Non-operative viva Flashcards

Question

What are psychomotor seizures?

Answer 1

Alteration of awareness with automatisms and aura (usually epigastric rising sensation)

Answer 2

Olfactory hallucinations - cacosmia = perception of a bad odour

Answer 3

Spatial memory (dominant), verbal memory (non-dominant) and learning concepts

Answer 4

Behavioural arrest, staring, oral automatisms, posturing of the contralateral arm. Seizures last a few minutes and post-ictal confusion, amnesia and aphasia (if dominant side).

Answer 5

Rhythmic theta (4-8 Hz) maximal in basal temporal electrodes

Answer 6

Atonic seizures resulting in drop attacks Medically refractory Valproate reduces seizure frequency by 50% **_Corpus callosotomy is the treatment of choice_**

Answer 7

Sleep deprivation Hyperventilation Photic stimulation Infections / Drugs / Metabolic disturbances Trauma / Stroke

Answer 8

Post-ictal weakness due to involvement of the motor cortex in the functional deficit zone

Answer 9

Barbiturates - phenobarbital Benzodiazepines - lorazepam / diazepam GABA analogues - gabapentin Voltage-gated sodium channel blockage - phenytoin / carbamazepine Synaptic vesicle protein (SV2A) blockage - levetiracetam

Answer 10

Valproate and Phenytoin

Answer 11

Valproate Phenytoin Levetiracetam

Answer 12

Carbamazepine Phenytoin Levetiracetam (Valproate is second line)

Answer 13

Voltage-gated sodium channel blocker Calcium channel 'T current' blocker

Answer 14

1st order (eliminiation proportional to concentration) then zero-order (elimination at constant rate i.e. elimination saturated). Half-life 24 hours. Aim for therapeutic levels 10-20 mcg/ml. Serum binding is affected by urea and albumin levels i.e. in hypoalbuminaemia the active phenytoin level is higher than expected (because 90% is protein bound). The correction is calculated by the Sheiner-Tozer equation.

Answer 15

Absorption is decreased by 70% when given with NG feeds. The feed should be held for 2 hours before and 1 hour after.

Answer 16

Hypotension Arrhythmias - bradycardia (Should be given as slow IV with cardiac monitoring and BP check at a max rate of 50 mg/min). Note the loading dose is 18 mg/kg and maintenance is 300-500 mg per day i.e. 100 mg TDS.

Answer 17

Fosphenytoin is a prodrug that is converted to phenytoin Less venous irritation Can be given IM Fewer arrhythmias and can be given 2x as fast as phenytoin, therefore.

Answer 18

Purple glove syndrome in the elderly Diffuse maculopapular rash Cognitive slowing SLE-like syndrome Megaloblastic anaemia Cerebellar degeneration Gingival hypertrophy Neonatal haemorrhage TEN / Steven-Johnsons Osteoporosis / rickets Teratogenic

Answer 19

Albumin and Ureamia (Renal failure without uraemia does not need adjustment) **_Scheiner-Tozer equation_**

Answer 20

**_Auto-induction_** - induces the hepatic enzymes to increase metabolism of itself and other drugs

Answer 21

Diplopia Ataxia Drowsiness Marrow suppression - Leucocytopenia SIADH Steven-Johnsons syndrome

Answer 22

No need for monitoring No Cytochrome P450 induction so minimal drug interactions BD dosing Linear kinetics Fewer side effects

Answer 23

Causes neural tube defects

Answer 24

Ethosuximide

Answer 25

History / examination Bloods to rule out infectious or metabolic causes EEG +/- sleep deprivation EEG MRI

Answer 26

In severe head injury, phenytoin reduces the risk of seizures by 73% for the first week but does not affect long term seizure rates. (Ref Temkin et al NEJM 1990 Double-blinded RCT)

Answer 27

Arching of the back Asychronous movements Forced eye closure Bilateral shaking with preserved awareness Weeping

Answer 28

Seizure \>5 minutes or persistent activity after 1st and 2nd line AEDs

Answer 29

ABCs Bloods incl glucose, electrolytes & AED levels Lorzepam / midazolam / diazepam \> phenytoin / levetiracetam / valproate \> I&V midazolam or propofol \> If continues to sz despite above then phenobarbital CT head \*\* If low glucose give thiamine first before dextrose to prevent wernicke's encephalopathy

Answer 30

Blocks voltage-gated Na channels. Risk of drowsiness, diplopia, ataxia, marrow suppression, stevens johns syndrome and hepatitis.

