Emergency Flashcards
1
Q
Define acute bronchitis
A
Lower respiratory tract infection which causes inflammation int he bronchial airways
2
Q
What are the sings and symptoms of acute bronchitis?
A
Cough
±sputum, wheeze, SOB
Chest pain when coughing
Mildly ill
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
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
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
6
Q
What are the types of acute coronary syndrome?
A
- Unstable angina
- ST Elevation MI
- Non-ST elevation MI
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
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
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
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
11
Q
What are the causes of raised troponin?
A
- Myocardial ischaemia
- Chronic Renal failure
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
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
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
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%
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
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.
17
Q
What is the presentation of Dressler’s syndrome?
A
Pleuritic chest pain Low grade fever Pericardial rub Pericardial effusion Pericardial tamponade
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
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
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
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
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
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
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
25
What are the investigations for AKI?
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
26
What is the management of AKI?
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)
27
What are the complications of AKI?
Hyperkalaemia
Fluid overload, HF, pulmonary oedema
Metabolic acidosis
Uraemia can lead to encephalopathy or pericarditis
28
What are the different classifications of the hypersensitivity reactions?
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.
29
What are the investigations for allergies?
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.
30
What are the treatments for post allergic exposure?
Antihistamines
Steroids
IM adrenaline in anaphylaxis
31
Define anaphylaxis
Caused by a severe type 1 hypersensitivity reaction. IgE stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals (mast cell degranulation).
32
Describe the presentation of anaphylaxis
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
33
What is the management for anaphylaxis?
ABCDE
- IM adrenaline (repeat after 5 mins if required)
- Antihistamines such as oral chlorphenamine or cetirizine
- Steroids (IV hydrocortisone)
34
What should you measure after an anaphylaxis?
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
35
Define abdominal aortic aneurysm
It is a dilated abdominal aorta. Ruptured AAA is when the aneurysm "pops" and starts bleeding into the abdominal cavity.
36
Describe the presentation of a AAA
- 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
37
Describe the management of AAA
- treat reversible risk factors
- monitoring size
- treating peripheral arterial disease
- surgical (usually considered >5.5cm)
- - endovascular stenting
- - laparoscopic repair
- - open surgical repair
38
Describe the presentation of a ruptured AAA
- known AAA or pulsatile mass in abdo
- severe abdo pain (non-specific, radiating to back or loin)
- haemodynamically unstable
39
What are the four cardiac arrest rhythms?
Shockable:
- ventricular tachycardia
- ventricular fibrillation
Non-shockable:
- Pulseless electrical activity
- Asystole
40
What is the treatment for tachycardia in an unstable patient?
Consider up to 3 synchronised shocks
Consider an amiodarone infusion
41
What is the treatment for tachycardia in a stable patient?
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
42
Define atrial flutter
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.
43
What are the conditions associated with atrial flutter?
- Hypertension
- Ischaemic heart disease
- Cardiomyopathy
- Thyrotoxicosis
44
What is the treatment for atrial flutter?
- 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
45
What is supraventricular tachycardias?
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.
46
What is paroxysmal SVT?
A situation where SVT reoccurs and remits in the same patient over time
47
What are the different types of SVT?
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
What is the acute management of stable patients with SVT?
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
What is the long term management of patients with paroxysmal SVT?
Medication: beta blockers, calcium channel blockers or amiodarone
Radiofrequency ablation
50
What is the aetiology of wolff-parkinson white syndrome?
Caused by an extra electrical pathway connecting the atria and ventricles.
51
What is the definitive treatment for Wolff-Parkinson White syndrome?
Radiofrequency ablation of the alternative pathway
52
What are the ECG changes seen in Wolff-Parkinson White syndrome?
```
Short PR interval <0.12s
Wide WRS complex >0.2s
Delta wave (slurred upstroke of QRS complex)
```
53
What is Torsades de Pointes?
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
What are the causes of prolonged QT syndrome
Long QT syndrome
Medications: antipsychotics, citallopram, flecanide
Electrolyte disturbance
55
What is the acute management of Torsades de pointes?
