Module 21 – Flashcard
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What Is Midlife? Erickson?
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40s the new 30, 50s the new 40 . . . Men and women ages 45-65 Developmental focus shifts to generativity vs. stagnation (Erikson) Generativity: focus on sharing wisdom and skills with the younger generation and leaving a legacy (family members/mentor to coworkers) Stagnation: maintenance of the status quo (Erikson)
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leading cause of death midlife
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Cancer (lung, colorectal, breast) Heart disease Unintentional injury (MVA) HIV diseases Suicide Homicide Obstructive lung disease Diabetes
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Take a Thorough History for midlife Medical history
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Acute and chronic illnesses (hospitalization and transfusions) Risk factors (CHD, diabetes, cancer, asthma, mental illness) Allergies and reactions Immunization status Recommended physical, dental, vision and hearing screenings
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What to screen for in midlife?
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Obesity Tobacco/alcohol use Depression High blood pressure Osteoporosis (women) Breast cancer (women) Colorectal cancer Cervical cancer (women) Lipid disorders (men) Chlamydia infections (women) Diabetes mellitus (type 2) In adults with HTN/dyslipidemia Prostate cancer (men)
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General Health Screening
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Obesity Screen all adults. Tobacco use Screen all adults. Alcohol use Screen all adults. Depression Screen all adults, but make sure there is support for the patient.
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Cardiovascular Risks
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Cigarette smoking/sedentary lifestyle/obesity Lifestyle modifications Screen all patients: Blood pressure and hypertension (BP >140/90 mmHg or on antihypertensive medication) (increased risk) Recommended to screen every 2 years Diabetes mellitus Screen based on risk factors (HTN, dyslipidemia, obesity) No specific time line given as to when to screen (USPSTF) Increased prevalence of lipid abnormalities Postmenopausal women with type 2 DM 3 times more likely to develop CVD/stroke and 4 times more likely to die from MI
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CV screening - Lipid profile recommendations
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Lipid profile USPSTF (2008) recommends screening at age 35 years in men and 45 years in women who have increased risk factors. USPSTF (2008) makes no recommendation for/against screening women with no risk factors over age 20. All patients with CHD or CHD risk equivalents (PAD, AAA, CAD, DM, and patients with multiple risk factors)
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Thyroid screening
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USPSTF (insufficient evidence to screen) Currently reevaluating the guidelines for screening The American Thyroid Association recommends adults be screened beginning at age 35 years and every 5 years thereafter
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Glaucoma screening
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USPSTF (insufficient evidence to screen) Perform glaucoma screening every 2-4 years before age 60 and every 2 years after (AAO)
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Oral Health Screening
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Important to consider Cavities? Oral hygiene Regular dental check-ups
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Additional Health Screening
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HIV and STIs U/A periodically after age 60 Vitamin D deficiency? USPSTF screening? Still researching (2013) Safety concerns: domestic violence
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Colorectal Cancer: increased risk??
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About 1 in 19 people will develop cancer of the colon or rectum at some point in their lifetime. Screening could potentially save 18,800 lives/year (USPSTF). Regular screening and removal of polyps can reduce risk by up to 90%. Increased risk: heredity component, age, race (AA more likely), diet (diet in processed meats and red meat), sedentary lifestyle (increased exercise reduces risk).
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Colorectal Cancer Screening
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Women and men over age 50 with average risk of colorectal cancer USPSTF Guidelines (2008) Begin screening men/women at age 50 with FOBT (annual), colonoscopy (q10years) or sigmoidoscopy (q5y with q3y high sensitivity FOBT), continuing to age 75.
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Immunizations for midlife folks
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Herpes Zoster (Recommended for persons 60 years and older) single dose 0.65ml SQ Tetanus, diphtheria, pertussis (Td/Tdap) Given every 10 years (1 dose Td booster) MMR (1 dose) If born before 1957, considered immune Influenza (yearly) Hepatitis A (two doses) if at risk Hepatitis B (three doses) if at risk
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Screening for women in midlife
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Obesity, smoking, depression, alcohol Cardiovascular risks (HTN, DM) Osteoporosis Breast cancer Endometrial cancer Ovarian cancer Cervical cancer Colorectal cancer
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Breast Cancer Screening
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Second leading cause of cancer deaths to women (lung #1) Tumors of the breast typically metastasize late in the preclinical course (before detectable size) Mammography detects 80-90% of breast cancers Screening for BRCA1/BRCA2 gene (only if sufficient risk factors identified)
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Genetic Testing for breast CA
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Women who are known BRCA1/BRCA2 mutation carriers have a 40-80% lifetime risk of developing breast cancer. Recommendation of clinical BE every 6 months, annual mammography and breast MRI.
