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170 Cards in this Set

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Day 18 of gestation -> how big is the embryo?
What shape is it?
About 1-2mm
Oval disc shaped
What are the three layers of the embryonic disc at day 18?
What will each layer become?
- Endoderm (lower) -> will form the visceral structures
- Mesoderm (middle) -> muscles, BVs and connective tissues
- Ectoderm (upper) -> skin and CNS
At what day of gestation do we see the first morphological sings of CNS?
day 18 - start to see the neural plate
What sort of epithelium is the neural plate?
Columnar pseudo strat ep
Describe the process of formation of the neural tube
- Day 18 -> the neural plate starts to invaginate along its longitudinal axis
- Neural folds (on either side) start moving up and towards each other at the same time
- Two neural folds meet dorsally and fus --> we have an enclosed tube
- Closure - starts in the middle. Top closes around day 24, bottom (2nd sacral level) closes around day 26
- From S2 to coccygeal region -> doesn't form by fusion of the neural folds, but rather it develops from block of tissue at the end of the closed neural tube
What are primary and secondary neurulation?
Primary = neural plate folding in and then fusing to form the neural tube
Secondary = formation of the bottom bit (from S2 to coccygeal region) - develops from block of tissue at the end of the closed tube
What do the neural crest cells form?
Sensory neurons of the DRG
Cell bodies of the symp and parasymp ganglia
Melanocytes and adrenal chromaffin
What is anencephaly? What happens?
Failure of closure of the anterior neuropore
--> skull can't grow over the brain -> it degenerates a fair bit in utero then so much when they're born that they die shortly after birth
What is spina bifida?
Neural tube fails to close (in any region, but most commonly in lumbo-sacral region)
What is the ventricular zone?
Proliferating layer adjacent to the lumen of the neural tube - where lots of cells are dividing
By what time in gestation do we have four columns formed running the length of the spinal cord? What are these columns?
What are the two columns separated by?
Two dorsal (alar) columns -> will form sensory interneurons
Two ventral (basal) columns -> future motor neurons
They're separated by the sulcus limitans
Neuronal proliferation in most parts of the brain is finished by when?
What's the exception?
Mostly finished by about wk 16 of gestation
Exception = the cerebellum - production of neurons in the internal granular layer occurs in the first year of post-natal life
What are the two big types of spina bifida?
SB cystica
SB occulta
What are the two types of spina bifida cystica?
Which is the most common
Myelomeningocele (most common - responsible for 90% of all SP cysticas)
Meningocele
** They are NOT caused by the same problem!!
What happens in myelomeningocele?
The caudal neural tube fails to close --> the neural tissue is exposed to the exterior, CSF can leak (skin hasn't been able to close over because neural folds haven't fused)
There's a cyst containing meninges and spinal cord!
What happens in meningocele?
The neuropore is closed, but the vertebrae haven't formed properly --> cyst containing meninges
What happens in spina bifida occulta?
There's no cyst, nothing herniating through the skin
But the spinous process hasn't formed properly
Often have a tuft of hair, dimple, pigmented skin etc over the area
Completely asymptomatic, affects 10-20% of the population
At what week does the defect form in myelomeningocele and meningocele?
Myelomeningocele --> the posterior neuropore hasn't closed (week 4 ie approx day 26)
Meningocele - the neuropore is closed properly, but the bones haven't properly formed around (occurs in weeks 5-12!)
Define hydrocephalus
Increase in CSF volume
(nothing in the definition re pressure!) can be high, low or normal pressure
What type of tissue does the notochord originate from?
What's its job?
Notochord is derived from mesoderm
It sits ventral to the neural plate - releases signals that tell the part of the ectoderm that will become CNS to thicken and then start folding
At approx what day does the middle of the neural tube close?
The anterior part? Posterior?
Middle = 22
Anterior = 24-26
Posterior = 26-28
Early on in the neural tube, what are the three bulges calleD?
- Prosencephalon
- Mesencephalon
- Rhombencephalon
What does the prosencephalon form? Divides?
