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99 Cards in this Set
- Front
- Back
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Etiology |
Search for the causes of illness and other health states |
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Mucositis |
Inflammation of the buccal mucosa, can be caused by radiation because it cases the cells to die |
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Incidence |
Number of new cases of illness occurring during a certain time period among those who do not already have the illness in a specified time period -new cases/population/year - ex. estimated 191,300 new cases of cancer and 76,600 deaths from cancer will occur in Canada in 2012 |
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Prevalence |
% population (new and old) that has illness at given point in time, normally expressed /100,000 living w illness -important for looking at illnesses of chronic nature that will require care for long period of time |
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Natural History (disease progression) |
Unaltered course that illness takes without any intervention such as therapy or lifestyle change -vital in determining etiology, establishing therapeutic interventions, developing preventative measures or screening practices that will affect outcome of illness |
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Morbidity |
Costs in terms of money, impact of illness ex. hospitalization costs, days-lost from work, school |
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Mortality |
Number persons dying at given point in time in total population dying at the time -ex. of all deaths in 2011, 30% were from cancer |
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Management |
Strategies to prevent, treat and control illness (the disease is not treatable but you can control it, getting chemo for terminal cancer) -independent nursing strategies -collaborative nursing, medical -pharmacology |
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Pharmacotherapy |
Using medicine to treat, providing therapy with drugs, in contrast to surgery, if you have cancer you can cut it out or use chemotherapy |
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DRUGS |
anything with a DIN (drug identity number) considered a drug, sunscreen even has a DIN, chemical, interacts with body, produces response, can be natural, sythetic, prescription and OTC |
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Canadian Drug Laws |
Therapeutic products directorate oversees drug control in Canada, food and drug regulations determine whether drugs are prescription or not, all drugs requiring prescription listed in Schedule F, provinces may have different rules, govern manufactures, distribution, advertising and sale |
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Controlled drugs and substances act |
control and sales of narcotics, controlled substances, substances of misuse, 8 schedules for punishment, FDA is American |
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Drug Identification number (DIN) |
eight digit number, preceded with the letters DIN, drug reviewed by Health Canada, natural health products have natural product number (NPN), homeopathic medicine number (DIN-HM) |
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Drug standards (health Canada) |
ideal drug should be effective (most important), demonstrated in clinical trials), safe and not toxic, selective with minimal side effects (does only what it is supposed to do, but no drug is 100% effective) |
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Therapeutic objective of a drug |
drug therapy should provide maximal benefit with minimal harm |
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Drug classification |
by chemical structure of active ingredient or by pharmacological action (function) chemotherapeutic drugs- used to cure infectious diseases and cancer, same class achieve a similar function but they have different mechanisms, have common stems or syllables that are used to identify the different drug classes |
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Pharmacokinetics |
Movement of the drug through the body, what the body does to the drug -ADME (absorption, distribution, metabolic, elimination) |
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Pharmacodynamics |
What the drugs do to the body |
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Pharmacogenomics |
study of individual variations to drugs, genetic variations between individuals and their influences on efficacy and adverse effects of drugs -customizing drugs, certain drugs work better for certain genetic make up (Asian people could respond better to one drug than the other) -focus =drug metabolism -improves safety and efficacy |
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Pharmacotherapeutics |
Use of drugs to prevent, diagnose and treat diseases, therapy based on individual patient disease status, establish and monitor desired therapeutic outcomes, important to understand patient physiological variables and influence of pathophysiological differences on pharmacokinetics and pharmacodynamics |
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Toxicology |
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Absorption -where are drugs primarily absorbed from? |
