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N402 1 The physiology of inflammation (KP1) Response of vascular tissues to harmful stimuli Pathogens Damaged cells Other irritants The response is structured to eliminate Cause of cell injury Necrotic cells and tissues Involves Host cells Blood vessels Proteins and mediators Initiates process of repair Classic signs Pain Heat Redness Swelling Loss of function 2 Inflammation and infection (KP2) 3 Role of prostaglandins (KP2) Group of lipids created at site of injury or infections Act as signals to control specific processes Cause inflammation, pain, fever as part of healing process Also involved in vasoconstriction, brochodilation/-constriction, gastric acid secretion, uterine contraction 4 Nonpharmacologic treatment of inflammation (KP3) Rest ↑Ω3 ↓Ω6 Inflammation Heat/ cold H20 Ω3 = (fish, grass-fed, walnuts, flaxseed) Ω6 (meat, dairy, grains) 5 Primary classes of drugs used to treat inflammation (KP4) NSAIDs Salicylates (ASA) COX2 Inhib. Ibu & Ibu-like Glucocorticoids Various: Cortisone Dexamethasone Methylprednisolone Prednisone Triamcinolone 6 Function of NSAIDs (KP4) Have multiple functions: Analgesia Anti-inflammatory Anti-pyretic Used for mild-moderate inflammation ASA—antiplatelet, can cause GI bleeding Celecoxib (Celebrex)—increased risk of thrombosis, MI, stroke Ibuprofen (Advil, etc.)—GI bleeding, heart failure, blood dyscrasias 7 Function of salicylates (KP4) 1897—scientists at Bayer investigated aspirin as a less irritating form of salicylates Binds to COX-1 and COX-2, prevents from forming prostaglandins May affect platelet for entire life-span (811days (must d/c prior to surgery) 8 Function of COX-2 inhibitors (KP4) Do not have as many adverse effects on GI system because they do not inhibit COX-1 (protective of gastric lining) Moderate to severe inflammation Early form (Vioxx) associated with stroke and heart attack risk 9 Function of Ibuprofen and Ibu-like NSAIDs (KP4) Inhibit both COX-1 and COX-2 Ibu and Naproxen available OTC Variability of patient response to various formats (e.g., ibuprofen, naproxen) Adverse GI effects, especially in the elderly 10 Function of glucocorticoids (KP4) Drug form doses are much higher than levels occurring naturally in the body Inhibit prostaglandins Serious adverse effects Hyperglycemia Mood changes Osteoporosis Cushing’s (↑cortisol → rapid central obesity, polyuria, HTN) Short term treatment If long term required, low dose, alternate days Discontinue gradually (wean) 11 General strategies: treatment of inflammation (KP5) First concern is to identify and treat the cause Inflammation serves a healing purpose; use nonpharmacologic approaches first Topical forms have fewer side effects Corticosteroids used only in severe cases Used only 1-3 weeks to control inflammation Patient then switched to NSAIDs 12 Treating fever (KP6) Fever naturally occurring defense Elevated fever kills bacteria Prolonged fever can be problematic for younger children Consider drugs as cause of fever if there is no other cause evident: Antibiotics SSRIs Antipsychotics Anaesthetics Chemotherapy drugs 13 Common medications to treat fever (KP6) Aspirin Ibuprofen Acetaminophen Can cause severe, fatal liver damage Contraindicated in chronic alcoholism 14 Terms you must know! (KP7) Pathogenicity—ability of an organism to cause disease (qualitative) Virulence—the degree of pathology or disease caused by an organism (quantitative) 15 Methods of classifying bacteria (KP8) Gram stain • Gram + • Thick wall • Retain color • Gram • Thin wall • Don’t retain color Cellular shape • Bacilli (rods) • Cocci (spheres) • Spirilla (spirals) Use of oxygen • Aerobic (live in O2rich environment) • Anaerobic (live without O2) 16 Broad classes of anti-infectives (KP8) Abx Anti-virals Anti-virals Antihelminthics Anti-TB Antifungals 17 Acquired resistance (KP9) First line antibiotics selected based on safety, availability, and cost Second line antibiotics are broader, greater risk : benefit ratio (less safe), more costly Some forms of a microorganism are able to survive exposure to a first or second line antiinfective Antibiotic resistance is now a major threat to public health (WHO) 18 Teaching points: preventing drug resistance (KP9&26) Prevent infections from occurring Use correct drug for the infection Use antibiotics only when medically necessary Instruct to complete full course of therapy Prevent transmission of pathogen 19 Selection of effective antibiotic (KP10) Often selected “empirically” Laboratory testing prior to initiating (not always possible—see above!) C&S testing Start with broad spectrum, then… Switch to narrow spectrum after C&S results obtained 20 Host factors (KP11) Host defenses Local Tissue Conditions The patient’s Antibiotic must natural immunity be able to cross any barriers: Goal is to inter- ∙Blood-brain ∙↓ Circulation fere with infec∙Pus tion enough so ∙Hematomas that natural ∙Intracellular vs body defenses can take over extracellular Allergy history Other variables Requires drug history Age Pregnancy Genetics Be sure to ask what type of reaction occurred with suspected antibiotic use 21 Classifications of antibacterial drugs (1) (KP12) Drug class Mechanism of action Nursing considerations