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NR511 Final ExamStudy GuideSee Midterm and Week 1 Study Guide for content covering weeks 1, 2 & 3Common InfectionsImpetigoImpetigo is a superficial bacterial infection of the skin. It is classified into primary impetigo when there is a direct bacterial invasion of previously normal skin or secondary impetigo when the infection arises at sites of minor skin trauma. The occurrence of secondary impetigo is referred to as impetiginization. Impetigo is most frequently observed in children ages 2–5 years of age, although older children of any age and adults may also be affected. The infection usually occurs in warm, humid conditions and is easily spread among individuals in close contact. Risk factors include poverty, crowding, poor hygiene, and underlying scabies. Impetigo is primarily caused by S. aureus. Group A Streptococcus (GAS) causes a minority of cases, either alone or in combination with S. aureus. Occasionally, MRSA is detected in some cases of impetigo. Variants of impetigo include nonbullous impetigo, bullous impetigo, and ecthyma. ?Nonbullous impetigo—most common form of impetigo and begins as papules that progress to vesicles surrounded by erythema. Within a week, the papules eventually become pustules that enlarge, break down, and form thick, adherent crusts with a characteristic golden appearance. Lesions usually involve the face and extremities. Regional lymphadenitis may occur, although systemic symptoms are usually absent. ?Bullous impetigo—Bullous impetigo is seen primarily in young children in which the vesicles enlarge to form flaccid bullae with clear yellow fluid, which later becomes darker and ruptures, leaving a thin brown crust. The trunk is more frequently affected. Bullous impetigo in an adult with appropriate demographic risk factors should prompt an investigation for previously undiagnosed human immunodeficiency virus (HIV) infection.?Ecthyma—This form of impetigo, caused by group A, beta-hemolytic Streptococcus (Streptococcus pyogenes), consists of an ulcerative form in which the lesions extend through the epidermis and deep into the dermis. Ecthyma resembles "punched-out" ulcers covered with yellow crust surrounded by raised violaceous margins. Poststreptococcal glomerulonephritis is a serious complication of impetigo (ecthyma). This condition develops within 1–2 weeks following infection. Poststreptococcal glomerulonephritis manifests with edema, hypertension, fever, and hematuria. The diagnosis of impetigo often can be made on the basis of clinical manifestations.A Gram stain and culture of pus or exudate is recommended to identify whether S. aureus and/or a beta-hemolytic Streptococcus is the cause. However, treatment may be initiated without these studies in patients with typical clinical presentations. Bullous and nonbullous impetigo can be treated with either topical or oral therapy. Topical therapy is used for patients with limited skin involvement whereas oral therapy is recommended for patients with numerous lesions. Unlike impetigo, ecthyma should always be treated with oral therapy. Benefits of topical therapy include fewer side effects and lower risk for contributing to bacterial resistance compared with oral therapy. Topical choices to treat impetigo include the following medications for 5 days.?Mupirocin three times daily?Retapamulin twice daily Extensive impetigo and ecthyma should be treated with an antibiotic effective for both S. aureus and streptococcal infections unless cultures reveal only streptococci. Dicloxacillin and cephalexin are appropriate treatments. A 7-day course of oral antibiotic treatment is recommended. If only streptococci are detected in extensive impetigo or ecthyma, oral penicillin is the preferred therapy. MRSA impetigo can be treated with doxycycline, clindamycin, or trimethoprim-sulfamethoxazole (Bactrim). Crusted lesions can be washed gently. Children can return to school 24 hours after beginning an effective antimicrobial therapy. Draining lesions should be kept covered.Quiz: Sally, aged 25, presents with impetigo that has been diagnosed as infected with staphylococcus. The clinical presentation is pruritic tender, red vesicles surrounded by erythema with a rash that is ulcerating. She has not been adequately treated recently. Which type of impetigo is this?a. Bullous impetigob. Staphylococcal scalded skin syndrome (SSSS)c. Nonbullous impetigod. EcthymaStaphylococcal Scalded Skin SyndromeCaused by Staphylococcus aureus, it’s a variant of bullous impetigo: Epidermal necrosis caused by bacterial exotoxins, resulting in the epithelial layer peeling off in large, sheet-like pieces; mimics scalded-skin thermal burn. This serious infection is more commonly seen in children and usually begins in the intertriginous areas.CellulitisCellulitis is an acute infection as a result of bacterial entry via breaches in the skin barrier. As the bacteria enter the subcutaneous tissues, their toxins are released which causes an inflammatory response. Cellulitis and erysipelas is almost always a unilateral infection with the most common site of infection being the lower extremities. Cellulitis involves the deeper dermis and subcutaneous fat. Cellulitis is observed most frequently among middle-aged individuals and older adults. The vast majority of pathogens associated with cellulitis are from either Streptococcus or Staphlococcus bacteria. The most common are beta-hemolytic streptococci (groups A, B, C, G, and F), and S. aureus (gram +) Both erysipelas and cellulitis manifest with areas of skin erythema, edema, warmth and pain. Fever may be present. Additional manifestations of cellulitis and erysipelas include lymphangitis and inflammation of regional lymph nodes. Edema surrounding the hair follicles may lead to dimpling in the skin, creating an appearance reminiscent of an orange peel texture called "peau d'orange".Cellulitis may present with or without purulencepatients with cellulitis tend to have a more indolent course with development of localized symptoms over a few days.Many patients with cellulitis have underlying such as tinea pedis, lymphedema, and chronic venous insufficiency. In such patients, treatment should be directed at both the infection and the predisposing condition if modifiable.Patients with cellulitis or erysipelas in the absence of abscess or purulent drainage should be managed with empiric antibiotic therapy. Patients with drainable abscess should undergo incision and drainage.Describe an appropriate empiric antibiotic treatment plan for cellulitisshould be managed with empiric therapy for infection due to beta-hemolytic streptococci and methicillin-susceptible Staphylococcus aureus (MSSA) with:?Cephalexin 500 mg four times daily (alternative for mild penicillin allergy)?Clindamycin 300 mg to 450 mg four times daily (alternative for severe penicillin allergy) Good choices for uncomplicated cases of cellulitis that are not associated with human or animal bites include dicloxacillin or cephalexin for 10 to 14 days.If pt has severe PCN allergy rx erythromycinIf caused by animal or human bite: amoxicillin-clavulanic acid (augmentin) for 2 weeksThe coverage for MRSA is achieved by adding to amoxicillin one of the following:Bactrim DS twice dailyDoxycycline 100 mg twice dailyMinocycline 200 mg orally once, then 100 mg orally every 12 hoursIf clindamycin is used, no additional MRSA coverage is needed.Risk factors for community-associated methicillin-resistant S. aureus (CA-MRSA) include the following.?Antibiotic use secondary to antibiotic selective pressure. Use of cephalosporins and fluoroquinolones strongly correlates with the risk for MRSA colonization and infection.?HIV infection?Hemodialysis?Long-term care facilitiesPatients with drainable abscess should undergo incision and drainage. For patients undergoing incision and drainage of a skin abscess, some experts suggest antibiotic treatment under some conditions.?Single abscess ≥2 cm?Multiple lesions?Extensive surrounding cellulitis?Associated immunosuppression or other comorbidities?Systemic signs of toxicity (fever >100.5° F/38° C)?Presence of an indwelling medical device (such as prosthetic joint, vascular graft, or pacemaker)?High risk for transmission of aureus to others (such as in athletes or military personnel)Quiz: Ian, age 62, presents with a wide, diffuse area of erythematous skin on his left lower leg that