Emergency medicine Flashcards

1
Q

What should you look for when assessing of breathing? (B)

A

signs of resp. distress

RR

Assess depth/quality of breathing

chest deformity, raised JVP abdominal distension

Record FiO2 and SpO2

Listen near face: wheeze, coughing, stridor

Palpate, percuss, auscultate

Trachea position

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2
Q

How can hyperventilation affect ventilation?

A

Reduces the level of ventilation achieved (just gets rid of CO2)

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3
Q

What signs may indicate resp. distress?

A

Increased RR (in SEVERE resp. distress - can become hypoventilation)
accessory muscle use, intercostal and subcostal recession
Agitation (untreated hyperaemia - cerebrally irritated)
Sweating
Pallor/redness/cyanosis
Wheeze

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4
Q

What RR indicates that pt. may be near death?

A

> 27

Or v. low

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5
Q

What may chest deformity tell you about pt?

A

Existing disease (eg. barrel chest, COPD)

Cause of breathlessness - abdominal breathing, broken ribs, restrictive disease etc.

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6
Q

Why is JVP important in resp.?

A

Cardiac cause of resp. problem (pulmonary oedema)

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7
Q

What things can cause tracheal deviation?

A

Large pleural effusions

tension pneumothorax

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8
Q

What treatments can you give breathless pt.?

A

Oxygen
Salbutamol nebs
GTN or furosemide (in pulmonary oedema - esp. if near arrest)
ABX and steroids (Later management, once pt. stable)

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9
Q

Flow rate of Oxygen that can be given when using nasal cannula. What percentage oxygen is delivered?

A

2-6L (usually 4L)/min

24-30%

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10
Q

Flow rate of Oxygen that can be given when using Hudson Mask. What percentage oxygen is delivered?

A

5-10L/min

30-40%

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11
Q

Flow rate of Oxygen that can be given with non-rebreathe mask. What conc. of oxygen is delivered?

A

12-15L

85% (ideally, would be 100%)

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12
Q

What is a benefit of a bag-valve mask?

A

Delivers positive pressure

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13
Q

What are CPAP/BiPAP?

A

Types of non-invasive ventilation

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14
Q

Should you prescribe O2 for someone who is breathless, but has normal-range O2 sats?

A

NO.

If they do not have oxygen requirement, THEY DO NOT NEED TO BE GIVEN SUPPLEMENTARY OXYGEN

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15
Q

What is normal range of sats in COPD pt.?

A

88-92%

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16
Q

What is normal range of sats in non-COPD pt.?

A

94-98%

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17
Q
62  yr M
COPD
SOB
Productive cough, fever, pleuritic chest pain
O2 sats 90%

Does he need Oxygen?

A

NO.

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18
Q
25 yr M
Operative repair of femur #
No PMH
ABCDE confirms he's not critically unwell
Sats 90%
Differentials
What is his O2 target range?
Does he need supplementary O2?
What delivery system should you use?
Why is ABCDE normal?
A

Fat embolism
Hospital-acquired pneumonia

O2 target range: 94-98%

Yes he needs O2

What delivery system? Nasal cannula (commencing on 1L/min up to max of 6L/min) - start small, increase!

ABCDE has shown he’s not critically unwell as he is ACUTELY unwell, not CRITICALLY unwell (critical means near-death). You have time to manage him before he turns critical.

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19
Q

What are features of fat embolism?

A

SOB, reduced sats, usually cerebrally confused

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20
Q
19Yr M
Collapsed at home
Vomiting
Pyrexial
Florid non-blanching purpuric rash
Critically unwell 
Sats on 99% on face mask

Does he need Oxygen?
How should it be delivered?

A

Critically unwell - therefore even if sats in range, need to be on 15L

non-rebreathe reservoir mask

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21
Q
78 yr F
COPD
Long-term O2 therapy
Collapse
Reduced consciousness
In extremis (about to have cardiac arrest)
Slow-intermirrent gasping breaths
Sats are unrecordable 
O2 target range?
Does she need supplementary O2?
What O2 delivery system would you choose?
What might her ABG look like?
What do you need to consider?
A

88-92%

Yes

She needs a bag and valve mask - she isn’t breathing, therefore needs ventilation (+ve pressure of bag and valve mask)

Low O2, high CO2 - possible resp. acidosis

Whether she may have a DNACPR, therefore, what you do re. withdrawng care/ continuing resuscitation

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22
Q
48 Yr M
Pneumonia on ward
Increasing SOB
On O2 (nasal cannula 6L/min
ABCDE: not critically unwell
Sats 93%

Does he need O2?
If so, via which O2 delivery system?

A

Yes

Simple fase mask (5L/min - although reduction, this would probably be enough via this method. If not working, titrate up)

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23
Q
28 Yr M
CF
Recovering from pneumonia 
ABCDE: not acutely unwell
Sats: 86% 
on 60% venturi (V60) mask 

What is his target range? Why?
Does he need O2?
Via which delivery system?
Who else might you want involved?

A

88-92
Yes
Non-rebreathe mask
Critical care review, if not HDU (as he is deteriorating and requiring high-flow Oxygen and aggressive treatment)

*in leeds, can’t be in normal ward if you’re on non-rebreathe

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24
Q

Who should get a blood gas?

A

ANYONE who’s Critically ill
Unexpected/inappropriate hyperaemia (Sp O2 <94%) Or requiring O2 to maintain normal sats

Deteriorating O2 sats

Increasing SOB with previously stable hyperaemia

Deteriorating pt. who now requires O2 to maintain constant O2 sats

RF for hypercapnia resp. failure, develops acute SOB, reduced O2 sats, drowsiness or other Sx of CO2 retention

SOB and thought to be at risk of metabolic conditions

Acute SOB or critical illness and poor peripheral circulation in whom reliable oximetry cannot be obtained

ANY OTHER EVIDENCE THAT WOULD INDICATE THAT BG WOULD BE USEFUL

Any reduction in O2 sats of 3% or more (even if within target range)

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25
Q

What are the benefits of ABG over VBG?

A

ABG is gold standard for determining the arterial metabolic parameters

Can determine PaO2 (can’t do this on VBG)

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26
Q

What is a normal pH range on a BG? What is it called if value is:

a) below range
b) above range?

A
  1. 35-7.45
    a) acidaemia
    b) alkalaemia
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27
Q

What is a normal PaO2 range on a BG? What is it called if value is:

a) below range
b) above range?

A

> 10kPA

a) hypoxaemia
b) hyperoxaemia

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28
Q

What is a normal PaCO2 range on a BG? What is it called if value is:

a) below range
b) above range?

A

4-6

a) respiratory alkalosis
b) respiratory acidosis

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29
Q

What is a normal HCO3 range on a BG? What is it called if value is:

a) below range
b) above range?

A

22-30

a) metabolic acidosis
b) metabolic alkalosis

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30
Q

What is a normal BXS range on a BG? What is it called if value is:

a) below range
b) above range?

A
  • 2 to +2
    a) metabolic acidosis
    b) metabolic alkalosis
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31
Q

Outline the process of blood gas interpretation

A
How is pt. clinically
O2
pH
PaCO2
BXS or bicarb
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32
Q

Outline blood gas interpretation

A
How is pt. clinically - KNOW CLINICAL SCENARIO (incl. FiO2)
O2
pH
PaCO2
BXS or bicarb

Does your interpretation fit clinical picture

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33
Q
20 yr M
Tachypnoea
Abdo pain
Vomiting
Confusion

What are differentials?

vomit has to be suctioned from airway

RR 28
SpO2 99% on air
AE L=R
Pulse 128
BP 95/60
HS I + II + 0
No other obvious abnormal signs
A

Differentials:
DKA
Pneumonia
Sepsis

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34
Q
20 yr M
Tachypnoea
Abdo pain
Vomiting
Confusion

What are differentials?

vomit has to be suctioned from airway

RR 28
SpO2 99% on air
AE L=R
Pulse 128
BP 95/60
HS I + II + 0
No other obvious abnormal signs

Knowing this, What other differentials might you come up with?

GCS 13/15
ES V4 M6

can he have blood gas?

VBG:
pH 6.9
PO2 11.5
PCo2 3.5
HCO3 8
BXS 12

What does this tell you?
Are the results a surprise?

A

Differentials 1:
DKA
Pneumonia
Sepsis

Differentials 2:
Septic shock
Hypovolaemic shock

He needs blood gas: shock and ?metabolic illness

Metabolic acidosis

No, results fit clinical picture

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35
Q

What are signs of C02 retention?

A

Cyanosis

Confusion

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36
Q

What is the definition of shock?

A

Clinical syndrome caused by inadequate tissue perfusion and oxygenation leading to abnormal metabolic function

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37
Q

What are the different types of shock?

A

Cardiogenic

Hypovolaemic

Obstructive

Neurogenic

Anaphylactic

Septic

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38
Q

What are the physiological effects of shock and re-perfusion?

A

Intracellular calcium overload leading to ↓myocardial contractility, ATP reduction & degradation of ion pumps via free radicals.

H+ excess causing ↓ catecholamine effect and ↓ myocardial function

Metabolism becomes glycolysis dependent leading to↑ FFA and
↑lactic acid

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39
Q

What are common causes of hypovolaemic shock

A

fluid loss eg. excess urination, reduced intake, vomiting, burns
haemorrhage (haemorrhage shock)

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40
Q

How should you treat hypovolaemic shock

A

IV access
IV fluids +/- blood
Treat cause (stop bleeding)
Monitor response

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41
Q

What is an anaphylactic shock?

A

Sudden onset generalised immune condition caused by exposure to a causative substance in a sensitised
person

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42
Q

How long after exposure to substance, do Sx of anaphylaxis begin?

A

depends what source is/route of contact (generally 30 mins)
topical 10-15 mins
eaten 30 mins
IV = matter of minutes

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43
Q

How would you treat anaphylactic shock?

A

1) Adrenaline (IM = thigh, elevate leg)
2) Crystalloid fluids (DO NOT GIVE COLLOID)
3) Hydrocortisone (prevent bi-phasic reactions)
4) Chloramphenamine (anti-histamine)
Ranitidine (H2 blocker)
May need to repeat IM adrenaline after 5 mins

Continue to deteriorate - IV adrenaline bolus (BY A SENIOR)

All anaphylaxis pts. are admitted - at risk of biphasic shock within around 6 hours

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44
Q

What is septic shock?

A

Sepsis accompanied by hypotension and perfusion abnormalities despite adequate fluid resuscitation

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45
Q

What is syncope?

A

transient loss of consciousness
(usually without warning)

Transient global cerebral hypotension

Rapid onset

WITH SPONTANEOUS COMPLETE RECOVERY (if you have lasting Sx, IT IS NOT SYNCOPE)

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46
Q

Can a pt. lose consciousness with TIA?

A

Unlikely that unconsciousness would occur TIA (as would need to effect both halves of brain blood supply at same time)

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47
Q

What are the main general categories of causes of TRUE syncope?

A

Cardiac
orthostatic
neurogenic

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48
Q

What are the San Francisco syncope rules? What do they help you decide?

A

CHESS - IF YOU THINK Pt HAS HAD SYNCOPE, helps you decide who is safe to go home.

Hx of congestive HF
Haematocrit <30%
Abnormal ECG
SOB
Triage systolic BP < 90

Any of these - high risk of having had cardiac event. Need to be admitted.

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49
Q

What is the OESIL risk score?

A

Risk score

Point score of following RF:
Age >65 (1)
Hx of Cv disease (1)
Syncope with prodromes (1)
Abnormal ECG (1)

Score of 2 or more implies increased risk of cardiac death

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50
Q

What are some more unusual Sx of syncope? How can each of these be told apart from a seizure?

A

Twitching (for about 5-10 seconds - convulsive syncope)

Tongue biting (at tip - unlikely to be seizure. Tongue biting at side, more likely to be seizure)

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51
Q

What should you include in a neurological assessment in a pt. with collapse?

A
Cranial nerves
Peripheral nerves    
Cerebellar
Gait
AMTS - best done on first meeting
Fundi
NIHSS
GCS
Pupils
Lateralising signs 
Capillary glucose
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52
Q

What is the NIHSS? What is it used for?

A

NIH stroke scale

Scale used to decide whether someone can be thrombolysed

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53
Q

What are common causes of hypoglycaemia in diabetic pts.

A

Hypoglycaemic agents
Decreased glucose intake
Increased glucose utilisation (increased exercise)
Increased insulin sensitivity (weight loss, increased exercise)
Reduced insulin clearance (renal failure)

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54
Q

Why would you do CXR if you think pt has PE?

A

May see wedge infarct

Rule out differentials (eg. pneumothorax)

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55
Q

What are the main two investigations for PE?

A
CTPA
VQ scan (looking for VQ mismatch)
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56
Q

Which direction do shoulder dislocations most commonly occur in? What are two key things associated with anterior shoulder dislocation that you should make sure you assess/document?

A

Anterior dislocations

test regimental badge and document radial artery

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57
Q

What are people given when they have been poisoned (if this has occurred within the last hour)?

A

Charcoal (drink)

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58
Q

What are the classical features of an opiate toxidrome?

A

pin point pupils
resp depression
reduced GCS

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59
Q

What can be used to reverse benzo toxicity? Why might you not do this?

A

flumazanil

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60
Q

Why might you NOT give a full dose of naloxone to someone who has suffered a heroine overdose?

A

Naloxone could recover their RR before the heroin has worn off, therefore pt may leave before the effects of heroin have worn off and you’ve been able to treat properly

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61
Q

What is a common s/e of poppers?

A

methaemoglobinaemia

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62
Q

w

A

w

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63
Q

What scoring system is used for PE? (other than Well’s score)

A

PERC

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64
Q

How should you approach a pt. who is acutely unwell?

A
Focussed Hx
Collateral Hx
Focussed examination
Investigation
Working diagnosis, initial treatment
management plan (incl. referral to correct ward)
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65
Q

How should you approach a pt. who is critical unwell?

A

ABCDE approach (treat at each stage)
Investigations
Working diagnosis, further initial treatment

Once stable: focussed Hx
focussed Ex
Longer-term management plan (incl. referral to correct ward)

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66
Q

List what should be done in A of ABCDE?

A

Look for signs of airway obstruction

TREAT obstruction (adjuncts)

Give oxygen (if sats require it)

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67
Q

List what should be done in B of ABCDE?

A
Look for resp distress
RR
Quality of breathing
Chest deformity 
FiO2 and spO2
Listen near face
palpate, percuss and auscultate
Tracheal deviation 

Initiate treatment

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68
Q

List what should be done in C of ABCDE?

A
HR 
BP
Fluids (if low BP/CO)
Look at cardiac monitor
Look/feel hands
assess peripheral and central CRT
Assess venous filling (cap. refill)
Central and peripheral pulses
Listen to heart
Look for signs of poor cardiac output, haemorrhage

Treat cause of cardiovascular collapse

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69
Q

List what should be done in D of ABCDE?

A

Review and treat ABC - sats and BP esp.

GCS/AVPU
Drug chart (drug-induced reduced GCS)
Pupils
Lateralising signs
Capillary glucose
Ensure airway protection
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70
Q

List what should be done in E of ABCDE?

A

Examine pt: bruising, breaks etc.

Temp

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71
Q

What should you do after you’ve done ABCDE assessment of pt.?

A
Take Hx
Review notes
Review results
Consider which level of care required
Reassess response
Documentation
Definitive treatment
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72
Q

How can causes of collapse be classified to help diagnosis?

A

Head
Heart
Vessels
Drugs

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73
Q

What are ‘head’ causes of collapse?

A
Hypoxia 
Hypoglycaemia
Epilepsy
Affective
Dysfunction of brain stem eg. verterbrobasilar stroke, TIA or migraine
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74
Q

What are ‘heart’ causes of collapse?

A
IHD
Emboli
Aortic obstruction (eg. stenosis, HOCM)
Rhythm disorders
Tachyarrhythmias (VT, SVT, QT syndrome)
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75
Q

What are ‘vessel’ causes of collapse?

A
Vasovagal
ENT: BBPV, labyrinthitis, meniere's
Situational: micturition/cough syncope
Sensitive carotid sinus
Ectopic pregnancy
Low vascular tone
Subclavian steal
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76
Q

What are ‘drug’ causes of collapse?

A

Anti-Hypertensives eg. beta blockers

‘Street’ drugs

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77
Q

What questions do you want to ask a pt. who has come in with collapse?

A
What were you doing at time?
Any associated Sx
Witnesses 
Recent illness
On-going illness
Medication 
Previous episodes
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78
Q

What systems do you want to examine in pt. who has come in with collapse?

A
General appearance (sats,
BP/HR/RR)
CV
resp
neuro
head and neck
abdo and pelvis
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79
Q

What investigations might you want to do for pt. who has come in with collapse?

A

blood glucose

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80
Q

What is cariogenic shock?

A

Heart unable to pump enough blood to meet body’s needs

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81
Q

What is neurogenic shock?

A

Shock caused by disruption of autonomic pathways within spinal cord

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82
Q

What is hypovolaemic shock?

A

Fluid loss means heart cannot pump enough blood around body to meet its needs

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83
Q

What is anaphylactic shock?

A

Severe allergic reaction

mediators released in allergic reaction cause vasodilation, bronchial restriction, leaky blood valves, depressed HR

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84
Q

What is obstructive shock?

A

Physical obstruction of great vessels or heart itself

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85
Q

What is septic shock?

A

Inflammatory markers and organ damage lead to lowered blood pressure and abnormal cellular metabolism

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86
Q

What are some common causes of cariogenic shock?

A

MI

Malignant dysrhythmia

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87
Q

What are some common causes of obstructive shock?

A

tension pneumothorax

cardiac tamponade

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88
Q

What types of shock fall under the term ‘distributive shock’?

A

septic shock
anaphylaxis
neurogenic shock

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89
Q

What might you find on ABC examination of a pt. suffering from an anaphylactic shock?

A

A: swelling, hoarseness, stridor
B: rapid breathing, wheeze, fatigue, cyanosis, sats < 92%, confusion
C: pale, clammy, low BP, faintness, drowsy/coma

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90
Q

What ratio of adrenaline is given in anaphylactic shock?

A

1:1000

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91
Q

What dose (and volume) of adrenaline is given to adults in anaphylaxis?

A

500 micrograms IM

0.5 mL

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92
Q

What dose (and volume) of adrenaline is given to children over 12 in anaphylaxis?

A

500 micrograms IM

0.5 mL

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93
Q

What dose (and volume) of adrenaline is given to children 6-12 yrs in anaphylaxis?

A

300 micrograms IM

0.3 mL

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94
Q

What dose (and volume) of adrenaline is given to children under 6 in anaphylaxis?

A

150 micrograms IM (0.15 mL)

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95
Q

What volume of CRYSTALLOID fluid is given to a) adults and b) children?

