Memory

Question 1

Awareness

Answer 1

1) neuroscientists, philosophers - only Subjective experience
2) clinical anesthesiologist - consciousness + explict episodic memory.

Question 2

Connected / disconnected consciousness

Answer 2

1) Connected - the experience of environmental stimuli ( surgery )
2) Disconnected - endogenous experience

Question 3

Consciousness / responsiveness

Answer 3

A person may fully experience a stimulus (“ Open your eyes “ ) but not be able to respond (a patient is paralyzed but conscious during surgery )

Question 4

Brainstem. LC

Answer 4

Locus ceruleus. Norepinephrine is synthesized in the LC , located in the
pons and projects widely throughout the cortex . LC activity is highest during waking consciousness , decreased during NREM sleep , nadir REM sleep.
Role of norepinephrine: barbiturate anesthesia time is increased By antagonizing norepinephrine and reduced by agonizing it.
LC noradreneregic neurons modulate the state of isoflurane anesthesia as well as emergence therefrom.

Question 5

Brainstem :LDT /PPT

Answer 5

Laterodorsal/pedunculopontine tegmentum (LDT/PPT) the pons are the brain’s source of acetylcholine. Max activity during REM sleep,during which the cortex is aroused. Activation of cholinergic neuron in LDT or PPT induces REM sleep. Both states of cortical activation across the seep- wake cycle are associated with high cholinergic tone.
General anesthetic modulate cholinergic projection from the LDT /PPT

Question 6

Brainstem. PRF

Answer 6

Pontine reticular formation. GABA - primary inhibitory neurotransmitter in the brain, the actions Of GABA in the PFR are associated with cortical arousal. (increased time spent in the waking state when the GABAa receptor agonist muscimol is microinjected in the PFR.
Decreased levels of GABA in the PFR correlated with isoflurane-induced unconsciousness, muscular hypotonia, and decreased respiratory rate, sinse the effects of anesthetics are normally associated with a potentiation of GABA activity.
.

Question 7

Brainstem. VTA

Answer 7

Ventral tegmental area . Dopaminergic neurons of the VTA in the midbrain have not classically been considered key mediators of the sleep-wake cycle because of relatively less evidence of state - dependent changes compared with neurons in other brainstem nuclei. Electrical stimulation of VTA dopaminergic neurons can reverse anesthetic - induced unconsciousness

Question 8

Hypothalamus. VLPO

Answer 8

Ventrolateral preoptic nucleus. Neurons of VLPO max activity during NREM and REM sleep, the median preoptic nucleus ( MnPO ) is also active during sleep., correlated with inhibition of other arousal centers in the brainstem and hypothalamus. Given its potentially central role as a mediator of sleep, VLP0 became an attractive candidate as a mediator of anesthetic - induced unconsciousness, but that the effects of sleep deprivation associated with chronic VLPO lesions could overwhelm this role.
These neurons are depolarized ( activated ) propofol, pentothlal ,isoflurane.

Question 9

Hypothalamus. Orexinergic neurons.

Answer 9

Orexinergic neurons are found in the lateral hypothalamus and provide an important arousal stimulus for the cortex. Types : Orexin A and B. Orexinergic neurons inneverate other arousalb centers in the brainstem and basal forebrain. Fire maximally in the waking State, are suppressed during NREM sleep, show occasional bursts during phasic REM sleep. Dysfunctional of the Orexinergic system is associated with narcolepsy.
Orexin attenuate the effects of isoflurane, propofol, retained and barbiturate.

Question 10

Hypothalamus. TMN

Answer 10

Tuberomammillary nucleus (/TMN). located in the caudal hypothalamus and is the brain’s source of histamine, an arousal -promoting transmitter. TMN activity and histamine levels are highest during wakefulness and lowest during sleep. The TMN is thought to have a relationship of reciprocal inhibition with the sep- promoting GABA - ergic neurons of the VLPO.
Systemic administration of propofol , pentothat , and the GABA agonist muscimol result in decreased activity in the TMN.

