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Year 4 revision > ACC revision > Flashcards

ACC revision Flashcards

1
Q

how to treat an airway obstruction (in RRAPID)

A

give 15L oxygen NRBM

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2
Q

what does stridor at rest infer

A

reduction of airway diameter of >50%

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3
Q

how is hypotension defined in the ED

A

SBP <90mmHg, MAP <60mmHg OR decrease in greater than 40mmHg of 30% from patient’s baseline MAP or combination

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4
Q

4 ways hypoxia is classified

A
  • hypoxic hypoxia (reduced O2 supply)
  • anaemic hypoxia (reduced Hb function = less O2 delivered)
  • stagnant hypoxia (blood and O2 can’t get to tissues)
  • histotoxic hypoxia (alcohol, drugs, poisons)
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5
Q

how is hypovolaemic shock treated

A

fluids +/- blood (usually over a litre of warmed crystalloids then switch to blood products)

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6
Q

what is cariogenic shock

A

tissue hypo perfusion due to damage/insufficiency of the heart

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7
Q

most common cause of cardiogenic shock

A

MI

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8
Q

confusion assessment method (CAM) of diagnosing delirium

A
  1. onset and fluctuating course - change from baseline
  2. inattention - easily distracted
  3. disorganised thinking - rambling/irrelevant conversations/illogical flow of ideas
  4. altered level of consciousness
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9
Q

antidote for benzodiazepine toxicity

A

flumanezil

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10
Q

antidote for hyperkalaemia

A

dextrose + insulin

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11
Q

antidote for LA toxicity

A

20% lipid emulsion

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12
Q

antidote for bradycardias

A

atropine

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13
Q

2 shockable rhythms

A 
V fib 
pulseless VT (no cardiac output)
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14
Q

what does pulseless electrical activity look like

A

fairly normal ECG but there is NO pulse

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15
Q

which medications to ask specifically about in a pre-op assessment

A

anticoagulants
antiplatelets
insulin
anticonvulsants

drug allergies and OTC

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16
Q

questions to ask in a pre-op assessment if someone has rheumatoid arthritis

A

Joints:

  • TMJ: problems with jaw
  • crico-arythenoid joints: glottic arthritis (problems with throat?)

CVS:
- asymptomatic pericardial effusion

RS:
- pulmonary nodules/fibrosis

anaemia, renal impairment, peripheral neuropathy

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17
Q

tests to do for diabetics pre-op

A

BM, urine glucose and ketones
ECG
electrolytes
first on the list

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18
Q

characteristics of pre-oxygenation for RSI

A
  • 3 minutes pre-oxygenation
  • 5 full vital capacity breaths over 30 seconds
  • EtO2 concentration >90

this is to replace forced respiratory capacity with oxygen

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19
Q

causes of bradycardia

A
  • normal (athletes)
  • MI, myotonic dystrophy, sick sinus syndrome
  • endocarditis
  • hypothyroid, hypo/hyperkalaemia
  • Cushing’s response (to trauma)
  • drugs
  • anorexia nervosa
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20
Q

location of MI most likely to cause bradycardia

A

inferior MI

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21
Q

drugs which can cause bradycardia

A
  • beta blockers
  • CCBs
  • digoxin
  • clonidine
  • opiates
  • amiodarone
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22
Q

what is Cushing’s reflex

A

physiological response to increased ICP:

  • bradycardia
  • widened pulse pressure (increased SBP, decreased DBP)
  • irregular respirations
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23
Q

4 main signs of reduced end-organ perfusion/ haemodynamic instability (from bradycardia?)

A
  • shock
  • syncope
  • MI
  • heart failure
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24
Q

treatment of bradycardia if there are adverse features of HD instability

A

atropine 500mcg - if doesn’t work:

  • atropine 500mcg IV repeat up to 3mg OR
  • isoprenaline 5mcg/min IV
  • adrenaline 2-10mcg/min IV etc.
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25
Q

when might glucagon be used for bradycardia

A

if it is due to beta blockers or CCBs

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26
Q

how does atropine work

A

blocks effects of vagus nerve = increases HR (prevents parasympathetic input)

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27
Q

drugs used during RSI

A
  • Thiopentone: 4-5mg/kg with onset of 15-30 seconds, lasting 4-8 minutes
  • Propofol: 1.5-2.5mg/kg, onset in 30 seconds, duration 2-6 minutes
  • Rocuronium: 1mg/kg, DOA: 6 minutes OR Suzemethonium: 1-1.5mg/kg, DOA 6 minutes
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28
Q

3 steps in the technique for RSI

A
  1. Cricoid pressure: 10-30N
  2. Apnoeic ventilation
  3. Confirm tube positioning- Co2
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29
Q

safe dose of lignocaine with vs without adrenaline

A 
without = 3mg/kg
with = 7mg/kg
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30
Q

characteristics for pre-oxygenation for RSI

A
  • 3 minutes pre-oxygenation
  • 5 full viral capacity breaths over 30 seconds
  • EtO2 concentration >90

this is to replace forced expiratory capacity with oxygen

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31
Q

normal AV node delay

A

120m/s

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32
Q

why does Cushing’s reflex cause bradycardia

A

inappropriate stimulation of baroreceptors during cerebral artery dilation

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33
Q

specific treatment of bradycardia if there are adverse features of HD instability (shock, MI, syncope, HF)