A

a) 500mL-1000mL

b) 20 mL/Kg

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96
Q

What dose of hydrocortisone is given to pts (IM or slow IV) in anaphylaxis?

a) adult or child >12 yrs
b) child 6-12 yrs
c) child 6 mths - 6 yrs
d) child < 6 mths

A

a) 200mg
b) 100 mg
c) 50 mg
d) 25 mg

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97
Q

What dose of chloramphenamine is given to pts (IM or slow IV) in anaphylaxis?

a) adult or child >12 yrs
b) child 6-12 yrs
c) child 6 mths - 6 yrs
d) child < 6 mths

A

a) 10mg
b) 5 mg
c) 2.5 mg
d) 250 micrograms/Kg

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98
Q

What is BUFALO and what does it stand for? What timeframe should it be completed in?

A
Septic pt. management:
Blood cultures and septic screen
Urine output (monitor hourly)
Fluid resuscitation
Antibiotics IV
Lactate measurement (ABG)
Oxygen - to correct hypoxia

Try to complete within one hour (ASAP)

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99
Q

What are the problems with ABGs? (which might make you consider getting a VBG)

A
painful
increased risk of bleeding and haematoma (compared to VBG)
risk of pseudo aneurysm  and AV fistula
Increased risk of infection 
Nerve injury
Digital ischaemia
Can cause delays in care
Serial exams may be needed

(some of these problems are still the case in VBGs)

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100
Q

Which elements of a VBG are usually adequate to aid decision making and have good correlation with ABG findings?

A

pH
PCO2 (if normocapnic - if PvCO2 normal in VBG, then PaCO2 is definitely normal)
HCO3
BXS

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101
Q

Other than hypercapnia, when might PCO2 from VBG not be as reliable as an ABG?

A

severe shock

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102
Q

What results on an ABG might indicate metabolic acidosis? What on the ABG might indicate respiratory compensation?

A

Metabolic acidosis: pH low, HCO3 low, Base excess high

Resp. compensation: CO2 low - pt. is blowing CO2 to try and reduce acidity of blood

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103
Q

What results on an ABG might indicate respiratory acidosis? What on the ABG might indicate metabolic compensation?

A

Resp acidosis: pH low, PaCO2 high

Metabolic compensation: HCO3 high - kidneys retain more bicarb in order to reduce acidity of blood

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104
Q

What results on an ABG might indicate respiratory alkalosis? What on the ABG might indicate metabolic compensation?

A

Resp alkalosis: pH high, PaCO2 low

Metabolic compensation: HCO3 is low - protein buffering in cells (acute) or kidneys excrete more bicarb to increase acidity of blood (chronic)

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105
Q

What results on an ABG might indicate metabolic alkalosis? What on the ABG might indicate metabolic compensation?

A

Metabolic alkalosis: pH high, HCO3 high, BXS low

Respiratory compensation: high CO2 - hypoventilation to increase acid in blood

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106
Q

What is included on an ABG?

A
pH
paO2
paCO2
HCO3
BXC
Lactate
Sodium
Potassium
Hb
glucose
CO
Methaemoglobin
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107
Q

Flow rate of Oxygen that can be given with venturi mask? What conc. of oxygen is delivered? What is a benefit of the venturi?

A

Flow rate depends on what type (based on colour)
24-60%

More specific percentage of oxygen can be delivered to pt. (you can be more certain that pt. is getting prescribed %)

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108
Q

What are the different flow rates (and %O2 delivered) of the different types of venturi?

A
Blue: 2-4L/min = 24% 
White: 4-6L/min = 28%
Yellow: 8-10L/min = 35%
Red: 10-12L/min = 40%
Green: 12-15L/min = 60%
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109
Q

When might you use a nasal cannula?

A

non-acute ward or if pt. mildly hypoxic

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110
Q

When might you use a Hudson mask?

A

Step up from nasal cannula

Doesn’t deliver specific % of oxygen like venturi

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111
Q

When might you use a venturi?

A

COPD

When you want to deliver a more specific amount of O2 to a pt.

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112
Q

When would you use a non-rebreathe mask?

A

acutely unwell pts.

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113
Q

When might you use CPAP?

A

sleep apnoea

heart failure

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114
Q

When might you use BiPAP?

A

COPD and atelectasis

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115
Q

What percentage oxygen is given in invasive ventilation? when might this be used?

A

100%

Used in theatre and in intensive care (when pt. in resp. arrest)

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116
Q

What should you do if O2 therapy is being use maximally and O2 levels continue to drop?

A

Involve ICU: view to use non-invasive ventilation, intubation and ventilation

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117
Q

Below what level O2 sats should you do an ABG?

A

92%

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118
Q

Why is an Oxygen saturation of below 90% such a big problem?

A

below sats less than 90%, the oxygen-Hb saturation curve drops significantly - therefore haemoglobin will rapidly become significantly less saturated with small changes in oxygen partial pressure

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119
Q

Which patients could be considered ‘CO2 retainers’? What happens to these pts?

A

severe obstructive lung disease (COPD, bronchiectasis and CF)

severe restrictive lung diseases (neuromuscular, severe kyphoscolliosis, severe obesity)

Respiratory drive is normally driven by CO2 levels, but CO2 retainers are desensitised to hypercapnia - rely on hypoxia to stimulate respiratory drive

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120
Q

What is the aim of oxygen therapy in CO2-retaining patients?

A

Increase oxygen level
WITHOUT
causing respiratory drive to decrease
(which will increase CO2, worsening resp. acidosis)

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121
Q

What is ACS (acute coronary syndrome)? What are the main classifications within ACS?

A

Range of heart conditions caused by lack of blood flow to myocardium
2 main divisions:
ST elevation ACS (STE-ACS)

Non-ST elevation ACS (NSTE-ACS) (which can be further divided in to unstable angina and NSTEMI)

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122
Q

What is the difference between unstable angina and an MI?

A

Unstable angina: blood clot or artery narrowing limits blood flow, but does not block it completely - therefore there is NO INFARCT in unstable angina

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123
Q

What is the difference between STE-ACS and NSTE-ACS?

A

STE-ACS: chest pain + ST elevation for >20mins. Most go on to develop STEMI

NSTE-ACS: chest pain WITHOUT persistent ST elevation
Other changes may be present on ECG

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124
Q

What features may be present on an ECG in NSTE-ACS?

A
persistent or transient ST-segment depression 
T-wave inversion
Flat T waves
Pseudo-normalisation of T waves
no ECG changes at presentation
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125
Q

What are risk factors for ACS?

A

Non-modifiable RF for atherosclerosis: age, male, family Hx of premature coronary heart disease, premature menopause.

Modifiable RF for atherosclerosis: smoking, diabetes mellitus (and impaired glucose tolerance), hypertension, dyslipidaemia (raised low-density lipoprotein (LDL) cholesterol, reduced high-density lipoprotein (HDL) cholesterol); obesity, physical inactivity.

Consider non-atherosclerotic causes in younger patients or if there is no evidence of atherosclerosis: coronary emboli from sources such as an infected cardiac valve, coronary occlusion (secondary to vasculitis), coronary artery spasm, cocaine use, congenital coronary anomalies, coronary trauma, increased oxygen requirement (eg, hyperthyroidism) or decreased oxygen delivery (eg, severe anaemia).

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126
Q

How might ACS present/what might be important to ask about in the Hx?

A
Chest pain (>15 mins) at rest
Pain in arms, back jaw
sweating
nausea
vomiting
fatigue
SOB
palpitations
syncope
tachycardia OR bradycardia
extra heart sounds 
murmur
hypotension
pulmonary oedema
narrowed pulse pressure
raised JVP

Limitation of daily activities due to angina (pain on less exertion than previous, pain lasting longer etc.)
Hx of angina
Hx of MI
Cardiovascular RF: smoking, BP, FHx, exercise, diet/weight, kidney problems, Previous cardiac problems/investigations, diabetes

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127
Q

Which patients may be less likely to have pain or chest tightness during a STEMI or an NSTEMI? How might this present instead?

A

Elderly
Diabetic

Syncope
Pulmonary oedema
Epigastric pain
Vomiting
Acute confusional state
Stroke
Diabetic hyperglycaemia
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128
Q

What investigations do you need to do in ACS?

A

ECG
Echocardiography
CXR (cardiomegaly, pulmonary oedema, widened mediastinum)
Coronary angiography

Bloods: Troponin I&amp;T (raised (2X) 3-6 hours post-infraction, remain raised for 14 days). Test at 6 and 12 hours after onset of pain. Levels usually raised for about a week.
FBC
Blood glucose
Renal function
Electrolytes 
TFTs
CRP
CK (raised in muscle trauma)
Lipids

Diagnosis: 2/3 - Hx, ECG changes and raised troponin

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129
Q

How would you initially manage a patient presenting with symptoms of ACS?

A

ABCDE assessment (incl. BP, RR, HR etc.)

A: secure airway if necessary

B: Oxygen (if necessary, 15L non-rebreathe). Get ABG. GTN sublingual (unless BP<90 or HR<50)

C: Get IV access. Get ECG if not done already. Take bloods. Cardiac exam.

Anti-platelet/anti-coagulant - 300 mg aspirin + Ticagralor 180mg loading dose
Fondaparinux (unless angiography due within 24 hours, then give unfractionated heparin)

D: Pain relief - GTN spray (unless R ventricular infarct)
If that doesn’t work, IV opioid (+ anti-emetic)
5-10mg morphine + metoclopramide 10mg IV

STEMI: thrombolysis (best within 12 hours) - streptokinase

Beta-blocker - atenolol 5mg IV
ACEi (in STEMI)
Statin

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130
Q

What is a normal RR in an adult?

A

12-20 breaths/min

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131
Q

What might you see on an ECG during an episode of unstable angina?

A

T wave inversion
ST depression
Normal

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132
Q

What risk-scoring system is used to predict risk of pt. having future cardiovascular event and six-month mortality?

A

GRACE score

Global Registry of Acute Cardiac Events

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133
Q

What is an important factor to bear in mind at each stage of ACS management (particularly in terms of prescribing drugs)?

A

Bleeding risk

ask re medications eg. warfarin, NOACs etc.

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134
Q

When might you consider use of PCI OR CABG in a patient with unstable angina/risk of MI? What are the risks associated with this?

A

If pt. has a high risk of recurrence

Risk of procedure-related MI or bleeding

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135
Q

After stabilising the pt., what would your more definitive treatment be of a patient who had a medium risk GRACE score? When else might this intervention be offered?

A

early in-hospital coronary angiography

angiography may also be offered in pts. whose risk is low, but are having recurrent episodes

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136
Q

What other differentials might you consider for a pt with ACS-like symptoms?

A

Cardiovascular: acute pericarditis, myocarditis, aortic stenosis, aortic dissection, pulmonary embolism.

Respiratory: pneumonia, pneumothorax.

Gastrointestinal: oesophageal spasm, gastro-oesophageal reflux disease, acute gastritis, cholecystitis, acute pancreatitis.

Musculoskeletal chest pain.

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137
Q

What are features of acute severe asthma?

A
any one of:
RR >=25/min
HR >=110/min
Inability to complete sentences in one breath
PEF 33-50% best or predicted
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138
Q

What are features of life-threatening asthma? (symptoms and signs)

A

Any one of:
Resp distress/poor resp effort
Silent chest
Cyanosis
Collapse
tachycardia, Arrhythmia, bradycardia, hypotension
Exhaustion, altered conscious level, coma

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139
Q

What investigations would you want to do in pt. presenting with features of acute asthma attack?

A

Pulse oximetry
ABG (if pt has ANY life-threatening features or SpO2<92%)
PEF (not always necessary)

(ECG and CXR in very specific circumstances)

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140
Q

What results would you find from investigations in life-threatening/near-fatal asthma?

A

Pulse oximetry: Sp O2<92%

PEF <33% previous best or predicted
(severe: 33-50%, moderate: 50-75%)

ABG: PaO2<8kPa
PaCO2 > 6.0 (near-fatal)
Low pH

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141
Q

What is the immediate management for acute severe asthma in adults?

A

A: check airway patent

B: O2 sats, RR, listen to apices and bases, look for cyanosis, ABG, (if well enough: PEF)

Prescribe: Oxygen (15L non-rebreathe): SpO2<94%

Salbutamol (5mg) or terbutaline (10mg) nebuliser (oxygen-driven). Repeat at 15-20 minute intervals

Ipratropium bromide (0.5mg) nebuliser (4-6 hourly)

Write up:
Prednisolone tabs (40-50mg) OR IV hydrocortisone (100mg)
(depends on how ill pt. is)

C: check HR, BP, cap refill
Cannulate
Bloods: FBC, U&Es, glucose
?ECG

D: fingers, toes, eyes, GCS

E: CALVES, rashes, temp.

CXR (once stable)

If life-threatening: discuss with senior clinician/ICU (consider aminophylline infusion)
Consider IV magnesium sulphate (1.2-2g) infusion over 20 mins
salbutamol 10mg continuously hourly

REASSESS

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142
Q

What single investigation do you need in pts with life-threatening asthma?

A

ABG

No other investigations are necessary for immediate management

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143
Q

What are the key features of asthma?

A
SOB
Cough (worse at night)
Chest tightness
WHEEZE (usually expiratory, but can also be inspiratory in severe asthma)
Poor Hx of control/recent increase of inhaler use
Possible resp. tract infection
Respiratory distress: Cyanosis
increased RR
Accessory muscle use

tachycardia (increased salbutamol use)
prolonged expiratory phase

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144
Q

After initial management of severe acute asthma, what should you do?

A

REASSESS

Pt improving:
Oxygen to maintain SpO2
Prednisolone 40-50mg daily OR IV hydrocortisone 100mg 6 hourly
Nebuliser beta-agonist and ipratropium 4-6 hourly

Pt not improving after 15-30 mins:
Continue oxygen and steroids
Continuous nebulisation of salbutamol (5-10mg/hour)
Continue ipatropium 0.5 mg 4-6 hourly until pt. is improving

Pt still not improving:
Discuss with senior and ICU, the use of:
IV Magnesium sulphate 1.2-2g over 20 minutes
IV beta agonist or IV aminophylline
Non-invasive and mechanical ventilation
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145
Q

What monitoring should be done in pt. with acute severe asthma?

A

PEF 15-30 mins after starting treatment. Do one before and after B2 agonist treatment and QDS during hospital stay

Oximetry

ABG within 1 hour of starting treatment if:
PaO2 <8 (unless subsequent SO2>92%)
PaCO2 normal/raised
Pt deteriorates

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146
Q

When should you transfer a pt. with severe acute asthma to ICU?

A
Deteriorating PEF
Worsening or persisting hypoxia or hypercapnoea
Exhaustion
Altered consciousness
Poor resp. effort or resp. arrest
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147
Q

What should patients with acute severe asthma have in order to ensure they can be discharged from hospital safely?

A

Pt. should have been on discharge medication for at least 24 hours
Check inhaler technique
PEF > 75% of best or predicted AND PEF diurnal variability <25%
Oral and inhaled steroids (in addition to bronchodilators)
own PEF meter and written asthma plan
GP follow up arranged for within 2 working days
Follow up with respiratory clinic within 4 weeks

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148
Q

What (in basic terms) is the treatment for an acute asthma attack?

A

OSHITME

All together:
Oxygen
Salbutamol 2.5-5mg NEB
Hydrocortisone 100mg IV (or prednisolone 40 mg PO)
Ipratropium 500mcg NEB

With senior input:
Theophylline: aminophylline infusion 1g in 1L saline (0.5ml/Kg/h)
Magnesium sulphate 2g IV over 20 mins
Escalate care (intubation and ventilation)

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149
Q

What are the key features of life-threatening asthma?

A

33, 92, chest

33: PEF <33% best/predicted
SpO2 < 92%
Cyanosis
Hypotension
Exhaustion
Silent chest
tachycardia
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150
Q

What PEFR would indicate mild asthma?

A

> 75%

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151
Q

What PEFR would indicate moderate asthma?

A

< 75%

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152
Q

How would you treat an acute COPD exacerbation?

A

OSHIT
BUT
Give controlled oxygen: 24-28% venturi mask
Consider BiPAP if sats don’t improve (and in type 2 resp failure)

ABG after 15 mins
Regular ABGs

ABX: Doxycycline 100mg OD (200mg loading dose)

Chest physio

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153
Q

What investigations would you do in someone with exacerbation of COPD?

A

CXR
ABG
ECG

Bloods: FBC, U&Es, blood cultures

Sputum microscopy and culture

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154
Q

What symptoms might you expect from someone with exacerbation of COPD?

A

Increased cough/sputum production/SOB
Reduced exercise tolerance
Resp distress: accessory muscle use, tachypnoea, cyanosis, wheeze
Confusion
Upper airway symptoms: colds, coughs etc.
Fluid retention
Increased fatigue/malaise

Resp failure

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155
Q

How would you manage COPD?

A

A: check airway patent

B: sats, RR, ABG, auscultate (apices and bases)
Oxygen (venturi 24-28%)
Salbutamol (5mg) NEB 15-20 mins. Air driven.
Ipratropium bromide (500 mpg) NEB. Air-driven.
Hydrocortisone (100mg) IV and Prednisilone (30mg) PO
Theophylline: aminophylline
CXR

C: HR, Cap refill, BP, Cannula, Bloods (incl. blood culture) - FBC, U&Es and glucose.
ECG

D: fingers, toes, pupils, GCS

E: temp, CALVES, Sacrum

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156
Q

What should you ask a pt. with COPD in A&E?

A
Assess COPD severity:
Oxygen/nebulisers at home
No. of exacerbations a year/in winter
Do you have a rescue pack
Ever been in to hospital with exacerbation before
Ever been admitted to ICU
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157
Q

When should you use the PERC (Pulmonary embolism rule-out criteria) score for PE? What is the aim of the PERC score?

A

Low-risk/pt. unlikely to have PE

Aim of score is to rule out PE.
Pt with score of 0 = rule out PE (<2% chance of PE). Its do not need a D-dimer.
CANNOT rule PE out safely if ANY of criteria are positive

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158
Q

What criteria are included in the PERC scale?

A
Age >= 50 yrs
HR >= 100
SpO2 on rom air < 95%
Prior Hx of DVT/PE
Recent trauma or surgery
Haemoptysis
Exogenous oestrogen (OCP, HRT)
Unilateral leg swelling
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159
Q

What are the symptoms of PE?

A
sudden onset SOB
Shortness of breath
Haemoptysis
Syncope
Cardiovascular collapse (tachycardia, hypotension)
Raised JVP
Hypoxia
(CXR often normal)
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160
Q

What scoring systems can you use to help you decide on investigations and management in PE?

A

Don’t think pt. has PE: PERC

Think pt. might have PE: Wells score

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161
Q

What is included in the PE Wells score? (how many points are given)

A

DVT Sx (3)
PE primary diagnosis (no alternative diagnosis more likely) (3)
HR >100 (1.5)
Immobile > 3 days or surgery < 4 weeks (1.5)
Previous PE or DVT (1.5)
Haemoptysis (1)
Malignancy (1)

<2 = low probability
2-6 = moderate probability
>6 = high probability
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162
Q

For what PE wells score range would you do D-dimer? What would you do after this?

