The Nursing Process
The Nursing Process NUR 220
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Date Created: 02/03/15
NUR 22101 Pathopharmacology II Final Examination Study Guide Spinal Cord Disorder and Drugs for Muscle Spasm and Spasticitv 1 What is the role of the sympathetic and parasympathetic nervous system in relation to the spinal cord Svaathetic nervous system receives innervation from cell bodies in the ThoracoLumbar region first thoracic through the second lumbar vertebrae ParastDathetic nervous system functions to conserve and restore energy Rest or restore response Defecation digestion diuresis a What is the primary neurotransmitter Acetylcholine b What is the role of the somatic nervous system Responsible for interaction with the external environment receives sensation from skin muscles and joints Sends motor impulses to skeletal muscles Controls voluntary muscle movement c Differentiate between cervical thoracic lumbar and sacral nerve function Cervical C1C8 back of head neck and shoulders arms and hands diaphragm Thoracic TlT12 chest muscles some muscles of the back parts of abdomen Lumbar LlL5 lower abdomenback buttocks some external genital organs parts of leg Sacral gSlSS thighs and lower parts of legs area around the anus most external genital organs feet 1 How do the afferent and efferent pathways function Afferent transmit information from peripheral receptors to the cerebral cortex Efferent transmit information from cerebral cortex to brain stem or spinal cord 2 Describe the most common etiologies of spinal cord injury a Who is most at risk 81 males Average age 334 years Motor vehicle accidents falls sport related injuries amp Violence b What areas of the spine are most commonly affected Why Most mobile portions of vertebral column locations where the spinal cord occupies largest portion of the vertebral canal Most common Cervical C1 C2 C4C7 and Thoracolumbar T10L2 c Differentiate between i Simple fracture Single break affecting transverse or spinous process ii Compressed fracture Wedge fracture vertebral body compressed anteriorly iii Comminuted fracture Burst fracture vertebral body shattered into fragments iv Dislocation Vertebrae move out of alignment 3 Differentiate between primary injury and secondary injury Primary injury Concussion temporary disruption of cordmediated function usually 2448 hours Contusion bruising of neural tissue resulting in edema and temporary loss of function Compression pressure on cord causing ischemia to tissues must be decompressed to prevent damage to cord Laceration tearing of the neural tissues of the spinal cord may be reversible only if slight damage to neural tissues permanent loss of function if spinal pathways are disrupted Transection severing of spinal cordpermanent loss of function Secondarv iniurv Hemorrhage bleeding into neural tissue due to rupture of blood vessel no major loss of function Obstruction of blood supply causes local ischemia Excitotoxicity are of injury gets ooded with excitatory neurotransmitter Glutamatecan kill nerve cells Invasion of the immune response cytokines exert a malignant in uence on nerve cells Oxygen free radicals highly reactive oxygen molecules disable cell membranes and inhibit cell growth Apoptosis nerve cells destruct kills oligodendrocites a What is the difference between complete and incomplete lesions Incomplete lesion implies preservation of the motor or sensory fibers or both below the level of the lesion Complete lesion implies total loss of voluntary muscle control and sensation below the level of the lesion i Anterior Cord Syndrome loss of motor function below the level of injury loss of pain and temperature sensation touch pressure position and vibration remains intact ii Central Cord Syndrome most often caused by hyperextension injury motor deficit in upper extremities especially the hands less pronounced deficit in lower extremities varying degrees of bladder dysfunction iii BrownSequard Syndrome Most commonly associated with penetrating injury hyperextension exion and compression fractures Ipsilateral paralysis Ipsilateral loss of touch pressure Vibration and position sense contralateral loss of pain and temperature sensation iv Posterior Cord Syndrome loss of pain proprioception loss of tactile sensation v Cauda Equine Syndrome compression of nerve roots below