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57 Cards in this Set
- Front
- Back
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Humoral Immunity
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mediated by B cells; the aspect of immunity that is mediated by secreted antibodies produced in the cells of the B lymphocytes. B Cells (with co-stimulation) transform into plasma cells which secrete antibodies. Co-stimulation of the B cell can come from another antigen presenting cell. This entire process is aided by CD4+ T-helper 2 cells, which provide co-stimulation. Secreted antibodies bind to antigens on surfaces of invading microbes (such as viruses or bacteria), which flags them for destruction. Humoral immunity is so named because it involves substances found in the humors, or body fluids.
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Cellular Immunity
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mediated by T cells & does not involve antibodies but rather the activation of macrophages, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes & release of various cytokines (small cell-signaling protein molecules) in response to an antigen.
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azathioprine (Imuran)
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Used as an adjunct medication to prevent rejection of kidney transplants
Also used in the treatment of rheumatoid arthritis |
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cyclosporine (Sandimmune)
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Primary drug used for the prevention of kidney, liver, heart, & bone marrow transplant rejection
May be used for other autoimmune disorders *grapefruit juice |
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tacrolimus (Prograf)
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Used only for the prevention of liver transplant rejection
Others uses are unlabeled uses |
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glatiramer acetate (Copaxome)
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The only immunosuppressant drug used for the treatment of multiple sclerosis (MS)
Used to reduce the frequency of MS relapses (exacerbations) in relapsing-remitting multiple sclerosis (RRMS) |
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Immunomodulators (IMs)
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Immunosuppressants
Immunizing drugs Biologic response modifiers (BRMs) -Hematopoietic drugs -Immunomodulating drugs |
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Interferons (IFNs)
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proteins made & released by host cells in response to presence of pathogens; allow communication between cells to trigger the immune system
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Monoclonal antibodies
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produced to specifically bind to a substance
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Interleukin receptor agonists & antagonists
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function of immune system depends in a large part on interleukins, Majority synthesized by helper CD4+ T lymphocytes, & through monocytes, macrophages, & endothelial cells. They promote development & differentiation of T, B, & hematopoietic cells.
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BRMs: Mechanisms of Action
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Enhancing or restoring the host’s immune system defenses against the tumor
Using drugs that are directly toxic to tumor cells, causing them to rupture (lyse) Modifying the tumor’s biology -Tumor cells cannot survive & reproduce |
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Humoral Immune System
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B-lymphocytes (B cells)
Antibody-antigen complex Memory cells Antibodies also known as immunoglobulins (Ig) Monoclonal antibodies Five major types of naturally occurring immunoglobulins: IgA, IgD, IgE, IgG, IgM |
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Cell-Mediated Immune System
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Cytotoxic T cells
T-helper cells T-suppressor cells Macrophages (derived from monocytes) Natural killer (NK) cells Polymorphonuclear (PMN) leukocytes (neutrophils) |
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Hematopoietic Drugs: Mech
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HDs promote synthesis of various types of major blood components by promoting growth, or differentiation, & function of precursor cells in bone marrow
Produced by rDNA technology HDs are used to: Decrease the duration of chemotherapy-induced anemia, neutropenia, & thrombocytopenia Decrease bone marrow recovery time after transplantation or irradiation Enable higher doses of chemotherapy to be given Stimulate other cells in the immune system to destroy or inhibit the growth of cancer cells Other uses |
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Hematopoietic Drugs
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Erythropoietic drugs RBCs
Colony-stimulating factors (CSFs) WBCs Platelet-promoting drugs Epoetin alfa (Epogen, Procrit) |
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darbepoetin alfa (Aranesp)
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Longer-acting form of epoetin alfa
Also used to stimulate RBC production |
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filgrastim (Neupogen)
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Granulocyte colony-stimulating factor (G-CSF)
Stimulates precursor cells for the type of WBCs known as granulocytes |
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pegfilgrastim (Neulasta)
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Longer-acting form of filgrastim
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sargramostim (Leukine)
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Stimulates bone marrow precursor cells that make both granulocytes & phagocytic (cell-eating) cells; known as monocytes
Granulocyte-macrophage colony-stimulating factor (GM-CSF) |
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oprelvekin (Neumega)
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Also classified as an interleukin (IL-11)
Stimulates bone marrow cells (megakaryocytes) that eventually become platelets |
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Hematopoietic Drugs: Indications
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Used in patients who have experienced destruction of bone marrow cells as a result of cytotoxic chemotherapy