A

4=> (PE unlikely)

D-dimer -ve: reassure
D-dimer +ve: LMWH (1.5mg/Kg)
CTPA when possible

CTPA -ve: stop LMWH
CTPA +ve: continue LMWH and start warfarin for 6 months
(Stop LMWH 5-7 days of dual therapy and when INR 2-3)

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163
Q

For what PE wells score would you NOT d-dimer?

A

5=< (PE likely)
Wouldn’t bother with D-dimer, JUST TREAT
LMWH (1.5 mg/Kg)
CTPA when possible

CTPA -ve: stop LMWH
CTPA +ve: continue LMWH and start warfarin for 6 months
(Stop LMWH 5-7 days of dual therapy and when INR 2-3)

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164
Q

If you can’t do a CTPA on a patient, what other scan could you do to confirm/exclude PE?

A

V/Q scan

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165
Q

What investigations can you do to check for severity of PE?

A

ECG (tachycardia, RV strain: T-wave inversion in R and inferior leads, RBBB, R axis deviation, S1Q3T3, RA enlargement: P pulmonale, RV dilation: dominant R in V1)
CXR (wedge infarcts, regional oligaemia, enlarged pulmonary artery, effusion)
echocardiogram (R heart strain/overload)
bilateral leg doppler (look for DVTs)

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166
Q

How would you manage a PE acutely?

A

A: check airway patent. Sit patient up.

B: RR, sats, ABG, auscultate
Oxygen 15L non-rebreathe

C: HR, BP, cap refill, cardiac monitor
Cannula
Fluid bolus
?inotropic support

D: fingers, toes, eyes

E: temp, CALVES
LMWH

Send for CTPA once stable

Call senior
Consider thrombolysis in:
Massive PE (SBP<90, puleslessness or persistent bradycardia) = STRAIGHT to thrombolysis
Submassive PE (RV dysfunction ot myocardial necrosis) = give LMWH and consider thrombolysis

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167
Q

What are some causes of pulmonary oedema?

A

Ischaemic heart disease: MI/ACS, LV failure
Murmurs: aortic regurg, mitral regurg, SEVERE aortic stenosis
PE
Arrhythmia
Cardiac tamponade
Cardiomyopathy
AKI or CKD
Iatrogenic fluid overload
High-output heart failure eg. sepsis, anaemia etc.
Liver failure, fat embolism, ARDS
neurogenic (after neurological insult e.g. status epileptics, head injury, stroke)

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168
Q

What are features of anaphylactic shock?

A

A: laryngeal/pharyngeal oedema, bronchospasm (stridor), hoarse voice

B: SOB, increased RR, wheeze

C: shock (pale, clammy), hypotension (dizziness, collapse), tachycardia

D: confusion, tiredness, agitation, LOC

E: rash/flushing
urticaria
angio-oedema
hypotension and shock
nausea, vomiting or diarrhoea

Three key criteria make anaphylaxis v. likely:

  • Rapid onset and progression of symptoms
  • life-threatening Airway, breathing or circulation problems
  • Skin and/or mucosal changes
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169
Q

How would you manage anaphylaxis?

A

Call for help 2222 (at very least anaesthetist)
Lie pt. flat
Raise pt.’s leg (try to raise BP)
Adrenaline 0.5mg IM (0.5mLs of 1:1000). Repeat every 5 minutes.

A: establish airway (nasopharyngeal/LMA/intubation)

B: RR, Sats, auscultation, air entry
15L non-rebreathe (may need intubation)
Wheeze: salbutamol (as in asthma)

C: HR, BP, cap refill
Cannula
Attach cardiac monitor
1) Adrenaline (IM) 1:1000 - 500 micrograms (0.5mL)
2) IV fluid challenge: 500-1000mL (Hartmann’s or NaCl)
3) Cloramphenamine 10mg IM (or slow IV)
4) Hydrocortisone 200 mg IM (or slow IV)
Bloods: FBC, U&Es, LFTs, calcium and glucose)
May need inotropes/vasosupressors

D: GCS, pupils, fingers, toes, glucose level

E: Feel abdo
Calves
Temp

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170
Q

What would you do for a patient with anaphylactic shock, once they’re stable?

A

Mast cell tryptase (venom-related, drug-related, idiopathic): ASAP after emergency, 1-2 hours after onset, 24 hours after or in f/u.

Observe pt. for 6 hours (risk of another reaction)
WARN PATIENT
Some may need 24 hrs observation

Adrenaline injector as interim measure (before specialist appointment)

Anti-histamine and steroid therapy for up to 3 days

Reassure pt.
Info about how to manage anaphylaxis (incl. how to use adrenaline injector)
Info about biphasic reaction

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171
Q

What things would you need to write in the notes re. anaphylactic shock and its management?

A
Clinical features 
Time of onset
Circumstances immediately before onset of symptoms
Treatments administered 
Results of any tests
Obs
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172
Q

What differentials might you think about in someone with anaphylaxis-like symptoms?

A

asthma (esp. in children)
septic shock

vasovagal episode
panic attack
breath-holding episode
non-allergic urticaria or angioedma

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173
Q

Which pts. may need observing for 24 hours

A
Severe reactions with slow onset
severe asthma
Hx of biphasic reactions
Pts presenting at evening or night
Pts where access to emergency care is limited
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174
Q

What are common features of pulmonary oedema?

A
Dyspnoea
Orthopnoea
Pink frothy sputum
Pale, sweaty, distressed pt. 
Increased jugular venous pressure
Inspiratory crackles
Wheeze (cardiac asthma)
Triple/gallop rhythm (S3 sounds - fluid overload)
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175
Q

What findings might you see on an X-ray?

A

Cardiomegaly
Fluffy bilateral shadowing with peripheral sparing (bats wings)
Kerley B lines
Pleural effusions

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176
Q

What is the CURB-65 score used for? What are its components?

A

estimates mortality for CAP

Confusion (1)
Urea >7 (1)
RR >30 (1)
SBP >90 or DBP<60
Age 65 =
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177
Q

What are the differentials you might consider for someone with shortness of breath (in ED)?

A
Exacerbation of COPD
Asthma
PE
Pneumothorax
Pneumonia
Pulmonary oedema
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178
Q

How would you manage a patient with pulmonary oedema?

A

A: sit pt. upright, check airway is patent
B: RR, sats, ABG (if in resp. distress), auscultate, tracheal deviation
O2 (15L NRB)
Salbutamol NEB if wheeze present
C: HR, BP, cap refill, cardiac monitor, CXR
Venous access, bloods - ?culture, FBC, LFTs, U&E, glucose
Treat any arrhythmias
2 sprays GTN or buccal suscard 2-5mg (if SBP>90)
Diamorphine 2.5mg IV (slowly)
Furosemide 40-80mg IV (slowly)
GTN IV 50mg in 50mls 0.9% NaCl 2ml/hr, titrate up to 20ml/hour. Maintain BP at 90
D: GCS, pupils, drug chart and notes
E: calves, abdo, temp

Reassess: no B improvement - CPAP
Senior/critical care outreach/anaesthetists/ICU

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179
Q

What are then different types of pneumothorax?

A

Spontaneous: primary and secondary
Traumatic: following penetrative chest trauma
Iatrogenic: following procedures eg. invasive ventilation, central line placement, biopsy etc.
Catamenial: pneumothorax around time of menstruation due to endometriosis
TENSION PNEUMOTHORAX

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180
Q

What are the different types of spontaneous pneumothorax?

A

Primary: no apparent underlying cause. Occur in young fit people.
Secondary: Associated with underlying lung disease - eg, COPD, TB, sarcoidosis, CF, malignancy, and idiopathic pulmonary fibrosis

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181
Q

Why is it important to establish whether a spontaneous pneumothorax is primary or secondary?

A

The consequences of a pneumothorax in patients with pre-existing lung disease are significantly greater and the management is potentially more difficult.

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182
Q

What are the BTS guidelines of working out whether pneumothorax is primary or secondary?

A

Age > 50 and significant smoking history

Evidence of underlying lung disease on exam or CXR?

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183
Q

What are symptoms of pneumothorax?

A

Primary spontaneous pneumothorax: Sx minimal or absent

Secondary spontaneous pneumothorax: greater than primary

Sudden onset pain
May be SOB
Can be Sx-less
Distressed and sweating

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184
Q

What might you find on examination of a pt. with pneumothorax?

A

A: airway may be patent

B: Resp distress
Reduced chest expansion on one side
tracheal deviation (towards side of pneumothorax)
Hyper-resonance on percussion over areas of collapse
breath sounds reduced/absent

C: Cyanosis
Tachycardia (>135 = tension)
pluses paradoxical (slows on inspiration)
HypoTN

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185
Q

How would you investigate a NON-tension pneumothorax?

A

CXR
CT in uncertain cases
ABG (if sats <92%)

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186
Q

What differentials might you consider in someone with pneumothorax-like symptoms?

A

Pleural effusion (slower onset and dullness to percussion)
PE (haemoptysis, more common in lower lobes)
Pleuritis

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187
Q

How would you measure the size of a pneumothorax on a CXR?

A

Measure the distance between pleural surface and lung edge (at level of hilum)
2cm or more = pneumothorax of at least 50% of hemithorax. This indicates need for drainage

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188
Q

What should you do in the following scenario?

Primary pneumothorax
Size >2cm and/or SOB

If this improves the situation (<2cm and breathing improves), what should you do?

If this does not improve the situation, what should you do?

A

Aspirate using 16-18g. cannula
Aspirate <2.5L

Consider discharge
R/v in OPD in 2-4 weeks

Chest drain
Admit pt.

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189
Q

What should you do in the following scenario?

Primary pneumothorax
Size <2cm and/or not SOB

A

Consider discharge

R/v in OPD in 2-4 weeks

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190
Q

What should you do in the following scenario?

Secondary pneumothorax
Size >2cm and/or SOB

A

Chest drain

Admit pt.

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191
Q

What should you do in the following scenario?

Secondary pneumothorax
Size <2cm (1-2cm) or not SOB

If this improves the situation (<1cm and breathing improves), what should you do?

If this does not improve the situation, what should you do?

A

Aspirate using 16-18g. cannula
Aspirate <2.5L

Admit
High flow oxygen
Observe for 24 hours

Chest drain
Admit pt.

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192
Q

What should you do in the following scenario?

Secondary pneumothorax
Size <1cm or not SOB

A

Admit
High flow oxygen
Observe for 24 hours

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193
Q

What are KEY features of TENSION pneumothorax?

A

Same Sx as above (reduced unilateral expansion etc.)
Hypotension
Trachea deviated AWAY from side of collapse
Distended neck veins

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194
Q

How would you manage someone with tension pneumothorax?

A
A: airway patent
B: RR, sats, AUSCULTATION, CHEST EXPANSION, PRECUSSION, TRACHEAL DEVIATION
15L Oxygen NRB
?ABG
C: HR, BP, cap refill
Confirmed diagnosis: Needle decompression 14-16g cannula, 2nd intercostal space, mid-clavicular line, leave in place
D: GCS, eyes, fingers etc.
E: calves, abdo etc.
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195
Q

What is the definition of HAP?

A

Pneumonia developed 48 hours after hospital admission

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196
Q

Which type of pneumonia has worse prognosis? why?

A

HAP - generally more comorbidities

Bugs more resistant

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197
Q

What are the common organisms for CAP?

A

Streptococcus pneumoniae, haemophilus influenzae

Anaerobes are rare

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198
Q

What are the common organisms for HAP?

A

Gram negative bacilli, staphylococcus aureus

Drug resistant organisms are more common, and more dangerous

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199
Q

What are the rarer causes of CAP?

A

Chlamydia pneumoniae (common in institutions – e.g. collegues, military camps – mild)
mycoplasma pneumonia
legionella

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200
Q

What are common precipitating factors for pneumonia?

A
Strep pneumoniae infection often follows viral infection with influenza or parainfluenza.
Hospitalisation
Cigarette smoking 
Alcohol excess
Bronchiectesis (e.g. in CF)
Bronchial obstruction (e.g. carcinoma)
Immunosupression
IV drug use
Dysphagia (both oesophageal and co-ordination disorders – leading to aspiration)
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201
Q

What are symptoms of a pneumonia?

A
Similar for HAP and CAP cases
SOB
Tachypnoea
Reduced oxygen sats
Tachycardia
Cough (purulent sputum, can be dry in infants and elderly)
Fever
Riggers
Vomiting
Headache 
Loss of appetite 
Pleuritic chest pain, may radiate to shoulder (if diaphragm is involved)
Upper abdo pain
Increased secretions
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202
Q

What investigations might you do for someone you suspect has pneumonia? What might you see?

A
BTS guidelines:
Pulse oximetry (may need ABG)

CXR: consolidation (may not be present for first 48 hours, but can be present for up to 6-weeks).
Repeat weekly as inpt, then 6 weeks after as f/u (community and hospital)
(may not need initial CXR if in community, if sure of diagnosis and no risk of underlying lung pathology)
ALL suspected CAP in hospital, should be investigated with CXR

Bloods: 
FBC
WCC (raised)
ESR and CRP (raised)
LFTs
Anaemia
Microbiological:
Blood cultures (moderate to high severity - start empirical ABX)
Sputum culture (in pts. who do not respond to empirical ABX)

Urine antigen investigations (if pneumococcal and legionella suspected)
Pleural fluid aspiration (if they have an effusion))

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203
Q

What scoring system would you use to assess the severity of pneumonia?

A

CURB 65

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204
Q

List some complications of pneumonia?

A
Sepsis: resp failure, hypotension
pleural effusion
empyema
Lung absences
Lobar collapse/pneumothorax
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205
Q

what should you do for a pt. with CURB-65 score of 0-1?

A

0-1: low severity

Other reason to admit = hospital
No reason to admit = home treatment

Amoxicillin 500mg TDS PO
(or doxycycline 200mg loading dose, 100mg PO)
Can have same dose IV if unable to do PO.

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206
Q

what should you do for a pt. with CURB-65 score of 2?

A

2: moderate severity

Hospital admission (short stay)

Supportive care: Oxygen, fluids, neb saline, chest physio, VTE prophylaxis, analgesia (NSAIDS or paracetamol)

ABX: amoxicillin 500mg-1g TDS PO + clarithromycin 500mg BD PO

Unable to use PO: amoxicillin 500mg TDS IV PLUS clarithromycin 500mg BD IV
(or doxycycline 200mg loading dose, 100mg PO)

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207
Q

what should you do for a pt. with CURB-65 score of 3-5?

A

3-5: high severity

Urgent hospital admission (and senior review)

Supportive care: Oxygen, fluids, neb saline, chest physio, VTE prophylaxis, analgesia (NSAIDS or paracetamol)

ABX: Antibiotics given as soon as possible
Co-amoxiclav 1.2 g tds IV plus clarithromycin 500 mg bd IV
(If legionella strongly suspected, consider adding levofloxacin)

Consider referral to critical care (if score 4/5)

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208
Q

What monitoring and follow up would you want to do in a patient with pneumonia?

A

Inpatient -
Repeat: bloods, X-rays etc after 3 days
24 hours after discharge, obs
6 WEEK FOLLOW-UP INCL. RPT.CXR.

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209
Q

What are the different types of aortic dissection?

A
Stanford classification: 
Type A (involving the ascending aorta, can extend ad infinitum)
Type B  (not involving the ascending aorta - aorta beyond subclavian artery only)

(less used) DeBakey Classification:
Type I: aorta, aortic arch, and descending aorta.
Type II: ascending aorta only.
Type III: descending aorta distal to left subclavian.

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210
Q

What are some risk factors for aortic dissection?

A
HTN
smoking
raised cholesterol
pre-existing aortic diseases
aortic valve disease
FHx or aortic diseases
Hx of cardiac surgery 
blunt chest trauma 
use of IV drugs

Marfan’s
Ehlers-Danlos syndrome

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211
Q

What is an aortic dissection?

A

Tear in inside of aorta

Blood flow between layers of wall of aorta, forcing layers apart

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212
Q

How might aortic dissection present?

A
Chest pain/back pain (ripping/sharp)... also groin. SUDDEN ONSET
MAXIMAL AT ONSET
MIGRATES (as dissection progresses)
Proximal dissections: retrosternal pain
Distal dissections: between scapulae
aortic regurg

angina/MI: involvement of coronary arteries

CCF

Pleural effusions

Syncope

Neurological symptoms (acute paraplegia, U/L limb ischaemic neuropathy): involvement of spinal arteries or carotid or distal aortic involvement

AKI

Often presents in two phases:
1st event: severe pain, pulse loss
2nd event: rupture = cardiac tamponde, pleural space or mediastinum

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213
Q

What might be a typical presentation of someone with chest pain?

A
man in 60s
HTN
SUDDEN onset chest pain (also groin or back)
retrosternal or between scapulae
'ripping' or 'sharp'
Maximum pain at the beginning
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214
Q

What differentials might you think about in a patient with ?aortic dissection?

A
ACS (can occur with dissection)
aortic regurg
aortic aneurysms
MSK
pericarditis 
mediastinal tumours
pleuritis
PE
cholecystitis
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215
Q

What investigations would you do on someone with ?aortic dissection?

A

ECG - MI, normal or non-specific ST-T segment changes

CXR (will not exclude, but may see widened mediastinum)
US echocardiography in unstable pt. (site and extent)
CT angiography is investigation of choice.

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216
Q

How is aortic dissection treated?

A

A and B as necessary

C: control BP and HR (prevent disease extension)
aim: SBP<120 and HR 60
Cannulate
Labetalol IV

analgesia eg. morphine

type a: surgery (stent or graft)

type b: not generally for surgery (managed just by BP) except:
Persistent pain, branch occlusion, leak, continues extension

*risk of paraplegia with surgery

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217
Q

What is type A more likely to end up malperfusing?

A
brain
coronary artery
spinal cord
liver
bowel
kidneys
legs
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218
Q

What is type B aortic dissection more likely to end up malperfusing?

A
JUST
spinal cord
liver
bowel
kidneys
legs
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219
Q

What are risk factors for aneurysms?

A
Hypertension
Smoking
Age
Diabetes
Obesity
High LDL levels
Sedentary lifestyle
Genetic factors 
Co-arctation of the aorta
Marfan’s syndrome, and other connective tissue disorders
Previous aortic surgery
Pregnancy (particularly 3rd trimester)
Trauma
Male
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220
Q

How might AAA present?

A
Unruptured: no Sx
Pain in back, abdo, loin, groin
(*severe lumbar pain, recent onset = think ?impending rupture)
pulsatile abdo swelling
limb ischaemia
ureterohydronephrosis
Collapse, syncope or shock (hypotension)
epigastric pain:
radiating to back
(may also get pain in groin, iliac fosse and testicles)
Constant or intermittent 

rupture into peritoneal space: dramatic, death on arrival
rupture into retroperitoneal space: contained (temporary seal formed)

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221
Q

What clinical signs might you find on examination of someone with ?AAA?

