Understanding Glaucoma, Diabetes, and Hypertension: Symptoms, Treatments, and Management, Exams of Health sciences

Download Understanding Glaucoma, Diabetes, and Hypertension: Symptoms, Treatments, and Management and more Exams Health sciences in PDF only on Docsity! 1 NSG 331 Exam 2 Study Guide, Best Solution..Latest Visual and Auditory Problems module (1 part) not as heavily covered as other 2 mods WebEx Notes o Eyes and ears not part of Final exam o Glaucoma, MD, Cataracts - know treatment, clinical manifestations o Hearing- know nursing care of the hearing impaired • Glaucoma *pressure & peripheral vision* • [Lewis Table 20.12, 20.13] o Normal intraocular pressure: 10 to 21 mm Hg o Can lead to structural damage. ▪ Optic nerve damage ▪ Loss of peripheral vision o Inflow > outflow  IOP increases  vision loss o Risk Factors ▪ Black people over 40 ▪ All persons over 60 ▪ Family history!! • Strong genetic link ▪ Open angle • Blockage is NOT at the entrance , but inside • Primary Open-Angle Glaucoma (POAG) o Most common: 60% of all glaucoma o Slow onset- S/S are often unnoticed because no pain or pressure. o Usually bilateral, leads to tunnel vision o Common in diabetics o Cause o Blockage of aqueous fluid drainage  increasing IOP  cupping of the optic disc  destroys retinal nerve fibers  painless vision loss. o IOP: 22 – 32 mm Hg • Symptoms o Asymptomatic early o Change in peripheral vision o Bumping into objects o Many assume normal aging changes o Dx: elevated IOP (22-32mm/Hg), visual field loss, cupping of optic nerve • Treatment o Medications ▪ Miotic Drops • pupil constriction and reduce formation of aqueous humor • Sx: burning, blurred vision ▪ Beta Blockers 2 • Decreases production of aqueous humor • Sx: burning, tearing, slowed HR, fatigue ▪ Topical Steroids 5 ▪ Diabetes mellitus o Common ▪ 25% of population, over 55. Over 22 million globally o Myths ▪ Not caused by over-using eyes, Not contagious or R/T cancer, Not a film or coating, Not spread from eye-to-eye o Symptoms ▪ No known means to reverse clouding ▪ Usually bilateral ▪ Like looking through foggy window ▪ Painless, progressive loss of vision ▪ Abnormal color vision ▪ Glare, esp at night • Bad for night driving ▪ Amount of vision loss R/T location & degree of clouding o Treatment ▪ Prescription glasses • Central vision is corrected, peripheral vision is distorted • 30% magnification o Adjustment needed for ADL’s (judging distances) ▪ Surgery • Must assess vision of un-operative eye • Outpatient, one eye at a time • Removal of the clouded lens and replaced with an intraocular lens implant (IOL). o Allows the eye to focus again clearly • Proper eyewear can further enhance vision ▪ Sometimes informing and reassuring the patient about the disease process makes the patient comfortable about choosing nonsurgical measures, at least temporarily. o Post-op Care & Complications ▪ Care • After sedatives wear off, patients are usually go home. • Permanent glasses prescribed after 3 months • Usually discharged with eye drops • Call MD if increased pain in operative eye o PT SHOULD NOT HAVE PAIN • Avoid increase of IOP o Activities: bending or stooping, coughing, or lifting. • Clean inner  outer • Shaded lenses, eye shield o Nighttime eye shielding • Showers, hair washed with head held backward • Sex in 6-8 weeks • Postoperative medications o Antibiotic drops (prevent infection) o Corticosteroid drops (decrease post-op inflammation) • During each postoperative examination, the ophthalmologist will measure the patient’s visual acuity, check anterior chamber depth, assess corneal clarity, and measure IOP. ▪ Complications 6 • Hemorrhage into anterior chamber • Vitreous prolapse o Can lead to retinal detachment. Surgery needed • Intraocular infection o S/S: throbbing or painful eye, drainage