Pharm 2060B Module 14A

Front 1

neurons transmit information through _____ and _____ signalling

Back 1

neurons transmit information through electrical and chemical signalling

Front 2

explain what happens during depolarization and repolarization.

Back 2

the resting potential of -70 goes super positive. How? an action potential causes an infllux of Na+ through voltage gated sodium channels. During repolarization, these channels close and potassium channels open, allowing potassium to leave and the cell returns to resting potential

Front 3

when an action potential reaches a pre synaptic cleft, it causes an influx of what? what does this cause?

Back 3

it causes an influx of calcium. This calcium forces the neurotransmitter vesicles release the neurotransmitter into the synaptic cleft, which then bind to the postsynaptic membrane, propogating the action potential.

Front 4

What are the 5 ways drugs can treat CNS disorders?

Back 4

1. replacement

2. inhibiting breakdown

3. inhibiting reuptake

4. agonism/antagonism

5. nerve stimulation

Front 5

name 6 symptoms of parkinsons

Back 5

1. tremor

2. rigidity

3. masklike face

4. bradykinesia

5. postural instability

6. dementia

Front 6

parkinsons is a chronic movement disorder caused by a disorder in the amount of _____ and _____ in the brain

Back 6

parkinsons is a chronic movement disorder caused by a discord in the amount of dopamine and acetylcholine in the brain

Front 7

How does the imbalance of acetylcholine and dopamine specifically cause the symptoms of parkinsons?

Back 7

1. not enough dopamine means less GABA inhibition

2. too much acetylcholine means more GABA activity

3. high GABA activity leads to the symptoms of parkinsons

Front 8

how can illicit drug use lead to parkinsons?

Back 8

drugs can produce a by product called MPTP which can permanently destroy dopamine neurons

Front 9

T/F environmental toxins, oxidative stress and brain trauma can cause parkiees

Back 9

true

Front 10

drug treatment of PD improves dope acetylcholine balance by?

Back 10

increasing dope, decreasing ass

Front 11

What are the 5 classes of drugs that increase dopamine neurotransmision to treat PD?

Back 11

1. dopamine replacement (L- Dopa)

2. Dopamine agonist

3. dopamine replacer

4. catecholamine-O-Methyltransferase inhibitor

5. MAO-B inhibitor

Front 12

what is the most effective drug for treating PD?

Back 12

L-Dopa

Front 13

T/F

a) FX of L-Dopa increase as disease progresses

b) L-Dopa passively travels to the brain through the BBB

c) L-Dopa is metabolized into dopamine in the brain

Back 13

a) false. FX decrease

b) false. l-dopa is transported to the brain through the BBB via a transport protein

c) L-dopa is metabolized into dopamine in the braine, true

Front 14

what cofactor speeds up the conversion of L-dopa into dopamine in the brain?

Back 14

vitamin b6

Front 15

why give l-dopa instead of straight dopamine? 2 reasons.

Back 15

1. dopamine does not cross the BBB

2. dopamine has a very short half life in the blood

Front 16

why does l-dopa cause nausea?

Back 16

dopamine mediated activation of the chemoreceptor trigger zone in the medulla

Front 17

why can l-dopa cause cardiac dysrhythmias?

Back 17

conversion of l-dopa to dopamine can cause activation of cardiac beta-1 receptors

Front 18

t/f l-dopa can cause dyskinesia, orthostatic hypotension, and psychosis

Back 18

true true and true

Front 19

l-dopa given alone is mostly metabolized in the

Back 19

peripheral tissue (i.e. intestine)

Front 20

why is l-dopa almost always given with _____

Back 20

l-dopa is almost always given with carbidopa because carbidopa inhibits peripheral tissue metabolism of l-dopa, allowing more to pass through the BBB, reaching the brain

Front 21

t/f carbidopa decreases the incidence of diskinesia and psychosis

Back 21

false. carbidopa decreases the incidence of caridac dysrhythmias, nausea and vomiting

Front 22

what are the two types of loss of effect someone taking l-dopa may experience

Back 22

1. wearing off. gradual loss of effect

2. on-off. abrupt loss of effect

Front 23

when does the wearing off effect of l-dopa occur and what are three ways it can be minimized?

