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Pharmacology > Module 14 > Flashcards

Module 14 Flashcards

1
Q

Alzheimer’s Disease - prevalent gender

A
  • Women (75%)
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2
Q

Alzheimer’s Disease - symptoms (general)

A

memory loss
problems conducting routine tasks
problems with language, judgment, behaviour, intelligence)

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3
Q

Alzheimer’s Disease - early symptoms

A
  • confusion
  • memory loss
  • problems conducting routine tasks
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4
Q

Alzheimer’s Disease - severe symptoms

A

= difficulty performing daily living activities (eating, bathing, speaking, controlling bowel and bladder function)

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5
Q

Pathophysiology of Alzheimer’s Disease

A
  • Degeneration of cholinergic neurons in hippocampus (early) then in cerebral cortex (late)
  • advanced Alzheimer’s = 10% of cholinergic nerve function
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6
Q

Alzheimer’s Disease - diagnosis

A
  • obtained after death (when brain sample is analyzed)
  • look for
    • neurofibrillary tangles
    • neuritic plaques
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7
Q

Neurofibrillary tangles

A
  • form inside neurons when microtubule arangement is disrupted
  • cause = abnormal production of a protein called Tau
  • can cause alzheimers
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8
Q

Tau

A
  • a protein responsible for forming cross-bridges between microtubules keeping their structure
  • abnormal formation –> alzheimers
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9
Q

Neuritic Plaques

A
  • found outside of neurons –> composed of a core of protein fragments called beta amyloid
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10
Q

Beta amyloid

A
  • make up core of neuritic plaques

- has been shown to kill hipocampal cells + cause Alzheimer-like symptoms (when injected into monkeys)

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11
Q

Etiology of Alzheimer’s Disease

A
  • usually unknown
  • 20% = genetic
  • head injury = also a factor
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12
Q

Alzheimer’s Disease - genetic predisposition (2)

A
  • two copies of apoplipoprotein E4 (ApoE4) –> propotes formation of neuritic plaques by binding to beta amyloid
  • Mutations in amyloid precursor gene (involved in production of beta amyloid)
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13
Q

Alzheimer’s Disease - drug treatment

A

1) Cholinesterase inhibitors (inhibit breakdown of acetylcholine)
2) NMDA receptor antagonists (block NMDA mediated increases in intracellular calcium)

only minimal improvement in symptoms

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14
Q

Cholinesterase inhibitors - target disease

A
  • treat alzheimers disease
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15
Q

Cholinesterase inhibitors - mechanism of action

A
  • inhibit metabolism of acetylcholine by enzyme acetylcholinesterase
  • allows more acetylcholine to remain in the synaptic cleft to exert its actions
  • only able to enhance cholinergic neurotransmission in the remaining healthy neurons
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16
Q

Cholinesterase inhibitors - effectiveness

A
  • display minimal benefit on some measures of memorry

- only effective in 25% of patients

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17
Q

Cholinesterase inhibitors - adverse effects (3)

A
  • nausea and vomiting
  • diarrhea
  • insomnia
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18
Q

NMDA receptor antagonists - target disorder

A

alzheimers

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19
Q

NMDA receptor - function

A
  • NDMA receptor = calcium channel blocked by magnesium at rest
  • when glutamate binds to the NDMA receptor, magnesium dissociates allowing calcium to enter post-synaptic neuron (when glutamate leaves, magnesium returns)
  • normal calcium influx is important in process of learning of memory
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20
Q

NMDA receptor and Alzheimers

A
  • Alzheimers = excess glutamate release,
  • NMDA receptor remains open –>
  • excess calcium enters the cell
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21
Q

detriments of excess calcium influx - NMDA receptors (2)

A

1) detrimental to learning and memory (overpowers normal calcium signal)
2) causes degradation of neurons (too much calcium is toxic)

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22
Q

NMDA receptor antagonists - mechanism of action

A
  • NMDA receptor antagonists block calcium influx into the post-synaptic neuron
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23
Q

NMDA receptor antagonists - adverse effects

A
  • well tolerated

- side effects observed in clinical trials had same incidence as patients taking placebo

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24
Q

Schizophrenia

A
  • disorder that makes it hard to differentiate between real and unreal experiences, to think logically, to have normal emotional responses, and to behave normally in social situations
  • affects 1`% of worlds population
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25
Q

Schizophrenia - age of onset

A

adolescence or early adulthood (16-30)

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26
Q

Symptoms of Schizophrenia (classifications)

A
  • Positive symptoms (exaggerate or distort normal neuro function)
  • Negative symptoms (where there is a loss of normal neurological function)
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27
Q

Symptoms of Schizophrenia - positive symptoms (7)

A 
symptoms that exaggerate or distort normal neurological function
EX
- delusions
- Hallucinations
- agitation
- paranoia
- combativeness
- disorganized speech
- disorganized thinking
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28
Q

Symptoms of Schizophrenia - negative symptoms (8)

A 
symptoms are those where there is a loss of normal neurological function
EX
- Social withdrawal
- poverty of speech
- poor self care
- poor insight
- poor judgment
- emotional withdrawal
- blunted affect
- lack of motivation
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29
Q

Etiology of Schizophrenia

A

largely unknown, a few factors that increase risk

  • Family history
  • Drug abuse
  • Low birth weight
  • Low IQ
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30
Q

Etiology of Schizophrenia - family history

A
  • 10% of schizophrenics have a parent with the disease

- both parents with schizophrenia –> 25% chance their children will have it

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31
Q

Etiology of Schizophrenia - drug abuse

A
  • methamphetaine (crystal meth), phencyclidine (PCP, angel dust) and lysergic acid diethylamid (LSD)
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32
Q

