Neuro Exam 1 questions Flashcards
A patient reports loss of pain and temperature in the right leg. Lesion of which of the following structures will best explain this sensory loss?
Left spinothalamic tract
Pick the correct statement about group 1 fibers
They process proprioception sensation from muscles spindles and golgi tendon organs
Plasticity occurs in the adult somatosensory cortex following?
Amputation of a limb or digit
Repetitive behavior/ overuse of particular digits
Cell bodies of the first order neurons processing proprioception information from the facial area are located in the:
Mesencephalic nucleus of the trigeminal complex
Which of the following nerves process somatosensory information from the posterior 1/3 third of the tongue?
Glossopharyngeal nerve
Which of the following pathways carriers mechanosensory information from the legs?
Dorsal column medial lemniscal pathway
Which of the following sensory fibers has the slowest conduction velocity?
C fibers= Slowest conduction
A fibers= Fastest
B fibers= intermediate
Which of the following skin areas has the smallest two-point discrimination threshold?
Finger tips
** The hand has one of the greatest receptor densities. Remember; the smaller the two point discrimination, the greater the receptor density in the body (smaller two point discrimination)
Receptor potential in a Pacinian corpuscle is generated predominantly by the influx of:
Na+
What statement is true about sensory transduction?
Generator potential of a critical threshold initiates action potential
Which of the following mechanoreceptors are most helpful in processing fine tactile sensations?
Merkel discs
Where does CSF flow?
In subarachnoid space
Blood supply to the brain is more reliable than other organs because:
Circle of willis (arterial anastomosis) creates redundancy in circulation
A 62 year old women is admitted to the hospital after suffering an embolic stroke secondary to previously undiagnosed arterial fibrillation
Middle cerebral artery
A 21 year old college student is brought to the ER by his roommate. He started feeling sick last night with a headache and fever. In the morning, he vomitted and complained of a stiff neck before becoming lethargic. CT of the brain revealed no lesions of bleeding. The physician prepares to perform a lumber puncture. What is true about this procedure?
The correct intervertebral space can be found by drawing a line connecting the posterior superior lilac crest
Efferent division:
Motor pathways
Preganglionic neuron:
Cell body located in the CNS
Neurons emerge from the brain stem or spinal cord
Form synapse at the ganglia
What is a ganglia:
Collection of nerve bodies
Postganglionic neurons:
Cell body located in the ganglia
Non-mylelinate neurons
Terminates on effector organs> smooth muscles, cardiac muscles, exocrine glands
T/F: Sympathetic preganglionic fiber will be long
False. Sympathetic preganglionic fiber will be short
*Remember: SSL (Sympathetic; short (pre), long (post)
where are sympathetic preganglionic neurons located?
T1-L3 spinal cord
Where are sympathetic postganglionic neurons located?
paravertebral or preortic ganglion
Tizanidine:
MOA:
Agonist alpha 2 adrenoreceptors in spinal cord> Bind to Upper motor neuron
-Tone deceased by blocking the release of excitatory neurons (i.e. epi, NE, glu)
-increasing the inhibition of presynaptic motor neurons> leads to reduced release of excitatory amino acids from the spinal interneurons
Clinical use of Tizanidine:
Reduces spasticity (muscle spasms) in patients with ALS or MS
Adverse effects of Tizanidine:
Sedation
Hypotension
Xerostomia
Dizziness
Muscles weakness
Hallucinations
Hepatotoxicity
Benzodiazepines:
-Postitive allosteric modulators (PAM)
-I.e. Diazepam (Valium) and Midazolam (versed)
MOA for Benzodiazepines:
Benzodiazepines drugs will signal for inhibitory interneurons to release GABA. Once GABA is released, GABA will cause Cl channels to open. Cl channel opening will lead to hyperpolarization of the cell.
