NURSING N490 Medical Surgical Final Exam Blueprint (65 Q&A from all the topics)>>100% Guaranteed Pass.

N490 SPRING Final Exam Blueprint 65 questions on the following topics: GENETICS In all nursing practice settings, nurses have five main tasks: • Help collect and interpret relevant family and medical histories • Identify patients and families who need further genetics evaluation and counseling and refer them to appropriategenetics services • Offer genetics information and resources to patients and families • Collaborate with genetics specialists • Participate in the management and coordination of care of patients with genetic conditions. Genetics-related nursing practice involves the care of people who have genetic conditions, those who may be predisposed to develop or pass on genetic conditions, and those who are seeking genetics information and referral for additional genetics services. Nurses support patients and families with genetics related and genomics-related health concerns by ensuring that their health choices are informed ones and by advocating for the privacy and confidentiality of genetic and genomic information and for equal access to genetic testing and treatments BONE MARROW TRANSPLANT Peripheral Stem Cell Transplantation – effective, lifesaving procedures for treatment of number of malignant or nonmalignant diseases - Safe use of high doses of chemotherapy agents and radiation therapy in patients whose tumor developed resistance or failed to respond to standard doses - GOAL IS TO CURE – if it can’t be achieved, it can result in period of remission - Commonly used to treat leukemia and lymphoma and also other cancers - Treatment is very damaging to bone marrow – without donation the patient can DIE TYPES OF DONOR STEM CELLS - ALLOGENEIC: a donor with matching HLA tissue typing o Can be from parents, siblings and unrelated matching donor o More at risk for graft vs. host - SYNGENEIC: stem cell from identical twin – perfect match o Graft vs. Host does not occur - AUTOLOGOUS: Most common – donation from self, stored and frozen for later use PROCEDURE - Harvesting: Two different methods o Harvesting stem cell residing in bone marrow ▪ Aspiration with large bore needle from ILIAC CREST OR STERNUM ▪ Takes 1-2 hours, can be discharged after recovery ▪ Pain may last for 7 days o Harvesting with cell separator equipment ▪ Takes 2-4 hours, but might take longer ▪ Would need drugs for mobilization of stem cells (see chart above) – harvested after 4-5 days - Conditioning phase: o Total body irradication of all malignant cells and create space in bone marrow for engraftment of new marrow - Transplantation: o Stem cell infusion administered BY IV SLOWLY INTO CENTRAL LINE o Usually 2-4 weeks required for transplanted marrow to start producing hematopoietic blood cells o RISK FOR PANCYTOPENIA – protect from sun exposure and supply them with electrolytes, nutrition and blood transfusion if needed ▪ Usually required patient to stay in hospital for 2-4 weeks to prevent infection COMPLICATIONS - INFECTIONS – need to use prophylactic antibiotic therapy - GRAFT VS. HOST – immunosuppressive therapy - Phlebitis – may occur 1 month after transplant – Need to monitor for jaundice, abdominal pain and liver. LYMPHOMA TWO TYPES: HODGKINS and NON-HODGKINS - Hodgkins – REED-STERNBERG, spreads in orderly fashion – upper body, cervical mantle region (NECK) - Non-Hodgkins – enlarged lymph nodes from multiple sites and extra nodal locations HODGKIN’S LYMPHOMA - Malignant condition characterized by proliferation of abnormal giant, multinucleated cells located in lymph nodes – REED- STERNBERG CELLS – know this! - Occurs mostly in 15-35 years of age and above 50 – more common in men WHAT IS THIS REALLY? - Cause is unknown, factors include Epstein-Barr Virus, genetics and exposure to toxins - Incidence increase among HIV patients - Disease arise from one location and spread to adjacent lymphatic – FROM CERVICAL LYMPH NODES - Eventually infiltrates to other organs – LUNGS, SPLEEN, LIVER o Above diaphragm – remains confine to lymph node for variable time o Below diaphragm – frequently spread to extra lymphoid sites such as LIVER WHAT CAN WE SEE? - Onset of symptoms usually insidious – PAINLESS lymph nodes enlargement usually in the NECK o IF PAINLESS SWELLING IS >1 INCH AND LASTS >6 WEEKS – CALL PROVIDER - Initial development most often in cervical, axillary, or inguinal; mediastinal node mass is 2nd most common location - Patient may notice weight loss, fatigue, weakness, fever, chills, tachycardia and night sweats - 2 types of staging symptoms o STAGE A: Asymptomatic o STAGE B: Unexplained weight loss >10% in 6 months, FEVER, and night sweats - Further down the road – Hepatomegaly and splenomegaly DIAGNOSTIC AND STAGING STUDIES - Peripheral blood analysis, excisional lymph nodes biopsy and bone marrow examination - PET SCAN – can detect malignant tumor in cells in the body o A small amount of radioactive glucose injected into vein and then scanner rotates around the body taking pictures o More glucose is metabolized by malignant tumor cells than normal – will be brighter in the scan - COTSWOLD STAGING CLASSIFICATION: o STAGE I: CONFINED TO ONE NODE REGION OR LYMPHOID STRUCTURE o STAGE II: 2 OR MORE NODAL REGIONS/SAME SIDE OF DIAPHRAGM o STAGE III: LYMPHOID REGIONS ON BOTH SIDE OF DIAPHRAGM o STAGE IV: EXTRA NODAL SITES – LIVER, BONE MARROW - STAGING can be classified with STAGE A and B symptoms HOW DO WE TREAT THIS? Treatment depends on the stage of Hodgkin’s disease: SURVIAL RATE IS GOOD - Stage I & II: o Chemotherapy with/without radiation therapy o 95% - complete remission o 90 – 95% have 5 year survival & 20 years for 70-80& - Stage III & IV: o Chemotherapy o Partial remission o Follow up with radiation drugs o 90% have 5 year survival rate - Chemotherapy and radiation: LOOK AT OTHER SECTION - Drugs: o Standard chemotherapy is AVBD – ADRIAMYCIN, BLEOMYCIN, VINBLASTINE, DACARBAZINE o A common regimen is BE A COPP ▪ BLEOMYCIN, ETOPOSIDE, ADRIAMYCIN, CYCLOPHOSPHAMIDE, ONCOVIN, PROCARBAZINE, PREDNISONE ▪ Take the prednisone in the morning! COMPLICATIONS - Late effects: thyroid, heart and lungs and also increase risk for other cancers o May appear years later: important for them to have regular follow-ups - NEED TO MANAGE PANCYTOPENIA - Fertility issues: need to address this concern (sperm bank, or have another dude nail your wife?) NON-HODGKIN’S LYMPHOMA – MORE COMMON THAN HL - Heterogeneous group of malignant neoplasms of primarily B, T or natural killer cell origin affecting all ages - Two types: o Low-grade: indolent – SILENT o Intermediate and high grade – aggressive WHAT IS THIS REALLY? SAME THING AS HL EXCEPT: - Multiple possible virus and bacteria include: o HTLV-1, EBV, HPV, HEP B and C, H. PYLORI, and BIG BACTERIA NAMES probably not on exam – BET ON IT! - Environmental involves chemicals and air pollution - Inherited syndromes or chemotherapy drugs - Involves lymphocytes arrested in various stages of development and mimics leukemia - BURKITT’s LYMPHOMA – high aggressive disease from B-cell blasts in lymph nodes WHAT DO WE SEE? - NO PATTERN, UNPREDICTABLE , most common is PAINLESS lymph node enlargement - LYMPHADENOPATHY – related to obstruction - Can manifest into more complications: Airway obstruction, spinal cord compression, hyperuricemia, tumor lysis syndrome and pericardial tamponade - Also similar staging as HL DIAGNOSTIC STUDIES - Almost the same as HL (PET), but more studies o MRI to rule out CNS or bone marrow infiltration o Barium enema o Upper endoscopy o CT to suspect GI involvement - Prognosis for NHL is based on HISTOPATHOLOGY SO…WE DO THE SAME THING AS HL? - Involves chemotherapy and radiation therapy o Indolent lymphoma have naturally long course but are difficult to effectively treat – may live 10 years without treatment - Infection lymphomas may be treated with antibiotics or antiviral therapy - Drug: Rituximab o Monitor patient for signs of severe hypersensitivity infusion reactions, AFTER