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General Flashcards

1
Q

Myasthenia gravis are sensitive to depolarising NMB

A

MG resistant to suxamethonium (double dose)

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2
Q

TNF is associated with

A

Cytokine

Poor outcome

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3
Q

Extradural space may contain

A 
Fat 
Spinal nerve roots 
Lymphatic 
Connective tissue 
Batsons plexus
Spinal arteries 
Epidural venous plexus
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4
Q

ECT current

A

30-45 Up to 100j

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5
Q

Autonomic response to ECT

A

Initial parasympathetic response ie bradycardia hypotension sometimes asystole

Followed by sympathetic response hypertension and tachycardia

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6
Q

Compliance greater under static or dynamic conditions

A

Static

Static is periods when no gas flow. Dynamic is when there is flow ie active respiration…. need to overcome airway resistance so dynamic compliance will be less.

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7
Q

Complain when greater with water or air

A

Water (liquid) - more pressure needed to distend lung with air than liquid

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8
Q

Compliance is greatest at FRC or TLC

A

FRC

TLC is top of pressure volume curve so little compliance

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9
Q

Acclimatisation to altitude includes what changes

A

Increased 23dpg
Compensated respiratory alkalosis (I.e loss of hco3)
Increased blood viscosity
Increased diffusing capacity co2
Cardiac output initially increases but settles once acclimatised

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10
Q

Where does sympathetic outflow arise

A

T1-L2 (sympathetic chain runs parallel to spinal column)

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11
Q

Where does parasympathetic outflow arise

A

Cranial sacral

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12
Q

Which cranial never have parasympathetic nuclei

A

III, VII, IX, X

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13
Q

Where is larynx located

A

Anterior neck, level c4-c6

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14
Q

Narrowest part of larynx adults vs infants

A

Adults glottis

Infants cricoid

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15
Q

Recurrent laryngeal nerve innervates what intrinsic muscles

A

All except cricothyroid

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16
Q

Sensory inner action larynx

A

Superior laryngeal never above cords

Recurrent laryngeal nerve below cords

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17
Q

How does adrenaline effect glucose levels

A

Adrenaline causes hyperglycemia

a receptors Stimulation inhibit insulin secretion, stimulate gycogenolysis and glycolysis

B receptors stimulation results in glycogen secretion in pancreas, increased ACTH, and increased lipomas is

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18
Q

Do thiazides cause hyperglycemia

A

Yes possibly by insulin resistance

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19
Q

Lumbar plexus roots

A

L1-4 sometimes with t12 and l5 input

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20
Q

Lumbar plexus nerves

A 
Femoral 
Obturator 
Ilioinguinal 
Iliofemoral 
Lateral cutaneous 
Genitofemoral
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21
Q

Tributaries of internal jugular vein

A

Medical school lets fun people in

Middle thyroid 
Superior thyroid 
Lingual 
Facial 
Pharyngeal 
Inferior petrosal
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22
Q

Major haemorrhage definitions

A

Loss of all blood volume in 24 hours (5liters or 70ml/kg in adults)

Loss of half circulating volume in 3 hours

Loss of 150ml/min

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23
Q

Genetics of malignant hyperthermia

A

Malignant hyperthermia is autosomal dominant

Error in RyR1 (Ryanodine receptor) on chromosome 19

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24
Q

Early signs of MH

A

Increase in co2
Increase in heart rate and oxygen consumption

Late sign is high temp

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25
Q

Mortality of MH

A

5% with introduction of dantrolene

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26
Q

What is cause of renal failure in ALF

A

Acute tubular necrosis

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27
Q

Association of chronic pain with
depression
Anxiety

A

Depression 30-40%

Anxiety 25%

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28
Q

What opiods can you do skin prick testing in

A

Fentanyl and remifentanil

Morphine codeine and diamorphine have significant direct mast cell degranulation without Ige so skin prick testing not appropriate

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29
Q

Mast cell tryptase measurements and why

A

Measure at time, 3hours and 24 hours

Mast cell tryptase is spontaneously released so need to see serial and rise and fall in anaphylaxis for confirmed diagnosis

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30
Q

What apart from anaphylaxis can cause raised mast cell tryptase

A

Typtase may be raised in mastocytosis, aml, myelodysplastic syndromes

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31
Q

What effect do volatiles have on venous admixture

A

Venous admixture is the lowering of arterial po2 from ideal level due to shunt. Volatiles impair HPV therefore increase venous admixture

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32
Q

Where is bilirubin produced

A

Bilirubin is produced in reticuloendothelial system in the spleen, bone marrow and hepatic kipper cells
Bilirubin is produced by macrophages by reduction of biliverdin

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33
Q

How is bilirubin transported to the liver

A

Bilirubin is bound to albumin as its insoluble

Conjugation makes bilirubin soluble

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34
Q

What is the concentration of intralipid

A

20%

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35
Q

What is the dose of intralipid on initial dose

A

1.5ml/kg

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36
Q

What is ongoing treatment with intralipid in LAST

A

Infusion intralipid 15ml/kg/hr
Two repeat boluses 1.5ml/kg (5 minutes between)
Increase infusion to 30ml/kg/hr (at 5 mins)

If CV stability not restored or deteriorates

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37
Q

Maximum dose of intralipid

A

12ml/kg

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38
Q

How does plasma site vary from effect site

A

Plasma site

Effect site has extra contant keo is effectively a 4th compartment but with negotiable volume
Time delay in equilibration between plasma and effect site as takes into account keo
In effect site need to overshoot CP then reduce to allow cp and Ce to equilibrate
Keo calculated by complex pharmacological modelling

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39
Q

Discuss marsh model for TCI

A

Marsh is based on weight
Safest to use in Cp as uses very large bolus in ce initially
Best for young people

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40
Q

Discuss Schneider model TCI

A

Snider uses age and lean weight (sex adjusted)
Always use in Ce
Beneficial in elderly
Smaller bolus doses

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41
Q

How can you minimise awareness in TIVA

A 
Concurrent use of remifentanil 
Depth of anaesthesia monitoring ie BIS 
One way valves 
Anti Syphon valves 
Adequate equipment training 
Avoid muscle relaxant 
Alarms on pump ie. low high pressure, battery
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42
Q

