Term
|
Definition
| a change in a cell's structure or function |
|
|
Term
|
Definition
| study of disease, its cause and development |
|
|
Term
| What is the path of pathology? |
|
Definition
| cause/etiology - pathogenesis (cell change - body's response) - signs/symptoms - outcome |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What are the 2 parts of pathogenesis? |
|
Definition
| cell change, body's response |
|
|
Term
| What is the pathology of a torn ligament? |
|
Definition
| trauma - cells die - acute inflammation/repair - pain, red, swelling - resolve |
|
|
Term
| What is the pathology of acne? |
|
Definition
| bacteria - cells die - acute inflammation/repair - pain, red, swelling - resolve |
|
|
Term
| How many etiologies are there? |
|
Definition
|
|
Term
| How many pathogenic reponses are there? |
|
Definition
|
|
Term
| How many diseases are there? |
|
Definition
|
|
Term
| List some etiologies and their meanings |
|
Definition
| physical mechanisms, aging, idiopathic, nutritional factors, genetic factors, immunologic reactions, infectious agents, chemical agents, hypoxia, ischemia |
|
|
Term
| List body responses to non-lethal cell injury and stress |
|
Definition
| cell adaptation, edema, neoplasia, repair, acute inflammation, chronic inflammation, thrombosis, hemorrhage |
|
|
Term
| List and describe common non-lethal cellular responses to injury and stress |
|
Definition
| atrophy (reduction in cell size due to loss of intracellular organelles from decreased activity = physiologic or denervation = pathogenic), hypertrophy (increase in cell size), hyperplasia (increase in number of cells), metaplasia (change from one mature cell type to another) |
|
|
Term
| What is a body response to a lethal cell injury? |
|
Definition
|
|
Term
| What 4 cell systmes are especially vulnerable to injury? |
|
Definition
| genetic material/nucleus, cell membrane for permeability, mitochondria for ATP, protein makers like golgi and rough endoplasmic reticulum |
|
|
Term
| What are the common biochemical mechanisms of cell injury? |
|
Definition
| loss of atp: cells can't do what they need to do (ex. Na pump is broken and na comes in with water, causing cell to swell) |
|
|
Term
| How do different cell types respond to pathogenesis? |
|
Definition
| metabolically active cells like neurons and heart cells are damaged first bc they need lots of atp |
|
|
Term
| When is cell injury irreversible? |
|
Definition
|
|
Term
| What are the 2 types of cell death? |
|
Definition
|
|
Term
|
Definition
| cell death caused by exogenous source; visible |
|
|
Term
| What are the types of necrosis? |
|
Definition
| coagulative, liquifactive, caseous, fat |
|
|
Term
| What is coagulative necrosis? |
|
Definition
| nucleus condenses (pyknosis), karyhorrexis, occurs from hypoxia, cell coagulates |
|
|
Term
| What is liquifactive necrosis? |
|
Definition
| occurs when lytic enzymes destroy forming pus in acute finflammation |
|
|
Term
| What is caseous necrosis? |
|
Definition
|
|
Term
|
Definition
| nucleus condenses and becomes darker |
|
|
Term
|
Definition
| cell membrane splits cell into bite sized pieces |
|
|
Term
|
Definition
|
|
Term
| What are the 4 types of cell adaptations to etiologies? |
|
Definition
| atrophy, hypertrophy, hyperplasia, metaplasia |
|
|
Term
| What are the types of body responses to non-lethal cell stress? |
|
Definition
| cell adaptations, acute inflammation, chronic inflammation, repair, edema, hemorrhage, thrombosis, neoplasia, necrosis |
|
|
Term
| What is the definition of inflammation? |
|
Definition
| automatic, steroptyed responses of living tissue to all forms of injury. Localized, protective response of body to foreign invasion and to cellular injury; designed to destory and and remove both the injurious agent and the injured tissue. Activates the subsequent healing and repair |
|
|
Term
| What is the difference between acute and chronic inflammation |
|
Definition
| acute = abrupt onset and short duration; chronic = slow onset and longer duration |
|
|
Term
| How is inflammation beneficial? |
|
Definition
| by preventing or limiting disease |
|
|
Term
| How is inflammation harmful? |
|
Definition
| can cause cell injury or disease |
|
|
Term
| What is the suffix for inflammatory diseases? |
|
Definition
|
|
Term
| What are the 4 types of inflammatory cells? |
|
Definition
| neutrophils, macrophages, lymphocytes, and mast cells |
|
|
Term
|
Definition
| chunked, segmented, lobed nucleus |
|
|
Term
|
Definition
|
|
Term
|
Definition
| small with big, dark nucleus |
|
|
Term
| what are the major characteristics of acute inflammation? |
|
Definition
| early response to injury/invasion, rapid onset (minutes to hours), resolves quickly (hours to days) |
|
|
Term
| what cells are involved in acute inflammation? |
|
Definition
|
|
Term
| what etiologies lead to acute inflammation? |
|
Definition
| infections, physical, necrosis, immune |
|
|
Term
| what are the signs/symptoms of acute inflammation |
|
Definition
| redness, pain, swelling, heat |
|
|
Term
| what are the outcomes of acute inflammation? |
|
Definition
| resolve to normal, abscess, chronic inflammation, repair |
|
|
Term
| what are the steps of pathogenesis of acute inflammation? |
|
Definition
| injury occurs, macrophage discovers injury and sends out chemical mediators, chemical mediators cause vasodilation and increase in blood flow, chemical mediators increase blood vessel permeability to release water from blood vessel, chemical mediators recruit neutrophils, chemical mediators recruit more macrophages, the etiology is destroyed by phagocytosis (the release of lytic enzymes) |
|
|
Term
| which mediators are released by macrophages to increase vasodilation? |
|
Definition
| histamine, prostaglandins |
|
|
Term
| what signs/symptoms are caused by the vasodilation of blood vessels? |
|
Definition
|
|
Term
| what mediator is released by macrophage to increase blood vessel permeability? |
|
Definition
|
|
Term
| what signs/symptoms are caused by the increase in permeability of blood vessels? |
|
Definition
| plasma fluid transudate and edema (swelling, pain) |
|
|
Term
| what mediator is released by macrophages to recruit neutrophils? |
|
Definition
|
|
Term
| how do neutrophils arrive at the area of injury? |
|
Definition
|
|
Term
| what is the result of neutrophils in an area of injury? |
|
Definition
|
|
Term
| what mediators cause phagocytosis? |
|
Definition
|
|
Term
| where are chemical mediators synthesized? |
|
Definition
| a variety of cells such as leukocytes, blood vessels, liver, etc. |
|
|
Term
| when mediators act locally, what are the signs and symptoms? |
|
Definition
| reness, pain, heat, swelling |
|
|
Term
| when mediators act systemically on the brain, what are the signs and symptoms? |
|
Definition
| fever, lethargy, loss of appetite |
|
|
Term
|
Definition
|
|
Term
|
Definition
| vasodilation, increased permeability |
|
|
Term
|
Definition
|
|
Term
|
Definition
| many molecules, many roles |
|
|
Term
|
Definition
| pain, fever, vasodilation |
|
|
Term
|
Definition
| increased permeability, chemotaxis |
|
|
Term
|
Definition
