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PathopharmA 2

chapter 67, 69, 73-75

chapter 67
Review of the Immune System
Natural immunity (innate) Physical barriers (skin), phagocytic and natural killer cells • Nonspecific, present before exposure
Specific acquired immunity Only after exposure • Cell-mediated  Table 67-1, p.811 • Antibody-mediated: Humoral  IgA, IgD, IgE, IgG, IgM Table 67-2, p.812
ANTIBODIES SPECIFIC TO PARTICULAR ANTIGEN Immunoglobulins(W/ BLOOD)  Gamma globulins Mediate humoral immunity,RELATED TO GLYCOGEN Produced by B lymphocytes CLASSES: IgA, IgD, IgE, IgG, IgM
Antigens RECOGNIZE AND BIND TO IT SEEN IT THROUGH IMMUNIZATION OR SICKNESS May trigger production of antibodies or cytotoxic T cells, or both More than one antibody can bind to the antigen
Characteristic Features of the Immune Response  Selectivity for antigens of nonself origin  Targets only foreign antigens (normal conditions) Specificity  Immune responses are triggered by specific antigens  Diversity  Millions of different antigenic determinants  Memory RAPID RESPONSE reexposure produces a faster, greater, and more prolonged response  Time limitation
Phases of the Immune Response Recognition phase  Antigen recognition by B cells and T cells Activation phase  Proliferation -MORE CELLS CREATED  Differentiation of activated lymphocytes Effector phase  Elimination of antigen
Autoimmunity When the ability to discriminate between self and nonself fails, the immune system can attack the body’s own cells. LIKE IN HIV,
A patient asks the nurse to explain how antibodies protect the body against bacterial diseases. Which statement is an accurate response by the nurse? “Antibodies attach to the antigens (or large molecules) on the bacteria surface, creating a way for white blood cells to attach and destroy the bacteria.” MOST ANTIBBODIES IGA PROTECT BODY IGG ATTACK ANTIGENS-opsoninS
The nurse knows that the production of memory T and B cells will do what? Increase the intensity of the immune response. Memory T- and B-cell production increases both the speed and the intensity of the immune response.
A patient receives an organ transplant. Which component of the immune system will recognize self from nonself (the transplanted organ) in this patient? Major histocompatibility complex molecules
Immunosuppressants Inhibit immune response  Uses  Prevention of organ rejection  Treatment of autoimmune diseases Toxicity  Increased risk of infection  Increased risk of neoplasms
Calcineurin Inhibitors POST-TRANSPLANT= PREVENT ORGAN REJECTION transplant recipients Cyclosporine, tacrolimus, (pimecrolimus): Most effective immunosuppressants available  Cyclosporine was developed first and is used more than tacrolimus
Cyclosporine [Sandimmune]  Some autoimmune diseases NON-BODY RECEPTOR PRODUCE BY INMMUNE RESPONSE Mechanism  Suppresses the production of IL-2, interferon gamma, and other cytokines (nonantibody mediator produced by immune cells) T.USE  Drug of choice for organ rejection (kidney, liver, and heart) of an allogenic transplant
Cyclosporine [Sandimmune] Adverse effects Nephrotoxicity .  Infection ,  Hepatotoxicity.  Lymphoma.  Hypertension  Tremor  Hirsutism  Leukopenia, gingival hyperplasia, gynecomastia, sinusitis, hyperkalemia  Anaphylactic reactions
Glucocorticoids Used to widely suppress immune response  Suppression of allograft rejection, treatment of asthma, rheumatoid arthritis, systemic lupus erythematosus (SLE), and multiple sclerosis, ORGAN TRASPLANT
GLUCOCORTICOID CANT STOP ABRUPTLY Large doses used to prevent rejection  Increased risk of infection, thinning of skin, bone dissolution with fracture, impaired growth in children, and suppression of hypothalamic-pituitary-adrenal axis INCREASE BLOOD SUGAR, RISK FOR INFECTION