Decrease the duration of low neutrophil counts, thus reducing the incidence & duration of infections Enhance the functioning of mature cells of the immune system, resulting in greater ability to kill cancer cells as well as viral- & fungal-infected cells Also enhance RBC & platelet counts in patients with bone marrow suppression resulting from chemotherapy Allow for higher doses of chemotherapy, resulting in the destruction of a greater number of cancer cells |
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Interferons: Indications
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Viral infections
-Genital warts, hepatitis Cancer -Chronic myelogenous leukemia, follicular lymphoma, hairy-cell leukemia, Kaposi’s -sarcoma, malignant melanoma Autoimmune disorders -Multiple sclerosis, others |
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Monoclonal Antibodies (MABs)
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Produced in the laboratory & designed to recognize and bind to specific antigens
Monotherapy or used in combination with chemo/other Used to target specifically cancer cells Block tumor growth &/or alert immune system to attack Minimal effect on healthy cells Fewer adverse effects than traditional antineoplastic meds Used to treat cancers & rheumatoid arthritis Were classified as biologic response modifiers; now thought of as targeted therapies specifically with cancer Changing the way cancer is treated |
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Aldesleukin
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acts indirectly to stimulate or restore immune response
Aids in causing T cells to multiply, including lymphokine-activated killer (LAK) cells LAK cells recognize & destroy only cancer cells, & ignore normal cells Used for metastatic renal cell carcinoma & malignant melanoma Under study for use in other types of cancer |
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denileukin diftitox
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IL-2 receptor antagonist (IL-2Ra)
Binds to cell-surface IL-2 receptors on normal as well as certain malignant cells Causes cell death |
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anakinra (Kineret)
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IL-1 receptor antagonist
Used to control symptoms of rheumatoid arthritis |
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Antirheumatoid Arthritis Drugs
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Also known as disease-modifying antirheumatic drugs (DMARDs)
Slow onset of action—several weeks May take 3 to 6 months to see full effects Can have much more toxic adverse effects than NSAIDs Antiinflammatory, antiarthritic, immunomodulating effects |
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etanercept (Enbrel)
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Used to treat rheumatoid arthritis (including juvenile RA) & psoriasis
Patients must be screened for latex allergy (some dosage forms may contain latex) Onset of action: 1 to 2 weeks Contraindicated in presence of active infections - Reactivation of hepatitis & TB have been reported |
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abatacept (Orencia)
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Used to treat rheumatoid arthritis
Caution if history of recurrent infections or COPD Patients must be up-to-date on immunizations before starting therapy May increase risk of infections associated with live vaccines May decrease response to vaccines |
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Sodium Bicarbonate
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Highly soluble
Buffers the acidic properties of HCl Quick onset, but short duration May cause metabolic alkalosis Sodium content may cause problems in patients with HF, hypertension, or renal insufficiency |
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Antiflatulents
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used to relieve the painful symptoms associated with gas
-activated charcoal -simethicone (gas-x) |
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H2 Antagonists: Mechanism of Action
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Block histamine at the (H2) receptors of
acid-producing parietal cells Production of hydrogen ions is reduced, resulting in decreased production of HCl |
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cimetidine (Tagamet)
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Binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs & increased drug levels
All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for absorption Smoking has been shown to decrease the effectiveness of H2 blockers |
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Proton Pump Inhibitors: Mechanism of Action
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Irreversibly bind to H+/K+ ATPase enzyme
Bond prevents the movement of hydrogen ions from the parietal cell into the stomach Results in achlorhydria—ALL gastric acid secretion is temporarily blocked - To return to normal acid secretion, the parietal cell must synthesize new H+/K+ ATPase |
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Proton Pump Inhibitors: Indications
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GERD maintenance therapy
Erosive esophagitis Short-term treatment of active duodenal & benign gastric ulcers Zollinger-Ellison syndrome: a rare disorder that causes tumors to form in pancreas or duodenum. may cause ulcers to develop in stomach & duodenum. Tumors are called gastrinomas & secrete a large amount of gastrin which causes an excessive production of stomach acid Treatment of H. pylori–induced ulcers - Given with an antibiotic |
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Sucralfate(Carafate)
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Cytoprotective drug
Used for stress ulcers, peptic ulcer disease Attracted to & binds to base of ulcers & erosions, forming a protective barrier over areas Protects areas from pepsin, which normally breaks down proteins (making ulcers worse) Little absorption from the gut May cause constipation, nausea, & dry mouth May impair absorption of other drugs—give other drugs at least 2 hours before sucralfate Do not administer with other medications Binds with phosphate; may be used in chronic renal failure to reduce phosphate levels |
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Misoprostol (Cytotec)
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Synthetic prostaglandin analog
Prostaglandins have cytoprotective activity Protect gastric mucosa from injury by enhancing local production of mucus or bicarbonate Promote local cell regeneration Help to maintain mucosal blood flow Used for prevention of NSAID-induced gastric ulcers Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea |
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Adsorbents
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Coat the walls of the GI tract
Bind to the causative bacteria or toxin, which is then eliminated through the stool Examples: bismuth subsalicylate (Pepto-Bismol), activated charcoal, aluminum hydroxide, others |
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Antimotility drugs: anticholinergics
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Decrease intestinal muscle tone & peristalsis of GI tract
Result: slows the movement of fecal matter through the GI tract Examples: belladonna alkaloids (atropine, hyoscyamine) |
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Antimotility drugs: opiates
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Decrease bowel motility & relieve rectal spasms
Decrease transit time through the bowel, allowing more time for water & electrolytes to be absorbed Reduce pain by relief of rectal spasms Examples: paregoric, opium tincture, codeine, loperamide (over the counter), diphenoxylate |
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Intestinal flora modifiers
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Probiotics or bacterial replacement drugs
Bacterial cultures of Lactobacillus organisms work by: Supplying missing bacteria to the GI tract Suppressing the growth of diarrhea-causing bacteria Example: L. acidophilus (Lactinex) |
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Antidiarrheals: Interactions
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Adsorbents decrease the absorption of many drugs, including digoxin, clindamycin, quinidine, hypoglycemic drugs, others
Adsorbents cause increased bleeding time & bruising when given with anticoagulants Antacids can decrease effects of anticholinergic antidiarrheal drugs Many other interactions |
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Laxatives
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Bulk forming
Emollient Hyperosmotic Saline Stimulant Peripherally acting opioid antagonists |
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Bulk forming
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examples psyllium (Metamucil) & methylcellulose (Citrucel)
High fiber Absorb water to increase bulk Distend bowel to initiate reflex bowel activity |
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Emollient
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examples Stool softeners: docusate salts (Colace, Surfak) & Lubricants: mineral oil
Stool softeners & lubricants Promote more water & fat in the stools Lubricate the fecal material & intestinal walls |
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Hyperosmotic
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Increase fecal water content
Results in bowel distention, increased peristalsis, & evacuation |
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Saline
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Increase osmotic pressure within the intestinal tract, causing more water to enter the intestines
Results in bowel distention, increased peristalsis, & evacuation |
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Stimulant
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Increases peristalsis via intestinal nerve stimulation
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Peripherally Acting Opioid Antagonists
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Treatment of constipation related to opioid use & bowel resection therapy
Block entrance of opioid into bowel Strict regulations for use Allow bowel to function normally with continued opioid use |
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Antiemetics & Antinausea Drugs: Mechanism of Action
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Many different mechanisms of action
Most work by blocking one of the vomiting pathways, thus blocking the stimulus that induces vomiting |
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Anticholinergic drugs (ACh blockers)
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Bind to & block acetylcholine (ACh) receptors in the inner ear labyrinth
Block transmission of nauseating stimuli to CTZ Also block transmission of nauseating stimuli from the reticular formation to the VC Scopolamine Also used for motion sickness (transdermal patch) |
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Antihistamine drugs (H1 receptor blockers)
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Inhibit ACh by binding to H1 receptors
Prevent cholinergic stimulation in vestibular & reticular areas, thus preventing nausea & vomiting Also used for motion sickness, nonproductive cough, allergy symptoms, sedation |
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Antidopaminergic drugs
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Block dopamine receptors on the CTZ
Also used for psychotic disorders, intractable hiccups prochlorperazine (Compazine) promethazine (Phenergan) droperidol (Inapsine): Use is controversial because of associated cardiac dysrhythmia Others |
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Prokinetic drugs
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Block dopamine in the CTZ
Cause CTZ to be desensitized to impulses it receives from the GI tract Also stimulate peristalsis in GI tract, enhancing emptying of stomach contents Also used for GERD, delayed gastric emptying metoclopramide (Reglan) Long-term use may cause irreversible tardive dyskinesia |
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Serotonin blockers
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Block serotonin receptors in the GI tract, CTZ, & VC
Used for nausea & vomiting in patients receiving chemotherapy & for postoperative nausea & vomiting |
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Tetrahydrocannabinoids
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Major psychoactive substance in marijuana
Inhibitory effects on reticular formation, thalamus, cerebral cortex Alter mood & body’s perception of its surroundings dronabinol (Marinol) Used for nausea & vomiting associated with chemotherapy, & anorexia associated with weight loss in AIDS patients |
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Ginger
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Used for nausea & vomiting including that caused by chemotherapy, morning sickness, & motion sickness
Adverse effects Anorexia, nausea & vomiting, skin reactions Drug interactions May increase absorption of oral medications Increase bleeding risk with anticoagulants |
