DRUG ACTING ON IMMUNE SYSTEM  Green tea (camellia sinensis) may enhance antitumor effects of

doxorubin
ANTINEOPLASTIC AGENT  Garlic (anticlotting properties, may decrease effects of chemotherapy)
4. PLANT ALKALOIDS
 Cancer is broad term encompassing a group of disease that are  Are derived from natural products that are CCS.
characterized by cellular transformation (by genetic mutation, controlled  Vincristine (Oncovin) developed from the periwinkle plant, was
cellular growth, possible invasion into surrounding tissue and metastasis originally approved by the FDA in the 1960's to treat Wilms' tumor in
the other organ) children.
5. BIOLOGIC RESPONSE MODIFIER
CANCER CHEMOTHERAPY
 These drugs alter the body response to disease such as cancer and
 Anticancer drugs are not selective autoimmune, inflammatory and infectious disease
 Usually administered systematically for cancer that has spread to other  enhancement of hematopoietic function
partsl  Regulation or enhancement of the immune response, including
 Chemotherapy administration is guided by specific protocols that were cytotoxic or cystatic activity against cancer cell.
developed based on the results of controlled.  Inhibition of metastasis, prevention of cell division or inhibition of cell
 The type and extent of the malignancy, type of chemotherapy given maturation.
 Amt. of time that normal cells need to recover. a. Colony Stimulating Factor(CSF)
cell cycle specific-  Work by binding to receptors on the surfaces of specialized
progenitor cells in the bone marrow
GENERAL SIDE EFFECTS OF CHEMOTHERAPY  When hepatopoietic drug binds to a progenitor cell surface, the
1. Fatigue immature progenitor cell
2. Nausea and vomiting  Filgrastim- is a colony stimulating factor that stimulates
3. Constipation or diarrhea progenitor cells for the subset of WBC's known as
4. Alopecia granulocytes
5. Mouth sores b. Interferons
6. Anemia and bleeding problems  Are proteins that have 3 basic properties
7. Infection  Antiviral
8. Myelosuppression- decrease in funtion of bone marrow  Antitumor
 Immunomodulating
TYPES OF ANTICANCER
 There are 3 different groups of interferons drugs each with its
1. ALKYLATING DRUGS own antigenic
 Cause cross-linking of DNA strands, abnormal base pairing or DNA strand  Alpha interferon
breaks, thus preventing the cell from dividing.  Beta interferon
 Cyclophosphamide  Gamma interferon
2. ANTIMETABOLITES
 Classified as CCS 6. IMMUNOSUPPRESSANT DRUG
 Disrupts metabolic processes and can inhibit enzyme synthesis  Use for those who have immuno disease
 Small amt. of the drug is excreted in the urine and up to 80% is excreted by  Decrease/prevent an immune response, hence response and suppress the
the lungs as carbon dioxide immune system.
 Fluorouracil  Selectively suppress T lymphocytes
3. ANTITUMOR ANTIBIOTIC  Cyclosporine
 It inhibit protein and RNA synthesis and bind DNA causing fragmentation.
7. IMMUNIZING DRUGS NURSING INTERVENTION
 Biologic antimicrobial drugs are substances such as antitoxins, antisera,
toxoids, vaccines that are used to prevent... 1. Always check and recheck the specific protocols and schedules of admin
ACTIVE IMMUNIZATION 2. Provide individuals receiving any immunizing drug with the proper instructions
a. TOXOID and updated written materials
 Have been detoxified/weakened with chemicals or heat, 3. Educate the patient receiving vaccine
which renders them nontoxic and unable to revert back a 4. Always provide the patient with written record of immunization
toxic form. 5. Administer all immunizing drugs as prescribed, using route specified
 These antibodies can then neutralize the same exotoxin upon 6. If discomforts appears, apply warm compress administer analgesic, antipyretic
any future exposure. and anti-inflammatory.