Cytotoxic Drugs Suppress immune response by killing B -BONE MARROW and T lymphocytes undergoing proliferation  Nonspecific: Toxic to all proliferating ceLLS
ADR  Bone marrow suppression • Neutropenia • Thrombocytopenia  GI disturbances  Reduced fertility  Alopecia Cytotoxic Drugs
Azathioprine [Imuran] T.USE Adjuvant treatment with transplants  Autoimmune disorders Adverse effects  Blood dyscrasias  Nausea and vomiting  Mutagenic and teratogenic  Neoplasms  Pancreatitis
OTHER CYTOTOXIC DRUG Cyclophosphamide  Anticancer drug  Methotrexate [Rheumatrex, Trexall]  Rheumatoid arthritis  Psoriasis  Suppression of B and T lymphocytes by interfering with folate metabolism
OTHER CYTOTOXIC DRUG Mitoxantrone [Novantrone]  Anticancer agent  Reduction of neurologic disability and clinical relapse for multiple sclerosis (MS) patients  Hazardous drug reserved for patients who are not responsive to safer drugs
Antibodies Basiliximab  Monoclonal antibodies  Blocks activation of T cells by IL-2  Prophylaxis of acute organ rejection after renal transplantation  ADR not increase the risk of oppoT. infections, and no cancers have been observed 1ys after treatmt
After receiving an allograft liver transplant, a patient is prescribed cyclosporine [Sandimmune] oral solution. What is the most critical component of patient teaching that the nurse should stress? Allograft recipients must take immunosuppressants for life to prevent transplant rejection. The other concepts are important to teach the patient but are not as high a priority.
When caring for a 21-year-old female patient, post kidney transplantation, who is taking cyclosporine [Sandimmune] and repaglinide [Prandin], what should the nurse do? Assess the patient for signs and symptoms of infection. increases the risk of infections, which develop in 74% of those treated. Activation of latent infection with the BK virus can result in kidney damage, primarily in kidney recipients. Patientbe warned about early s/s of infection (fever, sore throat)
chapter 73
Pathophysiology of Rheumatoid arthritis RA- IS CONFUSED WITH OSTEOARTHRITIS RA AFFECT SMALL JOINTS-BONES Immune system attacks synovial tissue(line joint)  Arthritis is in the name but RA has systemic manifestations  If untreated, the articular cartilage is completely destroyed causing bone to bone contact and eventually the bones fuse.
Rheumatoid arthritis (RA)-SEEN IN WOMEN Autoimmune inflammatory disorder Treatment  Relieve symptoms  Maintain joint function  Minimize systemic involvement  Delay progression of disease  Nondrug measures
 First-generation NSAIDs: Inhibit COX-1 and COX-2 Risk of thrombotic events and gastrointestinal (GI) ulceration and bleeding Safety: All prescription-strength NSAIDs carry a boxed warning regarding
Second-generation NSAIDs (coxibs): Selectively inhibit COX-2 (Celecoxib)
Glucocorticoids Generalized symptoms: Oral glucocorticoids  One or two joints are affected: Intra-articular injections  Adverse effects HYPERGLYCEMIA, RISK FOR INFECTION  Prednisone and prednisolone
Glucocorticoids USE FOR FLARE UP IN ADL
DMARDs  Disease-modifying antirheumatic drugs
Nonbiologic DMARDs (traditional DMARDs)-PRIMARILY USED Methotrexate-can cause thrombocytopenia FREQUENT LAB WORK-Q6W BUN, CREATINE AND CBC Most rapid-acting DMARD  Therapeutic effect: 3 to 6 weeks ORAL/SUBQ  Adverse effects  Hepatic fibrosis  Bone marrow suppression  GI ulceration  Pneumonitis GI-N/V, DIARRHEA
Sulfasalazine Used to treat inflammatory bowel disease (IBD); now used for RA as well  Anti-inflammatory and immunomodulatory actions  Can slow progression of joint deterioration  GI side effects may be intolerable
DMARDs I :Major Nonbiologic DMARDs-OTHERS Leflunomide [Arava]  Hydroxychloroquine [Plaquenil]  Minocycline [Minocin]  Penicillamine  Azathioprine [Imuran]  Cyclosporine  Prosorba column