Define aspiration

A

Inhalation of material below true cords

Commonly quoted 25ml and ph less than 7.2 comes from studies on monkeys extrapolated to humans

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43
Q

Kidneys cardiac output

A

25%

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44
Q

Kidneys glomerular filtrate volume

A

180l day

70 percent reabsorbed by pct

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45
Q

Renal perfusion ml/min/100g

A

Cortex 500, outer medulla 100, inner 20

Cortex least metabolically active so is a luxury blood supply in excess of requirement

Medullais very metabolically active, oxygen requirement is tight and is at risk of ischaemic injury

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46
Q

What matching required for cadeveric renal donors

A

Size, blood group and MHC complex

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47
Q

Side effects of ciclosporin

A

Ciclosporin causes hypertension, tremor, reduced egfr, encephalopathy

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48
Q

Why was glycine used for TURP

A

Doesn’t conduct electricity

TURP syndrome glycine level over 60mmol/l

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49
Q

TURP how high doe you need block

A

T9

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50
Q

Sickle cell genetics

A

Autosomal recessive most of the time
Trait carries some protective properties but phenotypically normal
Carried on chromosome 11
Abnormal B globin chain forms HbS which precipitated out of solution when deoxygenated
Heterozygotes 30% hbs (some protective from p.falciparum)
Homozygotes 100% hbs

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51
Q

Genetics of thalassemia

A

Group of heridatory anaemia causes by ineffective a or B chain formation.
Heterozygotes mild anaemia
Homozygotes severe
May be compensatory extramedullary haematopoesis

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52
Q

Diagnosis sickle cell

A

Sickledex but cannot distinguish between sickle trait and sickle cell
Blood film
Haemaglobin electrophoresis

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53
Q

Presentations of sickle cell

A

A/b - dypnoea, haemoptysis, chest pain (pulmonary infractions) - acute chest syndrome
Functional asplenism hypertrophy of other lymphoid tissue and osa
C- cardiomegaly due to anaemia or CCF, pulmonary heart failure
d- increase Tia and stroke, microvascualr changes in eye
E- automfarction pf spleen, pigment gallstones
f- renal failure
H- marrow hyperplasia frontal bossing and maxilla
Acute decreases in hb by infection induced myelosuppresion (ie parvovirus)
Bone marrow failure

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54
Q

Treatment sickle cell

A

Patient education re hydration, exercise, alcohol
Vaccinations
Folic acid
Hydroxyurea (increases fetal hb)

Acute
Analgesia
Rehydration
Remember acute abdomen differential is sickle cell

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55
Q

Sickle cell requiring op considerations

A

Pre op tests assessing organ dysfunction
Rehydrated
Hb and transfusion

Avoid adrenaline in Local
Positioning to avoid venous stasis
Tourniquets must be justified
Analgesia

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56
Q

Thalasseemia pre op considerations

A

Consider if could have sickle cell too
Haematocrit
Splenomegaly and thrombocytopenia
Facial changes and frontal bossing

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57
Q

Drugs with potential anti carcinogenic effects

A

Regional (directly from reduced sympathetic stress response or via reducing opiod consumption)
LA (possible direct immunomodulatory effect)
Propofol TIVA (as abolishes ischaemic reconditioning, increases apoptosis and decrease invasion migration and proliferation, more preserved NK function)
NSAIDS (reducing prostaglandin effects which is pro progression of neoplasia via IL6 IL4 ….. cox2 is higher in some cancers )

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58
Q

Drugs with potential pro carcinogenic effects

A 
Inhalation  agents ( promote tumour GF including HIF and IGF, reduction of NK cells.... overall promote tumour growth, invasiveness, migration) 
Opiods (some reduction via reduced stress response) (some evidence that reducing doses may reduce angiogenesis and a cancer recurrence)
Steroids (immunosuppressant reduces NK cells and other T cell subtypes) so,e studies refute thus
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59
Q

Surgical indications for TIVA

A 
Cancer surgery 
Tubeless ent or thoracic surgery 
Neurosurgery 
Surgery requiring neuromuscular monitoring ie scoliosis 
Day case surgery 
Non theatre environment
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60
Q

Patent indications TIVA

A 
MH 
PONV 
Long QT
Patient choice 
NM issues ie MG 
Anticipated difficult intubation or extubation
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61
Q

Checklist TCI systems

A

Only dedicated TCI pumps
Trained in use of pump and model
Pumps serviced last 12m
Ensure pumps plugged into mains
Ensure batteries are charged
Ensure drug dilutions correct and entered into pump
Ensure correct syringe type and mounted correctly
Ensure pump programmed for drug it is programmed for
Ensure high and low pressure alarms set
Ensure correct patient details entered
Consider if targets set are appropriate for asa and age
What is plan b if pumps fail

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62
Q

Recommendations to prevent technical problems with TIVA

A

Secure cannula
TCI system checklist
Keep cannula visible
Only use dedicated two way tap set includes anti siphon valves, non return on IV fluids, minimal dead’s peace
Only use Leur lock syringes when admin drugs
Don’t label remi until drug is in
Flush Tuva drug from dead space of three way way before connection and flush out at end

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63
Q

Potential problems with tiva

A

Awareness
Morbid obesity - marsh model will result in overdosing, snider based on LBW and once Bmi reaches a critical level the infusion rate is insufficiently corrected and may result in large bolus. Minto above certain bmi reduced bolus and inadequate analgesia
Analgesia and hyperalgesia
Propofol related infusion syndrome (metabolic acidosis with cardiac dysfunction plus possible rhabdo, hyper triglyceride, renal failure)

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64
Q

Nap 1

A

Supervisory role of consultant anaesthetists

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65
Q

Nap 2

A

Place of M&M meetings

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66
Q

Nap 3

A

Complications of central neuroaxial block in the uk

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67
Q

Nap 4

A

Major complications of airway management in the uk

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68
Q

Nap5

A

Accidental awareness during GA

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69
Q

Nap 6

A

Perioperstuve anaphylaxis

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70
Q

Nap7

A

Perioperative cardiac arrest

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71
Q

Why choice of agents in tiva

A

Remi and propofol synergistic effect
Short CSHT
Predictable pharmacological profile

