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24 Cards in this Set
- Front
- Back
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Describe the physiologic manner by which local anesthetics work |
- Suppress pain by blocking sodium channels, thereby blocking impulse conduction along axons - Only in neurons located near the site of administration - Suppress pain without generalized depression of nervous system |
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Differentiate between ester and amide types of local anesthetics in terms of mechanisms of action, mechanisms by which they are eliminated from the body, and adverse effects. |
Ester (eg. Procaine)- injection only: Metabolized in the blood by enzymes Adverse effects: less commonly used bc of greater risk of reaction
Amide (eg. Lidocaine): Metabolized in the liver by enzymes Adverse effects: less risk for allergic reaction |
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Adverse effects for local anesthetics. (procaine and lidocaine) |
- CNS (depression (coma) to excitation) - Cardiovascular- decrease in cardiac function --> brady, less CO, vasodilation, and hypotension - Allergic reaction- more common during ester type - labor + deliver- can cross placenta and get to fetus so not best for labor |
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Describe s/s of systemic local anesthetic toxicity, how to recognize them, and how to manage them |
- CNS- brief period of excitement possibly including convulsions followed by CNS depression (respiratory depression) - Cardio-toxicity- bradycardia, AV block, or cardiac arrest -Management: monitor bp, pulse rate, respiratory rate, and state of consciousness. Have room for CPR if needed. Manage CNS excitation with IV diazepam or thiopental |
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State the roles of the mu, kappa, and delta opioid receptors in causing analgesia respiratory depression, and euphoria. |
Mu- responses to activation of mu receptors include analgesia, respiratory depression, euphoria, and sedation. (+ decreased GI motility and physical dependence) Kappa- activation of kappa receptors = analgesia and sedation. (+ decreased GI motility) |
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Distinguish among pure opioid agonists, and antagonists in terms of their mechanism of action; also, place various named drugs in the appropriate category. |
Pure opioid agonists- relieve pain by mimicking the actions of endogenous opioid peptides- primarily at mu receptors, and partly at kappa receptors (eg. morphine) Antagonist- acts a mu and kappa receptors. (ex. Naloxone) - can reverse respiratory depression, coma, analgesia, and most other effects of pure opioid agonists. Mostly used to treat ODs. |
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Discuss the therapeutic uses for opioid agonists, agonist-antagonists, and antagonists. |
Agonists- relieve pain, sedation, euphoria Agonist-antagonists- produce less analgesia than morphine and have lower potential for abuse Antagonist- treat opioid OD. If someone is physically dependent on opioids though- and you give them a high does you'll send them into withdrawals |
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Discuss the adverse effects of opioids and both their pharmacologic and nondrug management. |
-Respiratory depression (resp. rate below 12 don't give morphine) (tolerance to resp. depression can develop, can compromise pt. with resp issues- COPD, asthma, etc.) (see slides), constipation, orthostatic hypotension, cough suppression, emesis, sedation, urinary retention, euphoria, sedation, miosis - Tolerance + physical dependence |
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Discuss opioid drug-related factors that contribute to the development of physical psychologic dependence. |
- if drug is given at high dose for 20+ days physical dependence may develop. Need to tapper pt. of drug slowly for 3 days to prevent abstinence syndrome. - If pt. dependence is esp. high (addict or someone that's been on opioids for a long time) then withdraw over 7-10 days. |
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Morphine Toxicity |
Clinical manifestations: classic triad = 1. coma, respiratory depression, pinpoint pupils Tx: ventilatory support, antagonist- naloxone (NARCAN)- short half life- give every 2 hrs- may need repeated dose depending on how much they OD'd with General guidelines: - monitor full vitals before giving - give med on a fixed schedule |
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Compare and contrast acute withdrawal from an opioid with the withdrawal signs/symptoms, and likely outcomes of unsupervised withdrawal from barbiturates, alcohol, and benzos. |
Although withdrawal from an opioid is unpleasant -it is not dangerous like it is when you w/d from etoh, benzos, etc. -Lasts 7-10 days if untreated. |
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Describe the similarities or differences b/t COX-1 and COX-2 pathways and state which physiologic process is mainly responsible for analgesia; anti-inflammatory activity; antipyresis; bleeding tendencies; and gastric mucosal damage. |
COX-1 (Good)- mediates beneficial processes; protecting gastric mucosa, supporting renal function, and promoting renal function.
