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Finals > Emergency > Flashcards

Emergency Flashcards

1
Q

Define acute bronchitis

A

Lower respiratory tract infection which causes inflammation int he bronchial airways

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2
Q

What are the sings and symptoms of acute bronchitis?

A

Cough
±sputum, wheeze, SOB
Chest pain when coughing
Mildly ill

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3
Q

What is the management of acute bronchitis?

A

Self-care:

  • OTC medications
  • stop smoking

Acute bronchitis is usually self-limiting with cough lasting 3-4 weeks

Abs if systemically unwell or if higher risk of complications or if CRP >100mg/L

If abs: doxycycline first line or amoxicillin if pregnant

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4
Q

Describe the pathophysiology of acute coronary syndrome

A

Usually the result of a thrombus from a plaque blocking a coronary artery.

When a thrombus forms in a fast lowing artery it is made up mostly of platelets.

This is why anti-platelet medications are mainstay treatment

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5
Q

Give a description of the coronary arteries

A

The left coronary artery becomes the circumflex and left anterior descending arteries

Right coronary artery curves around the right side and under the heart and supplies the:

  • R atrium and ventricle
  • Inferior aspect of L ventricle
  • Posterior septal area

Circumflex artery curves around the top, left and back of the heart and supplies the:

  • left atrium
  • posterior aspect of left ventriclee

Left anterior descending travels down the middle of the heart and supples the:

  • anterior aspect of the left ventricle
  • anterior aspect of the septum
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6
Q

What are the types of acute coronary syndrome?

A
  1. Unstable angina
  2. ST Elevation MI
  3. Non-ST elevation MI
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7
Q

Describe the diagnosis of acute coronary syndrome

A

If ST elevation or left BBB = STEMI

If no ST elevation, then perform troponin:

  • If raised troponin or other ECG changes = NSTEMI
  • if troponin normal and ECG normal = unstable angina or MSK
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8
Q

What are the symptoms with acute coronary syndrome?

A

Central constricting chest pain with:

  • nausea and vomiting
  • sweating and clamminess
  • feeling of impending doom
  • SOB
  • Palpitations
  • Pain radiating to jaw or arms

Symptoms should continue at rest for more than 20 mins, if they settle consider angina

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9
Q

Describe the ECG changes in acute coronary syndrome

A

STEMI:

  • ST segment elevation
  • New LBBB

NSTEMI:

  • ST segment depression
  • Deep T wave inversion
  • Pathological Q waves
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10
Q

What are the arteries and corresponding heart areas and ECG leads in ACS?

A

Left coronary artery - anterolateral - 1,aVL, V3-6

LAD - anterior - V1-4

Circumflex - Lateral - 1, aVL, V5-6

Right coronary artery - inferior - 2, 3, aVF

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11
Q

What are the causes of raised troponin?

A
  • Myocardial ischaemia
  • Chronic Renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
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12
Q

What are the investigations for ACS?

A
  • ECG
  • FBC (anaemia)
  • U+Es
  • LFTs
  • Lipid profile
  • TFTs
  • HbA1c

Plus:
CXR, CT coronary angiogram, Echo

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13
Q

Describe the treatment for acute STEMI

A

Primary PCI: if available within 2 hours of presentation

Thrombolysis if PCI not available within 2 hours

MONA

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14
Q

Describe the treatment for acute NSTEMI

A

BATMAN

Beta blockers unless contraindicated

Aspirin 300mg stat

Ticagretor 180mg stat or clopidogrel 300mg

Morphine

Anticoagulant: LMWH

Nitrates

Oxygen only if <95%

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15
Q

What are the complications of MI?

A

DREAD

Death

Rupture of the heart septum or papillary muscles

Edema (heart failure)

Arrhythmia or anuerysm

Dressler’s syndrome

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16
Q

What is Dressler’s syndrome? (definition and cause)

A

Usually occurs around 2-3 weeks post MI.