lumbar 1 caused by fracture dislocation or herniated disk lower extremity motor deficit variable sensor motor dysfunction variable re ex dysfunction variable bowel bladder and sexual dysfunction 4 Differentiate between the functional limitations of quadriplegia and paraplegia a What symptoms will you see in the patient with injuries to different levels of the spinal cord Quadriplegia occurs when injury is above the first thoracic vertebra paralysis usually affects the cervical spinal nerves paralysis of all four limbs weakening of abdominal and chest muscles will result in weakened breathing and the inability to properly cough and clear the chest Paraplegia occurs when the level of the injury is below the first thoracic spinal nerve degree to which the person is paralyzed can vary from the impairment of leg movement to complete paralysis of the legs and abdomen up to the nipple line paraplegic usually have use of their arms and hands b What are the goals of care Stabalize prevent further damage save tissue function prevent complications 5 What is the Frankel Classification System Class A complete transection of cord with complete loss of function Class B incomplete transection with preserved sensation only Class C Incomplete transection with nonuseful motor function Class D incomplete transection with useful motor function Class E Complete recovery 6 Describe spinal shock a When does it occur An immediate response to spinal cord injury Lasts 720 days b What symptoms do the patient present that indicate spinal shock is resolving Reappearance of re ex that has been depressed after injury sign spinal shock is resolving 7 What is Autonomic Dysreflexia Massive uncompensated cardiovascular response to stimulation of the sympathetic nervous system serious medical emergencylife threatening situation a Which patients are most at risk Patients with lesions at or above T6 b What are the presenting symptoms paraoxysmal hypertension up to 300 mmHg pounding headache 10 blurred vision sweating and ushing above level of lesion cold extremities and goose esh below level of lesion due to vasoconstriction Bradycardia attempt by body to cause vasodilation and lower blood pressure c How is it treated Removal of stimuli and lowering the blood pressure 1 What is the risk if left untreated Death How can muscle spasm be treated Centrally acting muscle relaxants treat localized muscle spasm Drugs for spasticity Groups are not interchangeable drugs for muscle spasm DO NOT treat spasticity drugs for spasticity do not treat muscle spasm What are the two groups of drugs which cause skeletal muscle relaxation a Which group is primarily used to treat muscle spasm Centrallyacting muscle relaxants NSAIDS Describe the mechanism of action route of administration therapeutic use and adverse effects associated with the centrally acting muscle relaxants Muscle Relaxants MOA Unclear Therapeutic Use Adverse effects Relieve local muscle spasm decrease local muscle pain increase ROM Generalized CNS depression drowsiness dizziness lightheadedness hepatic toxicity physical dependence cannot be withdrawn from abruptly I Diazepam enhancing effects of GABA I Tizanidine agonist action at presynaptic alpha2 receptor 11 12 Define spasticity Movement disorders of CNS origin Most common causes upper motor neuron damage multiple sclerosis cerebral palsy spinal cord injury stroke Characteristics include heightened muscle tone spasm clonis loss of dexterity Describe the mechanism of action route of administration therapeutic use and adverse effects associated with a baclofen Lioresal b diazepam Valium c dantrolene Dantrium Baclofen Lioresal MOA Acts in the spinal cord suppresses hyperactive re exes may mimic the action of GABA on spinal neurons Route of Administration Therapeutic Use Adverse Effects PO or Intrathecal Multiple sclerosis spinal cord injury cerebral palsy NOT WITH STROKE decreases exor and extensor spasms suppresses resistance to passive movement no direct effect on skeletal muscle does not decrease muscle strength CNS depressant drowsiness dizziness weakness fatigue gt Symptoms diminish with repeated use Should be increase gradually Other symptoms nausea constipation urinary retention DO NOT TAKE WITH ALCOHOL Diazepam Valium MOA Acts in CNS mimics action of GABA ROA PO TU Adverse effects Sedation Dantrolene Dantrium