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111 Cards in this Set
- Front
- Back
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Lymphocytes |
-white blood cells -recognize antigens -produce antibodies -kill infected host cells -B cell=> antibodies -T cell=> cytokines
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Phagocytes |
-white blood cells -macrophages and neutrophils -recognize damaged tissues and pathogens -recruit reparative cells -serve as antigen |
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Auxiliary Cells |
-soluble immunoglobin -recognizes and binds to specific antigens -destroy or neutralize antigens (made by B lymphocytes in response to an antigen) -inflammatory mediators -Mast cells: release histamine -Platelets: important for blood clotting |
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Cytokine |
-signaling molecule for communication between inflammatory cells -produced by virally infected macrophages and activated T lymphocytes |
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Interleukins |
-group of specific cytokines -stimulate other cells to divide (reproduce) and differentiate (becomes mature, stable form) -stimulate B-Lymphocytes to differentiate so they can make antibodies |
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Humoral Immunity |
-related to antibodies -T Lymphocyte: release cytokines T helper cells to help B lymphocytes differentiate -IgG antibodies coat bacteria and make them "tasty" to phagocytes |
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Cell-Mediated Immunity |
-involves the direct killing of organisms by defensive cells; usually by phagocytosis -Macrophages kill bacteria -Neutrophils kill bacteria -Natural Killer cells kill virus-infected cells and tumor cells -T Lymphocytes => Cytotoxic T cells (CD8+) attack and destroy infected host cells and tumor cells directly |
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Reactive Oxygen Species |
-activation of phagocytic cell results in activation of=> -Oxidase complex on the cell surface -produces ROS and hydrogen peroxide -toxic products that kill organisms and other cells -oxygen radicals pull electrons from other molecules -can damage DNA or other molecules leading to death of the target |
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Phopholipase A2 |
-activation of phagocytic cell results in activation of this -results in production of: -Prostaglandins: cause a variety of effects on blood vessels, nerves, inflammatory cells, increase sensitivity of pain receptors -Leukotrienes: inflammatory mediators with a variety of effects on other cells- severe retraction of bronchioles in asthma |
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Allergies |
-present as chronic sinusitis, recurrent OM, or itchy ears -B lymphocytes can be induced by T helper cells to release IgE & IgG antibodies (related to allergic reactions) -IgE binds to mast cells in tissues to await next exposure to antigen (need exposure) |
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Histamine |
-intercellular signaling molecule -released from Mast cells in response to antigen binding to cell-bound IgE -binds to Histamine receptors H1 and H2 |
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H1 Receptors |
-mediate allergic reactions -result in: vasodilation, increase in vascular permeability, visceral smooth muscle contraction -antagonists used to treat allergies |
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H2 Receptors |
-increase gastric acid secretion in stomach -antagonists used to treat acid reflux |
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Antihistamines |
-H1 receptor antagonists -anti-cholinergic effects: ethanolamines, piperazines, phenothaizi -sedative effects: ethanolamines, alkyl amines, piperazines. if cross blood brain barrier [decrease conduction though RF- slow vestibular-cerebellar pathway conduction, can be used to treat vertigo] |
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Glucocorticoids |
-aka: glucocorticosteroids, corticosteroids -endogenous anti-inflammatory agent -produced in adrenal cortex, released in response to ACTH -stress hormones => help adapt to perceived stress -chronic use for chronic inflammatory or AID=> Cushing's Syndrome -anti-inflammatory: decrease production of cytokines, increase production of lipocortin, inhibits phospholipase A2 to decrease production of prostaglandins & leukotreienes -anti-bacterial: decrease macrophage bactericidal activity, decrease T & B lymphocyte proliferation |
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Aspirin (ASA) |
