Brainscape's Knowledge GenomeTM

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


See full index

Semester 5 PMNM Exam 5 > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

which area of the limbic system is associated with the regulation of fear?

A

amygdala

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

this area of the limibic system is asosciated with memory, emotional processing, regulation of stress, emotions and mood

A

hippocampus

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

fxn of Ach

A

voluntary muscle movements

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

major excitatory NT

A

Glutamate! (gas pedal)

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

term for too much glutamate?

A

excitotoxicity - causes damage to the CNS

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

major inhibitory NT

A

gaba (brake of car)

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

drugs that increase GABA produce what? (5)

A

1) relaxation
2) sedation
3) sleep
4) reduced anxiety
5) muscle relaxation

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

3 limitations of chemical antidepressant drugs

A

1) drugs don’t work for all pt’s (only work for 50-70%)
2) takes weeks or months for drugs to start working
3) side effects limit usage

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

3 current available treatments for depression

A

psychotherapy, chemical antidepressants, ECT

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

Monoamine hypothesis of depression

A

depression may be related to a deficiency of primarily NE and serotonin (also dopamine), therefore drugs aim to increase NE and 5HT

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

neurotrophic hypothesis of depression

A

depression may be related t oa loss of neurotrophic growth factors such as brain-derived neurotrophic factor, which leads to neuronal atrophy and death. This all may be due to a decrease in NE and 5HT and increased glucocorticoid levels from stress. Antidepressant drugs aim to increase BDNF

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

3 types of antidepressant drugs

A

1) Tricyclics (TCAs)
2) Monoamine oxidase inhibitors (MAOIs)
3) SSRIs/SNRIs

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

which antidepressant drugs are 1st gen?

A

TCAs and MAOIs

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

which antidepressant drugs are 2nd gen?

A

SSRIs/SNRIs

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

main difference between 1st and 2nd gen antidep drugs?

A

side effects are worse in 1st gen drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

2 mechanisms of antidepressant drugs (lay terms definition)

A

1) bock re-uptake of NE and seratonin via SSRIs

2) block metabolism of NT’s via MAOIs (MAO is what breaks down NE and serotonin so we block MAO via MAOIs)

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

2 mechanisms of antidepressant drugs (from slides)

A
  • overall goal is to increase monoamine levels (NE and 5HT in the synapse
    1) block enzyme breakdown by monoamine oxidase via MAOIs
    2) block re-uptake into presynaptic terminal by inhibition of transporters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name 3 TCAs

A

imipramine, desipramine, amitriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TCAs: info about treatment

A
  • used to be standard treatment for depression

- now 2nd or 3rd treatment choice due to bad side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

mechanism of action of TCAs

A
  • block reuptake of NE and 5HT into the presynaptic terminal

- increase NE and 5HT in synaptic cleft

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

adverse effects of TCAS

A

sedation, anticholinergic effects (consitpation etc), arrhythmias, ORTHOSTATIC HYPOTENSION. overdose = fatal

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

the hip breaker drug

A

TCAs! due to orthostatic hypotension

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

name 3 MAOIs

A

phenelzine, tranylcypromine selegiline

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

info about MAOIs

A
  • 1st modern class of antidepressants

- not used much now because of toxciity and food issue

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

mechanism of action of MAOIs

A

increase synaptic availibility of NE and 5HT by blocking their breakdown via inhibition of MAO enzyme

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

Adverse effects of MAOIs

A
  • CNS excitation (restless, irritable), anticholinergic effects
  • increased BP – hypertensive crisis
  • Tyramine-rich foods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

expand upon tyramine-rich foods and MAOIs

A
  • tyramine-rich foods trigger the release of catecholamines which cause VC and hypertensive crisis that can be fatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

name 6 SSRIs

A
  • fluoxetine
  • sertraline
  • citalopram
  • escitalopram
  • paroxetine
  • fluvoxamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Current 1st line of antideprresant drugs are

A

SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

SSRI info

A
  • not more effective than older drugs, just fewer side effects
  • more useful in long term management of depression
31
Q

mechanism of action of SSRIs

A

block reuptake of 5HT (serotonin)

also increase abilibilty of 5HT in synaptic cleft

32
Q

adverse effects of SSRis

A
  • GI irritation (usually resolves after taking drug 1-2wks), insomnia, sexual dysfunction, nervousness, agitation, weight loss or gain
33
Q

Concerns for PT’s in patients who are depressed

A
  • be aware of potential comorbid depression
  • sedation, muscle weakness, ataxia
  • orthostatic hypotension!!
34
Q

name the 3 subtypes of partial seizures

A

1) simple partial
2) complex partial
3) partial becoming generalized

35
Q

define simple partial seizure

A

the person is alert and can remember what happens. it is limited to one area of the brain. the person whill show minimal signs that the seizure is occurring. it is the least robust type of seizure

36
Q

define complex partial seizure

A

starts in a small area of temporal/frontal lobe but can spread to other areas that affect alertness/awakeness

37
Q

define partial becoming generalized

A

partial seizure that spreads through the entire brain

38
Q

which area of the brain is involved in a generalized epileptic seizure?