is warm and tender to palpation. There is some edema involved. You suspect:a. Necrotizing fasciitis. c. Cellulitis.b. Kaposi's sarcoma. d. A diabetic ulcer.ErysipelasCellulitis and erysipelas are two of the most common skin and soft tissue infections. Erysipelas involves the upper dermis, and there is clear demarcation between involved and uninvolved tissue.An older name for erysipelas is “St. Anthony’s fire.” Despite the superficial nature of this infection, erysipelas should not be taken lightly, because it can be fatal if it is not treated promptly (especially in the very young and the elderly). Erysipelas is sometimes seen after an episode of strep throat.The most common sites of involvement are the face (especially the cheeks) and the lower legs. Erysipelas occurs in young children and older adults.Erysipelas results almost always results from a group A strep infection.erysipelas is non-purulent.Patients with erysipelas tend to have acute onset of symptoms with systemic manifestations including fever and chills Classic descriptions of erysipelas note "butterfly" involvement of the face. Involvement of the ear (Milian's ear sign) is a distinguishing feature for erysipelas, since this region does not contain deeper dermis tissue.Quiz: Which of the following types of cellulitis is a streptococcal infection of the superficial layers of the skin which does not involve the subcutaneous layers?a. Necrotizing fasciitis c. Erysipelasb. Periorbital cellulitis d. "Flesh-eating" cellulitisNecrotizing fasciitisConsidered as a severe case of cellulitis must refer to ER, can be a differential diagnosis of cellulitisDefined as deep infection that results in progressive destruction of the muscle fascia. The affected area may be erythematous, swollen, warm, and exquisitely tender. Pain out of proportion to exam findings may be observed.The hallmark of this infection is its rapid progression and the severity of the symptoms. The progress of the infection is measured in terms of hours instead of days, and the border can be seen to literally spread in just a few hours. This infection is caused by “flesh-eating bacteria,” and loss of life or limb is a potential complication.Quiz: Mark has necrotizing fasciitis of his left lower extremity. Pressure on the skin reveals crepitus due to gas production by which anaerobic bacteria?a. Staphylococcal aureus c. S. pyrogenesb. Clostridium perfringens d. StreptococcusMammalian bitesSoft tissue trauma caused by animal and human bites have serious clinical implications because of the potential for complications.Bite wounds should be irrigated copiously with sterile saline, and grossly visible debris should be removed. Prophylactic antibiotics are administered to patients who present for evaluation of a bite wound who do not yet have signs or symptoms of infection in the following circumstances.?Deep puncture wounds (especially due to cat bites)?Wounds requiring surgical repair?Moderate to severe wounds with associated crush injury?Wounds in areas of underlying venous and/or lymphatic compromise?Wounds on the hand(s) or in close proximity to a bone or joint?Wounds on the face or in the genital area?Wounds in immunocompromised hosts Amoxicillin/clavulanate 875 mg/125 mg twice daily is the agent of choice. Alternative antibiotics include one of the following agents with activity against Pasteurella.?Doxycycline 100 mg twice daily?Bactrim DS twice daily?Penicillin VK 500 mg four times daily?Ciprofloxacin 500 mg twice dailyPlus one of the following agents with anaerobic activity.?Metronidazole 500 mg three times daily?Clindamycin 450 mg three times daily First-generation cephalosporins and macrolides should be avoided. The duration of prophylactic oral antibiotics is 3–5 days, with close follow-up. Tetanus toxoid should be given to those who have completed a primary immunization series but who received the most recent booster 5 or more years ago. Patients with mild infection can be treated initially with the same prophylactic antibiotics for 5 to 14 days of therapy.Infection with Pasteurella multocida characteristically develops rapidly following cat or dog bites with erythema, swelling, and intense pain evident as early as 12 to 24 hours after the biteWound cultures of uninfected bite wounds are not useful. Wound cultures are not indicated in clinically uninfected bite wounds as results do not correlate with likelihood of infection or the pathogen that is present in patients with subsequent infection. If a bite wound appears to be infectedThe laboratory requisition should note that an animal or human bite wound is the culture source because Eikenella corrodens and Pasteurella multocida are fastidious organisms.Identify the likely pathogen associated with cats bites, human bites and dog bites.Human BitesPathogensStaph aureusStrepAgent of choice: Amoxicillin/clavulanate 875/125 2xday Cat & Dog BitesPathogensPasturella multocida & capnocytophaga canimorsisAlternative ATB w/ activity against PasturellaDoxycycline 100mg 2xdayBactrim DS 2xdayPCN VK 500mg 4xdayCiprofloxacin 500mg 2xdayPLUSMetronidazole 500mg 3xdayClindamycin 450mg 3xdayUrologyHematuria- 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.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, antispasmodicsb. 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, narcoticsc. Overflow: Failure to empty due to underactive detrusor, outlet obstruction, diabetes mellitus Medications: Anticholinergics, disopyramide, antihistamines, calcium channel blockersd. Functional: Delirium, fecal impaction, manual dexterity and immobilityMedications: diuretics, hypnotics, alcohol, narcotics, decongestantsRx: 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.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- The most accurate way to quantify the amount of protein in the urine is a 24-hour urine collection; however, a spot urine albumin to urine creatinine ratio can be measured and is a close approximation of the 24-hour urine measurement. A 24-hour urine with more than 165 mg of protein is considered abnormal and a specimen with more than 3.5 g is indicative of a nephrotic problem. A urine albumin to urine creatinine ratio of less than 0.2 is normal and corresponds to an excretion of less than 200 mg/dL of protein.- Causes of benign, or functional, proteinuria include orthostatic proteinuria, exercise, environmental conditions, fever, and acute illnesses. Orthostatic proteinuria occurs when the protein level is elevated only when the patient has been standing but not while he or she has been reclining. Exercise-induced proteinuria may occur in athletes such as runners or boxers; it may be accompanied by elevated catecholamines, hemoglobinuria, or hematuria. Proteinuria caused by environmental conditions such as emotional stress, exposure to cold, prolonged lordotic posture, and excess in the body’s norepinephrine level will resolve spontaneously when the precipitating element is eliminated or removed. A mild, transient proteinuria may result from an albumin infusion or acute illnesses such as fever, congestive heart failure, acute pulmonary edema, head injury, or cerebrovascular accident; this type of proteinuria typically resolves as the medical condition improves.- When proteinuria is identified in a low-risk (nondiabetic or nonpregnant) patient, the urine should be tested for Bence Jones protein, the presence of which suggests multiple myeloma.Cystitis & UTI- Cystitis: inflamed bladder, lower UTI: bladder/urethra- Causes: - bacterial infection (most common)- Fungal Infections- Trauma- Chemical Irritants- Foreign bodies (kidney stones)- UTI upper: kidneys and ureters- UTI lower: bladder and urethra- Common causes UTI: Gram – most common E. Coli, Gram + Staph seprophyticus 2nd most common affects young women, sexually active- Risk factors UTI: sexual intercourse, female gender, post menopause (decrease of estrogen causes a loss of protective vaginal flora increasing the risk for UTI), DM, infant boys with foreskin?, impaired bladder emptying- S/S: UTI: - suprapubic pain- urgency- dysuria (pain with urination- frequent urinationInfants: fussy, fever, feed poorlyOlder Adults: fatigue, incontinence, dementia- symptoms not usually seens due to being systemic: fever, N/V, pain at costovertebral angle)- Dx: urinalysis pyuria (WBC in urine), urine looks cloudy; urine dipstick: leukocyte esterase, nitrites (gram – E coli converts nitrate into nitrite); Ucx is the gold-standard for dx if >100,000 from clean catch urine- If pt has pyuria (WBC in urine and culture was negative-> sterile pyuria **suggest urethritis (inflammation of urethra) Most common cause STI: Neisseria gonorrhea or Chlamydia trochamatis- Tx: Thus, both TMP-SMX and nitrofurantoin may be used as empiric therapy for uncomplicated UTI only and, in fact, may prove to be inadequate.