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NUR 265 Exam 2 Study Guide & Exams questions and answers ➢ What drug is hyperthyroidism treated with? o Propylthiouracil (prO-pill-thigh-O-your-uh-sil)... [Show More] (PTU) o What does this do? ▪ Prevent iodine from binding in the thyroid to reduce symptoms o What is PTU’s black box warning against? ▪ Liver injury ➢ What drug is used to treat hypothyroidism? o Levothyroxine (lev-O-thigh-rocks-in) (Synthroid) o What should the nurse teach the patient about taking Levothyroxine? ▪ To take it every day at the same time, before breakfast o What condition is caused by an overdose of Levothyroxine (lev-O- thigh-rocks-in) (Synthroid)? ▪ Hyperthyroidism ▪ Name 3 symptoms of Levothyroxine (Synthroid) overdose? ➢ Chest pain, palpitations, excessive sweating ➢ What is the most important educational need for a patient with hypothyroidism about hormone replacement therapy? o That is life-long ➢ What is a myxedema coma? o The hypothyroid version of thyroid storm; the heart becomes flabby and the chambers enlarge resulting in decreased cardiac output o What can treat this? ▪ Synthroid ➢ Should you monitor a patient with hyper- or hypothyroidism for eyelid or global lag? o Hyperthyroidism ➢ A patient is returning from a thyroidectomy, so what 4 items are important to have available? Why? o (1) Oxygen – in case of respiratory distress from swelling or laryngeal spasm (2) Suction equipment – in case of increased secretions (3) Emergency tracheotomy – in case of hemorrhage or edema that blocks the airway (4) Calcium Gluconate – to treat hypocalcemia and tetany in case the parathyroids were injured ▪ What are the signs of hypocalcemia? ● Muscle twitching, numbness, and tingling ➢ What should a nurse take notice to that is an alert for laryngeal nerve damage? o Hoarse, weak voice [Show Less]
NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS • Nephrotic Syndrome: o NS is a condition of increased glomerular permeability that allows larg... [Show More] er molecules to pass through the membrane into the urine and then be excreted. o Immunological Kidney disorder o This causes massive loss of protein in the urine, edema formation, and decreased plasma albumin levels. ▪ Proteinuria- severe protein loss more than 3.5 g in 24- hour urine sample. o Key features: ▪ Massive proteinuria >3.5g / 24hrs ▪ Hypoalbuminemia <3g/dL ▪ Edema (facial and periorbital) ▪ Lipiduria ▪ Hyperlipidemia ▪ Increased coagulation (renal vein thrombosis) ▪ Reduced kidney function (↑ BUN, ↑ Cr, ↓ GFR) o Treatment- immunosuppressant agents (if immunity based). ▪ ACE inhibitors (to decreased protein loss in urine & ↓BP) ▪ Statins (improve blood lipid levels). ▪ Heparin (↑ coagulation / risk of thrombosis → treat vascular effects and improve kidney function) o Diet: ▪ If GFR is normal- dietary intake of complete proteins is needed ▪ If GFR is decreased- dietary protein is decreased, diuretics and sodium restriction. • Acute Kidney Injury: o AKI is rapid reduction in kidney function resulting in a failure to maintain fluid and electrolyte balance, and acid-base balance. ▪ Can occur over a few hours or days o Severity of AKI is based on serum creatinine increase, and decreased urine output- an increase in specific gravity (meaning urine is more concentrated or the patient is dehydrated). o GFR isn’t used to measure acute injury or illness—only chronic kidney disease. o 3 types of AKI ▪ prerenal - conditions that reduce blood flow / oxygen to the kidney → decreased perfusion to kidneys • azotemia- nitrogenous waste/toxin build up o effects LOC, mood, change in personality o related directly to reduced perfusion to the kidneys • examples of perfusion reduction: o blood/fluid loss- (surgery, sepsis, hypovolemic shock) o blood pressure drugs resulting in hypotension o MI or HF → low ejection fraction → low cardiac output o NSAIDs, ASA o Anaphylaxis o Severe burns o Severe dehydration o Renal artery stenosis o Bleeding or clotting in kidney blood vessels o Atherosclerosis (cholesterol deposits obstructing blood flow to the kidneys) ▪ Intra-renal failure- tissue damage to the actual kidneys • Intra-renal- reflects injury to the glomeruli, nephrons, or tubules • Examples of intra-renal failure: o Bleeding in the kidney o Glomerulonephritis or inflammation of the glomeruli o Pyelonephritis o Thrombi or emboli in the kidney blood vessels o TTP → platelet disorder ↑ clotting o Sepsis or local infection o Lupus o Multiple myeloma o Scleroderma o Chemo/ ABTs / nephrotoxic drugs o Ischemia in kidney failure, including hypoxemia from respiratory and cardiac arrest ▪ Post-renal failure- Urine flow obstruction • Post-renal failure examples: o Bladder cancer o Colon cancer o Prostate cancer o Cervical cancer o Enlarged prostate o Kidney stones o Blood clots in urinary tract o Neurogenic bladder →Nerve damage o Mean atrial pressure is important in determining adequate kidney perfusion!!! ▪ MAP= (systolic+ 2[diastolic])/3 Mean atrial pressure of 65 is needed to perfuse the kidney!! ➢ Manifestations (s/s) of AKI o Oliguria o Fluid Volume Overload ▪ Crackles ▪ Edema ▪ Anasarca (generalized edema) ▪ ↓ 02 sats ▪ ↑ RR o LOC changes o Labs (↑BUN, ↑Cr, urine specific gravity >1.030) o Nursing considerations / Interventions for AKI: ▪ Prevention is key! - urge patients to drink 2-3 L of water daily. • Monitor Fluid status (I&O, weight, ↑ hydration, characteristic of urine) • Report Output <0.5mL/kg/hr if persists >2hr <30mL/hr • Monitor for kidney functions o Labs (BUN, Cr, GFR, electrolytes, osmolarity) o I&Os ▪ You want output to be more than input ▪ Sodium, potassium, and specific gravity determine hydration status. o Contrast dyes o MAP > 65 mmHg • Diuretic therapy- happens after AKI is starting to be resolved! (Releasing extra fluid through the urine - This is a good sign!!! - Watch for dehydration! - Its normal to have fluids hanging during the diuretic phase! - Titrate fluids!) • Nutrition during AKI: o Low protein ▪ Because protein molecules are huge and put on the strain to process o Low sodium ▪ Since the body has high sodium concentration due to AKI • Fluid restriction o if AKI was due to anything except for perfusion problem • Hemodynamic Monitoring o Temporary Kidney Replacement Therapy ▪ → for Symptomatic Uremia (critical electrolytes, toxicity, metabolic acidosis, fluid overload that inhibits tissue perfusion) ▪ Removes toxins ▪ Requires immediate vascular access • If RRT occurs for 4 weeks or less, then there is no loss of kidney function • If RRT occurs for 3 months or more it is considered kidney failure • Chronic Kidney Disease o CKD- progressive, irreversible disorder and kidney function doesn’t recover. o Focus / Teach on reducing risk factors to slow Progression! o CKD is normally a result of another condition that compromises the kidneys and takes years to progress ▪ Hypertension ▪ Uncontrolled diabetes ▪ Renal stenosis ▪ Infection ▪ Glomerulonephritis ▪ Polycystic kidney disease ▪ African Americans are 4 times more likely to get it o Azotemia- nitrogenous waste build up o Uremia- azotemia with clinical manifestations ▪ Manifestations of uremia • Metallic taste in mouth • Anorexia • Nausea/vomiting • Muscle cramps • Uremic frost on skin • Itching • Fatigue and lethargy • Hiccups • Edema • Dyspnea • Paresthesia o Stages of chronic kidney disease: ▪ o effects of CKD on the kidneys: ▪ decreased urinary output • urine output decreases as the patient progresses through CKD until they reach oliguria ▪ increased potassium, BUN, Creatinine • put patient on tele monitor if they are in hyperkalemia!!! ▪ Decreased GFR ▪ Maintains homeostasis until late signs ▪ Salt wasting: • In early stages of CKD patients will lose the sodium and the water won’t follow!! So, excess fluid and hyponatremia • In late stages CKD- no urine output so salt and water stay and hypernatremia occurs! o Metabolic changes of CKD: • Urea and creatinine build up • Hyponatremia- early stages • Hypernatremia- late stages o Hyperkalemia- late stages → due to kidneys not excreting potassium though the urine. • Acid-base balance- o Metabolic acidosis occurs due to lack of urine excretion, and the body becomes more acidic! → kussmaul respirations! (deep rapid resp) → pt is compensating! o Patient is normally in a slight acidic state all the time. o Effects of CKD on the body: ▪ Cardiac- • Hypertension • Hyperlipidemia • Heart failure • Crackles • Pulmonary edema (pink frothy sputum) • Tachypnea • hyperpnea • Pericarditis, cardiac tamponade ▪ Integumentary • Uremic frost! - causes patient to be itchy! o Keep cold o Tepid water ▪ Hematological • Anemia (fatigued, SOB) →from lack of RBCs → from Ø erythropoietin o Put on fall precautions!!!- orthostatic hypotension ▪ Musculoskeletal • Bone pain • Muscle weakness • Pathological fx (↓Ca) ▪ Gastrointestinal • Stomatitis- huge ulcers in the mouth o Patient won’t want to eat o NG tube • PUD- GI bleeds • Uremic Fetor o Dietary restrictions of CKD ▪ Depends on the severity of the CKD and how well their kidneys are function • Protein: o Restriction early during the disease prevents complications of CKD, and preserves kidney function (↑ for dialysis) Monitor BUN and Albumin o Based on GFR and type of treatment being used • Fluid- May have restrictions! • Potassium- restriction! o Salt substitute is potassium! It is a big no no! o Kayexelate- excrete potassium in GI- diarrhea! • Give / ↑ Calcium, Vit D & Vit B • Magnesium o Avoid Mg and Mg containing antacids • Sodium o Restrict late, not early o ↑ for dialysis • Phosphorus o Restrict early in CKD! o Phosphate binders- GI excretion o Nursing Considerations / Interventions: ▪ Assess for FVO q4hr ▪ Daily weights (same time q day) 1 kg = 1 L of fluid ▪ Strict I&O ▪ Diuretics (do Not help in ESRD) ▪ Monitor Electrolytes ▪ Treat HTN → ACEs, CCBs, thiazides o Hemodialysis ▪ Most common Kidney replacement Therapy in ESKD ▪ Normally no urine output at all ▪ 3x a week- 4-5 hours. At clinic and go home ▪ pull blood [Show Less]
Labs • Hbg 12-18 • Hct 37-52% • WBC 5-10 • RBC 4.2-6.1 • PLT 150-400 • PT 11-12.5 sec (1.5-2.5x normal on Coumadin = 16.5-31.25 sec) •... [Show More] INR 0.9-1.2 sec (Therapeutic level 2-3x normal = 1.8-3.6 sec) • PTT 60-70 sec (1.5-2.5x normal on Heparin = 90-175) • Na 135-145 • K+ 3.5-5 • Creatinine 0.5-1.2 • BUN 10-20 • Albumin 3.5-5 • Mg 1.5-2.5 • Ca 9-10.5 • Cl 98-106 • Phosphorus 2-4.5 • Specific Gravity 1.005-1.030 Discoid lupus • Affects only the skin and is not lethal - Caused by UV rays • Macular Rash & Discoid Rash • Skin biopsy to dx Systemic Lupus Erythematosus (313-317) ***TEMPERATURE*** • Chronic, progressive, inflammatory connective tissue disorder that affects multiple body systems &organs o REMISSIONS/EXACCERBATIONS (can end up in the ICU) - Autoimmune o Attracted to KIDNEY’s—Lupus Nephritis is leading cause of death; this is direct damage to the kidneys • Poor survival associated with high creatinine, low hematocrit, proteinuria o Young Women of child bearing age 20-40 Y (primary AA women) o SLE & DLE both share a disfiguring and embarrassing rash!! • Clinical manifestations o Malar rash – red flat or raised rash over cheeks sparing nasolabial folds “butterfly rash” o Discoid rash – Red raised