| fever, lethargy, loss of appetite |
|
|
Term
|
Definition
| fever, lethargy, loss of appetite |
|
|
Term
|
Definition
| kill microbes, damage neighborhood |
|
|
Term
|
Definition
| non-steroidal anti-inflammatory drugs |
|
|
Term
| what are the 4 effects of NSAIDS? |
|
Definition
| anti-inflammatory, anti pyretic (fever reducers), analgesic, anti-coaculation |
|
|
Term
| What are some NCSAIDS that are nonselective COX inhibitors? |
|
Definition
| aspirin, iburofen, indomethacin, naproxen |
|
|
Term
| what are some NSAIDS that are selective COX2 inhibitors? |
|
Definition
|
|
Term
| what are the 2 normal metabolic pathways for prostaglandin synthesis? |
|
Definition
| cyclooxygenase 1 for synthesis of beneficial prostaglandins and cyclooxygenase 2 for synthesis of inflammatory prostaglandins |
|
|
Term
| what is the mechanism of action of NSAIDS? |
|
Definition
| inhibit production of prostaglandins by inhibiting cycoloxygenase |
|
|
Term
| what do nonselective inhbitors inhibit? |
|
Definition
| both cyclooxygenase 1 and 2, so both beneficial and inflammatory prostaglandins |
|
|
Term
| what do selective inhibitors inhibit? |
|
Definition
| only cyclooxygenase 2 so only inflammatory prostaglandins |
|
|
Term
| what are the adverse effects of nonselective inhibitors? |
|
Definition
| stomac lining damage, slows bone healing |
|
|
Term
| what are the adverse effects of selective inhibitors? |
|
Definition
| promotes thrombosis (clotting) |
|
|
Term
| what is an example of a health cell that makes beneficial prostaglandin? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| how is neutrophilia determined |
|
Definition
| complete blood count that shows increase of neutrophils in blood |
|
|
Term
|
Definition
| colleciton of neutrophils that the body walls off and leaves alone |
|
|
Term
| the body is under constant threat of what? |
|
Definition
| invasion by foreign materials/nonself/antigen |
|
|
Term
| what is the 1st line of defense? |
|
Definition
| antigen-non-specific, innate physical barrier (thick skin, low pH, mucous) |
|
|
Term
| what is the 2nd line of defense? |
|
Definition
| antigen-non-specific, innate acute inflammation |
|
|
Term
| what is the 3rd line of defense? |
|
Definition
| antigen specific immune response like chronic inflammation |
|
|
Term
| What are some of the body's responses to an etiology? |
|
Definition
| cell adaptations, acute inflammation, chronic inflammation, repair, edema, hemorrhage, thrombosis, neoplasia, necrosis |
|
|
Term
|
Definition
| automatic, steroptyped responses of living tissue to all forms of injury. Localized, protective response of body to foreign invasion and to cellular injury; designed to destroy and remove both the injurious agent and the injured tisue. Activates subsequent healing and repair. |
|
|
Term
| Acute inflammation is the body's which line of defense? |
|
Definition
|
|
Term
| Chronic inflammation is the body's what line of defense? |
|
Definition
|
|
Term
| how is inflammation beneficial? |
|
Definition
|
|
Term
| how is inflammation harmful? |
|
Definition
| can cause cell injury/disease |
|
|
Term
| suffix of inflammatory diseases |
|
Definition
|
|
Term
| what are inflammatory cells? |
|
Definition
| white blood cells/leukocytes = neutrophils, macrophages, lymphocytes, mast cells |
|
|
Term
| characteristics of chronic inflammation |
|
Definition
| slow, later onset (takes days, like TB test) |
|
|
Term
| what cells are inolved in chronic inflammation? |
|
Definition
|
|
Term
| characteristics of lymphocytes |
|
Definition
| mononuclear, large nucleus |
|
|
Term
| when does chronic inflammation occur? |
|
Definition
| after acute inflammation or directly after an etiology |
|
|
Term
| what etiologies cause the body to respond with chronic inflammation? |
|
Definition
| agent is in a cell: infection (virus) |
|
|
Term
| what are signs/symptoms of chronic inflammation? |
|
Definition
| pain, fever, sleepiness, lack of appetite, muscle pain, redness, others |
|
|
Term
|
Definition
|
|
Term
| what are the possible outcomes of chronic inflammation |
|
Definition
| resolve, continue, repair |
|
|
Term
| what are the events of pathogenesis of chronic inflammation? |
|
Definition
|
|
Term
|
Definition
| accumulation of macrophages |
|
|
Term
| what etiologies lead to granulomas? |
|
Definition
| inedible etiologies like sutures, talk, silicon; TB; some fungi; sarcoidosis |
|
|
Term
|
Definition
| mediators of chronic inflammation |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| fever, lethargy, loss of appetite; induce prostaglandin synthesis |
|
|
Term
|
Definition
| fever, lethargy, loss of appetite; induce prostaglandin synthesis |
|
|
Term
|
Definition
| many molecules, many roles |
|
|
Term
|
Definition
| pain, fever, vasodilation |
|
|
Term
|
Definition
| increase permeability, chemotaxis |
|
|
Term
|
Definition
|
|
Term
|
Definition
| kill microbes, damage neighborhood |
|
|
Term
| what does anti-inflammatory pharmacology try to do? |
|
Definition
|
|
Term
| what are glucocorticoids? |
|
Definition
| a family of homrones produced naturally in the adrenal gland |
|
|
Term
| what is the primary family member of glucocorticoids? |
|
Definition
| cortisol = hydrocortisone = prednisone |
|
|
Term
| what are natural levels of glucocorticoids like? |
|
Definition
| vary throughout day, peak at 8am, trough at midnight; levels increase above baseline with any type of stress |
|
|
Term
| what do medicinal glucocorticoids mimic? |
|
Definition
|
|
Term
| what is the anti-inflammatory mechanism of action of hormones and drugs? |
|
Definition
| enters cell and turns genes on or off |
|
|
Term
| what is the effect of anti-inflammatory drugs? |
|
Definition
| suppress acute and chronic inflammation and consequently suppress the immune system |
|
|
Term
| examples of medical uses of glucocortoids |
|
Definition
| halt allergic, autoimmune, osteoarthritis ctiondiaseses and prevent transplant re |
|
|
Term
| do anti-inflammatory drugs cure diseases or treat symptoms? |
|
Definition
|
|
Term
| adverse effects of glucocortocoids |
|
Definition
| adrenal gland stops producing cortisol (must taper off drug to return to normal cortisol production) |
|
|
Term
| why does cushing syndrome occur? |
|
Definition
| too much cortisol, causes catabolic effects on muscle, tendon, ligaments, bone, skin |
|
|
Term
| how does a complete blood count indicate chronic inflammatoin |
|
Definition
| increased lymphocytes in blood (lymphocytosis) from increased lymphocyte recruitment |
|
|
Term
| examples of chronic inflammatory diseases |
|
Definition
|
|
Term
| good use of chronic inflammation |
|
Definition
|
|
Term
| negative use of chronic inflammation |
|
Definition
| results in transplant rejection |
|
|
Term
|
Definition
|
|
Term
| why doesn't AIDS cause a chronic inflammatory response? |
|
Definition
| macrophages and lymphocytes are not available to respond |
|
|
Term
|
Definition
| make people more sucscepitble to virus infections, cancer, fungi |
|
|
Term
|
Definition
| the study of drugs, their mechanism of action, absorption, distribution, metabolism, effectiveness and compare to effectiveness of other dugs, toxicology, side effects, economics |
