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PHAR 123* > CNS Pathology > Flashcards

CNS Pathology Flashcards

1
Q

What is are the basic functional units for the nervous system?

A

Neurons, they are highly specialized cells

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2
Q

What is the purpose of the Blood Brain Barrier?

A

It is represented by the tight junctions that prevent larger and water soluble substances from entering the cells (infections, water soluble chemicals)

Water-soluble drugs have a hard time getting across the BBB

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3
Q

Do neurons divide in an adult?

A

No, neurons are nondividing, postmitotic, and permanent cells

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4
Q

What are glial cells?

A

They serve a supporting role. They are able to divide (unlike neurons)

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5
Q

How does damage to the brain affect its functions?

A

Specific loss of functions is associated with damage to specific areas of the Brian

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6
Q

What are the energy and nutrient demands of the brain?

A

Accounts for 2% of body weight, but its burden on metabolism is much greater

15% of cardiac output
20% of O2 consumption
25% of total body glucose utilization

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7
Q

Is the brain susceptible to toxicity despite the BBB?

A

Yes, largely due to the activity level of the brain. The brain is largely made form fats, so fat-soluble subsistences that are able to cross the BBB can build up in the brain

The brain also contains high amounts of sulfur-containing amino acids (can bind and transport heavy meals to the brain)

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8
Q

What are the reaction of neurons to injury?

A

The axon and/or cell body may become swollen upon injury. Rapid death results in phagocytosis. Axons may be regenerated

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9
Q

What happens to oligodendrocytes following brain injury?

A

These myelinating cells do not regenerate

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10
Q

What happens to astrocytes in response to brain injury?

A

Undergo hypertrophy and hyperplasia with just about any brain injury (this process is called gliosis)

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11
Q

What happens to ependymal cells following brain injury?

A

These cells line the ventricles (CSF container) and they do not regenerate

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12
Q

Does fibrosis occur in the brain?

A

No, there is no scarring. Rather a hole is left behind following a brain injury

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13
Q

What happens to microglia following a brain injury?

A

Transform into phagocytic cells once activated by chemotactic factors

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14
Q

What is global ischemia?

A

NOt enough oxygen gets to the brain tissue

Ex. Patients with chronic heart failure or due to atherosclerotic disease

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15
Q

What is a cerebral infarct?

A

This is a hemorrhagic stroke (clot blocks carotid artery)

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16
Q

What is intracerebral hemorrhage?

A

Bleeding in the brain such as a malformed vessel if that is weak (can be due to an aneurysm)

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17
Q

What is a fat embolism?

A

It is the presence of fat globules in the blood supply blocking flow

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18
Q

What is a mid-line shift in the brain?

A

This is the location of the corpus callousum

In forms of brain injury, the midline can shift towards one side due to injury on the other side

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19
Q

What are some risk factors associated with stroke?

A

HTN
Afib
Diabetes
Family history for stroke
High LDL
Increasing age
heart disease and poor blood flow

overweight, drinking heavily, eating too much fat or salt, smoking and cocaine, and other illegal drugs

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20
Q

What are the FAST symptoms seen in strokes?

A

FAST

Face: one side of the face is drooping

Arms: one or both arms have muscle weakness

Speech: difficult speaking

Time to call help and get EMS over to hospital

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21
Q

What are some factors that increase risk of dying following a hemorrhagic stroke?

A

Lots of intracranial bleeding
Coma
Advanced age
Oral anticoagulant use
Higher INR

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22
Q

What are some symptoms of a stroke?

A

Change in alertness
Changes in senses (impairment)
Clumsiness, confusion, or memory loss
Lack of control over bladder or bowels
Unilateral symptoms
Soured speech and/or trouble comprehending others
Trouble walking

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23
Q

What percentage of strokes are ischemic?

A

80% are ischemic, while the remaining 20% are hemorrhagic

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24
Q

How many hemorrhagic strokes are due to trauma?