FIRST INFUSION o S/Sx: hypotension, bronchospasm, dysrhythmias, angioedema and cardiogenic shock o Screen patient for history of hepatitis - Complete remission uncommon – but majority respond with improvement of symptoms - Psychosocial considerations are important: o Help family understand the disease, treatment and expected side effects – encourage expression of feelings and relaxation techniques o Identify infections related to bone marrow suppression o Body image disturbance – advise wig use or long sleeve shirts to cover skin changes ▪ GOT TO GIVE THEM CONTROL – let them cut hair themselves o Reproductive issues – sperm banking CHEMOTHERAPY AND VESICANTS - Chemotherapy usually administered by IV, but major concern is EXTRAVASATION – infiltration of drugs into tissue surrounding infusion site causing local tissue damage o Irritant – will damage veins, causing phlebitis and sclerosis BUT REVERSIBLE o VESICANTS – infiltrated into the skin, causing NECROSIS LIST OF VESICANTS Akylating Agents Anthracyclines (DNA) Mitomycin C (DNA) Vinca Alkaloid (non- Taxanes (Non-DNA) (DNA) Doxorubicin DNA) Docetaxel Bendamustine Daunorubicin Vincristine Paclitaxel Mechorlethamine Epirubicin Vinblastine THE PATIENT IS ACTING UP! WHAT DO I DO?!! - Identify the signs and take immediate action o WHEN PATIENT SAYS – SHEEEEEIT!!! MY HAND IS BURNING!!!! o Pain, but sometimes no pain is indicated o Swelling, redness and vesicles on the skin o After few days, ulceration and necrosis o Complications – sepsis, scarring, contractures, joint pain and nerve loss - SO NOW WHAT? o STOP INFUSION IMMEDIATELY o ASPIRATE THE CHEMO AGENT – DO NOT REMOVE IV YET o DO NOT FLUSH THE LINE! – can buffer with sodium bicarbonate o Remove needle and apply compression – BUT DON’T APPLY TOO MUCH, CAN CAUSE MORE DAMAGE o Mark the extravasation site and monitor - USE OF HOT AND COLD COMPRESSION o HOT – vasodilation/Disperse - vinca alkaloids, Taxanes, NON-DNA DRUGS o COLD – Vasoconstriction/Localize – Anthracyclines, mitomycin C, DNA DRUGS - To minimize physical discomforts, infections, IV can be given by central venous access device HEPATITIS Inflammation of the liver - NOTE: HEP A and E – ORAL FECAL – AMERICAN EAGLE - NOTE: MUST HAVE HEP B to HAVE HEP D – USE THE BATHROOM TO TAKE A DUMP HEP A - RNA virus transmitted through ORAL-FECAL route - Caused by dirty foods or water, crowded situations, DAYCARES, or cooks who don’t wash hands - Can lead to acute liver failure - Can be transmitted by people who have undetectable subclinical infections o Greatest risk of transmission occurs before clinical symptoms are apparent o HAV found in feces 2 or more weeks before onset of symptoms and up to 1 week after onset of jaundice - HEP A IgM – INDICATES ACUTE HAV - HEP A IgG – INDICATES PAST INFECTION - WASH HANDS BEST MEASURE TO PREVENT OUTBREAK HEP B - DNA virus – INFECTED BLOOD OR BODY FLUIDS enters someone’s body who has no vaccination 5 o Perinatally by mothers with HBV o IV drugs, needles, or unprotected sex(gay sex is most common) o Kissing can spread HBV by saliva o No evidence that urine, non-GI bleeding stools, tears, breast milk can transmit HBV - HBV can live on dry surface for up to 7 DAYS! More infectious than HIV! - HBsAg INDICATES INFECTION - Anti-HBs INDICATES IMMUNITY HEP C - Can be both acute and chronic, can be asymptomatic and difficult to detect - MOST COMMON CAUSE – DRUG USE, GAY SEX FROM HIV + MEN o People at risk for HCV also at risk for HBV and HIV - 20-30% chance of developing cirrhosis and is the most common cause of chronic liver disease o NEED LIVER TRANSPLANT o NO VACCINATION HEP D - Defective single stranded RNA virus that cannot survive on its own – NEED HEP B TO REPLICATE - Transmitted percutaneously – can cause asymptomatic chronic carrier state to acute liver failure - ALSO NO VACCINE! HEP E - RNA virus – THE OTHER FECAL ORAL ONE - Can get it from dirty water – usually occurs in developing countries CLINICAL MANIFESTATIONS - ACUTE PHASE – 1 to 4 months o Incubation period: Malaise, anorexia, weight loss, fatigue, N/V, and RUQ discomfort o May find food repugnant/smokers might think cigarettes are disgusting? o PERIOD OF MAXIMAL INFECTIVITY - Acute phase maybe icteric (JAUNDICE) or anicteric o Yellow like The Simpsons – alteration in bilirubin metabolism or flow of bile o Urine may be dark – excess bilirubin being excreted o IF BILIRUBIN CAN’T FLOW OUT OF LIVER – POOP WILL BE LIGHT OR CLAY COLOR o Pruritis can occur with jaundice - Convalescent phase: Jaundice fades and lasts for 2 to 4 months o Malaise and easily fatigued o Hepatomegaly, but splenomegaly subsides COMPLICATIONS - Most with acute hepatitis recover completely, HOWEVER complications occur including acute liver failure, chronic hepatitis, and cancer o HEP A – viral relapse after 2-3 months o Disappearance of jaundice does not mean patient has recovered o Chronic HBV more likely to develop in infant born to infected mothers and those who acquire infection before 5 years old o HCV more likely to become chronic ▪ RISK FACTORS: DRINKING, MALE, HIGH CHOLESTEROL, OBESITY and DM DIAGNOSTIC STUDIES - DEFINITIVE WAY – testing patient’s blood for specific antigen or antibody - HVC testing – if antibody testing is positive: HCV RNA test for chronic infection o May be helpful for immunocompromised patients - VIRAL GENOTYPE TESTING – for HBV and HCV patients undergoing drug therapy - Physical assessment – palpate liver – one hand on right ribcage and the other pressing down GENTLY COLLABORATIVE CARE - Most patients can be managed at home: MAIN GOAL IS REST AND NUTRITION – promotes liver healing - AVOID ALCOHOL – STOP DRINKING DRUG THERAPY - No drug therapy for Hepatitis A - Treatment for Acute Hepatitis B – only patients with severe hepatitis and liver failure - Acute Hepatitis C – PEGYLATED INTERFERON WITHIN FIRST 12 to 24 WEEKS – decrease chance of becoming chronic - Chronic Hepatitis B o To decrease viral load and liver enzymes – slowing the rate of disease progression – PREVENT CIRRHOSIS, LIVER FAILURE and CANCER o FIRST LINE OF DRUG: INTERFERON AND NUCELOSIDE ▪ Interferon – blocks viral entry to cells, synthesizes the viral proteins • Standard: Intron A – short half life – given 3 time a week • Pegylated: Long-acting – subcut. 1 times a week – BETTER WITH LONG DOSE • Effect: reduction in HBV DNA levels, normalize ALT and loss of HBeAg = response to treatment depends on viral genotype • CBC and LFTs done every 4 to 6 weeks! ▪ Nucleoside and Nucleotide Analogs: • Tricks HBV into thinking they are normal building blocks for DNA; thus virus not able to reproduce • Medications: lamivudine (Epivir), adefovir (Hepsera), entecavir (Baraclude), telbivudine (Tyzeka), and tenofovir (Viread • BENEFICIAL for lowering vial dose, decreasing liver damage and decreasing enzymes • LFTs for several month after medication is stopped o Chronic Hepatitis C ▪ PEGYLATED INTERFERON WITH RIBAVIRIN (REBETOL, COPEGUS) • RIVAVIRIN: MAKE SURE THE PATIENT ISNT PREGNANT – HARMFUL TO NEONATES! ▪ Careful when giving HIV patients – can lower their CD4 counts – WATCH FOR ANEMIA AND LEUKOPENIA ▪ ALSO WATCH FOR MOOD CHANGES – DEPRESSION NUTRITIONAL THERAPY - No special diet – BUT ATI SAYS – LOW CARB, LOW FAT, LOW PROTEIN, FREQUENT MEALS – promotes healing - VITAMIN K if needed - If anorexia, N/V are severe – IV solutions of glucose HEALTH PROMOTION - CONTROL AND PREVENT - HEP A: o HAND WASHING – IMPORTANT – AFTER TAKING A DUMP o Vaccination is BEST PROTECTION – IM IN DELTOID – Booster 6-12 months after primary dose o Isolation NOT required – private room if patient has crazy poop or personal hygiene o IG effective in preventing if given within 2 weeks of exposure - Hepatitis B o Best way to reduce: SCREENING, AND VACCINATION o GOOD HYGEINE – don’t share razors, toothbrush or cucumbers, USE CONDOMS o VACCINE IS BEST PREVENTION: 3 IM injections ▪ First dose: within one month of birth ▪ Recommended for chronic kidney disease patients – keep their antibody titers for dialysis o Postexposure prophylaxis – HBIG ▪ Used incase of needle stick injuries, or sexual exposures for infant born to mothers who are positive HBsAG - Hepatitis C o NO VACCINES!!!!! Primary measure is screening of blood, organs and tissue donors o After exposure: have anti-HCV testing done, baseline ALT levels should be measures with follow-up 4-6 months o Testing HCV RNA – 4-6 weeks ACUTE INTERVENTIONS - ASSESS FOR JAUNDICE o Fair skin people: sclera of eye or skin o Dark skin people: hard palate of mouth, inner canthus of eues o Urine may be dark brown – bilirubin being pissed out - Ensure adequate nutrition o Small frequent meals, and give them what they enjoy o Avoid hot drinks and soda o FLUID – 2.5 to 3 L/day is important! AMBULATORY CARE - Assess knowledge of nutrition and provide teaching - Vital to teach them how to prevent transmission to others - Assess foe manifestation of complications: o Bleeding with increasing PT values, symptoms of encephalopathy, or elevated LFTs - AVOID ALCOHOL!!!!! - Adhere to medication regimen - Make sure patients with positive HBsAg or HCV antibodies can’t donate blood… LAB VALUES FOR LIVER FUNCTION - ATI VALUES TEST NORMAL VALUES ABNORMAL FINDINGS INDICATION OF WHAT? Alanine aminotransferase ALT 3 to 35 IU/L INCREASED Liver cell injury Aspartate aminotransferase AST 5 to 40 units/L INCREASED Liver cell injury Gamma glutamyl transpeptidase GGT 0 to 45 units/L INCREASED Liver cell injury Alkaline phosphatase 44 to 147 IU/L INCREASED Impaired excretory function of liver Gamma globulin 3 to 12% of total proteins INCREASED Impaired clearance from liver Serum albumin 3.5 to 5g/dL DECREASED Liver cell damage Serum bilirubin 0.1 to 1.0 mg/dL INCREASED Liver cell damage Serum protein 6 to 8 g/dL DECREASED Lack of hepatic synthesis Prothrombin 11 to 12.5 seconds PROLONGED Decreased PT production by liver Ammonia 11 to 32 umol/L INCREASED Cirrhosis HEPATITIS TITERS (PRESENT AND PAST INFECTIONS) HEPATITIS LETTERS PRESENT INFECTION PAST INFECTIONS HEP A Anti-HAV IgM – ACUTE INFECTION Anti-HAV IgG – PREVIOUS INFECTION or immunization HEP B HBsAg – in acute or chronic infection, + in chronic carriers HBeAg – HIGH INFECTIVITY Anti-HBc IgM – ACUTE – blank after vaccination Anti-HBc IgG – ONGOING or PAST HBV DNA quanitation – active ongoing viral replication, indicates the effectiveness of therapy Anti-HBs – previous or immunization – MARKER OF POSITIVE RESPONSE TO VACCINATION! Anti-HBe – low viral load or infectivity in chronic HBV Anti-HBc IgG – Previous infection HEP C Anti-HCV – acute/chronic infection HCV RNA quantitation – active ongoing viral replication HEP D Anti-HDV – PRESENT/PAST HDV Ag – present within few days of infection Anti-HVD HEP E Anti-HEV igM and IgG – 1 week to 2 months after illness onset HEV RNA quantitation – active ongoing viral replication HIV/AIDS A retrovirus that causes immunosuppression - Can be transmitted: o UNPROTECTED Sexual activity with infected partner – blood, semen, vaginal secretions – GAY MEN SEX AT MOST RISK! o CONTACT WITH BLOOD PRODUCTS – NEEDLE SHARING, JUNKIES, BLOOD BROTHERS, VAMPIRES ▪ Puncture wound most common in work related HIV – AS AN RN – WE WASH WITH SOAP WITH WATER AND QUICKLY REPORT TO SUPERVISOR TO EMPLOYEE HEALTH • Given antivirals as option and stay on pills on 9 months until cleared -3 months each test o Perinatal transmissions - can be infected during pregnancy, deliver or breastfeeding - Variables that influence whether infection will establish after an exposure includes: o Duration and frequency of contact with organism o Volume, virulence, and concentration of organism o Host immune status ANYWAY, WHAT IS HIV? - It is an RNA virus – reverse transcriptase – killing off CD4+ T cells - Clinical symptoms may not appear for a long time – can go 10 years with no symptoms - NORMAL CD4 COUNT – 800-1200 o Normal lifespan if CD4 is 100 days, but in HIV it dies in 2 DAYS - Immune problems starts when it drops below 500 - <200 would indicate AIDS WHAT DO WE SEE? Important to remember that disease progression is highly individualized so the prognosis is unpredictable - ACUTE INFECTIONS: o Fever, SWOLLEN LYMPH NODES, sore throat, headache, malaise, nausea, muscle and joint pain, diarrhea or rash(SEROCONVERSION) o Neurologic complications – aseptic meningitis, peripheral neuropathy, facial palsy, Guillian-Barre syndrome o Can be mistaken sometimes as a bad flu - CHRONIC HIV INFECTIONS: o Often asymptomatic – CD4 remains about 500 ▪ Fatigue, headache, low grade fever, night sweats and lympadenopathy ▪ Patient might not be aware they are infected o Symptomatic infection: CD4 drops around 200-500 ▪ Persistent fever, frequent night sweats, chronic diarrhea, recurrent headaches, fatigue ▪ MOST COMMON – ORAL CANDIDIASIS or THRUSH ▪ Other infection include: shingles, vaginal candida infection, herpes, Kaposi sarcoma ▪ Oral hairy leukoplakia – painless, white, raised lesions on tongue AIDS - <200 CD4 count - Organisms that do not cause severe diseases in normal people can cause debilitating, disseminated and life threatening infections during this stage DIAGNOSTIC STUDIES - Test for HIV antibodies or antigen in blood – oral or blood specimen o Can take several week after the infection before antibody can be detected on screen test – WINDOW PERIOD - Rapid HIV antibody can be done in office and results in 20 minutes o Can also be done at home - A positive test should be followed by WESTERN BLOT test o EIA positive – REPEAT, if positive again, WESTERN BLOT - Lab tests measures viral levels and provides an assessment of disease progression o If undetectable – does not mean virus has been eliminated – can still transmit HIV to others - Two types of resistance test can be determines if patient’s HIV is resistant to ART therapy o Genotype assay detects drug resistant viral mutation that are present in reverse transcriptase and protease genes o Phenotype assay measure the growth of HIV in various concentration of antiretroviral drugs HOW DO WE CARE FOR THIS TYPE OF PATIENT? Collaborative care focuses on: - Monitoring HIV disease progression and immune function - Initiating and monitoring ART - Preventing the development of opportunistic diseases - Detecting and treating opportunistic diseases - Managing symptoms - Preventing or decreasing complications of treatment - Preventing further transmission of HIV Initial patient visit provide opportunity to gather baseline data to start establishing rapport - Remember: Newly diagnosed people won’t listen – MUST BE CLEAR DRUG THERAPY - Goal is to: o Decrease viral load, maintain or increase CD4 count, prevent HIV related symptoms and opportunistic diseases, delay diseas progression and prevent HIV transmission - Antiretroviral therapy – HIV CAN’T BE CURE , but ART can delay disease progression by deceasing viral replication o Major advantage of using different classes of drugs – can inhibit viral replication making it difficult for virus to recover and decreasing likelihood of drug resistance o Drugs has LETHAL INTERACTION with OTC drugs and herbs – ST. JOHN WORTs - SUSTIVA!!!!!! o Don’t use in pregnant ladies, large does can be fatal to babies o Once a day dose should be taken at bed time to cope with side effects – dizziness and confusion o Common to have bizarre dreams - Drug therapy for opportunistic diseases: o Prophylactic medicines can significantly decrease morbidity and mortality rate - Preventing transmission of HIV o Preexposure prophylaxis (PrEP) – reduce risk of sexually acquired HIV in adults at high risk ▪ Safe sex practice, risk reduction counseling and regular HIV testing o Emtricitabine and tenofovir can be used for PrEP ▪ Truvada is the first drug approved to reduce the risk of HIV infection in uninfected individual who are at high risk of HIV infection and who may engage in sexual activity with HIV infected partners ▪ Truvada is currently used in combination with other antiretroviral agents for the treatment of HIV-infected people. NURSING MANAGEMENT - Assessment: o Identify behaviors for people at