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Weeks 5-8 content Week Topics 5 Dunphy: Chapter 58: Diabetes Mellitus p. 909-938 Kennedy: ➢ Chapter 14: Endocrine, Metabolic, and Nutritional Disorders (p.369- 376) ➢ Obesity (p. 392-39... 6) Glucose metabolism disorders Types of diabetes (prediabetes, type 1 and type 2) * PreDmM = glucose intolerance, Islet cell–specific antibodies, Screening for prediabetes and DM should be considered in all individuals who are overweight or obese, regardless of age, and for all adults aged 45 years and older. * Type I - severe insulin deficiency resulting from beta cell destruction, which produces hyperglycemia due to the altered metabolism of lipids, carbohydrates, and proteins * Type II - abnormal secretion of insulin, resistance to the action of insulin in the target tissues, and/or an inadequate response at the level of the insulin receptor. Types of diabetes- Two types: Type 1 and Type 2- Improper function of the hormone insulin, secreted by the pancreas. Hyperglycemia is a hallmark sign of diabetes. Prediabetes: Impaired glucose tolerance (IGT) describes a prediabetic state of hyperglycemia where a 2-hour post-glucose load glycemic level is 140 to 199 mg/dL. * Type 1 (insulin deficiency)- Presents mostly during childhood. Genetic predisposition plus some sort of environmental trigger. Results in an auto-immune disorder in which the immune system attacks the beta cells of the pancreas to prevent them from producing insulin (decreases production). Inhibits this first step in the insulin pathway. * Type 2- Presents mostly during adulthood. Strongly associated with a genetic predisposition. Accompanied with other predisposing conditions, such as obesity or hypertension. Inability of these cells throughout the body to respond to insulin. The pancreas continues to secrete insulin. The cells throughout the body that are unable to adequately respond to it. * Miscellaneous * Drug-induced diabetes- caused by medications Most commonly occurs with a group of medications that are known as glucocorticoids (steroids) such as in asthma or chrons. * Gestational diabetes Presentation: acute, subacute, and asymptomatic * Acute: most severe presenting situation and can be life threatening for both type I and type II diabetes. very sick over a relatively short period of time, usually only a couple of days. S/S: nausea, vomiting, and abdominal pain leads to severe dehydration. Confusion or unconscious as a result. In type I diabetes, this is known as diabetic ketoacidosis. 30% of individuals with type I diabetes will initially present before diagnosis. DKA- acidotic due to the production of ketoacids Type 2 diabetes: 2% of individuals hyperosmolar nonketotic state- ketones are not produced. Can occur with either type I or type II diabetes. * Subacute: mild to moderate presentation that occurs over a period of weeks to months. S/S: Generally, just not feeling as well. Fatigue, increased thirst, frequent urination, or even weight loss. Most common form of presentation in Type 1 diabetes (70%). * Asymptomatic screening tests: Type II diabetes affects nearly 10% of the population. Those with the risk factors of type II diabetes should be routinely screened. Most common means by which type II diabetes is diagnosed. * Diagnostic criteria - ADA criteria for diagnosing DM- * Random BG >200 (week 5 quiz question) * 3 Ps of DM: polyphagia, polydipsia, polyuria (week 5 quiz question) * FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hrs * 2-h PG ≥200 mg/dL (11.1 mmol/L) during OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75-g anhydrous glucose load dissolved in water. * A1C ≥6.5% (48 mmol/mol). The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay. * In a patient with classic s/s of hyperglycemia or hyperglycemic crisis (polyuria, poly dipsia, weight loss), a random plasma glucose ≥200 mg/dL (11.1 mmol/L) Current guidelines for the diagnosis of DM include any one of the following: • Glycosylated hemoglobin (A1C) of 6.5% or higher • Symptoms of diabetes (e.g., polyuria, polydipsia, weight loss) plus a random plasma glucose level of 200 mg/dL or higher • Fasting plasma glucose level of 126 mg/dL or higher (following 8 hours of no caloric intake) • Two-hour plasma glucose level of 200 mg/dL or higher during an oral glucose tolerance test (OGTT) with a 75-g glucose load Diagnostic testing: laboratory tests. The hyperglycemia and the hemoglobin A1C are tested for in the blood to aid in the diagnosis of diabetes mellitus. Hemoglobin A1C: greater than or equal to 6.5% Blood glucose levels: greater than or equal to 200 mg/dL. * Random- cannot be used to diagnose pre-diabetes. * Fasting- slightly lower, then the level is 126 mg/dL. * Two-hour glucose tolerance test * Initial treatment recommendations * If FPG is above 126, next action: order A1C (week 5 quiz question) * Treatment goals for older adults (Kennedy table 14-2) * Hbg A1C goals based on complications (Dunphy p.925) * An A1C value of less than 7% indicates strong control; however, a value of less than 6.5% has been shown to significantly decrease the occurrence of complications, provided this can be achieved without hypoglycemia or other adverse effect. * Weight loss recommendations (Kennedy) * modest weight loss of 5% can improve glycemic control Risk factors (Dunphy p.922) * Family history (first-degree relative) * Body mass index >25 kg/m2 (lower for Asian Americans) * Age >45 years * Impaired fasting glucose or A1C >5.7% * History of gestational diabetes * Hypertension (> 140/90 mm Hg or on antihypertensive therapy) * Hyperlipidemia (high-density lipoprotein <35 mg/dL, triglycerides >250 mg/dL) * Women with polycystic ovarian syndrome * Race/Ethnicity • African American • Latino • Native American • Asian American • Pacific Islander Complications (Dunphy p.919) * Type 1 DM, the risk of development or progression of retinopathy, nephropathy, hyperlipidemia, and neuropathy * Most common s/e of DM: Yeast infections (week 5 quiz question) : page 932 Dunphy • Retinopathy - Optimizing blood pressure and lipid levels can reduce the risk or slow the progression of retinopathy. • Hyperlipidemia - an annual fasting lipid profile, including serum cholesterol, triglyceride, HDL, and calculated LDL cholesterol measurements. Lifestyle management (i.e., modifications to diet and physical activity), pharmacologic therapy. The purpose of treatment is to reduce cardiovascular events. • Diabetic Kidney disease - A routine spot UACR (normal < 30 mcg albumin/mg creatinine) and eGFR should be performed annually on all diabetic patients. Maintaining normal serum glucose levels, controlling BP is the most effective method to slow or reduce the risk of diabetic kidney disease. ACEIs or ARBs are the recommended treatment for patients with DM and hypertension, abnormally high UACR, or a lower than normal eGFR. • Hypertension - Systolic blood pressure should be less than 140 mm Hg and diastolic blood pressure below 90 mm Hg. A lower blood pressure goal of 130/80 mm Hg may be appropriate for patients at high risk for cardiovascular events. Treatment can be with ACEIs, ARBs, thiazide-like diuretics, or dihydropyridine calcium channel blockers. • Macrovascular disease - Evidence of uncontrolled angina, carotid bruits, or ECG abnormalities may require advanced intervention and calls for referral to a cardiologist. Daily aspirin is recommended for cardiac prophylaxis in patients with a 10-year risk of CVD greater than 10% at a dose of 81 to 165 mg/day. Given the increased risk of bleeding due to its antiplatelet effects, aspirin is not recommended in low-risk patients with a 10-year CVD risk of less than 5%. • Neuropathy - All patients should be screened for neuropathic symptoms at the time of diagnosis and then at least annually. Patients with significant urinary symptoms or impotence should be referred to a urologist. • Pregnancy- every pregnancy in a woman with type 2 DM should be planned. Insulin is the first-line medication for the treatment of diabetes in pregnancy. • Hypoglycemia • DKA – Dunphy pg 914 table 58.2 • HHS – Dunphy pg 920 table 58.4 Treatments for complications * Metformin – contraindicated in renal disease, abnormal creatinine clearance, acute MI, or septicemia (week 5 quiz question) Hypoglycemia is a medical emergency because of the seriousness of potential sequelae (e.g., seizures, coma, cardiovascular dysfunction, death). Initial testing for suspected hypoglycemia includes measurement of the blood glucose level. Hypoglycemia is typically diagnosed if the patient experiences a decrease in blood glucose concentration of greater than 100 mg/dL per hour or a blood glucose level of less than 50 mg/dL at any point during the test. The treatment of acute hypoglycemia for alert patients who can ingest by mouth is 6 to 12 ounces of orange juice or other fruit juice without additional sugar. The long-term management of hypoglycemia includes treatment of its underlying causes and dietary modifications as needed. SMBG is the cornerstone of long-term self-management of hypoglycemia. Treatment of choice for insulinoma is surgical resection Obesity o Comorbidities related to obesity * type 2 diabetes, hypertension, sleep apnea, nonalcoholic fatty liver disease, hyperlipidemia, osteoarthritis, or heart disease Coronary heart disease/congestive heart failure • Hypertension • Dyslipidemia/hyperlipidemia • Type 2 diabetes mellitus/insulin resistance • Metabolic syndrome • Sleep apnea • Restrictive lung disease • Asthma • Varicose veins and venous insufficiency • Gout/hyperuricemia • Osteoarthritis • Reflux esophagitis • Gallbladder disease • Thromboembolic disease • Cancers: Endometrial, breast, prostate, colon o BMI classifications (Kennedy) Overweight is defined as a BMI of 25 to 29. Obesity is defined as a BMI >30 with morbid obesity as a BMI >40. • <18.5 Underweight • 18.5-24.9 Normal • 25.0-29.9 Overweight • 30.0-34-9 Class I obesity • 35.0-39.9 Class II obesity • >40.0 Class III extreme obesity Facts: If an individual has symptoms of diabetes, then only one positive test, either the blood glucose or the hemoglobin A1C is necessary for the diagnosis of diabetes mellitus. If the individual is asymptomatic, then a diagnosis of diabetes mellitus requires two positive tests that are separated by at least one week of time. Often individuals will have a test result that is above the normal level however not severe enough to be considered diabetes and this is known as pre-diabetes. As the blood glucose levels in the body rise, this is sensed by the beta cells in the pancreas (secrete the hormone insulin). Insulin then acts on cells throughout the body to take the glucose from the blood up and thus lower the blood glucose levels. In diabetes mellitus, this insulin pathway is not working properly, therefore the body is not able to lower blood glucose levels. This results in increased blood glucose (hyperglycemia), characteristic finding of diabetes mellitus. A side effect of hyperglycemia is a process known as glycosylation, which is the non-enzymatic attachment of glucose to proteins. And one protein that this occurs with that is of importance in diabetes mellitus is the protein hemoglobin (located within red blood cells). In the presence of hyperglycemia, glucose will attach itself to an abnormally high percentage of hemoglobin within the red blood cells (known as glycosylated hemoglobin, or hemoglobin). The complications of inadequately treated DM include cardiovascular and peripheral vascular disease (PVD), decreased immune system functioning, renal failure, retinopathy, and nephropathy 6 Dunphy: ➢ Incontinence p. 628- 635 ➢ Lower Urinary Tract Disorders p. 636- 642 ➢ Menopause p. 716- 724 ➢ Erectile dysfunction p.761-767 ➢ Advanced Assessment 43.1 Urinalysis p. 624 Kennedy: ➢ Chapter 5: Symptoms and Syndromes (Urinary Incontinence section only) p. 83-87 ➢ Chapter 11: Urological and Gynecological Disorders: o Atrophic vaginitis p. 282-284 o Cystitis p.289-291 o Erectile dysfunction p.297-299 Urology and aging (Kennedy) Complicated UTI * acute or chronic infection with factors that predispose a patient to the infection or make treatment more difficult, such as instrumentation (e.g., indwelling, suprapubic, or intermittent catheterization), underlying chronic disease, systemic symptoms, or pregnancy. Uncomplicated UTI * Resolves without addressing other factors and is localized to the lower urinary tract UTI risk factors, differences based on gender * Women = gram-negative rod bacterium Escherichia coli. * Second most common is gram-positive coccus Staphylococcus saprophyticus * Men - abnormal urethral anatomy or inadequate treatment of prostatitis * asymptomatic bacteriuria, patients experience no obvious clinical symptoms or signs of UTI * dysuria–pyuria syndrome (also called “acute urethral syndrome”) is characterized by painful urination with WBCs on microscopic urinalysis in the absence of a positive bacterial culture (possibly Chlamydia) * contamination from the patient’s own gastrointestinal tract. * Bacteria from fecal contamination secondary to poor perineal hygiene, unprotected sexual (particularly anal) intercourse, and/or an anatomically shortened urethra in women UTI risk factors: Indwelling Catheters, urethral or condom catheters, incontinence (urinary and fecal), cognitive impairment, neurological conditions that impair bladder emptying, and diabetes. Sexual intercourse, functionality disability, sickle cell, prior antibiotic use, genetic predisposition, functional or structural genitourinary tract abnormalities. Differences based on gender: Women have a higher percentage of UTI. This is due to the Urethra being shorter in women than men. UTI pathophysiology- common bacterial causes * Escherichia coli * Staphylococcus saprophyticus * Proteus mirabilis, Klebsiella, Enterobacter, Serratia, and Pseudomonas. * Enterococcus * Staphylococcus aureus * Fungi, particularly Candida * Urease gene, expressed by certain gram-negative bacteria such as Proteus, Klebsiella, Ureaplasma, Providencia, and Pseudomonas species. UTI Pathophysiology: Cystitis is a pathogenic invasion of the wall of the bladder, usually resulting from an ascending infection via the urethra, of bowel flora organisms from the perineum . Common Bacterial Causes- E.- coli. (Most common), Klebsiela,Proteus,andEnterococcus. UTI diagnostic criteria and when to treat (review discussion) * presence of bacteria, especially if more than 100,000 organisms/mL * Urine culture is gold standard * UA with pyuria (greater then 10 neutrophils & RBCs * Interstitial cystitis – dx by potassium sensitivity test (put 40mL of sterile water in bladder by foley, wait 5 min determine level of pain 0-5, then put 0.4M of KCL, wait 5min & see if pain). UTI diagnostic criteria and when to treat- Urinalysis with culture, Treatment is based on the need of patient. Incontinence - Urinary incontinence * Involuntary loss of urine from the bladder * So common in women many consider it normal * Common in older men w/ enlarged prostate * Can affect quality of life * Significance-One of the most common complains w/ older adults, Distress & embarrassment, Cost burden to pt & society as a whole, Not life-threatening, may effect QOL, PCP essential to educating individuals * Epidemiology- Increased prevalence w/ age in men & women, Nursing home population – 40-70%, Often a factor in placement * URGENCY UI is greater in men * STRESS UI is greater in women * Overflow incontinence is usually associated with: Bladder outlet obstruction * Meds * Oxybutynin (anticholinergic/antispasmodic) – urge, stress & OAB * Flomax (Alpha1 blocker)– BPH * Amitriptyline (tricyclic antidepressant) – OAB, Urge * Botox - OAB * Terminology * UI- Unintentional voiding, loss or leakage of urine * Continuous incontinence-Continuous loss or leak of urine * Increased daytime frequency-More frequent during day than considered normal * Nocturia-Interruption of sleep one or more times due to the need to urinate – increases in frequency after age 50 * Urgency-Sudden, compelling desire to pass urine that’s difficult to prevent * Overactive bladder syndrome- Urgency, frequency, nocturia w/ or w/o incontinence Incontinence: Urinaryincontinence(UI)isaninvoluntarylosofurine. Stress incontinence-Urineleakageasociatedwithincreasedabdominalpresurefrom laughing,sneezing,coughing,climbingstairs,orotherphysicalstresorsincreasingabdominal presure Urge incontinence-Urineleakageasociatedbyorimmediatelyprecededbythefeelingofan urgentneedtovoid Overflow- Urineleakagewhenthebladderisover-distendedandmayresultinincomplete bladderemptyingSymptomscanpresentasconstantdribbling,frequency,hesitationwhen initiatingurination,andnocturiaOftenasociatedwithbladderoutletobstruction,suchas benignprostatichypertrophyinmenandpelvicorganprolapseinwomen Functional-Theinabilitytoholdurineduetoreasonsotherthanneurologicalandlower urinarytractdysfunctionincludingdelirium,psychiatricdisorders,UTI,impairedmobility Mixed-Acombinationofstresandurgeincontinence,markedbyinvoluntaryleakage asociatedwithurgencyandalsowithexertion,effort,snezing,orcoughing Dysuria * Pain & burning with urination * r/t inflammatory lesion or bladder/urethral infection * most common lower UTI * Meds that cause Dysuria: SSRI, Opiates, Scopalamine * Less common causes: tumor, renal failure, nephrolithiasis, STDs Causes of hematuria and proteinuria * Hematuria – blood in urine (3 RBCs or more) * Gross (can be seen in urine) or Occult (visible by microscope) * Transient – on occasion or Persistent – two or more consecutive occasions * Athletes (long distance runners) common to get hematuria * Foods that mimic hematuria – beets. * Causes – caffeine, spices, tomatoes, chocolate, alcohol, citrus, soy sauce, some herbal meds * Meds that cause – beta-lactam abx, sulfonamides, NSAIDs, cipro, Allopurinol, Tagamet, Dilantin * Anticoags to consider – warfarin, heparin, Asa, NSAIDs * Hematuria in men over 50 – work up for risk of urinary tract malignancy * Hematuria with Cast = indicate a renal origin Causes of Hematuria: Dietary substances such as beets mimic hematuria only , medications, Urolithiasis, and menses. * Proteinuria * Typically renal pathology (Glomerular) * Functional r/t illness, stress or exercise * Mild transient – r/t fever, CHF, acute pulm edema, head injury or stroke (will improve at pt improves) * Can result from overproduction of filterable plasma protein, assoc w/ multiple myeloma * Bence Jones proteins r/t multiple myeloma, lymphosarcoma, leukemia and Hodgkin’s disease. * Urine dip is most sensitive to larger proteins like albumin not Bence Jones proteins * BEST Test is 24-hr urine (↑160mg of protein in 24hrs is abnormal) * More than 3.5G is indicative of nephrotic disease * Nonfunctional proteinuria do 24hr urine (protein & creatine), if excretion is above 3.0-3.5G per day, pt has nephrotic syndrome (refer to nephrology) * Diff Dx = orthostatic proteinuria, exercise, environmental conditions, fever, acute illness, albumin transfusion, heart failure, acute pulmonary edema, cerebral vascular accident or head injury. Causes of proteinuria: Proteinuria can be functional- related to illness, stress or