Caused by a localised immune response and causes pericarditis.

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17
Q

What is the presentation of Dressler’s syndrome?

A 
Pleuritic chest pain
Low grade fever
Pericardial rub
Pericardial effusion
Pericardial tamponade
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18
Q

What is the diagnosis and management of dressler’s syndrome?

A

ECG: global ST elevation and T wave inversion

Echo: pericardial effusion

Raised inflammatory markers (CRP and ESR)

Management: NSAIDs –> steroids (prednisolone) –> pericardiocentesis

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19
Q

What is the secondary prevention medical management of acute coronary syndrome?

A

6As

Aspirin 75mg daily
Another antiplatelet (clopidorel or ticagretor)
Atorvastatin 80mg daily
ACEi
Atenolol
Aldosterone antagonist
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20
Q

What is the secondary prevention lifestyle for acute coronary syndrome/

A 
Stop smoking
Reduce alcohol
Mediterranean diet
Cardiac rehab
Optimise treatment of other medical conditions
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21
Q

What are the types of MI?

A

Type 1: Traditional MI due to acute coronary event

Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotention)

Type 3: sudden cardiac death or cardiac arrest suggestive of an ischaemic event

Type 4: MI associated with PCI/coronary stunting/ CABG

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22
Q

Define Acute Kidney injury

A

An acute drop in kidney function. Diagnosed by measuring serum creatinine.

NICE:

  • Rise in creatinine of >25micromol/L in 48 hours
  • Rise in creatinine of >50% in 7 days
  • Urine output of <0.5ml/kg/hour for >6 hours
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23
Q

What are the risk factors for AKI?

A
  • CKD
  • HF
  • Diabetes
  • Liver disease
  • Older age (>65)
  • Cognitive impairment
  • Nephrotoxic medications such as NSAIDs and ACEi
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24
Q

What are the causes of AKI?

A

Pre renal: most common cause and is due to inadequate blood supply to kidneys

  • dehydration
  • hypotension shock)
  • HF

Renal: where intrinsic disease in the kidney leads to reduced filtration:

  • glomerulonephitis
  • interstitial nephritis
  • acute tubular necrosis

Post-renal: caused by obstruction to the outflow of urine from the kidney causing back pressure into kidney (obstructive uropathy)

  • kidney stones
  • masses such as cancer in abdo or pelvis
  • ureter or urethral strictures
  • enlarged prostate or prostate cancer
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25
Q

What are the investigations for AKI?

A

Urinalysis for protein, blood, leucocytes, nitrates and glucose:

  • Leucocytes and nitrates suggest infection
  • Protein and blood suggest acute nephritis
  • Glucose suggests diabetes

US of the urinary tract is used to look for obstruction

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26
Q

What is the management of AKI?

A
  1. Correct underlying cause:
    - Fluid rehydration with IV fluids in pre-renal
    - Stop nephrotoxic medications that reduce filtration pressure
    - Relieve obstruction in post renal (e.g. catheter)
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27
Q

What are the complications of AKI?

A

Hyperkalaemia

Fluid overload, HF, pulmonary oedema

Metabolic acidosis

Uraemia can lead to encephalopathy or pericarditis

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28
Q

What are the different classifications of the hypersensitivity reactions?

A

Type 1: IgE antibodies trigger mast cells and basophils to release histamines. Immediate reaction.

Type 2: IgG and IgM react and activate complement system leading to direct damage of local cells. Eg: haemolytic disease of the newborn and transfusion reactions.

Type 3: immune complexes accumulate and cause damage to local tissues. Eg: autoimmune conditions such as SLE, RA, HSP

Type 4: Cell mediated hypersensitivity reactions caused by T lymphocytes. E.g. Organ transplant rejection and contact dermatitis.

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29
Q

What are the investigations for allergies?