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Risk Assessment in Breast Cancer
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Individuals with one first-degree relative with breast cancer have twofold risk, with two first-degree relatives have a threefold risk. Risk increases if bilateral breast cancer. Prolonged duration of menses can increase risk. More dense breast tissue increases risk.
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Risk Assessment Models: Gail model Claus model
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Gail model Age of menarche Number of breast biopsies Number of first-degree relatives with breast cancer Age at first live birth Claus model Predicts probability for development of breast cancer who has family history Useful in younger women
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Guidelines: Breast Cancer Screening
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USPSTF 2009 recommended screening every 2 years for women over the age of 40 if increased risk factors. USPSTF 2009 recommended screening every 2 years for women 50-74 (regardless of risk factors). Insufficient evidence for or against recommendation on SBE The American Cancer Society (ACS) recommends annual mammogram screenings at age 40, as well as CBE.
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Endometrial Cancer
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Endometrium is the inner glandular lining of the muscle of the uterus. Most common female genital tract cancer and fourth-most common malignant neoplasm in women. Mean age of diagnosis is 61. Most common presentation is postmenopausal bleeding. Pelvic u/s evaluates the thickness of the endometrial lining (should be Refer to GYN for biopsy.
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Uterine/Endometrial Cancer Screening: risk factors?
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Risk factors: Incidence increases with age Hx of endometrial hyperplasia (increase in cells in the lining of the uterus) Hormone therapy (using estrogen without progesterone) (increased exposure to estrogen) Obesity Tamoxifen (used to treat/prevent breast cancer) Race (white women more likely than African American)
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Ovarian Cancer - Increased Risk
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Risk increases with age Family hx of ovarian cancer Fertility drugs Menopausal hormone therapy Personal hx of breast and/or colon cancer BRACA1 mutation (20-60% risk) BRACA2 mutation (10-35% risk)
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Ovarian Cancer - decreased Risk
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Oral contraceptives (longer the use, lower the risk) Childbearing and breast-feeding Tubal ligation or hysterectomy Surgical removal (prophylactic)
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Detection for CA Ovarian CA
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Once pelvic performed, a transvaginal u/s should be ordered. If pelvic mass found, then serum cancer antigen 125 (CA-125) ordered.
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Other causes of elevation of CA-125
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Acute PID Endometriosis Functional ovarian cyst Ovarian hyperstimulation Renal disease Chronic liver disease Systemic lupus erythematosus Poorly controlled DM
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Ovarian Cancer: Screening Recommendations
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In 1996 USPSTF recommended against screening for ovarian cancer (no new recommendations). The American Cancer Society (ACS) states to only screen women with strong family hx of disease (transvaginal u/s and CA-125). ACOG recommends being vigilant looking for early signs sx (unexplained weight loss, abdominal or pelvic pain). If warranted: pelvic, transvaginal u/s and CA-125.
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Cervical Cancer
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Median age for diagnosis is 48 years. Incidence 1.5x greater for African American women than Caucasian women. Death rate for black women is twice that of white women. 75% of all cervical cancers are squamous cell carcinomas. HPV is the precursor. High-risk types 16 and 18 account for 70% of all cervical cancers. Perform a Pap test; refer to GYN for biopsy/colposcopy. ACOG 2013 guidelines: Agrees with current USPSTF guidelines Screen ages 30-65 every 5 years with cotesting (Pap and HPV testing) if 3 consecutive Paps nl No need to screen s/p hysterectomy
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Cervical Cancer symptoms
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SX: abnormal uterine bleeding, foul vaginal discharge (thin/watery), leg pain, GU/GI symptoms.
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Osteoporesis Screening
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Risks for fracture: Advanced age Smoker Low calcium or vitamin D intake More than two alcoholic drinks/day Hip fracture in parent Thinness or low BMI Increased fall risk (impaired vision, dementia, poor health, low physical activity) Chronic corticosteroid treatments
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Osteoporesis - Skeletal System Effects
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Bone loss starts in fourth decade at the hip. Bone loss from spine closely related to estrogen deficiency (starts about 2 years before last menses). Risk for osteoporesis increases after menopause.