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72
Q

When does propofol reach steady state concentration

A

20 hours

When all 3 compartments reach steady state concentration,

TCI matches elimination (k10)

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73
Q

Key components of TCI

A

User interface
Microprocessor
Infusion pump (up to 1200ml/hr)
Visual and audible safety systems and alarms

Calculates bolus dose required
Calculations repeated every 10s and infusion rate adjusted until Cpt

Diffusion to brain is exponential with first order rate constant keo

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74
Q

Marsh model fixed variable parameters and parameter determined by

A

Marsh model fixed rate constant
Variable v123

Parameter determined by weight

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75
Q

Schneider model fixed variable parameter and determined by parameter

A

Fixed in Schneider v1 v3 k13 and k31

Variable in Schneider V2

Parameter determined by age, weight, lean body mass

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76
Q

Minto model fixed and variable parameters and parameter determined by

A

Minto model v3 fixed

V1 v2 and rate constants variable

Model determined by weight and lean body mass

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77
Q

Stress response to surgery two broad categories

A

Neuroendocrine metabolic response

Inflammatory immune response

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78
Q

Surgery with largest stress response

A

Major open vascular and abdominal

Joint replacement cardiac on CPB

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79
Q

Describe neuroendocrine metabolic stress response to surgery

A

Sympathetic nervous system

  • PVN nucleus detects changes ie hypotension
  • impulses from site injury via limbic system
  • PVN fibres into posterior pituitary and control anterior pituitary functions
  • adrenaline secreted directly in response to hypothalmic activation and this increases sympathetic response
  • heart rate and vascular sm time increased
  • mobilised cho and fat stores
  • glyogenolysis and lipolysis = hyperglycemia
  • increased coag

Endocrine

  • increased CRH stimulates HPA
  • Increased ACTH which increases cortisol secretion in zone fasciculata
  • uktradian pulsation increase
  • chronic activation hpa leads to dysfunction with surgery - age and fragility risk factors and can get pre existing dysfunction ie in anxiety and depression.
  • GH increases hepatic glycogenolysis leading to hyperglycemia
  • increased in ADH, increased prolactin, reduced testosterone, thyroxine and t3

Metabolic response
Hyper metabolism and hylercatabolism
Glucose from all sources, and insulin ins inhibited and insulin resistance

Renin activates which eventually leads to increased aldosterone- retention of salt and water

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80
Q

Describe inflammatory immune stress response to surgery

A

Innate and cell mediated immunity

Macrophages, NK cells move into wounds and cause inflammatory mediators
Cytokines include ILS TNF interferons and cytokines

Early inflam cytokines IL6 TNFa IL8

Anti inflammatory il4il10

Acute phase response is increase in serum proteins stir by cytokines esp IL6
Ie crp, d dimmer, macroglobulins
IL6 and CrP can be linked to magnitude of surgical stress

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81
Q

Ways to modulate stress response to surgery

A

IV vs volatiles - volatiles may inhibit endocrine responses but other propofol lowest proteolytic effect
Benzodiazepine - inhibit cortisol at level HPA
A2 agonists - inhibit surgical stress response
Opiods - reduce acth and GH. Morphine fentanyl remi have immimo modulators role
Regional - blocks HPa axis response via afferent

Surgical techniques - minimally invasive surgery techniques, duration and extent surgery
Eras programmes
Early nutrition
Early mobilisation

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82
Q

Glucocorticoids and surgical stress response

A

Varied literature
Reduced CRP and IL6
Reduced post op ventilation, hyperthermia, infection and ,engage of stay
Caution in diabetes s

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83
Q

Define gbs and name subtypes

A

Guillian barre is and acute inflammatory polyneuropathy (ascending )

Types are 
Acute inflammatory demyelination polyradiculopathy 
Miller fisher variant 
Acute motor axonal neuropathy 
Acute motor sensory axonal neuropathy
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84
Q

GBS signs

A 
Motor difficulty / paralysis 
Loss deep tension reflexes 
Paraesthesia without sensory loss 
Muscle wasting 
Urinary retention 
Ptosis 
Autonomic 
Speech problems 
Respiratory distress
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85
Q

Investigations in gbs

A

Nerve conduction studies
LP
LTFS
Spirometers (vc less than 15ml/kg indication for intubation)

Also consider serology, stool culture, HIV, spinal MRI
Anti ganglioside antibodies

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86
Q

Treatment GBS

A 
Ventilator support 25%
- facial bulbar laryngeal weakness 
-inability to clear secretions 
- resp and diaphragm muscle weakness 
- pulmonary infections 
Often nocturnal decompensation 
Regular VC and constant oximetry 
Physio therapy 
Psychology 
Immmunoglobulin 
Plasmapheresis 
Nutrition 
Analgesia

Not steroids

Outcome GBS mortality 10%

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87
Q

Indications intubation in GBS

A

V1c less than 20
max inspiratory pressure of less than 30
Max exp pressure of more than 40
Decreased more than 30% of above

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88
Q

One MET

A

One met Represents the oxygen consumption of an adult at rest (approx 3.5ml kg min)

A person should be able to perform more than 4 mets which is equivalent of climbing one flight of stairs

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89
Q

Contraindications to CPET

A 
Absolute contraindications to cpet 
Acute MI 
Unstable angina 
Uncontrolled arrhythmias
Syncope 
Active endocarditis 
Myocarditis or pericarditis 
Severe AS 
Suspected dissecting aneurysm 
Uncontrolled asthma 
Room seats less than 85% 
Resp failure 
Relative 
Left main condo art stenosis 
Moderate stenosis valve 
Severe hypertension sbp 200 dbp 120 
HOCM 
Pulmonary hypertension 
Advanced or complicated pregnancy 
Electrolyte disorders
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90
Q

CPET timings

A

3 mins baseline
1-3mins unloaded
Increasing resistance
Full monitoring for ten mins cessation of exercise

