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Provide education - Many manifestations of radiation therapy do not develop until approximately 10-14 days. And some do not subside until several weeks after treatment. - The nurse explains the procedure, delivery of radiation, describe the equipment, the duration and the possible need of immobilizing the patient 2. Minimize side effects - In women of child bearing age, RT may cause prolonged or permanent infertility - In prostate radiotherapy, when radioactive seeds have been implanted, there is low, weakly penetrating radiation for others. - Therefore the client should use a condom for sexual intercourse in the first few weeks after the procedure. - Also the client should avoid close contact (<6 feet) contact with pregnant women and young children (younger than 3 years) for more than 5 minutes a day during the first 2 months following implantation. - If systemic symptoms occur, such as weakness and fatigue occur, the patient may need assistance with ADL and personal hygiene. - When a patient has a radioactive implant in place, nurses and other health care personnel need to protect themselves as well as the patient from the effects of radiation. 3. Provide a non-stressful environment - Some people who receive radiation to the head and neck experiences redness and irritation in the mouth, a dry mouth, difficulty in swallowing, changes in taste or nausea. - Other possible side effects include a loss of taste, earaches and swelling - Skin texture might change and jaws may feel stiff 4. Dental care - If you wear dentures, they may no longer fit well because of swollen gums. If your dentures can cause gum sores, you may need to stop wearing them until your radiation therapy is over because sores can become infected. - Clean teeth and gums thoroughly with a very soft toothbrush after meals and at least once a day each day. - Use fluoride toothpaste that contains no abrasives. - Use unwaxed dental tape to gently floss between once a day. - Rinse your mouth well with cool water or a baking soda solution after brushing. Use 1 tsp. baking soda in 1 quart of water. - Apply fluoride regularly as prescribed by your dentist. 5. Many patients feel tired due to the radiation therapy which can affect their emotions 6. Patients might feel depressed, afraid, angry, frustrated, alone or helpless - Peer support groups may meet at your hospital
Emotional and spiritual encouragement also is important to the healing process.
7. Side effects can include eating and digestion problems. You may completely lose interest in food during your treatment. - Even if you are not hungry, it is important to keep your protein and calorie intake high. - Doctors have found that patients who eat can better handle their cancers and side effects. - Eat when you are hungry, even when it is not meal time. - Eat several small meals during the day rather than 2 or 3 large meals. - Vary your diet and try new recipes. - If you don’t drink alcohol, ask your doctor if you should avoid alcohol during your treatment. - Keep healthful snacks close by nibbling when you get the urge. Drink milkshakes or prepared liquid supplements between meals. Patient receives a low residue diet to prevent frequent bowel movements. Radiation therapy may cause anorexia which may lead to inadequate nutrition and hydration so small frequent feedings or use of nutritional supplements may be required to maintain adequate nutrition. In radiation therapy, fatigue or malaise also contribute to poor nutritional intake thus planned rest periods may provide relief of fatigue providing increased energy for meal preparation or consumption. Nutrition – to promote retention of nutrients, administer antiemetics as prescribed. Encourage high calorie meals when child is least likely to be nauseated. Praise a child’s effort to eat. Provide foods identified by child as special favorites. Serve easy to swallow food at tolerable temperature. If mucous membrane of mouth, pharynx or esophagus is irradiated, modification of diet to bland, soft, or liquid foods will be necessary; mouth is rinsed frequently with a mild alkaline mouthwash; teeth are gently cleansed with absorbent cotton or gauze rather than the usual brush. Avoids foods that are dry and thick. 8. For lactating mothers undergoing radiation therapy. - Advise pt. not to breastfeed to prevent adverse effects to fetus. - Advise pt. to drink plenty of fluids to prevent dehydration. - Monitor nutritional status. 9. Miscellaneous. - A urinary catheter will be in place (if ordered) and must be inspected frequently to ensure that it drains properly. - Any profuse discharge should be reported immediately to the radiation oncologist or gynecologic surgeon.
Observing the patient for temperature elevation, nausea, and vomiting. The symptoms may indicate such complications as infection. Patient teaching includes informing the patient that abdominal fullness, cramping, backache, and the urge to void are normal feelings during therapy. Severe should not occur. Mild opioid agents, muscle relaxants or sedative medications may be helpful. Private room, with private bathroom and facilities Room previously occupied with patients previously treated with radionuclide treatment should not be used until the room has been cleansed and surveyed for residual contamination. Items such as bedpans, urinals and basins if disposable may be disposed of as radioactive waste. If these items are not disposable, they shall be thoroughly washed with soap and running water. Any vomitus, gastric contents collected during the first 24 hours by nasogastric aspiration or excessive sputum should be collected in a waterproof container and held for disposal by radiation safety division personnel. Wearing of lead apron The nurse must deal safety with radioactive body discharges by wearing gloves and in some instances placing excreta in containers for special disposal. For a child receiving radiation therapy Provide ample time to answer questions of children undergoing radiation therapy Advise client to wear loose clothing as skin in the area being treated might become more sensitive to touch. Skin changes: The patient is observed for possible reactions: Slight redness for a brief period Transitory epilation Erythema with temporary sweat gland activity suppression Dry desquamation For large doses or sensitive skin; observe the following: Marked erythema followed by purple discoloration Blister formation and moist desquamation Slow healing, leaving skin atrophied, thin and very sensitive to heat, cold and trauma. Permanent epilation and sweat gland destruction After treatment, the area is gently cleansed with tepid water and patted dry; soap is not used and brisk rubbing is avoided. Alcohol, powders, oils, lotions, creams, ointments, deodorants are not used unless prescribed by the doctor. The site is kept dry and may be covered lightly with smooth cloth/cotton but adhesive tape is contraindicated, used an alternative instead. If larynx is treated with radiation, the patient is closely observed 3-4 days for any difficulty in breathing; edema may develop and occlude airway necessitating prompt intubation or a tracheostomy.
Frequent blood cell counts are done because the hemapoetic tissue is extremely sensitive to radiation. Contact with persons with an infection should be avoided especially with respiratory infection because of the patients lowered resistance. Patient should have an extra rest, increased fluid intake and a high calorie, high protein, high vitamin diet. If the patient is allowed to go home, the importance of keeping the appointments for his treatments is stressed. Internal Radiation Therapy: - Patient should receive a simple explanation of the procedure and necessary precautions so he will know what to expect and what is expected of him. - Time is taken to answer his questions and dispel misconceptions. - After implantation, temperature is taken every 4 hours, an increase over 38 degrees is perorted. - Any radioactive material should be handled with a long forceps, never with hands. - All dressings should be checked before disposal. - Patient’s visitors are required to maintain a 3 feet distance from the patient. - Health workers should know the time at which the radioactive implant is to be removed and should have necessary equipment in advance and to remind the person responsible for removal. Nursing responsibilities for the patient receiving radiation therapy
Teletherapy The radiation source is exterior to the tumor such as the use of linear accelerator. 1. Remove all opaque objects such as pins, buttons and hairpins and replace clothing with a gown for body X-rays. 2. Have patient perfectly still; maintain position with the use of foam, plastic, plaster (material) devices and/or variety of other materials that can conform to the patient’s anatomy. 3. Tell the patient there will be no sensation or pain accompanying radiation therapy. 4. Advise the patient that he will be alone in the room for the protection of the technician, but will be in voice contact. 5. Determine from the physician what has been told to the patient about radiation therapy 6. If series of treatments are to be given, include the patient in the planning phase. Brachytherapy - The radiation source is used for surface, interstitial, or intracavity applications 1. The nurse should inform the patient that some skin reaction can be expected but that varies from patient to patient. 2. Do not apply lotions, ointments, cosmetics, etc. to the site of radiation unless prescribed by the physician. Cornstarch may be used when the skin
is dry and or itchy. Discourage vigorous rubbing or scratching. It may destroy skin cells. Techniques while working with patients undergoing radiation therapy: 1. Put on shoe covers and protective gloves before entering patients room. 2. Work quickly but effectively and courteously. Minimize your time in the room. 3. Note: No matter how long you are in the room, you will not receive a radiation exposure large enough to cause adverse effects. 4. Leave all trash, linens, and food trays in the room 5. After leaving the room, wash your hands. 6. Personnel should not smoke, eat or drink in areas where unencapsulated radio active is used in patient treatment or if the possibilities of contamination of the hands persist. General procedures for obtaining specimens from therapy patients 1. Read the instructions posted in the door. 2. Specimen containers must be labeled with radioactive material labels or tape to identify them as radioactive. 3. Put on a face mask if the patient has a tracheostomy or has symptoms of a respiratory infection. 4. Never use sink for handwashing/ use telephone/ cellphones while in the room. Nursing considerations in external radiotherapy: 1. It is important that the patient receive an explanation of the procedure and precautions. 2. Orient the patient and his family in advance, answer their questions and reassure them that the treatments are well controlled and adequate protection is used. 3. Following the treatment, observe for possible reactions. 4. Instruct and suggest care of the skin 5. Avoid patient to contact with other persons with infections 6. General supportive care applicable to all patients receiving radiotherapy include extra rest, an increase fluid intake and a high calorie, high protein, high vitamin diet 7. When reaction develops, reassure that they are not unexpected and are not an indication of a recurrence or worsening of his cancerous disease. Nursing responsibilities in internal radiotherapy: 1. An explanation to the patient of the procedure and the precautions 2. Place the patient in isolation in a single room and indicate that no visitors are allowed 3. Provide a telephone and radio or television and reading materials 4. In close contact with patient always wear a lead apron or gown and rubber gloves 5. Wear a monitoring badge which records the amount of radiation received by the patient 6. Visit patient once in a while 7. Nurse should wash hands thoroughly after any contact with patient and other equipment
Assure patients and the child that during the treatment. . no lotion should be applied to radiation areas until the treatment series is completed. . . leading to a constantly dry mouth.If creams contain any metal.To make this approach affective.Nurses must make sure they understand treatment and the precautions they need to take.Nurses must deal safely with radioactive body discharges by wearing gloves and in some instances placing excreta in containers for special disposal. . During treatment: .The nurse who is in close contact with such clients also needs to wear a lead apron. . keep the child fairly active early in the day and introduce activities after the sedative is administered. . .Children undergoing radiation therapy need their leukocytes and platelet counts monitored periodically for changes.These clients need emotional support to deal with the precautions and will likely accept treatments and precautions better when they know what will happen. a dental consult may be suggested. . alopecia (hair loss) may result. Linens. . needles and other treatment equipment are monitored before being returned.Exposure of the reproductive organs of mice and rabbits to X rays has caused gene mutations that resulted in malformed offsprings and geneticist believe that comfortable effects can occur in humans.Radiation to the head may reduce salivary gland function. just as there is no sensation from x-ray exposure. these could distort or interfere with the entrance of radiation.Radiation to bone marrow may depress blood cell and platelet production. . For clients undergoing radiation: . .8. when and why. .Infants are usually prescribed a sedative or conscious sedation before therapy to ensure that they be still during the procedure.Clients with radioactive implants are a source of radiation to the immediate environment.The nurse must wash gloved hands well before and after removing the gloves and placed contaminated materials in a special containers for special disposal. .Tooth growth may be halted due to root therapy.No cream. . syringes. This can slow healing of a tooth extraction.If head is involved in therapy.If the head will be irradiated. dishes. For infants and children .Require them to be still for a period of time possibly on an uncomfortable table. . After treatment: . . the child may will experience no sensation from radiation exposure. Often such clients are restricted to bed or to a confined area to protect others.