- TMP-SMX is a sulfonamide CI with sulfa allergy- Nitrofurantoin CI in 3rd trimester, or renal function impairment. Take with food and will darken urinePyelonephritis- Inflammation of the kidney possibly due to bacterial infection.- Type of upper urinary infection: renal pelvis, tubules, or interstitial tissue; may be unilateral or bilateral.Risk factors: -female sex- indwelling catheter- Sexual intercourse- DM-urinary tract obstruction- VUR- Common pathogens: E coli, proteus, and Enterobacter (common in bowel flora)- Acute pyelonephritis usually unilaterally - S/S: - WBC in urine-WBC cast - leukocytosis (inc WBC in blood)- fever - N/V, chills- flank pain at cosovertebral angleDx: urinalysis: positive for bacteria, proteinuria, leukocyte esterase, urinary nitrites, hematuria, pyuria, and specifically white blood cell (WBC) casts (reflecting the passage of neutrophils through the renal tubules)Urine Cx: demonstrates greater than 100,000 cfu/mL, allowing for identification of the causative organism.?-Tx: abx and hydrationFirst-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.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.CystitisFrequency, urgency, may have gross hematuriaRecent sexual intercourse, risk factors present (see?Table 2)15 to 20% have suprapubic tenderness; no costovertebral angle tendernessUsually positive for pyuria and sometimes also positive for bacteriuria and nitriteSubclinical pyelonephritisFrequency, urgency, may have gross hematuriaRisk factors present (see?Table 5)May have suprapubic tenderness; no costovertebral angle tendernessUsually positive for pyuria and sometimes also positive for bacteriuria and nitrite; positive renal cortical scintigraphy, urine culture usually > 105colony-forming units per mL of urineAcute pyelonephritisNausea, emesis, fever, sepsis, back/flank painMay have had concurrent or preceding cystitis symptoms (see?Table 5)Costovertebral angle tenderness, deep right or left upper quadrant tendernessPyuria usually present with casts of white blood cells; obtain urine culture and sensitivityInterstitial cystitisFrequency, urgency, gross hematuria (20%)Often middle-aged; longstanding symptoms with negative culturesNo costovertebral angle tenderness; may have suprapubic tendernessUrinalysis negative for white blood cells or bacteria; positive for glomerulations on cystoscopyVaginitisExternal irritation, vaginal discharge or pruritus, dyspareunia; no hematuriaPremenstrual exaggeration of symptoms; sexual activity or recent antibiotic exposure or post-menopausal and not receiving estrogen replacement therapyVaginal discharge, inflamed vaginal mucosa (absent in bacterial vaginosis), inflamed cervix (Trichomonas), vaginal atrophy (postmenopausal)Positive potassium hydroxide or vaginal saline preparation; elevated pH (bacterial vaginosis or Trichomonas)Genital herpesDysuria, fever, headache, myalgias, neck pain, vulvar pain, photophobiaSexually active; may have vaginal dischargeGrouped vesicles usually on cervix or pubic area, but may be vaginal; tender inguinal adenopathyViral culture optionalUrethritisUsually asymptomatic; if symptoms develop, they are usually delayed (>1 week)History of unprotected sexual exposureNo suprapubic pain unless associated with pelvic inflammatory disease; rarely, visible urethral dischargeUrethral swab positive for white blood cells; obtain Gram stain to detect intracellular gram-negative diplococci and DNA probe for Chlamydia and gonorrheaRenal calculi- Forms when solid in urine precipitate and is crystalized, due to dehydration or increased in solutes- Calcium oxalate and calcium phosphate stones account for 65% to 85% of all cases of renal calculi.Most common causes: Calcium oxalate (forms in acidic urine) black to dark brown stone, radiopaque on X-ray (white spot)*Most common in men- Risk factors hyperoxaluria: - genetic defect: increase in oxalate excretion- defect in liver metabolism- diet heavy on oxalate rich foods: rhubarb, spinach, chocolate, nuts and beer2. Calcium phosphate (forms in alkaline urine) dirty white stone, also seen as radiopaque on X-ray)Risk factors hypercalcemiaRisk factors hypercalciuriaIncreased absorption in GI tractimpaired renal tubular reabsorptionHormonal causes like primary hyperparathyroidismLow calcium diet: increased oxaluria due to less oxalate bound to calcium in GI tract- vasectomy- hypertension- LasixUric acid stones (red-brown radiolucent on X-ray; transparent to X-ray)- consuming lots of prurines which have high levels of uric acid causing also gouty arthritis. Foods: shellfish, anchovies, red meat, organ meatQuiz: The clinician should question the patient with suspected gout about use of which of these medications that may be a risk factor? Low-dose aspirinThiazide diureticsEthambutol (abx for TB tx)D) All of the aboveStruvite Stones (infection stones, dirty white and radiopaque on X-ray)* Most common in women- caused by bacteria, leading to urease then urea combined with CO2 making urine alkaline- Risk factors UTI, VUR, obstructive uropathiesCystine Stones (yellow or light pink, radiopaque on X-ray)Xanthine Stones (red-brown, radiolucent on X-ray)Urinary tract cancer- Gross painless hematuria is a cardinal symptom of certain malignancies such as bladder cancer.- in a UA glucose and protein positive- Renal tumors are responsible for approximately 3% of all adult malignancies. The incidence is higher in men (although the difference in incidence has been decreasing over time), with onset between ages 55 and 70 years and rarely occurring in people younger than 35 years of age. These cancers are curable in more than 90% of patients if they are superficial and/or localized in the renal pelvis or ureter. Tumors that are invasive have a 10% to 15% chance of being cured. In children, nephroblastoma (Wilms’ tumor) is common, comprising 5% of primary tumors, whereas sickle cell disease has a known, albeit rare, association with carcinoma of the renal medulla. - Cigarette smoking has a 25% to 30% correlation with the development of renal cell carcinoma.- Early signs of tumor growth are silent: Approximately 60% of the time, patients present with gross hematuria as the only symptom. The patient complains of a dull, achy flank pain or abdominal mass in approximately 30% of cases. In 10% to 15% of patients, the triad of flank pain, hematuria, and abdominal mass is found, which is often a sign of advanced disease.- Tx: Treatment for a renal neoplasm is primarily surgical with a partial or total nephrectomy, chemotherapy is not effective with this type of cancer; however, immunotherapy using lymphokine-activated killer cells with or without interleukin-2 may be helpful for selected patients. Radiation therapy is controversial but may be used in combination with nephrectomy or for palliative effects in patients with bone metastasis.Male ComplaintsTesticular torsion 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 includeepididymitis;acute varicocele;acute hydrocele;incarcerated hernia; andtraumatic 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.Benign Prostatic HyperplasiaThe prostate gland, is a walnut size gland positioned at the base of the bladder and in front of the rectum that begins to enlarge as a man ages.? It surrounds the urethra and as the prostate gets larger, it can squeeze or partly cause obstruction. BPH is the common name for nodular hyperplasia and is one of the most common conditions affecting men >40yrs old.? As many as 50% of men experience symptoms of enlarged prostate by age 60 and 90% of men will report symptoms by age 85The causes of BPH are not fully understood.? Aging is a risk factor and genetic predisposition may play a role.? Androgens are thought to play a key role.? There has been no concrete evidence that diet, environment, or sexual practices increase the risk for developing BPH. Obesity though does increase the risk of development.Symptoms of BPH usually involve a combination of obstructive and irritative voiding complaints.? BPH is not