A

Bimanual palpation of abdo: pulsatile
Abdo bruit
retroperitoneal haemorrhage: Grey Turner’s sign

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222
Q

What investigations might you do for someone ?AAA (non-urgent)?

A
Bloods:
FBC
Clotting screen
renal function
liver function
cross-match (if surgery planned)
ESR/CRP

ECG, CXR

US
CT
MRI angiography

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223
Q

What investigations might you do for someone ?AAA (urgent)?

A

Bloods:
FBC
Group and save/cross-match
U&Es

Plain abdo x-ray
US (may not need if emergency, may go straight to theatre)
CT angiography

224
Q

How would you manage someone with ruptured AAA?

A

large bore IV access
group and cross-match

*SURGICAL REFERRAL IMMEDIATELY - emergency endovascular aneurysm repair

225
Q

How would you manage a patient with uncomplicated AAA?

A

<5.5cm: monitor (US)
>5.5cm:surgery

manage risk factors: statins, anti-platelets (if not at risk of bleed)

Other indications for surgery: onset of sinister symptoms (back or abode pain), rapid expansion and RUPTURE

226
Q

How might alcohol withdrawal present?

A

Hx of alcohol abuse
Collapse

Within a few hours: Tremor
Nausea
Sweating
Agitation
Tachycardia
Palpitations
Hypertension
after 24-48 hours:
Delusions
Confusion
Diarrhoea
convulsions
auditory hallucinatinos

After 48 hours:
delirium tremens

227
Q

How might delirium tremens present?

A

Someone (generally) with a v. long drinking history - can also occur after a few months of drinking

3-4 days after withdrawal

Sx: 
Restlessness
Fear
Paranoia 
Confusion/reduced consciousness
Terror-stricken face
Sweaty/tachycardia/pyrexia/flushing/pallor
Visual hallucinations (lilliputian), formication
Auditory hallucinations
228
Q

How do you treat delirium tremens?

A

MEDICAL EMERGENCY: DEATH IN 10-15% (35% if untreated)

Benzo: sedation and anti-convulsant. Give up to 10 days, at night - avoid nightmares
B vitamins (pabrinex): reduce risk of encephalopathy
Fluid replacement
Dextrose (avoid hypoglycaemia)
Be aware of infection and head injury

On recovery: check for signs of alcohol brain damage, assess motivation for permanent change

229
Q

what causes death in delirium tremens?

A

Epileptic seizure
self-injury
infection

230
Q

How long does delirium tremens usually go on for?

A

3-4 days

Anxiety can go on for months

231
Q

Why does delirium tremens occur?

A

Long term changes occur in the brain with long-term/excessive alcohol use: decrease in GABA receptors (as tolerance develops)

When alcohol is withdrawn, patient is left with a v. low number of inhibitory receptors and nothing acting on them

This is why there is over-activity of the CNS

232
Q

What is Wernicke’s encephalopathy? what are the symptoms?

A

Acute syndrome (neurological symptoms) caused by thiamine deficiency

Ocular palsies (esp. abducens nerve)
Ataxic gait
Nausea
Memory problems

(can be caused by all types of thiamine deficiency, not just alcohol)

If someone presents with Wernicke’s, and it continues chronically, it becomes Korsakov’s syndrome. Can also present at same time as Korsakov’s = wernicke-korsakov syndrome

233
Q

What is Wernicke’s triad?

A

eye signs: nystagmus and ophthalmoplegia
Ataxic gait
Confusion

234
Q

What is korsakov’s syndrome and how does it present?

A

Chronic condition caused by thiamine deficiency (also called korsakov’s psychosis) - impaired memory function following signs of Wernicke’s encephalopathy.

Anterograde memory disorder (can’t consolidate new memories). Able to recall facts immediately, within a few minutes. No ability to get this info in to long-term memory.

Little/distorted sense of time
Make up events (confabulation)
Anser questions in a very laid-back manner
Memory recall for events before the syndrome are usually fine
No clouding of consciousness
Peripheral neuropathy

235
Q

What are the differentials for alcohol/alcohol-withdrawal problems?

A

Withdrawal (no dangerous features)
Delirium tremens (more common than Wernicke’s - no neurological symptoms)
Wernicke’s encephalopathy
Korsakov’s syndrome
Acute brain syndromes of miscellaneous cause
Chronic brain syndromes (different pattern of memory loss - incl. long-term memory)

Chronic alcohol intake can lead to chronic brain syndrome due to atrophy of the cerebrum

236
Q

How would you treat Wernicke’s encephalopathy?

A

Thiamine and other B vitamins (IM or IV) - PABRINEX

Sedation (benzodiazepines) - chlordiazepoxide

Fluids/electrolytes

237
Q

How would you treat Korsakov’s?

A

Life-long chronic illness
No real treatment
Thiamine supplements don’t really help after acute phase
Eventually, patients will require care

238
Q

What’s the prognosis of wernicke’s and other alcohol related brain syndromes?

A

Palsies: usually clear with appropriate treatment

Ataxia: usually resolve on its own over several months

Neuropathy: resolve slowly

Amnesia: 1/2 all patients recover from this

239
Q

What are features of opiate withdrawal?

A
Dilated pupils
High BP
Sweaty
Runny nose
Cramps
240
Q

What are features of benzo withdrawal?

A

Hypersensitivity
Hyper-reflexia
Depersonalisation

241
Q

What are features of psychostimulant withdrawal?

A

Agitation

restlessness

242
Q

What are features of heroin withdrawal?

A

Cold/shivery
flu-like symptoms
Body pain
CANNOT KILL YOU

243
Q

What are symptoms of third degree (complete) heart block?

A
Light-headedness
Dizziness
Fainting 
Fatigue
Chest pain
bradycardia
Palpitations
244
Q

What is complete heart block?

A

Electrical signal can’t pass normally from the atria to the ventricles.

P and QRS waves conducted at different speeds, no connections between them

245
Q

What are the features of complete heart block on an ECG?

A

P waves about 90/min (more P waves than QRS waves). Regular.

QRS about 36/min
Regular.

BUT NO LINK BETWEEN THE TWO.

Variable PR intervals

Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles. Generally broad.

Right axis deviation.

246
Q

What are different causes of complete heart block?

A

MI
Chronic - fibrosis of bundle of His or BBB in both branches (eg. old age)

Fibrosis more common than ischaemia

247
Q

How would you investigate whether someone may have complete heart block?

A

ECG

If well enough to go home, 24 hour tape

248
Q

How would you treat heart block?

A

Withdraw any medications that may be causing, aggravating condition eg.
Anti-hypertensives/anginal/anti-arrhythmic and heart failure medications cause AV block

Oxygen (if necessary)
Monitor ECG, BP, SpO2
Bloods: ABG, FBC, U&Es,
Identify and treat reversible causes (drug chart, electrolytes etc.)

if have adverse features (shock, syncope, MI or heart failure):
ATROPINE 500 mcg IV

If no response: repeat atropine 500 mcg IV to max of 3 mg
alternatives to this:
isoprenaline or adrenaline
Transcutaneous pacing

If successful: observe (unless risk of: systole, mobitz-type-2 block, broad QRS and ventricular pause >3 secs - then complete above)

Long term: pacemaker

249
Q

What alternative drugs can be given to atropine in complete heart block?

A

isoprenaline and adrenaline
Glycopyrrolate

aminophylline
dopamine

GLUCAGON (if beta-blocker or CCB overdose)

250
Q

What are the different classifications of hypoxia?

A

Hypoxic hypoxia - reduced O2 supply
Anaemic hypoxia - reduced haemoglobin function
Stagnant hypoxia - inadequate circulation
Histotoxic hypoxia - impaired cellular O2 metabolism (eg. carbon monoxide/cyanide poisoning)

251
Q

What is the oxygen delivery equation?

A

delivery of oxygen = cardiac output x conc. of oxygen in the blood

252
Q

How can you maximise oxygen delivery in trauma?

A

Increase cardiac output:
fluids
oxygen
BLOOD (reduce risk of coagulopathy)

253
Q

What is the triad of death?

A
Coagulopathy (causes lactic acidosis)
metabolic acidosis (causes decreased myocardial performance, causing hypothermia) 
hypothermia (halts the coagulation cascade = COAGULOPATHY)
254
Q

What is clinically significant hypothermia?

A

Body temp <36 for 4 hours or more

255
Q

What is cerebral perfusion pressure (CPP)?

A

pressure gradient causing cerebral blood flow (CBF) such that CBF=CPP/CVR

(CVR: cerebrovascular resistance)

OR MORE COMMONLY AS:
CPP = MAP-ICP

256
Q

How do you work out MAP?

A

(2 x diastolic BP + systolic BP)/3

257
Q

What is the Monro-Kellie Doctrine?

A

Cranial compartment volume is fixed

Cranium and its constituents (blood, CSF and brain) are in a state of volume equilibrium

Increased volume in one of the cranial constants must be compensated by a decrease in volume of another

258
Q

What are the main buffers in the MKD?

A

CSF
(to a lesser extent) blood volume

If there is an increase in volume requirement (eg. extradural haematom), there will be downward displacement of CSF in to the spinal canal, reduction in cerebral venous blood and stretch of falx cerebri between hemispheres and the tentorium between the hemispheres and the cerebellum.

These compensatory changes able to maintain normal ICP for changes in volume of less than 100-120mL

259
Q

What does the Monro-Kellie Doctrine tell us about changes in volume?

A

Small increases do not lead to an immediate increase in ICP.

Once ICP reaches about 25mmHg, small increases in brain volume can lead to marked increases in ICP as threshold for intracranial compliance is passed (CRITICAL VOLUME)

260
Q

What are some features of raised ICP?

A

Changes in LOC
Eyes: papilloedema, pupillary changes, impaired eye movement
Posturing: decerebrate, corticate, flaccid
Changes in speech
Headache
Seizures
Impaired sensory and motor function
Changes in vital signs - cushion’s triad: High systolic BP, low pulse, irregular resp.
Vomiting

261
Q

What is Cushing’s triad? Why does it happen? What does it tell you?

A

High systolic BP
Low HR
irregular breathing pattern

Body trying to increase CPP by raising BP and dilating cerebral blood vessels, but this increases intracranial haemorrhage, which raises ICP further

Very close to dying

262
Q

Why is raised ICP associated with higher mortality rates in TBI?

A

Raised ICP = cerebral ischaemia = infarction

263
Q

What can a very high ICP caused by a unilateral space-occupying lesion (eg. haematoma) result in?

A

Midline shift
Hydrocephalus or brain herniation

Herniation is usually uncle or tonsillar

Brainstem compressed = coning

264
Q

What clinical signs might you begin finding in someone with raised ICP?

A

Dilated pupil - sluggish then fixed (CNIII palsy)

Aphasia

265
Q

How would you manage a TBI clinically?

A

ABCDE - URGENT INTUBATION is first priority

Prevent secondary brain injury

266
Q

How might you prevent secondary brain injury?

A

Prevent: hypoxia
hypocarbia
hypoglycaemia
hypotension

267
Q

Who should you immobilise following a head injury/trauma? How long should they remain immobilised for?

A
GCS < 15 
Neck pain or tenderness
Focal neurological deficit
Paraesthesia in extremities
Any clinical suspicion of cervical spine injury

Remain immobilised until full risk assessment incl. clinical assessment and imaging (if necessary) have deemed it is safe to remove immobilisation device

268
Q

What is the purpose of the Canadian C-spine rules?

A

Assessment tool used to RULE OUT cervical spine injury in LOW-RISK patients (obviating need for radiography)

Use for all alert (GCS 15) and stable trauma patients where cervical spine injury is a concern

269
Q

What are the high-risk factors which mandate radiography of C-spine (according to C-spine rules)?

A

Age >= 65 years
Dangerous mechanism
Parasthesia in extremities

Yes to any one of these = radiography necessary

No to all of these, move on to consider low-risk factors

270
Q

What are the low-risk factors which allow safe assessment of range of motion? (according to Canadian c-spine rules)

A

Simple rear-end motor vehicle collision

Sitting position in ED

Ambulatory at any time

Delayed onset neck pain

Absence of midline c-spine tenderness

If patient doesn’t have these features, they are at risk of having a cervical spine injury, radiography is needed.

If they do have one of these features, move on to consider whether they can actively rotate their neck

271
Q

Does a patient need radiographic imaging if they are able to rotate neck 45 degrees L and R?

A

No (if other criteria have been fulfilled eg. no high risk and some low risk features)

Radiography needed if unable to move neck

272
Q

Outline the Canadian c-spine rules.

A
  1. any high-risk factor which mandates radiography (age >=65 years, dangerous mechanism or parasthesia in extremities)
  2. any low-risk factors which allow safe assessment of range of motion (simples rear-end MVC, sitting position in ED, ambulatory at any time, delayed onset neck pain, absence of midline c-spine tenderness)
  3. Assess whether able to actively rotate neck 45 degrees L and R
273
Q

How should you manage someone with a head injury?

A

ABC - stabilise these
GCS <8 - involve anaesthetist very urgently

Assess whether at high risk of brain injury or cervical spine injury - decide whether to image or not (using Canadian C-spine/NICE guidelines). Assess neck movement IF APPROPRIATE

If decide not to image, re-assess patient in one hour

Manage pain (as this can lead to raised ICP) - small doses of IV opioids

274
Q

What are the criteria for performing a CT head scan in someone with a head injury?

A

Any of the following risk factors = perform a CT head scan within one hour of risk being identified:

GCS less than 13 on initial assessment at ED

GCS less than 15 at two hours post-injury

Suspected skull fracture

Any sign of basal skull fracture: haemotympanum, panda eyes, cerebrospinal fluid leakage from ear to nose, Battle’s sign)

Post-traumatic seizure

Focal neurological deficit

More than one (SEPARATE) episodes of vomiting

If patient is on warfarin treatment

OR any of the following risk factor with LOC or amnesia since injury:

65yrs or older
Any Hx of bleeding or clotting disorders
Dangerous mechanism of injury
more than 30 mins retrograde amnesia of events immediately before the head injury

275
Q

What are the NICE criteria for performing a CT cervical spine in adults following a head injury?

A

Any of the following risk factors = CT should be completed within one hour

GCS < 13 on initial assessment
Pt. intubated
Plain X-rays technically inadequate 
Plain x-ray suspicious/abnormal
Need definite diagnosis
High risk Canadian c-spine factors
276
Q

When would you admit someone with a head injury?

A

Patients with new, clinically significant abnormalities on imaging

Patients whose GCS has not returned to 15 after imaging, regardless of imaging results

Pt has indications for CT scanning, but this cannot be done within appropriate period
Continuing worrying signs eg. persistent vomiting, severe headaches)
Other causes for concern eg. drug/alcohol intoxication etc.

277
Q

What are symptoms and key features of hyperglycaemic hyperosmolar state?

A
Generally T2DM
v. high blood sugar levels 
increased urination, thirst
nausea
dry skin
disorientation, drowsiness and LoC
weakness, leg cramps, visual impairment

Key features:
Hypovolaemia (eg. confusion, sunken eyes, longitudinal furrows of tonge, extremity weakness, raised urea, tachycardia, hypotension)
Hyperglycaemia (BG 30 or more)
WITHOUT hyperketonaemia (<3) OR acidosis (pH>7.3, bicarb >15)
Osmolality usually >320

May get HHS and DKA at same time

278
Q

what are the goals of treatment of HHS?

A
normalise osmolality
Replace fluid and electrolyte losses
Normalise blood glucose
Prevent arterial/vnous thrombosis
Prevent other complications
Prevent foot ulceration
279
Q

How do you calculate osmolality?

A

2Na + glucose + urea

280
Q

How would you manage a patient with HHS?

A

A - ensure airway is stable

B - RR, sats, oxygen if desaturating. ?CXR if suspect chest infection

C - cannula, fluids, bloods, BP, HR etc. listen to heart sounds. ECG. Fluid output. urinalysis.

D - GCS, pupils, BLOOD GLUCOSE. Neuroexamination

E - full body exposure, looking for infection/rashes or abdo problems
Check for thyroid enlargement
Temp.

Address fluid balance, give 0.9% saline (with potassium if required)
Calculate osmolality every hour
Try to replace half of fluid (3-6L) loss within first 12 hours, and other half in second 12 hours

Aim for decrease in glucose of 4-6 mmol/Hr

Target glucose: 10-15.
Aim for normalisation within 72 hours

No ketonaemia = no insulin
Only start insulin if BG does not decrease following fluid replacement therapy.

Potassium over 5.5 = do not infuse saline with potassium
Potassium 3.5-5.5 = 40mmol/L infusion
below 3.5 = senior review/HDU

LMWH for full duration of admission

281
Q

What investigations would you do for someone with probable HHS?

A
Bloods: 
FBC
U&amp;E
ABG/VBG
blood glucose 
CRP (looking for infective source)
blood cultures

Urine: urinalysis
urine dip

CXR
ECG

282
Q

What are common differentials for HHS?

A

delirium
Poisoning
Sepsis
Lactic acidosis or other causes of metabolic acidosis

283
Q

What are some complications of HHS?

A

Ischaemia of any organ esp. MI or cerebral
DVT/PE
ARDS
SIC
Rhabdomyolysis
Fluid overload/hypoglycaemia (caused iatrogenically)

284
Q

What are some causes of HHS?

A
MI
Infections
stroke/TIA
Hyper/hypothermia
PE
AKI
Acute abdo
Burns
Medication: metformin, diuretics, beta blockers, H2 receptor antagonists
CCB
APs
steroids
Anti-convulsants
Substance misuse

First presentation of diabetes
Poor diabetic control/non-compliance

285
Q

What are some risk factors for seizures?

A

Fever
Head injury
Alcohol/drugs - excessive or withdrawal
Brain infection
Ischaemic stroke or intracranial haemorrhage
eclampsia
pro-convulsive drugs (tramadol, theophylline, baclofen)

Specific stimuli: strobe lights, reading, psychological stress or sleep deprivation

286
Q

Following a suspected seizure, what examinations should you do for a patient?

A

cardiac
neurological
mental state

287
Q

what are some features of a seizure?

A

Temporal lobe: feeling frightened, deja vu, strange taste/smell, rising sensation in stomach, staring, lip-smacking, confusion

Frontal lobe: moving head or eyes to one side, not being aware of surroundings, screaming/swearing/laughing, unusual body movements, repeated movements

Parietal lobe: numbness, tingling, sexual sensations, sensation of body distortion, feeling out of your body, feeling dizzy, seeing things, language difficulty

Occipital lobe: seeing things, visual changes, seeing image repeatedly, eye pain, uncontrollable sideways movement of eyes, nystagmus

Aura: focal seizures acting as a warning of generalised seizure

generalised seizure: rigid muscles
Voilent muscle contractions
Loss of consciousness
Biting cheek/tongue
Clenched teeth or jaw
Incontinence
Stopped/difficulty breathing
Blue skin colour
After seizure: confusion
drowsiness
amnesia
headache
weakness on one side of body (mins-hours. Todd's paresis)
288
Q

What are some differential diagnoses for

A
syncope (post-anoxic convulsion)
TIA (although no LoC generally)
Metabolic encephalopathy
Night terrors
Sleep-walking
Migraines
Arrhythmias
Psychogenic non-epileptic seizures
289
Q

How would you investigate a seizure?