A

Close to 25%, most hemorrhagic strokes are not due to external trauma

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25
Q

Does ischemia take a while to have an effect on brain tissue?

A

No, ischemia affects the brain rapidly because it does not store glucose (severely limits how long brain tissue can survive without constant perfusion)

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26
Q

What are some factors that can impact the severity of a stroke?

A

Duration of ischemia (longer is worse)

Collateral circulation (more is better)

BP affects overall perfusion (more is better)

Haematological factors (prone to more clotting is bad)

Temperature (cooler is better. Slows down brain metabolism and extent of injury)

Glucose metabolism (hyper or hypoglycemia may affect infarction size ) (more is better)

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27
Q

What happens to the appearance of brain tissues following a stroke?

A

No major changes are seen until about 5-6h after infarction. Then there is slight discolouration and a fuzziness of the usual clear border between gray and white matter

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28
Q

What happens to damaged brain tissue?

A

It necroses, which results in liquefaction and subsequent hole formation

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29
Q

What exactly causes cell death follwing ischemia?

A

Influx of Ca2+ and Na+; and activation of destructive processes that lead to cell death

These changes cause inflammation and endothelial cell reaction, leading to capillary plugging and increased vascular permeability

This results in cell death via necrosis and apoptosis

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30
Q

Review slide 23 for acute stroke treatment pathway

A
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31
Q

How is hemorrhagic stroke treated?

A
  1. BP control and supportive care to reduce intracranial
  2. Reduce further risk (reverse anti-clotting)
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32
Q

How are the different antiplatelet, antithrombotic, and thrombolytic agents reversed?

A

Antiplatelets: Platelet transfusion, Desmopressin

Warfarin: Vitamin K and fresh frozen plasma

Heparin: Protamine sulfate

Thrombolytics: Fresh frozen plasma and/or cryopreciptate

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33
Q

What are some types of physical brain injury?

A

Brain concussion: widespread, microscopic

Brain contusion: localized, macroscopic bruise and/or bleeding

Laceration: tearing of tissue

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34
Q

What are some types of neck and spinal cord injuries?

A

Spinal cord gets pinched by vertebral bones due to jerking motion:

Hyperextension injury
Hyper flex ion injury

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35
Q

What are some symptoms of concussions?

A

May be fatigued, confused, and have headaches for a long period of time. Recovery is a long process in concussions.

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36
Q

How are intracranial hemorrhages classified?

A

Location (epidural, subdural, subarachnoid or intracebral)

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37
Q

What are some causes of intracerebral hemorrhages?

A

Common complication of head trauma

Rupture of intracerebral vessels

Gunshot wounds

Non-traumatic forms

Common in hematologic diseases (leukaemia)

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38
Q

What are some types of CNS infections?

A

Encephalitis
Myelitis
Cerebral abscess
Meningitis
Neurosyphillis
AIDS-related CNS lesions

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39
Q

What is encephalitis?

A

It is an inflammation of the brain and spinal cord usually caused by viral infection

Can be caused by diseases such as rabies, polomelitis, and herpes encephalitis are all caused by a viral infection

Measles, mumps, and rubella are childhood illnesses that can lead to secondary encephalitis

West NIle, La Crosse, St. Louis, western and eastern equine encephalitis care all caused by mosquito-borne viruses

HSV-1 (Herpesvirus encephalitis) can cause encephalitis in the very young and very old

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40
Q

What is the clinical presentation of encephalitis?

A

Flu-like symptoms and headache

Severe cases: Severe headache, sudden high fever, drowsiness, vomiting, confusion, seizures, abnormal sensations (visual, auditory, olfactory) or movements

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41
Q

What are the different types of encephalitis?

A

Infectious encephalitis (viral infection)

Post-infectious: (inflammation due to immune system reactions to previous infection or vaccine)

Autoimmune: inflammation due to immune system reacting to a non-infections cause)

Chronic: inflammation build slowly over many months (can be due to HIV or unknown cause)

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42
Q

What are some severe symptoms of encephalitis?