exercise. Mild transient proteinuria can result from fever, congestive heart failure, acute pulmonary edema, head injury or stroke. Proteinuria can develop from an overproduction of filterable plasma protein, which may be associated with multiple myeloma. UA dip interpretation Advanced Assessment 43.1: Urinalysis Urinalysis Result Finding/Abnormal Value Common Differential Diagnosis Appearance Colorless Dark Cloudy Pink/red Orange/yellow Brown/black Green Foamy Diabetes insipidus, diuretic agents, fluid overload Hematuria, malignancy, stones, acidic urine Urinary tract infection, hematuria, bilirubin, mucus Hematuria, hemoglobin, myoglobin, beets, food coloring Phenazopyridine (Pyridium), rifampin (rifampicin), bile pigments Myoglobin, bile pigments, melanin, cascara (laxative), iron preparation Bile pigments, methylene blue, indigo carmine (food dye) Proteinuria, bile salts Specific gravity Increased Decreased Dehydration, congestive heart failure, adrenal insufficiency, diabetes mellitus, nephrosis, antidiuretic hormone Diabetes insipidus, pyelonephritis, glomerulonephritis, excess fluid intake pH Acidic Alkaline Diet, medications, acidosis, ketoacidosis, chronic obstructive pulmonary disease Diet, sodium bicarbonate, vomiting, metabolic alkalosis, urinary tract infection Bilirubin Positive Jaundice, hepatitis Blood Positive Kidney stones, tumors, kidney disease, trauma, infection, injury from instrumentation, coagulation problems, menses Glucose Positive Diabetes mellitus, pancreatitis, Cushing’s disease, shock, burns, corticosteroids, renal disease, hyperthyroidism, cancer Ketones Positive Starvation, diet, ketoacidosis, vomiting, diarrhea, pregnancy Nitrate Positive Infection Protein Positive Kidney disease, pregnancy, congestive heart failure, diabetes mellitus, cancer, benign cause Leukocyte esterase Positive Infection Reducing substance Positive Signifies the presence of glucose, fructose, or galactose, lactose, pentose May also signify certain medications (e.g., salicylates, levodopa, ascorbic acid, nalidixic acid, tetracyclines) Liver disease, hyperthyroidism Sexuality and aging (Dunphy ch51) STIs * Common STIs include herpes simplex virus (HSV), human immunodeficiency virus (HIV), human papillomavirus (HPV), Chlamydia trachomatis, Neisseria gonorrhoeae, Trichomonas vaginalis, and Treponema pallidum (the causative agent of syphilis). * Less common STIs include chancroid (Haemophilus ducreyi), donovanosis or granuloma inguinale (Klebsiella granulomatis), mycoplasma genitalium, and lymphogranuloma venereum. In addition, hepatitis B virus (HBV), hepatitis C virus (HCV), molluscum contagiosum, pediculosis pubis, scabies, and methicillin-resistant Staphylococcus aureus * Common vaginal infections, such as Candida infections and bacterial vaginosis (BV) TABLE 51.1 Sexually Transmitted Infections CDC Treatment Pathogen Clinical Presentation Diagnostic Reasoning Recommendations (2015) Chancroid Haemophilus ducreyi LGV Chlamydia trachomatis Painful, irregularly shaped, deep red ulcer with red halo and undermined edges. Found on the penis, labia, fourchette, and vaginal walls. Painful inguinal adenopathy with buboes. Females may have multiple lesions and may be asymptomatic. Primary lesion: small painless erosion that heals quickly Inguinal stage: inguinal lymphadenopathy; may have headache, fever, and polymyalgia Late stage: anorectal swelling, perirectal abscesses, fistulae, swelling and Risk factors: coinfection with HIV, HSV, or syphilis. Test patients for HIV at time of diagnosis. Definitive diagnosis is obtained with culture (no FDA- approved PCR test available in United States). Risk factors: history of travel and sexual contact in endemically infected area. Diagnosis is confirmed with serological LGV complement fixation test; suspect if titer Azithromycin 1 g orall single dose OR Ceftriaxone 250-mg intramuscular injection single dose OR Ciprofloxacin 500 mg orally twice a day for 3 days OR Erythromycin base 500 mg orally four times a day for 7 days Doxycycline 100 mg orally twice a day for 2 days OR Erythromycin base 500 mg orally four times a day for 21 days. Granuloma inguinale (donovanosis) Klebsiella granulomatis Genital HSV ulcerations on labia Initial papule progresses into a painless, broad, superficial ulcer with clean, sharp rolled edges; may spread to inguinal folds. Lesion may be friable. Genital edema may occur. Late development of perianal fistulae and abscesses. Multiple painful above 1:16 and diagnostic if titer above 1:64. Risk factors: history of travel and sexual contact in endemically infected area. Diagnosis: Cannot be cultured; most reliable diagnostic method is direct visualization of Donovan bodies (i.e., rod-shaped, oval bacteria in the cytoplasm of mononuclear phagocytes or histiocytes) on stained tissue samples. NAAT (PCR assays Azithromycin 1 g orall weekly for 3 weeks or 500 mg daily for 3 wee OR Doxycycline 100 mg orally twice a day for 3 weeks OR Ciprofloxacin 750 mg orally twice a day for 3 weeks OR Trimethoprim- sulfamethoxazole 160 mg/800 mg one tablet orally twice a day for 3 weeks OR Erythromycin base 500 mg orally twice a day f 4 weeks First episode: vesicular or ulcerated for HSV DNA) Acyclovir 400 mg orall lesions that may last 12 Type-specific three times a day for 7– days in the initial outbreak or 4–5 days in serology testing is available and useful 10 days OR recurrent outbreaks. when developing Acyclovir 200 mg orall Flu-like symptoms plan of care. five times per day for 7 (common with first outbreak), adenopathy, and tingling at the site 10 days OR Valacyclovir 1 g orally before outbreak. twice a day for 7–10 da OR Famciclovir 250 mg orally three times a day for 7–10 days Recurrent episodes: Acyclovir regimens 400 mg orally three tim a day for 5 days 800 mg orally twice a day for 5 days 800 mg orally three tim a day for 2 days OR Valacyclovir regimens 500 mg orally twice a day for 3 days 1 g orally once a day fo 5 days OR Famciclovir regimens 125 mg orally twice a day for 5 days 1 g orally twice a day f 1 day 500 mg orally on e and then 250 mg orally twice a day for × 2 days Suppression therapy: Acyclovir 400 mg orall twice a day OR Valacyclovir 500 mg orally once a day OR Valacyclovir 1 g orally once a day OR Famciclovir 250 mg orally twice a day Evaluate after 1 year fo recurrent episodes. Molluscum contagiosum Pox virus Usually asymptomatic Pearly, raised, painless, flesh-colored lesions (mollusca) with Diagnosis is based on visual inspection of characteristic lesions. No treatment; lesions may last months to yea and often heal spontaneously. umbilicated (dimpled) Once healed, the patien centers; may be diffuse has lifetime immunity t or singular; may be self-limited the virus. Physical treatments to remove lesions, such as cryotherapy or curettag may be considered in extreme cases or for lesions in unsightly areas, but these method may lead to scarring. Syphilis Treponema Primary: painless ulcer at initial site of contact Risk factors: test all patients for HIV Treatment is driven by staging. Primary and pallidum (chancre), adenopathy and other common secondary or early laten Secondary: STIs. Definitive (<1 year since infection maculopapular rash on diagnosis: dark- Benzathine PCN G 2.4 the palms and soles, field microscopy million units flu-like symptoms, positive for intramuscularly one tim mucocutaneous lesions, lymphadenopathy Tertiary/late: cardiac, neurologic, ophthalmic, auditory, and gummatous lesions spirochetes. Presumptive diagnosis: 1. Nontreponemal test (VDRL or RPR) 2. Confirmation with treponemal test (e.g., FTA- ABS, TP-PA) If PCN allergy: Doxycycline 100 mg orally twice a day for 1 days OR Tetracycline 500 mg orally four times a day for 14 days OR Ceftriaxone 1 g intramuscularly or intravenously daily for 8–10 days Late latent, latent of unknown duration, or tertiary with normal cerebrovascular fluid examination: Benzathin penicillin B 2.4 units intramuscularly once a week for 3 doses If PCN allergy: Tetracycline 400 mg orally four times a day for 4 weeks OR Doxycycline 100 mg orally twice a day for 4 weeks Neurosyphilis and ocul syphilis: Aqueous crystalline penicillin G 3–4 million units intravenously every 4 hours for 10–14 days (o continuous infusion). Alternate therapy if compliance is assured: Procaine penicillin 2.4 million units intramuscularly daily PLUS Probenecid 500 mg orally four times a day for 10-14 days If PCN allergy: Desensitize and treat with penicillin as above OR Ceftriaxone 2 g intramuscularly/intrave ously once a day for 10 14 days Trichomoniasis Most infected persons Vaginal pH >5; Metronidazole 2 g orall Trichomonas vaginalis have minimal or no symptoms. cervical smear wet mount shows for one dose OR Some infected women motile protozoa and Tinidazole 2 g orally fo Urethritis Neisseria gonorrhoeae (most common) may have diffuse, frothy, malodorous, or yellow-green discharge and vulvar irritation. Infected men may have symptoms of urethritis, epididymitis, or prostatitis. May be asymptomatic Dysuria, urethral pruritus, mucoid or purulent discharge WBCs. Strawberry cervix may rarely be noted on examination. NAAT is highly sensitive: APTIMA T. vaginalis assay, amplified DNA Assay. In men, obtain penile-meatal swab. Rapid testing is available. Microscopic examination of urethral secretions will show WBCs one dose OR Metronidazole 500 mg orally twice a day for 7 days Avoid alcohol consumption during treatment with metronidazole. Treat with drug regime recommended for gonorrhoeae and trachomatis. Nongonococcal and GNID or M. genitalium responds Urethritis (NGU) Chlamydia trachomatis, Mycoplasma genitalium Gonorrhea Neiss eria gonorrhoeae Usually asymptomatic. Partner may have an MB/GV purple intracellular diplococci. Test all patients for C. trachomatis; test men with NGU for HIV and syphilis. In men, complications of NGU include epididymitis, prostatitis, and reactive arthritis. No FDA-approved test for M. genitalium. Gonococcal culture and NAAT better to azithromycin than doxycycline. Primary therapy: Ceftriaxone 250 mg infection, requiring Women: intramuscularly for one treatment. Women may report endocervical swab Men: urethral swab dose PLUS purulent, yellow, or green vaginal Azithromycin 1 g orall for one dose Alternativ discharge; bleeding or therapy (less effective): pain with intercourse; Cefixime 400 mg orally and pelvic pain; may have inflammation of Skene’s and Bartholin’s glands. Men may report inflammation of the for one dose PLUS Azithromycin 1 g orall for one dose If azithromycin allergy: Doxycycline 100 mg orally twice a day for 7 urethra, discharge, and days AND test of cure i dysuria. 