General Flashcards
(239 cards)
1
Q
Myasthenia gravis are sensitive to depolarising NMB
A
MG resistant to suxamethonium (double dose)
2
Q
TNF is associated with
A
Cytokine
Poor outcome
3
Q
Extradural space may contain
A
Fat Spinal nerve roots Lymphatic Connective tissue Batsons plexus Spinal arteries Epidural venous plexus
4
Q
ECT current
A
30-45 Up to 100j
5
Q
Autonomic response to ECT
A
Initial parasympathetic response ie bradycardia hypotension sometimes asystole
Followed by sympathetic response hypertension and tachycardia
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.
7
Q
Complain when greater with water or air
A
Water (liquid) - more pressure needed to distend lung with air than liquid
8
Q
Compliance is greatest at FRC or TLC
A
FRC
TLC is top of pressure volume curve so little compliance
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
10
Q
Where does sympathetic outflow arise
A
T1-L2 (sympathetic chain runs parallel to spinal column)
11
Q
Where does parasympathetic outflow arise
A
Cranial sacral
12
Q
Which cranial never have parasympathetic nuclei
A
III, VII, IX, X
13
Q
Where is larynx located
A
Anterior neck, level c4-c6
14
Q
Narrowest part of larynx adults vs infants
A
Adults glottis
Infants cricoid
15
Q
Recurrent laryngeal nerve innervates what intrinsic muscles
A
All except cricothyroid
16
Q
Sensory inner action larynx
A
Superior laryngeal never above cords
Recurrent laryngeal nerve below cords
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
18
Q
Do thiazides cause hyperglycemia
A
Yes possibly by insulin resistance
19
Q
Lumbar plexus roots
A
L1-4 sometimes with t12 and l5 input
20
Q
Lumbar plexus nerves
A
Femoral Obturator Ilioinguinal Iliofemoral Lateral cutaneous Genitofemoral
21
Q
Tributaries of internal jugular vein
A
Medical school lets fun people in
Middle thyroid Superior thyroid Lingual Facial Pharyngeal Inferior petrosal
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
23
Q
Genetics of malignant hyperthermia
A
Malignant hyperthermia is autosomal dominant
Error in RyR1 (Ryanodine receptor) on chromosome 19
24
Q
Early signs of MH
A
Increase in co2
Increase in heart rate and oxygen consumption
Late sign is high temp
25
Mortality of MH
5% with introduction of dantrolene
26
What is cause of renal failure in ALF
Acute tubular necrosis
27
Association of chronic pain with
depression
Anxiety
Depression 30-40%
| Anxiety 25%
28
What opiods can you do skin prick testing in
Fentanyl and remifentanil
Morphine codeine and diamorphine have significant direct mast cell degranulation without Ige so skin prick testing not appropriate
29
Mast cell tryptase measurements and why
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
30
What apart from anaphylaxis can cause raised mast cell tryptase
Typtase may be raised in mastocytosis, aml, myelodysplastic syndromes
31
What effect do volatiles have on venous admixture
Venous admixture is the lowering of arterial po2 from ideal level due to shunt. Volatiles impair HPV therefore increase venous admixture
32
Where is bilirubin produced
Bilirubin is produced in reticuloendothelial system in the spleen, bone marrow and hepatic kipper cells
Bilirubin is produced by macrophages by reduction of biliverdin
33
How is bilirubin transported to the liver
Bilirubin is bound to albumin as its insoluble
Conjugation makes bilirubin soluble
34
What is the concentration of intralipid
20%
35
What is the dose of intralipid on initial dose
1.5ml/kg
36
What is ongoing treatment with intralipid in LAST
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
37
Maximum dose of intralipid
12ml/kg
38
How does plasma site vary from effect site
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
39
Discuss marsh model for TCI
Marsh is based on weight
Safest to use in Cp as uses very large bolus in ce initially
Best for young people
40
Discuss Schneider model TCI
Snider uses age and lean weight (sex adjusted)
Always use in Ce
Beneficial in elderly
Smaller bolus doses
41
How can you minimise awareness in TIVA
```
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
```
42
Define aspiration
Inhalation of material below true cords
Commonly quoted 25ml and ph less than 7.2 comes from studies on monkeys extrapolated to humans
43
Kidneys cardiac output
25%
44
Kidneys glomerular filtrate volume
180l day
| 70 percent reabsorbed by pct
45
Renal perfusion ml/min/100g
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
46
What matching required for cadeveric renal donors
Size, blood group and MHC complex
47
Side effects of ciclosporin
Ciclosporin causes hypertension, tremor, reduced egfr, encephalopathy
48
Why was glycine used for TURP
Doesn’t conduct electricity
TURP syndrome glycine level over 60mmol/l
49
TURP how high doe you need block
T9
50
Sickle cell genetics
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
51
Genetics of thalassemia
Group of heridatory anaemia causes by ineffective a or B chain formation.
