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Part 2 exam > General Periop > Flashcards

General Periop Flashcards

1
Q

What is Marfan’s syndrome?

A

Autosomal dominant, multisystem connective tissue disease

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2
Q

What are the symptoms of marfan’s syndrome?

A

Subluxation
Dislocation of joints
Dilated aorta
Valvular heart disease
Pneumothorax
Reduced exercise tolerance

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3
Q

What are the anaesthetic implications of marfan’s syndrome?

A
  • Cardiac disease i.e aortic dilation, valvular disease (MR or AR), heart failure, conduction abnormalities
  • Pulmonary hypertension and its effects
  • Can have restrictive lung disease due to kyphoscoliosis
  • Can get pneumothorax secondary to emphesema, bronchogenic cysts, therefore need lung protection ventilation
  • May be difficult airways due to physical characteristics
  • Need haemodynamic control during intubation, pneumoperitoneum and extubation
  • Proper positioning due to risk of dislocation including TMJ during laryngoscopy!
  • Full/fast/forward if MVP/MR/AR (maintain preload, avoid bradycardia, reduced afterload)
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4
Q

What investigations are you interested in for Marfan’s syndrome?

A
  • ECG - bundle branch block
  • TTE - MV prolapse, MR, TV prolapse, AR, dilation of aortic root
  • CXR - pneumothorax, cardiolomeagly, pulmonary oedema
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5
Q

What is autonomic dysreflexia?

A
  • Medical emergency characterised by uncontrolled sympathetic response due to a precipitant
  • Occurs in up to 90% of patients with spinal cord injury at T6 or above
  • Occurs weeks to ~1 year after injury but can continue after this
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6
Q

What are the triggers of autonomic dysreflexia?

A
  • Bladder distention
  • Bowel - distension, constipation, fissures
  • Other - Surgical stimulation, skin infection
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7
Q

What is the pathophysiology of autonomic dysreflexia?

A
  • Stimulus below level of lesion
  • Afferent impulses transmitted to spinal cord but unable to pass level of injury
  • Sympathetic reflex below level of injury which causes vasoconstriction and hypertension
  • Detected by baroreceptors –> bradycardia, but nil parasympathetic stimulation can get down further so unopposed sympathetic activation
  • Above level of lesion will get parasympathetic stimulation (flushing, sweating)
  • Often presents with headaches
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8
Q

What are the clinical features of malignant hyperthermia?

A

Early: - prolonged masseter spasm after sux, raised EtCO2, unexplained tachypnoea or hyxpoxia, unexplained tachycardia/arrhythma

Developing: - hyperthermia (increased 0.5 degrees q15min)
- progressive resp then metabolic acidosis
- Hyperkalaemia
- Diaphoresis
- Haemodynamic instability
- Desaturation
- Generalised muscle rigidity

Late:

  • Cola colour urine
  • Rhabdomyolysis
  • Increased CK
  • Coagulopathy
  • Cardiac arrest
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9
Q

What is the immediate managment of malignant hyperthermia?

A
  • Call for help and get MH box
  • 100% O2 and high flows
  • High MV
  • Cease volatile change to TIVA
  • Give dantrolene 2.5mg/kg, then 1mg/kg Q10-15min
  • Active cooling
  • Gain IV access and adequate monitoring (CVC/IDC/Art line if available people)
  • Treat hyperkaelamia (calcium, insulin/dextrose)
  • Seek out adequate amount of dantrolene
  • Treat arrhythmias
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10
Q

How much dantrolene should a hospital have?

A

24 vials on site
Remote 36 vials

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11
Q

What is the immediate post anaphylaxis management?

A
  • Disposition - finish surgery vs cancel, ?post op disposition
  • Further treatement - IV steroids, oral antihistamines
  • Investigations - serial mast cell tryptase collected at 1,4,24 hrs
  • MCT >50mcg/L = anaphylaxis
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12
Q

What is the longer term post anaphylaxis management?

A
  • refer for allergy testing, usually 4-6 weeks post to allow mast cells to replenish histamine
  • letter for patient (3 copies, 1 for patient, 1 for GP 1 for medical records
  • Event reporting (eg WebAIRS and M+M meeting)
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13
Q

What is the pathophysiology of fat embolism syndrome?