Prosencephalon = greek for forebrain
It divides into telencephalon (forms the cortex, hippo, amygdala, CN1) and the diencephalon (forms everything ending in -thalamus as well as the retina)
Telen -> lateral ventricles
Diencephalon -> 3rd ventricle
What does the mesencephalon form?
Midbrain
And the cerebral aqueduct
From what vesicle does the 3rd ventricle develop?
Diencephalon
from what vesicle does the cerebral aqueduct develop?
Mesencephalon
What does the rhombencephalon form? Divides?
Divides into the mesencephalon (-> pons and cerebellum) and the myelencephalon (-> medulla)
Both also give rise to the 4th ventricle
What is responsible for dorso-ventral differentiation of the neural tube?
Shh from the NOTOCHORD - the ventral part of the neural tube will get high conc of Shh -> turns on TFs that give it its motor character. Dorsal -> low conc of Shh -> sensory character
What molecule is responsible for helping the dorsal parts of the neural tube to develop their sensory character?
BMP = bone morphogenic protein It's produced by the epidermis --> the lateral parts of the neural plate get high conc
What produces Shh during neural tube development?
The notochord
Where do we get BMP from during neural tube development?
Epidermis
What is the first (non-mitotic) cell type produced in the development of the CNS?
Radial glial cell
What's the function of the radial glial cells?
They have radial processes that attach them superficially and deep -> the new neurons grab onto the radial glial cells and climb out
What's the ventricular zone?
Area where new neurons are born
What is the mantle / marginal zone (MZ)?
As new neurons grow out from the ventricular zone, they grow into the MZ (grow along the radial glial cells!)
When does proliferation of neurons end?
About week 16
Cortex proliferation starts and ends later than a lot of the other areas
How do axons make contact with their target?
Distance is often too great for the axon to grow directly there --> we have intermediate targets - they release attractant molecules -> axon grows towards. Once the axon is there, there's a change in receptor expression so that the axon is now repelled away and grows towards the final target
Also have repulsant molecules along the way as well - deter the axon from growing in the wrong direction
What are the 7 phases of brain development?
1 Mitosis / proliferation (ventricular zone. Spinal cord and brainstem proliferate first, cortex is a fair bit later. finished by week 16)
2 Migration (migrate out of VZ on radial glial cells)
3 Differentiation
4 Synaptogenesis (make lots of random connections first)
5 Neuron death
6 Synapse rearrangement (get rid of all the dodgy / unwanted connections)
7 Myelination
After the huge and random synaptogenesis, how do we get rid of the unwanted connections?
Survival of the fittest scenario
The target structures release NEUROTROPHINS in an activity dependent manner -> if the axon is properly interacting with the target, will get lots of neurotrophins and grow and survive. If not, it will die
When is the male embryo exposed to high levels of testosterone?
What happens to the developing brain if this doesn't occur?
Weeks 8-20 -> high levels of testosterone (peaks around week 15)
If you don't have it, the male brain won't identify itself as male -> female brain
In how pregnancies do we get anencephaly? SB?
1/1000 for both
What % of SB cases will be picked up on US?
Amniocentesis?
What's a third way of detecting SB?
US --> pick up 80%
Amniocentesis -> pick up 99%

Third way of detecting = measuring the levels of alpha-fetoprotein in the mother (produced by fetal liver - if they have open neural tube, conc will be increased in the mother)
What % of mothers will abort when they find out they have a baby with SB? Anencephaly?
SB - only 30% abort
Anencephaly - 80% abort
At what spinal level is spina bifida occulta common?
L5-S1
In what week of gestation does SB occulta occur?
Weeks 5-12
(Problem with the vertebral column)
What % decrease is there in neural tube defects with folic acid supplementation?
70-80% decrease
How much do anti-convulsants increase your risk of neural tube defects?
Which is the worst one?
Does increased folic acid help remove this risk?
Increase 6 fold
Valproic acid is the worst

Extra folic acid does not help remove the risk! Ie they're independent risk factors
What's the impact of obesity on risk of neural tube defects?