o Tx: antibiotics • Meniere's disease [Lewis table 21.11] o Disorder that affects both vestibular and auditory function o Onset 30-60 years of age o Caused by excess endolymph in vestibular and semicircular canals o Remission and relapses without apparent causes o Aural: feeling of fullness in ear o S/sx: sudden attacks of vertigo, tinnitus, hearing loss, N&V o After attack: vertigo 2-4 hrs, dizziness, unsteadiness, gait changes, depression, moody, vital signs within normal limits, hearing loss o Care ▪ Bedrest ▪ Diuretics, corticosteroids, Na, caffeine, nicotine, alcohol restriction ▪ Stress reduction techniques ▪ Surgical • Endolymphatic sac decompression or shunt • Labyrinthectomy • Vestibular nerve section ▪ Drug therapy • Antihistamine, anticholinergics, benzos, antiemetics, antivertigo • Hearing loss [Lewis Table 21.14] o Conductive ▪ Outer or middle ear conditions prevent transmission of sound via air to inner ear ▪ Causes: otitis media, mastoiditis, impaction, foreign bodies, otosclerosis, presence of bone-air gap ▪ Person speaks softly ▪ Hearing aid o Sensorineural ▪ Impaired function of inner ear or vestibulocochlear nerve (CN VIII) ▪ Causes: hereditary, trauma, infection, immune dz, DM ▪ Sounds muffled ▪ Hearing aids may only make sounds louder, not clearer Diabetes Module (2 parts) Lewis Tables 48.1, 48.2, 48.10, 48.14, 48.15, 48.16, 48.17, 48.18, 48.19, 48.20, 48.21 WebEx Notes o Knowing type 1 and 2, hypo and hyperglycemia – what does it look like, what do we do for these, what teaching can we do (lot of teaching with DM) o Diabetes insipidus- has NOTHING to do with blood sugar- has more to do with fluids o Know normal blood sugar ranges, A1C, some electrolytes that play into this 7 Table 48.1: Differences between Type 1 & 2 pg. 1109 Table 48.2: Interprofessional Care • Diagnostic Assessment o History and physical exam o Blood tests: fasting BG, postprandial BG, A1C, fructosamine, lipid profile, BUN and serum creatnine, elecrrolytes, islet of cell autoantibodies o Urine analysis o BP o ECG (if indicated) o Funduscopic exam (dilated eye exam) o Dental exam o Neurological exam o Ankle-brachial index (ABI) o Food (podiatric) exam o Monitoring of weight • Management o Pt and caregiver teaching & follow-up programs o Nutrition therapy o Exercise therapy o Self-monitoring BG • Drug Therapy o Insulin o OA Type 1 diabetes • Cause o Autoimmune disorder in which the body develops antibodies against insulin and/or the pancreatic β cells that produce insulin. This eventually results in not enough insulin for a person to survive. o Autoantibodies to the islet cells cause a reduction of 80% to 90% of normal function before hyperglycemia and other manifestations occur. ▪ May take months to years before S/S occur • Clinical Manifestations o Onset is rapid, 1st manifestations are usually acute o Polyuria, polydipsia & polyphagia (3 P’s) ▪ Osmotic fx of excess glucose  polydipsia & polyuria ▪ Cellular malnourishment from insulin deficiency prevents cells from using glucose for energy  polyphagia o Weight loss b/c body breakdowns fat for energy ▪ Ketoacidosis can occur b/c of this • Insulin o Storage of insulin ▪ Do not heat/freeze ▪ In-use vials may be lef t at room temperature up to 30 days ▪ Extra insulin should be refrigerated ▪ Avoid exposure to direct sunlight, extreme heat or cold ▪ Store prefilled syringes upright for 10 ▪ Prolonged wound healing ▪ Vision problems • Collaborative care including oral anti-diabetic meds o OAs and noninsulin injectable agents work to improve the mechanisms by which insulin and glucose are produced and used by the body. o These drugs work on three defects of type 2 diabetes: ▪ (1) insulin resistance ▪ (2) decreased insulin production ▪ (3) increased hepatic glucose production. o Recommend holding oral