Question 11

Thalamus

Answer 11

The thalamus has been proposed as an ON/OFF switch for anesthetic state transitions. The hyperpolarization of the thalamus would shift tonic firing to burst firing that - a with sleep - would prevent afferent sensory stimuli from arousing the cortex.
Spontaneous activation of th thalamus alon with other subcortical structures is correlated with recovery from anesthesia, suggest the involvement of the thalamus in the primitive or “core” consciousness observed at emergence. Thus if the mechanism of anesthetic -induced unconsciousness was achieved primarily by a suppression of cortical computation, a depressed thalamus should be the result.
Propofol induction/sevoflurane ⇒ concurrent suppression of thalamus and cortex.
Action Propofol on GABA receptors in the nucleus reticularis generates a hypersynchronous alpha rhythm (8-13 Hz) with the frontal cortex that blocks sensory input.
Alpha synchronization between thalamus and medial prefrontal cortex during propofol induction.

Question 12

Cortical -subcortical connectivity

Answer 12

1) Propofol - disruption connectivity between the thalamus and lateral frontal -parietal networks . NONSPECIFIC nuclei and the cortex best accountEd for a reduction in the level of consciousness by propofol
2) Sevofluran - functionally disconnect the thalamus and cortex , exp. frontal cortex
3)

Question 13

Consecutive stages of unconsciousness

Answer 13

1) Sedation - increase of local/regional signal synchrony and consequent breakdown of global connectivity.
2) Deep surgical anesthesia or disorder of consciousness -collapse of both local /regional synchrony and global connectivity

Question 14

Declarative memory

Answer 14

representation of prior events and knowledge that is accessible to consciousness and can be manipulated by attention and executive function.

Question 15

Episodic memory

Answer 15

1)recollection of events with clear spatiotemporal context ( as when recalling autobiographical events with a distinct sense of personal experience, time , place)
2) fast-mapping and highly dependent on the MTL as well as frontal and parietal structures.
3) Episodic memory - Recollection ⇒ involves remembering specific qualitative contextual details about a prior event. Familiarity ⇒ judgment - sense that an item has been encountered previously, but beyond that there are no added contextual details.

Question 16

Semantic memory

Answer 16

1)the capacity to recall and apply meaning , facts and knowledge without any sense of time and place for the acquisition of that knowledges
2) seowere and involves distributed cortical region that closely map to the default mode network, a large -scale system that is active during the resting state and flow of spontaneous cognition

Question 17

Procedural memory

Answer 17

Dependent on the caudate nucleus

Question 18

Working memory

Answer 18

1) refers to the capacity to maintain limited amounts of information in the Stream of consciousness , which can be manipulated to perform complex cognitive tasks such as reasoning, comprehension, and learning.
2) Current understanding of working memory suggest that it is served by persistent activity and flexible resource allocation in a distributed cortical network , with a critical hab in the dorsolatereal prefrontal cortex ( DLPFC ) interconnected with parietal cortex , thalamus, caudate, globus pallidus
3) Depends on declarative memory representations to provide semantic meaning and context. During working memory tasks, cortical perceptual areas ascotiated with representations of declarative memory become activated and show increased synchorny with prefrontal regions.
4) The transition of memory from short-term stores through to stable long_term stores is experienced as continuousus and was assumed to reflect sequential transfer across systems
5) Recent studies have reinforced the view Inot memories are formed in multiple system in parallel.

Question 19

Long- term potentiation, synaptic taggin, and the consolidation model of memory

Answer 19

1) Retroactive interference - temporally graded such that the susceptibility of the memoryis greatest immediately after learning and decreases with time
2) Cellular models - functional changes in synaptic strength can Occur in the absence of any structural change in dencherie spines.
3 ) synchronized hippocampah theta oscillations ( 4-8 Hz) appear critical to successful memory behaviors
4) The induction of most forms of Long-term potentiation (LTP) - activation of post- synaptic N- methyl - D - aspartame (NMDA ) receptors ⇒ influx Of Na +, Ca 2+. Rise in intracellular Ca2+ - critical trigger for LTP. Calcium - calmodulin _ dependent kinase II (Ca Mk II ) - then activated and autophosphorylated ⇒ cytoskeletal reconfiguration. > protein synthesis in soma and dendrites ⇒enduring structural change at the synapse. (Protein synthesis inhibitors prevent sustained LTP in vitro and learning in vivo..
LTP: early LTP (E-LTP) _ independent of protein synthesis, canbe sustained across an interval of min to hours. Late LTP .(L-LTP) dependent on intracellular signaling, protein synthesis, can be sustained across many days
.

