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214.201 > Nervous > Flashcards

Nervous Flashcards

1
Q

What is in the central nervous system (CNS)?

A

Brain & spinal cord

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2
Q

What is in the peripheral nervous system?

A

Everything apart from the brain & spinal cord

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3
Q

What does the motor efferent division do?

A

Conducts impulses from CNS to effectors with somatic and visceral sensory nerve fibres

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4
Q

What does the sensory afferent division do?

A

Conducts impulses from receptors to CNS with motor nerve fibres

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5
Q

What does the somatic nervous system do?

A

Conducts impulses from the CNS to skeletal muscles

- Somatic motor (voluntary)

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6
Q

What does the autonomic nervous system do?

A

Conducts impulses from the CNS to the cardiac muscles, smooth muscles and glands
- Visceral motor (involuntary)

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7
Q

What does the sympathetic division do?

A

Mobilises body systems during activity

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8
Q

What does the parasympathetic division do?

A

Conserves energy; promotes housekeeping functions during rest

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9
Q

What do neurons do?

A
  • Communicate by electronic and chemical receptors and transmitters
  • Messengers of the brain
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10
Q

What are the neurotransmitters in the brain?

A
  • Acetylcholine
  • Dopamine
  • Noradrenaline/adrenaline
  • Serotonin
  • GABA
  • Beta-endorphins
  • Gluatamine
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11
Q

What are low levels of acetylcholine associated with?

A

Alzheimers

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12
Q

What are low levels of dopamine associated with?

A
  • Parkinson’s disease

- Dopamine hypothesis for schizophrenia

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13
Q

What are varied levels of noradrenaline/adrenaline associated with?

A
  • Elevated levels with arousal & excitement

- Low levels in depression

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14
Q

What are low levels of serotonin associated with?

A

Depression

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15
Q

What are low levels of GABA associated with?

A

Convulsions & epilepsy

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16
Q

What is over activation of glutamine associated with?

A
  • Neural damage and death

- Damage from stroke

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17
Q

What stroke is more common?

A

Ischaemic stroke

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18
Q

What is an ischaemic stroke?

A

A blood clots stop the blood of blood to an area of the brain

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19
Q

What are causes of an ischaemic stroke?

A
  • Thrombus (blood clot, damage to inside of blood vessel, fatty streak, plaque platelets stick to)
  • Atheroma (atherosclerosis clot)
  • Tumour (squeeze and press on blood vessels)
  • Embolus (clot that travels from somewhere else)
  • Atrial fibrillation (uncoordinated contraction of heart causing blood to recirculate and clot)
  • DVT (deep vein thrombosis)
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20
Q

What is a hemorrhagic stroke?

A

Bursting blood vessel in the brain

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21
Q

What causes a hemorrhagic stroke?

A
  • Aneurysm (abnormal dilation of the artery wall causes bursting leads to a brain bleed leading to apoptosis killing further cells surrounding)
  • Congenital arteriovenous malformation - abnormal connection between arteries and veins
  • Trauma
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22
Q

What is the difference between stroke and MI?

A
  • A stroke is when neurons die

- A MI is when heart muscle dies

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23
Q

What is the pathophysiology of a hemorrhagic stroke?

A
  • Blood leaks out of the cerebral circulation
  • Nowhere for blood to go inside the enclosed cranial cavity
  • Increased pressure on delicate neurons and blood vessels
  • Less blood for perfusion of downstream tissue
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24
Q

What weakens the artery wall?

A
  • Atheroma
  • Destruction of elastin by proteolytic enzymes
  • Continue high pressure on the collagen matrix due to hypertension
  • Marfan’s syndrome
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25
Q

What is decussation?

A

Brain controls opposites side of the body

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26
Q

What are signs and symptoms of a stroke?

A
  • FAST (Face dropping, Arm weakness, Speech difficulty, Time)
  • Gait (ataxia) difficulties, balance
  • Dysphagia
  • Cognitive issues
  • Anxiety
  • Hemi-neglect
  • Visual field changes
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27
Q

What is a TIA?

A
  • Transient ischaemic attack

- Result when cerebral artery is temporarily blocked, decreasing blood flow to brain

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28
Q

What are some stroke risk factors?