1 week. Follow CDC guidelines for complicated or refractory gonorrhea; consider EPT. Chlamydia Chlamydia trachomatis Asymptomatic infection is common in men and women. Women may report dysuria and mucopurulent vaginal discharge. Men may report purulent urethral discharge, dysuria, or pain/swelling of testicle(s). NAAT Women: vaginal swab Men: urethral or rectal swab or first-catch urine specimen Primary therapy: Azithromycin 1 g orall in a single dose OR Doxycycline 100 mg orally twice a day for 7 days Alternate therapy: Erythromycin base 500 mg orally four times a day for 7 days OR Ofloxacin 300 mg orall twice a day for 7 days OR Levofloxacin 500 mg orally once a day for 7 days HPV May infect Lesions are usually Risk factors: Preventive: the urethra, penis, asymptomatic. Early sexual debut, Gardasil, Gardasil 9, or groin, scrotum, Men and women may multiple sex Cervarix vulva, perineum, report itching or pain, partners. HPV vaccine times thre external anus, and perianal area, including depending on location. External warts are flat, papular or Diagnosis by visual inspection is based on characteristics doses Patient-applied: Podofilox 0.5% solutio anogenital warts pedunculated lesions, of lesion. or gel applied twice dai single or multiple, and Cervical and three times per week fo of varying sizes. intravaginal lesions are identified during colposcopy weeks OR Imiquimod 3.75% or 5 following an cream applied at bedtim abnormal Pap test three times per week fo or a normal Pap test 16 weeks in the presence of high-risk HPV serotype infection. OR Sinecatechins 15% ointment applied three times a day for 16 week Provider-administered: Cryotherapy with liquid nitrogen or cryoprobe, repeated every 1–2 weeks OR Surgical removal by excision, curettage, lase or electrosurgery OR TCA or BCA 80%–90% solution applied weekly Alternate therapy for external genital warts: Podophyllin resin 10% 25% in compound tincture of benzoin applied to each wart; may repeat weekly; stri application guidelines f provider-administered therapy must be followed. HIV Initial presentation of acute retroviral syndrome with fever, malaise, adenopathy, and maculopapular rash may occur. HIV: Malaise, headache, lymphadenopathy, gastritis, weight losws, Positive enzyme- linked immunosorbent assay is confirmed by positive Western blot. Treat concurrent STIs and opportunistic infections as recommended by CDC refer to specialist. Offer long-term counseling and management. HAART is key for the treatment of HIV; bloody diarrhea, initiation of therapy is a vaginal infections, function of T-cell count thrush. viral load, and concurre AIDS: Encephalitis, meningitis, blindness, Pneumocysti s pneumonia, tuberculosis, skin cancer. symptoms. Treatment i heavily influenced by t ability to comply with treatment regimens Age related changes * x GSM (Kennedy, NAMS videos) Signs and symptoms * genital symptoms (e.g., dryness, burning, and irritation), * sexual symptoms (e.g., dryness, discomfort, pain with intercourse), * urinary symptoms (e.g., urgency, dysuria, recurring urinary tract infections). SIGNS-Vaginal dryness, painful sex, burning, irritation, lack of lubrication, SYMPTOMS: urgency, dysuria, recurrent urinary tract infection, Diagnosis * complain of genital symptoms, a physical examination, cervical cytology, vaginal culture and pH measurement, and urinalysis should be done to assess whether the symptoms are related to estrogen deficiency and not to abnormal cellular changes or infection * Pelvic examination with speculum examination and Pap smear (may do wet mount and KOH preparation if infection is suspected) * UA to rule out UTI if symptoms When to treat, common treatments When to treat: This is whenever patients come to ask provider or provider starts conversation. Common treatments: moisturizers and lubricants, low dose vaginal estrogen (tablet, cream or vaginal ring), pelvic pt, * most effective treatment for vulvovaginal atrophy is intravaginal estrogen, which is available as a tablet, vaginal ring, or cream * NAMS position statement on HT recognizes HT as the most effective treatment for vasomotor symptoms and genitourinary symptoms of menopause. * healthy menopausal women younger than 60 years and who are within 10 years of menopause, HT is a reasonable option * ET: In most cases, estrogen-only therapy is used in women who do not have a uterus or are treating genitourinary symptoms with low-dose topical preparations * Estrogen plus progestin therapy (EPT): Combination therapy is used in women who have a uterus to prevent endometrial hyperplasia. EPT can be taken continuously (taking both estrogen and progestin daily) or cycled to mimic a menstrual cycle using a continuous-sequential (CS-EPT) or continuous- combined (CC-EPT) method. When using the CS-EPT method, estrogen is given on cycle days 1 to 21 of each month, and a progestin is given on cycle days 7 to 21. HT is withheld on cycle days 22 to 30, causing endometrial sloughing and bleeding. When using the CC-EPT method, estrogen and a progestin are taken daily. Patients may experience intermittent spotting for a few months, but this should subside once the endometrium thins in response to the HT. * Meds: Oral Estrogen (Premarin), Transdermal (Minivelle), Vaginal (Estrace cream or Premarin), Oral Estrogen+Progestin (Angeliq), Oral Estrogen+Testosterone (Covarys) Atrophic vaginitis Dunphy p. 282-284 * Symptoms: Vaginal dryness, dysuria, vulvar and vaginal itching, urinary frequency, blood-tinged vaginal discharge, dyspareunia * First-line therapies for atrophic vaginitis include nonhormonal lubricants with intercourse and possible regular use of long-acting vaginal moisturizers. * For symptomatic women with moderate to severe symptoms or those who don’t respond to lubricants/moisturizers, vaginal or low-dose systemic estrogen is the therapeutic standard. Menopause (Dunphy) Menstrual changes physiology * permanent cessation of menses resulting from loss of ovarian follicular function, 12 consecutive months of amenorrhea * symptoms of menopause include vaginal dryness, joint pain, diminished libido, and cognitive changes Menopause: menopauseisthepermanentcesationofmensesresultingfromlosofovarian folicularfunction.Itisdefinedasthefinalmenstrualperiod(FMP)andisreachedwhenthere haveben12consecutivemonthsofamenorhea.Menopausemostoftenoccursduetoaging andrepresentsthepermanentdeclineofsexhormonelevels.Inadditiontoaging,menopause canalsobeinducedsurgicaly(i.e.,bilateraloophorectomy)ormedicaly(e.g.,dueto chemotherapyorpelviciradiation)atanyage. Menstrual changes: Withthedepletionofovarianfoliclesthatareabletorespondto gonadotropins,bothfoliculardevelopmentandcyclicalestrogenproductionceaseduring menopause.FSHlevelsriseasthebodytriesunsuccesfulytostimulatefolicularproduction ofestrogen.FSHlevelsabove40IU/mLsignaltheapproachofmenopause,eventhougha womanmaystilexperienceoccasionalmenstrualbleeding.LHconcentrationisalsoelevated, butmenopausalevelsaredifficultodistinguishfromLHelevationseenduringpreovulatory gonadotropinsurgesinthenormalmenstrualcycle. Symptom management * lifestyle modification – aerobic exercise * SSRI, SNRI, hormone therapy * cognitive behavioral therapy, hypnosis, acupuncture, and oral supplements * Black cohosh (Cimicifuga racemose or Actaea racemose) has been used for many years to treat menopausal symptoms. Treatmentofmenopausefocusesonsymptommanagementandwilvarydependingondegree ofsymptomintensity,medicalhistory,typeofmenopausalsymptoms,andpersonal preference.Lifestylemodificationsareoftensufficientomanagemildhotflashes.Simple interventionsthatcanbehelpfulincludeusingfans,loweringroomtemperature,dresingin layers,andavoidingtrigersuchastres,caffeine,andalcohol. WomenwithmoderatevasomotorsymptomsmaybenefitfromtreatmentwithSRIsand SNRIs,asbothcanbeeffectiveinreducingthefrequencyofhotflushes.Menopausalhormone therapy(HT)isappropriateforwomenwithmoderatetoseveresymptomswhohaveno contraindicationsuchasbreastcancer,aswelasalowriskofcoronaryarterydisease,DVT, andstroke.Theantihypertensivemedicationclonidine100to150mcgdailycanbegiven oralyortransdermalytorelievehotflashes,cognitivebehavioraltherapy,hypnosis, acupuncture,andoralsupplementsmaybetried.Inadditionaltopharmacologictherapies, regularaerobicexerciseimprovescognitivefunction,enhancesmood,andpromotesdaytime alertnesandnocturnalslepines.Recentstudieshaveshownthatabriskdailywalkenhances welnesandpromotesasenseofwel-being.MenopausalHormonalTherapyhasbeen approvedbytheU.S.FoodandDrugAdministration(FDA)forthepreventionofosteoporosis, reliefofvasomotorsymptoms,andthetreatmentofvulvovaginalatrophyasociatedwith