Answer 31

Voltage gated Na channels GABA action T-type Ca channels Side effects are teratogenicity, thrombocytopaenia, hepatotoxicity and high ammonia

Answer 32

Voltage-gated Ca channel blockade GABA-B receptor blockade

Answer 33

T-type Ca currents in the thalamus. Used for absence seizures!

Answer 34

AMPA antagonist

Answer 35

Voltage-gated Na channel blockade

Answer 36

Monotherapy with the lowest possible dose of carbamazepine (focal) and lamotrigine or Keppra (generalised). Proper seizure control is the primary goal. The risk of maternal and fetal hypoxia/acidosis with seizures outweighs the risk of teratogenicity from AEDs. Give 5 mg/day (normal dose is 400 mcg) of folic acid prior to conception and continue the intake until at least the end of the first trimester.

Answer 37

= 2x ([Na] + [K]) + urea + glucose in mmol/l

Answer 38

0.9% which means 9g per litre

Answer 39

Hypotonic hyponatraemia with serum osmo \<275 (dilute) and inappropriately concentrated urine with urine osmo \>100.

Answer 40

CSW has extracellular fluid depletion due to renal sodium loss. Renal [Na] \>20.

Answer 41

Mild \<135, Moderate \<130 and Severe \<125

Answer 42

Hyperglycaemia or mannitol administration

Answer 43

If urine osmo dilute (urine osmo \<100) then psychogenic polydipsia or low Na intake. If urine osmo conc (urine osmo \>100) then check volume status. If dry and urine Na \>20 then CSW / diuretics / Addison's disease. If dry and urine Na \<20 then extrarenal losses of Na such as GI tract or burns etc. If euvolemic then SIADH If hypervolaemic and urine Na \>20 then renal failure or hypothyroidism. If hypervolaemic and urine Na \<20 then CHF and cirrhosis.

Answer 44

Fluid restriction

Answer 45

Volume replacement and Na replacement Fludrocortisone can be used for low Na if refractory

Answer 46

SIADH 35% and CSW 20%

Answer 47

Osmo 275-295: pseudohyponatraemia due to hyperlipidaemia or hyperparaproteinaemia;

Answer 48

Osmo \>295: Hyperglycaemia / mannitol administration

Answer 49

Osmo \<275: Urine osmo \<100 - psychogenic polydipsia Urine osmo \>100 - depends on fluid status Hypervolaemic: Renal failure if urine Na \>20 and CHF / cirrhosis if urine Na \<10 Euvolaemic: SIADH Hypovolaemic: CSW / Addisons if urine Na \>20 and GI tract or skin losses if urine Na \<10

Answer 50

Malignancy Infection (meningitis / encephalitis / TB) Pulmonary disorders Endocrine disturbances (adrenal insufficiency / hypothyroidism) Drugs

Answer 51

Serum osmo \<275 (hypotonic) Urine osmo \>100 (inappropriately conc urine) Clinically euvolaemic Urinary Na \>40 Normal thyroid and adrenal function No diuretic use

Answer 52

8 mmol/24 hours

Answer 53

\>100 mOsm/kg

Answer 54

Water load test: Give a water load of 20ml/Kg (max 1.5L). Urine output should be 2/3 of the water load at 4 hours, otherwise the patient has SIADH.

Answer 55

Na\<125 or symptomatic hyponatraemia

Answer 56

ICU transfer 3% saline (1-2 ml/h/kg body weight) with 20mg Frusemide Check Na every 2 hours and adjust 3% saline infusion rate Replace K Max correction 8mEq/24 hours

Answer 57

Fluid restriction based on the solute ratio For refractory cases consider demeclocycline (partial antagonist to ADH in the renal tubules) or conivaptan (vasopressin receptor antagonist)

Answer 58

CVP, volume status and serum K (raised in CSW but not SIADH). Haematocrit is raised as patient is dry.

Answer 59

0.9% or 3% saline; salt can also be administered orally. Other treatments include fludrocortisone, hydrocortisone

Answer 60

Lack or insensitivity to ADH causing hypertonic serum osmo (patient is dry) with dilute urine (urine osmo \<200 mOsmol/Kg OR urine SG \<1.003). This leads to a high serum Na.