life-threatening but it is life altering.? It is important to note that symptoms are not specific to BPH (since many conditions result in an overlap of symptoms) so a complete work-up needs to be completed.Obstructive symptoms includedecreased streamhesitancypostvoid dribblingsensation of incomplete bladder emptyingoverflow incontinenceinability to voluntarily stop the urine streamurinary retentionstrainingIrritative symptoms includenocturiaurinary frequencyurinary urgencydysuriaurge incontinenceDRE is done to determine the size of the prostate gland.? The prostate in BPH is usually smooth and enlarged.? If the prostate is nodular or unusually firm, cancer should be suspected.? Also, the size of the prostate does not correlate with the severity of symptoms.Quiz: During a digital rectal exam (DRE) on a 75-year-old man, the clinician suspects the patient has prostate cancer. What physical finding should make the clinician suspicious? An enlarged rubbery glandThe DDx for BPH is extensive but the diagnoses can be categorized into 1 of the 3 following types:bladder outlet obstruction (cancer, stricture, bladder neck contracture),nonobstructive etiologies (neurogenic bladder, DM, Parkinson’s, Medications)irritative symptoms (neoplasm, bladder cancer, prostatitis, uti)Diagnostic testingurinalysis and urine C&S is done to exclude infection and hematuriaPSA is done to assess for prostate cancerurine cytology is done to exclude bladder cancerthe AUA no longer recommends a serum creatinine on the initial evaluation should be done on subsequent visits or if obstructive uropathy is present.Keep in mind that there may be an elevation in the PSA in BPH just as it occurs in cancer so the PSA is NOT diagnostic of either.More advanced diagnostics include, should be done by an urologist:urodynamic studies to identify difficulties in emptying the bladderpost-void residual urine test (PVR)cystoscopyA patient with mild to moderate symptoms and minimal PVR may only require monitoring as long as more serious conditions have been ruled out. Avoidance of caffeine and alcohol, both known to be bladder irritants, should be recommended.Once prostatic cancer has been ruled out, medications may be tried to treat BPH symptoms.? This approach is typically taken when there is not a strong indication for surgical resection or if the patient is not a good surgical candidate.MedicationsMedication therapy typically includes Alpha 1A Blockers (relaxes the smooth muscle around the bladder neck) and 5-alpha-reductase inhibitors (block the conversion of testosterone to DHT)Alpha 1A BlockersCommon A1A medications prescribed include:Tamsulosin (Flomax) 0.4mg-0.8mg QDDoxazosin (Cardura) 4-8mg QDSilodosin (Rapaflo) 4-8mg QD5-alpha-reductase inhibitors that are commonly prescribed are:Finasteride (Proscar) 5mg QD alone or in combination with DoxazosinDutasteride (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.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:Obstructive: weak stream, incomplete bladder emptying, dribblingIrritative: 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:Fever, chills, malaiseLBPDysuriaArthralgia (joint pain)myalgia (muscle pain)Urgency, frequencynocturiabladder outlet obstruction- Chronic Bacterial s/s:* symptoms often are abscentPerineal painLBPDysuriaScrotal/penile painlower abd painIrritative voiding- When we look at the DRE results for the three conditions, we can expect to see the following.Acute bacterialChronic bacterialNonbacterialWarm, tense, swollen, boggy, and very tender prostateNormal (may be a little boggy or focally indurated)Normal or tender prostate- Antibiotics—ABP: Current CDC guidelines recommend (sta/tg2015/urethritis-and-cervicitis.htm?(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 hoursLevofloxacin 500 mg dailyOfloxin 400 mg Q 12 hoursNorfloxin 400 mg Q 12 hoursAlternatives to a fluoroquinolone includedoxycycline 100 mg Q 12 hours; andTMP-SMX [160 mg/800 mg] (Bactrim DS) one tab Q 12 hoursSTD Coverage—ABPFluoroquinolone 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 includessingle-dose IM ceftriaxone 250 mg; plussingle dose oral Azithromycin 1 gm or doxycycline 100 mg BID × 7 days.Supportive Measures—ABPantipyretics, NSAIDS, hydration, stool softeners as neededurinary analgesics such as phenazopyridine and flavoxate are also used.urology referral to ensure eradication and prevent relapseNocturia- Having to wake at night one or more times to void, each time being preceded and followed by sleep- Adult men normally void five to six times during the day and once or not at all during the night. As men age, nocturia is usually a sign of a prostate problem, most often benign prostatic hyperplasia (BPH)- a type of irritative symptom in BPH- Typically, 50% of men older than age 50 years have BPH, and the rate increases by 10% for every 10 years of age (i.e., to 60% of men older than age 60 years, to 70% of men older than age 70 years, and so on).- Medications, such as methyldopa, phenothiazines, diazepam, excessive vitamin D, and diuretics, may also cause nocturia, as well as precipitate or aggravate incontinence. Drugs that cause urinary retention include alpha-adrenergic agents, androgens, and sympathomimetic agents such as ephedrine and pseudoephedrine. Urinary retention can cause nocturia and incontinence.Erectile dysfunction- Or also referred as impotence, is the failure to consistently maintain a sufficiently rigid erect penis to allow for sexual intercourse and is considered a facet of male sexual dysfunction. ED can also manifest as a lack of sexual desire or inability to ejaculate. ED can result from many causes, including physiological, psychological, endocrine, vascular, and neurological.- ED is classified as mild if the patient fails to achieve a satisfactory erection in 2 out of 10 attempts. If all attempts at satisfactory erection fail, the ED is classed as severe. Moderate ED is somewhere in between mild and severe.- Some common medications that can cause ED: methyldopa (BP), spironolactone, beta-blockers. The use of alcohol, tobacco, and recreational drugs increases the risk of sexual dysfunction.- The development of drugs that decrease the breakdown of 5-cyclic guanosine monophosphate (cGMP) has revolutionized ED treatment. cGMP is the intracellular second messenger of nitric oxide, which is the primary vasodilator and neurotransmitter involved in the erectile response. The first of these drugs was sildenafil citrate (Viagra). - - Sildenafil is an orally active cGMP-specific phosphodiesterase inhibitor. It results in an increased blood flow necessary for successful penile erection. The standard dose is sildenafil 50 mg taken orally at least 1 hour before sexual activity.- Prolonged erection (priapism) occurs rarely, but the patient should be instructed to seek medical attention if this does occur.- Hormone Replacement: Parenteral agents: testosterone cypionate (Depo-Testosterone) testosterone enanthate (Delatestryl) CI: Do not use in patients with serious liver, kidney, or cardiac disease, prostate or breast cancer, or in those with mercury allergy. The peak and trough effects that may lead to aggression, feelings of well-being, energy, and increased libido within 72 hours of injection. As the peak level falls, the patient may experience depressed mood and loss of libido; Transdermal testosterone patch: Androderm, Testoderm. Considerations: NOT to be applied to the scrotum. Should be applied to the arm, back, abdomen, or thigh. May cause local irritation.- Oral agents: sildenafil (Viagra) vardenafil (Levitra) tadalafil (Cialis) avanafil (Stendra) SE: Headache, flushing, dyspepsia, nasal congestion, visual color changes, back, lower limb pain for all phosphodiesterase-5 inhibitors (PDE5); CI: None of these agents should be used in patients taking nitrates or alpha blockers. Must wait 24 hours before giving a nitrate after sildenafil or vardenafil can cause severe hypotensive effects. The duration of action for tadalafil is 36 hours. Must wait 48 hours before giving a nitrate.