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Semester 3 > Case 10 - Yaffas Part 2 > Flashcards

Case 10 - Yaffas Part 2 Flashcards

1
Q

what are the two main forms of cholinesterase

A

acetylcholinesterase (AChE)

butyrylcholinesterase (BuChE)

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2
Q

what is AChE

A

mainly membrane bound
relatively specific for acetylcholine
responsible for rapid acetylcholine hydrolysis at cholinergic synapses

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3
Q

what is BuChE

A

relatively non-selective
occurs in plasma and many tissues

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4
Q

what is the clinical use of anti cholinesterase drugs

A

To reverse the action of non-depolarising neuromuscular-blocking drugs at the end of an operation (neostigmine).
Atropine/Glycopyrrolate must be given to limit parasympathomimetic effects.
To treat myasthenia gravis (neostigmine).

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5
Q

what are the autonomic side effects of cholinesterase inhibitors

A

bradycardia
hypotension
bronchocontriction

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6
Q

what are the muscular side effects

A

Muscle fasciculation
Twitch tension
Depolarisation block

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7
Q

what is the mechanism of action of neostigmine

A

blocks acetylcholinesterase

increases Ach in the neuromuscular junction (both nicotinic and muscarinic)

increases muscular junction

acts to reverse effects of muscle relaxants

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8
Q

what are examples of muscarinic receptor antagonists

A

atropine and glycopyrrolate

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9
Q

what do muscarinic receptor anatagonists do

A

antagonise the muscarinic receptor and thus inhibit cholinergic transmission

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10
Q

what can atropine do that glycopyrolate cannot

A

atropine can cross the blood brain barrier whereas glycopryrolate cannot

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11
Q

what are muscarinic receptor antagonists used to do

A

limit parasympathethomimetic effects caused by neostigmine

it prevents neostigmine muscarinic effect such as bradycardia

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12
Q

what is mannitol

A

an osmotic diuretic

it is inert in humans but it occurs naturally

the drug is used to treat raised intracranial pressure

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13
Q

what is the mechanism of action of mannitol

A

These are pharmacologically inert substances that are filtered in the glomerulus but not reabsorbed by the nephron.
They cause diuresis because they increase the solute content of the fluid in the proximal tubule and collecting tubules.
This draws fluid from the body into the proximal tubule, thus decreasing the volume of fluid inside the body.
The result of this is that less water is reabsorbed and also less sodium.
This leads to a decrease in extracellular fluid volume.

Also, they increase the plasma osmolality.
This increases the flow of water from tissues (brain and CSF included) into the interstitial fluid and plasma.
This reduces the intracranial pressure.

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14
Q

what is sleep

A

a state of physiological reversible unconsciousness

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15
Q

what is the change from sleep to wakefulness mediated by

A

the reticular activating mechanism

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16
Q

what is the change from wakefulness to sleep affected by

A

it is an active process affected by an arousal inhibitory mechanism based on a partial blockade of the thalamus and upper brainstem

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17
Q

what is the cognitive change between sleep and wakefulness accompanied by

A

changes in the autonomic system, the cerebral blood flow and cerebral metabolism

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18
Q

what is instant awareness

A

the ability to integrate all sensory information from the external environment and the internal environment of the body

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19
Q

what is awareness a function of

A

the thalami-cortical network in the cerebral hemispheres, which forms the final path of the sleep/wake mechanism

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20
Q

what is awareness an essential component of

A

total consciousness (defined as continuous awareness of the external and internal environment, both past and present, together with the emotions arising from it)

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21
Q

what is the circadian clock

A

Human sleep occurs with circadian periodicity. The biological clock detects decreases in light levels as night approaches.
Ganglion cells containing melanopsin are depolarized by light.
Projections run via axons running the retino-hypothalamic tract, which projects to the suprachiasmatic nucleus (SCN) of the anterior hypothalamus, the site of the circadian control of homeostatic functions.