Increased risk
What are some of the disabilities you get with SB?
- Limited or no use of legs
- Loss of bowel / bladder control
- Learning difficulties (we don't really know why)
- Often develop latex allergies
What is a chiari type II malformation?
When the cerebellum and brainstem sit lower than normal
It can block the CSF from exiting fourth ventricle -> hydrocephalus
What are the two theories for why chiari type II malformations are so common in myelomenigocele babies?
- Because their CNS isn't a closed system (CSF leaking out), there's not high P in the cranial cavity -> posterior fossa never really grows big enough
- Spinal cord tethering - ie the spinal cord and vertebral column are attached --> as column grows down, it pulls the spinal cord (and hence brainstem) with it
What happens in 80% of myelomenigocele babies when we patch up their hole?
They have chiari type II malformation -> CSF has problems leaving the IV ventricle - this is OK when it can travel down the central canal and leak out
But when we close this off, will get sudden build up in CSF volume = hydrocephalus!
How do we fix the hydrocephalus in SB babies after we've repaired the hole?
- Shunt
- Third ventrculostomy (make a hole in the base of the III vent -> CSF can leak into the basal cisterns)
In what weeks do we have proliferation of neurons for most of the brain except cortex? Which weeks do we have cortex proliferation?
Which area of the brain continues proliferation after birth
Majority of the brain -> wks 4-10
Cortex -> wks 7-16
Cerebellum - proliferation occurs in first week of life
What features do we see in kids with FAS?
- Small head
- Small size and weight at birth (and continues into life)
- Irritable and hyperactive
- Poor motor skills, low IQ
- FACE: small, short palpebral fissure (eye isn't very wide -> space between eyes appears bigger, short nose and it's upturned, flat mid face, thin upper lip)
Smaller brain
How many drinks p/day does a mum have during pregnancy to -> FAS?
8-10
How many drinks p/ day does mum have during pregnancy to -> fetal alcohol effects (more subtle than FAS)
4-6 p/day
How many drinks are safe p/day for the fetus?
No more than 2 drinks per day
What's the total volume of CSF?
About 120mL
How much CSF is produced p/day ?
P/hour?
About 500 mL per day
(20mL p/hour)
Describe the distribution of CSF (ie how many mLs in each area)?
TOTAL = 120mL
Lateral ventricles - 25mL
Third + fourth vents - 5mL
Cranial sub-arach space - 25mL
Spinal subarach space - 75mL
How does CSF differ from plasma in terms of PROTEIN and GLUCOSE content?
0.5% protein cf plasma
Less glucose (not so signtly less though)
How does CSF differ from plasma in terms of chloride and H+ content?
More Cl- and H+ in CSF cf plasma
What cell type lines the ventricles?
Ependymal cells
Cerebral aqueduct derives from what part of the neural tube?
The mesencephalon
Lateral ventricles derive from what part of the neural tube?
Telencephalon
Fourth ventricle derives from what part of the neural tube?
Rhombencephalon (both parts!)
Sub-arachnoid space = actual or potential space?
Sub-dural?
SA = actual (filled with CSF)
S.D = potential space
What anchors the arachnoid mater to the pia mater?
Weblike arachnoid extensions
What are the 'cisterns'?
The pia mater follows the brain exactly down all the contours etc. The arachnoid doesn't --> get cisterns = large spaces when pia's gone down and arachnoid hasn't
Structure of BBB?
- Tight junctions, no intracellular clefts or fenestrae
- Capillaries encased by glial foot processes of astrocytes
What cells make up the choroid plexus? What's special about them?
They're MODIFIED ependymal cells
Modified because they have tight junctions (normally between them = gap junctions) and they contain the enzyme carbonic anhydrase
What % of CSF production is from the choroid plexus?
80%
What increases CSF production?
- Symp denervation
- Cholinergic stimulation
- Cholera toxin application
What decreases CSF production?
- Symp stimulation
- Ventriculitis (infection of the ventricles)
- Acetazolamide (carbonic anhydrase inhibitor)
How does CSF get reabsorbed?