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?PLUSsingle dose oral Azithromycin 1gm or Doxycycline 100mg BID x 7dIf 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 finishedSupportive 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.447675209550Varicocele & 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.?Diagnosis of a varicocele is mostly clinical and is again typically found incidentally on a work-up for infertility. Men with varicoceles tend to have low sperm counts, and the motility of their sperm is decreased. Because a urologist or reproduction specialist is usually the one to find a varicocele, testing is not often done in primary care. However, a scrotal ultrasound, venography, or thermography all can confirm the diagnosis.Grade 1 varicocele is one that is palpable only when the patient performs the Valsalva maneuver.Grade 2 varicocele is palpable when the patient is standing.Grade 3 varicocele may be assessed with light palpation and visual inspection?The differential or varicocele should includehydrocele;spermatocele;testicular tumor; andepididymal cyst.?Most varicoceles are minor, but a referral to a surgeon is indicated. Embolization or ligation of the spermatic vein can be performed. Conservative treatment is the preferred management for older men with only minor pain or for whom fertility is no longer an issue.A hydrocele is a collection of peritoneal fluid within the scrotum between the two-layered sac that holds the testes and spermatic cord. Hydroceles are also uncommon (<1% of adult men), but most occur in males >40 years old.Causes of hydrocele includeacute epididymitis;teste trauma;testicular tumors; andsequelae of radiation therapy complications.?History findings will complain of swelling in the scrotum or inguinal canal. They are usually painless and are reported as a sense of heaviness in the scrotum.?The physical exam should include an examination of the scrotum, testes, abdomen, and groin. Additionally, transillumination of the scrotum should be performed. To do this, in a darkened room, place a penlight up against the scrotum. The trapped fluid from a hydrocele will appear light pink, yellow, or red. The testes themselves do not illuminate, and neither does a hematoma. This is typically considered a diagnostic finding.?Diagnosis of a hydrocele is a clinical one. If a hydrocele cannot be confirmed by H&P alone, the patient should have an inguino-scrotal ultrasound performed to rule out inguinal hernia. At this point if diagnosis is still unclear, a referral to a urologist is recommended where additional testing with abdominal X-rays or nuclear scan may be warranted.?DDx for hydrocele should includeindirect inguinal hernia;orchitis (infection of testes);epididymitis; andTreatment: For adults, no treatment is required in most cases. If the hydrocele is painful, large, unsightly, or uncomfortable, several outpatient surgical procedures can be performed by an urologist.Testicular cancerCompared with other types of cancer, testicular cancer is rare and is highly treatable. Testicular cancer is the most common cancer in American males between the ages of 15 and 35.?There is no clear cause-and-effect relationship for testicular cancer, but risk factors includeHIV infection;Caucasian race; andhistory of cryptorchidism (undescended testes).?Other risk factors that have been identified includehigher social status;being unmarried; andliving in a rural area.?Testicular cancer is usually found based on the symptoms a person is experiencing or when the patient or their partner finds a lump in one of the testicles not previously noted. Typically, the patient will report a painless lump in one of their testicles or a feeling of heaviness in the affected scrotum. As many as 10% of patients with testicular cancer will be asymptomatic whereas another 10% will present with manifestations of metastasis, which may include LBP, generalized fatigue, swollen lymph nodes noted in 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 includeepididymitis;hydrocele;varicocele;hematoma; andQuiz: A 22-year-old male is seen in the clinic because he found a hard lump in his testicle when performing testicular self-examination (TSE). Which of the following should be included in the list of differential diagnoses?A) Testicular cancer, B) Inguinal hernia, C) Varicocele, D) All of the aboveTo 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 fingersFeel for lumps or irregularities.Like all cancers, the earlier the diagnosis is made, the better the patient outcome.M/SRange of motion and strength testing- ROM shoulder:Forward flexion: Normal is to 180 degrees.Extension: Normal is to 40 degrees.Abduction: Normal is to 120 degrees with the palm down, 180 degrees with the palm up.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.External rotation: Normal is to 90 degrees.- ROM elbow:The flexion should be between 140–150 degrees.Extension 0–5 degrees.Pronation 90 degrees.Supination 90 degreesM/S examination & diagnostic testing- A useful approach to the initial patient encounter for any musculoskeletal complaint is to determine if the complaint isacute or chronic;articular or nonarticular;inflammatory or noninflammatory; orlocalized or systemic in distributionAcute PainLess than 3 months in durationSharp/throbbing/pulsing/electric/paresthesia/burning (peripheral/nociceptive/neurogenic pain systems) in qualityModerate to severe intensity at first and decreases predictably over time (based on type of tissue injury)Edema is common and decreases predictably over timePain disappears once healing is completeMood tends to not change the patient’s complaintsPain provocation tests produce the patient’s initial complaintsPain is localized to site of injury or can present in standard referral patternsResults from something specific, such as an injury or inflammationChronic pain:Greater than 3 months in durationPain symptoms become more generalized topographically and less localized to the site of injury or initial complaintPain referral patterns that shift in location as well as intensity, frequency, and qualityPain that does not change with movement, rest, or over timePatients usually report pain as constant or continuous (less like to be intermittent).Mood or current psychological status tends to affect or worsen the pain complaints.Articular structures include the following.SynoviumSynovial fluidArticular cartridgeIntra-articular ligamentsJoint capsuleJuxta-articular boneDisorders of these structures are typically characterized by the following.Deep or diffuse painLimited AROM and PROM on movementSwellingCrepitationInstabilityLockingDeformityArticular disorders are classified based on the number of involved joints.Monoarticular: One jointPeriarticular: Two to four jointsPolyarticular: Four or more jointsQuiz: You have detetected the presence of crepitus on examination of a patient with a musculoskeletal complaint. Additionally, there is limited range of motion (ROM) with both active and passive movement. These findings suggest that the origin of the musculoskel244347947305etal complaint is: A)Articular B) Inflammatory C) Nonarticular D)A and BNonarticular disorders structures include the following.LigamentsTendonsBursaeMuscleFasciaBoneNerveOverlying skinDisorders of these structures are typically characterized by the following.Painful AROM but not PROMDemonstrated point or focal tendernessPhysical findings far from the joint capsuleUnlikely to see crepitus, instability, or deformityNonarticular disorders are described as either focal or widespread.Inflammatory disorders can be idiopathic or infectious and usually present with all or some of the four cardinal signs of inflammation.Erythema3. WarmthPain4. SwellingSystemic signs of inflammation may be presents including the following.FatigueWeight lossMorning stiffnessFeverElevated ESRElevated C-reactive proteinAnemia of chronic diseaseHypoalbuminemiaThrombocytosis Noninflammatory disorders tend to be related totrauma (i.e., meniscus tear);ineffective repair (OA);neoplasm; andpain amplification (i.e., fibromyalgia). There may be pain without swelling or warmth, absence of inflammatory or systemic features, minimal or absent morning stiffness, and normal for age laboratory testing.Quiz: What is the most common cause of generalized musculoskeletal pain in women aged 20 to 55 years? Fibromyalgia syndrome (FMS)Quiz: Which of the following statements is true concerning the musculoskeletal exam? The uninvolved side should be examined initially and compared to the involved sideAdhesive capsulitis (frozen shoulder)- There are four stages of recuperation, which ranges from 1 month to 24 months. By the time it is at stage 4, it is almost resolved. Initially, it is a gradual onset of diffusely painful shoulder, which can be significantly 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.