Etiology of Schizophrenia - low birth weight

A

babies born at less than 5.5 pounds have increased risk of developing schizophrenia

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33
Q

Etiology of Schizophrenia - low IQ

A

lower IQ = greater risk of developing schizophrenia

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34
Q

Brain regions affected by Schizophrenia (6)

A
  • Basal ganglia
  • Frontal lobe
  • Limbic system
  • Auditory system
  • occipital lobe
  • hippocampus
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35
Q

Brain regions affected by Schizophrenia - basal ganglia

A
  • normal = movement and emotions

- abnormal = abnormal activity –> paranoia and hallucinations

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36
Q

Brain regions affected by Schizophrenia - frontal lobe

A
  • normal = problem solving and insight

- Abnormal - associated with difficulty planning actions and organizing thoughts

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37
Q

Brain regions affected by Schizophrenia - Limbic System

A
  • normal = emotions

- Schizophrenia = contributes to agitation

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38
Q

Brain regions affected by Schizophrenia - Auditory system

A
  • overactivity –> hallucinations
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39
Q

Brain regions affected by Schizophrenia - occipital lobe

A
  • normal = processes visual info

- Abnormal = involved with interpreting images, reading emotion on other;s faces and recognizing motion

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40
Q

Brain regions affected by Schizophrenia - hippocampus

A
  • normal = mediates learning and memory

- abnormal = learning and memory hindered

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41
Q

Pathophysiology of Schizophrenia (3)

A
  • increased dopaminergic nerve transmission (opposite side of Parkinson’s spectrum) = increased domaminergic neurotransmision and increased binding of dopamine to D2 receptors
  • 5-HT (seretonin) imbalance… decreased number of 5HT 2A receptors, increase in 5-HT 1A receptors –> impact symptoms
  • Glutamate - patients with schizophrenia have a decreased number of NMDA receptors in some regions of their brain –> symptoms of schizophrenia
    • PCP (angel dust) = antagonist of NMDA receptor
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42
Q

Schizophrenia - how is it diagnosed?

A
  • no definitive test

- diagnosis made by psychiatrist after interviewing patient and family

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43
Q

Schizophrenia - diagnostic criteria (5)

A

1) changes in function from before illness
2) developmental bacground
3) family history’
4) response to meds
5) brain scans (enlarged ventricles, decreased frontal lobe brain activity)

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44
Q

Drug treatment of Schizophrenia

A
  • blocking dopamine and/or serotonin neurotransmission in the brain
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45
Q

Drug treatment of schizophrenia - classification (2)

A
  • conventional antipsychotics

- atypical antipsychotics

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46
Q

Conventional antipsychotics - mechanism of action

A
  • work primarily by blocking dopamine 2 (D2) receptors primarily in the mesolimbic area of the brain
    • lesser degree - also block receptors for acetylcholine, histamine, norepinephrine
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47
Q

Conventional antipsychotics - potency

A

directly proportional to thier ability to inhibit D2 receptors

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48
Q

Conventional antipsychotics - efficacy

A
  • mostly efficient at treating positive symptoms of schizophrenia than the negative symptoms
  • initial effects seen in 1-2 days, substantial improvement takes 2-4 weeks
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49
Q

Conventional antipsychotics - adverse effects (6)

A

1) extrapyramidal symptoms
2) sudden high fever
3) anticholinergic effects
4) orthostatic hypotension
5) sedation
6) skin reactions

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50
Q

Extrapyramidal symptoms (what, pathophysiology, 4 types)

A
  • movement disorders that resemble the symptoms of parkinson’s disorder
  • due to blockade of D2 receptors
  • 4 types = acute dystonia, parkinsonism, akathesia, tardive dyskinesia
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51
Q

Acute Dystonia

A
  • an extrapyramidal symptoms

- involuntary spasm of the muscles in the face tongue, neck or back. typically occurs early in therapy

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52
Q

Parkinsonism (what,, symptoms (4), treatment)

A
  • a type of extrapyramidal symptoms (EPS)
  • bradykinesia, mask-like face, rigitity, stooped posture
  • treated with anticholinergic drug (avoid L-DOPA)
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53
Q

Akathesia

A
  • an extrapyramidal symptom
  • pacing, squirming, desire to continually be in motion
  • typically occurs early in treatment
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54
Q

Tardive Dyskinesia

A
  • an extrapyramidal symtom
  • occurs in 20% of patients on longterm therapy
  • irreversible (early detection is essential)
  • involuntary twisting and writhing of the face and tonuge, lip smacking
  • switch medications immediately
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55
Q

Atypical antipsychotics - mechanism of action

A
  • block both dopamine D2 receptors and 5-HT-2A receptors

- can block D2 receptors, but affinity is very low…. Therapeutic action is due to blockade of 5-HT receptors

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56
Q

Which is better - conventional antipsychotics or atypical antipsychotics

A

atypical psychotics…

1) same efficacy versus positive symptoms of schizophrenia
2) much greater efficacy versus negative symptoms of schizophrenia
3) much lower risk of developing extrapyramidal symptoms

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57
Q

Atypical antipsychotics - adverse effects (5)

A
  • sedation
  • orthostatic hypotension
  • weight gain (sometimes severe)
  • risk of developing type II diabetes
  • anticholinergic effects
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58
Q

Epilepsy

A
  • neurological disorder that produces brief disturbances in the normal electrical activity in the brain
  • Characterized by sudden, brief seizures (vary from person to person)
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59
Q