movement of drug from site of administration into blood, determined by drug's physicochemical properties, formulation, route of administration, drugs must be in solution to be absorbed, concepts of bio-availability and first pass effect intertwine w route -most absorbed through passive absorption -lipid soluble and non-ionized drugs absorbed faster -drugs given orally must survive low pH and numerous GI secretions, including potentially degrading enzymes |
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First-pass effect |
If the drug gets passed through the liver acts as a middle man in a drug deal looking for a finders fee, end person=systemic circulation (bitch looking for addy) who gets less because you bought it from a sucker who stole part of the pill and decreases amount of active medication present in body |
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Bio availability |
How fast drug enters systemic circulation (rate of absorption) and how much of the nominal strength enters body (extent of absorption) -active drug or metabolite enters systemic circulation-->site of action -primarily determined by properties of form of drug |
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Variables of drug absorption |
-lipid solubility--> cells have fatty acid layer so drugs that are more lipid in content are absorbed more rapidly -richer blood supply the quicker the absorption, when working out blood only in vital organs so GI tracts isn't going to get much blood flow -pH--> acid likes acid, bases like bases, presences of bile and mucus cause drug to be absorbed faster -thinner the epithelial membrane faster absorbed -pain and stress--> blood flow diverted to vitals because HR=up so drugs absorbed slowly -Natural health products--> enhance and decrease drug absorption |
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Enterohepatic circulation of drugs |
Associated with half life, whatever is retained after the drug goes through the liver, recycling of the drug, going back through circulation, drug-->liver-->bile-->goes through the systemic circuit again |
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Factors influencing Bio-availability |
-Product preparations: if drug is in form that is difficult to absorb, if coded takes longer to release -Route of admin: places more highly vascularized faster it's absorbed -Food: can delay if there's a lot of food instomach, sometimes you need food in system to facilitate regular absorption -First-pass effect: bio availability dependent on this, after liver how much drug is being administered? |
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First-pass effect and drug routes |
rectal route of administration can have first pass effect sometimes, some can be absorbed without going through GI tract first though, other first pass -hepatic arterial -oral, portal venous -Injections surpass this |
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Cytochrome P450 |
hepatic metabolism involves the activity of this large class of enzymes, also known as microsomal enzymes, control variety of reactions that aid in the metabolism of medications, largely targeted against lipid soluble drugs (non polar or no charge) |
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Enteral route |
Sublingual and buccal routes, by mouth and has first pass effect, drug is absorbed into the systemic circulation through the mucosa of the stomach, small/large intestine |
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Parenteral Route |
by vessel, most of this is not absorbed by GI tract so no first pass effect -intradermal -subcut -IV -IM -intrathecally -Intraarticularly -intra-arterially |
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Topical route |
on the skin, transdermal route |
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Minimum effective concentration (MEC) |
when the drug starts to kick in, lowest concentration a drug will have to relieve the symptoms, when you take a Tylenol and it finally kicks in |
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Minimum toxic concentration (MTC) |
minimum cocnetration for the drug to be toxic, the gap between these two are the therapeutic index (TI), you want a large TI because it takes a small amount of drug to have effect and not dangerous because you can control dosage better |
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Potent vs efficacious drugs |
When concentration of the drug is higher in a shorter amount of time verses a efficacious drug when it takes more time to reach min effective concentration and is ind of time bc it has the potential to reach a higher effect |
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Distribution |
Movement of drug from intravascular to body tissues, influenced by organ perfusion, organ size, binding of the drug to various components of blood and tissue, permeability of tissue membrane (e.g., walls of capillaries are thin so highly permeable) -look at diagram, do you understand it? PP slide 53 week 1 part 2 -movement of drugs through body to target site, drugs interact with receptors during distribution, may travel attached to albumin -more fat soluble drug is, better able to cross cell membrane |
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Hydrophilic vs hydrophobic |
Hydrophilic drugs are going to be lipophobic and vice versa, is drug water or lipid soluble? -Lipid soluble can pass through cells, volume of distribution in your body is therefor very high -Implications on the distribution of the drug, if drug can pass into cell, (majority of our body) it would have a high volume of distribution, if it is high distribution it can reach toxicity level quickly |
