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Carroll Pharm Lect 2
Anti-Inflam: NSAIDS, DMAARDS, Steroids, & Gout
| Question | Answer |
|---|---|
| What are the 5 signs of inflammation? | SHARP: Swelling, heat, altered function, redness, and pain |
| What are the physiological signs of inflammation? | 1. Vasodilation 2. Increased permeability of blood vessels 3. Recruitment of neutrophils and macrophages |
| What is the Triple Response of Lewis? | 1. Immediate red scratch mark 2. red flare around scratch mark 3. red swollen area around flare |
| What are mediators of actute inflammation? | histamine, bradykinin, prostoglandins, and leukotrienes |
| 1. What are mediators or inflammation? 2. What is known to inhibit this mediator? | 1. Protoglanins 2. Aspirin |
| What are prostaglandins derived from? | Derived from arachidonic acid from the diet and stored until needed |
| What role do prostaglandins play in disease? | -inflammation (inc swelling and perm) -pain (inc sensitivity of pain receptors) -fever (inc body temp) -dysmenorrhea (pms) -Thrombus formation-blood clotting -Asthma, diabetes, cardiovascular disorders |
| What do anti-inflammatory drugs do? | PREVENT synthesis of prostaglandins |
| What are three usefull effects of anti-inflammatory medication? | 1. Suppression of inflmmation 2. Relief of pain3. Reduction of fever |
| What are three adverse effects of anti-inflammatory medications? | 1. Gastric ulceration 2. suprresion of platlet aggregation (good for heart, bad for clotting) 3. induction of acture renal failure |
| What are prostaglandins derived from? | Derived from arachidonic acid from the diet and stored until needed |
| What role do prostaglandins play in disease? | -inflammation (inc swelling and perm) -pain (inc sensitivity of pain receptors) -fever (inc body temp) -dysmenorrhea (pms) -Thrombus formation-blood clotting -Asthma, diabetes, cardiovascular disorders |
| What do anti-inflammatory drugs do? | PREVENT synthesis of prostaglandins |
| What are three usefull effects of anti-inflammatory medication? | 1. Suppression of inflmmation 2. Relief of pain3. Reduction of fever |
| What are three adverse effects of anti-inflammatory medications? | 1. Gastric ulceration 2. suprresion of platlet aggregation (good for heart, bad for clotting) 3. induction of acture renal failure |
| What are therapeutic agents for inflammation? | 1. NSAIDS (nonsteroidal anti-inflammatory drugs) 2. glucocorticcoids (steroids) 3. DMARDs (Disease-modifying antirheumatic drugs) |
| What is LOX? What does it lead to from Arachidonic acid? | lipoxygenase - leukotrienes |
| What is COX? What does it lead to from Arachidonic acid? | cyclooxygenage - prostaglandins |
| What is an NSAIDs mechanism of action? | To block COX *figure of pathway |
| What are some characteristics of COX-1? | Responsible for mediating normal cell activity and maintaining homeostasis. (Housekeeping, always turned on, platelet, kidney, stomach) Stomach: protect stomach lining from gastric acid. Kidney: maintain renal function. Platelet: regulating normal ac |
| What are some characteristics of COX-2? | Produced primarily in injured cells. (inflammation process, rapidly induced, no effects on stomach) **Emergency cell component** |
| What are 8 prototypes of NSAIDS? | 1.*Aspirin 2.*Ibuprofen (Advil, Motrin, Nuprin)*Naproxen(aleve, Naprosyn) 3.Ketoroloc(Torodol) 4.*Piroxicam(Feldene) 5.*Indomethacin(Indocin) 6.*Celecoxib(Celebrex) 7.Rofecoxib(Vioxx) 8.*Acetaminophen(Tylenol)-->analgesic |
| What are 4 actions of aspirin? | 1.Analgesic(low intensity pain killing) 2.anti-pyretic(decr fever) 3.anti-inflammatory(in large doses) 4.anti-platelet(interfers with clotting, inc risk of hemorrhage) |
| What are some therapeutic uses of aspirin? | -Suppression of inflammation/arthitis -analgesia(mild to mod) -Reduces fever(not with children with chicken pox or influenza) -dysmenorrhea -suppression of platelet aggregation |
| What is the mechanism of action for aspirin? | Irrevesibily inhibits COX |