Answer 61

Neurogenic is a lack of ADH release; Nephrogenic is insensitivity to ADH in the kidneys

Answer 62

Lithium, demeclocycine, colchicine; also caused by chronic renal failure, sarcoidosis and sjorgren's syndrome

Answer 63

Iatrogenic following transsphenoidal surgery (most common after craniopharyngioma) Pituitary apoplexy Encephalitis / meningitis

Answer 64

1 - injury to posterior pituitary causes reduced SIADH release (polyuria and polydipsia) 2 - cell death causes excess SIADH release (SIADH symptoms) 3 - chronic reduction in ADH release due to loss of cells in post. pituitary

Answer 65

Polyuria with \>250ml/h for 2 or more hours Dilute urine with urine osmo \<200 or SG \<1.003 High serum Na Normal adrenal function

Answer 66

Polydipsia because there is appropriately diluted urine

Answer 67

In suspected cases of DI stop the patient from drinking / IV input. In a normal patient the urine output should decrease the urine osmo will rise to \>600 mOsm/kg. In DI the urine will remain dilute.

Answer 68

If mild - drink to thirst If severe - desmopressin

Answer 69

Water absorption from the collecting ducts through Aquaporin channels

Answer 70

An irreversible loss of consciousness

Answer 71

Neurological injury when the brainstem has been irreversibly damaged but the heart is still beating and the body is kept alive by a ventilator

Answer 72

Confirmation of absence of brainstem reflexes and apnea testing

Answer 73

5 minutes - long enough for irreversible brainstem death

Answer 74

Irreversible loss of capacity to breath Irreversible loss of consciousness No need for ancillary tests

Answer 75

Receptivity to signals from the environment

Answer 76

Deeply unconscious Mechanically ventilated Irreversible brain damage of known aetiology No reversible influences e.g. sedatives, hypothermia, endocrine or metabolic (electrolytes and glucose) abnormalities

Answer 77

Period of observation for short acting drugs Administration of reversal agents (naloxone / flumezenil) Plasma levels for long acting or unpredictable clearance (e.g. thiopental) Confirmatory tests can be used e.g. DSA showing no flow

Answer 78

NMJ blockers High cervical cord injury

Answer 79

Performed twice by independent practitioners: Pupil response (CN2 and 3) Corneal response (CN5 and 7) Oculovestibular reflex (CN8 and CN3/4/6) - visualise TM and undertake cold water caloric testing Painful response (CN5 and CN7) - supraorbital pain Gag reflex (CN9 and 10) Cough reflex (CN10) - suctioning After the above then apnoea testing to produce a pH\<7.4 without hypoxia by reducing the RR until PCO2 = 6. Observe for 5 minutes.

Answer 80

EEG DSA/CTA/TCD BSAER These are used where a comprehensive neurological examination cannot be carried out e.g. facial trauma, when sedatives cannot be excluded or high cervical injuries.

Answer 81

If \>2 months old then same as adults If \< 2 months old then more difficult as preconditions are rarely met If \<37/40 then cannot be done.

Answer 82

Age \>50 years History of cancer - unexplained weight loss Night pain Immunosuppression / HIV / Steroids / Organ transplant Infection - fever, night sweats, foreign travel Bowel / bladder dysfunction Trauma Neurological symptoms

Answer 83

Leg pain worse with standing or walking for a set distance Gets better when sitting / leaning forward Leg gives way Dermatomal numbness

Answer 84

Calf pain with walking Worse with activity progressing to rest pain when advanced. Worse at night - wakes from sleep. Hangs their leg out of bed. Reduced pulses Skin changes Pallor on elevation

Answer 85

The cortical micturition centre is found in the mesial prefrontal lobes / anterior cingulate. It inhibits the pontine micturition centre in the locus coeruleus. The locus coeruleus sends descending control over the sympathetic fibres in the intermediolateral nucleus of the spine (T12-L2) and parasympathetic fibres in Onuf's nucleus in the sacrum S2-4. The sympathetic fibres travel on the hypogastric nerves to relax the detrusor muscle and constrict the internal urethral sphincter via alpha-2-adrenergic R. This allows bladder filling. The parasympathetic fibres travel along the pelvic splanchnic nerves (nervi erigentes) and cause relaxation of the internal urethral sphincter and detrusor constriction through the action of mAch R. Somatic efferents from the S2-4 control the relaxation of the external urethral sphincter. Sensory stretch fibres in the bladder wall travel to the conus via the pudenal, hypogastric and pelvic nerves and ascend in the spinothalamic tract.

