Term
| Name 4 characteristics of NSAIDs |
|
Definition
-Decrease Inflammation
-Analgesia
-Decrease Fever (antipyresis)
-Decrease Blood Clotting (anticoagulation) |
|
|
Term
| Useful in treating pain and inflammation associated with acute or chronic musculoskeletal disorders |
|
Definition
|
|
Term
| The best known NSAID. Inhibits the synthesis of prostaglandins |
|
Definition
|
|
Term
| Prostaglandins, thromboxanes, and leukotrienes are collectiely known as what? |
|
Definition
|
|
Term
| Help to regulate cell function under normal or pathological conditions. |
|
Definition
|
|
Term
| Formed by arachidonic acid which is a fatty acid stored in cell membranes |
|
Definition
|
|
Term
| Influence cardiovascular, respiratory, renal, GI, nervous, and reproductive systems |
|
Definition
|
|
Term
| What is the role of prostaglandins (6) |
|
Definition
-Inflammation (erythema, edema, increase blood flow, increase capillary permeability, increase histamine and bradykinin)
-Pain
-Fever
-Dysmenorrhea
-Thrombus Formation (increase platelet aggregation)
-Others (HTN, asthma, MS, DM, colon cancer) |
|
|
Term
| (3) Mechanisms of action for NSAIDS |
|
Definition
-Inhibit cycloxygenase (COX) enzyme
-COX enzyme participates in the synthesis of prostaglandins
-Inhibition of the COX enzyme is the key to NSAID benefit |
|
|
Term
| COX enzyme exists in 2 forms. What does COX1 do? |
|
Definition
| Mediates normal cell activity |
|
|
Term
| COX enzyme exists in 2 forms. What does COX2 do? |
|
Definition
| Produces prostaglandins in pathological cells which mediate pain and inflammation |
|
|
Term
| Aspirin and most NSAIDS inhibit what? |
|
Definition
|
|
Term
| If NSAIDs inhibit COX enzymes, then what benefit is lost? |
|
Definition
|
|
Term
| Selective COX2 inhibitors should do what? |
|
Definition
| Reduce the effects of COX2 enzyme while not effecting the COX1 enzyme |
|
|
Term
| Name 5 uses of Aspirin and other NSAIDS |
|
Definition
1. Treat pain and inflammation
2. Avoid side-effects of opioids
3. Treat fever except in children (aspirin has been associated with Reye Syndrome)
4. Treat vascular disorders (blood clots, HA, TIAs)
5. Cancer prevention |
|
|
Term
| Name some NSAID side effects |
|
Definition
GI problems
Liver dz
Renal dz
Reye Syndrome in children
Delays tissue healing by inhibiting connective tissue formation |
|
|
Term
| Is there any evidence that an NSAID has a better therapeutic effect than aspirin? |
|
Definition
| No but some may have fewer side effects |
|
|
Term
| Name 2 common COX2 inibitors |
|
Definition
Celebrex
Vioxx (removed from market) |
|
|
Term
| Decrease in GI problems and do not inhibit platelet function. Decrease in side effects due to lack of COX1 inhibition. |
|
Definition
|
|
Term
| Is acetominophen an NSAID? |
|
Definition
|
|
Term
-Has some analgesic and antipyretic effects but does not reduce inflammation.
-Used in non-inflammatory disorders to treat pain
-Also used as a substitute for aspirin in children to avoid Reye Syndrome |
|
Definition
|
|
Term
| How are most NSAIDs administered? |
|
Definition
|
|
Term
NSAIDs:
-Dose
-Absorption
-Distribution |
|
Definition
Dose varies
Absorbs in stomach and small intestine
Distribution: plasma proteins and throughout the body |
|
|
Term
| How are NSAIDs metabolized and excreted? |
|
Definition
Metabolized via biotransformation in bloodstream and liver.