Correct the cause (electrolyte disturbance or meds)
Magnesium infusion (even if normal mg)
Defibrillation if VT occurs
56
What is the long term management of prolonged QT syndrome?
Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers
Pacemaker
57
Give the ECG presentations of Heart Block
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
What is the treatment for bradycardias/AV node blocks?
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
What is the ABG in salicylate overdose?
Mixed respiratory alkalosis and metabolic acidosis
60
What are the features of salicylate overdose/
```
Hyperventilation
Tinnitus
Lethargy
Sweating, pyrexia
N+V
Hyperglycaemia and hypoglycaemia
Seizures
Coma
```
61
What is the treatment of salicylate overdose?
General: ABC, charcoal
Urinary alkalinization with IV sodium bicarbonate
Haemodialysis
62
What is the indication for haemodyalisis in salicylate overdose?
```
Serum concentration >700mg/L
Metabolic acidosis resistant to treatment
Acute renal failure
Pulmonary oedema
Seizures
Coma
```
63
What are the triggers for left ventricular heart failure?
Iatrogenic
Sepsis
MI
Arrhythmias
64
What is the presentation of acute left ventricular failure?
Sudden SOB worse lying flat and improves sitting up
Type 1 respiratory failure (low O2)
3rd Heart sound
bibasal crackles
65
What are the investigations in left ventricular heart failure?
If clinical presentation is acute LVF then treat before diagnosis
BNP
Echo (ejection fraction >50% is normal)
CXR
66
What is the management of left ventricular failure
Pour SOD
Pour away (stop) their IV fluids
Sit up
Oxygen
Diuretics
67
What is the presentation of chronic heart failure?
```
Exertional SOB
Cough ± frothy sputum
Orthopnoea
Paroxysmal nocturnal dyspnoea
Peripheral oedema
```
68
What is the diagnosis of chronic heart failure?
Clinical presentation
BNP
Echo
ECG
69
What are the causes of chronic heart failure?
Ischaemic heart disease
Valvular heart disease - aortic stenosis
HTN
Arrhythmias - AF
70
What is the first line medical treatment for chronic heart faillure?
ABAL
ACEi
Beta blocker
Aldosterone antagonist when A+B not working
Loop diuretics improves symptoms
71
What is Cor pulmonale?
Right sided heart failure caused by respiratory disease
72
What are the causes of cor pulmonale?
```
COPD - most common
PE
Interstitial lung disease
CF
Primary pulmonary HTN
```
73
What is the signs and symptoms of cor pulmonale?
SOB
Peripheral oedema
Syncope
```
Hypoxia
Raised JVP
3rd heart sound
Murmurs
Hepatomegaly
```
74
What is the diagnosis of COPD?
Clinical presentation and spirometry
FEV1/FVC <0.7
Does not show reversibility to salbutamol
75
What is the management of COPD?
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
What is the rule for giving oxygen in COPD?
If retaining CO2 aim for 88-92% titrated by venturi mask
If not retaining co2 and their bicarbonate normal then >94%
77
What is the medical treatment for a COPD exacerbation?
HOME:
Prenisolone
Regular inhalers/nebulisers
Antibiotics
```
HOSPITAL:
Nebulised bronchodillators
Steroids
Antibiotics
Physiotherapy
```
```
STEP UP:
IV aminophyline
NIV
Intubation and ventilation
Doxapram
```
78
Which fractures carry the biggest risk for compartment syndrome?
Supracondylar and tibial shaft fractures
79
What is the diagnosis of compartment syndrome?
intracompartmental pressure >20mmHg are abnormal and >40mmHg is DIAGNOSTIC
80
What is the treatment for compartment syndrome?
Prompt fasciotomy
| Death of muscle groups within 4-6hrs
81
What is the presentation of a DVT?
```
Unilateral
Calf/leg swelling
Dilated superficial veins
Tenderness to calf
Oedema
Colour change
```
82
What is the investigation of DVT?
