Exam (elaborations) NR 601 FINAL EXAM STUDY GUIDE

Exam (elaborations) NR 601 FINAL EXAM STUDY GUIDE of DM 1. Type 1- severe insulin deficiency resulting in reduction or absence of functioning beta cells in the pancreatic islets of Langerhans. This leads to hyperglycemia due to altered metabolism of lipids, carbs, and proteins. Initial s/s of hyperglycemia. Subjective findings- polyuria, polydipsia, nocturnal enuresis and polyphagia with paradoxical weight loss, visual changes and fatigue. Objective-dehydration(poor skin turgor and dry mucous), wt loss despite normal/increase appetite, reduction in muscle mass. DKA-fatigue, cramping, abnormal breathing 2. Type 2- Type 2 DM is characterized by the 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. A patient may, however, present with pruritus, fatigue, neuropathic complaints such as numbness and tingling, or blurred vision. 3. Prediabetic- fasting glucose consistently elevated above the normal range but less than 100-125. Impaired glucose tolerance (IGT) state of hyperglycemia where 2 hr post glucose load glycemic level is 140-199 Diagnostic criteria- there are 4 lab-based criteria to confirm DM: A1C, random plasma glucose, fasting plasma glucose, and 2-hr post load plasma glucose  AIC of 6.5 or higher=diabetes  Random plasma glucose level of 200 WITH classic symptoms of hyperglycemia or a hyperglycemic crisis  Fasting plasma glucose level of 126 or higher on TWO occasions(fasting is defined as no caloric intake for at least 8 hrs  2-hour post load plasma glucose level of 200 or higher during an OGTT, following consumption of a glucose load containing the equivalent of 75g of anhydrous glucose dissolved in water (OGTT is also used to screen for diabetes during pregnancy) *** In the absence of unequivocal hyperglycemia results should be confirmed by repeat testing on a new blood sample without delay, preferably using the same type of test.***  *All above-but confirmation of type 2 diabetes mellitus requires: two fasting blood glucoses ≥126 mg/dL or two random blood glucoses ≥200 mg/dL.  You do not screen for type 1 diabetes but you do screen for type 2 if an individual is overweight or obese, regardless of age, and for all adults aged 45 years and older. Tests should be repeated at a minimum of 3 year intervals Initial TreatmentType 1- FIRST LINE: INSULIN. The initial goal of treatment for type 1 DM is to normalize the elevated blood glucose level. This is best accomplished by intensive insulin regimens to achieve the following goals: plasma glucose levels of 80 to 130 mg/dL before meals, peak postprandial 1 NR 601 FINAL EXAM STUDY GUIDE (1–2 hours after the beginning of a meal) glucose levels of less than 180 mg/dL, and an A1C below 7% for adults with type 1 DM. A comprehensive treatment plan requires exogenous insulin, frequent self-monitoring of blood glucose (SMBG), medical nutrition therapy, regular exercise, continuing education in prevention and treatment of diabetic complications, and the periodic reassessment of treatment goals. (Type 1A: insulin dependent, Type 1B: variably insulin dependent). The ADA Standards of medical care in diabetes states that the majority of patients with type 1 DM, should be treated with multiple daily injections of prandial insulin and daily basal insulin or with a continuous subcutaneous insulin infusion pump. INITIATION OF INSULIN THERAPY IN NEWLY DIAGNOSED TYPE 1 DM, SHOULD BE MANAGED BY OR IN CLOSE COLLABORATION WITH AN ENDOCRINOLOGIST. Type 2-FIRST LINE: LIFESTYLE MANAGEMENT. Interventions should include treatments directed at both risk reduction and glycemic control. Lifestyle management is an important part of treatment and comprises nutrition therapy, activity prescriptions for exercise, decreased prolonged sitting, and in older adults, training in balance and flexibility. Lifestyle management should focus on mental health, sleep, and smoking cessation. Obesity management has become a high-level target in the treatment of pts with type 2 DM. ADA states that every patient should receive diabetes self-management education and diabetes self-management support at the time of diagnosis. Pharmacological therapy for type 2 DM is required when lifestyle management does not result in adequate blood glucose control. Drug therapy should always be considered an adjunctive therapy to lifestyle management, as the latter is typically initiated first. The ADA and AACE recommend metformin if there are no contraindications, such as renal disease or abnormal creatinine clearance, acute myocardial infarction, or septicemia. The AACE recommends adding a second agent to lifestyle treatment and metformin if the A1C is more than 7.5% at the time of diagnosis or after 3 months of monotherapy without achievement of the patient’s blood glucose goals. Metformin can be used as a monotherapy unless the patient has contraindications or