scrub or scratch the skin in the treatment area. after is over. Nursing Diagnoses and its Nursing Interventions - - Nursing Diagnosis: Impairment of skin integrity due to irradiation Nurisng interevntions: . ask the doctor or nurses how long you should continue to take extra precautions in the sun. Avoid putting anything that is hot or cold.Patient education . Nausea and vomiting are most likely to occur when the radiation dose is high or if the abdomen or another part of the digestive tract is irradiated. and providing interventions. When washing. ointments. . doses and reactions is required. Ask the doctor or nurse to recommend skin care products that will not cause skin irritation.For patients with xerostomia undergoing irradiation . Compazine. education and support. great care is taken to protect both the nurse and patient from unnecessary exposure. pat dry. This nurses can suggest the following: Avoid irritatitng treated skin. body oils. Do not rub. Sometimes nausea and vomiting occur after radiation to other regions. use only lukewarm water and mild soap. . take naps and get extra sleep at night. such as heating pad or ice packs on treagted skin. lotions or home remedies in the treatment area while you’re being treated and for several weeks afterward unless approved by the doctor. during and after a course of head and neck irradiation. but in these cases the symptoms usually disappear within a few hours after treatment.Nursing care involves assesing the physical and emotional aspects of the patient before. Do not apply skin lotion within 2 hours of treatment. Chemotherapy and radiation therapy: knowledge of the appropriate routes. Avoid rubbing or scratching the area the nurse needs to explain that during treatment.- Knowing these. Avoid extremes of temperature Avoid rough and tight garments. deodorants. perfumes. Tigan or Zafran. creams. Do not use any powders. Nausea and vomiting can be treated with antacids. Do not wear tight clothing over the area. the patient must stay in absolute bedrest. Avoid exposing the radiated area to the sun during treatment. Infection control: nurses must be aware of standard infection control precautions. Fatigue frequently starts after the 2nd week therapy and may continue until about 2 weeks after the therapy is finished. the patient should be very gentle with the skin in the treatment area. Patients may need help to limit their activities.During radiation therapy.
No hot or cold is applied on the site and must be protected from direct sunlight. Try not to rub. Dry the irradiated area with potting motions rather than rubbing motions. using a clean. • This is an acute phenomenon that correlates with the depletion of actively proliferating basal cells in the epidermal layer of the skin. - . The skin and oral mucosa are assesses frequently for changes. • Remaining basal cells are stimulated and their cell cycle shortened. Do not wear tight clothing over the treatment area. to destroy blood producing tissue. a tendency to develop cataracts. nutritional status and general feeling of well being. lotions. Use only luke warm water and mild soap. Mild erythema to moist desquamation similar to appearance to a second-degree burn. wear protective clothing and sunscreen. scrub or scratch any sensitive spots. If you expect to be in the sun for more than a few minutes. The nurse assesses the patient’s skin.2) and is caused by obliteration of sebaceous glands within the field. Avoid exposure of the irradiated area to the sun. or creams on your skin at the radiation site unless they are prescribed by your radiologist. Use your hand rather than a washcloth to be more gentle. The skin is protected from irritation and the patient is instructed to avoid using ointments. Just let water run over the treated area. Wear soft clothing over the skin at the radiation site. or cornstarch. Ask your doctor or nurse about using sunscreen lotions. you may suggest application of plain calamine lotion without phenol. A void heat exposure. a tendency to develop cancer.- Nurses should know also that over exposure to radiation may include burning and scarring of the skin or lungs. Do not rub. Take care not to remove the markings that indicate exactly where the beam of radiation is to be focused. Avoid exposing the area to the sun during treatment and for at least 1 year after the treatment is completed. lotion or powder on the area. ointments. • Subsequent peeling of the skin is defined as dry desquamation. Rinse soap thoroughly from your skin. soft towel Use no powders. a fixed percentage of which die with each dose fraction of irradiation. Wash the irritated area gently each day with sitter water alone on a mild soap and water. • Dryness and pruritus may occur at an accumulated dose of 2000 to 28000 Cgy (1. Pressure is avoided by avoiding tight clothing’s and prolonged lying on the area of treatment. • The skin becomes dry and patient may notice itching and burning sensations. If itching and irritation accompanying erythema.
.Monitor weight weekly or daily .Sip cool drinks often throughout the day.Eat or chew sugar free candy or gum to help keep your mouth moist .Use direct pressure over injection sites until bleeding stops Nursing Diagnosis: Activity intolerance due to anemia Nursing intervention: . . . .Teach person to avoid physical trauma and aspirin while platelets are low .Assess person’s understanding of nutrition and teach as necessary Nursing Diagnosis: Alteration in mucous membranes due to irradiation Nursing interventions: .Avoid foods that are dry and thick Care of the teeth.Encourage good nutrition and plenty of rest Nursing Diagnosis: Alteration in Nutrition: Less than body requirements due to anemia Nursing intervention: . Nursing Diagnosis: Potentials for infection due to bone marrow depression Nursing Intervention: .Monitor oral cavity daily . chew tobacco or drink alcohol because tobacco and alcohol can further irritate mouth sores. no smoking. hygiene and good habits. . Nursing Diagnosis: Potential for bleeding due to BM depression: Nursing Interventions: . gums.• Dry skin is susceptible to further injury through scratching and/or formation of fissures – augmenting the risk of infection and tissue necrosis. no alcohol .Avoid spices and coarse foods such as raw vegetables.Good oral hygiene and saline rinses every 2 hours while awake may help .Contact dietitian if indicated .Ask your doctor or nurse to recommend a good mouthwash. dry crackers and nuts .Ensure professional dental care .Monitor platelet counts weekly .Discuss fatigue and its causes with person . mouth and throat .Do not eat or drink very hot foods .Monitor stool.Stay away from sugary foods and snacks.Monitor diet for efficient calories .Teach persons signs of infection to report to physician. The alcohol content in some mouthwashes has a drying effect on mouth tissues.Do not smoke. integument for signs of hemorrhage . .Monitor blood counts weekly.Encourage bland diet.Teach person to avoid infection by frequent handwashing and good nutrition.Teach person signs of hemorrhage to report to physician .
Give low residue diet/antidiarrhea medication as prescribed. prevent irritation and promote healing Mucositis: do not remove membrane Nursing Diagnosis: Alteration in bowel elimination: diarrhea due to irradiation Nursing interventions: .Gentle oral hygiene is essential to remove debris.Administer antiemetics as prescribed .Encourage telephone calls .Stop by door to say “hello” HYPERSENSITIVITY REACTIONS . hats.Monitor for dysuria or urinary frequency .Encourage verbalization of feelings .Instruct person on hair care Nursing Diagnosis: Alteration in urinary elimination patterns due to irradiation Nursing interventions: . Nursing Diagnosis: Alteration in comfort and vomiting due to irradiation Nursing interventions: . radio or tape player .Encourage fluid intake Nursing Diagnosis: Social isolation due to irradiation Nursing Interventions: . etc .Monitor stool .Administer analgesics as prescribed Nursing Diagnosis: Disturbance in self concept due to alopecia Nursing interventions: .Explain and discuss irradiation precaution . scarf’s.Plan rest periods before and after meals . .Moisten food with gravies and sauces to make eating easier.Monitor fluids and electrolytes Nursing Diagnosis: Alteration in comfort: headache due to irradiation Nursing Interventions: .Suggest use of wigs..Monitor pain .Suggest television.Monitor urine for blood .
occupational chemicals. clothings. examine all labels of new prepared foods for presence of allergens. nuts. sneezing. urticaria. fur. angioedema. rash: diarrhea. anaphylaxis Sensitizing Dose – initial contact with allergen that triggers the synthesis of specific antiallergenic IgE antibodies Shocking. shock therapy 2. indi exhibits the symptoms of Type I Nursing Process: Assessment – history taking Diagnostic Test – skin test. Increase in vascular permeability – urticaria(hives or tissue edema 3. report side effects of prescribed medication . animal dander. cosmetics. pollens. hematopoietic suppression. malaise. joint pains. Constriction of smooth muscles in the bronchi – bronchospasm 2. graft rejections TYPE I – Anaphylactic / Immediate Hypersensitivity Reaction Common antigens: Insect bites. drugs. one-week food diary test Nursing Diagnosis: Alerted health maintenance. fever. food. Control the environment – house dust. mold spore. x-ray contrast medium Signs and Symptoms: Urticaria(hives) caused by foods. Allergen immunotherapy 3. plant oils. Challenging Dose – subsequent contact with allergen. avoid eating unknown foods when travelling.• • Exaggerated or inappropriate response to specific antigen Anaphylaxis. Knowledge deficit Implementation: 1.eggs. radioallergosorbent test. use gloves to handle allergen. changes in temperature and stress Pathophysiology: IgE attach to the surface of mast cells and basophils providing a site for allergens to bond the cells. read all labels of nonprescription drugs before taking the new drug. fish . use non allergenic soaps and cosmetics – coat nickel containing jewelry with clean nailpolish. Atopy means inherited hypersensitivity. pollens. animal dander Contactants – fibers in wool. This causes the cells to releases vasoactive substances including histamine leading to: 1. perfumes. osaps. Common Antigens include: Inhalants – dust. nickel in jewelry. transfusion reactions. Benadryl. Facilitate learning – remind physician of allergy if new medications are prescribed. allergies. Increase in mucus secretions – hay fever and asthma Symptoms: wheezing. pollen. Prevent anaphylactic reaction . nylon. rhinitis with conjunctivitis. tracheal intubation. drugs Atopic allergies – less severe and more common form seen in about 15% of the population. aminophylline. hair dyes.Epinephrine. fungus 4.