Back 23

wearing off effect occurs when the end of the dosing interval is near

can be minimized by

1. shortening the dosing interval

2. give a COMT that inhibits l-dopa metabolism

3. add a dopamine agonist to the therapy

Front 24

t/f wearing off effect can occur when l-dopa levels are high

Back 24

false. on-off effect can occur when l-dopa levels are high

Front 25

what are 3 ways the on-off loss of effect of l-dopa can be minimized?

Back 25

1. taking more frequent doses per day

2. using a controlled release formulation

3. move protein containing meals to the evening

Front 26

what is the mechanism of action of dopamine agonists

Back 26

literally just bind to dopamine receptors and activate them, just like dopamine would. not as effective as l-dopa, but used as a first line treatment for those with milder symptoms

Front 27

name 3 adverse effects of dopamine agonists

Back 27

1. hallucinations

2. orthostatic hypotension

3. daytime drowsiness

Front 28

what are the three mechanisms of action of dopamine releasers?

Back 28

1. releases more dopamine from the presynaptic neuron into the synaptic cleft

2. blocks dopamine reuptake into presynaptic neuron

3. blocks NMDA receptors. this decreases dyskinesia effect of l-dopa

Front 29

why is l-dopa usually given with a dopamine releaser

Back 29

dopamine releaser block nmda receptors which reduce diskinesia effect of l-dopa

Front 30

name 3 adverse fx of dopamine releaser

Back 30

nausae, vomiting, dizziness

Front 31

what is the mechanism of action of COMT inhibitors?

Back 31

COMT adds a methyl group to l dopa and dopamine, rendering them inactive. this inhibits that enzyme and allows more l-dopa to be converted to dopamine

Front 32

note: all 4 other dopamine increasers can be combined with l-dopa

Back 32

c

Front 33

what is the mechanism of action of MAO B inhibitors

Back 33

MAO B metabolizes dopamine and l-dopa through oxidation in the brain. MAO B inhibitors stop that

Front 34

what are the 2 effects of MAO B inhibitors on dopamine?

Back 34

1. allows more dopamine to be converted from l-dopa

2. allows more dopamine to be available in the presynaptic cleft

Front 35

t/f At!therapeutic!doses, MAOCB!inhibitors!used!to!treat!Parkinson’s do!not!inhibit!MAOCA!in!the!liver!and!therefore!do!not!cause!hypertensive!crisis!when!patients!eat!tyramineCcontaining foods (

Back 35

true

Front 36

what are the three symptoms of excess acetylcholine specifically? (parkinsons)

Back 36

1. diaphoresis (excess sweating)

2. salivation

3. urinary incontinence

Front 37

what is the mechanism of action of cholinergic antagonists for parkinsons, and what three symptoms do they decrease?

Back 37

they block acetylcholine receptors. they actually increase effectiveness of l-dopa.

they decrease diaphoresis, salivation, and urinary incontinence (pissing involuntarily)

Front 38

name 2 side FX of anticholinergic drugs

Back 38

1. dry mouth

2. urinary retention

Front 39

anticholinergic drugs are reserved for _____ patients

Back 39

anticholinergic drugs are reserved for younger patients because older patients may experience hallucinations or delirium

Front 40

who has alzheimers more, men or women?

Back 40

women

Front 41

alzheimers is characterized by a degeneration of ____ neurons in the ______ (brain region) early on

Back 41

alzheimers is characterized by a degeneration of cholinergic neurons in the hippocampus early on

Front 42

t/f a diagnosis of alzheimers cannot be given until after death

Back 42

true

Front 43

what are the two hallmarks of alzheimers?

Back 43

neurofibrillary tangles and neuritic plaques

Front 44

how are neurofibrillary tangles formed?

Back 44

abnormal production of Tau, a MAP that is responsible for forming cross bridges between microtubules

Front 45

what are neuritic plaques and how do they contribute to alzheimers?

Back 45

neuritic plaques are found outside of neurons and contain beta amyloids. beta amyloids kill hippcampal cells

Front 46

t/f mutations in dna can cause alzheimers

Back 46

true

Front 47

those with two copies of ______ are at risk of getting alz. why?

Back 47

those with two copies of ApoE4 are at higher risk of getting alz. ApoE4 binds to beta amyloids forming neural plaques

Front 48

patients with mutations in the _____ precursor gene are at higher risk of alz. why?