|
|
Term
| what are the goals of drug therapy? |
|
Definition
| relief of symptoms, quality of life, prevent symptoms of disease, reverse or delay pathophysiological effects, decrease side effects, decrease cost |
|
|
Term
| describe relief of symptoms as goal of drug therapy |
|
Definition
| get rid of headache, osteoarthritis pain, anxiety |
|
|
Term
| describe quality of life as goal of drug therapy |
|
Definition
| sleeping pilss, rest from anxiety, analgesics |
|
|
Term
| how does drug therapy prevent symptoms of disease |
|
Definition
| decrease blood pressure, heart disease, cholesterol, insulin |
|
|
Term
| how does drug therapy reverse or delay pathophysiological effects |
|
Definition
| cholesterol lowering meds reduce atherosclerosis which over time reduces riskof heart atack |
|
|
Term
| what are the steps of using drug therapy to accomplish PT consult |
|
Definition
| 1. swallow pill; 2. med disintegrates in GI tract and dissolves with help of GI acid; 3. med is absorbed from small intestine to capillaries of GI tract; 4. everything that leaves GI tract goes next to liver where it is broken down; 5. med goes into general circulation; 6. goes to site ofinterest; 7. finds receptor site of action; 8. increase range of motion in PT consult |
|
|
Term
| in taking a pill orally, which part goes slowly and which part goes quickly? |
|
Definition
| takes a longer time to get into circulation (disintegration, absorption, breakdown in liver); goes quickly to receptor site after getting into circulation |
|
|
Term
|
Definition
| fits with drug like lock and key, in order for a drug to work it has to find its relative site of action |
|
|
Term
| what is a median effective dose |
|
Definition
| the does where 50% of people have not yet felt effects of drug but 50% have |
|
|
Term
| what is the median toxic dose |
|
Definition
| dose where 50% of people have not felt drug's toxicity but 50% have |
|
|
Term
| what is the therapeutic index? |
|
Definition
| median toxic dose/median effective dose |
|
|
Term
| do we want therapeutic index to be large or small? |
|
Definition
|
|
Term
| which has higher therapeutic index, OTC or RX drugs? |
|
Definition
|
|
Term
|
Definition
| causes measurable effect; provokes cellular/enzymatic change |
|
|
Term
|
Definition
| can block unintended pharmacological effect of agonist |
|
|
Term
| why do we have to repeat doses? |
|
Definition
| drugs bind to receptors transiently and then float away |
|
|
Term
|
Definition
|
|
Term
| describe how prilosec works |
|
Definition
| blocks/antagonizes receptor without causing cellular change; diminishes effect on stomach lining by NSAIDS |
|
|
Term
|
Definition
| antihistamines, which lock H1 receptors to reduce inflammation |
|
|
Term
|
Definition
| small population (less than 50), identify rational doses, usually done in normal volunteers in order to understand toxicology |
|
|
Term
|
Definition
| disease is present in volunteers, 50-200 people |
|
|
Term
|
Definition
| thousands of people, finally get drug approved after 2 randomized clinical trials, severe side effects emerge |
|
|
Term
| what factors can make a difference in individual responses to drugs? (ie why would one person achieve full range of motion with 100mg ibuprofen while another achieves full range of motion at 400mg?) |
|
Definition
| 1. drug interaction: could be taking a 2nd drug that antagonizes ibuprofen (can overcome this by increasing dose of ibuprofen), 2. First Pass: liver may metabolize more ibuprofen because there are more active sites/enzymes in liver cells, 3. there may be oral absorption differences in the two patients (take the drug by iv to reduce this effect), 4. characteristics such as age, volume, activity level |
|
|
Term
| in a blood/serum concentration vs. time after does graph, what do we call the increase in concentration side of the curve? |
|
Definition
|
|
Term
| in the graph, what do we call the decrease in blood concentration? |
|
Definition
|
|
Term
| what do we call the time between absoprtion phase and elimination phase? |
|
Definition
|
|
Term
| what is done to turn a blood concentration specimen into serum fluid? |
|
Definition
|
|
Term
| what do we call the highest concentration on the serum conc vs. time after does graph? |
|
Definition
|
|
Term
| which will be higher, Cmax for IV drugs or Cmax for oral drugs? |
|
Definition
|
|
Term
| what other changes do we see in a conc vs. time graph for IV instead of PO? |
|
Definition
| With IV, absorption phase is faster and curve goes higher. Elimination phase looks the same whether drug is given PO or IV |
|
|
Term
| what is the time at which Cmax happens? |
|
Definition
|
|
Term
| how is Tmax different for IV from PO? |
|
Definition
| Tmax is faster for IV than for PO |
|
|
Term
| why is Cmax for PO lower than Cmax for IV |
|
Definition
| loss of drug to liver with PO (first pass.) all oral drugs pass through liver first, but only some IV drugs pass through liver |
|
|
Term
| comparing IV to PO concentration shows us what? |
|
Definition
| measurement of absorption/bioavailability for PO |
|
|
Term
| how do we calculate bioavailability for a drug PO? |
|
Definition
| assume bioavailability for IV drug si 100% bc it is injected into bloodstream. Bioavailability = (area under curve for PO)/(area under curve for IV) |
|
|
Term
| what does a PO bioavailability of 10-20% mean? |
|
Definition
| this bioavailability is too low and drug will not be given PO |
|
|
Term
| what kind of information can we get from the measurement of the rate of elimination? |
|
Definition
|
|
Term
| what is a drug's half life? |
|
Definition
| the time it takes the drug concentration to decrease by half |
|
|
Term
| does a drug have the same half life in all people? |
|
Definition
| no, different people have different half lives for the same drug |
|
|
Term
| what happens if we give a 2nd dose to someone whose serum concentration has not yet returned to 0? |
|
Definition
| raises their Cmax (need to watch out for toxicity) |
|
|
Term
| half life is a measurement of what? |
|
Definition
|
|
Term
| what affects molecular elimination of a drug? |
|
Definition
|
|
Term
| where does metabolism of a drug occur? |
|
Definition
| mostly by enzymes in the liver |
|
|
Term
| what does metabolism do to a drug? |
|
Definition
| change the drug molecule (breaks it down and adds oxygen, hydrogen, and glucose-like molecules) |
|
|
Term
| why does changing the molecule affect its drug actions? |
|
Definition
| if the molecule is changed, it may no longer fit with the receptor, making it inactive. Or it can be changed but still work |
|
|
Term
| what do we call metabolized drugs? |
|
Definition
|
|
Term
| metabolites have increased water solubility, which causes what? |
|
Definition
| increased elimination by the kidney (renal filtration and urine excretion increased) |
|
|
Term
| what are the possible outcomes for a metabolite? |
|
Definition
| 1. becomes active or inactive (either way increases water solubility), 2. goes to blood for elimination by kidney or recirculation, 3. goes to bile then liver then GI tract and can possibly return to body |