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. 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.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.ROM of the lumbar spine including flexion, extension, and rotation to determine limitations and reproduction of painPalpation of the lumbar spine and paraspinal muscles to assess for tenderness and muscle spasmPalpation of the sciatic notch and hips with testing of hip ROMMuscle strength of the lower extremities including flexors and extensors of the hips, knees, and feetDTRsGait including heel and toe walkingSLR (straight leg raise test) and sensation should be assessed paying attention to dermatomal patterns as this may indicate nerve root compression (A diagnosis of disk compression is likely if pain radiates from the buttock to below the knee when the angle of the leg is between 30 and 60 degrees)- Differential DiagnosisLBP 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 spondylitisDrug-seeking behaviorVisceral organ diseaseCancer with metastasis to spine or spinal tumorSpinal infection of epidural spaceQuiz: Sam is a 25-year-old man who has been diagnosed with low back strain based on his history of localized low back pain and muscle spasm along with a normal neurological examination. As the clinician, you explain to Sam that low back pain is a diagnosis of exclusion. Which of the following symptoms would alert the clinician to the more serious finding of a herniated nucleus pulposus or ruptured disc? Unilateral radicular pain symptoms that extend below the knee and are equal to or greater than the back pain- TreatmentAcute 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.Radicular pain- 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.- For sciatic nerve syndrome: Sciatic nerve syndrome is back pain that radiates into the buttocks and produces tingling in the posterior thigh and posterolateral calf to the lateral malleolus. Often the cause is a herniated disc, spinal stenosis, obturator neuritis, sciatic nerve irritation, direct trauma, or osteoarthritis. The pain may also be secondary to lumbar sacral strain but does not necessarily indicate disc herniation or prolapse. Sciatic nerve compression may result from tumors in the pelvis or from prolonged sitting or lying on the buttocks. The history may reveal twisting, bending, or heavy lifting .The physical exam includes evaluating for point tenderness and ROM in the back. With the patient supine, perform straight-leg raising. A positive finding is radicular pain that occurs below the knee at less than 60 degrees of limb elevation, with pain in the buttock or posterior thigh. Treatment is usually conservative. Any change in bowel or bladder function (cauda equina syndrome) constitutes an emergency and needs immediate intervention.- For cervical radiculopathy: commonly caused by compression of the cervical nerve roots, when the cervical discs place stress on the vertebral bodies. It usually is the result of age-related changes, cervical spondylosis, or a herniated disc. The most commonly involved nerve roots are C6 and C7, which produce paresthesias into the lower lateral arm, thumb, and middle finger. Diagnostic tests include radiological assessment of the cervical spine, and if radicular pain is severe or if there is motor or sensory deficit or hyporeflexia, MRI is indicated. If only radiculopathy is present, a conservative trial of cervical traction as in the use of a soft cervical collar may be warranted.- For lumbar spinal stenosis: Lumbar spinal stenosis is narrowing of one or more levels of the lumbar spinal canal and subsequent compression of the nerve roots. In the order of descending likelihood, L4 to L5, L3 to L4, and L1 to L2 are the levels most commonly involved. Onset of symptoms may follow a lifting incident or minor trauma or may gradually emerge. Often there is pseudoclaudication causing radicular complaints (with or without associated back pain) in the calves, buttocks, and upper thighs of one or both legs. Symptoms progress from a proximal to distal direction. Walking or prolonged standing causes pain and weakness in the legs and buttocks. In cases of vascular claudication, the pain stops when the patient stops walking, but pseudoclaudication does not immediately subside when walking stops. The patient may obtain short-term relief by leaning forward (manifested as “stooping”); when grocery shopping, the patient will be leaning on the cart. Relief after sitting is variable, depending on the degree of neural compression. Patients who sleep on their backs, meaning with the spine extended, might awaken after several hours with back and leg pain. Lumbosacral pain is associated with walking and standing. A vague aching in the legs or leg weakness may also be present. Spondylolisthesis (degenerative or spondylolytic), vascular insufficiency, and osteoarthritis of the hips are often associated with spinal stenosis, as well as obesity.Herniated discLumbar Disc Herniation- Herniated nucleus propulsus (HNP) is the medical term for what is commonly known as a herniated or slipped disk. Between each bony vertebra lies a disc that provides cushion, support, and flexibility within the spine. Each disk is named for the vertebrae above and below it, so the disk between the L4 and L5 bones is referred to as the L4–5 disc. The discs are filled with a gelatinous substance that is like a cushiony sac. As part of the normal aging process, the discs degenerate over time and start to become less absorbent. When a small tear occurs in the disc, the inner most portion of that gel-like substance can ooze out of the disc. Typical pain associated with HNP occurs when the contents compress the nerve root on one or both sides. Pain can be mild to debilitating.- History and Physical: The history and physical for suspected HNP is the same as for spinal stenosis. Questions regarding acute injury should be asked as trauma can contribute. Most patients can recall the time when the pain occurred and an inciting event. Some may experience a gradual onset of symptoms. Straight leg test usually reproduces pain on the affected side between the angle of 30 and 60 degrees. With knee extended, raise leg until pain is reproduced, then slowly lower leg until pain is gone. Provider should ensure the foot is dorsiflexed for testing accuracy. The sensitivity is 91%; the specificity is 26%.Quiz: Which of the following statements is true concerning the management of the client with a herniated disc? intolerable pain for more than a 3-month period is an indication for surgical intervention.Gaenslen’s Sign- Hip joint is flexed maximally on one side and the opposite hip joint is extended, stressing both sacroiliac joints simultaneously. This test is considered positive if the patient experiences pain while this test is performed- weak clinical testPatrick’s Maneuver/FABER TestThis is a test for the hip or sacroiliac joint; it isolates spasm to the iliopsoas muscle. The provider will flex, abduct, and externally rotate the hip. Pain while completing maneuver is positive. The sensitivity is at 77%; specificity is 100%.- SymptomsWhen nerve compression occurs, symptoms typically include the following.Leg pain > back painPain that travels in a dermatomal pattern of the nerve root that is compressed (L1-L3 produces radiation of pain to the hip and/or anterior thigh, etc.)NumbnessWeaknessTinglingDiminished reflexes in the legs- Diagnosis and TreatmentMost patients with acute uncomplicated low back pain (i.e., no red flags) do not require imaging, blood tests, or other diagnostic tests, and 4–6 weeks of treatment is appropriate before consideration of imaging studies. In fact, many insurances will deny a request for advanced imaging if failure of conservative treatment is not shown because rapid or routine MRI in the early care of patient’s increases cost without significantly improving pain or long-term function.Treatment: In most patients, symptoms of lumbar disc herniation with imaging-confirmed neurologic involvement will improve with conservative management alone, which includes oral analgesics, physical therapy, ESIs and exercise.Quiz: Which of the following is not a maneuver test to assess for lumbosacral pain? Straight leg raise Gaenslen’s Hawkins FaberCauda Equina SyndromeThe cauda equina is a continuation of the spinal cord below the first lumbar level in the adult. The “horse’s tail” consists of an array of nerves that exit the conus of the spinal cord and continue down the lumbar spine, exiting at different lumbar and sacral levels through foramina. These nerves are responsible for specific sensory and motor functions, including perineal sensation and both bladder and anal sphincter function. In some instances, an acute herniation of the disc at the L5 to S1 level may cause acute cauda equina compression characterized by bilateral lower extremity weakness, anesthesia, or paresthesia of the perineum and buttocks (saddle anesthesia) and bowel or bladder retention and/or incontinence. This is a medical emergency and requires immediate decompression.Quiz: Janet is a 30-year-old woman who has been recently diagnosed with a herniated disc at the level of L5-S1. She is currently in the emergency room with suspicion of cauda equina compression. Which of the following is a sign or symptom of cauda equina compression? Paresthesia of the perineum and buttocksKnee pain & examination- most common knee conditions that you will see in primary care. These include patellofemoral syndrome, OA, ligament sprain, and meniscus tear.