A

Bloods: glucose, U&E, calcium, renal function, liver function, urine biochem)
12 lead ECG

CT/MRI

EEG - within 24-48 hours of first seizure or see-deprived
If to support diagnosis of epilepsy, do after second seizure
DO NOT PERFORM IN PROBABLE SYNCOPE because possible false-positive produced

290
Q

How would you manage a seizure acutely?

A

Keep pt from falling, guide them to floor, move objects that might cause them harm
TIME THE SEIZURE
Try to get them on to their side, but don’t be too hard
Pay close attention to what is happening
(in community, after 5 mins, ring ambulance and give buccal midazolam if pt. has it)

Post seizure: get pt on side if not already, loosen clothing around neck and waist
move anything from front of mouth out
wait with patient until come around fully

291
Q

What would you have to tell the patient/patient’s family?

A

How to recognise and manage seizures
Reporting further attacks
Stop driving
Avoid swimming or bathing without supervision

Driving is permitted after one year’s freedom from seizures after an unprovoked seizure and on a case-by-case basis on provoked seizures

Commercial driving not usually allowed for 10 years freedom from seizure with AED

292
Q

How would you manage someone with a seizure in the long term?

A

investigations

refer to specialist in management of epilepsies

patient education

293
Q

How do you manage status epileptics?

A

A - ?nasopharyngeal

B - oxygen 15L NRB

C - IV access, bloods: FBC, U&E, LFTs, calcium, magnesium, glucose

294
Q

How do you manage status epileptics?

A

A - ?nasopharyngeal

B - oxygen 15L NRB

C - IV access, bloods: FBC, U&E, LFTs, calcium, magnesium, glucose, blood cultures if suspect sepsis

D - pupils, AVPU

E - injuries, temperature etc.

Time the seizure
After 5 mins: 1-2mg lorazepam IV
Repeat after 5 mins if necessary (max of 4 mg can be given).

If seizures continue: IV phenytoin 20mg/Kg (max 2g), give at 50mg/min. Monitor ECG and BP

Continues seizures: anaesthetic sedation.

295
Q

What causes appendicitis? What happens if it is untreated?

A

Obstruction of appendical lumen - once obstructed, there can be: bacterial overgrowth, distention, ischaemia and inflammation

If untreated: necrosis, perforation, abscess formation and gangrene

296
Q

What are the clinical features of someone with appendicitis?

A

‘classic’ symptoms only in about 50% of patients

Pain: usually Epigastric or periumbilical THEN localises to RLQ
Pain migration due to different innervation of layers.

Peritonitis: wash-board rigidity. Pain exacerbated by slightest movement.

Rebound tenderness at McBurney’s point (2/3 of way along imaginary line from umbilicus to R anterior superior iliac spine)

Rousing’s sign: pain in LRQ when LLQ palpated

Psoas sign: increased pain on passive extension of right hip

Obturator sign: pain felt on passive internal rotation of flexed hip

Nausea/vomiting
Anorexia
Low-grade fever
Reduced bowel movements
Urine dip may show WBC or RBCs
297
Q

What investigations might you want to do for someone with ?appendicitis?

A

Bloods: FBC, U&E, LFTs, CRP

Pregnancy test

Urine dip

USS ( would see aperistaltic and non-compressible structure with diameter >6 mm)

Contrast CT (good sensitivity and specificity, able to diagnose other differentials BUT takes time to arrange)

Laparotomy

298
Q

How would you manage a patient with appendicitis?

A

Pain relief!

Appendectomy under GA
Keyhole or open
Contraindicated in IBD involving the caecum and possibly elderly or severely ill.

Unable to have appendectomy: IV antibiotics (not curative, reduce mortality in 50%, therefore buy time).

May consider IV ABX and appendectomy a few weeks later if patient has an appendix mass (fatty mass around appendix)

299
Q

What are the complications associated with appendicitis?

A

Perforation with/without peritonitis

Abscess formation

300
Q

What are the differentials for someone with ?appendicitis?

A
Gastroenteritis
IBS
constipation
bladder or urine infections
Crohn's disease
pelvic infection

ECTOPIC PREGNANCY

301
Q

What are the two different types of appendicitis?

A

Simple appendicitis—Inflamed appendix, in the absence of gangrene, perforation, or abscess around the appendix

Complicated appendicitis—Perforated or gangrenous appendicitis or the presence of periappendicular abscess

302
Q

what are some risk factors for cholecystitis?

A
GALL STONES or biliary sludge
Female gender
Age
Obesity
Rapid weight loss
Pregnancy
Crohn's disease
Hyperlipidaemia
303
Q

how might cholecystitis present?

A
epigastric or RUQ pain
vomiting
fever (high-swinging fever - riggers and chills)
raised WCC
Jaundice
Murphy's sign 

chariot’s triad: RUQ pain, jaundice, fever

304
Q

What investigations might you do for someone with ?cholecystitis?

A

FBC - WCC raised
LFTs (often mildly abnormal)
U&Es

USS - thickened GB wall, pericholecystic fluid or air
(thickened GB wall, but no gallstones = calculus cholecystitis)

305
Q

What are risk factors for gall stones?

A
Fair
Fat 
Fertile
Female
Forty (increasing age)
\+ve family history
Sudden weight loss
diabetes
Oral contraception
306
Q

How might someone present with gall stones?

A

biliary colic (most common presentation - cause by gallstone impacting in cystic duct or ampulla of Vater)

cholecystitis (second most common presentation, caused by distention of GB)

pancreatitis
obstructive jaundice

307
Q

How does biliary colic present?

A

Sudden onset pain in epigastrium or RUQ, may radiate from back into intrascapular region

subsides spontaneously with analgesics

nausea or vomiting

308
Q

What are differentials for biliary-tract obstructions/infections?

A

reflux
ulcers
IBS
pancreatitis

309
Q

How would you manage biliary colic and acute cholecystitis?

A

Pain relief: morphine, pethidine parenterally or diclofenac suppository

IV ABX
Fluids (if electrolyte/hydration imbalance)

refer for laprascopic cholecystectomy

unfit for cholecystectomy: percutaneous cholecystectomy (surgical drainage of GB)

310
Q

Which intestine is more likely to become obstructed? Large or small?

A

Small bowel

311
Q

What are some risk factors for small intestinal obstruction?

A

adhesions (from prior operations)
strangulated hernia
malignancy (usually caecum)
volvulus

312
Q

What are some risk factors for large intestinal obstruction?

A
colorectal malignancy (worse the lower down the bowel)
older age

risk of perforation

313
Q

What are some risk factors for sigmoid and caecal volvulus? (rotation of gut)

A

elderly
psychiatric illness
African/Asian (higher incidence)

314
Q

What are some risk factors for paralytic ileus? (condition in which bowel ceases to function - no peristalsis)

Intestinal pseudo-obstruction = ogilvie’s syndrome

A
Chest infection
Acute MI
Stroke
AKI
Puerperium 
Trauma
Severe hypothyroidism
Electrolyte disturbance
Diabetic ketoacidosis

Post-operative

315
Q

What are different types of bowel obstruction?

A

mechanical obstruction eg. adhesions, malignancies etc.

volvulus (rotation of gut)

paralytic ileus/ogilvie’s syndrome (lack of peristalsis)

316
Q

What are symptoms of bowel obstruction?

A

nausea/vomiting:
early in presentation =high-level obstruction
faeculant vomiting = low obstruction

dysphagia

abdo pain - diffuse, colicky, central (may be less/absent in paralytic ileus)
Severe pain and tension: suggest ischaemia or perforation

failure to pass bowel movements = earlier in lower obstruction
No flatus and no bowel movement: paralytic illeus

abdo distention:
Lower the level of obstruction = more

tympani

high-pitched bowel sounds

pseudo-obstruction presents like large bowel obstruction, but other medical history may indicate true nature.

317
Q

What might you find on examination in ?bowel obstruction?

A

Dehydration: poor peripheral perfusion, tachycardia, hypotension

pyrexia - perforation or infarction of bowel

Abdo distension
Peristalsis may be visible

Distended bowel: resonant on percussion
Abdo mass may be palpable

Peritonism (tenderness and guarding) = strangulation or perforation

Hernial orifices

Tinkling bowel sounds = obstruction
Silence = reduced OR SILENT bowel sounds

318
Q

How might you investigate someone for ?bowel obstruction?

A

Fluid charts - monitor fluid input and output
NG tube

Bloods: FBC
U&amp;Es
Creatinine
Group and cross-match
Glucose
Amylase (rule out pancreatitis)

Abdo X-ray (supine and erect)
US (to exclude small bowel obstruction)

ct scanning

319
Q

What differentials might you consider for someone presenting with symptoms of ?bowel obstruction?

A

Gastroenteritis (wouldn’t necessarily get bloating and reduced bowel movement)

ischaemia of gut - usually bloody diarrhoea

Acute pancreatitis (can get associated paralytic ileus)

peptic ulcer, perforated diverticular disease, perforated carcinoma

TB

MI (small bowel) 
Ovarian cancer (large bowel)
320
Q

How would you manage bowel obstruction?

A

All:

ABCDE management

Uncomplicated: conservative - fluid resuscitation, electrolyte replacement, intestinal decompression (via NG tube) and bowel rest, analgesia, anti-emetic

Antibiotics (prophylactic against bacteria)

Steroids (if inflammatory cause)

Illeus: stop medications that slow colonic motility

Endoscopy: decompression, dilation of strictures, stents
^ final treatment OR to allow for delay until elective surgical therapy

Emergency surgery (eg. complete small-bowel obstruction, closed loop obstructions, TOXIC MEGACOLON, bowel ischaemia and volvulus = surgical emergencies). Consider surgery if any signs of ischaemia, perforation, peritonitis

321
Q

What are symptoms/features of toxic megacolon?

A

Symptoms may come on suddenly
Background of IBD

Abdo pain
distended abdo
abdo tenderness
fever
tachycardia
shock
bloody or profuse diarrhoea
painful bowel movements
322
Q

What is diverticulitis?

A

diverticular inflammation with or without localised symptoms and signs

323
Q

What are the symptoms/features of diverticulitis?

A
LLQ pain (asians: RLQ)
intermittent or constant 
change in bowel habit
fever
tachycardia 
(hypotension and shock are unusual)
Anorexia, nausea and vomiting may occur
Localised tenderness, palpable mass

Bowel sounds may be normal or increased

Rectal examination may show tenderness or a mass

may present with complications of diverticulitis

324
Q

What are the complications of diverticulitis? (pts may present with these)

A

perforation: peritonitis
abscess: tender mass or persistent fever despite ABX
fistula
stricture/obstruction
Colovesical fistulas: pneumaturia (bubbles and dysuria) or faecaluria
colovaginal fistulas: frequent vaginal infections or copious vaginal discharge

bleeding - GI haemorrhage. abrupt painless bleeding, cramps, bloody stool

325
Q

What examinations would you do for someone with ?diverticulitis?

A
Bloods: 
FBC (WBC raised in diverticulitis, raised platelets, anaemia)
CRP
LFTs
U&amp;Es

CXR - detect pneumoperitoneum

Abdo xray - demonstrate small or large bowel dilation/obstruction, ileum, pneumoperitoneum, soft-tissue density (abscesses)

pelvic ultrasound (in women - investigate gynae problems)

?colonoscopy (or risk of perforation)

CT

326
Q

How would you manage a patient with diverticulitis?

A

Mostly managed at home: ABX, paracetamol, fluid-only diet for 2/3 days, followed by low-fibre diet (reduce faeces produced)

admit if: pain cannot be controlled by paracetamol
unable to drink enough fluids to keep hydrated
unable to take ABX PO
general health is poor
weakened immune system
suspected complications
symptoms failing to improve at home

ABCDE

Rehydration, symptomatic relief (pain killlers), IV ABX (metronidazole)

drainage of abscesses
elective surgery for removal of diverticula (4-6 weeks after diverticulitis attack)

emergency surgery: peritonitis, visceral perforation, sepsis, undrainable abscess, bowel obstruction or lack of improvement/deterioration with initial medical management

327
Q

What is pancreatitis?

A

acute inflammation of pancreas
release of exocrine enzymes which cause auto digestion of the organ.

Other local tissues and distant organs can also be involved

328
Q

What are the most common causes of pancreatitis?

A
I GET SMASHED
idiopathic/iatrogenic
gall bladder disease
excess alcohol consumption 
trauma (post ERCP, blunt)
Steroids 
Mumps
autoimmune
scorpion stings
Hyperlipidaemia, hyperparathyroidism (hypercalcaemia))
ERCP
drugs 

Ischaemia
IBD

329
Q

How does acute pancreatitis present?

A
Symptoms: 
upper abdo pain (LUQ), penetrates to back (could also be general abdo)
sudden onset
vomiting
pain increases over 72 hours
Signs: temperature (generally raised)
tachycardia, pt. unwell and dehydrated
jaundice may be present
abdo rigidity (epigastric or general)
bowel sounds usually present in early phase. Can get paralytic ileum (causing absent bowel sounds)

Severe cases: hypotension, pyrexia, tachypnoea, ascites, pleural effusion, Cullen’s sign, Grey Turner’s sign (due to retroperitoneal haemorrhage… pancreas is the retroperitoneum)
hypoxaemia

330
Q

What investigations would you want to do on a patient with ?acute pancreatitis?

A
Bloods:
FBC
U&amp;Es
glucose
CRP
ABG (PaO2 and calcium - for GLASGOW score and may also get hypocalcaemia)
LFTs (raised bilirubin and/or serum aminotransferase suggest gallstones)
May see hypocalcaemia
Amylase (3x normal or more)
Lipase (more sensitive and specific)

Abdo xray - exclude other causes, may see calcification, elevated hemidiaphragm, pleural effusion

CT scan

US - see presence of gall stones (but otherwise not that helpful)
Endoscopic ultrasound

331
Q

How would you manage a patient with mild acute pancreatitis?

A

Manage on general ward

Pain relief: pethidine or buprenorphine with/without benzos
NOT MORPHINE.

IV fluids, nil by mouth
NG tube for severe vomiting

ABX for specific infections

No other treatment, No CT necessary

pain, Sx and bloods under control: oral fluids, then solids resumed. Gallstones are the cause = consider common bile duct clearance

332
Q

How would you manage a patient with severe acute pancreatitis?

A

Treat in ITU or HDU

Fluids (maintain urine output >0.5 ml/kg)

Oxygen if necessary

IV ABX for 7-14 days (cef and met or AMG) if there is necrosis

Evidence of pancreatic necrosis, IV antibiotics

NG tube feeding

ERCP for patients with co-existing cholangitis or biliary obstruction

Surgery (if there is infection and necrosis)
Percutaneous catheter drainage

333
Q

What are the complications of pancreatitis?

A
pancreatic necrosis
infected necrosis
acute fluid collections
pancreatic abscess
acute pseudo-cyst
pancreatic ascities
acute cholecystitis
334
Q

How does paracetamol overdose cause toxicity?

A

Paracetamol metabolised by P450 system: 95% metabolised into harmless metabolites
5% becomes NAPQI

glutathione makes NAPQI harmless

Overdose increases NAPQI levels, run out of glutathione

NAPQI builds up

Hepatocytes damaged

335
Q

What should you do for patients presenting with paracetamol overdose?

A

ABCDE
Hx from patient
Look on toxbase (might need to make phonemail to NPIS - national poisons information services)

management of overdose depends on time after ingestion

Consider sectioning under 5(2) MHA (if on acutes, cannot do in ED)

336
Q

What are the important parts of the history?

A
HPC: How much has been taken
Time of first tablet (to last tablet)
Any other substances taken
what happened - fell, unconscious etc.
Precipitating factors 

Current symptoms: N+V, LOC, RUG pain

DH: Any regular meds, O/C
illicit drugs or alcohol alongside or regularly
ANYTHING INTERACTING WITH P450

PMH: anorexia, alcoholism (reduced glutathione stores)

PSYCH and social Hx

337
Q

How would you treat paracetamol overdose?

A

< 1 hour since start of overdose: CHARCOAL

have to wait until 4 hours to take PCM level

4-8 hours: take level
higher than line on graph, treat with parvolex

8 hours or more: start on parvolex treatment
take PCM measurement
If above line, continue treatment
If below line, stop treatment

15+ hours: treat with parvolex
no need to do PCM level

338
Q

What investigations would you want to do on a patient presenting with paracetamol overdose?

A

FBC
U&E
LFTs
PCM level - whether need to give parvolex
CLOTTING FACTORS (INR) - tells you about synthetic function of liver

339
Q

Under what circumstances can you use the PCM level graph?

A

UNstaggered overdose (taken within less than an hour)
Know time of first tablet
After 4 hours

340
Q

What is the treatment regimen for Parvolex in paracetamol overdose?

A

first bag: over 15mins
second bag: over 4 hours
third bag: over 16 hours (may need to give several of the third bags, until clotting returns to normal)

341
Q

What adverse reactions might you see in a patient who has been given parvolex? How would you manage this?

A

mock allergic reaction (red and itchy)

Piriton
Start parvolex at half dose

342
Q

What signs might you see in a patient with paracetamol overdose?

A

N+V within 24 hours
24-72 hours: jaundice
72 + hours: jaundice, bleeding and encephalopathy

343
Q

What are some red flags of lower back pain?

A

TUNAFISH

T: TRAUMA, TB
U: UNEXPLAINED WEIGHT LOSS, NIGHT SWEATS
N: NEUROLOGICAL DEFICIT, INCONTINENCE or retention, saddle anaesthesia, hip/leg weakness, NIGHT PAIN
A: AGE (<20 or >55)
F: FEVER
I: IVDU, infection
S: STEROID USE OR IMMUNOSUPPRESSED
H: Hx OF CANCER, EARLY MORNING STIFFNESS (pain at rest)

344
Q

What symptoms would make you think a patient might have a spinal cord compression? how would you treat this?

A
back pain
leg weakness
limb numbness
ataxia (+ve Romberg's)
urinary retention (with overflow)
hyper-reflexia
extensor plantars
clonus

Where possible: decompression of the spinal cord

345
Q

What symptoms would make you think a patient had caudal equina?

A
bilateral leg pain
back pain
urinary retention
perianal sensory loss
erectile dysfunction
reduced anal tone
346
Q

How would you investigate a patient that you thought might have a serious back problem (presented with red flags)?

A

Myeloma screen

Bloods: FBC
U+E
Calcium 
CRP
ESR

plain Xray (esp. if suspect osteoporosis/infection - not routine)

MRI

(CT if MRI not available)

347
Q

What are some causes of acute low back pain?

