NURS 316 AHI Recap Exam II [Recommended/detailed]

NURS 316 AHI Recap Exam II Be sure to sure to use all of your resources to study: ATI, course notes and the course textbook. Priority & Delegation (5 questions) May use ATI Book from Fundamentals (p.25-28). You may also refer to see scanned pages on Blackboard *Priority & Delegation (5), SATA (5), and dosage & calculation (5) questions are a requirement for all professional phase nursing exams Dyslipidemia Risk factors for the development of HTN and hyperlipidemia HTN: Primary (Essential)- Obesity, smoking, stress, family history, age, & diet Secondary- Health conditions such as renal disease, Cushing’s syndrome, primary aldosteronism, pheochromocytoma, & also medications. Hyperlipidemia: Familial hypercholesterolemia, diabetes, HTN, smoking, abdominal obesity, strong family hx of premature cardiovascular disease (CVD) Dietary requirements for clients with elevated cholesterol. Avoid saturated fats and sodium DASH diet: soluble fiber, fruits, vegetables, & fish Anticipated assessment findings by the nurse for a client with PAD and PVD. PAD (affects arteries)- Result of systemic atherosclerosis. Chronic condition in which partial or total arterial occlusion (blockage) decreases PERFUSION to the extremities: Pain, stops at rest Pallor (pale) Pulselessness Paresthesia Paralysis Poikilothermia (coolness) Loss of hair, thickened nails Ulcers on toes, feet with possible gangrene & pain PVD (affects ANY blood vessel)- Alters natural flow of blood through arteries and veins of peripheral circulation  decreased PERFUSION to the extremities. Affects legs much more often. Usually implies PAD rather than venous involvement, but pts can have both. PAD Venous insufficiency Ache on dependency Pulses WNL Normal or cyanotic color Normal or slightly cool temp Edema present Brown pigmentation at ankles, skin thickened Ulcers on ankles with no gangrene or severe pain Cholesterol: less than 200 mg/dL Triglycerides: less than 150 mg/dL HDL cholesterol: 60 mg/dL (low is bad) LDL cholesterol: 60-130 mg/dL (high is bad) HTN Which medications discussed in Unit I: Fluids and Electrolytes are related to the treatment of patients diagnosed with HTN? What medication instructions are important to include? diuretics -get BP checked by HCP often (every 2 weeks) -encourage K rich diet (citrus fruits, potatoes) -check K labs (if K labs have not been drawn, suggest it to provider) -WATCH FOR IRREGULAR HEART RATE How is HTN identified and diagnosed? What are presenting clinical manifestations? Pregnancy, Cushing’s syndrome, chronic renal failure, diabetes, hypo/hyperthyroidism, & high BP x3 with same HCP. -usually none until it causes organ damage, sometimes an occipital headache may present but this is rare What are modifiable and non-modifiable risk factors for HTN as referenced in the textbook? smoking, stress (reduce stress response), & diet: avoid foods high in Na & cholesterol (red meat and visible fat); use EVOO and DASH diet race/genetics, family history, & age List blood pressure ranges for normotension (normal blood pressure), pre-HTN, Stage 1 and Stage 2 HTN as referenced in the textbook? Normotension: less than (less than 120)/(less than 80) Pre-HTN: (120-129)/(less than 80) Stage 1: (130-139)/(80-89) Stage 2: (140 )/(90 ) Identify treatment interventions for patients with normotension, pre-HTN, Stage 1 and Stage 2 HTN. What cardiovascular assessment parameters should the nurse follow when administering these medications? * Review HTN handout on Blackboard. -normotension: keep up good work -preHTN: life-style changes -stage 1 HTN: diuretics (combination) -stage 2 HTN: Anti HTN drugs and diuretics Assess vital signs: HR & BP. List common causes for primary HTN and secondary HTN discussed in class. Essential- not caused by an existing health problem. Lifestyle & genetics. Secondary- Caused by an existing health problem. List complications of HTN discussed in class, and key interventions to avoid each complication. HF, renal disease, arterial