Fever. fever. Febrile. Graft-versus-Host Disease_Pt. stomatitis.Involves antigens. where they activate complement and cause inflammation . headache. shock and possible cardiac arrest 5.Anxiety. Occurs when allergens are taken up by antigen-presenting cells that migrate to lymph nodes and present the allergen to Tcells.Antihistamines and salicylates. vascular collapse.Infusion of ABO incompatible with blood. The reaction of antibodies and antigens usually leads to activation of the complement system. flushing. anxiety. Chills. ARF. rash. muscle pain 3. urticaria. Non Hemolytic ( most common) . nausea. low back pain. anemia. difficulty swallowing.Immunodeficient person receives lymphocytes begin to reject cells 4-30 days after the transfusion. flushing. Acute hemolytic Reaction/hemolytic transfusion reaction .Sudden chills and fever. . high fever. cardiac arrest. wheezing.Flushing. the immune complexes are small enough to escape phagocytosis. bleeding. hemoglobinuria 6. back pains. tightness and pain chest. progressing to cyanosis. which then proliferate.Infusion of IgA protein to IgA deficient recipient who has developed IgA antibody . Sensitization to RBC antigen not ABO system .Glomerulonephritis and rheumatoid arthritis . Damage cells by causing lysis as in compatible blood transfusion reactions Types of Transfusion Reactions: 1. where .Anorexia. epinephrine TYPE IV – Cell mediated or Delayed Hypersensitivity Reaction . Mild Allergic reaction involves sensitivity to foreign plasma proteins . platelets or plasma proteins . When certain ratios of antigen to antibody occur. chills. tachycardia.Usually appears 12-72 hours after exposure to an allergen. steroids – prednisone. RBCs or components containing 10 ml or more RBC’s antibodies in the recipients plasma attach to the antigens on transfused RBC’S ---RBC destruction. hypotension. Delayed hemolytic reaction .TYPE II – Cytotoxic Hypersensitivity • • Caused by antibodies (IgG and IgM) directed against antigens on a person’s red blood cells.An amnestic immune response that occurs 7-14 days after transfusion.Sensitization to donor’s WBC’s. shock. lymphocytes or platelets or tissue cells. tachypnea. . diarrhea. liver dysfunction Prevention of transfusion Reaction: Accurate laboratory testing. antibodies (IgG and IgM) and the complement system. itching. jaundice. hemoglobinuria. careful blood administration TYPE III – Hypersensitivitis/Immune Complex . Some of the new Tcells return to the site of allergen entry into the body. urticaria 4. death 2. but they become trapped in the basement membrane under the endothelium of blood vessels. Anaphylactic reaction .
prevent graft movement. functional ability. direct sloughing off tissue Organ Transplantation for end stage or failure and do not respond to conventional therapy Recipient: free of irreversible of infection or malignancy End stage of failure and do not respond to conventional therapy No anatomical problem that would lead to difficulty of transplantation Therapeutic or benefit of the patient Ability of the family to pay costs. free of infection/ cover dressing during the 1 st 24 hours within mesh gauze until the site is dried up. family support system. flee graft Pre-op and Post-op Care Recipient Site: free of infection. tissue implanted will now shed off Second set rejection: no vascularization. Synthetic Graft.Graft and - they produce gamma interferon. nutrition - Tissue Rejection – healthy defense mechanism of the body First set rejection: recipient receives unmatched skin 2-3 days the body accepts the skin. acute. prevent infection. family with no history of death of unknown causes Types of Rejection: hyper acute. Mycobacterium tuberculosis. prevent fluid loss Forms of Graft: skin graft. there is vascularization 6 . prevention of infection. no malignancy. psychological status. no transmissible disease. ALG Immunosuppressive drugs. flap graft. no existing disease. promote circulation. which stimulates an inflammatory response. which activates macrophages. chronic Therapies to prevent Rejection: azaththjioprine. cyclosporine.10TH day + lympadenopathy 10 – 14th day + appearance of rejection taking place with the appearance of macrophages and T lymphocytes on the site of transplant 12 – 40th day + necrosis. good vascularization in the area. rehabilitation potential. poison ivy Organ Donation Types: Isograft/syngraft: Autograft. ability to buy post transplantation regimen Donor: cadaver-brain death. . analgesics. Xenograft: Allograft Purposes: Art/Aesthetic. and tumor necrosis factor. cleaned aseptically before surgery/ prevent fluid collection on the graft. promote adequate circulation in the area Donor Site: celan site. ability to return to work. glucocorticoids. age.
what medications taken. asthma Type 2 Cytotoxic and Cytolytic IgG. any contact with animal or animal products. RBC Type 3 Immune Complex IgG. vaccination history Clinical Manifestations: 1. stings (+) wheal and flare within 30 minutes Secondary to prostaglandin. histamine Systemic anaphylaxis. any animal or insect bites. edema Acute inflammatory reagent Serum sickness Type 4 Cell Mediated or Delayed Response T cells.Summary of Hypersensitivity Reactions Property Type I Anaphylactic IgE. Assess for clinical manifestation of infection . serotonin. organ donation DISRUPTIVE INFLAMMATORY RESPONSES COMMUNICABLE DISEASE IN CHILDREN Nursing Process Overview Assessment: History Taking: Local or systemic infection. Ca Tissue induration Tissue destruction Mediators Allergens Response to Skin Test Pathophysiolog y and effect Examples ABO incompatibility TB. macrophages PTB. Baasophils mast cells Drugs. any illnesses that compromises body defenses. bradykinin. complement sytem BT Not done Destruction of cells. IgM Soluble agents like drugs Erythema. history of travel. IgM. IgG.
Potential for spread of infection 5. Measure to prevent cross contamination of infection 4. Altered thermoregulatory status 3. Assist with spinal aspiration of lumbar tap. Enhance coping mechanism to promote adaptation Immunization – receiving immunity against a number of dangerous infections. pyrogenic exudates for bacteriologic studies 3. Fluid and electrolyte imbalance 2. Artificially Acquired Active Immunity – when pathogens are artificially injected into the child by immunization. Obtain specimens of blood. nasal secretions. Potential for serious systemic complications 8. urine. Passive Immunity – IgG antibodies that a woman possesses. Ineffective coping and social isolations 9. sputum. Secure/Assist in securing blood smears or other materials for microscopic studies 4. passive or active Active Immunity – when the child produces antibodies after the natural invasion of a pathogen Naturally Acquired Active Immunity – ability to produce antibodies rapidly should be specific antigen invade again. Carry out appropriate skin tests for specific diagnostic reactions as directed Nursing Diagnosis: 1. Naturally Acquired Passive Immunity – fetus does not make antibodies but received them. .2. BM or any other fluids or tissues for cytologic. Ensure hemostasis 3. lasting. Immunity – ability to combat a particular antigen. Artificially Acquired Passive Immunity – injection of antibodies made synthetically or obtained from animal serum to the child to give rapid immunity lasting approximately for six weeks. throat swabbing. Fever 4. serologic or bacteriologic study 5. Implement therapeutic plan to treat infection 2. Should be specific antigen enter again. Altered elimination status 7. Knowledge deficit Planning and Implementation: 1. Prevent overwhelming infection in the immunocompromised patient 5. stool. Relief of symptoms of infection 6. either through immunization or through having a disease are transferred across the placenta to a fetus in utero. Altered respiratory status 6. antibodies are produced against the pathogen that are just as lasting as those produced are in naturally acquired active immunity.
“I wish to buy 12 articles at 7 pence each. Note: Retrograde amnesia – loss of memory of events leading up to a brain injury or insult. or 7 random numbers.g.5 ml) 0.Immunization Schedule Vaccine BCG (1 dose at birth) DPT (3 doses) OPV HEP B (3 doses) MEASLES 9 months Indication Tuberculo sis Age At birth School entrant Dose 1 dose (0. . fever Fever. fever None Local reaction – swelling. duration of hospital stay or recent events in the news. fever. RECENT memory – ask patient to describe present illness. REMOTE memory – ask about events or circumstances of occurring more than 5 years previously. local reaction 3x 3x 3x 0. deltoid. e. IMMEDIATE memory – Digit span – Ask patient to repeat a sequence of 5.5 cc Frequenc y 2x Route Intradermal deltoid IM vastus lateralis oral IM vastus lateralis Subcutaneo us. How much change will I receive from L1? Ask patient to reverse 3 or 4 random numbers. VERBAL memory – ask patient to remember a sentence or a short story and test after 15 minutes. Post traumatic amnesia – permanent loss of memory of events for a period following a head injury. VISUAL memory – ask patient to remember objects on a tray and test after 15 minutes. The examiner must compare patient’s present reasoning ability with expected abilities based on job history and/or schoolwork.5 ml 2 drops 0. Ask patient to sort cards into suits. local abscess Swelling. 6.5 cc once EXAMINATION – HIGHER CEREBRAL FUNCTION MEMORY TEST Testing requires alertness and is not possible in a confused or dysphasic patient. gluteal Side effects Pain. Ask patient to explain proverbs. REASONING AND PROBLEM SOLVING Test patient with two-step calculation.
serial 7 test. may awake.” Ask the patient to name objects Does the patient read correctly? Does the patient write correctly? Ask the patient to perform numerical calculation.g.fluent Does the patient understand simple/complex spoken commands? e. Can the patient recognize objects? E.g. quick. e. “Hold up both arms. ask the patient to select an object from a group. ask the patient to forma star with matches or copy a drawing of a cube.g. Can the patient dress himself? Note the patient’s ability to copy a geometric pattern. disorders Note patients ability to find his way around the ward or his home. may be aroused quickly but easily falls . normal response to tactile. e. clear mentation. touch the right ear with the left fifth finger.g. Dominant hemisphere disorders Expressive dysphasia Receptive dysphasia Receptive dysphasia Nominal dysphasia Dyslexia Dysgraphia Dyscalculia Agnosia Non. stimuli responds to stimulus.Dominant hemisphere Geographical agnosia Dressing apraxia Constructional apraxia Mild mental function tests and Functional activity questionnaire are used in the assessment of DEMENTIA MENTAL BEHAVIOR Level of Consciousness: Alert verbal. painful Drowsy asleep.EMOTIONAL STATE Note: Anxiety or excitement Depression or apathy Emotional behavior Uninhibited behavior Slowness of movement or responses Personally type or change COGNITIVE SKILL Listen to language pattern – hesitant . where 7 is subtracted serially from 100.