| What are some side effects of aspirin? | GI: blocks protective prostaglandins (ulcers, heartburn) BLOOD: increases bleeding UTERUS: decreases contractions KIDNEY: promotes retension RESPIRATION: stimulates |
| What are the symptoms of aspirin toxicity? | GI ulcers, hypersensitivity/lung constriction, overdose (nausea, vomitting, deafness, dehydration) Prolonged labor, Reye's syndrome, alcohol |
| What is Reye's syndrome? | marked by a high fever, vomitting, liver dysfunction, and increasing undresponsivness, |
| What are some drug interactions to be aware of with aspirin? | Warfin, glucocorticoids (inc gastric ulceration), Alcohol (inc gastric bleeding), Ibuprofen (decr antiplatelet, negate effect) |
| What are some implications of aspirin poising? | 20-25 g in adults, 4 grams in children death from respiritory failure (respiratory alkalosis from inc CO2), treat with ventilator, external cooling, bicarb, IV fluids |
| What things are contraindicated by aspirin? | Kidney problems, preexisting bleeding disorder, history of peptic ulccer/asthma. In combo with anticoagulants, glucocorticoids(inc ulcers), or alcohol; pregnancy-anemia/hemorrhage |
| Aspirin is considered a salicylate, what are examples of others? | Magnesium Salicylate (Doan's) and Topical (Ben-Gay) |
| What is the mechanism of action for Ibuprofen/Naproxen? | Inhibits COX |
| What is a difference between inboprofen and naproxen? | Ibuprofen has a shorter duration of action |
| What are three actions of Ibuprofen/Naproxen? | 1.Anti-inflammatory 2.Antipyretic 3.Analgesic |
| What are some therapeutic uses of Ibuprofen/Naproxen? | Suppression on inflammation, rheumatoid arthritis, moderate pain, fever, dysmenorrhea, naproxen only-bursitis/tendonitis, better tolerated NSAIDs, Ibupprofen-safe to use with anticoagulants |
| What is the mechanism of action for Piroxicam(Feldane)? | inhibits COX |
| What are some characteristics of Piroxicam? | decs free radical production at [high], half life of 50-60 hours-so 1x/day; antiplatelet like aspirin, Rheumatoid arthritis & OA, 9.5 higher risk for peptic ulcer and bleeding, Antiplatelet-prolongs bleeding time |
| What is the mechanism of action of Indomethacin (Indocin)? | Inhibits COX |
| What are some uses of Indomethacin? | Antiplatelet like aspirin, decs pain & fever but not used for this; arthritis, bursitis, tenonitis, gouty arthritis, close ductus arteriosus in premies |
| What is the mechanism of action for Celecoxib (Celebrex)? | Selective COX-2 inhibition |
| What are some uses of Celecoxib? | OA & RA |
| What are three actions of Celecoxib? | anti-inflammatory, anti-pyretic, and analgesic |
| What are side effects of Celecoxib? | Renal impairment, sulfa allergy, 3rd trimester, inc anticoagulation of Warfin, NO PLATELET aggregation |
| What is the mechanism of action of Acetaminophen? | WEAK inhibition of COX |
| How is Acetaminophen different from other NSAIDs? | It is only able to inhibit prostaglandins in the CNS, other go into PNS too |
| What are the actions of Acetaminophen? | Analgesic and antipyretic |
| What are some characteristics of acetaminophen? | Not an anti-inflammatory agent, categorized as an analgesic; does not cause GI bleeding or inhibit platelets, rarely causes hypersensitivity, and increases liver injury with alcoholics |
| What are some characteristics of RA? | Autoimmune inflammatory disease (inflam of memb & goes over cartilage, enzymes destroy overgrowth until cartilage is completely destroyed); joint stiffness & pain, wt loss, fever, weakness. Want to decrease inflammation and stop progression |
| What are DMARDs? | Disease-modifying antirheumatic drugs used to treat RA. Drug effects take 6 weeks to 6 months to be evident. The drugs shorten life and decrease quality of life. |
| What are some prototypes of DMARDs? | Mthotrexate(Rheumatrx-chemo), Sulfasalazine(Azulfidine), Leflunomide(Arava), Entranercept(Enbrel) |
| What are the characteristics of Methrotrexate? | Rapid acting (3-6 weeks), inhibit cytoines, low cost, administered once per week so inc compliance |