A

Respiratory arrest

Coma

Death

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43
Q

What are some chronic symptoms of encephalitis?

A

Fatigue

Mood disorders

Memory problems

Intellectual disabilities

Lack of muscle coordination

Paralysis

Hearing or vision loss

Speech impairments

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44
Q

What causes “Covid-19 related brain fog”?

A

Severe inflammation outside the brain (lungs and other organs) while enduring Covid-19, causes immune system activation

This activation causes brain fog, anosmia/dysguesia (loss of taste), impaired cognition, memory, and mood

These symptoms can persist for many months after the infection

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45
Q

What are some factors that can improve the outcomes of neurogenerative disease?

A

Hearing aids, continual education, physical activity, and social interactions all help stave off neurogenerative disease

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46
Q

What is dementia?

A

It is a general, non-specific term to describe the cognitive, memory, and communication impairment associated with neurogenerative diseases

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47
Q

What are some specific skills that can become impaired n dementia?

A

Focus, reasoning, judgement, control of emotions, and motor skills can also become impaired

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48
Q

Is dementia a normal part of aging?

A

No, not everyone does not develop dementia

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49
Q

How are dementias diagnosed?

A

In addition to a medical history, family history and physical exam the following can be performed

Special tests of memory, language skills, math ability, and mental functioning

Lab tests to rule out infection, vitamin deficiency, or tumour

Psychiatric evaluation to rule out depression and other affective disorders

Genetic testing for specific disorders like Huntington’s

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50
Q

What are some neurodegenerative diseases?

A

Alzheimer’s disease

Parkinson’s disease

Amyotrophic lateral sclerosis

Pick’s disease

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51
Q

What is Alzheimer’s disease (AD)?

A

It is a degenerative brain disorder that develops in mid-to-late adulthood. It results in a progressive and irreversible decline in memory and deterioration of various other cognitive abilities

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52
Q

Who does Alzheimer’s disease disproportionately affect?

A

Usually elderly citizens and urban populations

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53
Q

What are some factor that increase the risk of Alzheimer’s disease?

A

HEavy MEtals

Environmental factors (Tobacco, Smoke, PEsticides)

Genetics (mutations in APP, PSEN1, and PSEN2)

Aging

CV disease

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54
Q

What is the physiopathology of Alzheimer’s disease?

A

Atrophy of the cortical parts of the frontal and temporal regions of the brain (cognitive and judgement impairment)

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55
Q

What is dementia?

A

Progressive loss of cognitive functions and a functional decline (loss of memory predominates)

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56
Q

What are some modifiable risk factor for Alzheimer’s disease?

A

Social engagement

Physical activity

Educational level

Mental actvity

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57
Q

What are some non modifiable risk factors for Alzheimer’s disease?

A

Family history

Genetics (Apo E2 gene)

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58
Q

Is there a connection between CV risk factors and Alzheimer’s disease risk?

A

The following are under investigation for their impact on Alzheimer’s disease:

Vascular disease
Heart disease
Stroke
HTN
Diabetes
Obesity

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59
Q

What is the pathology of Alzheimer’s disease?

A

The development of neurofibrillary tangles. They contain amyloid protein. Amyloid protein is toxic, compressing, and destroys normal brain tissue

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60
Q

Do amyloid plaques also cause damage that can lead to the development of Alzheimer’s disease?

A

They are not the direct cause of neuronal dysfunction. Some patients with amyloid plaques do not have dementia

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61
Q

What areas of the brain are particularly affected by Alzheimer’s disease?

A

Hippocampus (new memories)

Frontal lobe (behaviour, cognition, judgement)

Parietal lobe (language)

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62
Q

Review slide 47 to examine the differences between normal and early Alzheimer’s symptoms

A
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63
Q

What are the three stages of Alzheimer’s disease?