DMARDs II Major Biologi-USED WHEN PATIENT ISNT RESPONDING TO THE NON-BIOLOGIC TREATMENTS Tumor necrosis factor (TNF) inhibitors  Suppress immune function  Pose risk of serious infection  Work by neutralizing TNF-PRIMARILY MEDIATOR IN RHEUMATOID ARTHRITIS AND OTHER IV INFUSING Q6-8WS, OR QW
DRUGS Etanercept [Enbrel] • Adalimumab [Humira] • Certolizumab pegol [Cimzia] • Golimumab [Simponi] • Golimumab [Simponi Aria] • Infliximab [Remicade]
A patient with rheumatoid arthritis is prescribed methotrexate [Rheumatrex]. The nurse will expect to observe therapeutic effects with this drug in which time period? Methotrexate acts faster than all other disease-modifying antirheumatic drugs. Therapeutic effects may develop in 3 to 6 weeks
Which statement about enteracept does the nurse identify as true? Enteracept can cause liver injury. Live vaccines canNOT be administered with enteracept OR W/ IMMUNOSUPPRESANT
Injection-site reactions redness, swelling, itching, pain are common with these drugs. Inform patients that symptoms usually subside in a few days, and advise them to contact the prescriber if the reaction persists.
NF antagonists may increase the risk of acquiring or transmitting infection after immunization with a live vaccine. Accordingly, live vaccines should be avoided. Inform parents that pediatric vaccinations should be current before therapy with a TNF antagonist starts.
Gout Causes  Excessive production of uric acid  Impaired renal excretion of uric acid Recurrent inflammatory disorder Seen mainly in men  Hyperuricemia Uric acid level greater than 7 mg/dL in men or greater than 6 mg/dL in women  Uric acid crystals deposited in joints Episodes of severe joint pain (typically in large toe)
Short term to relieve symptoms of attack CONTROL AND TREAT SYMPTOMS Infrequent flare-ups (fewer than 3 times/year)  NSAIDs: First-line agents  Glucocorticoids also used COLCHICINE WAS USED FOR ACUTE, BUT NSAID IS BETTER STILL POSSIBLE HAVE ATTACK EVEN ON LONG-TERM MED
NSAID Indomethacin [Indocin]  Naproxen [Naprosyn]  Diclofenac [Voltaren] Agents of first choice for acute gouty arthritis  Better tolerated and more predictable than colchicine  Relief should be occur within 24 hours; swelling subsides over the next few days
ADVERSE REACTION Gastrointestinal (GI) ulceration, decreased renal function, fluid retention, increased risk of cardiovascular events
Glucocorticoids (PREDISONE) Highly effective in relieving pain Useful for patients who are hypersensitive to, are unresponsive to, or have medical conditions that contraindicate the use of NSAIDs I.EGASTRIC ULCER OR RENAL SUFFICIENCY Avoid in patients prone to hyperglycemia
Colchicine Anti-inflammatory agent  No longer the first-line drug  Now reserved for patients who are unresponsive to or intolerant of safer agents  Not effective against other anti-inflammatory disorders
Colchicine- Uses  Treats acute gouty attack  Reduces incidences of attack  Aborts an impending attack
ADR  Gastrointestinal*  Myelosuppression  Myopathy Drug interaction  Statins  P-glycoprotein (PGP) inhibitors  Inhibitors of CYP3A4
Precautions and contraindications  Older adults  Debilitated patients  Patients with cardiac, renal, hepatic, and GI disease  Pregnant patients
Long term to lower blood levels of uric acid Three or more times per year  Uricosuric drugs
Drug Therapy for Hyperuricemia NOT USED IN ACUTE GOUTY ATTACK, LACK ANTI-INFLAMMATORY OR ANALGESICS PROPERTIES Goals of therapy  Promote dissolution of urate crystals  Prevent new crystal formation  Prevent disease progression  Reduce frequency of acute attacks  Improve quality of life
Allopurinol  Inhibits uric acid formation Reduces blood levels of uric acid  Inhibits xanthine oxidase (XO), an enzyme required for uric acid formation=DAMAGE OF JOINT Uses  Chronic tophaceous gout  Hyperuricemia due to chemotherapy