vigorous. movement are absent except for muscle reflex contraction state of mental confusion and excitement lack of emotional response a sensory phenomenon that may precede a convulsion. Responsive only to deep painful stimulation no response to any stimulation. When stimulated. referring usually to antero-lateral pathways that transmit pain Hypoglycoorrhakia Pleocytosis Xaantochromia Macrocephalous Microcephalous - CSF low sugar in CSF increased WBC in CSF yellowish discoloration of the CSF HEAD having an unusually large head having an unusually small head . or ringing bells. HANDOUT IN NEUROLOGIC NURSING Abberration Decerebrate Denervate drug Contrecoupinjury the - NOMENCLATURE deviation from normal structure of behavior deprived of cerebral function to interrupt motor/sensory nerve supply to a party by injection or operation injury to the brain produced on the side opposite that of primary injury brain injury resulting from violent jarring of the to the head. he Semi-comatose Comatose some Confusion Apathy Aura flash of - but movements are not purposely. often stimuli are necessary to arouse the patient. can be aroused and responsive. fall Cerebral Concussion brain due to blow Craniotomy Craniectomy Chordotomy the SURGICAL PROCEDURE surgical opening through the cranium the surgical removal of a part of the skull division of the long tract of the spinal cord.Obtunded falls back Stuporous painful move yawn frequently. fall asleep during meal or lengthy conversation. but he’s usually confused and to sleep as soon as he is not directly stimulated does not respond spontaneously to environment. such as light.
movement is slowed flexion of the knee and hip joint is slowly and imperfectly performed. involuntary short. He cannot accurately place one foot in front of the other and leg movement is jerky and uncoordinated: tends to fall on one side. eventually forcing the patient. trunk developing a forward list. Retropulsion Scissors other Emprosthothonus forehead and Opisthotonus head on the floor Pleurothotonus to one side Orthotonus line - titanic spasm marked by rigidity of the body in a straight MOVEMENTS. with his difficulty in stepping. TONE . the patient affected foot higher than normal and the foot tends to downward. associated with spastic weakness. He may be unable to stabilize his trunk in the vertical posture so that he tends to jerk back and forth (titubation) + Rombryg test (sensory) staggering gait morbid acceleration of gait tendency to push or fall forward in walking walking backward. to have to run forward to “catch up” with the center of gravity.Cephalococle Cephalhematoma “Foot drop” gait elevates the point Spastic gait and - protrusion of the brain from the cranial cavity subcutaneous swelling containing blood found in the head GAIT due to weakness in dorsiflexing the ankle. short-stepped. Propulsion 2. The patient has to swing the affected leg around (circunduct) since he cannot flex and elevate it. 2. slow steps. COORDINATION. affected arm is characteristically held in semiflexion at the elbow and wrist. titanic spasm in which the body position is arched Parkinson Gait with the Ataxic - Titubation Festination 1. an arched position of the body with the feet and or bed. patient show either or both of these abnormalities: 1. with legs alternately crossing over each POSITION lying with the body in curved and resting upon the feet with face downward. the patient shows loss of arm swing. affected leg tends to remain adducted.
neck or shoulder muscles that may be involuntary or the result of a habit rhythmic quivering: involuntary movement of a part of the - - resulting from the alternate contraction of opposing muscles 1. . rapid. coordinated. undershoots or overshoots tendency to veer to one side of tip of nose or finger to touch it extreme slowness of movement involuntary. Fine Tremors – rapid.) 2. movements serial order instead of being made together inability to fix the range of a movement. sudden movement or muscular produce localized. Clonic movement . characterized by oscillation of 810 times per second Twitching convulsions quick spasmodic contraction of muscles paroxysm of involuntary muscular contractions and relaxations 1. defect in voluntary movements absence of muscle lack of coordination between muscle groups. ex. Coarse Tremors – oscillations are relatively slow (6-7 per sec. involuntary twitching of muscle group while muscles are at rest. squirming. writhing. Tonic – one which the contractions are maintained for a time which usually draw joints into position of flesion/extension Chorea/Choreiform hallmark of chorea. Flexing and extending fingers Ballismus quick jerky shaking movement Hemiballismus quick jerky movement involving half of the body Athetosis repeated involuntary movement of slow. incoordinated. are purposeless. jerky usually involving the movements extremities and trunk with facial grimacing. stereotyped spasmodic muscular contraction face. muscles alternately contract and relax 2.one having intermittent contractions.Coordination complex Apraxia movements Dyskinesia Akinesia synergia are in Dysmetria Pass-pointings when trying Bradykinesia Spasm contraction Fasciculation a single Tic of the Tremor body - harmonious action of muscle groups in performing movement inability to perform certain acts or purposeful - without motor loss.
giving in Muscular resistance is characteristically intermittent when muscles are palpated. no motor stiffness of the neck temporary suspension or permanent loss of voluntary sensation in a body part involved part of the body is in a state of muscular rigidity tenseness involved part is completely relaxed or limp paralysis of the lower half of the body paralysis of the longitudinal half of the body paralysis of like parts on either side of the body paralysis of the four extremities muscle weakness of partial or incomplete paralysis dropping of the upper eyelid SENSATION peculiar sensation of numbness. Tactile – inability to distinguish objects by using sense of touch is the inability to recognize familiar objects by - Asteriognosis touch or Diplopia Anopsia Homonymous eye Anosmia Dysarthria Dysphasia - manipulation double vision loss of vision in one eye Hemianopsialoss of one-half of the field of vision in one absence of the sense of smell SPEECH AND LANGUAGE difficulty in articulation impairment in speech . softness and flabbiness. tingling. prickling. unusual sensitivity to pain or sensory stimuli severe Lancination pain along the course of a nerve muscular pain loss of comprehension of audio-v.Nystagmus Rigidity Spasticity Cogwheel Rigidity the Rest Tremors Intention Tremors Hypotonia Flaccidity response Nuchal rigidity Paralysis motion and Spastic Paralysis or Flaccid Paralysis Paraplegia Hemiplegia Diplegia Quadriplegia Paresis Blepharopthosis Paresthesia Hyperesthesia Neuralgia Myalgia Agnosia sensation - twisting type. visual or other 1. Auditory – inability to interpret sounds 2. involuntary muscle movement at rest involuntary movement seen when doing something decreased muscle tone muscular weakness. Optic – inability to interpret images seen 3. involuntary movement of the eyeballs resistance all through the ROM resistance of movement at the beginning then.
Frontal Lobe – aphasia A. Sensory (receptive aphasia) – inability to comprehend or understand oral or written communication 2. Optic – inability to copy words INTRACRANIAL HEMORRHAGE bleeding beneath the cranium and outside the dura. Convulsion 7.Aphasia written - loss or the inability to use or understand spoken or Alexia Agraphua - language. incontinence/retention C. it may exist without intellectual impairment 1. word blindness inability to express oneself in writing 1. Motor deficits – weakness or paralysis of any part of the body 3. Other signs and symptoms which may or may not develop: 1. Awkwardness – may mean weakness. Auditory aphasia – difficulty of understanding spoken word 5. Speech disturbances 6. Motor. hemorrhage between the dura and arachnoid. Nominal aphasia – inability to attach meaning to words read inability to read. Localizing Symptoms 1. write although can comprehend 3. Acoustic – inability to write words head 3. personality changes maybe the first noticeable sign Subarachnoid Hemorrhage hemorrhage between the arachnoid and pia mater into CSF NEUROLOGIC SIGNS increasing or widening pulse pressure Decreasing PR Increasing headache Pappil edema Decreased mental awareness Decreased in RR B.inability to write due to muscle coordination 5. Extradural/Epidural frequently Subdural Hemorrhage increasing ICP develop slowly. Sensory Disturbances of any part of the body 4. difficulty or coordination 5. Vomiting – may or not be projectile 2. Global aphasia – an almost total language loss manifested in minimal response in every phase of language 4. Cardinal symptoms: . Absolute – complete inability to write 2. Cerebral – inability to express thoughts in writing 4. Motor (broca’s) aphasia can’t speak.
rubber 4. it becomes small ↓ Also. nystagmus. the liver is apt to be large and its cells loaded with fat ↓ Later as replacing scar tissue contracts.Confusion Changes in personality Jacksonian convulsion. bec the scar within it is disposed in coarse bundles. sensory disturbance. 3. taste or hearing. Basal Ganglia Athetosis. chorea. smell of burning Occipital Lobe – visual disturbance Cerebellum Ataxia – muscle coordination especially manifested when voluntary muscular movements are attempted. its surface often becomes rough.convulsion begins in one part of the body and 2. spread in orderly manner to all of the body parts. exposure to certain chemicals or infectious schistosomiasis ↓ Episodes of necrosis involving the liver cells ↓ Destroyed liver cells are replaced by scar tissue. which contract and pull in the capsule at certain points and cause the island of residual normal tissue and of new regenerating liver tissue to project in the little lumps ↓ Liver Enlargement → Activity Intolerance r/t fatigue ↓ Portal Obstruction and Ascites → Ineffective Breathing Pattern r/t ↓ intra. the amount of which in time may exceed that of the functioning liver tissue ↓ Early in the disease. hemiballismus. Parietal Lobe – convulsion.abdominal fluid collection (ascites) . asteriognosis Temporal Lobe – defects in visual field. 5. Tremors. hypotonia 6. tremor Pathopysiology Cause: excessive alcohol consumption. reduced protein intake.
overt 5.overt 7. Activity Intolerance r/t fatigue .abdominal fluid collection (ascites) overt 3.Infection and peritonitis compromised ↓ Gastrointestinal varices altered clotting ↓ Edema compromised ↓ Vit deficiency and anemia ↓ liver Mental deterioration inability of the liver Body Image Disturbed r/t personal vulnerability → Impaired Skin Integrity r/t immunologic status → Risk for Injury and bleeding r/t Mechanism → Fluid Volume Excess r/t → regulatory mechanism Nutrition Imbalanced: less than body requirements r/t oral intolerance and Cirrhosis → Risk for acute confusion r/t to detoxify certain enzymes or drugs Prioritization of Problems: 1.overt 2. Fluid Volume Excess r/t compromised regulatory mechanism . Risk for acute confusion r/t inability of the liver to detoxify certain enzymes or drugs – covert . Ineffective Breathing Pattern r/t intra.overt 6. Body Image Disturbed r/t personal vulnerability . Impaired Skin Integrity r/t compromised immunologic status . Risk for Injury and bleeding r/t altered clotting mechanism -covert 8.overt 4. Nutrition Imbalanced: less than body requirements r/t oral intolerance and liver cirrhosis .
cyanosis. Indicative of onset infection ex. Pneumonia Evaluation STO: fully met pt is no longer dyspheric and O2 is no longer needed Factors: Pt is very cooperative and willing to participate in any therapy LTO: fully met if pt will establish a normal or effective respiratory pattern Auscultate breath sounds.Assessment S: “Nahihirapan akong huminga” O: v/s Temp: 36. reduced protein intake. exposure to certain chemicals and infectious schistosomiais Necrosis of liver cells Destroyed liver cells are replaced by scar tissue Scar tissue exceeds that of functioning liver tissue Objectives STO: After 8 hours of health care interventions pt will be free of dyspnea. rhonchi Investigate changes in level of consciousness Portal obstruction and ascites Ineffective Breathing Pattern Monitor temp.7°C BP: 110/60 mmHg PR: 94/min RR: 18/min Conscious: dyspheric Prefers to be in bed Prefers to sleep Assisted w/ ADL by SO Easily fatigued: pallor Appears weak and restless On O2 at 12\LPM/NC Irritable thus changes position once in a while (+) coughing. increased coughing. note presence of chills. nonproductive Enlarged Pathophysiolog y Cause: excessive alcohol consumption. changes in color/character of sputum Monitor serial ABG’s pulse oximetry. chest x-rays Tx: keep head of bed elevated. vital capacity measurements. depth and effort Rationale Rapid shallow respirations/dyspne smay be present bec. Of hypoxia and or fluid accumulation in abdomen Indicates developing complications. wheezes. increasing risk of infection Changes in mentation may reflect hypoxemia and respiratory failure w/c often accompany hepatic coma. w/ ABG’s and vital capacity w/in acceptable range LTO: After 2 weeks of health care intervention pt will establish a normal effective respiratory pattern Intervention DX: Monitor respiratory rate. Reveals changes in respiratory status developing pulmonary complications . noting crackles.
