Final Flashcards
How do meds interfere with action potentials and nerve conduction? (3)
- Alter axonal conduction (local anesthetics)
- Alter synaptic transmission of signal
- Receptor agonism or antagonism
Define receptor agonism
Drug causes same effect as naturally occurs => receptor activation
Define receptor antagonism
Drug reduces or causes opposite effect => receptor deactivation/blockade.
Ways drug agonists work (4)
- Increase synthesis of neurotransmitter molecules
- Decrease degrading enzymes
- Increase the release of these neurotransmitters into the synaptic cleft
- block the inhibitory effect on neurotransmitter release
Ways drug antagonists work (3)
- block the synthesis of neurotransmitter molecules
- Cause the neurotransmitters to leak from the vesicles so that enzymes can degrade them
- block the release of the neurotransmitter into the synaptic cleft
Common side effects associated with neuro drugs (5)
- Affect movement (limit movement or cause abnormal involuntary movements
- Induce sleep or arousal
- Treat anxiety, depression, and other psychiatric conditions, cognition and mental well being
- Affect memory and short term memory
- Increase attention and focus
What does the BBB do?
-The blood brain barrier prevents passage of foreign substances into the brain and therefore preserves the integrity of this imperative organ.
How is the BBB formed?
-The blood brain barrier is formed by capillary endothelial cells that are connected by tight junctions with an extremely high electrical resistivity.
•These tight junctions do not exist in normal circulation.
How BBB can be affected to allow easier entry? (4)
- At birth-not fully formed
- Post-radiation
- Infectious agents present
- Trauma, ischemia & inflammation
spasticity is defined as a “motor disorder characterized by a ____ increase in tonic stretch reflexes…”
- Velocity dependent
- Passively stretched muscle or muscle groups respond with an increase in resistance
What types of diagnoses are associated with spasticity? (5)
- Multiple Sclerosis
- Traumatic Brain Injury
- Cerebral Vascular Accident
- SCI
- CP
How is spasticity managed? (6)
- Therapeutic modalities
- Oral Medications
- Nerve blocks and chemical neurolysis
- Surgery: orthopedic procedures
- Intrathecal Medications
- Medical Marijuana
Muscle Relaxants
- MOA
- Side Effects (3)
- Decrease somatic motor activity and reduce muscle tone. (not long lasting)
- CNS depression
- Sedation
- Anticholinergic side effects
- CNS depression
What are Anticholinergic side effects? (5)
- dry mouth
- blurred vision
- memory impairment
- hallucinations
- drowsiness
especially in elderly
Botox
- MOA
- Side Effects
- Acts on peripheral cholinergic neurons to inhibit acetylcholine release, which reduces contractions and relaxes the muscle.
- Localized: Hematoma and bruising. Muscle weakness near injection site, Low risk botulism.
What is an intrathecal baclofen pump?
Delivers small doses of baclofen into the spinal canal. Fewer side effects and more effective for spasticity esp. in LE.
- Onset .5 - 1 hrs
- Peak effect ~4 hours lasing 4-8
- Refilled every 3 months
Differences between recreational and medical MR?
Recreational marijuana tends to be high THC because THC acts on the parts of the brain that cause euphoria or pleasure.
Most medical marijuana instead contains small amounts of THC but high amounts of cannabidiol.
Medical marijuana is different from recreational marijuana and requires a healthcare provider prescription associated with a medical condition.
What are characteristics of Parkinsons disease?
- A degenerative and progressive disorder.
- Non-motor effects: Cognitive (verbal fluency, abstract reasoning, executive function, memeory) and Behavioral (Anxiety, Apathy, Depression)
- Dementia
- Disturbance of ANS (urinating)
- Tremor at rest
- Rigidity
- Akinesia (inability to movie)
- Bradykinesia (slow movment)
What is the etiology of PD?
Associated with consequences of decreased Dopamine (DA) levels produced by Substantia Nigra nueron loss.
Levodopa
- MOA
- Purpose
- Side Effects
- Able to cross BBB and is converted to dopamine
- Most effectivve single drug for PD
- Side Effects: GI, CV, psych, hypotension, dyskinesa and neuropathy after prolonged use.
Carbidopa
- MOA
- Purpose
- Side Effects
- Administered with Levodopa to prevent conversion in the periphery preventing nausea.
- Carbidopa inhibits peripheral decarboxlase enzyme so that levodopa can cross the BBB intact.
- Side Effects: GI upset; nausea and vomiting, CV problems (orthostatic hypotension), Dyskinesias.
COMT inhibitors
- MOA
- Purpose
- Side Effects
Inhibitis action of enzyme that degrades dopamine to increase its availability.
- 2nd line agent used only in combination with levodopa/carbidopa
- Side Effects: Nausea, vomiting, diarrhea, abdominal pain, dyskinesias
DA Agonists
- MOA
- Purpose
- Side Effects
-Used in the early stages of PD to reduce symptoms. May prolong or decrease need for levodopa
-Stimulates, agonize, DA receptors in the absence of DA.
Side Effects: N/V, orthostatic hypotension, droswiness, dizziness, hallucinations, confusion, unsteadiness, dyskinesias, hypersexuality, compulsive gampling
Amatadine
- Class
- MOA
- Purpose
- Side Effects
-Dopamine agonist, also anti-viral effects.
-DA agonist, glutamate antagonist
Side Effects: blurred vision, dizziness, trouble sleeping; depression/anxiety; swelling feet/hands; SOB. difficulty urinating.