Adverse effects (generally well tolerated) Hypersensitivity syndrome (rare but potentially fatal)  GI effects  Neurologic effects  Initial therapy may elicit an acute gouty attack
Allopurinol [Zyloprim] drug of choice for chronic tophaceous gout  Reduces blood uric acid levels  Prevents new tophus formation and causes regression of tophi that have already formed  Allows joint function to improve
Allopurinol [Zyloprim] Reversal of hyperuricemia also decreases the risk of nephropathy from deposition of urate crystals in the kidney
Other uses Hyperuricemia that develops secondary to cancer chemotherapy  Certain blood dyscrasias: Polycythemia vera, myeloid metaplasia, leukemia
Probenecid (Generic Only) Increases uric acid excretion Acts on renal tubules to inhibit reabsorption of uric acid  Prevents formation of new tophi and helps diminish existing tophi  May exacerbate acute episodes of gout  Add indomethacin for relief-FOR GOUT
ADVERSE REACTION Usually well tolerated, but mild GI effects occasionally occur; take with food  Risk of kidney damage can be minimized by alkalinizing urine and drinking 2.5 to 3 L of fluid daily during the first few days of treatment
Drug interactions  Aspirin  Other salicylates
OTHER LONG-TERM MEDICATIONS Febuxostat  Inhibits uric acid formation Pegloticase  Converts uric acid to allantoin, a compound readily excreted by the kidney
A patient with acute gouty arthritis requests information on the preferred drug to take to treat a painful flare-up. The nurse should recommend which medication? NSAIDs and glucocorticoids are preferred drugs for treating acute gouty attacks. LONG-TERM DECREASE URIC ACID AND PREVENT GOUTY ATTACK-ATTACK CAN OCCUR PERIODICALY , EVEN WITH LONG-TERM MEDS
A patient is prescribed allopurinol for chronic tophaceous gout. The patient develops a rash. What is the priority intervention by the nurse? Stop the medication and assess the patient for liver and kidney failure. A serious toxic reaction to allopurinol is hypersensitivity syndrome. the patient should be observed for rash, fever, eosinophilia, and liver and kidney dysfunction.
Calcium Physiology Critical to function of the skeletal, nervous, muscular, and cardiovascular systems Body stores  Bones: More than 98% stored in the bones, 2% FLOWS IN BLOOD  Blood: Total serum calcium = 10 mg/dL
ABSORPTION  Occurs in the small intestine  Increased by parathyroid hormone and vitamin D  Glucocorticoids decrease absorption
EXCRETION Calcitonin augments calcium elimination
Parathyroid hormone Promotes calcium resorption from bone  Promotes tubular reabsorption of calcium that had been filtered by the kidney glomerulus  Promotes activation of vitamin D, and thereby promotes increased absorption of calcium from the intestine
Vitamin D Increases calcium resorption from bone  Decreases calcium excretion by the kidney  Increases calcium absorption from the intestine
Calcitonin Released from the thyroid gland when calcium levels in the blood rise too high  Lowers calcium levels by inhibiting resorption of calcium from bone and increasing calcium excretion by the kidney  Does not influence calcium absorption
Hypercalcemia-- Usually asymptomatic  If symptoms are present: Kidney, gastrointestinal (GI) tract, CNS  Causes  Cancer  Hyperparathyroidism  Vitamin D intoxication  Sarcoidosis  Use of thiazide diuretics
Treatment DRUG THAT : promote urinary excretion of calcium decrease mobilization of calcium from bone decrease intestinal absorption of calcium form complexes with free calcium in the blood  IV saline Then diuresis with a loop diuretic
Drugs Furosemide  Glucocorticoids  Gallium nitrate  Bisphosphonates  Inorganic phosphates  Edetate disodium Glucocorticoids  Calcitonin  Bisphosphonates  Cinacalcet (Sensipar): Suppresses parathyroid hormone (PTH) secretion; used for hypercalcemia associated with hyperparathyroidism
