Download NR511 FINAL EXAM STUDY GUIDE LATEST UPDATE and more Study Guides, Projects, Research Nursing in PDF only on Docsity! NR511 FINAL EXAM STUDY GUIDE LATEST UPDATE See Midterm and Week 1 Study Guide for content covering weeks 1, 2 & 3 Common Infections 1. Impetigo 2. Staphylococcal Scalded Skin Syndrome 3. Cellulitis 4. Erysipelas 5. Necrotizing fasciitis 6. Mammalian bites 1. Hematuria Urology - Hematuria is defined as blood in the urine and can be visible (gross) or occult (microscopic) - the ingestion of beets can color the urine red to pink, and medications such as rifampin and phenazopyridine (Pyridium) can give urine a reddish-orange color. The presence of porphyrins, hemoglobin, or myoglobin can color the urine reddish-brown. Pus in the urine is indicative of bacterial infection, such as cystitis, urethritis, or prostatitis. - Menstrual history is always important in a female patient, as well as history of recent strenuous exercise, streptococcal infection (especially poststreptococcal glomerulonephritis), or nephrolithiasis; family history (e.g., of polycystic kidney disease); and recent travel (potential exposure to parasitic infections). Gross painless hematuria is a cardinal symptom of certain malignancies such as bladder cancer. 2. Incontinence & overactive bladder - Urinary incontinence (UI) is the involuntary loss of urine from the bladder. Incontinence is so frequent in women that many consider it normal. Incontinence is also common in older men as a result of an enlarging prostate. Incontinence can affect a person’s quality of life and may be psychologically devastating. a. Stress: Failure to store due to hypermobility of bladder neck, intrinsic sphincter deficiency, neurogenic sphincter deficiency Medications: Sedatives, hypnotics, antispasmodics b. Urge: Failure to store due to urinary tract infection; vaginitis; bladder stones and tumors; cortical, subcortical, and suprasacral lesions; cerebrovascular accident; dementia; multiple sclerosis; Parkinson’s disease; spinal cord transection Medications: Diuretics, narcotics c. Overflow: Failure to empty due to underactive detrusor, outlet obstruction, diabetes mellitus Medications: Anticholinergics, disopyramide, antihistamines, calcium channel blockers d. Functional: Delirium, fecal impaction, manual dexterity and immobility Medications: diuretics, hypnotics, alcohol, narcotics, decongestants Rx: Anticholinergic/Antispasmodic Agents: ex: tolterodine (Detrol LA) or oxybutynin (Ditropan XL) for urge, overactive bladder and stress incontinence. Contraindications: Closed-angle glaucoma, Myasthenia gravis. - Tricyclic Antidepressants: Imipramine (Tofranil) amitriptyline (Elavil) for OAB and Urge incontinence - The term overactive bladder (OAB) is often used interchangeably with the term urge incontinence; however, they are different conditions. OAB is a syndrome of symptoms that include urgency, frequency, and nocturia, all of which are associated with involuntary contractions of the detrusor muscle. Urge incontinence may or may not be a feature of this syndrome; about one-third have urge incontinence. 3. Proteinuria - Proteinuria is usually indicative of a renal pathology, most often of glomerular origin. Proteinuria can be functional as a result of acute illness, emotional stress, or excessive exercise and is a benign process. It can also develop from overproduction of filterable plasma proteins, especially Bence Jones proteins associated with multiple myeloma -Tx: abx and hydration First-line therapy ciprofloxacin (Cipro) 500 mg two times daily for 7 days, or levofloxacin (Levaquin) 750 mg daily for 5 days. In second-line therapy, trimethoprim-sulfamethoxazole (TMP-SMX) (Bactrim DS, Septra DS) taken orally for 14 days may be as effective as amoxicillin- clavulanate for 14 days in young women with their first pyelonephritis and without anatomical abnormalities. However, given the prevalence of sulfonamide and ampicillin resistance among common uropathogens, TMP-SMX and amoxicillin are likely to be ineffective in cases of recurrent or moderate to severe pyelonephritis (except in cases of Enterococcus infection, which calls for the addition of amoxicillin [Amoxil] 500 mg PO three times daily). Nitrofurantoin should be avoided because it does not achieve adequate tissue levels. Other effective choices are third generation cephalosporins (e.g., cefixime, cefpodoxime, ceftriaxone), aminoglycosides (e.g., gentamicin, tobramycin), or aztreonam, with fluoroquinolones reserved for antibiotic-resistant organisms, hence the critical need for early urine culture to guide pharmacotherapy. 6. Urethritis - Infections of the lower urinary tract can occur in the urethra, bladder, and prostate. Infection of the urethra (urethritis) and infection of the urinary bladder (cystitis) usually occur together. - Common causes: E. coli, chlamydia or gonorrhea, trichomonas, HSV - Pus in the urine is indicative of bacterial infection, such as cystitis, urethritis, or prostatitis. - Suprapubic tenderness is indicative of a bladder etiology, whereas urethral discharge indicates a urethritis. - Acute cystitis and urethritis produce gross hematuria and are more common in women. - Hematuria is also often present in lower and upper UTI, but not in vaginitis or urethritis. - Urethritis in men is rare; if left untreated or treated inadequately, it can lead to complications such as urethral strictures, periurethral abscess, urethral diverticuli, and fissures. - Vaginal discharge in women and urethral discharge in men may suggest sexually transmitted diseases (STDs). Purulent urethral discharge (Neisseria gonorrhoeae) or