A
compression fractures to spine from osteoporosis
Cancer involving spine
fracture of spinal cord
muscle spasm
rupture or herniated disk
sciatica
spinal stenosis
spine curvatures
strain or tears to muscles or ligaments supporting back
AAA leaking
Arthritis conditions
Infection of spine 
Kidney infection or kidney stones
pregnancy
Conditions affecting female reproductive organs
348
Q

What would you recommend for someone who has lower back pain, but does not appear to be due to sinister causes?

A

Stay as active as possible
exercises and stretches for back pain
NSAIDS (if safe)
Hot or cold compression packs for short term relied

Physiotherapists

349
Q

How would you treat caudal equina?

A

URGENT surgery - relieve pressure on nerves

Other treatment depends on cause eg. infections = ABX, cancer = radiotherapy

350
Q

What are the Ottawa ankle rules?

A

Guidelines for clinicians to help decide whether patient needs X-ray for foot or ankle:

Ankle - pain in the malleolar zone and any one of the following:
- Bone tenderness along the distal 6 cm of the posterior edge of the tibia or tip of the medial malleolus
OR
- Bone tenderness along the distal 6 cm of the posterior edge of the fibula or tip of the lateral malleolus
OR
- An inability to bear weight both immediately and in the emergency department for four steps.

Foot - any pain in the midfoot zone and any one of the following:

  • Bone tenderness at the base of the fifth metatarsal (for foot injuries)
    OR
  • Bone tenderness at the navicular bone (for foot injuries)
    OR
  • An inability to bear weight both immediately and in the emergency department for four steps.
351
Q

What does the surviving sepsis campaign bundle say should be completed within three hours of presentation?

A

Measure lactate level
Blood cultures (X2)
Administer broad-spectrum antibiotics - one hour in septic shock/severe sepsis
Administer crystalloid for hypotension or lactate >=4.

Essentially, buffalo

352
Q

What are red flag features for herniated nucleus pulpous?

A

Major muscle weakness

foot drop

353
Q

What can cause peptic ulcer disease?

A
H. pylori 
NSAIDS
pepsin
smoking
alcohol
bile acids
steroids
stress
354
Q

How might peptic ulcer disease present?

A
epigastric pain and tenderness (usually 1-3 hours postprandial)
Pain may wake patient at night
Pain may radiate to back
relieved by food
Nausea
Oral flatulence
bloating
distention
intolerance of fatty food (like in gall stones)
Heartburn (may be GORD)
Pain may be relieved by antacids
succussion splash on auscultation of abode
355
Q

What are the differential diagnoses for someone with ?peptic ulcer disease?

A
AAA
GORD
Gastric cancer
Gall stones
Chronic pancreatitis
Crohn's disease
Diverticular disease
IBS
Drub-induced dyspepsia
Hepatitis
Acute ulcers
Zollinger-Ellison syndrome
Coronary heart disease
356
Q

What investigations might you do for someone with suspected peptic ulcer disease?

A
Bloods: 
FBC (may show iron-deficiency anaemia)
U+Es
LFTs
CRP

Carbon-13 urea breath test or stool antigen (to test for H. pylori)

Endoscopy - only necessary if patient presenting for the first time is 55yrs< or warning signs:
iron-deficiency anaemia
chronic blood loss
weight loss
progressive dysphagia
persistent vomiting
epigastric mass
In pts. aged over 55 (not presenting for first time), also do endoscopy if:
previous gastric ulcer
previous gastric surgery
pernicious anaemia
NSAID use
family history of gastric carcinoma
357
Q

How would you manage a patient with peptic ulcer disease?

A

Stop or replace causative drugs/ ask patient to take with food or alendrotnic acid
Cardiac risk pts: continue low-dose aspirin and full-dose naproxen

encourage cessation of smoking

H.pylori positive: eradication therapy

NSAID-induced: first line - PPI for two months
Second line - 8/52 of standard dose H2-receptor antagonist (ranitidine 150mg BD)

not H. pylori or drug-induced: may need sample of ulcer

Bleeding ulcer: endoscopic intervention with ablative/mechanical treatment

follow up endoscopy 6-8 weeks later

358
Q

What are the first-line drugs recommended for eradication therapy (for H. pylori)?

A

7 day PPI plus amoxicillin 1g and either clarithromycin 500mg or metronidazole 400mg (all BD). Clarithro + metro if pt. penicillin allergic

359
Q

what are some risk factors for urinary tract stones?

A
abnormal kidneys/ureters
FHx
HTN
gout
Hyperparathyroidism
Immobilisation
Relative dehydration
increased excretion of solutes
cystinuria
drugs: diuretics and vit D supplements
360
Q

How might renal colic present (if symptoms are present)?

A

sudden onset severe pain (may begin as dull ache)
loin pain, moves to groin
tenderness of login or renal angle
haematuria
stone high (in renal capsule): flank pain
pain may radiate down to testis, scrotum, labia and anterior thigh

rigors and fever (if infection is present)
dysuria
haematuria
urinary retention
nausea and vomiting
hypotension may be present
361
Q

What investigations might you want to do for someone with ?renal colic?

A

Bloods: FBC, CRP, renal function, electrolytes, calcium, phosphate, rate and creatinine
Prothrombin time and INR (if intervention planned)

Urine:
urine dip for blood, white cells, nitrites, ph<7 (urea-splitting organisms) ,<5 (uric acid stones)
microscopy, culture and sensitivities

US
CT
KUB

362
Q

How would you manage a patient with renal colic (at hospital)?

A

NSAIDS: diclofenac IM or PR = first line

opiates only if severe pain NOT PETHIDINE

Anti-emetics

Conservative management for up to 3 weeks (unless infection of obstruction is present)

Medical expulsive therapy to help passage of stone: nifedipine or tamsulosin + steroid

May need surgical removal:
stent (if obstruction present)
extracorporeal shock wave lithotripsy (ESWL - shock waves break up stones)
other types of surgery available too.

363
Q

For what reasons would you admit someone with renal colic?

A

fever
solitary kidney
inadequate pain relief or persistent pain
inability to take fluids due to nausea and vomiting
anuria
pregnancy
poor social support
inability to arrange outpatient follow-up
over 60 yrs if concerned about clinical condition

364
Q

When might you consider managing a patient with renal colic as an outpatient?

A

patient has been relieved
patient able to drink large amounts of volume
good social circumstances
no complications evident

365
Q

what complications can be associated with renal colic?

A

reduced eGFR
sepsis
ureteric stricture
pyelonephritis

366
Q

What is a lower UTI?

A

Infection of bladder (cystitis)

367
Q

What is an upper UTI?

A

pyelitis and pyelonephritis

368
Q

What’s an uncomplicated UTI?

A

infection by usual pathogen in a person with usual urinary tract with normal kidney function

369
Q

What’s a complicated UTI?

A

anatomical, functional or pharmacological factors predispose patient to persistent infection, recurrent infection OR treatment failure

370
Q

What pathogens most commonly cause UTI?

A

E. coli
Staphylococcus saprophticus
proteus mirabilis
enterococci

371
Q

What are less common causes of UTI? (eg. in patient with predisposition)

A

Klebsiella
Proteus vulgaris
Candida albicans
Pseudomonas

372
Q

What are some risk factors for UTI?

A
Increasing age
female 
instrumentation in renal tract
abnormality of renal tract
incomplete bladder emptying
sexual activity
use of spermicide
diabetes
catheter
institutionalisation
pregnancy
immunosupression 
genetic
373
Q

What are some common symptoms of UTI?

A
frequency
painful frequent passing of small amounts of urine
dysuria
haematuria
foul-smelling +/- cloudy urine
urgency
incontinence
suprapubic or loin pain
riggers
pyrexia
N+V
acute confusional state (esp. in elderly patients)
374
Q

How would you investigate someone for UTI?

A

Dipstick analysis of urine
(not for catheters). Treat fas bacteria if positive for nitrites and/or leukocytes

Urine microscopy

Urine culture (to exclude diagnosis, or high-risk, or failing to respond to empirical treatment)

ultrasound of upper UT (rule out obstruction and renal stone disease in acute pyelonephritis)

Febrile 72 hours post treatment: further imaging (?CT)

375
Q

Which patients with UTI should be refered for imaging or cystoscopy?

A

Persistently not responded to treatment

Hx of renal tract disease or anomaly

Haematuria

WOMEN with recurrent infections, not responding to preventative measures

MEN with 2=< episodes in 3 mths

376
Q

When might you investigate a patient for cancer if they present with UTI-like symptoms? How would you investigate this?

A

MALE nocturne, urinary frequency, hesitancy, urgency or retention OR visible haematuria: DRE and PSA

Refer under 2-week wait if: person under 45 has had unexplained visible haematuria without UTI OR visible haematuria which persists after successful treatment of UTI OR
60 or over unexplained non-visible haematuria and either dysuria or raised WCC on blood test OR
over 60 with recurrent/unexplained UTI

377
Q

How would you treat a UTI?

A

lower UTI: Trimethoprim or nitrofurantoin

3 days in uncomplicated women
7 days for men

Pyelonephritis: ciprofloxacin 7-10 days. Co-amoxiclav is an alternative.

Asymptomatic bacteria should not be treated in adults with catheters or non-pregnant women

378
Q

What can cause an acute ischaemic leg?

A

Embolism - gas, solid or liquid (most commonly of cardiac origin)
Thrombosis - peripheral vascular disease

Rarely: dissection or trauma

379
Q

What are symptoms and signs of acute limb ischaemia?

A
Pain
Pallor (but could also be red)
Paresthesias
Perishingly cold
Pulelesness
Paralysis

Skin changes: mottling (signifies irreversible changes)
Development of gangrene (late sign)

380
Q

How long may a patient have had limb ischaemia for it to be called ‘acute’?

A

Less than 2 weeks

381
Q

What investigations would you do for someone who you suspected had an acute ischaemic leg?

A

Bloods: FBC (ischaemia is aggravated by anaemia)
U+E (dehydration, K+ usually raised if tissue necrosis is occurring)
ESR (inflammatory disease causing ischaemia)
CK (raised if ischaemia has occurred)
Glucose
Lipids
Thrombophilia screen (clotting)
Group and save

ABG/VBG (acidosis secondary to ischaemia)

HAND-HELD DOPPLER US scan

Diagnosis in doubt: angiography (CT)

ECG (source of emboli)
Echo
Aortic ultrasound
Popliteal and femoral artery ultrasound

382
Q

How would initially manage an acute ischaemic leg in the emergency department?

A

Analgesia: IV morphine

Oxygen

IV Heparin

IV fluids

tPA (tissue plasminogen activator) - given for 8-24 hours via Fogarty Catheter (arterial catheter) <2 weeks.

Refer to vascular specialist urgently. Delay risks the limb (if sensorimotor impairment). Thrombolysis or surgery!

383
Q

What are the different stages of the Rutherford classification for acute limb ischaemia?

A

Stage 0: asymptomatic
Stage 1: mild claudication (salvageable)
Stage 2: moderate claudication (salvageable with immediate reconstruction)
Stage 3: severe claudication (major tissue loss or permanent nerve damage)
Stage 4: rest pain
Stage 5: ischaemic ulceration (not exceeding ulcer of digits of foot)
Stage 6: sever ischaemic ulcers or frank gangrene

384
Q

How can you tell the difference between thrombosis end embolism in lower limb ischaemia (generally)?

A

Thrombosis onset: hours to days
Embolism onset: minutes

Upper limb effected: thrombosis = rarely, embolus = commonly

Multiple sites affected: not usually in thrombus
can occur in embolus

Previous claudication usually present with thrombus

Obstruction usually complete in embolus (no collaterals), but collaterals in thrombosis

385
Q

What are some symptoms and symptoms might you see in someone with cellulitis?

A
Swollen area
Red
Well-defined border
Warm
Tender to touch/pressure
Usually unilateral
Pain onset: gradual
Malaise
Chills
Fever
Tachycardia
Tachypnoea
Hypotension
Skin sloughing
Skin anaesthesia or high levels of pain
Violaceaous bullae
Lymphangitis spread
386
Q

What elements of previous medical history might be in-keeping with a diagnosis of cellulitis?

A
General debility
Immunocompromised
Hx of infection
DM (esp. if ulcerated or cut foot)
Cancer
Venous stasis
Chronic liver disease
Peripheral arterial disease
CKD
387
Q

What investigations would you do for someone you suspected have cellulitis?

A
Bloods: blood culture
FBC, U+E and LFTs (baseline level)
Creatinine (high)
creatinine phosphokinase (high)
CRP (high)
VBG - bicarb (low)

Purulent lesion: debride and culture

Imaging: US
X-ray
CT (if concerned about necrotising fasciitis)

388
Q

How would you manage a patient with cellulitis?

A

MARK AREA WITH SKIN-MARKING PEN

Analgesia (NSAIDS)

ABX: flucloxacillin 500mg QDS = first line
Erythromycin 500mg QDS if patient is penicillin allergic

Clindamycin is second-line treatment

Steroids (for anti-inflammatory)

Emollient

hydration

389
Q

What is the difference between gout and pseudo gout? How can you tell this difference?

A

Gout: urate crystals
Psuedogout: calcium phosphate crystals

Differentiate by aspirating the joint

390
Q

What is gout?

A

Crystal arthritis

High concentration of uric acid in blood stream

Not all patients with high blood urate level get gout

Low blood urate level doesn’t rule out diagnosis

391
Q

What causes gout?

A
genetic susceptibility
diet: meat and alcohol, food with high conc. of purine
SE status
Larger BMI
Drugs: diuretic (esp. thiazide)
392
Q

How might gout present?

A

mono arthritis - v. hot, red, swollen joint.
MTP is join affected in most patients (also PIP and DIP)

wakes patient at night

Tophi (urate crystal deposits in skin) - if long term

Synovitis

Pyrexia

Stone formation in kidney and bladder (may cause other symptoms)

393
Q

What investigations might you do for someone you suspected had gout?

A
Bloods: FBC (WCC raised), U+E 
Serum urate (raised in 60% of cases)
ESR (often raised)

Synovial fluid aspiration

x-ray (if assessing long-term damage)

394
Q

How would you manage a patient with gout?

A

NSAIDSs
Colchicine

(allopurinol once episode has passed)

remove triggers

395
Q

How does pseduogout usually present? How would you investigate this? How would you manage it?

A

Presents like gout
BUT knee most commonly affected (and bigger joints)

Joint aspiration
Radiographs (may show chondrocalcinosis)

Treatment: NSAIDS less effective than in gout
INTRA-ARTICLUAR INJECTIONS OF STEROIS useful in treating acute presentation

396
Q

What are the symptoms of amphetamine overdose?

A
Tachycardia and arrhythmias
Mydriasis
Euphoria
Formication
Agitation or pacing
Tremor
Dilated pupils (sluggish response to light)
Convulsions
Hypertension
HYPERTHERMIA (can get dangerously high)
clenched jaw/jaw rigidity 
rapid speech
Flushed face
Hyper vigilance and paranoia
397
Q

How would you investigate someone with suspected amphetamine toxicity?

A

A: airway

B: RR etc.

C: Bloods: U+Es
Renal function
LFTs
creatine phosphokinase
ECG
Urine dipstick

D: blood sugar
CT head if Hx of head injury or altered consciousness

Assess for serotonin toxicity

398
Q

How would you manage a patient with amphetamine toxicity?

A

A-E assessment
sedation: benzodiazepines

Fluids

Airway management, Oxygen, rapid calling etc. if necessary. Seizure control with benzodiazepines

399
Q

How would opioid overdose present?

A

Opioid overdose triad:
pinpoint pupils
unconsciousness
respiratory depression

400
Q

How should you manage a patient with opioid overdose?

A

A-E assessment
Naloxone (IV, IM, SC or intranasal). Start low (0.04-2mg IV) can give up to 4mg at a tim (if pt. severely poisoned)

IM if patient threatening to self-discharge

Can also be given as an infusion

Toxbase

401
Q

How would you investigate a patient with opioid toxicity?

A

Urine drugs test

Bloods (baseline): FBC, metabolic screen, SK and ABG

CXR if pulmonary oedema suspected

ECG

402
Q

How might tricyclic antidepressant overdose present?

A
Sedation (+/- apnoea)
Confusion/delerium
Arrhythmia
Seizure
Hypotension
Anticholinergic effects: hyperthermia, flushing, dilated pupils
nausea and vomiting
headache
403
Q

How would you investigate someone with TCA overdose?

A

ECG: sinus tacky, prolonged QRS, unusual R wave, prolonged QTc

Bloods: FBC
U+E
LFTs
(baseline)
ABG/VBG
404
Q

How would you manage a patient with TCA overdose?

A

Airway management: may require intubation (GCS>8)

B: hyperventilate pt. to blow off CO2

C: IV access - sodium bicarb rapid bolus. Repeat until ECG changes seen. May want to set up infusion.
May need to give magnesium.
Fluids to raise BP, may need vasopressors (noradrenaline)
IV bentos for seizures

D: NG tube

E: temp

405
Q

What is testicular torsion?

A

Torsion of spermatic cord
Occlusion of testicular blood vessels
Rapidly lead to ischaemia and loss of testis

406
Q

How might testicular torsion present?

A

Usual neonatal or post-pubertal (but can be any age)
L more common than R
Bilateral = rare

Acute swelling of scrotum
Sudden onset, severe pain
Lower abdo pain
Pain onset during physical activity
May be history of this happening before and resolving 
Nausea and vomiting
407
Q

What might you see in testicular torsion, when examining the testicle?

A

Redenning scrotal skin
Swollen, tender testis, retracted upwards
Lifting testis over symphysis increases pain
epididymis may be in anterior position
‘bell-clapper position’
Absence of cremasteric reflex

408
Q

What investigations would you do for someone with suspected testicular torsion?

A

COLOUR DOPPLER
MRI
Urinalysis (eliminate other differentials)

Clinical suspicion high, surgical intervention should not be delayed

409
Q

How would you manage a patient with suspected testicular torsion?

A

surgical exploration for anyone with high suspicion of torsion
Pt should be NBM
may be able to reduce torsion manually
Bilateral orchiopexy to fix testis in place

410
Q

How might an ankle sprain present?

A

Severity depends on severity of sprain

Tenderness and swelling
Bruising
Functional loss (eg. pain on weight-bearing)
Mechanical instability (if severe)
Marked bruising (may indicate ligament tear or fracture)

411
Q

What are differentials of acute ankle pain?

A
Achilles tendon injury
Joint pathology
Tendon injury
Stress fractures
Fracture
412
Q

How can you classify (lateral) ankle sprains? (lateral ankle sprains make up 85% of sprains)

A

Grade I-III

Grade 1: ligament stretched mild swelling
no/little functional loss
no joint instability.
Pt can partially weight bear.

Grade 2: ligament stretched,
partial tearing,
swelling mod-severe, moderate function loss, mild-mod joint instability. Difficulty weight-bearing.