| What are the side effects of Methrotrexate and what is contraindicated? | SE: liver fibrosis, bone marrow suppression CONTRA: Pregnancy |
| What are the characteristics of Sulfasalazine? | Treats inflammatory bowel disease, retards progressoin of joint deterioration |
| What are the side effects of Sulfasalazine? | GI problems and rash |
| Waht are the char'tics of Leflunominde? | Slow formation of bone erosion, well tolerated, benefits seen in one month |
| What are the side effects of leflunomide? | GI distress, rash, liver function |
| What is the mechanism of action for leflunomide? | Stops lymphocyte activation |
| What is the mechanism of action of Etanercept? What are its side effects? | Anti TNF drug (TNF = tumor necrosis factor); SE: increased risk of infection |
| What do cytokines play a central role in? | Inflammation and immune response |
| What does TNF do? | produced by macrophages & activated by T-cells, alpha stimulates the release of cytokines |
| What is the most potent and affective drug against chronic inflammation? | Steroids |
| What is the first line of treatment for asthma? | inhaled steroids |
| What is prednisone? | A steroid used for arthritis |
| What is the mechanism of action for steroids? | 1. Binds to a receptor 2. Activates a complex 3. localizes to nucleus 4. Causes induction or repression of target genes |
| What do steroids do for inflammation? | -Inhibit cytokines (also mediators of inflam) -increase synthesis of annexin I which inhibits phopholipase A2 (no prostaglandin) - cleaves arachindonic acid from the membs, no acid no pros'n synth |
| What are some problems with chronic steroid use? | fractures, infections, cataracts, diabetes, hypertension |
| What are the char'tcs of osteoarthritis? | Intrinsic defect in the joint cartilage, NOT immune response; more prevalent then RA (50-80%>65y/o; 100%>75) |
| What is drug rx used for OA? | To manage pain and maintain active lifestyle (NOT treat inflammation), acetaminophen/NSAIDS-symptomatic, Viscosupplementation - restore lubrication in joints with injection of hyaluronan (benefits for 6 mo -1 yr); Glucosamine & Chondroitin Sulfate - decre |
| What are some special concerns in Rehab with OA? | Stop jt dysfxn & inc Strength; -Glucocorticoids-effects muscle, tendons, bone, & skin; ROM & strengthening programs - becareful of fractures & soft-tissue injuries; Prevent skin breakdown(splints,etc) |
| What is gout? | caused by deposits of urate in the jints and cartilage; phagocytosis of urate crystals leads to the secretion of inflammatory mediators; leukocytes migrate and amp inflam |
| What does the treatment of gout include? | 1. Suppress different phases of leukocyte activation(Colchicine) 2.Inhibit urate crystal phagocytosis(Indomethacine) 3.Decrease the pool of urate available(Probenacid) |
| What are the char'cs of Colchicine? | Prophylaxis of recurrent episodes of gouty arthritis, binds to tubulin (inhib migration of leukocytes) |
| What is a side effect of Colchicine? | Diarrhea |
| How are NSAIDs used to treat gout? | Inhibit prostaglandin synthesis and inhibit urate phagocytosis; initial treatment of gout, most often used for acute gout |
| How does Probenacid treat gout? | Stop the take up of uric acid; decreases the net reabsoption by affecting the transport sites, need large urin volume to minimize kidney stones |
| What are opiods? | Agents which alleviate pain INDEPENDENTLY of any anti-inflammatory effect. Strickly work on pain. |
| What do narcotic include? | Any drug that dulls a person's perception of pain and induces sleep. |
| What are types of endogenous opioids? | Enkephalins(NS), endorphines(hypothal), dynorphins(hypothal & pituitary) |
| What are the 3 receptors for opioids? | Mu, Kappa, and Delta |
| What is the primary therapeutic effects for the Mu receptor? | Spinal and supraspinal analgesia - Others: sedation, respiratory depression, inhibits Ach & dop, increases prolactin & growth hormone |
| What is the primary therapeutic effects for the Kappa receptor? | Spinal & supraspinal analgesia - other: sedation, constipation, pschotic effects |