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91
Q

CPET measurements

A 
Work in watts 
Metabolic gas exchange ie vo2 and vco2 
Respiratory exchange ratio 
Anaerobic threshold 
Hr 
12 lead ecg 
Nibp 
Oxygen pulse (vo2/hr) 
Ve 
Vt 
Rr 
Spo2 
Ventilator equivalents for oxygen

Computer software calculated expected for height age weight sex

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92
Q

9 panel plot

A

Graphical representation of CPET is called 9 panel plot
235 cardiovascular
147 ventilation
689 Ventilation perfusion

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93
Q

Vo2 max

A

As work rate 8ncreases exercise muscle requires more oxygen to generate adequate levels of ATP

Increase in oxygen consumption met by increasing CO

Vo2 = co x arterial venous oxygen difference

Co therefore increases linearly with vo2 as does the av difference until a peak oxygens extraction reached

Vo2 max is the maximum o2 consumption of the body (attainable by athletes)

Vo2 peak is the peak o2 consumption when test is not completed ie age fragility deconditioned

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94
Q

Anaerobic threshold

A

With imcreasing exercise oxygen demand exceeds supply and atp is generated anaerobically
Produces lactic acid- buffered with hco3- produces co2
Sudden increase of vco2 more than vo2 and rer becomes more than 1

AT usually reached about half way through test
Doesn’t vary with patient motivation or age

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95
Q

Safe AT and VO2 peak for surgery

A

At 11ml/kg/min

Vo2 peak 30

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96
Q

Functional walk test

A

6minute walk test (500-600m, says hr and Borg scale of dyspnoea and leg fatigue)
Incremental shuttle test (speed increases every minute - failure to reach come in next tone or exhaustion terminates test)

Both correlate well with peak vo2

97
Q

Innervation of knee

A 
Hilton’s law 
Femoral 
Obturator 
Common and recurrent perineal 
Tibial

The femoral nerve via its Soph branch and to vastus supplies suprpatella recess, patellar periosteum, anterior medial and anteriolateral joint capsule

Tibial never supplies medial lateral posterior joint capsule, infrapatellar fat pad, tibial periosteum

CPN supplies anteriolateral capsule

Recurrent peroneal - tibfib joint

Obturator - posteriormedial capsule

Cutaneous innervation anterior femoral

98
Q

Independent predictors severe post op pain knee arthoplasty

A

Young age
Pre op pain
Depression

99
Q

Cause of pain in knee surgery

A

Prostaglandins and bradykinin realised at site of injury

Nociecotive fibres travel STT (nmda receptors)

100
Q

Prep knee surgery

A

Joint school

Preemptive analgesia nsaids good evidence, gabapentin unclear

101
Q

RA for knee arthoplasty

A

Regional associated with reduction in post op complications including dot pulmonary embolism blood transfusion respiratory depression

Spinal (plus femoral nerve block and sciatic block)
Epidural
Femoral nerve block
Adductor canal block (contains saph nerve and posterior obturator nerve medial knee only)
Local infiltration analgesia

Novel techniques
I pack block (infiltration between popliteal artery and capsule of posterior knee)
Nerve to vastus lateralis

102
Q

Adjuncts in knee surgery

A

Dexamethasone reduces acute phase reactants such as CRP and IL6
Avoid knee haematoma with TXA

103
Q

Post op pain management knee surgery

A 
Multimodal 
PCA 
Continuous LA infusion ie elastomeric 
Gabapentin? 
Cryocuff
104
Q

Types of cognitive impairment after surgery

A

Preexisting or progression of existing neurocognitive disorder

Mild NCD- noticeable decline in cognitive function but maintains independence
Major NCD - impairs daily living

Acute onset of delirium (less than 7 days post operative)

Delayed neurocognitive recovery (first 30 days)

Post operative cognitive dysfunction (within a year)

105
Q

Cognitive domains evaluated in NCD

A 
Learning and memory (learn and recall new infor) 
Language 
Perceptual motor 
Social cognition 
Complex attention 
Executive function (planning) 
Delirium
106
Q

Delirium

A

Fluctuating changes in attention, consciousness and cognitive f7nctuin within hours or days of event
Hypo or hyperactive

107
Q

Post operative cognitive dysfunction

A

Describes a decline in cognitive ability from baseline that starts in the days after surgery.
May be in one or more cognitive domain
Timeframe remains undefined but can be detected after 7 days - transient effects after surgery are multi factorial and so can’t really test or attribute to POCD until this time

Can effect any age but more profound sequelae in elderly

108
Q

Tools to diagnose POCD

A

Mmse not great as doesn’t detect subtle changes
Addie brookes cognitive examination
Montreal cognitive assessment tool

Needs to be dynamic and pre operative too

109
Q

Cause of POCD

A

Unclear
? Neuronal death neuroinflammation and micro emboli
? Anticholinergic pathways

110
Q

Patient Risk factors POCD

A 
Age 
Lower education level 
History of cerebrovascular accident 
Preoperative mild cognitive impairment 
Cognitive dysfunction at discharge
111
Q

Anaesthetic risk factors for POCD

A 
Ga vs ra - suggestion is ra benefit but no evidence
Propofol better than sevo 
EEG or BIS may reduce risk 
No association with abnormal physiology ie hypoxia 
Dexmed protective 
Ketamine may be protective 
Steroids no effect 
NSAIDs may be protective 
Other risk factors include 
Long anaesthetic time 
Post op infection 
Multiple surgeries 
Respiratory complications
112
Q

Drug reactions A to E

A 
A is acute 
B is bizarre ie idiosyncratic 
C is chronic 
D is delayed ie cardiomyopathy secondary to chemo ten years later 
E is end of treatment Ie withdrawal
113
Q

Sickle cell genetics

A

Sickle cell inherited haemoglobinopathy
Mutation on chromosome 11
Results in glutamate for valine at position 6 on beta chain