-prototypic NSAID -analgesic, anti-pyretic, anti-inflammatory -irreversibly binds to and inhibits COX enzyme -Salycylism toxicity: salicylates enter perilymph by active transport => reversible tinnitus, flat or HF SNHL, loss of SOAEs, decrease cochlear AP -permanent loss associated with renal failure -Salicylate poisoning: respiratory depression, acidosis, death |
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Aspirin Ototoxicity |
-with HIGH doses of ASA -inhibition of COX and decreased prostaglandin production => vasoconstriction and ischemia in stria vascularis => impaired cochlear nerve conduction and altered OHC function |
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Non-Specific Cox Inhibitors |
-inhibits COX1: decrease prostaglandin that protects gastric lining; increase risk of GI bleeding -decrease vasodilatory prostaglandin synthesis in kidney; therefore increased risk of renal damage (due to excessive vasoconstriction) -decreased risk of ototoxicity than with ASA [if occurs, typically reversible] -naproxen (aleve)- not generally reversible |
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Quinines |
-treat drug resistant malaria, heart arrhythmias, rheumatoid arthritis -can cause Cinchonism => mechanism unknown- binds to DNA and inhibits many enzymes- vasoconstriction and ischemia in spiral ligament, stria vascularis, BM, HC => high pitched tinnitus => bilateral flat SNHL => vertigo effects are reversible, but can become permanent with prolonged use
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Cytotoxic Drugs |
-kill most rapidly dividing cells (normal and abnormal cells) -anti-cancer or chronic inflammatory -used in low doses to kill lymphocytes when patient cannot tolerate other drugs -no active reversal agent
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Arteries |
-carry blood away from heart (oxygenated, except pulmonary] -smooth muscles in walls constrict & dilate -SANS sets vasomotor tone via A1 adrenoceptors (A1= constrict, B1= dilate) -muscarinic receptors, but no PANS innervation -sets total peripheral resistance (TPR) |
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Capillaries |
-tiniest blood vessels -link arterioles to venules -site of exchange between blood and tissue |
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Veins |
-carry blood back to the heart [oxygenated except pulmonary] -little smooth muscle in walls constricts and dilates -SANS sets vasomotor tone via A1 adrenoceptors (A1= constrict, B1= dilate) -muscarinic receptors, but no PANS innervation -holds ~50% total blood volume -constriction => significant increase in venous return |
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Left Side of Heart |
-high pressure system [keeps blood moving through system] -oxygenated blood from pulmonary vein enters left atrium -blood from left ventricle goes through aorta to rest of body to deliver O2 & nutrients -deoxygenated blood returns from tissues via the veins through the vena canvas to right atrium |
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Right Side of Heart |
-low pressure system [prevents fluid from entering airway] -deoxygenated blood from vena cavas enters right atrium -deoxygenated blood from right ventricle goes through pulmonary artery to lungs to pick up O2 and release CO2 -oxygenated blood returns via pulmonary veins to left atrium |
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Cardiac Output |
-volume of blood pumped by heart heart per minute -increased by: increased heart rate and increased venous return (provides more blood to pump) |
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Sinoatrial Node (SA) |
-pacemaker -cells undergo spontaneous depolarization -influences by: PANS (muscarinic cholinoceptors) and CN 10 (vagus) & SANS (B1 adrenoceptors) -rate: 70 beats/min -SA propagates signal to AV then to bundle of hiss then splits and propagates flow to both sides equally |
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Atrioentricular Node (AV) |
-potential secondary pacemaker (if necessary) -capable of spontaneous depolarization -conduction influenced by: PANS & SANS -rate: 40-50 beats/min -SA propagates signal to AV then to bundle of hiss then splits and propagates flow to both sides equally |
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Bundle of Hiss |
-conducts action potential down septum of heart to both ventricles -able to spontaneously depolarize -potential last resort pacemaker -rate 30 beats/min -SA propagates signal to AV then to bundle of hiss then splits and propagates flow to both sides equally |
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Perkinje Fibers |
