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RCPCH TAS/ AKP > Emergency Medicine > Flashcards

Emergency Medicine Flashcards

1
Q

What strength of adrenaline in anaphylaxis?
+ Doses

A

1:1000
- <6y: 150 micrograms
- 6-12y: 300 micrograms
- >12y: 500 micrograms

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2
Q

Presentation of anaphylaxis

A

Mins after exposure
- Urticaria, angioedema
- Upper airway obstruction
- Abdominal cramping / diarrhoea
- Shock

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3
Q

What are the phases of bone healing?

A
  1. Inflammatory phase (hours-days): Inflammation, formation of haematoma –> primary calculus
  2. Reparative phase (days-weeks): Thick callus forms around bone.
  3. Remodelling phase (months-years): Osteoblastic / osteoclastic activity
    May need to repeat xray - see callus formation
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4
Q

Types of shock

A
  • Hypovolaemic - haemorrhage
  • Distributive - Sepsis, anaphylaxis
  • Cardiogenic - Arrhythmia
  • Dissociative - Profound anaemia
  • Obstructive - PE, tamponade, pneumothorax
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5
Q

What is pre-load?

A

Tension in ventricular wall at end of diastole (“Stretch”)

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6
Q

What is afterload?

A

Tension in left ventricular wall required to push blood into aorta (“Squeeze”)

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7
Q

What is myocardial contractility?

A

The ability of the heart to react to pre-load and after-load

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8
Q

Noradrenaline/ adrenaline mechanism of action

A
  • Alpha-1 receptors
  • Increased vasc. resistance (increased HR / SV / CO)
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9
Q

Dopamine mechanism of action

A
  • Alpha-1, Dopamine-1 receptors
  • Increased vascular resistance
  • Selective vasodilation: renal, cerebral, coronary, mesentry
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10
Q

Dobutamine mechanism of action

A
  • Beta-1/2 receptors
  • Increased HR and CO
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11
Q

Vasopressin mechanism of action

A
  • V1/2 receptors
  • Increased vasc. resistance due to reduced UO and vasoconstriction
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12
Q

What are the reversible causes of cardiac arrest?

A

4 H’s: Hypotension, Hypoxia, Hypothermia, Hypo/hyperkalaemia
4 T’s: Tamponade, toxins, tension pneumothorax, Thrombus

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13
Q

How is cardiac output calculated?

A

CO = HR x SV

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14
Q

How is BP calculated?

A

BP = SV x Vascular resistance

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15
Q

Description of superficial (simple erythema) burns

A

Erythema. No blistering. +/- peeling
Epidermis only
1 week healing.

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16
Q

Description of Superficial partial thickness burn

A

Wet erythema and blistering. Painful. Usually no scarring. 2w to heal.
Epidermis and upper 1/3 dermis.

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17
Q

Description of Deep partial thickness burn

A

Yellow / white. Blistering. Less painful that superficial. Risk scarring. Takes 8 weeks to heal.
Deeper layers of dermis

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18
Q

Description of full thickness burn

A

White/ brown. Painless. Scarring / contractures.
All layers of skin.

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19
Q

How to calculate fluid resus in burns

A

4 x body weight x % area of burn
In 24 hours

50% in 1st 8 hours, maintenance fluid given on top of this.

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20
Q

Burns criteria for referral to a specialist centre

A
  • > 5% total SA
    Burns to face, hands, feet, genitalia, perineum
  • Full thickness
  • Electrical / chemical burns
  • Inhalation
  • Circumferential burns
  • Suspicious
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21
Q

What is Cushing’s Reflex?

A

Result of raised ICP
- Irregular respirations
- Bradycardia
- Hypertension

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22
Q

Presentation raised ICP

A
  • Cushing’s response
  • Reduced GCS
  • Headache - morning / coughing / sneezing
  • Focal neurology
  • Retinal haemorrhage
  • Sunset sign - downward looking pupils
  • Papilloedema
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23
Q

Treatment raised ICP

A
  • Elevation of bed 30 degrees (improved venous return)
  • Supportive
  • Fluid restriction
  • Mannitol 20%/ 3% saline
  • Surgical decompression
  • Strict regulation ventilation / temp
24
Q

Indications for CT Head

A
  • Suspicion NAI
  • Post-traumatic seizure
  • GCS <14 on arrival, <15 2 after injury
  • Open, depressed, basal skull fracture
  • Focal neuro deficit
  • Bruise / swelling >5cm in <1 y/o
    >1 of: LOC >5 mins, drowsiness, amnesia >5mins, >2 x vomits, dangerous mechanism
25
Q

Presentation spinal cord injury

A

Loss of motor / sensation function
Unopposed parasympathetic response –> bradycardia / hypotension

26
Q

Pathophysiology drowning

A
  1. Submersion / immersion in liquid
  2. Asphyxia +/- aspiration
  3. Hypoxia + ischaemia
  4. Multisystem failure
27
Q

What is diving reflex?