-Patellofemoral syndrome is a broad term used to describe pain in front of the knee and around the patella. It is sometimes referred to as “runner’s knee” or “jumper’s knee” because it is common in people who play sports. However, the condition can occur in non-athletes, as well. The condition occurs when nerves sense pain in the soft tissues and bone around the patella. These soft tissues include the tendons, the fat pad beneath the patella, and the synovial tissue that lines the knee joints. In many cases, PFS is caused by vigorous physical activity or a sudden change in the activity or intensity of an activity. Pain is typically in the anterior aspect of the knee that occurs after periods of strenuous activity but is relieved with rest.- Diagnosis is made by history, and on physical, the pain can be reproduced with the patient asked to squat. X-ray may identify osteochondritis, which has a similar presentation. - Treatment is conservative and includes activity modification, muscle strengthening, and PT.OA of the knee is a progressive disease of the joints that occurs when articular cartilage that covers the ends of bones gradually wear away. Where there once was smooth articular cartilage that made the bones move smoothly, there is now a frayed and rough surface. Joint motion along this exposed surface is painful. OA can affect any joint in the body, and symptoms can range from mild to disabling. OA of the knee is the most common and is characterized by recurrent knee pain that worsens with activity. It may also be associated with crepitus and knee instability. - Imaging: Plain radiography is considered the “gold standard” for morphological assessment of knee OA.- Treatment: Acetaminophen is recommended as first-line therapy. Cortisone injections provide short-term benefits. Hyalurinoc acids may be helpful, but the evidence is conflicting. Indications for total joint replacement include refractory pain (when meds are not helping) and disability and radiographic evidence of knee OA.Ligament sprains and tears of the knee most of these end up being referred to orthopedics for treatment. However, it is important to understand the signs and symptoms of each condition as well as the maneuvers to test them. Ligament sprain or tears occur after some sort of injury. Symptoms include acute pain, swelling, and possible instability. Physical exam should include the valgus and varus stress tests, which test the MCL and LCL respectively, and are performed at 30 and 0 degrees. The ACL and PCL are tested using the anterior drawer and posterior drawer tests.Maneuver testing video for valgus and varus test Maneuver testing video for posterior and anterior test: anterior or posterior cruciate ligament tear: - Imaging should start with X-rays, and an MRI should be performed if there is a high index of suspicion for ligament tear. Treatment for partial tears include aspiration of bloody effusion, possible arthroscopy, immobilization, padded splint knee immobilizer, and circular cast for 3–4 weeks; then, begin vigorous rehab of quadriceps and hamstrings. For a complete tear, surgical repair should be attempted as soon as possible, best done within 48 hours, although it is possible even 10 days post-injury. Meniscus TearThe symptoms typically exhibited by these patients include knee pain, swelling, knee locking, sensation of giving way, painful snapping or clicking. McMurray’s test (positive with a click or pop with associated pain see below) and the Apley compression test are performed to evaluate the meniscus.Imaging: MRI evidence of meniscal tears is very common in asymptomatic patients and patients with osteoarthritis. - Treatment: Arthroscopic surgery for degenerative meniscal tears does not improve pain more than conservative treatment in patients with mild or no concurrent osteoarthritis.Quiz: John is a 16-year-old boy who presents to the emergency room after hurting his knee in a football game. He described twisting his knee and then being unable to extend it completely. John tells the clinician that he heard a pop when the injury occurred and has been experiencing localized pain. The clinician suspects a meniscal tear. Which test would be most appropriate to assess for the presence of a meniscal tear? McMurray’s Lastly, we will discuss common ankle and foot disorders that you will see in your practice. The most common injuries are ankle sprain, plantar fasciitis, Achilles rupture, bunion, and toe fracture.Ankle sprain 809625652145- Occurs after some injury and is a tearing of the ligaments of the ankle when the ligament is stretched beyond its limitations. The most common ankle sprain occurs on the outer (lateral) ankle. Injuries where the ankle is rolled inward (inversion) will produce a lateral ankle injury. Whereas, outward or eversion injuries produce medial ankle injuries. - Ankle X-rays are only required if pain is in malleolar zone and any of the following.Bone tenderness at posterior edge or tip of lateral malleolusBone tenderness at posterior edge or tip of medial malleolusInability to bear weight both immediately and in emergency department- The history and physical exam are key. Treatment involves PRICE (protection, rest, ice, compression, and elevation). Acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce pain.Plantar FasciitisPlantar fasciitis is an overuse injury that affects the thick band of tissue (fascia) connecting your heel bone to the base of your toes. The condition typically starts gradually with mild pain at the heel bone that is often referred to as a “stone bruise” and is more likely to be felt after exercise. Plantar fasciitis is a clinical diagnosis, and the hallmark symptom includes pain with the first morning steps or after a period of sitting. Treatment includes stretching, shoe inserts, arch supports, orthopedic shoes, night splints, NSAIDs, and possibly steroid injection. Achilles Tendon Rupture Complete tear of the tendon and typically affects men over the age of 40 who are involved in a recreational sport. Symptoms include a sudden, sharp pain in the Achilles tendon. A loud snapping noise or bang may also be heard. A gap of 4 to 5 cm in the tendon can be felt immediately after the injury but may be less obvious later as swelling increases. There is a considerable loss of function, and the patient usually needs to limp but may still be capable of walking. This is also a clinical diagnosis. This is usually a clinical diagnosis that requires a MRI if uncertain. Should this type of injury present to the clinic, an immediate surgical consult is needed because the sooner that it takes place, the higher the chance of success. If the injury is >2 days old, the chances of a successful outcome decreaseCarpal Tunnel SyndromeCTS occur when the median nerve, which runs from the forearm into the palm of the hand, becomes constricted. The carpal tunnel is a narrow passageway of the ligaments and bones at the base of the hand that houses the median nerves and the tendons that bend the fingers. The median nerve provides feeling to the palm side of the thumb and to the index, middle, and ring fingers but not to the little finger. A common cause of CTS is repetitive activity with the hands that cause irritated tendons, causing compression of the median nerve. Symptoms may include burning, tingling, or itching numbness of the hand and fingers, especially the thumb, middle, and index fingers. Symptoms usually start gradually, and the classic presentation is the patient will complain of waking up feeling the need to “shake out” the hand or wrist because of numbness. This is because most of us sleep with our wrists flexed. As the condition progresses, symptoms may occur during the day, and weakness ensues, making it difficult to grasp small objects or perform manual tasks. In untreated cases, the muscle at the base of the thumb loses innervation and atrophies.