Calcitonin Inhibits the activity of osteoclasts  Decreases bone resorption  Inhibits tubular resorption of calcium  Increases calcium excretion  Therapeutic uses: Osteoporosis (treatment not prevention), Paget’s disease
Bisphosphonates-Structural analogs of pyrophosphate  Inhibit bone resorption by decreasing activity of osteoclasts  Indications: Postmenopausal osteoporosis, osteoporosis in men, glucocorticoid-induced osteoporosis, Paget’s disease of bone, hypercalcemia of malignancy
Adverse effects: ocular inflammation, osteonecrosis of the jaw (ONJ), atypical femur fractures, atrial fibrillation (A-fib)
lendronate [Fosamax, Fosamax Plus D]- SAFE Most widely used oral ADR esophageal ulceration, atypical femoral fracture, esophageal cancer, musculoskeletal pain, ocular problems, ONJ, hyperparathyroidism, A-fib Take with a full glass of H2O, Remain upright for at least 30 minutes
Hypocalcemia-- Increases neuromuscular excitability  Clinical presentation  Tetany, convulsions, and spasm of the pharynx
Causes Deficiency of PTH  Deficiency of vitamin D  Deficiency of calcium  Chronic renal failure  Long-term use of certain medications, such as magnesium- based laxatives, and drugs used to manage osteoporosis (eg, bisphosphonates and denosumab)
Treatment Intravenous calcium supplementation (calcium gluconate)  Once calcium levels have been restored: Calcium citrate for maintenance  Vitamin D
Calcium salts Oral • Mild hypocalcemia, dietary supplements Adverse effects: Hypercalcemia • Esp. with high vitamin D  Drug interactions: Corticosteroids, tetracycline, fluoroquinolone, thyroid hormone, phenytoin, bisphosphonates, loop diuretics, thiazide diuretics
Parenteral: Calcium chloride and calcium gluconate Severe hypocalcemia  Adverse effects: Highly irritating; do not give IM; can cause IV extravasation  Drug interaction: Digoxin • Severe bradycardia
Vitamin D Important regulator of calcium and phosphorus homeostasis  Health benefits  Vitamin D deficiency • Less than 20ng/mL  Activation of vitamin D • Determined by calcium availability
Vitamin D toxicity Early symptoms: Weakness, fatigue, nausea, vomiting, anorexia, abdominal cramping, constipation  Later symptoms: Kidney function is affected, resulting in polyuria, nocturia, and proteinuria  Neurologic: Seizures, confusion, ataxia
Vitamin D toxicity Cardiac dysrhythmia  Coma  Calcium deposition in soft tissues  Decalcification of bone despite high blood calcium levels
Other Disorders Involving Calcium
Rickets (usually children)  Stress on softened bones caused by bearing weight results in deformity Treatment: Vitamin D replacement therapy Vitamin D deficiency results in reduced calcium absorption  PTH is released  PTH restores serum calcium by promoting calcium resorption from bone, thereby causing bones to soften
Osteomalacia (adult counterpart of rickets) Absence of vitamin D  Impaired mineralization of bone  Bowing of the legs  Fractures of the long bones  Kyphosis (“hunchback” curvature of the spine)  Diffuse, dull, aching bone pain  Treatment: Vitamin D replacement therapy
Paget’s disease of bone Increased bone resorption and replacement of resorbed bone with abnormal bone  Pelvis, femur, spine, skull, tibia  Pain, skeletal deformity, fracture  Treatment: Pain management and bisphosphonates to suppress bone resorption
Hypoparathyroidism Cause: Inadvertent removal of parathyroid glands during surgery on the thyroid gland  Lack of PTH: Hypocalcemia, paresthesias, tetany, skeletal muscle spasm, laryngospasm, convulsions  Treatment: Calcium supplements
Primary hyperparathyroidism Cause: Usually results from a benign parathyroid adenoma  Increase in PTH secretion: Hypercalcemia and hypophosphatemia
ADR Skeletal muscle weakness, constipation, CNS symptoms, renal calculi, bone abnormalities Treatment Surgical resection of parathyroid glands; calcium-lowering drugs—cinacalcet [Sensipar]