A

Skin prick testing
RAST testing
Food challenge testing

Food challenge testing is the gold standard but it requires a lot of time and resources and isn’t available everywhere.

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30
Q

What are the treatments for post allergic exposure?

A

Antihistamines
Steroids
IM adrenaline in anaphylaxis

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31
Q

Define anaphylaxis

A

Caused by a severe type 1 hypersensitivity reaction. IgE stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals (mast cell degranulation).

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32
Q

Describe the presentation of anaphylaxis

A

Rapid onset:

  • urticaria
  • itching
  • angio-oedema with swelling around lips and eyes
  • abdominal pain

Additional symptoms:

  • SOB
  • Wheeze
  • Swelling of the larynx, causing stridor
  • tachycardia
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33
Q

What is the management for anaphylaxis?

A

ABCDE

  • IM adrenaline (repeat after 5 mins if required)
  • Antihistamines such as oral chlorphenamine or cetirizine
  • Steroids (IV hydrocortisone)
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34
Q

What should you measure after an anaphylaxis?

A

Serum mast cell tryptasse within 6 hours of the event.

Tryptase is released during mast cell degranulation and stays in the blood for 6 hours before gradually disappearing

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35
Q

Define abdominal aortic aneurysm

A

It is a dilated abdominal aorta. Ruptured AAA is when the aneurysm “pops” and starts bleeding into the abdominal cavity.

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36
Q

Describe the presentation of a AAA

A
  • often asymptomatic
  • symptoms of peripheral vascular disease
  • non-specific abdo pain
  • palpable expansile pulsation in the abdomen when palpated with both hands
  • found incidentally on abdo x-ray
  • diagnosis by US or angiography
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37
Q

Describe the management of AAA

A
  • treat reversible risk factors
  • monitoring size
  • treating peripheral arterial disease
  • surgical (usually considered >5.5cm)
    • endovascular stenting
    • laparoscopic repair
    • open surgical repair
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38
Q

Describe the presentation of a ruptured AAA

A
  • known AAA or pulsatile mass in abdo
  • severe abdo pain (non-specific, radiating to back or loin)
  • haemodynamically unstable
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39
Q

What are the four cardiac arrest rhythms?

A

Shockable:

  • ventricular tachycardia
  • ventricular fibrillation

Non-shockable:

  • Pulseless electrical activity
  • Asystole
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40
Q

What is the treatment for tachycardia in an unstable patient?

A

Consider up to 3 synchronised shocks

Consider an amiodarone infusion

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41
Q

What is the treatment for tachycardia in a stable patient?

A

Narrow complex (QRS<0.12s):

  • AF: rate control with beta blocker or dilitiazem
  • Atrial flutter: rate control with beta blocker
  • supraventricular tachycardia: vagal manoeuvres and adenosine

Broad complex (QRS>0.12s):

  • ventricular tachycardiaa: amiodarone infusion
  • if known SVT with BBB: treat as normal SVT
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42
Q

Define atrial flutter

A

Atrial flutter is caused by a “re-entrant rhythm” in either atrium. Where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway.

The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300bpm. The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node causing 150bpm ventricular contraction.

This gives a “sawtooth appearance” on the ECG with P wave after P wave.

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43
Q

What are the conditions associated with atrial flutter?

A
  • Hypertension
  • Ischaemic heart disease
  • Cardiomyopathy
  • Thyrotoxicosis
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44
Q

What is the treatment for atrial flutter?

A
  • rate/rhythm control with beta blockers or cardioeversion
  • treat the reversible underlying condition
  • radiofrequency ablation of the re-entrant rhythm
  • anticoagulation based on CHA2DS2VASc score
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45
Q

What is supraventricular tachycardias?

A

Caused by the electrical signal re-entering the atria from the ventricles. Once the signal is back in the atria, it travels back through the AV node and causes another ventricular contraction.

This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia.

It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

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46
Q

What is paroxysmal SVT?