Measure circumference of calf 10cm below tibial tuberosity.
>3cm difference is significant
83
What is the diagnosis of DVT?
D-dimer is sensitive but not specific.
US Doppler = DIAGNOSTIC
84
What is the management of DVT?
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
Give the management of tonic clonic seizures?
1. Sodium valproate
| 2. Lamotrigine or carbamazepine
86
What are focal seizures?
Start in the temporal lobes and affect hearing speech memory and emotions
87
How do focal seizures present?
Hallucinations
Memory flashbacks
Deja vu
Doing strange things on autopilot
88
What is the management of focal seizures?
Reverse tonic clonic seizure meds
1. Carbamazepine or lamotrigine
2. Sodium valproate or levetiracetam
89
What is the management of absent seizures?
Sodium valproate or ethosuximide
90
What are the investigations and diagnosis of seizures?
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
What is status epilepticus and what do you do?
Seizure lasting more than 5 minutes or more than 3 seizures in one hour
Buccal midazolam
Rectal diazepam
92
What is the cause of hyperthermia?
Excess release of calcium from sarcoplasmic reticulum
Halothane
Suxamethonium
93
What is the investigation and management of hyperthermia?
Investigation:
CK raised
Contracture tests with halothane and caffeine
Management:
Dantrolene (prevents calcium release)
94
What are the investigations in hypothermia/
```
Temp
ECG: J waves or osborn waves
Bloods (+Glucose)
ABG
Coagulation
```
95
What are the common causes of bacterial meningitis in children, adults and neonates?
Children + Adults:
Neisseria meningitidis and Step pneumonia
Neonates:
Group B strep
96
What is the management of meningitis?
Community: IM or IV Benzyllpenicillin
Hospital:
blood culture and LP
<3mths: cefotaxime + amoxicillin
>3mths: ceftriaxone
Consider adding vancomycin and steroids
97
What is the most common cause of viral meningitis?
HSV
Enterovirus
Varicella zoster virus
98
How do you differentiate between bacterial and viral CSF in meningitis?
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
What is the causative organism of necrotising fascitis?
Type 1: anaerobes and aerobes
| Type 2: Strep pyogenes
100
What is the management of pain from raised ICP?
Treat underlying cause
Standard analgesics in stepwise
Trial dexamethasone 8-16mg daily (discontinue if no effect in 3 days)
101
What is the sepsis 6 protocol?
```
Blood lactate level
Blood cultures
Urine output
Oxygen
Empirical antibiotics
IV fluids
```
102
What is neutropenic sepsis?
It is sepsis in a patient with low neutrophil count
103
What is the management of neutropenic sepsis?
Low threshold - suspect neutropenic sepsis in patients taking immunosuppressants
Broad spectrum antibiotics such as piperacillin with tazobactam
104
What are the features of spinal cord compression?
Back pain (worse on lying down and coughing)
Lower limb weakness
Sensory loss and numbness
Neurological signs
105
What is the investigation for spinal cord compression?
Urgent MRI of whole spine within 24hr of presentation
106
What is the management of spinal cord compression?
High dose oral dexamethasone
| Consider radiotherapy or surgery
107
What are the features of tricylcic overdose?
```
Dry mouth
Dilated pupils
Agitation
Sinus tacchy
Blurred vision
```
108
What are the ECG changes seen in tricyclic overdose?
Sinus tachycardia
Widening QRS
Prolongation of QT interval
109
What is the management of tricyclic overdose?
IV bicarbonate
| IV lipid emulsion
110
What is the management for benzodiazepine overdose?
Flumazenil
111
What is the management of lithium overdose
```
Normal saline (mild-moderate)
Haemodialysis (severe)
```
112
What is the management of beta-blocker overdose?
```
Bradycardic = atropine
Resistant = glucagon
```
113
What is the management of methanol poisoning (windshield washer fluid)
Fomepizole or ethanol
| haemodialysis
114
What is the treatment for human and animal bites>
Co-amoxiclav