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Osteoporesis - treatment
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Treatment Diet and exercise! Medication Recommend dexa scan if >65 or at high risk
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Nutritional Supplements: Calcium
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Requirements increase with menopause due to bone resorption rate increase. Calcium absorption may be limited due to a lack of vitamin D. Recommended: adults age 50+ = 1,200 mg/d Other dietary factors that limit absorption are oxalic acid (spinach, rhubarb, and other leafy green vegetables).
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Nutritional Supplements: Vitamin D
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Target vitamin D status: serum 25(OH)D >30 ng/ml Usually achieved with at least 600-800 IU/d >800 IU/d with calcium can reduce the rate of postmenopausal bone loss Sources: oily fish (salmon), wild fish better than farm raised; milk (100 iu/8oz)
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Osteoporosis Treatment - Bisphosphonates
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Alendronate (Fosamax): 5 mg/d or 35 mg/week (prevention); 10 mg/d or 70 mg/week (treatment) Alendronate + Vit. D (Fosamax plus): 70 mg + 2,800 IU/wk (treatment) Must stand or sit upright for at least 30 min after taking Risedronate (Actonel): 5 mg/d or 35 mg/week 75 mg in 2 consecutive d/mo; 150 mg/mo Ibandronate (Boniva): 150 mg/mo (can be IV q 3 mo) Etidronate (Didrocal): 400 mg/d for 14 days every 3 mo Zoledronic acid (Reclast): IV 5 mg/2yr
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Definition: Menopause
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Permanent cessation of menstruation resulting from the loss of ovarian follicular activity Natural menopause: no menstrual period for 1 full year and experience cessation of ovulation
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What ages do women experience menopause in Western countries? Is there a relationship between a woman's age at menarche and her age at menopause?
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experience between ages 45 and 55 (median age 50-52). No known relationship between a woman's age at menarche and her age at menopause.
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Factors Affecting Age of Menopause
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Genetic variations Environmental exposure Smoking accelerates menopause by 1.5 to 2 years. Childhood cancers (ovarian exposure to radiation, Hodgkin's lymphoma) have 8% change of premature menopause. Other factors Nulliparity Type I DM (experience it earlier) Epilepsy
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Different Types of menopause
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1. Induced menopause: abrupt stop of menstruation due to bilateral oophorectomy or chemotherapy *Causes abrupt cessation of ovarian function *Decrease in estradiol, testosterone, and dehydroepiandrosterone *Noted to have increased vasomotor symptoms 2. Premature: occurs before age 40 3. Genetic or autoimmune factors 4. Premature ovarian failure (POF): full or intermittent loss of ovarian function in women younger than 40 years *Affects approx. 1% of women under 40
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Pathophysiology of menopause
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*Changing levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, estrone, and adrenal steroids *Elevated FSH first measurable sign of reproductive aging (>10 IU/L) *Increased FSH recruit more follicles per cycle (leads to follicular atresia) *Overproduction of estradiol by this enlarged cohort of recruited follicles may be responsible for perimenopausal symptoms (bloating, irritability, mastalgia, menorrhagia, growth of uterine fibroids)
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perimenopausal symptoms include what?
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bloating, irritability, mastalgia, menorrhagia, growth of uterine fibroids
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Clinical Symptoms of menopause
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Cardiovascular changes Hot flashes Sleep disturbances Vulvovaginal symptoms Sexual function Fertility issues Urinary issues
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Hot Flashes
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Vasomotor: Second-most common symptom, experienced by 85% of postmenopausal women. Patho still not understood (thought to be related to decreased estrogen levels). More frequent and severe at night or during times of stress.
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How could you offer help for hot flashes?
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Encourage lifestyle changes such as wearing light-colored clothing; lowering thermostat; avoiding spicy foods, caffeine, and alcohol; relaxation techniques.