If respiration/oxygena tion inadequate/ mechanical ventilation maybe required Reduces metabolic and oxygen requirements Conserve pt’s strength by providing rest periods and assisting with activities Change position in every 2 hours Assist with paracentesis or thoracentesis as indicated Ed Encourage frequent repositioning and deep breathing exercises/cough ing as appropriate Demonstrate Promotes expansion and oxygenation of all areas of the lungs Paracentesis and thoracentesis are performed to remove fluid from the abdominal and thoracic cavities respectively.abdomen (ascites) A: Ineffective Breathing Pattern r/t Ascites Position on sides Provide supplemental o2 as indicated Facilitates breathing by reducing pressure on the diaphragm and minimizes risk of aspiration of secretions Maybe necessary to treat/prevent hypoxia. .
7°C BP: 110/60 mmHg PR: 94/min RR: 18/min Conscious Always in bed and asleep Appears weak and restless Globular or enlarged abdomen Pathophysiolog y Cause: excessive alcohol consumption. exposure to certain chemicals and infectious schistosomiais Necrosis of liver cells Destroyed liver cells are replaced by scar tissue Scar tissue Objectives STO: After 8 hours of health care intervention pt will be able to demonstrate progressive weight gain toward goal with pt appropriate normalization of laboratory values LTO: After 1 month of health care interventions pt will attain desirable weight with optimal Intervention DX: Measure dietary intake by calorie count Weigh as indicated. Skin fold measurement are useful in assessing changes in muscle mass and . recent weight history. skin fold measurement. compare changes in fluid status. enhance mobilization of secretions Assessment S: “wala akong ganang kumain” O: v/s Temp: 36. reduced protein intake. Rationale Evaluation STO: not met Pt was not able to demonstrate progressive weight gain Factors: Pt doesn’t like to eat because he claims that he is already full Recommendation : Pt needs encouragement NGT insertion Provide information about intake needs or deficiencies It maybe difficult to use weight as indicator of nutritional status in view of edema and ascites.with respiratory adjuncts Aids in lung expansion and mobilizing secretion Reduces incidence of atelectasis.
sparing protein for healing LTO: fully met if pt will attain desirable body weight with optimal maintenance of health Not met: If pt will not attain desirable body weight with optimal maintenance of health Offer smaller. more frequent meals Provide salt substitutes. Provide calories for energy. bloating Salt substitutes enhance the flavor of foods and aid in increasing appetite ammonia potentiates risk for encephalopathy. subcutaneous fat reserves. if allowed.Prominent abdominal veins Tenderness on all quadrants Dull abdomen upon percussion Anorexia: food intolerance Slender body built Increased bowel sounds Oral intolerance (-) nausea and vomiting (-) fever (-) diarrhea exceeds that of functioning liver tissue Vit deficiency and anemia Nutrient imbalanced: less than body requirement maintenance of health Tx: Provide diet high in carbohydrates with protein intake consistent with liver function Elevate head of bed during meals. gas producing or spicy and excessively hot or cold foods. Decreases feeling of fullness. Reduces discomfort from abdominal distention and decreases sense of fullness produced by pressure of abdominal contents and ascites in the stomach. avoid those containing ammonia Restrict intake of caffeine. Aids in reducing gastric irtrtation/diarrhe .
Hemorrhage form esophageal varices may occur in advanced cirrhosis. Reduces excessive gastric stimulation and risk of irritation or bleeding. Encourage pt to eat meals and supplementary feedings a and abdominal discomfort that may impair oral intake and digestion. Conserving energy reduces metabolic demands on the liver and promotes cellular regeneration. avoiding roughage if indicated. . Promotes appetite and sense of wellbeing. Promote undisturbed rest periods especially before meals Provide oral hygiene before meals aesthetically pleasing setting at mealtime Ed: Suggest soft foods. Encouragement is essential fo the pt w/ anorexia and gastrointestinal discomfort. Recommend cessation of smoking.
thrombosis).Is an inflammation of the arachnoid. The infection spreads throughout the subarachnoid space about the brain and spinal cord and usually involves the ventricles. engorgement with blood. especially in the basal cisterns.. changes in subarachnoid arteries (e.g. Almost any bacteria can enter the body causing meningitis o The most common are: Meningoccocus (Neisseria meningitides) Pneumococcus (Streptoccous pneumonia) Haemophilus influence These organisms are often present in nasopharynx. Little change occurs in brain structures in the early stages. and intervening CSF. Clinical manifestations Headache Prostration Chills Fever N/V . FACTORS PREDISPOSING TO BACTERIAL MENINGITIS head trauma systemic infection post surgical infection meningeal infection other systemic illness When pathogenic organisms enter the subarachnoid space >inflammatory reaction (CFS clouding. The pia arachnoid becomes thickened and adhesions form. rapture. pia. and congestion of adjacent tissues.NEUROLOGIC INFECTIONS BACTERIAL MENINGITIS . It is not known how they enter the blood stream and the subarachnoid space. exudates formation.
bacterial. Backpain Stiff neck Generalized seizures Later stage. stuporous. or hemorrhagic rash may develop The patient may be irritable at first. yeast) Exudate forms ↓ Meningeal irritation/inflammation ↓ Cortical inflammation ↓ Cerebral edema ↓ Increased ICP ↓ Vasculitis Increased infection Petechial Hemorrhages Neuritis Hydrocephalos ↓ ↓ ↓ ↓ ↓ Cortical Brain abscess Septic Emboli Cranial nerve Increased Necrosis Septicemias involvement ICP ↓ ↓ ↓ Adrenal DIC Seizures Compression of Hemorrhage brain structures Hemorrhage Inadequate perfusion Shock ↓ DEATH Hypoxia . or semicomatose. petechial. confused. but as the infection progresses the sensorium becomes clouded and coma may develop o Signs of meningeal irritation: Nuchal rigidity (rigidity of the neck) Positive finding of Brudzinski’s sign Positive finding of Kernig’s sign MENINGITIS infectious organisms gain access to meninges and subarachnoid spaces (viral.
food containing beta-phenylethylamine o Chocolate o Cheese o Citrus fruits o Coffee o Pork products o Dairy products Familial tendency .Are paroxysmal disorders characterized by recurrent throbbing headaches .Intense throbbing headache is due to dilation of extracranial and intranial branches of the external carotid artery Psychological factors influence migraine headache o Perfectionist o Fatigue o Excess sleep o Hunger o Refractive errors o Bright light o Surprises o Mental and emotional excitement o Excessive smoking o High altitudes o Drinking alcoholic beverages Certain foods that seem to precipitate migraine episodes. nose. severe HPN.Constriction of intracranial vessels > neurologic symptoms . frequency varies from several times a week to several times a year PATHOPHYSIOLOGY (vascular theory is currently accepted) . Serious disorders that typically produce headache include intracranial tumors and infection. throat.They decrease in frequency and severity with advancing years . The cause must be identified so that appropriate treatment can be given.Episodes begin during puberty or ages 20-40 years .Occurs at irregular intervals. COMMON TYPES OF HEADACHES I. cerebral hypoxia. the nurse should encourage clients with persistent or recurrent headaches to seek neurologic assessment. ear. Most headaches do not indicate serious disease however.Is a symptom of an underlying disorder rather than a disease itself. bacterial or viral meningitis. Clients often-self treat headaches with OTC medication without prescription. acute or chronic diseases of the eye. head injuries.Women are more susceptible than men are .Affects 5-10% of the population . Migraine .
3. Lying in a dark. 4. diplopia). I. restlss. Cluster headaches (Histamine headaches) . distorted vision. II. scalp may be very tender. I. vertigo. and excessive tearing of the eyes. Ergot must be taken before the vessels become rigid from edema in their walls. diphenhydramine hydrochloride (Benadryl). o Unilateral and may be localized to the front. It gradually increases in severity until the pain becomes intense and all-encompassing. may be generalized or unilateral. and may or may not be accompanied by N/V. or hammering.1. abdominal pain. o General sensitivity of all sensory organs and client withdraws from light and sound. . pressing. nausea. MANAGEMENT: 1. biofeedback. N/V. flashes of lights. 6. Treat the two phases of migraine.>mild discomfort.Once the migraine becomes intense ergot is of little value.. avoid food and beverages that contain tyramine and have vasoactive qualities. bright spots. o Pain described as dull and boring. or extremities). 2. Apply pressure on the common carotid artery and the affected superficial artery. diarrhea. quiet room with ice on the back of the neck during acute episodes. or side of the head. analgesics such as acetaminophen may relieve mild H/A. diarrhea. >prostrating. redness. Severe headaches respond to ergot preparations but only if they are taking 30-60 minutes after headache onset. Atypical or Common Migraine o Begins suddenly with or without prodromal symptoms.g. vasoconstriction and vasodilation. o Acute migraine episodes lasts 4-6 hours (accompanied by photophobia. 5. stronger analgesic such as codeine sulfate. and swelling of the nasal mucosa (sometimes accompanied by epistaxis) may occur. back. It can occur during menstruation. Follow a restrictive diet. Oral contraceptive may exacerbate migraines or induce their onset in women previously free from significant headaches. irritable. may lasts a few minutes or several hours. swelling. tremor. o Arteries of the head may become prominent and the amplitude of their pulsation increase. throbbing.Prescribed orally IV or rectally . e. Classic or Typical Migraine o Preceded by an aura or prodromal phase in which the client may feel depressed. vertigo. throbbing pain >seclusion and lie in bed in a darkened room. Relaxation techniques. and perhaps anorexic o May experience transient neurologic disturbances (visual phenomena. o Has a “cresendo” quality. often the temple and eye areas.2. paresthesis (numbness of tingling of lips. or counseling directed at preventing episodes by helping the client understand tensions and resolve major life conflicts. excessive sweating or chilliness). face.