patches with scaling follicle plugging o Photosensitivity– discoid skin rash from sun exposure - pt should wear sunscreen or protective clothing o Oral ulcers–usually painless o Polyarthritis-multiple joints affected • Small joints and knees inflamed • Osteonecrosis from chronic steroid use (5y+) o Pleuritis with pleural effusion or pericarditis o Fever is the major sign of exacerbation o Generalized weakness, fatigue, anorexia, weight loss o Renal disorders–proteinuria, cellular casts o Neurologic disorders – seizures, psychosis and also peripheral neuropathies o Raynaud’s phenomena • Exposure to cold or extreme stress – red, white, blue & pain of digits o Alopecia or hair loss common • Diagnostic Tests o ANA most sensitive but antinuclear antibodies not specific to SLE o C reactive protein can help differentiate SLE flare from an infection (remains normal if SLE flare) o CBC shows pancytopenia (a decrease in all cell types) • Medical Management o Topical steroids for skin lesions o Acetaminophen or NSAIDS (caution with kidneys) – tx joint & muscle pain & inflammation o Hydroxychloroquine (anti-malarial agent) – dec absorption of ultraviolet light by skin, dec skin lesions ▪ Frequent eye exams – b4 starting and q 6 mon o Glucocorticoids – Chronic steroid therapy ▪ Take in the am b4 breakfast ▪ Take Ca to prevent osteoporosis ▪ Maintain skin integrity o Immuno-suppressants – methotrexate, azathioprine o Belimumab – do not receive live vaccines for 30 days b4 tx • Teaching • Protect the skin o Limit sun/ultraviolet light exposure to prevent exacerbation (fluorescent light too) ▪ Long sleeves, lg-brimmed hat, SPF 30+ o Clean skin with mild soap, pat dry and apply lotion o Cosmetics ok w/ moisturizers and sun protection, no excess powder or drying substances • Monitor temperature – first sign of exacerbation • Avoid large crowds and people who are ill, bc immunosuppressed • Avoid harsh hair tx (permanents or highlights) • Pregnancy can cause exacerbation Systemic Sclerosis (Scleroderma) ***SWALOWING PROBLEM*** • Uncommon, chronic, inflammatory, autoimmune connective tissue disease. • Similar to SLE, but w/a higher mortality rate • Doesn’t respond to steroids or immunosuppressants, why mortality higher than SLE • Inflamed tissue becomes fibrotic and then sclerotic (hard) – renal involvement leading cause of death • Women 25-55, most in 40s • Diffuse cutaneous *Major organ problems o First sx – hand and forearm edema w/ or w/o bilateral carpal tunnel syndrome o Skin thickening on trunk, face, and proximal and distal extremities (most of the body) o Painless symmetric pitting edema of hands & fingers (sausage like fingers) o Changes of pigmentation with loss of skin folds & face can become mask like o Develop early problems w/ GI tract (GERD to dysphagia), heart(myocardial fibrosis), lungs (fibrosis & PAH), & kidneys (malignant HTN) o Complications can be rapid • Limited cutaneous *Esophagus o Skin thickening limited to sites distal to face, neck and distal extremities o Organ changes rare or late o CREST Syndrome ▪ Calcinosis – calcium deposits in tissues ▪ Raynaud’s Phenomenon – intermittent vasospasm of finger tips - first CREST symptom that develops ▪ Esophageal dysmotility - **Dysphagia** ▪ Sclerodactyly – scleroderma of digits – fingers stiff, shiny, and no skin folds ▪ Telangiectasia – capillary dilations that form vascular lesions on face, lips & fingers • Medical Management o Medications – Tx sx ▪ Vasoactive agents – CCB for Raynaud’s symptoms ▪ Anti – inflammatory meds - steroids ▪ Immunosuppressants o Reduce renal complications ▪ ACE inhibitors and HTN control o Treat PAH (Pulmonary Artery Hypertension) ▪ Bosentan - endothelin receptor antagonist – Liver toxic • Nursing Management o Keep HOB elevated 60 degrees during meals and at least an hour after o Maintain skin integrity– esp with steroids & vasospasm o Small frequent meals w/semisoft foods – avoid liquids (thick it) due r/f choking – small amounts & chew well o Teach to avoid foods that include gastric secretion–spices, caffeine, pepper o Promote bowel elimination – have both constipation & diarrhea • Client Education o How to dress in cold weather-gloves, socks, etc. o Eliminate alcohol, cigarettes, extreme stress, and caffeine (vasoconstrictive) o Biofeedback for stress management o Disease process – Only gets worse Fibromyalgia ***SLEEP & STRETCHING*** • Chronic pain syndrome, NOT inflammatory or autoimmune • Pain stiffness and tenderness in trigger points – back of neck, upper chest, trunk, low back, and extremities • Burning and gnawing that comes and goes, worsen w/stress, include activity, and weather conditions • Women between 30 -50 years, Lyme disease, trauma, & flu-like illness • Clinical Manifestations o Fatigue – most common manifestation o Morning stiffness o Non refreshing sleep because of lack of stage 4 sleep- most do not get REM sleep o Post exertional muscle pain o 1/3 of patients have irritable bowel, tension headaches, PMS, numbness & tingling & Raynaud’s phenomena o Depression – common with chronic pain • Medical Management—Directed at symptom relief o L tryptophan-used to enhance sleep o TCAs (amitriptyline, nortriptyline) inhibit serotonin uptake - antidepressant o Benzodiazepines for anxiety associated w/ depression o NSAIDS for pain control but may need stronger meds if pain not well controlled o Pregabalin (Lyrica) – FDA approved for fibromyalgia pain o **LOW INTENSITY EXERCISE WILL DECREASE PAIN** ▪ Stretching, walking, swimming, rowing, biking, and water exercise o Anticonvulsants like carbamazepine (Tegretol) & gabapentin (Neurontin) to