2nd module - a bit more neuro (stroke, MS, park, vestibular)

Question 1

Cerebrum

Answer 1

cerebral cortex; motor, sensory, conscious function

Question 2

basal ganglia

Answer 2

control of motor activities

Question 3

diencephalon

Answer 3

thalamus and hypothalamus

Question 4

mescencephalon and brain stem

Answer 4

vital function

Question 5

cerebellum

Answer 5

coordination

Question 6

limbic system

Answer 6

emotional and behavior

Question 7

spinal cord

Answer 7

spinal cord

Question 8

blood brain barrier

Answer 8

CNS capillaries lack the gaps that are seen in peripheral capillaries and instead hold tight junctions that prevent many substances from entering the brain and spinal cord.
Drugs attempting to exert their effects on the CNS must be able to pass from bloodstream into the brain and SC.
nonpolar, lipid soluble drugs able to cross by passive diffusion
polar and lipophobic copaounds are usually unable to enter.
other drugs may be able to enter by active transport or by endocytosis.
active transport systems exist that are responsible for removing drugs and toxins from the brain. This makes it difficult for drugs to ahve therapeutic levels.

Question 9

Review of presynaptic neuro and postsynaptic neuron

Answer 9

action potential, synthesis, storage, release, reuptake, degradation, postsynaptic receptor, presynaptic “auto receptor”, membrane (drugs can affect all these areas)

Question 10

ACH

Answer 10

acetyloholine, in cerebral cortex (many areas), basal ganglia, limbic and thalamic regions, spinal interactions, for excitation

Question 11

ACH locations

Answer 11

cerebral cortex (many areas), basal ganglia, limbic and thalamic regions, spinal interactions

Question 12

ACH general effects

Answer 12

EXCITATION

Question 13

Norepinepherine

Answer 13

CNS location: neurons originating in brainstem and hypothalamus that project throughout other areas of brain
General effects: inhibition

Question 14

Dopamine

Answer 14

CNS location: basal ganglia, limbic system
General effects: inhibition

Question 15

neurotransmitter serotonin

Answer 15

CNS location: neurons originating in brain stem that project upward (to hypothalamus) and downward (to spinal cord)
General effects: inhibition

Question 16

Neurotransmitter GABA (gamma-aminobutyric acid)

Answer 16

CNS location: interneurons throughout the spinal cord, cerebellum, basal ganglia, cerebral cortex
General effects: inhibition

Question 17

neurotransmitter glycine

Answer 17

CNS location : interneurons in spinal cord and brainstem
General effects: inhibition

Question 18

glutamate, aspartame neurotransmitter

Answer 18

CNS location: interneurons throughout brain and spinal cord
General effects: excitation

Question 19

Substance P neurotransmitter

Answer 19

CNS location : pathways in spinal cord and brain that mediate painful stimuli
General effects: excitation

Question 20

enkephalins neurotransmitter

Answer 20

CNS location : pain suppression pathways in spinal cord and brain
General effects: excitation

Question 21

Stroke Drugs list

Answer 21

Thrombolytics
Anticoagulants
Antiplatelet Therapy
Antihypertensive agents
Angiotensin II receptor antagonists
anticholesterol agents/statins
antispasmodics/spasmolytics
antispastics
anticonvulsants
GABA receptor antagonists
Neurotoxins
Antidepressants

Question 22

Ischemic stroke: blood clot
Drugs used

Answer 22

Thrombolytic Drugs
Tissue plasminogen Activator(T-PA) <> IV Alteplase
Converts plasminogen to plasmin -> degrades clot bound fibrin.

