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Fundamentals of Pharmacology > Week 9 > Flashcards

Week 9 Flashcards

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1
Q

Is the heart’s electrical system different to the brains?

A

Yes, the brain is different to the heart where the electrical signals spread across the entire tissue in synchronization (brain must remain isolated – specific pathways that do not interfere with each other)

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2
Q

Briefly explain the regulation of electrical activity at a single neuron level?

A

The neuron begins in a resting state and then it becomes activated and we see the movement of ions into the cell.

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3
Q

Briefly explain the regulation of electrical activity of complex neural networks?

A
  • A > B signalling pathway
  • Neuron C activating is undesired
    Use of GABA to inhibit neuronal firing
    Hyperpolarization
  • Surround inhibition
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4
Q

What is a seizure?

A

“rapid, synchronous, and uncontrolled spread of electrical activity”

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5
Q

What are the causes of a seizure?

A

PRIMARY: genetic
SECONDARY: structural damage (stroke, tumour), pyrexia, infection, toxins and drugs

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6
Q

What are the classifications of focal seizures?

A

Aware, impaired awareness and focal to bilateral tonic-clonic

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7
Q

Is consciousness preserves in an aware focal seizure?

A

Yes

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8
Q

What are the symptoms of an aware focal seizure?

A

Involuntary, repetitive movement, paraesthesia’s and flashing lights

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9
Q

What is the effect on consciousness of impaired awareness focal seizures?

A

Altered, usually preceded by aura

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10
Q

What are the symptoms of impaired awareness focal seizures?

A

vague, confused or dreamlike. Automatisms, after there is a period of confusion and little, if any memory

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11
Q

What is the effect of consciousness of focal to bilateral tonic-clonic seizures?

A

Loss of consciousness, usually preceded by aura

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12
Q

What are the symptoms of a focal to bilateral tonic-clonic seizure?

A

Initially symptoms of the above which typically evolves into tonic-clonic seizure 9contraction and rhythmic movement of all limbs)

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13
Q

What is aura in terms of seizures?

A

the sensation before a seizure

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14
Q

What are the warnings of spread of a seizure?

A
  • Sensory: numbness, tingling, burning
  • Motor: jerking of limb, twitching of face
  • Autonomic: blushing, pallor, increased heart rate, nausea
  • Psychic: DeJa’Vu, hallucinations, fear
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15
Q

Does epilepsy cause a pathological increase in CNS activity?

A

Yes

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16
Q

What are the two main regulators of CNS activity?

A
  • Glutamate – general activator
  • GABA – general suppressor
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17
Q

What is the NMDA channel?

A
  • Increases nerve depolarization
  • Glutamate is a general nerve activator, just as GABA is considered a general nerve suppressor
  • Glutamate activates the NMDA channel
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18
Q

What is the ratio between NMDA and GABA?

A

GABA channel activity divided by NMDA channel activity // this determines overall nervous system activity

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19
Q

How is epilepsy classified?

A

Disorder characterized by potential for recurrent seizures:
- At least 2 unprovoked seizures > 24 hours apart
- 1 unprovoked seizure and potential for more after 2 seizures
- Diagnosis of an epilepsy syndrome

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20
Q

What are some triggers of epilepsy?

A
  • Flashing lights
  • Flickering of screens
  • Sudden loud noises or repetitive sounds
  • Alcohol consumption
  • Cigarette smoking
  • Stress
  • Headache
  • Lack of sleep
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21
Q

What is the rationale for epilepsy drug use?

A

Treat or prevent seizures and prevent complications
- Stabilise the abnormally hyperexcitable epileptogenic focus of neurons
- Prevent spread of the seizure discharge to surrounding areas of the brain
Many of the drugs have multiple actions, precise mechanisms are not fully understood (newer drugs in particular)

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22
Q

When do you start treatment for epilepsy?

A

When impact of further seizures outweighs risk of treatment
- After first seizure or second seizure
Start treatment with 1 first-line drug
- Exhaust all reasonable options before considering combining >1 drug

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23
Q

What are the historical antiepileptics?

A

Phenobarbital, primidone

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24
Q

What is the MOA of phenobarbital and primidone?

