Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > Chapter 14A > Flashcards

Chapter 14A Flashcards

1
Q

Neuropharmacology

A

The study of how drugs affect the function of the CNS

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

When an action potential reaches the pre-synaptic nerve terminal it causes influx of __

A

Calcium

Which then causes vesicles with neurotransmitter to fuse to membrane

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

What are the classes of neurotransmitters?

A

Monoamines
Amino acids
Other

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

Examples of monoamine neurotransmitters:

A

Norepinephrine
Epinephrine
Dopamine
Serotonin

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

Examples of amino acid neurotransmitters:

A

Excitatory - glutamate and aspartate

Inhibitory - GABA and glycine

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

Example of other neurotransmitters:

A

acetylcholine

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

What are the 5 different basic mechanisms of CNS drugs:

A

1) Replacement
2) Agonist/antagonist
3) Inhibiting neurotransmitter breakdown
4) Blocking reuptake
5) Nerve stimulation

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

Describe Parkinson’s Disease

A

Discovered by James Parkinson in 1817
Progressive loss of dopaminergic neurons in substantia nigra (70-80%)
Without treatment - in 5-10 years patient cannot care for themselves
Chronic movement disorder caused by too much acetylcholine and too little dopamine

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

Symptoms of Parkinson’s

A

1) Tremor (extremities)
2) Rigidity (joint stiffness and increased muscle tone)
3) Bradykinesia (initiating movements)
4) Masklike face (difficulty blinking and swallowing)
5) Postural instability
6) Dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Symptoms of Parkinson’r arise because of what three things:

A

1) Decrease dopamine - not enough to inhibit GABA release
2) Relative excess of acetylcholine - activates GABA release
3) Excess GABA causes the movement disorders

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

Is the etiology of Parkinson’s largely known or unknown? What is thought to be caused by?

A

unknown

1) Street drugs that have MPTP
2) Genetics - mutation in 4 genes (alpha synuclein, parkin, UCHL1, DJ1)
3) Environmental toxins
4) Brain trauma
5) Oxidative stress

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

What are the 5 major classes of drugs used to treat Parkinson’s?

A

1) Dopamine replacement - L-dopa
2) Dopamine agonist
3) Dopamine releaser
4) Catecholamine-O-methyltransferase inhibitor
5) Monoamine oxidaseB inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Levodopa and what does it do?

A

Most effective drug for treating PD (benefits decrease over time)
Crosses blood brain barrier by active transport protein and is inactive until converted to dopamine in dopaminergic nerve terminals
This conversion is mediated by decarboxylase enzymes in the brain
Cofactor pyridoxine (vitamin B6) speeds up this reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why can we not just give someone with PD dopamine?

A

Because it cannot cross the BBB and has a very short half-life in the blood

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

Side effects of L-DOPA:

A 
Nausea and vomiting
Dyskinesias
Cardiac dysrhythmias - conversion to dopamine in periphery can result in activation of cardiac beta 1 receptors
Orthostatic hypotension 
Psychosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Peripheral Metabolism of L-DOPA

A

Only 1% of LDOPA reaches the brain
Almost always given with carbidopa (decarboxylase inhibitor) so that 10% reaches the brain
It also decreases cardiac dysrhythmias, nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the two types of loss of effect that patients taking LDOPA might experience?

A
  1. Wearing off (gradual)

2. On-off (abrupt loss of effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is we wearing off? How can it be minimized?

A

Occurs at end of dosing interval and indicates drug levels might be low

Minimized by:

  • shorter dosing interval
  • drug that inhibits LDOPA metabolism (e.g COMT)
  • add dopamine agonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is On-off loss of effect? How can it be minimized?

A

Can occur when drug levels are high

Minimized by:

  • divide medication into 3-6 doses/day
  • use controlled release formulation
  • move protein containing meals to evening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What do dopamine agonists do?

A

Produce effects by directly activating dopamine receptors on post-synaptic membrane
Not as effective as LDOPA (for patients with milder conditions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Adverse effects of dopamine agonists:

A

Hallucinations
Daytime drowsiness
Orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do dopamine releasers do?