114
Q

Physiological factors promoting sickling in sickle cell disease

A 
Hypoxia 
Hypothermia 
Pain 
Dehydration 
Infection
115
Q

Sickle dex test Reagent and limitations

A

Reagan’s is sodium metabisulphate

Test doesn’t differentiate between trait and disease

116
Q

Parameters for exchange transfusion in sickle cell

A

Hb 10
Hb a more than 70%
Hb s more than 30%

117
Q

Long term complications of sickle cell

A 
Vasoocllusive sequels ie ulcers 
Haemolytic anaemia 
Functional asplenism 
Cardiomegaly 
Chronic pain 
Bone marrow failure 
Hypertrophic of lymphoid tissue
118
Q

Cystic fibrosis genetics

A

Autosomal recessive
Single gene mutation on chromosome 7
1 in 2500
Results in failure to transport chloride ions across the cell membrane resulting in vscid mucus that can’t be cleared by cilia

119
Q

Respiratory pathogens in CF

A

Pseudomonas spp
Staph aureus
Haemophilus influenzae
Burkholderia cepacia

120
Q

Non respiratory manifestations of CF

A

Malabsorption
Diabetes
Infertility
Nasal polyps

121
Q

Preooptimise CF

A 
Pre optimise CF 
Physio
Nutrition 
Mucolytics and nebulisers 
Protective isolation 
Prophylactic antibiotics
122
Q

Tailor GA for CF

A 
Consider carefully re intubation - do you need suction facilitaton of ETT 
Lung protective strategies 
Good analgesia deep breathing 
Opiate sparing 
Ensure adequate reversal
123
Q

Mechanism of action of antiemetics

Dex 
Ondansetron 
Metoclopramide 
Cyclizine
Droperidol 
Aprepitant 
Scopolamine 
Midazolam
A 
Dex is steroid 
Ondansetron 5ht3 antagonist 
Cyclizine histamine 1 antangonist 
Metaclopramide dopamine antagonist 
Droperidol dopamine antagonist 
Apprepitant neurokinin antagonist 
Scopolamine anticholinergic 
Midazolam benzo
124
Q

Adult PONV scoring system

A

Apfel

Provoc in children

125
Q

Causes of secondar6 hypertension

A 
Phaeo 
Conns syndrome 
Renal artery stenosis 
Endocrine disorder ie Cushing hypo and hyperthyroidism 
PCKD 
Diabetic nephropathy 
Cv causes like coactation
126
Q

End organ effects hypertension

A

Cardiac LVH
Renal ESRF
Optahlmic hypertensive retinopathy
Neuro cva hypertensive encephalopathy

127
Q

Aagbi guidance for BP for elective surgery

A

Primary care BP less than 160/100

Secondary care ie pre op less than 180/110

128
Q

Hypertensive treatment algorithm step1 - over 55 or afrocaribean

A

Calcium channel blocker

129
Q

Hypertension treatment algorithm under 55 or diabetes

A

Ace I

130
Q

Second line treatment hypertension

A

Ace I or calcium channel whatever not on yet

Thiazides diuretic

131
Q

Third line hypertension

A

ACD all 3

132
Q

4th line hypertension

A

Seen in tertiary care

Spiro or a blocker

133
Q

Perioperative complications hypertension

A 
Labilecardiovascular 
Relative hypovolemia 
Exaggerated response to press or 
Post operative cognitive dysfunction 
Cardiovascular events ie mi
134
Q

Define carcinoid syndrome

A

Carcinoid is a syndrome caused by release of serotonin histamine bradykinin prostaglandins by a slow growin* neuro endocrine tumour

135
Q

What is serotonin

A

Monoamine neurotransmitter

136
Q

Signs and symptoms of carcinoid

A

Symptoms flushing sob diarrhoea nausea

Signs bronchospasm sweating hypertension

137
Q

Treatment carcinoid

A

Symptom control with serotonin receptors antangknists ie ondansetron

Somatostatin analogues ie octreotide

Surgical excision tumour

138
Q

What pharm agents can manipulate serotonin

A

SSRIS
MAOI
Antiemetics
Sumatriptan

139
Q

What are phaechromocytomas and what diseases are they associated with

A

Functionally active tumours secreting catecholamines (adrenaline, noradrenaline) mainly located in adrenals
Associated with MEN 2 VHL NF1

140
Q

Clinical features phaeo

A 
Hypertension 
Tachycardia 
Headaches 
Palpitations
Sweating 
Ischaemia 
End organ damage
141
Q

Preoperative assessment phaeo

A 
Check end organ damage ie LVH
BP control
Control of arrhythmias
Volume status 
Glycemic control 
Electrolytes
142
Q

Pre op treatments phaeo

A

Alpha block ie phenyoxybenzamine
B block ie propranolol
Sometimes calcium channel antagonists

143
Q

Intraoperative goals

A

Avoid hypertension ie arterial line, phentolamine, gtn

Prevent tachyarrythmias ie remifentanil esmolol

Hypotension post tumour removal fluids and vasopressors

144
Q

Post op complications phaeo

A

Significant hypotension
Persistent hypertension
Hypoglycaemia
Hypoadrenalism

145
Q

Cardiovascular features of autonomic neuropathy

A

Postural hypotension
Bradycardia
Resting tachycardia
Prolonged qtc

146
Q

Respiratory features of autonomic neuropathy

A

Blunted chemoreceptors response to hypoxia

Post operative hypoventation

147
Q

GI effects of autonomic neuropathy

A

Gastroparesis

Diarrhoea or constipation

148
Q

Endocrine effects of autonomic neuropathy

A

Abnormal thermoregulation

149
Q

Common causes of autonomic neuropathy

A 
Diabetes 
Gillian barre 
Alcohol 
Drug induced ie chemo 
Nutritional ie b12 
Autoimmune
150
Q

Anaesthetic considerations perioperatively autonomic neuropathy

A

Lability BP
Reflux
Abnormal temp control
Atelectasis and blunted response to hypoxia

151
Q

Positives of low flow anaesthesia

A

Cost
Environment
Humidification

152
Q

Negatives of low flow anaesthesia

A 
Exhausts soda lime quickly can mean rebreathe get
Potential for hypoxic mixture 
Accumulation toxic intermediates 
Less real time effects 
Doesn’t compensate for leaks
153
Q