 Toxoids were first developed in 1923 at the Pasteur Institute 7. Have epinephrine ready.
by Gaston Ramon and his associates
LINES OF DEFENSE
b. VACCINE
 Suspensions of live, attenuated or kills microorganism that 1: Mechanical, chemical barrier
can stimulate production of antibodies against particular
organism. 2: inflammation and phagocytosis
 Developed by Edward Jenner during 1749
3: Specific immune response and natural killer cell
 People vaccinated with live bacteria/viruses enjoy lifelong
immunity against particular disease PAIN AND INFLAMMATORY AGENTS
 They stimulate the humoral immune system.
MECHANISM OF ACTION Inflammation- localized protective response stimulated by injury to tissues, which
 Active immunizing drugs consist of vaccines and toxoids serves to destroy, dilute or wall off both the injurious agent and the injured tissue.
that may be given either orally or IM and work by Classic sign and symptoms of inflammation include pain, fever, loss of function,
stimulating humoral Immune system. redness and swelling.
 Immunoglobulin attack and kill foreign substances that CHEMICAL MEDIATORS:
may invade the body.
1. Histamines- dilates interior and capillary capability.
2. Kinins- bredikinins- sensation of pain
3. Prostaglandins- vasodilators: increased cellular permeability and may cause
PASSIVE IMMUNIZATION
fever.
a. ANTITOXIN
 Is purified antiserum that is usually obtained from horses inoculated by 2 phases:
toxin. 1. Vascular- 10-15 mins. after an injury (temporal construct and then prolong
b. ANTIVENIN dilatation.
 Antiserum containing antibodies against venom, which is poison
secreted by an animal such as a reptile, insects/arthropod ANTI- INFLSMMATION AGENTS
 Obtained from animals that have been injected with particular venom
 The serum contains immunoglobulin that can neutralize... - Relieves pain (analgesic), redole elevated body temp. (antipy ) and inhibit
MECHANISM OF ACTION platelet aggregation (anti-coagulation)
 Passive immunization drugs are the actual antibodies that can
ASPIRIN- oldest known anti inflammation.
kill/inactivate pathogen
 Provided by the immunizing drugs MECHANISM OF ACTION
 Last shorter in time.
- The NSAIDs (Non-steroidal Anti-inflammatory drugs) work through inhibition of the - Aspirin like but have stronger effect and create less GI irritation
leukotriche pathway, the prostaglandin pathway or both. - Highly protein bound
- Better tolerated than other
NSAIDs relieve pain, headache.  Feaprofen cal (nalfon)
 Naproxen (naprosya)
 Ketoprofen (orudis)
COX1  Flurbiprofen (ansaid)
- Protects stomach lining  Oxaprozin ()
- Decrease fever 5. FEREMATES
- Promote platelet aggregation - Used for acute and chronic arthritis
COX2 - Common Side effect- GI irritation: patient with peptic ulcer should avoid
- triggers pain and inflammation taking this drug
- Other side effect include edema, dizziness, tinnitus, pruritus
Aspirins and NSAIDS blocks COX1 and 2 -
Inhibit COX1 6. OXICAMS (PINOXICAM) FELDESE
- loss stomach lining protection (ulcer) - For long term arthritic condition such as rheumatoid and osteo
- Prevent blood cloth (e.g. Celecoxid) - Well tolerated
Inhibit COX2 - Major advantage are other NSAIDS is by half-life which allow to be taken
- reduces pain only once daily, take 1-2 weeks
- Supress inflammation a. Check patient’s history
b. Obtain drug and herbal history and report any possible drug-
NSAIDS drug/herbal-drug interaction
1. SALICYLATES c. Assess patient for GI upset and peripheral edema.
- aspirin is known chemically as acetylsalicylic acid (ASA) Intervention:
- Developed in 1899 by Adolp Bayer a. Obseve patient for bleeding gums, petechiae, ecchymoses, and black
- Has antiplatelet activity- prevents blood from clumping together stool.