|
|
Term
| what might affect a person's metabolism? |
|
Definition
| age, renal function (serum creatinine - as creatinine increases, filtration decreases), body size, diabetes, other diseases |
|
|
Term
| what happens to serum concentration if we give regular doses? |
|
Definition
| we get constant peaks and troughs of serum concentration |
|
|
Term
|
Definition
| when time between peaks or troughs is constant |
|
|
Term
| what factors can make a difference in individual responses to drugs? (ie why would one person achieve full range of motion with 100mg ibuprofen while another achieves full range of motion at 400mg?) |
|
Definition
| 1. drug interaction: could be taking a 2nd drug that antagonizes ibuprofen (can overcome this by increasing dose of ibuprofen), 2. First Pass: liver may metabolize more ibuprofen because there are more active sites/enzymes in liver cells, 3. there may be oral absorption differences in the two patients (take the drug by iv to reduce this effect), 4. characteristics such as age, volume, activity level |
|
|
Term
| in a blood/serum concentration vs. time after does graph, what do we call the increase in concentration side of the curve? |
|
Definition
|
|
Term
| in the graph, what do we call the decrease in blood concentration? |
|
Definition
|
|
Term
| what do we call the time between absoprtion phase and elimination phase? |
|
Definition
|
|
Term
| what is done to turn a blood concentration specimen into serum fluid? |
|
Definition
|
|
Term
| what do we call the highest concentration on the serum conc vs. time after does graph? |
|
Definition
|
|
Term
| which will be higher, Cmax for IV drugs or Cmax for oral drugs? |
|
Definition
|
|
Term
| what other changes do we see in a conc vs. time graph for IV instead of PO? |
|
Definition
| With IV, absorption phase is faster and curve goes higher. Elimination phase looks the same whether drug is given PO or IV |
|
|
Term
| what is the time at which Cmax happens? |
|
Definition
|
|
Term
| how is Tmax different for IV from PO? |
|
Definition
| Tmax is faster for IV than for PO |
|
|
Term
| why is Cmax for PO lower than Cmax for IV |
|
Definition
| loss of drug to liver with PO (first pass.) all oral drugs pass through liver first, but only some IV drugs pass through liver |
|
|
Term
| comparing IV to PO concentration shows us what? |
|
Definition
| measurement of absorption/bioavailability for PO |
|
|
Term
| how do we calculate bioavailability for a drug PO? |
|
Definition
| assume bioavailability for IV drug si 100% bc it is injected into bloodstream. Bioavailability = (area under curve for PO)/(area under curve for IV) |
|
|
Term
| what does a PO bioavailability of 10-20% mean? |
|
Definition
| this bioavailability is too low and drug will not be given PO |
|
|
Term
| what kind of information can we get from the measurement of the rate of elimination? |
|
Definition
|
|
Term
| what is a drug's half life? |
|
Definition
| the time it takes the drug concentration to decrease by half |
|
|
Term
| does a drug have the same half life in all people? |
|
Definition
| no, different people have different half lives for the same drug |
|
|
Term
| what happens if we give a 2nd dose to someone whose serum concentration has not yet returned to 0? |
|
Definition
| raises their Cmax (need to watch out for toxicity) |
|
|
Term
| half life is a measurement of what? |
|
Definition
|
|
Term
| what affects molecular elimination of a drug? |
|
Definition
|
|
Term
| where does metabolism of a drug occur? |
|
Definition
| mostly by enzymes in the liver |
|
|
Term
| what does metabolism do to a drug? |
|
Definition
| change the drug molecule (breaks it down and adds oxygen, hydrogen, and glucose-like molecules) |
|
|
Term
| why does changing the molecule affect its drug actions? |
|
Definition
| if the molecule is changed, it may no longer fit with the receptor, making it inactive. Or it can be changed but still work |
|
|
Term
| what do we call metabolized drugs? |
|
Definition
|
|
Term
| metabolites have increased water solubility, which causes what? |
|
Definition
| increased elimination by the kidney (renal filtration and urine excretion increased) |
|
|
Term
| what are the possible outcomes for a metabolite? |
|
Definition
| 1. becomes active or inactive (either way increases water solubility), 2. goes to blood for elimination by kidney or recirculation, 3. goes to bile then liver then GI tract and can possibly return to body |
|
|
Term
| what might affect a person's metabolism? |
|
Definition
| age, renal function (serum creatinine - as creatinine increases, filtration decreases), body size, diabetes, other diseases |
|
|
Term
| what happens to serum concentration if we give regular doses? |
|
Definition
| we get constant peaks and troughs of serum concentration |
|
|
Term
|
Definition
| when time between peaks or troughs is constant |
|
|
Term
| how are immune cells, tissues, and organs like the police/army to prtoect the body from invasion? |
|
Definition
| 1. patrol to detect invasion, 2. recruit and activate immune cells when invasion is detected, 3. destroy the foreign material |
|
|
Term
|
Definition
| foreign material/non-self |
|
|
Term
|
Definition
| antigens which cause disease |
|
|
Term
| what are the 2 major subtypes of chornic inflammation? |
|
Definition
| humoral immune response, cell mediated immune response |
|
|
Term
| what cells are involved in the 3rd line of defense/chronic inflammation? |
|
Definition
| lymphocytes, plasma cells, macrophages, mast cells, eosinophils, basophils |
|
|
Term
| what are the steps of pathogenesis for chornic inflammation? |
|
Definition
| lymphocytes, macrophages release mediators to recruit more cells, activate cells, and destroy etiology |
|
|
Term
| how do our immune cells distinguish between self and nonself cells? |
|
Definition
| self cells all have the same membrane proteins/id tags |
|
|
Term
| what are the two types of self membrane proteins/id tags? |
|
Definition
| major histocompatability complex and human leukocyte antigen |
|
|
Term
| what is the job of macrophages in chronic inflammation |
|
Definition
| coordinator = first one there, lets everyone else know to come here; phagocytic = can kill cells |
|
|
Term
| what types of B lymphocytes do we have? |
|
Definition
| B memory cells for patrolling and plasma cells to make antibodies |
|
|
Term
| once a B lymphocyte is activated, what are its two choices? |
|
Definition
| 1. continue looking like B lymphoctes and leave site to return to patrolling, 2. change appearance and bceome plasma cells that make antibodies to destroy specific antigens |
|
|
Term
| What are the 3 types of T lymphocytes? |
|
Definition
| T memory = patrols, can recognize 1 antigen; T helper = coordinator that releases cytokines (also called CD4); T cytotixic = destroys cells (also called CD8) |
|
|
Term
| what type of antigen causes a humoral-meidated immune response? |
|
Definition
| microorganisms, especially bacteria and viruses |
|
|
Term
| what cells are involved in humarl-mediated immune responses? |
|
Definition