A

Mild/Early: lasts 2-4 years

Moderate/Middle: lasts 2-10 years

Severe/Late: 1-3+ years

64
Q

What two drug classes are used to treat Alzheimer’s disease?

A

Cholinesterase inhibtors

NDMA receptor antagonists

65
Q

What is the signal-to-noise ratio in Alzheimer’s disease?

A

It is describing the electrical “noise” generated by continual over-activation of NDMA receptors by b-amyloid oligomers.

As the “noise” increases, it makes it difficult to detect a proper synaptic signals (important for less ringing/plasticity). The neurons die due to excitotoxicty

66
Q

What is an example of a NMDA receptor antagonsists?

A

Memantine can prevent chronic activation, -which in turn reduces the amount of cell death and progression of Alzheimer’s disease

67
Q

What are some monoclonal antibodies available for Alzheimer’s disease?

A

Aducanumab

Lecanumab (approved by FDA):
Reduced cognitive decline by 27%

Cost: 30-50k/year

68
Q

What is etiology of Pick’s disease ?

A

Etiology:
Several genes can be mutated
Rare disease starts in middle age (40-60)
5% of cases of frontotemporal dementia

69
Q

What is the pathogenesis of Pick’s disease?

A

Abnormal accumulation of tau protein in swollen neurons

Loss of cortical neurons, severe atrophy, gliosis. Particularly in the frontal lobe, with slow loss of function

Frontal and temporal lobes particularly affected

70
Q

What are the clinical manifestations of frontotemporal dementia?

A

Impulsive, Inappropriate Behaviours and Speech

Loss of Interpersonal Skills and/or Empathy

Apathy

Decreasing Self-awareness and personal hygiene

Repetitive compulsive behaviours

Inability to plan or concentrate

Sudden and frequent mood changes

Speech and language difficulties

Balance and movement problems

71
Q

How can frontotemporal dementia be effectively managed?

A

Avoid medications that can worsen confusion

Mood management

Treat underlying comorbidities

72
Q

What is Lewy body disease?

A

Also known as Dementia with Lewy bodies (DLB), is a type of dementia that is closely allied to both Alzheimer’s and Parkinson’s diseases

It is characterized by the presence of Lewy bodies (clumps of alpha-synuclein and ubiquitin protein in the neurons)

73
Q

What is the pathology of Lewy body disease?

A

Abnormal deposits of a-synuclein in the brain, the location determines the symptoms

Cerebral cortex: impaired information processing, perception, thought, and language

Limbic cortex: plays a major role in emotions and behaviour

Hippocampus: essential to forming new memories

Midbrain and basal ganglia: involved in movement

Brain stem: important in regulations sleep and maintaining alertness

74
Q

What are the differences between Alzheimer’s and Lewy Body Dementia?

A

Women have a higher chance of developing Alzheimer’s, while men have a higher chance of developing Lewy Body Dementia

Alzheimer’s survival age is 85 yo, for Lewy Body it is 80

Alzheimer is caused by neurofibrillary tangles, while Lewy Body is due to build up of a-synuclein

75
Q

What are some clinical manifestations of dementia with Lewy bodies?

A

Balance and motor control

Intermittent issues with memory

Flat affect (limited emotion)

Visual hallucinations

May act out what they are dreaming

Dysregulated autonomic nervous system (hypotension, dizziness, falls)

DO NOT GIVE ANTI-PYSCHOTICS

76
Q

What are some treatment options for Lewy Body Disease?

A

There is no single treatment, may need to be on multiple drugs for symptomatic treatment

Cognitive: Cholinesterase inhibitors or NMDA receptor antagonists (Alzheimer’s disease drugs)

Motor symptoms: Carbidopa/levodopa

Behavioural symptoms: Antidepressants

Sleep symptoms: Melatonin or Clonezapam

Autonomic symptoms: Fludrocortisone and Midocrine

77
Q

What is the epidemiology of Parkinson’s disease?