2. PARA-CHLOROBENZOIC ACID b. Report if patient has GI discomforts. Administer NSAIDS
- 1st NSAIDS introduced c. Monitor vital signs
- Used from rheumatoid, gouty arthritis and osteoporosis (COX2 inhibitors vecome available in the market in the last several years to decrease
- Potent prostagenator inhibitor inflammation and pain)
- Highly protein bound (90%) and displaced other protein bound resulting in 7. CORTICOSTEROID
potential toxicity - Controls inflammation by suppressing or preventing any of the opponents
- Indomethacin is very irritating to the stomach and should be taken with of the inflammatory process at the injured site.
food - The half-life of a corticosteroid is long and it is administered once a day in a
 INDOMETHACIN large prescribed dose.
3. PHENYLACETIC ACID DERIVATIVE
- Analgesic and inflammatory effect similar to those aspirins, but is minimal Disease Modifying Anti-Rheumatic Drug (DMARDS)
to antipyretic effect 1. IMMUNO SUPPRESSANTS
- Management for short-term pain - To treat refracting rheumatoid arthritis
- For IM/IV - Drugs such as azathioprine (Imuran), cyclophosphamide (Cytoxan) and
- Used in rheumatoid arthritis and osteoporosis methotrexate () are primarily used to supress the inflammatory process of
 Diclofenac (pain), ketorolac (postsurgical) RA.
4. PROPIONIC ACID DERIVATIVE 2. IMMUNOMODULATOR
- Treat moderate to severe rheumatoid arthritis by disrupting the Signs:
inflammatory process and delaying disease progression d. Non-opioid and Opioid Analgesic Drugs
- Interleukins(IL-1) receptor antagonist and tumor necrosis factor blockers Pain- unpleasant sensory/emotional experience associated with either
are two groups of drugs classified as immunomodulation actual/potential tissue damage.
 Cytokines - It is very personal and individual experience
 Limpkins - Define as whatever the patient says it is, and it exist when
 Monokines patient says it does
 Chemokines - Involves physical , psychological and even cultural factor
 Interleukins Acute- suddenly and responds to treatment
a. Anakinra () Chronic- 6 months and is difficult to treat
- Receptor antagonist blocks activity of IL-1 by inhibiting it from Cancer- pressure on nerves and organ
binding to interleukin receptor located in cartilage and bones Somatic- skeletal, ligaments and joints
b. Antanercept (Enbrel) Vascular- headache/migraine
- Was the first TNF blocker developed Visceral- smooth muscle/organ
- Administered SQ
c. Other TNF blockers include infliximab (Remicade), Adalimumab Pain threshold- decrease in pain, the higher the pain
(Humira), leflunomide (Arava) Pain tolerance- endurance
3. ANTI-MALARIAL 1. Transduction
- Take 4-12 weeks to become apparent 2. Transmission
- Usually used in combination with NSAIDS whose arthritis is not under 3. Perception of pain
control 4. Modulation
- It is still unclear  Endorphins
4. ANTI-GOUT DRUGS  Oxytocin
Gout- attacks joints, tendons and other tissues Non –Opioid analgesic
- Is characterized by an uric acid nutrient disorder and a defect in purine - Less potent than Opioid drugs