A
  • Causes systemic (ARDS, coagulopathy) and localised effects (eg petechiae)
  • Biochemical theory: Fat breaks down into toxic intermediates eg Free fatty acids, causes ARDS, release of cytokines
  • Mechanical theory: causes pulmonary vascular occlusion as well as systemic occlusion if gets across
  • Presents with hypoxia/neurological/rash
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14
Q

What are the clinical features of serotonin syndrome?

A

Triad:
-Changes in mental status: Restlessness, agitation, seizures, confusion, delayed emergence
- Neuromuscular abnormalities: Myoclonus, hyperreflexia, shivering, tremor, rigidity, nystasgmus
- Autonomic hyperactivity: Diaphoresis, diarrhoea, temp >38, severe haemodynamic fluctuations (hypertension, tachycardia)

  • Sudden onset within 24-48hrs of expsosure to triggering agent
  • Hunter’s criteria is used for diagnosis
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15
Q

What are the risk factors for serotonin syndrome?

A

Patient:
○ Pt taking drugs that increase serotonin activity eg SSRIs, MAOi, TCA, tramadol
○ Recent changes to dosing or initiations of these drugs

Surgical:
○ Administration of methylene blue (has some MAO inhibition - MAO metabolises serotonin)

Anaesthetic:
○ Fentanyl (agonist for Serotonin receptors)
○ Use of tramadol

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16
Q

What is the management of serotonin syndrome?

A

○ Cease serotonergic agents
○ Monitor in high dependency area
○ Supportive management
- Agitation management eg benzodiazepines
- Seizure management
- Cooling if needed
- BP control (usually short acting beta blockers such as esmolol, GTN - avoid hydralazine is a MAOi)

○ Cyproheptadine is a serotonin antagonist used in severe cases
○ Dexmedetomidine inhibits serotonin release, is sedating and stablises haemodynamics

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17
Q

What is the diagnosis triad of DKA?

A
  • Ketones >3mmol/L
  • Blood glucose > 11
  • Bicarb <15 or pH <7.3
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18
Q

What are the causes of DKA?

A
  • Underlying infection
  • Missed insulin treatment
  • First presentation of Diabetes
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19
Q

What is the initial management of DKA?

A
  • ABC approach
  • Goals:
  • Fluid resuscitation: Aggressive crystalloid resus (1L over first hour, then 500ml/hr for 4hrs, then 250ml/hr for 4 hrs)
  • Insulin administration: fixed weight rate infusion of actrapid 0.1unit/kg/hr (make up 50 units in 50mls then run 1ml/hr for every 10kg) until pH >7.3, bicarb >15, ketones <0.6
  • Electrolyte management: Potassium may be high/low/normal initially but there is a total body deficit (due to exchange with H+ which is taken into the cell and potassium exchanged out)
    ○ Initial bag doesn’t need potassium, but provided K <5.5 and urine is being produced, 40mmol/L of potassium should be in subsequent potassium
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20
Q

What are risk factors for peri-operative stroke?

A

-Patient:
Age >70
female
comorbidities eg HTN/diabetes/smoking/PVD/IHD/AF/malignancy
Previous stroke
Carotid stenosis

-Surgical:
Type of surgery (cardiac, CEA, vascular)
Emeregency surgery
Long surgery
Long bone #

-Anaesthetic:
Haemodynamic instability
Hypoglycaemia
Beach chair positioning

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21
Q

What are the measures to minimise perioperative stroke?

A
  • Risk stratification and modification: delay surgery if recent stroke, treatment of carotid disease before procedure, anticoagulant/antiplatelet meds
  • DVT/VTE prophylaxis eg LMWH, calf compressors
  • Regional if possible
  • If GA maintain normal haemodynamics and glycaemia, normal CO2
  • Careful patient positioning and monitoring of BP in beach chair
  • Neurological monitoring eg EEG
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22
Q

What are issues associated with prolonged procedures/anaesthesia?

A
  • Positoning - pressure care, nerve palsies
  • Monitoring - need for art line, IDC, temperature
  • Equipment - ETT, multiple cannulas, Calf compresison
  • Physiological - temperature homeostasis, temp management
  • Staff safety - maintaining vigilance, managing fatigue, handovers between staff
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23
Q

What are periop issues with bariatric patients?