whitish-mucoid discharge (Chlamydia trachomatis) should be treated aggressively with the appropriate antibiotic therapy. Cystitis Frequency, urgency, may have gross hematuria Recent sexual intercourse, risk factors present (see Table 2 ) 15 to 20% have suprapubic tenderness; no costovertebral angle tenderness Usually positive for pyuria and sometimes also positive for bacteriuria and nitrite Subclinical Frequency, Risk factors May have Usually positive pyelonephritis urgency, may present suprapubic for pyuria and have gross (see Table 5 ) tenderness; no sometimes also hematuria costovertebral positive for angle tenderness bacteriuria and nitrite; positive renal cortical scintigraphy, urine culture usually > 105colony- forming units per mL of urine Acute Nausea, May have had Costovertebral Pyuria usually pyelonephritis emesis, fever, concurrent or angle tenderness, present with sepsis, preceding deep right or left casts of white back/flank cystitis upper quadrant blood cells; pain symptoms (see Table 5) tenderness obtain urine culture and sensitivity Interstiti al cystitis Frequency, urgency, gross hematuria (20%) Often middle- aged; longstandin g symptoms with negative cultures No costovertebral angle tenderness; may have suprapubic tenderness Urinalysis negative for white blood cells or bacteria; positive for glomerulatio ns on cystoscopy Vaginitis External Premenstrual Vaginal discharge, Positive irritation, exaggeration inflamed vaginal potassium vaginal of symptoms; mucosa (absent in hydroxide or discharge or sexual activity bacterial vaginal saline pruritus, or recent vaginosis), preparation; dyspareunia; antibiotic inflamed cervix elevated pH no hematuria exposure or (Trichomonas), (bacterial post- vaginal atrophy vaginosis or menopausal (postmenopausal) Trichomonas) and not receiving estrogen replacement therapy Genital Dysuria, fever, Sexually Grouped vesicles Viral culture herpes headache, active; may usually on cervix optional myalgias, neck have vaginal or pubic area, but pain, vulvar discharge may be vaginal; pain, tender inguinal photophobia adenopathy Urethritis Usually History of No suprapubic Urethral swab 1. Testicular torsion Male Complaints Testicular torsion is a twisting or rotation of the testes around the spermatic cord, which is the blood supply to the testes. The lack of blood supply to the testes results in acute ischemia. This condition is considered a urological emergency, so in the primary care setting, you must be able to recognize this and immediately refer the patient to the ER. Compression of the testicular vessels will lead to ischemic necrosis within 6 hours, so failure to recognize the torsion and intervene immediately can result in loss of the testicle. Testicular torsion can happen at any age, even to newborns and older men; however, the majority of cases are seen in adolescent and young adult males. It is not a common condition and its etiology is really not clear, but one theory is that contraction of the cremasteric muscle may contribute. Things that can cause contraction of the muscle include trauma, exercise (most frequent in runners), extreme cold, and sexual stimulation. The most common symptom in testicular torsion is sudden, severe pain accompanied by swelling of the affected testis. The patient may have pain for several days without seeking medical attention. The most common finding on clinical exam is the absence of the cremasteric reflex(striking of inner thigh contracts the testicle on same side) and unlike in epididymitis elevation of the affected testis does not relieve the pain (Phren’s sign). This finding is not enough to differentiate between the two conditions, but rather they can support your suspicion. The DDx for torsion should include ● epididymitis; ● acute varicocele; ● acute hydrocele; ● incarcerated hernia; and ● traumatic hematoma. Diagnosis is a clinical one, meaning it is based solely on the history and physical findings. The only assessment that is required is the physical exam of the scrotum, testes, abdomen, and groin. Again, because this is considered an emergency, if the patient presents to you in primary care and you have a high level of suspicion, send the patient to the ER and call ahead with a brief H&P to the ER provider. In the ER, manual reduction of the testis is usually performed and if not successful will be followed by surgical exploration and may require removal of a nonviable testis. Viability of the testicle is directly related to the duration of torsion, so again, time is of the essence. If torsion occurred more than 6 hours prior, the likelihood of viability falls to 10–15%. Beyond 24 hours, the viability rate falls below 10%. There is also a reduced rate of sperm production in patients who have had torsion, whereby reproduction may be affected. 2. Benign Prostatic Hyperplasia The prostate gland, is a walnut size gland positioned at the base of the bladder and in front of the Fever, chills, malaise LBP Dysuria ● Tamsulosin (Flomax) 0.4mg-0.8mg QD ● Doxazosin (Cardura) 4-8mg QD ● Silodosin (Rapaflo) 4-8mg QD 5-alpha-reductase inhibitors that are commonly prescribed are: ● Finasteride (Proscar) 5mg QD alone or in combination with Doxazosin ● Dutasteride (Avodart) 0.5mg QD * Erectile dysfunction should be assessed on patient taking finasteride. Surgery may be indicated when there is urinary retention or when other symptoms are unmanageable in which case a transurethral resection of the prostate (TURP) is performed. 