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Semester 5 PMNM Exam 5 > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

(85 cards)

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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
BBB - what can cross
no charge | lipophilic
26
Affective or Mood disorders are classified based on
whether patient experiences manic episodes or not
27
Major Depressive Disorder or Unipolar Depression
No manic episodes | Tx with antidepressants
28
Bipolar Disorder
Periods of depression with periods of mania | Tx with mood stabilizing drugs - LITHIUM
29
Currently available tx for depression
Psychotherapy Chemical antidepressants ElectroConvulsive Therapy
30
Chemical antidepressants - effectiveness
improve sx in 50-70% of patients with MDD
31
Chemical antidepressants - two bad things
Delay of therapeutic effect - takes weeks or months | Side effects can limit usage
32
Hypothesis of Depression (2)
Monoamine/Biogenic Amine Hypothesis | Neurotrophic Hypothesis
33
Hypothesis of Depression - Monoamine/Biogenic Amine Hypothesis
Deficiency in the level of 5HT, NE, DA | All currently available antidepressants enhance the synaptic availability of monoamines
34
Hypothesis of Depression - Neurotrophic Hypothesis
Loss of neurotrophic support (BDNF) and related signlaing play a role in cell survival and synaptic plasticity
35
Major antidepressant drugs
TCAs MAOIs 2nd generation antidepressants - SSRIs and SNRIs
36
Antidepressant MOA (4)
Block degradation of monoamine oxidase Block reuptake of 5HT and/or NE Block presynaptic autoreceptors Bind postsynaptic 5HT receptors
37
Antidepressent side effects depend on
receptor affinity
38
Examples of TCAs include
Imipramine Desipramine Amitriptyline
39
TCAs - what line of treatment
now is 2nd or 3rd line because of sever side effects
40
Adverse effect of TCA important for PTs
Orthostatic hypotension | Definitely don't want an elderly individual on these
41
MAOIs - examples
Phenelzine Tranylcypromie Selegiline
42
Adverse effects with MAOIs
Tyramine rich foods - triggers release of catecholamines and thus VC - can lead to a hypertensive crisis that can be fatal
43
SSRIs examples
``` Fluoxetine Setraline Citalopram Escitalopram Paroxetine Fluvoxamine ```
44
Depression - concerns for the DPT
Sedation, mm weakness, ataxia will slow progress with tx | Orthostatic hypotension! More so with TCAs or MAOIs than SSRIs
45
Seizure =
sudden, transient alteration of bx due to abnormally excessive, synchronous, and rhythmic firing of certain hyperexcitable neurons in the brain
46
Underlying causes of a seizure
``` altered excitation thresholds of certain neurons Congenital abnormalities Head trauma Genetic factors Infections hypoglycemia, hypoxia ```
47
Epileptic seizures are categorized according to
clinical and electrophysiological manifestations
48
Treatment options for epilepsy
Antiepileptic meds | Surgery
49
Partial Epileptic Seizures - types
Simple Partial Complex Partial Partial become generalized
50
Partial Epileptic Seizures - types - Simple Partial
Person remains alert and can remember what happens, limited sensory or motor signs
51
Partial Epileptic Seizures - types - Complex Partial
Usually start in small area of temporal or frontal lobe but quickly involve other areas that impact alertness
52
Partial Epileptic Seizures - types - Partial becoming generalized
Partial seizures that spread throughout the brain
53
Epileptic Seizures - Generalized
The whole brain is involved | Impaired consciousness and distorted electrical activity of a larger portion of the brain
54
Epleptic Seizures - Generalized - Types
Absence (Petit Mal) | Tonic - Clonic (Grand Mal)
55
Epleptic Seizures - Generalized - Absence (petit mal)
Sudden, bried loss of consciousness, ranges from no motor signs to symmetrical jerking movement of entire body
56
Epileptic Seizures - Generalized - Tonic - Clonic (Grand mal)
Major convulsions of entire body, loss of consciousness
57
Epileptic Seizures - Generalized - Tonic =
Loss of consciousness and mm tensing
58
Epileptic Seizures - Generalized - Clonic =
mm contractions and relaxation, convulsions
59
Epileptic Seizures - Generalized - Tonic - Clonic steps
Aura Tonic Clonic Sleep
60
Antiepileptic Drug Therapy - function by doing what
inc effects of GABA Dec effects of glutamate Alter neuronal activation by altering mvmnt of Na and Ca
61
Examples of drugs used to treat epilepsy
``` Phenobarbital (acute tx) Diazepam (acute tx) Phenytoin (partial or gen) Carbamazepine (partial or gen) Ethosuximide (petit mal) Valproic acid (petit mal) ```
62
Epilepsy - concerns for DPT
Seizures must always be a concern | Dizziness, ataxia, sedation, rashes
63
Neurodegenerative disorders - pathology includes
cellular aggregation of misfolded proteins
64
Neurodegenerative disorders - pathologies
Parknsons Disease and Huntingtons Alzheimers ALS
65
PD (3)
Usually begins in 50s or 60s Progressive loss of DA containing neurons in BG Total loss of motor function and mm control
66
Cardinal s/s with PD
Bradykinesia Muscular rigidity Resting tremor Postural instability
67
Pathophysiology of PD
Degeneration/loss of dopaminergic neurons in substantia nigra that project to striatum Accompanied by increased activity of cholinergic pathways in BG
68
PD - Genetic factors
Alpha synuclein accumulation, formation of lewy bodies, increased production of free radicals`
69
BG - role in motor control and PD pathophysiology
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
PD - treatment strategies
``` DA replacement DA receptor agonists L DOPA degradation inhibitors Inc in DA release Anticholinergic agents ```
71
Examples of drugs for PD
Levodopa
72
Side effects from Levodopa
Postural hypotension Confusion Dyskinesias GI effects
73
Problem with L DOPA
Benefits of treatment decline after 3 or 4 years of therapy with it - they become less responsive to it
74
L DOPA is often given with what and why
Carbidopa - it inhibits the dopa decaroxylase in the periphery so that more can make it to the brain
75
Dopamine replacement - adverse effects to L DOPA
Dyskinesias Response fluctuations - wearing off rxns and end of dose failure, and on/off phenomenon - drug holiday
76
Concerns for the DPT - dopamine replacement
If possible time therapy with peak effects of drug Be aware of orthostatic hypotension Dizziness, syncope
77
Two types of treatments for muscle spasms
Diazepam | Polysynaptic inhibitors
78
Diazepam is a ___ - how does it work (muscle spasm)
Benzodiazepine | Potentiate the action of GABA and increase the frequency of chloride ion influx
79
Diazepam works by
increasing the central inhibitory actions of GABA on alpha motor neurons
80
Muscle spasms - examples of polysynaptic inhibitors
Carisoprodol Cyclobenzaprine Methocarbamol
81
Polysynaptic inhibitors are agroup of drugs used to
enhance muscle relaxation and decrease muscle spasms
82
Muscle spasticity treatment - examples of medications
``` Baclofen Diazepam Dantrolene Gabapentin Tizanidine Botulinum Toxin ```
83
Baclofen activates what
GABA b receptors
84
Benzos activate what
GABA a
85
Concerns for the DPT with muscle spasticity or spasms
Sedation and mm weakness | Schedule PT when sedative effects are minimal

Semester 5 PMNM Exam 5 (4 decks)

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