risk o Basic questions you can ask: ▪ Have you ever had a blood transfusion or used clotting factor? ▪ Have you ever shared needles with another person ▪ Have you ever had sexual experience in which your sexual organs touched other person’s sexual organs? ▪ Have you ever had a sexually transmitted infection? NURSING IMPLEMENTATION Health promotion: - PREVENTION IS ONLY WAY TO CONTROL EPIDEMIC - Encourage early detection and if primary prevention has failed, early intervention initiated - Prevention of HIV Infection: o Goal is to develop safer, healthier and less risky behavior - condoms and decreasing number of sex partners - Decreasing risk related to sexual intercourse: o Abstinence is the most effective way – listened by no one ever o Limiting sexual behaviors which the penis, mouth, vagina, or ass does not come into contact with partner’s same organs – eliminates contact with blood, semen or secretions o Safe activities – Masturbation, mutual masturbation – “hand job” – whoever wrote this in the textbook must be laughing his/her ass off. o USE CONDOM – PROMOTE IT – EXPENSIVE? THERE ARE FREE ONES! - Decreasing risk related to drug use: o Alcohol and tobacco is harmful – again listened by no one ever ▪ Can cause immunosuppression, poor nutrition and mental problems ▪ Major risk is sharing needles, not the drug itself o Basic risk reduction includes: ▪ DO NOT DO DRUGS ▪ IF DOING DRUGS, DON’T SHARE NEEDLES ▪ Do not have sex while on drugs o Safest way: DON’T DO DRUGS, but if you REALLY NEED TO – sterile equipment… - Decreasing risk of perinatal transmission: o Best way to prevention infection in infants is to prevent HIV infection in women o Ask them about their reproductive desires o Optimal ART therapy and counseling helps - Decreasing Risk at work: o Should exposure occur, PrEP with combination of ART can significantly decrease the risk of infection o Need for timely treatment and counseling make it even more critical for nurses to report all blood exposures – REPORT TO SUPERVISOR ASAP!!! - HIV testing: o Many people don’t know that they are infected o CDC recommends, universal, voluntary testing for all ages 13- 64 regardless of status o Goal: normalize the test and decrease new case of infection o ALSO, it is a crime not to tell your partners that you are infected with HIV ACUTE INTERVENTION - Early detection of symptoms, opportunist diseases and mental problems - Initial response to diagnosis of HIV: o Anxiety, fear, depression, denial, hopelessness, anger and guild - Antiretroviral Therapy: o ART can significantly slow clinical progression of HIV. However, this is very expensive and can cause problems with adherence to treatment. o Interventions include teaching about: ▪ Advantages and disadvantages of new treatment ▪ Dangers of poor adherence to therapeutic regimens ▪ How and when to take each drug ▪ Drug interactions to avoid ▪ Side effects that must be reported to health care provider o Issues to consider when selecting an initial drug regimen: ability of patient’s HIV to resist specific drug, potential medication side effects, existing co-morbidities and dosing schedule ▪ Critical because first treatment regimen is generally the patient’s best chance for success ▪ Most important is patient readiness ▪ Adherence to ART is critical component of successful drug therapy for people with HIV infection • MISSING ONE DOES CAN LEAD TO DRUG RESISTANCE!!!!! • Need reminders, beepers, timer pillboxes and calendar • IF MISS FOR ANY REASON, REPORT TO PCP 13 o Group support and individual counseling can help – best approach to learn about patient’s life and assist with problem solving related to taking medication within the confines of life. - Delaying Disease Progression o Useful interventions for delaying HIV ▪ Getting nutritional support to maintain lean body mass and ensure appropriate levels of vitamins and micronutrients – MILKSHAKE? ▪ Moderating or eliminating alcohol, tobacco and drugs ▪ Keeping up to date with recommended vaccines ▪ Getting adequate rest and exercise ▪ Avoiding exposure to new infectious agents ▪ Accessing mental health counseling ▪ Getting involved in support groups and community activities ▪ Developing a consistent relationship with healthcare providers, including attendance at regular appointment o Teach patient to recognize signs and symptoms that may indicate disease progression or drug side effects (CHART ABOVE) - Acute Exacerbations o Best way to prevent opportunistic disease is to ensure that patient is adhering to effective ART regimen, and taking prophylactic medications ▪ If a person has PNEOMOCYSTIS PNEUMONIA (PCP), nursing intervention can ensure adequate oxygenation ▪ If the patient has crytococcal meningitis, an important nursing concern is maintaining a safe environment for a confused patient AMBULATORY AND HOME CARE - Many cases HIV leads to death because of no cure - Affects the entire range of person’s life from physical health to social, emotional, economic, and spiritual well being - Stigma of HIV o HIV infected patients share problems experienced by all individuals with chronic diseases, but these problems are exacerbated by negative social constructs surrounding HIV o Some people may believe they brought HIV upon themselves, immoral (homosexuality), or illegal (drug use) o There is constant fear that HIV may spread to other people o HIV stigma is a global problem often more severe for women o Discrimination can lead to social isolation, dependence, frustration, low self image, loss of control, and economic pressures - Disease and Drug Side effects: o Patients on ART for a long time can develop metabolic disorders that changes their body shape because of lipodystrophy, hyperlipidemia, insulin resistance and hyperglycemia, osteoporosis, lactic acidosis and renal and cardiovascular diseases o Management: early detection, dealing with symptoms, and helping with patients cope with emerging problems and change to treatment regimens - End of Life Care o Keep patient comfortable, facilitating emotional and spiritual acceptance of finite nature of life, helping patients significant other deal with loss and maintaining a safe environment GERENTOLOGICAL CONSIDERATIONS - HIV on the rise – need to assess them carefully because they might be too ashamed to admit infection CUSHING SYNDROME Results from chronic exposure to excess corticosteroids, particularly glucocorticoids CAUSES - iatrogenic administration of exogenous corticosteroids e.g. prednisone - ACTH-secreting pituitary adenoma (Cushing disease) - adrenal tumors - ectopic ACTH production by tumors (usually of the lung or pancreas) Cushing disease and primary adrenal tumors are more common in women between 20s and 40s Ectopic ACTH production is more common in men MANIFESTATIONS - accumulation of adipose tissue in the trunk, face, and cervical spine area  weight gain - cortisol-induced insulin resistance and gluconeogenesis by the liver  hyperglycemia - muscle wasting  muscle weakness - loss of bone matrix  osteoporosis, back pain - loss of collagen  weak and thin skin, easily bruised - catabolic processes  delay in wound healing - mineralocorticoid excess  HTN - adrenal androgen excess  severe acne, virilization in women, feminization in men - first indication of Cushing syndrome may be truncal or generalized obesity, moon face w/ facial plethora, purplish red striae, hirsutism and menstrual disorders in women, HTN, and unexplained hypokalemia DIAGNOSTIC - plasma cortisol levels may be ↑ w/ loss of diurnal variation - collect a 24-hr urine collection for free cortisol - urine cortisol > 80 to 120 mcg/24 hr = Cushing syndrome - if results are borderline  low-dose dexamethasone suppression test - false-positive results can occur in pts with depression and those taking certain meds, including phenytoin, rifampicin - urine levels of 17-ketosteroids may be ↑ - high or normal ACTH levels = Cushing disease - low or undetectable ACTH levels = adrenal or med etiology COLLABORATIVE CARE - if cause is pituitary adenoma  