insufficiency, & venous insufficiency Na restriction, weight maintenance, diet, & complementary & alternative therapy. Explain the procedure for taking a two-step blood pressure measurement. How are the systolic blood pressure and a palpable blood pressure related? If only patient's carotid pulse is palpable, the systolic BP is 60-70 mm Hg. if carotid and femoral pulses are palpable, the systolic BP is 70-80 mm Hg. If the radial pulse is also palpable, the systolic BP is more than 80 mm Hg How do meds ending in ‘pril’ and ‘olol’ correspond to classifications of anti-HTN meds discussed in class? Which CV assessment parameters should the nurse follow when administering these meds? -pril (lisinopril): ACE inhibitors - Check K blood levels b4 administering. *Low K diet. -olol (Atenolol): Beta blockers- HR should be monitored bc cardio-selective Which dietary instructions should be included for clients taking anti-HTN medications? Dietary Approaches to Stop HTN (DASH) List key nursing interventions for HTN patients receiving ACE inhibitors. -assess for cough -avoid K substitutes (ACE inhibitors cause body to retain K ) -compliance (NEVER suddenly stop taking med to avoid rebound HTN) -take this med 1 hour BEFORE meals More common name for lipid-lowering meds aka HMG-CoA reductase inhibitors? 3 generic med exs of statin meds, 5 common side effects, and 5 nursing interventions? Statins 3 Generic Medications Atorvastatin (Lipitor) Simvastatin (Zocor) Lovastatin (Mevacor) 5 Common side effects: Abdominal cramps, constipation, diarrhea, heartburn, & rashes. 5 Nursing interventions: Evaluate serum cholesterol and triglyceride levels b4 initiating & periodically. Monitor liver function tests b4 initiating. If pt develops muscle tenderness during therapy, monitor CK (creatinine kinase) levels; if greatly elevated, discontinue med. Administer lovastatin w/ food at dinner. Avoid large amounts of grapefruit juice. HTN management (ABCD): Angiotensin-converting enzyme inhibitors/Angiotensin II receptor blockers (Can cause HYPERKALEMIA)- lisinoPRIL (ACE), ValsarTAN (ARB) Beta blockers- atenoLOL (BB- Not for use in HF or bronchial asthma) Calcium channel blockers- AmlodiPINE (CCB- ^ DIGOXIN levels) Diuretics- HydrochloroTHIAZIDE (diuretic) *electrolyte disturbances Secondary HTN causes: (ABCDE) Aldosterone/Apnea Bad kidney/Bruits Catecholamines/Cushing syndrome Drugs/Diet Endocrine HTN nursing interventions (DIURETIC) Daily weight Intake and output Urine output Response of blood pressure Electrolytes Take pulses Ischemic episodes (transient ischemic attack) Complications (four Cs) Coronary artery disease (CAD) Coronary rheumatic fever Congestive heart failure (CHF) Cardiovascular accident (CVA) Review Laboratory Profile (Chart 33-2) p.656 Immune/Hypersensitivity Reactions Discuss the nursing care for procedures and tests that diagnose hypersensitivity reactions. skin patch- done to determine which specific allergens, if any, cause an allergic reaction; they can also test for irritation place patch on arm or back for 48 hours and avoid activities that cause excessive sweating skin injection (intradermal test)- small amount of allergen is injected into skin the site should be examined for a reaction (the 5 ORs) after 15 mins -weal may form (looks like mosquito bite): glucocorticoids can be used to treat this -anaphylaxis may develop so the nurse should have the pt remain nearby for 20-30 min to be sure they will not go into shock blood tests (RAST test and WBC): can test for x reactions at once. Blood test that evaluates the severity of an allergy by measuring how much IgE reacts with the allergen. On a scale of 0 to 5 (higher the # the likely for a reaction to allergen) Discuss the anatomic locations and functions of immunoglobulins synthesized in response to allergens: IgA, IgD, IgE, IgG, IgM. IgA (Active, have disease)- located in secretions such as mucous membranes and intestinal mucosa prevents infection in upper and lower respiratory tract, GI, and GU tract IgD- found