menopause. Erectile Dysfunction (Dunphy) Erectiledysfunction(ED)istheinabilitytoachieveormaintainanerectionthatisufficient forsatisfactorysexualperformance.EDcanalsomanifestasalackofsexualdesireoran inabilitytoejaculate.EDcanresultfrommanycauses,includingphysiological,psychological, endocrinological,vascular,andneurologicetiologies. Diagnosis * Labs - fasting blood sugar to rule out diabetes mellitus, a lipid profile to rule out dyslipidemia, thyroid-stimulating hormone (TSH), and a testosterone level. * If the testosterone level is below 300 ng/dL, a serum prolactin level is warranted. Treatment – medications * Nonpharmacologic interventions including vacuum constriction devices, vasoactive therapy, penile prostheses, and penile revascularization * Pharmacologic: Treatment of ED Medications: Hormone therapy (Testosterone), Do not use in patients with serious liver, kidney or cardiac disease, prostate or breast cancer or allergy to mercury. Will increased libido 72 hours. after injection. Oral agents are not recommended. Skin gel or patch is harmful to women of child bearing age. Vasoactive therapy (Viagra, ) Do not take with nitrates or alpha blockers, Caverject-Taking with anticoagulants can increase bleeding. Can be used every 24 hrs 2-3 times a week. After injection last 30-60 min. DRUG ADVERSE REACTIONS PRESCRIBING CONSIDERATIONS Hormone Therapy Parenteral agents: Testosterone cypionate (Depo- Testosterone) Testosterone enanthate (Delatestryl) Sodium retention with dependent edema, increased risk of bleeding, pain at injection site, mild gynecomastia, mood swings, lipid abnormalities Do not use in patients with serious liver, kidney, or cardiac disease, prostate or breast cancer, or in those with mercury allergy. Peak and trough effects may lead to aggression, feelings of well-being, energy, and increased libido within 72 hours of injection. As peak level falls, patient may experience depressed mood and loss of libido. Oral agents: Fluoxymesterone (Halotestin) Methyltestosterone (Android, Methitest, Testred, Virilon) Same as for parenteral agents Not used as much as transdermal or parenteral formulations because of difficulty in Oral agents are not generally recommended because of hepatotoxicity and unreliable androgenic effects. achieving adequate blood levels due to high first-pass metabolism in the liver Transdermal testosterone patch (Androderm, Testoderm) Local irritation; burn-like blistering or irritation of skin where transdermal patch is applied NOT to be applied to the scrotum. Should be applied to the arm, back, abdomen, or thigh. May cause local irritation. Transdermal testosterone topical gel or solution (AndroGel 1%, 2.5–5 g packets) (Testim 1% Gel, 5– 10 g packets) (Axiron solution, 60–120 mg) Burn-like blistering or irritation of skin where gel is applied Problems with urination Apply to the axilla, upper arm, or shoulder, but NOT the scrotum. May transfer to partner during intimate skin-to-skin contact. Testosterone implantable pellets (Testopel, 150–450 mg) Infection at implantation site and pellet extrusion Produces steady blood levels; must be implanted in subcutaneous tissue every 3–4 months Less flexibility in dose adjustment Testosterone buccal system (Striant, 30 mg) Mouth or gum irritation Allergic reactions Swelling of ankles or legs Breathing disturbances, including those associated with sleep Liver damage Insertion twice daily in the morning and evening provides continuous systemic delivery of testosterone Vasoactive Therapy Oral agents: Sildenafil (Viagra) Vardenafil (Levitra) Tadalafil (Cialis) Avanafil (Stendra) Headache, flushing, dyspepsia, nasal congestion, and visual color changes Back and lower limb pain for all PDE5 inhibitors None of these agents should be used in patients taking nitrates or alpha blockers. Must wait 24 hours before giving nitrate medication after sildenafil or vardenafil and 48 hours for tadalafil. Injectables: Alprostadil (Caverject, Edex) Penile pain, prolonged erection, penile fibrosis, injection site hematoma, Taking along with anticoagulants or heparin may increase risk of bleeding. Should not be used in patients with sickle cell anemia, penile fibrosis, coagulopathy, severe cardiovascular numbness, yeast infection, and priapism May also cause upper respiratory infection, headache, dizziness, and hypotension disease, myeloma, leukemia, penile deformity, morbid obesity, or penile implants. Can be used only once every 24 hours and a maximum of three times a week. Patient should be instructed to choose injection site along side of proximal one-third of penis, alternate injection sites, and avoid visible veins. Transurethral suppositories: Alprostadil (Muse) May cause urethral irritation As above. Should not be used if partner is pregnant unless a condom is used. Suppository is inserted in penis to approximately 1 inch, after the patient urinates. Button on top of applicator is pushed to release suppository; gentle rocking motion will separate suppository from applicator. After applicator is removed, patient should massage penis firmly for approximately 10 seconds while standing. Erection will begin in 5–10 minutes. half-lives of medications * x Medication interactions * x Comorbid diagnoses * x 7 Dunphy: ➢ Alzheimer’s Disease p. 105-110 Kennedy: ➢ Chapter 16: Psychological Disorders o Delirium (p.439- 443) o Dementia (p.443- 451) o Depression (p.45- 456) o Elder abuse (pp.456- 458) Elder Abuse o Types of abuse o Provider responsibilities in suspected abuse Types of elder abuse: Elder abuse is any form of mistreatment resulting in harm to a vulnerable person. • Physical abuse: physical pain or injuring a vulnerable person • Sexual abuse: sexual contact with a vulnerable elder without his or her consent • Neglect: Failing to provide food, shelter, health care or protection for a vulnerable elder • Exploitation: the taking of funds, property, or any assets of a vulnerable elder without legal consent and not for the benefit of the elder. The example used was family member moving into grandma’s house and using her home and ssi check or their income to provide for themselves, and not providing for grandmas needs. • Emotional abuse: using verbal or nonverbal means to cause mental pain, anguish or distress in an elder. If patient seems less interactive do not only think cognitive changes- keep abuse as a differential. • Abandonment: deserting the vulnerable elder once someone has assumed responsibility for that individual • Self- neglect: the elder fails to perform the needed activities to protect his or her own health and safety (lacks food/utilities, refuses medications, hoards, lives in unsafe conditions, neglects grooming/ appearance, is unable to handle finances, is isolated, is disoriented, develops a dependence on drugs/ alcohol). Example would be if patient was living alone and could not provide for own needs. Elder Abuse Types of Abuse: 1. Physical Abuse: Causing physical pain or injuring a vulnerable elder. 2. Sexual Abuse: Sexual contact with a vulnerable elder without his/her consent. 3. Neglect: Failing to provide food, water, shelter, health care, or protection for a vulnerable elder. 4. Exploitation: the taking of funds, property, or any assets of a vulnerable elder without legal consent and not for the benefit of the elder. 5. Emotional Abuse: Using verbal/ nonverbal means to cause mental pain, anguish, or distress in an elder. 6. Abandonment: deserting the vulnerable elder once someone has assumed responsibility for that individual. 7. Self-Neglect: The elder fails to perform the needed activities to protect his/her own health and safety (lacks food/ utilities, refuses meds, hoards, lives in unsafe conditions, neglects his/her grooming/ appearance, or unable to handle finances, is isolated, is disoriented, develops a dependence on drugs and/ or alcohol) Provider responsibility: If elder abuse is suspected, it is health professional’s responsibility and, in most cases, legal obligation to report it to either 911 or state elder abuse hotline. Health care professionals should incorporate routine screening for at risk elder population. Tell- tale signs of abuse may include bruises, broken bones, poor personal hygiene, abrupt changes in finances, sudden withdrawal from normal activities, unexplained weight loss, and excessive power or control by a close family member or friend. Providers Responsibility in Suspected Abuse: 1. If elder abuse is suspected, the health-care provider’s responsibility is to report this to either 911 or the state elder abuse hotline. 2. They must carefully collect information regarding the patient, using physical findings, patient’s functional abilities, testing results, and verbal information from the patient and his/her caregivers. Use the interdisciplinary team and speak with social workers, nursing staff and others who may have interacted with the patient and caregiver. 3. Document all findings, because they may be required to be presented in court later. Especially document any differences in verbal accounts between the patient and his/her caregiver. 4. Photograph suspicious injuries as well as measuring or comparing size of injury with a familiar object if a ruler is not available. 