Anaesthetic machine check

A

Self inflating bag present
Automatic manufacturers machine self check
Power supply - plugged in switched on battery
Supplies and suction- tug test, cylinder, hypoxic guard flow meters, flush, suction
Breathing system- 2 bag test, vaporisers, soda lime, common gas outlet
Ventilator - working
Scavenging - working
Monitors - working
Airway equipment

Recorded in patients notes

154
Q

2 bag test

A

Attach a test lung to patients end

Fresh gas flow 5lmin, ventilate, check unidirectional valves and system patent. Check apl by squeezing both bags

Turn on ventilator, turn off fgf
One each vaporiser in turn and make sure no loss in system

155
Q

Benefits HFNO2

A

Warmed humidified — secretion clearance

PEEP — prevention atelectasis and recruitment

High gas flow —oxygen reservoir, co2 washout

156
Q

Indications HFNO2

A 
Type 1 resp failure 
Awake fibreoptic intubation 
Apnoeic ventilation 
THRIVE 
Tubeless surgery 
Extubation 
Unable to tolerate FM 
High secretion load
157
Q

Contraindications to HFNO2

A 
Any contraindications to PEEP 
Basal skull fracture
Epistaxis 
Recent neurosurgery 
Facial injury 
Agitation 
Patient refusal
158
Q

Guidelines re pain fractured nof

A

Pain assessed on admission, 30 mins after analgesia and hourly until pain controlled then routinely throughout admission

Analgesia to allow for investigations and nursing care

Paracetamol 6 hourly

Avoid nsaids

Nerve block in ED and at some of surgery

159
Q

Causes of falls that may impact on anaesthesia

A 
Postural hypotension
Arrhythmias 
Infection 
Abnormal electrolytes 
Cognitive dysfunction 
Valvular heart disease
160
Q

Transfusion triggers in hip surgery

A

Less than 9

Less than10 if ischaemia heart disease

161
Q

Reasons for delay fractured nof

A

Have to be correctable

Ie k less than 2.8 or more than 6 
Na less than 120 or more than 150
Hb less than 8 
Reversible coagulaopathy 
Uncontrolled diabetes 
Untreated heart failure 
Chest infection with sepsis
162
Q

Risk factors for BCIS

A

Age
Male sex
Diuretics
Cardiopulmonary disease

Should consider uncenented prosthesis

163
Q

Surgical role to reduce risk bcis

A 
Tell anaesthetist when BC 
Wash and dry femeoral cabal 
Lavage clean and deep suction 
Retrograde cement 
Don’t use extra pressure
164
Q

Anaesthesia role BCIS

A

Hydrated before
Vigilance when surgeon states cementing
Aim map within 20%
Vasopressors and fluid

165
Q

GI and renal causes low magnesium

A

Diahhorea
Reduced dietary intake
Renal losses

166
Q

Pharma causes low magnesium

A

Diuretics
Ace I
Chemotherapy

167
Q

Patient factors associated low magnesium

A 
Age 
Type 2 diabetes 
Alcohol dependence 
Coeliac 
Crohns
168
Q

Cardiovascular effects low magnesium

A

Arrhythmias

High SVR

169
Q

Neuro effects low magnesium

A

Seizures

Myoclonus

170
Q

Non obs uses magnesium

A 
Asthma
Arrhythmias 
Pain
SAH 
Phaeos
Tetanus
171
Q

Management magnesium toxicity

A

Calcium gucomate 10% over 10mins

172
Q

Mechanism magnesium

A

Magnesium displaces calcium in synaptic endings reducing neuro transmitter transmission
Nmda antagonist
Magnesium blocks calcium = vasolidayikn of sm

173
Q

What is myotonic dystrophy

A

Multisystem
Progressive muscle weakness and myotonia
Autosomal dominant

174
Q

Perioperative concerns myotonic dystrophy

A 
Consent and capacity 
Avoiding nm blockade 
Bulbar weakness 
Reflux 
OSA 
Diabetes 
Cardiomyopathy 
Arrhythmias
175
Q

Pre op assessment myotonic dystrophy

A 
Functional assessment 
ECG 
ECHO 
Glucose and diabetes management 
Pacemaker
176
Q

Intraoperative management MD

A 
RSI with rocurinium 
Short acting agents ie remifentanil 
Opiate sparing 
Full reversal but care TOF 
Pacemaker management 
Glucose momitoring
Invasive monitoring ie arterial line 
Early extubation 
Hdu care
177
Q

Never event

A

Adverse safety incident that is serious largely preventable and of concern to public and Heath. Are providers

178
Q

Examples of never events in anaesthesia and icu

A 
Wrong site block 
Wrong strength midazolam 
IV admin of epidural medication 
Misplaced NG 
Miselevtion potassium solution 
Overdosed insulin due to abbreviations 
Unintentional connection of patient to flow meter

Suspended currently oesophageal intubation

179
Q

Risk factors OSA

A 
Male 
Smoker
Obesity 
Age over 50 
Neck circ over 40 
Alcohol 
Pregnancy 
Neuro muscular disease
180
Q

AHI levels

A

Apnoea or hyponoease more than ten seconds, more than 5 times in an hour

More than 5 mild
More than 15 moderate
More than 30 severe

181
Q

Stop bang

A

Snoring
Tired
Observed
Pressure ie hypertension

Bmi
Age over 50
Neck over 40
Gender male

Over 3 high risk

182
Q

Medical consequences OSA

A 
Hypertension 
Tachy Brady arrhythmia 
MI 
Pulmonary hypertension Simon 
CCF 
Mortality 
Endocrine ie glucose tolerance 
Raised cortisol and acth 
Dyslipidemia
183
Q

Management OSA

A

Prehabilitation, if severe and elective consider referral for sleep studies and 3 months CPAP prior

Difficult intubation

Regional where possible

Short acting agents

Opiate sparing analgesia

Extubation safe place awake

CPAP for recovery

Does patient need HDU

184
Q

Steroid 2020 guidelines for primary adrenal failure

A

100mg hydrocortisone on induction then immediately start 200mg over 24 hours

Start enteral feeding ASAP and change to double dose of normal steroid for 48 hours (up to a week)

This is the case for all surgery including regional and IVF egg retrieval.