A
  • Increased age
  • Gender (male)
  • Ethnicity (more in non-europeans)
  • Heredity
  • Excessive alcohol and cigarette consumption → kills blood cells; increases BP
  • High blood cholesterol levels (high ratio of LDL vs HDL; fatty acids)
  • Diabetes → hypertension, hyperglycaemia
  • Hypercoagulability
  • Hypertension
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29
Q

What are modifiable risk factors?

A
  • Excessive alcohol + cigarette consumption
  • Cholesterol levels
  • Hypertension
  • Type 2 diabetes
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30
Q

How do you diagnose a stroke?

A
  • Angiogram

- MRI

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31
Q

How do you treat ischaemic stroke?

A

The objective - remove obstruction & reperfusion

- t-PA tissue plasminogen activator, activate plasmin to dissolve clot e.g. Atleplase

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32
Q

How do you treat haemorrhagic stroke?

A

The objective - stop bleeding, stabilise intracranial pressure

  • Decrease BP, anti-seizure meds, drain/evacuate, clip/coil aneurysm
  • Sit the patient up to decrease pressure in head
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33
Q

What is a contusion?

A

Bruising/bleeding which is visible in imaging at the surface of the brain and also the back

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34
Q

What is a concussion?

A

Microscopic damage not visible on imaging with an expected full recovery

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35
Q

Why is mannitol given for brain damage?

A
  • It is a diuretic

- Increased fluid loss lowers pressure in the brain

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36
Q

What is a epidural hematoma?

A

Bleeding between dura mater and skull

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37
Q

What is a subdural hematoma?

A

Bleeding between arachnoid mater and dura mater

38
Q

What is coup/contrecoup?

A

Impact/damage on front of brain then rebound against back of skull causing further damage

39
Q

What is expected with a concussion?

A
  • Brief disruption in LOC, amnesia
  • Microscopic changes to neurons and neuroglia
  • Brain imaging is usually negative
  • May show post-concussion syndrome but full recovery is expected
  • Recurrent concussions can cause permanent damage
40
Q

What is expected with a contusion?

A
  • Bruising of the brain visible with imaging
  • Brain cells will die and effects vary according to area impacted
  • Full recovery may not occur
41
Q

What are signs of increasing intracranial pressure?

A
  • Increased BP (to provide more oxygen)
  • Decreased HR (Mary’s law, inverse reaction between HR and BP)
  • Pupillary response (increased pressure on oculomotor nerve affects pupillary response)
  • LOC (pressure on brain can change consciousness)
  • Temperature (pressure of hypothalamus can change temperature)
42
Q

What is Cushing’s reflex?

A

Increased BP, decreased HR

43
Q

What is the tentorium?

A

A fold in the dura mater which separates the cerebrum and cerebellum. The upper brain stem passes through an opening in the tentorium

44
Q

What is tentorial herniation (coning)?

A
  • Increased pressure forces part of the temporal lobe through the tentorial opening, squeezing the brain stem and damaging blood supply
  • This affects the reticular formation and results in a coma
45
Q

What occurs with tentorial herniation (coning)?

A
  • Nerve III (oculomotor nerve) may be damaged resulting in a fixed and dilated pupil, first on the side of herniation and then alter on the other side
  • Permanent ischemic damage occurs if the herniation reduces oxygenated blood below a critical threshold for more than a few minutes
46
Q

What is Alzheimer’s disease?

A
  • Progressive, degenerative
  • Diffuse atrophy of the cortex
  • Widespread loss of cholinergic neurons
47
Q

What occurs if the hippocampus degenerates?

A

Impaired memory and learning

48
Q

What occurs if the amygdala degenerates?

A

Inappropriate emotions & anxiety

49
Q

What occurs if the frontal lobe degenerates?

A

Impaired speech, reasoning, personality (can be agitated, aggressive)

50
Q

What is the pathophysiology of Alzheimer’s?

A
  • Neuritic/senile plaques (Abnormal clusters of protein fragments, build up between nerve cells)
  • Neurofibrillary tangles (in dead/dying nerve cells, twisted strands of proteins)
  • Loss of up to 95% of cholinergic innervation on the cortex
  • Decline of enzyme that produces acetylcholine
51
Q

What is treatment of Alzheimer’s?