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Metabolism |
Done primarily in liver, deals with a lot of fatty things so drugs that are more lipid soluble, drugs that re more water soluble are in the kidney -water soluble drugs are easier to excrete -therapeutic consequences= accelerated drug excretion, drug inactivation, activation of prodrugs, increased therapeutic action, toxicity variations |
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Elimation |
Removal or drugs from the body, kidney via three processes -glomerular filtration -passive tubular resorption -active tubular secretion |
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Loading dose vs maintenance dose |
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Pharmacokinetics |
length of time until the onset and peak of action and the duration of action play important part in determining the peak level (highest blood level) and trough level (lowest) of a drug, if peak blood level is too high, drug toxicity may occur |
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Half-life |
the time for the amount of drug in the body to decrease by 50% |
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Pharmacodynamics |
action of drug on body and how, includes receptor interactions, dose-response phenomena and mechanisms of therapeutic and toxic action -action vs effect -min amount drug w max response -max efficacy is largest effect drug can produce -relative potency=amount of drug needed to produce an effect |
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Drug receptors |
Any functional macromolecule in a cell to which a drug binds to produce its effect, like a lock and key or light switch to turn on and be activated, specific receptor |
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Protein binding drugs |
drug molecule must be bound to cells and tissues to produce effect, most drugs produce effect by binding to proteins (receptors) |
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Drug action |
direct effect on proteins, proteins act as enzymes or receptors, ion channels or transporters, once interaction occurs, then pharmacologic effects become evident |
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Drug agonist |
mimics or enhances action of receptor, has both affinity (ability to bind to receptor) plus intrinsic activity (ability to produce measurable effect) |
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Drug antagonist |
has affinity for the receptor but no effect, so blocks the receptor and prevents binding of agonist so ability of drug to produce a physiologic effect is dependent on receptor occupancy and intrinsic activity |
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Therapeutic index |
Measure of drugs safety, goal to keep drug between MEC and MTC |
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Adverse drug reactions |
adverse drug reaction is defined as a noxious, unintended and undesired effect that occurs at normal drug doses |
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Drug tolerance |
Decreased responsiveness to a drug due to repeated drug administration |
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Nonspecific defense |
First line of defense -->anatomic barriers= skin, mucous membrane and secretions of skin and cilliated epithelia, chemical barriers, gastric acid and lysozymes Second line of defense -->phagocytic WBCs, defensive proteins and inflammatory response, lymphatic system |
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Specific defense (immune system) |
Third line of defense --> lymphocytes and antibodies -->lymphatic system |
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Inflammation |
to neutralize or destroy foreign material, restrict tissue damage, alert individual to impending threat of tissue injury, prepare injured area for healing |
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Acute inflammation |
Of relatively short duration, nonspecific early response to injury and aimed primarily at removing the injurious agent and limiting tissue damage |
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Chronic inflammation |
longer duration lasting for days to years, a recurrent or progressive acute inflammatory process or a low grade smoldering response that fails to evoke an acute response |
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Chronic vs acute inflammation |
acute inflammation is self limited, of short duration and infiltration of neutrophils, exudate Chronic inflammation is self perpetuating and may last weeks-years, infiltration by mononuclear cells (macrophages) and lymphocytes, proliferation of fibroblasts (scaring) |
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Leukocytes |
neutrophils (acute), macrophages, lymphocytes, eosinophils, mast cells (chronic) -inflammatory mediators worked to amplify the initial response and influence its evolution in vascular and cellular responses |
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Endothelial cellls |
regulate blood flow, as barrier, synthesis of inflammatory mediators, regulate immune cells proliferation, produces growth factors for angiogenisis (repair) synthesis of EC matrix -regulate blood flow because they dilate the blood vessels and synthesize inflammatory mediators endiogenisis=growth of new blood vessels |