A

atropine 500mcg

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34
Q

what is 1st degree heart block

A

consistent prolonged PR interval (>120m/s)

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35
Q

3 causes of 1st degree heart block

A
  • normal physiology (athletes)
  • inferior MI
  • electrolyte disturbances
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36
Q

when does 1st degree heart block become a problem and how is it managed

A

haemodynamically unstable - give atropine 500mcg IV or TC pacing

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37
Q

causes of 2nd degree heart block Mobitz type 1 (Wenckeback) - increasingly prolonged PR interval followed by dropped QRS

A
  • drugs: CCBs, BBs, amiodarone, digoxin
  • inferior MI
  • electrolyte disturbances
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38
Q

main pathological cause of 2nd degree heart block type 2

A

Purkinje fibre dysfunction - often due to anterior/septal MI, fibrosis (surgery), SLE, systemic sclerosis

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39
Q

how is mobitz type 2 treated

A

permanent pacemaker - much more likely to be clinically problematic (haemodynamically unstable)

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40
Q

how to treat complete heart block

A
  • TC pacing followed by pacemaker

- atropine if broad QRS

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41
Q

what is a broad complex tachycardia vs narrow complex

A

tachycardia >100bpm with broad QRS >120m/s (2 small squares)

narrow complex = <120m/s

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42
Q

treatment for broad complex tachycardia if there are adverse features of shock (including VT)

A

synchronised DC shock

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43
Q

treatment for broad complex tachycardia if there are NO adverse features of shock (including VT)

A

amiodarone 300mcg IV over 1 hour (900mg IV over 24 hours)

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44
Q

treatment for narrow complex tachycardia if there are adverse features of shock

A

synchronised DC shock

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45
Q

treatment for narrow complex tachycardia if there are NO adverse features of shock

A
  1. vasovagal manoeuvres
  2. IV adenosine (6mg IV bolus) - further 2 x 12mg if no effect
  3. if still no effect - consider high dose BBs (verapamil) and call for cardiologist
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46
Q

most common cause of VT (type of broad complex tachycardia)

A

ischaemic heart disease

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47
Q

what drugs can lead to VT

A
  • macrolides
  • fluoroquinolones
  • digoxin
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48
Q

what must first be done if VT is recognised

A

check pulse - can be an arrest rhythm so must check

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49
Q

main causes of V fib

A
  • CAD
  • Previous MI: scar tissue
  • Myocarditis
  • Cardiomyopathy
  • Congenital heart disease
  • WPW
  • Long QTc syndrome
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50
Q

management of V fib

A
  • ABCDE
  • synchronised DC shock
  • 1mg IV adrenaline + amiodarone 300mg IV then 900mg over 24 hours
  • more amiodarone
  • lignocaine 1mg/kg
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51
Q

what is the seldinger technique

A

general way lines are inserted into arteries or veins - needle goes in, then guide wire through needle

then catheter is fed around the guide wire

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52
Q

arterial line waveforms - what does the maximum height show and the minimum height show

A 
maximum = SBP
minimum = DBP
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53
Q

what does the upstroke of the curve in arterial line waveforms show

A

cardiac contractility

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54
Q

what does the area under the curve in arterial line waveforms show

A

cardiac output

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55
Q

typical abnormal findings of arterial line waveform in cariogenic failure

A
  • reduced gradient of upstroke
  • reduced peak height
  • altered position of dichrotic notch
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56
Q

most common site of central venous line

A

internal jugular vein

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57
Q

what is the Trendelenburg position

A

entire bed is tilted with head of bed LOWER than foot of bed

facilitates venous return - used when inserting central venous lines

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58
Q

how long is the central venous line

A

16cm long - MUST be inserted under US guidance

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59
Q

how is the positioning of a central venous line confirmed before use

A

must have CXR to confirm positioning and to check for any pneumothorax

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60
Q

normal central venous pressure

A

5-10mmHg

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61
Q

indications of central venous lines

A
  • TPN
  • monitoring of central venous pressure
  • resuscitation with blood/fluids
  • delivery of irritant drugs: vasopressors, amiodarone
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62
Q

complications of central venous catheter insertion

A
  • failure
  • accidental injury/cannulation of artery
  • arrhythmias - guidewire irritation of heart
  • pneumothorax
  • air embolism
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63
Q

what does aldosterone do

A

Na+ and Cl- reabsorption = water follows to be reabsorbed (osmosis)

also excretion of K+ into urine

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64
Q

describe RAAS system

A
  1. drop in BP = detected by juxtaglomerular apparatus = renin secretion
  2. renin converted to angiotensin I by angiotensinogen from liver
  3. angiotensin I converted to angiotensin II by ACE in the lungs
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65
Q

effects of angiotensin II on BP

A
  • increased sympathetic activity
  • adrenal gland secretion of aldosterone = Cl- and Na+ and water reabsorption
  • arteriole vasoconstriction
  • pituitary release of ADH = H20 reabsorption
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66
Q

