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Clinical Modules > Emergency Medicine > Flashcards

Emergency Medicine Flashcards

1
Q

1st line for opiod overdose

A

Naloxone

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2
Q

1st line for opiod detoxification

A

Methadone/ buprenorphine

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3
Q

Posterior hip dislocation presentation

A

Shortened, adducted and internally rotated leg

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4
Q

Anterior hip dislocation

A

Abducted and externally rotated leg, no leg shortening

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5
Q

Achilles tendon rupture presentation

A
  • increased resting ankle dorsiflexion in a prone position with knees bent
  • a palpable gap above the heel
  • a lack of plantar flexion when the calf is squeezed (Thompson’s test positive)
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6
Q

Achilles tendon rupture investigation

A

Ultrasound scan

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7
Q

Pulmonary embolism presentation

A
  • pleuritic chest pain
  • dyspnoea
  • haemoptysis
    Signs:
  • tachypnea
  • crackles
  • tachycardia
  • fever
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8
Q

Left ventricular free wall rupture presentation

A

Sudden heart failure, raised JVP, pulsus parodoxus, recent MI

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9
Q

Multiple myeloma presentation

A
  • around 70yrs old
  • C - Hypercalcaemia
  • R - Renal damage (dehydration/ thrist)
  • A - Anaemia
  • B - Bleeding/ bruising
  • B - Bones (pain, fractures)
  • I - Infection
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10
Q

Multiple myeloma investigations

A
  • full blood count: anaemia
  • peripheral blood film: rouleaux formation
  • urea and electrolytes: renal failure
  • bone profile: hypercalcaemia
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11
Q

Anaphylaxis presentation

A
  • lips/ tongue/ airway swelling
  • dyspnoea
  • wheeze
  • chest tightness
  • pruritus
  • erythmema
  • urticaria
  • peripheral vasodilation
  • N/V, diarrhoea
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12
Q

Anaphylaxis management

A
  • give oxygen
  • open and maintain airway
  • 0.5mg IM adrenaline
  • nebulised salbutamol for bronchospasm
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13
Q

Diabetic ketoacidosis aetiology

A
  • insulin deficiency:
    – undiagnosed DM
    – interrupted insulin therapy
    – intercurrent illness - eg. infection or surgery
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14
Q

Diabetic ketoacidosis pathophysiology

A
  • insufficient insulin -> increased hepatic gluconeogenesis -> high blood glucose -> osmotic diuresis -> dehydration
  • increase in peripheral lipolysis -> free fatty acids -> liver converts to ketones -> metabolic (keto)acidosis
  • no insulin to drive K into cells -> high serum K, low body K -> potassium imbalance
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15
Q

Diabetic ketoacidosis presentation

A
  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Acetone smell to their breath
  • Kussmaul respiration (deep hyperventilation)
  • Dehydration
  • Weight loss
  • Hypotension (low blood pressure)
  • Altered consciousness
  • Abdominal pain
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16
Q

Diabetic ketoacidosis diagnostic criteria

A
  • Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
  • Ketosis (e.g., blood ketones above 3 mmol/L)
  • Acidosis (e.g., pH below 7.3)
    (metabolic acidosis with a low bicarbonate)
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17
Q

Diabetic ketoacidosis invesstigations

A
  • blood glucose
  • blood ketones
  • venous blood gas
  • urine dipstick
  • U & Es
  • FBC
  • identifying a precipitating cause (eg blood cultures/ MSU for infection)
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18
Q

Diabetic ketoacidosis management

A
  • IV fluid resus with normal saline (1L/1st hour-> 1L/2hourly)
  • fixed-dose IV insulin therapy (0.1units/kg/hr)
  • monitor blood glucose, if < 14mmol/L add 10% dextrose at 125ml/hr
  • add KCl to fluids if needed (K<5.5) upto 20mmol/hr
  • treat underlying triggers (eg infection)
  • monitor blood ketones, pH and bicarbonate
  • continue long-acting, stop short-acting insulin
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19
Q

Diabetic ketoacidosis resolution

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
  • pt should be eating/ drinking
  • pt should have started regular SC insulin
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20
Q