Question 20

Mathematical modeling of anesthetic amnesia

Answer 20

-Ψ
Mt = λt
λ reflects the initial memory strength (an index of encoding)
Ψ express the rate of decay (an index of consolidation)
1) Propofol - archetypal amnestic drug - permits robust encoding of material, but the information undergoe accelerated decay because if a failure of consolidation.
2) Dexmedetomidine - archetypally causes memory impairment because of a failure of information to be strongly encoded but has little /no effect on the subsequent consolidation of memories that are encoded.
3) Midazolam - like a propofol at lower doses;with >doses a significant encoding impairment emerges.
4 ) Tiopental - causes marked encoding failure but demonstrates minimal effect on consolidation

Question 21

General anesthesia including

Answer 21

1) Hypnosis (ie, loss of consciousness)

2) Amnesia (ie, lack of recall)

3) Analgesia (ie, pain relief, antinociceptive properties) [2]

4) Akinesia (ie, immobility)

5)Autonomic and somatic block

Question 22

MAC value-it is…

Answer 22

MAC value – The MAC value is the concentration of an inhalation agent in the alveoli required to prevent movement in response to a noxious stimulus in 50 percent of subjects after allowing sufficient time for uptake and redistribution of the inhalation agent to reach a steady state

Question 23

Definition of minimum alveolar concentration (MAC) values

Answer 23

0.3 MAC -MACawake (MAC value below this will allow the patient to become conscious)
1 MAC- End-tidal concentration of anesthetic agent necessary to prevent movement in response to a surgical stimulus in 50% of patients
1.5 MAC- MAC value where 90% of patients will not move in response to a surgical stimulus
2.0 MAC- MAC-BAR (MAC value required to block autonomic responses to a surgical stimulus in 50% of patients)

Question 24

1 MAC for inhalation anesthetic

Answer 24

1) Nitrous oxide 104
2) Desflurane 6.6
3) Sevoflurane 1.8
4) Isoflurane 1.17
5) Halothane 0.75

Question 25

Factors that increase MAC

Answer 25

1)Chronic alcohol use
2)Infancy (highest MAC at 6 months)
3)Hypernatremia
4)Hyperthermia
5)Amphetamines
6)Cocaine
7)Ephedrine

Question 26

Factors that decrease MAC

Answer 26

1) Acute alcohol use
2) Older age
3) Hyponatremia
4) Hypothermia
5) Anemia (Hgb <5 g/dL)
6) Hypercarbia
7) Hypoxia
8) Metabolic acidosis
9) Pregnancy
10) Nitrous oxide
11) Opioids
12) Benzodiazepines
13) Propofol
14) Alpha2 agonists
15) Intravenous lidocaine

Question 27

Stage 1 of anesthesia depth

Answer 27

Analgesia state: Patient is conscious and rational, with decreased perception of pain.

Question 28

Stage 2 of anesthesia depth

Answer 28

Delirium stage: Patient is unconscious; body responds reflexively; irregular breathing pattern with breathholding

Question 29

Stage 3 of anesthesia depth

Answer 29

Surgical anesthesia: Increasing degrees of muscle relaxation; unable to protect airway

Question 30

Stage 4 of anesthesia depth

Answer 30

Medullary depression: There is depression of cardiovascular and respiratory centers

Question 31

Composition of salivary

Answer 31

1) Rate 100-100° CC/ day
2) Na - 50, K_20; Cl 40

Question 32

Composition of basal gastric secretion

Answer 32

1) volume_1000 CC/day
2) Na 100 ;KL10,Cl 140

Question 33

Composition of stimulated gastric secretion

Answer 33

1) volume 4300
2) Concentrations: Na 30
K10
Cl 140
H + 100

Question 34

Composition of bile

Answer 34

1) Volume % 500-1000
2) Na 140
K 5
Cl 100

Question 35

Composition of pancreatic

Answer 35

1) Volume 1000
2) Na 140
K 5
Cl 75
Bicarbonate-rich

Question 36

Composition of duodenum Secretion

Answer 36

1) Volume 1000-2000
2) Na 140
K 5
Cl 80

Question 37

Composition of duodenum Secretion

Answer 37

1) Volume 1000-2000
2) Na 140
K 5
Cl 80

Question 38

Composition of ileum secretion

Answer 38

1) Volume 100-2000
2) Na 140
K 5
Cl 70

Question 39

Composition of colon secretion

Answer 39

1) Volume -
2) Na 60
K 70
Cl 15