mostly on surface of B-lymphocytes plays a role in B cell activation and works w/ IgM so they are both present in low blood concentrations IgE (Everywhere)- acts as a mediator of many allergic responses by inactivating the allergen least concentrated immunoglobulin. defends against parasitic invasions IgG (Gone, don’t have disease)- most abundant of IGs (makes up 75%) levels increase on 2nd and subsequent exposure to allergen to provide LONG TERM IMMUNITY enhances neutrophils and macrophage actions IgM (immediate, not sure if have disease)- initial antibody produced after an infection) makes up 10-15% of all immunoglobulins and is the largest performs agglutination and precipitation activates complement pathway Describe with examples types of immunity: natural, artificial (acquired), active, passive Natural- exposure to disease or microorganism, producing antibodies. Natural active- exposure to a live pathogen, develops the disease, and becomes immune ex: chicken pox Natural passive- something else or someone else makes antibodies Ex: babies can get antibodies from mom through placenta or breast milk Artificial/acquired- Purposely inject antigen so immune system can respond and make antibodies Artificial/acquired active- vaccine Artificial/acquired passive- injecting antibodies Active- antibodies develop after exposure to an antigen thru disease or vaccine. Passive- antibodies produced artificially are being injected List strategies that promote antibody-mediated immunity. Children ***FOLLOW IMMUNIZATION SCHEDULE -get Heb B shot at birth (within 24 hours of life), again at 2 months, and again at 1 year -also at 2 months: get TDAP, Hib, IPV, PCV, RV Adults- **FOLLOW IMMUNIZATION SCHEDULE -age 60 and older: get herpes zoster (shingles) vaccine -age 65 and older: get pneumococcal vaccine (get it when younger if smoker) -get flu shot every 6 months Discuss nursing interventions for the client admitted to the nursing unit with a latex allergy. Mild- contact dermatitis: rash, urticaria, itching, and/or redness Severe- anaphylaxis; usually occurs due to an inhalation reaction Nursing interventions: -educate pt about S&S of latex reaction and products that contain latex -pt should have ID band stating they have a latex allergy -latex free room (aka avoidance therapy) -sign should be posted above room door and above bed stating allergy -manage allergic reaction (proper meds, EpiPen, & all members of healthcare team should be notified) Describe clinical manifestations and immune system components/cells involved in Type I, Type II, Type III, and Type IV hypersensitivity reactions. Type I (Rapid hypersensitivity reactions/Atopic allergy)- immediate (occurs within minutes) or IgE-mediated. IgE antibodies attached themselves to mast cell receptors which causes the mast cell to release histamine and other inflammatory mediators that is toxic to both the allergen and host cells. Typically causes anaphylactic shock. *Mast cells Latex allergy Clinical manifestations: -Most common- rhinitis -clear rhinorrhea -sneezing and sinus pressure -itchy, watery eyes -headache and itching Type II (Cytotoxic reactions)- antibody-dependent process in which specific antibodies bind to antigens, resulting in tissue damage or destruction. Hemolytic anemias Immune thrombocytopenic purpura – (ITP) Hemolytic transfusion reactions Goodpasture’s syndrome (glomerulonephritis) Type III (immune complex reactions- rheumatoid arthritis or systemic lupus erythematosus)- Excess antigens cause immune complexes to form in blood. Circulating complexes lodge in small blood vessels. Clinical manifestations: Kidneys, skin, joints - inflammation and tissue damage. Type IV (delayed/ t-cell mediated)- T-lymphocytes cause a reaction. Clinical manifestation: edema, redness, fever, and tissue damage. 