intolerance. Although metformin is the first-line medication recommended by the ADA and the AACE for DM type 2, it should be used only in patients with adequate renal function and should not be used in patients with an eGFR below 45 mL/min/1.73 m2 . • Immediately upon diagnosis of type 2 DM, begin lifestyle therapy with medically assisted obesity treatment. • If glycemic goals are still not met 3 months later, begin single-agent or dual therapy with oral antidiabetic agents, depending on whether A1C is less than or greater than 7.5%. • If glycemic goals are not met in 3 months, initiate triple therapy. • If after 3 additional months (or at the time of diagnosis) A1C is 9.0% or higher and the patient is symptomatic, add insulin therapy.  A1c-Gyycemic level over 2-3months and is helpful is documenting control and continuing care.  A1c less than 7% indicate strong control  6.5%or less decrease occurrence of complications achieved w/o hypoglycemia or other adverse effect. 2 Medication Side Effects -Type 1: Hypoglycemia is a common occurrence in patients with type 1 DM and occurs for a variety of reasons: excessive exogenous insulin, missed meals or inadequate food intake, excessive exercise, alcohol ingestion, drug interactions, or decreases in liver or kidney function. Signs and symptoms: diaphoresis, tachycardia, hunger, shakiness, altered mentation (ranging from an inability to concentrate to frank coma), slurred speech, and seizures. The ADA classifies hypoglycemia as a plasma glucose level of < 54 as serious, clinically significant hypoglycemia. A blood glucose level of 70 is considered a threshold level that requires intervention. Examples of appropriate foods: #1 choice: pure glucose, ½ cup fruit juice, 6oz regular soda (not diet or sugarless), 1 cup milk, or glucose tabs. Candy is only a last resort. Recheck glucose 15 minutes after treatment. Additional carbs can be given if glucose is still less than 70 -Type 2: Metformin can cause: hypoglycemia esp in older adults, adverse reactions such as GI disturbances and metallic taste, and is contraindicated in renal disease so assess renal function prior to prescribing. - Metformin also has a boxed warning in its FDA-approved prescribing information for lactic acidosis, although this side effect is very rare. Metformin should be discontinued 24 to 48 hours before diagnostic and surgical procedures due to the risk of decreased kidney function, and its administration should not be resumed for at least 6 hours after these procedures or until the patient is adequately hydrated. Initial dosing is 500 mg once a day with breakfast or dinner for 1 week, then twice daily with breakfast and dinner. Several weeks of therapy may be needed to achieve maximum effects of the given dose. Common adverse reactions include diarrhea, nausea, anorexia, and abdominal discomfort, which usually resolve with a gradual increase of dosage. Metformin has been shown to cause decreased vitamin B12 absorption, and patients on long-term metformin therapy should undergo periodic testing for B12 deficiency, especially if the patient complains of peripheral neuropathy. At the maximum dose, the monthly cost of metformin in the United States is approximately $4 on many generic formularies. Metformin is currently found in 20 combination formulations with other medications. *For other noninsulin agent adverse reactions see pg 929 Dunphy book* SINGLE-DOSE THERAPY Single Injection • Intermediate or long-acting insulin with or without regular insulin in the morning or Intermediate or long-acting insulin at bedtime • Recommend at a minimum SMBG in the morning and at bedtime CONVENTIONAL SPLIT-DOSE THERAPY Two Injections • Mixture of NPH and regular insulin in the morning and evening • Recommend at a minimum SMBG before each dosing and at bedtime INTENSIVE INSULIN THERAPY 3 Three Injections • NPH and regular insulin in the morning; regular insulin at dinner; NPH insulin at bedtime • Monitor for increased risk of hypoglycemic episodes Four Injections • Regular or lispro insulin before meals and long-acting insulin to maintain basal insulin levels • Monitor for increased risk of hypoglycemic episodes Treatment goals for older adults (Kennedy table 14-2).  Healthy (few chronic illnesses) A1C <7.5, Fasting glucose 90-130, Bedtime 90-150, BP < 140/90, for lipids use statin unless contraindicated or not tolerated  Complex (multiple chronic illnesses, ADL impairment, cognitive impairment) A1C <8.0%, fasting 90-150, bedtime 100-180, BP same as above, for lipids use statin unless contraindicated or not tolerated  Very complex (LTC or end stage illnesses) A1C <8.5%, fasting 100-180, bedtime 110-200, BP <150/90, consider likelihood of benefit with statin (secondary prevention more so than primary) Hbg A1C goals based on complications - An A1C value of less than 7% indicates a 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 effects - Maintaining an A1C of less than 6.0% during pregnancy is recommended to prevent adverse fetal outcomes, although this goal increases the risk of hypoglycemia Weight loss recommendation: Lifestyle modifications of weight loss and exercise are particularly important in lowering Hb A1c. exercise of even a modest nature can be beneficial in decreasing insulin resistance.  