| T helper lymphocytes, B lymphocytes, lasma cells |
|
|
Term
| what are the steps of humoral-mediated immune response? |
|
Definition
| 1. B lymphocyte detects antigen, 2. B lymphocyte sends out cytocines to recruit T Helper, 3. T Helpber sends out cytokines to recruit B lymphocytes and to encourage intital B lymphocyte to undergo mitosis, 3. B lymphocyte turns into plasma B cells, 4. plasma B cells make antibodies, 5. antiobodies tag antigen for destruction |
|
|
Term
| how does the B lymphocte detect an antigen? |
|
Definition
| it has an antibody that is used as a "feeler" to find antigen |
|
|
Term
| what is used to tag the antigen for destruction? |
|
Definition
| antibody = immunoglobulin |
|
|
Term
| what are the 3 types of immunoglobulin that we need to know? |
|
Definition
| IgM = 1st type produced, disappears; IgG = 2nd type produced, remains for years as immunity to antigen (kind of antibody vaccines are designed to produce); IgE used in Type 1 hypersensitivity |
|
|
Term
| which cells are involved in cell-mediated immune response? |
|
Definition
| T Hleper lymphocytes, macrophages, T cytotixic lymphocytes |
|
|
Term
| what are the antigens of cell mediated immune response |
|
Definition
| cells (viruses in our cells, cancer cells, transplanted cells, non-degradable cells) |
|
|
Term
| what are the steps of cell-mediated immune responses? |
|
Definition
| 1. T cytotixic of macrophage identifies antigen cell, 2. T cytotoxic sends out cytockines to recruit T helpers, 3. T helpers send out cytokines to recruit macrphages and T cytotoxic, 4. T cytotoxics and macrophages kill antigen cell |
|
|
Term
| how is the antigen destroyed in cell mediated immunity? |
|
Definition
| T cytotoxics or macrophages form hole in antigen cell membrane causing water to rush in and cell dies OR T cytotoxics and macrophages trigger apoptosis so antigen cell kills itself |
|
|
Term
| what is Type I humoral immunity? |
|
Definition
| hypersensitivity = allergies |
|
|
Term
| describe Type 2 hypersensitivity |
|
Definition
| a humoral immunity I which an antigen is on a cell's surface, an antibody (IgG) binds and tags cell, a complement recognizes the tag/antigen, the complement kills cell by poking holes in cell, or nothing kills cell and the antigne sits there blocking the cell's function |
|
|
Term
| what is another name for Type 1 Hypersensitivity? |
|
Definition
|
|
Term
| What is another name for Type 2 Hypersensitivity? |
|
Definition
| Cytotixic reactions to Ag |
|
|
Term
| What is another name for Type III Hypersensitivity? |
|
Definition
|
|
Term
| What are some diseases caused by Type I hypersensitivity |
|
Definition
| allergies, hayfever, asthma, anaphylaxis |
|
|
Term
| what are some diseases caused by Type II hypersensitivity |
|
Definition
| myesthenia gravis, transfusion reaction, graft rejection, kill tumors |
|
|
Term
| describe what is happening in myesthenia gravis |
|
Definition
| an antibody sits on an antigen on a cell and blocks function (muscle cell cant contract) |
|
|
Term
| describe type 3 hypersensitivity |
|
Definition
| a humoral immunity in which antigens and antibodies in the blood get stuck together, causing an acute inflammation response which kills the neighborhood and makes people sick |
|
|
Term
| what diseases are caused by type 3 hypersensitivity? |
|
Definition
| lupus, rheumatoid arthritis, glomerulonephritis |
|
|
Term
| what is another name of type 4 hypersensitivity? |
|
Definition
| delayed = cell-mediated immunity |
|
|
Term
| what dieseases are caused by cell mediated immunity? |
|
Definition
| contact dermatitis, TB test, graft rejection, kill tumors |
|
|
Term
| what are normal and healthy immune responses? |
|
Definition
| acute inflammation, chronic inflammation |
|
|
Term
| how do normal and healthy immune responses make us sick? |
|
Definition
| mediators, cytokines, damage to neighborhood |
|
|
Term
| what are the two types of immunodeficiency diseases? |
|
Definition
|
|
Term
| what are the 3 types of congenital immunodeficiency diseases |
|
Definition
| B cell, T cell, combined B and T cell |
|
|
Term
| what is a B cell immunodeficiency disease? |
|
Definition
| born with no B cells; can't make antibodies; compromises humoral immunity |
|
|
Term
| what is a T cell immunodeficiency disease? |
|
Definition
| born with no T cells; compromises humoral AND cell mediated immunity; will get many viral infections and cancers |
|
|
Term
| ddescrbe combined B and T cell immunodeficiency disease |
|
Definition
| born with no B and T cells; must live in a bubble that is a completely sterile environment |
|
|
Term
| what is an acquired immunodeficiency dieases |
|
Definition
| AIDS; infects macrophages and T helpbers; compromises humoral and cell-mediated immunity |
|
|
Term
| what are 3 drugs that cause acquired immunosuppression? |
|
Definition
| steroids, chemotherapy, anti-rejection drugs |
|
|
Term
| describe increased immune responses |
|
Definition
| hypersensitivity diseases (allergic diseases, etc.), hummoral immunity and cell-mediated immunity, causes allergies and autoimmune diseases |
|
|
Term
| describe misdirected immune responses |
|
Definition
| autoimmune diseases; antigen is our self; immune responses to our own body |
|
|
Term
| what are some examples of immune neoplasms |
|
Definition
| cancer, lymphoma, leukemia |
|
|
Term
| definition of immunocompromised |
|
Definition
| having an immune system that has been impaired or weakened by disease or treatement |
|
|
Term
|
Definition
| intended or unintended suppressino of the immune rsponse, as by drugs or radiation |
|
|
Term
|
Definition
| state in which the immune system's ability to fight infections is compromised or entirely absent |
|
|
Term
| what is an anti-nuclear antibody? |
|
Definition
| an antibody made for nuclear proteins that are antigens; we make these to use when cells die and their interior cell contents are distributed |
|
|
Term
| how are immune cells, tissues, and organs like the police/army to prtoect the body from invasion? |
|
Definition
| 1. patrol to detect invasion, 2. recruit and activate immune cells when invasion is detected, 3. destroy the foreign material |
|
|
Term
|
Definition
| foreign material/non-self |
|
|
Term
|
Definition
| antigens which cause disease |
|
|
Term
| what are the 2 major subtypes of chornic inflammation? |
|
Definition
| humoral immune response, cell mediated immune response |
|
|
Term
| what cells are involved in the 3rd line of defense/chronic inflammation? |
|
Definition
| lymphocytes, plasma cells, macrophages, mast cells, eosinophils, basophils |
|
|
Term
| what are the steps of pathogenesis for chornic inflammation? |
|
Definition
| lymphocytes, macrophages release mediators to recruit more cells, activate cells, and destroy etiology |
|
|
Term
| how do our immune cells distinguish between self and nonself cells? |
|
Definition
| self cells all have the same membrane proteins/id tags |
|
|
Term
| what are the two types of self membrane proteins/id tags? |
|
Definition
| major histocompatability complex and human leukocyte antigen |
|
|
Term
| what is the job of macrophages in chronic inflammation |
|