months or years. wearing a hat or exposure to cold . Some feel they cannot survive another episode.Onset is gradual. III. anxiety and depression. Cluster headache may recur at irregular intervals for many years. . Tension headaches (muscle Contraction Headaches) . They may increase significantly in menopause. Intervention is ineffective because of shortness of episodes. Excruciating painful. Tricyclic antidepressant 4.Maybe unrelieved for weeks. throbbing. could also be accompanied by dizziness. Supportive care – clients tend to become depressed over their condition and fearful recurrent episodes. often related to times of stress anxiety. Lying in a dark. or emotional upset. The nose and affected eye water. Episodes may occur within a few days.Pain could be precipitated by combing the hair. There is usually no aura. These headaches were formerly believed to be caused by sensitivity to histamine. Indomethacin (Indocin) medication of choice 3. Men are affected five times more often than are women. the client experiences: Excruciating. MANAGEMENT: 1. and tend to occur in clusters. quiet room with ice on the back of the neck during acute episodes. Pre-menstrual headaches are of this type. but more so in the occipital and upper cervical regions and extends diffusely over the top of the head .Begin in adolescence but occur most often in middle age. Episodes usually begin in middle life and are often worsened by alcoholic consumption. and neck and upper back.- - Sometimes classified as a form of migraine. around and behind the eye on the affected side. Then the headaches again recur in clusters. During episode.Pain is steady. tinnitus or lacrimation .Vasodilation of associated cranial arteries may also contribute to muscle irritability and head pain . weeks. Most clients experiencing cluster headaches do not have a history of migraine headaches. .) . and the skin reddens on the affected side Nasal congestion and conjunctival infection are common. face. or steady pain arising high in the nostril and spreading to one side of the forehead. followed by a remission with no symptoms for months or years. or occasionally months.Results from the long-sustained contraction of skeletal muscles around the scalp. The mechanism underlying cluster headache is not well understood but is believed to be in vascular origin. with N/V (late reaction). non-pulsatile ache (unilateral or bilateral) in any region of the head. 2.Muscles become tender → client tenses more (primary source of many headaches associated with excessive emotional tension. . unilateral .
Psychotherapy for those with prolonged and recurrent muscle tension headaches of psychological in origin 3. apply local heat. Heat intolerance (such as vacationing in warm climates) may increase headaches. coffee. small frequent meals may avert headaches. a larger dose may be required during these times. The lack of eating may lower blood sugar and may lead to headache. If stressors cannot be reduced. the dose of medication can be adjusted. Alcohol increases the size of blood vessels (vasodilation) and may increase headache. CLIENT EDUCATION GUIDE PREVENTING MIGRAINE HEADACHES Many things can trigger a migraine headache. Adjusting Medications During Menstrual Cycles. cheese. Eliminate source of stimulation (diseased teeth) 2. or car hoods. then medications may need to be increased. Adjusting Dietary Triggers. It is important for the client to find out what triggers the headache and avoid the trigger.. roads. and bright sunlight causing a glare from water. citrus fruits. Some foods contain betaphenlethylamine and should be considered possible triggers.g. rest and various relaxation techniques 4. occasionally a stronger analgesic is needed (e. Responds well to a combination of non-narcotic analgesic with an anxiety relieving drug.MANAGEMENT: 1. Other factors related to stress that might trigger headaches include fatigue. Stress may trigger migraines. excess sleep. If medications are taken for migraines. In this case. Codeine sulfate). These items include chocolate. Symptomatic relief: massage affected muscles. pork products and dairy products. if possible. . if avoidance of the trigger is not possible. Menstruation and ovulation may trigger migraines. Identifying the Role of Stress.
Hereditary coagulation disorder. both hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency) are inherited as sex linked recessive disorder and are therefore almost exclusive for males. X-linked recessive disease – it means that. Hereditary and limited to males. it is common to males but is being transmitted by females. Hemophilia A (Classic Hemophilia) • 80% hemophiliacs • Factor VIII deficiency (anti hemophilic factor) . All daughters of hemophiliacs become carrier. Transmitted by a female trait carrier Absence deficiency or malfunction of any one of clotting factors TRANSMISSION OF HEMOPHILIA Genotype of parents N Carrier+N male N female+Hemophiliac Carrier+hemophiliac 50% 0% 0% Female Carrier 50% 100% 50% Hemophili ac 0% 0% 50% Male N Hemophilia c 50% 50% 100% 0% 50% 50% COMMON TYPES OF HEMOPHILIA 1.HEMOPHILIA • • • • • • • A disorder characterized by impaired coagulation of blood and a tendency to bleed.
elevation and topical coagulants such as fibrin foam and thrombin) • Since the deficient factors are contained in the plasma. Blood Factor replacement Therapy FFP: all clotting factors present Cryoprecipitate: factor VIII. Moderate:2 to 5 % • More frequent bleeding episodes. tendency to nose/gum bleeding 2. • In major hemorrhage. Hemophilia B (Christmas Factor) • Factor IX deficiency (Plasma Thromboplastin component) 3.2. excessive bleeding after surgery or trauma 3. severe bleeding • Hemarthrosis MANIFESTATIONS: • Diagnosed usually in infancy or early childhood • History of excessive bleeding into any part of the body sponataneoulsy following trauma • History of excessive bleeding following circumcision and dental extraction • PTT of Hemophilia A and hemophilia B is prolonged • Platelet count and prothrombin time is normal TREATMENT • Replace deficient coagulation factor when bleeding episodes do not respond to local treatment (ice bags. Severe: 1% or less • Spontaneous bleeding. • In classic hemophilia. fresh plasma and blood or fresh frozen plasma Is given. Mild: clotting factor level 6 to 30% • Bruise easily. fibrinogen . immobilization. adequate blood levels were difficult to maintain without overloading person’s circulation with large volumes of blood and plasma. treatment of choice in acute bleeding is infusion of concentrate of antihemophilic factor (Factor VII) • Concentrates prevent circulatory overload and produce fewer adverse effects • Usually people who are being transfused with Factor VIII concentrates are easy to acquire AIDS because donors are not screened that well MANAGEMENT: I. manual pressure or dressing. Hemophila C • Factor XI deficiency (Plasma Thromboplastin antecedent) STAGES 1.
Desmopessin for Mild Hemophilia A It triggers the release of Factor VIII CLOTTING FACTORS 1. Lyophilized factor VIII concentrates Vit. IX. Factor IX – Plasma thromboplastin component (PTC) 9. stabile factor. K dependent complex: Factor VIII. Factor IV – Calcium 5.Stuart power factor 10. Factor VI – omitted 7. prothrombin II. Factor III – Thromboplastin 4. accelerator globulin 6.Factor XIII – Fibrin Stabilizing Factor Extrinsic System Factor III Factor VII Intrinsic System Factor XII Factor XI Factor IX Factor VIII Scheme of clotting Mechanism Platelet lysis Factor X Factor V Calcium Prothrombin Thrombin . Factor II – Prothrombin 3.Factor XII – Hageman Factor (HF) 12. serum prothrombin conversion accelerator (SPCA) 8. Factor X . Factor I – Fibrinogen 2. labile factor.Factor XI – Plasma Thromboplastin antecedent (PTA) 11. Factor VII – Proconvertin. XI. Factor V – Proaccelerin.
quicker to perform. more sensitive. V. frequently used to monitor heparin therapy and hemoglobin NORMAL VALUES 2 to 9 minutes Clotting time (CT) Prothrombin Time (PT) 5 to 10 minutes 11 to 16 seconds Partial Thromboplastin Time (PTT) Activated Partial Thromboplastin (APTT) 60 to 90 seconds 26 to 42 seconds . VII and X) -more sensitive test than PT to evaluate adequacy of intrinsic coagulation pathway (Fibrin formation) -modified PTT. II.Plasminogen Activator Urokinase Plasminogen Plasmin COMMON BLEEDING AND COAGULATION BLOOD TESTS TEST Bleeding time DESCRIPTION -Evaluation of vascular platelet factors – the time it takes for a small stab wound to stop bleeding -time required for solid clot to form (less sensitive test than PTT) -indicates rapidity of blood clotting (indicates adequacy of extrinsic coagulation pathways for factors I.
Cardiac output b. which Is greater dependent on body sodium • Thus. . itself dependent on the thickness of the arteriolar wall and the effects of neural and hormonal influences that either constrict or dilate these vessels. • About 90-95 of hypertension is idiopathic and apparently primary (Essential hypertension) • Of the remaining 5-10%. sodium homoestasis is central to blood pressure regulation TOTAL PERIPHERAL RESISTANCE: • Predominantly determined at the level of the arterioles and depends on lumen size. most is secondary to renal disease or less often. to narrowing of the renal artery. REGULATION OF NORMAL BLOOD PRESSURE: The magnitude of the arterial blood pressure depends on two hemodynamic variables: a. usually by an atheromatous plaque (Renovascular hypertension) • Infrequently. secondary hypertension is the result of disease related to the adrenal glands.HYPERTENSION: • Elevated blood pressure • A sustained blood pressure greater than 90 mmHg or a sustained systolic pressure in excess of 140 mmHg is considered to constitute hypertension. Total peripheral resistance CARDIAC OUTPUT: • Influenced by blood volume.