Seizure

A

a sudden alteration of behaviour caused by CNS dysfunction

- transient and sudden

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60
Q

Epileptic seizure

A
  • a seizure caused by primary CNS dysfunction

- due to excess depolarization and hypersynchronization of neurons

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61
Q

Non-epileptic seizure

A
  • a seizure-like episode that is not the result of abnormal electrical activity in the brain
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62
Q

Epilepsy (definition)

A
  • a tendency for recurrent spontaneous epileptic seizures
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63
Q

Status epilepticus

A
  • a single unremitting epileptic seizure of duration longer than 30 minute OR
  • frequent seizure without recovery of awareness in between

EMERGENCY

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64
Q

Categories of seizures (2)

A
  • epileptic

- non-epileptic

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65
Q

Categories of Epileptic seizures (3)

A
  • focal/partial seizure
  • generalized seizure
  • secondary generalized seizure
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66
Q

categories of focal/partial seizure (2)

A
  • complex

- simple

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67
Q

Categories of generalized seizure (5)

A
  • abscence seizure
  • tonic/clonic seizure
  • myoclonic seizure
  • tonic seizure
  • atonic seizure
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68
Q

Focal/partial seizure

A
  • arise in one area of the brain
  • 2 types
    • simple partial seizure
    • complex partial seizure
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69
Q

Simple partial seizure

A
  • no loss of consciousness
  • symptoms depend on where the seizure activity is arising from
  • EX - L motor strip oglidendroglioma –> clonic movement of right arm, then right face, then right leg. No impairment of consciousness, lasts 45 seconds`
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70
Q

Complex partial seizure

A
  • loss of consciousness (patient may appear to be awake but are not aware of surroundings)
  • symptoms depend on where seizure is taking place
  • EX - right temporal lobe epilepsy –> whistling, bicicling movements in left leg, rising epigastric sensation with nausea, normal ictal speech, no memory of events post ictally (after seizure), lasting 30-45 seconds
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71
Q

Generalized seizures

A
  • bilateral diffuse onset, seeming to arise form all areas of the brain at once
  • 5 types
    • abscence seizure
    • tonic/clonic seizures
    • myoclonic seizures
    • tonic seizures
    • atonic seizures
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72
Q

Absence seizures - symtoms

A
  • loss of consciousness, behavioural arrest, staring

- rarely associated with automatisms (unusual purposless movements)

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73
Q

Absence seizure - frequency and timing

A
  • usually brief

- may occur multiple times in a day

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74
Q

Absence seizures - population

A

more common in childhood

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75
Q

Tonic/Clonic seizures - symptoms

A
  • abrupt loss of consiousness
  • a tonic period (muscles become rigid) lasting 1 minute)
  • a clonic period (involuntary muscle contractions) lasting 2-3 minutes
  • patient may become incontinent and have tongue biting
  • post-ictal –> drowsy, confusion, frequently complaining of headaches
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76
Q

Tonic - definition

A

muscles become rigid

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77
Q

Clonic - definition

A

involuntary muscle contractions

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78
Q

Myoclonic seizures

A
  • sudden, brief muscle contractions that can involve any muscle group
  • usually no loss of consciousness
  • sometimes associated with a later developemnt of generalized tonic/clonic seizures
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79
Q

Tonic seizures

A
  • sudden msucle stiffening (rigidity)

- often involve impaired consiousness

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80
Q

Atonic seizures

A
  • sudden loss of muscle tone
  • brief (15 seconds)
  • aka drop seizures (patients drop to the grund)
  • risk for falling injuries
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81
Q

Secondary generalized seizure

A
  • a seizure that begins in one area of the brain (like a focal seizure) then spread throughout the brain
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82
Q

an “aura”

A
  • preliminary focal phase of a secondary seizure
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83
Q

Localizing focal seizures

A

evaluating the patients symptoms vs what we know about vaious regions of the brain

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84
Q

Focal seizures - frontal lobe (3)

A
  • simple repetitive motor movements involving a localized muscle group –> seizure activity in the contralateral primary motor cortex
  • tonic posturing affecting entire side of the body –> seizure in contralateral Supplemental Motor Area (SMA) + other higher level motor structures
  • Very complex behaiour automatisms involving bilateral movment (swimming, bicycle riding movements) = seizure in higher areas of frontal cortex, may involve vocalizations (laughter, crying)
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85
Q

Where is the seizure? - simple repetitive motor movements involving a localized muscle group

A
  • frontal lobe (primary motor cortex)
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86
Q

Where is the seizure? = tonic posturing affecting entire side of the body

A

Frontal lobe (Contralateral Supplemental motor area/ other higher level motor structures)

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87
Q

Where is the seizure - Very complex behavioural automatisms involving bilateral moment (swimming, bicycle riding movements), may involve vocalizations (laughter, crying)

A

Frontal lobe (higher areas of the frontal cortex)

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88
Q

Focal Seizures - Temporal Lobe

A
  • typically associated with auditory hallucinations (buzzing, voices talking), olfactory (smell), gustatory (taste) hallucinations
  • more ocmplex sensory phenomena (visual distortions, paresthesias (numbness) and autonomic disturbances
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89
Q

Where is the seizure? - auditory, olfactory, gustatory hallucinations

A

temporal lobe

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90
Q

Where is the seizure? - paresthesias, autonomic disturbanes

A

temporal lobe

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91
Q

Focal Seizures - Parietal Lobe (3)

A
  • localized paresthesias = numbness, “pins and needles” = somatosensory cortex
  • complex/widespread paresthesias = somatosensory association cortex
  • complex multi-sensory hallucinations and illusions = higher order sensory association (difficult to distinguish from the more common temporal lobe seizure)
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92
Q