Grade 3: ligament is completely ruptured
swelling is immediate and severe
ecchymosis
Patient cannot weight bear or not without SEVERE pain
Mod-severe instability of the joint

413
Q

How would you manage someone with an ankle sprain?

A
Pain relief
Functional support (rather than immobilisation, unless severe e.g.. grade 3)

For the first 72 hours: PRICE

P: protection from further injury (eg. bandage, ankle tape, brace, high-top lace shoes)

R: rest ankle joint for 48-72 hours after injury. Consider crutches in this period.

I: apply ICE for about 10-30 mins after injury (NOT directly next to skin). Limits pain, inflammation and bruising)
Try for 15 mins every 2 hours (NOT during sleep)

C: compression bandage, limit swelling

E: elevation to limit and reduce any swelling

Range of motion exercises once not too painful

grade 3 spain may recover better with period of immobilisation first

advise to go to GP if no improvement

414
Q

What things should you advise a patient to avoid in ankle sprain?

A

HARM

Heat
Alcohol
Running
Massage

All increase bleeding and swelling risk

415
Q

What is the common cause of a Colle’s fracture?

A

FOOSH

416
Q

How would a Colle’s fracture present?

A

Dorsal displacement and deformity (dinner fork deformity)

Ulnar styloid tenderness

417
Q

Other than the obvious dinner-fork deformity, what else should you check in a patient with ?Colle’s fracture?

A
Ulnar styloid for tenderness
Examine elbow (for co-exisiting radial head fracture)
Neuromuscular function
418
Q

How would you investigate a Colle’s fracture?

A

Xray (at least lateral view)

419
Q

How would you manage a Colle’s fracture?

A

Analgesia (but careful as pt. may need to be NBM)

Reduce in emergency department (under sedation): longitudinal traction (pulling wrist) and dorsal pressure
Sedation: midazolam +/- fentanyl (ketamine in children)

Apply back slab

RE-XRAY to check bone alignment (may need to repeat if it is not)

Severely displaced/open-fracture: open surgical repair

Healing time 6-8 weeks

420
Q

What are the complications of Colle’s fracture?

A

Medial and ulnar nerve damage
acute carpal tunnel syndrome
compartment syndrome
malunion/non-union

long term: deformity/loss of function/osteoarthiritis

421
Q

How would you investigate someone with suspected hip fracture?

A
Bloods: FBC
U+Es
LFTs
Group and save
INR (if on warfarin)
Clotting

ECG

X-ray hip and pelvis

422
Q

How might a hip fracture present?

A

Hip pain
Hx of fall/trauma
Leg: shortened and externally rotated

423
Q

How would you manage someone with hip fracture?

A

Urgent X-ray of the pelvis
(within an hour)

Pain relief +++ (fascia iliac block - local nerve block)

Minimal movement

Pressure sore care

Fluids etc. if necessary

C-spine immobilisation (if trauma)

call to surgeons - hemiarthroplasty

VTE prophylaxis (stockings)

424
Q

What is Gardener’s classification of hip fractures?

A

Categorises fractures into severity, guiding management

Also predicts development of AVN

Garden stage I : undisplaced incomplete, including valgus impacted fractures.

Garden stage II : undisplayed complete

^ stable fractures, treated with internal fixation

Garden stage III : complete fracture, incompletely displaced

Garden stage IV : complete fracture, completely displaced

^unstable fractures treated with arthroplasty (semi or total)

425
Q

What is septic arthritis?

A

Infection producing inflammation in native or prosthetic joint

Can be acute or chronic

426
Q

Which groups might be more likely to get septic arthritis?

A
Children (under 5)
Immunosuppressed 
Diabetics
IVDU
Prosthetic joints/joint surgery 
(old)
427
Q

How might septic arthritis present?

A
single swollen joint with pain on active or passive movement
warm joint
Fevers or rigors may be present
vomiting 
hypotension
may have an abscess
bacteraemia
chest wall pain (if infected joint around chest)

Triad of fever, pain and impaired range of motion

OFTEN PRESENTS IN THE KNEE

immunosuppressive disease
recent steroid injection
STD
IVDU

428
Q

What are the differential diagnoses of septic arthritis?

A
rheumatological disorders
gout/pseudogout
vasculitis
drug-induced arthritis 
reactive arthritis
lyme disease
infective endocarditis
429
Q

How would you investigate a patient with ?septic arthritis?

A

Bloods: FBC (raised WCC)
ESR and CRP

Synovial fluid examination:
aspirate - crystals, white cells and culture
DON’T ASPIRATE PROSTHETIC

Blood culture
Tissue culture
PCR
Test for lyme disease
Immunology

?imaging (X-ray, then ?CT) (for prosthetic joint)

430
Q

How would you manage a patient with septic arthritis?

A

Consult microbiologist

Prescribe broad spectrum ABX that covers S. aureus and strep. Flucloxacillin, clindamycin if penicillin allergic.
MRSA - vancomycin
IV 2-3 weeks, switched to oral for 2-4 weeks

431
Q

How might otitis media present?

A

More common in children

Ear features: Acute onset ear pain (otalgia)
Middle ear inflammation

Eardrum features:
Effusion or Purulent discharge (can be bloody) - reduce pain once this occurs
Bulging or erythematous tympanic membrane
Fluid level behind tympanic membrane
Perforated tympanic membrane

Hearing features:
Conductive deafness
Tinnitus

Other general features:
previous URTI
Fever
Imbalance

432
Q

How would you manage a patient with otitis media?

A

Analgesia (NSAIDS etc).

Early otitis media:
Symptomatic treatment
+/- ABX (if pt. is well, analgesia and symptomatic relief)
ABX: co-amoxiclav

Bulging otitis media:
ABX (co-amoxiclav)
If these fail (or recurrent) = myringectomy (incise tympanic membrane to release fluid build up)

Discharging otitis media:
Antibiotics based on swab and culture

(most resolve within 7-14 days)

Recurrent = gromit insertion

433
Q

What are common causes of otitis media?

A

Strep

H. influenza

434
Q

What are common causes of tonsillitis?

A

30% bacterial
70% viral
(99% will recover without antibiotics)

Group A streptococcus

435
Q

What are the symptoms of tonsillitis?

A

Sore throat, red and inflamed
Enlarged tonsils
Fever
Malaise/lethargy

436
Q

What investigations might you do for someone with tonsillitis?

A

Generally no investigations done

throat swab, but this takes time

437
Q

What investigations might you do for someone with tonsillitis?

A

Generally no investigations done
throat swab, but this takes time

General obs (check for systemic illness)

438
Q

How would you manage patient with tonsillitis?

A

Paracetamol and ibuprofen
Avoid giving ABX unless meet censor criteria OR systemically unwell

Penicillin V (phenoxymethylpenicillin) used if meet criteria
Erythromycin if penicillin-allergic
439
Q

Which ABX should you not give to a patient with tonsillitis? Why?

A

Amoxicillin

Can cause rash if patient has glandular fever

440
Q

What are the red flags of tonsilitis/sore throat?

A
Persistent sore throat for > 6 weeks
Excessive drooling
Trismus
Unilateral facial swelling
Dysphagia
Dyspnoea
Immunosuppressant medication such as carbimazole
Persistent unilateral tonsillar enlargement
Neck stiffness
Photophobia
Non-blanching rash

cancer, agranulocytosis

441
Q

What are the two main presentations of meningococcal disease?

A

Meningococcal meningitis

Meningococcal septicaemia

442
Q

What are the features of a meningitis prodrome?

A

Fever
Nausea and vomiting
Malaise
Lethargy

443
Q

What are the features of meningococcal meningitis?

A

Severe headache
Neck stiffness (not always present in young children)
Photophobia
Drowsiness/confusion/impaired consciousness
Seizures (late sign)
Focal neurological deficit, incl. cranial nerve involvement and dilated/unequal/poorly-reactive pupils (late sign)

444
Q

What generally kills people with meningococcal meningitis?

A

Raised ICP

445
Q

What are features of meningococcal septicaemia?

A
Limb/joint pain
Cold hands and feet
Prolonged cap refill
Plae/blue/mottled skin
Tachycardia
Tachypnoea, labour breathing, hypoxia
Riggers
Oliguria/thirst
Rash (non-blanching)
Abdominal pain (+/- diarrhoea)
Drowsiness/confusion/impaired consciousness
Hypotension
Rapid deterioration
446
Q

What generally kills people with meningococcal septicaemia?

A

Cardiovascular failure

447
Q

How would you manage a patient with meningococcal septicaemia or meningitis?

A

A: airway may be needed

B: 15L NRB O2 (acutely unwell)
Breathing sounds 
RR
Sats
ABG
C: blood cultures
Cannula
IV ABX - ceftriaxone +/- vancomycin (travel abroad or long-term ABX use). Up to 7 days.
Fluids (restrict if raised ICP)
Anticoagulants if patient has DIC
corticosteroids

D: Neurological assessment (incl. pupils)
Blood glucose
AVPU/GCS

E: expose to look at/for rash
feel abdo

May need HDU/ICU bed

448
Q

On top of treating the patient with meningococcal disease, what else must you do as a clinician?

A

Contact consultant in communicable disease control or public health medicine

Prescribe ciprofloxacin to close contacts + vaccinations
(prevents further spread FROM contacts as opposed TO contacts)

449
Q

What investigations might you do on someone who’s ?mengingococcal disease

A
Blood cultures
FBC (WCC and platelets )
CRP
U+Es
Renal function tests
LFTs
Clotting (aPTT, fibrinogen) - investigating ?DIC

PCR for N. meningitidis (use earliest sample possible)

Pharyngeal swab

Lumbar puncture (once stable) - check for ICP. Microscopy, culture, glucose and PCR. DO THIS EARLY IF MENINGITIS SUSPECTED, LATER IF SEPTICAEMIA

450
Q

Which signs in meningococcal disease require URGENT review by senior +/- critical care review?

A

Rapidly progressive rash
Capillary refill time > 4 secs,
oliguria or systolic BP
< 90mmHg
Respiratory rate < 8 or >30
Pulse rate < 40 or >140
Acidosis pH < 7.3 or Base excess worse than -5
White blood cell count <4x109/L
Lactate > 4 mmol/L
Glasgow coma scale <12 or a drop of 2 points
Poor response to initial fluid resuscitation

451
Q

what are some causes of diarrhoea?

A

Short-term:
virus
Bacterial (eg. food poisoning)
parasites (eg. giardiasis)

Anxiety
Alcohol excess
Allergy
Appendicitis
Radiotherapy
Drugs:
ABX
Antacids (containing magnesium)
Chemo
NSAIDS
SSRIs
Statins
Laxatives
Long term:
IBS
IBD
Coeliac disease
Bile acid malabsorption
Chronic pancreatitis
Diverticular disease
Bowel cancer
452
Q

What counts as diarrhoea?

A

Stools more than 3 times a day

Stools become loose or watery

453
Q

How would you manage diarrhoea?

A

Fluids (if dehydrated)

Loperamide

454
Q

What is giant cell arteritis?

A

systemic immune-mediated vasculitis affecting medium and large-sized arteries

455
Q

How might giant cell arteritis present?

A

Temporal headache (recent onset). Severe. Sometimes worse at night.
myalgia
malaise
fever
Jaw or tongue claudication
Enlarged, beaded or pulseless temporal artery
Scalp tenderness
Raised ESR
Anaemia
Visual disturbance (inflammation of ophthalmic artery, ischaemic optic neuritis): blurred vision, amaurosis fugax, transient or permanent visual loss, diplopia. Ischaemic changes may be seen on fundoscopy)

Classic presentation:
over age of 50
scalp tenderness 
transient visual symptoms
unexplained facial pain

CAN RESULT IN LOSS OF VISION

Systemic symptoms: weight loss, fever, sweats, carotid bruits

456
Q

What investigations might you do for someone with ?GCA?

A

Bloods: FBC (normocytic normochromic anaemia)
LFTs
ESR
CRP

Temporal artery biopsy

Colour duplex ultrasonography

457
Q

What criteria must be present to diagnose someone with GCA? How many need to be met to make the diagnosis?

A

Age of disease onset: >=50 yrs

New onset headache

Temporal artery abnormality

ESR >= 50 mm/hr

Abnormal artery biopsy

3/5 must be present to make the diagnosis

458
Q

How would you manage a patient with GCA?

A

High dose corticosteroids
40mg prednisilone daily unless patient has iscahemic symptoms
Claudication/ischaemic symptoms: 60 mg
Visual symptoms: IV methyprednisilone

Once symptoms reduce - reduce slowly.

Low dose aspirin 75mg + PPI

459
Q

How does a subarachnoid haemorrhage present?

A
Sudden onset headache (usually occipital)
INTENSE from start
Neck stiffness
Vomiting
Extensor plantar responses 
Impaired consciousness (usually shortly after onset, but can be after several hours)
Cranial nerve signs
Hemiplegia
Hypertension

(sentinel headache)

Symptoms of stroke (following vasospasm after SAH - causing ischaemia)

460
Q

What investigation would you do for someone with ?SAH?

A

CT (able to detect >90% lesions within 48 hours of onset). NON-CONTRAST

bleed found: angiography

Lumbar puncture (if CT negative, but strong clinical suspicion) - looking for xanthochromia (yellow CSF)

ECG

Bloods: Billirubin

461
Q

How should you manage a a patient with SAH?

A

Call:
Med reg
neurosurgeon on call
anaesthetist (depending on GCS)

Stabilise patient haemodynamically

A-E

Prevent re-bleeding: nimodipine 60mg 4-hrly
low dose nitroprusside (vasodilator) and labetalol - maintain cerebral perfusion (but not enough to encourage re-bleeding)

Analgesia
Anti-emetics

Surgery: clipping (craniotomy) and coiling (clips around aneurysm via femoral catheterisation)

462
Q

What is a stroke?

A

Sudden onset of brain dysfunction

Caused by alteration in cerebrovascular blood supply

463
Q

How might a stroke present? (generally speaking)

A

Rapid, acute onset neurological changes eg. hemiplegia

464
Q

What are the two main types of stroke?

A
Brain ischaemia (80-90%)
Haemorrhage (10-20%)
465
Q

What are the main causes of stroke?

A

Arterial embolism

Haemorrhage (cerebrum itself or SAH)

466
Q

What are some risk factors for stroke?

A
Afro-carribean/asian
Male
Age
HTN
Smoking
AF
Diabetes
Alcohol
hypercholesterolaemia/hyperlipideamie
Obesity
heart disease
FHx
467
Q

When do most strokes occur?

A

BP lowered during the night whilst asleep

On waking, BP rises, more likely to dislodge any embolism

468
Q

Where is the most common location for cerebral infarct to occur? How would this present?

A

Middle cerebral artery

Hemiparesis
hemiplegia
floppy limbs, lack reflexes reduced/absent
Facial weakness
hemianopia
aphasia

symptoms usually develop rapidly. Recovery will occur gradually, over days, weeks etc. Longer time = worse prognosis

not usually a headache (if present, implies swelling, implies haemorrhage)
not usually any LOC
seizure v. rare

Reflexes reappear, but exaggerated
Extensor plantar response

469
Q

What symptoms might you see in patient with anterior cerebral artery infarct?

A

weak leg +/- shoulder

CONTRALATERAL side

470
Q

What symptoms might you see in patient with posterior cerebral artery infarct?

A

eye problems

471
Q

What symptoms might you see in patient with a brainstem infarct?

A

(depends on location, but selection of symptoms):

semi/tetraparesis
sensory loss
diplopia
facial numbness
facial weakness
nystagmus and vertigo
dysphagia and dysarthria
hornet's syndrome
altered consciousness

coma
locked-in syndrome (loss of all motor neurone function)
pseudo bulbar palsy (dysarthria and dysphagia)

472
Q

What symptoms may present with lacunar infarct?

A

Often symptomless
Very localised symptoms eg. purely sensory or purely motor

aphasia
hemiparesis
hemisensory loss
unilateral ataxia

473
Q

How would you investigate suspected stroke?

A

CT:
infarctions = wedge shape
haemorrhage = blood appears bright white initially, gets darker over time. 1-2 weeks later = indistinguishable from normal brain tissue

New stroke <2 hours old, may not show up at all. 6-12 hours, will be clearly visible.

BP (manage)
ECG (looking for AF)
CXR (heart size), echo

Blood (rule out differentials):
ESR (raised - ?GCA)
FBC/platelets/clotting
glucose
cholesterol/lipids
474
Q

How might a cerebral haemorrhage present?

A

Similar to infarct picture BUT
more likely to lose consciousness, headache
progressive neurological defects

Hydrocephalus (blood leaks in to ventricular system)

475
Q

How would you manage ischaemic stroke?

A

A-E

Thrombolysis (if possible)

If unable to thrombolyse: 300mg aspirin for 2 weeks then 75mg a day (if not aspirin, clopidogrel)

Dipyridamole

Warfarin or NOAC in long-term

476
Q

How would you manage haemorrhage stroke?

A

A-E

Mostly supportive

If anticoagulants and antiplatelets have been given, reverse with fit K, fresh frozen plasma and platelet transfusions

haemorrhagic mass >3cm = surgery (drain or craniotomy)

Manage BP is SBP>185mmHg

477
Q

What are the clinical features of a DVT?

A

(result of obstruction to venous drainage)

Limb pain
Tenderness along line of deep veins
Swelling of calf or thigh (usually unilateral)
Bilateral - thrombosis in iliac bifurcation, pelvis veins or vena cava
Pitting oedema
Distension of superficial veins
Warm limb
Skin discolouration (erythema or cyanosed)
Palpable cord (hard, thick palpable vein)

Severe DVT: cellulitis-like
can also have cellulitis (as secondary to DVT or primary, leading to DVT)

478
Q

What differentials might present similar to DVT?

A
Trauma
Superficial thrombophlebitiis
peripheral oedema, heart failure, cirrhosis, nephrotic syndrome
venous/lymphatic obstruction
vasculitis
cellulitis
septic arthritis
479
Q

How would you investigate a patient with suspected DVT?

A

Depends on level of risk (calculated by a two-level Well’s score)

General bloods:
FBC
PT
INR/APTT
Renal function
LFTs
480
Q

How would you investigate a patient who has suspected DVT and a LIKELY two-level DVT Well’s score? (>=3)

A

Doppler US leg

D-dimer (if doppler -ve)

481
Q

How would you investigate a patient who is at low risk of DVT? (<3 on two-level Well’s score)

A

D-dimer test

If positive: doppler US leg
(wouldn’t be done if D-dimer was negative)

If doppler US is negative and Wells score 1-2, reassess using US scan in 5-7 days time.

482
Q

How would you manage someone with DVT?

A

Analgesics (avoid aspirin and NSAIDS)

LMWH (deltaparin, enoxaparin, tinzaparin) - start this immediately if diagnosis of DVT is likely on clinical grounds before definitive investigation
OR
Fondaparinux
For at least 5 days (or until INR 2

483
Q

What are some contra-indications to anticoagulation that you need to consider when prescribing LMWH?