AEIOU indications for renal replacement therapy

A 
A = acidosis 
E = electrolyte disturbances - resistant hyperkalaemia
I = ingestion of toxins (alcohol, lithium, theophylline, barbiturates, valproate)
O = overload of fluid 
U = uraemia symptoms (encephalopathy, pericarditis)
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67
Q

anticoagulant complications of RRT

A
  • hypocalcaemia
  • bleeding
  • thrombocytopenia
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68
Q

circuit related complications of RRT

A

-Air embolism
-Clotting of circuit
-DIC
-Anaemia
-Thrombocytopaenia
-Hypothermia
-Hypotension
-Electrolyte disturbance
Dialysis Disequilibrium Syndrome (DDS)

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69
Q

3 things you should ask before carrying out an ABG

A
  • do you take any anticoagulants
  • do you experience Raynaud’s
  • have you ever had any LN or axillary clearance in this arm
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70
Q

what do base excess values mean

A

below -2 = metabolic acidosis

above +2 = metabolic alkalosis

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71
Q

2 things which can cause respiratory alkalosis

A
  • hyperventilation

- T1RF

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72
Q

what effect can acidosis have on the heart

A

negative chronotrophic effect = BRADYCARDIA

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73
Q

what anaesthetic should be used in non-emergency blood gases

A

lidocaine 0.5-1ml SC 1% via orange 25G needle

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74
Q

what is diaphragmatic/ respiratory splinting

A

when a patient breathes in v shallowly in an attempt to avoid inspiratory pain

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75
Q

What percentage of oxygen is delivered at:

a) . 1 Litre
b) . 2 Litre
c) . 3 Litre
d) . 4 litre
e) . 5 litres

A

a) . 1 litre = 24%
b) . 2 litres = 28%
c) . 3 Litres = 32%
d) . 4 Litres = 36%
e) . 5 litres = 40%

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76
Q

What percentage of oxygen is delivered at:

a) . 6L
b) . 7L
c) . 8L
d) . 9L
e) . 10L

A

a) . 6L = 44%
b) . 7L = 48%
c) . 8L= 52%
d) . 9L= 56%
e) . 10L = 60%

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77
Q

what must be done before a NRBM is used

A

finger over the valve in the mask to allow it to inflate the bag

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78
Q

which concentrations of O2 are often given to patients with chronic lung disease

A

24-28%

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79
Q

What percentage/litre of O2 does each venturi valve deliver?

a) . Blue
b) . White
c) . Yellow
d) . Red
e) . Green

A

a) . Blue = 2/L- 24%
b) . White = 4/L - 28%
c) . Yellow = 8/L - 35%
d) . Red = 10/L - 40%
e) . Green = 15/L - 60%

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80
Q

how many litres of O2 does a bag-valve mask deliver

A

15L flow rate (+ positive pressure)

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81
Q

how many litres of O2 can a CPAP machine or ventilator deliver

A

1-15L O2

ventilator = 1-15L via invasive positive pressure

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82
Q

most important cause of pulmonary oedema

A

cardiac

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83
Q

scale used to assess severity of COPD

A

MRC dyspnoea scale

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84
Q

what is the MRC dyspnoea scale

A 
1 = breathless with strenuous exercise
2 = SOB when hurrying on a level or walking up slight hill
3 = walks slower than people of same age due to SOB
4 = stops for breath after walking 100 years (90m)
5 = too breathless to leave the house or breathless when dressing/undressing
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85
Q

what should be done for COPD exacerbation if there is no change with bronchodilator + O2

A

NIV

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86
Q

4 contraindications for NIV

A
  • untrained pneumothorax
  • facial burns
  • fixed upper airway obstruction
  • at least 2 weeks after oesophagectomy
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87
Q

1st line tool for recognising delirium

A

SQiD - single question to identify delirium

‘is this person more confused than normal’

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88
Q

what is used after SQiD if the answer is yes (for delirium)

A

AMT4 (abbreviated mental test 4):

  • age
  • DOB
  • location
  • year
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89
Q

what medications can cause delirium

A
  • STEROIDS
  • Benzodiazepines (sedatives)
  • Analgesia- opiates can cause constipation
  • Cimetidine (H2 antagonist)
  • Anticholinergics
  • Digoxin
  • Muscle relaxants
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90
Q

when would epithelial cells be found in a urine sample

A

when it has touched the skin - invalidated

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91
Q

normal levels of WBCs in MSU

A

normal = <40

elevated = pyuria/infection or inflammation??