Definition
| coordinator = first one there, lets everyone else know to come here; phagocytic = can kill cells |
|
|
Term
| what types of B lymphocytes do we have? |
|
Definition
| B memory cells for patrolling and plasma cells to make antibodies |
|
|
Term
| once a B lymphocyte is activated, what are its two choices? |
|
Definition
| 1. continue looking like B lymphoctes and leave site to return to patrolling, 2. change appearance and bceome plasma cells that make antibodies to destroy specific antigens |
|
|
Term
| What are the 3 types of T lymphocytes? |
|
Definition
| T memory = patrols, can recognize 1 antigen; T helper = coordinator that releases cytokines (also called CD4); T cytotixic = destroys cells (also called CD8) |
|
|
Term
| what type of antigen causes a humoral-meidated immune response? |
|
Definition
| microorganisms, especially bacteria and viruses |
|
|
Term
| what cells are involved in humarl-mediated immune responses? |
|
Definition
| T helper lymphocytes, B lymphocytes, lasma cells |
|
|
Term
| what are the steps of humoral-mediated immune response? |
|
Definition
| 1. B lymphocyte detects antigen, 2. B lymphocyte sends out cytocines to recruit T Helper, 3. T Helpber sends out cytokines to recruit B lymphocytes and to encourage intital B lymphocyte to undergo mitosis, 3. B lymphocyte turns into plasma B cells, 4. plasma B cells make antibodies, 5. antiobodies tag antigen for destruction |
|
|
Term
| how does the B lymphocte detect an antigen? |
|
Definition
| it has an antibody that is used as a "feeler" to find antigen |
|
|
Term
| what is used to tag the antigen for destruction? |
|
Definition
| antibody = immunoglobulin |
|
|
Term
| what are the 3 types of immunoglobulin that we need to know? |
|
Definition
| IgM = 1st type produced, disappears; IgG = 2nd type produced, remains for years as immunity to antigen (kind of antibody vaccines are designed to produce); IgE used in Type 1 hypersensitivity |
|
|
Term
| which cells are involved in cell-mediated immune response? |
|
Definition
| T Hleper lymphocytes, macrophages, T cytotixic lymphocytes |
|
|
Term
| what are the antigens of cell mediated immune response |
|
Definition
| cells (viruses in our cells, cancer cells, transplanted cells, non-degradable cells) |
|
|
Term
| what are the steps of cell-mediated immune responses? |
|
Definition
| 1. T cytotixic of macrophage identifies antigen cell, 2. T cytotoxic sends out cytockines to recruit T helpers, 3. T helpers send out cytokines to recruit macrphages and T cytotoxic, 4. T cytotoxics and macrophages kill antigen cell |
|
|
Term
| how is the antigen destroyed in cell mediated immunity? |
|
Definition
| T cytotoxics or macrophages form hole in antigen cell membrane causing water to rush in and cell dies OR T cytotoxics and macrophages trigger apoptosis so antigen cell kills itself |
|
|
Term
| what is Type I humoral immunity? |
|
Definition
| hypersensitivity = allergies |
|
|
Term
| describe Type 2 hypersensitivity |
|
Definition
| a humoral immunity I which an antigen is on a cell's surface, an antibody (IgG) binds and tags cell, a complement recognizes the tag/antigen, the complement kills cell by poking holes in cell, or nothing kills cell and the antigne sits there blocking the cell's function |
|
|
Term
| what is another name for Type 1 Hypersensitivity? |
|
Definition
|
|
Term
| What is another name for Type 2 Hypersensitivity? |
|
Definition
| Cytotixic reactions to Ag |
|
|
Term
| What is another name for Type III Hypersensitivity? |
|
Definition
|
|
Term
| What are some diseases caused by Type I hypersensitivity |
|
Definition
| allergies, hayfever, asthma, anaphylaxis |
|
|
Term
| what are some diseases caused by Type II hypersensitivity |
|
Definition
| myesthenia gravis, transfusion reaction, graft rejection, kill tumors |
|
|
Term
| describe what is happening in myesthenia gravis |
|
Definition
| an antibody sits on an antigen on a cell and blocks function (muscle cell cant contract) |
|
|
Term
| describe type 3 hypersensitivity |
|
Definition
| a humoral immunity in which antigens and antibodies in the blood get stuck together, causing an acute inflammation response which kills the neighborhood and makes people sick |
|
|
Term
| what diseases are caused by type 3 hypersensitivity? |
|
Definition
| lupus, rheumatoid arthritis, glomerulonephritis |
|
|
Term
| what is another name of type 4 hypersensitivity? |
|
Definition
| delayed = cell-mediated immunity |
|
|
Term
| what dieseases are caused by cell mediated immunity? |
|
Definition
| contact dermatitis, TB test, graft rejection, kill tumors |
|
|
Term
| what are normal and healthy immune responses? |
|
Definition
| acute inflammation, chronic inflammation |
|
|
Term
| how do normal and healthy immune responses make us sick? |
|
Definition
| mediators, cytokines, damage to neighborhood |
|
|
Term
| what are the two types of immunodeficiency diseases? |
|
Definition
|
|
Term
| what are the 3 types of congenital immunodeficiency diseases |
|
Definition
| B cell, T cell, combined B and T cell |
|
|
Term
| what is a B cell immunodeficiency disease? |
|
Definition
| born with no B cells; can't make antibodies; compromises humoral immunity |
|
|
Term
| what is a T cell immunodeficiency disease? |
|
Definition
| born with no T cells; compromises humoral AND cell mediated immunity; will get many viral infections and cancers |
|
|
Term
| ddescrbe combined B and T cell immunodeficiency disease |
|
Definition
| born with no B and T cells; must live in a bubble that is a completely sterile environment |
|
|
Term
| what is an acquired immunodeficiency dieases |
|
Definition
| AIDS; infects macrophages and T helpbers; compromises humoral and cell-mediated immunity |
|
|
Term
| what are 3 drugs that cause acquired immunosuppression? |
|
Definition
| steroids, chemotherapy, anti-rejection drugs |
|
|
Term
| describe increased immune responses |
|
Definition
| hypersensitivity diseases (allergic diseases, etc.), hummoral immunity and cell-mediated immunity, causes allergies and autoimmune diseases |
|
|
Term
| describe misdirected immune responses |
|
Definition
| autoimmune diseases; antigen is our self; immune responses to our own body |
|
|
Term
| what are some examples of immune neoplasms |
|
Definition
| cancer, lymphoma, leukemia |
|
|
Term
| definition of immunocompromised |
|
Definition
| having an immune system that has been impaired or weakened by disease or treatement |
|
|
Term
|
Definition
| intended or unintended suppressino of the immune rsponse, as by drugs or radiation |
|
|
Term
|
Definition
| state in which the immune system's ability to fight infections is compromised or entirely absent |
|
|
Term
| what is an anti-nuclear antibody? |
|
Definition
| an antibody made for nuclear proteins that are antigens; we make these to use when cells die and their interior cell contents are distributed |
|
|
Term
|
Definition
| replacement of dead/necrotic cells with viable ones; restoration of tissue architecture and function after an injury |
|
|
Term
| what are the 3 options of repair? |
|
Definition
| regeneration, scar (fibrosis), regeneration AND scar |