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22
Q

what is the activation of the SCN

A

Activation evokes responses in neurons whose axons first synapse in the paraventricular nucleus (PVN) of the hypothalamus.
These neurons descend to the preganglionic sympathetic neurons in the intermediolateral zone (IML) in the lateral horns of the thoracic spinal cord.
These preganglionic neurons modulate neurons in the superior cervical ganglia (SCG) whose postganglionic axons project to the pineal gland.
This causes secretion of melatonin into the bloodstream.

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23
Q

when is melatonin increased

A

as the light in the environment decreases. in the elderly, the pineal gland produces less melatonin

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24
Q

where is melatonin found

A

the pineal gland

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25
Q

what is the ascending arousal system

A

increases arousal and mediates wakefulness

flows from the brainstem through the thalamus, hypothalamus and basal forebrain to the cerebral cortex

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26
Q

what is the first component of the ascending arousal system

A

Through the thalamus to the cerebral cortex.

These projections activate relay neurons and reticular nuclei (in the thalamus) essential for thalamocortical transmission.

Two cholinergic structures (PPT/LDT) in the brainstem and basal forebrainserve as the origin of these projections.

PPT/LDT neurons are most active during wakefulness and rapid eye movement (REM) sleep and discharge more slowly during non-REM (NREM) sleep, a period when cortical activity is reduced.

Transmission to the reticular nucleus promotes a state of excitability and wakefulness (“reticular activating system”).

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27
Q

what do projection to the thalamus use

A

acetylcholine

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28
Q

what is the second component of the ascending arousal system

A

Through the lateral hypothalamus (LH) and basal forebrain (BF) to the cerebral cortex.
It comprises a number of monoaminergic cell populations, including:
Noradrenergic neurons of the locus coeruleus (LC)
Serotoninergic (5-HT) dorsal and median raphe nuclei
Dopaminergic neurons of the ventral periaqueductal grey matter
Histaminergic neurons from TMN

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29
Q

features of neurones in the monoaminergic systems

A

have broad action potentials, discharging most rapidly during wakefulness, slowing during NREM sleep and showing little activity during REM sleep

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30
Q

what is orexin

A

a neurotransmitter that regulates arousal, wakefulness and appetite

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31
Q

orexin nucleus activity during wakefulness

A

strongly excite various brain nuclei with important roles in wakefulness including the dopamine, norepinephrine, histamine and acetylcholine system.

also helps stabilise wakefulness and sleep

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32
Q

what happens to orexin activity during sleep

A

the activity is reduced

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33
Q

what are the stages of sleep

A

consist of non-REM stages that vary clinically with an REM stage during which the EEG cycles between a desynchronised state and a synchronised state

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34
Q

how many sleep cycles are there in an 8hr period of sleep

A

4-6 sleep cycles

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35
Q

how much of the sleep cycle is spent in non-REM sleep

A

80% - amount decreases with each cycle

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36
Q

how much of the sleep cycle is spent in REM sleep

A

20% - and increased with each cycle

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37
Q

what is non-REM sleep induced by

A

“non-REM-on” GABA neurons in the hypothalamus.
Serotonin from the raphe nuclei.

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38
Q

what has decreased activity during non-REM sleep

A

brainstem noradrenergic neurones

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39
Q

what is non-REM sleep characterised by

A

progressively synchronised EEG

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40
Q

four stages of non-REM sleep

A
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41
Q

what happens to skeletal muscles during non-REM sleep

A

skeletal muscles relax but maintain their tone

42
Q

features of parasympathetic nervous system during non-REM sleep

A

is active and promotes gastric motility and a decease in heart rate and BP

43
Q

what is REM sleep characterised by

A

sudden conversion from a synchronized to a desynchronized EEG, resembling that of the awake state combined with a loss of muscle tone (atonia), which results in an active nervous system in an inactive body.