A

A - Difficult BMV, can be difficult intubation (not always), increased asp risk if reflux or previous baritric surgery

B - Quickly desats - due to reduced FRC, higher ventilation pressures due to decreased chest wall compliance, Post op resp failure - increased risk of OSA, OHV, atelectasis, poor mobilisation

C - Increased ventricular work (increased blood volume, increased cardiac output), risk of comorbidities, practical issues i.e vascular access, NIBP monitoring

D - Drug dosing ideal vs lean, vs adjusted vs total

E - Positioning if diffiicult, risk of patient sliding in steep positions

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24
Q

How do you manage agitation/confusion in PACU?

A
  • Keep patient and staff safe first
  • A - ensure patent
  • B - treat hypoxia, treat hypercarbia i.e naloxone, flumanzenil, ensure reversed completely, rule out APO
  • C - treat hypo/hyper, treat arrhythmia, treat ischaemia, check electrolytes with bloods
  • D - check GCS and pupils, exlcude ICH, delirium, hypoglycaemia, Hyponatraemia, hypothermia
  • E - Check bladder distension (IDC not draining)
  • F - check analgesia ?pain

Other rarer causes:
- Stroke
- Post ictal
- TURP syndrome
- Medication side effects eg ketamine

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25
Q

What issues do you consider when anaesthetising someone with multiple sclerosis?

A
  • Local anaesthetics may exaccerbate symptoms due to increased sensitivity to local anaesthetic toxicity
  • Non-depolarizing NMB safe
  • Caution with sux if debalitated (Hyperkalamia risk)
  • Maintain normothermia as heat my trigger sx
  • If severe they may have pseudobulbar palsies or swallowing difficulties/high aspiration risk
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26
Q

What issues do you consider when anaesthetising someone with motor neurone disease?

A
  • loss of innervation leads to extra-junctional ACho receptors
  • avoid sux
  • reduce dose of Non depol NMB as increased sensitivity
  • high risk of post op respiratory complications
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27
Q

What issues do you consider when anaesthetising someone with gulian barre syndrome?

A
  • risk of autonomic instability -> requires invasive BP monitoring
  • avoid Sux, may need reduced dose of non depol NMB
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28
Q

What are the ECG criteria for ventricular hypertrophy?

A

RVH = V1 R wave >3 big boxes
V6 S wave > 1 big box

LVH = V1 S wave > 3 big boxes
V6 R wave > 5 big boxes

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29
Q

What are ECG changes of WPW?

A
  • Shortened PR interval
  • Delta wave
  • Discordant ST segements V1-3
  • PR depression
  • Widened QRS
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30
Q

Why is preop functional testing important?

A
  • adverse events are linked to the functional inability of patients to meet extra metabolic demands required when having major surgery
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31
Q

What is Duke activity status index (DASI)?

A

Simple patient questionaire that ascertains the maximum level of activity an individual can perform

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32
Q

What is a MET?

A

Metabolic equivalent = oxygen consumption of an adult at rest.

= 3.5mls/kg/min oxygen

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33
Q

What is monitored during a CPET?

A
  • inspired and expired gases
  • HR
  • ECG
  • NIBP
  • O2 sats
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34
Q

What is measured during a CPET?

A
  • work rate
  • VO2 = O2 consumption, roughly matches cardiac output
  • VCO2 = CO2 production
  • Resp exchange ratio
  • Anerobic threshold
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35
Q

What is the resp exchange ratio?

A
  • ratio of volume of CO2 being produced by the body and the amount of O2 being consumed
    -This value of this ratio gives us an indication as to whether the body is operating aerobically or anaerobically.
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36
Q

What is the anerobic threshold?

A
  • marker of combined efficiency of lungs, heart and circulation
  • VO2 at the point at which CO2 production occurs (representing anerobic metabolism)
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37
Q

What is the pathophysiology of the anerobic threshold?

A
  • the point at which the oxygen demand of the muscle is greater than oxygen supplied
  • muscle changes to anerobic metabolism which produces lactic acid
  • when increased lactic acid is buffered by bicarb it becomes CO2. AT is the VO2 at the point at which this occurs
  • This is also when RER >1
38
Q

Why is the anerobic threshold useful compared to VO2 max?

A
  • Does not vary with age very much
  • Occurs part way through the test so does not vary with patient effort
  • Varies with organ impairment
  • therefore provides a reliable, repeatable, patient-specific
    measurement of dynamic functional capacity
39
Q

What is the safe anaerobic threshold for major surgery?