3. Acute & chronic prostatitis - prostatitis accounts for about 25% of all office visits in men and over 50% of men will experience prostatitis in their lifetime - most common chronic non-bacterial prostatitis (8x mre frequent than bacterial prostatitis), complains and PE similar to those with chronic bacterial prostatitis but urine cx will be negative. - acute bacterial prostatitis has an abrupt onset, and always associated with an UTI most predominant in sexually active men between ages 30-50. - Symptom classification: a. Obstructive: weak stream, incomplete bladder emptying, dribbling b. Irritative: urinary complains (frequency, urgency, nocturia, dysuria), pain and discomfort (LBP, penile scrotal pain, fever, chills malaise or painful ejaculation) - Acute Bacterial and non-bacterial will have same s/s: Arthralgia (joint pain) myalgia (muscle pain) Urgency, frequency nocturia bladder outlet obstruction - Chronic Bacterial s/s:* symptoms often are abscent Perineal pain LBP Dysuria Scrotal/penile pain lower abd pain Irritative voiding - When we look at the DRE results for the three conditions, we can expect to see the following. Acute bacterial Chronic bacterial Nonbacterial Warm, tense, swollen, boggy, and very tender prostate Normal (may be a little boggy or focally indurated) Normal or tender prostate - Antibiotics—ABP: Current CDC guidelines recommend (www.cdc.gov/sta/tg2015/urethritis-and- cervicitis.htm (Links to an external site.)Links to an external site. ) a 14 to 28 day regimen of one of the following fluoroquinolone antibiotics for ABP. ● Ciprofloxacin 500 mg Q 12 hours ● Levofloxacin 500 mg daily ● Ofloxin 400 mg Q 12 hours ● Norfloxin 400 mg Q 12 hours Alternatives to a fluoroquinolone include ● doxycycline 100 mg Q 12 hours; and ● TMP-SMX [160 mg/800 mg] (Bactrim DS) one tab Q 12 hours STD Coverage—ABP Fluoroquinolone antibiotics are no longer recommended for the treatment of gonococcal infections in the United States due to high antibiotic resistance rates. Co-treatment of Chlamydia is essential because the two often coexist. Treatment includes ● single-dose IM ceftriaxone 250 mg; plus ● single dose oral Azithromycin 1 gm or doxycycline 100 mg BID × 7 days. Supportive Measures—ABP ● antipyretics, NSAIDS, hydration, stool softeners as needed ● urinary analgesics such as phenazopyridine and flavoxate are also used. ● urology referral to ensure eradication and prevent relapse 4. Nocturia 6. Epididymitis - Epididymitis can affect males of any age and is inflammation of the epididymis at the back of the testicle that stores and carries sperm. - There is a predisposition to epididymitis for patients with a history of unprotected intercourse, a new sexual partner, history of UTI, or urinary discharge. Symptoms can also occur following heavy lifting and or straining, trauma, medical procedures that affect the urinary tract and an uncircumcised penis. - Causes of epididymitis in males younger than 35 years are usually due to STIs such as gonorrhea and chlamydia. Chlamydia is responsible for approximately two thirds of acute cases, followed by Neisseria gonorrhea, and E. coli. - In nonsexually active males and men over the age of 35, causes of epididymitis is most commonly due to E. coli, and sometimes Pseudomonas aeruginosa and Staphylococcus aureus. It is also associated with distal urinary tract obstruction or any cause that can cause bacteria to spread from the infected site to the epididymis (prostatitis, surgical procedures, etc.). - S/S: unilateral scrotal pain that often radiates along the spermatic cord or to the flank.Pain may be experienced in the tip of the penis and typical symptoms of UTI are present (dysuria, cloudy urine, hematuria, etc.). With severe infections, fever and chills occur. - The physical examination should include an abdominal examination to detect a distended bladder and costovertebral angle tenderness, a genital examination, and a digital rectal examination. - Scrotal swelling will be present, and the testis may be indistinguishable from the epididymis. Enlarged lymph nodes in the groin or a lump on the testis may be palpated. Rectal exam will reveal a tender prostate, but the hallmark characteristic is relief of discomfort with elevation of the testis and epididymis. It is important to discern epididymitis from testicular torsion by checking for the Prehn sign during the examination. By elevating the affected hemi-scrotum, the pain of epididymitis will be relieved but would exacerbate the pain of torsion. - The CDC guidelines for the treatment of Epididymitis essentially recommend the same antibiotics that treat for GC & CT. Again, fluoroquinolone antibiotics are no longer recommended for the treatment of gonococcal infections in the US due to high antibiotic resistance rates. Co-treatment of Chlamydia is essential since the 2 often coexist. Treatment includes: ● single-dose IM Ceftriaxone 250mg PLUS ● single dose oral Azithromycin 1gm or Doxycycline 100mg BID x 7d If the cause is an STI, the patient’s sexual partner needs to be treated, and the patient should avoid sexual contact until the treatment is finished Supportive treatments include pain medication (NSAIDS are effective in reducing swelling, pain, and fever), rest, scrotal support with an athletic strap, ice packs, and the avoidance of lifting heavy objects are additional treatment options. In severe cases a spermatic block with local anesthetics may be necessary. 