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