A

> 11 mls/kg/min

40
Q

What are CPET predictors of poor outcome in thoractomy patients?

A
  • Low AT
  • Low Peak VO2
41
Q

What is the 6min walk test?

A
  • How far people can walk on the flat in 6 mins (usually down a hallway and they turn around cones)
42
Q

What are normal vaules for a 6 min walk test?

A

500-600 m
<300 m is high risk

43
Q

What is the VO2 peak and what value is considered higher risk?

A
  • maximum oxygen consumption, usually at the end of the test
  • VO2 peak < 15 mls/kg/min is high risk
44
Q

What is CPET?

A
  • a quantitative, reliable and non invasive measure of functional capacity
  • Looks at incremental increases in exercise and the response to this
45
Q

What is ASA score?

A
  • Risk score for population based mortality
  • Classed 1 - 6
  • High ASA score is predictive of increased post op complications and mortality
46
Q

What is the Lee’s revised cardiac risk index?

A
  • risk score for devleopment of cardiac complications after major non-cardiac operations:
  • High risk surgery
  • IHD
  • CCF
  • Cerebral vascular disease
  • Inulin therapy
  • CKD (creat > 176)
47
Q

What is the main risk score for post op pulmonary complications?

A
  • ARISCAT
  • uses a 7 varibale regression model to stratifiy patients into low, intermediate or high risk
  • Includes patient factors: Age, preop Sats, recent resp infections, preop anaemia
    and surgical factors: incision location, surgery location, duration and emergency surgery
48
Q

Whats the difference between risk prediction models and risk scores?

A
  • Risk scores assign a weighting to factors indentified as independent predictors of outcome, simple to use
  • Risk prediction models estimate an individual probability by entering patients data into a multivariate risk prediction model, complex to use
49
Q

What are some common risk prediction models?

A
  • P-Possum: 12 physiological variables and 6 surgical to calculate 30 day mortality
  • NELA: national emergency laparotomy audit: 30 day mortality
  • Surgical outcome risk tool (SORT): 30 day mortality in non-cardiac, non neuroloical inpatient surgery
  • American college of surgeons national surgical quality improvment project universal surgical risk calculator: predicts 30 day morbidity and mortality
50
Q

What is used to classify acute liver failure?

A

O’Grady classification
Time from jaundice to hepatic encephalopathy
<1 week = hyperacute
4 weeks = acute
12 = subacute

51
Q

What is chronic liver disease?

A

Progressive deterioration of hepatic function over a period longer than 28 days

52
Q

What are the types of chronic liver disease?

A

Compensated
Decompensated (jaundice, ascites, hepatic encephalopathy, variceal haemorrhage)

53
Q

What are the extra-hepatic manifestations of chronic liver disease?

A

CVS: Hyperdynamic circulation with high cardiac output and low SVR, cirrhotic cardiomyopathy

Resp:
- Mechanical compression of lungs eg ascites
- Hepatopulmonary sydrome
- Portopulmonary hypertension

GI:
Portal hypertension
SBP

Renal:
Acute/chronic renal dysfunction
Hepatorenal syndrome

CNS:
Hepatic encephalopathy

Haemtological:
Hypoalbuminuemia
Coagulopathy
Anaemia
Thrombocytopaenia
Hypofibrinogenaemia

54
Q

What are the signs/symptoms of anterior ischaemic optic neuropathy?

A
  • Painless, progressive vision loss
  • Oedematous optic disc +/- flame haemorrhage
55
Q

What are the signs/symptoms of posterior ischaemic optic neuropathy?

A

Acute painless unilateral or bilateral
Normal optic disc

56
Q

What are signs/symptoms of central retinal artery occlusion?

A
  • painless, unilatearl
  • Pale retina with cherry red spot at macula
57
Q

What is the difference between anaesthesia induced rhabdomyolysis and MH?

A
  • AIR has no muscle rigidity
  • Otherwise similar triggers (Volatile)
  • AIR has more myalgias and muscle weakness
  • Can both get rhabdomyolysis
58
Q

How do you calculate transpulmonary gradient?

A

mPAP - PCWP (if its > 12)

59
Q

What is the most common inherited bleeding disorder?

A

Von Willebrand disease

60
Q

What is von willebrand disease?

