the cardiovascular system to provide adequate blood flow to the extremities and vital organs

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15
Q

Aetiology of cardiogenic shock

A

True cardiac - MI, arrhythmia, valve failure

Extracardiac - Obstructive
Prevent inflow- Tension pneumothorax, Tamponade
Prevent outflow - Pulmonary embolus

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16
Q

Assessment and investigations for suspected cardiac shock

A

A to E
ABG, CXR,
Bloods - FBC, U&E, Glucose, clotting, crossmatch
ECG, Echocardiogram

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17
Q

Management of cardiogenic shock

A

A to E
Treat the underlying cause eg. Revascularisation
Cautious fluid resuscitation - 250ml
Early ICU involvement - inotropes and vasopressors

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18
Q

Description of hypovolemic shock

A

Insufficient circulating volume in the intravascular space to adequately perfuse end organs due to fluid loss

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19
Q

Aetiology of hypovolemic shock

A

Haemorrhage - On the floor and 4 more
Chest, Abdomen, Pelvis, Long bones.

Salt or fluid loss - Vomiting, Diarrhoea

Third spacing - Ascities

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20
Q

Assessment and investigation of suspected hypovolemic shock

A 
A to E 
ABG - ?DKA ?Pancreatitis
CXR - ?Haemothorax
Bloods - FBC, U&E, LFT, Amylase, Coag, X-match
ECG - ischaemia 
FAST Scan - ruptured AAA
Pelvic x-ray - fractures

Urine Osmolality - Diabetes insipidus
Stool MC&S

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21
Q

Management of hypovolemic shock

A 
A to E 
Fluid resuscitation with 0.9% NaCl
Treat the underlying cause  
Correct electrolyte disturbances 
?Massive Haemorrhage protocol
22
Q

Description of acute respiratory failure

A

Type 1 respiratory failure is a Pa02 <8kPa caused by a ventilation-perfusion mismatch

Type 2 respiratory failure is a Pa02 <8kPa with hypercapnia PaCO2 >6kPa caused by failure of ventilation

23
Q

Aetiology of Type 1 respiratory failure

A 
The 4 Ps + Asthma
Pulmonary embolus 
Pulmonary oedema 
Pneumothorax
Pneumonia
24
Q

Aetiology of Type 2 respiratory failure

A

Respiratory - COPD, Life threatening Asthma

Neurological - Drugs, MND, Guillian-Barre

MSK - Myasthenia gravis, obesity, kyphoscolioisis

25
Q

Complications of Type 1 respiratory failure

A

Prolonged hypoxia
Invasive ventilation and the risks associated with it.
Multiorgaan failure and death

26
Q

Complications of Type 2 respiratory failure

A

Prolonged hypoxia
Prolonged hypercapnia
Multiorgan failure and death

27
Q

Assessment and investigation of suspected Type 1 respiratory failure

A 
A to E assessment
Peak Expiratory Flow 
ABG - pa02 <8kPa 
CXR - pneumonia, pneumothorax
ECG - Pulmonary embolus
28
Q

Assessment and investigation of suspected Type 2 respiratory failure

A

A to E assessment
ABG - pa02 <8kPa, PaCo2 >6kPa
CXR
Send sputum

29
Q

Management of Type 1 respiratory failure

A 
Treat the cause 
- 15L Non rebreathe
- Continuous Positive Airway Pressure 
- Invasive Ventilation 
Monitor for progression to type 2
30
Q

Management of Type 2 respiratory failure

A

Treat the cause
COPD - Controlled 02, aim sats 88-92%
White Venturi 28% to start
Consider non invasive ventilation with bilevel positive airway pressure

31
Q

Reversible causes of cardiac arrest

A

Hypoxia
Hypovolaemia
Hypo/perkaleamia
Hypothermia

Thrombosis
Tension pneumothorax
Tamponade
Toxins

32
Q

Shockable and non shockable rhythms during cardiac arrest

A

Ventricular Fibrillation
pulseless Ventricular tachycardia

Pulseless electrical activity and asystole

33
Q

When are drugs given during advanced life support

A

Give adrenaline 1mg 1:10,000 IV every 3-5 minutes

Give amiodarone 300mg IV after 3 shocks

34
Q

Aetiology of falls in the elderly

A

B - Hypoxia, PE
C - MI, dysrhythmia, Sepsis, Shock
D - Hypoglycaemia, Seziures, CVI

Mechanical
Ataxia
Syncope - postural hypotension, vasovagal, situational

35
Q

Hx taking for falls in the elderly

A

Before - events, symptoms, speed of onset
During - LOC? Head injury? Incontinence? Time on the floor?
After - Speed of recovery? Helped up?
Previous falls + ICE
PMH - Cardiac, DM, Neuro
DH - New? antihypertensives? hypoglycemics? Anticoagulants
SH - Circumstances, Mobility, vision?