7. Varicocele & Hydrocele A varicocele is an abnormal degree of venous dilation in the vasculature above the testes. Varicocele incidence is around 10–20%, and there is no particular age group who are predisposed to it. Varicoceles are caused by weak walls and vascular engorgement in the spermatic cord. You can think of it as varicose veins of the testes. Patients may present with pain or engorgement of the testes, however, it is usually noted as part of a work-up for infertility. The hallmark characteristic of varicocele is the sensation that the testes feel like a “bag of worms.” Varicocele can be bilateral, but if it is unilateral it is almost always on the left side due to the anatomy of the vasculature drainage in the testes. On physical exam with the patient sitting upright, tortuous veins located posterior and above the testes can be seen. Venous engorgement may increase with the Valsalva maneuver. When the patient lies down in the recumbent position, the distension will resolve. the groin area, and weight loss. On physical exam a firm, nontender mass is usually distinct from the spermatic cord. Differential diagnosis of testicular cancer should include ● epididymitis; ● hydrocele; ● varicocele; ● hematoma; and To confirm a diagnosis of testicular cancer: ● An ultrasound is often the first test done. ● Some blood tests can help diagnose testicular tumors. Many testicular cancers make high levels of certain proteins called tumor markers, such as alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG). When these tumor markers are in the blood, it suggests that there is a testicular tumor. ● A testicular tumor might also increase the levels of an enzyme called lactate dehydrogenase (LDH). It is important to remember, however, that a high LDH level often indicates widespread disease in many other conditions other than cancer. ● To make a definitive diagnosis of testicular cancer, the patient will need a biopsy of the lump found in the patient’s testicle. ● A CT, MRI, and a PET scan can be used to determine if the cancer has spread to other areas of the body. Treatment for testicular cancer is determined based on the TNMS staging system. (T stands for tumor, N stands for node, M stands for metastasis, and S stands for serum tumor marker). Treatment of testicular cancer usually starts with surgery to remove the testicle with cancer, called radical inguinal orchiectomy. The entire testicle and most of the spermatic cord are removed. Follow up with chemotherapy and radiation are typically recommended. A multidisciplinary team that includes a urologist and a medical oncologist will create the patient’s treatment plan. Most often, testicular cancer can be successfully treated with surgery, chemotherapy, and/or radiation. Your role as an NP will be focused around providing the patient with answers to their many questions and making sure that the patient gets the proper referral connections needed, along with providing the patient and family with support. In addition, you may be involved in helping to manage the patient’s side effects associated with treatment. Males particularly have concerns regarding how their treatment will affect their sexual function, fertility, and quality of life. Prevention is important for all men in this age range. Teaching about a monthly self-exam is extremely important and cannot be stressed enough. All males age 15 to 40 years old should be instructed to perform monthly TSEs, and technique should be demonstrated during routine preventative medical exams. The patient should perform a self-testicular exam during a warm bath or shower or right after a warm bath/shower. The warmth relaxes the scrotum making the exam easier. It is normal for one testicle to seem larger or longer than the other. ● Cup one testicle at a time using both hands. ● Examine by rolling the testicle between the thumb and the fingers ● Feel for lumps or irregularities. ● Like all cancers, the earlier the diagnosis is made, the better the patient outcome. M/S 1. Range of motion and strength testing - ROM shoulder: o Forward flexion: Normal is to 180 degrees. o Extension: Normal is to 40 degrees. o Abduction: Normal is to 120 degrees with the palm down, 180 degrees with the palm up. o Internal rotation: Ask the patient to rotate his arm across his back and walk the fingers as far up the back as possible, recording this by vertebral level. As a guide, the inferior border of the scapula is located at about T7 or 60–90 degrees. o External rotation: Normal is to 90 degrees. - ROM elbow: o The flexion should be between 140–150 degrees. o Extension 0–5 degrees. o Pronation 90 degrees. o Supination 90 degrees 2. M/S examination & diagnostic testing - A useful approach to the initial patient encounter for any musculoskeletal complaint is to determine if the complaint is I. acute or chronic; II. articular or nonarticular; III. inflammatory or noninflammatory; or IV. localized or systemic in distribution Acute Pain o Less than 3 months in duration o Sharp/throbbing/pulsing/electric/paresthesia/ burning (peripheral/nociceptive/neurogenic pain systems) in quality o Moderate to severe intensity at first and decreases predictably over restricted, then transitions to passive and active motion in all planes. - Imaging: This is not routinely indicated; MRI is only recommended in reoperative assessment for proper prognosis. - Treatment: The patient should treat pain with NSAIDs and progressive range of motion exercises. Intra-articular steroid injections may be helpful during painful freezing phase. Prolonged immobilization should be avoided. 