Heterozygotes mild anaemia
Homozygotes severe
May be compensatory extramedullary haematopoesis
52
Diagnosis sickle cell
Sickledex but cannot distinguish between sickle trait and sickle cell
Blood film
Haemaglobin electrophoresis
53
Presentations of sickle cell
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
54
Treatment sickle cell
Patient education re hydration, exercise, alcohol
Vaccinations
Folic acid
Hydroxyurea (increases fetal hb)
Acute
Analgesia
Rehydration
Remember acute abdomen differential is sickle cell
55
Sickle cell requiring op considerations
Pre op tests assessing organ dysfunction
Rehydrated
Hb and transfusion
Avoid adrenaline in Local
Positioning to avoid venous stasis
Tourniquets must be justified
Analgesia
56
Thalasseemia pre op considerations
Consider if could have sickle cell too
Haematocrit
Splenomegaly and thrombocytopenia
Facial changes and frontal bossing
57
Drugs with potential anti carcinogenic effects
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 )
58
Drugs with potential pro carcinogenic effects
```
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
```
59
Surgical indications for TIVA
```
Cancer surgery
Tubeless ent or thoracic surgery
Neurosurgery
Surgery requiring neuromuscular monitoring ie scoliosis
Day case surgery
Non theatre environment
```
60
Patent indications TIVA
```
MH
PONV
Long QT
Patient choice
NM issues ie MG
Anticipated difficult intubation or extubation
```
61
Checklist TCI systems
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
62
Recommendations to prevent technical problems with TIVA
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
63
Potential problems with tiva
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)
64
Nap 1
Supervisory role of consultant anaesthetists
65
Nap 2
Place of M&M meetings
66
Nap 3
Complications of central neuroaxial block in the uk
67
Nap 4
Major complications of airway management in the uk
68
Nap5
Accidental awareness during GA
69
Nap 6
Perioperstuve anaphylaxis
70
Nap7
Perioperative cardiac arrest
71
Why choice of agents in tiva
Remi and propofol synergistic effect
Short CSHT
Predictable pharmacological profile
72
When does propofol reach steady state concentration
20 hours
When all 3 compartments reach steady state concentration,
TCI matches elimination (k10)
73
Key components of TCI
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
74
Marsh model fixed variable parameters and parameter determined by
Marsh model fixed rate constant
Variable v123
Parameter determined by weight
75
Schneider model fixed variable parameter and determined by parameter
Fixed in Schneider v1 v3 k13 and k31
Variable in Schneider V2
Parameter determined by age, weight, lean body mass
76
Minto model fixed and variable parameters and parameter determined by
Minto model v3 fixed
V1 v2 and rate constants variable
Model determined by weight and lean body mass
77
Stress response to surgery two broad categories
Neuroendocrine metabolic response
Inflammatory immune response
78
Surgery with largest stress response
Major open vascular and abdominal
| Joint replacement cardiac on CPB
79
Describe neuroendocrine metabolic stress response to surgery
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
80
Describe inflammatory immune stress response to surgery
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
81
Ways to modulate stress response to surgery
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
82
Glucocorticoids and surgical stress response
Varied literature
Reduced CRP and IL6
Reduced post op ventilation, hyperthermia, infection and ,engage of stay
Caution in diabetes s
83
Define gbs and name subtypes
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
```
84
GBS signs
```
Motor difficulty / paralysis
Loss deep tension reflexes
Paraesthesia without sensory loss
Muscle wasting
Urinary retention
Ptosis
Autonomic
Speech problems
Respiratory distress
```
85
Investigations in gbs
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
86
Treatment GBS
```
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%
87
Indications intubation in GBS
V1c less than 20
max inspiratory pressure of less than 30
Max exp pressure of more than 40
Decreased more than 30% of above
88
One MET
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
89
Contraindications to CPET