Answer 86

Top trace is over central sulcus (C3) - N19 - primary sensory cortex (+ so downward deflection) and P22 is motor cortex (- so upward deflection) Middle trace is placed over the cervical region and shows activity at the root entry zone. Bottom trace is with electrode placed over the brachial plexus (Erb's point) and shows the stimulation passing through the brachial plexus

Answer 87

L5-T12 shows activity in the lumbar plexus (positive deflection P22) Cv7 (cervical electrode) shows activity in the dorsal columns - N27 Cz - shows P40 activity at the sensory cortex

Answer 88

Vitale checklist: 1 - Technical considerations (check connections and contacts etc) 2 - Pause surgery and alert anaesthetist 3 - Anaesthetic optimization with MAP, pCO2, temperature and pH corrections. Check drugs administered (paralytics / inhalational agents) 4 - Surgical considerations - Remove retractors / last surgical step when monitoring was lost e.g. remove spinal screw etc or papaverin if vasospasm 5 - Stagnara wake up test if all else fails to normalise IONM

Answer 89

The anaesthetic is weaned intraoperatively to a point where the patient can obey commands such as moving fingers / toes.

Answer 90

Stimulation of a motor nerve also causes antidromic APs which cause the anterior horn to fire and cause a delayed (much smaller amplitude) orthodromic F-wave. This may be delayed in radiculopathy but is not sensitive. Normal F-wave \<33 ms.

Answer 91

Is a monosynaptic reflex with stimulation of the sensory nerve causing an orthodromic action potential stimulating the gastrocnemius. This is only useful for S1 root and gives the same information as the ankle jerk reflex.

Answer 92

DML between 4.5-6.5 with SNAPs present = Moderate CTS on the Canterbury scale

Answer 93

0 - normal 1 - very mild, only detected on two sensitive tests 2 - mild, SNCV \<40 m/s with DML\<4.5 ms 3 - moderate, DML 4.5-6.5 with preserved SNAP 4 - severe, DML 4.5-65 with absent SNAP 5 - very severe, DML\>6.5 with absent SNAP 6 - Absent SNAP with CMAP\<0.2mV

Answer 94

lumbrical/interossei DML comparison Median to ulnar latency comparison or median to radial CV comparison Inching study across the carpal tunnel

Answer 95

Lack of sensory input from the bladder wall leads to stretching and overflow incontinence without feeling

Answer 96

Efferent lesions from cortex to sacrum cause loss of cortical inhibition and reflex contraction of the bladder

Answer 97

Loss of inhibition of the pontine voiding reflex. Results in involuntary reflex bladder contraction and voiding as sensation is intact. Treat with anticholinergics

Answer 98

Initially - spinal shock causes an areflexic bladder and retention. After this the bladder becomes hyperreflexic. Treat with intermittent catheterisation and anticholinergics

Answer 99

With cauda equina lesion

Answer 100

Urodynamic testing, sphincter EMG and micturating cystourethrogram.

Answer 101

antimuscarinics e.g. oxybutynin, these relax the bladder wall and increase capacity so should be combined with a timed voiding regime.

Answer 102

Intermittent self catheterisation / indwelling. Start Tamsulosin. Check post-void residuals. If \<75ml then no need for catheter.

Answer 103

Apathy, abulia, eye deviation if frontal eye fields involved (looks to the side of the lesion!). Involvement of the prefrontal region results in impulsiveness and disinhibited behaviour.

Answer 104

Gerstmann's syndrome, aphasia and bilateral astereognosis (inability to identify objects by touch), hemianopsia and neglect

Answer 105

Spatial memory loss, loss of self awareness (anosognosia) and dressing apraxia, hemianopsia and neglect

Answer 106

Hemispheric = Ataxia in ipsilateral limbs Vermis = Ataxia in trunk

Answer 107

The perception of a noxious stimulus

Answer 108

Lateral transmit pain and temperature Anterior transmit crude touch and pressure

Answer 109

Described by Melzack and Wall in 1965, it describes the modulation of pain transmission to the brain. Sensory inputs (Abeta) from the surrounding area can inhibit the pain signal (Adelta and C) in the substantia gelatinosa by hyperpolarising the dorsal horn.