A

the entire brain

39
Q

2 types of generalized seizures

A

absence (petit mal) and tonic-clonic (grand mal)

40
Q

absence/petit mal seizure

A

sudden, brief loss of consciousness, ranges from no motor signs to symetrical jerking mvmt of entire body

41
Q

tonic-clonic grand mal

A

major convulsions of entire body and loss of consciousness
tonic = loss of consciousness and mucle tension
clonic = muscle contracts and relaxes aka convulsions

42
Q

4 phases of tonic clonic seizure

A

1) aura: visual distrubances that occur before the seizure. tells person seixure is coming
2) tonic: muscle contractions
3) clonic: convulsions
4) sleep

43
Q

goals of antiepileptic drugs

A

inhibit firing of hyperexcitable cerebral neurons

44
Q

3 ways antiepileptic drugs work

A

1) increase inhibitory effects of gaba
2) decrease glutamate
3) alter neuron acitvation by altering mvmt of Na Ca (this is needed for depolarization of neurons) (blockks APs)

45
Q

name 6 epileptic durgs

A

phenobarbital, diazepam, phenytoin, carbamazepine, ethosuximide, valproic acid

46
Q

these 2 epileptic drugs produce sedation by increasin gaba

A

phenobarbital and diazepam (valium and zanex)

47
Q

this drug is used to treat status epilepticus (ongoing seizure)

A

diazepam

48
Q

these 2 drugs can be used to treat a variety of seizures

A

phenytoin, carbamazepine (work by blocking sodium channels)

49
Q

these 2 drugs are most commonly used for petit mal seizures

A

ethosuximide and valproic acid

50
Q

side effects of epileptic drugs PT’s need to be aware of

A

dizziness, ataxia, sedation, rashes

51
Q

simple pathology of parkinson’s

A

loss of dopaminergic neurons in basal ganglia.. also includes misfolded proteins that build up and eventually destroy cells

52
Q

main protien involed in parkison

A

alpha-synuclein

53
Q

parkinsons pts lose neurons that contain what NT

A

dopamine!

54
Q

4 sx/sy of PD

A

bradykinesia, muscle rigidity, resting tremor, postural instability

55
Q

pathophys of PD from slide

A

degeneration/loss of dopamine nuerons in substantia nigra that project to striatum. accompanied by increased activity of ACH in BG. result = decreased ability of BG to modify muscle cotnraction and activiation

56
Q

basic idea of PD treatmetn

A

increase dopamine and decrease ACH

57
Q

genetic factors of PD

A

alpha synuclein accumulation (protein), formulation of LEwy bodies and increased production of free rads all itnerfere with neuron fxn leading to neuron death

58
Q

more pathopys of PD

A

degeneration of SN leads to overactivity in indirect pathway. Net effect = neruons in SN become mroe active and increase inhbition to the thalamus

59
Q

PD: you lose dopamine in SN. These effect the indrect pathway, so you are losing inhibiton, causing the indirect pathway to be over-active. the end result is increased activation of GP and pars reticulata of the SN which increase gaba input to the thalamus.. this results in decreased excitatory input to the cortex for motor mvmts

A

:)

60
Q

most common drug given for PD

A

L-DOPA. Can’t give dopamine b/c it doesn’t cross BBB, but L-DOPA does.

61
Q

downsides of L-DOPA

A
  • some patient’s can’t tolerate the drug or don’t respond to it
  • benefits of treatment decrease after 3-4 years
62
Q

L-DOPA is usually given with what drug

A

Carbidopa, which inhibits dopa decarboxylase (the substance that breaks down Ldopa) so that it can make it into the brain so less is metabolized in the periphery

63
Q

adverse effects of LDOPA

A
  • dyskinesias that increase the longer you are on the drug

- response fluctuations (wearing off)

64
Q

dyskinesias from ldopa include what

A

choreiform mvmts, athetosis, ballismus, dystonias

65
Q

describe the wearing off of LDOPA

A

drug wears off after it is given (after a certain amount of time) so time your treatments to shortly after the drug has been given (don’t wait to treat until the end of the day)

66
Q

idea of combating effects of LDOPA

A

drug holiday! stop taking drug for a period of time to improve response fluctuation issue

67
Q

main sx to be worreid about with LDOPA

A

orthostatic hypotension

68
Q

2 types of drugs for spasms

A

diazepam and polysnaptic inhibitors

69
Q

how does diazepam work

A

increases gaba in the spinal cord and shuts down acivity of motor neurons to decrease spasm

70
Q

name 3 drugs for spasms

A

Carisoprodol, cyclobenzaprine, methocarbamol

  • decrease MN activity
  • adverse effects = sedation, dizziness, ataxia
71
Q

6 drugs for spasticity

A

baclofen, diazepam, dantrolene, gabapentin, tizanidine, botulinum toxin

72
Q

MOA of baclofen

A

gaba B receptor agonist

73
Q

dantrolene works at the ____

A

muscle to decrease spasticity

74
Q

side effects of spasm/spasticity drugs

A

sedation, muscle weakness, dizziness ataxia orthostatic hypotension

Semester 5 PMNM Exam 5 (2 decks)

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