```
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
```
90
CPET timings
3 mins baseline
1-3mins unloaded
Increasing resistance
Full monitoring for ten mins cessation of exercise
91
CPET measurements
```
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
92
9 panel plot
Graphical representation of CPET is called 9 panel plot
235 cardiovascular
147 ventilation
689 Ventilation perfusion
93
Vo2 max
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
94
Anaerobic threshold
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
95
Safe AT and VO2 peak for surgery
At 11ml/kg/min
| Vo2 peak 30
96
Functional walk test
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
Innervation of knee
```
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
Independent predictors severe post op pain knee arthoplasty
Young age
Pre op pain
Depression
99
Cause of pain in knee surgery
Prostaglandins and bradykinin realised at site of injury
| Nociecotive fibres travel STT (nmda receptors)
100
Prep knee surgery
Joint school
| Preemptive analgesia nsaids good evidence, gabapentin unclear
101
RA for knee arthoplasty
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
Adjuncts in knee surgery
Dexamethasone reduces acute phase reactants such as CRP and IL6
Avoid knee haematoma with TXA
103
Post op pain management knee surgery
```
Multimodal
PCA
Continuous LA infusion ie elastomeric
Gabapentin?
Cryocuff
```
104
Types of cognitive impairment after surgery
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
Cognitive domains evaluated in NCD
```
Learning and memory (learn and recall new infor)
Language
Perceptual motor
Social cognition
Complex attention
Executive function (planning)
Delirium
```
106
Delirium
Fluctuating changes in attention, consciousness and cognitive f7nctuin within hours or days of event
Hypo or hyperactive
107
Post operative cognitive dysfunction
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
Tools to diagnose POCD
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
Cause of POCD
Unclear
? Neuronal death neuroinflammation and micro emboli
? Anticholinergic pathways
110
Patient Risk factors POCD
```
Age
Lower education level
History of cerebrovascular accident
Preoperative mild cognitive impairment
Cognitive dysfunction at discharge
```
111
Anaesthetic risk factors for POCD
```
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
Drug reactions A to E
```
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
Sickle cell genetics
Sickle cell inherited haemoglobinopathy
Mutation on chromosome 11
Results in glutamate for valine at position 6 on beta chain
114
Physiological factors promoting sickling in sickle cell disease
```
Hypoxia
Hypothermia
Pain
Dehydration
Infection
```
115
Sickle dex test Reagent and limitations
Reagan’s is sodium metabisulphate
| Test doesn’t differentiate between trait and disease
116
Parameters for exchange transfusion in sickle cell
Hb 10
Hb a more than 70%
Hb s more than 30%
117
Long term complications of sickle cell
```
Vasoocllusive sequels ie ulcers
Haemolytic anaemia
Functional asplenism
Cardiomegaly
Chronic pain
Bone marrow failure
Hypertrophic of lymphoid tissue
```
118
Cystic fibrosis genetics
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
Respiratory pathogens in CF
Pseudomonas spp
Staph aureus
Haemophilus influenzae
Burkholderia cepacia
120
Non respiratory manifestations of CF
Malabsorption
Diabetes
Infertility
Nasal polyps
121
Preooptimise CF
```
Pre optimise CF
Physio
Nutrition
Mucolytics and nebulisers
Protective isolation
Prophylactic antibiotics
```
122
Tailor GA for CF
```
Consider carefully re intubation - do you need suction facilitaton of ETT
Lung protective strategies
Good analgesia deep breathing
Opiate sparing
Ensure adequate reversal
```
123
Mechanism of action of antiemetics
```
Dex
Ondansetron
Metoclopramide
Cyclizine
Droperidol
Aprepitant
Scopolamine
Midazolam
```
```
Dex is steroid
Ondansetron 5ht3 antagonist
Cyclizine histamine 1 antangonist
Metaclopramide dopamine antagonist
Droperidol dopamine antagonist
Apprepitant neurokinin antagonist
Scopolamine anticholinergic
Midazolam benzo
```
124
Adult PONV scoring system
Apfel
Provoc in children
125
Causes of secondar6 hypertension
```
Phaeo
Conns syndrome
Renal artery stenosis
Endocrine disorder ie Cushing hypo and hyperthyroidism