A

A situation where SVT reoccurs and remits in the same patient over time

47
Q

What are the different types of SVT?

A

Atrioventricular nodal re-entral tachycardia: when the re-entry point is back through the AV node

Atrioventricular re-entrant tachycardia: when the re-entry point is an accessory pathway (WPW syndrome)

Atrial tachycardia: where the electrical signal originates in the atria somewhere other than the SA node. Caused by abnormally generated electrical activity in the atria.

48
Q

What is the acute management of stable patients with SVT?

A

Stepwise approach - so look at the ECG see if its worked before moving on

  1. Valsalva manoeuvre
  2. Carotid sinus massage
  3. Adenosine
  4. Alternative to adenosine (verapamil)
  5. Direct current cardioversion
49
Q

What is the long term management of patients with paroxysmal SVT?

A

Medication: beta blockers, calcium channel blockers or amiodarone

Radiofrequency ablation

50
Q

What is the aetiology of wolff-parkinson white syndrome?

A

Caused by an extra electrical pathway connecting the atria and ventricles.

51
Q

What is the definitive treatment for Wolff-Parkinson White syndrome?

A

Radiofrequency ablation of the alternative pathway

52
Q

What are the ECG changes seen in Wolff-Parkinson White syndrome?

A 
Short PR interval <0.12s
Wide WRS complex  >0.2s
Delta wave (slurred upstroke of QRS complex)
53
Q

What is Torsades de Pointes?

A

A type of polymorphic ventricular tachycardia.
Occurs in people with prolonged QT interval.

Either it will terminate spontaneously and revert back to sinus rhythm or progress into ventricular tachycardia

54
Q

What are the causes of prolonged QT syndrome

A

Long QT syndrome
Medications: antipsychotics, citallopram, flecanide
Electrolyte disturbance

55
Q

What is the acute management of Torsades de pointes?

A

Correct the cause (electrolyte disturbance or meds)
Magnesium infusion (even if normal mg)
Defibrillation if VT occurs

56
Q

What is the long term management of prolonged QT syndrome?

A

Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers
Pacemaker

57
Q

Give the ECG presentations of Heart Block

A

1st degree: PR interval >0.2s

Mobitz 1: Increase PR interval until P wave no longer followed by QRS

Mobits 2: Missing WRS complexes e.g. for every 3 P waves, there is one WRS therefore 3:1 block

3rd degree: no relationship between P wave and QRS

58
Q

What is the treatment for bradycardias/AV node blocks?

A

Stabe: Observe

Unstable or at risk of asystole (Mobitz 2, 3rd degree block or previous asystole):
1. Atropine 500mcg IV
If no improvement:
2. Atropine 500mcg IV repeated up to 6 doses
3. Other inotropes e.g. NA
4. Transcutaneous cardiac pacing using a defib

59
Q

What is the ABG in salicylate overdose?

A

Mixed respiratory alkalosis and metabolic acidosis

60
Q

What are the features of salicylate overdose/

A 
Hyperventilation
Tinnitus
Lethargy
Sweating, pyrexia
N+V
Hyperglycaemia and hypoglycaemia
Seizures
Coma
61
Q

What is the treatment of salicylate overdose?

A

General: ABC, charcoal
Urinary alkalinization with IV sodium bicarbonate
Haemodialysis

62
Q

What is the indication for haemodyalisis in salicylate overdose?

A 
Serum concentration >700mg/L
Metabolic acidosis resistant to treatment
Acute renal  failure
Pulmonary oedema
Seizures
Coma
63
Q

What are the triggers for left ventricular heart failure?

A

Iatrogenic
Sepsis
MI
Arrhythmias

64
Q

What is the presentation of acute left ventricular failure?

A

Sudden SOB worse lying flat and improves sitting up

Type 1 respiratory failure (low O2)

3rd Heart sound

bibasal crackles

65
Q

What are the investigations in left ventricular heart failure?