Where is the seizure? - numbness, “pins and needles”

A

parietal lobe (somatosensory cortex)

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93
Q

Where is the seizure? - complex/widespread parenthesis

A

Parietal lobe (somatosensory association cortex)

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94
Q

Where is the seizure - complex multi-sensory hallucinations and illusions

A

Parietal lobe (higher order sensory association areas)/temporal lobe

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95
Q

Focal seizures - occipital lobe

A
  • Visual hallucinations (flashing.repeated pattern in the environment, rather than organized objects such as people or faces)
  • Temporary blindness/decreased vision, sensation of eye movement, nystagmus (involuntary eye movement)
  • can be mistaken for migraine headaches
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96
Q

Where is the seizure? - Visual hallucinations (flashing.repeated pattern in the environment

A

occipital lobe

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97
Q

Where is the seizure? - Temporary blindness/decreased vision, sensation of eye movement, nystagmus (involuntary eye movement)

A

Occipital lobe

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98
Q

Epileptogenesis (3)

A

1) symptomatic epilepsy
2) idiopathic epilepsy
3) cryptogenic epilepsy

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99
Q

Symptomatic epilepsy

A

epilepsy arising from an identified physical cause (ex brain tumour, stroke, infection, other injury)

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100
Q

Idiopathic epilepsy

A

epilepsy that does not have identifiable cause; often there is a family history of seizures, genetics likely play a role

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101
Q

Cryptogenic epilepsy

A

epilepsy that is likely to have an underlying cause that has not been identified

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102
Q

The seizure threshold (2)

A
  • thought of as the balance between excitable and inhibitory forces in the brain
  • everybody has a seizure threshold –> affects how susceptible a patient is to having a seizure
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103
Q

The Seizure threshold - contributing factors (~7)

A
  • Determining factors - anything that causes changes in electrical activity/affects firing of action potentials
  • EX: stroke, head injury, drug/alcohol withdrawal, infection, tumour, severe fever, visual stimuli (flashing lights)
104
Q

Anti-epileptic drugs - categories

A

1) blocking sodium channels
2) blocking voltage-gated calcium channels
3) glutamate antagonists
4) potentiating the actions of GABA

105
Q

Anti-epileptic drugs - blocking sodium channels - mechanism of action

A
  • recall - sodium influx contributes to generation of action potential
    • NORMAL - after sodium enters the cell, sodium channel enters inactive
      state where sodium entry to cell is prevented…return to normal active state
      very quickly
  • Sodium channel blocker AEDs prolong inactivation state of sodium channel = don’t allow to fire at high frequency
106
Q

Phenytoin - function

A
  • most widely used anti-epileptic drug
107
Q

Phenytoin - mechanism of action

A

blocks sodium channels

108
Q

Phenytoin - indications for use

A

useful in the treatment of all types of epileptic seizures except absence seizures

109
Q

Phenytoin - metabolism and effect

A
  • metabolism of the liver is limited –> non-linear kinetics
  • small increase in dose = large increase in plasma concentration
  • narrow therapeutic range –> drug monitoring
110
Q

Phenytoin - adverse effects

A
  • sedation
  • gingival hyperplasia
  • skin rash
  • teratogenic
111
Q

Anti-epileptic drugs - blocking voltage dependent calcium channels

A
  • NORMAL - influx of calcium through VG calcium channels promotes neurotransmitter release from pre-synaptic nerve terminal
  • inhibition of calcium suppresses neurotransmitter release
112
Q

Glutamate antagonists - mechanism of action (2)

A
  • Glutamate = an excitatory CNS neurotransmitter
  • block glutamate in two places –> dereased CNS excitation
    - NMDA receptor blockage
    - AMPA receptors blockage
113
Q

GABA receptor (what, mechanism of action, result)

A
  • inhibitory CNS neurotransmitter
  • binding of GABA to its receptor causes negatively charged chloride ions to rush into the cell
  • result = makes it more difficult for threshold to be reached + difficult to have an action potential
114
Q

Potentiating the actions of GABA - anti-epileptic drug

A
  • potentiate actions of GABA –> increase inhibitory stimuli –> suppress seizure activity
115
Q

Potentiating the actions of GABA - anti-epileptic drug - 4 ways to mediate

A

1) enhancing binding of GABA to its receptor
2) stimulating GABA release
3) Inhibiting GABA re-uptake
4) inhibiting GABA metabolism

116
Q

Anti-epileptic dug - classififications (2)

A
  • Traditional = phenytoin, valpoic acid

- Newer = lamotrigine

117
Q

Classifications of anti-epileptic drugs - differences

A

1) effectiveness is similar

2) newer AEDs have decreased side effects + decreased propensity to induce hepatic drug metabolizing enzymes

118
Q

Depression

A
  • when symptoms of depression are prolonged and interfere with everyday life
  • 1/3 people will experience depression at some time in their life
  • current estimate = 3% currently have depression
119
Q

Diagnosis of depression (9)

A

5 of the following symptoms

  • depressed mood most of the day, nearly everyday
  • loss of interest or pleasure in all or almost all activities
  • significant weight loss (no diet) or weight gain
  • insomnia or hypersomnia
  • psychomotor agitation or retardation
  • fatigue and energy loss
  • feelings of worthlessness or excessive guilt
  • decreased ability to think, concentrate, excessive indecisiveness
  • recurrent thoughts of death or suicidal ideations`
120
Q

Types of depression (2)

A

2 main types =

  • exogenous
  • endogenous
121
Q

Exogenous depression

A
  • triggered by external stimuli
122
Q

endogenous depression

A

may or may not be related to external events

123
Q

Exogenous depression - classifications (2)

A
  • pathological grief

- adjustment disorder

124
Q

Pathological grief (what, treatment)

A
  • prolonged grieving coupled with excessive guilt.

