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what are the adverse physiological and cardiac effects of pain
- Pulmonary : atelectasis, V/Q mismatch, arterial hypoxemia, hypercarbia, pneumonia
- Cardiac: increased catecholmines release leading to htn, tachycardia, MI, dysrhtymias
what are the adverse immune system and endocrine effects of pain?
- Endocrine: hyperglycemia, Na and H20 retention, protein catabolism
- Immune system: decreased function
what are the adverse physiological effects of pain for the Gi/Gu system and coagulation?
- Caogulation: increased platelet adhesion, decrease fibrinolysis, increase coagulation increase DVT's
- GI/GU systems: decrease peristalsis, urniary retention
what is the upside of pain?
protection: being able to feel Pain can help avoid dangerous situations
What are the psychological risk factors for Pain?
abuse history, depression, personality disorders, coping with major psychological trauma, physical and secual abuse, emotional neglect, abandonment and chemical dependence
what is allodynia?
what is hyperalgesia?
- allodynia-perception of ordinarily non noxious stimuli as painful (clothing or sheet on legs)
- Hyperalgesia- increased repsonse to noxious stimuli
what is analgesia?
what is anesthesia?
- absence of pain perception
- Anesthesia- absence of sensation
what is hypoalgesia?
what is hyperesthesia?
- hypoalgesia- diminished response to noxious stimuli
- hyperesthesia- increase resonse to MILD stimulus
what is neuralgia?
what is paresthesia?
what is radiculopathy?
- Neuralgia- pain in a distributing nerve or gtoup of nerves
- Paresthesia- abnormal sensation perceived without apparent stimulus
- Radiculopathy-functional abnormality of one or more nerve roots
what does nociception serve as? what 4 types is it divided into?
- serves to detect, localize and limit tissue damage
what is transduction? what are the types of stimuli? what neurotransmitters are released once tissue is damaged?
- transduction-perception of noxious stimuli into electrical energy
- Types of stimuli include chemical, mechanical and thermal
- Neurotransmitters released are bradykinin, serotonin, substance P
what do the neurotransmitters substance P, bradykinin and serotnoin do once released?
activate the arachidonic acid cascade which leads to inflammation which leads to the generation of a nerve impulse
what happens during transmission?
- 1st order neurons transmit signals to the spinal cord via the dorsal root ganglia
- 1st order neurons synapse with second order neurons whose axons cross the midline and ascend to the thalamus via the spinothalamic tract
- 2 order neurons synapse in the thalamic nuclei with 3rd order neurons that send signals to the cerebral cortex
what are the 2 types of nerve fibers? myelniated or unmyelintaed? fast or slow? 1st or 2nd? what type of pain is felt? diffuse or localized?
- A delta fibers- Myelinated-1st/fast pain-well localized (sharp, stinging, pricking)
- C fibers-UNMYELINATED-2nd slow pain-diffuse-burning, aching, throbbing
what is the dorsal horn organized into?
Layers known as Rexeds lamina (specifically the first 6 laminae)
where do C fibers terminate primarily?
in superficial lamina 1 and 2. Interneurons transmit C fiber impulses to lamina V
where do primary afferents terminate?
in a highly organized way in the dorsal horn on the same side of the body of the origin
where do A delta fibers terminate?
what is the major neurotransmitter released from A delta? from C fibers?
- in lamina 1,3 to 5 after leaving the tract of Lissauer
- Gluatamate(which binds to AMPA receptors) from a delta fibers
- Substance P is released from C fibers(binds to NK-1 receptors) on the post synaptic membrane
what is convergence?
termination of somatic and visceral afferents in the same lamina can result in convergence and referred pain as WDR neurons receive input from both sources
where are the cell bodies located in 2nd order neurons? what are the 2 types of 2 order neurons?
Located in the dorsal horn. 2 types of second order neurons are WDR(wide dynamic range) and NS
where do the axons of 2nd order neuron A delta and C fibers go?
cross the midline of the cord, gather into bundles of ascending fibers in the contralateral anterolateral spinal region and then ascend to brainstem targets where they synapse with 3rd order neurons
spinothalamic tract is what?
the most common ascending pathway involved in normal perception of pain
2 groups of cells in dorsal horn are what? where are they located?
- NS( nociceptive specific) located primarily in Lamina 1
- (WDR) wide dynamic range are located in lamina V (smaller amts in 1 & X)
where do WDR receive input from? how are they activated?