help w/ chronic pain mgmt. o Biofeedback– esp. helpful with pain syndrome o Oral Mag helpful with muscle pain Lyme’s Disease ***NO DARK CLOTHING*** • Tick born disease • Considered a connective tissue disease because the skin, joints, nervous system, and heart are involved • Sx begin w/i 3-30 days post bite • Easy to treat when found in time • Signs and Symptoms o 1st - Red flat rash that clears in the center (bulls-eye lesion)- near the area of the bite o Flu-like sx - Severe HA, Fever, Chills, Severe malaise, Fatigue, Stiff neck, & Joint pain • Medical Management o Doxycycline is the most common antibiotic used to treat (14-21 days) o Severe disease- IV antibiotics for 30 days (ceftriaxone or cefotaxime) o Neurologic abnormalities may occur if tx is ineffective o Intra-joint steroids & NSAIDS may be used for joint inflammation & pain o Long term effects include fatigue & arthralgias for many years after initial infection • Prevention & Early Detection o Avoid dark clothing, long-sleeved tops and long pants, tuck in shirt and pants into boots o Insect repellant w/DEET o Remove with gloves or tissue, do not squeeze or burn, flush down the toilet. Clean area with alcohol o Wait 4-6 weeks after being bitten b4 being tested, testing b4 is not reliable Allergy (348-358) ***EPI PEN, STOP INFUSION, LATEX CONDOM USE*** • “Hypersensitivity” inc immune response to the presence of an allergen “antigen” • Diagnosis o Allergy skin testing – Has to be red & raised ▪ avoid antihistamines & corticosteroid inhalers 2 weeks before testing ▪ Emergency equipment (resuscitation bag, suction, IV, drugs) for anaphylaxis o RAST (radioallerosorbent test) or fluroenzyme blood tests used to measure IgE levels to specific allergens o Pulmonary function measurements for allergic asthma o Blood test measuring levels of IgE (normal 39 IU/ml) o CBC may show inc eosinophils (normal 1-2%) • Allergic Disorders o Allergic Rhinitis ▪ Histamine causes capillary leak, nasal & conjunctival mucus secretion, & itching w/redness ▪ Allergic rhinitis has rhinorrhea (runny nose), stuffy nose, & itchy, watery eyes ▪ Clear or white nasal drainage, HA or feel pressure o Food allergy vs food intolerance ▪ 8 foods 90% of true food allergies – milk, eggs, peanut, tree nuts, shellfish, fish, soybeans & wheat ▪ Diagnosis & treatment are avoidance o Atopic dermatitis ▪ No cure but goal is to control symptoms with antihistamines & topical steroids ▪ Lesions red, itchy, contain exudates – may be drier in elderly ▪ Lesions typically found on cheeks, scalp, & forehead o Urticaria “hives” ▪ Papules or plaques that often fade within 24 hrs. ▪ If hives last over 6 weeks – chronic urticaria ▪ ASA & NSAIDS can exacerbate hives- ▪ Antihistamines mainstay of treatment o Anaphylaxis (Distributed Vasodilated Shock) ▪ Most common causes drugs, food, latex exposure, insect bites & stings (BEES) ▪ Symptoms • Often present with hives, angioedema, dyspnea & wheezing • Syncope, hypotension • N&V, diarrhea, abd pain • Flushing, headache, rhinitis, itching • CV collapse, shock, resp tract obstruction ▪ Symptoms can begin 5-30 min after encountering trigger or be delayed an hour or more ▪ Treatment • Assess respiratory status, airway & O2 sat (do not run and get a probe) • Call the Rapid Response Team • Oxygen via non rebreather 90-100% and have intubation/tracheostomy equipment ready • 1st - Immediately discontinue IV drug and changing the tubing and hang NS • Prepare to administer Epinephrine IV OR EPI PEN • Elevate HOB 45 degrees if BP normal, 10 degrees if hypotensive • Reassure patient frequently • Medical/Nursing Management o Identify allergen & avoid if possible o Medications ▪ Antihistamines - diphenhydramine – 2nd line drugs (angioedema & urticaria) ▪ Decongestants – most OTC – are sympathomimetic ▪ Steroids – 2nd line drugs • Nasal sprays – beclomethasone, triamcinolone, fluticasone (limit 5 days at a time) • Topical creams for dermatitis - hydrocortisone • Oral – have systemic effects also - prednisone • Inhaled steroids for allergic asthma – fluticasone, salmeterol o Desensitization – allergy shots • Latex Allergy o Type 1 hypersensitivity reaction o People at greatest risk for developing a latex allergy are those with high exposure to natural latex products like patients with spina bifida, frequent use of latex condoms and healthcare workers. o Allergic to bananas, avocados, and some nuts more likely to have latex allergy HIV/AIDS • Infection w/ human immunodeficiency virus (HIV) results in destruction of the body’s defenses & immune system • Risk Factors o Virus is spread through sexual practice (primary), exposure to blood & body fluids and through perinatal o Male homosexual activity still greatest risk for most Americans o Increased risk with IV drug users, women & heterosexuals noted recently o Women over 50 acquire HIV primarily through heterosexual contact o IV drug use accounts for largest number of HIV infections through exposure to infected blood o Accidental needle stick exposure poses greatest hazard to healthcare workers o Standard Precautions markedly reduce healthcare workers exposure • Pathophysiology o Retrovirus infects T helper cells, macrophages & B cells o Normal CD4+ T cell level is 500 – 1600/mm3 – Decrease w/age o With CD4+ T cell level < 200/mm3 - infection is likely to develop o Antiretrovirals inhibit ability of virus to enter cells or replicate, reduce amount circulating virus & halting its destructive activity o Usually at least two to three drug protocol o 5 % of HIV people after 10 y show no progression and are called long-term non-progressors (LTNP’s) o Main target