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Sleep Disturbances
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Early morning waking responsive to estrogen therapy (ET) Poor sleep (inadequate quantity or poor quality) Can lead to performance deficits, muscle aches, inability to concentrate, irritability Women on hormone therapy have shorter sleep latency and more frequent rapid eye movement (REM) sleep
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Vulvovaginal Symptoms during menopause
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Urogenital atrophy Caused by decreased estrogen levels Increased vaginal pH, thinning vaginal mucosa, reduced vaginal secretions, reduced compressibility of the urethra Vaginal walls are thin, pale, dry, and possibly inflamed Leads to vaginal irritation, dryness, itching, and irritation of the vulva, pain during intercourse, urinary incontinence
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Want to rule out vulvar cancer with what finding? What is usually associated with a lump on the GYN exam? Refer to GYN for evaluation and biopsy
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Urogenital atrophy
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Sexual Function during menopause
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Sexual desire decreases with age in late 40s-50s. Decreased estrogen causes a rapid change in epithelial lining of the vagina. Decreased elasticity can result in discomfort during sex. Leads to vascular, muscular, and connective tissue changes over time Decreased vascularization makes engorgement and lubrication difficult Impairing touch and vibration perception Delaying orgasm → reducing satisfaction
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Fertility during menopause
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Begins to decline around age 35-38 or 10-15 years before menopause. Associated with increased risks of chromosomal abnormalities and complications (premature labor and fetal mortality). Age-related uterine changes may contribute to decreased fertility without any changes in menstrual cycle.
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Urinary Issues - Two different types of incontinence
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Stress - Occurs with cough, laugh, sneeze, exercise Due to poor urethral support and urethral sphincter weakness Urge - Leaking due to sudden urgency to get to bathroom Due to detrusor instability (bladder muscle overactivity)
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which type of incontinence is due to detrusor instability (bladder muscle overactivity)
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Urge incontinence
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which type of incontinence is due to poor urethral support and urethral sphincter weakness
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Stress incontinence
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Overactive bladder
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Urinary urgency with frequency (>8 voids/24 hr) and nocturia
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Possible causes of overactive bladder:
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Behavioral causes Neuromuscular problems (never damage to lower spine) UTIs (symptomatic vs. asymptomatic) Interstitial cystitis (chronic pelvic pain) Bladder cancer
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Treatment Options for overactive bladder
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Determine the type of incontinence Discuss how bothersome symptoms are to the patient *Behavioral modification Avoiding bladder irritants Timed voidings Hydration Constipation management *Kegel, kegel, kegel! *Medications Detrol LA, Ditropan, Toviaz, Sanctura, VESicare, Enablex, Oxytrol (patch), Gelnique (solution) All anticholinergics that quiet bladder spasms and decrease urgency to void SE: dry mouth, constipation Myrbetriq Newer medication, beta-3 agonist (targets bladder in a different way, but quiets bladder spasms)
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What did the Women's Health Initiative (2002) warn women?:
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WHI: warned that HRT leads to higher risks for breast cancer, CV events, blood clots, cognitive decline.
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What did the Heart and Estrogen/Progestin Replacement Study show?
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(HERS) - Showed an increased risk in heart disease that was reversible.
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What did the HERSII Study show?
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HERS II reevaluated benefit of HRT as cardioprotectant and found no benefit.
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2004 Women's Health Initiative Memory Study (WHIMS) showed what?
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WHIMS: Showed that women >65 who were started on HRT had a negative effect on cognition (worse if already had decline).
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Another study on hormone therapy showed what?
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that women who were on HRT ages 50-63 had a lower risk of developing Alzheimer's disease.
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Hormone Therapy Now says what?
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HT is initiated within 10 years of menopause or in women Age of starting HT is important. (Younger is better; shorter duration is better.) HT can increase risk for adverse outcomes in women who have heart disease or high risk. Prolonged use (>5 years) can increase risk of breast cancer (although decreases risk of colon cancer and osteoporosis).
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Please note how we refer to menopause therapy now:
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We do not use the term hormone replacement therapy anymore. It's now referred to as hormone therapy.
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Cardiovascular Effects of hormone therapy
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Increased risk after menopause (suggesting estrogen has a cardioprotective benefit) Difference in data collection, reevaluation of the WHI study (observational and preclinical vs. RCT; time of initiation of ET (younger vs. older) Data very susceptible to interpretation! Be careful!
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HT Recommendations: What does the USPSTF recommend?
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1. against the use of combined estrogen and progestin for the prevention of chronic conditions in postmenopausal women. 2. Recommends against use of estrogen for the prevention of chronic conditions in post menopausal women who have had a hysterectomy.
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HT Recommendations: What does the North American Menopause Society (NAMS) (Guidelines 2012) recommend?
