Neurotransmitters Flashcards

1
Q

Acetylcholine

A

Low in Alzheimers - memory function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dopamine

A

V levels in basal ganglia - Parkinsons

Schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adrenaline and noradrenaine

A

V in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Serotonin

A

V in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GABA

A

V in epilepsy

V in Huntingtons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glutamine

A

From damage in stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Stroke

A

Ischaemic
•Obstruction of blood supply to a region of the brain
–Thrombosis (causes?)
–Atheroma (causes?)
–Tumour?
–Embolus (causes: atrial fibrillation, DVT, tumour fragment, infective endocarditis)
Stroke and Brain Damage
REMEMBER if motor or sensory cortex has the lesion, the opposite side of the body is affected! – “Decussation” or crossing over of fibers.
FAST
Face/Arms/Speech/Time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TIA = transient ischaemic attack

A

Temporarily blocked arteries

Cells weakened but don’t die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stroke Risk Factors

A
  • Age (more in older age group)
  • Gender (more in males)
  • Ethnicity (more in non-Europeans)
  • Heredity (family history present)
  • Excessive alcohol and cigarette consumption
  • High blood cholesterol levels
  • Diabetes mellitus
  • Hypercoagulability
  • Hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aneurysm

A

•An aneurysm is an abnormal dilation of the artery wall…bursting leads to a brain bleed
•The artery wall may be weakened by:
–Atheroma
–Destruction of elastin by proteolytic enzymes
–Continued high pressure on the collagen matrix due to hypertension
–Marfan’s syndrome

Treatment
- metal clip or wrapped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Head trauma

A

Glasgow coma scale
Vital signs
Blunt force
Coup/contrecoup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Concussion

A
  • Signs are a brief disruption in level of consciousness and amnesia. Full recovery is expected.
  • Recurrent concussions can cause permanent damage.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Contusion

A
  • Bruising of the brain.
  • Brain cells will die and effects vary according to area impacted.
  • Full recovery may not occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What changes would you notice with increased intracranial pressure for:

A
  • blood pressure ^
  • heart rate/pulse
  • temperature
  • pupils - fixed dilated
  • level of consciousness v

Treatment Mannitol
Diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tentorial Herniation (Coning)

A
  • The tentorium is a fold in the dura mater which separates the cerebrum and cerebellum. The upper brain stem passes through an opening in the tentorium.
  • With herniation, increased pressure above the tentorium forces part of the temporal lobe thru an opening, which squeezes the brain stem and damages its blood supply
  • This affects the reticular formation and results in coma.
  • Nerve III (oculomotor nerve) may be damaged due to increased pressure resulting in a fixed and dilated pupil, first on the side of herniation and then later on the other side as well
  • Permanent ischemic damage occurs if herniation reduces oxygenated blood below a critical threshold for more than a few minutes (especially if there is a reduction in blood pressure as well)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Alzheimer’s Disease

A

Impact
•Progressive, degenerative
•Diffuse atrophy of the cortex
•Widespread loss of cholinergic neurons Hippocampus – impaired memory, learning Amygdala – inappropriate emotions/ anxiety Frontal lobe – impaired speech, reasoning, personality (can be agitated, aggressive)
Alzheimer’s - Pathophysiology
•Neuritic/senile plaques
•Neurofibrillary tangles
•Loss of up to 95% of cholinergic innervation in the cortex
•Plus – decline of enzyme that produces acetylcholine
Alzheimer’s - Treatment
Cholinesterase inhibitor

17
Q

Parkinson’s Disease

A

•Progressive degeneration of dopaminergic neurons from substantia nigra
•Leads to reduction in dopamine activity in basal ganglia affecting:
–Learned, automatic movement
–Monitoring and smoothing of voluntary movements initiated by motor cortex
–Inhibition of antagonistic or unnecessary movements

18
Q

Tremor

A

Unilateral, pill rolling hand tremor.

May affect other limbs and head. - at rest

19
Q

Rigidity

A

1st general slowing and stiffness - leadpipe
Expressionless face
v swallowing

20
Q

Bradykinesia

A

Slowness of movement
slow speech - quieter/monotonous
less spontaneous
shuffling walk

21
Q

Huntingtons disease

A
  • Autosomal dominant
  • Progressive loss of neurons in the basal ganglia
  • Get increased motor output – “choreiform movements”
  • Usually presents 20-50 y
  • Personality and cognitive changes in later stages
22
Q

Multiple Sclerosis

A
  • Autoimmune, progressive, demyelination
  • Get neurodegeneration in later stages
  • Diagnosis usually 20-40y, more in females
  • Symptoms: Motor (limb weakness, loss of bladder/bowel control, speech), Sensory (numbness, pain), Visual (double vision, loss of vision), Cognitive (thinking)
23
Q