modest weight loss of 5% can improve glycemic control Risk factorsDm Type 1  Autoimmune,  Genetics (chromosome 6p)  1-5% of monogenic forms Diabetes Mellitus Type 2 - 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 4 • African American • Latino • Native American • Asian American • Pacific Islander Complications  Type 2 DM is the leading cause of acquired blindness in adults aged 20-74 and up to 25% of newly diagnosed patient may present with retinopathy at the time of diagnosis.  Metformin is contraindicated in patients with renal insufficiency because the risk of lactic acidosis is increased in these patients and, while uncommon, has a very high mortality rate.  Acute complications requiring immediate attention include diabetic ketoacidosis, recurring fasting hyperglycemia of greater than 300 mg/dL, Hb A1c of greater than 13%, or severe hypoglycemia with changes in sensorium, altered behavior, seizures, or coma. Complications resulting from prolonged hyperglycemia include renal failure, blindness, coronary artery disease, stroke, peripheral vascular disease, slow-healing wounds, autonomic neuropathies, hypertension, sexual problems, and genitourinary system disorders. Macrovascular complications from diabetes substantially increase the risk of morbidity and death from coronary artery disease, stroke, and peripheral vascular disease. Treatment for complications - Hyperlipidemia: use of statins as antihyperlipidemia therapy is indicated with these patients with nutritional treatment (diet modification) initiated as first line therapy. (hyperlipidemia: LDL greater than 100 Referrals  Initial diagnosis: referral to dietician and a certified diabetes educator  DM patient should have annual exam of feet and eyes (funcuscopy)  Endocrinologist  Annual eye and oral examination Obesity  Comorbidities related to obesity- Obesity is considered a risk factor for the development of a number of illnesses or diseases. Being overweight or obese explains almost 50% of cardiovascular outcomes (ie coronary heart disease, stroke) and contributes of blood pressure, dyslipidemia, and glucose concentration.  The obese patient is more likely to develop coronary artery disease, hypertension, and hyperlipidemia. There is an increased risk of developing type 2 diabetes mellitus, cerebrovascular disease, and CKD. The obese patient is more likely to develop physical disability, sexual dysfunction, lower UTIs, and impaired cognitive function and dementia. Certain types of cancer such as colon, breast, endometrium, liver, kidney, esophagus, gastric, pancreatic, 5 gallbladder, and leukemia are also associated with obesity. Obese patients are also more likely to develop obstructive sleep apnea, gallbladder disease, fatty liver disease, and osteoarthritis. They will often have symptomatic varicose veins or GERD.  Obesity is defined as a BMI >30 with morbid obesity as a BMI >40. Overweight is defined as a BMI of 25 to 29. The CDC provides a BMI calculator on their Healthy Weight Web site (CDC, 2015b). BMI DEFINITION <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 Week 6: Urology and aging UTI - Urethritis and cystitis usually occur together - Infections can be acute, chronic, recurrent, complicated, or uncomplicated. - UTIs become chronic because of obstructions, antibiotic-resistant bacteria, or the presence of multiple strains of bacteria that are not susceptible to the antibiotic therapy prescribed. - A complicated UTI is either an acute or chronic infection that is accompanied by factors that predispose a patient to the infection or make treatment more difficult such as instrumentation (ie indwelling, suprapubic, or intermittent cath), underlying chronic disease, systemic symptoms, or pregnancy. Risk factors- Predisposing factors to the development of cystitis in older adults include indwelling catheters, urethral or condom catheters, incontinence (urinary and fecal), cognitive impairment, neurological conditions that impair bladder emptying, and diabetes (high pH=more alkaline), which can lead to neurogenic bladder. Poor hygiene, unprotected anal intercourse, sexual intercourse, immunosuppression, functional disability, sickle cell disease, prior antibiotic therapy, genetic predisposition, and functional or structural genitourinary tract abnormalities (including urethral strictures, uterine or bladder prolapse, ureteral weakness, and vesicoureteral reflux or renal calculi) Gender: 6  UTI rarely occurs in men younger than 50yo unless caused by urinary caths, anatomical abnormalities, of urinary tract, unprotected anal intercourse, or vaginal intercourse with a woman who has a bacterial infection.  