Auto regulation leads to an increase in peripheral resistance. ENVIRONMENTAL FACTORS: Environmental factors are thought to contribute to expression of the genetic determinants of increased pressure. • • • . however. physical inactivity. In the face of an increasing cardiac output. MECHANISMS: • What then are the primary defect in essential hypertension? • Two overlapping pathways are proposed: a. and along with it an elevation of blood pressure. Hydrogen ions c.• Normal vascular tone depends on the competition between: a) Vasoconstricting influences Angiotensin II Catecholamines Thromboxane Leukotrienes Endothelin b) Vasodilators: Kinins Prostaglandins Nitric oxide • Certain metabolic products…. and heavy consumption of salt have all been implicated as exogenous factors in hypertension. Lactic acid b. a. In both the major pathways for hypertension – primary renal and primary vascular defects – heavy sodium intake augments hypertension. Stress. Renal retention of excess sodium The existence of genetic factors that result in reduced renal sodium excretion – in the presence of normal arterial pressure – as the initiating event. Decreased in sodium excretion leads to an increased in fluid volume and a high cardiac output. obesity. Adenosine And hypoxia…can also function as local vasodilators! • GENETIC FACTORS: It is now thought that essential hypertension results from an interaction of genetic and environmental that affect cardiac output or both. peripheral vasoconstriction occurs as a result of auto regulation to prevent the over perfusion of tissues that would ensue from an increase cardiac output.
Such vasoconstrictive influences. hyperplasia and matrix deposition. Hyperplasia of smooth muscle cells Leading to thickened wall and narrowed lumen or by both effects. At the higher setting of blood pressure. salt intake. or repeatedly may themselves cause structural thickening of the resistance vessels. catecholamines. Angiotensin II) also function as growth factors causing smooth muscle hypertrophy. enough additional sodium can be excreted by the kidneys to equal intake and prevent fluid retention. Remodeling b. Vasoconstriction and vascular hypertrophy Such increased resistance is caused either by factors that induce functional vasoconstriction or by stimuli that induce structural changes in the vessel wall like a. thus perpetuating increased blood pressure. Increase released of vasoconstrictor agents (eg. Thus. Certain vasoconstrictors (eg. VASCULAR PATHOLOGY: . endothelin) 3. estrogens… Which affect the variables that control blood pressure in the genetically predisposed individual. Increased sensitivity of vascular smooth muscle to constricting agents. SUMMARY: • Essential hypertension is a complex disorder that almost certainly has more than one cause. both increased cardiac output and increased peripheral resistance contribute to the increased pressure. • In established hypertension. Rennin. • It may be initiated by environmental factors – stress. Conversely. if exerted chronically. preceding rather than strictly secondary to the vasoconstriction. Hypertrophy c. Such evidence has led to a hypothesis that genetic or environmentally induced defects in intracellular signaling in smooth muscle cells affect cell cycle genes and ion fluxes that modulate both smooth cell growth and increased vascular tone resulting in wall thickening and vasoconstriction respectively. an altered but steady state of sodium excretion is achieved (resetting of pressure natriuresis) but at the expense of stable increases in blood pressure b. Behavioral or neurogenic factors – as exemplified by the reduction of blood pressure achieved by meditation (therelaxation response 2. there is evidence that structural changes in the vessel wall may occur early in the hypertension. Vasoconstrictive influences may consist of: 1.
Note: • The kidneys play a very important role in blood pressure regulation. hyaline arteriosclerosis is a major morphologic characteristic of benign nephroscerosis in which the arteriolar narrowing causes diffuse renal ischemia of the kidneys. Hypertension is associated with two forms of small blood vessel disease. the chronic hemodynamic stress of hypertension or a metabolic stress in diabetes accentuates endothelial injury. • Thus. . • The narrowing of the arterial lumens causes impairment of the blood supply to affected organs particularly well exemplified in the kidneys. HYALINE ARTERIOSCLEROSIS: • The vascular lesion consist of homogenous. concentrated laminated thickening of the walls of arterioles with progressive narrowing of the lumens. • Renal dysfunction is essential for the development and maintenance of both essential and secondary hypertension. • This form of arteriolar disease can be identified with the light microscopy by virtue of its onion skin. but other causes may also be involved. thus resulting in leakage and hyaline deposition. • Presumably.• • Hypertension accelerates atherogenesis and causes structural changes in the walls of blood vessels that potentiate both aortic dissection and cerebral hemorrhage. • Rennin elaborated by the juxtaglomerular cells of the kidney transforms plasma angiotensin to angiotension I. HYPERPLASTIC ARTERIOSCLEROSIS: • Related to more acute or severe elevation of blood pressure and is therefore characteristic of but not limited to malignant hypertension (diastolic pressure more than 110 mmHg). • Increasing peripheral resistance is achieved largely by its ability to cause vasoconstriction through direct action on vascular smooth muscle. • The kidney influences both peripheral resistance and sodium homeostasis. pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. a. • It is believed that the lesions reflect leakage of plasma components across vascular endothelium and increasing extracellular matrix production by smooth muscle cells. • angiotension I is converted to angiotension II by angiotension converting enzyme (ACE) • angiotension II alters blood pressure by increasing both peripheral resistance and blood volume. Hyperplastic arteriosclerosis Both lesions are related to elevations of blood pressure. Hyaline arteriosclerosis b. and the rennin-angiotensin system appears central to these influences.
GFR – independent natriueretic factors. --. Abnormalities in these renal mechanisms are implicated in the pathogenesis of secondary hypertension in a variety of renal diseases. a peptide secreted by heart atria in response to volume expansion. • In renovascular hypertension. of water. akinesia. The kidney produces a variety of vasodepressor or antihypertensive substances that presumably counterbalance the vasopressor effects of angiotensin. • This initiates angiotension II induced vasoconstriction --. Urinary kalikrein – kinin system d. including atrial natriuretic factor (ANF).• • • • • Blood volume is increased by stimulation of aldosterone secretion --. with muscle rigidity.increased peripheral resistance. but they also play important roles in essential hypertension. • In Pheochromocytoma. inhibit sodium reabsorption in distal tubules and cause vasodilation.increased sodium reabsorption and increased blood volume. a tumor of the adrenal medulla. the GPR falls. PARKINSON’S DISEASE Brain disorder causing progressive deterioration.which increases distal tubular reabsorption of sodium and thus. this. These include: a. PATHOGENESIS OF ESSENTIAL HYPERTENSION: • Arterial Hypertension occurs when changes develop that after the relationship between blood volume and total peripheral resistance. in turn leads to increased reabsorption of sodium by the proximal tubules in an attempt to conserve sodium and expand blood volume. Platelet activating factor c. and voluntary tremors Usual cause of death: aspiration pneumonia One of the most common crippling diseases in the United States . catecholamines produced by tumor cells cause episodic vasoconstriction and thus induce hypertension. Prostaglandins b. renal artery stenosis causes decreased glomerular flow and pressure in the afferent arteriole of the glomerulos and induces rennin secretion by the juxtaglomerular cells. through the aldosterone mechanism. Nitric oxide When blood volume is reduced.
anticholinergics. neck. Oxidative stress is believed to: Alter the brain’s iron content Impair mitochondrial function Alter antioxidant and protective systems Reduce glutathione . skin breakdown Assessment: Insidrous (unilateral pill-roll) tremor. frequent meals and high-bulk food • Physical therapy and assistive devices to aid ambulation • Medication: Dopamine replacement drugs. and trunk Increased perspiration and insomnia. urinary tract infections. antiviral agents. monotonous voice. causing loss of available dopamine • Dopamine deficiency prevents affected brain cells from performing their normal inhibitory function • Excess excitatory acetylcholine occurs at synapses • Nondopaminergic receptors are also involved • Motor neurons are depressed Causes: • Usually unknown • Exposure to such toxins as manganese dust and carbon monoxide Common Characteristics: Muscle rigidity and tremor Resistance to passive muscle stretching Akinesia and dysarthria and drooling High-pitched. which increases during stress or anxiety and decreases with purposeful movement and sleep Dysphagia Fatigue with activities of daily living (ADLs) Muscle cramps of legs. food aspiration. and loss of posture control Excessive sweating and decreased GI motility Orthostatic hypotension and oily skin and eyes fixed upward Complications: injury from falls. enzyme-inhibiting agents and tricyclic antidepressants • Surgery used when drug therapy fails • Destruction of ventrolateral nucleus of thalamus New research on the pathogensis of Parkinson’s disease focuses on damage to the substantia nigra from oxidative stress. mood changes Treatment: • Small. Affects more men than women Occurs in middle age or later Pathophysiology: • Dopaminergic neurons degenerate.
verbal communication • Ineffective coping and risk for injury The patient will: Perform ADLs and develop alternative means of communicating Avoid injury and maintain adequate calorie intake Express positive feelings about himself Develop adequate coping behaviors and seek support resources Nursing Interventions: • Take measures to prevent aspiration • Protect the patient from injury • Stress the importance of rest periods between activities • Ensure adequate nutrition • Provide frequent warm baths and massage • Encourage the patient to enroll in a physical therapy program • Provide emotional and psychological support • Encourage the patient to be independent Monitor: Vital signs. proteins. Damage lipids. intake and output Drug therapy and adverse reactions to medications Postoperatively: signs of hemorrhage and increased intracranial pressure MYASTHENIA GRAVIS Abnormal fatigability of striated (skeletal) muscles Sporadic but progressive weakness . social interaction. and deoxyribonucleic acid Nursing Diagnoses: • Interrupted family processes • Imbalanced nutrition: less than body requirements • Bathing or hygiene self-care deficit • Disturbed body image • Chronic low self-esteem • Constipation • Dressing or grooming self-care deficit • Feeding self-care deficit • Impaired physical mobility.
and with infections Physical Findings: Sleepy. destroy. ptosis and Diplopia Skeletal muscle weakness. after emotional stress. may be life-threatening Spontaneous remissions in about 25% of patients Occurs at any age Three times more common in women than men Highest in women ages 18 to 25. or weaken neuroreceptors (which transmit nerve impulses) • The result is failure in transmission of nerve impulses at the neuromuscular junction Causes: • Autoimmune disorder associated with the thymus gland • Accompanies other immune and thyroid disorders Common Characteristics: Weak eye closure. Muscle weakness exacerbations by exercise and repetitive movement Muscle weakness improved by anticholinesterase drugs Initial symptoms related to cranial nerves With respiratory system involvement. aspiration Assessment: Varying assessment findings Progressive muscle weakness Extreme weakness and fatigue (cardiac symptoms) Ptosis and diplopia (the most common sign and symptom) Difficulty chewing and swallowing Jaw hanging open (especially when tired) and Head bobbing Symptoms milder on awakening worsen as the day progresses Short rest periods that becomes more intense during menses. paralysis Complications in respiratory distress. after prolonged exposure to sunlight or cold. in men ages. masklike expression . pneumonia. 50 to 60 Transient myasthenia in about 20%of infants born to myasthenic mothers Pathophysiology: • Blood cells and thymus gland produce antibosies that block.