PCKD
Diabetic nephropathy
Cv causes like coactation
```
126
End organ effects hypertension
Cardiac LVH
Renal ESRF
Optahlmic hypertensive retinopathy
Neuro cva hypertensive encephalopathy
127
Aagbi guidance for BP for elective surgery
Primary care BP less than 160/100
Secondary care ie pre op less than 180/110
128
Hypertensive treatment algorithm step1 - over 55 or afrocaribean
Calcium channel blocker
129
Hypertension treatment algorithm under 55 or diabetes
Ace I
130
Second line treatment hypertension
Ace I or calcium channel whatever not on yet
| Thiazides diuretic
131
Third line hypertension
ACD all 3
132
4th line hypertension
Seen in tertiary care
| Spiro or a blocker
133
Perioperative complications hypertension
```
Labilecardiovascular
Relative hypovolemia
Exaggerated response to press or
Post operative cognitive dysfunction
Cardiovascular events ie mi
```
134
Define carcinoid syndrome
Carcinoid is a syndrome caused by release of serotonin histamine bradykinin prostaglandins by a slow growin* neuro endocrine tumour
135
What is serotonin
Monoamine neurotransmitter
136
Signs and symptoms of carcinoid
Symptoms flushing sob diarrhoea nausea
Signs bronchospasm sweating hypertension
137
Treatment carcinoid
Symptom control with serotonin receptors antangknists ie ondansetron
Somatostatin analogues ie octreotide
Surgical excision tumour
138
What pharm agents can manipulate serotonin
SSRIS
MAOI
Antiemetics
Sumatriptan
139
What are phaechromocytomas and what diseases are they associated with
Functionally active tumours secreting catecholamines (adrenaline, noradrenaline) mainly located in adrenals
Associated with MEN 2 VHL NF1
140
Clinical features phaeo
```
Hypertension
Tachycardia
Headaches
Palpitations
Sweating
Ischaemia
End organ damage
```
141
Preoperative assessment phaeo
```
Check end organ damage ie LVH
BP control
Control of arrhythmias
Volume status
Glycemic control
Electrolytes
```
142
Pre op treatments phaeo
Alpha block ie phenyoxybenzamine
B block ie propranolol
Sometimes calcium channel antagonists
143
Intraoperative goals
Avoid hypertension ie arterial line, phentolamine, gtn
Prevent tachyarrythmias ie remifentanil esmolol
Hypotension post tumour removal fluids and vasopressors
144
Post op complications phaeo
Significant hypotension
Persistent hypertension
Hypoglycaemia
Hypoadrenalism
145
Cardiovascular features of autonomic neuropathy
Postural hypotension
Bradycardia
Resting tachycardia
Prolonged qtc
146
Respiratory features of autonomic neuropathy
Blunted chemoreceptors response to hypoxia
| Post operative hypoventation
147
GI effects of autonomic neuropathy
Gastroparesis
| Diarrhoea or constipation
148
Endocrine effects of autonomic neuropathy
Abnormal thermoregulation
149
Common causes of autonomic neuropathy
```
Diabetes
Gillian barre
Alcohol
Drug induced ie chemo
Nutritional ie b12
Autoimmune
```
150
Anaesthetic considerations perioperatively autonomic neuropathy
Lability BP
Reflux
Abnormal temp control
Atelectasis and blunted response to hypoxia
151
Positives of low flow anaesthesia
Cost
Environment
Humidification
152
Negatives of low flow anaesthesia
```
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
Anaesthetic machine check
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
2 bag test
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
Benefits HFNO2
Warmed humidified — secretion clearance
PEEP — prevention atelectasis and recruitment
High gas flow —oxygen reservoir, co2 washout
156
Indications HFNO2
```
Type 1 resp failure
Awake fibreoptic intubation
Apnoeic ventilation
THRIVE
Tubeless surgery
Extubation
Unable to tolerate FM
High secretion load
```
157
Contraindications to HFNO2
```
Any contraindications to PEEP
Basal skull fracture
Epistaxis
Recent neurosurgery
Facial injury
Agitation
Patient refusal
```
158
Guidelines re pain fractured nof
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
Causes of falls that may impact on anaesthesia
```
Postural hypotension
Arrhythmias
Infection
Abnormal electrolytes
Cognitive dysfunction
Valvular heart disease
```
160
Transfusion triggers in hip surgery
Less than 9
Less than10 if ischaemia heart disease
161
Reasons for delay fractured nof
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
Risk factors for BCIS
Age
Male sex
Diuretics
Cardiopulmonary disease