4. Low back strain/sprain - Back pain is often recurrent, misunderstood, and mistreated. Moreover, the term sciatica is loosely used for all back pain that radiates, which is theoretically not right, but because the sciatic nerve roots are the most commonly affected, it is coincidentally correct most of the times. - LBP also known as low back sprain, lumbar sprain or strain simply refers to an injury to the paravertebral spinal muscles. In acute LBP, there is an activity intolerance due to back or back-leg symptoms of less than 3-months duration whereas symptoms persist > 3 months in chronic low back pain. - LBP occurs in nearly 70% of adults at some point in their lives and is one of the most frequent reasons patients seek treatment from a primary care provider. Most cases are self-limiting, but there is a high rate of reoccurrence. - There are two categories of risk factors that influence low back pain: occupational and patient related. a. Occupations that require repeated lifting, bending, twisting, prolonged sitting, or motions that cause jarring of the spine (such as horseback riding and jack- hammer use) are common culprits. b. Patient-related factors such as obesity, sedentary lifestyle, weak core muscles, smoking, age and psychosocial factors such as depression, anxiety, and stress also contribute. Sometimes an inciting event such as cough, sneeze, or exercise can result in LBP. - Symptoms of LBP are typically exhibited by diffused back pain and difficulty with standing erect. Back pain may be accompanied by hip or buttock pain. Pain that is mechanical in nature worsens with activities such as bending, stooping, or twisting and improves with rest. Stiffness is common. - Pain resulting from nerve root compression is termed sciatica and involves radicular pain (or pain that radiates down the leg in a dermatomal pattern). Radicular pain may be continuous or intermittent and tends to wax and wane in intensity. There may be associated numbness and tingling in the dermatome of the nerve root affected or decreased muscle strength in the muscles that are innervated by the nerve root being compressed. It is extremely important to assess for pain that may be related to visceral organ disease such as pyelonephritis, renal calculi, ovarian cysts, pancreatitis, or AAA. - Imaging: Not indicated in patients with nonspecific low back pain - Treatment: Conservative treatment for 4–6 weeks on NSAIDs - Physical exam of the low back should include the following. Ø ROM of the lumbar spine including flexion, extension, and rotation to determine limitations and reproduction of pain Ø Palpation of the lumbar spine and paraspinal muscles to assess for tenderness and muscle spasm Ø Palpation of the sciatic notch and hips with testing of hip ROM Ø Muscle strength of the lower extremities including flexors and extensors of the hips, knees, and feet Ø DTRs Ø Gait including heel and toe walking Ø SLR (straight leg raise test) and sensation should be assessed paying attention to dermatomal patterns as this may indicate nerve root compression - Differential Diagnosis · LBP is a diagnosis of exclusion based on history and compatible physical examination. The differential includes the following. • Fracture of the vertebral body (seen on plain X-rays) • HNP or ruptured disk (unilateral or bilateral radicular pain with leg pain > back pain) • Ankylosing spondylitis • Drug-seeking behavior • Visceral organ disease • Cancer with metastasis to spine or spinal tumor • Spinal infection of epidural space - Treatment Acute low back pain does not warrant radiographic imaging unless there is evidence of neurological dysfunction, significant trauma, osteoporosis, fever >38.5 for >48 hours, suspicion of cancer, or chronic oral steroid use. For chronic low back pain, plan AP and lateral films are appropriate and may show age- related changes such as osteophyte formation and reduced height due to disk degeneration on lateral view. MRI is appropriate after failure of conservative treatment for LBP with radicular symptoms or if neurological deficits such as LE weakness is observed. 5. Radicular pain 2. Thyroid testing National organizations differ in their recommendations for routine screening in asymptomatic patients. In 2004 the U.S. Preventive Services Task Force (USPSTF) concluded that there was insufficient evidence for or against routine screening for thyroid disease in adults without symptoms, and the USPSTF has not updated this recommendation. If the patient is symptomatic or in a high-risk category, such as having a family history of thyroid disease or previous history of thyroid disease or autoimmune disorders, screening is appropriate. The initial screening tests for suspected hyperthyroidism are measurement of the serum-sensitive TSH assay to detect suppressed levels in the setting of elevated thyroid hormones, T4 and T3. Laboratory protocols that add free thyroxine immunoassay (FT4) and T3 if the TSH is low can avoid additional blood draws and expense. If the protocol is not in place, an FT4 and T3 should be tested next. The sensitive TSH assay has a functional sensitivity of 0.02 mcg/dL or less, although units for this test are typically expressed as mIU/L or mcIU/mL. A 24-hour radioactive iodine uptake (RAIU) test can differentiate Graves’ disease from subacute thyroiditis and toxic nodular goiters, thereby refining treatment recommendations. spots, within the gland. Patients with toxic nodular goiter and Graves’ disease have a high RAIU, whereas in subacute thyroiditis, iodine uptake is low. A thyroid scan is critical to determining functionality of any dominant thyroid nodule in a patient presenting with thyrotoxicosis, because cold nodules are highly suspicious for concomitant malignancy and must be evaluated further. An ultrasound of the thyroid will assist in differentiating a cyst from a nodule A fine-needle biopsy is the preferred initial diagnostic technique for evaluation of thyroid masses, particularly