Clinical Indications/Implications:
Recognize signs of stroke: “BE FAST”
Determine ischemic or hemorrhagic
Ischemic: 3 -4.5 hours since onset
used for lysis of thrombi in arteries, pulmonary emboli, thrombi in stroke
Clinical Implications
Risk of hemorrhaging; look for signs of bleeding
Monitor vital signs, especially with aerobic exercise
Use of compression stocking, compression pumps

Drug <> Drug interactions
Antiplatelet therapy: Aspirin
recommended within 24 - 48 hours of AIS. delayed 24 hours if TPA was administered

Question 23

Flaccid

Answer 23

complete a sense of resistance to elongation

Question 24

hypotonia

Answer 24

decreased resistance to elongation

Question 25

spastic hypertonia

Answer 25

increased resistance to elongation that increases with FASTER stretch (VELOCITY DEPENDENT), usually more predominant in muscle on one side of affected joints in stroke/TBI (or in both agonists and antagonists in affected areas following SCI) and more obvious toward the end of the range when the muscle is on maximal stretch

Question 26

Rigid hypertonia

Answer 26

increased resistance to elongation that does not increase with faster stretch (present even at slow speeds) often present in muscles on both sides of the joint and present through the range (though it may show a “cog - wheel pattern)

Question 27

Spastic hypertonia is ________ dependent

Answer 27

velocity

Question 28

Baclofen (Tone drug?)

Answer 28

MOA: acts as a GABA agonist, inhibits transmission at SC: inhhibitory effect on excitatory neurons that synapse with the alpha motor neuron (presynaptic inhibition) Adverse reactions: dizziness, fatigue, weakness, drowsiness Clinical Implications: monitor changes in spasticity, strength, or mood/behavior blood pressure Drug <> Drug: CNS depression with other CNS depressants

Question 29

Dantrolene Sodium/Dantrium (Tone drug?)

Answer 29

MOA: Ca 2+ release is inhibited when dantrium binds to ryanodine type 1 receptor on the calcium channels in SKELETAL muscle SR Adverse reactions: drowsiness, weakness, diarrhea, hepatotoxicity Clinical Implications: monitor signs of hepatotoxicity, spasticity, dizziness, Drug <> Drug: CNS depression with other CNS depressants, hepatotoxicity, risk of arrhythmia. Use cautiously with cardiac, pulmonary or previous liver disease

Question 30

Diazepam/Valium

Answer 30

Classification: anti anxiety, anticonvulsants, muscle relaxant sedative MOA: depresses the CNS, potentiating GABA. Skeletal muscle relaxation by inhibiting spinal polysynaptic afferent pathways. Adverse reactions: dizziness, drowsiness, lethargy Clinical Implications: assess spasms, pain, ROM, dizziness, drowsiness, BP can acuse physical dependence Drug <> Drug: CNS depression with other CNS depressants/antihistamines/opioids, fluoxetine/metoprolol/propoxyphene/propranolol/valproic acid may decrease metabolsimf of diazepam. may decrease the efficacy of levodopa

Question 31

Gabapentin

Answer 31

Classification: analgesic adjunct, anticonvulsant MOA: debatable. Gaba agonist, allowing Cl- into cell vs inhibiting specific calcium channels in presynaptic terminal -> decreases release of glutamate and other (+) NT. Adverse reactions: confusion, depression, drowsiness, ataxia Clinical Implications: monitor signs of drowsiness, confusion, dizziness, monitor pain, paresthesias, may increase risk of suicidal ideation, Drug <> Drug: antacids may decrease absorption, risk of CNS depression, morphine increases gabapentin levels -> risk of toxicity

Question 32

Tizanidine

Answer 32

Classification: anti spasticity (pharm: adrenergic) MOA: debatable. alpha-adrenergic agonist, reduces spasticity by increasing presynaptic inhibition of motor neurons. Adverse reactions: anxiety, depression, dizziness, sedation, weakness, hypotension, abdominal pain, skin ulcers, back pain, paresthesia. May slow recovery in acute phase of stroke or TBI Clinical Implications: monitor signs of spasticity, back pain, paresthesias, dizziness, depression, hallucinations, BP. Has been used for chronic pain as well. Drug <> Drug: risk of hypotension with other alpha adrenergic antihypertensives, CNS depression,