agents during acute illness and changing the patient to insulin management during their hospitalization. ▪ Prior to discharge, the patient is converted back to their oral agent regimen. o Many oral agents need to be timed with the meal patterns of the patient. o Oral Agents ▪ Sulfonylureas: Glyburide • Increase insulin production from the pancreas. • Major Sx: hypoglycemia ▪ Biguanides: Metformin • Reduces glucose production by liver • Enhances insulin sensitivity • Improves glucose transport • May cause weight loss • Discontinue metformin before surgery or the radiologic procedures w/ a contrast medium o Do not resume taking until 48 hours after and after their creatinine has been checked and is normal ▪ Alpha Glucosidase inhibitors: Acarbose • Aka starch blockers • work by slowing down the absorption of carbs in small intestine • Take with first bite of food ▪ Meglitinides: repaglinide • Increase insulin similar to sulfas but at slower rate o Less likely to cause hypoglycemia ▪ Thiazolidinedione: pioglitazone ▪ Dipephdyl Peptidase -4 Inhibitors: sitagliptin ▪ SGLT2 inhibitors: dapagliflozin • HHS – CMs, treatment, risks fluid & electrolyte imbalances o Extremely BS: >600 o S&S: hypotension, profound dehydration, tachycardia, decrease in sensorium o TX: IV NS till BP and UO stable ▪ Correct abnormal electrolytes (esp. watch potassium levels) ▪ IV saline with insulin drip, lower slowly towards 250 then add D5 to solution to prevent cerebral edema and hypoglycemia ▪ Note: If you are unsure if pt is hypo or hyperglycemic---treat as hypoglycemic Diagnostics for DM o A1C: 6.5% or higher o Fasting plasma glucose: 126 mg/dL or higher o 2-hr plasma glucose level: 200 mg/dL or higher 11 ▪ Oral glucose tolerance testing is no longer recommended for routine clinical use. Tests to distinguish Type 1 vs 2 o Presence of endogenous insulin = Type 2 ▪ Endogenous insulin is absent in Type 1 o Islet cell antibody testing ▪ Positive = Type 1 Teaching for Diabetic Pts • Nutritional therapy • Drug therapy • Exercise o Lowers BSL by increasing uptake of glucose by muscles o Improves circulation & muscle tone, facilitates wt loss o Pts with uroketones should NOT exercise ▪ If BSL > 250, no exercise if ketones present o 150 min/wk of moderate aerobic activity o Concern: hypoglycemia ▪ Do accuchecks before, during, & after ▪ If BSL < 100, eat 10-15 g carb and recheck in 15-30 min o Wait to exercise 1 hr post meal • Self-monitoring of blood glucose o Self-monitoring of Blood Glucose o Do comparison of results with lab every 6-12 months o 2-4 times/day o Need to keep a log o Puncture on side of finger o Urine: check ketones for type 1, during sickness & pregnancy o Type 1 diabetes ▪ Often test their blood glucose before meals. ▪ Checking blood glucose 2hrs after the first bite of food  determine if the bolus dose was adequate o During illness: check blood glucose levels at 4-hour intervals • Diet, exercise, and weight loss may be sufficient for Type 2 • Decrease o Lipid levels o Calories & fat to have normal glucose, lipid, & B/P levels ▪ Even a 10% weight reduction can cause large improvements in glucose levels • Alcohol: Main danger is hypoglycemia • Insulin to carb ratio: 1 units: 6 gm carbs Acute complications of Diabetes • Hypoglycemia o BS <70mg o Causes: too much insulin, too little food, or too much exercise. o S&S: sweating, tremor, increase HR, hunger, HA, confusion, numb tongue. ▪ Severe: loss of consciousness, seizures o TX: give 15-20 g CHO 12 ▪ Repeat BS in 15 min, if still low/symptomatic repeat. If BS rising, give meal within hour o If patient not alert: give IM glucagon or 20-50 ml D50 IVP, recheck BS and monitor: follow with meal once alert ▪ Nausea is a common reaction after glucagon injection. ▪ To prevent aspiration  turn the patient on the side