Case 10 Flashcards
what does cognitive mean
interlectual functioning, mood, memory (perception, storage, retrieval), perception
general anasethesia
medically induced coma, loss of protective reflexes resulting from GA agents.
purposes of general anasthesia
Analgesia, amnesia, immobility, unconciousness, muscle relaxation. inhibition of midbrain reticular formation, thalamic sensory relay nuclei and cortex cause unconsciousness and analgesia. inhibition at the spinal level cause loss of reflex. causes short term amnesia.
premedication before GA
not everyone requires it, compliments GA. benzodiazepines, opiods, anticholinergics, antibiotic, antacids
induction of GA
there is an excitment stage, may be irregular heart rate and breathing. can be via inhalation, injection IV IM subcutaneous. oral or rectal. faster with IV, 10 sec. avoids excitary phase. Propofol, sodium thiopentone, etomidate and ketamine often used.
IV induction
injected, travels to brain, highly lipid soluble, rapidly enters brain, onset in one arm - brain time. initial recovery by redistribution, ultimate recovery elimination.
Inhilation induction
vapour breathed into lungs, enters blood, travels to brain, highly lipid soluble, initial and ultimate recovery exhalation. Minimal amount metabolised.
maintanence of GA
duration of IV would be 10 mins without maintanence. Breathe O2 NO and anasthetic agent - isoflurane. or propofol continuous IV. usually with opiods fentanyl. Muscle relaxants used which prevent Ach binding, atracurium, suxamthonium, tubocurarine. artificial resp/ reversed by acetylcholinesterase drugs.
reversal of GA
stop anasthetics. neostigmine or glycopyrrolate reverse muscle relaxants.
GABA receptor
ionotropic receptor, Cl channels. 5 subunits, each unit has 4 transmembrane regions. a 1-6 b 1-3 y 1-3 delta etc. benzodiazepine sensitive a1-2, 2xb y 2/3. binds between a/y. a1 sleep, a2/3 anxiety. barbituates between b/y or a/y. anasthetics mainly work on extrasynaptic GABAa recep.
two pore demain K channels
leak channels. inhalation inducing agents activate these channels causing hyperpolarisation. analgesic hyonitic and immobilising effects. not affected by intravenous agents.
Potency of inhaled anaesthetic agents
potency is expresed as the minimal alveolar concentration MAC. conc of vapour in the lungs that can prevent movement in 50% patients in respoce to surgical stimulus. Potency inc with inc lipid solubility.
propofol
IV used in induction. induce unconsciousness, rapid onset and rate of distribution. rapidly metabolised to inactive metabolites giving rapid recovery. 60L/kg. Pos modulation of inhibitory function of GABA through GABAa recept. SE: hypotension bradycardia respiratory depression nausea. can also used as maintain.
Isoflurane
volatile anaesthetic, inhalation inducing agent used for maintanance. with O2 and NO. binds GABA NMDA and glycine receptors. SE hypotension vasodilation respiratory depression.
Fentanyl
narcotic, similar to morphine but more rapid onset and shorter duration. dose 0.05mg/ml IV. agonsit at u opiod receptor. inhibits adenylate cyclase causes inhibition release of nociceptive substances sub P GABA dopamine.
Non depolarising neuromuscular blocking agents
competitive antagonists at Ach receptor at motor endplate. also block facilitatory presynaptic autoreceptors so inhibit release Ach in repetitive stim of motor nerve. most are metabolised in the liver or excreted via kidney except atracurium which hydrolyses spontaneously in plasma. Motor paralysis - helps facilitate endotracheal intubation. SE hypotension, bronchospasm, ganglion block.
depolarising neuromuscular blocking agent
suxamethonium/succinylcholine. muscle relaxant. duration 3 - 5 mins. persistent depolarisation at neuromusc junction, caused by mimiking effect of Ach without being rapidly hydrolised by acetylcholinesterase. leads to desensitisation. hydrolised by plasma cholinesterase (BuChE) butyrylcholinesterase. SE bradychardia and hyperkalemia. Inc intraoc pressure. Postop pain.
Cholinesterase inhibiting drugs
acetylcholinesterase and BuChE. used to reverse action of non depolarising neuromusc blocking drugs at the end of op (neostigmine). Cholinesterase inhibitors affect periphery and central cholinergic synapses so atropine or glucopyrrolate given to limit parasymp effects - antagonise muscarinic recept inhibit cholinergic transmission, atropine can cross BBB, prevents neostigmines muscarinic effects like bradycardia.
osmotic diuretics
Mannitol, treat raised intracranial pressure/cerebral oedema. inc solute conc in proximal tubule draw fluid from body and less water reabsorbed. also inc plasma osmolality inc flow of water from tissues into interstitial fluid and plasma.