- psychotherapy is usually more effective than drugs

125
Q

Adjustment disorder (what)

A

prolonged depression following failure or rejection (i.e. losing your job, failing out of school

126
Q

Adjustment disorder (common symptoms)

A

hypersomnia (excess sleep), hyperphagia (overeating)

127
Q

Adjustment disorder (treatment)

A
  • psychotherapy is often more effective than drug therapy
128
Q

Endogenous depression - categories (7)

A
  • major depression
  • severe depression
  • atypical depression
  • dysthymia
  • seasonal affective disorder (SAD)
  • postpartum depression
  • bipolar disorder
129
Q

Major depression (symptoms) 3

A
  • loss of interest and lack of response to positive stimuli
  • symptoms usually worse in the morning
  • insomnia and weight loss are typical
130
Q

Severe depression (symptoms) (~6)

A
  • similar symptoms to major depression (- loss of interest and lack of response to positive stimuli; symptoms usually worse in the morning; insomnia and weight loss are typical)
  • severe suicidal ideation
  • psychoses
131
Q

Atypical depression

A
  • similar to symptoms of major depression (loss of interest and lack of response to positive stimuli; symptoms usually worse in the morning)
  • BUT atypical symptoms of hypersomnia and hyperphagia
  • often patients with atypical depression are obese
132
Q

Dysthymia (symptoms, treatment)

A
  • patient’s mood is regularly low but symptoms are not as severe as major depression
  • symptoms are more noticeable to family members/close friends than they are to the patient
  • usually responds better to psychotherapy than drugs
133
Q

Seasonal affective disorder

A
  • mild or moderate symptoms of depression related to the lack of sunlight
  • usually affects people only in the winter months
134
Q

Postpartum depression

A
  • moderate to severe depression in women after they give birth
  • usually occurs within 3 months of delivery but may occur up to a year after birth
135
Q

Bipolar disorder (depression)

A
  • alternating periods of elevated or irritable mood and periods of depression
136
Q

The monoamine hypothesis

A
  • depression - exact cause and pathophysiology is unknown

- THEORY = altered monoamine release, receptor sensitivity, post-synaptic function lead to symptoms of depression

137
Q

Antidepressants - function

A
  • act to increase synaptic levels of one or more monoamine neurotransmitters
138
Q

Antidepressants - efficacy

A
  • difficult to assess since it often take months for effects to occur
  • results from placebo-controlled clinical trials = 40% effects observed may be attributed to the placebo effect
139
Q

Antidepressants - mechanisms of action

A
  • act to increase synaptic levels of one or more monoamine neurotransmitters
    1) inhibiting monoamine reuptake
    2) inhibiting monoamine metabolism
140
Q

Classes of antidepressant drugs (4)

A

1) tricyclic antidepressants
2) selective serotonin reuptake inhibitors (SSRIs)
3) selective serotonin/norepinephrine reuptake inhibitors
4) monoamine oxidase inhibitors (MAOIs)

141
Q

Tricyclic antidepressants (mechanism of action)

A
  • inhibit reuptake of both serotonin and norepinephrine
142
Q

Tricyclic antidepressants - target population

A

effective in treatment of major depression

143
Q

Tricyclic antidepressants - adverse effects (7)

A
  • anticholinergic effects
  • sedation
  • orthostatic hypotension
  • decreased seizure threshold
  • cardiac toxicity (rare but potentially serious)
  • weight gain
  • sexual dysfunction
144
Q

Selective serotonin reuptake inhibitors (SSRIs) - mechanism of action

A
  • block serotonin reuptake
145
Q

Selective serotonin reuptake inhibitors (SSRIs) - when used

A
  • most commonly used
  • similar efficacy to Tryciclic antidepressants, but incidence of side effects are lower
  • most commonly used in major depression
146
Q

Selective serotonin reuptake inhibitors (SSRIs) - adverse effects (4)

A
  • weight gain
  • sexual dysfunction
  • insomnia
  • Serotonin syndrome (agitation, confusion, anxiety, hallucinations, incoordination occurring within 3 days of initial therapy disappearing when drug is stopped)
147
Q

Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) - mechanism of action

A
  • block re-uptake of both norepinephrine and serotonin (similar mechanism to TCAs)
148
Q

Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) - onset of action

A
  • FASTER (huge advantage)
149
Q

Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) vs Tryciclic antidepressants

A
  • TCAs have three-ringed structure

- SNRIs do not and have faster onset

150
Q

Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) - adverse effects

A
  • nausea
  • diastolic hypertension
  • sexual dysfunction
151
Q

Monoamine Oxidase

A
  • an enzyme that inactivate monoamine neurotransmitters
152
Q

Monoamine Oxidase - 2 types, what they (M)

A
  • MAO-A: metabolizes serotonin and norepinephrine

- MAO-B: metabolizes dopamine

153
Q

Monoamine Oxidase Inhibitors (MAOIs) - mechanism of action

A
  • inactivates MAO, which are enzymes that inactivate monoamine neurotransmitters
  • non-selective = inhibit both MAO-A and MAO-B
  • RESULT = inhibits metabolism of monoamines in the pre-synaptic neuron
154
Q

Monoamine Oxidase Inhibitors (MAOIs) - population to treat

A
  • atypical depression and dysthymia
155
Q

Monoamine Oxidase Inhibitors (MAOIs) - adverse effects (3)

A
  • CNS excitation - anxiety, insomnia, agitation
  • orthostatic hypotension
  • hypertensive crisis if taken with tyramine containing foods
156
Q