A

It has its onset at 50-70 yo

Affects about 1-2% of the North American population

Men are more affected than women

78
Q

What is the etiology of Parkinson’s disease?

A

Usually sporadic (novel development), but there are rare cases of inherited defects in the alpha-synnuclein gene that causes early onset

Fibrilogenesis is implicated

Oxidative stress produced during melanin production in the substantia nigra causes neuronal injury via protein misfolding of alpha-synuclein and the formation of filamentous inclusions

Parkinson’s is one of many neurodegenerative diseases that involve the accumulation of filamentous alpha-synuclein inclusions

79
Q

What is the clinical presentation of Parkinson’s disease?

A

Resting tremor

Rigidity

Bradykinesia

Mask-like facial expression

Shuffling small-steps gait

And more… (review slide 64, 66)

80
Q

What is the first-line treatment for Parkinson’s disease?

A

Levadopa/Carbidopa

Levadopa is a prodrug of dopamine that can cross the BBB

Carbidopa reduces systemic metabolism of levodopa so that can reach the brain

81
Q

What are some other drugs used in Parkinson’s disease?

A
  1. Blocking peripheral metabolism of levodopa into dopamine (carbidopa)
  2. Blocking breakdown of dopamine at the neuron. These agents have notable side effects (MAOi, selegiline, rasagiline)
  3. Reducing reuptake of dopamine (amandatine)
  4. Direct dopamine agonists (bromcriptine, pramipexole, and ropinirole)
82
Q

What is the prevalence of depression and anxiety?

A

The global prevalence of depression is 4.4%, women are more effected by depression vs. men

83
Q

What are some physical symptoms associated with generalized anxiety?

A

Fatigue

Trouble sleeping

Muscle tension or aches

Trembling, feeling twitchy

NErvousness

Sweating

Nausea, diarrhea or IBS

Irritability

84
Q

Is pharmacological alone sufficient for effective therapy in depression and anxiety?

A

No, depression and anxiety are complex disorders with many underlying mechanisms, so drug therapy alone is usually not effective on its own.

Drug therapy needs to be coupled with counselling

85
Q

What activities does serotonin help modulate?

A

Mood

Emotion

Learning

Memory

Personality

Affect

Appetite

Aggression

Motor function

Temperature regulation

Sexual activity

Pain perception

Sleep induction

86
Q

What is the serotonergic system?

A

It is very diverse in terms of the activities it helps regulates, has 14 sub-types of receptors organized into 7 classes.

87
Q

What is the role of serotonin in the brain specifically?

A

It helps modulate mood, happiness, and sleep

88
Q

What is the relationship between platelets and serotonin?

A

Serotonin activates 5HT1 receptors (serotonin receptors), which causes NO release with subsequent vasodilation. This action effectively reduces BP

When serotonin activates 5HT2 receptors (diff. Serotonin receptor), it results in both platelet aggregation and vasoconstriction

89
Q

How does sertoninergic signalling work?

A
  1. Depolarization of pre-synaptic neuron cases entry of Ca2+ and Na+ into the neuron
  2. Vesicles are now full of serotonin (5HT) and they start to fuse with the plasma membrane and release serotonin into the synaptic cleft
  3. Once the serotonin crosses the cleft, it binds with a serotonin receptor on the postsynaptic neuron (many different kinds of receptors exist)
  4. Intracellular signalling then occurs in the postsynaptic nerve
90
Q

What is the monoamine hypothesis of depression?

A

Depletion of monoamines causes depressive symptoms. By restoring monoamines, it can improve depression in most cases.

Ex. Norepinephrine, serotonin, and dopamine

91
Q

Review slide 81 for the roles of epinephrine, serotonin, and motivation

A
92
Q

What are neurotrophic factors in terms of depression?

A

An example would be brain-derived neurotrophic factor (BDNF). IT regulates neural plasticity, resilience, and neurogenesis

Stress and pain decrease BDNF, this has been linked to be responsible for Neurotropic

93
Q

What is the efficacy of using electroshock therapy for sever depression?