36
Q

Assessment and investigations for fall in the elderly

A 
Full set of observations + CPG
Check for head injury and C spine tenderness
Cardiovascular and Neurological exam
Lying and standing BP 
Hourly neuro obs for 4 hours

Ix: ECG at bedside
Bloods - FBC, U&Es, CRP, BM, Troponin?
CT head - if criteria
Radiograph - if suspicious of fracture

37
Q

CT head guidelines for adults following head injury within 1 hour

A 
GCS < 13 on initial assessment 
GCS < 15 at 2 hours after injury
Focal neurological deficit 
More than one episode of vomiting
Suspected skull fracture
Any sign of Basal soul fracture 
Post traumatic seizures
38
Q

CT head guidelines for adults following head injury within 8 hour

A

Always if anti-coagulated

LOC or amnesia following injury +

  • 65yrs or older
  • Previous bleeding/clotting disorder
  • Dangerous mechanism
  • > 30mins retrograde amnesia of before injury
39
Q

Hx taking and risk assessment following overdose

A 
Drugs taken + Dose + Number?
Time taken + Staggered?
With alcohol?
Symptoms - vomiting, tinitus, dizziness
Before - Events, trigger, planned, note writing
During - who, what, where, intent
After - how discovered? Guilt? 
RISK - Feeling now? Plans? Protective?
Previous attempts + Psych Hx
Social Hx + Current stressors
40
Q

Pathophysiology of paracetamol overdose

A

Normal pathways of conjugation with the sulfate and glucuronide become saturated, so more paracetamol is shunted to the cytochrome P450 system to produce NAPQI. Hepatocellular supplies of glutathione become depleted and NAPQI remains in its toxic form in the liver. NAPQI damages cellular membranes resulting in widespread hepatocyte damage and death, leading to acute liver necrosis

41
Q

Investigations of paracetamol overdose

A

Paracetamol levels after 4 hours
Bloods: FBC, U&E, LFTs, Clotting, Bicarbonate
If Bicarbonate abnormal then do ABG

42
Q

Management of paracetamol overdose

A

Single OD above treatment line (>150mg/kg)
Staggered overdose
Paracetamol levels not known at 8hrs
N-acetyl-cysteine in 5% Dextrose
Bag 1 = 150mg/kg in 200ml over 1h
Bag 2 = 50mg/kg in 500ml over 4h
Bag 3 = 100mg/kg in 1000ml over 16h.
If anaphylactoid reaction - Chlorphenamine + slow IV
Psychiatric assessment
If liver failure, discuss with hepatologist

43
Q

Presentation of salicylate overdose

A

Tinnitus or hearing impairment
Vomiting, Sweating, Fever,
Drowsiness, Dizziness, Blurred vision
Hyperventilation - due to direct stimulation of respiratory centre, causes respiratory alkalosis

44
Q

Assessment and investigation of suspected Salicylate overdose

A 
ABG - respiratory alkalosis
Progresses to metabolic acidosis
U&amp;Es -  decreased K+, deranged Na+
BM - Deranged due to uncoupling of oxidative phosphorylation 
Salicylate levels raised
Paracetamol levels incase mixed
45
Q

Management of salicylate poisoning

A

IV rehydration and potassium replacement

If severe then consider:
Urinary alkalisation with IV sodium bicarbonate
Heamodialysis

46
Q

Presentation of Tricyclic overdose

A

Anticholinergic features
Dsyrhythmia +/- hypotension
Mycolonic jerking, Reduced GCS

47
Q

Assessment and investigation of tricyclic overdose

A

ABG - Metabolic acidosis

ECG - Prolonged PR, QRS widening

48
Q

Management of tricyclic overdose

A

Cardiac monitoring or serial ECGs
Alkalisation with sodium bicarbonate

IV glucagon or vasopressors for hypotension
Control seizures with benzodiazepines

49
Q

Presentation of iron overload

A 
First stage - GI irritation 
Nausea, vomiting, diarrhoea 
Second stage - 24 -48 hrs after OD
Dehydration, Metabolic acidosis 
Liver failure
50
Q

Investigation of iron overload

A

ABG - ?metabolic acidosis
Bloods: FBC, Serum iron, Glucose
AXR - tablets can be counted

51
Q

Management of iron overload

A

Desferrioxamine IV infusion

5th Year (10 decks)

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