| What is the primary therapeutic effects for the Delta receptor? | Spinal & supraspinal analgesia - Other: increases growth hormone, inhibits dopamine |
| What do opioid agonists result in? | a decrease in the release of neurotransmitters |
| What are opioids linked to? What does they affect? | Linked to G-proteins; affect ion gating, intracellular Ca2+, and protein phosphorylation |
| Where are opioid receptors located? | Present on spinal cord & relay primary afferents that relay pain message to spinal cord. Drugs are given directly to spinal cord so they have no peripheral actions. |
| What are the affects of opioid agonists? | Anagesia, euphoria, sedation, constipation, cough spression, respiratory depression, nausea, pupil constriction |
| What are the therapeutic uses of opioids? | Analgesia, acute pulonary edema, cough, diarrhea, anesthesia, rectal suppositories |
| What are effective for alleviating moderate and severe pain? | codeine, oxycodone, & tramadol |
| What are some characteristics of Morphine? | Principle alkaloid in opium, Mu agonist, does not reach the brain quickly, lasts 4-5 hours (long time), relieves pain |
| What are some side effects of morphine? | Mental clouding, orthostatic hypotension, constipation, pupil constriction, respiratory depression, urinary retension, Emesis, elevated intracranial pressure, tolerance & phyiscal dependence |
| When should Morphine be used? | Only with patient with painful disorders and sharp stabbing pain |
| What should be done with a Morphine overdose? | ventilation and give opioid antagonist |
| What drug interactions should be avoided with Morphine? why? | Alcohol, barbiturates, & antihistamines - all increase repiratory depression |
| What are the char'cs of Heroin? | Gets into the brain quicker than morphine, no evidence that it is more effective than morphine, high abuse potential, legal in europe for pain relief |
| What are the char'cs of codeine? | mild to moderate pain (no morphine like efficacy), side effects limit the maximum tolerated, often used in combo with aspirin or acetaminophen |
| What are the char'cs of oxycodone? | never achieve morphine like efficacy, schedule II drug, crushed and snort powder |
| What are some char'cs of Meperidine (demerol)? | Shorter duration of action than morphine, forms a toxic metabolite that can accumulate, widely used, contraindicated in those with heart problems |
| What are some char'cs of Fentanyl? | Mu agonist, 100x more potent than morphine, short acting (1-1.5 hours), synthetic heroin - health professionals abuse. Parental for anethesia, transdermal for chronic pain |
| What are some char'cs of Tramadol? | WEAK Mu agonist, mild to moderate pain, may cause seizures, and useful in chronic neuropathic pain |
| What are two cough suppressants? | Codeine & dextromethorphan |
| What is used to treat opioid overdoses? | Naloxone as a mu antagonist |
| What is useful in the treament of alcoholism? | Naltrexone - block endogenous opioids giving feeling of euphoria |
| What is an opioid agonist-antagonist? | Agonist at kappa; antagonist at mu, less powerful but also less addictive |
| What are some char'cs of Nalbuphine? | Moderate pain, less side effects than agonist, produce more psychotropic effects |
| What occurs with tolerance in opioids? | Rapid nausea & vomitting, moderate rate-euphoria and analgesic effects(lose high & pain relief), little or no tolerance-sonstipation and pupil constriction |
| What occurs with physical dependance of opioids? | The body fxns abnormally when administration stops, occurs as early as 6 hours post withdrawl |
| What are symptoms of withdrawl/physical dependance with opioids? | Restlessness, sweating, yawning, irritability, tremor, anorexia, depression, weakness, vomitting, inc heart rate, dehydration |
| What are char'cs of opioid abuse? | Craving, drug seeking behavior, withdrawl (get rid of tolerance so takes less to get high again), treat with drugs or behavioral therapy |