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92
Q

what can RBCs in the urine indicate

A

infection
trauma
malignancy
renal stones

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93
Q

3 cancers associated with cannonball lung mets

A

prostate
renal cell
sarcoma

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94
Q

how many seconds is one small square on ECG

A

0.04 seconds (one large square = 0.2 seconds because is 5 small squares)

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95
Q

how long is normal PR interval

A

3-5 small squares (0.12-0.2 seconds)

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96
Q

how long is a normal QRS

A

<0.12 seconds (<3 small squares)

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97
Q

where do the limb leads on ECG go

A

RIDE
YOUR
GREEN
BICYCLE

R: R- upper left arm
Y: Left- upper left arm
Green: Left lower limb
B: Right lower limb

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98
Q

3 most common causes of right axis deviation

A

increased RV workload:

  • right ventricular hypertrophy
  • PE
  • COPD
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99
Q

most common causes of left axis deviation

A

conduction defects

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100
Q

in which leads do you look for RBBB and LBBB

A 
RBBB = leads V1 and V2
LBBB = leads V1 and V6
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101
Q

how can DKA lead to hyperkalaemia

A

hyperglycaemia = hypertonia = shift of K+ out of cells into blood

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102
Q

top 3 causes of DKA

A
  • INFECTION
  • poor diabetic control and use of insulin
  • unknown diagnosis - 1st presentation of T1DM
103
Q

2 other conditions which can cause DKA

A

stroke

steroids

104
Q

type of shock in DKA

A

hypovolaemia - severe dehydration

severe dehydration = hyponatraemia

105
Q

rate of insulin needed for DKA

A

FIXED rate IV insulin 0.1 units/kg/hour

106
Q

what should be done for DKA if blood glucose falls below 15

A

infusion of 10% dextrose along with insulin

107
Q

what dose of fluids to use in DKA

A
  • 500ml bolus over 10-15 mins if not hypotensive

- 1L over 1 hour if hypotensive

108
Q

when would K+ be infused with saline in DKA

A

when it falls below 5.5

this happens because glucose uptake into cells is co-transported with potassium = hypokalaemia

109
Q

4 main metabolic treatment targets in DKA

A
  1. Reduction of blood ketones by 0.5mmol/L/hour
  2. Increase of venous bicarb by 3.0mmol/L/hour
  3. Reduction of cap glucose by 3.0ml/hour
  4. Maintain K+ between 4-5.5mmol/L
110
Q

risk of fluid resuscitation in children and young adults with DKA

A

cerebral oedema

111
Q

how can AKI present

A
  • Can be ASYMPTOMATIC
  • N&V, diarrhoea
  • Dehydration: reduced skin turgour, dry mucous membranes
  • Fatigue
  • Oliguria/anuria
  • Can have signs of uraemia later on: anorexia & nausea, encephalopathy, asterixis, pericarditis, platelet dysfunction
112
Q

DIAMOND HAL - nephrotoxic drugs

A 
diuretics
iodine contrast/IV contrast
ACEi/ARB
metformin
opioids
NSAIDs
digoxin

heparin
aminoglycosides (gentamicin)
lithium

113
Q

STOP treatment for AKI

A
  1. SEPSIS: complete sepsis 6 if suspected (BUFALO)
  2. Toxins: avoid or stop any nephrotoxins the patient is on
  3. Optimise BP: give crystalloid fluids if the patient is hypotensive
  4. Volume assessment:
  5. Prevent harm: treat complications such as hyperkalaemia, identify cause, review medications, fluid balance

Also review medication doses in medications excreted by kidneys

114
Q

when would RRT be considered in AKI

A
  • Intractable hyperkalaemia
  • pH <7.1
  • Intractable pulmonary oedema
  • Uraemic pericarditis
  • Encephalopathy
115
Q

complications of AKI

A
  • Hyperkalaemia
  • Electrolyte imabalances: Hyperphosphataemia, hyponatraemia, hypermagnesia
  • Metabolic acidosis
  • Volume overlode: peripheral and pulmonary oedema
  • Uraemia
  • CKD
116
Q

how long does an induction agent take to start working

A

1-2 brain-arm circulations i.e. 10-20 seconds

117
Q

4 main induction agents

A

propofol (most common)
thiopentone (barbiturate)
ketamine
etomidate

118
Q

2 benefits of propofol

A
  • excellent airway suppression reflexes

- decreases incidence of PON+V

119
Q

3 unwanted effects of propofol

A
  • drop in HR and BP
  • pain on injection
  • involuntary movements
120
Q

dose of propofol

A

1.5-2.5 mg/kg

121
Q

3 benefits of thiopentone

A
  • faster than propofol
  • used mainly for RSI
  • antiepileptic properties - protects brain
122
Q

3 unwanted effects of thiopentone

A
  • Drops HR BUT rise in BP
  • Rash/bronchospasm
  • Vasospasm can cause thrombosis and gangrene distally if injected intra-arterial
123
Q

what is contraindicated in thiopentone

A

porphyria

124
Q

dose of thiopentone

A

4-5mg/kg

125
Q

3 features of ketamine

A
  • slow onset 90 seconds
  • bronchodilation
  • rise in HR and BP = good for when circulation is compromised
126
Q

dose of ketamine

A

1-1.5mg/kg

127
Q

3 benefits of etomidate

A
  • rapid onset
  • haemodynamic stability
  • lowest incidence of hypersensitivity

useful for patients with limited cardiac reserve (elderly, heart failure etc)

128
Q

4 unwanted effects of etomidate

A
  • Pain on injection
  • Spontaneous movements
  • Adreno-corticol suppression for 72 hours
  • High incidence of PONV
129
Q

why can etomidate lead to high mortality

A

Critically ill patients such as in septic shock need adrenocorticoids to deal with the stress