Question 33

Botox

Answer 33

Normal Phys: Protein receptors direct vesicles to fuse with the surface and allow AcH to be released. MOA: inhibits the release of acetylcholine which decreases local muscle activity. Used to inhibit contraction of intrafusal muscle fibers in the skeletal muscle, some literature in effects on CNS. Adverse reactions: headache, nausea, local muscle weakness, allergic reactions Clinical Implications: education, effects last 2-3 months, to maximize effects engage in serial casting/ROM etc to maintain muscle range.

Question 34

Parkinson’s disease

Answer 34

Neurodegenerative condition that progresses as a slow degeneration of dopamine-secreting neurons in the basal ganglia. Issues with medical management Dopamine does not cross the blood brain barrier

Question 35

Which drug does not cross the blood brain barrier, relative to parkinsons?

Answer 35

dopamine

Question 36

Parkinson’s disease Usual drug that treats this

Answer 36

Primary Drug: Carbidopa-Levodopa (sinemet) Levodopa - precursor to dopamine, able to cross BBB. Carbidopa: decarboxylase inhibitor, prevents premature levodopa breakdown. Adverse Reactions: Gi issues: nausea/vomiting, arrhythmias, dyskinesias: chorea, athetosis, ballismus, dystonia, behavioral changes, diminished response, on/off phenomenon

Question 37

Parkinsons disease Other drugs that treat it

Answer 37

Dopamine Agonists: Bromocriptine, ropinirole (table 10-2), apomorphine: use in advanced PD, Clinical implications: sometimes used alone in early Parkinsonism, used alongside sinemet can produce optimal results with smaller dosage, Adverse reactions: GI issues, confusion, hallucinations Anticholinergic Drugs: deficiency in striatal dopamine is associated with increased activity in cholinergic pathways in the BG. Clinical implications: drugs that limit AcH transmission can help with symptoms of tremor and rigidity. Adverse reactions: AcH agents are nonselective which may result in CNS side effects, cardiac irregularities, dry mouth, and urinary retention. Amantadine: useful in reducing dyskinesias and motor complications with levodopa and advanced PD. MOA: effects likely from blocking NMDA receptor in brain -> inhibiting glutamate. More research underway Monoamine Oxidase B Inhibitors: selegiline, rasagiline MOA: inhibit the MAO-B enzyme which is responsible for breaking down dopamine. Inhibiting the enzyme prolongs the local effects of dopamine at the synapse. Catechol-o-methyltransferase inhibitors: entacapone, tolcapone MOA: inhibit the enzyme catechol-o-methyltransferase (COMT) which converts levodopa to an inactive metabolite. Prevent levodopa conversion in peripheral tissues. Clinical implications: may prolong “on” times. Adverse reactions: dyskinesias

Question 38

Multiple sclerosis

Answer 38

autoimmune disease - inflammation, selective demyelination of the CNS

Question 39

guillain barre syndrome definition

Answer 39

autoimmune disease - inflammation, selective demyelination of the PNS

Question 40

MS management

Answer 40

Corticosteroids: used to treat acute relapses because of their anti-inflammartory and immunosuppressive effects. Plasmapharesis: Remove harmful antibodies in the blood. Mainly used for RRMS. Disease-modifying therapeutic agents: Prevent future progression of disease but do not return function. Includes interferons which slow down the immune system byblocking activated T cells from crossing blood brain barrier Ocrevus: monoclonal antibody that binds to a molecule on the surface of B cells and depletes them from circulation

Question 41

Vestibular and inner ear disorder treatment drug

Answer 41

Meclizine: Antivert Classification: Antiemetic, antihistamine MOA: central anticholinergic, CNS depressant and antihistaminic properties. Decreases excitability and conduction between the middle ear and cerebellar pathways. Clinical implications: Long term use can limit vestibular recovery.