44
Q

when does REM sleep commence

A

only after non-REM sleep progresses through stages 1-4 and back to state 2, a cycle that lasts about 90. mins

45
Q

what initiates REM sleep

A

brainstem cholinergic neurones in the ascending arousal system act on ‘REM-on’ cells

46
Q

what is activated during REM sleep

A

inhibitory medullary reticulospinal neurones, causing skeletal muscles to become flaccid and muscle stretch reflexes to be absent

47
Q

what are the only muscles to remain active

A

the ocular, respiration and middle ear muscles

48
Q

are all sensory systems inhibited during REM sleep

A

yes

49
Q

what is there an increase of during REM sleep

A

increase in BP, metabolism, and blood flow to the brain

50
Q

what are penile and clitorial erections features of

A

REM sleep

51
Q

when do most dreams occur

A

during REM sleep, and the visual images precieved during dreaming are associated with PGO waves int he EEG

52
Q

what initiates a transition from REM sleep back to non-REM sleep

A

noradrenergic and serotenergic neurones act as ‘REM-off’ cells initiating the transition

53
Q

what does the amount of daily REM sleep decrease with

A

age

54
Q

what type of sleep do we need to survive

A

need non-REM sleep in order to survive

55
Q

what is the theory of restoration

A

rest and recover
prepare to be awake again
no exactly certain what is restored - cortex can achieve some form of essential rest during non-REM phases

56
Q

what is the theory of adaptions

A

less obvious - sleep to hide from predators - out most vulnerable state

adaption for conserving energy

57
Q

what is consciousness defined as

A

an alert cognitive state in which you are aware continually aware of the external and internal environment, both past and present, together with the emotions arising fro it

it is also the maitenance of an alert state

58
Q

what does someone have to have in order to be fully conscious

A

have an intact ascending reticular activating system (awake) in the brainstem and a functioning cerebral cortex (aware)

59
Q

what is a coma

A

profound state of unconsciousness that is associated with depressed cerebral activity from which the individual cannot be aorused

60
Q

what is a vegetative state

A

is a clinical condition, in which the patient is unaware of self or surroundings, breathes spontaneously and has stable circulation and shows patterns of eye closure and opening that may simulate sleep.
However, there is no intelligent communication coming from the patient.
A persistent vegetative state is irreversible.
A person is said to be in a persistent vegetative state if they are still in one 12 months after a head injury.

61
Q

what is a generalised seizure

A

involves the entire cerebral cortex, of both hemispheres

62
Q

what is a partial seizure

A

involves only a limited area of the cortex, but it can spreaf

63
Q

what happens in both types of seizures

A

the neurones within the affected areas fire with a synchrony that never occurs during normal behaviour

this is why seizures are usually accompanied by very large EEG pattens

64
Q

what Is the condition known as when a person experienced repeated seizures

A

epilepsy

65
Q

what are potent convulsants

A

drugs that block GABA

66
Q

what drugs are potent convulsants

A

drugs that block GABA receptors

67
Q

how do anticonvulsants work

A

Prolonging the inhibitory actions of GABA (e.g. barbiturates, benzodiazepines).
Decrease the tendency for certain neurons to fire high-frequency action potentials (e.g. phenytoin, carbamazepine).

68
Q

what do the behavioural features of a seizure depend on

A

the neurones involved and the patterns of their activity

69
Q

how is behavioural disrupted during generalised seizures

A

virtually all corticalneurones participate, so behaviour is completely disrupted for many mintues

70
Q

what is the tonic-clonic seizure

A

consciousness is lost, while all muscle groups may be driven by tonic (ongoing) activity or by clonic (rhythmic) patterns, or by both in sequence

71
Q

what can partial seizures be

A

instructive

72
Q

what happens if partial seizures begin in a small area of the motor cortex

A

they can cause clonic movement of part of a limb

73
Q

what can happen if seizures begin in a sensory area,

A

they can trigger an abnormal sensation or aura such as an odd smell or sparkling lights

74
Q

what are the early signs of elevated ICP

A

drowsiness and a diminished Level of consciousness

75
Q

what are late signs of raised ICP

A

coma and unilateral pupillary changes

76
Q

what is emergent treatment of elevated ICP most quickly achieved by

A

intubation and hyperventilation which causes vasoconstriction and reduces cerebral blood volume

77
Q

what is sometimes used for refractory elevations of ICP, although these have a significant side effect and not been proven to improve outcome

A

high dose barbiturates, decompressive hemicraniacetomy or hypothermia

78
Q

what are the two principles of oedema

A

Vasogenic oedema refers to the influx of fluid and solutes into the brain through an incompetent blood-brain barrier (BBB).
Cytotoxic oedema refers to cellular swelling.