5. Be sure to follow-up with case workers to determine the outcome of the case. It sometimes takes several reports before the true picture of neglect, exploitation, or abuse can be investigated thoroughly, and the elder individual is moved to a safe environment. If you suspect elder abuse perform a physical exam and order any necessary tests, include a cognitive screen and include what patient says and objective findings. May interview patient and caregiver separate. Alzheimer's (Kennedy) o Distinguishing features- symptoms, subjective complaints, objective findings Staging guidelines (Kennedy p.444) Distinguishing Features: 1. Cognitive changes including: confusion, disorientation (as to place, person, and time) 2. Impaired short-term memory 3. Personality changes 4. Psychiatric symptoms 5. Problem behaviors 6. Changes in daily function 7. Diffuse cerebral plaques, neurtitc plaques and tangles, neurons and synapse loss o Treatment Delirium (Kennedy) Definition: Change in mental status, confusion, disorientation (time, place, person), agitation. The DSM-5 differentiates delirium into the following categories: 1. Substance intoxication delirium 2. Substance withdrawal delirium 3. Medication-induced delirium 4. Delirium due to another medical condition 5. Delirium due to multiple etiologies Delirium should also be specified as acute or persistent, as well as hyperactive, hypoactive, or mixed level activity. o Distinguishing features- symptoms, subjective complaints, objective findings Distinguishing features: The onset of the disturbance is rapid (hours to days) and typically fluctuates over the course of the day. Cognitive changes (poor memory, disorientation, speech disturbance) and/or perceptual disturbances are distinct from a pre-existing, established, or evolving neurocognitive disorder. Although there are common cognitive disturbances in delirium and dementia, a primary difference is that the patient with dementia usually is alert, whereas the patient with delirium manifests overt disturbances of consciousness or arousal. The rapid onset and course of cognitive impairments and the reversibility of symptoms are helpful in distinguishing between delirium and dementia. The severity of delirium symptoms typically fluctuates over the course of a day, whereas dementia symptoms generally do not fluctuate. Delirium can happen in any medically ill patient, and older adults are more prone to delirium due to pre-existing conditions, aging processes, and greater vulnerability to multiple precipitating factors. Males tend to have a higher incidence rate, and the male gender appears to be an independent risk factor for delirium. Symptoms of delirium: confusion; difficulty sustaining and shifting attention; extreme distractibility; disorganized thinking; rambling, irrelevant, pressured, and incoherent speech; impaired reasoning ability and goal-directed behavior; disorientation to time and place; impairment of recent memory; misperceptions about the environment, including illusions and hallucinations; emotional instability; and psychomotor activity that fluctuates between agitation, purposeless movements, and a vegetative state. Disorientation to other persons occurs commonly. Dysarthria is a frequent speech and language disturbance, and dysnomia (impaired ability to name objects), dysgraphia (impaired ability to write), or aphasia may be observed. Commonly associated features of delirium include disturbances in the sleep–wake cycle, such as daytime sleepiness, nighttime agitation, and disturbances in sleep continuity. Complete reversal of the sleep–wake cycle or fragmentation of the circadian sleep–wake pattern can occur. Emotional disturbances may include anxiety, fear, depression, irritability, anger, euphoria, and apathy. Affective lability (rapid and unpredictable shifts from one emotional state to another) may occur. Emotional disturbances may include anxiety, fear, depression, irritability, anger, euphoria, and apathy. Affective lability (rapid and unpredictable shifts from one emotional state to another) may occur. Symptoms of subclinical delirium, such as restlessness, anxiety, irritability, distractibility, or sleep disturbance, may be manifested in the days before the onset of overt delirium and may progress to full-blown delirium over the course of a few days. The duration of delirium can range from less than 1 week to more than 2 months and typically resolves within 10 to 12 days. However, for some older persons persistent delirium can last for years. Although delirium was once thought to be reversible, evidence supports that delirium may result in permanent neuronal damage to the brain and increased mortality Subjective complaints: family members report the s/s of dementia. Objective findings: Possible physical and autonomic signs associated with delirium include tachycardia, sweating, flushed face, dilated pupils, and elevated blood pressure. o Common causes * Causes of delirium are numerous and in elderly hospitalized patients there are often multiple etiologies, including metabolic, infection, cardiac, neurological, pulmonary, sensory impairments, medications, and toxins. * Regardless of cause, a consistent finding is significant reduction in regional cerebral perfusion during periods of delirium in comparison with blood flow patterns after recovery. * A possible neurological common pathway may involve acetylcholine and dopamine, and the disruption in the sleep-wake cycle in delirium indicates melatonin as a possible factor. (Kennedy-Malone 59) There is usually evidence from the history, physical examination, or laboratory tests of a direct physiological etiology of a general medical condition, substance intoxication or withdrawal, use of a medication, toxin exposure, or a combination of these factors. Causes of delirium are numerous, and in older adult hospitalized patients there are often multiple etiologies: ■ Metabolic: renal failure, hepatic failure, anemia, hypoxia, hypoglycemia, thiamine deficiency, electrolyte abnormalities ■ Infection: meningitis, encephalitis, sepsis, urinary tract infection (UTI), respiratory infection ■ Cardiac: myocardial infarction, congestive heart failure, arrhythmia ■ Neurological: stroke, intracranial hemorrhage, head trauma, seizures, undiagnosed pain ■ Pulmonary: respiratory failure, COPD causing hypoxia ■ Sensory impairment: visual and/or hearing deficits ■ Medications: benzodiazepines, sedative-hypnotics, opioids, anticholinergics, antihypertensives, corticosteroids, lithium ■ Toxins: alcohol, amphetamines, cocaine, substance intoxication or withdrawal Because the cause of delirium is multifactorial, no single neuropathology of delirium has been identified. Possible neurological pathways may involve oxidative stress, inflammatory responses, and neurotransmitter deficiencies in acetylcholine and melatonin; excesses of norepinephrine, dopamine, and glutamate; and abnormalities in serotonin, histamine, and y-aminobutyric acid. A careful medical evaluation that includes attention to level of oxygenation, possible occult infection (e.g., UTI), and the role of medications is essential. Although many medications can be a causative factor, those with anticholinergic effects are frequently responsible o Prevention strategies A careful medical evaluation that includes attention to level of oxygenation, possible occult infection (e.g., UTI), and the role of medications is essential. Although many medications can be a causative factor, those with anticholinergic effects are frequently responsible. Preventive measures to lessen the likelihood of delirium include elimination or minimization of risk factors. These measures include judicious use of high-risk medications (Beers list; STOPP/START), timely management and good control of acute and chronic medical disease processes, correction of sensory deficits (eyeglasses, magnifying glasses, adequate lighting, hearing aids, cerumen removal), promotion of normal sleep patterns through good sleep hygiene measures, provision of adequate nutrition and hydration with oral/parenteral supplementation as necessary, prompt attention to elimination needs, participation in activities that maintain and stimulate cognitive and physical functioning, and provision of general supportive measures (environmental modifications, reality orientation, control of external stimuli). For hospitalized elders and long-term care residents, encourage frequent visits by family members to provide familiarity, reality orientation, reassurance, and comfort. Treatment: Appropriate treatment for delirium involves discovering the causes, many of which are reversible, and preventing complications through prompt treatment of specific, identified disorders. A thorough, comprehensive assessment; evaluation of medications, interactions, and contraindications and ordering of laboratory work will assist in ruling out/in the many etiologies of delirium. While assessing for probable etiology and definitive treatment, management should focus on ensuring safety from behavioral disturbances by combining environmental, behavioral, and pharmacological therapies. Quality improvement models of care, such as the Hospitalized Elder Life Program (HELP), a prevention model, use a multicomponent strategy with the overall purpose of promoting independence in hospitalized older persons. Protocols are implemented to screen for delirium, treat the underlying cause, and prevent cognitive and functional decline. Acute care for the elderly units in the hospital setting and the designation of delirium beds within these units is another strategy to manage delirium. The framework for using the ABCDE (Awakening and Breathing coordinating, Choice of sedatives, Delirium identification, and Early exercise and mobility) Bundle is also used in critical care settings Nonpharmacological Interventions: A therapeutic environment would include frequent reassurance