A
Active peptic ulceration
alcohol excess
liver disease
PT>2 secs beyond normal range
Thrombocytopenia (platelets <80)
Uncontrolled hypertension (>180/100)
Ophthalmic/neurosurgical intervention recently
Hx of haemorrhage stroke
biopsies
pregnancy
484
Q

What is included in Two-level DVT Wells score?

A

Each score one point, except final point, which is -2

Active cancer (treatment on-going or within 6 months OR palliative)

Paralysis, paresis or recent plaster immobilisation

Recently bed-ridden for 3 days or more
Major surgery within 12 weeks, requiring general or regional anaesthesia

Localised tenderness long distribution of deep venous system

Entire leg swollen

Calf swelling at least 3x larger than asymptomatic leg

Collateral superficial veins (non-varicose)

Previously documented DVT

An alternative diagnosis is at least as likely as DVT (-2)

485
Q

What can cause vasovagal syncope?

A

Emotional: feat, pain, phobia, sudden unexpected sight sound or smell

Orthostatic: prolonged standing, hot places

486
Q

What might people described in a history of vasovagal syncope?

A

Brief LOC

Warning: light-headedness, nausea, sweating, weakness, visual disturbance

No chest pain or SOB, not during exercise

Almost immediate restoration of appropriate behaviour and orientation (pt. might be v. tired)

Might be Hx of new medications

Syncope may be more likely in morning

487
Q

Differential diagnosis?

A
Other causes of syncope
Epilepsy
Narcolepsy
Drop attacks
TIA
488
Q

How would you investigate a patient with ?vasovagal syncope?

A

Many investigations to rule-out serious causes of harm.

BP measurement (lying and standing)

Bloods: FBC, blood glucose

ECG

489
Q

What would you want to know about a patient to determine risk of severe cardiac problems in syncope?

A
coronary heart disease
ECG changes (broad QRS, prolonged QT interval, non-sustained VT)
Syncope during exercise or supine
palpitations
FHx of sudden cardiac death
HR<50
490
Q

How would you manage a patient with Vasovagal syncope?

A

Reassure and educate:

Avoid prolonged standing in warm environments
Avoid hot baths

At first sign of collapse: Lie down, legs in air
Sit agains wall, head between knees
squat down on heels
get up very carefully, return to position if feeling unwell again

491
Q

How would you manage someone with high-risk NSTEMI or STEMI?

A

A-E assessment and management

MONAT

Morphine 
Oxygen  (if sats <94% or 90% (COPD))
Nitrates (usually IV in NSTEMI/unstable angina)
Aspirin (300 mg)
Ticagrelor 

After acute event, when stable:
beta-blocker
ACEi
Statins

492
Q

How would you manage a patient with unstable angina?

A

A-E assessment and management

MONA

Morphine
Oxygen (if sats <94% or 90% (COPD))
Nitrates
Aspirin

493
Q

What should your first actions be in cardiac arrest?

A

Call for help (ask them to call 2222)

Begin CPR

Administer oxygen if available

Attach defib, establish rhythm

494
Q

Which rhythms are shockable in cardiac arrest?

A

VF

VT

495
Q

If after sticking on Defib, you are told your rhythm is shockable, what should you do?

A

administer defibrillation

Immediately resume CPR for 2 mins

Establish vascular access

Recheck shockable rhythm after 2 mins. Shockable: shock.
Give 1mg IV adrenaline every 3-5 mins
Consider ET tube

Continue CPR for 2 mins

Check shockable rhythm: shock
CPR 2 mins
Amiodarone 300mg (after 3rd shock)
Establish and treat reversible cause

496
Q

Which rhythms aren’t shockable?

A

PEA

Asystole

497
Q

Once you’ve found out a rhythm isn’t shockable in cardiac arrest, what would you do?

A

Resume CPR for 2 mins
Establish IV access
Give IV adrenaline 1mg every 3-5 mins
Consider ET tube

Check whether rhythm shockable: no = return to CPR for 2 mins
establish and treat reversible causes

Continue to give IV adrenaline 1mg every 3-5 mins
Repeat process until shockable rhythm, ROSC or calling

498
Q

What should you do if your rhythm suddenly becomes shockable/un-shockable in cardiac arrest?

A

Switch to other half of algorithm

499
Q

What are the key drugs and doses to remember in cardiac arrest?

A

Adrenaline 1 mg every 3-5 mins
(give immediately in non-shockable, give after 2 shocks in shockable)

Amiodarone 300 mg first dose
2nd dose 150 mg
Give after third shock

500
Q

What are the reversible causes of cardiac arrest?

A

5 H’s and T’s

H
Hypoxia
Hypovolaemia
Hydrogen ions (acidosis)
Hypo/hyperkalaemia
Hypothermia
T
Tamponade
Tension pneumothorax
Toxins
Thrombosis (cardiac or pulmonary)
Trauma
501
Q

How would you manage a patient with HR>=150 (with pulse) with adverse features? (shock, syncope, MI or heart failure)

A

Cardioversion - synchronised DC shock. Up to 3 attempts.

After this, seek expert help.

Give amiodarone 300 mg IV over 10-20 mins
Repeat shock
Give amiodarone 900mg IV over 24 hours

502
Q

How would you manage a patient with a regular broad QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure)

A

VT (or uncertain rhythm):
amiodarone 300mg IV over 20-60 mins
THEN
900mg over 24 hours

(If SVT+BBB, treat like narrow-complex tachy)

503
Q

How would you manage a patient with a irregular broad QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure)

A

CALL FOR HELP

504
Q

How would you manage a patient with a regular narrow QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure). What are the likely causes of this rhythm?

A
Vagal manoeuvre: head down or blow in to syringe
Adenosine 6mg rapid IV bolus
no effect: 12 mg
No effect: 12 mg
(monitor with ECG continuously)

Sinus rhythm achieved -
record ECG of sinus rhythm
consider anti-arrhythmic prophylaxis
Probably re-entry paroxysmal SVT

If sinus rhythm NOT achieved - seek expert help
Consider rate control (beta-blocker)
?consider cardioversion
Probable atrial flutter

505
Q

How would you manage a patient with a irregular narrow QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure). Which rhythm is likely to cause this?

A

AF

Control rate with beta blocker or diltiazem

In heart failure: digoxin or amiodarone

Assess VTE risk, consider anticoagulation

506
Q

What are the different types of SVT?

A
Regular: 
sinus tachy
atrial flutter
Sinus node re-entrant tachy
Atrioventricular re-entry tachycardia (AVRT eg. WPW syndrome)
AV nodal re-entry tachycardia (AVNRT)
Automatic junctional tachycardia

Irregular:
AF
atrial flutter with variable block

507
Q

How would you initially treat someone with bradycardia with adverse features? (shock, syncope, myocardial ischaemia, heart failure)

A
A-E assessment
Oxygen
IV access
ECG
BP
SpO2 
Identify and treat reversible causes.

Atropine 500 mcg IV

508
Q

How would you initially treat someone with bradycardia with NO adverse features? (shock, syncope, myocardial ischaemia, heart failure)

A
A-E assessment
Oxygen
IV access
ECG
BP
SpO2 
Identify and treat reversible causes.
Work out risk of asystole:
recent asystole
mobitxz II AV block
Complete heart block with broad QRS
Ventricular pause >3s

No risk: observe

Risk: Atropine 500 mcg IV repeat to max of 3mg 
OR
Isoprenaline 5mcg/min IV
Adrenaline 2-10mcg/min IV
alternative drugs
OR
transcutaneous pacing

Seek expert help

509
Q

What would you do if initial management of someone with symptomatic bradycardia (atropine 500mcg IV), didn’t work?

A
Atropine 500 mcg IV repeat to max of 3mg 
OR
Isoprenaline 5mcg/min IV
Adrenaline 2-10mcg/min IV
alternative drugs
OR
transcutaneous pacing

Seek expert help

510
Q

How might shoulder dislocation present?

A

Hx of trauma
Pain

Anterior: Externally rotated arm
loss of shoulder roundness
anterior bulge
humeral head palpable anteriorly
abduction and internal rotation are resisted
may have loss of sensation in regimental badge area

Posterior: arm adducted and internally rotated
Posterior bulge
humour head palpable below acromion process
abduction and external rotation are painful
inability to externally rotate to neutral position and supinate

511
Q

What things should you check on examination of someone with ?anterior shoulder dislocation?

A

radial pulse (assess vascular injury)

regimental badge area (axillary nerve damage)

thumb, wrist and elbow weakness on extensions and sensation on dorm of hand (radial nerve function)

rotator cuff (once joint is reduced)

512
Q

How would you investigate shoulder dislocation?

A

x ray (AP and axillary or transcapular view)

513
Q

How would you manage someone with shoulder dislocation?

A

Analgesia and sedation:
opiate and benzo

reduction

fracture dislocation: surgery

514
Q

List some causes of AF

A
Cardiac: 
HF
MI
hypertension
mitral  valve disease
congenital 

Pulmonary:
PE
pneumonia
bronchocarcinoma

Other:
hyperthyroidism
alcohol
post-op
sepsis
caffeine
anti-arrhythmias
hypoK
hyperMg

LONE

515
Q

How might AF present?

A
palpitations
chest pain
SOB
dizziness
syncope

Irregularly irregular pulse
apical pulse rate > radial pulse rate
signs of LV dysfunction

516
Q

What might you find on an ECG of someone with AF?

A
no P waves
irregular QRS - regular shape
HT 75-190 bpm
normal T waves
V1 looks like atrial flutter
517
Q

What investigations should you do for someone with AF?

A

ECG

Bloods: FBC (rule out anaemia as cause of palpitations)
U+Es
TFTs
Cardiac enzyme

Echo

518
Q

How might you manage someone with an acute presentation of AF?

A

<48 hours after onset of symptoms

A-E
treat underlying cause
Control rate
Initiate anticoagulation (heparin)

Consider DC or chemical cardioversion

Acutely unwell: cardioversion in ITU with sedation

519
Q

what drug is given for chemical cardioversion in AF?

A

Amiodarone IV 5mg/Kg in 1 hr, then 900mg-1.2g in a 24 hour period

Amiodarone PO 200mg/8hr for 1 week then 200mg/12hr for one week then 200mg/day maintenance

Can also use flecainide

520
Q

What can cause atrial flutter?

A
atrial dilation 
open heart surgery
HTN
obesity 
alcohol abuse
COPD
cardiomyopathy 
atrial myxoma
pericarditis
thyrotoxicosis
electrolyte imbalance
sleep apnoea
521
Q

How might atrial flutter present?

A
palpitations
fatigue
dyspnoea
chest pain
dizziness 
syncope 
heart failure
TIA/stroke
Pulse may be regular or irregular or regular pulse tachycardia
signs of underlying cause 
HF
hypotension
522
Q

How would you investigate someone for ?atrial flutter?

A
Bloods: FBC
U+E
TFTs
ESR
LFTs 
coagulation screen

ECG: saw-tooth flutter waves II, III and aVF

Echo

523
Q

How would you manage a patient with atrial flutter?

A

rate control - medications or cardioversion

treat underlying conditions

anticoagulation (like in AF)

524
Q

What is cerebral venous sinus thrombosis?

A

acute thrombosis in dural venous sinuses (which drain blood from brain)

525
Q

List some symptoms of cerebral venous sinus thrombosis

A

Headache (sudden to gradual onset)
ophthalmoplegia (papilloedema) and/or diplopia (usually unilateral to start with)
seizures (can be unilateral)
stroke-like symptoms: hemiparesis, lower limb weakness, aphasia and ataxia
Facial pain
pulsatile proptosis
hornet’s syndrome

Raised ICP: reduced consciousness, HTN, reduced HR

526
Q

List some causes of venous sinus thrombosis

A
thrombophilia
nephrotic syndrome
chronic inflammatory diseases
pregnancy and puerperium 
oestrogen-containing contraception
meningitis and ENT infections
527
Q

How would you investigate someone with ?cerebral venous sinus thrombosis?

A

Bloods: FBC (Hb may be elevated, WCC and platelets may be elevated)
U+E
LFTs
D-dimer

Urine dip

CT venogram (normal CT often appears normal)

ECG

528
Q

How would you manage a patient with venous sinus thrombosis?

A

Elevate hear 30-40 degrees to help reduce intracranial pressure

anti-convulsants if seizures present

LMWH initially IV or SC
warfarin once patient stable

Severe: thrombectomy, endovascular therapy

529
Q

What are signs of raised ICP?

A

headache: nocturnal, starting on waking, worse on coughing or moving head, altered mental state

Changes to mental state: lethargy, irritability, slow decision making, abnormal social behaviour

Vomiting

Pupillary changes
Fundoycopic changes eg. blurred disc margins, haemorrhages

unilateral ptosis

hemiparesis

raised BP, widened pulse pressure

bradycardia

530
Q

How can raised ICP present acutely?

A
Head injury
syncope
headache
meningism
focal neuro deficit
seizures

talk and deteriorate - talk and then go in to coma

531
Q

How would you investigate a patient with suspected raised ICP?

A

GCS

CT scan

532
Q

How would you manage a patient with raised ICP?

A
avoid pyrexia (hypothermia)
manage seizures
CSF drainage (intraventricular catheter)
elevation of head
analgesia and sedation 
neuromuscular blockade (reduce muscle activity, which can cause raised ICP)

Mannitol: intravascular osmotic agent

Hypertonic saline (3-30%)

Hyperventilation

decompressive craniotomy

533
Q

How might a space-occupying lesion in the cerebellum present?

A
cerebellar ataxia
intention tremor
past-pointing
dysdiadochokinesis
nystagmus
staccato speech
534
Q

How might a space-occupying lesion in the temporal lobe present?

A
depersonalisation
epilepsy
deja vu
dysphasia 
visual field defects
forgetfulness 
fugue
535
Q

How might a space-occupying lesion in the frontal lobe present?

A

anosmia
change in personality
dysphasia
hemiparesis or fits on contralateral side

536
Q

How might a space-occupying lesion in the parietal lobe present?

A
hemisensory loss
two-point discrimination 
stereognosis
extinction
neglect
dysphasia
537
Q

How might a space-occupying lesion in the occipital lobe present?

A

visual defeat - specific one depends on whereabouts lesion is

538
Q

How might a pituitary tumour present?

A

homonymous hemianopia

endocrine changes

539
Q

How would you investigate someone for a space-occupying lesion?

A
Bloods: 
FBC
U&amp;E
LFTs
CT head
Biopsy of lesion

If unsure of primary tumour: CXR
mammography/ultrasound

540
Q

Causes of space-occupying lesions:

A
malignancy
haematoma
hydrocephalus
cerebral abscesses (RF: COPD)
Cysts
541
Q

How would manage a space-occupying lesion?

A

treat underlying cause
manage raised ICP
treat complications and symptoms of raised ICP

542
Q

What is AKI?

A

Rise in serum creatinine >26 within 48 hours
OR
rise in serum creatinine 1.5 x baseline value within 1 week
OR
urine output <0.5ml/Kg/hr for 6 consecutive hours

543
Q

What are the criteria for stage 1 AKI?

A

Rise in serum creatinine greater than 26 µmol/L within 48 hours
or
Rise in serum creatinine greater than 1.5-1.9 × baseline value
or
Urine output less than 0.5 ml/kg/hr for 6 hours

544
Q

What are the criteria for stage 2 AKI?

A

Rise in serum creatinine greater than 2-2.9 × baseline value
or
Urine output less than 0.5 ml/kg/hr for 12 hours

545
Q

What are the criteria for stage 3 AKI?

A

Rise in serum creatinine greater than 3 × baseline value
or
Rise of serum creatinine greater than 354 µmol/L
or
Commenced on renal replacement therapy
or
Urine output less than 0.3 ml/kg/hr for 24 hours or anuric for 12 hours

546
Q

What are some risk factors for AKI?

A

Age greater than 75 years
Chronic kidney disease (estimated glomerular filtration rate < 30)
Hypertension (one or more anti-hypertensive drugs)
Cardiac failure
Liver disease
Diabetes Mellitus
Nephrotoxins (e.g. NSAIDs, gentamicin, iodinated contrast)
Hypovolaemia
Sepsis

547
Q

List some pre-renal causes of AKI:

A

Hypovolaemia (vomiting, diarrhoea, burns, haemorrhage)
Hypotension
Sepsis
Cardiac failure

548
Q

List some intrinsic caused of AKI:

A
Prolonged hypo-perfusion
Nephrotoxins
Glomerulonephritis
Vasculitis
Interstitial nephritis
549
Q

List some post-renal causes of AKI:

A

Obstruction (renal stones, retro-peritoneal fibrosis, bladder cancer, pelvic mass, enlarged prostate)

550
Q

How might AKI present?

A

Reduce urine output

Other signs of hypovolaemia: Hypovolaemia - assess volume status (capillary refill time, pulse, blood pressure, jugular venous pressure, skin turgor, pulmonary oedema, peripheral oedema, urine output, weight)

Palpable bladder?

Signs of vasculitis (weight loss, fever, rash, uveitis, haemoptysis, joint swelling)

Bruits (renal artery stenosis)

551
Q

How would you investigate someone you suspect has AKI?

A
FBC
U&amp;Es
Bicarbonate
LFTs
Calcium
Phosphate
Consider blood cultures if sepsis suspected

Urine dipstick (presence of blood and protein suggests infection or vasculitis)

Chest X-Ray (pulmonary infiltrates could indicate fluid, infection or haemorrhage)

Renal tract ultrasound (assess renal anatomy and exclude renal tract obstruction)

552
Q

How would you manage someone with AKI?

A

STOP V:

Sepsis - complete BUFALO if suspected

Toxins - stop/avoid nephrotoxins eg. gentamicin, NSAIDS, iodinated contrast

Optimise blood pressure

Prevent harm - treat complications eg. hyperkalaemia, pulmonary oedema, acidosis, pericarditis
identify cause and treat
review all medications and doses
refer if renal replacement therapy necessary
monitor: daily volume assessment, fluid balance, U+Es and bicarbonate

553
Q

What are common indications for renal replacement therapy?

A
intractable hyperkalaemis
pH <7.15
intractable pulmonary oedema
uraemia pericarditis
encephalopathy
554
Q

What is acute urinary retention? How might it present

A

inability to urinate in presence of painful bladder
Bladder might be distended, dull to percussion
well above symphysis pubis, almost at level of umbilicus
infected or malformed genitals
faecal impaction
reduced lower limb power and perineal sensation (cord compression or prolapsed disc)

555
Q

What are common causes of acute urinary retention?

A

children: abdo pain, drugs

young people/adults: drugs, surgery, UTI, trauma, haematuria, constipation, kidney injury

elderly: surgery, tumour, BPH, kidney injury

556
Q

How would you investigate someone for acute urinary retention?

A

Bloods: FBC
U+Es
creatinine

Urine: MSU

Bladder scan (quantify urine retained)

cystography

urodynamics

557
Q

How would you manage someone in acute urinary retention?

A

catheterisation

treat underlying cause