conducts action potential thought ventricles |
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Blood Pressure Regulation- Baroreceptors |
-increase in BP => increase in baroreceptor firing -increase vagal tone => decrease HR -decrease sympathetic tones => decrease cardiac output, decrease TPR
-decrease in BP => decrease in baroreceptor firing -decrease vagal tone => increase heart rate -increase sympathetic tone=> increase cardiac output and TPR |
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Blood Pressure Regulation- PANS & SANS |
-changes in CNS output to heart and blood vessels via SANS and PANS -baroreceptors in carotid sinus => cardiovascular center => PANS & SANS => heart and conduction rates altered -PANS: muscarinic receptors in heart -SANS: B1 in heart, A1 on blood vessels, Nn on adrenal medulla |
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Anemia |
-low O2 carrying capacity of blood -inadequate BP to perfuse and oxygenate brain -due to: 1. blood: inadequate volume 2. heart: inadequate cardiac output 3. blood vessels: inadequate venous return, leads to low |
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Arrhythmia |
-abnormal HR due to abnormal rate or rhythm -due to abnormal impulse generation at SA node or abnormal impulse conduction -treatment: medications to restore normal cardiac rhythm and prevent recurrence- or electrical defribillation, surgery, pacemakers |
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Quindine- Arrythmia |
-K+ & Na+ channel blocker -inhibits spontaneous depolarization & slows cardiac conduction -prevents propagation of spontaneous depolarizations from secondary pacemaker cells -Cinchonism |
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Phenytoin- Arrythmia |
-Na+ channel blocker -inhibits depolarization of cardiac neurons -side effects: ataxia, vertigo, abnormal VNG -can be used as vestibular suppressant at low doses |
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Beta Blockers- Arrythmia |
-propanolol: B1 & 2, affects heart, blood vessels, airway of lungs -metopropol: B1 specific -slow spontaneous depolarization of SA node and slow conduction through AV node |
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Calcium Channel Blockers- Arrythmia |
-Cardiac: slow spontaneous depolarization of SA node, slow AV conduction & conduction through other neurons of heart, decrease strength of contractions of cardiac muscle -Vascular: vasodilation of coronary arteries to increase blood to heart. vasodilation of peripheral vessels to decrease TPR. results in decrease workload for heart- decrease BP. can cause dizziness |
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Angina |
-cardiac pain due to decrease blood flow & inadequate O2 supply to heart muscle -caused by plaque or small clot on vessel wall -treatment: aspirin, platelet aggregation inhibitors, Ca2+ channel blockers, Beta blockers |
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Congestive Heart Failure |
-impaired cardiac function & reduced tolerance for exercise -chronic weakness, fatigue, unexplained syncope -causes: ischemic heart disease, hypertension, valvular disease, cardiomyopathy -3 to 4 drug classes for each stage of disease |
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Diuretics- CHF |
-excretion of excess fluid volume to reduce workload of heart |
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Nitrovasodilators- CHF |
-acts directly on vascular smooth muscle to cause dilation -may cause dizziness due to decreased venous return & decreased cardiac output |
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Digoxin-CHF |
-cardiac glycoside -increases strength of myocardial contraction -increase in vagal firing => slow heart rate and causes dizziness, fatigue, bradycardia |
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ACE Inhibitors- CHF |
-decrease level of angiotensin II & aldosterone -less Na+ and water reabsorbed -reduced blood flow -decrease vasoconstriction -decreased TPR & venous return -decreased workload for heart -X pril |
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Combination Diuretics- CHF |
-lasix or thiazide + alderstone -K+ sparing
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Hypertension |
-elevated blood pressure -associated with organ damage -typically cause cannot be identified -may be due to: increased cardiac output, peripheral resistance, blood volume (or combo) -diuretics= 1st drug of choice -adrenergic blockers=2nd drug of choice -all drugs reduce cardiac output- therefore share similar side effects [orthostatic hypotension, dizziness, lightheadedness] |