surgical removal of pituitary tumor using the transphenoidal approach or radiation - if adrenal tumors or hyperplasia  adrenalectomy (laparascopic if benign, open surgery if cancer) - if poor candidate for surgery  drugs - ketoconazole (Nizoral), aminoglutethimide (Cytadren), mitotane (Lysodren) o often toxic at the dosages needed to ↓ cortisol secretion - hydrocortisone or prednisone o may be needed to avoid adrenal insufficiency - mifepristone (Korlym) o may be used to control hyperglycemia in pts w/ DM-2 - if cause is corticosteroid therapy  o gradual discontinuance of CS therapy o or reduction of CS dose o or conversion to alternate-day regimen ▪ twice the daily dosage of a shorter-acting CS every other morning NURSING MANAGEMENT - focus on s/sx of hormone and drug toxicity and complicating conditions e.g. CV disease, DM, infection - assess and monitor VS, daily weight, glucose, and possible infection - s/sx of inflammation may be minimal or absent - monitor s/sx of abnormal thromboembolic events such as PE - emotional support - Preoperative care o pt should be brought to optimal physical condition o preop teaching - Postoperative care o adrenal glands are vascular  high risk of hemorrhage o may have NG tube, urinary catheter, IV catheter, CVP monitoring, and leg sequential compression devices to prevent emboli o manipulation of glandular tissue during surgery may release large amts of hormones into the circulation  marked fluctuations in the metabolic processes  unstable BP, fluid balance and electrolyte levels o high doses of CS e.g. hydrocortisone are administered IV during surgery and for several days afterward to ensure adequate responses to the stress of the procedure  ↑ susceptibility to infection and delay wound healing o large amts of endogenous hormones in circulation  HTN, ↑ risk of hemorrhage o critical period for circulatory instability ranges from 24 to 48 hrs postop o keep IV line open for quick admin of CS or vasopressors o obtain AM urine samples (at the same time each AM) for cortisol measurement to evaluate surgery’s effectiveness o tapering CS too rapidly  acute adrenal insufficiency  hypocortisolism (vomiting, ↑ weakness, dehydration, hypotension), painful joints, pruritus, peeling skin, severe emotional disturbances o after surgery, pt is usually maintained on bed rest until BP stabilizes o prevent infection AMBULATORY & HOME CARE - consider home health nurse referral - wear Medic Alert bracelet at all times and carry medical identification and instructions - avoid exposure to extreme temperatures, infections, and emotional disturbances - teach pt to adjust their CS replacement therapy in accordance w/ their stress level - many pts require lifetime replacement therapy - prepare pt to take several months to adjust the hormone dose satisfactorily ADDISON’S DISEASE ETIOLOGY & PATHO - causes adrenocortical insufficiency (hypofunction of the adrenal cortex) - ↓ glucocorticoids, mineralocorticoids, and androgens - most common cause is autoimmune (most common in white females) - adrenal tissue is destroyed by antibodies against the pt’s own adrenal cortex - other causes: o infarction o fungal infections e.g. histoplasmosis o AIDS o metastatic cancer o iatrogenic may be due to adrenal hemorrhage - adrenal insufficiency most often occurs in adults < 60 yrs MANIFESTATIONS - evident when adrenal cortex is 90% destroyed - insidious onset - progressive weakness - fatigue - weight loss - anorexia - ↑ ACTH  bronze-colored skin hyperpigmentation – primarily seen in sun-exposed areas, pressure points, over joints, and in the creases, esp palmar creases - orthostatic hypotension - hyponatremia - salt craving - hyperkalemia - N/V/D - irritability, depression – primary adrenal hypofunction COMPLICATIONS - Addisonian crisis o acute adrenal insufficiency o triggered by: ▪ stress e.g. infection, surgery, psychologic distress ▪ sudden withdrawal of corticosteroid hormone therapy ▪ adrenal surgery ▪ sudden pituitary gland destruction o severe manifestations of glucocorticoid and mineralocorticoid deficiencies includeing hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, confusion o hypotension may lead to shock o circulatory collapse associated with adrenal insufficiency is often unresponsive to usual tx (vasopressors and fluid replacement) o GI manifestations: severe vomiting, diarrhea, and pain abdomen o pain may occur in lower back or legs DIAGNOSTICS - depressed serum and urinary cortisol levels - ↓ urine level of aldosterone - ACTH ↑ in primary adrenal insufficiency and ↓ in secondary disease - primary disease if cortisol levels fail to rise over basal levels with an ACTH stimulation test - secondary disease if a positive response to ACTH stimulation test indicates a functioning adrenal gland - ↑ K, BUN - ↓ Cl, Na, glucose - anemia - ECG may show low voltage and peaked T waves caused by hyperkalemia - CT and MRI scans to identify other causes e.g. tumor, fungal infections, TB, or adrenal calcification COLLABORATIVE CARE - hormone therapy o glucocorticoid ▪ hydrocortisone – has both glucocorticoid and mineralocorticoid properties ▪ during stressful situations, ↑ dose to prevent addisonian crisis ▪ dosage is given 2/3 in the morning and 1/3 in the afternoon o mineralocorticoid ▪ fludrocortisone (Florinef) daily, preferably AM (reflect normal circadian rhythm and ↓ side effects) - ↑ salt in diet - Addisonian crisis o shock management o high-dose hydrocortisone replacement o large volumes of 0.9% saline and 5% dextrose NURSING MANAGEMENT - if pt is hospital o monitor and correct fluid & electrolyte balance o assess VS and signs of fluid volume deficit o monitor serum glucose, Na, K o establish baseline data for mental status, VS, and weight o obtain a complete med hx to determine potential interactions (oral hypoglycemic, cardiac glycosides, oral contraceptives, anticoagulants, NSAIDs) o note s/sx of Cushing syndrome (changes in BP, weight gain, weakness, etc) o protect against infection o assist w/ daily hygiene o protect from noise, light, and env’t temp extremes AMBULATORY & HOME CARE - stress management - teach s/sx of corticosteroid deficiency and excess (Cushing syndrome) and to report to MD to adjust dose - wear Medic Alert and carry a wallet card stating the pt has Addison’s - meds that cause a need to ↑ glucocorticoid dose – phenytoin, barbiturates, rifampin, antacids, etc - meds that cause a need to ↓ glucocorticoid dose – estrogen, etc - carry emergency kit that contains 100 mg of IM hydrocortisone, syringes, and instructions for use TRANSPHENOIDAL HYPOPHYSECTOMY - offers the best chance for a cure - surgery produces an immediate reduction in GH levels followed by a drop in IGF-1 levels w/in a few weeks - when the entire pituitary gland is removed  permanent loss of all pituitary hormones - replace with essential hormones instead (glucocorticoids, thyroid hormone, and sex hormones) - hormonal therapy for life - large tumors or if GH > 45 ng/mL  adjuvant radiation or drug therapy - can treat Cushing syndrome that is caused by pituitary adenoma - Surgical removal of the hypophysis (pituitary gland) – best option for a cure for small adenomas - POST-SURGERY EDUCATION! o Elevating HOB 30 degrees – decreases headaches and pressure on sella turcica o Monitor pulillary response, speech patterns and extremity strength – detect neurologic complications o MOUTH CARE Q4H o AVOID BRUSHING TEETH FOR 10 DAYS – PROTECT SUTURE LINES o Observe for any signs of bleeding o AVOID HARD COUGHING OR SNEEZING OR POOPING TOO HARD – prevent CFS leakage ▪ CLEAR nasal drainage need to be tested for glucose - >30mg/dL INDICATES CSF LEAKAGE! IS AT RISK FOR MENINGITIS o BUT! CSF leakage usually resolves within 72 hours when head elevated and bed rest. o CHECK URINE OUTPUT! PHEOCROMOCYTOMA A rare condition caused by a tumor in the adrenal medulla affecting the chromaffin cells  excess production of catecholamines (epinephrine, norepinephrine) MANIFESTATIONS - most dangerous immediate effect is severe