Bipolar disorder

A
  • severe illness - recurrent fluctuations between episodes of mania and depression
157
Q

Bipolar disorder - onset

A
  • symptoms begin in adolescence or early adulhood
158
Q

Bipolar disorder - mania (6)

A
  • irritation
  • inflated self-esteem (delusions of grandeur)
  • little need for sleep
  • poor control of temper
  • reckless behaviour (binge eating, drinking, drug use)
  • easily distracted
159
Q

Patterns of mood episodes - bipolar

A
  • cycles vary (some experience repeat mania with occasional depression, others repeated depression with occasional mania)
  • Average = 2 episodes every 5 years
160
Q

Drug treatment of bipolar disorder (3)

A

1) mood stabilizers
2) antipsychotics
3) antidepressants

161
Q

Mood stabilizers - function

A

1) relieve symptoms during manic or depressive episodes
2) prevent recurrence of manic or depressive episodes
3) do not worsen symptoms of mania or depression and do not alter rate of cycling

162
Q

Mood stabilizers - bipolar disorder (2)

A
  • lithium

- valproic acid (anti-epileptic drug)

163
Q

Lithium - mechanism of action

A
  • unclear

- alters uptake and release of glutamate and blocking binding of serotonin

164
Q

dangers of lithium (2)

A

1) narrow therapeutic range
2) plasma concentrations may be altered by sodium
- agents that increase sodium loss from body (diuretics) increase lithium concentrations and may produce toxicity

165
Q

Symptoms of lithium toxicity

A
  • GI upset
  • tremor
  • sedation
  • hypotension
166
Q

Antipsychotics - use for bipolar

A
  • acute = control mania symptoms, longterm to stabilize mood
  • benefit patients even if they don’t have psychotic symptoms
  • preference for atypical antipsychotics (lower risk of extrapyramidal symptoms)
167
Q

Antidepressants and bipolar disorder

A
  • used in bipolar disease to treat depressive episodes
  • always combined with a mood stabilizer (used alone, they may preciptate mania)
  • no good evidence for which one works best
168
Q

Anxiety

A
  • normal physiological response to stress
  • normal before an exam or before a first date
  • turns into a disorder when symptoms create functional impairment in a patients daily living
  • linked with depression
169
Q

Types of anxiety (7)

A
  • generalized anxiety disorder
  • panic disorder
  • agoraphobia
  • obsessive-compulsive disorder
  • social anxiety disorder
  • post-traumatic stress disorder
  • simple phobia
170
Q

Generalized anxiety disorder

A
  • patient is overwhelmed with uncontrollable worrying

- unrealistic or excessive worry about several activities lasting 6 months or longer

171
Q

Panic disorder

A
  • patients have a sense of impending doom that is unrelated to stressors
  • panic attacks (sudden onset of heart palpiltations, chest pain, shortness of breath, dizziness [mimic heart attack])
172
Q

Agoraphobia

A
  • anxiety where the patient feels judged or a situational anxiety where escaping would be difficult or embarrassing
173
Q

Obsessive-compulsive disorder

A
  • persistent obsession and compulsions that interfere with daily life (hand-washing, checking locks, etc)
174
Q

Social anxiety disorder

A
  • anxiety in social situations

- patients may not be able to talk (or stop talking), eat in front of others or use public washrooms

175
Q

Post-traumatic stress disorder

A
  • anxiety occurring after experiencing a traumatic event

- symptoms = re-experiencing the event and severe insomnia

176
Q

Simple phobia

A

symtoms related to a specific fear (spiders, elevators)

177
Q

Drug treatment for anxiety (3)

A
  • benzodiazepines (BDZs)
  • buspirone
  • antidepressants
178
Q

Benzodiazepines (target disorder)

A
  • first line of therapy for anxiety
179
Q

Benzodiazepines - mechanism of action

A
  • work by potentiating the actions of GABA at GABA receptor
  • note: NOT GABA agonists….bind to a different site on the GABA receptor and cause increased binding of GABA to the receptor
  • GABA binds to the receptor, opening a channel, so chloride ions move into the cell –>CNS depression
  • note: BZD amplify endogenous GABA there is a limit to the CNS depression they may produce making them much safer than Barbituates
180
Q

Therapeutic uses for benzodiazepines (5)

A

1) anxiety
2) seizures
3) insomnia
4) alcohol withdrawal
5) muscle spasm

181
Q

Dosing a benzodiazepine

A
  • different dose = different effects

- EX - higher dose of BD is used to treat insomnia than anxiety

182
Q

Benzodiazepines - target disorders

A
  • treat generalized anxiety and social anxiety disorders
183
Q

Benzodiazepines - adverse effects (6)

A
  • CNS depression - drowsiness, difficulty concentrating,
  • Anterogade amnesia - impaired memory of events that occur following dosing
  • respiratory depression (rare, but more common if combined with alcohol)
  • teratogenic
  • tolerance
  • withdrawal (should be tapered slowly
184
Q

Buspirone - mechanism of action

A
  • not a CNS depressant

- mechanism UNCLEAR –> modulation of serotonergic and/or dopaminergic neurotransmission

185
Q

Buspirone - target population

A
  • useful in patients who use alcohol

- generalized anxiety disorder (ineffective for other types such as panic disorder or OCD)

186
Q

Buspirone - advantages (4)

A
  • not a CNS depressant = can be used in patients who use alcohol
  • no signs of tolerance or physical dependence
  • few adverse effects
  • non-sedating
187
Q

Buspirone - disadvantage

A
  • anxiolytic effects develop slowly = ineffective at treating symptoms that require immediate relief
188
Q