A

It is fairly effective and “resets” the brain

94
Q

How long do anti-depressants drugs take to have an effect?

A

Treatment with antidepressants increases monoamine levels quickly, but the anti depressive effect lags by several weeks.

This lag is due to the the time required to up-regulate the expression of neurotrophic factors

95
Q

What are some drugs that can affect serotonergic signalling?

A

Reserpine: prevents vesicular accumulation of serotonin

Triptans: reduce pain signals and reduce vasodilation

MAOIs: not used anymore (too many side effects and drug interactions)

SSRIs, SNRIs, TCAs: block 5HT reuptake at the synaptic cleft

Buspirone: partial agonist at 5HT1A (different receptor form SSRIs)

Antipsychotic drugs: block 5HT 2A/C receptors

Anti-emetics: block 5HT3 receptors (ex. Odansetron)

96
Q

What are some indications for SSRIs?

A

Major depression, anxiety, panic attacks, OCD, and PTSD

97
Q

How exactly do SSRIs work?

A

They inhibit serotonin reuptake via SERT and a reduction in auto receptors in the axon and terminus of the pre-synaptic nerve (effectively preventing them from reducing serotonin release)

98
Q

What drugs should patients avoid when using SSRIs?

A

St. John’s Wort and other serotonergic drugs (can cause serotonin syndrome)

99
Q

What are some side effects seen with SSRIs?

A

Insomnia

Anxiety

Reduced libido

GI (nausea, diarrhea)

100
Q

What are some examples of SSRIs?

A

Sertraline, Citalopram, Fluoxetine, Paroxetine

101
Q

What are some indications for Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)?

A

Used for major depression, generalized anxiety disorder, and an adjunct therapy for chronic pain

102
Q

How exactly do SNRIs work?

A

They work similarly to SSRIs, except SNRIs also inhibit norepinephrine reuptake via NET transporter

103
Q

What are some side effects seen in SNRIs?

A

CV (HTN)

Insomnia

Anxiety

Reduced libido

GI (nausea, diarrhea)

104
Q

What is an example of a SNRI?

A

Venlafaxine

105
Q

How do serotonin receptor antagonists work?

A

They block 5HT2 receptors, preventing serotonin from binding.

106
Q

What are some indications for serotonin receptor antagonists?

A

Depression and anxiety, with insomnia

107
Q

What is the efficacy of Serotonin Receptor Antagonists vs. SSRIs/SNRIs?

A

Serotonin Receptor Antagonists are less effective, but they are useful when combined with other antidepressants. Serotonin Receptor Antagonsists can help reduce insomnia side effects

Not first line for mono therapy in major depression

108
Q

What are some side effects associated with Serotonin Receptor Antagonists?

A

CV (HTN)

Somnolence (State of drowsiness)

Increases appetite and weight gain

Agranulocytosis (esp. with mirtazipine)

Hepatotoxicity (esp. with nefazodone)

109
Q

What are some indications for Bupropion?

A

Primarily used in smoking cessation

But it can also be used in ADHD and acts as an antidepressant

110
Q

How does Bupropion work?

A

Bupropion inhibits NET (norepinephrine reuptake), DAT (dopamine receptor), and alters VMAT2 to increase norepinephrine and dopamine

DOES NOT INCRREASE SEROTONIN (great for patients that have not reacted well to other agents that increase serotonin)

111
Q

What is the efficacy of Bupropion?

A

Similar to SSRIs and SNRIs, but has a lag time for effect.

Bupropion also has a lot of side effects

112
Q

What are some side effects associated with Bupropion use?

A

CV (tachycardia and HTN)

Muscarinic (dry mouth, urinary retention, confusion)

Agitation and aggression

Insomnia

Anxiety

Reduced libido

GI (nausea, diarrhea)

Seizure (rare)

113
Q

What are some indications for Tricyclic Antidepressants (TCAs)?