of HIV is immune system but also damages other parts of body as a result of HIV in body tissues ▪ Cranial & peripheral neuropathies ▪ Cardiomyopathy ▪ Pneumonitis ▪ Malabsorption in small intestine ▪ Nephritis ▪ Arthritis, psoriasis ▪ Adrenalitis ▪ Anemia, granulocytopenia, thrombocytopenia • Clinical Manifestations—Must know o Classification based on: ▪ CD4+ T cell counts, viral load (amount of virus present in the body) ▪ Clinical presentation o Primary infection–initial period after a person acquires HIV ▪ Fever, fatigue, lymphadenopathy, N/V ▪ HA, truncal rash, ulcers of mouth & genitals, thrush, pharyngitis, diarrhea, hepatomegaly, myalgia, arthralgia, leukopenia ▪ CD4+ count may rapidly drop to below 100/mm3 (But rebounds) ▪ This is the time when antibodies are developed but not detected for 4-12 weeks – seroconversion • HIV enzyme immunoassay – if positive Western Blot is performed to confirm HIV infection ▪ Preliminary studies show that starting retrovirals at this time can prevent damage to the immune system and other body systems • Once you start the antiretrovirals you cannot come off of them ▪ Some not dx bc of mild sx, not seeking medical attention or healthcare professional does not recognize & take adequate hx (symptoms can mimic mono) • AIDS criteria o CDC definition - patient has AIDS if he or she is infected with HIV & presents with ONE of the following: o A CD4+ T-cell count < 200 OR o Patient has one of the defining illnesses ***NO DROPLET OR CONTACT, ONLY STANDARD*** ▪ Candidiasis of lung, bronchi, or esophagus; Coccidioidomycosis; Cryptosporidiosis; CMV; TB; Histoplasmosis; Kaposi’s sarcoma (cancer); Pneumocystis Jiroveci Pneumonia (kills most AIDS pt.) ▪ Defining illnesses usually do not make us sick, with a heathy Immune system (standard precautions) EXCEPT for TB which needs airborne and standard. • Until parameters other than a skin test come back negative for TB in a pt w/ AIDS who has TB sx, maintain airborne precautions along with standard precautions. • Complications o Opportunistic infections–CMV(visual disturbances), pneumocystis o Kaposi’s sarcoma ▪ Most common AIDS related malignancy ▪ Small, purplish brown, raised lesions on skin or mucous membranes, not painful or itchy • Painful if large lesions, open, and weeping ▪ Make-up ok if lesions are closed ▪ With HAART therapy many lesions will disappear o AIDS dementia– most antiretrovirals do not cross the blood brain barrier o Wasting syndrome– HIV affect absorption in small intestine • Clinical Management o Medication administration ▪ Antiretrovirals • Inhibits viral replication, but doesn’t kill the virus • Offer treatment asymptomatic with CD4+ < 250-300 • CD4+ >350 can defer if asymptomatic or consider if viral load is high • Buffalo humps or cervical (neck) fat development & lg abd fat accumulations ▪ HAART – Highly Active Antiretroviral Therapy, uses 4 classes of antiretroviral to reduce viral load, improve CD4+ T-cell counts, and slow disease progression • Multiple drugs taken to prevent drug resistance • Drugs need to be taken correctly 90% of the time forever • Missed doses of drugs contributes to drug resistance due to inc viral replication • Drawbacks o Expensive, food and timing requirements, significant s/e o IRIS – Immune Reconstruction Inflammatory Syndrome ▪ T-cells slowly rebound and generate inflammatory reaction from opportunistic infections ▪ High fever, chills, and worsening of infection (ex. TB becomes worse) ▪ Tx with short term corticosteroids to reduce inflammatory response o Preventing infection (when neutropenic, low WBCs) ▪ Clean toothbrush weekly by running it through dishwasher or bleaching ▪ Avoid fresh fruits and veges; undercooked meats, fish, and eggs; and pepper and paprika ▪ Do NOT drink water, milk, juice that have been standing for longer than 1 hour ▪ Do not change pet litter boxes, if unavoidable, use gloves & wash hands ▪ Take temp once a day and report if > 100, have persistent cough, cloudy urine, etc. ▪ Do not dig in garden or work with houseplants o Pain management - esp. with neuropathies ▪ Pregabalin (Lyrica), TCAs- amitriptyline (Elavil) ▪ Anticonvulsants- gabapentin (Neurontin), phenytoin (Dilantin), carbamazepine (Duragesic) ▪ Opioids – hydrocodone, tramadol, or codeine, oxycodone, morphine, hydromorphone or fentanyl o Maintenance of skin integrity • Client education o Recurrent labs o Annual TB test o PAP test- every 6 months o Chest x-rays o Long term medication, dosing, S/E, timing around the clock o Diet high in calories and protein, 2-3 L H2O, avoid fatty foods (causes diarrhea) due to intolerance from s/e of antiretrovirals. • Home care and infection spreading control o Do not share razors or toothbrushes o Wipe up body fluids, flush, and clean area with bleach o Needles or sharps in coffee can or bleach bottle & decontaminate when full w/bleach, seal w/tape, place in paper bag, and put in regular trash o Condoms all the time Organ Transplants • Contraindications to Transplant o Presence of active systemic infection o HIV/AIDS o Malignant disease(except skin cancer) o Active peptic ulcer disease o Active abuse of alcohol or other substances o Severe damage to organ systems other than one to be transplanted (ex. Cardiac Disease) o Severe psychiatric disease- to where they can’t understand and follow the post-transplant protocol o Demonstration of past or current inability to comply with a prescribed medical regimen o Lack of a functional social support system o Lack of resources to pay for surgery, hospitalization, medication, and follow up care • Nurses Role in Organ Donation o Identifying