Goes through arachnoid villi (= from the sub arach space into the venous sinuses) - they clump together -> arachnoid granulations
Hydrostatic gradient pulls the CSF into the sinus (passive transport)
Is CSF production dependent on pressure?
Reabsorption?
Production - NOT dependent on pressure
Reabsorption - IS dependent on pressure
What's the normal hydrostatic gradient between the sub arach space and the venous sinus?
20-50mmH20
What are some secondary sites of CSF reabsorption?
Cranial and spinal nerve root sleeves
-> drains into the lymphatics

(relatively impt most of the time, but might be of more importance at higher pressures)
What sort of epithelium is the choroid plexus?
Cuboidal / columnar
Where is the majority of teh choroid plexus located?
In the lateral ventricles
(There's some in III and IV too though)
What enzyme is impt in CSF secretion?
Carbonic anhydrase
What's the normal CSF pressure?
Is it constant?
5-12mmHg
(=7-15cmCSF)
Pressure is pulsatile (changes with arterial P and respiration)
Where would you usually do a lumbar puncture?
Between 3rd and 4th lumbar vertebrae
(Can't do it unless you've excluded a space occupying lesion!)
What's the difference between communicating and non-communicating hydrocephalus?
Communicating = non-obstructive. Due to impaired reabsorption
Non-communicating -> obstruction of the ventricular system
What do you see in someone with acute obstructive hydrocephalus?
Headache
Nausea
Vomiting
Then lethargy, drowsiness, stuper, coma
Signs - papilloedema, diplopia.
Sunset eyes (eyes go down)
What is the characteristic triad in normal pressure hydrocephalus?
Gait disturbance
Dementia
Urinary Incontinence
What is pseudotumour cerebri?
Increased ICP in the absence of mass lesion or hydrocephalus
Also called 'idiopathic IC hypertension' or 'benign IC HT'
Common in overweight young females (16-30)
Describe AMPA and NMDA Rs
NMDA = tetramer - made of NR1 and NR2. NR1 binds lysine, NR2 binds glutamate (need both binding for activation)
Then it opens rapidly -> influx of Na+ (and some allow Ca2+). Don't stay open for long, don't have huge influx
AMPA - they also tetramer, don't need lysine binding though. Slower activation (the small depol from NMDA removes Mg2+ molecule that was blocking the channel) -> Ca2+ and Na+ can flow. Open for longer
Which opens first - AMPA or NMDA ?
NMDA faster to open
What is long term potentiation?
= when there are activity dependent changes in synaptic activity
(includes changes in R number and activity)
How does excess glutamate --> cell death?
(ie excito-toxicity)
Excess glutamate release --> excess stimulation of glutamate Rs --> lots of Ca2+ influx into the cells
--> activation of proteases, lipases, endonucleases, NO synthase etc
--> CELL DEATH (by apoptosis or necrosis)
What happens when GABA binds to its R?
Cl- influx -> hyper-polarisation
How is GABA synthesised?
In the GABA shunt:
One of the intermediates in the KREB cycle (=alpha-ketoglutarate) can be converted to glutamate and that can then be converted to GABA
What's the intermediate from which GABA is synthesised?
Alpha-ketoglutarate
What Rs do benzos act on (specifically)?
GABA-A Rs that contain alpha1, alpha2, alpha3, alpha5 or gamma subunits
(approx 30% of all GABA A Rs)
What is bisculline?
A competitive antagonist of GABA-a Rs -> turns them off ie decreased inhibition
What Rs do barbiturates bind to?
All GABA-a Rs
What Rs does ethanol bind to at different blood concs?
Low -> delta subunit of GABA-a Rs
Higher -> gamma-2L subunit
Higher still -> loses specificity --> binds to all GABA a Rs
How do benzos and barbiturates work?
They both act on GABA a Rs
Benzos -> increased FREQUENCY of opening
Barbiturates -> open for longer
How do we diagnose epilepsy?
At least ONE unprovoked seizure
What % of people will have a seizure in their lifetime?