| What are char'cs of patient-controlled analgesics? | Self administer small amount on freq basis, better pain control with smaller quantities, provided through a pump |
| What occurs with opioids and athletes? | impairment of hand-eye coordination, failure to recognize serious injury (cause drowsiness) |
| What is histamine involved in when it comes to normal regulation of physiological functions? | 1.A mediator in allergic reactions 2.A mediator in the tissue response to injury 3.Mediator of gastric acid secretion 4.May serve in CNS neural modulation |
| How can histamine release be inhibited? | 1.Cromolyn Sodium-stabilizes mast cells & prevents release of contents 2.Epi-drug for analphylactic shock 3.Terbetaline-acute asthma attacks 4.Theophylline-2nd line Rx 5.Corticosteriods-Most often used for asthma treatment |
| What are some char'cs of Cromolyn Sodium? (Nasalcrom) Side effects? | Takes 2-3 weeks to be effective; SE: burning, itching, sneezing, coughing |
| What are the H1 receptors for histamine? | located on vascular, respiratory, and GI smooth muscle; |
| What are the H2 receptors for histamine? | regulation of gastric acid secretion |
| What occurs with H1 receptor activation? | Increase perm, drops in BP, contract bronchioles, nerve endings-pain and itch, temperature regulation, arousal, appetite, pain perception |
| What occurs with H2 receptor activation? | Increase in HR, drops in BP, RELAXES the bronchioles, gastric acid secretion*, temperature regulation |
| What do H2 blockers do? | Inhibits gastric acid secretion, relieves Sx of ulcer |
| What are the uses of H1 blockers? | Common cold-symptomatic relief, local allergic manifestations, motion sickness, sedative/hypnotic-OTC sleep remedy |
| Of the two major classes of H1 blockers, what do the first generation do? | Penetrate the CNS, more side effects such as blurred vision, dry mouth, etc |
| What are the difference char'cs of H2 blockers? | The newer drugs are less sedating |
| What are two examples of first generation H1 blockers? | Diphenhydramine (Benadryl) & dimenhydrinate (Dramamine) |
| What are some second generation H1 blockers? | Fexofenadine (Allegra), Loratidine (Claritin) |
| What are some char'cs of Diphenhyramine? What is the trade name? | Benadryl - allergies, Antiemetic (prevents nausea & vomitting), causes sedation in 50%, peak level in 1 hour, lasts 4 hours, available OTC |
| What are some char'cs of Dimenhydrinate? What is the trade name? | Dramamine - motion sickness, causes muscular weakness/drowsiness, no idea the mechanism of action |
| What are some char'cs of Fexofenadine? What is the trade name? | Allegra - allergies, causes less drowsiness, the active metabolite of Terfenadine so does NOT cause toxic cardiac effects |
| What are soem char'cs of Loratidine? What is the trade name? | Claritin - allergies, less sedating, once a day, extended release formulas |
| What are some uses of H2 blockers? | Inhibit gastric acid secretion, reduce volume of gastric acid secreition, relief Sx of peptic ulcers, GERD (gastroesophageal reflux) |
| What is a char'c of Cimetidine? Trade name? | Tagament - inhibits cytochrome P450 metabolism of other drugs (not good with anything else) |
| What are the side effects of Cimetidine? | Causes headaches, impotence, and gynecomastia (breast formation in men) |
| What are the char'cs of Ranitidine and Damotidine? Trade names? | Ran: Zantac, Famo: Pepcid - heart burn and gastric acid reliefe, Zollinger-Ellison Syndrome |
| What is the path of hormones? | Synthesized and released into the blood. Then transported dto a distant organ where it then binds to a receptor. |
| What are the three types of hormones? | -Endocrine: to distant organ -Paracrine: to a neighbor organ -Neurocrine: to a nerve |
| Are steroids hydrophobic or hydrophillic? | Hydrophobic |
| What are the three types of adrenocortical steroid hormones? | Glucocorticoids, mineralocorticoids, and androgens |
| What are Glucocorticoids? | steroids that influeence carbohydrate metabolism |
| What are mineralocorticoids? | Steroids that Modulate salt and water balance |