|
|
Term
|
Definition
|
|
Term
|
Definition
| DNA synthesis and replication to prepare for mitosis |
|
|
Term
|
Definition
| cell growth preparing for mitosis |
|
|
Term
|
Definition
|
|
Term
|
Definition
| exit cycle when not dividing |
|
|
Term
| what are the 3 categories of proliferative capacities of cells based on mitotic capacity? |
|
Definition
| labile, stable, permanent |
|
|
Term
|
Definition
| cells which normally continuously divide, meaning they regularly undergo mitosis and continuously moe through cell cycle (don't go to Go) |
|
|
Term
| what type of repair would result from labile cells? |
|
Definition
| regeneration and return of function |
|
|
Term
|
Definition
| by mitosis from mature cells or from stem cells |
|
|
Term
|
Definition
| immature/undifferentiated cells with large mitotic/proliferative capacity |
|
|
Term
| what are embryonic stem cells? |
|
Definition
| from early embryo; have capacity to grow into many different cell types |
|
|
Term
| what are adult stem cells? |
|
Definition
| from adults; have capacity to grow into fewer different cell types |
|
|
Term
| what are examples of labile cells? |
|
Definition
| epithelium = cells that cover surfaces/line cells like skin, GI lining, respiratory;genital/vascular/urinary TUBES, blood cells |
|
|
Term
|
Definition
| cell type that do not normally undergo mitosis but can if injured; spend most of their time in Go phase of cell cycle but can return to cycle if told to do so |
|
|
Term
| what is the type of repair of stable cells? |
|
Definition
|
|
Term
| what are examples of stable cells? |
|
Definition
| bone, cartilage, liver cells, solid structures |
|
|
Term
|
Definition
| cell types with poor mitotic capabilities even after injury, spend their lives in Go and very reluctant to leave |
|
|
Term
| what type of repair results from permanent cells? |
|
Definition
|
|
Term
| what are some examples of permanent cells? |
|
Definition
| cardiac muscle (heart attack), neurons/nervous system (stroke, alzheimer's), skeletal muscle sometimes |
|
|
Term
| what types of etiologies lead to necrosis? |
|
Definition
| any etiologies from day 1, including trauma, decreased oxygen, inflammatio |
|
|
Term
| what is the pathogenesis of repair |
|
Definition
|
|
Term
| most of our cells are which type of cells? |
|
Definition
|
|
Term
| what is the outcome when cells regenerate and replace following necrosis? |
|
Definition
|
|
Term
| what types of cells lead to regeneration? |
|
Definition
|
|
Term
| what types of cells lead to scars? |
|
Definition
|
|
Term
|
Definition
| necrotic cells are replaced with connective tissue |
|
|
Term
| what is connective tissue composed of? |
|
Definition
| cells and extracellular matrix |
|
|
Term
| what type of cells are found in connective tissue and what do those cells do? |
|
Definition
| fibroblasts, make extracellular matrix |
|
|
Term
| what kind of fibers are in the extrcellular matrix? |
|
Definition
| collagen fibers for strength |
|
|
Term
| what are the steps of the body response in scarring? |
|
Definition
| macrophage comes in to eat dead (necrotic) cells; granulation tissue forms new blood cells (neovascularization/angiogenesis); fibroblasts make extracellular matrix/collagen; collagen and fibroblasts line up to be stronger |
|
|
Term
| what color is a scar 3-5 days after it is formed? |
|
Definition
| pink because of vascularization |
|
|
Term
| what color is a scar weeks after it is formed? |
|
Definition
|
|
Term
|
Definition
| cehmical mediator that causes a cell to enter cell cycle of mitosis and also increases survival of new cells by decreasing apoptosis. Secreted by many cell types, inluding macrophages |
|
|
Term
| what is the function of epidermal growth factor? |
|
Definition
| mitosis of fibroblasts and skin cells (keratinocytes_ |
|
|
Term
| what is the function of fibroblast growth factor? |
|
Definition
| mitosis of fibroblasts and skin cells (keratinocytes), angiogenesis, scar remodeling |
|
|
Term
| what is the function of transforming growth factor |
|
Definition
| mitosis of many cell types, angiogenesis |
|
|
Term
| what is the functio of vascular endothelial growth factor? |
|
Definition
| mitosos of endothelial cells (blood vessel cells) for angiogenesis |
|
|
Term
| what is healing by first intention |
|
Definition
| healing of a clean, curgical incision closed with sutures |
|
|
Term
| what is happening in a 1st intention wound in less than 24 hours? |
|
Definition
| necrosis, acute inflammation |
|
|
Term
| what is happening in a 1st intention wound in 1-3 days? |
|
Definition
| repair, reapithelialization, macrophages and phagocytes enter |
|
|
Term
| hwat is happening in a 1st intention wound in 3-7 days? |
|
Definition
| formation of granulation tissue |
|
|
Term
| how strong is a 1st intention wound in less than 24 hours (has sutures)? |
|
Definition
|
|
Term
| how strong is a 1st intention wound after sutures are removed |
|
Definition
|
|
Term
| how strong will a 1st intention wound become after healing |
|
Definition
|
|
Term
| what happens weeks to months after a 1st intention wound? |
|
Definition
| epidermis is regenerated, dermis is scarred, as a remodeled, organized scar |
|
|
Term
| what is healing by 2nd intention? |
|
Definition
| healing of a larger, necrotic wound without sutures |
|
|
Term
| how does healing by 2nd intention differ from healing by 1st intention? |
|
Definition
| larger wound leads to longer repair time; re-epithelializtion is less succesful leading ot larer scar |
|
|
Term
| what is a pathologic aspect of repair? |
|
Definition
| keloid = excessive scar tissue formation |
|
|
Term
| what is an infectious disease? |
|
Definition
| disease caused by a specific pathogenic microorganism tha tmay be capable of being transmitted to another individual through direct or indirect contact |
|
|
Term
| example of infectious disease that can be transmitted |
|
Definition
|
|
Term
| example of infectious disease that cannot be transmitted human to human |
|
Definition
| rocky mountain spotted fever |
|
|
Term
| what is a community acquired fectious disease? |
|
Definition
| an ID acquired in a community not related to medical profession |
|
|
Term
|
Definition
| ID induced by a physician's words or therapy such as a catheter, IV, surgery (infection) |
|
|
Term
|
Definition
| ID acquired in the hospital such as by wound infections, pneumonia, etc., not from procedures, more individual such as from a sneeze or poor handwashing |
|
|
Term
|
Definition
| non-living protein (mad cow disease) |
|
|
Term
| what is the major cause of infectious disease |
|
Definition
|
|
Term
| what is the second most common cause of infectious disease? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| what are potential reservoirs of ID |
|
Definition
| non-animal vectors such as plants, food, soil, water; animal ,vectors such as insects, mammals; humans such as in secreations (blood, tears, semen) or excretions (urine, feces) |
|
|
Term
| how are IDs transmitted to us? |
|
Definition
| indirect contact through a non-human vector; direct contact human to human |
|
|
Term