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NAMS (Guidelines 2012) Support the initiation of HT around the time of menopause to tx menopause related sx and to prevent osteoporosis in high risk women. Use of the lowest dose for the least amount of time should be used. Treatment should be reevaluated annually.
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Nurse Practitioners in Women's Health (NPWH) recommends what for HT?
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No stance against/for HT. Stance against bioidentical hormones (2005).
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What are some Effects of HT?
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HT remains the most effective treatment available for menopausal symptoms (hot flashes, night sweats, impaired quality of life). If a pt has blood clots, heart disease, stroke, or breast cancer, may not be in best interest to tx pt. Most healthy women Increased risk of stroke and blood clots (PE) 1/1,000
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What are some goals of hormone therapy?
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1. reduce estrogen depletion symptoms (vasomotor symptoms, sleep disturbances, lethargy, depressed mood), prevent osteoporosis, and minimize SE 2. Helps to manage - Vasomotor sx, vaginal sx, sexual fxn, urinary health, bone density, reduce risk for DM type II
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What are some benefits of Estrogen-only therapy (ET)?
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Estrogen-only therapy (ET) Used by women who have had a hysterectomy
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What are some benefits of Estrogen-plus-progestin (EPT)
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Usually used by women with a uterus to reduce risk of endometrial hyperplasia and cancer associated with ET
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What are the Three main types of estrogen In the body these are all produced from androgens through actions of enzymes.
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Estrone (E1), estradiol (E2), and estriol (E3)
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What is the predominant form in nonpregnant females
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Estradiol (E2)
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Which estrogen is produced during menopause
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Estrone
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Which estrogen is the primary estrogen of pregnancy.
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Estriol
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From menarche to menopause the primary estrogen is which one?
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17β-estradiol.
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In postmenopausal women which type of estrogen is more present?
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more estrone is present than estradiol in postmenopausal women.
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Which estrogen is produced from testosterone and which one from androstenedione by aromatase.
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Estradiol (testosterone) estrone (androstenedione by aromatase.)
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Progesterones include what?
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Progesterone (hormone secreted by the ovary and placenta) Progestins (synthetic steroids that mimic the actions of endogenous progesterone) Range in formation (Provera, Cycrin, Amen) Prevent overproliferation of endometrial tissue, which occurs in the presence of unopposed estrogen (which can result in endometrial hyperplasia and endometrial cancer) Can be used to help with irregular bleeding from uterus and restore normal menses (younger women)
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What can be used to help with irregular bleeding from uterus and restore normal menses (younger women)
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Progesterones
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Most commonly used ET therapy:
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ET therapy: Premarin tablets (0.3 mg, 0.45 mg, 0.625 mg, 0.9 mg, 1.25 mg/d) Femtrace tablets (0.45 mg, 0.9 mg, 1.8 mg/d)
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Most commonly used Progestin therapy::
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Provera tablets (2.5 mg, 5 mg, 10 mg/d)
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Most commonly used Progesterone therapy:
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Prometrium tablets (100 mg, 200 mg/d)
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Most commonly used ET +P:
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Prempase (0.625 mgE +5.0 mg P/d) Prempro (0.625 mgE +2.5 or 5.0 mg P)
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Vaginal Hormone Therapy
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Dispensed in cream, tablet, ring formulations. Vaginal estrogen causes only a slight increase in blood E2 level, has fewer contraindications and adverse systemic effects than oral HT. No progesterone needed. Local estrogen has minimal systemic absorption (no effect on vasomotor symptoms or bone density).
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What are some benefits from Vaginal Hormone Therapy
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causes only a slight increase in blood E2 level, has fewer contraindications and adverse systemic effects than oral HT. minimal systemic absorption (no effect on vasomotor symptoms or bone density).
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What are some Vaginal Estrogen Therapies
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Premarin cream (0.625 mg) conjugated estrogen cream Loading dose 2-4 g/day x 2 weeks, then 0.5-1.0 g up to 3x/week Vagifem tablet (25 mcg of 17 beta-estradiol in a matrix) One tablet inserted into vagina 2x/week. The tablet matrix hydrates once inserted and adheres to the vaginal wall, where E2 is gradually released and absorbed into vaginal epithelium.
