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Semester 5 PMNM Exam 5 > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

1
Q

Forebrain is involved in

A

Movement and sensory processing, thinking, planning, and problem solving

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2
Q

Forebrain structures include

A 
Cerebral cortex
Thalamus
Hypothalamus
Limbic System
Basal Ganglia
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3
Q

Thalamus function

A

Relay states for information for coming into the brain

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4
Q

Hypothalamus function

A

Stress and emotional responses
Hormonal responses and homeostasis
Temp and appetite

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5
Q

Limbic system function

A

Amygdala - regulation of fear

Hippocampus - memory formation and regulation of stress responses, emotions, and overall mood

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6
Q

Hippocampus - what is special about the memory component

A

important in covnerting short term memories into long term memory

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7
Q

Basal Ganglia includes what

A

Striatum (caudate, putamen)
Globus Pallidus
Lentiform nucleus
Substantia nigra

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8
Q

Basal ganglia function

A

Control of motor activities and movement

Regulation of reward and pleasure sensations

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9
Q

Hindbrain includes what

A

Brainstem

Cerebellum

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10
Q

Brainstem function

A

Pons and Medulla - control of respiration and CV function

Reticular formation - control of consciousness, arousal, alertness

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11
Q

Cerebellum function

A

Planning and coordination of motor mvmnts

Balance and posture

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12
Q

NTs - Ach - function

A 
Voluntary mm mvmnts
Memory and learning
Attention
Control of sleep stages
Mostly excitatory fxn
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13
Q

NTs - Monoamines

A

Dopamine
Norepinephrine
Serotonin

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14
Q

NTs - Monoamines - Dopamine

A

Movement and hormonal responses

Psychiatric manifestations - altered mental states and/or mental illness

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15
Q

NTs - Monoamines - Norepinephrine

A

Learning and memory, control of alertness vs. sleep

Fight or flight responses

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16
Q

NTs - Monoamines - Serotonin

A

COntrol of emotional states and mood

Depression and anxiety

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17
Q

Glutamate is

A

excitatory

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18
Q

Excitotoxicity

A

Can damage CNS if get excitotoxicity from too much glutamate

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19
Q

GABA is

A

inhibitory

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20
Q

Drugs that increase GABA produce

A 
relaxation
sedation
sleep
reduced anxiety
muscle relaxation
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21
Q

Neuropeptides

A

Substance P - excitatory involved in spinal pain processing

Endogenous opioids - inhibit pain sensation

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22
Q

BBB - function of

A

tight junction between endothelial cells on CNS capillaries

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23
Q

BBB - selective filter

A

prevents many substances from entering the brain and spinal cord

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24
Q

BBB - does not let what cross

A

Polar and lipophobic compounds

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25
Q

BBB - what can cross

A

no charge

lipophilic

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26
Q

Affective or Mood disorders are classified based on

A

whether patient experiences manic episodes or not

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27
Q

Major Depressive Disorder or Unipolar Depression

A

No manic episodes

Tx with antidepressants

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28
Q

Bipolar Disorder

A

Periods of depression with periods of mania

Tx with mood stabilizing drugs - LITHIUM

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29
Q

Currently available tx for depression

A

Psychotherapy
Chemical antidepressants
ElectroConvulsive Therapy

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30
Q

Chemical antidepressants - effectiveness

A

improve sx in 50-70% of patients with MDD

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31
Q

Chemical antidepressants - two bad things

A

Delay of therapeutic effect - takes weeks or months

Side effects can limit usage

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32
Q

Hypothesis of Depression (2)

A

Monoamine/Biogenic Amine Hypothesis

Neurotrophic Hypothesis

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33
Q

Hypothesis of Depression - Monoamine/Biogenic Amine Hypothesis

A

Deficiency in the level of 5HT, NE, DA

All currently available antidepressants enhance the synaptic availability of monoamines

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34
Q

Hypothesis of Depression - Neurotrophic Hypothesis

A

Loss of neurotrophic support (BDNF) and related signlaing play a role in cell survival and synaptic plasticity

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35
Q

Major antidepressant drugs

A

TCAs
MAOIs
2nd generation antidepressants - SSRIs and SNRIs

36
Q

Antidepressant MOA (4)

A

Block degradation of monoamine oxidase
Block reuptake of 5HT and/or NE
Block presynaptic autoreceptors
Bind postsynaptic 5HT receptors

37
Q

Antidepressent side effects depend on

A

receptor affinity

38
Q

Examples of TCAs include

A

Imipramine
Desipramine
Amitriptyline

39
Q

TCAs - what line of treatment

A

now is 2nd or 3rd line because of sever side effects

40
Q

Adverse effect of TCA important for PTs

A

Orthostatic hypotension

Definitely don’t want an elderly individual on these

41
Q

MAOIs - examples

A

Phenelzine
Tranylcypromie
Selegiline

42
Q

Adverse effects with MAOIs

A

Tyramine rich foods - triggers release of catecholamines and thus VC - can lead to a hypertensive crisis that can be fatal

43
Q

SSRIs examples

A 
Fluoxetine
Setraline
Citalopram
Escitalopram 
Paroxetine
Fluvoxamine
44
Q

Depression - concerns for the DPT

A

Sedation, mm weakness, ataxia will slow progress with tx

Orthostatic hypotension! More so with TCAs or MAOIs than SSRIs

45
Q

Seizure =

A

sudden, transient alteration of bx due to abnormally excessive, synchronous, and rhythmic firing of certain hyperexcitable neurons in the brain