MOA Acts directly on skeletal muscle suppresses the release of calcium from the sarcoplasmic reticulum SR ROA TU Spasticity associated with multiple sclerosis cerebral Adverse effects palsy spinal cord injury Malignant hyperthermia potentially fatal condition caused by succinylcholine and general anesthetics Hepatic toxicity occurs most commonly with women over 35 muscle weakness drowsiness diarrhea acne like rash Learning Obiectives for Musculoskeletal Disorders Understand pathophysiology of RA LEHNE 920 I Exact etiology is unknown Chronic autoimmune disease synovial space in joints infiltrated with in ammatory cells macrophage tcells plasma cells these release cytokines I cell proliferation Pannus formation an abnormal layer of granulation tissue in amed proliferating synovial membrane invades cartilage and bone ultimately destroys the joint Recognize the clinical presentations of RA Joint in ammation I joint destruction disfigurement hands wrists feet fever weakness and fatigue weight loss thinning of the skin in ammation of the sclera and corneal ulcers vasculitis nodules under the skin Four must be present for diagnosis morning stiffness for more than 1 hours will be stiff in the momingafter they get up and start moving around they will loosen up Symmetric arthritis Rheumatoid nodules Serum RF increased rheumatoid factor in the blood Arthritis of hands or wrist joints Arthritis of more than 3 joints Radiographic changes Must be present for six weeks List at least four differences between RA and 0A RA Age of onset Any age Above 40 Disease Distribution Systemic Localized In ammation Present Absent or mild Joint involvement Symmetric Maybe asymmetric Pannus Present Absent Presentation Malaisefatigue Deep pain fever Identify four appropriate nonpharmacological interventions for RA Physical theraDV massage warm baths topical heat warm and dry feels good Exercise balance between exercise and rest want to keep people moving but want to balance with rest Rest is IMPORTANT Surgery joint replacement ex bionic knee Identify the appropriate reasons for use of NSAIDs DMARDs and glucocorticoids NSAIDs fast relief of symptoms but do not prevent joint damagedisease progression alter platelet aggregation Glucocorticoids rapid relief of symptoms slow disease progression longterm can cause serious toxicity if you need a quick fix this might be a good way to go DMARDs diseasemodifying antirheumatic drugs slowly reduce joint destruction amp disease progression more toxic than NSAIDs takes a few months for the DMARDs to work NSAIDs or glucocorticoids in the meantime Learning Obiectives for Drugs for Bone disorders 0 Identify common risk factors for osteoporosis 0 What is osteoporosis 0 Thinning of the density and strength of bones 0 Common risk factors 0 Non modifiable versus potentially modifiable 0 Non modifiable risk factors 0 Caucasian 0 HO adult fractures 0 Family hx of fractures 0 Advanced age old age 0 Dementia 0 Female gender 0 Poor healthfrailty 0 Potentially modifiable risk factors 0 Low calcium intake 0 Postmenopausal Estrogen de ciency 0 Estrogen limits the life span of osteoclasts 0 Most common risk menopause 0 Why 0 Estrogen limits the lifespan of osteoclasts as we age there is less estrogen which causes an increase in osteoclasts 0 Inadequate exercise 0 Wgt 127 0 Anorexia nervosa 0 Cigarette smoking 0 Alcoholism and caffeine consumption 0 Deficiency in Vitamin D and calcium 0 Nutritional disorders 0 Thyroid disorders 0 Disrupt bone building 0 Decreased level of hormones 0 Estrogen and testosterone Types of Osteoporosis Primary Osteoporosis both are related to aging 0 Type I 0 Postmenopausal 0 Related to aging 0 Type II 0 Senile 0 Already at an advanced old age 0 Related to zinc deficiency Secondary Osteoporosis 0 Secondary to medical conditions 0 Bone marrow disorders 0 Metabolic disorders 0 GI diseases 0 Malignancies 0 Rheumatic disease 0 OR secondary to medications 0 Glucocorticoids 0 Anticonvulsants 0 Excess thyroid hormone 0 Heparin 0 Medroxyprogesterone 0 Protonpump inhibitors 0 Used for acid re ex 0 Stomach is naturally acidic 0 TUMS is a common medication used for heartburn 0 Main ingredient 0 CALCIUM Explain nonpharmacologic therapies used to treat osteoporosis Limit alcohol and caffeine consumption Exercise Smoking cessation 12 mg of element calciumday 4001000 IU of Vitamin