Secondary hyperparathyroidism  Cause: Common complication of chronic kidney disease (CKD)  High levels of PTH and disturbances of calcium and phosphorus homeostasis
Treatment Vitamin D sterol (eg, paricalcitol) and calcium-containing phosphate-binding agents • Cinacalcet [Sensipar]: Can reduce PTH and has a positive effect on calcium and phosphorus levels
Osteoporosis POSTMENOPAUSAL WOMEN DUE TO NO ESTROGEN(MAKE BONE STRONG)-MEN CAN HAVE IT TO Most common disorder of calcium metabolism  Low bone mass and increased bone fragility  Primary prevention  Calcium, vitamin D, lifestyle  Diagnosis  Measurement of bone mineral density (BMD)  Dual-energy x-ray absorptiometry (DEXA)
Treating Osteoporosis in Women Agents that decrease bone resorption: Estrogen, raloxifene, bisphosphonates, calcitonin, denosumab; sufficient calcium and vitamin D are important  Agent that promotes bone formation: Teriparatide (Forteo)
Treating Osteoporosis in Women Agents that reduce fractures: Teriparatide, denosumab, zoledronate
Raloxifene [Evista] Selective Estrogen Receptor Modulator (SERM) Structurally similar to estrogen and binds to estrogen receptors  Comparison to estrogen  Therapeutic uses • Osteoporosis • Breast cancer
Adverse effects Thromboembolic events, such as deep vein thrombosis (DVT), pulmonary embolism, and stroke, and fetal harm
Teriparatide [Forteo] Form of PTH  Produced by recombinant DNA  Only drug that increases bone formation  Generally well tolerated  Nausea, headache, back pain, leg cramps
A nurse has been asked to present a talk on drug therapy for osteoporosis to a group of adults. When preparing the talk, what should the nurse include for the mechanism of action and the adverse effects of the bisphosphonates? Bisphosphonates help decrease the breakdown of the microstructure of bone. Side effects of bisphosphonates include stomach pain, difficulty swallowing, esophageal inflammation, esophageal reflux, and ulcer formation.
What information should the nurse include to reduce adverse effects of bisphosphonates? To reduce ADR , the patient should avoid using aspirin, nonsteroidal anti- inflammatory agents, and antacids when taking bisphosphonates. In addition, the patient should not sit or lie down for 30 minutes after taking the bisphosphonate
Along with the use of drugs for the treatment of osteoporosis, what other measures can help prevent the development of osteoporosis? The nurse should inform the group that adequate calcium and vitamin D intake, as well as not smoking, avoiding alcohol, and performing weight-bearing exercises, can prevent the development of osteoporosis.
The nurse should advise patients who are taking calcium to avoid consumption of which food? SPINACH Calcium absorption is reduced by consumption of foods containing oxalic acid (spinach, rhubarb, Swiss chard, and beets) and phytic acid (bran and whole-grain cereals).
A patient with hyperparathyroidism has a calcium level of 13.2 mg/dL. What medication does the nurse anticipate being prescribed? Salmon calcitonin [Calcimar] Salmon calcitonin is administered for hypercalcemia related to hyperparathyroidism. Calcium levels are lowered by inhibition of bone resorption and increased excretion of calcium by the kidneys.
When preparing to administer intravenous calcium chloride, the nurse should do what? Warm the solution to body temperature. Calcium solutions should be warmed to body temperature before IV dosing. Perform IV injections of calcium chloride slowly (0.5 to 2 mL/min).
arenteral calcium may cause severe bradycardia in patients taking digoxin; infuse calcium slowly and cautiously in these patients. Evaluate the patient for reductions in tetany, muscle spasm, laryngospasm, paresthesias, and other symptoms of severe hypocalcemia.
Created by: Seka_nurse
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