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Vaginal Estrogen Therapies: Vaginal Rings
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Vaginal ring: Estring delivers 7.5 mcg of E2 consistently over 24 hours Worn continuously for 3 months E2 blood levels not raised significantly by the ring (FSH, LH, and E2 levels remain in menopause range) Femring (estradiol acetate containing ring) Available in two-dose strengths: 0.05 and 0.1 mg/day Worn continuously for 3 months
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Other Vaginal Lubricants
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K-Y jelly Replens (OTC) Reduce urogenital symptoms (helps with maturation of the vaginal epithelium) Reduces the pH of vaginal secretions (reduces episodes of atrophic vaginitis and UTIs) Valera Organic, increases lubrication
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Bioidenticals for menopause
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Preparations compounded for an individual according to prescription Questioned purity, quality, and consistency of the substance Not FDA approved However, there are a few commercially available hormones that are approved by the FDA and are considered by proponents to be bioidentical based on formulation Controversial (not recommended by NAMS, the Endocrine Society, or the FDA)
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Bioidentical Hormones for menopause
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*17B-Estradiol (E2) is the most studied bioidentical estrogen - Approved by the FDA for management of menopausal symptoms. *DHEA: bioidentical hormone? Precursor to testosterone, many hope that it might provide some improvement in sexual function. *Testosterone: approved by FDA for palliative tx of metastatic breast cancer and in combo with estrogen for management of menopausal vasomotor symptoms Controversial use.
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Herbal Medications for menopause
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Soy Plant estrogens found in beans, particularly soybeans. High isoflavone intake (about 50 grams of soy protein per day) may be helpful in the short term (2 years or less) in relieving hot flashes and night sweats. Taken over the long term, it also may have beneficial effects on cholesterol and bones. St. John's wort May be helpful in the short term (2 years or less) to treat mild to moderate depression in women (when given in doses of less than 1.2 milligrams a day) Others: Black cohosh, Red clover, Ashwagandha, wild yam
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What are the herbs: Black cohosh, Red clover, Ashwagandha, wild yam used for
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menopause
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What herbal remedies may be helpful in the short term (2 years or less) in relieving hot flashes and night sweats
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High isoflavone intake (about 50 grams of soy protein per day)
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What diet changes may be beneficial for menopause?
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Adding more protein High-quality fats Limit refined carbs, sugar, gluten, and processed foods
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Screening for middle aged male
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Obesity, smoking, depression, alcohol Cardiovascular risks (HTN, DM) Osteoporosis Colorectal cancer Prostate cancer
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Hypertension and Diabetes in middle aged male race?
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Men are at greater risk for HTN and DM Race (AA, Latino, Asian American or Island Pacific) noted increased risk Decreased sleep (can raise sugar levels) Low testosterone (4x more likely to develop DM, according to Hopkins study)
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Osteoporosis in middle aged male. What factors increase risk? such as
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20% of those affected by osteoporosis are men - Each year 80,000 men break a hip.. *family history, taking steroid medicines, not exercising, smoking, drinking too much alcohol or having low testosterone levels can increase risk. low estrogen levels in men can lead to bone loss.
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What can you order if suspect increased risk of osteoporosis?.
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order a bone density
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What can decrease osteoporosis risk.
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Exercise and proper diet (calcium and vitamin D)
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Colorectal Cancer Screening in middle age male [stats]
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In the United States 70,651 men (68,883 women) are diagnosed with colorectal cancer each year. Each year in the United States 28,471 men (28,132 women) die from colorectal cancer. 90% of all cases of colorectal cancer are diagnosed in people age 50 or older. The 5-year relative survival rate for colorectal cancer is 90% if the disease is found and treated early.
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Shown to be increased risk of colon cancer if what?
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diabetic and male.
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Prostate Cancer
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Each year more than 217,000 men in the United States are diagnosed with prostate cancer. 1 in 6 men will be diagnosed with prostate cancer during their lifetime. 1 in 35 men will die from the disease. Incidence varies by race (evidence starting to question this). African American men are 1.5x's more likely than Caucasian.
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To draw PSA or not to draw PSA?
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No reduction of mortality with combined PSA and DRE screening over 11 years f/u Increased incidence of finding prostate cancer in the screened arm
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Practice Guidelines for PSA
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USPSTF recommends against screening. AUA best practice guidelines: begin screening at age 55 and then every 2 years. American Cancer Society recommends active discussion with provider (screening at age 50 PSA/DRE, increased risk begins at age 40).
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PSA: What Is It?