Penicillins Disruption of bacterial cell Generally safe wall Allergy is common Cross-allergy common Cephalosporins (cefazolin) Disrupt cell wall of gramnegative infections Multiple generations 10% PCN-allergic pts have Ceph-allergy Tetracyclines Inhibit protein synthesis GI upset; take with food, not with milk Photosensitivity Broad spectrum* Not for patients < 8 years Macrolides (erythromycin) Inhibit protein synthesis Most gram-positives Some gram-negatives Low-dose=bacteriostatic High-dose=bacteriocidal Broad spectrum* 22 Classifications of antibacterial drugs (2) (KP12) Drug class Mechanism of action Nursing considerations Aminoglycosides (Gentamycin) Inhibit protein synthesis Bacteriocidal Gram-negative Used for serious systemic infections Inner ear, renal toxicity Fluoroquinolones (Cipro, levoflaxacin) Affect DNA synthesis All work against gm-neg Newer against gm-pos Well-absorbed orally Do not take with MVI Assoc with tendon injury in pts > 60 Sulfonamides (sulfamethoxazole) Gram-positive and gram- Overuse → resistance negative effectiveness UTIs Inhibit folic acid synthesis Used in MRSA Other: Metronidazole Effective against anaerobes in abscesses and deep wounds; some parasites Minor side effects High doses may be neurotoxic 23 Drug treatment of tuberculosis (KP 13) Majority of cases are urban Half cases are Asian; 1/3 are Hispanic Increasing drug resistance Slow growing microorganism Therapy needs to continue for 6-12 months Requires treatment with 2-4 drugs Chemoprophylaxis for close contacts First line drug is isoniazid (INH) 24 Fungal, protozoan, and helminthic infections (KP14) Fungal Protozoan • Spores found in soil • Lungs • Skin • Hair • Nails • Found in water • Poor sanitation and hygiene Helminthic • Parasitic worms • Not common in North America 25 Drugs for fungal, protozoan, and helminthic infections (KP15-16;18) Drug class Mechanism of action Nursing considerations Antifungals (amphotericin B) Interfere with cell membrane synthesis, causing leaky membrane Little-to-no antibacterial activity *Treatment may be months Nephrotoxicity, blood dyscrasias Antiprotozoan (chloroquine) Especially malaria; interrupt protozoal life cycle Rare in US Preventive treatment for high-risk travel Antihelminthic (mebendazole) Interrupt life cycle locally and systemically Some are broad spectrum Resistance not a factor 26 Notes on superficial fungal infection (KP17) Not exclusive to immune-suppressed patients Examples: Vaginal candidiasis Tinea pedis (athlete’s foot) Tinea cruris (jock itch) Generally safe: poor penetration to deeper layers Often available OTC Example: nystatin 27 Characteristics of viruses (KP19) Non-living Structurally simple Method of action Enter target cell Use own viral enzymes, and Replicate using structural components of target cell Many are self-limiting Rapid rate of mutation Drugs aimed at viral enzymes 28 Simple pathophysiology of HIV (KP20) Exposure to infected bodily fluids (“introduction”) HIV seeks out T-cell host (“viral attachment”) HIV injects own enzymes into cellular fluid (“viral fusion”) Protective coating of RNA is dissolved (“uncoating”) RNA converts to DNA (“reverse transcription”) New DNA integrates into T-cell nucleus (“integration”) Cells separate into new HIV (“final assembly”) HIV enters circulation, starts over (“budding”) 29 Principles of HIV therapy (KP21) Early treatment will delay progression to AIDS Expensive Long-term treatment may cause resistance Start if AIDS symptoms or when T-cell count is < 200 cells/mcl Monitor viral load (amount HIV RNA in blood) regularly Viral load goal is < 75 copies/ml 30 Postexposure prophylaxis (PEP) after occupational HIV exposure (KP22) If patient is known HIV-positive, start PEP within 24 to 36 hours If HIV status unknown and exposure severe, PEP until patient is tested If long-term treatment required, continue for 4 week period Also monitor for hepatitis, syphilis exposure 31 Principles of Herpes virus pharmacotherapy (KP23) Acquired through direct physical contact HSV resides in nerve ganglia May remain latent for many years Lesions may occur with physical or emotional stress Virus stays with patient for lifetime Shingles vaccine recommended after age 60 (Zostavax) 32 Examples of shingles 33 Principles of influenza pharmacotherapy (KP24) Best approach is prevention—flu vaccine LTC residents Chronic cardiopulmonary disease Children ages 5 years and younger Pregnant women in 2nd and 3rd trimesters Adults over age 65 Health care workers Antivirals should start within 48 hours of symptoms starting Will shorten duration only Are not useful against common cold! 34 Sidebar: cold or flu??? Cold Flu Begins with sore throat More severe, comes on quickly Nasal symptoms follow Sore throat, fever, cough Cough 4th or 5th day Muscle aches and pains, headache Fever uncommon; may be slight May progress to pneumonia 35 Principles of viral hepatitis pharmacotherapy (KP25) Three primary types: A, B, C A spread by oral-fecal route B spread through blood and body fluids C spread through blood and body fluids Best treatment is prevention Hep A and Hep B vaccines are available; not for Hep C Non-A/non-B viruses include hepatitis C, D, E, and G Interferon and antivirals are primary drugs 36