What is the breakdown of causes of these seizures?
About 10-15%

About 1/3 of these = febrile convulsion, another 1/3 = patients having a single seizure, the final 1/3 is epilepsy
What is the prevalence of epilepsy?
0.5-1%
Define prevalence
= how many cases there are at a given time
Define seizure
= Clinical manifestation of an abnormal and excessive excitation of a population of cortical neurons
Describe partial seizures
Partial seizures = focal ie excitation of neurons in a relatively small, discrete region
They often have an AURA
Describe generalised seizures
Both hemispheres are involved, there's widespread neuronal activation
Usually patients don't get an aura
Describe Grand-mal seizures
= the most common type of generalised seizures
Tonic clonic (ie rigid phase for about 10 seconds then rhythmic jerky contractions = clonic phase)
They don't get an aura. Have post-ictal confusion. Often bit their tongue, be incontinent of urine
Describe a petit-mal seizure (is it a generalised or partial seizure?)
Petit-mal = generalised! They usually don't get an aura
Have a period of absence that usually lasts about 10 seconds and then they're fine afterwards
Most common in childhood
List 5 types of generalised seizures
grand mal
petit mal
tonic
clonic
myoclonic
Describe simple partial seizure
There is no LOC
They usually get an aura
The signs / symptoms depend on which area of the brain is affected. Can get positive signs (eg twitching of a limb) or negative (eg loss of speech)
Usually they're find afterwards
Describe a complex partial seizure
They do lose consciousness (this can vary between being quite mild to being fairly severe). LOC means that the electrical activity is affecting more of the cortex cf simple partial seizures or that it's affecting the deep brainstem / diencephalon-areas
Often get automatisms (eg smacking lips)
Most common = temporal seizure
What's the most common type of complex partial seizure?
What aura do they get with this?
Most common = in the temporal lobe
Aura -> indescribable sensation, epigastric, emotional and/or olfactory phenomena, or they can also get deja vu
What is secondary generalisation of a seizure
= when a partial seizure spreads across to the other hemisphere -> now a generalised seizure
in which type of seizure do you often see automatisms?
Complex partial seizure
In what % of epilepsy cases are we able to define a cause?
Only about 1/3 of cases
What are the two age peaks of new-onset epilepsy?
Infancy/childhood
And older adult
In infants / young children, what are some common causes of epilepsy onset?
Birth injury
Congenital malforamtion
What's the most common type of seizure in infants?
Febrile convulsion
What are some common causes of epilepsy onset in older adults?
Stroke
Brain tumour
Neuro-degenerative disease
When is absence epilepsy most common?
In children aged about 6-7
Describe childhood absence epilepsy
- Peak onset of 6-7 years
- Get remission in 80% of cases (ie they grow out of it)
- Fine after the absence ie no post-ictal confusion
- Can be commonly triggered by hyper-ventilation, strobe lights, sleep deprivation
Describe juvenile myoclonic epilepsy
Teenage onset
Particularly common early in the morning
Quite a lot of them have absence seizures as well
Most of them never grow out of it
Teenage onset of epilepsy, happens most in the mornings. They don't usually collapse, but drop what they're holding etc
-> what is it? What will we treat them with? Prognosis? Grow out of it?
Juvenile myoclonic epilepsy

Most don't grow out of it
Treat them with sodium valproate -> good outcome (90% are well controlled)
Is familial association stronger with generalised seizures or partial seizures?
Stronger with generalised
- If person has generalised epilepsy -> 10% risk to other siblings
- Partial epilepsy -> 5% risk
Describe generalised epilepsy with febrile seizures plus
It's an autosomal dominant disorder! (ie GENETIC)
Basically, they're having abnormal febrile seizures (eg they might last longer than normal 15 minutes, happen more frequently than normal (more than one in 24 hrs), have focal features, outside the normal age bracket (3m-6y))
What % of people who have their first seizure will have a recurrence (ie a second seizure)? When do most recurrences occur?