sleep
state of physiological reversible unconciousness. the change from sleep to wake is mediated by reticular activating mech. wake to sleep is active proocess by arousal inhibitory mechanism based on partial blockage of thalamus and upper brainstem. Arousal system inhibited by sleep active GABAergic and gelaninergic neurons of ventrolateral preoptic nucleus, like off switch.
wakefulness
instant awareness - ability to integrate all sensory info from ecternal and internal environment. may be function of thalamocortical network. total conciousness: continuous awareness of eternal and internal environ both past and present with emotions rising from it.
circadian clock
biological clock detects dec in light. ganglion cells containing melanopsin are depolarised by light. projections run via axons in retino hypothalmic tract which project to suprachiasmatic nucleus SCN of ant hypothal.
activation of SCN
activation evokes responses in neurons whose axons first synapse in paraventricular nucleus of hypothalamus. these descend to preganglionic symp neurons in intermediolateral zone IML in lateral horns of thoracic spinal cord. these modulate neurons in superior cervical ganglia SCG whos postgang acons go to pineal gland causing secretion of melatonin. Melatonin inc as light dec, in elderly pineal gland produces less malatonin. SCN also govern BT, hormone sec, BP, urine.
retinohypothalmic tract, SCN neurons are GABA so inc light inc GABA pineal gland less active dec melatonin.
wakefulness - ascending arousal system
inc arousal and mediates wakefulness. flows from brainstem to thalamus hypo, basal forebrain and cortex. it has 2 components: through thalamus to corte - activate relay neurons and reticular nuclei essential for thalamocortical trans. two cholinergic structures PPT/LDT in BS and forebrain serve as origin. PPT/LDT neurons most active in wake and REM sleep. Use Ach.
Through lateral hypo and basal forebrain to cortes: moradrem of locus coeruleus, seratoninergic dorsal and median raphe nuclei, dopaminergic neurons of pariaqueductal grey matter, histaminergic from TMN. discharge most rapidly in wakefulness.
Orexin
neurotransmitter that regulates arousal wakefulness and appetite. strongly excite brain nuclei inc dopamine noradren histamine and Ach systems important in wake. in sleep Orexin is reduced.
sleep definition
readily reversible state of reduced responsiveness to and interaction with the environment. Coma and GA are not readily reversible so arent sleep.
stages of sleep
Usually 4-6 cycles in 8h. 80% is in non REM, dec with each cycle.
Non REM sleep
induced by nonREM on GABA neurons in hypothalamus and seratonin from raphe nuclei. Brainstem noradrenergic neurons show dec activity. Synchronised EEG. 4 stages: NREM1 light sleep, between wake and sleep EEG 4Hz, Theta waves. NREM2 deeper sleep, bruxism occurs-involuntary grinding of teeth. EEG 10Hz Theta and sleep spindles. NREM3 and 4, deepest NREM sleep, sleepwalking night terrors bedwetting. slowwave sleeo. less responsive to environ. EEG 3Hz. Delta waves.
skeletal muscles relaxed but maintain their tone. parasymp active promotes dec HR BP. Need for survival.
REM sleep
Desynchronized EEG, resembles awake state but with loss muscle tone-atonia. Comes after NREM has done 1-4 then 2-90mins. Brainstem cholinergic neurons in ascending arousal syst act as REMon cells. Inhibitory medullary reticulospinal neurons activated causing skeletal musc become flaccid and reflexes absent. only ocular resp and middle ear muscles active. all sens systems inhibited. inc BP metabolism and BF to brain. Dreams occur, PGO waves in EEG. Noradrenergic and serotonergic neurons REMoff back to NREM. Dec age. Integrates and consolidates memories, less REM could impede learning abilities.
Theories of sleep
Restoration theory: rest and recover. prepare to be awake again. cortex essential rest.
Adaptation theory: hide preditors, conserve energy, protective for some species.
adenosine
inhibitory effect on Ach Ne 5HT, which promotes sleep, it dec as sleep duration inc until modulatory systems arent inhibited and wakefulness resume.
Melatonin
secreated pineal body above the tectum, derivative of tryptophan. released in dark. helps initiate and maintain sleep.
zeitgebers
environmental time cues. absense keep 24 hour cycle.
conciousness
alert cognitive state in which you are aware continually of the external and internal environment both past and present with emotions arising from it. Unconciousness is lacking normal arareness of self or environment.
concussion
reversible state of unconsciousness thats bried without anu structural or pathological alteration.
coma
profound state of unconsciousness thats associated with depressed cerebral activity and the individual cant be aroused. usually occurs when theres dysfunction or injury involving both cerebral hemispheres or reticular formation.
stuporose
unconscious but can be roused by verbal command or pain for short periods and produce verbal responces
glasgow coma scale
used to assess depression of conciousness. eye, verbal and motor responce. score of less than 8 are in a coma. score greater than 12 is only minor head injury
vegetative state
unaware of self or surroundings, breathes spontaneously and has stable circulation and shows patterns of eye opening and closure that may stimulate sleep. a persistent vegetative state is irreversible-12 months after a head injury.
types of conciousness/coma
toxic metabolic encephalopathy. Locked in syndrome. minimally concious state, persistent vegetative state. chronic coma, come =after 6 hours. brain death. medically induced.