hypertension o if left untreated, may lead to hypertensive encephalopathy, DM, cardiomyopathy, and death - most common in young to middle-aged adults - may be inherited in persons with multiple endocrine neoplasia - severe, episodic HTN accompanied by classic manifestations of severe, pounding headache; tachycardia with palpitations, profuse sweating, and unexplained abdominal or chest pain - attacks may be provoked by many meds, including antihypertensives, opioids, radiologic contrast media, and TCA – attacks may last from a few mins to several hrs DIAGNOSIS - is often missed - uncommon cause of HTN - the simplest and most reliable test is measurement of urinary fractionated metanephrines (catecholamine metabolites) and fractionated catecholamines and Cr – usually done as a 24-hr urine collection o values are elevated in 95% of the pts - serum catecholamines may be elevated during an attack - CT scans and MRI to diagnose for tumors - avoid palpating abdomen of pt suspected with pheochromocytoma as this may cause sudden release of catecholamines and severe HTN! TREATMENT & NURSING MANAGEMENT - primary tx is surgical removal of the tumor - give α and β-adrenergic receptor blockers preop to control BP and prevent intraoperative hypertensive crisis - α-adrenergic receptor blocker (phenoxybenzamine [Dibenzyline]) is given 7 to 10 days preop to ↓ BP and alleviate other sc of catecholamine excess - then, β-adrenergic blockers (e.g. propranolol) are used to ↓ tachycardia and other dysrhythmias o if β blockers are started too early, unopposed α-adrenergic stimulation could precipitate hypertensive crisis - they can cause orthostatic hypotension - surgery is usually done laparoscopically - alternative option is giving metyrosine (Demser) to ↓ catecholamine production by the tumor o adverse effect is orthostatic hypotension - identify classic triad of sx: severe pounding headache, tachycardia, and profuse sweating - pt need rest, nourishing food, and emotional support - HTN may persist even after tumor removal BRAIN ATTACK (look at Hauck’s outline) - PREVENTIVE DRUG THERAPY - antiplatelet drugs for pts who have had a TIA: o Aspirin (81 to 325 mg/day) o ticlopidine (Ticlid) o clopidogrel (Plavix) o dipyridamole (Persantine) o combined dipyridamole and aspirin (Aggrenox) - statins for pts w/ hx of TIA - anticoagulants for pts who have A Fib: o warfarin o rivaorxaan (Xarelto) o dabigatran etexilate (Pradaxa) ACUTE CARE FOR ISCHEMIC STROKE - Most important is the time of onset of symptoms!!! - Goals: preserving life, preventing further brain damage, reducing disability - Acute care begins with ABC - Need baseline neurologic assessment - ~25% of pts worsen in the first 24 to 48 hrs - ↑ BP is common immediately after a stroke and may be a protective response to maintain cerebral perfusion – but it can be detrimental! o ↓ BP if markedly increased (systolic BP > 220 or diastolic > 120) and if pt is NOT on fibrinolytic therapy o if pt IS on fibrinolytic therapy, then BP needs to be < 185/110 and then maintained at or below 180/105 for at least 24 hrs after fibrinolytic therapy o IV antihypertensives such as labetalol and nicardipine are preferred - Correct hypotension and hypovolemia if present, but unlikely - Control fluid and electrolyte balance carefully o keep pt adequately hydrated via IV, oral, or tube feeding to promote perfusion – priority! o overhydration may increase cerebral edema o monitor urine output to prevent dehydration - if ADH ↑  urine ouput ↓ and fluid is retained  hyponatremia - AVOID IV solutions of glucose and water b/c they are hypotonic and may further ↑ cerebral edema and ICP o prevent hyperglycemia - ↑ ICP o more likely with hemorrhagic stroke o usually peaks in 72 hrs and may cause brain herniation o prevent by elevating HOB, maintaining head alignment, and avoiding hip flexion, managing hyperthermia, drug therapy to prevent seizures, pain management, avoidance of hypervolemia, and management of constipation o drain CSF DRUG THERAPY FOR ISCHEMIC STROKE Recombinant tissue plasminogen activator (tPA) - produce localized fibrinolysis by binding to the fibrin in the thrombi - other fibrinolytic agents CANNOT be substituted for tPA - administered IV to reestablish blood flow thru a blocked artery to prevent cell death in pts with acute onset of ischemic stroke - must be administered within 3 to 4 ½ hrs of onset of clinical signs of ischemic stroke - Screening: o noncontrast CT or MRI scan to rule out hemorrhagic stroke o blood tests for glucose level and coagulation disorders o recent hx of GI bleeding, stroke, or head trauma w/in the past 3 months, or surgery w/in 14 days - insert a urinary catheter, NG tube, and multiple IVs before tPA administration - during infusion, closely monitor VS and neurologic status - control of BP is critical during tx and for 24 hrs following!!!! - intraarterial infusion of tPA o can be administered up to 6 hrs after onset of stroke sx o neurovascular specialist inserts a thin, flexible catheter into an artery (usually femoral artery) and guides to area of clot by angiogram o tPA is administered thru catheter and immediately targets the clot o less tPA is needed Anticoagulants generally NOT recommended after an ischemic stroke due to risk for intracranial hemorrhage - anticoagulants and platelet inhibitors can be used if pt is stabilized and stroke is caused by thrombi and emboli - platelet inhibitors = aspirin, ticlopidine, clopidogrel, dipyridamole - for pts with A fib – warfarin, rivaroxaban, and dabigatran etexilate Asprin 325 mg may be initiated within 24 to 48 hrs after onset of ischemic stroke – beware of hx of PUD Statins SURGICAL THERAPY FOR ISCHEMIC STROKE - stent retrievers e.g. Solitaire FR, Trevo - mechanical embolus removal in cerebral ischemia (MERCI) retriever ACUTE CARE FOR HEMORRHAGIC STROKE Drug Therapy - anticoagulants and antiplatelet inhibitors are CONTRAINDICATED - main drug therapy is management of HTN with oral or IV agents to maintain normal BP - seizure prophylaxis in acute period after intracerebral and subarachnoid hemorrhage is situation specific Surgical Therapy - immediate evacuation of aneurysm-induced hematomas or cerebellar hematomas larger than 3 cm - if arteriovenous malformation (AVM) ruptures  tx with surgical resection and/or radiosurgery - tx aneurysms by clipping or coiling to prevent rebleeding NURSING INTERVENTIONS Respiratory - risk of aspiration pneumonia is high b/c of impaired consciousness or dysphagia - dysphagia after stroke is common - airway obstruction from chewing and swallowing, food pocketing, and tongue falling back - may require ET intubation or mechanical ventilation initially o oral care at least q 2 hr to reduce risk of ventilator-assisted pneumonia - enteral tube feedings place pt at risk for aspiration pneumonia - screen all pts for ability to swallow and keep NPO until dysphagia is ruled out 1) frequently assess airway patency and function, 2) provide oxygenation, 3) suction, 4) promote pt mobility, 5) position pt to prevent aspiration, and encourage deep breathing Neurologic - National Institutes of Health Stroke Scale (NIHSS) – measures stroke severity, predictor of short- and long-term outcomes of stroke pts - closely monitor VS - neurologic assessment - ↓ LOC may indicate ↑ ICP Cardiovascular - Aimed at maintaining homeostasis - Cardiac efficiency may be further compromised by fluid retention, overhydration, dehydration, or BP variations - CVP, PAP, or hemodynamic monitoring may be used as indicatiors of fluid balalnce or cardiac function in the CCU 1) Monitor VS frequently, 2) monitor cardiac rhythms, 3) calculate I&O and noting imbalances, 4) regulate IV infusions, 5) adjust fluid intake to individual needs, 6) monitor lung sounds for crackles and rhonchi indicating pulmonary congestion, 7) monitor heart sounds for murmurs or for S3 or S4 - monitor for orthostatic hypotension before ambulating pt for the first time - pt is at risk for VTE – keep pt moving! – assess for signs of VTE