| Question |
Answer |
| How is ANS controlled? |
unconscious |
| What are the two systems of the autonomic system? |
parasympathetic or sympathetic |
| What is the response of the sympathetic system? |
fight or flight |
| WHat does activation of the sympathetic nervous system cause? |
1. pupillary dilation 2. increased heart rate 3. dilation of airways 4. dilation of blood vessels in skeletal muscle 5. sweat glands 6. constriction of blood vessels in gut |
| What is the response of the parasympathetic system? |
vegetative functions |
| What does activation of the parasympathetic system cause? |
1. pupillary constriction 2. decreased ehart rate 3. airway constrxtion 4. dilation of vessels in the gut and mucous membranes 5. gut motility (smooth muscle contrxn) 6. secretions in gut, saliva and mucous membranes 7. no paras. innerv of skeletal muscle |
| The actual state of being is determined by what? |
balance between the 2 systems |
| What type of neuronal chain syst. exists in these two systems? |
1. cell body of 1st neuron is in brain or spinal cord (preganglionic) 2. cell body of 2nd neuron is autonomic ganglion (postganglionic neuron) |
| What makes up the cranial-sacral system of the parasympathetic system? |
1.fibers from cranial nerves iii, Vii, IX, and X and sacral cord (S2,3,4 and intermediate grey matter) |
| Where are the ganglia of the cranio-sacral system located? |
in or near the organ that's innervated so first axon is long, second axon is short |
| What are the innervations of cranial nerves III, VII, IX, and X? |
III = pupil VII = salivary glands (sublingual, submandibular), mucous membranes of head IX = parotid (salivary) gland X = all viscera up to left colic fracture |
| What does the sacral portion of the cranio-sacral system? |
from left colic flexure onward in gut and all pelvic viscera |
| Where are the ganglia located in abdominal organs? |
in the wall of the organ |
| Where are the large plexi formed? |
in abdomen |
| What are the neurotransmitters of the parasympathetic system? |
1st synapse (ganglionic) is cholinergic (nicotinic); synapse onto effector is also cholinergic (muscarinic) |
| Where is the thoraco-lumbar system of the sympathetic syst. derived from? |
T1-L2 |
| Where does the thoracolumbar syst exit? |
spinal nerve |
| How does the thoracolumbar enter the sympathetic chain? |
white ramus |
| What are the options for the 2nd nerve? |
1. synapse on ganglion, exit on spinal n. (via grey ramus) 2. innervate abdominal organs 3. innervate UE and LE 4. innervation of head 5. intestines and pelvic organ |
| How does the thoracolumbar syst unnervate abdominal organs? |
come off lower thoracic ganglia, form splanchnics (synapse at preaortic ganglia) innerv. abd. organs |
| How does the thoraco-lumnar syst. innervate the UE and LE? |
innerve UE + LE via spin. n above/below T1-L2 (preganglionic descending or ascending chain, synapse in ganglion at the level of the spinal n., then ride spinal n. to periphery into the limb |
| How does the thoracolumbar syst. innervate the head? |
ascend sympathetic chain, synapse in a cervical ganglion and exit chain to rid blood vessels to destination in head |
| How does the thoracolumbar syst. innervate the intestines and pelvic organ? |
innervated by lumbar splanchnics that exits L1 or L2 and synapse in superior or inferior mesenteric ganglia. |
| How far does the sympathetic chain span? |
extends the length of vertebral column even though the levels of origin from spinal cord are only T1-L2 |
| What are the neurotransmitters of the sympathetic nervous system? |
1. 1st synapse between pre- and postganglionic neurons is cholinergic (nicotinic) 2. 2nd synapse between postganglionic neuron and effector is noradrenergic (norepinephrine) |
| What is the difference in length between the first and second axon? |
first is short, second is long |
| What is Horner's syndrome? |
from severence of sympathetic chain in the neck |
| What are the signs of horner's syndrome? |
1. ptosis of eyelid 2. sinking of the eye in the orbit (endophthalmus) 3. vasodilation of the face 4. lack of sweating in the face (anhidrosis) 5. pupillary constriction |
| What is autonomic dysreflexia? |
occurs with spinal cord injury esp. with quadraplegia and high paraplegia above T4-T6; due to unregulated autonomic reflexes, esp. those asociated with splanchnic nerves |
| What are symptoms of dysreflexia? |
drastic change in BP (250-300/140-160), weating, SOB and headache |
| What might trigger dysreflexia? |
often triggered by bowel or bladder needs or noxious stimulus |
| What is complex regional pain syndrome? (Reflex sympathetic dystrophy) |
burning pain (causalgia), tenderness, pain with light touch (allodynia), swelling discoloration, decreased skin temp, decreased capillary refill |
| What makes pain worse with complex regional pain syndrome? |
movement and cold |
| What happens in later stages os of complex regional pain syndrome? |
trophic changes in nails and skin (shiny, decreased subcutaneous tiss.), loss of hair, bone loss (demineralization, osteoporosis) |
| What is the epidemiolog and etiology? |
M=F, no age preference; >50% of the time a result of trauma (fx's, sprains, trivial soft tissue injury). 1-15% of peripheral n injuries result in this |
| What is the pathophysiology of CRPS? |
thought to be an overactivation of the sympathetic nervous system in the spinal cord due to chronic incoming painful stimuli |
| Treatment for CRPS? |
sympathetic nerve blocks (sympathetic and peripheral). Pain meds like neurontine, morphine, dilaudid. PT mobilization of area |
| What happens if pt. becomes resistant to nerve blocks? |
pain will be permanent and debilatating, indication of CNS has maladapted |
| What is prophylaxis for CRPS? |
early mobilzation and aggressive, early treatment of pain |
| Amine neurotransmitters |
acetylcholine, catecholamines, dopamine, norepinephrine, serotonin |
| amino acid neurotransmitters |
glutamate, aspartate, GABA, Glycine |
| neuropeptide neurotransmitters |
angiotensin II, Beta Endorphin, Enkephalin, Substance P |
| What type of receptors do neurotransmitters attach to? |
ion channel or 2nd messenger |
| What type of effects do receptors associated with ion channels have? |
fast excitatory or inhibitory effects |
| What are agonist types of drugs? |
act like neurotransmitters (Morphine-opiod agonist) |
| What are antagonist drugs |
bind to receptor and block neurotransmitter (beta blockers) |
| What are inhibitors of catabolic enzymes? (MAOIs) |
decrease degradation; the class of antidepressants that inhibit the breakdown of norepinephrine and make more transmitters available to postsynaptic receptors |
| What are SSRIs? |
selective serotonin Reuptake inhibitors, prevent uptake and reuptake (decrease degredation |
| What does botulinum toxin affect? |
prevent release of transmitter (decrease available transmitter); affects molecules in synaptic terminal where synaptic vesicles bind to release trnsmitter; prevents release of Ach at myoneural jxn |
| What can drugs be selective for? |
certain receptor subtypes depending on their molecular structure |
| what is excitotoxicity? |
is cell toxicity that results from excessive glutamate release; glutamate binds with NMDA rec. subtype (assoc. with Ca++), cell then flooded with Ca++ which can kill the cell |
| Where does excitotoxicity occur? |
occurs with trauma to CNS (brain, injury, stroke and other diseases |
Vanessa Kennedy
on 2009-10-15
BIOL3326 Forms