Bowel procedures IV fluids and 100mg hydrocortisone

Dex is not ok for primary as no mineralocorticoid action

185
Q

Steroids 2020 guidelines for those on steroids

A

Steroids of more than 5 mg over 4 weeks duration

100mg hydrocortisone at induction then 200mg over 24 hours
Major intermediate labour and and c section

Resume enteral at normal dose if uncomplicated Otherwise double

Alternative dex 6-8mg will give cover for 24 hours (not for labour)

2mg/kg in children then infusion based on weight

186
Q

Steroid conversion

A

100mh hydrocortisone = 20mg pred = 1mg dex

187
Q

2020 hip fracture mamagement main guidance

A 
Anaesthesia integral to MDT 
Appropriately experiences anaesthetist and surgeon 
Facilitate surgery with 36 hours 
Agreed standards for hospital 
Involvement in pathways
188
Q

Hip fracture guidance re analgesia

A

Assessed for single shot in Ed then theatre if more than 6 hours
Femoral or FIB
USS may help
Continuous has nit been assessed

189
Q

Hip fracture guidance

Assessment scoring devices

A 
Nottingham rip fracture score 
(National hip database tool) 
Frailty score 
4 AT 
(NH risk)
190
Q

Hip fracture guidance 2020

Reasons for delay

A 
Na less than 120 more than 150 
K less than 2.8 more than 6 
Uncontrolled arrhythmia more than 120 
Hb less than 8 
Uncontrolled diabetes 
Uncontrolled left ventricular failure 
Chest infection with sepsis 
Reversible coagulopathy
191
Q

Transfusion triggers in hip fractures

A

Hb less than 9

Hb less than 10 if ischaemia heart disease or not mobilised on first day

192
Q

Post op pulmonary complications

A

Pulmonary abnormalities that lead to identifiable disease or dysfunction

Atelectasis 
Pneumonia 
Respiratory failure 
Pleural effusion
Pneumothorax 
Aspiration pneumonitis
193
Q

Patient risk factors for post op pulmonary complications

A 
Age over 60 
ASA 2
Functional dependence 
OSA (obesity actually isn’t risk factor in its,ef) 
Smoking 
Alcohol 
Pulmonary hypertension 
CCF 
COPD 
Albumin less than 30 
Hb less than 100 
Sats less than 90
194
Q

Anaesthesia risk factors for post op complications

A

Ga

Use nmb

195
Q

Surgical risk factors for post op pulmonary complications

A

More than 3 hours
Thoracic abdominal head and neck vascular
Emergency surgery

196
Q

Strategies to reduce risk post op pulmonary complications

A

Pre op
Smoking cessation
Resp disease optimised
Inspiratory muscle training

Intraoperative 
Lung protective ventilation 
Minimally invasive surgery 
Avoid NG where possible 
Short acting NMB 
Neurocial 
Goal directed fluid 
Post op
Early mobilisation 
Effective analgesia 
Lung expansion techniques 
Physio
197
Q

Diagnosis in myasthenia gravis

A

Clinical fatigue biliary

Anti achR and TFTs first
Anti musk
Anti LRP4

Neurophysiology - reduction in compound motor action potentials on repetitive stimulation
CT MRI

NOT EDROPHUM TEST

198
Q

Mamagement myasthenia

A

Symptomatic ie pyridostigmine

Immune suppression

Plasmapheresis or IVig

Thymectomy

199
Q

Assesment MG

A 
Preoperative optimal control 
Bulbar symptoms, previous crisis 
Consider prep IVg or pex if severe 
Keep meds going 
Extra steroids if on

Investigations inc FVC
Consider and discuss post op ventilation (risk factors, long disease bulbar symptoms, high doses pyridostigmine, vital capacity less than 2, high antibody titres)

Intraoperative 
Short acting 
Regional where possible 
Careful upper limb blocks and neuro axial as don’t want to lose accessory muscles or phrenic 
Short acting agents
TIVA is good
If need paralysis 1/10 roc and Suggamadex 
Sv for short, iPpv for long 
Emergence tof more than 0.95
200
Q

Drugs to avoid in myasethenia

A 
Aminoglycosides 
B blockers
Iodine contrast 
Magnesium 
Macrolides 
Statin
201
Q

Myasthenia crisis

A

Severe resp or bulbar weakness that requires intubation

Vc less than 20ml per kg

202
Q

Ch9linergic crisis

A

Rare, precipated by anticholinesterases ie neostigmine with pyridostimine
Bradycardia hypotension lacrimation sweating vomiting

203
Q

Pregnancy and MG

A

Optimise before conception
Epidural great
Care spinal if severe resp involvement or bulbar disease
Transient MG in neonate

Preeclampsia care with drugs
Use methylpred or hydralazine
Caution with magnesium

204
Q

Treatment acute adrenal insufficiency

A

Steroids 100mg the ph 200mg over 24 hours
Cautious spresus as may have had excess fluids
Do a random cortisol and when stable can consider short synacthen if borderline

205
Q

Treatment of thyroid storm

A 
Propylthiouravil or carbimazole 
Steroids 
B blockers for symptomatic relief 
Caution with fluids 
Temperature control

Plus or minus
Plasma exchange
Dialysis
Emergency thryoidectomy

206
Q

Management myoxedema coma

A

Often in women with low consciousness level and signs hypothyroidism

Tsh up, t3 t4 down ck up glucose down
Sinus bradycardia

Treat giving thyroxine
IV t3
Mechanical ventilation
Consider steroids

207
Q

Management pituitary apoplexy

A

Test all anterior pituitary hormones
Trigger hypertension drugs trauma

Can mimic sah so need CT or mri

Steroid replacement before thyroxine

208
Q

Presentation DI

A

High volumes urine over 3 l day
Dehydrated
Hypernatremia

Urine dilute so not many osm ie l3ss than 300

Plasma concentration ie many osm ie more than 300

Cranial vs neprhogenic vs pregnancy placenta related (vassopressinase)