Answer 110

Allows morphine dose to be more effective even though the actual dose is less (1-4 mg/day) and delivered with less systemic S/E (drowsiness, respiratory depression etc) by delivering the opiates to the subarachnoid space. Here it can directly on Mu-opioid receptors in the CNS.

Answer 111

Mostly performed percutaneously at C1/2 using CT guidance. Palliative procedure in patients with \<6 months prognosis. A radiofrequency needle is inserted into the anterior lateral cord and an ablation is performed within the lateral spinothalamic tract. There is a somatotopy to the tract with C = anterior and S = posterior.

Answer 112

Mannitol is a sugar that acts as an osmotic diruretic. It also changes the rheology of the blood by reducing the viscosity and haematocrit. It reduced ICP by reducing CBF. Complications include renal failure, hyperosmolar state, hypotension and electrolyte derangement.

Answer 113

Mnemonic = SCAND Slurred speech Confusion - CNS depression Asterixis Nystagmus Diplopia Also: SIADH, bone marrow suppression hepatitis and Steven-Johnson syndrome

Answer 114

As it is a potent enzyme inducer and increases its own metabolism.

Answer 115

Movement disorders (PD, ET and dystonia) Epilepsy (ANT, Centromedian, Hippocampus) Pain (Thalamus) Psychiatric (OCD, Tourette's, depression)

Answer 116

1. Retractory to medical therapy 2. Levodopa-induced dyskinesia 3. Gait and postural instability (PPN)

Answer 117

Dementia Risk of ICH (coagulopathy / uncontrolled hypertension) Ipsilateral hemianopsia (due risk of complete blindness) Age \>85 years Secondary Parkinson's (MSA / PSP / olivopontocerebellar atrophy)

Answer 118

Dyskinesia (due to drug reduction) 90% Bradykinesia 85% Rigidity 75% Tremor 60%

Answer 119

Paraesthesia (too posterior - stimulation of lemniscal fibres entering the ventralis caudalis nucleus) Dysequilibrium (due to ZI stim) Dysarthria (too medial - stimulation of the medial Vim) or too lateral if also associated with muscle contractions - stimulation of the internal capsule) Ataxia (too ventral and medial - stimulation fo the brachium conjunctivum) High voltages needed for tremor suppression (too anterior due to stimulation of the ventralis oralis posterior) Phosphenes (too deep - optic tract stimulation)

Answer 120

a - electrode is too anterior and within the VOP - requires high voltages to induce tremor suppression b - electrode is too short within the Vim - will likely not to result in any tremor suppression. c - electrode too posteroir and within the ventralis caudalis nucleus - will likely results in paraesthesias due to leminiscal fibre stimulation

Answer 121

a - medial location within the Vim. Likely to result in dyarthria. b - deep location stimulating the ZI and brachium conjunctivum. Likely to cause ataxia. c - lateral location so within the internal capsule. Likely to cause dysarthria and facial pulling movements/dystonia.

Answer 122

Superior = ventralis oralis anterior / ZI (stim results in tremor suppression) Inferior = Substantia nigra (stim results in akinesia) Medial and deep = midbrain / CN3 nuclus (double vision and gaze deviation) Anterior or Lateral = internal capsule (dysarthria and muscle contraction) Posterior = (perspiration and mydriasis)

Answer 123

Based on the target: STN / VIM / GPi

Answer 124

Platinum iridium contacts 1.5 mm length spaced by 1.5 mm. Diameter 1.2 mm. Stimulation parameters: pulse width 75 μs, frequency 150 Hz. With a well-placed electrode, tremor arrest can be achieved at 0.5 to 2.0 volts. Suppression thresholds of 4 volts or greater suggest that repositioning of the electrode may be necessary.

Answer 125

Relative loss of dopamine-mediated inhibition (i.e. overactivation) of the effects of acetylcholine on the basal ganglia

Answer 126

Bradykinesia Tremor Rigidity (also have postural and gait disturbances, Micrographia, mask-like facies and emotional lability)

Answer 127

Primary - gradual onset bradykinesia and tremor which is asymmetrical and responds well to levodopa. Secondary - rapidly progressive with poor response to levodopa. Early midline symptoms eg. gait, balance, sphinter disturbance etc and associated with dementia, orthostatic hypotension and extra-ocular muscle weakness