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Alpha Adrenergic Blockers- Hypertension |
-beta: acts to decrease heart rate => decrease cardiac output and decreases renin release from kidney to decrease angiotensin 2 production
-alpha (not used frequently due to side effects- orthostatic hypertension, syncope, dizziness): block A1 receptors on arteries and veins so they don't constrict with SANS stimulation. decrease TPR to decrease cardiac output |
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Ca2+ Channel Blockers- Hypertension |
-decrease SA node firing rate, decrease AV conduction, decrease strength of myocardial contraction => decreases cardiac output & systolic BP -promotes vasodilation to decrease TPR, diastolic BP, and venous return => decreased cardiac output |
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Vasodilators- Hypertension |
-dilate blood vessels -decrease diastolic BP & venous return -decreases cardiac output |
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Ace Inhibitors- Hypertension |
-inhibit production of angiotensin 2 & alderosterone release -reduces Na+ & fluid in the body due to increased renal excretion therefore decrease blood volume -reduces vasoconstriction from angiotensin 2 therefore reduces venous return & cardiac output |
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Kidney Functions |
-excretion of nitrogenous waste products & most drugs [either unaltered or after processed by kidney] -regulation of extracellular fluid volume -regulation of electrolyte concentrations -regulation of blood pH |
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Ultrafiltrate |
-blood is filtered at glomulus -ultrafiltrate (similar to plasma w/o proteins) is formed at glomerulus -ultrafiltrate is modified along nephron => absorption => secretion -final adjustment of content & concentration in ultrafiltrate is made at collecting ducts |
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Transport Mechanisms |
-Simple Diffusion: uses electro-chemical gradient of molecule for transport -Facilitated Diffusion: uses saturable channels or carriers. substances travel down concentration gradient -Active Transport: process is powered by ATP |
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Diuretics |
-increase renal excretion of Na+ & water -different groups have different mechanisms for producing diuresis => most act by decreasing reabsorption of Na+ from the ultrafiltrate => increase water excretion -some are ototoxic or facilitate development of ototoxicity -can be used to treat Meniere's Disease |
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Osmotic Diuretics |
-increase osmotic pressure for water in the lumen along the length of the tubule -water is not reabsorbed, so it is excreted -system adjusts easily, may not be effective after 1-2 uses -not used often because leads to dehydration of other tissues |
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Carbonic Anhydrase Inhibitors |
-inhibit carbonic anhydrase intracellularly -block Na+ & HCO-3 reabsorption in proximal convoluted tubule- increased Na+& water are excreted -inhibit H+ secretion at collecting duct -less effective than loop -used for: glaucoma, altitude sickness
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Loop Diuretics |
-block Na+ reabsorption from thick ascending limb of Loop of Henle [block sodium reabsorption, Na+ will be in urine,water will follow] -blocks Na+/K+/2Cl- cotransporter in Loop of Henle therefore more Na+, Cl-, H20, K+, H+ are excreted -adverse effects: nephrotoxicity, ototoxicity |
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Thiazide Diuretics |
-block Na+ reabsorption from early distal convoluted tubule => water follows -inhibits Na+/Cl- cotransporter -used for hypertension, Meniere's -can cause vertigo/dizziness -can increase risk of ototoxicity from other drugs [increase concentration of drug in IE] |
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Potassium Sparing Diuretics |
-some are aldosterone antagonists -some block lumen Na+ channels in distal convoluted tubule & collecting duct -block Na+ reabsorption, do not increase K+ excretion |
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Ototoxicity of Loop Diuretics |
-flat bilateral HL, tinnitus, rarely vertigo due to decrease in 8th nerve action potentials -reversible if low doses -permanent if high doses, rapid IV injection, administered with other ototoxic drugs -high risks: patients with renal failure, neonates *Edecrin most ototoxic, Loop 2nd -mechanism: fluid accumulation in stria vascularis, Na+ levels increase in endolymph. Na+/K+/2Cl- cotransporter in basolateral membrane of the strial marginal cells => impaired K+ secretion |