209
Q

Acute hypercalcemia causes

A

Primary hyperparathyroidism and malignancy

Other bit d toxicity, thyroxicosis, lithium, tpn

210
Q

Signs of acute hypercalcemia

A

Above 3

Weakness fatigue abdominal pain thirst polyuria vomiting stones

Above 3.5 arrthymias

211
Q

Management hypercalcemia

A

Parathyroid

Fluids
Bisphosphinates

Dialysis
Urgent parathyroidectimy

212
Q

Cell salvage principles

A

Specific suction
Washing swabs IV saline in clean area

Processed via cebtrifuge
Separated in fixed or variable bowl

Washed in sodium chloride
Reinfused within 6 hours, flush lin3s before drugs ie paracetamol causes red cells to clump
Consider filters ie leukocyte depleting filters in cancer or malignancy

213
Q

Positives cell salvage

A 
Reduced requirement allogenjc blood 
Superior oxygen delivery 
Plasma explosion
Transfusion triggers irrelevant 
Moral option in some groups

? Reduced morbidity and length of stay

214
Q

Negatives cell salvage

A

Labour intensive
High costs
Reinfused hypotension
Time to process

215
Q

Contraindications to cell salvage

A

Refusal
Sickle cell

Care with suction 
Antibiotics not licences jv 
Iodine
Chlorhexidine 
Topics, clotting agents 
Fibrin glue Orthopaedic unset cement
216
Q

Iron deficiency

A

Ferritin less than 30

Or

Ferritin less than 100 with raised crp or tsats less than 20%

217
Q

Preoperative target haemoglobin

A

130 men and women (who says 120 women)

218
Q

How to replace iron

A

Oral iron if more than 6-8 weeks
(Delay if non urgent)
Low dose
Repeat test 4 weeks prior to surgery

IV iron if doesn’t respond, side effects or less than 6 weeks

219
Q

Iron deficiency without anaemia

A

May benefit from iron and should consider investigating cause

220
Q

What is hepcidin

A

Hepcidin regulates iron
Inhibits iron being released by cells into circulation and may prevent absorption

Hepcidin increased by 
High iron levels (hence why use low dose oral iron or may have counteract effect on hepcidin) 
Infection 
Inflammation 
Cancer

Hepcidin reduced by
Low stores
Anaemia
Hypoxia

221
Q

Goals anaesthesia laparotomy

A

Rapid secure of airway

Management of fluid and haemodynamic support

Protective lung ventilation

Analgesia a

Post operative care

222
Q

RAG indicators NELA

A

CT report before surgery
Risk death documented
Timing theatre appropriate
Consultant surgeon and anaesthetist when NELA more than 5%
Icu if risk of death more than 10%
Care by older person specialist over age 75

223
Q

National laparotomy pathway quality improvement care bundle (NLP QuIC)

A 
Early assessment and resuscitation 
Early antibiotics 
Early scan and surgery 
Goal directed therapy 
Icu all patients
224
Q

Frailty

A

Frailty is a state of increased vulnerability to poor resolution (not being able to recover) homeostasis after a stressor

225
Q

Frailty scores

A

Edmonton frailty score

Clinical frailty scale

226
Q

TEG

A

Point of care testing
360 micro blood into 2 heated cups. The cups have wire place in
Cups rotate 4degree 45 for ten seconds each direction
Increasing clot strength measured by torsion on wire

Kaolin to activate clotting

Different Reagants to take heparin out, test plate tests etc

R time 4-8 minutes is time for initiation until 2mm amplitude and is influenced by clotting factors

K 1-4 mins 2 to 20mm clot kinetics

A angle 47 to 74 degrees build up of fibrin and cross linking

MA maximum amplitude max clot strength - platelets and fibrinogen

CY30 and 60 clot stability

227
Q

Rotem

A

Rotem is point of care testing

300micro blood in corvette,
Heated 37 degrees
Pin and ball immersed, and rotates (corvette stays stationary)

Activated by tissue factor or contact factors

228
Q

Patient blood management aims

A

Clinical concept main aim to avoid unnecessary blood transfusions

229
Q

Pillars of patient blood management

A

)optimiseRed cell mass and erythropoiesis

2) minimise blood loss
3) manage post op anaemia

230
Q

Nice blood transfusion guidelines (all products)

A

Fe before and after
TXA
Cell salvage

Red blood cells 70-90gl post transfusion
Single transfusion only

Platetekts less than 10 and single

FFP only if bleeding and abnormal coagulation tests

PCC warfarin and bleeding or head injury

Cryo if fibrinogen less than 1, 2 pools

Safety

Consent and information

231
Q

Phaeo pre op

A

BP co tool and success
Volume status
End organ damage
Other syndromes ie calcium?

232
Q

Pre surgical treatment phaeo

A

Phenoxybenzamine 10mg long acting irreversible

B1 selective blockade

May consider specific a 1 antagonists ie doxazocin

233
Q

Tests for phaeo

A

Urinary vma and metenephrine

234
Q

Carcinoid

A

Enterochromaffin cells
Secrete serotonin Bradykinin histamine neurokinin dopamine prostaglandins

Originate from embryonic divisions of gut but can be bronchus to rectum and liver

Carcinoid symptoms if met or in liver

235
Q

Symptoms of carcinoid

A 
Flushing 
Diarrhoea 
Lacrimagiom 
Wheezing 
Hypo and hypertension
236
Q

Diagnosis carcinoid

A

Urinary 5 Hiaa

Ct

237
Q

Anaesthetic management carcinoid

A

Consider as a multi system disease
Dehydration anaemia electrolytes

CV history ie heart failure
Hormone release resulting in hypo and hypertension

238
Q

Treatment of carcinoid pre theatre

A

OCTREOTIDE (syndpnethetic somatostatin which reduced growth horomone and serotonin)
Can give further 50 mic boluses Intraoperative if issues

239
Q

Carcinoid Intraoperative mamagement

A

Epidural
Avoid BP variation
Avoid morphine and atracurium where possible due to histamine release
Invasive cardiac monitoring
Liver resection keep CVP low to prevent venous bleeding
Phenyleprhine dpvasopressor of choice

Hdu 48 hours post op

Final Written (12 decks)

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