D Discuss drug treatments for osteoporosis Basis of bone remodeling 0 Osteoblasts bone building cells 0 Osteoclasts cause bone demineralization 0 Using this information in treatment 0 2 methods 0 Encourage osteoblasts OR 0 Decrease the lifespan of osteoclasts 0 Calcium Daily Recommendation 0 What is the recommendation for my age 1124 0 1200 mgday 0 Some is good but more is not necessarily better 0 Should NOT exceed 2000 mgday 0 Sources of Calcium 0 Dairy products 0 Salmon 0 Orange Juice 0 Almonds 0 Broccoli 0 Calcium supplements 0 Calcium carbonate 0 Caltrate OsCal and TUMS 0 Should be taken with food 0 Calcium citrate 0 Citracal 0 Does not need to be taken with food 0 Naturally occurring calcium 0 Should not be taken due to lead exposure 0 What facilitates absorption of calcium in the small intestine 0 Vitamin D 0 Sources of Vitamin D 0 Fish and dairy products 0 Who is most at risk for deficiency 0 Postmenopausal women 0 Pregnant women Infants Elderly 0 Know a representative drug in class MOA adverse effects 0 Bisphosphonates 0 MOA suppress osteoclast activity 0 Prototype Alendronate sodium Fosamax 0 Low bioavailability 0 Take on empty stomach with a full glass of water 0 Eat nothing for 30 minutes after administration 0 Remain upright after administration 0 Adverse effects 0 Esophageal ulceration 0 Patient should take drug While in an upright position to prevent 0 Esophagitis 0 Rare 0 Osteonecrosis of the jaw ONJ 0 rare 0 Nursing Implications 0 Coffee and orange juice should be avoided When taking this drug 0 Why 0 Can decrease absorption 0 Calcitonin Miacalcin Fortical O MOA inhibits osteoclasts 0 Source salmon 0 Route of Administration intranasal nasal spray 0 One sprayday alternate nostrils each day 0 Dose 200 IU per spray Side Effects 0 Nasal irritation 0 Post Menopausal HRT 0 SERMS selective estrogen receptor modulators 0 Raloxifene Evista 0 MOA blocks estrogen receptors in the breasts and uterus 0 Limits osteoclast activity 0 Side effects 0 Increase risk of blood clots 0 Increased hot ashes 0 Nursing implications 0 Should not be taken concurrently With HRT 0 Teriparatide Forteo 0 MOA increases bone formation 0 ONLY drug to stimulate osteoblasts 0 Route of administration Sub Q 0 Black box warning 0 Can cause osteosarcoma bone cancer 0 Therefore patients With bone cancer or increased risk for bone cancer should avoid this drug Biology of Cancer and Cancer Chemotherapy Study Guide 1 Define Carcinogenesis Why is cancer predominantly a disease of aging a Carcinogenesis i A normal cell turns into a cancer cell b Cancer is predominately a disease of aging i Cancer develops due to multiple mutations ii The more times our cells replicate themselves the more likely there Will be errors in the copying of those cells iii As we age our cells replicate more and more leads to a likelihood of more mutations Describe environmental risk factors that can lead to cancer development What role can the nurse play in decreasing cancer risk due to environmental factors a Environmental risk factors i Tobacco 1 Includes second hand smoke 2 Includes cigarette cigar and pipe smoking ii Diet 1 30 of overall risk factors a Xenobiotics i Hydrocarbons and amines produced during cooking of meat protein 2 Some foods may decrease the risk of cancer Fruits and vegetables Fiber Foods containing vitamins and folate Whole grains Lycopene Legumes and nuts 3 Some foods may increase the risk of cancer weeps Foods high in calcium Refined grains a Fat b High glycemic carbohydrates c Food With high amount of preservatives d Alcohol e Grilled and blackened foods f Fried foods g h iii Obesity 1 Abdominal obesity can be associated With insulin resistance and cause hyperinsulinemia iv Alcohol consumption 1 Risk is even more increased With cigarette smoking 2 Genetic predispositions v Ionizing radiation 1 Emission from Xrays 2 Increased use of diagnostic tests 3 What does exposure cause a Cell death b Gene mutations c Chromosome aberrations vi Ultraviolet radiation 1 Causes skin cancer a Skin in ammation b Release of free radical and TNF in epidermis 2 Main source is from sunlight UVA and UVB vii Electromagnetic radiation EMR 1 Nonionizing lowfrequency radiation 2 Sources a Microwaves b Radars c Cell phones d Electricity radio waves e Fluorescent lights f Computers viii Sexual reproductive behavior 1 HPV a Present in 997 