A

They were used historically for major depression (we have better suited agents now)

At low doses, they are good adjunct therapies for insomnia and pain (ex. Amitriptyline)

114
Q

How do Tricyclic Antidepressants (TCAs) work?

A

They inhibit SERT and NET, but also have affinity for H1, 5HT2, alpha-1, M1-3 receptors

Therefore TCAs have lots of side effects because they can disrupt so many pathways

115
Q

What are some side effects associated with TCAs?

A

CV (tachycardia, orthostatic HTN)

Muscarinic (dry mouth, urinary retention, confusion)

Histaminergic (sedating)

Insomnia

Anxiety

Reduced libido

GI (Nausea, diarrhea)

Weight gain

Lowered seizure thresholds

116
Q

What are some unique features of TCAs regarding metabolism?

A

They depend on CYP2D6 for metabolism. CYP2D6 function is variable across people, so drug dose has to be adjusted for each individual

117
Q

How do MAOIs work?

A

They inhibit both MAOa and MAOb, thus preventing metabolism of biogenic amines (Norephinephrine, Dopamine, Serotonin, and tyramine)

These biogenic amines are allowed to buildup

118
Q

What are some drug and food interactions with MAOIs?

A

Sympathomimetics, TCAs, opioids, and certain foods like hard cheese and red wine

119
Q

What are MAOIs indicated for?

A

They were used for depression, but no longer due to the availbility of safer agents

They are presently used in low doses for preventing the metabolism of dopamine in Parkinson’s disease

120
Q

Do the effects of MAOIs wear off in a few days?

A

No, many MAOIs are irreversible inhibitors. It can take up to 2 weeks for a fresh supply of MAO.

This has implications for how HCPs switch drugs

121
Q

How do benzodiazepines work?

A

They bind to GABA receptors, resulting in hyperpolarization and thus refractoriness to excitiation

122
Q

What are some indications for Benzodiazepines?

A

Due to the abuse potential, they are not used for anxiety and other long-term use

They are used for short-term events like post-op anxiety or panic attacks

123
Q

What are some examples of benzodiazepines?

A

Lorazepam, diazepam, clonazepam, oxazepam, etc.

124
Q

How does buspirone work?

A

Partial agonist at pre-synaptic 5HT-1 receptors. Buspirone causes serotonin release to increase.

125
Q

Is buspirone addictive?

A

No, unlike benzodiazepines

126
Q

What are some indications for Buspirone?

A

Indicated for generalized anxiety disorder, but it is not first line

127
Q

What are some side effects associated with buspirone use?

A

Nervousness

Overexcitement

Restlessness

Nausea

Headaches

Weird dreams

Dizziness

Lightheadedness

Blurred vision

Tiredness, avoid alcohol

128
Q

What is a drug interaction with Buspirone?

A

Do not take with alcohol

129
Q

What is a seizure?

A

It is a rapid, synchronous, uncontrolled spread of electtical activity due to abnormal function of ion channels and dysregulation of neural networks

130
Q

What is epilepsy?

A

This is a sereies of conditions in which patients have a tendency to reccurent seizures

131
Q

What is the prevalence of epilepsy?

A

About 1% of Canadians are affected.

50 million people worldwide

Greatest prevalanec between 18-44 years old (75% are diagnmosed before the age of 30)

132
Q

Can epilepsy be well controlled via therapy?

A

Yes, 65-85% of patients with epilepsy enter long-term remission with treatment

133
Q

What are some potential causes of epilepsy?

A

Genetic predisposition

Secondary to tumours, infection, head injury, lack of oxygen at birth, metabolic factors, alcohol abuse, and stroke)

But, in over 50% of cases, the cause is unknown

134
Q

What are the main types of epilepsy according to the newer guidelines?

A

The newer classification based on the area affected. Each type can be broken down into motor and non-motor seizures

Focal onset (small spot affected)

Generalized onset (both hemispheres are involved)

Unknown onset (idiopathic)

135
Q

What are tonic seizures?