cortiscosteroids.V. Drooping jaw Ptosis Decreased breath sounds and tidal volume Respiratory distress and myathenic crisis Treatment: Plasmapheresis Emergency airway and ventilation management Diet as tolerated Activity as tolerated. I. exercise may exacerbate symptoms Medication: Anticholinesterase drugs. immune globulin Surgery: Thymectomy • • MULTIPLE SCLEROSIS Progressive demyellination of white matter of brain and spinal cord Characterized by exacerbations and remissions .
contractures. resulting in widespread and varied neurologic dysfunction Causes: • Exact cause unknown • Slowly acting viral infection • An autoimmune response of the nervous system • Allergic response • Events that precede the onset: Emotional distress Overwork Fatigue Pregnancy Acute respiratory tract infections • Generic factors possibly also involved Risk Factors: • Trauma. urinary tract infections. in higher socioeconomic groups Family history increases with living in a cold. constipation.• • • • • May progress rapidly. causing death within months Prognosis varies (70% lead active lives with prolonged remissions Highest in women. pressure ulcers and pneumonia • Multiple Sclerosis (MS)described as: . and toxins • Nutritional deficiencies • Vascular lesions • Anorexia nervosa Common Characteristics: • Dependent on the extent and site of myelin destruction • Sensory impairment • Muscle dysfunction • Bladder and bowel disturbances • Speech problems and fatigue • Complications in injuries from falls. damp climate Major cause of chronic disability in young adults ages 20 to 40 Pathophysiology: • Sporadic patches of demyelination occur in the central nervous system (CNS). among people in northern urban areas. Anoxia.
extent of remyelination and adequacy of subsequent restored synaptic transmission • Visual problems and sensory impairment (the 1st signs) • Blurred vision or diplopia • Urinary problems • Emotional lability • Dysphagia • Bowel disturbances (involuntary evacuation or constipation) • Fatigue (typically the most disabling symptom) • Poor articulation • Muscle weakness of the involved area • Spasticity. thyroid disease and chronic fatigue syndrome Assessment: • Symptoms related to extent and site of myelin destruction. biological response modifiers Nursing Diagnoses: • Activity intolerance • Interrupted family processes . antimetabolics. Elapsing remitting – clear elapses with full recovery lasting disability. syphilis or another infection. acute attacks. immunosuppresants. multiple small strokes. hyperreflexia • Intention tremor and gait ataxia • Paralysis. alkylating drugs. ranging from monoplegia to quadriplegia • Nystagmus scotoma • Optic neuritis and Ophthalmoplegia Treatment: General for acute exacerbations. the disease doesn’t worsen Primary progressive – steady progression or worsening of the disease from the onset with minor recovery or plateaus Secondary progressive begins as a pattern of clear-cut relapses and recovery but becomes steadily progressive and worsens between acute attacks Progressive relapsing – steadily progressive from the onset but also has clear. Differential diagnosis must rule out spinal cord.V. for the disease process and for related signs and symptoms High fluid and fiber intake in case of constipation Frequent rest periods Medications: I. steroids followed by oral steroids. Between attacks.
• • • • • • • • • • • • Imbalanced nutrition: less than body requirements Ineffective role performances Disturbed thought processes Impaired urinary elimination Chronic low self-esteem Constipation Fatigue Impaired physical mobility Compromised family coping Ineffective coping Deficient knowledge chronic pain Risk for infection and injury The patient will: Perform activities of daily living Remain free from infection Maintain joint mobility And range of motion Express feelings of increased energy and decreased fatigue Develop regular bowel and bladder habit Use support systems and coping mechanism Nursing Intervention: • Provide emotional and psychological support • Assist with physical therapy program • Provide adequate rest periods • Promote emotional stability • Keep the bedpan or urinal readily available because the need to void is immediate • Provide bowel and bladder training if indicated • Administer medications • Monitor: o Response to medications o Adverse drug reactions o Sensory drug reactions o Muscle dysfunction o Energy level o Signs and symptoms of infection o Speech o Elimination patterns vision changes o Laboratory results .
progressive and deliberating disease that’s invariably fatal No cure Also known as Lou Gehrig’s disease 3 times more common in men than in women Affects people ages 40 to 70 Pathophysiology: • An excitatory neurotransmitter that accumulates to toxic levels • Motor units that no longer innervate • Progressive degeneration of axons that cause loss of myelin • Progressive degeneration of upper and lower motor neurons • Progressive degeneration of motor nuclei in the cerebral cortex and corticospinal tracts Causes: • Exact cause unknown • 10% of patients with amyotrophic lateral sclerosis (ALS) inherit the disease as an autosomal dominant trait • Virus that creates metabolic disturbances in motor neurons • Immune complexes such as those formed in autoimmune disorders Precipitating factor that cause acute deterioration: • Severe stress. such as myocardial infraction • Traumatic injury • Viral infections • Physical exhaustion Common Characteristics: • Muscle weakness • Atrophy • Fasciculations • Respiratory tract infections • Complications of physical immobility Assessment: Mental function intact . AMYOTROPHIC LATERAL SCLEROSI Most common motor neuron disease of muscular atrophy Chronic.
chewing.V. legs and trunk Brisk and overactive stretch reflexes Difficulty talking. Baclofen I. swallowing and breathing Shortness of breath and occasional drooling Treatment: Rehabilitation May need tube feedings No restrictions : as tolerated Medication: muscle relaxants. dantrolene. or intrathecal administration of thyrotropin-releasing hormone Nursing Diagnoses: Imbaanced nutrition: less than body requirements Anticipatory grieving Anxiety Bathing or hygiene self-care deficit Dressing or grooming self-care deficit Feeding self-care deficit Hopelessness Impaired physical mobility Impaired airway clearance Ineffective breathing pattern Ineffective coping Compromised family coping Deficient knowledge (ALS) Risk for impaired skin integrity Risk for infection The patient will: • Maintain a patent airway and adequate ventilation • Maintain joint mobility and range of motion (ROM) • Maintain daily calorie requirements . Family history of ALS Asymmetrical weakness 1st noticed in one limb Easy fatigue and easy cramping in the affected muscles Physical Findings: Location of affected motor neurons Severity of the disease Fasciculations in the affected muscles Progressive weakness in muscles of the arms.
. a draw sheet to help him move up in bed. • Recommend devices to ease the patient’s and caregiver’s work such as extra pillows or wedge pillows to help the patient sit up. keeping stairs well lit. • Help the patient adjust to changes in the environment. a commode. Encourage independence. or oxygen equipment. • Discuss the need for rearranging the furniture moving items in or out of patient’s care area. such as keeping stairs and pathways free from clutter. installing handrails in stairwells and the shower. and obtaining such equipment as a hospital bed. using nonskid mats in the bathroom and in place of loose throw rugs. tub and toilet areas and removing electrical and telephone cords from traffic areas. or a bell for calling the caregiver.• • Seek support systems and exhibit adequate coping behaviors Remain free from infections Nursing Interventions: Provide emotional and psychological support Teach about active exercises and ROM exercises Promote independence Teach about meticulous skin care Turn and reposition the patient frequently Administer ordered medication Teach how to perform deep-breathing and coughing exercises Provide airway and respiratory management Promote nutrition Teach about swallowing regimens and aspirations precautions Monitor: o Muscle weakness o Respiratory status o Speech o Swallowing ability o Skin integrity o Nutritional status o Response to treatment o Complications o Signs and symptoms of infection • Modifying the home for a Patient with ALS Guidelines: • Explain basic safety precautions. a lap tray for eating.
rapidly progressive. and potentiaaly fatal Three • • • Phases: Acute – lasting from 1st symptoms. extends over 4 to 3 years.• Advise the patient to keep suction due to handy to reduce the fear of choking due to secretion accumulation and dysphagia. preventing normal transmission of electrical impulses Sensorimotor nerve roots are affected. autonomic nerve transmission may also be affected Causes: Unknown Virus can cause cell-mediated immunologic attack on peripheral nerves Risk Factors: Surgery Rabies or swine influenza vaccination Viral illness Hodgkin’s or some other malignant disease Lupus erythematosus Common Characteristics: Symmetrical muscle weakness initially in lower extremities and progressing to upper extremities Parethesia Diplegia Dyshagia Hypotonia Areflexia . GUILLAIN-BARRE SYNDROME A form of polyneuritis Acute. ending in 1 to 3 weeks Plateau – lasting several days to 2 weeks Recovery – coincides with remyelination and axonal process regrowth. Teach him to suction himself. recovery possibly not complete Pathophysiology: Segmented demyclination of peripheral nerves occurs.
Complications: Thrombophlebitis Pressure ulcers. the face Stiffness and pain in the calves Physical Findings: Muscle weakness (major neurologic sign) Sensory loss. beta-adrenergic blockers and parasympatholytics I. an elevated protein count and in severe disease.V. chewing and swallowing Paralysis of the ocular.V. facial and oropharyngeal muscles Loss of position sense Diminishes or absent deep tendon reflexes Diagnostic Procedures: • Cerebrospinal fluid (CSF) analysis may slow a normal white blood cell count. Others: • Electromyography may demonstrate repeated firing of the same motor unit instead of widespread sectional stimulation • Nerve conduction studies show marked slowing of nerve conduction velocities Treatment: Primarily supportive Possible endocrinal intubation or tracheotomy Volume replacement Plasmapheresis Possible tube feeding with endotracheal intubation Adequate calorie intake Exercise program to prevent contractures I. immune globulin and possible tracheostomy . trunk and finally. increased CSF pressure. usually in the legs (spreads to arms) Difficulty in taking. contractures and muscle wasting Aspiration and respiratory and cardiac compromise Assessment: Minor febrile illness 1 to 4 weeks before symptoms Tingling and numbness (paresthesia) in the legs Progression of symptoms to arms.
provide eye and mouth care Prevent constipation Provide emotional support Administer medications. Possible gastrotomy or jejunotomy feeding tube insertion Nursing Diagnoses: • Imbalanced nutrition: less than body requirements • Impaired urinary elimination • Anxiety and fear • Impaired gas exchange and impaired physical mobility • Impaired verbal communication and ineffective breathing pattern The patient will: Maintain a patent airway and adequate ventilation Develop alternate means of expressing self Maintain required calorie intake daily Establish routine urinary elimination patterns Maintain joint mobility and range of motion (ROM) Nursing Interventions: Establish a means of communication before intubation is required Turn and reposition the patient Encourage coughing and deep breathing Begin respiratory support at the first sign of dyspnea Provide meticulous skin care Administer passive ROM exercises In case of facial paralysis. as ordered Monitor: o Vital signs o Breath sounds o Arterial blood gas measurements o Level of consciousness o Continual respiratory function o Pulse oximetry o Signs of thrombophlebitis o Signs of urine retention o Response to medications .
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