potential donors, notifying OPO, assisting in management of donor ▪ In Kentucky & S. Indiana all hospital deaths must be called to KODA ▪ Potential brain death with low GCS must be called prior to death o Preparation of recipient – organs have limited viability outside the body ▪ Heart 4 - 5 hrs ▪ Lung 4 - 6 hrs ▪ Liver 24 - 30 hrs ▪ Pancreas - 24 hrs ▪ Kidney – 48 – 72 hours- often a 72 hr kidney will need dialysis before it starts on its own • Hyperacute Graf t Rejection o Within 48 hrs after surgery o Caused by presence of antibodies – results in organ necrosis o Prevented by histocompatibility testing, crossmatching & PRA (preformed reactive antibody) testing o Tx w/ plasmapheresis - but if it fails the patient needs a new organ transplant o Diagnosis is made based on serologic labs, physical assessment data & hemodynamic measures • Acute Graf t Rejection o W/i first three months after transplant o Either a cellular immune response mediated by T cells or an antibody mediated response or a combination o Diagnosis is made based on clinical manifestations, labs & results of a biopsy o S/S of acute graft rejection ▪ Fever ▪ Graft tenderness ▪ Fatigue ▪ Heart – SOA, irregular heartbeat ▪ Lung – SOA ▪ Liver- tachycardia, RUQ or flank pain, diminished bile drainage, change in bile color, inc jaundice ▪ Pancreas- kidney issues occur before pancreatic problems; high glucose levels is a late sign ▪ Abnormal Labs • Kidney – inc BUN & creatinine • Liver - inc total bilirubin & liver enzyme levels (AST and ALT) • Pancreas – inc urine amylase/lipase, inc creatinine • Heart- BNP ▪ Diagnosis of rejection is by organ biopsy (both acute & chronic rejection) ▪ Treatment of acute rejection is called rescue therapy and includes: DON’T NEED TO KNOW NAMES • High dose steroids • Muromonab-CD3 (Orthoclone OKT3) • Antilymphocyte globulin • Includes 2-3 antirejection meds, to further immunosuppress - high risk for infection • Chronic Rejection o Gradually during period of months to years, after the first 3 months after transplantation o May be a result of frequent acute rejection episodes, increased ischemic time, or CMV infection o Usually slow progressive loss of graft function o Transplanted organ develops persistent perivascular inflammation associated with local myocyte necrosis o Treated like acute rejection & new organ transplant may be needed • Other Post Transplant Issues o Infection ▪ Leading cause of morbidity & mortality after transplant ▪ Results from immunosuppression or altered immune defenses ▪ First month postop – nosocomial infections common ▪ 1-6 months – opportunistic infections - pneumocystis carinii, candida, & CMV ▪ Lungs are most common infection site followed by blood, urine, & GI tract o Malignancy ▪ Development of post-transplant malignancy is well documented ▪ Basal cell & squamous cell skin & lip cancer, Ca of vulva, perineum & lungs ▪ All patients should be screened for [Show Less]
NUR 265 Exam 3 Study Guide & Exam Questions and Answers Increased ICP (939-940, chart 941) • Normal ICP 10-15 mmHg, pressures >20 mmHg impair cerebral ... [Show More] circulation • IICP is leading cause of death from head trauma in pts who reach the hospital alive. • Cerebral Perfusion Pressure (CPP) o Blood flow required to provide adequate oxygenation & glucose for brain metabolism o Maintenance above 70 mmHg o CPP= MAP-ICP ▪ MAP= (2xD) + S MAP NEEDS TO BE ATLEAST 80 3 • Compensation o First Response – CSF is shunted or displaced into the spine (compliance) o Next – Reduction of blood volume in the brain (autoregulation) o As ICP continues to increase cerebral perfusion decreases leading to brain tissue ischemia, edema, vasodilation then acidosis which causes further increases ICP o In edema remains untreated the brain may herniate into spinal canal – death from brain stem compression • Assessment Findings o Changes in LOC – First sign of IICP is declining LOC & includes restlessness or confusion to Stuporous ▪ W/o glucose & 02, brain shuts down. Ex. Pt knew who you were in am & now don’t remember o Headache – Quite environment may have photophobia so keep room lights very low. o Change in speech pattern – Aphasia, Slurred Speech o Changes in pupil size – 2 cm change in either direction is significant, dilated or constricted, Notify Dr ▪ Normal is 6 mm. Getting better if going back toward normal from dilated or constricted ▪ Uneven pupils tx as IICP until proven otherwise; pinpoint - brain stem (pons) dysfunction o Abnormal Posturing – Decorticate (flexion) or Decerebrate (extensor) ▪ Decorticate – arms drawn to core, legs straight ▪ Decerebrate – arms straight and stiff, pts rarely survive o Hyperthermia – followed later by hypothermia ▪ When hypothermic – BE CONCERNED, pressure on hypothalamus located next to brain stem o Cardiac & respiratory rate/rhythm changes ▪ Tachy first – Increased HR & RR before brady HR & RR o N/V – Common in IICP o Cushing’s Triad – Severe HTN, Widened Pulse Pressure, Bradycardia ▪ Late response & indicates severe IICP w/loss of autoregulation, Imminent death ▪ Systolic BP increases bc decreased blood flow to brain ▪ Pressure on Vagus nerve and brainstem = bradycardia • Managing IICP o Elevate HOB 30-45 degrees (unless contraindicated) ▪ If hypotension, elevate HOB where CPP >70 o Maintain head in a midline neutral position o Avoid sudden and acute hip or neck flexion during positioning – Log roll pt o Avoid clustering of care (bath followed by linen change) o Coughing and suctioning increase ICP o Decrease cerebral edema – osmotic diuretics (mannitol) & fluid restriction ▪ Mannitol is hypertonic- pulling fluid into