Answer 128

Pars compacta of the substantia nigra

Answer 129

In normal circumstances the direct pathway causes movement and the indirect pathway prevents movement. Direct pathway - motor cortex stimulates the striatum (Caudate + putamen). The striatal GABA release inhibits the GPi. The GPi release of GABA on the thalamus is reduced so excitign the motor cortex and allowing movement. The STN excites the SNc. DA neurons from the SNc then release DA on the D1 striatal neurons and increases the GABA release on the GPi. There is negative feedback between the SNc and STN. \*The DA from the SNc on the D1 in the striatum amplifies the DIRECT pathway

Answer 130

Indirect pathway inhibits motor movement. Motor cortex stimulates the striatum. The striatum GABA inhibits the GPe. The GPe release of GABA on the STN is therefore reduced so the STN activation of the GPi increases. The GPi inhibition of the thalamus increases which then inhibits the motor cortex. This prevents movement. The STN activity also stimulates the SNc. The SNc then releases DA on the striatum and activates the DIRECT pathway i.e. negative feedback loop.

Answer 131

D1-R activate the DIRECT pathway and therefore causes movement D2-R activate the INDIRECT pathway and therefore prevents movement

Answer 132

Eosinophilic intraneuronal hyaline inclusions composed of alpha-synuclein

Answer 133

Olivopontocerebellar degeneration Striatonigral degeneration Post-encephalitic parkinsonism PSP MSA Drug induced

Answer 134

Parkinsonism + postural hypotension or other signs of autonomic dysfunction. Do not respond to L-Dopa. Associated with degeneration of neurones in the lateral horn of the thoracic spine.

Answer 135

Progressive vertical gaze palsy (Doll's eye remains the same) Pseudobulbar palsy (dysarthria / dysphasia / hyperactive jaw jerk) Axial dystonia (neck and upper trunk)

Answer 136

1) Assess functional status and cognition 2) Start drugs when PD seriously interferes with life - use the lowest dose that provides symptom relief Start with L-Dopa (dopamine precursor) and a Dopa-decarboxylase inhibitor (carbidopa). The carbidopa acts peripherally and cannot cross the BBB so prevents the conversion of L-Dopa to dopamine preventing the peripheral effects of dopamine. Dopamine cannot cross the BBB. (100 mg L-Dopa : 25 mg Carbidopa TDS). COMT inhibitors can be used in conjunction to prevent peripheral L-Dopa breakdown. MAO-B inhibitors are used to manage 'end of dose' off-effects of L-Dopa. 3) After a few years, the L-dopa becomes less effective. May help to start slow-release L-Dopa and add in Dopamine-3 agonists e.g ropinorole / cabergoline / pramipexole / Pergolide. These may be used as first-line in younger patients to reserve L-Dopa. Anti-muscarinics can be used to help with extrapyramidal symptoms but are associated with cognitive impairment. 4) Advanced disease may be treated with an apomorphine pump 5) DBS

Answer 137

1) L-Dopa (dopamine precursor) with dopa decarboxylase inhibitor (e.g. co-careldopa) 2) Dopamine agonists (cabergoline, bromocriptine, pramipexole, ropinirole, apomorphine and pergolide) 3) COMT inhibitors e.g. entacapone, for patients that have motor fluctuations 4) MAO-B inhibitors e.g. selegiline, for those that have end of dose off periods 5) Antimuscarinics e.g. procyclidine, trihexyphenidyl

Answer 138

Nausea / vomiting Dyskinesia and fluctuation in motor performances Palpitations / postural hypotension Drowsiness Anxiety / depression / psychosis

Answer 139

Drowsiness / hypotension / Nausea / constipation / headache Pulmonary and retroperitoneal fibrosis Cardiac valvular disease and pericarditis Dyskinesias Loss of inhibitions and impulsivity - increased libido and gambling Peripheral vasospasm so don't use in Raynaud's syndrome

Answer 140

Potent glucocorticoid effect with minimal mineralocorticoid effect. 25x more potent than hydrocortisol. It increases hepatic gluconeogenesis, lipolysis and muscle catabolism. Metabolised in the liver with a T1/2 3 hours.

Answer 141

The NASCIS trials showed no benefit for high dose steroids following SCI.

Answer 142

Oedema Pericavity necrosis Wound dehiscence / infection

Answer 143

Based on the mental capacity act 2005: They understand the information They can retain the information They can weigh up the information - risks and benefits - to make a decision They communicate the decision

Answer 144

By law, they are presumed to have capacity and be competent to consent for themselves. It is best practice to involve the parents in the decision making. They can consent to treatment but cannot refuse it.