46
Q

Underlying causes of a seizure

A 
altered excitation thresholds of certain neurons
Congenital abnormalities
Head trauma
Genetic factors
Infections hypoglycemia, hypoxia
47
Q

Epileptic seizures are categorized according to

A

clinical and electrophysiological manifestations

48
Q

Treatment options for epilepsy

A

Antiepileptic meds

Surgery

49
Q

Partial Epileptic Seizures - types

A

Simple Partial
Complex Partial
Partial become generalized

50
Q

Partial Epileptic Seizures - types - Simple Partial

A

Person remains alert and can remember what happens, limited sensory or motor signs

51
Q

Partial Epileptic Seizures - types - Complex Partial

A

Usually start in small area of temporal or frontal lobe but quickly involve other areas that impact alertness

52
Q

Partial Epileptic Seizures - types - Partial becoming generalized

A

Partial seizures that spread throughout the brain

53
Q

Epileptic Seizures - Generalized

A

The whole brain is involved

Impaired consciousness and distorted electrical activity of a larger portion of the brain

54
Q

Epleptic Seizures - Generalized - Types

A

Absence (Petit Mal)

Tonic - Clonic (Grand Mal)

55
Q

Epleptic Seizures - Generalized - Absence (petit mal)

A

Sudden, bried loss of consciousness, ranges from no motor signs to symmetrical jerking movement of entire body

56
Q

Epileptic Seizures - Generalized - Tonic - Clonic (Grand mal)

A

Major convulsions of entire body, loss of consciousness

57
Q

Epileptic Seizures - Generalized - Tonic =

A

Loss of consciousness and mm tensing

58
Q

Epileptic Seizures - Generalized - Clonic =

A

mm contractions and relaxation, convulsions

59
Q

Epileptic Seizures - Generalized - Tonic - Clonic steps

A

Aura
Tonic
Clonic
Sleep

60
Q

Antiepileptic Drug Therapy - function by doing what

A

inc effects of GABA
Dec effects of glutamate
Alter neuronal activation by altering mvmnt of Na and Ca

61
Q

Examples of drugs used to treat epilepsy

A 
Phenobarbital (acute tx)
Diazepam (acute tx)
Phenytoin (partial or gen)
Carbamazepine (partial or gen)
Ethosuximide (petit mal)
Valproic acid (petit mal)
62
Q

Epilepsy - concerns for DPT

A

Seizures must always be a concern

Dizziness, ataxia, sedation, rashes

63
Q

Neurodegenerative disorders - pathology includes

A

cellular aggregation of misfolded proteins

64
Q

Neurodegenerative disorders - pathologies

A

Parknsons Disease and Huntingtons
Alzheimers
ALS

65
Q

PD (3)

A

Usually begins in 50s or 60s
Progressive loss of DA containing neurons in BG
Total loss of motor function and mm control

66
Q

Cardinal s/s with PD

A

Bradykinesia
Muscular rigidity
Resting tremor
Postural instability

67
Q

Pathophysiology of PD

A

Degeneration/loss of dopaminergic neurons in substantia nigra that project to striatum
Accompanied by increased activity of cholinergic pathways in BG

68
Q

PD - Genetic factors

A

Alpha synuclein accumulation, formation of lewy bodies, increased production of free radicals`

69
Q

BG - role in motor control and PD pathophysiology

A

In PD, degneration of SN pars compacta leads to overactivity in the indirect pathway and inc glutaminergic activity by subthalamic nucleus
Reduced excitatory to cortex

70
Q

PD - treatment strategies

A 
DA replacement
DA receptor agonists
L DOPA degradation inhibitors
Inc in DA release
Anticholinergic agents
71
Q

Examples of drugs for PD

72
Q

Side effects from Levodopa

A

Postural hypotension
Confusion
Dyskinesias
GI effects

73
Q

Problem with L DOPA

A

Benefits of treatment decline after 3 or 4 years of therapy with it - they become less responsive to it

74
Q

L DOPA is often given with what and why

A

Carbidopa - it inhibits the dopa decaroxylase in the periphery so that more can make it to the brain

75
Q

Dopamine replacement - adverse effects to L DOPA

A

Dyskinesias
Response fluctuations - wearing off rxns and end of dose failure, and on/off phenomenon
- drug holiday

76
Q

Concerns for the DPT - dopamine replacement

A

If possible time therapy with peak effects of drug
Be aware of orthostatic hypotension
Dizziness, syncope

77
Q

Two types of treatments for muscle spasms

A

Diazepam

Polysynaptic inhibitors

78
Q

Diazepam is a ___ - how does it work (muscle spasm)

A

Benzodiazepine

Potentiate the action of GABA and increase the frequency of chloride ion influx

79
Q

Diazepam works by

A

increasing the central inhibitory actions of GABA on alpha motor neurons

80
Q

Muscle spasms - examples of polysynaptic inhibitors

A

Carisoprodol
Cyclobenzaprine
Methocarbamol

81
Q

Polysynaptic inhibitors are agroup of drugs used to

A

enhance muscle relaxation and decrease muscle spasms

82
Q

Muscle spasticity treatment - examples of medications

A 
Baclofen
Diazepam
Dantrolene
Gabapentin
Tizanidine
Botulinum Toxin
83
Q

Baclofen activates what

A

GABA b receptors

84
Q

Benzos activate what

85
Q

Concerns for the DPT with muscle spasticity or spasms

A

Sedation and mm weakness

Schedule PT when sedative effects are minimal

Semester 5 PMNM Exam 5 (4 decks)

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