Pathophysiology and Pharmacology Unit 1 – Flashcards

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What is Pathophysiology?
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a science that provides understanding of disease mechanism and how/why physiology changes in body structure and function lead to clinical manifestations of disease.
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pathology
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study of disease
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physiology
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study of functions of living organism
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Prevention: Primary
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health promotion and protection to reduce/prevent incidence of disease ei: immunization, diet, exercise
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Prevention: Secondary
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early detection of disease to alter outcome ei: screening-cholesterol, education, breast exam
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Prevention: Tertiary
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treatment and rehab of illness to avoid/postphone complications, sequelae ei: stroke rehab, diabetes management
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Pharmaco- -ology
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science of the origin, nature, effect, chemistry, and uses of drugs the study of
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Pharmacology
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the study of drugs and their interactions with living systems
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Ideal Properties: Effectiveness
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the desire reponse acheive
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Ideal Properties: Safety
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the drug dosen't produce harmful effect even at high dose
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Ideal Properties: Selectivity
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only achieve a response at it given, no side effects ei: antihistamine causes drowsiness
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Intensity of Responses
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-Pharmacokinetics -Pharmacodynamics -Pharmacogenomics
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Pharmacokinetics Process:
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the actions of the body on a drug Determine drug concentration at site of action: 1)absorption 2)distribution 3)metabolism 4)excretion
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Pharmacokinetics: Absorption
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movement of drug from its site of administration to the blood
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Pharmacokinetics: Absorption Affected by:
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Affected by: -Rated of Dissolution -Surface Area (Larger=better) -Blood flow(^flow=flows faster) -Lipid Solubility(easily to cross membrane) -pH Partitioning
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Pharmacokinetics: Absorption Infuenced by routes of administration
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-Enteral -Via. Gl tract (anything in side GI tract) -Oral, mouth, GI Tube, PO -Parenteral -outside the GL tract -"by injection" -IV,IM,SQ/SC
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Pharmacokinetics: Distributions
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-movement of the drug thoughout the body
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Pharmacokinetics: Distributions Determined by:
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Determined by: -blood flow to tissues -ability to exit vascular system -ability of drug to enter cells
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Pharmacokinetics: Distributions -Blood flow to tissues
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-Blood brain barrier: might block the drug from entering the brain -Placental drug transfer: lipid-solubility can transfer material to baby -ei:alcohol -Protein binding: drugs form reversible bond with protein
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Pharmacokinetics: Metabolism
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-Biotransfermation (metabolizing) -Hepatic Drug: Metabolizing Enzymes
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Pharmacokinetics: Metabolism -Factors affecting Drug Metabolism -Prodrug -First Pass effect -Individual response
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Factors affecting Drug Metabolism -Prodrug: become active when in the body but inactive outside the body -First Pass effect: rapid inactivation of a drug when the drug is absorb in the GI Tract -Individual response: every1 is different
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Pharmacokinetics: Excretion
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removal of the drug from the body
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Pharmacokinetics: Excretion Renal System: 1) Glomerular Filtration 2) Passive Tubular Reabsorption 3) Active Tubular Secrection
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Renal System: 1) Glomerular Filtration: blood to tubular to urine 2) Passive Tubular Reabsorption: from tubular back to the blood 3) Active Tubular Secrection: active transfer pump from the blood to the tubular, some urine gets reabsorbed
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Pharmacokinetics: Time Course of Drug Responses -Minimum Effective Concentration -Toxic Concentration -Therapeutic range
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Responses -Minimum Effective Concentration: when response occur -Toxic Concentration: when levels are too high -Therapeutic range: eough of the drug present to have theri therapeutic response
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Pharmacokinetics: Time Course of Drug Responses -Plateau Drug Levels -Loading dose -Maintenance dose -Decline from Plateau
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-Plateau Drug Levels: steady dose /remaining constant (average drug level) -Loading dose: large, initial dose make the plateau dose more effective -Maintenance dose: smaller dose use to maintance the plateau dose -Decline from Plateau- most drug takes 4 half live to get it out of the system
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Pharmacokinetics: Role of the cell membrane Phospholipid Molecule:
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Hydrophilic head: water loving head Hydrophobic tail: water hating tails
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Pharmacokinetics: Movement across cell membrane -Channels/Pores -Transport systems -Directly crossing membrane
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-Channels/Pores: small comound can escape -Transport systems: move stuffs from one side to another -Directly crossing membrane: direct cross the membrane( must be lipid
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Pharmacodynamics
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Definition: the process by which drugs influence cell physiology to achieve desired result -how a drug changes the body -what drug do to the body and how they do it
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Pharmacodynamics Concepts -Maximal efficacy -Relative Potency -Drug Receptors
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Concepts -Maximal efficacy: largest effect that the drug can produces -Relative Potency: amount of drug that must given to get an effect -Drug Receptors: any fuction marcomolecule to which a drug is to bing to be effective
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Receptor Theory
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-drugs generally attach to cell receptors to elicit celluar response(it can block or make it work) -2nd messager response -drug-> receptor-> cellular response -
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Agonist
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-activate receptors, mimic(ei: nervous transmitter)
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partial agonist