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Platelets (thrombocytes) |
help with vascular permeability and secrete neutrophils and monocytes are part of phagocytosis activated-->inflammatory response-->vascular permeability and endothelial protelytic properties (role of inflammatory disease) |
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Cell adhesion molecules |
involved in leukocyte recruitement and trafficking (they're pimps) -selectins: refers to three groups of proteins with similar structures, function in adhesion of leukocytes to endothelial cells -integrins: family of 30 structurally similar proteins, promotes cell to cell and cell to extracellular matric interactions, integrates signals of EC lignads with cytoskeleton-dependent motility, shape, change and phagocytic responses of immune cells -immunoglobin super family: anything ending in "AM" e.g., ICAM1, interacts w integrins on leukocytes to mediate their recruitment |
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Vascular phase (acute inflammation) |
Lasts for minutes to hours 1. Increase blood flow from nitric oxide and histamine bc they increase blood flow endothelial cells-->nitric oxide/histamine-->dilation-->increase blood flow 2. increase vascular permeability endothelial cells-->mediators-->contraction of endothelial cells--> leads to gaps, larger vessels that lead to gaps plasma can now leak out and swelling occurs |
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Cellular phase (acute inflammation) |
Emigration of leukocytes, chemotaxis and phagocytosis -phagocytosis would be the removal of invading organisms and the beginning of the healing process |
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5 signs inflammation |
1. heat (calor) 2. redness (rubor) 3. swelling (tumour) 4. loss of function (funtio laesa) 5. pain (dolar) caused by bradykinin bc stimulation nerve endings from the swelling |
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Vasodilation (hyperemia) |
increased blood flow to the damaged area resulting in redness and warmth (heat) |
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Swelling |
swelling is from leakage of plasma proteins (exudate-pus is a type of this), normal part of inflammation *clear exudate is expected from inflammation but if it is foul smelling it's something to worry about |
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Who's responsible for pain? |
Tenderness and pain as a result of release of prostaglandins and bradykinin or from swelling |
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Exudate |
may flush away other content and helps with cellular repair, drain to local lymphatic channels, pulls H2O from plasma -fibrinogen in exudate significant pp that is activated to fibrin (strengthens clot) -clot traps bacteria, prevents spread, helps with healing -net result of vascular response--> formation of exudate at damaged site |
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Purulent Exudate vs Serous exudate |
Serous- ulceration is where the sight of inflammation has become necrotic center on the epithelial surface, yellow stuff is healthy tissue growing Purulent- more considered as pus, degraded WBC and tissue debris are present in purulent exudates whereas serous is more protein and water, drainage looks necrotic bc drainage isn't clear, keep close eye on this |
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Cellulitis |
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Cellular response hallmark |
if sufficient damage occurs or infection the appearance of inflammatory cells such as neutrophils decreased velocity of blood flow to site-->increased expression of vascular endothelial adhesion molecules-->increase vascular permeability (precipitated cellular phase because end of vascular phase) |
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Migration of leukocytes |
Influx phaocytic cells into tissues 1. activation of neutrophil 2. rolling on endothelial cells to find spot to enter tissue 3. firm adhesion to endothelial cells 4. spreading of endothelial cell 5. diapediesis (entering of neutrophil into tissue) 6. Chemotaxis- chemokines attract the leukocytes (student follows pizza smell) PEUDES HACERLO |
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Leukocyte adhesion cascade |
immuno-super family responsible for adhesion of leukocytes (neutrophils for acute inflammation, macrophages for chronic) to endothelial cell (look at diagram on slide 56, lecture 3) |
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Diapedesis |
Neutrophil entering the damaged, acute inflamed tissue through the endothelial cells |
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Chemotaxis |
Leukocytes follow the higher concentration of chemokines to damaged tissue |
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Margination |
Neutrophil attaching to the endothelial wall |
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Monocyte |
Arrive second, develops into a macrophage and has longer life span than neutrophil |
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Compliment |
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Histamine and serotonin |
first mediators, dilate arterioles, increase vascular permeability |
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Prostaglandins |
Induce inflammation, potentiates histamine, thromboxane (platelet aggregation) |