Excreted via kidneys |
|
|
Term
| Can be toxic to the liver in high doses |
|
Definition
|
|
Term
| The most common medication administered to the PT population |
|
Definition
|
|
Term
| 2 primary conditions that affect joints |
|
Definition
|
|
Term
| A chronic, systemic disorder that affects various tissues but mainly synovium and articular tissue |
|
Definition
|
|
Term
| RA diagnostic criteria include: (7) |
|
Definition
Morning Stiffness
Arthritis in 3+ joints
Hand joint arthritis
Symmetric arthritis
Rheumatoid nodules
Serum rheumatoid factor
Radiograph change |
|
|
Term
| Caused by an autoimmune response in genetically susceptible patients. Formation of antibodies that initiate phagocytes and lymphocytes. Phagocytes and lymphocytes cause production of cytokines, eicosanoids, and destructive enzymes (proteases, collagenases) |
|
Definition
|
|
Term
| Drugs have 2 goals in treating RA |
|
Definition
Decrease Inflammation
Slow/stop disease progression |
|
|
Term
| Name the 3 categories of RA drugs |
|
Definition
NSAIDs
Glucocorticoids (corticosteroids)
Disease-modigying antirheumatic drugs |
|
|
Term
| Name the 2 most common medications for RA |
|
Definition
|
|
Term
| Adverse effects of NSAIDs |
|
Definition
| Primarily gastric ulcer or hemorrhage |
|
|
Term
| Extremely effective in treating inflammation. Does not slow disease progression. Increases anti-inflammatory protein production and inhibits pro-inflammatory substances production. |
|
Definition
|
|
Term
| Blocks pro-inflammatory prostaglandin production. Also inhibits macrophages and T lymphocytes |
|
Definition
|
|
Term
| Name some adverse effects of Glucocorticoids |
|
Definition
-Breaks down muscle, tendon, and bone
-Osteoporosis
-Can cause ms weakness, atrophy, HTN, DM, glaucoma, and cataracts |
|
|
Term
| Do DMARDS (Disease-Modifying antirheumatic drugs)alter RA progression? |
|
Definition
|
|
Term
| Most of these inhibit the function of monocytes and lymphocytes that are responsible for joint inflammation and destruction. |
|
Definition
|
|
Term
|
Definition
Antimalarial Drugs
Azathioprine (Imuran)
Etanercept (Enbrel)
Gold Therapy
Leflunominde (Arava)
Methotrexate
Penicillamine |
|
|
Term
| Which form of arthritis is more common? |
|
Definition
|
|
Term
| Virtually everyone over 75 has this to some degree. Only mild inflammation in most cases. Articular/cartilage damage is the primary concern |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Hyaluronan is injected into the joint to restore synovial fluid viscosity. |
|
Definition
|
|
Term
| Used to produce GAGs, proteoglycans, and hyaluronic acid |
|
Definition
| Glucosamine and Chondroitin |
|
|
Term
| A sustained, reproducible increase in BP. Can lead to CVA, HF, Renal dz and blindness |
|
Definition
|
|
Term
| Short-term control of BP is by the what? |
|
Definition
|
|
Term
| Long term control of BP is by what? |
|
Definition
| kidney control of fluid balance |
|
|
Term
| Cardiac Output X Total Peripheral Resistance = |
|
Definition
|
|
Term
| What are common causes of HTN? |
|
Definition
| Exact cause unknown. Maybe a combo of internal and external factors such as diet, stress, predisposition, smoking, and alcohol abuse |
|
|
Term
| Once HTN is diagnosed it seems to progress: (3) |
|
Definition
-Decrease baroreceptor refex sensitivity
-Increased kidney discharge
-Increased vascular resistance |
|
|
Term
| Increases the formation/excretion of urine, thus decreases vascular fluid volume to serve as an antihypertensive |
|
Definition
|
|
Term
| Inhibits Na reabsorption thus increasing fluid excretion |
|
Definition
|
|
Term
| Inhibits Na and Cl reabsorption thus increasing fluid excretion |
|
Definition
|
|
Term
| Prevents K from being excreted from kidneys; prevents Na reabsorption; increases fluid excretion |
|
Definition
|
|
Term
|
Definition
| Hypnatremia and hypokalemia can result in cardiac and metabolic problems, weakness, and fatigue |
|
|
Term
| Decreases HR thus reduces CO |
|
Definition
|
|
Term
| What are some side effects of beta blockers |
|
Definition
| Bronchoconstriction (asthma) and depressed HR |
|
|
Term
| Blocks vascular smooth muscle receptors thus decreases vascular resistance |
|
Definition
|
|
Term
| What are some side effects of alpha blockers? |
|
Definition
| Reflex tachycardia and orthostatic HTN |
|
|
Term