Musculoskeletal - prevent joint contractures and muscular atrophy - ROM and positioning - special attention to paralyzed or weak side 1) trochanter roll at the hip to prevent external rotation, 2) hand cones (not rolled washcloths) to prevent hand contractures 3) arm supports with slings and lap boards to prevent shoulder displacement 4) avoidance of pulling the pt by arm to avoid shoulder displacement 5) posterior leg splints, footboards, or high-top tennis shoes to prevent foot-drop 6) hand splints to reduce spasticity Integumentary 1) pressure relief by position changes, special mattresses, or wheelchair cushions o side-backside q 2 hr o positon on weak/paralyzed side for only 30 mins o epidermis and dermis are damaged if redness does not go away for 15 mins o do not massage damage area o pillows under lower extremities 2) good skin hygiene 3) emollients applied to dry skin 4) early mobility Gastrointestinal - most common problem is constipation - may need bowel retraining Urinary - poor bladder control  incontinence - promote normal bladder function and avoid indwelling catheters o long term use is associated with CAUTI - avoid bladder overdistention - bladder retraining program: o adequate fluid intake with most of it given between 7 AM and 7 PM o scheduled toileting q 2 hrs using bedpan, commode, or bathroom while encouraging usual position for urinating o observe for signs of restlessness, which may indicate need for urination o assessment for bladder distention by palpation - ultrasound measures how much urine is in bladder after voiding – incomplete emptying may cause UTI Nutrition - assess for gag reflex before feeding o usually speech therapist or occupational therapist is the one responsible to create exercises to stimulate swallowing - severe impairment may require enteral or parenteral nutrition support - mouth care before feeding helps stimulate sensory awareness and salivation and can facilitate swallowing - remain in high Fowler’s position for feeding and for 30 mins afterward - foods should be easy to swallow and provide enough texture, temperature, and flavor to stimulate swallow reflex - crushed ice can be a stimulant - pureed foods not recommended - thin liquids are difficult to swallow and may promote coughing - avoid milk products - PEG tube if inadequate oral diet or dysphagia persists - promote self-feeding Communication - support psychological needs - assess ability to speak and to understand - use gestures to support verbal cues - collaborate with speech therapist to assess Sensory-Perceptual Alterations - Right side stroke pt o high risk for injury due to mobility difficulties o verbal directions o break task down into simple steps o environmental control o provide nonslip socks o assist or remind pt to dress weak or paralyzed side or shave forgotten side of the face (one-sided neglect) - Left side stroke pt o nonverbal cues and instructions are helpful for comprehension - homonymous hemianopsia (blindness in the same half of each visual field) o initially, arrange environment within pt’s perceptual field o later, let pt learn to compensate - safety measures such as closely observing pt, elevate side rails, lower height of the bed, using video monitors - use eye patch if diplopia - if corneal reflex is absent, observe closely and protect against eye injuries – artificial tears or gel, eye shield at night - ptosis is generally not treated b/c it does not inhibit vision Coping - provide information and emotional support AMBULATORY AND HOME CARE - critical factor in discharge planning is the pt’s level of independence in performing ADLs - prepare pt and caregiver for discharge thru teaching, demonstration and return demonstration, practice, and evaluation of self-care skills - plan follow-up care - identify community resources to provide recreational activities, group support, spiritual assistance, respite care, adult day care, and home assistance based on needs Rehabilitation - goal: maximize pt’s abilities - most pts see maximum benefit in the 1st yr of recovery after a stroke - physical therapy focuses on mobility, progressive ambulation, transfer techniques, and equipment needed for mobility - occupational therapy emphasizes retraining for skills of daily living such as eating, dressing, hygiene, and cooking – occupational therapists are skilled in cognitive and perceptual evaluation and training - speech therapy focuses on speech, communication, cognition, and eating abilities Musculoskeletal function - most pts begin to show signs of spasticity with exaggerated reflexes within 48 hrs after the stroke – denotes progress toward recovery - as improvement continues, small voluntary movements of the hip or shoulder may be accompanied by involuntary movements in the rest of the extremity (synergy) - the final stage of recovery occurs when pt has voluntary control of isolated muscle groups - balance training - assess whether pt autocorrect their posture when sitting on edge of bed - Bobath method – help pt gain control over patterns of spasticity by inhibiting abnormal reflex patterns - constraint-induced movement therapy (CIMT) – encourages pt to use weakened extremity by restricting movement of normal extremity - supportive or assistive equipment Stroke Survivorship & Coping - often exhibit emotional responses inappropriate or atypical for the situation 1) distract pt who suddenly becomes emotional 2) explain to the pt and family that emotional outbursts may occur after a stroke 3) maintain a calm env’t 4) avoid shaming or scolding pt during emotional outbursts Sexual Function - teach about optional positioning of partners, timing for peak energy times, and pt and partner counseling ACUTE RENAL FAILURE - Prerenal causes: - factors that ↓ systemic circulation  ↓ glomerular perfusion and filtration of the kidneys (tubular and glomerular function is preserved) - in prerenal oliguria, there is no damage to the kidney tissue (parenchyma) – different from intrarenal oliguria - oliguria is caused by ↓ circulating blood volume - prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged Intrarenal causes: - include conditions that cause direct damage to the parenchyma, resulting in impaired nephron function - damage usually results from prolonged ischemia, nephrotoxins (e.g. AG antibiotics, contrast media), hgb released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells - nephrotoxins  obstruction of intrarenal structures by crystallizing or by causing damage to the epithelial cells of tubules - hgb and myoglobin can block tubules and cause renal vasoconstriction - Acute tubular necrosis (ATN) – most common intrarenal cause of AKI and is primarily result of ischemia, nephrotoxins, or sepsis o potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates o most common cause of AKI for hospitalized pts Postrenal causes: - involve mechanical obstruction in the outflow of urine  urine refluxes into the renal pelvis  impairing kidney function - bilateral ureteral obstruction  hydrohephrosis (kidney dilation), ↑ in hydrostatic pressure, and tubular blockage  progressive decline in kidney function o if relieved w/in 48 hrs of onset, complete recovery is likely o after 12 weeks, recovery is unlikely - prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis MANIFESTATIONS - AKI has a prolonged course when parenchymal is damage - prerenal and postrenal AKI that has not caused intrarenal damage usually resolves quickly with tx of the cause - when pt does not recover from AKI  CKD - RIFLE classification is used to describe the stages of AKI (Table 47-3) - AKI may progress thru phases: o oliguric phase – most common manifestations: ▪ urinary changes • oliguria – reduction in urine output to < 400mL/day – occurs within 1 to 7 days of the injury to kidneys • if cause is ischemia, often occurs within 24 hrs • if nephrotoxic drugs are involved, onset may be delayed for as long as 1 wk • nonoliguria > 400 mL/day – about 50% of pts (makes initial diagnosis difficult) • lasts on average 10 