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-moderate agonist activity (not a complete mimic)
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anatgonist
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-prevent receptor activity (blocking it)
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Interpatient Variablity -LD 50 -ED 50 -Therapeutic Index
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-LD 50: dose lethal in 50% animals( dose that casues 50/100 animal to die) -ED 50: average effective dose(dose that have effecet in 50% of the popluation) -Therapeutic Index: ratio of average lethal(LD 50) dose to effective dose (ED 50)
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Variation in Patient Response
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-Individual Characteristics: age, race, body composition, diet, compliance -abnormal physiology -tolerance -drug formulation -genetics
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Pharmacogenomics
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the study of how gentic indivdual effects to the drug
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Genetics: Pharmacogenomics -can alter:
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-Metabolism -Drug Targets -Immune response
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Benefits of Pharmacogenomics
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-can increase efficacy and safety of drugs -create better drugs -increase quality of care -better disease management -decrease cost of health care
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Cellular Adaption
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-Genomics -Adaptations
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Cellular Adaptation: Atrophy
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-decrease of size of cells ei:thymus gland gest small in child, adnormal= smaller cell size in the heart due to workload
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Cellular Adaptation: Atrophy -Physiology -Pathologic -Disuse
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-Physiology: ei: thymus gland gets smaller as child grows -Pathologic: blood supply, nutrition -Disuse: individual can't move or in bed(immobilize)
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Cellular Adaptation: Hypertrophy Types -physiologic -pathologic Triggers -Mechanical -Trophic
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-increase in the side of cells ei: the heart Types -physiologic: -pathologic: Triggers -Mechanical:stressing of muscle -Trophic: growing factors
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Cellular Adaptation: Hyperplasia -Compensatory -Hormonal -Pathologic
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-Increase amount of cells -Compensatory: regrow of cells -Hormonal:estrogen, ei:when the girl get pregnant -Pathologic:increase cells related to disease
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Cellular Adaptation: Maladaption -Neoplasia
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-trait that is (or has become) more harmful than helpful -Neoplasia:abnormal pattern of growth/abnormal proliferation of cells
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Cellular Adaptation:Metaplasia
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-replacement of one mature cell type with another -reprogramming of stem cells due to noxious stimulus -if cells has injury the cells can regrow
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Cellular Adaptation:Dysplasia(atypical hyperplasia)
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-Abnormal size, shape, organization of mature cells -low to high grade -remove dysplastic tissue/ remove stimulus -common in the urine due to inflammation
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Cellular Injury
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-most diseases start with cell injury -cell unable to maintain homeostasis or adapt -injured cells have capacity to recover(reversible injury/recover), or die (irreversible/ possible for cellular death)
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Casues of Cellular Injury
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-Ischemia -Hypoxia -Free radicals -Chemical agents
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Hypoxic Injury -Hypoxia -Ischemia -Anoxia
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Hypoxia- insufficient to tissues (most common cause of cellular injury) Ischemia (reduced blood supply) most common cause of hypoxia Anoxia-lack of oxygen to tissues(no oxygen) ei: heart failure
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Hypoxic Cellular Injury
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1) ischemia-> decrease in oxygen in mitochondria-> decrease ATP 2)decrease ATP-> alters NA/K pump and NA/CA exchange (altered membrane permeability) 3) increase intracellular NA and CA -> K moves out of the cell 4) water enters cell -> swelling and ER dilation 5) ribosomes detach with decrease protein synthesis 6) vacuolation 7) cell membrane damage if oxygen is restored-reversible/recover if not restored- irreversible cell injury/ not recover
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Reperfusion injury/ Oxidative injury can occur with restoration of blood flow and oxygenation
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-free radicals generated leading to additional cellular damage - unstable atom group steals electron -bond formations-injurious -target mitochondria
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other sources of oxidation injury
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-extreme energy expose (uv, radiation) -endogenous reactions -chemical exposure -aging
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Damage Cause by Free Radicals 1)Lipid peroxidation 2)alters ion pumps/ transport mechanisms 3)fragments DNA 4) mitochondrial damage
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1)Lipid peroxidation: the lipid bilayer went bad 2)alters ion pumps/ transport mechanisms: damage the pump 3)fragments DNA: decrease protein sythesis 4) mitochondrial damage: Ca is release cause membrane break down
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Mechanisms of Chemical Injury
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-direct -exaggerated response -biologic activation -hypersensitivity -rare toxicites
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Examples of Chemical Agents(cause chemical injury)
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-lead -carbon monoxide -ethanol -social "street drug" -OTC, prescription drugs -insecticides -chronic air pollution exposure -mercury
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Outcomes of Cellular Injury -Necrosis -Apoptosis -Autophagy
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-Necrosis: cells are not longer able to function -Apoptosis: self destruction (ei: cancer, DNA damage) -Autophagy: cell self eating itself (ei: cell is starving or lack of nutrition)
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Neoplasia
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-Tumor/ abnormal cell growth/ new growth -"new growth" -tumor -benign -malignant -carcionma in situ
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Benign Tumor
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-well organized -encapsulated( surrounded by capsule) -normal cell structure -well differentiated (easily find) -non invasive -slow growing -localized - -oma
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Malignant Tumor
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-grow rapidly; high mitotic rate -loss of differentiation; Anaplasia -disorganized tissue -pleomorphic -not encapsulated -invasive -metastasize -named for tissue of origin -less specialize
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Tumor Nomenclature: Malignant -Carcinoma -Adenocarcinoma -Sarcome -Lymphoma -Leukemia
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-Carcinoma: epithelial tissue -Adenocarcinoma: ducts or glangs -Sarcome: connective tissue -Lymphoma: lymph -Leukemia: blood forming cells
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Classification of Tumors
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-Appearance of tissue -Genetic analysis -Molecular analysis
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