130
Q

best induction agent for patient needing burns dressing on ward

A

ketamine

131
Q

best induction agent for a patient having an LMA

A

propofol (good airway suppression for LMA)

132
Q

2 main options for maintenance anaesthesia

A
  • propofol infusion

- inhalation agents (started AFTER induction)

133
Q

4 main maintenance inhalation anaesthetics

A

isoflurane
desflurane
sevoflurane
enflurane

134
Q

definition of MAC

A

Concentration of vapour that prevent reaction to a standard surgical stimulus
- In 50% of subjects (50% pain free, 100% amnesia)

135
Q

what percentage of … is 1 MAC:

  • NO
  • sevoflurane
  • isoflurane
  • desflurane
  • enflurane
A
  • NO = 104%
  • sevoflurane = 2%
  • isoflurane = 1.15%
  • desflurane = 6%
  • enflurane = 1.6%
136
Q

best maintenance for a child with no IV access

A

sevoflurane - sweet smelling, inhalation induction

137
Q

best maintenance for a long 8 hour finger reimplantation

A

desflurane - low lipid solubility, rapid onset and offset, LONG OPERATIONS

138
Q

best maintenance for organ retrieval

A

isoflurane - least effect on organ blood so can be used for organ donation

139
Q

3 main short acting opiates in order of strength

for suppressing response to laryngoscopy and airway insertion

A

remifentanil - alfentanil - fentanyl

140
Q

2 main long acting opioids

for intra and post-op analgesia

A 
morphine 
oxycodone (can use in renal failure)
141
Q

when are analgesics administered in surgery

A

before amnesic - 1-5 minutes for onset and peak is slower than amnesic agents

142
Q

2 advantages of tramadol

A
  • can be used for both nociceptive and neuropathic pain

- can be used with morphine

143
Q

2 side effects of tramadol

A
  • N+V

- confusion

144
Q

2 IV NSAIDs

A
  • ketorolac

- parecoxib

145
Q

how do depolarising muscle relaxants work

A

act similarly to Ach - binds to nicotinic receptors on post-synaptic membrane

slowly broken down by acetylcholinesterase

146
Q

how do non-depolarising muscle relaxants work

A

block nicotinic receptors - so Ach can’t get to receptors

147
Q

main depolarising muscle relaxant

A

suxamethonium (used for RSI - 1-1.5mg/kg)

148
Q

5 side effects of suxamethonium

A
  • muscle pain
  • fasciculations
  • hyperkalaemia (muscle breakdown)
  • malignant hyperthermia
  • rise in ICP, IOP and gastric pressure
149
Q

short acting non-depolarising muscle relaxant

A

mivacurium

150
Q

3 intermediate acting non-depolarising muscle relaxants

A

vecuronium
rocuronium
atracurium

151
Q

long acting non-depolarising muscle relaxant

A

pancuronium

152
Q

2 muscle relaxant reversal agents

A

neostigmine

glycopyrrolate

153
Q

what can cause intraoperative hypertension and how is it treated

A

inadequate anaesthesia

increase anaesthesia +/- analgesic OR increase amnesia

154
Q

3 most common vasoactive drugs

A

ephedrine
phenylephrine
metaraminol

155
Q

3 main vasoactive drugs used in severe hypotension/ICU

A

adrenaline
noradrenaline
dobutamine

156
Q

best vasoactive drug for low BP and low HR

A

ephedrine

157
Q

best vasoactive drugs for low BP and high HR

A

metaraminol

phenylephrine

158
Q

5 main antiemetics used in PONV

A
  1. 5HT3 blockers: Ondansetron
  2. Anti-histamine: Cyclizine
  3. Steroids: Dexamethasone
  4. Phenothiazine: Prochlorperazine (Stemetil)
  5. Anti-dopamidergic: Metoclopramide
159
Q

usual order of use of antiemetics in PONV

A
  1. ondansetron
  2. dexamethasone
  3. cyclizine
  4. prochlorperazine
160
Q

features of neostigmine and why isn’t it used on its own

A
  • Anti-cholinesterase
  • Prevents breakdown of ACh
  • Muscarinic effects of ACh leads to PROFOUND BRADYCARDIA

SO much be combined with Glycopyrrolate

161
Q

3 downsides of neostigmine

A
  • N+V
  • inability to reverse profound block
  • slow onset to peak: 7-11 minutes
162
Q

another reversal agent is

A

sugammadex

163
Q

how does sugammadex work

A

It has a hydrophobic core (the donut hole part) and a hydrophilic exterior. The rocuronium (or other NMB) gets stuck in the hole and this keeps it away from the Ach receptor. It forms a 1:1 complex with the NMB and is eliminated in the kidneys in this form.

