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62 Cards in this Set

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What classes of antidepressents are there?
1)MAO x = Ipronazid, Selegiline (A=5HT, B=DA/NA)
2)Tricyclics = Amitryptiline, Doxepin, Despramine (Blocks monoamine reuptake)NB- can cause cardiotoxicity.
3) SSRIs- Fluxetine (Prosac)-less side effects than tricyclics.
4)Mixed uptake inhibitor- Venlafaxine (used in severe)
5) SSRI + 5HT antag- Trazedone (reduced Side effects)
What is the treatment for bipolar disorder?
Carbamazepine or Lithium then Sodium Valproate.
What is the treatment for Partial siezures in epilepsy, and how does it work?
Carbamazepine. Sodium channel blocker
What is the treatment for generalised epileptic siezures? How does this work?
Sodium valproate. Potentiates GABA, and blocks Sodium channels.
What are other Epilepsy treatments?
1)GABA pentin- Calcium blocker
2)Benzodiazepines- Potentiate GABA
3)Vigabatrin- Inhibits GABA breakdown (GABAT)
4)Tiagabine- Inhibits GABA reuptake.
5)Phenytoin- Sodium and Calcium blocker.
6)Diazepam- used for status epilepticus.
What are the main general anaesthetics?
*Premed-sedatives
*Induction- propofol
*Maintainance- N2O or Isoflurane
*Analgesia- Opiates
*Muscle relaxants- Atracurium
*Muscarinic antag- Atropine
How do general anaesthetics work?
*Inhibit Na and Ca channels
*Activate K channels
*Enhance GABA
*Block NMDA/AMPA receptors
*Decrease transmitter release
What are the classes of anxiolytic drugs?
1)Benzodiazepines-Diazepam, lorazepam, Triazolam. (physical dependance- Increase GABA affinity and potential for opening of channel)
2)5HT agonist- Busiprone (no tolerence/dependence).
3)Beta antagonists- Propanolol- reduce peripheral effects in mild anxiety.
How do local anaesthetics work?
Uncharged for passes through membrane and binds to Sodium channel in charged form. Block Na channel and prolongs the inactivation.
Do local anaesthetics show use dependance?
Yes- excpet benzocaine which acts via a different pathway. (lidocain, procaine etc do).
How much of local anaesthetics are unionised at pH 7.4, and how does decreasing the pH affect this.
20%, decreasing pH lowers this proportion.
How can you prolong the activation of local anaesthetics, and when should you not do this?
Give adrenaline- but never in peripheral surgeries, due to ischemia.
How does cocaine work? (and crack)
Blocks dopamine reuptake.
Crack cocaine has higher pH and more unionised drug, so gets into systems faster.
Hows does amphetamine work? What are the effects?
Increases dopamine release, blocks reuptake and also blocks MAO degredation.
- Elevated mood, alertness, insomnia, agression, anorexia, psychosis, increased HR and BP.
How does MDMA (ecstacy) work? How do the effects compare to amphetamine?
Increases 5HT release, and blocks reuptake. Same as amphetamine but no agression and added effects of increased thirst and body temperature. Degredation on 5HT neurones is debatable.
How do LSD and Ketamine work?
LSD=5HT agonist
Ketamine = NMDA antagonist
What are the symptoms of parkinson's disease?
Hypokinetic movements, Freezing, Rigidity, Resting-pill rolling tremor, Bradykinesia, Dysphagia, Micrographia, shuffling gait.
What causes parkinsons disease?
Degredation of nigrostriatal pathway dopamine release. (70% loss = symptoms)
What are the treatments available for parkinsons disease?
*LDOPA- requires carbidopa (decarboxylase inhibitor). SE-dyskinesia, nausea, postural hypotension.
*Anticholinergic-Benztropine (tremor)
*Amatadine- antiviral with dopamine agonist properties, and also inhibits catecholamine reuptake.
*MAOB inhibitor- Selegiline
*Dopamine agonists (lots of side effects)
What are the antipsychotics and how do they work?
*Phenothiazines-Thiroridazine
*Butyrophenones-Haloperidol/pimozide
*Atypicals-dibenzodiazepines
Work by increasing dopamine (and maybe 5HT, and also decreasing glutamate).
How do opiates (morphine etc) work?
G protien coupled receptor:
-inhibits neuronal firing (increase K)
-Inhibits transmitter release (decrease Ca)
-disinhibition of dopamine
-Decrease excitability of cells
What are the side effects of opiates?
Euphoria, constipation, sedation, cough surpression, respiratory depression, nausea and vomiting, tolerance, physical and psychological dependance.
What are the different types of haemorrage?
*Extradural-middle meningeal
*Subdural-Bridging veins
*Subarachnoid-Basal vessels
*Parenchymal-diffuse axonial injury
What are the features of multiple sclerosis?
*Affects young people usually
*Weakness, sensory losses, optic neuritis, vertigo.
*relapse and remission
*Active plaques-lymphocytes and maxrophages
*Inactive plaques-glial scar
*Shallow plaque-remylelination
What type of nerve fibres carry pain?
C and Adelta, mainly unmyelinated fibres.
How is the pain threshold changed during inflammation?
Lowered because of lowered pH and bradykinins.
How does the wind up pain phenomina occur?
NMDA-enhances depolarisation
Substance P-Increases NMDA activation.
CGRP- reduces substance P breakdown.