If you inhibit COX -1: Harmful effects: - gastric erosion and ulceration - bleeding tendencies - Renal impairment Beneficial effects: - protection against MI and stroke (secondary to reduced platelet aggregation)
COX-2 (Bad)- mediates harmful processes; mediates inflammation, sensitizes painful stimuli
inhibition of COX-2 = mostly beneficial
Beneficial effects: - suppression of inflammation - alleviation of pain - reduction of fever - protection against colorectal cancer Adverse effects: - renal impairment - promotion of MI and stroke (secondary to suppressing vasodilation) |
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Discuss the beneficial and adverse actions of NSAIDs and the basic mechanisms by which they occur.
(Celecoxib (Celebrex)) - second gen COX- 2 inhibitor - fewer adverse effects than first gen. - bc of cardiovascular risks, last choice for long term management of pain |
-used for: osteoarthritis, rheumatoid arthritis, acute pain, dysmenorrhea
Adverse effects: - dyspepsia - abdominal pain - renal toxicity - sulfonamide allergy - cardiovascular impact (stroke, MI) - avoid if hx - use in pregnancy |
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Discuss the beneficial and adverse actions of NSAIDs and the basic mechanisms by which they occur. (Aspirin) |
Inhibits COX-1(protection against MI +
Adverse effects (from inhibiting COX-1) - gastric ulceration - bleeding - renal impairment
Aspirin is irreversible- takes 7-10 days to get platelet aggregation again |
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Discuss the beneficial and adverse actions of NSAIDs and the basic mechanisms by which they occur. (Tylenol) - inhibits prostaglandin synthesis in CNS |
Therapeutic uses: - analgesic, antipyretic - does not have any anti-inflammatory or anti-rheumatic actions - not associated with Reye's syndrome
Adverse effects: - few at normal doses - hepatotoxicity- w/ OD or pt. with liver failure - OD- hepatic necrosis - s/s of liver failure, coma, death- early s/s= n/v, diarrhea, sweating, abdominal pain
Tx for OD = acetylcysteine (mucomyst) - converts metabolite to nontoxic form
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Identify situations in which aspirin should not be used. |
- if pt. has GI problems- increased ulceration risk - bleeding disorders - before surgery- bleeding risk - renal failure - bc of inhibiting COX-1 - toxic in children |
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Compare and contrast the signs and symptoms of acute poisoning with aspirin and with acetaminophen; the time course of the s/s and underlying causes; and the management of these conditions |
Aspirin S/S - respiratory excitation then resp. depression -acidosis - hyperthermia - sweating - dehydration - electrolyte imbalance - Stupor and coma
Tx - hospitalization - acute med emergency - mechanical ventilation for resp. depression - external cooling- sponging to correct hyperthermia - IV fluids to correct dehydration - slow infusion of bicarb to reverse acidosis - gastric lavage- charcoal - hemodialysis
Tylenol S/S - hepatic necrosis - liver failure, coma, death - early s/s = n/v, diarrhea, sweating, abdominal discomfort - not until 48-72 hrs after drug ingestion that indications of hepatic injury appear
Tx: - liver damage can be minimized by giving acetylcysteine (Mucomyst) - antidote- when given within 8-10 hours of OD it's 100% effective at preventing severe liver injury |
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Describe the general mechanism by which glucocorticoids cause their biologic effects. |
Physiologic effects (low doses) - modulation of glucose metabolism and adrenocortical insufficiency Pharm effects (high doses) - suppression of inflammation - reduce inflammation by suppressing 1. synthesis of inflammatory mediators (prostaglandins, leukotrienes, histamine 2. infiltration of phagocytes 3. release of lysosomal enzymes 4. proliferation of lymphocytes |
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In terms of mechanisms and targets of action, state why glucocorticoids have greater anti-inflammatory activity than NSAIDS |