A
  • Cholinesterase inhibitors

- Help manage symptoms of mild to moderate Alzheimer’s

52
Q

What is Parkinson’s disease?

A
  • Progressive degeneration of dopaminergic neurons from substantia nigra
  • Leads to reduction in dopamine activity in basal ganglia affecting:
    1) Learned, automatic movement
    2) Monitoring and smoothing of voluntary movement initiated by motor cortex
    3) Inhibition of antagonistic or unnecessary movements
53
Q

What are the primary motor symptoms of Parkinson’s disease?

A
  • Tremor - one sided, resting tremor, pill-rolling
  • Rigidity - cogwheel or lead-pipe
  • Bradykinesia - slow movements
54
Q

What is treatment for Parkinson’s disease?

A

Levodopa + carbidopa

  • Dopamine too large to cross blood brain barrier (BBB)
  • Administer Levodopa that can pass BBB where is converts to dopamine
  • Carbidopa added (decarboxylase inhibitor) that blocks conversion of levodopa to dopamine in the periphery so all the levodopa gets into the brain
55
Q

What is Huntington’s disease?

A
  • Autosomal dominant
  • Progressive loss of neurons in the basal ganglia
  • Increased motor output “choreiform movements”
  • Usually presents 20-50 years old
  • Personality and cognitive changes in later stages
56
Q

What is multiple sclerosis?

A
  • Autoimmune, progressive, demyelination
  • Gte neurodegeneration in later stages
  • Diagnosis usually 20-40 years old, more in females
57
Q

What are symptoms of multiple sclerosis?

A
  • Motor - limb weakness, loss of bladder/bowel control, speech
  • Sensory - numbness, pain
  • Visual - double vision, loss of vision
  • Cognitive degeneration - thinking
58
Q

What are different types of epilepsy?

A
  • Tonic/clonic
  • Grand mal
  • Petit mal
  • Temporal lobe
59
Q

What are common features of epilepsy?

A
  • Uncontrolled firing of a group of neurons

- Symptoms/presentation depend on location and extent of spread

60
Q

What are treatments for epilepsy?

A

Drugs that increase GABA (inhibitory neurotransmitter)

61
Q

What are risk factors of unipolar depression?

A
  • Personality traits
  • Monoamine depletion
  • Stress & HPA axis dysregulation
  • Changes in morphology or function of brain regions
  • Other medical conditions
  • Side effects of drugs
  • Post-natal
  • Social/environmental effects
  • Genetics
62
Q

What is the proposed mechanism of unipolar depression?

A
  • During stress - increased activation of hypothalamic-pituitary-adrenal axis → increasing CRH, ACTH, cortisol
  • Many metabolic effects of cortisol and decreased immunity, decreased appetite and sleep changes
  • Cortisol also binds to receptors in the hippocampus and may lead to decreased synapse formation & neurogenesis
63
Q

What does imaging show in depressed people?

A
  • Smaller hippocampus (Involved in memory and emotion) → impaired memory
  • Smaller frontal lobe (Involved in cognitive processing, concentration, suppressing negative thoughts) → impaired cognitive function
  • Increased activity of amygdala (involved in emotion, reactivity to “threatening stimuli”) → impaired ability to identify threat
64
Q

What is treatment for unipolar depression?

A

1) Aim is to reduce chronic stress
2) Drugs:
- SSRIs (selective serotonin reuptake inhibitor) - block reuptake of serotonin selectively
- MAOIs (Monoamine oxidase inhibitor) - non-selective, block noradrenaline and serotonin breakdown
- TCAs (Tricyclic antidepressants) - nonselective, block noradrenaline and serotonin reuptake

65
Q

What are the risks of unipolar depression medications?

A
  • Thereapuetic effect takes 2-6 weeks
  • Adverse effect can occur on the same day
    Therefore there is increased risk of suicide in the first few weeks
66
Q

What is schizophrenia?

A
  • Abnormal perception of reality therefore is a psychotic illness
  • Unknown cause
  • Imaging shows:
    1) Enlargement of ventricles in the brain
    2) Reduced size of temporal and frontal lobe
67
Q

What are some positive symptoms of schizophrenia?

A
  • Hallucinations

- Delusions

68
Q

What are some negative symptoms of schizophrenia?

A

Flattened mood

69
Q

How does dopamine affect symptoms of schizophrenia?