until he or she becomes alert o Follow the “Rule of 15” to treat hypoglycemia. ▪ 15g carbs ▪ Check after 15 min ▪ Still less than 70  15g more carbs Diabetes insipidus • Differences from diabetes mellitus and Management – F&E risks • Your body can't properly balance fluid levels • Characterized by large amounts of dilute urine and increased thirst. o Amount urine produced can be ~ 20 liters per day. • Complications may include dehydration or seizures. • Fluid imbalance makes you very thirsty even if you've had something to drink. • Can be caused by damage to hormone secreting organs, genetics, or medications Vascular disorders module (2 parts) Webex Notes • Aneurysms- how to prevent it o Surgery- what are potential complications and how to prevent them, what should we monitor? • PAD vs CVI o PAD = Arterial- worried about pulses and oxygenated blood getting to tissues. o CVI = Venous – worried about backup of fluid • DVT and PAD o Know differences between antiplatelets (aspirin, Clopidogrel) & anticoagulants (warfarin) o what should we teach pts, whats the risk, how do we manage it? Venous- worried about backup of fluid • Pulses, edema, dull aches or no pain, skin assess • Effects on system o hypercoagulability of blood, arterial fibrillation, immobility, HF, pregnancy, stroke, obesity • Diagnostic- lab tests, venous compression ultrasound, duplex ultrasound, CTV Arterial- worried about pulses and oxygenated blood getting to tissues. • Ischemia, pulses, skin, temp, color • Effects on system o Smoking, diabetes, elevated lipid levels and cholesterol, high BP • Diagnostic segmental bp, ABI, MRA, angiograft, chest x-ray, echocardiogram Hypertension Lewis Tables 32.2, 32.3, 32.4, 32.5, 32.6, 32.7, 32.12 15 o ABI: 0.9 or less • Collaborative Care o don’t cross legs, wear cotton socks, good hard-soled shoes with round toes o foot care: don’t soak, inspect, lubricate o protect from heat/cold o leg: level or slightly lower than heart o lifestyle modification o exercise o medication o the 1st treatment goal is to aggressively modify CVD risk factors regardless of the severity of symptoms. ▪ To manage lipids, both dietary interventions and drug therapy will be needed. • ACE Inhibitors (Statins) lower LDL & triglyceride levels and reduces CVD morbidity and mortality risks. o e.g. simvastatin (Zocor) • Anticoagulants: warfarin, heparin are NOT recommended o Walking is the most effective exercise for individuals with claudication ▪ 30 to 45 minutes daily, 3 times/week o Anticoagulants: warfarin / heparin are NOT recommended for prevention of CVD events in PAD patients o ACE inhibitors are used to treat patients with HTN who also have symptomatic PAD. o • Surgery o Check the operative extremity every 15 minutes initially and then hourly for ▪ Skin color and temperature, Capillary refill, Presence of peripheral pulses distal to the operative site, Sensation and movement of extremity o Loss of palpable pulses and/or a change in the Doppler sound  immediately notify physician or radiologist and prompt intervention. o Knee-flexed positions should be avoided except for exercise o Turn and position frequently o If edema develops- position the patient supine and elevate the leg above heart level. o Walking even short distances is desirable. ▪ A walker may be helpful, especially in frail, elderly patients. • Nursing management o Proper care of feet ▪ Keep feet clean by washing them with a mild soap in room temperature water ▪ Keep feet dry, especially the ankles and between toes ▪ Avoid injury – wear comfortable, well-fitting shoes. Never go without shoes ▪ Keep toenails clean and filed, cut toenails straight across ▪ Apply lubricating lotion to feet ▪ Never use a heating pad on your feet ▪ Avoid constricting garments ▪ If a problem develops see a podiatrist ▪ Avoid extended pressure on your feet or ankles o Promoting vasodilation ▪ Provide warmth through socks, insulated shoes, warm environment ▪ Never direct heat to limb – may cause burns due to decreased sensation in limb ▪ Avoid long periods of exposure to cold ▪ Drink adequate fluids ▪ Avoid vasoconstriction from stress, caffeine, and nicotine 16 • Vasoconstriction from smoking may last up to 1 hr Chronic Venous insufficiency • Venous wall/valves in leg veins not working effectively  blood can’t return to heart from legs  blood pools in veins  stasis o CVI = Venous – worried about backup of fluid • S/sx o Edema, leathery skin, increased pigmentation, varicosities, leg ulcers due to stasis ▪ Swelling in legs/ankles ▪ Brownish or darker skin discoloration from the release of hemosiderin from broken down RBCs. • ABI > 0.9 • Nursing management o Get rid of and control swelling ▪ Lower extremity elevation o Ulcer healing ▪ Must provide compression or wound will NOT heal! ▪ Moist environment dressings are the basis of wound care o TED hose over dressing Venous thromboembolism (VTE) • VTE represents spectrum of pathology from DVT to pulmonary embolism (PE) o Look up more about others on spectrum • Virchow’s triad: blood stasis, vessel damage, and increased blood hypercoagulability o need 2 of the 3 • Anticoagulants Lewis Table 37.8, 37.9, 37.10, 37.11, 37.13, 37.14 o Vitamin K antagonists- Warfarin ▪ Taken PO ▪ Give at same time each day ▪ INR - Used to monitor therapeutic levels • Therapeutic: 2-3 ▪ Antidote: Vit K o Thrombin inhibitors- Heparin ▪ Given subcutanesously ▪ DO NOT: expel air bubble from prefilled syringe, rub site, give IM ▪ Rotate sites ▪ aPPT- measures therapeutic levels • Therapeutic: 46-70 sec ▪ Antidote: Protamine o Factor Xa inhibitors ▪ Antidote: Andexanet alfa (Adexxa) Aortic aneurysms • Bulge in the wall of the aorta of 3cm or greater o ¾ are in the lower abdomen below renal arteries o Dilated aortic wall becomes lined with thrombi that can embolize ▪ Leads to acute ischemic symptoms • Types 17 o True: wall bulges with layers of vessel wall intact o False: wall bulges with disruption of all wall layers o Dissecting: torn intima with blood flow between layers • Rupture: high mortality rate! • Abdominal AA: most common cause is atherosclerosis. • Collaborative medical/surgical management an aortic aneurysm. o No smoking, BP and lipid reduction, beta-blockers, antibiotics o Open procedure with cross clamping and Dacron graft o Endovascular o Placed via femoral artery • Risk factors o Male o Age 65+ years o Tobacco o CAD or PAD o High BP o High cholesterol • Goal – prevent aneurysm from rupturing o Early detection/treatment imperative o Once detected- studies done to determine size and location • Manifestations o Abdominal ▪ Frequently asymptomatic ▪ Often found on routine exam or other unrelated x-ray procedures ▪ May note periumbilical pulsatile mass with +bruit ▪ Back and abdominal pain ▪ Blue toe syndrome with intact pedal pulses o Thoracic/arch ▪ Often asymptomatic ▪ Deep chest pain ▪ Angina ▪ Hoarseness ▪ Dysphagia ▪ JVD and SVC syndrome • Management o Conservative: risk factor modification ▪ Tobacco cessation, decreasing BP, optimizing lipid profile, and annual monitoring of aneurysm size using ultrasound, CT, or MRI. ▪ Growth rates may be lowered with β-Blockers (propranolol), statins, and antibiotics o Surgical ▪ Treatment of an aneurysm involves clipping or coiling the aneurysm to prevent rebleeding • Clip stays in place for life • May also use catheter ▪ Preop Care • Hydration • Stabilize electrolytes, coagulation, and hematocrit • Autotransfusion reduces need for blood transfusion during surgery • Bowel prep • NPO • Shower • IV antibiotics right before incision made ▪ Complications from graph- Endoleak- most common