Answer 145

Sufficient information is given to the patient (based on what a reasonable person would want to know), including the risks, benefits and alternative treatments. They are able to make a voluntary decision without any coercion. They have capacity to make the decision.

Answer 146

Prior to Montgomery vs Lanarkshire, the threshold for information was based on the Bolam test, which is based on what a body of professionals would do. In the Montgomery case, the patient had gestational diabetes and the 10% risk shoulder dystocia was not explained to the patient and the alternative of a C-section was not offered. The child was left with brain damage. The law now states that the information provided should be that of what a **_'reasonable person'_** would attach significance about the **_'material risks'_**.

Answer 147

This is the ability of a child \<16 years that has sufficient maturity to make medical decisions on their own without parental consent and keep this confidential. The framework for this is provided by the Frasier guidelines.

Answer 148

Mother and Married father All other people including unmarried fathers do not have parental responsibility unless bestowed upon them by a court.

Answer 149

Age / comorbidities Aetiology - MS / vessel conflict Previous treatment response including failure and intolerance to medications Patient choice

Answer 150

24-hour urine collection (the alternative is salivary cortisol) and low dose dexamethasone test. I would expect the 24-hour urinary cortisol to be raised and the low dose dexamethasone to suppress to \<5mcg/dl in a patient without a pituitary adenoma. 1mg of Dexamethasone is given at midnight and serum cortisol is measured at 8 am. If the low dose Dexamethasone does not suppress then I would perform a high dose dexamethasone test by administering 8mg at midnight. I would expect this to suppress the 8am cortisol in patients with an adenoma (CUSHINGS disease) but not with ectopic secretion. I would confirm this with inferior petrosal sinus sampling.

Answer 151

In Cushing's syndrome the diurnal variation in cortisol is lost (normally high in the morning and low in the evening). Salivary cortisol is more accurate at detecting cyclical Cushing's compared to 24-hour urine collections as cortisol day curves can be generated showing \>2 peaks in the cortisol levels with troughs that are below the upper limit of normal. Late-night salivary cortisol \>5 is highly suggestive of Cushing's syndrome.

Answer 152

ACTH (8 am cortisol if worried about low or 24 hour urine cortisol if worried about high). Prolactin IGF-1 TSH and T4 FH/LH and oestrodiol (F) and testosterone (M)

Answer 153

Cortisol - low and high dose dexamethasone test for Cushing's syndrome/disease AND short Synacthen test for cortisol reserve. GH - If IGF-1 is high then OGTT for Acromegaly and if IGF-1 is low then insulin tolerance test (ITT) Thyroid - If TSH low then stimulate with TRH. If TSH high then suppress with T3.

Answer 154

Measure cortisol on the 3rd morning (8am) and omit the dose from the night before, For a retained cortisol reserve 8 am cortisol should be \>350 micrograms/dl. For the success of surgery in Cushing's disease 8 am cortisol \<50 micrograms/dl.

Answer 155

Posterior extension of the ethmoidal air sinus to the sphenoid sinus. Risks damage to the optic nerve.

Answer 156

Induces panhypopituitarism Induces DI Loss of reproductive function

Answer 157

Following bilateral adrenalectomy for Cushing's disease. Characterised by hyperpigmentation, high ACTH and growth of pituitary adenoma. Treatment is transphenoidal hypophysectomy. Prophylactic radiation at the same time is protective. Medical therapies (ocreotide / temozolomide) are less effective.

Answer 158

Diagnosis = Acromegaly

Answer 159

\>6.8 U/ml

Answer 160

Does not suppress \<5 mcg/l

Answer 161

Bromocriptine / octreotide / pegvisomant (genetically modified analogue of human GH that acts as a selective antagonist)

Answer 162

Octreotide for \>3 months prior to surgery increased the rates of surgical remission in 4 RCTs

Answer 163

There is no gold standard but many would use: OGTT \<5 mcg/L or reduction in IGF-1 (delayed)

Answer 164

Previous bleed Single draining vein Flow aneurysm Diffuse morphology Small AVMs Deep drainage

Answer 165

SM grade 1/2 = surgery or SRS if eloquent 3 = multimodal treatment with embolisation to potentially down-grade the AVM 4/5 = no treatment. The Lawton-Young modification (takes the total to 10 with cut off for surgery =6): Age \<20 = 1, 20-40 = 2 and \>40 = 3 Bleed = 0 Compact = 0 / diffuse nidus = 1

Answer 166

Between 2-4% per year. The presence of high-risk features increases this to 8% per year. Lifetime risk = 105-age or = 1 - (risk of no haemorrhage)^years expected to live i.e. 1 - 0.98^20 where risk of no haemorrhage is 98% per year!

