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Neurological Pharmacology Flashcards

1
Q

what are 2 ways that medications can interfere with the nervous system ?

A

•Alter axonal
conduction (Local anesthetic)
•Alter synaptic transmission

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2
Q

What is receptor agonism

A

same effect as naturally occurs => receptor activation

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3
Q

What is receptor antagonism

A

drug reduces or causes opposite effect

receptor deactivation/blockade

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4
Q

what are the steps in synaptic transmission

A
  1. NT synthesis and storage
  2. Release of NT into cleft
  3. Post synaptic receptor binding
  4. inactivation of NT by reuptake, enzyme degradation, diffusion
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5
Q

what can drugs that affect the CNS do?

A

•Affect movement
(Limit movement
and Cause abnormal involuntary movements)
•Induce sleep or arousal
•Treat anxiety, depression, and other psychiatric conditions
•Affect memory
•Increase attention and focus

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6
Q

what limitation does the Blood Brain Barrier (BBB) create?

A
  • Protects against passage of foreign substances into the brain
  • damaging or therauetic drugs have hard time entering
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7
Q

what is a TIA and how do you decrease the risk ?

A
  • “mini-stroke”, without permanent damage

- asprin can decrease risk bc it is an antiplatelet

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8
Q

What is tPA ?

A
  • binds to fibrin in thrombus and breaks down clots
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9
Q

What is spasticity?

A

Velocity dependent increase in tonic stretch reflexes & exaggerated Deep Tendon Reflexes.

  • Hypertonia 2/2 Upper Motor Neuron lesion that affects descending motor tracts.
  • imbalance of excitatory and inhibitory input to α motor neuron
  • post-stroke; sarcomere shorter and stiffer
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10
Q

when are Muscle Relaxants used and what is the MOA?

A
  • Decrease somatic motor activity
  • Reduce muscle tone

Class side effects
•CNS depression
•Sedation
•Anticholinergic side effects, Especially in elderly

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11
Q

what is a mus relaxant example?

A

Baclofen, diazepam (valium),Dantrolene, Botox, canabis

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12
Q

what is Parkinson’s Disease

A 
•A degenerative and progressive disorder
•Unilateral>Bilateral > Balance Issues >restricted to walking cane or bed
-↓ DA levels produced by substantianigra
(SN) neuron loss
loss of movemetn and self expression

non motor effects:

  • Cognitive: verbal fluency, abstract reasoning, executive function & memory
  • Behavioral: anxiety, apathy, depression
  • Dementia
  • Disturbance of autonomic nervous system (difficulty in urinating)
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13
Q

what are Parkinson characteristics?

A

TRAP
•Tremor @ rest •Rigidity
•Akinesia, bradykinesia
•Postural instability

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14
Q

what is Levodopa?

A
  • Most effective single drug for PD bc it can cross BBB
  • GI, CV(postural hypotension), psych (Hallucinations, agitation), hypotension. Dyskinesia & neuropathy -↓after prolonged use
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15
Q

how can Levodopa be modified for an improved effect?

A

1) Controlled release formulation

2) Adding additional medications to regimen

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16
Q

what are concerns of Levodopa ?

A
  • dont take with high protein

- most of drug is metabolized in periphery, and little of it makes in to BBB, which causes nausea

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17
Q

What is carbidopa + levodopa ?

A

Sinemet
- prevent conversion in the periphery
- more drug crosses BB and less nausea
SE- pretty much the saem as levadopa
- can have a diminished response, Drug holidays can be taken
-question for whenmed should start being taken
- dosses given more often to cover “offs”

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18
Q

what advantage do COMT Inhibitors offer?

A
  • Inhibits action of enzyme that degrades NTs (L-dopa) to increase its availability
  • 2nd line
  • extends 1/2 life of levadopa
  • GI SE and Dyskinesias
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19
Q

when are Dopamine Agonists used?