solid masses, to rule out malignancy. Magnetic resonance imaging is the preferred test to assess for ophthalmopathy resulting from Graves’ disease 3. Graves’ disease It identifies areas of increased and decreased thyroid function, often termed hot and cold Graves’ disease is by far the most common cause of spontaneous hyperthyroidism in the United States. An autoimmune disorder characterized by autoreactive, agonistic antibodies to the thyroid-stimulating hormone (TSH) receptor, Graves’ disease accounts for 80% to 90% of hyperthyroid cases, peaking in young adults aged 20 to 40 years. It is also the most common form of hyperthyroidism occurring in pregnancy. A diffusely enlarged goiter involving both thyroid lobes, hyperthyroid ophthalmopathy (periorbital edema, conjunctival edema and injection known as chemosis, proptosis, lid lag, and even diplopia), and excessive uptake of radioactive iodine on diagnostic testing are all common characteristics. Subsequent Testing In Graves’ disease, antithyroglobulin and antimicrosomal antibodies are elevated. A TSH receptor antibody test is usually elevated in Graves’ disease and is part of subsequent testing. The diagnosis of thyrotoxicosis is considered in cases of hyperthyroidism when TSH levels are depressed and measurements of T4 are normal. The three treatment options for Graves’ disease are antithyroid drugs, radioactive iodine, or surgery. None of these treatments alters the underlying autoimmune process of Graves’ disease. The most successful treatment in achieving a permanent euthyroid state is surgery; however, it is rarely the preferred method of treatment unless the thyroid gland is extremely enlarged and is pressing on other structures in the neck. 4. Toxic multinodular goiter Toxic multinodular goiter (Plummer disease) is as common as subacute thyroiditis, accounting for 15% to 20% of thyrotoxicosis cases. This type of goiter is more common in older adults and is a complication of chronic, inactive nodular goiter. In fact, this condition may be asymptomatic at the time of diagnosis, especially in older individuals in whom the classic symptoms of hyperthyroidism This condition is more common in other parts of the world where dietary iodine deficiency is prevalent. A single, toxic thyroid adenoma is the next most common cause of thyrotoxicosis, accounting for 3% to 5% of all cases. Multinodular and uninodular goiters should be referred to an endocrinologist for evaluation of possible malignancy. Nonmalignant thyroid nodular disease with laboratory evaluations indicating hyperthyroidism is most often treated with radioactive iodine. 5. Subacute thyroiditis Subacute thyroiditis is the most common cause of thyrotoxicosis, accounting for 15% to 20% of cases. Characterized by glandular inflammation and follicular cell destruction, it is thought to be of viral etiology, frequently occurring following an acute viral infection. More common in middle-aged adults between 40 and 50 years, subacute thyroiditis is more likely to develop in women than in men. Silent thyroiditis is a form of subacute thyroiditis in which the thyroid gland is moderately enlarged and nontender. It usually occurs in adults between 30 and 40 years and is also more common in women. hus, unlike other common causes of thyrotoxicosis subacute thyroiditis demonstrates a very low uptake of radioactive iodine on diagnostic testing. In subacute thyroiditis, the patient will present with a firm, painful, thyroid gland enlargement, fatigue, and possibly a low-grade fever. An enlarged painful thyroid gland is also consistent with degeneration or hemorrhage into a thyroid nodule, as well as either granulomatous or suppurative thyroiditis. In contrast, in silent thyroiditis or subacute lymphocytic thyroiditis, the gland is swollen but not usually tende Subacute thyroiditis may also have laboratory abnormalities of elevated erythrocyte sedimentation rate and C-reactive protein. Mild anemia is also common. Subacute thyroiditis is a self-limiting condition treated with beta-adrenergic blocking medications and NSAIDs. If patients have moderate to severe symptoms or do not respond to beta blockers and NSAIDs, they are candidates for treatment with corticosteroids. 6. Thyroidtoxicosis The inappropriate use of thyroid replacement or treatment errors may also produce symptoms of hyperthyroidism. Thyrotoxicosis factitia is a form of thyrotoxicosis in which a patient takes excessive amounts of either thyroxine (T4) or triiodothyronine (T3). This condition should be considered in a patient with access to hormone supplements or with a psychiatric problem. Before initiation of antithyroid therapy, a baseline complete blood count and liver function tests including hepatic aminotransferases (aspartate aminotransferase, alanine aminotransferase) should be obtained. During therapy, the white blood cell count is checked every 2 weeks during the first month and then every 4 to 6 months thereafter. Liver enzymes should be evaluated every 3 to 6 months. Radioactive Iodine Radioactive iodine–131 ( 131 I; Iodotope) is the treatment of choice for hyperthyroidism in the United States, especially in middle-aged or older adults. Typically, a 24- hour radioiodine uptake dose of 75 to 200 mcCi per gram of estimated thyroid tissue is administered orally Women receiving radioactive iodine therapy should refrain from becoming pregnant for 4 months after therapy. T4 levels need to be checked monthly for 3 months after the administration of radioactive iodine in patients receiving radioactive thyroid ablation therapy. A nonradioactive alternative to thyroid radioablation