A

Stiffening of muscles

136
Q

What are atonic seizures?

A

Limp body (“wet noodle-esque”)

137
Q

What are clonic seizures?

A

Repeatd jerking movements

138
Q

What are absence seizures?

A

Interruption of conciousness, with blank stare, possibly with some motor symptoms

139
Q

What do motor seizures look like?

A

Stiff and jerking (tonic-clonic)

There may also be automatisms (repaeated automatic movements) like clapping or rubbing hands, lipsmacking or chewing, pacing in circles

140
Q

What do non-motor seizures look like?

A

Absence seizure (interruption of conciousness)

OR

Spread from focal to generalized seizure (tonic-clonic)

Other symptoms:
Changes in sensation, emotion, cognition, waves of heat and cold, goosebumps, heart racing

141
Q

What are some symptoms associated with a temporal lobe seizure?

A

Odd taste and/or smell

Tinnitus

Fear or panic

Deja vu

Abdominal discomfort

142
Q

What are some symptoms associated with a frontal lobe seizure?

A

Loss of motor control

Change in behaviour

Change in language expression

143
Q

What are some symptoms associated with an occipital lobe seizure?

A

Multi-coloured shapes (circles and flashes)

Temporary vision loss

144
Q

What are some symptoms associated with a parietal lobe seizure?

A

Feel numbness or tingling

Burning

Cold sensations

145
Q

What is the pathophysiology of seizure?

A

Two main pathways

Excessive excitation:
Inward Na+ and Ca2+ currents and the subsequent release of excitatory neurotransmitters (glutamate, spartate)

Not enough inhibition:
Insuffcient transport of Cl- into the cell and K+ release. This causes fewer inhibitry neurotransmtters to be released (GABA)

146
Q

What is surround inhibition?

A

This process effectively focuses signals by stimulating inhibitory GABAergic neurons to block excitation lateral to the main stimulus

147
Q

Review slide 106 to see where different anti-seizures work

A
148
Q

How do Na+ channel blockers work to prevent seizures?

A

They block the flow of sodium into the neurons (slowing down repolarization). This increases the refractory period, effecti vely reducing the maz number of action potentials in a given amount of time

149
Q

How do Ca2+ channel blockers prevent seizures?

A

Control the entry of Ca2+ into the presynaptic nerve terminal and regulates neurotransmitter releases such as glutamate and norepinephrine

ex. ethosuximide, valproic acid, gabapentin, pregablin

150
Q

What are the types of Ca2+ channel blockers used in seizures?

A

T type (slow): They are inactive in the awake state, but activate during absence seizures
ex. ethosuximide

High-voltage activated Ca2+ channel blocker:
Used mainly for focal seizures as an adjunct therapy

151
Q

How glutamate inhibitors prevent seizures?

A

These drugs prevent the excitatory neurotransmitter glutamate from binding to glutamate receptors (AMPA and NMDA) on the post-synaptic neuron

ex. lamotrigine, topiramate

152
Q

How do SV2a inhibitors prevent seizures?

A

Levetiracetam will bind to a SV2a protein, effectivly rpreventing the release of neurotransmitters

153
Q

How do GABA-related inhibition drugs prevent seizures?

A

These drugs increase the amount of surround inhibition by GABAergic neurons

ex. benzodiazepines (diazepam, lorazepam, clonazepam)

154
Q

What are some adverse effects associated with anti-seizure drugs?

A

All anti-seizure drugs gave the potential for adverse effectsm some of which are dose-related and others that occur randomly

Most symptioms are asociated with sedation and motor function abnormalities

155
Q

What are some changes in the brain that lead to reduced natural seizure inhibtion?

A

Damage and degeneration of GABAergic neurons

Abnormal ion gradients induced by space-occupying neurons

Gene mutations that alter channel function

PHAR 123* (11 decks)

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