79
Q

what does cranial oedema that is clinically significant usually represent

A

a combination of vasogenic and cellular components

80
Q

what is the treatment for cranial oedema

A

elevate head to 30 degrees

intubate and hyperventilate - reduce cerebral blood flow due to vasoconstriction

IV mannitol - osmotic diuretic

ventricular damage

81
Q

what is a craniotomy

A

this is a surgical removal of part of the cranium, performed to expose brain and meninges for inspection or biopsy or to relieve excessive intracrnaial pressure

82
Q

what is the procedure of a craniotomy

A

The hair is shaved, the scalp is cleaned with iodine solution, and an incision is then made to expose the skull.
Burr holes are drilled through the skull at several locations.
The burr holes are then joined together.
The bone flap is removed, exposing the dura.
The dura is then carefully opened and folded back.

83
Q

what is the blood supply to the scalp via

A

five pairs of arteries, two from the internal carotid and three from the external carotid

84
Q

whast are the two arteries from the internal carotid

A

Supratrochlear arteryto the midline forehead. The supratrochlear artery is a branch of the ophthalmic branch of the internal carotid artery.

Supraorbital arteryto the lateral forehead and scalp as far up as the vertex. The supraorbital artery is a branch of the ophthalmic branch of the ICA.

85
Q

what are the 3 arteries of the external carotid

A

Superficial temporal arterygives off frontal and parietal branches to supply much of the scalp.

Occipital arterywhich runs posteriorly to supply much of the posterior aspect of the scalp.

Posterior auricular artery ascends behind the auricle to supply the scalp above and behind the auricle.

86
Q

how can a small scalp wound bleed profusely

A

the walls of the blood vessels are firmly attached to the fibrous tissue of the supericial fascial layer, hence cut ends of the vessels here do not readily retract

87
Q

what is a compound fracture

A

when the skin is also broken

88
Q

types of fracture table

A
89
Q

what is a neuropsycholoigcal assessment (simple procedure)

A

Asking whether the patient is able to move and react to physical stimuli.
If so, the next question is whether the patient can respond in a meaningful way to questions and commands.
If so, the patient is asked for name, current location, and current day and time.
A patient who can answer all of these questions is said to be “oriented times three” (sometimes denoted “Ox3” on a medical chart), and is usually considered fully conscious.

90
Q

what is a complex neurological examination

A

A formal neurological examination runs through a precisely delineated series of tests, beginning with tests for basic sensorimotor reflexes, and culminating with tests for sophisticated use of language.

91
Q

what is cognition associated with

A

intellectual functioning

perception

memory

mood

speech and language

92
Q

what are the type types of assessment

A

descriptive:
- type and severity of the problem

predictive:
- to explain causes and consruwneces pf defect

93
Q

assessment

A

Intellectual Functioning
Higher executive functioning (WAIS-R).
Reduced accuracy / or speed in time pressure processing.
Reduced concentration span.

Perception
Visuo-perceptual (object recognition)
Audition (sound recognition, localisation)
Hallucinations
Altered olfactory, kinaesthetic or gustatory experiences

Memory
Impaired recent memory
Frequency estimation
Sequencing
Delayed response task

Mood
Lability (swings)
Aggression
Depression
Anxiety

Speech and Language
Lability (swings)
Aggression
Depression
Anxiety

Behaviour
Sexual disinhibition
Aggression
Uncharacteristic responses (described as personality change)

94
Q

what is the rehabilitation plan

A
95
Q

what does right temporal lobe damage and part removal do

A

memory/hearing/language understanding / info processing

96
Q

preoperative oedema consequences

A

additional damage to residual tissue

97
Q

what is dense hemioarwsus

A

on going disability / consequences

98
Q

what is esteem support

A

whereby other peppleincrease ones own self esteem

99
Q

what is informational support

A

whereby other people are available to offer advice

100
Q

what is compqnioshup

A

which involves support though activites

101
Q

what is instrumental support

A

involves physical help

102
Q

what does the stress buffering hypothesis suggest

A

that social support helps individuals to cope with stress

Semester 3 (94 decks)

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