Cystitis is rare in men because the increased length and drier environment around the urethra contribute to less frequent bacterial colonization. In addition, prostatic fluid has inherent antibacterial prosperities. Thus, when UTI does occur, it is often associated with abnormal urethral anatomy or inadequate treatment of prostatitis  -Men have a 20% incidence of UTI, with lifetime prevalence of 1% . After age 65 years, the rate of cystitis in men significantly increases, but is still approximately one-half that of.  Incidence in postmenopausal women can range from 0.07/women/year to 0.13/women/year in women greater than 85 years old with great degrees in prevalence.  -Community-dwelling men 70 years of age and older have a prevalence rate of ASB from 3.6% to 19%, whereas their institutionalized counterparts have a prevalence rate from 15% to 40%  -Community-dwelling women 70 years of age and older have a prevalence rate of ASB from 10.8% to 16%, whereas their institutionalized counterparts have Patho & Common bacteria  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  The most common organism in adults of all ages is E. coli, which transcends across community dwelling and long-term care residing older adults. In women, approx. 80-90% of cases of uncomplicated UTI are a result of E.Coli.  The second most common cause (5-20%) of uncomplicated bacterial infections=Staphylococcus saprophyticus  Other less common bacteria but more prevalent in complicated UTI’s: Proteus mirabilis, Klebsiella, Enterobacter, Serratia, and Pseudomonas Diagnostic Criteria  Diagnosis of lower UTI is made based on the subjective complaints of the patient and a cleancatch midstream urine sample showing the presence of bacteria, especially if more than 100,000 organisms/mL of the same morphology are present in a sample from a female patient.  UTI is currently defined as a urine sample with greater than 100 organisms/mL in the presence of characteristic clinical symptoms.  Although urine culture is considered the gold standard with the greatest sensitivity for lab confirmation of URI, urinalysis with microscopy is also helpful and provides rapid results. UA typically indicates pyuria (>10 neutrophils per hpf on microscopic exam) and often the presence of RBC. Hematuria is common in UTI but not with urethritis or vaginitis, however blood in the urine is not a marker of complicated infection.  Bacteriuria and pyuria are the main laboratory clinical manifestations of cystitis  older adult, the presence of localized genitourinary symptoms (see Signal Symptoms) and pyuria on urinalysis are required for diagnosis  The presence of greater than 10^ 5 colony-forming units/mL of a single bacterium in a culture of freshly voided urine is generally considered to be a significant bacteriuria Treatment 7  Uncomplicated UTI in women that highlighted nitrofurantoin 100 mg twice daily for 3 days over trimethoprim-sulfamethoxazole related rising resistance rates and nitrofurantoin’ s lesser side effect profile. And Fosfomycin given in a 3 g one-time dose o However, a 3 day course of Bactrim or a longer 10 day course of ampicillin. In pts with sulfa allergy or previous abx use in last 3 months, use nitrofurantoin (Macrobid)  Uncomplicated treatment of UTI in the adult male can be treated empirically for 7 days with a fluoroquinolone or sulfamethoxazole-trimethoprim DS.  In pregnancy, fluoroquinolones should be avoided due to concern for their effects on bone and cartilage formation in developing fetus and Bactrim should be avoided in first and third trimesters of pregnancy. However, treatment is important because a UTI during pregnancy increases premature delivery . Empirical therapy may include ampicillin or Keflex  The management of asymptomatic bacteriuria deserve s special mention: o Treat pregnant individuals out of risk of premature delivery o Treat asymptomatic young children due to high rate of recurrent asymptomatic infection without obvious sequelae o Treat pts before they undergo a urological procedure to avoid operating on a contaminated field, after removal of a bladder cath in place for less than 1 week, and in any pt with an underlying structural abnormality of the urinary tract, vesicoureteral reflux, or struvite stones. o In contrast, treatment of asymptomatic bacteriuria is not warranted in: adult men, nonpregnant women, the elderly, diabetic persons, and spinal cord patients with indwelling urinary catheters  Older men may require longer therapy for 10 to 14 days  *Untreated symptomatic cystitis can lead to pyelonephritis, sepsis, shock, and death* Incontinence : involuntary loss of urine and is generally the result of illness or the effects of medications and is self-limiting when the cause