of women WITH cervical cancer ix Chemicals and occupational hazards 1 Examples a Asbestos b Dyes paint c Rubber and rubber products d Explosives e Heavy metals f Air pollution i Outdoor v indoor 1 Outdoor a Emissions from industries 2 Indoor a Second hand smoke b Radon gas c Heat and cooking combustions d Asbestos e Inorganic arsenic poison x Viruses 1 HPV Hepatitis B and C EpsteinBarr Virus Kaposi sarcoma herpes virus human T cell leukemialymphoma virus xi Impairment of immune system 1 Factors that can impair the immune system a Antirejection drugs b High dose steroids c Stress d AIDS b What can decrease cancer risk i Physical activity 1 Decreases a Insulin growth activity b Obesity c In ammatory responses and free radicals 2 Increases a Gut motility 3 What role do viruses play in increasing cancer risk a Viruses trigger the immune system and impaired immune system can increase the cancer risk Certain viruses can also cause an impaired immune system b In ammatory cells release free radicals and promote mutation c Bacterial cause of cancer i H pylori 1 Chronic infections 2 Treated with Flagyl 4 Define neoplasm a new growth b Also called tumors i Any swelling caused by in ammation 5 Differentiate between benign and malignant tumors a Tumors can be benign or malignant both can cause significant damage 1 Benign a Noncancerous Grow slowly Well defined capsule Not invasive Well differentiated Low mitotic index Do not metastasize reactb0999 oma cancers 2 Malignant a Cancerous Grow rapidly Not encapsulated Invasive Poorly differentiated High mitotic index Can spread Metastasis Epithelial tumors i Carcinomas i Connective tissue tumors i Sarcomas j Lymphatic tissue tumors i Lymphomas k Bloodforming cell tumors i Leukemia 6 How are cancer cells different than normal cells a Autonomy i Free of normal cell control mechanisms b Anaplasia i Loss of differentiation FQOWPPPP ii without form c Pleomorphic i Variable size and shape d Uncontrolled Growth e Inability to differentiate fully i Means they are incapable of fully becoming mature f Loss of Contact Inhibition i Cancer cells do not have boundaries and continuously grow g Lack of Adhesion i Cancer cells don t adhere well so they oat around the body and go where they want h Ability to repair damage i Cancer cells are less able to repair tissue damage 1 Radiation tissue damage 7 Describe carcinoma in situ CIS What areas of the body are most commonly affected a Carcinoma in situ CIS i Preinvasive tumors precancer tumors 1 Can turn malignant ii Haven t yet invaded the surrounding stroma b Commonly affected areas i Cervix ii Skin iii Oral cavity iv Bronchus v Esophagus vi Breast vii Stomach viii Large bowel 8 How are tumor markers used in cancer care a Tumor markers i Substances produced by cancer cells 1 Or found on plasma cell membranes in blood CSF or urine ii What is found in these substances 1 Hormones 2 Enzymes 3 Genes 4 Antigens 5 Antibodies b How are tumor markers used in cancer cells i Screen and identify individualistic high risks for cancer ii Diagnose specific types of tumors iii Observe clinical course of cancer 9 Define the role of protooncogenes oncogenes and tumorsuppressor genes How do genes mutate a Prontooncogenes i Normal genes that direct protein synthesis and cellular growth b Oncogenes i Accelerators ii Mutant genes that accelerate cell proliferation c Tumorsuppressor genes also called antioncogenes i Brakes ii Encode proteins that in their normal state negatively regulate proliferation d How do genes mutate i Point mutation 1 Change in one or a few nucleotide base pairs ii Chromosome translocation 1 A piece in one chromosome is transferred to another iii Gene amplification 1 Duplication of a small piece of chromosome over and over 2 increased expression of an oncogene iv Mutation of tumorsuppressor genes 1 Unregulated cellular growth V Loss of heterozygosity 1 Both chromosome copies of a gene are inactivated Vi Gene silencing 1 Whole regions of chromosomes are shut off while the same regions in other cells remain active vii Chromosome instability 1 Increase in malignant cells 2 chromosome loss loss of heterozygosity and chromosome amplification 10 What is the Guardian of the Genome a Caretaker b Encode for proteins that are involved in repairing damaged DNA 1 1 Angiogenesis a Growth of new vessels b When the cancer is advanced