vascular space- will inc. fluid output & monitor BP for HTN ▪ Furosemide used in adjunct to reduce incidence of rebound from mannitol. Helps reduce edema & blood volume, decrease Na uptake by the brain, & decrease production of CSF at choroid plexus. o LOW CSF using intraventricular drain system o Control fever w/antipyretics or cooling blanket – do not allow pt to shiver as will increase ICP ▪ When febrile every cell in body needs more 02 and glucose o Oxygenation – Hyperventilate on a vent to decrease CO2 which causes vasodilation o Reduce cellular metabolic demands – barbiturates (-bital, -barbital) and/or sedation (coma) Traumatic Brain Injury (946-957) • Primary Brain Injury o Occurs at time of injury o Open – Head fractured or penetrated; Closed – Blunt trauma, shaken baby o Open Head Injuries ▪ Skull Fractures • Linear Fx – thin line on x-ray, no tx unless underlying brain tissue damaged • Depressed Fx – Brain damage from bruising (contusion), laceration from bone fragments • Basilar skull Fx – Fx of bones of the base of skull & results in CSF leak from nose & ears. o May not be seen on plain x-ray, R/F Infection w/ CSF leak o Manifested by bruises around eyes(raccoon eyes) or behind ears (Battle’s sign) o Has potential for hemorrhage if it damages the internal carotid o Closed Head Injuries ▪ Caused by blunt force trauma ▪ Contusion – Bruising to brain tissue @ site of impact (coup) or opposite (contercoup) ▪ Laceration – tearing of the cortical surface vessels, lead to secondary hemorrhage, cerebral edema and inflammation ▪ Diffuse Axonal Injury (DAI) – Tissue of entire brain from high speed acel/decel MVC • Impaired cognitive functioning, results in disorganization, impaired memory • Severe will present with immediate coma, survivors require lone-term care o Classified as ▪ Mild – GCS 13-15 (concussion) • Blow to head, transient confusion, or feeling dazed or disoriented • Loss of consciousness for up to 30 min, loss of memory before and after accident • No evidence of brain damage, sx resolve w/i 72 hrs • Sx: HA, N/V, Fatigue, Foggy, Balance off, Irritable, Sad, Nervous, Emotional, Visual probs ▪ Moderate – GCS 9-12 • Loss of consciousness 30 min – 6 hrs w/ memory loss up to 24 hrs. • Short hospital stay to prevent secondary injury • Memory loss up to 24 hrs. ▪ Severe – GCS 3-8 • Loss of consciousness >6 hrs • High risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion • Pupil changes, Bradycardia, Papilledema, HTN w/wide PP, Nuchal rigidity if CSF leak o Glasgow Coma Scale ▪ Score from 3-15; score 3-8 in a coma ▪ A change of 2 points requires immediate notification to HCP • Secondary Brain Injury o Any process that occurs after the initial injury and worsen or negatively influences patient outcomes. ▪ While trying to recover from initial event, something else happens (ex: meningitis) o Most common result from hypotension, hypoxia, IICP, & cerebral edema ▪ Damage to brain tissue due to delivery of O2 and glucose to brain is interrupted ▪ Low blood flow and hypoxemia contribute to cerebral edema o Hypotension & Hypoxia ▪ hypotension (MAP <70), hypoxia (PaO2 <80) ▪ Hypotension may be from shock & hypoxia from resp. failure, loss of airway, or impaired ventilation o Increased Intracranial Pressure (IICP) ▪ See Increased ICP section above o Hemorrhage ▪ Begins at moment of impact & potentially life threatening ▪ Epidural Hematoma – Arterial bleeding between dura and inner skull, from fx of temporal bone • Have “lucid intervals” – Pt awake & talking then momentary unconsciousness ▪ Subdural Hematoma – Venous bleeding into space beneath dura & above arachnoid • From laceration of brain tissue, bleeding is slower than epidural, Highest mortality rate • Acute SDH – w/i 48 hrs after impact • Subacute SDH – 48 hrs – 2 weeks • Chronic SDH – 2 weeks to several months ▪ A loss of consciousness from an epidural or subdural hematoma is a neurological emergency! o Hydrocephalus – abnormal increase in CSF volume ▪ Caused by impaired reabsorption or blockage with outflow of CSF, leads to IICP o Brain Herniation ▪ Uncus- dilated non-reactive pupils, ptosis, decreased LOC ▪ Central – Down shift brain stem – Cheyne-Stokes, Pinpoint & nonreactive pupils, hemodynamic instability. NOTIFY PHYSICIAL IMMEDIATELY • Etiology o Young males, play more sports, take more risks when driving (MVC), consume more alcohol o Falls most common in older adults. • Assessment/Interventions o Hx – Did pt lose consciousness? Drug or alcohol consumption? All screened for abuse/neglect o Physical ▪ First priority is assessment of ABCs - Report any sign of respiratory problems immediately! ▪ Suspect neck injury until proven otherwise, stabilize w/ C-Collar and backboard • Skin breakdown & pressure ulcer formation are concern with spine board & c-collar • Once board removed, spinal precautions maintained until HCP indicates it is safe o (1) Bedrest; (2) No neck flexion with a pillow or roll; (3)No thoracic or lumbar flexion w/HOB elevation (reverse T acceptable); (4) Manual control of C spine anytime collar removed; (5) Log roll ▪ Prevent secondary brain injury – O2 & lowering ICP, Vent if needed, do not want CO2 to rise as it causes vasodilation & IICP. o Vital Signs ▪ Monitor VS Q 1-2 hrs – May be hypotensive or hypertensive (IV fluids to maintain above 90) ▪ Central fever caused by hypothalamic damage – no sweating, high, last days-weeks • Responds better to cooling (sponge bath, cool air) • Fever from any cause is associated w/higher mortality rates ▪ Cushing’s Triad – HTN, Wide PP, & Bradycardia – late sign of IICP and indicates imminent death ▪ Hypotension and