is determined and addressed Different Types: - Stress: urine leakage associated with increased abdominal pressure from laughing, sneezing, coughing, climbing stairs, or other physical stressors increasing and pressure o Tx: lifestyle interventions, behavioral therapies, possible surgical procedures, alpha adrenergic meds, SNRI - Urge: urine leakage associated by or immediately preceded by the feeling of an urgent need to void o Tx: lifestyle interventions, behavioral therapies, consider trial of antimuscarinic (anticholinergic) medications - Mixed: a combo of stress and urge incontinence, marked by involuntary leakage associated with urgency and also with exertion, effort, sneezing, or coughing o Tx: same as stress and urge incontinence - Overflow: urine leakage when the bladder is over-distended and may result in incomplete bladder emptying. Symptoms can present as constant dribbling, frequency, hesitation when initiating urination, and nocturia. Often associated with bladder outlet obstruction, such as benign prostatic hypertrophy in men and pelvic organ prolapse in women (DING: TAMSULOSIN) 8 o Tx: Assess for cause ie. medication usage and fluid intake. Double voiding to empty residual urine from bladder - Functional: the inability to hold urine due to reasons other than neurological and lower urinary tract dysfunction including delirium, psychiatric disorders, UTI, impaired mobility o Tx: treat underlying cause Risk factors : pelvic muscle weakness, multiparity, estrogen depletion, pelvic organ prolapse, diabetes, stroke, multiple sclerosis, Parkinson’ s disease, spinal cord injury, benign prostatic hyperplasia, UTI, fecal impaction, poor fluid intake or excessive fluid intake, smoking, cognitive impairment, depression, immobility or impaired mobility, environmental barriers, impaired dexterity, visual impairment, obesity, and high-impact physical activities. Incontinence can be a side effect of many medications, including cholinergics, anticholinergics, diuretics, antispasmodics, opiates, hypnotics, calcium channel blockers, ACE inhibitors, alcohol, and caffeine. Gender: UI is twice as prevalent in women as in men, and the incidence increases with age, with institutionalized individuals, and those who have at least one deficit in ADLs ( Wagg et al., 2015 ; da Silva et al., 2012 ). Women are at higher risk for stress incontinence; however, overflow incontinence is more prevalent in men as a result of hyperplasia of the prostate gland. Pathophysiology: The causes and management of UI are multifactorial, depending on the type of incontinence and also the severity and impact on quality of life for the individual. Anatomical changes, factors related to the individual ’ s medical history, lifestyle, and acute and chronic illnesses, in addition to medications, can result in incontinence that can be either reversible or a permanent condition. Cognitive as well as chronic mental illness, depression, and functional barriers to continence can also affect an individual’ s ability to maintain urinary continence Dx and when to treat: urinalysis to rule out infection and renal abnormalities. presence of nitrites and leukocyte esterase in the urinalysis is usually indicative of an infectious process. culture and sensitivity should be ordered to ensure appropriate antimicrobial therapy. Incontinence Mnemonic:  DRIP ■ Delirium ■ Restricted mobility ■ Infection ■ Pharmaceuticals, polyuria  Mnemonic: DIAPERS ■ Delirium ■ Infection, impaction, inflammation ■ Atrophic vaginitis ■ Psychological, pharmaceuticals, psychotropics ■ Endocrine problem ■ Restricted mobility ■ Stool impaction Causes of hematuria and proteinuria: - Proteinuria: glomerular disease - Hematuria: may indicate a tumor - Hematuria may indicate a number of differential diagnoses, including infection, obstruction, kidney stones, or malignancy. Proteinuria is revealing for renal disease and is often associated with poorly controlled diabetes. Urologic changes in male/female: - Incontinence is common in older men because of their enlarging prostate 9 - Age-related changes that may affect urological functioning are decreased bladder capacity, increased postvoid residual urine volume (>50mL), increased disinhibition of bladder contractions (overactive bladder), increased nocturnal sodium and fluid excretion (nocturia), urinary overflow phenomena resulting from increased urethral resistance in men related to BPH, and weakness of the pelvic floor in women. Postmenopausal estrogen deficiency in women can result in decreased competence of the internal and external sphincters via atrophy of the urethral mucosa epithelium resulting in atrophic urethritis, loss of compliance, and a diminished urethral mucosal seal. It is important to note that normal aging does NOT cause UI. Sexuality and aging STIs/Age related changes: - Assumptions regarding lack of sexual expression in