and reality orientation; clear communication; caregiver consistency; decreased stimuli (noise reduction, adequate lighting, sufficient time to perform tasks); decreased stress and anxiety through frequent reassurance and provision of a daily routine; comfort maintenance (eyeglasses, hearing aids, personal belongings); reestablishment of a sleep– wake cycle by controlling nighttime noise and unnecessary disruptions; guarantee of adequate daily fluid intake; assurance that elimination needs are met; provision of space and programs for physical activity, ambulation, and range of motion; and avoidance of chemical or physical restraint. Medication should be used as a last resort. Pharmacotherapy: Data support the use of first-generation (e.g., haloperidol) and second-generation (e.g., olanzapine, risperidone, ziprasidone, and quetiapine) antipsychotic medications to control behavioral symptoms of delirium and prevent injury to self or others. Antipsychotic medications have significant side effects, especially for older persons with dementia, and should be prescribed at the lowest effective dose and only 1 to 2 days or the shortest interval possible depending upon the setting, such as surgery or intensive care. The avoidance of benzodiazepines except for specific indications (e.g., alcohol or g-hydroxybutyric acid [GHA] withdrawal delirium, delirium related to seizures) continues to be a recommendation. Dementia (Kennedy) Dementia is a neurocognitive disorder and is defined as a clinical syndrome with global cognitive decline from a previous level of baseline function that interferes with activities of daily living (ADLs). Alzheimer’s disease (AD) is the most common cause of dementia, so dementia is mainly referenced as AD. In the differential diagnosis, it is important to ascertain whether an individual has cognitive impairment or an illness with similar or overlapping signs and symptoms such as delirium, depression schizophrenia, bipolar disorder, or other neurological disorder. If there is cognitive impairment, then developmental delay, borderline intellectual functioning, mild cognitive impairment, and other related diagnoses must be ruled out. o Distinguishing features-symptoms, subjective complaints, objective findings : To meet the criteria for minor or major neurocognitive disorders according to the DSM-5, cognitive decline must be in at least one of the following cognitive domains including: complex attention, executive function, learning and memory, language, perceptual motor or social cognition. Once dementia is ruled in, the type of dementia can then be determined. Cognitive changes including confusion, disorientation (as to time, place, person), and impaired short-term memory. Personality changes, psychiatric symptoms, problem behaviors, and changes in daily functioning. AD has a gradual onset, and the course of illness and progression is typically slow. The duration of AD ranges from 3 to 20 years and averages 10 years as comorbidities complicate the course of illness. Symptoms vary from person to person, and cognitive deficits cause significant impairment in social and occupational functioning, impaired ability to care for oneself, and altered behavioral patterns. Signs and symptoms progress from memory loss to impaired executive functioning, language deficits, coordination, and perception with total or partial loss of the ability to recognize familiar people or objects. Impairment in memory and learning (amnestic) is the typical presentation for AD and neuropsychiatric symptoms almost always occur. Signs and Symptoms: Signs and symptoms vary according to the stage of dementia and disease progression. AD is a multiyear brain disease; it is thought to begin well before clinical manifestations appear. Preclinical changes in the brain can begin 10 to 20 years before symptoms present. These changes include diffuse cerebral plaques, neuritic plaques and tangles, neuron and synapse loss, and some cognitive impairment. The onset of clinical symptoms typically begins with memory loss. The duration of each stage varies, and functional changes usually occur late in the disease process. Many patients manifest noncognitive behavioral symptoms (NCBSs) years before being diagnosed with dementia. Once dementia is diagnosed, NCBSs may continue to manifest similarly or progress to symptoms more difficult to manage. Subjective complaints: Caregivers, significant others, or family members often report the following: Apathy, agitation, aggression, combativeness, delusions, hallucinations, depression, anxiety, disinhibition/sexual behaviors, emotional lability, irritability, wandering, sleep disturbances, and sundowning. Objective findings: See below for the clinical presentation of the most common types of dementia o Most common types Differentiation of Dementia: Dementia can be classified as vascular, Lewy body/Parkinson’s, frontotemporal lobe/Pick’s disease, or mixed (Alzheimer’s Association, 2016; APA, 2013). Vascular Dementia ■ Sequelae from transient ischemic attacks, mini-strokes, cerebrovascular accidents ■ No or little cortical shrinkage ■ Cognitive, behavioral, and functional losses defined by area of infarct ■ Stepwise deterioration over time Clinical Presentation: ■ Abnormal executive functioning ■ Impaired psychomotor performance ■ Changes in personality and mood ■ Disturbances in gait (slow and unsteady) ■ Hyper-reflexia, extensor plantar response ■ Urinary incontinence ■ Hemiparesis, including lower facial weakness ■ Hemisensory deficits ■ Visual problems (field defect, diplopia) ■ Pseudobulbar syndrome (e.g., dysarthria, dysphagia, emotional incontinence) ■ Focal deficits Lewy Body/Parkinson S Dementia ■ Diffuse presence of Lewy body proteins in brain, including cerebral cortex ■ Lewy bodies deplete dopamine ■ Acetylcholine is depleted, causing disruption of perception, thinking, and behavior ■ Resultant parkinsonian symptoms: stiff, shuffling gait, stiffness in arms and legs, tremors, frequent falls, masklike facies with blank stare, flat affect, stooped posture, drooling, runny nose Clinical Presentation: ■ Parkinsonian signs ■ Symptoms may fluctuate as often as moment to moment, hour to hour, or day-to-day ■ Fluctuating cognition, varying degrees of alertness and attention ■ Progressive memory loss ■ Visual hallucinations ■ Rapid eye movement (REM) sleep difficulties Frontotemporal Lobe Dementia/Pick’s Disease ■ Gradual and progressive changes in behavior—socially inappropriate, disinhibition, easily frustrated, impulsive, compulsive behaviors; or ■ Gradual and progressive language dysfunction—problems with expression of language, incorrect words, naming objects ■ Difficulties with reading and writing Mixed Dementia ■ More than one type of dementia (e.g., combination of AD and vascular dementia) Etiology: The etiology of dementia includes numerous systemic disorders; however, most cases of dementia are irreversible because dementia is a progressive disease process unto itself. ■ Central nervous system (CNS) disorders: mild cognitive impairment (MCI), AD (most common type of dementia, 60% to 80%; one-half of cases are mixed dementia related to other pathology), Lewy body dementia (10% to 25%), Parkinson’s disease (incidence one-tenth of AD), vascular dementia (10%), primary degenerative dementia, frontotemporal dementia or Pick’s disease (10% of persons 45 to 60 years old), Huntington’s disease, normal pressure hydrocephalus (5%) ■ Cardiovascular disease: cerebral hypoxia/anoxia, vascular insults to brain, cardiac arrhythmias, inflammatory blood vessel disease ■ Infectious processes: AIDS, Creutzfeldt-Jakob syndrome, neurosyphilis ■ Liver disease: chronic progressive hepatic encephalopathy ■ Neoplastic conditions: intracranial lesions, primary or metastasis ■ Pulmonary disease: respiratory encephalopathy, COPD/CO2 toxicity ■ Urinary tract disease: UTI, chronic or progressive uremic encephalopathy Age: Early-onset AD affects those 65 years old or younger, is usually familial, and represents less than 5% of AD cases. Late-onset AD affects those age 65 years and older and may or may not be related to family history. Gender: More women than men have dementia, primarily because women live longer. Ethnicity: African Americans and Hispanics are at highest risk of developing AD. African Americans are approximately twice as likely to develop AD than Caucasians, and Hispanics have approximately one and one-half times the risk of their Caucasian counterparts. Contributing Factors: Risk factors for AD are designated as actual and probable. Actual Risk Factors ■ Age ■ Genetics/family history ■ Gene mutations chromosomes 1, 14, 21 ■ A 50/50 chance of developing early-onset AD if one parent had AD ■ Apolipoprotein E (ApoE) gene on chromosome 19 ■ ApoE alleles e2, e3, e4 ■ Possibly chromosomes 9, 10, 12 ■ Microglial TREM2 gene triples the risk of AD ■ Down syndrome ■ Less than 5% of AD cases are caused by rare genetic variations found in a small number of families worldwide. In these inherited forms of AD, the disease tends to develop before age 65 years, sometimes in people as young as 30 years old. The genetic mutations involve the following chromosomes: ■ Chromosome 21 on the gene for the amyloid precursor protein ■ Chromosome 14 on the gene for the presenilin 1 protein ■ Chromosome 1 on the gene for presenilin 2 Probable Risk Factors ■ Low educational level, low lifetime achievements ■ More years of education (versus fewer years) provides a “cognitive reserve” that enables compensation for symptoms of AD/other dementia ■ Differences in education and dementia