to 14 days but can last months in some casese • the longer the oliguric phase lasts, the poorer the prognosis for complete recovery • changes in urine output generally do not correspond to changes in GFR – however, can be helpful in differentiating etiology of AKI o e.g. anuria is usually seen with UT obstruction, oliguria is commonly seen w/ prerenal etiologies, and nonoliguric AKI is seen w/ interstitial nephritis and ATN • urinalysis may show casts, RBCs, and WBCs o casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules • urinalysis may show a specific gravity fixed at around 1.010 and urine osmolality at about 300 mOsm/kg  same sp gravity and osmolality of plasma, thus reflecting tubular damage w/ loss of concentrating ability by the kidney • proteinuria – if kidney failure related to glomerular membrane dysfunction ▪ fluid volume • hypovolemia has the potential to exacerbate all forms of AKI • reversal w/ fluid replacement is often sufficient to tx many forms of AKI • when urine output ↓ fluid retention occurs • severity of sx depends on extent of fluid overload o e.g. distended neck veins w/ bounding pulses if anuria and oliguria o e.g. edema or HTN • fluid overload  HF, pulmonary edema, pericardial and pleural effusions ▪ metabolic acidosis • kidneys cannot synthesize ammonia or excrete acid products of metabolism • bicarb depleted in buffering H+ , defective reabsorption and regeneration of bicarb • Kussmaul respirations (rapid, deep respirations) may develop to compensate by ↑ exhalation of CO2 ▪ sodium balance • damaged tubules cannot conserve sodium  normal or ↓ serum Na • avoid excessive Na intake b/c it can lead to volume expansion, HTN, and HF • uncontrolled hyponatremia or water excess can lead to cerebral edema ▪ potassium excess • kidneys normally excrete 80% to 90% of K – but in AKI, kidney is impaired to excrete K • hyperkalemia is more of a risk if AKI is caused by massive tissue trauma b/c damaged cells release additional K into the EC fluid • bleeding and blood transfusions  cellular destruction  release of more K • acidosis worsens hyperkalemia – H+ ions enter the cells and drive K out • usually asymptomatic • pt may complain of weakness w/ severe hyperkalemia • peaked T waves, wide QRS complex, and ST segment depression on ECG • cardiac muscle is intolerant of acute ↑ in K, so tx is essential! ▪ hematologic disorders • hospital-acquired AKI often occurs in pts w/ multiorgan failure • leukocytosis is often present w/ AKI • most common cause of death in AKI is infection – most common sites are urinary and respiratory systems • CBC w/ eosinophilia suggest an allergic response and possibly interstitial nephritis, polyarteritis nodosa, or atheroemboli ▪ waste product accumulation • ↑ BUN and serum creatinine • ↑ BUN can be caused by dehydration, corticosteroids; or catabolism resulting from infections, fever, severe injury, or GI bleeding • best serum indicator of AKI is creatinine ▪ neurologic disorders • occur when nitrogenous waste products accumulate in brain and other nervous tissue • manifestations can be as mild as fatigue and difficulty concentrating , and then escalate to seizures, stupor, and coma • asterixis (flapping tremor when the wrist is extended ) o Diuretic phase ▪ daily urine output is usually around 1 to 3 L, but may reach 5 L or more ▪ nephrons are still not fully functional though ▪ high urine volume is caused by osmotic diuresis from high urea concentration in glomerular filtrate and inability of tubules to concentrate urine ▪ kidneys have recovered ability to excrete wastes, but not to concentrate urine ▪ hypovolemia and hypotension if massive fluid losses  monitor for hyponatremia, hypokalemia, and dehydration ▪ may last 1 to 3 weeks ▪ near end of this phase, acid-base, electrolyte, and waste product values begin to normalize o Recovery phase ▪ begins when GFR ↑, allowing BUN and serum Cr levels to plateau and then ↓ ▪ kidney function may take up to 12 months to stabilize ▪ some do not recover and progress to end-stage kidney disease ▪ elderly less likely to have complete recovery ▪ some scar tissue remains but no clinically significant loss of function DIAGNOSTIC STUDIES - need thorough hx - prerenal causes – if hx of dehydration, blood loss, or severe heart disease - intrarenal causes – if nephrotoxic drugs or recent hx of blood transfusion or radiologic study using contrast media - postrenal causes – if hx of changes in urinary stream, stones, BPH, or cancer of bladder or prostate - ↑ in serum Cr may not be evident until there is a loss of > 50% of kidney function - urinalysis – urine sediments, osmolality, Na content, Sp gravity - kidney ultrasound – for evaluating possible kidney disease and obstruction - renal scan – assess abnormalities in kidney blood flow, tubular function, and the collecting system - CT scan – identify lesions, masses, obstructions, and vascular anomalies - renal biopsy – best method for confirming intrarenal causes - MRI/MRA with contrast media gadolinium is a no no if pt has kidney failure COLLABORATIVE CARE (Look at Hauck’s outline) Renal Replacement Therapy (RRT) indicated in AKI if: 1) volume overload, resulting in compromised cardiac and/or pulmonary status 2) ↑ serum K 3) metabolic acidosis (serum bicarb < 15 mEq/L) 4) BUN > 120 mg/dL 5) significant change in mental status 6) pericarditis, pericardial effusion, or cardiac tamponade Continuous Renal Replacement Therapy (CRRT) - provided continuously over approx. 24 hrs thru cannulation of an artery and vein or cannulation of 2 veins Hemodialysis - method of choice when rapid changes are required in a short time - more complicated process - requires specialized staff and equipment, vascular access, anticoagulation therapy - rapid fluid shifts during HD may cause hypotension NUTRITION - goal in AKI is to maintain adequate caloric intake – 30 to 35 kcal/kg and 0.8 to 1.0 g of protein/kg of desired body weight - get adequate energy primarily from carbs and fat sources - restrict Na as needed to prevent edema - get 30% to 40% of total calories from fat, or use fat emulsion IV infusions - if pt cannot maintain adequate oral intake, then go for enteral nutrition - if GI tract not functional, go for parenteral nutrition (but may need daily HD or CRRT to remove excess fluid) (concentrated parenteral formulas available as substitute) NURSING INTERVENTIONS - Monitor VS, daily I&O, and fluid & electrolyte balance o 1 kg = 1000 mL of fluid - Assess: o urine for color, sp gravity, glucose, protein, blood, and sediment o general appearance, including skin color, edema, neck vein distention, and bruises o if dialysis, observe access site for inflammation and exudate o mental status, LOC o oral mucosa for dryness and inflammation o lungs for crackles and rhonchi or diminished breath sounds o S3 gallop, murmurs, or pericardial friction rub o dysrhythmias - Caution: o Aggressive diuretic therapy for fluid overload can lead to ↓ in renal blood flow!!! o Some OTC analgesics may worsen kidney function if pt has mild CKD o ACEi can ↓ perfusion pressure and cause hyperkalemia o However ACEi are frequently used to prevent proteinuria and progression of kidney disease, esp in diabetics - Infection is leading cause of death in AKI – infection precautions! - Mouth care to prevent stomatitis, which develops when ammonia (produced by bacterial breakdown of urea) in saliva irritates mucous membranes END STAGE RENAL DISEASE Chronic kidney disease (CKD) - progressive, irreversible loss of kidney function - either presence of kidney damage or GFR < 60 mL/min/1.73m2 for > 3months - last stage of kindey failure = end-stage kidney (renal) disease (ESKD) = GFR < 15 mL/min - RRT is required to maintain life if ESKD - leading causes are DM and HTN - CKD are frequently asymptomatic MANIFESTATIONS (look at Hauck’s outline) - uremia – syndrome in which kidney function declines to the point that sx may develop in multiple body systems - during early stages, no change in urine - as CKD progresses, ↑ diffic