A

If clinical presentation is acute LVF then treat before diagnosis

BNP
Echo (ejection fraction >50% is normal)
CXR

66
Q

What is the management of left ventricular failure

A

Pour SOD

Pour away (stop) their IV fluids
Sit up
Oxygen
Diuretics

67
Q

What is the presentation of chronic heart failure?

A 
Exertional SOB
Cough ± frothy sputum
Orthopnoea
Paroxysmal nocturnal dyspnoea
Peripheral oedema
68
Q

What is the diagnosis of chronic heart failure?

A

Clinical presentation
BNP
Echo
ECG

69
Q

What are the causes of chronic heart failure?

A

Ischaemic heart disease
Valvular heart disease - aortic stenosis
HTN
Arrhythmias - AF

70
Q

What is the first line medical treatment for chronic heart faillure?

A

ABAL

ACEi
Beta blocker
Aldosterone antagonist when A+B not working
Loop diuretics improves symptoms

71
Q

What is Cor pulmonale?

A

Right sided heart failure caused by respiratory disease

72
Q

What are the causes of cor pulmonale?

A 
COPD - most common
PE
Interstitial lung disease
CF
Primary pulmonary HTN
73
Q

What is the signs and symptoms of cor pulmonale?

A

SOB
Peripheral oedema
Syncope

Hypoxia
Raised JVP
3rd heart sound
Murmurs
Hepatomegaly
74
Q

What is the diagnosis of COPD?

A

Clinical presentation and spirometry

FEV1/FVC <0.7

Does not show reversibility to salbutamol

75
Q

What is the management of COPD?

A
  1. B-2-agonist (salbutamol) or short acting antimuscarinics (ipatropium bromide)
  2. IF no asthmatic or steroid response: LABA + LAMA

IF asthmatic response: LABA + ICS

76
Q

What is the rule for giving oxygen in COPD?

A

If retaining CO2 aim for 88-92% titrated by venturi mask

If not retaining co2 and their bicarbonate normal then >94%

77
Q

What is the medical treatment for a COPD exacerbation?

A

HOME:
Prenisolone
Regular inhalers/nebulisers
Antibiotics

HOSPITAL:
Nebulised bronchodillators
Steroids
Antibiotics
Physiotherapy
STEP UP:
IV aminophyline
NIV
Intubation and ventilation
Doxapram
78
Q

Which fractures carry the biggest risk for compartment syndrome?

A

Supracondylar and tibial shaft fractures

79
Q

What is the diagnosis of compartment syndrome?

A

intracompartmental pressure >20mmHg are abnormal and >40mmHg is DIAGNOSTIC

80
Q

What is the treatment for compartment syndrome?

A

Prompt fasciotomy

Death of muscle groups within 4-6hrs

81
Q

What is the presentation of a DVT?

A 
Unilateral
Calf/leg swelling
Dilated superficial veins
Tenderness to calf
Oedema
Colour change
82
Q

What is the investigation of DVT?

A

Measure circumference of calf 10cm below tibial tuberosity.

> 3cm difference is significant

83
Q

What is the diagnosis of DVT?

A

D-dimer is sensitive but not specific.

US Doppler = DIAGNOSTIC

84
Q

What is the management of DVT?

A

LMWH started before confirming diagnosis

Switch to long term anticoagulation
3 mnths if obvious cause
>3mths if cause unclear
6 mths in active cancer

85
Q

Give the management of tonic clonic seizures?

A
  1. Sodium valproate

2. Lamotrigine or carbamazepine

86
Q

What are focal seizures?

A

Start in the temporal lobes and affect hearing speech memory and emotions

87
Q

How do focal seizures present?

A

Hallucinations
Memory flashbacks
Deja vu
Doing strange things on autopilot

88
Q

What is the management of focal seizures?

A

Reverse tonic clonic seizure meds

  1. Carbamazepine or lamotrigine
  2. Sodium valproate or levetiracetam
89
Q

What is the management of absent seizures?

