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Spring '20/ L. A&P > sleep > Flashcards

sleep Flashcards

(48 cards)

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1
Q

Normal occurrence of REM
Adult
Child
Elderly

A

adult 4-5
child 4
elderly 3

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2
Q

sleep- wake cycle control in the brain

A

suprachiasmatic nucleus of hypothalamus

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3
Q

NREM sleep

A

(slow wave) non-rapid eye movements

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4
Q

REM sleep %

A

(fast wave) rapid eye movements [25%]

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5
Q

4 stages of NREM

A

Stage 1; Light Sleep [5%]
Stage 2; Deeper sleep [45%]
Stage 3-4 [25%]; Deepest , bed wetting, sleepwalking and night terror
Benzodiazepine decrease stage 4, useful for night terror and sleepwalking
Imipramine is used to treat enuresis since it decrease stage 4 sleep

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6
Q

REM Sleep characteristics

A

Every 90 min.
Beta wave ( like awake)
Increased and variable pulse
Dreams- you can tell the next moring
Tremendous loss of muscle tone- paralyzed
Erections
Decreases with benzodiazepines and old age

REM sleep is like sex: increase pulse , penile/clitoral erection, decrease with age

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7
Q

This condition is characterized by problem of insufficient sleep despite an adequate opportunity for sleep

A

insomnia

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8
Q

This is an intense and irresistible urge to sleep during daytime activities.

A

narcelopsy

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9
Q

This is an obstruction of respiratory air-ways during sleep

A

sleep apnea

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10
Q

In this condition REM sleep is entered directly from waking state and there is profound reduction of muscle tone and paralysis . This results fall on ground and inability to move

A

Cataplexy

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11
Q

Sleep Apnea due to extreme obesity

A

Pickwichian syndrome

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12
Q

This stage of sleep is related to bed-wetting

A

Stage 3 & Stage 4 of nonrem

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13
Q

Primary Motor Cortex“ motor strip”

A

Located in the precentral gyrus (area 4)
Composed of pyramidal cells whose axons make up the corticospinal tracts
Allows conscious control of precise, skilled, voluntary movements
Motor homunculus “little man” – represents areas of presentation of various organ in motor cortex

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14
Q

Primary motor cortex
damage
epileptic events

A

damage-stroke

epileptic events - jacksonian seizures

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15
Q

Premotor Cortex (area 6)

A

Located anterior to the precentral gyrus
Controls learned, repetitious, or patterned motor skills e.g. typing
Coordinates simultaneous or sequential actions
Involved in the planning and mental rehearsal of a movement

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16
Q

PYRAMIDAL (CORTICOSPINAL)

TRACT – Upper Motor Neurons

A

Most important output pathway from motor cortex to spinal cord
Fibers cross to opposite side –LCT
Fibers do not cross – VCT
Relay on interneurons and anterior horn cells of spinal cord

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17
Q

EXTRAPYRAMIDAL TRACTS

A 
All tracts other than pyramidal tract
Rubrospinal tract
Pontine reticulospinal tarct
Medullary reticulospinal tract
Lateral vestibulospinal tract
Tectospinal tract
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18
Q

Upper motor neuron lesions signs

A

Spastic paralysis, increased tendon reflexes, Bibinski sign +ve

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19
Q

Lower motor neuron lesion signs

A

Atrophy, flaccid paralysis, absent tendon reflex , Bibinski sign -ve

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20
Q

Coma

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A

non-arousal due to damage to RAS

21
Q

Decorticate Rigidity

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A

Damage to brain above cerebellum and brainstem

Upper extremity flexion and lower extremity extension

22
Q

Decerebrate Rigidity

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A

Damage to brainstem and cerebral lesions
Arms and legs extension
Mechanical ventilation is required

23
Q

Brown-Sequard’s Syndrome

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A

Hemisection (transection on only one side) of spinal cord.