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Platelet activating factor |
serotonin released, leukocyte adhesion, chemotaxis, stimulates synthesis of other mediators |
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plasma proteins |
clotting, complement (increase vascular permeability, phagocytosis) and kinin systems (vasodilation, pain) |
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Chemokines |
Attract cells from capillaries into the tissue space and bind to heparin -endothelial cells -monocytes -lymphocytes |
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Inflammatory cytokines |
attract cells from capillaries into the tissue space -monocytes -lymphocytes |
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Complement components |
opsonize microorganisms for efficient phagocytosis attract leukocytes, lyse bacterial membrane -monocytes/macrophages -cascade activated Group of proteins that require activation, cascade of actions, three pathways and ultimately produce key enzymes -classical -lectin -alternative three phases -initiative/activation -amplification of inflammation (becoming marked) -membrane attack response |
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C5a |
most potent complement protein triggering inflammation, causes mast cells to release vasodilators such as histamine, stimulates neutrophils and endothelial cells to express more adhesion molecules, attracts phagocytes, extremely potent at stimulating neutrophil chemotaxis, adherence, respiratory burst generation and degranulation |
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Opsonization |
Marking the cell to be killed |
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Chronic inflammation |
long term (days, months, years) infiltration with mononuclear cells (angiogenesis), proliferation of fibroblasts instead of exudates (risk for scarring and deformity), may be associated with cancer *different cells, more macrophages here bc they live longer, may see growth of new blood vessels and more scarring are biggest differences of chronic vs acute |
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Effects of chronic inflammation |
-diabetes -cancer -cardiovascular -alzheimer's disease -pulmonary disease -arthritis -autoimmune disease -neurological disease |
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Chronic inflammation causes |
-foreign bodies -viruses (hepatitis) -disease causing excessive and inappropriate activation of immune system (asthma) -obesity-->heart disease--> vascular related (plaque builds on vessels and when it becomes completely occluded) |
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Systemic manifestations of inflammation |
when infection isn't localized its everywhere Acute-phase response: release cytokines causing changes in concentration of plasma proteins, skeletal muscle catabolism, negative nitrogen balance, increased # leukocytes that leads to fever (immature neutrophils called bands) indication of acute systemic inflammation bc your body is trying to crank out more leukocytes than it can produce -fever, anorexia, somnolence and malaise |
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Somnolence |
tired and drowsiness |
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Malaise |
generally speaking you just don't feel well |
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Acute phase proteins |
from the liver, regulated by cytokines (TNFalpha) -Fibrinogen causes RBC to form stacks that sediment more rapidly to elevate ESR -C reactive protein binds to invading microorganisms, target for destruction by complement and phaocytosis -serum amplyoid A protein increases HDL from liver cells to macrophages (for energy) |
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Pyrexia |
FEVER- increase in temperature set point, cytokine induced (thermostatic center in the hypothalamus) nonspecific response, mediated by endogenous pyrogens released from host cells in response to infectious or non-infectious disorders -fever resolves when the intruding substance is gone |
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Prostoglandin |
Triggers your body to set a higher level temperature 1. release fever producing cytokines from inflammatory cells 2. resetting thermostatic set point 3. temp raising response- vasoconstriction, shivering, increased metabolism 4. core body temp reaches new set point 5. temp reducing response- vasodilation, sweating, increased ventilation |
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Systemic- WBC response |
increased neutrophils, more common with bacterial infection (excess demands of phagocytosis, increased bands (immature neutrophils) released) -eosinophilia: parasitic and allergic responses -decreased neutrophils and lymphocytosis=viral infection -leukopenia= overwhelming infections or impaired ability to produce WBC |
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Lymphadenitis |
reaction in lymph nodes to drain the affected area- palpable nodes that maybe painful, from increased WBC |
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Systemic inflammatory response syndrome (SIRS) |
occurs in sepsis, enormous quantities of inflammatory cytokines is released due to uncontrolled and overwhelming inflammatory response, BP drops bc all blood vessels dilated, patient in shock, doesn't matter what you put in the IV the BP is going to be low, and low volume means low delivery system |