Should consider uncenented prosthesis
163
Surgical role to reduce risk bcis
```
Tell anaesthetist when BC
Wash and dry femeoral cabal
Lavage clean and deep suction
Retrograde cement
Don’t use extra pressure
```
164
Anaesthesia role BCIS
Hydrated before
Vigilance when surgeon states cementing
Aim map within 20%
Vasopressors and fluid
165
GI and renal causes low magnesium
Diahhorea
Reduced dietary intake
Renal losses
166
Pharma causes low magnesium
Diuretics
Ace I
Chemotherapy
167
Patient factors associated low magnesium
```
Age
Type 2 diabetes
Alcohol dependence
Coeliac
Crohns
```
168
Cardiovascular effects low magnesium
Arrhythmias
| High SVR
169
Neuro effects low magnesium
Seizures
| Myoclonus
170
Non obs uses magnesium
```
Asthma
Arrhythmias
Pain
SAH
Phaeos
Tetanus
```
171
Management magnesium toxicity
Calcium gucomate 10% over 10mins
172
Mechanism magnesium
Magnesium displaces calcium in synaptic endings reducing neuro transmitter transmission
Nmda antagonist
Magnesium blocks calcium = vasolidayikn of sm
173
What is myotonic dystrophy
Multisystem
Progressive muscle weakness and myotonia
Autosomal dominant
174
Perioperative concerns myotonic dystrophy
```
Consent and capacity
Avoiding nm blockade
Bulbar weakness
Reflux
OSA
Diabetes
Cardiomyopathy
Arrhythmias
```
175
Pre op assessment myotonic dystrophy
```
Functional assessment
ECG
ECHO
Glucose and diabetes management
Pacemaker
```
176
Intraoperative management MD
```
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
Never event
Adverse safety incident that is serious largely preventable and of concern to public and Heath. Are providers
178
Examples of never events in anaesthesia and icu
```
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
Risk factors OSA
```
Male
Smoker
Obesity
Age over 50
Neck circ over 40
Alcohol
Pregnancy
Neuro muscular disease
```
180
AHI levels
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
Stop bang
Snoring
Tired
Observed
Pressure ie hypertension
Bmi
Age over 50
Neck over 40
Gender male
Over 3 high risk
182
Medical consequences OSA
```
Hypertension
Tachy Brady arrhythmia
MI
Pulmonary hypertension Simon
CCF
Mortality
Endocrine ie glucose tolerance
Raised cortisol and acth
Dyslipidemia
```
183
Management OSA
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
Steroid 2020 guidelines for primary adrenal failure
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
Steroids 2020 guidelines for those on steroids
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
Steroid conversion
100mh hydrocortisone = 20mg pred = 1mg dex
187
2020 hip fracture mamagement main guidance
```
Anaesthesia integral to MDT
Appropriately experiences anaesthetist and surgeon
Facilitate surgery with 36 hours
Agreed standards for hospital
Involvement in pathways
```
188
Hip fracture guidance re analgesia
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
Hip fracture guidance
Assessment scoring devices
```
Nottingham rip fracture score
(National hip database tool)
Frailty score
4 AT
(NH risk)
```
190
Hip fracture guidance 2020
Reasons for delay
```
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
Transfusion triggers in hip fractures
Hb less than 9
Hb less than 10 if ischaemia heart disease or not mobilised on first day
192
Post op pulmonary complications
Pulmonary abnormalities that lead to identifiable disease or dysfunction
```
Atelectasis
Pneumonia
Respiratory failure
Pleural effusion
Pneumothorax
Aspiration pneumonitis
```
193
Patient risk factors for post op pulmonary complications
```
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
Anaesthesia risk factors for post op complications
Ga
| Use nmb
195
Surgical risk factors for post op pulmonary complications
More than 3 hours
Thoracic abdominal head and neck vascular
Emergency surgery
196
Strategies to reduce risk post op pulmonary complications
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
Diagnosis in myasthenia gravis
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
Mamagement myasthenia
Symptomatic ie pyridostigmine
Immune suppression
Plasmapheresis or IVig
Thymectomy
199
Assesment MG
```
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
Drugs to avoid in myasethenia
```
Aminoglycosides
B blockers
Iodine contrast
Magnesium
Macrolides
Statin
```
201
Myasthenia crisis