the healthy older adult are unfounded. With the possibility of pregnancy eliminated, many mature adults feel less restraint. As a result of divorce or widowhood, they may seek satisfaction with new partners yet lack the knowledge to protect themselves from sexually transmitted diseases, especially HIV. More than 42% of those living with HIV in the United States in 2013 were in people more than 50 years old; 39% of deaths from HIV in 2014 were in adults older than 55yo. Older adults need to be taught methods for safe sex with use of a barrier to avoid sexually transmitted diseases, including HIV and hepatitis B. Using the patient’s sexual history, explore patient needs, preferences, and medical or psychological obstacles to sexual expression. This exploration facilitates counseling and interventions to promote healthy sexual behavior. - Male microabrasion in outer penis shaft serve as entry point for STI - Susceptibility is also influenced by aging and the presence of existing infection - Female pH change can disrupt the natural balance of flora and predispose the reproductive track to infection - Older women are prone to infection secondary to drying and thinning of the vaginal and vulvar tissue - Education methods of safe sex with the use of barriers to avoid STI (esp HIV and Hep B) - More than 42% living with HIV are over 50yo, 39% of deaths from HIV 55yo+ GSM: genitourinary syndrome of menopause  GSM incorporates VVA (vulvovaginal atrophy aka atrophic vaginitis). VVA really just describes estrogen deficiency changes of the vulva and vagina but GSM is a whole syndrome that involves symptoms of the vagina, the urinary tract, and sexual symptoms.  Signs and symptoms- main symptoms: pain with intercourse, vaginal dryness, postmenopausal o GSM is the #1 cause of discomfort with intercourse after menopause o All symptoms: vaginal dryness, dysuria, vulvar and vaginal itching, urinary frequency, blood-tinged vaginal discharge, dyspareunia, decreased vaginal secretions  Complaints of urinary frequency, urgency, and stress incontinence are common o On exam: pale, dry, nonrugated vaginal walls with patches of erythema or petechiae or both. The vaginal canal is short and narrow. A watery, white vaginal discharge without foul odor may be found. Estrogen deficiency can lead to loss of uterine support and subsequent uterine descensus. The exam may also reveal sparse vulvar hair, decreased 10 subcutaneous fat within the mons pubis and labia majora, volume reduction of labia minora, retracted clitoris and inadequate vaginal lubrication with pale, dry, and shiny introitus.  Diagnosis- estrogen deficiency leads to atrophy of vaginal and vulvar epithelium. o Diagnostic tests: pelvic exam with speculum and Pap smear (may do wet mount and KOH preparation if infection is suspected) : results if GSM: pale, dry, nonrugated vaginal mucosa; pap smear results should be normal, vaginal pH by litmus paper > or equal to 5. Urinalysis to rule out UTI if symptoms: results if GSM: variable, if dipstick is positive for WBCs and nitrates, a culture and sensitivity should be done. If negative, UTI is not cause of symptoms.  When to treat, common treatments –  Nonprescription therapies: FIRST LINE: over the counter moisturizers and lubricants plus regular sexual activity with a partner, device, or masturbation. Use products on a small patch of skin for 24 hrs before using intravaginally. Next step: pelvic physical therapy (PT). o Herbal alternatives (black cohosh and soy) have NO benefit on atrophic vaginitis  Prescription therapies: If these options do not work, hormonal therapy is the next option: lowdose vaginal estrogen, there's a tablet that's placed in the vagina twice weekly, creams that are placed in the vagina two or three times weekly, and it's very simple to use vaginal ring that's put the vagina for 3 months at a time. GSM often occurs in women with a history of breast cancer who reinitiate their sex lives. o Potential contraindications to vaginal estrogen are postmenopausal women with undiagnosed vaginal/uterine bleeding and controversial in women with estrogendependent breast or endometrial neoplasia.  Expected response is quick, with resolution of symptoms within 2-3 months. If this does not occur, the patient should be reevaluated and reexamined for other causes of symptoms.  The important message is that we have so many effective medications for general urinary syndrome of menopause (GSM) yet so many women aren’t on therapy often because we just are not asking. Every clinician needs to ask every postmenopausal patient at every well visit and every comprehensive visit if they have any vaginal dryness, discomfort with sexual activity, or any concerns about your sex life.  Education: Use water-soluble lubricants. Counsel patient regarding the benefits of regular sexual activity. Identify age-related difficulty associated with intrav