ACVPU scale

A
  • Alert
  • Confusion (new-onset)
  • Voice
  • Pain
  • Unresponsive
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21
Q

3 types of paracetamol overdose

A
  • Acute overdose: excess amounts of paracetamol ingested over less than one hour, usually in the context of self-harm
  • Staggered overdose: excess amounts of paracetamol ingested over longer than one hour, usually in the context of self-harm
  • Therapeutic excess: excess paracetamol ingested with the intent to treat pain or fever and without the intent of self-harm
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22
Q
A
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23
Q

Paracetamol overdose early presentation

A

Early (<12hrs):
* Potentially asymptomatic
* Nausea and vomiting
* Mild/moderate abdominal pain/tenderness

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24
Q

Paracetamol overdose pathophysiology

A
  • paracetamol metabolised by cytochrome P450 enzymes into toxic NAPQI
  • usually NAPQI conjugated with glutathione for excretion
  • excess NAPQI = insufficient glutathione -> NAPQI damages hepatocytes -> acute liver failure -> death
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25
Q

Paracetamol overdose late presentation

A

Late (12-36hrs):
* Moderate/severe abdominal pain
* Metabolic acidosis
* Jaundice
* Acute kidney injury
* Hepatic encephalopathy
* Coma
* Bruising or systemic haemorrhage may indicate coagulopathy secondary to impaired hepatic clotting factor production

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26
Q

Paracetamol overdose investigations

A
  • Paracetamol concentration
  • Liver function tests
  • INR
  • Urea and electrolytes
  • Plasma bicarbonate
  • Plasma glucose
  • Full blood count
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27
Q

Paracetamol overdose investigations

A
  • accurate history essential:
    – combination/ strength ingested
    – length of time ingested over
    – time since ingestion
  • activated charcoal if present within 1hr
  • IV acetylecysteine given over 1hr if:
    – staggered overdose
    – present 8-24hrs
    – present >24hrs if jaundiced/ hepatic tenderness
    – plasma paracetamol conc. on/ above single treatment line
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28
Q

Rhabdomyolysis pathophysiology

A

breakdown of skeletal muscle cells -> release of intracellular fluids (CK, myoglobin, urate, electrolytes) into circulation -> electrolyte imbalances/ AKI

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29
Q

Rhabdomyolysis aetiology

A
  • seizure (esp status epilepticus)
  • collapse/coma (prolonged immobilisation)
  • ecstasy
  • crush injury
  • McArdle’s syndrome (genetic disorder)
  • drugs: statins (especially if co-prescribed with clarithromycin)
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30
Q

Rhabdomyolysis presentation

A
  • AKI with raised creatinine
  • significantly elevated CK
  • myoglobinuria: (tea-coloured)
  • hypocalcaemia (myoglobin binds calcium)
  • elevated phosphate (released from myocytes)
  • hyperkalaemia (may develop before renal failure)
  • metabolic acidosis
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31
Q

Rhabdomyolysis management

A
  • IV fluids to maintain good urine output
  • manage any electrolyte disturbances
  • urinary alkalinization in severe cases (IV sodium bicarb)
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32
Q

Total anterior circulation stroke

A
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia (loss of half of the visual field in both eyes)
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
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33
Q

Partial anterior circulation stroke

A

TWO of the following:
* Unilateral weakness (and/or sensory deficit) of the face, arm and leg
* Homonymous hemianopia (loss of half of the visual field in both eyes)
* Higher cerebral dysfunction (dysphasia, visuospatial disorder)
OR higher cerebral dysfunction alone

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34
Q

Posterior circulation syndrome

A
  • Cranial nerve palsy with a contralateral motor or sensory deficit, or
  • Bilateral motor/sensory deficit, or
  • Conjugate eye movement disorder, or
  • Symptoms of cerebellar dysfunction such as vertigo, nystagmus or ataxia, or
  • Isolated homonymous hemianopia
35
Q

Stroke differentials

A
  • Seizures (Todd’s paresis)
  • Migraine
  • Bell’s palsy
  • Vestibular neuritis / BPPV
  • Head injuries
  • Exacerbation of an old stroke
  • Space-occupying lesions (e.g. tumours)
  • Demyelinating disorders (e.g. multiple sclerosis)
  • Delirium
  • Sepsis and central nervous system infections
  • Hypoglycaemia and hyperglycaemia
  • Intoxication with alcohol or drugs
36
Q