Buspirone - adverse effects (3)

A
  • well tolerated, non-sedating
  • dizziness
  • lightheadedness
  • excitement
189
Q

Antidepressants - anxiety

A

useful in certain types of anxiety

190
Q

Antidepressants + generalized anxiety disorder (which types x3)

A
  • SSRIs and SNRIs effective

- buspirone slow to enact their effect

191
Q

Antidepressants + panic disorder/agoraphobia (which ones (3) work, which one is prefered)

A
  • SSRIs, TCAs, MAOI are useful but effects take 6-12 weeks to appear
  • SSRIs preferred (better tolerated)
192
Q

Antidepressants + OCD

A
  • SSRIs = first line of therapy

- used in conjunction with behavioural therapy

193
Q

Antidepressants + social anxiety disorder

A
  • SSRI = first line of therapy, BDZ can also be used

BDZ = immediate relief, SSRIs = LT

194
Q

Neuropharmacology

A

study of how drugs affect the function of the central nervous system

195
Q

What is the brain composed of

A

millions of neurons

196
Q

neurons

A
  • excitable cells that transmit information by electrical and chemical signalling
197
Q

How is information transmitted in neurons

A 
Dendrite of neuron recieves signal from other neuron
Action potential (electric signal) propagates along axon of the neuron
AP reaches pre-symaptic nerve terminal, causes release of neurotransmitters (chemical signalling)
198
Q

Action potentials

A

A depolarization, positive charged Na+ ions enter cell through VG Na+ channels = membrane changes from -70mV to +35 mV

Na+ channels then close and potassium channels open allowing Na+ to leave cell during repolarization

overshoot (-70 mV)

199
Q

Synapse - transmitting the AP

A

send neurotransmitters

  • once AP reaches pre-synaptic neuron, Ca2+ influx
  • cause vesicles with Neurotransmitters to release into the synaptic cleft
200
Q

Neurotransmitters in the CNS that are monoamines (4)

A
  • norepinephrine
  • epinephrine
  • dopamine
  • seretonin
201
Q

Norepinephrine - associated disorders

A

depression and anxiety

202
Q

Epinephrine - associated disorders

A

anxiety

203
Q

Dopamine - associated disorders

A

parkinson’s + schizophrenia

204
Q

Norepinephrine - classification

A

monoamine

205
Q

Epinephrine - classification

A

monoamine

206
Q

dopamine - classification

A

monoamine

207
Q

Serotonin - classification

A

monoamine

208
Q

Neurotransmitters in the CNS - classifications (3)

A
  • Monoamines
  • Amino acids
  • other
209
Q

Neurotransmitters - amino acids - classification

A
  • Excitatory

- Inhibitory

210
Q

Neurotransmitters - excitatory amino acids - classification (2)v

A
  • Glutamate

- asparate

211
Q

Neurotransmitters - inhibitory amino acids - classification

A
  • GABA

- Glycine

212
Q

Glutamate - associated disorder

A
  • alzheimer’s
213
Q

Glutamate - classification

A

amino acid neurotransmitter

214
Q

Aspartate - associated disorder

A

Alzheimer’s

215
Q

Aspartate - classification

A

Amino Acid neurotransmitter

216
Q

GABA - associated disorder

A

Anxiety

217
Q

GABA - classification

A

amino acid neurotransmitter

218
Q

Glycine - associated disorder

A
  • anxiety
219
Q

Glycine - classification

A

amino acid neurotransmitter

220
Q

Acetylcholine - associated disease

A

Alzheimer’s and Parkinson’s

221
Q

Basic Mechanisms of CNS Drug action (5)

A

1) Replacement (what is low in disease)
2) agonists/antagonist (drug directly binds to receptors)
3) inhibiting neurotransmitter breakdown (inhibit metabolism)
4) blocking reuptake
5) nerve stimulation

222
Q

Parkinson’s Disease - pathology

A

Progressive loss of dopaminergic neurons in substantia nigra of the brain (70-80%)

progresses in 5-10 years to state where patients cant care for themselves

223
Q

Symptoms of Parkinson’s Disease (6)

A

1) Tremor (extremities = hands, arms, legs, jaw, face)
2) Rigidity
3) bradykinesia (slowness of movement/slow to initiate movement
4) masklike face (cant show expression + difficult blinking, swallow)
5) postural instability
6) dementia (later in disease)

224
Q

Parkinson’s disease - pathophysiology (3)

A
  • imbalance between acetylcholine and dopamine in the brain
    • dopamine release is decreased (not enough present to inhibit GABA
      release)
    • relative excess of acetylcholine compared to dopamine, resulting in
      increased GABA release
    • excess GABA causes movement disorders
225
Q

Etiology of parkinson’s disorder

A

largely unknown

226
Q

Parkinson’s Disorder - Risk factors (5)

A
  • Drugs (by product of street drug synthesis produces MPTP. MPTP causes irreversible death of dopaminergic neurons
  • Genetics - mutation in 4 genes (alpha sunuclein, parkin, UCHL1, DJ-1)
  • Environmental Toxins - pesticides –> PD
  • Brain trauma (from injury)
  • oxidative stress (reactive oxygen species…diabetes induced oxidative damage –> PD)
227
Q

Drug treatment of parkinson’s disease

A

reverse degeneration of dopaminergic neurons (ideal)

but. ….
1) Increase dopamine
2) decrease acetylcholine

228
Q

Drugs that increase Dopamine Neurotransmission

A

1) dopamine replacement
2) dopamine agonist
3) dopamine releaser
4) catecholamine-O-Methyltransferase inhibitor
5) Monoamine oxidase-B (MAO-B) inhibitor