| Inhibits the release of norepinephrine thus decreases excitation of heart and vascular smooth muscle |
|
Definition
| Presynaptic Adrenergic Inhibitors |
|
|
Term
| Causes vasodilation thus decreasing peripheral resistance. Side effects include reflex tachycardia, dizziness, weakness, nausea, HAs, and fluid retention |
|
Definition
|
|
Term
| Blocks the conversion of angiotensin I and II thus preventing vasoconstriction |
|
Definition
|
|
Term
| Inhibits vascular smooth muscle by preventing Ca influx, decreases vascular resistance, and decreases HR |
|
Definition
|
|
Term
| Beta Blockers have been shown to reduce what? |
|
Definition
|
|
Term
| A pain that results from ischemic heart dz. Causes chest compression/tightness and sometimes pain radiating to the jaw, left arm, or back. Caused by physical exertion but can occur at rest or sleep |
|
Definition
|
|
Term
| Dilate vascular smooth muscle; vasodilation causes decreased cardiac work; decreasing cardiac work decreases myocardial oxygen demand. |
|
Definition
|
|
Term
| The best known antianginal drug. Can be administered sublingually or transdermally. |
|
Definition
|
|
Term
| Block beta-1 receptors which decrease myocardial contraction; decreases HR and cardiac force output; decreases myocardial oxygen demand |
|
Definition
|
|
Term
| Blocks Ca entry into smooth vascular muscle. Decreases ms contraction, decreases cardiac work due to vasodilation, decreases myocardial oxygen demand, increases coronary artery blood flow, and increases myocardial oxygen supply. |
|
Definition
|
|
Term
| Name the 2 most common anticoagulants |
|
Definition
|
|
Term
| Any significant deviation from normal cardiac rhythm. If untreated, impaired cardiac pumping, CVA and/or heart failure may occur |
|
Definition
|
|
Term
| During cardiac ms contraction and relaxation, an exchange of K, Na, and Ca ions occurs. Why is this important for pharm? |
|
Definition
| Some drugs affect the movement of these ions to normalize arrhythmias |
|
|
Term
| Abnormal pulse generation - injury or dz may render the SA and AV nodes incapable. Abnormal pulse conduction - dz or damage may result in action potential delay or action. Simultaneous abnormalities of impulse generation and conduction - combination of both. |
|
Definition
|
|
Term
| Bind to Na channels that are open (activated) or closed (inactivated). Normalizes the rate of Na entry into cardiac tissue and normalizes rhythm. |
|
Definition
|
|
Term
| Decrease excitatory effects of the SNS (norepi and epi) on the heart. Results in deceased HR. Also slows down myocardium conduction. Side effects include poor cardiac pumping resulting in heart failure (rare) |
|
Definition
|
|
Term
| Delay repolarization of cardiac cells which lengthens the time between action potentials. Results in slowing/stabilizing the HR. Side effects include an initial increase in arrhythmia. |
|
Definition
| Drugs that prolong repolarization |
|
|
Term
| Controls arrhythmias by altering excitability and conduction of cardiac tissues. Blocks Ca entry into myocardial and vascular smooth muscle. |
|
Definition
|
|
Term
| What is the primary concern for people taking medications for cardiac arrhythmias?c |
|
Definition
| Common to increase arrhythmia. Must monitor closely |
|
|
Term
| A condition where the heart is unable to pump sufficient blood to peripheral tissues. Caused by some form of cadiac disease or dysfunction. Causes accumulation of fluid int he lungs and peripheral tissues. |
|
Definition
|
|
Term
| Symptoms include peripheral edema and decreased physical capacity. Caused by various mechanisms - cardiac cell disturbances, altered genetic myocardial proteins, changes in neurohormonal factors. |
|
Definition
|
|
Term
| Name the 2 basic goals in the pharmacology treatment of CHF> |
|
Definition
1. Improve pumping ability of heart
2. Decrease cardiac workload |
|
|
Term
| Name a common drug that works to increase myocardial contraction |
|
Definition
|
|
Term
| Improves cardiac pumping ability; increases CO; often used in combo with other drugs as well. Increases intracellular Ca thus increasing contractibility. Inhibits SNS thus decreasing heart stress/deman and relaxes vasculature smooth muscle. |
|
Definition
|
|
Term
| Side effects of digitalis |
|
Definition
| Toxicity. Signs include N&V and CNS disturbances (fatigue, confusion) |
|
|
Term
| Drug that works to decrease cardiac workload (4) |