Ischaemic stroke management

A
  • aspirin 300mg, cont. 2 weeks
  • thrombolysis with alteplase within 4.5hrs of onset
  • thrombectomy within 6-24hrs if confirmed PAC
  • stroke rehab if needed
    secondary prevention:
  • clopidogrel/ dipyridamole
  • treat modifiable RF (eg HTN)
37
Q

Burns immediate management (heat/ electrical/ chemical)

A
  • airway, breathing, circulation
  • burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb
  • electrical burns: switch off power supply, remove the person from the source
  • chemical burns: brush any powder off then irrigate with water
38
Q

How to assess the extent of a burn

A
  • Wallace’s Rule of Nines: head + neck = 9%, each arm = 9%, each anterior part of leg = 9%, each posterior part of leg = 9%, anterior chest = 9%, posterior chest = 9%, anterior abdomen = 9%, posterior abdomen = 9%
  • Palmar surface for smaller areas (SA of patients entire hand = 1%)
  • Lund and Browder chart: the most accurate method
39
Q

Burn depth classification

A
  • Superficial (1st degree): Only epidermis damaged
  • Superficial Partial (2nd degree): Epidermis & upper dermis damaged
  • Deep Partial (2nd degree): Epidermis, upper & lower dermis damaged
  • Full Thickness (3rd degree): All skin layers to subcutaneous tissues damaged
40
Q

How to assess the depth of a burn

A
  • superficial: Red and painful, dry, no blisters
  • superficial partial: Pale pink, painful, blistered. Slow capillary refill
  • deep partial: Typically white but may have patches of non-blanching erythema. Reduced sensation, painful to deep pressure
  • full thickness: White (‘waxy’)/brown (‘leathery’)/black in colour, no blisters, no pain
41
Q

Severe burns pathohysiology

A
  • local progressive tissue loss/ damage
  • loss of capillary membrane integrity -> plasma leakage into interstitial space -> hypovolaemic shock (up to 48h after injury) - decreased blood volume and increased haematocrit
  • Immunosuppression is common -> high risk of sepsis
42
Q

Severe burns management

A
  • stop burning process
  • assess airway - consider early intubation (eg smoke inhalation/ deep facial burns/ blisters to oropharynx)
  • IV fluids: children with burns >10% of total body surface area, adults with burns >15% TBSA
  • urinary catheterisation
  • analgesia
  • transfer to burns unit if complex
43
Q

8 reversible causes of cardiac arrest

A

4Hs and 4Ts:
* Hypoxia
* Hypokalaemia/hyperkalaemia
* Hypothermia/hyperthermia
* Hypovolaemia
* Tension pneumothorax
* Tamponade
* Thrombosis
* Toxins

44
Q

Salicylate examples

A
  • NSAIDs
  • Aspirin
  • Certain antacids and antidiarrhoeal meds
45
Q

Salicylate overdose pathophysiology

A
  • stimulate cerebral medulla -> hyperventilation -> respiratory alkalosis
  • salicylate metabolisation -> uncoupling of oxidative phosphorylation -> anaerobic respiration -> increased lactate -> metabolic acidosis
  • this results in a mixed respiratory alkalosis and metabolic acidosis
46
Q

Salicylate overdose presentation

A
  • hyperventilation (centrally stimulates respiration)
  • tinnitus
  • **lethargy
  • sweating, pyrexia **
  • nausea/vomiting
  • hyperglycaemia and hypoglycaemia
  • seizures
  • coma
47
Q

Salicylate overdose treatment

A
  • general (ABC, charcoal)
  • urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine
  • haemodialysis
48
Q

Describe the Monro-Kellie hypothesis

A
  • the skull has a fixed capacity and contains 3 main substances: brain tissue, CSF and blood
  • if the volume of 1 of these increases, the volume of one of the others must decrease to maintain a constant ICP (compliance)
  • eg bleed in the brain = reduced CSF production
  • once this compensatory compliance mechanism is overwhelmed, small increases in the volume of any one of the three substances will lead to dramatic increases in ICP
49
Q