for severe Graves’ disease or subacute thyroiditis involves administering a large quantity of concentrated iodine as a saturated solution of potassium iodide (SSKI, 35–50 mg iodide per drop, 1–2 gtts in water PO 2 times daily; Lugol solution, 8 mg iodide per drop, 3–5 gtts in water PO 3 times daily) or iopanoic acid (Telepaque, 1–3 g PO or 0.5 g PO 2 times daily). These concentrated iodine therapies effectively block the conversion of T4 to T3 and inhibit the release of thyroid hormones. Persons receiving radioactive iodine therapy should avoid contact with infants, children, and pregnant women for 7 days after ingestion. Women who receive this treatment postpartum must not breastfeed for at least 3 to 6 months, because radioactive iodine is excreted in breast milk and can ablate the infant’s thyroid. HYPOTHYROIDISM Common symptoms include hoarseness, deafness, confusion, frank psychosis, dementia, ataxia, depression, constipation, intolerance of cold temperatures, dry skin, or hair loss. Hashimoto’s thyroiditis, a type of primary hypothyroidism, is the most common form of autoimmune thyroid disease. This type of hypothyroidism occurs at least four times more often in women than in men, with the average age at onset from 30 to 60 years. Thyroid Association recommends measuring thyroid function in all adults starting at age 35 years and then at least every 5 years. The American College of Physicians recommends TSH measurement in women older than 50 with one or more general symptoms that could be caused by thyroid disease. All patients with a prior history of any medically or surgically treated thyroid disease should be screened with a serum TSH measurement yearly. In addition, patients with other autoimmune diseases and those with unexplained depression, diabetes mellitus (DM), cognitive dysfunction, prior external radiation to the head and neck, hypercholesterolemia, or other risk factors should be screened with TSH measurements. Women experiencing unexplained infertility should be screened for thyroid dysfunction, and postpartum women with vague complaints may benefit from screening. Patients with secondary or tertiary (central) hypothyroidism show a low, normal, or mildly elevated TSH level with low FT4 and T3 by radioimmunoassay. The laboratory values for patients with subclinical hypothyroidism show a mildly increased TSH (4.5–10 mIU/L) with a normal FT4 level. The diagnosis of hypothyroidism is made by measuring serum TSH. TSH and FT4 should be used to follow treatment. When autoimmune thyroiditis is the suspected underlying cause, it is helpful to confirm this via antithyroid antibody titers, either antimicrosomal antibody (antithyroid peroxidase [TPO] antibody) or antithyroglobulin antibody. Once a diagnosis of hypothyroidism is confirmed, additional testing may be necessary to determine the effect of the disease on other body systems. Because T3 is nonspecific and not sensitive, it is not routinely used as an initial diagnostic tool. Because anemia is a frequent complication of hypothyroidism, a complete blood count should be done. A complete blood chemistry profile should be done to assess for alterations in electrolytes, blood urea nitrogen, creatinine, serum osmolarity, and glucose, because a decreased glomerular filtration rate (affecting renal function) can occur. A complete urinalysis should also be performed, with specific attention to the presence of protein (indicating possible renal impairment). Changes in the chemistries may be an indication of deteriorating thyroid function leading to myxedema. 7. Subclinical hypothyroid Subclinical hypothyroidism is the presence of normal free thyroxine immunoassay (FT4) with an elevated thyroid-stimulating hormone (TSH). As many as 15% of patients older than age 65 years have these levels, as do many other adults. However, few of these patients report symptoms, or their symptoms are nonspecific The American Thyroid Association and the American Association of Clinical Endocrinologists recommend treating subclinical disease when there is presence of antithyroid antibodies, when evidence of atherosclerotic cardiovascular disease exists, when heart failure exists, or if the patient is symptomatic at this TSH level. Some patients with subclinical hypothyroidism feel better when treated with levothyroxine. Medication therapy has potentially dangerous adverse effects but may improve subtle abnormalities, prevent goiterous growth, and prevent the development of frank hypothyroidism. Therapy is advisable especially if thyroid autoantibodies are positive, because overt hypothyroidism frequently develops. in young patients or patients with goiter, consider initiating levothyroxine therapy. If the decision is made not to treat these patients, they should be evaluated at 6- to 12-month intervals for evidence of more severe clinical and biological loss of thyroid function. A lower dose (0.5–1.0 mcg/kg) could be given in the treatment of subclinical hypothyroidism. 