What is the pupillary light reflex?
Optic N->pre tectal nuc->edinger-westphal nuc-> occulomotor nerve-> cillary ganglion-> eye
What is the accomodation reflex?
Optic N->lateral geniculate nuc->visual cortex->edinger-westphal nucleus->occulomotor nerve->eye
What is the corneal reflex?
opthalmic division of CN5->main sensory and spinal nuc-> facial nuc->facial nerve->contraction of obicularis oculi
What is the gag reflex?
Glossopharyngeal n->nucleus of solitarty tract->nucleus ambiguous->vagus
What is the airway protection reflex?
Vagus->nucleus of solitary tract->nucleus ambiguous->vagus
What is the vestibular-occular reflex?
Vestibular nerve->Vestibular nuc->Abducens and occulomotor nuc->occulomotor and abducens nerves
What is the caloric test reflex?
Vestibularcochlear nerve->vestibular nucleus->abducens and occulomotor nucleus->abdu/occulomotor nerves =nystagmus towards (warm) and away(cold) from stimulus.
What does CN3 do?
Occulomotor :
*Moves eye- superior rectus, inferior rectus, medial rectus, inferior oblique, levator palpebrae, ciliary muscle, and iris sphincter
*Occulomotor and edinger-westphal nuclei
What does CN4 do?
*Trochlear nerve- Superior oblique muscle (trochlear nucleus)
What does CN5 do?
*Trigeminal:
-skin of membranes
-muscles of mastication
Spinal,main sensory and mesencephalic nuclei of CN5.
What does CN6 do?
-Abducens:
- lateral rectus muscle (abducens nucleus)
What does CN7 do?
Facial:
-tears and saliva- superior salivatory nuc
-taste ant 2/3- solitary tract nuc
-ear sensation-spinal nucleus
-facial expression- facial nucleus
What does CN8 do?
Vestibular cochlear:
-hearing and balance (cochlear and vestibular nuclei)
What does CN9 do?
glossopharyngeal:
-taste- post 1/3- solitary tract
-Ear sensation- spinal nuc
-Pharyngeal sense- solitary tract
-saliva- inf salivatory nucleus
Pharyngeal striated muscle-nucleus ambiguous
What does CN10 do?
Vagus-
-ear sensation-spinal nucleus
-pharyngeal sensation-solitary tract
-phayngeal muscle-nuc ambiguous
-taste-solitary tract
-autonomics- dorsal motor nucleus
What does CN11 do?
Hypoglossal-
-moves tounge- hypoglossal nuc
What does CN12 do?
Accessory nerve:
-moves larynx-nuc ambiguous
-moves respiratory accessory muscles- accessory nucleus
What does the cerebellum control?
Rate range force and direction of movements
What signs appear with cerebellar damage?
Ataxia, hypotonia, nystagmus, intention tremor
What is the nernst equation for an ion? and what is the resting membrane potential?
60log[x]outside
---
[x]inside
normal potential = -90mV
How do synapses work?
*Depolarisation
*Ca channels open
*Ca causes vesicle fusion with presynaptic membrane
*Neurotransmitter released
*Diffuses and binds to receptors on postsynaptic membrane.
What are excitatory and inhibitory transmitters?
*Excitatory-glutamate (cations)
*Inhibitory-GABA/glycine- Cl channels
Describe hearing transduction
*Stapes hits oval window
*Fluid displaces IHC
*K channel opens-influx K
*Depolarisation
*Ca channels open
*transmitter release
What are the potentials of endolymph and perilymph?
Endolymph=like ICF-80mV (bathes organ of corti)
Perilymph=like ECF = 0mV
What are the frequencies heard at the base and apex of the cochlear?
apex=low frequencies
Base = higher frequencies
What are the causes of a lower motor neurone lesion?
Motor neurone disease, poliomyelitis, spinal nerve root tumour, diabetes, vasculitis.
What are the signs of a lower motor neurone lesion?
Muscle weakness, wasting, hypotonia,fasiculations, loss of relex's.
What are the causes of an upper motor neurone lesion?
Spinal cord compression, stroke, MS, Motor neurone disease, poliomyelitis, syringomyelia (cavitation of cord)
What are the signs of an upper motor neurone lesion?
Muscle weakness, increased tone, brisk reflexs, babinski sign
What are the features of Brown-sequard syndrome?
Ipsilateral corticospinal and dorsal column loss(UMN signs and loss of touch and proprioception) and contralateral anterolateral tract- pain and temperature
What viruses cause meningitis?
Enteroviruses-echo, cocksakie, polio
*Mumps
*Herpes simplex type 2
What viruses cause encephalitis?
*Herpes simplex type 1
*VZoster (in HIV)
*MMR,
*Measles
*Rabies
What are the signs of stroke?
Variable- dysarthria (slurring), Dysphasia (jumbling of words), loss of vision, facial droop, hemiparesis, ataxia, dysphagia, numbness, pins and needles.
What are the risks for strokes?
*Age over 65
*Hypertension
*diabetes
*Cholesterol
*smoking
*alcoholism
*Clotting disease
*Contraceptive pill
*Infection
Describe visual trasduction.
*Retinal changes from cis to trans
*Opsin changes shape
*Decreases cGMP
*Na channels close=hyperpolarisation
*Decrease glutamate release
*depolarises bipolar cell
*excites ganglion cell
*via optic nerve to LGN or superior colliculus