A

Stimulate release of dopamine from dopaminergic neurons and also blocks dopamine reuptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Adverse effects of dopamine releaser:

A

Dizziness, nausea, vomiting, lethargy, and anticholinergic side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do catecholamine-o-methyltransferase (COMT) inhibitors do?

A

Enzyme that adds methyl group to both dopamine and LDOPA
When methylated they are inactive
Inhibiting COMT results in greater fraction of LDOPA that is available to become dopamine
Only moderately effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Adverse effects of COMT inhibitors:

A

Nausea
Orthostatic hypotension
Vivid dreams
Hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What do monoamine oxidaseB (MAO-B) Inhibitors do?

A

Enzyme that oxidatively metabolizes dopamine and LDOPA - inactivating them
Inhibiting metabolism allows more conversion to dopamine in the brain and remain in nerve terminals
Only moderately effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Adverse effects of MAOB inhibitors:

A

Insomnia
Orthostatic hypotension
Dizziness

28
Q

Excess acetylcholine causes:

A

Diaphoresis (excess sweating)
Salivation
Urinary incontinence

29
Q

What do anticholinergic drugs do?

A

Block the binding of acetylcholine to receptor
Increase effectiveness of LDOPA
Decrease effects of excess acetylcholine

30
Q

Adverse effects of anticholinergic drugs:

A 
Dry mouth
Blurred vision
Urinary retention
Constipation
Tachycardiac

Elderly patients experience hallucination, confusion and delirium so usually only for younger patients

31
Q

What is Alzheimer’s Disease?

A

Irreversible form of progressive dementia and is the most common
Over 500,000 Canadians
1/11 people older than 65
75% are women

32
Q

Symptoms of Alzheimer’s:

early vs. general

A 
Memory loss
Problems with language
Judgement 
Behaviors and intelligence
Difficulty eating, bathing and controlling bowel/bladder

Early symptoms:
confusion, memory loss and problems with routine tasks

33
Q

What is the pathophysiology of Alzheimer’s ?

A

Degeneration of cholinergic neurons in the hippocampus early in disease
Follower by degeneration of neurons in the cerebral cortex

34
Q

What are the hallmarks of Alzeimer’s and when can these be seen?

A

Neurofibrillary tangles and neuritic plaques

Seen after death

35
Q

What are neurofibrillary tangles?

A

Form inside neurons when microtubule arrangement is disrupted

Caused by abnormal production of protein “tau” that is responsible for forming cross-bridges between microtubules keeping their structure

36
Q

What are neuritic plaques?

A

Found outside of neurons
Composed of a core of a protein fragment called beta amyloid
Beta amyloid kills hippocampal cells and causes Alzheimer’s in monkeys

37
Q

Is the cause of Alzheimer’s known? What do we think causes it

A

No not known
20% run in family
Mutations in DNA - two copies of apolipoprotein E4
Mutation in amyloid precursor protein gene
Head injury

38
Q

What are the two classes of drugs used to treat Alzheimer’s?

A 
Cholinesterase inhibitors (inhibit breakdown of acetylcholine)
NMDA receptor antagonists
(block NMDA mediated increases in intracellular calcium)
39
Q

What do cholinesterase inhibitors do?

A

Inhibit metabolism of acetylcholine by acetylcholinesterase
Allows more acetylcholine to remain in cleft
Only able to help the remaining healthy neurons
Minimal benefit (25% effective)

40
Q

Adverse effects of cholinesterase inhibitors?

A

Nausea and vomiting
Diarrhea
Insomnia

41
Q

What do NMDA receptor antagonists do?

A

With Alzheimer’s there is excess glutamate release so the NMDA receptor remains open allowing calcium to enter the cell
Excess calcium is detrimental to learning and memory and it causes degradation of neurons
The NMDA receptor antagonist blocks the NMDA receptor when glutamate binds to remove magnesium

42
Q

Adverse effects of NMDA antagonist:

A

Well tolerated

43
Q

What is schizophrenia?