Water-soluble complex 1:1 with steroidal muscle relaxants

NO effect on nicotinic/muscarinic receptors

164
Q

which muscle relaxants is sugammadex compatible with

A

Rocuronium > Vecuronium >Pancuronium

165
Q

order of general anaesthesia with LMA

A
  1. Oxygenation
  2. Opioids: Fentanyl/Alfentanyl
  3. Induction agent: Propofol
  4. Inhalation agent: sevo/isoflurane
  5. Bag mask ventilation
  6. LMA insertion

if patient is then intubated, give muscle relaxant and then intubate

166
Q

how does paracetamol toxicity occur

A

In overdose the Glutathione is all used up due to high levels of NAPQI so NAPQI is not all safely mopped up by Glutathione causing liver toxicity - patients tend to be asymptomatic for 24 hours

167
Q

questions to ask when asking about paracetamol overdose

A
  • WHEN did they take the paracetamol?
  • Staggered or single overdose?
  • How much did they take?
  • Did they take any other drugs or alcohol?
  • Do they have any medical conditions- liver disease/poor nutrition
  • Are they taking any other medications?
168
Q

ATOM FC injuries which could compromise ventilation

A

Airway obstruction
Tension pneumothorax
Open chest wound
Massive haemothorax

Flail chest
Cardiac tamponade

169
Q

what does HEP B assess (in circulation)

A

Hands: temp, sweating, colour, CRT
End organ perfusion: consciousness urine output
Pulse: rate, quality, regularity

BP - hypotension is a late sign

170
Q

how is a secondary brain injury prevented

A
  • Opitimise oxygenation
  • Maintain cerebral perfusion with BP >90mmHg
  • Avoid hypoglycaemia
  • Avoid pyrexia
  • Definitive imaging and treatment
171
Q

what radiological investigation should be done within 30 mins of arrival at a MTC

A

full trauma CT

172
Q

what is positive predictive value

A

probability that a pt w/ a positive test truly has the disease.

The more specific a test, the higher its PPV
prevalence dependent: the higher the disease prevalence, the higher the PPV of the test for that disease

173
Q

what happens to the negative predictive value as the prevalence of the disease increases

A

NPV decreases

number of negative tests who do NOT have the condition

174
Q

5 causes of PE

A
  1. MAIN CAUSE: DVT which breaks off and travels to pulmonary vasculature
  2. Air emboli
  3. Fat emboli from large fractures (trauma)
  4. Talc due to IV drug use
  5. Amniotic fluid
175
Q

what is a provoked PE

A

PE which occurs within 3 months of a TRANSIENT risk factor:

  • Surgery
  • Trauma/major immobility/surgery
  • Pregnancy/puerperium
  • Hormonal contraception

NB: one without RFs or which are NOT transient e.g. thrombophilia = unprovoked PE

176
Q

what must be done before wither a CTPA or V/Q for PE

A

plain CXR to check for other pathology

177
Q

criteria for massive PE (= thrombolysis)

A
  • Hypotension 90/60 for >15 mins
    OR
  • Cardiac arrest
178
Q

criteria for sub-massive PE

A
  • Hypoxia/increased O2 demand
  • Cardiac echo/ECG shows right heart strain
  • +ve cardiac markers: troponin
179
Q

how is a sub-massive PE managed

A

RISK STRATIFICATION (VERY important)

  • using PESI score/modified PESI score
  • If the score is <85 then is low risk, higher should be admitted

If lower: anticoagulate [DOAC] and send home

180
Q

1st line anticoagulants for PE

A

DOACs - lower bleeding risk

181
Q

when should LMWH be used for PE instead of DOACs

A
  • pregnant
  • already on warfarin
  • clots present around metal work e.g. heart valves, stents
182
Q

how long should anticoagulants be used in provoked vs non-provoked PE

A

provoked = min. 3 months

unprovoked = beyond 3 months (risk of another PE)

183
Q

what investigations to carry out after an unprovoked PE

A

Should have limited investigations into whether there is any underlying malignancy:

  • FBC
  • U&E’s
  • Calcium/PSA
  • Clotting factors and LFT’s (liver mets)
  • Consider a breast/prostate/testicular examination
  • Systems review

ONLY do further investigations if clinical suspicion of cancer after all these tests

184
Q

PERC criteria - PE rule out criteria (if 0 don’t even do D-dimer!)

A

PERC: PE-rule out criteria:

  • Age <50 years
  • HR <100bpm
  • O2 sats >94% on air
  • NO unilateral leg swelling
  • No haemoptysis
  • No surgery/trauma in last 4 weeks
  • No Hx of VTE
  • No oestrogen use

if can’t rule out PE = do Well’s score

185
Q

which Well’s score is high and would bypass D dimer going straight to CTPA

A

4+

186
Q

4 examples of ester LAs

A

prilocaine
cocaine
benzocaine
tetracaine

187
Q

why are ester LAs not commonly used

A

high rates of hypersensitivity reactions

188
Q

5 examples of amide LAs

A 
lidocaine (lignocaine)
bupivacaine
prilocaine
levobupicaine
ropivacaine
189
Q

max safe dose of lidocaine with and without adrenaline

A 
without = 3mg/kg
with = 7mg/kg
190
Q

max safe dose of prilocaine

A

6mg/kg

191
Q

how to work out concentration of 0.25% bupivacaine

A

0.25 x 10 = 2.5mg/ml

192
Q

what are the 3 ligaments of the spinal cord which are passed through when doing a spinal anaesthetic