Severe resp or bulbar weakness that requires intubation
Vc less than 20ml per kg
202
Ch9linergic crisis
Rare, precipated by anticholinesterases ie neostigmine with pyridostimine
Bradycardia hypotension lacrimation sweating vomiting
203
Pregnancy and MG
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
Treatment acute adrenal insufficiency
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
Treatment of thyroid storm
```
Propylthiouravil or carbimazole
Steroids
B blockers for symptomatic relief
Caution with fluids
Temperature control
```
Plus or minus
Plasma exchange
Dialysis
Emergency thryoidectomy
206
Management myoxedema coma
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
Management pituitary apoplexy
Test all anterior pituitary hormones
Trigger hypertension drugs trauma
Can mimic sah so need CT or mri
Steroid replacement before thyroxine
208
Presentation DI
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
Acute hypercalcemia causes
Primary hyperparathyroidism and malignancy
| Other bit d toxicity, thyroxicosis, lithium, tpn
210
Signs of acute hypercalcemia
Above 3
Weakness fatigue abdominal pain thirst polyuria vomiting stones
Above 3.5 arrthymias
211
Management hypercalcemia
Parathyroid
Fluids
Bisphosphinates
Dialysis
Urgent parathyroidectimy
212
Cell salvage principles
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
Positives cell salvage
```
Reduced requirement allogenjc blood
Superior oxygen delivery
Plasma explosion
Transfusion triggers irrelevant
Moral option in some groups
```
? Reduced morbidity and length of stay
214
Negatives cell salvage
Labour intensive
High costs
Reinfused hypotension
Time to process
215
Contraindications to cell salvage
Refusal
Sickle cell
```
Care with suction
Antibiotics not licences jv
Iodine
Chlorhexidine
Topics, clotting agents
Fibrin glue Orthopaedic unset cement
```
216
Iron deficiency
Ferritin less than 30
Or
Ferritin less than 100 with raised crp or tsats less than 20%
217
Preoperative target haemoglobin
130 men and women (who says 120 women)
218
How to replace iron
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
Iron deficiency without anaemia
May benefit from iron and should consider investigating cause
220
What is hepcidin
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
Goals anaesthesia laparotomy
Rapid secure of airway
Management of fluid and haemodynamic support
Protective lung ventilation
Analgesia a
Post operative care
222
RAG indicators NELA
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
National laparotomy pathway quality improvement care bundle (NLP QuIC)
```
Early assessment and resuscitation
Early antibiotics
Early scan and surgery
Goal directed therapy
Icu all patients
```
224
Frailty
Frailty is a state of increased vulnerability to poor resolution (not being able to recover) homeostasis after a stressor
225
Frailty scores
Edmonton frailty score
Clinical frailty scale
226
TEG
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
Rotem
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
Patient blood management aims
Clinical concept main aim to avoid unnecessary blood transfusions
229
Pillars of patient blood management
)optimiseRed cell mass and erythropoiesis
2) minimise blood loss
3) manage post op anaemia
230
Nice blood transfusion guidelines (all products)
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
Phaeo pre op
BP co tool and success
Volume status
End organ damage
Other syndromes ie calcium?
232
Pre surgical treatment phaeo
Phenoxybenzamine 10mg long acting irreversible
B1 selective blockade
May consider specific a 1 antagonists ie doxazocin
233
Tests for phaeo
Urinary vma and metenephrine
234
Carcinoid
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
Symptoms of carcinoid
```
Flushing
Diarrhoea
Lacrimagiom
Wheezing
Hypo and hypertension
```
236
Diagnosis carcinoid
Urinary 5 Hiaa
Ct
237
Anaesthetic management carcinoid
Consider as a multi system disease
Dehydration anaemia electrolytes
CV history ie heart failure
Hormone release resulting in hypo and hypertension
238
Treatment of carcinoid pre theatre
OCTREOTIDE (syndpnethetic somatostatin which reduced growth horomone and serotonin)
Can give further 50 mic boluses Intraoperative if issues
239
Carcinoid Intraoperative mamagement
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