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Excretion of Loop Diuretics |
-Furosemide/Lasix: active secretion in proximal convoluted tubule kidney=> toxic in renal failure -Bumentanide/Torsemide: liver metabolism=> less toxic in RF -synergistic effect=> not predictable |
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Neoplasm |
-Abnormally growing group of cells- benign or malignant -usually genetic predisposition, extrinsic factors may initiate cancer growth -cancerous cells divide at normal rate, but do not die normally (immortalized) -metastasize via extension into surrounding tissue or by distribution through lymph or blood stream |
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Cell Cycle |
-Go Phase: resting stage, most adult differentiated cells found here -S Phase: DNA synthesis occurs here, 2 strands of DNA molecules replicate -M Phase: mitosis occurs, cell divides into 2 daughter cells -transcription: DNA to mRNA -translation: mRNA to protein -tightly regulated process, reparative enzymes correct errors |
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Cell Death |
1. Necrosis: due to severe cell stress or damage 2. Programmed Cell Death: due to molecular events pre-programmed to genes or molecular machinery 3. Apoptosis: due to induction of cascade of events that activate executioner proteases => caspases => leads to destruction of survival proteins |
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Apoptosis Pathways |
1. Mitochondrial: increase mitochondrial permeability & destruction. activated by radiation, chemotherapy drugs, oxidative stress, DNA damage, increase intracellular & mitochondrial Ca2+ levels 2. Death Receptor: uses membrane receptors related to tumor necrosis receptor family, activated by ligands |
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Oxidants |
-remove electrons from other molecules -generate ROS can induce apoptosis due to 1. damage to lipids, proteins, DNA 2. increase intracellular Ca2+ levels 3. decrease ATP production 4. induction of mitochondrial apoptotic path |
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Anti-Oxidants |
-reducing agents or electron donors -GSH is a normal intracellular antioxidant -nitric oxide synthetase makes nitric oxide an antioxidant => nitric oxide reacts with ROS it can produce reactive nitrogen species => very damaging |
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Antineoplastic Agents |
-designed to block or interfere with various phases of DNA replication, transcription, translation -disruption process results in failure of the cell to replicate correctly in the future or failure to thrive |
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Alkylating Agents |
*most ototoxic -act by causing oxidative damage to DNA -results in cross linking of DNA strands => DNA strands become unreadable to the enzymes involved in replication -calls most effected are rapidly reproducing cells (cancer, bone marrow, GI tract) |
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Cisplatin |
*most ototoxic -platinum based oxidizing agent -inactivated by blood proteins & covalent bonding to sulfhydryl group in glutathione -excreted by kidneys -adverse effects: nephrotoxicity, myleosuppression, decrease RBC, WBC, platelets, peripheral neuropathy, nausea, vomiting, ototoxicity, tinnitus |
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Cisplatin Ototoxicity |
-induced auditory sensory cell apoptosis -via induction of mitochondrial apoptotic pathway -due to free radical generation from lipid peroxidation -use antioxidants to protect hair cells=> prevents oxidative damage, but may reduce effectiveness of cisplatin as a chemotherapy agent -vestibulotoxicity is rare & cause unclear |
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Carboplatin |
-same anti tumor activity as cisplatin -less toxic to kidneys [less vomiting] -myleosuppressive -ototoxic: due to ROS & reactive nitrogen species
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Cyclophosphamide |
-ototoxic at high doses & in high risk patients -LF SNHL -may be used as an anti-inflammatory in rheumatoid arthritis or AIED |
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Tubulin Binding Agents |
-microtubules= structural proteins composed of tubular -critical for alignment & separation of chromosomes during replication -Vinca Alkaloids: disrupt microtubule function, therefore chromosome distribution to daughter cells becomes random 1. Vincristine: damage to HC & ganglion neurons [high dose may increase cisplatin toxicity] 2. Vinblastine: damage to HC only |
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Antibiotics |