tachycardia indicate hypovolemic shock o Neuro ▪ GCS ▪ Most important variable to assess w/any brain injury is LOC ▪ Dec or change in LOC is first sign of deterioration (behavior changes, restlessness, disorientation) ▪ Assess pupils • Pinpoint - & nonresponsive – Brainstem dysfunction @ level of ponds • Asymmetric, loss of light reaction, unilateral or bilateral dialed – herniation o Late signs of IICP – severe HA, N/V, seizures, papilledema - always sign of IICP ▪ Motor response - Decorticate or Decerebrate posturing o Psychosocial ▪ Personality changes – temper outbursts, depression, risk-taking, denial, talkative, outgoing o Therapeutic Hypothermia ▪ Rapidly cool pt to 89.6 – 93.2 for 24-48 hrs after primary injury to reduce brain metabolism and reduce secondary brain injury. o Mechanical ventilation ▪ Maintain PaCO2 at 35 to 38 to prevent IICP from vasodilation from CO2 ▪ Maintain PaO2 between 80-100 to prevent secondary injury ▪ Lidocaine given IV or endotracheally to suppress cough reflex; coughing increases ICP o Drug Therapy ▪ Mannitol through a filter • Reduces edema and blood volume, dec Na uptake by brain & dec CSF production • Used with furosemide to reduce rebound from Mannitol & enhances therapeutic action • Foley catheter for strict I&O, check serum (want 310-320) and urine osmolarity daily. ▪ NO Steroids are effective ▪ Propofol & dexmedetomidine – sedative agents with short ½ life ▪ Morphine or fentanyl in vented pts to dec agitation & restlessness if caused by pain. • Fentanyl is safer. Both reversed with naloxone. ▪ Antiepileptic drugs – phenytoin to prevent seizures ▪ Acetaminophen or aspirin for fever >101 if not from central fever (cooling only) ▪ Barbiturate Coma • Pentobarbital or thiopentone - For IICP that can’t be controlled • Dec metabolic demands of brain, requires vent, hemodynamic & ICP monitoring. • Complications – dec GI motility, dysrhythmias from hypokalemia, hypotension, fluctuations in body temp • Surgical Management o Insert ICP monitoring through burr hole (key hole craniotomy) - maintain w/strict sterile technique ▪ Be sure to provide head to toe assessment even though pt ICP being invasively monitored o Decompressive Craniotomy ▪ Removal of section of the skull – allows space for edema w/o Increasing ICP ▪ DO NOT LAY PT ON THE SIDE WHERE THE SKULL FRAGMENT WAS REMOVED. ▪ Pt must wear helmet when out of bed • Pt & Family Education for self-management – MILD BRAIN INJURY o Acetaminophen for HA Q 4 hrs o Avoid sedatives, alcohol, sleeping pills for at least 24 hrs o No strenuous activity for 48 hrs o Monitor or assist movement due to balance disturbances o If these sx occur bring back to ER ▪ Severe HA; Worsening HA; Persistent or severe N/V; Blurred vision; Drainage from ear or nose; Weakness; Slurred speech; Progressive sleepiness; Unequal pupil size • Interdisciplinary Care o Rehab specialists o Speech & Language Pathologists (SLP) o Dietitian o Rehab therapists o Severe brain injury requires lone-term case management & ongoing rehab o OT, PT, SLP, & home evaluations after discharge for severe Cerebral Aneurysm (chart 940) ● Intracranial aneurysm – weakness in a cerebral blood vessel wall, Saccular or berry most common in the head ● AV Malformations – Tangled arteries and veins, blood shunted from artery to a vein, can bleed or thrombose o Pt. present with HA, seizures, or focal deficits o Once bleeds, has 25% chance of bleeding again ● Surgery o Surgical ligation or resection (Open) ▪ Surgical removal of AVM or aneurysm, care same as craniotomy o Clip (Open) ▪ Clamp over aneurysm base to isolate, movement can occur ▪ Close attention on neuro to detect early rebleeding or migration of the clip. Changes in cognition or new focal neurologic deficits must be communicated urgently to the surgeon. o Coil: with stent assist; with balloon assist ▪ Detachable coils placed under fluoroscopy to occlude aneurysm w/o interrupting main vessel flow. ▪ Due to rebleeding risk, avoid drugs that interfere with the clotting during recovery ▪ Re-evaluation at 3, 6, and 12 months w/neurosurgeon to evaluate effectiveness ▪ Frequent neurologic assessments in first 24 hrs post procedure to detect intracranial bleeding. • Flow diversion o Shifting blood flow away from the vessel defect, resulting in a thrombosed (clotted) aneurysm over 5-6 mon o Full embolization takes 5-12 months, ongoing monitoring by the neurosurgery ▪ Teach pt to avoid strenuous activity or situations that create HTN while the prolonged embolization occurs • Liquid polymer embolization o AVMs only, used prior to surgical litigation or to tx small AVMs o may not provide definitive treatment ▪ Perform frequent neuro assessment in the 24 hours post-op to detect early signs of bleeding • Stereotactic Surgery o Microwave or radio beams are directed to the defective vessels to obliterate the defect. o Swelling around beam site may alter neurologic status o Inform neurosurgeon of ant deterioration in consciousness or new focal weakness or sensory changes. Brain Tumor (957-962) • Complications o Cerebral edema/brain tissue inflammation o IICP o Neurologic deficits o Hydrocephalus o Pituitary dysfunction – pressure causing SIADH or DI • Symptoms of a Brain Tumor o HA- more severe on awakening in the AM o N/V o Visual changes, diplopia o Seizures, Aphasia o Loss of balance or dizziness o Weakness or paralysis in one part or one side of the body o Changes in mentation or personality o Difficulty thinking, speaking, or articulating o Papilledema (swelling of the optic disc) indicating IICP [Show Less]
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