A
  • supraspinous ligament
  • interspinous ligament
  • ligamentum flavum
193
Q

describe a spinal block

A
  1. Patient sat sitting hunched forward- line between the 2 iliac crests is L2/3
  2. Skin infiltrated with 1% lidocaine
  3. 25g spinal needle into L3/4 space
  4. Free flow of CSF from the spinal needle indicates in correct place
  5. Attach marcain syringe (bupivacaine + glucose) and retract syringe slightly to see swirls of CSF in synringe
  6. Inject LA
  7. Lie patient down immediately and monitor Bp closely
194
Q

why is marcaine (bupivacaine + glucose) used in a spinal anaesthetic

A

heavier molecule = sinks to bottom of spinal cord = no sympathetic block of whole body

NB: blocking sympathetic chains = BP reduction with spinal anaesthesia

195
Q

describe an epidural catheter anaesthetic

A

Indwelling catheter into the epidural space: LA +/- opioid

  • Longer, slower onset= 15-20 minutes
    1. Hooked needle inserted into potential epidural space and NaCl injected to create a space
    2. spinal catheter in: should feel loss of resistance
    3. Inject 3ml and see if patient feels any systemic signs suggesting accidently into CSF
    4. If not then continue to inject through catheter- fluid should be sucked up by needle due to negative pressure
196
Q

how does ephedrine work

A

indirect general agonist; releases stored catecholamines (used for nasal decongestion, urinary incontinence, hypotension)

Direct and indirect action on Alpha & Beta receptors:
- Indirect action: agonist releasing stored catecholamines

Alpha: Vasoconstriction on V receptors
Beta: Increase HR (beta = beats)

197
Q

how do metaraminol and phenylephrine work

A

Metaraminol has direct and indirect effects on Alpha receptors causing vasoconstriction

Phenylephrine just has direct action on Alpha receptors causing vasoconstriction

198
Q

which organism tends to cause pneumonia AFTER influenza infection

A

staph aureus (gram +ve cocci)

199
Q

organisms causing severe CAP

A
  • gram +ve cocci = strep pneumoniae, staph aureus
  • gram -ves = H. influenzae
  • atypical = legionella, mycoplasma
200
Q

how is CURB score 0-1 pneumonia treated

A

doxycycline/amoxicillin

201
Q

how is CURB score 2 pneumonia treated

A

co-amoxiclav +/- clarithromycin OR still doxycycline

202
Q

how is CURB score 3-5 pneumonia treated

A

co-amoxiclav + clarithromycin

levofloxacin if allergic???

203
Q

specific antibiotic used for strep pneumonia

A

IV benzylpenicillin

204
Q

specific antibiotic used for s. aureus pneumonia

A

flucloxacillin

205
Q

main causes of HAP

A

same causes as CAP plus gram negatives - E. coli, pseudomonas

206
Q

antibiotics suitable for non-severe HAP

A

co-trimoxazole

207
Q

antibiotics suitable for severe HAP

A

linezolid + ciprofloxacin

208
Q

how is MRSA treated and when is a patient deemed MRSA free

A

Nasal mupirocin plus chlorahexidine body washes for 5 days

  • Once decolonised- send repeat MRSA swabs
  • 3 consecutive negative screens, each 48 hours apart is MRSA free
209
Q

what is a parapneumonic effusion

A

exudative pleural effusions that occur adjacent to a bacterial pneumonia and result from migration of excess interstitial lung fluid across the visceral pleura; although inflammatory cells are present, parapneumonic infections are STERILE

typically these are small and uncomplicated and resolve with resolution of the pnuemonia

if bacteria from the pneumonia invade the pleural space a complicated parapneumonic effusion or empyema will result***

210
Q

4 features of a simple parapneumonic effusion

A
  • Non-infective: no gram stain/culture positives
  • LDH <1000
  • pH >7.2
  • Glucose >2.2
211
Q

how are simple parapneumonic effusions managed

A

antibiotics alone

sometimes chest drain for symptom relief

212
Q

4 features of complication parapneumonic effusion

A
  • Infected effusion - positive gram stain/culture
  • LDH >1000
  • pH <7.2
  • Glucose <2.2 (bacteria eat it up)
213
Q

what is present in empyema

A

frank pus - don’t need to check pH

214
Q

when might a yeast empyema occur

A

after oesophageal rupture/anastomotic leak from GI tract

215
Q

1st line antibiotics for empyema /parapneumonic effusion

A

IV co-amoxiclav OR IV levofloxacin/ metronidazole if penicillin allergic

also need to do aspiration +/- chest drain insertion, could also do fibrinolysis

216
Q

minimum insertion length of an NG tube

A

55cm

217
Q

what does procalcitonin indicate

A

bacterial infection

218
Q

what is often raised in a GI bleed

A

urea: digested blood

219
Q

what antibiotics can cause muscle breakdown when someone is also taking a statin

A

macrolides: clarithromycin, clindamycin, erithromycin

220
Q

normal JVP is

A

less than 4cm

221
Q

common post-op airway problems

A
  • Decreased muscle tone due to certain drugs
  • Secretions
  • Sleep apnoea- body habitus larger
  • Laryngospasm
222
Q

some causes of hypoxia

A
  1. Alveolar hypoventilation
  2. V/Q mismatch- PE, Atelectasis, bronchopneumonia, aspiration pneumothorax, pulmonary oedema
  3. Circulatory problems:
    - Increased oxygen demand: sepsis
    - Low cardiac output states: hypotension
223
Q

signs of LA toxicity

A
  • tongue and Perioral tingling/numbness
  • tinnitus
  • light-headedness
  • speech slurring
  • confusion
  • restlessness
  • muscle twitching
  • diplopia
  • convulsions

excitatory due to inhibition of inhibitory neurone via GABA receptors

224
Q

safe dose of prilocaine (ester) with adrenaline

A

8mg/kg (6 without)

