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NURS 350 patho pain

Pain, temperature

QuestionAnswer
3 aspects of understanding pain sensory/descriminative, motivational/affective, cognitive/evaluative
what mediates sensory/descriminitive aspects of pain mediated by afferent nerves, spinal cord, brainstem, higher brain centers
name 3 types of pain fibers A-delta, Type C, A-Beta
what class of neurons are A-delta and Type C first order neurons, nociceptive
what class is A-Beta fiber non-nociceptive fiber that INHIBITS A-delta, Type C
type of stimuli and physical characteristics of A-Delta receives mechanical or thermal stimuli and conducts with fast, thick, myelinated axons for intense pain
type of stimuli and physical characteristics of Type C receives chemical, as well as mechanical and thermal bwo polymodal receptors which transmit on small, unmeyelinated fibers--> diffuse, throbbing, burning or chronic pain
somatogenic pain pain witha physical cause
psychogenic pain no KNOWN physical cause, but not imaginary (fibromyalgia)
most pain is a mixture of somatogenic and psychogenic pain
types of physical pain acute or chronic
properties of acute pain protective, begins suddenly-motivates to relieve cause, relieved when chemical mediators removed, associated with anxiety & hope of recovery
acute pain may manifest as somatic, vesceral or referred
what type of fibers contribute to acute pain A-Delta and Type C contribute
visceral pain manifests as poorly localized (except if stretch receptors in viscera activated, then acute), often radiates
visceral pain associated with n/v, hypoTN, restlessness, shock
referred pain characteristics impulse converge on same ascending neuron, brain cant discriminate
physiological responses to acute pain adrenergic response (inc HR, Resp, BP, flushin, diaphoresis, hyperglycemia, mydriasis)
physiological response to chronic pain sympathetic adapts over time --> normal HR, Resp, BP, may have intermittent acute pain episodes. associated with depression
pain threshold point at which stimulus perceived as pain
pain tolerance time or intensity individual will endure pain before initiating overt pain responses
pain neuroanatomy involves afferent pathways, CNS, efferent pathways
where do affernt pathways terminate dorsal horn of spinal cord
nociceptors equipped to receive stimuli from these channels traditional voltage gated, TRP channels = transient receptor potential channels
MOA of TRP channels reside on naked nerve endings and respond to variety of stimuli
what class of neurons act as pain gate 2nd order neurons = projection neuron, excitatory interneuron, inhibitory interneuron
what happens once 2nd order neurons gate the pain signal 2nd order neurons CROSS OVER in from dorsal horn in spinal cord to spinothalamic tract, then transmit to 3rd order -->periacueductal grey matter, thalamus, reticular formation, limbic system, sensory cortex
name 5 inflammatory mediators bradykinin, leukotrienes, prostaglandins, nitric oxide
exciatory transmitter glutamate, and others
inhibitory transmitters endogenous opioids, GABA
neuromodulators serotonin, others
name 4 endogenous opioids endomorphins, endorphins, dynorphins, enkephalins
MOA endogenous opioids inhibit release of excitatory glutamate et al right before gain at 1st order neuron
HOA of opiates bind opiate receptors to enhance natural endorphin response
how we increase endogenous opioids to raise pain threshold sex, stress, physical exertion, acupuncture
what disease state may involve circulating endorphins silent heart attack
once signal decussates to spinothalmic tract, how is it processed either goes to (brain stem OR reticular formation OR hypothalamus,thalamus), limbic, cerebral cortex
thalmus role when signal arrives discriminates and localizes pain
limbic and reticular systems functions for pain alert, arousal and motivating behaviros
medulla/hypothalamus functions for pain coping, flight/fight, cortisol release, CV response
what fibers in the efferent pathway are responsible for modulating pain sensation reticular formation -->midbrain-->sustantia gelantinosa in spinal cord-->taret effector organ
how is temperature regulation acheived balancing of heat production, heat conservation and heat loss
what mediates hormonal aspect of temp reg hypothalamus
if temp is low, hypothalamus triggers these responses heat production --- heat conservation
MOA of heat production - endocrine hypothal ---TSHRH---ant pit---TSH---thyroid---thyroxine---adrenal medulla----epi/norepi
heat production when epi/norepi released vasoCON shunts blood to core, increased glycolysis, increased metabolic rate
the chemical reactions of heat production induce skeletal muscle tone/contraction, chemical thermiogenesis
heat conservation MOA hypothal---sympathetic/adrenergic---shivering/vasocon shunt to core. ALSO relays to cortex, voluntary response to curl up, get blanket, etc.
if temp too high, body will decreased sympathetic response will reverse mechanisms of heat production, heat conservation AND involke mechanism of heat loss
3 mechanisms of heat loss radiation (off surface), conduction (by direct contact), convection (by gases)
other mechanisms of heat loss vasoDIL gets warm blood to perifpher, dec muscle tone, evaporation, increased resp, voluntary, adaptation to warm climates (increased ECF & plasma)
benefits of fever - microorganisms kills, affects growth, affects replication
benefits of fever - elements decreases serum Fe, Zn, Cu which are needed for bacterial replication
benefits of fever - misc lysosomal breakdown-->autodigestion of infected cells. Increases interferon, enhances phagocytosis
Created by: lorrelaws