Raised ICP presentation

A
  • Headache
  • Nausea and vomiting
  • Papilloedema
  • Restlessness, agitation or drowsiness
  • Slow slurred speech
  • Ipsilateral sluggish dilated pupil which then becomes fixed (“blown pupil”)
  • Cranial nerve palsy (e.g. CN III palsy with ‘down and out’ pupil)
  • Seizures
  • Reduced GCS
  • Abnormal respiratory pattern
  • Abnormal posturing, initially decorticate and then decerebrate
50
Q

Cushing’s Triad

A
  • Widening pulse pressure (inc. systolic, dec. diastolic)
  • Bradycardia
  • Irregular respirations
51
Q

How to calculate cerebral perfusion pressure

A
  • CPP = Mean Arterial Pressure (MAP) – ICP
52
Q

Head injury: CT head in 1hr

A
  • GCS < 13 on initial assessment
  • GCS < 15 at 2 hours post-injury
  • suspected open or depressed skull fracture
  • post-traumatic seizure.
  • focal neurological deficit.
  • more than 1 episode of vomiting
  • any sign of basal skull fracture
53
Q

Head injury: CT head within 8hrs

A

LOC/ amnesia since injury, plus any of:
* age 65 years or older
* any history of bleeding or clotting disorders including anticogulants
* dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
* more than 30 minutes’ retrograde amnesia of events immediately before the head injury

54
Q

Benzodiazepine overdose presentation

A
  • Reduced level of consciousness (including coma): if severe this can result in loss of airway tone and reflexes leading to hypoxia if left untreated.
  • Respiratory depression: decreased respiratory rate can result in hypoxia and inadequate tissue perfusion.
  • Hypotension
  • Bradycardia
  • Rhabdomyolysis
  • Hypothermia
55
Q

Benzodiazepine overdose presentation

A
  • Reduced level of consciousness (including coma): if severe this can result in loss of airway tone and reflexes leading to hypoxia if left untreated.
  • Respiratory depression: decreased respiratory rate can result in hypoxia and inadequate tissue perfusion.
  • Hypotension
  • Bradycardia
  • Rhabdomyolysis
  • Hypothermia
56
Q

Benzodiazepine overdose management

A

Flumazenil

57
Q

Pulmonary embolism risk factors

A
  • Recent surgery
  • Recent fractures
  • Recent immobility
  • Personal or family history of a clotting disorder or PE/DVT
  • Obesity
  • Malignancy
  • Infection
  • Pregnancy
  • Medications such as the combined oral contraceptive pill or hormone replacement therapy
58
Q

Pulmonary embolism presentation

A
  • Shortness of breath
  • Pleuritic chest pain
  • Cough
  • Haemoptysis: secondary to infarcted lung tissue.
  • Dizziness or syncope
    Signs:
  • Tachypnea
  • Crackles
  • Tachycardia
  • Fever
59
Q

Pulmonary embolism management

A

PE Wells Score
* PE likely (>4): CTPA, interim DOAC
* PE unlikely (4 or less): D-Dimer -> positive result -> CTPA

60
Q

Pneumothorax definition

A

collection of air between the parietal and visceral pleura of the lung

61
Q

Pneumothorax symptoms

A

sudden onset:
* dyspnoea
* chest pain: often pleuritic
* sweating
* tachypnoea
* tachycardia

62
Q

Pneumothorax management

A
  • no SOB, <2cm rim of air on CXR: no tx required, F/U in 2-4 weeks
  • SOB or >2cm rim of air on CXR: aspiration and reassess -> chest drain if needed
63
Q

Tension pneumothorax pathophysiology

A
  • thoracic trauma -> creates one-way valve, air let in but not out of pleural space
  • trapped air creates pressure inside thorax -> pushes mediastinum across -> kinks big vessels -> cardiorespiratory arrest
64
Q

Tension pneumothorax signs

A
  • Tracheal deviation away from the side of the pneumothorax
  • Reduced air entry on the affected side
  • Increased resonance to percussion on the affected side
  • Tachycardia
  • Hypotension
65
Q

