Therapeuticmeds
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| pathophysiology-the cell | 1.damage to cell 2.impairment of 1 or more cell structures 3. tissue/organ function affected 4. function of system affected 5. affects spead to another system 6. homeostatis disrupted
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| the cell adapts | shrink-become less active, decrease mitochondia demand(atrophy), grow-more active in response to demand(hypertrophy), change-hyperplasia(number), metaplasia(type), dysplasia(structure)
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| The cell dies | necrosis-cant meet demands of the nucleus
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| tissue healing | 1.regeneration-replace injured tissue w/normal tissue-integrity and func restored 2. scarring-injured cells replaced by connective tissue-integreaty restored not function,
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| three phases of healing | inflammation, proliferation and remodelling
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| Inflammatory phase | 1. hemostatis-immediate vasoconstriction, activate platelets, control blood loss, 2.Vascular response-vasodialtion, incrase cell permeability, plasa exit vessel enter damaged tissue(edema), 3.cellular respons WBC clear the area of bacteria and dead cells
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| Proliferation phase | close the tissue wound-fibroblasts secrete collagen-protien that binds to self and other tissue to create scar, tissue becomes vascularized and new tissue cells form
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| Remodeling phase | overlap with proliferation phase, tissue remodeling occurs while collagen still being laid, simultaneous breakdown & deposition of collagen bonds, final collagen strucure forms in response to forces experienced
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| Acute inflammation | 1.damaged cells release chemicals-histamine, bradykinins, prostaglandins, cause capillary dilation, increase cell permeability, 2reaction increase BF, plasma &protien enter interstitial space3.protiens in blood interact w.fibrin=collagen clot
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| acute inflammation 4+ | chemicals attract luekocytes-prolong inflammation-act as phagocytes, dissolve absorb damaged cells 5. an inflammation continues, increase pressue, blood flow to ara decreased, damage to healthy cells in area=secondary hypoxic injury
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| Chronic inflammation | result of long term chemcial irritation and mechanical stress, chemcial action and luekocytes-inhibits tissue healing, same s.s as acute-less intense, persissts until cause of cellular damage is removed
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| Signs and Symptoms of Inflammation | P!-tissue damage, inflammatory chemcisas, ischemia--Swelling, erthema, heat-increased blood flowk, plasma fluid in interstiial space-decreased function-p!, local muscle guarding, loos of movement--eccymosis-RBC in the tissue
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| NSAIDs-arachidonic acid | arachidonic-produces prostoglandins-basodilate &sensitize receptors to bradykinins& histamin-decrease p!threshold, increased sensiati vity to p!
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| lipoxygenase pathway | arachodoinic acid pathway-inflammation w/ asthma
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| cycloxygenase COX pathway | COX1 enzyme-production of prostoglandins rsponsible for protection of GI mucosa, maintian renal function, platelet aggregation--COX2 enzyme-production of prostaglandins responsible for inflammation, pain, febver, wound healing
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| Non-Selective/traditional NSAIDs | inhipit COX1/COX2 enzyme(inhibit prostoglandins), reduce p!, swelling, fever, prevent"good" prosotglandins tht protect stomach
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| Selevtive(celebrex, vioxx, Bextra) | Do not block COX1, COX2 inhibited
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| NSAIDs | used as-antiinflammatory, analgesic, antipyretic- lipid soluble:easily absorbed, stomach/sma intestin-produce effects w/in 15-30min, 7-10 days needd to evaluate effectiveness of drug-side effects-heart burn, nausea, diarrhea, constipation, GIbleed, ulscer
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| Corticosteriord | usted to treat-asthma, inflammatory bowel disease, tendonitis, bursitis, dermatolical conditions, allergic reactions-how-decreased inflammation by inhibiting synthesys of arachidonic acid-administerd-orally, inhal, inj, topical, transdermal
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| corticosteroid side effects | restlessness, dizziness, sleeplessnes, change skin color, unusual hair growth, eye pain, nausea, black stool, fluid retention, skin reaction, menstrual irregularities, prolonged sore throat, fever, tendon ruptures, decreased done density, GI disturbances
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| analgesics-acetaminophen | treats-midle/mod p!, fever--dosage-tablets, capsules, chewAVLE, SUPPORISTORES-side effects increase risk for liver toxivity, overdose-does not inhibit platelet aggregation like NSAIDs
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| analgesics-narcotics/opiates | treat-mod/sever p!, post-op, cancer--admin-oral, inj, rectal--side effects-drowsiness, euphoria, abuse, constipation--narcotics-oxycodone, demerol, opiates-morphone, codine
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| Antibiotics | treat-bacterial inf, admin-oral, IM, IV--side effects-allergic reaction, dependant on drug-interact w/ oral contraceptives-less effective, misuse has lead to MRSA
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| bactericidal antibiotics | inhibits synthesis of bacteria cell wall, works to kill invading bacteria
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| Bacteriostatic | keeps bacteria from reproducing, allowing the immune system time to kill bacteria-high doesse or in conjunction w/ other antibiotics can kill
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| Antihistamines | histamine-chemical mediator released during inflam, 3 types of histamine receptors-h1:respiratory tract, H2:stomach, H3:CSF,
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| H1 antihistamines | tret allergies, cold, flue, skin-1st generation: lip soluble, pass blood-brain barrier=drowsy(benadryl), 2nd generation-less lip soluble less drowsiness(claritin, allegra)
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| H2 antihistamines | reduce gastric acid production (H2 blockers)
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| Decongestants | used to treat-nasal congestionw/ allergies, common cold, how-vasoconstirc blood vessels in nasal passage to help reduce swelling of mucosal membrane, admin-oral(sutafed), nasal spray Afrin-only use 305 days- rebond congestion),
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| decongestant side effects | head ache, insomnia, restlessness, nervousness, do not use if HTN, heart diesase, raise heart rate, diabetics check with Md, may change insulin requirement
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| Bronchodilators | used to treat-asthma, expand airways, relax bronchial spasm, admin-oral, inhaled(actquicker, fewer side effects) Side effects-side effects-tachycarda, increased BP, increased bloodsugar, nausea, vomit, nervousness, restlessness, diuretic
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| Gastrointestinal drugs-antidiarrheals | treat symptoms od diarrhea, not underlying cause, opoids-decrease GI motility(immodium),absorbents-absorbs h2o, increase viscosity of stoll
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| GI drugs-laxatives | bulkform-fiber, swells when mixed w/h2o, stimlatesperistalsis-12-72 hrs, osmotic lax-draw h2o to intestinal lumen, increasae peristaltis 1-3 hrs, stimlant-increase bowelmotility, stomach cramps 6-10hrs, stool softeners-soften contents of bowel, prevention
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| Gi drugs-antacids | neurtalize stomach acid, used to treat peptic ulcer, heartburn, mild cases of GERD, take after meal, before bed, results:5-15 min, note:reduce absorption of other meds for 2 hrs
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| Proton Pump inhibitors(PPI) | decrease acid production, take 30 min prior to meal, dosage depends on condition being treated
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| H2 blockers | antagonists to histamine(h2), D acid production, dose dependant on condition being treated
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| Antifungals | used to treat-superficial(mucous membrane, skin hair, nailes), systemic-side effects:oral:nausea vomit, abp!, HA, topical:itching burning, skin irritation
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| Fungicidals | disrupt cell membrane kill fungus
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| Fungistatic | prevent cell prlication, allows immune system to manage infection
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| Antivirals | prescription only, used to treat/reduce the duration/severity of: herpes virus, inluenza
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