-agent produced by one microorganism that suppresses the growth of other microorganisms -ideally selective toxicity=> interferes with vital function of bacterium w/o affecting host cells -targets unique characteristics of bacteria -must be effective against infecting bacteria 1. Broad- many species 2. Narrow- few species |
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Bactericidal |
-agent that kills bacteria -rate and extent of bactericidal activity increases with increasing drug concentration above MBC up to PAE |
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Bacteriostatic |
Agent that inhibits the growth of bacteria, but does not kill them |
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Minimum Inhibitory Concentration |
-minimum concentration of a drug that prevents visible bacterial growth |
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Minimum Bactericidal Concentration |
-minimum concentration to reduce bacterial count by ≥99.9% |
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Post Antibiotic Effect |
-the persistent suppression of bacterial growth after exposure to antimicrobial agent [after agent has been removed] |
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Antibiotic Resistance |
-due to a mutation in the bacteria's DNA 1.Innate: intrinsic resistance to an antibiotic due to natural characteristics of the bacterium 2. Acquired: resistance due to the acquisition of a gene that changes the bacterium so it becomes resistant to the antibiotic -mechanisms: reduced membrane permeability, production of enzymes that alter the structure of the antibiotic, alteration of drug target site on the bacterium |
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Cell Wall Synthesis Inhibitors |
-bactericidal -inhibit the synthesis of the bacterial cell wall -time dependent killing -high therapeutic index (safe) -Glycopeptide=> Vancomycin gram+ bacteria ototoxicity reversible potentiates ototoxic effects of other drugs mechanism unknown
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Disruptors of Cell Membrane Function |
-bactericidal -usually used topically -very toxic -aerobic gram- bacilli |
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Inhibitors of Bacterial Protein Synthesis |
-bacteriostatic -inhibit protein synthesis in bacteria mostly, but also host -act at various sites for mRNA translation *Macrolides: erythromycin ototoxicity: usually reversible, tinnitus,flat SNHL, vertigo- mechanism unknown [increased risk with high doses] |
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Aminoglycosides |
-bactericidal -gram- -require oxygen dependent transporter to enter bacterium -resistance due to: alteration of O2 dependent transporter, production of aminoglycoside modifying enzymes -not metabolized by liver => excreted unchanged by kidneys -adverse effectes [correlated to duration of exposure]: nephrotoxicity (reversible) & ototoxicity (all except nebulized) |
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Aminoglycoside- Cochleotoxicity |
if pt is given for 7-10 days => strong likelihood of ototoxicity
1. Kanamycin 2. Neomycin [used to treat OE] 3. Amikacin 4. Tobramycin [eye drops]
average t1/2 for perilymph 10-15 hours (2-3 for blood) |
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Aminoglycoside- Vestibulotoxicity |
1. Streptomycin: rarely used clinically, except TB 2. Gentamycin: may be used in Meniere's to cause unilateral vestibularablation (injected)
damage to dark cells of crista ampullaris, Type 1 HC, Type 2 HC |
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Aminoglycoside- Ototoxicity Mechanisms |
-NMDA over activation=> excitotoxic damage -formation of ROS -apoptotic & necrotic cell death -ROS generation causes damage to mitochondrial membranes causing increased permeability 1. membrane ruptures- necrosis 2. membrane severely damaged- apoptosis |
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Tetracyclines |
-bacteriostatic -act inside cells to prevent from making required proteins -gram -/+ -resistance due to alteration in transporter -ototoxicity uncommon -vestibulotoxicity reversible |
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Inhibitors of Bacterial DNA Synthesis |
-bactericidal synthetic antibiotics -inhibit replication of bacterial DNA -gram -
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Inhibitors of Bacterial RNA Synthesis |
-inhibit transcription of DNA into RNA by targeting specific RNA polymerase -Rifamycin for TB, not ototoxic |
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Antifolates |
folates are required to make DNA [purines= subunits of DNA] |