| What are Androgens? | Steroids that are responsible for the expression of sexual characteristics |
| What is the term for referring to glucocorticoids & mineralocorticoids together? | Corticosteroids |
| what are steroid hormones synthesized from? | Cholesterol |
| What are anabolic steroids char'cs? | Synthetic, derivatives of testosterone; Exogenous testosterone often used by athletes |
| What are corticosteroids char'cs? | Steroid hormones, produced in adrenal cortex, athletes use to cover up anabolic steroids |
| What is the Hypthalamic-pituitary axis? | Hypothalamus (CRH) ---> Anterior pituitary (ATCH) ---> Target gland/adrenal gland ---> hormone/corticosteroid |
| Where is mineralocortioid produced? Glucocorticoid? | Min: outer cortex of adrenal gland Gluc: inner cortex of adrenal gland |
| What are some char'cs of glucocorticoids? | Increase avail of glucose, corticol is most important, hydrocortisone, prednisone, and prednisolone are often used |
| What are the physiological effects of Glucocorticoids? | Supplying the brain with glucose, promote glucose availibility, opp effect of insulin |
| What are the physiological effects of Glucocorticoids re: proteins? What can this lead to? | promotes protein breakdown providing AA for glucose synthesis -high levels for prolonged time leads to thinning of skin and muscle wasting |
| What are the physiological effects of Glucocorticoids re: fat breakdown? What can this lead to? | Promotes fat breakdown -high levels for prolonged peroid leads to fat distributions (mood face/buffalo hump) |
| What are the physiological effects of Glucocorticoids re: the vacular system? | Maintains fxn of vascular system -depressed levels lead to drop in blood pressure |
| What are the physiological effects of Glucocorticoids re: RBC & Hbg? | Increases RBC and hemoglobin |
| What are the physiological effects of Glucocorticoids re: muscles? | supports function of striated muscles by maintaining circulatory competence. |
| What are the physiological effects of Glucocorticoids re: mood and CNS? | Affects mood and CNS excitability - insufficient: depression, too much: euphoria |
| What are the physiological effects of Glucocorticoids re: stress? | Reponds to stress |
| What are the physiological effects of Glucocorticoids re: immune function? | immunosuppression -interferes with synthesis, release, and action of immunologic factors (organ transplant) |
| What are the physiological effects of Glucocorticoids re: inflammation? | Anti-inflammatory activity -stops the release of Phopholipase A2 (so no free arach acid) -inhibits COX-2 |
| How is regulation of glucocorticoid controlled? | Synthesis when needed, not stored; synthesis controlled by ACTH |
| What are some char'cs of Mineralocorticoids? | Influence renal processing of Na, K, and Hydrogen |
| What are the physiological effects of mineralocorticoids? | Aldosterone promotes Na reabsorption and K/Hydrogen excretion (Hyperkalemia - too much K, want a certain level of aldosterone) |
| How does regulation of mineralocorticoids occur? | Regulated by the renin=angiotension system-NOT ACTH -prossess salt-retaining properties |
| What are the most potent endogenous hormones of the gluco and mineralo? | Min: Aldosterone Gluco: Cortisol |
| What is Cushing's syndrome? Sx? Rx? | Hormone excess - A disease where a person has excess glucocortiocoids. Sx: obesity, muscle weakness, stretch marks, moon face, buffalo hump. Rx: Radiation and surgery |
| What is Primary Hyperaldosteronism? Sx? Rx? | Hormone excess - A disease with excessive secretion of aldosterone. Sx: Muscle weakness, metabolic aklalosis, hypokalemia. Rx: Surgery or aldosteron antagonist |
| What is the Rx for adrenocortical insufficiency? | Replacement therapy with corticosteroids. gluco always required & possibly mineralo. |
| What is a glucocorticoid medication? Mineralo? | Gluc: Hydrocortisone/cortisone Mineralo: fludrocortisone |
| What are the char'cs of hydrocortisone? | Similar to cortisol, replacement Rx, Also has mineralo properties, generally safe, also for allergic reaction |