Benefit of Benzodiazepines:
Benzodiazepines will enhance the binding of GABA’s allowing for a greater entry of Cl. Entry of Cl will make it more difficult for the cell to depolarize; reducing excitability
Clinical uses of Benzodiazepines:
-Treat muscle spasms due to cerebral palsy, stroke, spinal cord injury
-Generalized anxiety
-Panic disorders
-Sleep disorders
-Seizures
Route of administration for Benzodiazepines:
Oral
Adverse effects for Benzodiazepines:
CNS Depression> Sedation, anterograde amnesia
- Psychological and physiologic dependence
Botulinum Toxin (BoNT) drugs:
Incobotulinumtoxin A
Onabotulinumtoxin A
Abobotulinumtoxin A
Rimabotulinumtoxin B
MOA for BoNT:
- BoNT binds to receptor and endocytose (cell entry)
- Light chain gets released from heavy chain and disulfide bond
- Light chain cleaves synapatobrevin, SNAP25, and VAMP
- Synaptic fusion complex blocked
- ACh release blocked. No Postsynaptic excitatory occurs
T/F: BoNT induces flaccid paralysis of skeletal muscle
True. BoNT will also reduce activity of parasympathetic and sympathetic cholinergic synapses
Route of administration for BoNT:
Injection
Clinical uses of BoNT:
-Spasm due to cerebral palsy
-Multiple sclerosis
-Overactive bladder
-Hemifacial spasms
-Strabismus (crossed eye)
-Blepharospasm (uncontrolled twitching and blinking)
-Chronic migraine’s
Adverse effects of BoNT:
-Respiratory tract infections
-Muscle weakness
-Urinary incontinence
-Falls
-Fever
-Pain
Where is Epinephrine synthesized from:
Tyrosine inside of the adrenal medulla
How much of EPI and NE is released into the bloodstream?
80% EPI
20% NE
T/F: EPI interactions with both beta and alpha receptors?
True
Which receptors has a high dose vasoconstriction in regards to EPI?
Alpha has a high dose vasoconstriction while Beta has a low dose vasodilation on the vascular system
Actions of EPI for the cardiovascular system:
Increases:
-Contractility of myocardium
-Rate of contraction
-Cardiac output
-Renin release
-Constriction of arterioles in the skin
-Dilatation of vessels
-Systolic BP
-Decrease in diastolic BP
Actions of EPI for the respiratory system:
-Bronchodilation (B2)
-Relief of dyspnea (anaphylactic shock)
-Increase tidal volume
-Inhibition of release of allergic mediators (histamine and mast cells)
Therapeutic uses of EPI:
Bronchospasm (albuterol; drug of choice)
Anaphylactic shock> type 1 HPS
Anesthetics>allows to increase the duration of usage; EPI causes vasoconstriction at injection site
Cardiac arrest
Adverse effects of EPI:
-Anxiety
-Fear
-Tension
-Headache
-Tremor
-Cerebral hemorrhage from increased BP
-Cardiac arrhythmias
-Pulmonary edema
Interactions of EPI (hyperthyroidism):
Increased production of adrenoceptors on vasculature of hyperthyroid patients; Enhanced CV effects
Interactions of EPI (Cocaine):
Enhanced CV effects
Interactions of EPI (Diabetes):
Increase release of glucose ; insulin dose needs to be increased
Interactions of EPI (Beta blockers):
Will leave alpha receptors unopposed leading to increased peripheral resistance
Interactions of EPI (Inhalation anesthetics):
Leads to tachycardia
Norepinephrine:
Neuromediator of adrenergic nerves
Mostly alpha adrenergic effects
Norepinephrine affects on the cardiovascular:
Increase in PR due to vasoconstriction; more than EPI
Increase in systolic and diastolic BP
Baroreceptor reflex due to increase in BP reflex
Therapeutic effects of Norepinephrine:
Shock; NE increases vascular resistance and BP
Adverse effects of NE:
-Anxiety
-Fear
-Tension
-Headache
-Tremor
-Cerebral hemorrhage from increased BP
-Cardiac arrhythmias
-Pulmonary edema
Albuterol:
Direct acting, short acting agent
Mostly effective on Beta 2 receptors
Interact with both beta receptors
What does Albuterol induced?
bronchial smooth muscles relaxation (bronchodilation)
What does Albuterol inhibit?
Immediate hypersensitivity mediator release, mostly in mast cells
Clinical use of Albuterol:
COPD and asthma
Phentolamine:
-Blocks alpha 1 and alpha 2 (competitive)
-Produces postural hypotension
-Causes EPI reversal
-Reflex tachycardia (barorecptor)
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