A
  • Defeciency/defective vWF
  • Decreased factor VIII (carried by vWF)
61
Q

What are investigations for patients with von willebrands disease?

A
  • Normal Platelet and PT
  • Prolonged APTT
62
Q

What is the treatment of bleeding in von willebrand disease?

A
  • DDAVP (increases release of factor vIII) - only effective type 1 VWF disease (most common type)
  • TXA
  • Von willebrand factor/Factor VIII plasma concentrate
63
Q

What are some issues with managing parkinson’s disease patients?

A
  • Need to continue parkinson’s meds
  • Airway mx: - Increased secretions, dysphagia, gastroparesis, GORD
  • Ventilation: May have restrictive deficit
  • Circulation: difficulty monitoring due to tremor, autonomic instability
  • Anti-emetics: avoid dopamine antagonists
  • post op delirium
  • Rigidity can make positioning challenging
64
Q

What are the complications of withdrawal of parkinsons meds?

A
  • Parkinsonism-hyperpyrexia syndrome: similar to NMS (muscle rigidity, fever, altered mental state, CVS instability)
  • Dopamine agonist withdrawal syndrome: anxiety, nausea, depression, pain and orthostatic hypotension
65
Q

What are the goals of an anaesthetic with a patient with myasthenia gravis?

A
  1. Avoid exacerbation of muscle weakness
    1. Preserve respiratory function
66
Q

What is the reaction of patients with myasthenia gravis to muscle relaxants?

A
  • Resistant to sux
  • Sensitive to non-depol (10% of normal dose)
67
Q

What are some issues with patients with epilepsy?

A
  • continue antiepileptics
  • assess severity and stability of seizures
  • avoid drug interactions
  • avoid drugs that increase risk of seizure
68
Q

What are general issues with patients with neuromuscular disorders undergoing anaesthesia?

A
  • High risk resp complications (due to involvement of resp and pharyngeal muscles)
  • Potentially difficult airways due to progressive spinal deformities
  • Anaesthesia induced rhabdomyolysis can be caused by use of volatile anaesthetics and sux
  • Avoidance of suxamethonium
  • Dose reduction of non depol NMB
69
Q

What are anaesthetic implications for charcot-marie-tooth?

A
  • avoidance of sux due to denervated muscle
  • effects on nondepol may be prolonged
70
Q

What are anaesthetic implications for Fredrich’s ataxia?

A
  • Avoid sux
    • Risk of aspiration if bulbar function is impaired
    • Avoid negative inotropes and assess cardiac function pre op
71
Q

What are anaesthetic implications for muscular dystrophies?

A

-common issues is contractures, marked scoliosis, restrictive lung disease, arrythmias and cardiomyopathies
- Avoid sux
- Avoid volatiles
-Care with non depol NMB

72
Q

What are the clinical features of Myotonic dystrophy?

A

○ Myotonia (incomplete muscle relaxation)
○ muscle wasting
○ cardiac abnormalities (conduction, cardiomyopathy)
○ resp abnormalities (restrictive lung disease and OSA)

73
Q

What are the anaesthetic implications of myotonic dystrophy?

A
  • Avoid sux
  • May be sensitive to opioids and sedatives
    -Avoid use of standard reversal (eg neostigmine - cholinesterase inhibitor)
  • Prevent myotonias
  • May have bulbar involvement and risk of aspiration
  • May have conduction defects or cardiomyopathies
74
Q

What drugs are to be avoided in patients with mitochondrial myopathies?

A

-Propofol
- Local anaesthetics

75
Q

What are the anaesthetic implications of motor neurone disease

A
  • Loss of innervation leads to muscle atrophy and development of extra-junctional receptors
    • Avoid sux
    • Reduce dose of non-depol
      Resp complications are common
76
Q

What are the anaesthetic implications of multiple sclerosis?

A
  • Local anaesthetics may exacerbate symptoms due to increased sensitivity of demyelinated axons
    • Non depol NMB can be used at normal doses
    • Caution with sux if patient is debilitated
    • Avoid hyperthermia as neurones are sensitive to heat and symptoms can deteriorate
77
Q

What are the anaesthetic implications of Gullian barre syndrome

A
  • Risk of autonomic instability
  • Avoid sux even following recovery due to risk of hyperkalamic arrest
    -May be more sensitive to non depol NMB
78
Q

What are the anaesthetic implications of Eaton lambert syndrome?