- receive input from both A beta and nociceptive fibers
- can be activated by either tactile of noxious stimuli
- Have large compex receptive fields
- can contribute to pain perception
where do NS receive input from?
- responds exclusively to noxious stimuli and its physiological conditions
- limited receptive fields, confined to some fraction of a dermatome
where are 3rd order neurons located? where do the fibers extend?
- most cell bodies are located in the thalamus.
- extend in to the somatosensory areas of the parietal cortex where perception and localization of pain occur
what 4 centers of the brain give perception of pain?
- RAS- has extensive interconnections with other supraspinal sites
- Thalamus- is the "central station" of the brain
- Limbic system- Emotinal aspects of pain, stress, sleep
- Cerebral cortex- pereception of pain- SI section is believed to be most significant
Modulation of pain can occur where?
In multiple sites and can eithere inhibit or facilitate
How do ASA, NSAIDS, steroids and Tylenol work?
help eliminate prostaglandin, histamine, bradykinin, ascetylcholine, lactic acid, H and K in order to decrease pain
when can central modulation occur? is it inhibitory or excitatory? is it functional or dysfunctional?
can occur at any point in pain pathway, can be inhibitory or excitatory, can be functional or dysfunctional
what is wind up?
repeated firing of WDR neurons can lead to prolonged discharge even in the absence of C fiber input.
what is segmental inhibition? what theory does it represent?
- occurs when activation of large afferent fibers inhibits WDR neurons in spinothalamic tract
- Basis of gate theory?
what is supraspinal inhibition? where does it originate? what tract does it descend down?
- several structures send fibers down the spinal cord to inhibit pain in the dorsal horn
- originates in the periaquaductal gray, reticular formation, and nucleus raphe magnus
- descends down dorsolateral fasiculus to the dorsal horn
what neurons does a supraspinal work on? what neurotransmitter is released?
- presynaptically on 1st order neurons
- postsynaptically on 2 order neurons
- enkephalin is released, binds to first order neurons and inhibits release of substance P--> decreasing transmission of pain signals
why is pain management challenging?
because of psychological, cultural and other variable influences
what 4 ways is pain calssified as?
- duration- transient or chronic
- etiology- nociceptive, inflammatory, or neuropathic
- severity- mild, moderate, severe
- anatomy-somatic, visceral, referred
describe acute pain- what phase is it, how long does it last, what anatomy classifies it, what neurotransmitter is released, psychological issues?
phase 1 pain,short duration(2-6 months), usually resolves when underlying cause resloves, somatic and visceral, glutamate is major neurotransmitter, minimal psych symptoms
describe nociceptive pain? where is it transmitted, visceral or somatic? what 4 processes does it consist of?
- transmitter via normal pathways via Ad(1st fibers) and C fibers(2 pain), eithers somatic or visceral.
- consists of nociception
describe chronic pain? what phase is it? how long does it last? what is the anatomic classification? major neurotransmitter released?
Phase 2 pain, serves no protecive function, persist >3-6 months, can be nociceptive or neuropathic, major neurotransmitter is supstance P(also glutamate and aspartate), rarely treated effectively
what is tha pathophys of chronic pain?
occurs when dorsal horn has been bombarded by severe pain for a long time, the interneuron adjusts by adding fast pain receptors that amplify pain signal--> ascending tract, the cognitive and emotional centers of the brain receive a large pain signal and the brain perceives increasing pain
How is CRPS treated? 1st line medications? 2nd?
what enables PT to take place
- Physical therapy is more important treatment.
- 1st line therapies include steroids, NSAIDS, antidepressants, and anticonvulsants
- 2nd line include alpha adrenergic blockers(clonidine, prazosin, phenoxybenzamine)
- sympathetic blocks
what differentiates CRPS 1 from 2? what is the testing done to differentiate the 2?
an identifiable nerve lesion is present in type 2 not in type 1. the testing that can be done is EMG and nerve stimulating test
how do you differentiate between SIM(sympathetically independent pain) and SMP(sympathetic maintained pain)?
a stellate ganglion block or lumbar sympathetic block
what percentage of the IDDM pts have a neuropathy?
what are the 3 classifications of neuropathy? what is the most common?
- polyneuropathy, mononeuropathy, and autonomic neuropathy.
- the most common is polyneuropathy
what is the pathophysiology for Diabetic neuralgia?