|
Definition
1. Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors)
2. Beta Blockers
3. Diuretics
4. Vasodilators |
|
|
Term
| Inhibits vasoconstriction |
|
Definition
|
|
Term
| Reduce excessive sympathetic stimulation of the heart |
|
Definition
|
|
Term
| Decrease congestion in lungs and periphery by eliminating fluid; also decrease cardiac workload by decreasing fluid |
|
Definition
|
|
Term
| Decrease peripheral resistance; decreases the amount of blood returning to the heart resulting in decrease in workload |
|
Definition
|
|
Term
| Prevents excessive hemorrhage from damaged vessels. Inadequate blood clotting can lead to excessive blood loss and overactive clotting can cause thrombogenesis |
|
Definition
| Blood coagulation/hemostasis |
|
|
Term
| Influenced by hyperlipidemia which is a chronic increase in plasma lipids. |
|
Definition
|
|
Term
| Can cause cholesterol to be deposited on arterial walls (artherosclerosis) which can lead to thrombosis formation and infarction |
|
Definition
|
|
Term
| Involves the activation of various clotting factors; ultimately leads to conversion of prothrombin to thrombin; thrombin enzyme converts fibrinogen to fibrin which forms a mesh-like structure (clot) |
|
Definition
|
|
Term
| Tissue plasminogen activator converts plasminogen to plasmin; plasmin enzyme breaks down fibrin mesh; destroys clot. |
|
Definition
|
|
Term
| Primarily includes heparin and warfarin (Coumadin) |
|
Definition
|
|
Term
| Promoes the role of antithrombin III which binds to clotting factors and makes them inactive. |
|
Definition
|
|
Term
| Impairs hepatic synthesis of several clotting factors. Side effects include hemorrhage; joint/back pain may indicate hemorrhage; GI distress |
|
Definition
|
|
Term
| Inhibits synthesis of prostaglandins; prevents platelet-induced thrombus formation. Use to treat and prevent MI; prescrived to those who have risk factors for MI such as CAD. |
|
Definition
|
|
Term
| Breakdown and dissolve clots that have already formed. Converts plasminogen to plasmin. Very useful in treating acute MI; can re-establish blood flow caused by coronary occlusion; prevents or reverses damage. |
|
Definition
|
|
Term
| Is aspirin a thrombolytic drug or antithrombolytic drug? |
|
Definition
|
|
Term
| A hyperlipidemia drug that inhibits HMG-CoA reductase which is an enzyme that assists in the synthesis of cholesterol |
|
Definition
| HMG-CoA Reductase Inhibitor (Statins) |
|
|
Term
| The mechanisms of action is unclear for this hyperlipidemia drug. But may increase lipoprotein lipase enzyme activity; thus decreases triglyceride levels. |
|
Definition
|
|
Term
| Responsible for mediating gas exchange between the air and our bloodstream. |
|
Definition
|
|
Term
| These drugs treat symptomatic coughing and irritation from cold, allergies, and respiratory tract infections. |
|
Definition
| Respiratory tract irritation and secretion drugs |
|
|
Term
| Suppress coughing associated with cold and minor irritations. Recommended for short-term use only. Coughing is a defense mechanism that can help expel mucous and foreign material. |
|
Definition
|
|
Term
| Inhibits the cough reflex through a central mechanisms or inhibits the effects of histamine. Sedation is a common side effect. |
|
Definition
| Antitussives (Codeine, hydrocodone, hydromorphone) |
|
|
Term
| A decongestant that binds to alpha 1 receptors in blood vessels of the mucosa causing vasoconstriction; dries up the mucosal vasculature and decreases congestion. |
|
Definition
| Alpha 1 Adrenergic Agonists |
|
|
Term
| The side effects for Alpha 1 Adrenergic Agonists inlude headache, dizziness, nausea, HTN, and palpitations. What is a common one? |
|
Definition
|
|
Term
| Used to treat respiratory allergic response to allergies. |
|
Definition
|
|
Term
| Involved in normal regulation of physiological functions including allergic reactions. |
|
Definition
|
|
Term
| Binds to H1 receptors in the vascular and respiratory tissues |
|
Definition
|
|
Term
| Blocks histamine from binding to the H1 receptors; decrease the allergic response. Side effects can include sedation, fatigue, incoordination, N&V. |
|
Definition
| Antihistamines such as Tavist, Dramamine, Benadryl, Claritin, and Actifed |
|
|
Term
| Decrease viscosity of respiratory secretions |
|
Definition
|
|
Term
| Facilitate production and ejection of mucus |