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Prostate-specific antigen (PSA) - Protein produced by normal prostate cells Participates in the dissolution of the seminal fluid coagulum and plays important role in fertility Some PSA escapes the prostate and found in the serum Serum component has been used to track response to therapy in men and track prostate cancer.
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PSA: What Does It Mean?
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Standard level is 0-4 ng/nl Levels vary and can be falsely elevated if recent ejaculation, infection, or instrumentation
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What Other factors that can affect PSA level:
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Age, race Pharmacologic therapies Finasteride (Proscar)/Dutasteride (Avodart) Decrease PSA by 50% (after 3 months)
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Prostate Cancer: How Do We Treat?
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Different therapies Surveillance (watchful waiting) Androgen deprivation therapy Lupron, Zoladex, Trelstar, and Eligard May increase risk for colon cancer Radical prostectomy Open/RRP (radical retropubic prostatectomy) RALPH (robotic-assisted laproscopic prostatectomy)
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Prostate Cancer Screening: Where Are We Going?
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wo companies: Myriad Genetics and Genomic Health Measuring gene activity levels in tumors Compared or said to be better than the Gleason score (way of measuring severity of cancer after biopsy) Genomic Prostate Score - Will be unveiled at AUA meeting this May PCA 3 + (Progensa) - Measures concentration of prostate cancer gene and PSA RNA molecules
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Benign Prostatic Hyperplasia (BPH)
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Noncancerous enlargement of the prostate gland 20% of men >60 years have obstructive and irrigative symptoms that are severe enough to warrant treatment Clinical symptoms Obstructive: urinary hesitancy, decreased force of stream, postvoid dribbling Irritating: frequency, urgency, nocturia
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BPH - what to do in OV and what meds to check?
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Get a good history Check OTC and prescription meds Anticholinergics (impair bladder contractility) Sympathomimetics (increase outflow resistance) Diuretics (increase urine output) American Urological Association (AUA) Symptom Index for BPH sx (form patient completes)
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BPH - diagnostics, exam and diff. diagnosis
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Diagnostics Urinalysis (UTI, hematuria) Baseline serum creatinine PSA Exam DRE Possible bladder scan Differential diagnosis Bladder calculi, urethral stricture, UTI, neurologic disorder, cancer, bladder neck contracture
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BPH - Management and treatment options
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Management Goals Relief of symptoms Slow progression of disease Treatment options Finasteride (Proscar) 5 mg po qd Dutasteride (Avodart) 0.5 mg po qd Alpha-1 blockers (flomax 0.4 mg), (rapaflo 8 mg), (uroxatral 10 mg) Combination drug (Jalyn: Flomax + Avodart) Surgery (TURP, green-light laser)
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Hypogonadism (Low T)
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Low serum testosterone level coupled with any of the following signs/symptoms: Anemia Depressed mood Diminished bone density Diminished energy, sense of vitality, sense of well-being Diminished muscle mass and strength Impaired cognition Increased fatigue Sexual symptoms (decreased libido, ED, difficulty achieving orgasm, diminished penile sensation)
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What Causes Testerone Deficiency?
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Injury, infection, loss of testicles Chemotherapy or radiation treatment for cancer Genetic abnormalities (Klinefelter's syndrome) Hemochromatosis (increased iron in the body) Dysfunction of the pituitary gland Medications (hormones used to treat prostate cancer and corticosteroid drugs) Chronic kidney failure Liver cirrhosis
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What are the 3 variables involved in testosterone deficiency
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Sex hormonesThyroid functionAdrenal functionsex hormones
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Testosterone Measurement
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Total testosterone: normal (300-1,000 ng/dl) Draw between 8-11 a.m. due to circadian rhythm (yields highest level of circulating testosterone)
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Hypogonadism = what also should you check? ↑ LH, ↑ FHS = what? ↓ or nl LH = what?