A

Enhance GABA-mediated inhibition

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25
What are the major risk of using historical antiepileptics?
- Sedation, tolerance + dependence - Pregnancy: major risk of congenital malformations:  orofacial clefts, cardiac defects - Elderly: increased risk of adverse effects - Children: behavioral changes, hyperactivity - Skin reactions: stevens-Johnson syndrome, toxic epidermal necrolysis - Many drug interactions
26
What factors affect drug choice?
- Efficacy in treating syndrome - Pregnancy - Adverse Effects:  Body weight (valproate, topiramate)  Impaired cognition (topiramate, benzodiazepines, phenytoin)  Cosmetic (phenytoin, valproate)  Hypersensitivity (carbamazepine, phenytoin) - Drug interactions
27
What are the strategies and targets of epilepsy treatment?
Strategies and targets: - Increase inhibitory (GABAergic) transmission  GABA level or GABA channel - Modification of ion conductance  sodium and calcium channels - Decrease excitatory (glutamatergic) activity  NMDA channel
28
What are some examples of drugs that enhance GABA-mediated inhibition?
Clobazam and clonazepam
29
What is the MOA of GABA mediated inhibtion?
enhance GABA-mediated inhibition: - Potentiate effects of GABA binding - Inhibit enzymes that degrade GABA - Inhibit action potential - Increase surround inhibition
30
What are the adverse reactions of GABA mediated inhibition?
- Sedation - Tolerance
31
What are examples of drugs that enhance sodium channel mediated inhibition?
Phenytoin, carbamazepine, lamotrigine
32
What is the mechanism of drugs that enhance sodium channel mediated inhibition?
- Act directly on voltage gated Na+ channels - Slows recovery from inactivated state – prevents repetitive firing
33
What are the indications that can present for someone to go on phenytonin?
focal (partial) seizures, generalized tonic-clonic seizures
34
What are the adverse reactions of phenytonin?
ataxia, nystagmus, gingival hypertrophy, reduces BMD, hirsutism
35
Does phenytonin have a narrow therapeutic index?
Yes
36
What types of seizures is carbamazepine used for?
- Simple and complex focal seizures - Generalised tonic-clonic seizures
37
What are the adverse reactions of carbazepine?
Drowsiness, ataxia, dizziness, diplopia, reduces BMD
38
What types of seizures in lamotrigine used for?
Focal (partial) or generalized tonic-clonic seizures
39
What are the adverse reactions of lamotrigine?
- Skin reactions: stevens-johnson syndrome and toxic epidermal necrolysis - Diplopia, dizziness, ataxia, headache
40
What is the MOA of valproate?
- Prolongs Na channel inactivation - Inhibits T-type calcium channels - Enhances GABA effects
41
What are the adverse reactions of valproate?
- Weight gain, tremor, hair loss/ thinning - Reduced BMD with long term use
42
is valproate recommended for females of childbearing potential?
No it is a known teratogen: increased risk of neural tube defects (spina bifida) and other congenital malformations (cleft palate)
43
What is the mechanism of action of topirmate?
- Block Na channels - Block AMPA receptor - Inhibit HVA Ca ion channels - Enhance GABA effects
44
What are the adverse reactions of topiramate?
- Somnolence, fatigue, weight loss
45
What is the mechanism of action of levetiracetam?
exact mechanism unknown. May modulate neurotransmission by binding to synaptic vesicle protein 2A
46
What are the adverse reactions of levetiracetam?
- Behavioral effects, drowsiness, insomnia - Rarely: skin reactions (SJS/TEN)
47
What is the mechanism of action of cannabidol?
- May antagonize G-protein coupled receptor 55 in excitatory synapses and inhibit calcium release preventing excitatory signaling
48
What are the adverse reactions of cannabidol?
- Somnolence, sedation - Hypersalivation, drooling
49
What are some things a doctor will consider for ongoing epileptic treatment in pregnant women?
 Risk of congenital malformations: spina bifida, cleft palate – highest risk with valproate  ALL antiepileptics may be teratogenic  Dangers of uncontrolled epilepsy to mother and foetus
50
What are some diagnostic criteria of depression?
- Marked change in weight or appetite - Insomnia/ hypersomnia nearly every day - Psychomotor agitation/ retardation nearly every day - Fatigue/ loss of energy nearly every day - Feelings of worthlessness, excessive inappropriate guilt - Indecisiveness or diminished concentration - Feelings of hopelessness - Thoughts of death, suicidal ideation/ attempt
51
What is MILD depression?
distress and some difficulty with usual activities
52
What is MODERATE depression?
symptoms marked, considerable difficulty with activities
53
What are SEVERE depression classifications?
symptoms considerable, person is unable to continue activities beyond minimal extent
54
What are the goals for treatment of depression?
- Relieve psychological and physical symptoms - Improve functional capacity - Reduce the likelihood of self-harm or suicide
55
What are some lifestyle modifications that help manage depression?
Improved sleep, hygiene, regular exercise, healthy diet, minimise alcohol, and have daily routines
56
Before starting treatment you should seek explanation for distress with what factors?
- Grief - Alcohol/ illicit drug misuse - Hypothyroidism - Adverse effects of drugs (corticosteroids)
57
What does VMAT stand for?
vesicular monoamine transporter
58
What does MAO stand for?
monoamine oxidase enzyme
59
What is the MOA of escitalopram, paroxetine and sertaline?
- Selectively inhibit presynaptic reuptake of serotonin (5-HT)
60

Fundamentals of Pharmacology (4 decks)

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