NSAIDs suppress synthesis of prostaglandins via COX inhibition
Glucocorticoids can suppress inflammation by a number of ways. --> Reduce inflammation by suppressing 1. synthesis of inflammatory mediators (prostaglandins, leukotrienes, histamine 2. infiltration of phagocytes 3. release of lysosomal enzymes 4. proliferation of lymphocytes |
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State and describe the physiologic effects of glucose administration on 1. the metabolism 2. the cardiovascular system 3. the stress response 4. fluid and electrolytes and 5. the respiratory system in neonates. |
Metabolism: - elevate blood glucose by reducing amount of glucose taken up by muscle and adipose tissue - decrease muscle mass, bone mass, thinning skin - Cushing's syndrome Cardiovascular: -increase the # of circulating RBCs + leukocytes - decrease lymphocytes, eosinophils, basophils, and monocytes (immune system) Effects during Stress (trauma, infection, surgery): -maintain bp and glucose levels Fluid and Electrolytes: -act on kidney to promote retention of sodium and water, while increasing excretion of potassium - can result in hypernatremia, hypokalemia, and edema Respiratory: - during delivery- adrenals of full-term infant release a burst of glucocorticioids which hasten maturation of the lungs - if preterm infant- production is low and they might have respiratory distress |
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Describe the potential risks to and relative glucocorticoid requirements of patients who are under physiologic stress and during discontinuation of systemic glucocorticoids. |
- normally adrenal secrete large amounts of glucocorticoids during stress. but bc of adrenal suppression if stress is sufficiently severe- trauma or surgery- these glucocorticoids are essential for supporting life - if pts. receiving long term glucocorticoid therapy- you must give them some during increased times of stress. - once glucocorticoid use has ceased- supplemental doses are required whenever stress occurs until recovery of adrenal function is complete - pt. should carry emergency card - so dr. will know this in emergency |
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Discuss the etiology, patho, clinical presentation, and tx of gouty arthritis |
Etiology: -excessive production of uric acid - impaire renal excretion of uric acid Patho: -uric acid crystals in joint space -recurrent inflammatory disorder - more common in men - hyperuricema - uric acid level greater than 6 (women) greater than 7 (men) Clinical Presentation: - severe joint pain, usually in toes- esp. large toe |
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Discuss the first-line agents for relieving the pain of an acute gouty attack and explain when glucocorticoids and colchicine are acceptable alternatives. |
Acute Flare/Short term relief of symptom: - NSAIDs- first-line - glucocorticoids can also be used (NSAIDs preferred, but these are used on pts who are hypersensitive to NSAIDs, who have medical conditions that contraindicate NSAIDs, or pts. with severe gout that is unresponsive to NSAIDs. Avoid in pts. with hyperglycemia. - Colchicine- only reduces inflammation with gout. It does not provide analgesia. Second line bc other drugs give analgesia and are safer. |
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Summarize the mechanisms of action of allopurional and colchicine in the context of hyperuricemia, gouty arthritis. State where each fits into tx. plan for asymptomatic hyperuricemia, tx of acute gout, and prophylaxis of recurrent attacks and also when each should not be used. |
Colchicine: - can treat acute gout in high doses - can be use prophylactically to prevent attacks from occurring- can also abort impending attack - stop at first sign of diarrhea- can become severe
Allopurional: - doesn't work for acute gout (no analgesia or anti-inflammatory actions), but does reduce the frequency of acute attacks - used for chronic gout and hyperuricemia due to chemo - reduces blood levels of uric acid, inhibits uric acid formation
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