A

Facial contact with cold water –> bradycardia and vasoconstriction to preserve blood supply to vital organs

28
Q

Describe primary prevention

A

Removal of circumstances causing injury eg lock on medicine cupboard

29
Q

Describe secondary prevention

A

Reduce severity of injury eg bike helmet

30
Q

Describe tertiary prevention

A

Optimal treatment eg good first aid

31
Q

Paracetamol overdose: Mechanism and presentation

A

Mechanism: NAPQI produced by saturation of life CYP450, unable to conjugate to glutathione
Presentation: Abdo pain, vomiting, liver failure

32
Q

Paracetamol OD management

A

N-acetylcysteine
- Over Tx line
- Staggered >1 hour
- >150mg/kg

33
Q

Presentation and management of ingestion button batteries

A

Clear history
Abdominal pain +/- perforation
Tx: AXR / CXR, endoscopic removal

34
Q

Carbon monoxide poisoning: Mechanism and presentation

A

Mechanism: Binds to Hb –> lower o2 transport
Presentation: Headache, nausea, drowsy, confusion, coma
Worse prognosis in Preg, cardio conditions, (resp conditions)

35
Q

CO poisoning managment

A

High flow o2

36
Q

Salicylate OD: Mechanism and presentation

A

Mechanism: Stimulates resp. centre, uncouples oxidative phosphorylation
Presentation: Vomiting, tinnitus, resp. alkalosis (acidosis = late), hyperventilation, sweating, diplopia, dizziness

37
Q

Salicylate OD management

A

<1 hour - activated charcoal
Urine alkalinisation
Haemodialysis

38
Q

Symptoms of theophylline OD

A

Hyperventilation / resp. alkalosis
Vomiting
Agitation
Dilated pupils
Hyperglycaemia
Tachycardia.

39
Q

TCA OD: Mechanism and presentation
Eg amitriptylline

A

Mechanism: Interferes with cardiac conduction (blocks Na+ channels)
Presentation: Tachycardia, arrhythmia, drowsy, seizure

40
Q

TCA OD management

A

Sodium bicarb
Supportive

41
Q

Presentation organophosphate poisoning

A

Miosis - antimuscarinic eye effects

42
Q

Ethylene glycol poisoning: Mechanism and presentation
Eg antifreeze

A

Mechanism: Toxic metabolites interfere with cellular energy production
Presentation: Intoxication, tachycardia, severe met. acidosis, renal failure, HTN

43
Q

Ethylene glycol/ methanol poisoning management

A

Fomepizole
Alcohol
Competitive inhibitors of alcohol dehydrogenase

44
Q

Iron OD: Mechanism and presentation

A

Mechanisms: Corrosive –> disruption of oxidative phosphorylation –> free radicals
Presentation: Vomiting, diarrhoea, GIB, seizures, coma, gut strictures

45
Q

Iron OD Tx

A

IV Desferrioxamine (binds to free iron and enhances renal elimination)
Activated charcoal if <1 hour

46
Q

Amphetamine OD presentation and management

A

Dilated pupils
Hypertension, tachycardia
Skin pallor
Hyperexcitability, agitation
Hypokalaemia.
Hyperpyrexia
Rhabdomyolysis
Acute renal / liver failure
Tx: beta blockers, BDZ

47
Q

Treatment of beta-blocker OD

A

Atropine
Glucagon

48
Q

How is Anion gap calculated

A

[(Na+ + K+) - (HCO3- + Cl-)]

49
Q

Causes of raised anion gap (>16 mmol)

A

MUDPILES
Methanol
Uraemia
DKA
Propylene Glycol
Iron and Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates

50
Q

What is Klumpke’s palsy and how does it present?

A

Damage to T1 SNS chain –> ulnar and median nerves. Excessive abduction of arm.
Can move arm but not hand
Loss of sensation thumb, index and middle finger

51
Q

How to calculate cerebral perfusion pressure

A

Cerebral perfusion pressure = MAP - ICP

52
Q

Presentation of lead poisoning

A
  • Pica eg lead containing products, drinking water from old lead pipes
    Nausea
    Abdo pain
    Constipation
    Blue discolourationg of gums
    Neuropathy, GDD, impaired cognition
53
Q

Classification of hypovolaemic shock

A

I-II: <25%
III: 25-40%
IV: >40%

54
Q

Which nerve is most likely to be damaged in distal radius fracture?

A

Median nerve

55
Q

Describe features of Rheumatic fever

A

GAS infection
Mainly 4-15 years.
Common middle and east Asia, Eastern Europe and SA.
Fleeting migratory polyarthritis affecting large joints.

56
Q

What is “pulled elbow” / “Nursemaid’s elbow”?

A

Radial head subluxation. Presentation = holding arm to side with extended elbow and pronated forearm. Comfortable unless asked to move.
<6y (weak annular ligament). Caused by sudden pull on extended, pronated forearm.

RCPCH TAS/ AKP (20 decks)

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