- chronic hyperglycemia-->decrease blood flow to nerve--> nerve edema-->Increase thickness in basement membrane-->vessel becomes weak, leaks protein, slow blood flow-->cells and organs lose function
- Nerve degeneration begins in periphery-->axonal degeneration of large myelinated A fibers and small unmyelinated C fibers
what is the AN mgmt for diabetic neuropathy?
- glycemic control is the most effective treatment
- also may use ASA, opioids, tramadol, antidepressants, TENS, gabapentin, and capsacin ointment
what are the effects of autonomic neuropathy?
orthostatic hypotension, postural hypotension, impotence, anihydrosis, arrhtymias, urine retention,GI dysfunction
what are the key points of PHN?
PHN is most common and severe symptom of shingles, zostavax vaccine may decrease pain of shingles and PHN, wind up pain can last several months and involves the dorsal root ganglia and trigeminal nerve, treatment involves antidepressants, anticonvulsants and opioids
what positioing issues does someone with low back pain have? what can we do to relieve it?
- loss of normal lumbar curvature in supine position,.
- Place padding under lumbar spine, avoid flexion or extension of spine(Can cause spinal cord ischemia), uncross legs (may cause pressure on pernal and and sural nerve), avoid leg elevation
what differentiates primary from secondary headaches?
- primary headaces are tension, cluster or migraines
- secondary are sinusitis, tumor, OSA, craniofacial neuralgias,pheo
what are the treatment modalities for migraines?
what are the 2 common types of headaces in children?
tension(induced by stress) and migraine
what should we do preop in a pt who has chronic headaches?
detailed h&p, neuro exam, differentiate between acute and chronic, assess stressors
what is the drug tolerance, dependence and psychological dependence of cancer pts in pain? what may help prevent opioid withdrawl?
- drug tolerance requires increased dose
- psychological tolerance- cravings are RARE
- physical dependence occurs in ALL CA pts receiving opioids
- opioid antagonist may help(methylnaltrexone) prevent withdrawl
what is the major problem with intrathecal opioids in CA pain?
what AN mgmt for CA patients?
- take opioids preoperatively, have a PCA with a basal rate
what are the hallmarks of neuropathic pain? describe the pain?
- allodynia and hyperalgesia
- phase 3, pathologic in nature, produce from damage to central and peripheral nerves, exaggerated and can be spontaneous or innocuous
- may involve deaffernation with the central or peripheral nervous system
what conditions are often assoicated with neuropathic pain?
- Diabetes #1
- back, leg and hip problems
- HIV or aids
- facial nerve problems
what is the pathophsy of chronic inflammatory pain?
A beta fibers become activated(normally are inactive) by chronically inflamed nociceptors, these nociceptors pass a constant and powerful signal to cell bodies in the dorsal root ganglia-->new activated touch fibers pass signals to the dorsal root ganglia then to spinal cord as hyperalgesia,allodynia
what is the pathophys of neuropathic pain?
- C fibers are injured-->develop new adrenergic receptors--> ectopic neuronal pacemakers are formed along length of nerve--
- NA channels are different in these nerves
describe wind up and Long term potentiation(LTP)? how long does LTP last? what receptors do these 2 things effect? what drugs can block these 2 effects?
- thought to be part of the sensitization process involved in many chronic pain states LTP lasts at least 1 hr-several months
- NMDA type glutamate receptors are formed when dorsal horn is bomabarded with pain for a long time--> triggers a cascade of events leading to sensitization of dorsal horn WDR neurons-
- NMDA antagonists ketamine and dextromethorphan can block this cascade of events
Central Pain is aka as? what are the main criteria? what are the common causes of it?
- A.k.a thalamic pain syndrome, posterior thalamic syndrome, dejerine roussy syndrome, central post stroke syndrome.
- Main criteria is damage to the sensory nerce cells in the central nervous system anywhere from the thalamus down through the spinal cord(spinothalamic tract)
- Common Causes: Spinal cord injury, stroke, MS, cancer, physcial trauma, any demyelinating condition
what is the triad of central pain?
burning pain often with paradoxical cold, made worse by light tough or rubbing of clothing
what is radicular pain? what causes it? give examples
- pain "radiating" along the dermatome of a nerve, caused by compression,inflammation or injury to spinal nerve root
- ex. sciatica, low back pain, cervical radiculopathy
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