50%
Usually occur within 3-6 months
Aims of epilepsy Tx?
- Use a single drug
- Minimise S/Es while preventing another seizure
What % of epileptics have good prognosis (get good control and/or go into remission)? What % need regular meds and might still have occassional breakthrough seizures?
What % don't really respond at all to Tx?
70-80% -> good prognosis
About 20% might still have breakthrough seizures despite being on regular meds
About 5-10% don't respond well to Tx
Differences between syncope and seizure?
Syncope -> limp fall, need a precipitating factor (won't happen when you're asleep/supine), no incontinence or tongue bite, might have some convulsions, wake up totally fine / rapid recovery
Seizure - can happen when you're asleep (don't need ppting factor), don't recover rapidly
What's the most common surgery we do for epileptics?
What % get seizure freedom from this?
Temporal lobectomy
About 60-70% have total seizure freedom
What are the two tests that are useful in diagnosis of seizures?
EEG
Structural imagining (particularly MRI)
Do most people presenting with epilepsy have abnormal symptoms / signs between seizures?
NO!
-> their inter-ictal EEG will be normal
Do the majority of people presenting with seizures have abnormalities on MRI?
LT quoted a % of people with partial epilepsy who have structural features of MRI - what is it?
NO

Between 20-70% of people with partial epilepsyhave abnormalities on MRI
What do we do / need to think about when someone's had a single epileptic seizure?
- Key question = is this the first of many epileptic seizures? Or is it just a one off?
- EEG - unlikely to rule out epilepsy
- MRI - look for structural abnormalities
What are the sensitivity and specificity of inter-ictal EEGs?
specificity -> SPPIN. High (positive result -> we can rule IN epilepsy)
Sensitivity -> SNOUT. LOW. ie negative result -> we can't rule out epilepsy
How do we work out what type of epilepsy a patient has?
Most impt = HISTORY! From them and observers
Look at their EEG DURING A SEIZURE (might help work out where it's coming from)
No serial EEGs help in determining patient's response to anti-epileptic meds?
NO!
5 mechanisms of anti-convulsant drugs and egs of each
1. Increased inactivation of Na+ channels -> reduction of sustained frequency AP firing. EG phenytoin, carbamazepine (also decreases glutamate release)
2. Inhibition of T-type Ca2+ chs on pre-synaptic neurons -> decreased glutamate release. EG ethosuximide
3. Enhance activity of GABA. EG diazepam and phenobarbitone (also decreases glutamate release)
4. Inhibit GABA breakdown by enzyme GABA transaminase. EG vigabatrin
5. Inhibit GABA reuptake by GAT-1 EG tiagabine
How do gabapentin / pregabalin work?
They are GABA analogues. We don't exactly know how they work but they seem to increase conc of GABA in the CSF
How does PHENYTOIN work?
Increases inactivation phase of Na+ chs (needs channels to open first -> works best on rapidly firing neurons)
Limits frequency of nerve impulse conduction
How does PHENOBARBITONE work?
It's a barbiturate -> acts on GABA a Rs to increase opening time
Also reduces neuronal release of glutamate (partial agonist of adenosine Rs on pre-synaptic neurons)
How does CARBIMAZEPINE work?
It increases inactivation of the Na+ channels -> decreased firing of APS
Also reduces neuronal release of glutamate (partial agonist of adenosine Rs on pre-synaptic neurons)
How does DIAZEPAM work?
It's a benzo - acts on about 30% of GABA a Rs -> enhances action of GABA
How does TIAGABINE work?
It blocks the GAT-1 transporter - usually transports the GABA back into the neuron
-> increases GABA conc in the synapse
How does VIGABATRIN work?
Inhibits the metabolism of GABA by the enzyme GABA transaminase
(Ie vigabatrin is structurally similar to GABA -> binds to the enzyme so it now can't metabolise GABA)
How does sodium valproate work?
By mechanisms 1,2 and 4
IE increased inactivation of Na+ chs, decreased Ca2+ T-type channel opening on pre-synaptic neurons and decreased metabolism of GABA by gaba transaminase
What two mutations have been found in some epileptics?