risk may reflect increased risk for disease in general and less access to medical care in lower socioeconomic groups ■ Female gender, low estrogen levels ■ Framingham Study: Lifetime risk for any dementia in females who reached age 55 years = 21% and for males = 14% ■ Depression, brain injury ■ Cardiovascular disease, hypertension, type 2 diabetes mellitus, smoking, obesity o Duration of preclinical symptoms Duration of preclinical symptoms: The National Institute on Aging and the Alzheimer’s Association workgroup introduced diagnostic staging for AD, including preclinical, mild cognitive impairment due to AD, and dementia due to AD. TABLE 16-5 Stages of Alzheimer’s Disease and Associated Symptoms STAGE ASSOCIATED SYMPTOMS Preclinical Impaired memory, excused or covered Insidious instrumental ADLs losses (money handling, bills) Preserved basic ADLs Poor judgment and decisions Subtle personality changes Decreased spontaneity, sense of initiative Increased anxiety, socially normal Mild- Obvious memory impairment moderate Overt instrumental ADL impairment Basic ADLs failing Prominent behavioral difficulties Shortened attention span Language difficulty Variable social skills Supervision required Severe Memory fragments only No recognition of familiar people Assistance with basic ADLs required Fewer troublesome behaviors Reduced mobility Weight loss, infections Seizures, dysphagia Incontinence Groaning, moaning, grunting o Treatment (note black bx warnings) A comprehensive, multidimensional treatment plan for dementia includes biological, psychotherapeutic, social, family, and pharmacological interventions. Biological Interventions: Treat underlying medical disorders with medications, medical or surgical procedures, and ongoing evaluation and management as indicated. Psychotherapeutic Interventions: Include behavioral management, reminiscence therapy, validation therapy, supportive psychotherapy, sensory integration, simulated presence therapy, reality orientation, skills training, recreation and art therapy, exercise, and aromatherapy. Social Interventions: Include a functional and safety assessment, environmental modifications, assessment for abuse and neglect, provision of supervision and home health care, cleaning and meal services, assessment for appropriate level of care, financial and estate planning, and legal provisions for power of attorney. Family Interventions: Include caregiver education, training and support, respite care, and support groups. Pharmacotherapy: Cholinesterase inhibitors (ChEIs) are the cornerstone of pharmacological therapy, with the aim to enhance or preserve cognitive and behavioral status. Acetylcholine is important for the functioning of brain cells involved in memory, thought, and judgment, and brain levels are significantly decreased in those with AD. ChEIs inhibit breakdown of acetylcholine, which increases levels within the brain; this mechanism of action may improve or delay a decline in memory. ChEIs are effective in approximately 30% of patients and are not curative, preventive, or disease-reversing agents. The choice of ChEI is based on the patient’s clinical presentation and comorbid conditions.The three commonly prescribed ChEIs are donepezil, rivastigmine, and galantamine. Clinical and safety issues for ChEIs include medical and psychosocial factors before drug initiation, consideration of when to initiate the medication, and side effects, which are fewer with slower dose titration. Careful monitoring for efficacy and side effects is necessary. Common side effects of ChEIs are nausea, vomiting, dyspepsia, anorexia, diarrhea, insomnia, vivid dreams, fatigue, increased urination, and cramps. Uncommon side effects of ChEIs are syncope, bradycardia, confusion, depression, and agitation. Use cautiously in patients with liver or gastric disease, COPD, bradycardia, and inadequate supervision. Considerations regarding when to stop ChEIs may include intolerable side effects, new medical contraindications, poor compliance, lack of supervision, and rapid cognitive and/or functional decline. Any benefits of treatment are rapidly lost upon discontinuation. Long-term treatment may continue to offer advantages such as slowing of cognitive decline, continued ability to perform ADLs, fewer noncognitive behavioral symptoms, and decreased caregiver burden. Another medication approved to treat dementia is memantine (Namenda), an N-methyl-D-aspartate (NMDA) receptor antagonist. Memantine assists in regulating high levels of glutamate in the brain, typically found in AD. Common side effects include headache and constipation, and an uncommon side effect is confusion. Memantine is excreted through the kidneys, and caution is advised in patients with renal impairment. Combination therapy of memantine with a ChEI is a good strategy, because these medications work differently (NIA, 2016). Usually medications are started when AD severity is moderate, but they can be initiated earlier depending on individual patient clinical presentations (see Table 16-7). DONEPEZIL (ARICEPT) CHEI RIVASTIGMINE (EXCELON) CHEI GALANTAMINE (REMINYL) AND EXTENDED RELEASE (RAZADYNE) CHEI FDA approval 1996; mild, moderate, severe AD 2000; mild, moderate AD 2001; mild, moderate AD Benefit Typically well tolerated; improves cognitive and behavioral status, Improves cognitive, behavioral, and functional impairments; is more selective for Significantly improves cognitive, behavioral, and caregiver burden, and capacity for ADLs central processes and regions critical for cognition and memory functional symptoms of AD Dosage strengths (mg) 5, 10 1.5, 3, 4.5, 6 4, 8, 12 Extended Release: 8, 16, 24 Oral solution 1 mg/mL 2 mg/mL 4 mg/mL Starting dose 5 mg qd 1.5 mg bid 4 mg bid Maximum 10 mg qd 6 mg bid 8–10 mg bid recommended dose Extended Release: 16–24 mg qd TI/2 (hours) 73 5 6–8 Plasma protein binding CYP450 substrate of CYP450 inhibitor of 96% 40% 18% 2D63A4 NA 2D63A4 NA NA NA CLINICAL FEATURES DEMENTIA DELIRIUM DEPRESSIO Onset Insidious Rapid May be abrup Course Long, progressive Short, diurnal variation Situational Duration Months to years Hours to 1 month 2 weeks, mon Awareness Clear Reduced Clear Alertness Normal Impaired Normal Orientation Impaired Impaired Selective Thought process Poor, abstract thinking; diminished thoughts; poor judgment; difficulty with word finding/verbalizing Disorganized, distorted, fragmented, diminished or expansive thoughts, incoherence Intact, linear; hopelessness, self-esteem Perception Frequent misperceptions Distorted with illusions, delusions, hallucinations Intact Psychomotor Normal, apraxia Varies/mixed; Varies with re behavior hypokinetic, hyperkinetic agitation, reta Sleep-wake Fragmented, disturbed, reversed Disturbed, reversed Disturbed sle cycle (increased/de mid, late inso Associated Affect superficial, labile, Variable affective Affect and m features inappropriate; may be in attempt changes, increased increased som to conceal deficits arousal, personality preoccupation Mental status Increased effort to find exaggeration Distracted from task, Inability to fo testing appropriate replies, frequent inability to focus makes little ef 8 Dunphy: ➢ Ch.78 (Palliative Care and Pain Management p.1299-1309) ➢ Ch. 77 End of Life Decision Making only (p. 1293-1294) Kennedy: ➢ Chapter 19: Palliative Care and End-of-Life Care (The Dying Patient only) near-miss answers, word searching Ethical Issues and End of life care o Barriers to end of life care o Differences between palliative care and hospice Advanced directives/Advanced care planning (ACP) o Barriers to ACP o Durable power of attorney for healthcare POLST o Criteria Palliative care o eligibility criteria o Services offered o Length of eligibility o Symptom management (Kennedy table 19-4) Hospice o eligibility criteria o Services offered o Length of eligibility o Symptom management (Kennedy table 19-4) Pain management options in palliative and hospice care (Kennedy) • Indications- most appropriate medications for each type of pain • Onset of action for most common medications • Most effective pain medication for terminally ill patients • Medication side effects Types of pain- shows indiffe 1. Nociceptive pain represents a normal response to injury of tissue • Somatic pain, which is pain arising from muscles joints, and cutaneous tissue • Visceral pain, which is pain arising from organs and smooth muscle. • Appropriate medications: opioid analgesics and NSAID agents 2. Neuropathic pain is caused by somatosensory impulses in the nervous system - Diabetic neuropathy, postherpetic neuralgia, postamputation pain, and poststroke pain • Appropriate medications- antiepileptic drugs, antidepressants, and local anesthetics. Gabapentin is an antiepileptic medication that is effective for nerve pain. Amitriptyline is a tricyclic antidepressant that is effective for neuropathic pain as well • Methadone is also used for severe pain and may be effective for neuropathic pain. i. Methadone has a slow onset and long duration of action and half-life Morphine is considered the most effective medication for pain in terminally ill patients because it has fewer side effects Codeine is the most constipating opioid and is less effective than others when give alone Fentanyl is commonly used in transdermal preparations for severe chronic cancer pain. Chart 78:1 on 1306 has common pain medications, indications and prescribing info- including onset and side effects Grief (Kennedy) • Complicated- symptoms, duration • Uncomplicated- symptoms, duration [Show More]

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