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

sleep Flashcards

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

A

non-arousal due to damage to RAS

21
Q

Decorticate Rigidity

A

Damage to brain above cerebellum and brainstem

Upper extremity flexion and lower extremity extension

22
Q

Decerebrate Rigidity

A

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

23
Q

Brown-Sequard’s Syndrome

A

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

Gun shot wound

24
Q

brown-sequard syndrome

Findings below the lesion:

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
Q

horners syndrome

A

If lesion occurs above T1, presents with Horner’s syndrome

26
Q

Horner’s Syndrome

A

Due to destruction of stellate (superior cervical) ganglion
Loss of sympathetic tone and predominant parasympathetic tone

27
Q

Horner’s Syndrome

S/S (lesion above T1)

A 
Ptosis (slight drooping of eyelids)
Anhidrosis ( absence of sweating)
Miosis (pupil constriction)
Enophthalamos
Flushing ,  temp
Nasal congestion 
Ipsalateral of injury
28
Q

Autonomic Dysreflexia / Autonomic Hyperreflexia Anesthesia considerations

A 
Prevent further cord damage
High dose steroid
Head stabilization 
Monitor BP, CVP, PCWP
Regional and deep general anesthesia
29
Q

Autonomic Dysreflexia / Autonomic Hyperreflexia

A

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
Q

CEREBELLUM “Little Brain”
functions of cerebellum
Spinocerebellum

A

Spinocerebellum– control rate, force, range, and direction of movement

31
Q

Layers of cerebellum

A

Granular layer
Purkinje cell layer – out puts are inhibitory
Molecular layer

32
Q

Clinical disorders of cerebellum – ataxia

A

Lack of coordination , intention tremors

Poor execution of movement , inability to perform alternating movements

33
Q

BASAL GANGLIA

A

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
Q

Lesion of subthalamic nucleus

A

Release of inhibition leads wild, flinging movements (hemiballismus)

35
Q

Lesion of striatum

A

Release of inhibition leads to Huntington’s disease (dancing movements)

36
Q

Lesion of substantia nigra

A

Destruction of dopamine producing neurons leads Parkinson’s disease
Over all inhibitory
Lead-pipe rigidity, tremors and reduced voluntary movements

37
Q

Parkinson’s disease

A

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
Q

parkinsons treatment

A

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
Q

MAO-B Inhibitor

A

Selegiline (deprenyl) selectively inhibit MAO-B
increase dopamine level in brain
Use in Parkinson’s disease

40
Q

Language

R Vs. L Hemisphere

A

Right hemisphere is dominant in facial expression

The left hemisphere is usually dominated with respect to language. Its lesion causes aphasia.

41
Q

Brocas area

A

Damage to Broca’s Area causes motor aphasia, in which speech and writing is affected but understanding is intact.

42
Q

Wernicke’s Area

A

Damage to Wernicke’s Area causes sensory aphasia, in which there is difficulty understanding written or spoken language- “word salad”

43
Q

brocas vs. wernicke

A

Broca’s is nonfluent aphasia with intact comprehension (expressive aphasia). Wernicke’s is fluent aphasia with impaired comprehension (receptive aphasia)

44
Q

short term memory

A

Short-term memory involves synaptic changes

45
Q

long term memory

A

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
Q

functions of cerebellum- vestibulocerebellum

A

Vestibulocerebellum– control balance and eye movements

47
Q

CEREBELLUM “Little Brain”
functions of cerebellum
pontocerebellum

A

Pontocerebellum– planning and initiation of movement

48
Q

autonomic hyperreflexia

NT outflow

A

Unopposed sympathetic out flow norepinephrine, B-hydroxylase and dopamine

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

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