229
Q

Dopamine replacement - main drug name

A

Levodopa (L-Dopa)

230
Q

L-Dopa - use

A
  • treats Parkinson’s disease
  • most effective drug
  • use decreases with time
231
Q

Levodopa (L-DOpa) - transportation to site

A
  • crosses blood brain barrier by an active transport protein
232
Q

Levodopa (L-DOpa) - mechanism of action

A
  • inactive on its own, converted to dopamine in dopaminergic nerve terminals
  • reaction mediated by decarboxylase enzymes in the brain
  • cofactor pyridoxine (vit B6) speeds up this reaction
233
Q

Levodopa (L-DOpa) - why not just give dopamine

A
  • Dopamine does not cross blood brain barrier

- dopamine has a very short half-life in blood

234
Q

Levodopa (L-DOpa) - adverse effects (5)

A
  • nausea and vomiting (dopamine trigger chemoreceptor in medula of brain)
  • dyskinesias (abnormal involuntary movements)
  • cardiac dysrhythmias (dopamine in periphery can activate cardiac beta 1 receptors)
  • orthostatic hypotension
  • psychosis (20% of patients)
235
Q

Levodopa (L-DOpa) - peripheral metabolism (solution, impact)

A

only 1% of L-Dopa reaches brain, rest is metabolized in peripheral tissue

  • solution = give with carbidopa
236
Q

Carbidopa (what, function, effect)

A

carbidopa (decarboxylase inhibitor)
inhibits peripheral metabolism of L-DOPA

= 10% of L-DOPA reaches brain, less cardiac dysrhythmia, decreased N+V

237
Q

Levodopa (L-DOpa) - types of loss of effect (2)

A

1) wearing off - gradual loss

2) on-off - abrupt loss of effect

238
Q

Wearing off (L-DOPA)

A

a gradual loss of effect

usually occurs at the end of the dosing interval and indicates that drug levels might be low

239
Q

Wearing off (L-DOPA) - solutions

A
  • shorten dosing interval
  • give drug that inhibits L-DOPA metabolism (ie a COMT inhibitor)
  • add a dopamine agonist to the therapy
240
Q

On-off (L-DOPA) - what/when it occurs

A
  • abrupt loss of effect

- can occur even when drug levels are high

241
Q

On-off (L-DOPA) - solutions

A
  • divide med into 3-6 doses per dya
  • use a controlled release formulation
  • moving protein-containing meals to the evening
242
Q

Dopamine Agonist - mechanism of action

A
  • produce effects by directly activating dopamine receptors on the post-synaptic cell membrane
243
Q

Dopamine Agonist - indications for use-

A
  • not as effective as L-DOPA

- first line of treatment for patients with midler symptoms

244
Q

Dopamine Agonist - adverse effects (3)

A
  • hallucinations
  • daytime drowsiness
  • orthostatic hypotension
245
Q

Dopamine Releaser - mechanism of action (3)

A
  • stimulate release of dopamine from dopaminergic neurons
  • blocks dopamine reuptake into pre-synaptic nerve terminals
  • blocks NMDA receptors (decrease dyskinesia side effect of L-Dopa)
246
Q

Dopamine Releaser - indications for use

A
  • not as effective as L-dopa, used in combo with L-DOpa or alone in mild PD
247
Q

Dopamine Releaser - adverse effects (5)

A
  • dizziness,
  • nausea,
  • vomiting,
  • lethargy,
  • anticholinergic side effects
248
Q

Catecholamine-O-Methyltransferase Inhibitor (COMT) - mechanism of action

A
  • Inhibits COMT (enzyme that adds methyl group to dopamine and L-DOPA, rendering them inactive)
  • results in a greater fraction of Dopamine and L-Dopa that can be converted to dopamine
249
Q

Catecholamine-O-Methyltransferase Inhibitor (COMT) - indications for use

A
  • moderately effective in treating symptoms —> combine with L-DOPA
250
Q

Catecholamine-O-Methyltransferase Inhibitor (COMT) - adverse effects (4)

A
  • nausea
  • orthostatic hypotension
  • vivid dreams
  • hallucinations
251
Q

Monoamine oxidase-B (MAO-B) inhibitor - mechanism of action

A
  • inhibits MAO-B facilitated oxidation (metabolism) of dopamine and L-Dopa
  • Result = more L-DOPA conversion to dopamine, more dopamine in nerve terminals
252
Q

Monoamine oxidase-B (MAO-B) inhibitor - indications for use

A
  • moderately effective on their own at treating symptoms –> combine with L-DOPA
253
Q

Monoamine oxidase-B (MAO-B) inhibitor - adverse effects (3)

A
  • insomnia
  • orthostatic hypotension
  • dizziness
  • does not inhibit MAO-A in liver = dont cause hypertensive crisis in patients eating tyramine-containing fod
254
Q

Excess acetylcholine symptoms (3)

A
  • diaphoresis (excess sweat)
  • salivation
  • urinary incontinence
255
Q

Anticholinergic drugs - mechanism of action

A
  • block binding of acetylcholine to its receptor

- also called cholinergic antagonists

256
Q

Anticholinergic drugs - indications for use

A
  • may increase effectiveness of L-Dopa
  • may decrease incidence of diaphoresis, salivation, incontinence
  • NOT for elderly (more likely to experience severe CNS side effects)
257
Q

Anticholinergic drugs - adverse effects (6)

A
  • dry mouth
  • blurred vision
  • urinary retention
  • constipation
  • tachycardia

Elderly CNS effects = confusion, hallucination, deliriumm

Pharmacology (6 decks)

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