| what are portals of entry for an ID into a human |
|
Definition
| airborne/inhalation, enteric = fecal/oral; sexual (membrane lesions); skin (bites, lesions) |
|
|
Term
| how does it help to understand the transmission events for an organism? |
|
Definition
| to devise prevention methods |
|
|
Term
| what is the most important prevention of person to person infectious diseases? |
|
Definition
|
|
Term
|
Definition
| injection of pieces of the organismi that cause the body to create protective IgG and memory cells so that chronic inflammation will occur quickly at next exposure |
|
|
Term
| what is the path of infections? |
|
Definition
| enter through a barrier, cause localized leasion, multiply and spread locally OR enter blood to become widely disseminated |
|
|
Term
| what is the incubation period of an infectious disease? |
|
Definition
| time when organism has entered and is multiplying before we're aware that we're infected = happens during pathogenesis |
|
|
Term
| what are the pathogenic responses to infectiuos disease? |
|
Definition
| necrosis, acute inflammation, chronic inflammation, neoplasms |
|
|
Term
| when is an infectious disease transmitted? |
|
Definition
| during pathogenesis or signs/symptoms (before or during the time that symptoms are present) |
|
|
Term
| when is a clinical disease present |
|
Definition
| during signs/symptoms when the disease can be recognzied |
|
|
Term
| what are the outcomes of an infectious disease |
|
Definition
| recovery, complications, death |
|
|
Term
| how does ID cause cell and tissue injury? |
|
Definition
| direct injury of cells by microorganism, indirect injury by toxins produced by microorganism, trigger host response (inflammation) |
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Term
| how many viruses cause humanillness? |
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Definition
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Term
| what are viruses composed of? |
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Definition
| a few proteins + DNA or RNA |
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Term
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Definition
| must live in host cell; each virus can infect only one or a few cell types; patrolling cells discvoer virus because virus puts viral proteins on cell membranes |
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Term
| what is the body response to viral infections |
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Definition
| humarol, cellular chronic inflammation to kill our infected cells |
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Term
| superficial fungal infections |
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Definition
| low morbidity, ie tinea (ringworm, athlete's foot), candida (oral cavity, vagina) |
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Term
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Definition
| higher morbidity and mortality. More common in immunocompromised |
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Term
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Definition
| single celled microoganisms, mostly extracellular |
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Term
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Definition
| staphylococcus, streptococus |
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Term
| where do bacteria infect? |
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Definition
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Term
| what types of bacteria live in our bodies normally but make us sick if they go to the wrong place in our bodies? |
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Definition
| E. coli (GI tract), mycobacteria (TB family - lives in our cells) |
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Term
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Definition
| toxins secreted by the bacteria (cholera, salmonella) |
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Term
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Definition
| part of the bacteria cell wall that triggers many inflammation signals |
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Term
| what is the body's response to bacterial infections? |
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Definition
| acute inflammation or humoral chronic inflammation (to make antibodies to the bacteria) |
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Term
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Definition
| antibacterial drugs that are effetive in killing or limitng growth of pathogenic bacteria |
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Term
| what are important properties of antibacterial drugs? |
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Definition
| broad specturem that is effective against many different bacterai vs. specific/selective that is effectie against only one or a few types of bacteria; bactericidal that kills bacteria vs. bacteriostatic that limits the growth and proliferation of bacteria |
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Term
| what are the 3 basic mechanisms of antibacterial drug action? |
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Definition
| 1. inhibition of bacterial cell wall synthesis and function (bactericidal); 2. inhibition of bacterial protein synthesis (bactericidal and bacteriostatic); 3. inhibition of bacterial DNA/RNA function (bactericidal and bacteriostatic) |
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Term
| examples of bacterial cell wall inhibiting antibiotics |
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Definition
| penicillin, cephalosporins, polymyxin B |
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Term
| eamples of bacterial protein synthesis inhibiting antibiotics |
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Definition
| aminoglycosides, tetracycline, erythromycin |
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Term
| how do bacteria become resistant to an antibacterial drug? |
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Definition
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Term
| a given bacteria may develop what? |
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Definition
| single or multidrug resistance |
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Term
| mechanisms used in antibiotic resistance? |
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Definition
| bacteria develop ways to destroy the antibiotic, bacteria modify or mask site where antibitic binds to it, bacteria develop ways to keep drug out of its interior |
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Term
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Definition
| multidrug resistant staph aureus can kill a healthy person quickly |
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Term
| antibiotic adverse effects |
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Definition
| common = rash, UV hypersensitivity, GI complaints |
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