Case 10

Question 1

what does cognitive mean

Answer 1

interlectual functioning, mood, memory (perception, storage, retrieval), perception

Question 2

general anasethesia

Answer 2

medically induced coma, loss of protective reflexes resulting from GA agents.

Question 3

purposes of general anasthesia

Answer 3

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.

Question 4

premedication before GA

Answer 4

not everyone requires it, compliments GA. benzodiazepines, opiods, anticholinergics, antibiotic, antacids

Question 5

induction of GA

Answer 5

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.

Question 6

IV induction

Answer 6

injected, travels to brain, highly lipid soluble, rapidly enters brain, onset in one arm - brain time. initial recovery by redistribution, ultimate recovery elimination.

Question 7

Inhilation induction

Answer 7

vapour breathed into lungs, enters blood, travels to brain, highly lipid soluble, initial and ultimate recovery exhalation. Minimal amount metabolised.

Question 8

maintanence of GA

Answer 8

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.

Question 9

reversal of GA

Answer 9

stop anasthetics. neostigmine or glycopyrrolate reverse muscle relaxants.

Question 10

GABA receptor

Answer 10

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.

Question 11

two pore demain K channels

Answer 11

leak channels. inhalation inducing agents activate these channels causing hyperpolarisation. analgesic hyonitic and immobilising effects. not affected by intravenous agents.

Question 12

Potency of inhaled anaesthetic agents

Answer 12

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.

Question 13

propofol

Answer 13

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.

Question 14

Isoflurane

Answer 14

volatile anaesthetic, inhalation inducing agent used for maintanance. with O2 and NO. binds GABA NMDA and glycine receptors. SE hypotension vasodilation respiratory depression.

Question 15

Fentanyl

Answer 15

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.

Question 16

Non depolarising neuromuscular blocking agents

Answer 16

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.

Question 17

depolarising neuromuscular blocking agent

Answer 17

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.

Question 18

Cholinesterase inhibiting drugs

Answer 18

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.

Question 19

osmotic diuretics

Answer 19

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.

Question 20

sleep

Answer 20

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.

Question 21

wakefulness

Answer 21

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.

Question 22

circadian clock

Answer 22

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.

Question 23

activation of SCN

Answer 23

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.

Question 24

wakefulness - ascending arousal system

Answer 24

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.

Question 25

Orexin

Answer 25

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.

Question 26

sleep definition

Answer 26

readily reversible state of reduced responsiveness to and interaction with the environment. Coma and GA are not readily reversible so arent sleep.

Question 27

stages of sleep

Answer 27

Usually 4-6 cycles in 8h. 80% is in non REM, dec with each cycle.

Question 28

Non REM sleep

Answer 28

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.

Question 29

REM sleep

Answer 29

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.

Question 30

Theories of sleep

Answer 30

Restoration theory: rest and recover. prepare to be awake again. cortex essential rest.
Adaptation theory: hide preditors, conserve energy, protective for some species.

Question 31

adenosine

Answer 31

inhibitory effect on Ach Ne 5HT, which promotes sleep, it dec as sleep duration inc until modulatory systems arent inhibited and wakefulness resume.

Question 32

Melatonin

Answer 32

secreated pineal body above the tectum, derivative of tryptophan. released in dark. helps initiate and maintain sleep.

Question 33

zeitgebers

Answer 33

environmental time cues. absense keep 24 hour cycle.

Question 34

conciousness

Answer 34

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.

Question 35

concussion

Answer 35

reversible state of unconsciousness thats bried without anu structural or pathological alteration.

Question 36

coma

Answer 36

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.

Question 37

stuporose

Answer 37

unconscious but can be roused by verbal command or pain for short periods and produce verbal responces

Question 38

glasgow coma scale

Answer 38

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

Question 39

vegetative state

Answer 39

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.

Question 40

types of conciousness/coma

Answer 40

toxic metabolic encephalopathy. Locked in syndrome. minimally concious state, persistent vegetative state. chronic coma, come =after 6 hours. brain death. medically induced.

Question 41

Seizures

Answer 41

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

Question 42

post traumatic seizure

Answer 42

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.

Question 43

Elevated intercranial pressure

Answer 43

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.

Question 44

cranial oedema

Answer 44

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.

Question 45

3 sites where herniation tends to occur

Answer 45

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.

Question 46

pupil fixed and dilated

Answer 46

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.

Question 47

craniotomy

Answer 47

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.

Question 48

blood supply to the scalp

Answer 48

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.

Question 49

skull fractures

Answer 49

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.

Question 50

neuropsychological assessment

Answer 50

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.

Question 51

Neurocognitive assessment

Answer 51

cognition is associated with intellectual functioning, perception, memory, mood, speech and language. Descriptive-type and severity of problem. Predictive-causes and consequences.

Question 52

reasons for assessing cognitive function

Answer 52

provide differential diagnosis. Measure deficit. Guide rehab. Predict consequences of surgery. Monitor progress. Evaluate other interventions,pharmacology. Medico legal evaluation.

Question 53

Intellectual functioning tests

Answer 53

Higher excecutive functioning (WAIS-R) Reduced accuracy or speed of processing. Reduced concentration.

Question 54

Perception test

Answer 54

Visuo perception-object recognition. Audition-sound recog, localisation. Hallucinations. Altered olfactory kinaesthetic or gustatory experiences.

Question 55

Memory

Answer 55

impaired recent memory. frequency estimation. sequencing. delayed response task.

Question 56

mood

Answer 56

swings, aggressing, depression, anxiety

Question 57

behaviour

Answer 57

sexual disinhibition, aggression, uncharacteristic responces.

Question 58

right temporal lobe damage

Answer 58

memory, hearing, language understanding, info processing.

Question 59

Rehabilitation

Answer 59

holistic approach. multidisciplinary team. Biopsychosocial. Goal directed. Reinforced and tailored. Includes-pharmacology, behavioural therapy, social retaining, physical retaining, family therapy, cognition therapy.

Question 60

social support

Answer 60

Esteem support, informational, companionship, instrumental. main effect hypothesis SS itself is beneficial, absence is stressful. Stress buffering hypoth-helps cope with stress.

Question 61

naloxone

Answer 61

opiod antagonist. rapidly redistributed.