|
Definition
|
|
Term
| What is the primary mucolytic drug? |
|
Definition
|
|
Term
| What is the only expectorant listed by the FDA? |
|
Definition
|
|
Term
| What are the treatment goals for COPD drugs? |
|
Definition
| Reduce bronchial constriction |
|
|
Term
| Administered via inhaler or nebulizer. Stimulates Beta-2 receptors reslting in bronchodilation. Side effects = Prolonged use may increase bronchial response, cardiac irregularities, nervousness, tremors. |
|
Definition
| Beta-Adrenergic Agonists (Albuterol, Epinephrine) |
|
|
Term
| Results in bronchodilation. May inhibit phosphodiesterase (PDE) enzyme in bronchial smooth muscle; increase cAMP; cause bronchodilation. May also act as an adenosine antagonist; adenosine stimulates bronchocontriction |
|
Definition
|
|
Term
| Side effects of Xanthine Derivatives? |
|
Definition
| Toxicity, nausea, confusion, irritability, cardiac arrhythmias, seizures. |
|
|
Term
| Cause bronchodilation. Prevents acetylcholine (from the PSN) from binding to cholinergic mucosa receptors; preventing bronchoconstriction. Side effects include dry mouth, constipation, tachycardia, and confusion. |
|
Definition
| Anticholinergics (Atropine and Atrovent) |
|
|
Term
| Reduces inflammation associated with COPD disorders. Includes Cortisone, Dexamethasone, and Prednisone |
|
Definition
|
|
Term
| Prevent bronchospasm not bronchoconstriction in pts with asthma. Must be administered before asthma episode. |
|
Definition
|
|
Term
| May inhibit the release of inflammatory mediators (histamine, leukotrienes). Side effects are minimal. |
|
Definition
| Cromones (Cromolyn sodium and nedocrmil sodium) |
|
|
Term
| Treatment of bronchial asthma |
|
Definition
| Bronchodilators (beta-adrenergic agonist, xanthine derivatives, and glucocorticoids) |
|
|
Term
| Results in excessive viscous secretions. Results in pneumonia, pulmonary fibrosis, and infections. |
|
Definition
|
|
Term
|
Definition
| Bronchodilators, Mycolytic/Expectorants, and glucocorticoids |
|
|
Term
| 2 primary types of adrenocorticosteroids |
|
Definition
Glucocorticosteroids
Mineralcorticoids |
|
|
Term
| Controls glucose metabolism and body's ability to deal with stress. |
|
Definition
| Glucocorticoids (cortisol, corticosterone) |
|
|
Term
| Maintain fluid and electrolyte balance |
|
Definition
| Mineralocorticoids (aldosterone) |
|
|
Term
| The precursor of this is cholestrol. All steroid hormones share similar chemical structures. Adding a H+ ion to testosterone synthesis makes estradiol. By manipulating chemical side-groups, pharmacologists develop more effective drugs. |
|
Definition
|
|
Term
| Released on a cyclic basis peaking at 8 am in humans. Prepares human for increased activity. |
|
Definition
|
|
Term
| Alter protein synthesis by directly effecting the cell nucleus. Alters the transcription of DNA genes. Exert anti-inflammatory effects by increasing anti-inflammatory and decrease inflammatory protein synthesis |
|
Definition
|
|
Term
| Increase blood glucose and liver glycogen. This is the result of affecting glucose, fat, and protein metabolism |
|
Definition
| Glucocortcoid Physiological Effects |
|
|
Term
| They inhibit genetic stimulation of inflammatory cells. They inhibit production of pro-inflammatory protoglandins and leukotrienes. |
|
Definition
| Glucocorticoids anti-inflammatory effects |
|
|
Term
| Inhibit the immune response (immunosuppression) by the same means of inhibiting inflammation. Inhibit key components of immune response (T cells) |
|
Definition
|
|
Term
| 4 Clinical uses for glucocorticoids |
|
Definition
Replacement therapy
Evaluate endocrine dysfunction
Inflammation
Immunosuppression |
|
|
Term
| 3 Glucocorticoid Side effects |
|
Definition
| Adrenocortial suppression due to negative feedback, cushing syndrome, and tissue breakdown |
|
|
Term
|
Definition
|
|
Term
| Regulates/increases fluid and electrolyte levels. Increase levels of angiotensin II stimulate aldosterone production. Helps to prolong the antihypotensive effect. |
|
Definition
| Mineralocortoids (aldosterone) |
|
|
Term
| Why might you use mineralocorticoids? |
|
Definition
| To treat Addison Disease (replacement therapy) |
|
|
Term
| The primary male hormone is testosterone and is a what? |
|
Definition
|
|
Term
| estrogens (estradiol) and progestins (progesterone) |
|
Definition
|
|
Term