Epilepsy

A
  • Different types
  • Tonic/clonic
  • Grand mal
  • Petit mal
  • Temporal lobe
  • Common features – uncontrolled firing of a group of neurons; symptoms/presentation depend on location and extent of spread
  • Neurons – lowered seizure threshold or hypersensitive to hypoglycemia, hypernatremia, repeated sensory stimulation, fatigue, etc.
  • Drugs used to treat epilepsy increase levels of GABA (inhibitory neurotransmitter)
24
Q

Unipolar Depression

A

Along with decreased levels of noradrenaline and serotonin….
•Depressed may show dysfunction in limbic and frontal areas
•Chronic stress, with persistent high levels of corticotropin-releasing factor and cortisol leads to: insomnia, low appetite, decreased reproductive function, etc.

Aim to reduce chronic stress. DRUGS USED TO TREAT DEPRESSION:
SSRIS- block re-uptake of serotonin selectively MAOIs- non-selective- block noradrenaline breakdown TCAs- non-selective- block re-uptake
Selective serotonin reuptake inhibitor Monoamine oxidase inhibitor Tricyclic antidepressants

25
Q

Bipolar Depression

A

•Periods of deep depression are interrupted by bouts of mania
o Outbursts of over-activity, rapid speech and thinking, expansive optimistic ideas, possibly aggression and psychotic symptoms
o Mechanisms not as well understood: may be dysfunction in dopamine and/or glutamate activity

26
Q

Schizophrenia

A
  • Major psychotic illness – abnormal perception of reality
  • Cause unknown - genetic? drug induced? early neural development?
  • Positive symptoms: delusions, hallucinations, bizarre behaviour, paranoia
  • Negative symptoms: social withdrawal, low motivation, loss of affect, loss of speech
27
Q

Spina Bifida

A
  • Spina bifida means ‘split spine’
  • Results from an incomplete formation of the vertebral arches
  • Although can occur at any point along the vertebral column, is typically found in the lumbo-sacral region
  • Severe conditions may involve the spinal cord and cause spinal cord damage

•The more neurological structures contained within the sac the greater the neurological impairment
•Problems with infection are ongoing since the cyst wall is thin, porous and liable to rupture
•Spina bifida cystica is accompanied by hydrocephalus in 90% of cases
A number of environmental factors have been implicated as causing spina bifida. There appears to be a link between inadequate maternal levels of Folic acid and the incidence of spina bifida

28
Q

Lumbar disc herniation

A

• herniated discs can ‘push’ onto spinal nerves, compress spinal arteries reducing blood flow, directly damage the spinal cord etc causing spinal cord injury
Sciatica

29
Q

Spinal cord injury

A

Paralisys
Paraplegia - legs
Tetraplegia (aka quadriplegia) - arms and legs
Brown-Sequard syndrome- below injury level motor weakness or paralysis on one side of body.
Hemiplegia - one side paralysis

30
Q

poikilothermy

A

organism takes on the temperature of the environment.

v thermoregulation

31
Q

Pain

A

Three types
Nociceptive pain
- damaged tissue, starts in nociceptors
Inflammatory pain
- secretion of substances that lower pain threshold and amplify pain. Acute and chronic
Neuropathic pain
- caused by injury or disease to nervous system.

32
Q

A delta fibre

A

fast impulses - extreme stimulus - superficial - quick conduction - acute pain - protective response - localised- sharp/stabbing - reflex action.

33
Q

C fibres

A

Unmylinated - slow - respond to excessive heat - touch - chemicals - somatic - visceral - slower route - chronic pain - amplify local inflammation by releasing inflammatory chemicals.

34
Q

Three stimuli that activate nociceptors

A

Temperature
Pressure
Chemicals

35
Q

Sensory (1st order) neurons

A
  • Transmission of the electrical impulse to the dorsal horn of the spinal cord (1st order neuron)
  • Neurotransmitters released: glutamate, substance P, etc.
36
Q

Referred pain

A
  • Visceral and somatic pathways converge on the same spinal dorsal horn neurons projecting to the brain
  • Difficult for the brain to identify the original source of pain.

Heart in cheeks
Liver and lungs in neck/traps region

37
Q

Brain regions involved in perception and understanding of pain

A

Sharp pain - thalamus - hypothalamus

Dull/aching pain - Thalamus > primary somesthetic cortex > cortical centers - cognition anxiety insomnia.

38
Q

Gate theory and pain modulation

A

Pain can be modulated by simultaneous somatosensory input.