i Can secrete angiogenic factors VEGF 1 Vascular endothelial GF 2 Platelet derived GF 3 Basic fibroblast GF 12 What is the relationship between telomeres and chromosome immortality a Body cells AREN T immortal b Telomeres i Protective caps on each chromosome 1 Block cell division and prevent immortality c Telomeres get smaller with each cell division d Telomerase i Holds the telomeres to the chromosomes 1 Cancer cells can activate telomerase a Creates unlimited division 13 Describe the role of stem cells in cancer treatment a Stem cells selfrenew i Cell divisions create new stem cells b Stem cells are pluripotent i Ability to differentiate into multiple different cell types c Chemotherapy does not kill our cancer stem cells d Where are our normal stem cells located i Bone marrow 14 Differentiate between primary and metastatic disease a Primary v metastatic cancer i Primary cancer 1 Cancerous cells found in tissue of their origin ii Metastatic cancer 1 Cancerous cells found in tissue other than tissue of origin b How is metastasis diagnosed i Biopsy of the tissue c List common sites of metastasis of primary tumors i Primary tumor and site of metastasis 1 Breast lymph nodes lung liver bone chest wall brain Lung brain liver lymph nodes bone Brain spinal cord Ovary intraperitoneal Bone kidney uterus testes lung Colon pancreas stomach liver lung bone 7 Multiple myeloma bone 15 How is cancer staged a Stages i I no metastasis QMPPP ii 11 local invasion iii III spread to regional structures iv IV distant metastasis b Describe the World Health Organization s TNM system 1 T tumor spread 2 N node involvement 3 M presence of distant metastasis 16 List the common treatment modalities for cancer i Surgery ii Radiation iii Drug therapy Chemotherapy b What types of cancer are most amenable to chemotherapy i Disseminated cancers tumor is traveling within the body 1 Leukemia 2 Disseminated lymphomas 3 Widespread metastases 17 List the basic principles of cancer chemotherapy a Drug classes i Cytotoxic agents 1 Drugs will kill the cells directly 2 This is the group used for CHEMOTHERAPY ii Hormones and hormone antagonists 1 Directly affect hormones that feed cancer growth a Estrogen and progesterone iii Biologic response modifiers 1 Immune modifiers iv Targeted drugs 1 Bind with specific molecules a Promote cancer growth 18 Describe the cell cycle i G1 1 Cell prepares to make DNA ii S 1 DNA synthesis occurs iii G2 1 Preparation for cell division mitosis iv M 1 Mitosis 2 Creation of daughter cells 3 Cells begin with G1 to repeat the cycle or enter mitotic dormancy G0 b In what phase of the cell cycle is chemotherapy used i M mitotic phase c What is the difference between cellcycle specific drugs and cellcycle nonspecific drugs i Cellcycle specific drugs 1 Toxic to drugs only in a specific phase 2 Must be in blood continuously over a long period of time ii Cellcycle nonspecific drugs 1 Can act during any phase of the cell cycle 19 Define Growth Fraction i Ratio of proliferating cells cells undergoing mitosis to cells in dormancy cells in G0 b List cells that have a high ratio of growth fraction i Bone marrow ii Skin iii Hair follicles iv Sperm V Gastrointestinal tract c How does chemotherapy affect cells with a high growth fraction i Chemotherapy is toxic to tissue with high growth function 20 Describe the obstacles to successful chemotherapy i Toxicity to normal cells ii Cure requires 100 cell kill 1 Druginduced cell kill 2 Impossible to tell when the cell kill has been achieved a This is when we would need to go in and check things like the tumor markers iii Absence of truly early detection iv Solid tumors respond poorly V Drug resistance vi Heterogeneity of tumor cells 1 Differences of tumor cells 2 Cancer cells are heterogeneity meaning that all cancer cells can vary vii Limited drug access to tumor cells b How is the decision made when to treat i Benefits should outweigh risks ii Patient should be given the idea of the benefits of proposed therapy iii One of these three should be possible 1 Cure 2 Prolongation of life 3 Palliation 21 What strategies can be used to achieve maximum benefit from chemotherapy a Chemotherapy goal 100 cell kill while causing limited injury to normal tissue i Intermittent chemotherapy 1 On and off treatment 2 Limits damage to normal tissue 3 Cells have time to repopulate