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NURS 350 patho pain
Pain, temperature
| Question | Answer |
|---|---|
| 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 |