A
  • Early PD stages
  • 1st line therapy, can also be added in later stages
  • cant be used as main defnese bc of intese SE
  • Delays need for levodopa and delays motor fluctuations that occur with prolonged levodopa use (dyskinesias)
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20
Q

when is Apomorphine(Apokyn®) used

A
  • only in severe cases under med supervision for when the patient is stuck
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21
Q

what is a first line therapy for PD?

A

Selegiline/Eldepryl

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22
Q

What is dementia ?

A

Progressive disorder
•Neuronal degeneration
•Reduced Cholinergic (Ach) Transmission
-Amyloid plaques
loss of cognition and loss of at least one of the following abilities:
•to speak coherently and understand language
•to recognize or identify objects
•to execute motor activities
•to think abstractly, make sound judgment, and plan and carry out complex tasks; personality changes
•Clinical diagnosis rules out delirium

23
Q

what typre of pharmacological Treatment is avaiable for Alzheimers?

A

Cholinesterase inhibitors are helpful for ~ 1/3 of patients
•Will slow progression of disease, but NOT cure
- supplements: Vit E/C and ginkgo biloba

24
Q

How are Cholinesterase inhibitors helpful in AD?

A

ACh transmission in brain is 90% < non-AD brains
•ACh essential for forming memories
•AChE-I cN help mild-moderate patients