A
  • Sensitive to both depol and non depol NMB
    • Nil issues with cholinesterase inhibitors
  • Risk of autonomic dysfunction
79
Q

What are implications for pregnant patients with myotonic dystrophy?

A
  • C-section more common to due to uterine muscle dysfunction
  • Increased risk of PPH due uterine atony
  • Avoid high block with regional
80
Q

What are the symptoms of brown sequard syndrome?

A
  • Hemisection
  • Ipsilateral senosory and motor loss
  • Contralateral loss of pain and temperature
81
Q

What are the issues with an obstetric patient with spinal cord injury?

A
  • Autonomic dysrefelxia triggered by labour as well as contracted uterus post delivery
  • Urological problems eg pyelonephritis
  • Resp compromise due to effects of gravid uterus
  • High rate of C section -> difficult airway possibly ideally planned not emerg
  • Difficult epidural due to previous surgery -> usually spinal uncomplicated
82
Q

What is primary and secondary spinal cord injury?

A
  • Primary injury is the initial damage from direct cord compression, haemorrhage and traction forces
  • Secondary injury is from within minutes after injury, where haemorrhage and oedema within the spinal cord leads to spinal cord ischemia
  • Secondary injury spreads bi-directionally up and down the cord from the site of initial injury
83
Q

What is neurogenic shock?

A

Neurogenic shock is the interruption of autonomic pathways leading to hypotension and bradycardia, usually involving T2-5 which is cardiac sympathetic, can last from 24h to several weeks

84
Q

What are some of the anaesthetic issues with an acute spinal cord injury?

A
  • Airway: Maybe be difficult intubation due to MILS, as well as other oral secretions if trauma (blood, vomit etc.), usually RSI due to trauma and gastroparesis from trauma and spinal cord injury. Maintain oxygenation to prevent secondary injury
  • Breathing: If high injury will need ventilation (Above T1 removes intercostal function, after C3-5 then lose diaphragm too), cough will be impaired with higher injuries too. Ventilate better lying flat for first few days
  • Cardiovascular: Initially sympathetic surge with injury then becomes hypotensive and bradycardic as sympathetic tone is lost. With higher injuries will not be fluid responsive (as vagoplegic) so need vasopressors
85
Q

What are some goals for patients with acute spinal cord injuries?

A
  • Neuroprotection: Avoid hypoxia, hypotension and hypercarbia
    ○ Hypotension avoided with vasopressor support, some evidence for MAP >85mmHg for a week
  • Surgical decompression: If there is direct pressure on the spinal cord
  • Thromboprophylaxis: High risk of VTE and PEs due to immobility and trauma coagulopathy
  • Gastric protection: Unopposed vagal activity increases gastric acid and rates of peptic ulceration
86
Q

What are signs of diabetes insipidus?

A

○ Awake: polyuria, polydypsia, thirst
○ Asleep/Brain injured:
-Increased urine volume (>3000ml/24hr)
-High serum sodium (>145 mmol/L)
- High serum osmolality (>305 mmol/kg)
-Abnormally low urine osmolality (<350mmol/kg)

87
Q

What is diabetes insipidus?

A
  • associated with TBI, SAH, intracerebral haemorrhage and pituitary surgery
  • Failure of secretion of ADH -> impaired ability to concentrate urine
  • Subsequently produce large volumes of dilute urine -> hypernatraemia secondary to dehydration
88
Q

What is acromegaly?

A
  • excess of growth hormone due to hypersecretion from a functioning pituitary macroadenoma
89
Q

What are the anaesthetic implications of acromegaly?

A
  • Airway management: Difficult intubation due to macrognathia, macroglossia and expansion of soft tissues
  • OSA: associated resp and CVS effects as well as possibly difficult BMV
  • Kyphoscolosis: restrictive resp defect
    -CVS: LVH, hypertension, IHD, arrhythmias, conduction abnormalities, cardiomyopathy
90
Q

What is cerebral salt wasting syndrome?

A
  • renal loss of sodium resulting in polyuria, natriuesis, hyponatraemia and hypovolaemia (unlike SIADH which is HYPERvolaemia)
  • due to disruption of the hypothalamo-renal pathways
91
Q

What is the management of salt wasting syndrome?

A

volume and sodium resuscitation

92
Q
A

Part 2 exam (15 decks)

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