Gun shot wound

24
Q

brown-sequard syndrome

Findings below the lesion:

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A

Ipsilateral UMN signs (corticospinal tract)
Ipsilateral loss of fine touch, vibration, proprioception sense (dorsal column tract)
Contralateral loss of light touch, pain, temperature sense (spinothalamic tract)
Ipsilateral loss of all sensations at level of lesion.
LMN signs (e.g. flaccid paralysis) at level of lesion

25
horners syndrome
If lesion occurs above T1, presents with Horner’s syndrome
26
Horner’s Syndrome
Due to destruction of stellate (superior cervical) ganglion Loss of sympathetic tone and predominant parasympathetic tone
27
Horner's Syndrome | S/S (lesion above T1)
``` Ptosis (slight drooping of eyelids) Anhidrosis ( absence of sweating) Miosis (pupil constriction) Enophthalamos Flushing ,  temp Nasal congestion Ipsalateral of injury ```
28
Autonomic Dysreflexia / Autonomic Hyperreflexia Anesthesia considerations
``` Prevent further cord damage High dose steroid Head stabilization Monitor BP, CVP, PCWP Regional and deep general anesthesia ```
29
Autonomic Dysreflexia / Autonomic Hyperreflexia
Spinal cord injury at or above T6 (mid thoraric) Unopposed sympathetic out flow norepinephrine, -hydroxylase and dopamine Life threatening - hypertensive crisis, headache, vasoconstriction, skin pallor below the level of lesion Bradycardia due to baroreceptor reflex, profuse sweating, vasodilation and skin flushing above the level of lesion
30
CEREBELLUM “Little Brain” functions of cerebellum Spinocerebellum
Spinocerebellum– control rate, force, range, and direction of movement
31
Layers of cerebellum
Granular layer Purkinje cell layer – out puts are inhibitory Molecular layer
32
Clinical disorders of cerebellum – ataxia
Lack of coordination , intention tremors | Poor execution of movement , inability to perform alternating movements
33
BASAL GANGLIA
Consists of striatum, globus pallidus, subthalamic nuclei and substantia nigra Modulates thalamic out flow to motor cortex to plan and execute smooth movement Many synaptic connections are inhibitory and use GABA
34
Lesion of subthalamic nucleus
Release of inhibition leads wild, flinging movements (hemiballismus)
35
Lesion of striatum
Release of inhibition leads to Huntington’s disease (dancing movements)
36
Lesion of substantia nigra
Destruction of dopamine producing neurons leads Parkinson’s disease Over all inhibitory Lead-pipe rigidity, tremors and reduced voluntary movements
37
Parkinson’s disease
decrease dopamine Destruction of dopaminergic neurons of substantia nigra Antipsychotic drugs- MCC Resting Tremors, lead-pipe Rigidity, Akinesia ,Postural instability TRAP Mask-like face, shuffling gait, pill rolling tremors
38
parkinsons treatment
Levodopa (dopamine cannot cross BBB) + carbidopa (DOPA decorboxylase inhibitor) combination - Sinemet ® Dopamine-receptor agonists (bromocriptine, pramipexole) MAO-B inhibitor ; Selegiline to increase dopamine activity Amantadine (antiviral) Anticholinergic Benztropine To counteract excessive action of acetylcholine
39
MAO-B Inhibitor
Selegiline (deprenyl) selectively inhibit MAO-B increase dopamine level in brain Use in Parkinson’s disease
40
Language | R Vs. L Hemisphere
Right hemisphere is dominant in facial expression | The left hemisphere is usually dominated with respect to language. Its lesion causes aphasia.
41
Brocas area
Damage to Broca’s Area causes motor aphasia, in which speech and writing is affected but understanding is intact.
42
Wernicke’s Area
Damage to Wernicke’s Area causes sensory aphasia, in which there is difficulty understanding written or spoken language- “word salad”
43
brocas vs. wernicke
Broca’s is nonfluent aphasia with intact comprehension (expressive aphasia). Wernicke’s is fluent aphasia with impaired comprehension (receptive aphasia)
44
short term memory
Short-term memory involves synaptic changes
45
long term memory
Long-term memory involves structural changes in nervous system and is more stable Bilateral lesion of hippocampus block the ability to form new long-term memory
46
functions of cerebellum- vestibulocerebellum
Vestibulocerebellum– control balance and eye movements
47
CEREBELLUM “Little Brain” functions of cerebellum pontocerebellum
Pontocerebellum– planning and initiation of movement
48
autonomic hyperreflexia | NT outflow
Unopposed sympathetic out flow norepinephrine, B-hydroxylase and dopamine

Spring '20/ L. A&P (21 decks)

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