Back 48

patients with mutations in the amyloid precursor gene are at higher risk of getting alz. this is because this gene is involved with the production of beta amyloiid in neural plaques

Front 49

what are the 2 classes of drugs used to treat alz?

Back 49

cholinesterase inhibitors and NMDA receptor antagonists

Front 50

what is the mechanism of action of cholinesterase inhibitors

Back 50

they inhibit the enzyme acetylcholinesterase., allowing more acetylcholine to remain in the synaptic cleft to exert its actions

Front 51

t/f cholinesterase inhibitors can reverse alz

Back 51

false. they can only increase cholinergic transmission in the healthy neurons left.

Front 52

describe the action of the NMDA receptor in a non alz patient

Back 52

normally, NMDA receptors have calcium channels that are gated when magnesium is bound. when glutamate binds to another site, then magnesium leaves and there is calcium influx, which is necessary for learning and memory.

Front 53

describe the action of the NMDA receptor in an alz patient

Back 53

in an alz patient there is excess glutamate activity leading to high levels of calcium influx. this is detrimental because it can damage learning and memory and degrade neurons

Front 54

how do nmda receptor antagonists work?

Back 54

they block the calcium channel opening such that calcium cannot enter the cell even when there is excess glutamate activity

Front 55

t/f patients with shizo dont have multiple personalities but are violent

Back 55

false. niggaz with schiz dont have mult pers and arent violent

Front 56

positive symptoms ____ or _____ normal neurological function.

negative symptoms have a _____ of normal neurological function

Back 56

exaggerate or distort

have a loss of

Front 57

name 4 risk factors for schizophrenia

Back 57

1. family history

2. drug abuse - meth pcp and lsd

3. low birth weight

4. low iq

Front 58

how does schizo affect basal ganglia?

Back 58

thought to play a role in paranoi and hallucinations

Front 59

how does schizo affect frontal lobe?

Back 59

difficulty planning and organizing thoughts

Front 60

limbic system schiz?

Back 60

agitation

Front 61

occipital lobe schiz?

Back 61

reading images, recognizing motion

Front 62

auditory system schiz?

Back 62

hallucinations

Front 63

hippocamous schiz?

Back 63

learning and memory, which are decreased in schiz

Front 64

drugs that block the dopaminergic neurons increase/decrease some of the positive symptoms of schizo

Back 64

decrease some of the positive symptoms of schizo

Front 65

patients with schizo have more ____ receptors and less _____receptors in the _________

Back 65

patients with schizo have more 5HT1A receptors and less 5HT2A receptors in the frontal cortex

Front 66

patients with schizo have an increased/decreased number of NMDA receptors in their brain

Back 66

decreased number of nmda receptors in their brain

Front 67

in a brain scan for schiz, what would you expect the size of

a) ventricles

b) frontal lobe activity

Back 67

a) increased ventricle size

b) decreased frontal lobe activity

Front 68

what are the two classes of drugs used to treat schiz?

Back 68

conventional antipsychotics, atypical antipsychotics

Front 69

conventional antipsychotics act by blocking _____ receptors in the ______ region of the brain

Back 69

conventional antipsychotics act by blocking dopamine receptors in the mesolimbic region of the brain

Front 70

conventional antipsychotics are better at treating the postive/negative symptoms of schiz rather than the negative/positive ones

Back 70

positive

negative

Front 71

what are extrapyrimidal symptoms

Back 71

movement disorders that resemble the symptoms of parkinsons

Front 72

name 4 extrapyrimidal symtoms

Back 72

1. acute distonia

2. parkinsinism- treat with antichol not l dopa

3. akathesia

4. tardive diskinesia- switch to atypical antipsy

Front 73

what is the mechanism of action of atypical antipsychotics

Back 73

they block dopamine, 5ht1a and 5ht2a receptors.

Front 74

what receptors do atypical antipsychotics block the least

Back 74

dopamine

Front 75

what are 3 advatnages of atypical antipsychotics over conventional

Back 75

1. same efficacy against positive symptpms

2. more effective against negative symptoms

3. lower risk of extrapyrimidal symptoms

Front 76

t/f conventional antipsychotics cause weight gain

Back 76

false. antipsychotics do.