| What are the char'cs of fludrocortisone? | Only minaeral corticoid available for replacement therapy. Also gluco activity. If dose is too high, salt & water retension = weight gain, hypertension, hypokalemia, & edema |
| What is Fludrocortisone used to treat? | Addison's disease, hypoaldosteronism, & congenital adrenal hyperplasia. |
| What is Addison's disease? Sx? Rx? | Deficiency of gluco/mineralocorticoids. Sx: Weakness, pigmentation of skin, hyperkalemia, & hypoglycemia Rx: Hydrocortisone/cortisone & add fludrocortisone |
| What is Congenital Adrenal hyperplasia? Sx? Rx? | Deficiency of enzymes for glucocorticoid synthesis, (ATCh goes into overdrive.) Overcompensates with ACTH releasing androgens. Sx: increases masculization in girls; phallic enlargment in boys, adults height is deminished. Rx: Glucocorticoid administrat |
| What are other therapeutic uses for corticosteroids? | Adrenal insufficiency, sports injuries (tendonitis), asthma, arthritis-prednisone, allergic diseases, organ transplant, hyperthroidism, pain mang't in cancer, alcohol hepititis, meningitis, acute mnt sickness, hisuitism |
| What are some principles for administration of corticosteroids? | (Oral, injection, inhaler, topical, droplet, IV) -Therapeutic dose will change in course of Rx -single dose is usually not harmful -prolonged therapy has lethal potential -Abrupt discontinuation may be life-threatening b/c body doesn't know |
| What is a tapering regimen for corticosteroids? | -need to allow recovery of normal pituitary-adrenal response to endogenously produced corticosteroids -tapering dosaage may be necessary over 2 mo to 1 yr |
| What are Sx of corticosteroid withdrawl? | headach, dizziness, joint pian, nausea, vomitting, fever, hypoglycemia, and hypotension |
| What are the uses for corticosteroids in Acute conditions? | Collision, fall, twist; tears lead to inflammation; NSAIDs are commonly used; corticosteroids will NOT help in treating acute soft-tissue injuries |
| What are the uses for corticosteroids in chronic conditions? | Rotator cuff tendonitis, tennis elbow, achilles tenonitis; treatment throught NSAIDs, PT, & rest; corticosteroids used for CHRONIC soft-tissue injuries |
| What are the char'cs of steroid injections? | Mechanism unknown, generally last resort, not more than 3-4 injections/year b/c of side effects |
| What conditions are treated by steroid injections? | tennis elbow, golfer's elbow, joint pain of varying nature, bursitis of shoulder, hip, or knee, frozen shoulder, carpal tunnel syndrome, heriated disc and other back pain |
| How are inhaled corticosteroids used to treat asthma? | for pts with mod to severe asthma, reduces sensitivity of the airways to triggers and prevents swelling in airways. |
| Corticosteroid toxicity - What are some adverse side effects of: electrolytes? | Fluid electrolyte imbalances - sodium retension, edema |
| Corticosteroid toxicity - What are some adverse side effects of: GI? | Nausea/vomitting, weight loss/gain |
| Corticosteroid toxicity - What are some adverse side effects of: Endocrine? | Hypercorisolism (Cushing's disease), percipiatation of diabetes (not enought insulin for steroids) |
| Corticosteroid toxicity - What are some adverse side effects of: CV? | Hypertension |
| Corticosteroid toxicity - What are some adverse side effects of: Musculoskeletal? | Muscle pain or weakness, fractures |
| Corticosteroid toxicity - What are some adverse side effects of: neuro? | Headache, seizure |
| Corticosteroid toxicity - What are some adverse side effects of: Bone mass? | decrease amt of Calcium absorbed from food, exerts direct effect on cells responsible for bone maintenance (osteoclasts/blasts) |
| What changes with diabetes and treatment of bursitis? | Increase insulting because corticosteroids increase blood glucose levels (so need more insulin) |
| what is Steroid diabetes? | Development of diabetes from taking corticosteroids. |
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