Answer 167

Meta-analysis showed obliteration rate with embo+SRS = 50% and SRS alone 65%. Might be selection bias as embo only given to larger more complex AVMs.

Answer 168

POLLOCK-FLICKINGER SCORE Age Location Number of draining veins Volume Previous embolisation \*\*Spetzler Martin grade does not correlate with SRS outcome

Answer 169

Microsurgery - 97% complete removal. 95% chance of HB1/2 if intact before. 50% retention of hearing SRS - 90% stop growing. 98% chance of facial weakness if intact before. 75% retention of hearing.

Answer 170

Initial management is focused on the treatment of hydrocephalus as well as obtaining a diagnosis. In a patient presenting in extremis, I would perform an emergency EVD. I would also send serum and CSF tumours marks for AFP, HCG and PLAP. If the patient has hydrocephalus but is stable I would elect to perform an ETV and biopsy the next morning. I would request an MRI +/- Contrast and diffusion imaging as well as stealth sequence for neuronavigation.

Answer 171

Embryonal ca Yolk sac Immature teratomas Mixed GCT

Answer 172

Choriocarcinomas Germinomas with syncytiotrophoblasts

Answer 173

Germinomas are treated with radiation alone achieving 10-year survival \>90%. Some centres also give induction chemotherapy. Non-germinomatous GCTs are treated with chemo and radiotherapy. Surgery is reserved for mature teratomas or tumours that do not respond to chemo/radiotherapy.

Answer 174

Choriocarcinomas

Answer 175

Pineoblastoma = chemo- and radiotherapy to the whole neuroaxis (high risk of drop mets) Pineocytoma = surgical resection

Answer 176

In children, these should be treated if symptomatic or growing. In asymptomatic children surveillance imaging. In adults, cysts remain stable if \<1 cm. Surveillance imaging if \>1 cm. Can occasionally present with apoplexy and be treated with surgery.

Answer 177

Germinomas represent 80% of GCTs and 30% of these secrete bHCG. Only 5% of GCTs are choriocarcinomas. A tumour that secretes HCG is more likely to be a germinoma than choriocarcinoma, therefore.

Answer 178

RCT of over 2000 patients. A 7% absolute risk reduction of poor outcome (from 31% to 24%) was seen with coiling versus clipping (all-cause morbidity and mortality). 18 year follow up was published in 2015. At 10 years, there was a significantly greater chance of being independent with coiling.

Answer 179

1 - Mild headache 2 - Severe headache or CN3 palsy 3 - Confusion 4 - Stupor 5 - Deep coma

Answer 180

1 = GCS 15 2 = GCS 13-14 without deficit 3 = GCS 13-14 with deficit 4 = GCS 7-12 5 = GCS 3-6

Answer 181

For the following sized aneurysms = \<7; 7-12; 13-24 and \>25: Anterior circulation = 0; 2.5; 14.5 and 40 Posterior circulation = 2.5; 14.5; 18.4 and 50%

Answer 182

Combination or ISAT, BRAT and Finnish aneurysm trials. Rupture risk of an aneurysm is based on Population, Hypertension, Age, Site, Earlier SAH and Size.

Answer 183

1. Important health problem 2. Natural history should be understood 3. There should be a recognizable early stage 4. There should be a sensitive and specific test to identify the early stage that is acceptable 5. There should be an efficacious treatment. 6. Treatment should be more efficacious if provided earlier 7. Cost-effective In the context of aneurysms the natural history is not well understood regarding which aneurysms will rupture and screening with MRA can miss small aneuryms.

Answer 184

2 first degree relatives have aneurysms or bleeds. Screening should be with MRA. For incidental aneurysms or those treated with coiling, then yearly surveillance is performed.

Answer 185

12% in the first year (compared to 2-4% without rupture)

Answer 186

Hydromyelia = ependymal lining Syrinx = no ependymal lining