Seizures
most extreme form of synchronous brain activity, sign of pathology. Generalised - involves entire cortec, partial - limited area of cortex but can spread. neurons fire with synchrony, very large EEG. when its repeated its known as epilepsy. drugs that block GABA are convulsants. muscles are either tonic ongoing or clonic rhythmic so tonic clonic seizures. absense, tonic clonic.Partial seizures - in motor area clonic movement, sensory area abnormal sensation. deja vu. simple - no loss conciousness, complex, partial with secondary general. Febrile convulsions
post traumatic seizure
Immediate seizures are result of damage to cerebral cortex by excitotoxicity and iron from blood, cerebral oedema haemorrhage laceration. Late seizures due epileptogenesis in which neural networks are restructured so inc liklihood of being excited leading to seizures.
Elevated intercranial pressure
signs inc. drowsiness and diminished conciousness. Imaging show oedema. coma and unilateral pupillary changes are late signs and require immediate intervention. Initial treatment intubation and hyperventilation causing vasoconstriction and reducing blood vol. barbituates decomptessive hemicraniectomy or hypothermia used.
cranial oedema
vasogenic, influx of fluid and solutes through incomplete BBB. Cytotoxic oedema is cellular swelling. Treat - elevate head 30o, intubate and hyperventilate, IV mannitol, ventricular damage. osmotic and interstitial-hydrocephalus.
3 sites where herniation tends to occur
subfalcine-cingulated gyrus under falx cerebri. tentorial-uncus of temporal lope through tentorial notch. tonsillar-cerebral tonsils through foramen magnum onto resp and cardiac centres of medulla.
pupil fixed and dilated
sign of transtentorial herniation where medial temporal love herniated from middle into post fossa. the uncus is forced into the gap between the midbrain and edge of tentorium compressing occulomotor nerve causing fixed dilated pupil and collapeses post cerebral artery causing infrct.
craniotomy
surgical removal of part of the cranium, exposes brain and meninges for inpection and relive excessive pressure. hair shaved, scalp cleaned with iodine, incision made. Burr holes drilled and joined, bone flap removed and dura carefully folded back.
blood supply to the scalp
via 5 arteries, 2 from internal 3 from external carotid. Internal - supratrochlear, branch opthalmic. supraorbital also branch opthalmic.
external - superficial temporal, gives off frontal and parietal. Occipital. Post auricular. walls of BV attached to fibrous tissue of superficial fascial layer so cuts dont retract and bleed profusely.
skull fractures
If skin is broken known as compound fracture. Linear-most common, bends inwards so area around bends outwards. Diastatic-line transverses one or more sutures of skull causing a widening. Depressed-broken bone displaced inwards. High risk raised ICP, crushing tissue, requires surgery to lift pieces of bone off brain. Basilar-break at base of skull. blood in sinuses, CSF leak from nose or ears.
neuropsychological assessment
simple procedure: ask if can move, can respond in meaningfull way, asked name date, if can answer known as orientated x3 fully concious. Complex-reflexes, language etc.
Neurocognitive assessment
cognition is associated with intellectual functioning, perception, memory, mood, speech and language. Descriptive-type and severity of problem. Predictive-causes and consequences.
reasons for assessing cognitive function
provide differential diagnosis. Measure deficit. Guide rehab. Predict consequences of surgery. Monitor progress. Evaluate other interventions,pharmacology. Medico legal evaluation.
Intellectual functioning tests
Higher excecutive functioning (WAIS-R) Reduced accuracy or speed of processing. Reduced concentration.
Perception test
Visuo perception-object recognition. Audition-sound recog, localisation. Hallucinations. Altered olfactory kinaesthetic or gustatory experiences.
Memory
impaired recent memory. frequency estimation. sequencing. delayed response task.
mood
swings, aggressing, depression, anxiety
behaviour
sexual disinhibition, aggression, uncharacteristic responces.
right temporal lobe damage
memory, hearing, language understanding, info processing.
Rehabilitation
holistic approach. multidisciplinary team. Biopsychosocial. Goal directed. Reinforced and tailored. Includes-pharmacology, behavioural therapy, social retaining, physical retaining, family therapy, cognition therapy.
social support
Esteem support, informational, companionship, instrumental. main effect hypothesis SS itself is beneficial, absence is stressful. Stress buffering hypoth-helps cope with stress.
naloxone
opiod antagonist. rapidly redistributed.