3 common examples -contact dermatitis (Latex “allergy”- inflammation of skin d/t chemicals NOT latex) -Purified Protein Derivative (PPD): wheals may form -Local response to insect stings. -tissue transplant rejections Pain Management What is the purpose of a symptom analysis for pain assessment? to gather subjective data (most reliable indicator of pain. most comprehensive way of assessing pain OPQRSTUAAA How should the nurse validate the client's c/o severe pain? using objective data as well as a pain scale Define acute pain; define chronic pain. How are they similar? How are they different? Acute- pain that last for 3 months or less and has a sudden onset. usually linked to specific tissue injury Chronic- pain that is present for longer than 3-6 months Similar: Can be both a nursing dx and medical dx, nursing interventions for both are similar Different: Pt behavior may be different depending on whether or not pain is acute or chronic, vital signs different, timing different What is the purpose of acute pain? of chronic pain? warning sign that something is wrong none Describe 2 categories of nociceptive pain; give a postoperative example of each. Midline incision from surgery, goes from xiphiod process to top of umbilicus Debridement: done after burns to remove eschar (hardened slough that looks like leather; it is hard; traps bacteria. can be grey, green, yellow, and black) Describe 3 causes of postoperative neuropathic pain. -phantom limb pain (after amputation) -infection (can cause neuritis) -diabetic neuropathy Define 4 types of pain with respect to location. -nerve pain -somatic pain (skin, muscle, skeletal) -radiating pain (starts in one area and spreads until a larger area hurts) -referred pain (ex- pain from the pancreas, which is felt in the back.) Describe non-pharmacologic methods of pain relief. -prayer and meditation -repositioning -exercise/ physical therapy -music -TV (contraindicated in pt's with Meinere's disease) -cold (decreases swelling and functions as an anesthetic) and warm compresses (RICE) -deep breathing Discuss medication teaching instructions for the client who has been prescribed opioid analgesics for postoperative pain relief. can cause constipation: prevent Colace from working which is a laxative that makes you have a BM; PRUNE JUICE IS HIGH IN FIBER -FFA (fluids, fiber, ambulate) -respiratory assessment -assess pain -encourage pt to monitor who has access to his or her meds What are the most severe side effects of opioid analgesics? of NSAIDs? Opioid analgesics- respiratory depression NSAIDs- Renal failure, bleeding Discuss medication teaching instructions for the client who has been prescribed fentanyl patches for pain relief. -wash area w/ mild soap and water after removing old patch -DO NOT use alcohol to remove patch -dispose old patch in sharps Discuss best-practice procedures for the client receiving round-the-clock pain medication. Call HCP if pain gets worse or if it does not get better in about 3 days Discuss the nurse's role in assessing the client with a high pain tolerance, with a low pain tolerance. High- tell them they are doing well; appeal to culture or behaviors to get them more comfortable with you Low- get OBJECTIVE signs, listen to whatever pt says about pain (you must believe them) -they usually have anxiety so sit down with pt and use therapeutic use of touch and self and encourage deep breathing Adjuvant analgesics are effective against which type of pain? -antidepressants that are effective against neuropathic pain when prescribed with another milder analgesic. Discuss purpose and components of the WHO Analgesic Ladder. to classify pain and organize treatment -mild to moderate pain (1-3) **Non-opioids -aspirin -NSAIDs -paracetamol moderate to severe pain (4-7) -mild opioids (ex- codeine) with or without non-opioids severe pain (8-10) -Strong opioids (ex- morphine) with or without non-opioids Pain types Nociceptive pain- Normal pain as result of actual/potential tissue damage or inflammation. Somatic- arises from skin & musculoskeletal structures Visceral- arises from organs Neuropathic pain- Abnormal pain as a result of damage/dysfunction of PNS &/or CNS. “burning”, “shooting”, “tingling”, “feeling pins and needles”