25
How do Cholinesterase inhibitors (AChEI) work?
inhibits AChEbreakdown ↑level & duration of ACh
26
What are NMDA receptor Antagonist (Memantine) for?
For moderate to severe AD; partially blocks NMDA receptors | •Amyloid plaques may cause excess influx of Ca+ into neurons
27
what is Multiple Sclerosis
Unpredictable, progressive, degenerative of CNS myelin •(exacerbation & remission) •Onset: 20-50 yrs; Caucasians more common •Autoimmune disorder; antibodies attack myelin •Myelin loss!↓ nerve conduction of AP & ↓ function
28
what are primary and 2ndary symptoms of MS ?
Primary Symptom Treatment for MS disease-specific symps -Prevent relapse and MS progression Secondary Symptoms •Caused by primary symptoms •Example: Urinary tract infection due to urinary retention 3rd- pycho issues
29
What are Interferons?
•Family of naturally-occurring proteins secreted by immune system cells - used to Modulate immune system response in relapsing MS - SE: Flu like symps
30
what are Symptom Management Meds for MS ?
•Baclofen : for spasticity •Antidepressants: •Beta blockers for tremors •Antiseizure: for neuropathic pain •Anticholinergics: for bladder dysfunction •Corticosteroids (methylprednisone) for Acute exacerbations (vision loss, pins, needles, etc.)
31
What causes a seizure?
- neuronal activity, firing in the brain •Partial Seizures •Localized to one hemisphere of the brain * Generalized Seizures * Spread to the opposite hemisphere of the brain after initiation of seizure
32
what drugs can be used for seizures ?
Anti-Epileptic Drugs (AEDs)
33
what do Anti-Epileptic Drugs (AEDs) do?
-Prevention,manage symptoms/reduce frequency -Inhibit firing of specific neurons •↑ inhibitory effects of GABA •↓ effects of excitatory glutamate •Blocking action potentials (e.g. sodium influx)
34
what are Common side effects of Anti seizure meds ?
``` Dizziness, CNS depression drowsiness lethargy mental slowing weight gain glaucoma skin rash hepatotoxicity dyskinesia ```
35
what are types of sedatives ?
Benzodiazepines •Includes anti-anxiety drugs •Regarded as safer •Block GABA ``` Non-Benzodiazepines •Barbiturates •Smaller therapeutic Index •Quickly approach lethal doses •Abuse potential •Used more in past •Also potentiate GABA effects ```
36
What is CNS depression
- Occurs secondary to CNS dx (stroke, MS, etc | - Thought to result from deficiency of norepinephrine (NE) or serotonin
37
what do anti depressants do ?
- for CNS depression - Antidepressants ↑availability of one of both of NTs in the CNS synapse by inhibiting their reuptake by pre-synaptic neuron
38
what are signs of Major Depression?
* Depressed Mood or loss of interest in activities that usually produce pleasure (anhedonia) * Loss of energy, fatigue * Indecisiveness * Difficulty, thinking and concentrating * Inappropriate feelings of guilt and worthlessness * Loss or appetite or excess eating * Sleep disorders (hypersomnia or insomnia) * Obsession with death, thoughts of suicide
39
which meds are indicated for Major Depression?
SSRI First line, more tolerable than tricyclics Tricyclic Anti-Depressant (TCA) 2nd choice MAO Inhibitors Not usually front-line treatment
40
what are PT concerns for Antidepressant Drugs?
•Patient perception of the rehabilitation process being positively influenced by medications - May take up to 6 weeks for full effects (Zoloft); 3-6 weeks (Lexapro) effects to be seen •Active cooperation and continuity of treatment session may be compromised due to side effects •Fall prevention •HTN crisis •Suicidal tendencies
41
What are types of CNS stimulants and what are their indications?
Anorexiants: Stimulates the hypothalamus to release NE, thus reducing appetite ADHD: Stimulate the areas in the brain responsible for mental alertness and attentiveness by blocking the reuptake of DA and NE Narcolepsy: Increase mental alertness Caffeine: Migraine headaches, co-administered with other drugs, used to treat headaches. Vasoconstriction minimizes migraine pain
42
How do Amphetamines work?
Block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronalspace
43
how do CNS Stimulants work?
↑behavioral activity when administered •CNS stimulants act by facilitating initiation and transmission of Action Potentials (AP) to excite other neurons. •New drugs act selectively to inhibit reuptake of norepinephrine (NE) in the nervous system.
44
what is Acetaminophen - Tylenol used for?
- analgesic (pain reliever) - antipyretic (fever reducer) - gold standard for OA - works on CNS - efficacy, safety, low cost - side effect: liver toxicity
45
what is Ibuprofen - NSAID (non-steroidal anti-inflammatory drugs) used for?
- analgesic - antipyretic - anti-inflammatory - anticoagulant
46
what is the difference btwn cox 1 and 2
COX 1 - can cause stomach/intestinal ulcers - enzyme is predominantly found in endothelial cells in mucosal membranes COX 2 - does not cause ulcers - enzyme predominantly found in inflamed tissue following infection, tissue damage, or injuries
47
what are 2 SSRI medications
Escitalopram (Lexapro) | Sertraline(Zoloft)
48
what are SSRI medications side effects?
GI complaints Insomnia HA Sexual dysfunction
49
what is serotonin syndrome ?
Side effect of depression/ anxiety meds - Precipitated by over activation of serotonin or impaired metabolism —usually occurs 2‐72 hours after Rx onset - Mental status changes - hallucinations - agitation - coma -Autonomic instability (tachycardia, hyperthermia,changes in BP) Neuromuscular hyperactivity: hyperreflexia, incoordination, clonus, tremors, GI disturbances: N/V/D
50
what does ISPATHWARM stand for?
``` Warning signs of suicide: I deation S ubstance Abuse P urposelessness A nxiety T rapped H oplessness W ithdrawl A nger R ecklessness M ood Change ```
51
How do "off" periods change over the course of PD?
Over course of treatment, “off” periods increase (intensity and frequency)
52
what are types of MS?
``` Types: Relapse-Remitting Secondary progressive Primary progressive Progressive Relapsing ```
53
what is the MOA for Interferon beta? how is this different from Immunosuppressants ?
Naturally occurring glycoproteins Produced in response to viral and other biologic inducers Inhibits migration of proinflammatory leukocytes across BBB Suppresses T‐helper cell activity
54
what is the usage and side effects for Immunosuppressants ?
Usage Suppresses Production Of Immune System Cells (B-lymphocytes, T-lymphocytes, macrophages) =decreased destruction of myelin Clinical Use: cancer, MS types: Worsening relapsing‐remitting, Secondary progressive, Progressive‐relapsing ``` Side effects Myelosuppression Cardiotoxicity Irreversible hair loss GI irritation/ distress •Key Point: reserved for patients who cannot be treated with safer agents ```

Pharmacology (5 decks)

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