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If suspicion high, also check FSH, LH ↑ LH, ↑ FHS = primary testicular disorder ↓ or nl LH = secondary pituitary disease Consider checking: Sex binding hormone, LDH
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Testosterone Replacement Therapy
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Testim (5-g tube) - 1 tube/day (50 mg testosterone) Androgel - Gel packets Pump (4 pumps/day = 50 mg testosterone) Axiron - Under the arm 1 swipe = 30 mg (usual dose 60 mg) (each underarm) Injection - Testosterone (100 mg/ml) Inject IM every 2 weeks
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Side effects/risks of Testosterone Replacement Therapy treatment (including labs):
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Acne, oily skin, stimulation of prostate tissue (increased frequency), breast enlargement, decreased testicular size Increased risk of prostate cancer? Lab abnormalities Elevated LFTs (check labs 6 weeks after starting therapy Increase in RBC count Decrease in sperm count Increase in PSA
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Erectile Dysfunction
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Failure to consistently maintain a sufficiently rigid penis to allow for sexual intercourse May also present as a lack of sexual desire or inability to ejaculate (check testosterone) 10-30 million men diagnosed in United States (25% of men >65 years have ED) Half of all men will experience ED at some time and not considered pathologic (alcohol/drugs/stress/situational)
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some organic causes of ED non-organic?
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Organic causes: Arteriogenic inflammatory (prostatitis, stricture, urethritis) Post-op (never or vascular injury from prostatectomy) Occlusive (pelvic injury, atherosclerosis) Traumatic (pelvic fracture, urethral rupture) Mechanical (chordee, phimosis, peyronie's disease, obesity) Chemical (ETOH, prescription drugs, marijuana) Endocrine (testicular failure, pituitary failure) Neurogenic (neuropathy, multiple sclerosis, temporal lobe epilepsy Nonorganic causes of ED - Psychogenic
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when assessing ED -obtain what?
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Sexual history Onset, duration, circumstances Erection quality during intercourse, masturbation, and nocturnal erections Changes in ejaculation, libido, orgasms Multiple partners? Medical history PMH (diabetes, smoking, HTN, hyperlipidemia, liver, renal, vascular, psychiatric)
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Treatment Options for ED
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Penile pumps Inflatable (inserted via surgery) Malleable (feel rod in penis) External - Pills Viagra (25 mg, 50 mg, 100 mg prn) Cialis (2.5 mg, 5 mg daily), (10 mg, 20 mg q 3 days) Longer half life, "weekender" Levitra (10 mg, 20 mg prn) SE: headache, facial flushing, abnormal vision, risk for retinal problems Injectables (Alprostadil) (PGE) Caverjet: inject into penis (10 mcg, 20 mcg) EDEX: inject into penis (comes premixed): (10 mcg, 20 mcg, 40 mcg) Muse: injectable pellet into urethra (125 mcg, 250 mcg, 500 mcg, 1000 mcg) SE: pain in penis, redness, swelling, burning in perineal area, headache Refer for psychological counseling
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What are some SE from ED meds
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SE: headache, facial flushing, abnormal vision, risk for retinal problems
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Analyze the physiologic and clinical implications of abnormal liver function studies.
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Analyze the physiologic and clinical implications of abnormal renal studies.
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Analyze the physiologic and clinical implications of abnormal pancreatic studies.
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Correlate the abnormal hepatic, renal, or pancreatic value with the pathophysiology to develop a differential diagnosis.
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Discuss major clinical implication of deviation from normal liver, renal, and pancreatic values
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BUN: 30; Creat: 0.8 Na: 140, K 4.0, Cl 100, CO2 22 Hgb: 7.6, Hct: 22.8
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Normal BUN: 5 to 25 mg/dl, Normal Cr: adult male, the normal range is 0.6 to 1.2 mg/dl, or 53 to 106 μmol/L For the adult female, with her generally lower muscle mass, the normal range is 0.5 to 1.1 mg/dl, or 44 to 97 μmol/L Adequate, but there is an elevation of the BUN, indicating decrease filtration but with normal creatinine not significant impairment. Evidence of significant renal impairment due to the elevated BUN. Need to investigate further to assess the glomerular filtration rate
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Blood Urea Nitrogen (BUN)
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Normal: 5-25 mg/dL Urea produced by the liver as a waste product of protein metabolism Excreted by kidneys Azotemia: increase nitrogenous waste in the blood Uremia: toxic condition; kidney unable to excrete urea or other substances
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Blood Urea Nitrogen (BUN) - Elevation Causes
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Increase protein catabolism Decreased renal perfusion (prerenal) Intrarenal failure Nephrotic syndrome, medications Obstructive uropathy Any prerenal or intrarenal failure will produce a decrease in the glomerular filtration and decrease in urea excretion
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Elevation of BUN - Signs and symptoms
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Fatigue, muscle weakness, seizures Treatment Determine cause of elevation Prerenal: improve perfusion Intrarenal: stop offending medication, treat cause Hydration Dialysis