| Are all male and female hormones considered steroids? |
|
Definition
|
|
Term
| Clinical uses for androgens |
|
Definition
Replacement Therapy
Catabolic States or Pathologies
Delayed Puberty
Breast Cancer
Anemia
Hereditary Angioedema |
|
|
Term
| Primarily seen in athletes or weight lifters. Can promote strength and muscle growth (anabolic steroid). Liver damage, HF, cardiomyopathy, CVA, MI, behavior changes, impaired sperm production,e tc. |
|
Definition
|
|
Term
| Clinical uses for estrogen and progesterone |
|
Definition
-Primarily oral contraceptives
-Replacement therapy
-Hypogonadism
-Failed ovarian development
-Menstrual Irregularities
-Endometriosis
-Carcinoma |
|
|
Term
| Pancreatic endocrine function secretes 2 primary hormones |
|
Definition
|
|
Term
| What is primary role of insulin and glucagon? |
|
Definition
|
|
Term
| Also plays a role in fat and protein metabolism |
|
Definition
|
|
Term
| A defect in production and/or function of insulin. |
|
Definition
|
|
Term
| Primary role is to lower blood glucose by increasing glucose entry into peripheral tissues. |
|
Definition
|
|
Term
| Promotes storage of protein in muscle and lipids in adipose tissue. It encourages protein synthesis by increasing DNA activity in protein synthesis. Inhibits protein breakdown. |
|
Definition
|
|
Term
| Stimulates the production of triglycerides. Inhibits lipid breakdown. |
|
Definition
|
|
Term
| Considered to be the hormonal antagonist to insulin. Increases blood glucose levels and prevetns hypoglycemia. Increases glycogen breakdown in the liver which results in the increase in blood glucose |
|
Definition
|
|
Term
| Can cause damage to neural and vascular structures. |
|
Definition
|
|
Term
Increase Glucose = Increase Insulin
Decrease Glucose = _____Glucagon |
|
Definition
|
|
Term
| Lack of insuline produced |
|
Definition
|
|
Term
| The lack of adequate utilization of insulin in the peripheral tissues |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Can result in glycosuria (increase glucose excretion). Promotes fluid excretion thus dehydration. |
|
Definition
|
|
Term
| Can cause ketoacidosis which can result in coma or death |
|
Definition
|
|
Term
|
Definition
| Control blood glucose levels |
|
|
Term
| This is too large of a polypeptide to be absorbed orally. Typically injected into the subcutaneous tissue. May be adminisered intravenously in severe cases. |
|
Definition
|
|
Term
| Treats hypoglycemia induced by insulin or oral hypoglycemic drugs. Increases glucose release from liver. Administered by injection |
|
Definition
|
|
Term
| Marked by rapid, uncontrolled cell proliferation and conversion of normal cells to undifferentiated state. Excessive cell proliferation results in tumors/neoplasms. Can be benign or malignant. |
|
Definition
|
|
Term
| Limit cell proliferation by killing or altering the growth of cancer cells |
|
Definition
|
|
Term
| Attack healthy cells as well so there will be some adverse effects. Most inhibit DNA/RNA synthesis or inhibit cell division. |
|
Definition
|
|
Term
| Sometimes classified by whether they act at a specific phase of cell division. |
|
Definition
|
|
Term
| Exert effects at a certain stage of cell division |
|
Definition
| Cell-Cycle-Specific (CCS) |
|
|
Term
| Exert their effect during any stage of cell division. More general and effect overall tissues. |
|
Definition
| CCNS (Cell-Cycle-Nonspecific) |
|
|
Term
| % of proliferating cells to total neoplastic cells |
|
Definition
|
|
Term
| These cells are more susceptible to antineoplastics because they are the cells that are causing the problems. |
|
Definition
|
|
Term
| Every malignant tumor cell must be destroyed to eliminate cancer. |
|
Definition
|
|
Term
| These drugs affect good tissue as well as cancer tissue |
|
Definition
|
|
Term
| Induces binding of DNA strands; prevents DNA replication and function; kills cell |
|
Definition
|
|
Term
| Compee/interfere with normal metabolites during cell biosynthesis |
|
Definition
|
|
Term
| Known as the antimitotic drugs because they inhibit cell division |
|
Definition
|
|
Term
| Does not directly destroy cancer cells; affects the regulation of cell division or the immune system. |
|
Definition
| Interferons and Interleukin-2 |
|
|
Term
| Contain platinum. Form strong links in DNA strands; inhibits DNA replication and function. |
|
Definition
|
|
Term
|
Definition
|
|