8. Primary hypothyroid More than 95% of patients with hypothyroidism have primary or thyroidal hypothyroidism, involving dysfunction or atrophy of the thyroid gland. When the thyroid dysfunction is caused by failure of the pituitary gland, the hypothalamus, or both, it is known as central hypothyroidism. Interferon-α, thalidomide, and the antiretroviral agent stavudine have also been associated with primary hypothyroidism. Thyroid hormone deficiency beginning in early infancy and childhood is characterized by growth retardation, mental deficiency, and delayed dentition. Adolescents with primary hypothyroidism may manifest an enlarged sella turcica and, rarely, mg/day every 3–6 weeks to a maximum of 0.3 mg per day. Older adults require a beginning dose slightly lower. After therapy has been initiated with levothyroxine, the practitioner should check the patient’s levothyroxine levels in 4 to 8 weeks by evaluating the TSH level to determine whether adjustment of the levothyroxine dose is necessary. The target TSH level is 0.3 to 2.4 mIU/L. Increasing the levothyroxine dose more often than at 6- week intervals will probably lead to overreplacement. The patient should be examined annually for manifestations of thyrotoxicity (e.g., tachycardia, nervousness, or tremor) before increasing dosages. Laboratory values (FT4 and TSH levels) within normal limits and a satisfactory clinical exam suggest that treatment is adequate. For maintenance treatment, the medication should be titrated to the lowest dosage required to maintain euthyroidism, with a normal TSH and a normal or slightly elevated T4. Undetectable TSH levels suggest overtreatment; medication should be decreased in these patients. TSH levels greater than 10 mIU/L indicate undertreatment, and medication should be increased. Practitioners are encouraged to write prescriptions that do not allow substitution and use the same brand for the patient throughout treatment. The same brand of thyroid preparation is recommended because the bioavailability, stability, and content of the medication may vary with the different brands. 10. Obesity Obesity is an excess of adipose tissue (body fat) and is manifested by body mass index (BMI) of 2 30 kg/m or higher for adults and a BMI at or above the 95th percentile for children and adolescents. The two major types of obesity are upper body (apple-shape) and lower body (pear-shape) obesity. Patients with central or upper body obesity have excessive body fat in the abdomen and flank areas and are at a greater risk for type 2 DM, coronary artery disease, stroke, and early death than those with lower body obesity. Patients with lower body obesity have excessive adipose tissue in the buttocks and thighs. Overweight and obesity are epidemic in the United States today. Thirty-five percent of men and 36% of women are obese. Another 30% of Americans are overweight with a BMI between 25 and 2 29 kg/m . African American women are more likely to be obese than are white women. The incidence of obesity is higher in those of lower socioeconomic status regardless of race. Central and upper body obesity is more common in men, whereas lower body obesity is more common in women. The causes of obesity are categorized as essential and secondary. Essential obesity is the most prevalent type and is a result of the intake of more calories than are expended. This type of obesity results from the multiple interactions of genetic and environmental factors Secondary obesity is rare; possible causes include Cushing’s disease, polycystic ovary syndrome (PCOS), hypothalamic disease, hypothyroidism, and insulinoma. Some medications associated with weight gain include glucocorticoids, tricyclic antidepressants, and phenothiazines. Risk factors for development of obesity include diet, lifestyle, environment, and the interaction among the aforementioned causes. A diet high in fat contributes to obesity because dietary fat has more than twice the calories of carbohydrates or proteins. Obesity results when one’s intake of calories exceeds metabolic needs. The control of appetite and the mechanisms that govern food intake are complex and incompletely understood. The hypothalamus controls certain aspects of appetite and appears to have a role in an individual’s food preferences. Calculating Body Mass Index The most recent formula for calculating body mass index (BMI) was developed by a panel convened by the National Heart, Lung, and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Diseases. The equation for BMI is weight (kg) divided by height (m) squared (kg/m2). Classifying Obesity Classification Relative Weight BMI Overweight 100%–120% 25–29.9 kg/m2 Obesity 140%–200% 30–40 kg/m2 Severe (morbid) obesity Measurements of weight and height are used to calculate the BMI for the exact classification of obesity. BMI is calculated by taking the body weight in kilograms divided by the height in meters squared. Secondary causes of obesity must be ruled out before initiating a treatment plan with the patient. Cushing’s syndrome, hypothalamic injury, and hypothyroidism should be considered The patient should be questioned about any periods of rapid weight gain and environmental or psychosocial changes in lifestyle during these periods explored. An exercise history should also be obtained, A past medical history and complete medication profile are necessary, Initial assessment of the patient who is obese should include the following laboratory tests: thyroid- stimulating hormone (TSH), complete blood count, fasting glucose, liver function tests, and a lipid profile. An electrocardiogram (ECG) should also be obtained. The management plan should focus on reducing comorbidity and reducing visceral obesity, not solely on improving cosmetic outcomes. A weight-loss goal of 1 pound per week can be achieved by reducing caloric intake by 500 kcal daily, because 1 pound of fat accounts for about 3,500 kcal. The National Institutes of Health guidelines suggest that the ideal weekly weight-loss goal is 1 to 1.5 pounds. Assisting the patient to identify reasons for overeating may benefit the patient in managing his or her behavior. Being tired, anxious, and angry are major triggers for overeating. Remember the acronym HALT: hungry, angry, lonely, and tired.