nutrient w/c results in increase in urates (VA salts) and an accumulation - Treat mild, to moderate pain
of uric acid (hyperuricemia) infective clearance of uric acid - On the counter meds but COX-2 requires prescription
a. Colchicine a. NSAIDS
- Inhibits migration of leukocyte to other inflamed site 1. Acetaminophen- popular non-prescription drug for the relief of
- Alleviate acute symptoms pain, discomfort and fever
- Not effective in decreasing inflammation - Non-opioid, not inflammatory
- Does not inhibit uric acid synthesis and does not promote uric acid - E.g. Tylenol
excretion. Opioid Analgesics
- Concentration is w/n 2 hours - Treat moderate to severe pain
- Excreted in feces, and 20% in urine - Non- opioid- peripheral nervous system at the pain receptor site
- Oldest known treatment - Opioid acts in Central Nervous System
b. Uric Acid inhibitor 2 isomers
- Not anti-inflammatory drugs; it inhibits the final steps of uric acid o Levo- produce analgesic
biosynthesis, lowers serum (allopurinol) blocks hyposantin o Dextro—does not cause physical dependence
c. Uricosuric Drugs a. Morphine
- Increase rate of uric acid excretion by inhibiting its reabsorption - Extraction from opicea , is a potent opioid analgesic
- Effective in alleviating chronic gout, not use during acute attack - Effective against acute pain resulting myocardial infection, cancer,
- Avoid using aspirin dyspnea, pulmonary edema
- Avoid using aspirin - 3-4 hours duration
 - It may be used as a ______________ - Symptoms: irritability, diaphoresis, restlessness, muscle twitching and
Assessment: increase pulse rate and BP
1. Obtain medical history
2. Determine drug history (not take alcohol)
3. Assess vital signs
4. Monitor urinary output DRUGS ACTING CENTRAL NERVOUS SYSTEM
5. Assess type of pain, location, duration before giving opioid ANXIOLYTICS
NURSING DIAGNOSIS: - Used to treat anxiety and insomnia
1. Constipation - Metabolized in liver and excreted via urine
2. Risk for fall - Benzodiazepines not be discontinued because of withdrawal symptoms
3. Acute pain related to surgical tissue injury - Buspirone- first antianxiety
4. Ineffective reathing pattern ____ excess morphine dosage - Side effect: headache, blurry vision, dry mouth
NURSING INTERVENTION - Benzodiazepines- anticonvulsant, sedative and family group of hypnotic
1. Administer Morphine before pain reaches its peak to maximum Relaxation
effectiveness Pyschotherapy
2. Monitor VS Support System
3. Record patient urine output (600ml) SEDATIVE-HYPNOTIC
4. Check bowel sound (high fibre) - Have a calming effect that depress the CNS
5. Check for pupil changes and reaction - To reduce tension and anxiety
6. Have naloxone available - Inhibit transmission of nerve impulse
7. Validate dose of morphine by administration - Hypnotic cause sleepiness
PATIENT TEACHING
 Barbiturates- 1st benzodiazepines
1. Alleviate side railings
Sleep- transient, reversible and periodic state of rest in which there is
2. Assess presence of blurred vision and headache
decrease in physical and consciousness.