The mutations are in ion channels!
1. GABA-a R mutation in the gamma-2 subunit (mutation is in loop joining 2 TM domains) --> decreased Cl- influx -> decreased inhibition
2. Mutation in sodium channel - Nav1.1 channel = located on GABA interneurons. (mutation --> channel doesn't get transported properly to the surface) Decreased Na+ influx -> decreased excitation of the GABA interneuron -> decreased inhibition
Acute pain resolves after how long?
About 4-6 weeks
Chronic pain lasts how long?
More than 3 months
What is sub-acute pain?
Lasts between 4-12 weeks (ie somewhere between acute and chronic)
What percentage of males and females have chronic pain?
About 17% of males
20% females
What % of people with chronic pain report that their pain interferes with their ADLs?
About 60%
IE only about 40% of those with chronic pain are NOT signtly disabled by their pain
Who are Melzack and Wall? What theory did they come up with?
The gate control theory of pain! IE that pain isn't only due to the pain signal being transmitted directly up to the brain, but that it gets modulated in the spinal cord and higher centres
Ie pain perception is dependent on more than just the severity of the sensory input
What are the 6 psychological processes that affect pain perception?
- Attention (if you're busy paying attention to other things, eg war etc -> won't perceive the pain as super bad)
- Meaning
- Cognitive response
- Motivation
- Affect / mood (if you're depressed, pain will seem worse)
- Learning
Paediatric history -> what extra things do we have to include?
ADING
A = ante and perinatal history
D = development
I = immunisations
N = nutrition
G = growth
Adolescent history -> what's the special assessment we have to do?
HEADSS
H = home
E = education
A = activity
D = drugs
S = sex
S = suicide
What does it mean when we say that phenytoin has zero-order kinetics?
Means that elimination of the drug is NOT dependent on time or concentration! (because the liver enzymes get saturated)
Which anti-convulsant drug has zero-order kinetics?
Phenytoin
When would TDM not be useful?
- If we can measure the desired clinical endpoint (eg BP) - can't really do this with seizures
- When there isn't a good relationship between plasma conc and effect
- If the drug has many active metabolites (looking at plasma conc of teh drug alone won't give us an insight into the effect it's having)
What's therapeutic index? Do we want a big or small number?
Toxic dose / therapeutic dose
Want a big number
With which anti-convulsant drugs is TDM particularly useful?
WHY?
Phenytoin
Carbamazepine
Sodium valproate

Because the plasma conc : effect relationship is stronger than the dose:effect relationship
(for both efficacy and toxicity)
In what % of cases is poor compliance responsible for an anti-convulsant failing to control seizures?
more than 50% !
TDM is useful -we can look to see if they've been compliant
What three things do we need to know / have in order to get valuable results from TDM?
- need to know when the sample was taken in relation to most recent dose
- Need patient to be in steady state (ie can't have changed dose / drugs recently)
- need to have correctly documented dosing history from the patient
What happens to metabolism of phenytoin and carbamazepine during pregnancy?
Metabolism increases -> usually need to increases dose
Patient is taking 2+ anti-convulsants and getting S/Es -> how do we work out which drug is causing the S/Es>
TDM -> can look at the plasma conc of each drug.
And we have good clinical data on the relationship between plasma conc and adverse effects
What are the three subsets of stigmatisation?
- Legal discrimination (eg epileptic not allowed to be pilot / drive bus etc)
- Enacted stigma (eg not given a job in a bank because of your epilepsy)
- Perceived or felt stigma (the shame of being an epileptic and the feat of encountering enacted stigma)
Using epilepsy as an EG, what's the model of 'hidden stress'?
= When person with epilepsy is afraid of encountering stigma --> they actively don't disclose to people that they're epileptic
According to the LT, is it worse for most epileptics that people know they have epilepsy or that people see them have a seizure?
Worse that people see them have a seizure
What's more common - perceived stigma or enacted stigma?
Perceived! This results in the epileptic person avoiding social contacts etc