between rounds 4 In order to work noncancer cells must repopulate faster than malignant cells ii Combination chemotherapy 1 Combining two types of chemotherapy 2 Advantages a Suppress drug resistance b Increase cell kill c Reduce injury to normal tissues 3 Drug selection a Each drug must be effective alone b Each drug should have different MOA c Drug should have minimal overlapping toxicity iii Optimizing dosing schedules 1 To be effective a Choose the right drug b Dose schedule must maximize beneficial effects i Cell cycle specific vs nonspecific 1 Specific a During a specific phase 2 Nonspecific a During any phase 22 What administration hazards accompany the administration of chemotherapy i Bone marrow suppression 1 Neutropenia 2 Thrombocytopenia 3 Anemia ii Digestive tract injury stomatitis 1 Nausea 2 Vomiting 3 Diarrhea iii Alopecia 1 Hair loss iv Hyperuricemia 1 Excess uric acid in the blood v Reproductive toxicity vi Local injury from extravasation of vesicants 1 Vesicants agents that the chemotherapy is killing 2 Due to IV a Example Dilantin purple glove syndrome 3 Ports are used for chemotherapy and ONLY chemotherapy vii Carcinogenesis b How can the nurse be protected from administration hazards i Do not have direct contact can lead to local injury ii Should obtain certification in chemotherapy administration 23 Describe the use mechanism of action and side effects of the following cytotoxic drug classifications a Alkylating Agents i Use nonspecific 1 Given over a short period of time ii MOA 1 Alkalization of DNA iii Side effects 1 Drug resistance 2 Toxicity a In tissues of high growth fraction iv Prototypes 1 Nitrogen Mustards Cytoxan 2 Nitrosoureas BCNU b Platinum Compounds i Use nonspecific ii MOA produce cross links in DNA iii Prototype 1 PlatinolAQ c Antimetabolites i Use specific ii MOA disrupt metabolic processes iii Prototypes 1 Folic Acid Analog Methotrexate 2 Pyrimidine Analog CytosarU and Adrucil 3 Purine Analog Purinethol d Hypomethylating Agents i Use specific ii MOA incorporated into the DNA iii Prototypes 1 Vidaza e Antitumor Antibiotics i Use nonspecific ii MOA direct interaction With DNA iii Side effects 1 Poor GI absorption should be administered intravenously 2 Cause bone marrow suppression iv Prototypes 1 Anthracyclines Adriamycin a Damages heart muscles and induce HF 2 Nonanthracyclines Actinomycin D f Mitotic Inhibitors i Use specific ii MOA prevent cell division iii Side effects 1 Peripheral neuropathy iv Prototypes 1 Vinca alkaloids Vincristine 2 Taxanes Taxol g Hormonal Agents i MOA mimic or block the actions of endogenous hormones ii Side effects 1 Hot ashes Fluid retention Vaginal discharge Nausea and vomiting Menstrual irregularities 9593 iii Prototypes 1 Tamoxifen a Used with surgery b Suspect with breast cancer 2 Trastuzumab h Androgen Receptor Blockers i MOA block androgen receptors ii Prototype 1 Flutamide a Suspect prostate cancer 24 Targeted drugs a Angiogenesis Inhibitors i MOA 1 Inhibit growth of new blood vessels the blood vessels of the tumor a Tumors require their own blood supply for growth 2 Stabilize the tumor ii Side effects 1 Less than cytotoxic drugs iii Prototype 1 Avastin b Proteasome Inhibitors i MOA 1 Inhibit intracellular multienzyme complexes that degrade proteins ii Side effects 1 Weakness Nausea Diarrhea Thrombocytopenia Anemia Neutropenia Constipation 8 Anorexia iii Prototype Velcade 1 Multiple myeloma and mantle cell lymphoma 8091 25 How are the biologic response modifiers used a Interferon Alpha2a i Immunostimulant ii Alter host response to cancer iii Enhance immune attack against cancer cells b Glucocorticoids i When used for patients With cancer high doses are needed 1 ii Uses 1 2 PW 908091 9 With high does lots of severe side effects Combination therapy for lymphoid tissue Acute and chronic a Leukemia b Hodgkin s c Multiple myeloma Manage complications of cancer and cancer therapy Suppress chemotherapy a This Will induce nausea and vomiting Reduce cerebral edema Reduce pain Suppress hypercalcemia Can improve appetite Promote weight gain 26 Describe the use of dronabinol Marinol to increase appetite in patients undergoing chemotherapy a Active ingredient in marijuana b Use this in chemotherapy patients Who feel like not eating i This drug increases appetite
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