A

Hard to tell the difference between real and unreal experiences, think logically, have normal emotional responses and behave normally
NOT:
- have multiple personalities
- violent
1% of world’s population
Begins adolescence or early adulthood (16-30 years)

44
Q

What are the symptoms of schizophrenia?

A

Divided into positive or negative
Positive - exaggerate or distort normal neurological function
Negative - loss of normal neurological function

45
Q

What is the etiology of schizophrenia?

A

Family history
Drug abuse
Low birth weight
Low IQ

46
Q

What regions of the brain are affected by schizophrenia?

A 
Basal ganglia
Frontal lobe
Limbic system
Auditory system
Occipital lobe
Hippocampus
47
Q

Basal Ganglia

A

Involved in movement and emotions

Abnormal activity plays a role in paranoid and hallucinations

48
Q

Frontal lobe

A

Involved in problem solving and insight

With schizophrenia, involved in difficulty planning actions and organizing thoughts

49
Q

Limbic system

A

Involved with emotions

In schizophrenia contributes to agitation

50
Q

Auditory system

A

In schizophrenic patients, overactivity contributes to hallucinations

51
Q

Occipital lobe

A

Processes visual information

In schizophrenia, its involved in interpreting images, reading emotion on other faces, recognizing motion

52
Q

Hippocampus

A

Mediates learning and memory which are decreased in schizophrenia

53
Q

Pathophysiology of Schizophrenia

A

Increased dopaminergic nerve transmission
Excess of dopamine
Have decreased number of 5-HT2A and increased number of 5-HT1A in frontal cortex (serotonin)

Decreased number of NMDA receptors in some regions of their brain

54
Q

How is schizophrenia usually diagnosed?

A

Made by psychiatrist after interviewing patient and family
Evaluates:
1) Changes in function from before illness
2) Developmental background
3) Family history
4) Response to medication
5) Brain scans

55
Q

Three ways to treat schizophrenia

A

Block:

1) dopamine
2) serotonin
3) glutamate

56
Q

Drugs used to treat schizophrenia can be classified as __ or __

A

Conventional antipsychotics or atypical antipsychotics

57
Q

What do conventional antipsychotics do?

A

Act by blocking dopamine 2 (D2) receptors in the mesolimbic area of the brain
To a lesser degree, they also block receptors for acetylcholine, histamine and norepinephrine
More effective at treating positive symptoms
Initial effect in 1-2days; substantial improvement takes 2-4 weeks

58
Q

Potency of conventional antipsychotics is directly proportional to their ability to ___

A

Inhibit D2 receptors

59
Q

Adverse effects of conventional antipsychotics:

A 
Extrapyramidal symptoms
Sudden high fever
Anticholinergic effects
Orthostatic hypotension
Sedation
Skin reactions
60
Q

What are extrapyramidal symptoms (EPS)?

A

Movement disorders that resemble the symptoms of PD

1) Acute dystonia
2) Parkinsonism
3) Akathesia
4) Tardive dyskinesia

61
Q

Acute dystonia

A

Involuntary spasm of muscle in face, tongue, neck or back

62
Q

Parkinsonism

A

Bradykinesia, mask like faces, rigidity and stooped posture

63
Q

Akathesia

A

Pacing, squirming and a desire to continually be in motion

64
Q

Tardive dyskinesia

A

Irreversible - need early detection

Involuntary twisting and writhing of face and tongue along with lip smacking

65
Q

What do atypical antipsychotics do?

A

Block dopamine D2 (low affinity) receptors and 5HT1A and 5HT2A receptors

66
Q

Compare to conventional antipsychotics, atypical antipsychotics have:

A

1) Same efficacy versus positive symptoms
2) Much greater efficacy versus negative symptoms
3) Much lower risk of developing extrapyramidal symptoms - especially tardive dyskinesia

67
Q

Adverse effects of atypical antipsychotics:

A 
Sedation
Orthostatic hypotension
Weight gain 
Risk of developing type 2 diabetes
Anticholinergic effects

Pharm (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions