Categories
Drugs Acting on the Immune System Nursing Pharmacology

Anti-inflammatory Agents

Anti-inflammatory Agents

Inflammatory Response

  • Protects the body from injury and pathogens
  • Uses chemical mediators to produce the reaction that helps destroy pathogens and promote healing

Anti-inflammatory Agents

  • Block or alter the chemical reactions associated with the inflammatory response

Types of Anti-inflammatory Agents

  • Corticosteroids: used systemically to block the inflammatory and immune systems
  • Antihistamines: block the release of histamine in the initiation of the inflammatory response

Salicylates

  • Can block the inflammatory response
  • Have antipyretic (fever-blocking) properties
  • Have analgesic (pain-blocking) properties

NSAIDs

  • Provide strong anti-inflammatory and analgesic effects
  • Sold over the counter, which may lead to abuse

Common Salicylates

  • Aspirin (Bayer,etc.): treats inflammatory conditions
  • Balsalazide (Colazal): new drug that treats ulcerative colitis
  • Choline magnesium trisalicylate (Trilisate): treats mild pain and fevers as well as arthritis
  • Choline salicylate (Arthropan): treats mild pain and fevers as well as arthritis
  • Mesalamine (Pentasa, etc.): treats inflammation of the large intestine
  • Olsalazine (Dipentum): converted to mesalamine in the colon; has the same direct anti-inflammatory effects
  • Salsalate (Argesic, etc.): treats pain, fever, and inflammation
  • Sodium thiosalicylate (Rexolate): treats episodes of acute gout and muscular pain as well as rheumatic fever

Salicylates

  • Action/indication
    • Inhibit synthesis of prostaglandin; used to treat mild to moderate pain and fever
  • Pharmacokinetics
    • Absorbed from the stomach, peak in 5 to 30 min., metabolized in the liver, and excreted in the urine
  • Contraindications
    • Known allergy, bleeding abnormalities, and impaired renal function
  • Drug-to-drug interactions
    • Interact with other drugs by interfering with absorption

Salicylates—Adverse Effects

  • GI irritation
    • Nausea, dyspepsia, and heartburn
  • Clotting system
    • Blood loss and bleeding abnormalities
  • Eighth cranial nerve stimulation
  • Salicylism
    • Ringing in the ears
    • Acidosis
    • Nausea, vomiting, and diarrhea
    • Mental confusion and lassitude

Types of NSAIDs

  • Propionic acids
    • Fenoprofen
    • Ibuprofen
  • Acetic acids
    • Diclofenac
    • Etodolac
  • Fenamates
    • Mefenamic acid
  • Cyclooxygenase-2 inhibitors
    • Celecoxib

NSAIDs Indications

  • Relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis
  • Relief of mild to moderate pain
  • Treatment of primary dysmenorrhea
  • Fever reduction

Contraindications to NSAIDs

  • Presence of allergy to any NSAID or salicylate
  • Cardiovascular dysfunction or hypertension
  • Peptic ulcer or known GI bleeding
  • Pregnancy and lactation
  • Caution with renal or hepatic dysfunction

Other Anti-inflammatory Agents

  • Acetaminophen (Tylenol)
  • Gold compounds
  • Antiarthritic drugs

Acetaminophen

  • Action/indications
    • Acts directly on the thermoregulatory cells of the hypothalamus
    • Mechanism of action related to analgesic effects is not certain
    • Used to treat pain and fever
      • Treatment of pain and fever associated with a variety of conditions, including influenza
      • Prophylaxis of children receiving diphtheria–pertussis–tetanus (DPT) immunizations
      • Relief of musculoskeletal pain associated with arthritis
  • Pharmacokinetics
    • Absorbed from the GI tract
    • Peaks in ½ to 2 hours
    • Metabolized in the liver
    • Excreted in the urine
    • T½ is about 2 hours
  • Contraindications
    • Known allergy
    • Use with caution in pregnancy and lactation
  • Adverse reactions
      • Headache, hemolytic anemia, renal dysfunction, skin rash, fever, and hepatotoxicity
    • Drug-to-drug interactions
      • Oral anticoagulants increase bleeding

Gold Compounds

  • Action
    • Absorbed by macrophages, which results in inhibition of phagocytosis
  • Indication
    • Tissue destruction is decreased
  • Pharmacokinetics
    • Absorption varies based on the site of administration
    • Widely distributed throughout the body
  • Contraindications
      • Known allergy
      • Diabetes, CHF, and renal or hepatic impairment
    • Adverse reactions
      • Stomatitis, glossitis, gingivitis, bone marrow depression, and dermatitis
    • Drug-to-drug interactions
      • Penicillamine, antimalarials, cytotoxic drugs, and immunosuppressive agents

Other Antiarthritis Drugs

  • Etanercept (Enbrel)
  • Leflunomide (Arava)
  • Penicillamine (Depen)
  • Hyaluronidase derivative (Synvisc)
  • Sodium hyaluronate (Hyalgan)
  • Anakinra (Kineret)

Use of Anti-inflammatory Agents Across the Lifespan

Use of Anti-inflammatory Agents Across the Lifespan
Use of Anti-inflammatory Agents Across the Lifespan

 

 

Prototype Salicylates

Prototype Salicylates
Prototype Salicylates

 

 

Prototype NSAIDs

Prototype NSAIDs
Prototype NSAIDs

 

 

Prototype Acetaminophen

Prototype Acetaminophen
Prototype Acetaminophen

 

 

Prototype Gold Compound

Prototype Gold Compound
Prototype Gold Compound

 

 

Nursing Considerations for Salicylates

  • Assessment (history and physical exam)
  • Nursing diagnosis
  • Implementation
  • Evaluation

Nursing Considerations for NSAIDs

  • Assessment (history and physical exam)
  • Nursing diagnosis
  • Implementation
  • Evaluation
Categories
Drugs Acting on the Immune System Nursing

Introduction to the Immune Response and Inflammation

Introduction to the Immune Response and Inflammation

Body’s Defenses

  • Barrier defenses
  • Cellular defenses
  • Inflammatory response
  • Immune response

Barrier Defenses

  • Skin
    • Protects the internal tissues and organs of the body
  • Mucous membrane
    • Lines the areas of the body that are exposed to external influences but do not have skin protection
  • Gastric acid
    • Secreted by the stomach in response to many stimuli
  • Major histocompatibility complex
    • Distinguishes between self-cells and foreign cells

Types of Cellular Defenses

  • Mononuclear phagocyte system (MPS)
    • Composed of:
      • Thymus gland
      • Lymphatic tissue
      • Leukocytes
      • Lymphocytes
      • Numerous chemical mediators

Types of White Blood Cells—Leukocytes—Produced by the Body

Types of White Blood Cells Leukocytes Produced by the Body
Types of White Blood Cells Leukocytes Produced by the Body

 

 

Types of Leukocytes

Types of Leukocytes
Types of Leukocytes

 

 

The Inflammatory Response Hageman Factor (Factor XII)

  • A chemical in the plasma activated by cell injury
  • Responsible for activating three systems in the body
    • The kinin system
    • The clotting cascade: starts blood clotting
    • The plasminogen system: starts the dissolution of blood clots

The Role of Bradykinin

  • Causes local vasodilation
  • Stimulates nerve endings to cause pain
  • Causes the release of arachidonic acid
  • This release of arachidonic acid causes the release of autocoids

Types of Autocoids Released

  • Prostaglandins
    • Some augment the inflammatory reaction and some block it
  • Leukotrienes
    • Some can cause vasodilation and increased capillary permeability and some can block the reactions
  • Thromboxanes
    • Cause local vasoconstriction and facilitate platelet aggregation and blood coagulation

Clinical Presentation

  • Calor (heat)
    • Caused by increased blood flow
  • Tumor (swelling)
    • Caused by fluid that leaks into the tissues
  • Rubor (redness)
    • Caused by the increase in blood flow due to vasodilation
  • Dolor (pain)
    • Caused by the activation of pain fibers

Inflammatory Response

Inflammatory Response
Inflammatory Response

 

 

Immune Response

  • Specific invasions stimulate specific responses through the immune system
    • Lymphocytes produced in the bone marrow can develop into T lymphocytes or B lymphocytes
    • Other identified lymphocytes include natural killer cells and lymphokine-activated killer cells
      • These cells are aggressive against neoplastic or cancer cells and promote rapid cellular death

Types of T Cells

  • Effector or cytotoxic T cells
  • Helper T cells
  • Suppressor T cells

Function of T Cells

  • Effector or cytotoxic T cells
    • Found throughout the body
    • Aggressive against non-self cells
    • Can directly destroy foreign cells or mark cell so other cells can destroy them
  • Helper T cells
    • Stimulate the activity of B cells and effector T cells
  • Suppressor T cells
    • Monitor the chemical activity in the body
    • Act to suppress B-cell and T-cell activity when the foreign antigen is under control

Cell-Mediated Response

Cell-Mediated Response
Cell-Mediated Response

 

 

The Role of the B Cell

  • Programmed to identify specific proteins or antigens
  • Involved in humoral immunity
  • Produces antibodies or immunoglobulins

Humoral Immune Response

Humoral Immune Response
Humoral Immune Response

 

 

Response to the Varicella Virus

Response to the Varicella Virus
Response to the Varicella Virus

 

 

Other Mediators in the Immune Response

  • •nterferons
    • Prevent viral replication and suppress malignant cell replication and tumor growth
  • Interleukins
    • Chemicals secreted by active leukocytes to influence other leukocytes
  • Tumor necrosis factor (TNF)
    • Chemical released by macrophages; inhibits tumor growth and can cause tumor regression

Conditions That Cause Problems Involving the Immune System

  • Neoplasm
  • Viral invasion
  • Autoimmune disease
  • Transplant rejection

Theories of Autoimmune Disease

  • Result of response to a cell that was invaded by a virus, leading to antibody production to similar cells
  • In a state of immunosuppression, the suppressor T cells do not suppress autoantibody production
  • There is a genetic predisposition to develop autoantibodies
Categories
Chemotherapeutic Agents Nursing Pharmacology

Anti-infective Agents

Anti-infective Agents

Drug Therapy Across the Lifespan

Drug Therapy Across the Lifespan
Drug Therapy Across the Lifespan

Development of Anti-infective Therapy

  • 1920s
    • Paul Ehrlich worked on developing a synthetic chemical effective against infection-causing cells only
    • Scientists discovered penicillin in a mold sample
  • 1935
    • The sulfonamides were introduced

Mechanisms of Action

  • Interfere with biosynthesis of the bacterial cell wall
  • Prevent the cells of the invading organism from using substances essential to their growth and development
  • Interfere with steps involved in protein synthesis
  • Interfere with DNA synthesis
  • Alter the permeability of the cell membrane to allow essential cellular components to leak out

Mechanism of Anti-infective Agents

Mechanism of Anti infective Agents
Mechanism of Anti infective Agents

Anti-infective Activity

  • Anti-infectives vary in their effectiveness against invading organisms
  • Some are selective: they are effective only for a small number of organisms
  • Bactericidal: kill the cell
  • Bacteriostatic: prevent reproduction of the cell

Narrow Spectrum vs Broad Spectrum

  • Narrow spectrum of activity
    • Effective against only a few microorganisms with a very specific metabolic pathway or enzyme
  • Broad spectrum of activity
    • Useful in treating a wide variety of infections

Human Immune Response

  • Goal of anti-infective therapy is reduction of the population of the invading organism
  • Drugs that eliminate all traces of any invading pathogen might be toxic to the host as well
  • Immune response is a complex process involving chemical mediators, leukocytes, lymphocytes, antibodies, and locally released enzymes and chemicals

Problems With Treating Infections in Immunosuppressed Patients

  • Anti-infective drugs cannot totally eliminate the pathogen without causing severe toxicity in the host
  • These patients do not have the immune response in place to deal with even a few invading organisms

Resistance

  • Anti-infectives act on a specific enzyme system or biological process; many microorganisms that do not act on a specific system are not affected by the particular drug
  • This is considered natural or intrinsic resistance to that drug

Acquired Resistance

  • Microorganisms that were once sensitive to the particular drug have begun to develop acquired resistance
  • This results in serious clinical problems

Ways Resistance Develops

  • Producing an enzyme that deactivates the antimicrobial drug
  • Changing cellular permeability to prevent the drug from entering the cell
  • Altering transport systems to exclude the drug from active transport into the cell
  • Altering binding sites on the membranes or ribosomes, which then no longer accept the drug
  • Producing a chemical that acts as an antagonist to the drug

Preventing Resistance

  • Limit the use of antimicrobial agents to the treatment of specific pathogens sensitive to the drug being used
  • Make sure doses are high enough, and the duration of drug therapy long enough
  • Be cautious about the indiscriminate use of anti-infectives

Identification of the Pathogen

  • Identification of the infecting pathogen is done by culture
  • A culture of a tissue sample from the infected area is done
    • A swab of infected tissue is allowed to grow on an agar plate
    • Staining techniques and microscopic examination identify the bacterium
  • Stool can be examined for ova and parasites

Sensitivity of Pathogen

  • Shows which drugs are capable of controlling the particular microorganism
  • Important to be done for microorganisms that have known resistant strains
  • Along with a culture, identifies the pathogen and appropriate drug for treatment

Factors Affecting Prescribing Anti-infective Agents

  • Identification of the correct pathogen
  • Selection of the right drug
    • One that causes the least complications for that particular patient
    • One that is most effective against the pathogen involved

Combination Therapy

  • Use of a smaller dosage of each drug
  • Some drugs are synergistic
  • In infections caused by more than one organism, each pathogen may react to a different anti-infective agent
  • Sometimes, the combined effects of the different drugs delay the emergence of resistant strains

Adverse Reactions to Anti-infective Therapy

  • Kidney damage
  • Gastrointestinal (GI) tract toxicity
  • Neurotoxicity
  • Hypersensitivity reactions
  • Superinfections

Prophylaxis of Anti-infective Agents

  • People traveling to areas where malaria is endemic
  • Patients who are undergoing gastrointestinal or genitourinary surgery
  • Patients with known cardiac valve disease, valve replacements, and other conditions requiring invasive procedures