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Streptococcus Pneumoniae |
-normally found in nasopharynx -causative agent: meningitis, OM [>1/3 cases of acute OM & sinusitis], sinusitis -gram + -Penicillin V or Amoxicillin <20% infections will resolve w/o treatment
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Haemophilus Influenzae |
-normally found in oropharynx -gram - -capsulated (epiglottis, pneumonia, meningitis) or non-capsulated (w/ obstruction of eustachian tubes- pathogens of OM & sinusitis) -50% will resolve w/o treatment |
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Moraxella Catarrhalis |
-normally in nasopharynx -gram- -causative agent: laryngitis, bronchitis, pneumonia, meningitis -w/ obstruction of eustachian tube- pathogen of OM & sinusitis -70% will resolve w/o treatment |
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Acute OM |
-initial treatment: Amoxicillan -for penicillian allergic: erythromycin & clindamycin |
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Psedomonas Species |
-gram - -frequent ineffective agent in OE -antibiotic resistant |
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Proteus Species |
-gram- -frequent ineffective agent in OE -antibiotic resistant |
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Staphylococcus Aureus |
-gram + -frequent ineffective agent in OE -some strains are resistant to methicillin & vancomycin -community acquired MRSA |
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Viruses |
-parasites- can infect any organ -need a host to live/for replication -typically virus & host's response are asymptomatic & self-limiting
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Viral Infection |
-duration & severity range/ symptoms depend on host's response -not susceptible to antibiotics -develop resistance to anti-viral drugs due to nucleotide mutations- change in drug's binding site on the Viron -DNA Genome: incorporates DNA into chromosomal DNA of host & forces to replicate -RNA Genome: enzymes make proviral DNA copy of RNA & replicates outside of hist's nucleus |
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Vaccines |
-flu, hep, HPV [virustatic only- host must be immunocompetent] -contains attenuated/dead copies of Virons -given to activate host immune system=> makes antibodies=> produces B lymphocyte memory cells *viruses often mutate rapidly |
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Eustachian Tube |
-opening of eustachian be in lateral nasopharynx -diseases affecting nose & oral pharynx can effect ME |
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Rhinitis |
-acute or chronic inflammation of nasal mucosa -usually due to viral infection or IgE mediated allergic response [viral infection: stimulates inflammatory response in mucus membranes] [IgE bound to mast cells in tissues] |
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Rhinorrhea |
-excessive production of watery nasal secretions, often symptom of rhinitis -usually due to viral infection or IgE mediated allergic response [viral infection: stimulates inflammatory response in mucus membranes] [IgE bound to mast cells in tissues] |
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Inflammation of Nasal Passages |
-Virons: defensive inflammatory response -Allergens: bind to IgE already bound on mass cells in tissues -Trauma: defensive inflammatory response due to tissue damage |
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Pharyngitis |
-sore throat -cause: streptococcal -treatment: 1. Penicillins 2. Erthomycin (macrolide) |
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Sinusitis |
-infection of sinuses -cause: streptococcous, pneumonaie, H. influenzae, moraxella, carrhallis, gram- -treatment: penicillin |
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Fungi |
-opportunistic infective organisms -site dependent & altered by host's immune system -pathogenicity results from 1. mycotoxin production 2. allergenicity involving IgE 3. tissue invasion |
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Otomycosis |
-fungal infection of EAC -infecting fungi: candida albicans, aspergillus higer -not affected by antibacterial or antiviral drugs *host immune system fights if not immunocompromised |
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Anti-Fungal Drugs |
-fungicidal: kill fungi w/o help from host -Polyene Macrolides: act at cell membrane, destroy directly [Amphotericin] -Imidazoles & Triazoles: inhibit cytochrome P-450, blocks synthesis necessary for membrane development/maintenance => prevents synthesis -5-fluctyosine: nucleic acid synthesis, not effective alone |