A

Sodium valproate or ethosuximide

90
Q

What are the investigations and diagnosis of seizures?

A

EEG after second simple tonic clonic seizure

MRI brain in:
First seizure is in child <2yr
Focal seizures
No response to 1st line meds

91
Q

What is status epilepticus and what do you do?

A

Seizure lasting more than 5 minutes or more than 3 seizures in one hour

Buccal midazolam
Rectal diazepam

92
Q

What is the cause of hyperthermia?

A

Excess release of calcium from sarcoplasmic reticulum

Halothane
Suxamethonium

93
Q

What is the investigation and management of hyperthermia?

A

Investigation:
CK raised
Contracture tests with halothane and caffeine

Management:
Dantrolene (prevents calcium release)

94
Q

What are the investigations in hypothermia/

A 
Temp
ECG: J waves or osborn waves
Bloods (+Glucose)
ABG
Coagulation
95
Q

What are the common causes of bacterial meningitis in children, adults and neonates?

A

Children + Adults:
Neisseria meningitidis and Step pneumonia

Neonates:
Group B strep

96
Q

What is the management of meningitis?

A

Community: IM or IV Benzyllpenicillin

Hospital:
blood culture and LP
<3mths: cefotaxime + amoxicillin
>3mths: ceftriaxone

Consider adding vancomycin and steroids

97
Q

What is the most common cause of viral meningitis?

A

HSV
Enterovirus
Varicella zoster virus

98
Q

How do you differentiate between bacterial and viral CSF in meningitis?

A

Bacteria are cloudy, they release protein and suck up glucose. The body produces neutrophils in response

Virus are clear and release a little protein but don’t suck glucose. Body releases lymphocytes in response

99
Q

What is the causative organism of necrotising fascitis?

A

Type 1: anaerobes and aerobes

Type 2: Strep pyogenes

100
Q

What is the management of pain from raised ICP?

A

Treat underlying cause
Standard analgesics in stepwise
Trial dexamethasone 8-16mg daily (discontinue if no effect in 3 days)

101
Q

What is the sepsis 6 protocol?

A 
Blood lactate level
Blood cultures
Urine output
Oxygen 
Empirical antibiotics
IV fluids
102
Q

What is neutropenic sepsis?

A

It is sepsis in a patient with low neutrophil count

103
Q

What is the management of neutropenic sepsis?

A

Low threshold - suspect neutropenic sepsis in patients taking immunosuppressants

Broad spectrum antibiotics such as piperacillin with tazobactam

104
Q

What are the features of spinal cord compression?

A

Back pain (worse on lying down and coughing)
Lower limb weakness
Sensory loss and numbness
Neurological signs

105
Q

What is the investigation for spinal cord compression?

A

Urgent MRI of whole spine within 24hr of presentation

106
Q

What is the management of spinal cord compression?

A

High dose oral dexamethasone

Consider radiotherapy or surgery

107
Q

What are the features of tricylcic overdose?

A 
Dry mouth
Dilated pupils
Agitation
Sinus tacchy
Blurred vision
108
Q

What are the ECG changes seen in tricyclic overdose?

A

Sinus tachycardia
Widening QRS
Prolongation of QT interval

109
Q

What is the management of tricyclic overdose?

A

IV bicarbonate

IV lipid emulsion

110
Q

What is the management for benzodiazepine overdose?

A

Flumazenil

111
Q

What is the management of lithium overdose

A 
Normal saline (mild-moderate)
Haemodialysis (severe)
112
Q

What is the management of beta-blocker overdose?

A 
Bradycardic = atropine
Resistant = glucagon
113
Q

What is the management of methanol poisoning (windshield washer fluid)

A

Fomepizole or ethanol

haemodialysis

114
Q

What is the treatment for human and animal bites>

A

Co-amoxiclav

Finals (20 decks)

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