b. Meperidine
Non-REM Sleep
- 1st synthetic opioid
1. Dozing of feeling of shifting off sleep
- Demerol available in mid-1950’s
2. Relaxed but person on easily be awakened
- Schedule II drug- CSA
3. Deep sleep, difficulty to awaken
- Shorter duration than Morphine
4. Very difficult to awake
- Side effects: blood pressure drop
REM sleep
c. Hydromorphine
- With vivid dreams and breathing may be irregular
- Semisynthetic opioid similar to morphine
- Effect approximately 6 times more potent than morphine
Non-Pharmacological Management
- Has factor onset and shorter duration
1. Arise specific hour in morning
- Classified as Schedule II
2. Take few/ no daytime naps
ADVERSE EFFECT OF OPIOID ANALGESIC
3. Avoid drinks that contain caffeine and alcohol
1. Use Opioid analgesic (OA) is contraindicated for patient with head injuries
4. Avoid heavy meals
2. OA given to patient with Respiratory disorder only intensify the respiratory
5. Take warm bath, listen to music/perform other soothing activity by bed.
distress
6. Decrease exposure to noise
3. May cause hypotension and are not indicated for patient in shock for who
7. Drinking copious amount of water
have very low BP
BENZODIAZEPINES
WITHDRAWAL SYNDROME
- Most commonly prescribed sedative-hypnotic drugs
- Caused by physical dependence
 - Either sedative –hypnotic or anxiolytic depending on primary usage Mechanism of Action
Mechanism of Action - The majority of the muscle relaxants work within the CNS. Their beneficial
- Increase action of inhibiting neurotransmitter gamma-amino butyric and effects are believed to come from their sedative effects are rather than
GABA receptors. Neuron excitability is reduced. from direct muscle relaxation
- Their effects are the result of CNS depression in the brain primarily at the
BARBITURATES level of the brainstem, thalamus, and basal ganglia and also at the spinal
cord. The effects of muscle relaxants are relaxation of striated muscles,
- 1st introduced during 1930
mild weakness skeletal muscle, decreased force of muscle contraction and
- Standard drug for treating insomnia and producing sedation
muscle stiffness
- Forming have low therapeutic index
- Used during convulsions
DATROLENE
EPILEPSY- syndrome of CNS dysfunction that are cause symptoms ranging from
- Acts directly on the excitation- contraction coupling of muscle fibers and
momentary distributions to convulsive
not at the level of CNS
1. Primary- without identifiable cause
- Directly affects the skeletal muscles by decreasing the response of the
2. Secondary- with identifiable cause
muscle to stimuli.
- A seizure is brief episode of abnormal electrical act.
- Decrease the amount of calcium that released from storage sites in the
- Convulsion is more severe seizure characterized by involuntary spasmodic
sarcoplasmic reticulum.
contraction.
 Generalized on set (grandular)- all are moving simultaneously
LOCAL AND GENERAL ANESTHETIC AGENTS
 Tonic- Clonic seizure- muscular thorn out
- Anesthetic drugs that reduces or eliminates pain by depressing nerve
- Progressive contraction continued by relaxation
function in CNS and or the PNS
 Tonic seizure- w/o relaxation
- Reduced neurologic function is called Anesthesia
 Clonic- sudden drop
General Vs. Local
 Myoclonic- brief muscular jerky
- General anesthesia involves complete loss of consciousness, loss of body
 Absence seizure
reflexes, elimination and other sensations throughout the entire body, and
 Partial onset seizure skeletal system and smooth muscle paralysis
 Jaksonian seizure - Local anesthesia does not involve paralysis of respiratory function but does
not involve elimination of pain sensation in the tissue enervated by nerves.
ANTIEPILEPTIC AGENTS/ ANTICONVULSANTS Mechanism of Action:
- Prevent seizure - the lipid structure of cell membrane is altered, resulting to impaired
Mechanism of Action physiologic function
1. By suppressing sodium influx through the drug binding to the sodium - the inhibiting neurotransmitter GABA is activated to the GABA receptor
channel when it is inactivated, prolonging the channel inactivation and that pushes chloride ions into the neurons
thereby preventing neuron firing. - Ascending reticular activating system is altered and the neurons cease to
2. By suppressing the calcium influx preventing the electrical current transmit info to the brain.
generated by calcium ion to the t-type calcium channel (Valproic and Stages:
ethuxusimide interaction) 1. Stage of Analgesia (induction stage) - begins with consciousness and
3. By increasing the action of gamma amino butyric acid which inhibits ends with loss of consciousness. Speech difficult, sensation of smell and
neurotransmitter throughout the body pain is loss. Dreams and auditory and hallucination may occur
2. Excitement or Delirium- loss of consciousness caused by depression of
ANTIPARKINSONISM AGENT cerebral cortex.
- Muscle relaxant, centrally act in skeletal muscle relaxant 3. Surgical- surgical procedure is performed during this stage.
- Group of compounds that act predominantly within the CNS to relieve pain 4. Medullary paralysis- toxic stage of anesthesia. Resp. is loast and
associated with skeletal muscle spasm circulatory is collapse
Administration:
- INHALANTS
- IV
- TOIPCAL
- LOCAL ANESTHESIA
- SPINAL ANESTHESIA
Adverse:
- Myocardial depression
- Hepatoxicity
- Respiratory deprssion