A
  • Too much dopamine causes positive symptoms

- Too little dopamine causes negative symptoms

70
Q

How do dopamine antagonists treat positive symptoms of schizophrenia?

A

They block the dopamine receptors, lowering dopamine levels

71
Q

What is spina bifida?

A
  • Incomplete formation of the vertebral arches (“split spine”)
  • Occurs at any point of the vertebrae
  • The more neurological structure contained within the sac, the greater the neurological impairment
  • Problems with infection are ongoing since the cyst call in thin, porous and liable to rupture
  • Accompanied by hydrocephalus in 90% of cases
  • Links between environmental factors such as inadequate maternal folic acid level
72
Q

What treatment is therefore for spina bifida?

A

Surgery

73
Q

What would prevent spina bifida?

A

Sufficient amount of folic acid before and during pregnancy

74
Q

What is a lumber disc herniation?

A

Herniated disc pushing on spinal nerves, compressing spinal arteries reducing blood flow or directly damaging the spinal cord

75
Q

What types of spinal injury are there?

A
  • Paraplegia - no movement in legs and trunk
  • Quadriplegia - all four limbs and trunk affected
  • Monoplegia - 1 leg affected
  • Hemiplegia - one side either left or right
76
Q

What are signs of acute stage of spinal injury?

A
  • Flaccid paralysis, loss of reflexes, absence of somatic/visceral sensations below level of injury
  • Loss of bladder/bowel control
  • Possible reduction in sympathetic tone leading to vasodilation, hypotension, & decreased sweating
77
Q

Why might spasticity occur?

A
  • After acute period, spinal reflexes may occur below level of injury as these are mediated by the spinal cord.
  • Inhibitory messages from higher brain centres cannot be conducted past injured area of spinal cord
78
Q

What pathways are affected by anterior damage?

A

Prevention of motor function while maintaining sensory function

79
Q

Why is outflow from the sympathetic nervous system often disrupted in spinal cord injury?

A

Sympathetic ganglia lie alongside the spinal cord (vasodilation below LOI, decreased sweating below LOI)

80
Q

What other difficulties can be experienced with a spinal injury?

A
  • Problems with deep breathing/cough
  • Bladder/bowel function impaired
  • Sexual function possible affected
  • Integumentary - skin breakdown
81
Q

What is poikilothermy?

A

Taking on the temperature of the environment

82
Q

Why is there increased risk of DVT with a spinal injury?

A
  • Immobile - decreased skeletal pump
  • Pooling of blood and oedema
  • Increased clotting
83
Q

What are the first, second, and third-order neurons involved in the perception of pain?

A

1) Nociceptive - spinal cord
2) Spinal cord to thalamus
3) Thalamus to somatosensory

84
Q

How does referred pain occur?

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
85
Q

What stimuli active nociceptors (pain receptors)?

A
  • Extreme heat and cold
  • Pressure/cut, damage tissue
  • Histamine
86
Q

How does the body produce pain relief?

A

Block messages of pain getting to the brain

87
Q

What is visceral pain?

A

Pain from the organs

88
Q

What are two examples of referred pain?

A
  • Gallbladder and liver also has pain in right shoulder

- Heart also has pain in left arm

89
Q

What are the brain regions involved in perception and understanding of pain messages?

A
  • Somatosensory
  • Emotional centres (limbic system)
  • Frontal lobe
  • Hippocampus
90
Q

What are “A-delta” fibres?

A
  • Thinly myelinated, conduct fast impulses
  • Respond to heat and touch
  • Usually superficial, somatic
  • Quick conduction to thalamus & somatosensory cortex
  • “Fast”, “first”, “good”, “acute”, pain
  • Well-localized, shapr, stabbing pain
  • May lead to reflex withdrawal of affected body part for protection
91
Q

What are C fibres?

A
  • Unmyelinated and conduct impulses slowly
  • Respond to heat, touch or chemicals
  • Can be somatic or visceral
  • Slower, circuitous route through thalamus & limbic system
  • “Second” or “slow” pain
  • Poorly-localized, diffuse, buring, aching, itching, dull pain
  • More likely to transmit chronic pain and can also amplify local inflammation by releasing more inflammatory chemicals

214.201 (17 decks)

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