225
Q

colours of vessels, bones and soft tissues in USS

A
  • vessels and fluid = black (anechoic - don’t reflect the sound waves)
  • bones = white (hyper echoic - reflect all the sound waves back to probe)
  • soft tissues = grey (isoechoic - reflect some US waves)
226
Q

what do nerves look like on USS

A

honeycomb appearance - hypoechoic/hyperechoic

227
Q

features of high frequency transducers

A
  • 7-18MHz
  • High resolution but LOW DEPTH
  • Superficial vessels, muscles
228
Q

features of low frequency transducers

A
  • 2-6 MHz
  • Penetrate deeper but lower resolution
  • Cardiac, abdominal and obstetric uses
229
Q

what is gain in USS

A

the amount the amplifier increases the incoming signal - especially the brightness of the image

230
Q

colour of Doppler when signal is moving away and towards probe

A

signal from fluid moving AWAY from probe = lower frequency = blue

signal from fluid moving TOWARDS probe = higher frequency = red

231
Q

what is acoustic shadowing

A

The reduced echo intensity behind a highly attenuating or reflecting object such as a stone creating a shadow

Structure behind an object which reflects all the US waves looks black

232
Q

what is acoustic enhancement

A

Increased echo intensity behind a minimally attenuating object such as a cyst or blood vessel

Sounds waves going through fluid structure such as vessel- less are absorbed so tissues after fluid can look white (hyperechoic) but they shouldn’t

233
Q

4 ultrasound views of the heart

A
  • parasternal long
  • parasternal short
  • apical (4 chamber view)
  • suprasternal
234
Q

where to put ultrasound probe for parasternal view

A

left of sternum in 3/4th intercostal space

235
Q

where to put ultrasound probe for apical view

A

under left nipple

236
Q

preferred areas of guided peripheral vascular access

A
  • cephalic vein
  • basilic vein
  • brachial vein
237
Q

most common site of arterial cannulation

A

radial

can also do brachial, femoral or dorsals pedis

238
Q

what are vasopressors

A

Drugs which work on alpha 1 receptors to cause vasoconstriction and therefore increase BP

239
Q

what are inotropes

A

Drugs which increase myocardial contractility and HR

however this can lead to myocardial ischaemia due to increasing myocardial O2 demand

240
Q

3 examples of inotropes

A

adrenaline
dopamine
dobutamine

241
Q

4 examples of vasopressors

A

phenylephrine
metaraminol
adrenaline
noradrenaline

242
Q

side effect of vasopressors

A

increased after load = more stress on heart

hypertensive episodes = reduced blood flow to end organs

243
Q

role of B1 and B2 receptors

A

B1 = increase HR and cardiac contractility

B2 = vasodilation

244
Q

how does phenylephrine work

A

Works purely on alpha-1 receptors to cause vasoconstriction with no effect on heart

Good for when low BP and body has already compensated with tachycardia

245
Q

how does ephedrine work

A

Direct and indirect action on beta and alpha receptors due to release of stored catecholamines

Therefore increases HR and vasoconstriction

Good to use when Low BP and Low HR

246
Q

how does noradrenaline work

A

stimulates A1 and B1/2 receptors to cause vasoconstriction AND increased CO due to B1 action

247
Q

how does dopamine work

A

higher B1 affinity = increases HR and contractility

mild A1 vasoconstriction effect

248
Q

how does adrenaline work

A

strong B1 affinity and mild A1/B2 affinity = increases HR and contractility a lot

249
Q

how does dobutamine work

A

very high B1 affinity = increases HR and contractility

can initially have some hypotension due to B2 affinity

250
Q

what does paradoxical breathing indicate

A

complete airway obstruction

251
Q

2 main cautions for penicillins

A
  • renal impairment (dose reduction)

- using with methotrexate - reduces renal excretion = increases risk of toxicity

252
Q

what happens if you take allopurinol with penicillin

A

can increase likelihood of rash

253
Q

side effects of cephalosporins

A
  • GI upset: D&V
  • Antibiotic associated colitis
  • Hypersensitivity, especially if patient has penicillin allergy
  • Neurological toxicity in high doses/renal impairment
  • Agitation
  • Arthritis
  • Confusion & fatigue
  • Pruiritis
  • Transient hepatitis + jaundice
  • Increases INR and bleeding by inhibiting vitamin K dependent clotting factors (1972)
254
Q

2 interactions of cephalosporins

A
  1. Warfarin: enhances anticoagulant effect by killing normal gut flora which make Vitamin K
  2. Aminoglycosides: increases nephrotoxicity

Year 4 revision (5 decks)

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