Tension pneumothorax management

A

Insert a large bore cannula into the second intercostal space in the midclavicular line

66
Q

ACS presentation

A
  • Pain radiating to the jaw or arms
  • Nausea and vomiting
  • Sweating and clamminess
  • A feeling of impending doom
  • Shortness of breath
  • Palpitations
67
Q

ACS immediate management

A
  • M - IV morphine
  • O - oxygen if sats below 94 (aim 94-98)
  • N - nitrate
  • A - aspirin 300mg
68
Q

Status epilepticus medical management

A
  • 1st line: 4mg IV lorazepam (give buccal/ IM if no IV access)
  • Repeat after 10 minutes
  • Phenytoin/ levetiracetam/ sodium valproate infusion
69
Q

Status epilepticus general management

A
  • Secure airway (nasopharyngeal)
  • Position pt on left side (aspiration risk)
  • Give oxygen
  • Glucose/ thiamine if indicated
  • Medical management (BDZs)
70
Q

Phenytoin cautions

A
  • Risk of arrhythmias (avoid if cardiac problems)
71
Q

Causes of upper GI bleed

A
  • Peptic ulcers (the most common cause)
  • Mallory-Weiss tear (a tear of the oesophageal mucosa)
  • Oesophageal varices (secondary to portal hypertension in liver cirrhosis)
  • Stomach cancers
72
Q

Upper GI bleed presentation

A
  • Haematemesis (vomiting blood)
  • Coffee ground vomit (caused by vomiting digested blood with the appearance of coffee grounds)
  • Melaena (tar-like, black, greasy and offensive stools caused by digested blood)
73
Q

Glasgow-Blatchford Bleeding Score factors

A
  • Haemoglobin (falls in upper GI bleeding)
  • Urea (rises in upper GI bleeding)
  • Systolic blood pressure
  • Heart rate
  • Presence of melaena
  • Syncope
  • Liver disease
  • Heart failure
74
Q

Group and save vs Crossmatch

A
  • “Group and save”: the lab checks the patient’s blood group and saves a blood sample to match blood if needed
  • “Crossmatch”: the lab allocates units of blood, tests that it is compatible, and keeps it ready in the fridge
75
Q

Upper GI bleed initial management

A

ABATED:
A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 x large bore cannula)
T – Transfusions are required
E – Endoscopy (within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

76
Q

When to transfuse a pt

A
  • Massive haemorrhage
  • Active bleeding plus thrombocytopenia (plt<50)
  • Give prothrombin complex concentrate if active bleeding + warfarin
77
Q

Major haemorrhage definition

A
  • 50% blood loss within 3 hours
  • Blood loss at a rate >150ml/minute
  • Loss of one blood volume over 24 hours
    In an acute scenario, bleeding plus:
  • A blood pressure <90mmHg systolic
  • A heart rate >110bpm
78
Q

How to locate a haemorrhage

A
  • On the floor (external wound)
    and four more:
  • chest cavity (haemothorax)
  • abdominal cavity (injury to a solid organ/ major blood vessel)
  • pelvis (fracture)
  • long bones (fracture)
79
Q

Haemorrage management aims

A
  • Stopping the bleeding (direct pressure, medical/ surgical mx)
  • Replacing lost blood volume (give colloids, 1:1 ratio of units of plasma and RBC)
  • Avoid lethal triad (hypothermia, acidosis, coagulopathy - keep pt warm, maximise oxygenation, avoid crystalloids)
80
Q

COPD exacerbation management

A
  • oxygen
  • nebulised salbutamol/ ipratropium bromide
  • consider NIV
  • consider antibiotics
  • corticosteroids
81
Q

Moderate asthma attack features

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

82
Q

Severe asthma attack features

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

83
Q

Life-threatening asthma attack features

A

PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

84
Q

Acute asthma management

A
  • admit to hospital if life-threatening
  • give oxygen if hypoxaemic
  • SABA - nebulised if life-threatening
  • oral prednisolone for >5 days, in addition to ICS
  • ipratroprium bromide if no response to SABA/ steroids
  • IV magnesium sulfate/ aminophylline - senior management

Clinical Modules (11 decks)

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