- CTS is made primarily as a clinical diagnosis with attention to occupational and leisure activities. Physical exam should include testing of upper extremity strength and sensation as well as reflexes. A Phalen’s and Tinel test should also be performed. In the Tinel test, the provider taps over the median nerve of the affected wrist. The test is positive if tingling occurs in the affected fingers. Phalen’s maneuver, or wrist-flexion test, involves having the patient pressing the backs of their hands and fingers together with their wrists flexed as far as possible, ideally 90 degrees. The test is positive if tingling or numbness occurs in the affected fingers within 2–3 minutes (it may not happen immediately).Confirmatory testing can be done with an EMG or nerve conduction test, which can evaluate the severity of the neuropathy, but it is important to know that symptoms must be present for at least 3 months before an abnormality will be detected on EMG.Treatment starts conservatively with nocturnal wrist splints that extend the wrist upwards, taking pressure off the tunnel. Surgery is reasonable to offer after failure of conservative therapy for 3 months because delayed surgery appears as effective as immediate surgery with 94% versus 92% success rates. It is important to know that NSAIDs, vitamin B6, and diuretics are not effective.Osteoporosis- Osteoporosis is a generalized skeletal disorder characterized by normal bone mineralization (nomal amount of minerals to make bone) but low bone mass (bone mineral density-either makes little bone or or looses too much bone) and disruption of the bony architecture, both of which result in an increased risk of fragility fractures. Its chief clinical manifestations are vertebral and hip fractures, although fractures can occur at any skeletal site. This is contrasted with osteopenia, which is a less severe form of decreased bone mineral density, and osteomalacia, which denotes a decrease in actual bone mineralization.- Women are more likely to have osteoporosis, but men also suffer from this condition. White women are more susceptible than black women; the prevalence of osteoporosis in Hispanic and Asian women is similar to that of white women.- Bone loss after menopause is caused predominantly by estrogen deficiency and is most rapid (up to 7% per year) in the first decade after menopause. Postmenopausal osteoporosis is more prevalent in white and Asian women than in women of other races, with the majority of white women developing osteoporosis by the end of the first postmenopausal decade. By age 65, one-third of women will have had a vertebral fracture, and by the ninth decade of life, one in three will have had a hip fracture.Table 15.8?World Health Organization Diagnostic Criteria for?OsteoporosisDiagnosisDiagnostic FindingsNormalBMD within 1 SD of young adult reference meanOsteopeniaBMD >1 SD below young adult reference mean (21)OsteoporosisBMD >2.5 SD below young adult reference mean (22.5)Osteoporosis(severe)BMD >2.5 SD below young adult reference mean (22.5)?andpresence of osteoporotic fractures- Risk factors:LifestyleLow body weightCigarette smokingExcessive alcohol intakeLow dietary calcium intakeVitamin D deficiencyDisease-related risk factorsThyrotoxicosisHyperparathyroidismCushing’s diseaseHypogonadismRheumatoid arthritisInflammatory bowel diseaseChronic renal insufficiencyMalabsorptive diseasesSecondary estrogendeficiency resulting fromanorexiaor overexerciseMedication-related risk factorsGlucocorticoidsExcessive thyroxineLong-term use of phenytoinOther risk factorsAdvanced ageFamily history of osteoporosisPostmenopausalGenetic predisposition- Weight-bearing exercise, such as walking, is considered the best form of activity and is associated with higher bone density.- The importance of adequate calcium, phosphorus, and vitamin D intake for children, adolescents, and young adults should not be underestimated, because studies have indicated that women begin losing bone mass (albeit at a rate of less than 1% a year) in their early 30s.- There is increasing evidence that vitamin D deficiency is more prevalent than previously thought, particularly among individuals at increased risk, such as the elderly; those living in northern latitudes; and in individuals with poor nutrition, malabsorption, or chronic liver or renal disease. Modest vitamin D deficiency can lead to a compensatory, secondary hyperparathyroidism and is an important risk factor for osteoporosis and fractures.- As bone density decreases, microfractures of the anterior vertebral bodies in the thoracic spine are likely to accumulate over time, leading to the characteristic dorsal kyphosis (or “dowager’s hump”). The resultant exaggerated kyphosis produces a loss of height, which is generally not a “complaint,” per se, but may be only casually mentioned by a patient during the course of a health-care visit. This may be the only verbal cue the practitioner receives to help identify that patient as being at risk for having osteoporosis. As the kyphosis worsens over time, impairment of rib mobility, a decrease in lung volumes, and an increase in respiratory complaints may develop.Shoulder dislocations- Shoulder dislocations are a common injury, occurring most frequently in younger adults. The mechanism of injury may be direct or indirect, usually with the arm in extension. - There is often an obvious fullness of the anterior capsule on exam and a positive sulcus sign (space under the acromion). In an acute anterior dislocation, pain is severe and ROM is limited. The patient will usually hold the arm slightly abducted and externally rotated. There may be associated neurovascular and/or neurosensory trauma; therefore, the clinician should check the distal pulses and sensation, especially over the deltoid. Posterior dislocations are less common (2%) and less apparent. Deformity is minimal, but any motion of the extremity will cause severe pain. Recurrent dislocations can occur and do not require as severe a force as the initial injury. Reduction is usually the treatment of choice; occasionally, surgery is necessary.Quiz: Jennifer is an 18-year-old girl who comes to the emergency room after a fall during a soccer game. Jennifer explains that she fell on her left side and kept her arm out straight to break her fall. She has been experiencing severe pain and limited range of motion in her left shoulder. The clinician has diagnosed Jennifer with a dislocated shoulder. Which of the following statements are true concerning shoulder dislocation? There is a risk of neurovascular and neurosensory trauma, so the clinician should check for distal pulses.Systemic musculoskeletal symptomsSystemic signs of inflammation may be presents including the following.?Fatigue?Weight loss?Morning stiffness?Fever?Elevated ESR?Elevated C-reactive protein?Anemia of chronic disease?Hypoalbuminemia?Thrombocytosis Other important info not to miss:- maneuver test to confirm a cervical injury is Spurling’s test.Explain spinal stenosisNarrowing of the spinal canal w/ compression of nerve rootsCongenital or acquired (age)Most commonly from enlarging osteophytes at the facet joints, hypertrophy of the ligamentum flavum and protrusion/buldging of the intervertebral discsMay produce symptoms by directly pushing on nerve or interrupting the blood supply to nerveCommon source of chronic low back pain, seen most with aging. All older people have some degree of this. A common source of chronic low back pain, seen most with aging, is spinal stenosis.Spinal stenosis is caused by a narrowing of the spinal canal as a result of degeneration of the bony facet joints and the intervertebral disks. Bone spurs or osteophytes may also grow into the spinal canal. Facet joints become enlarged and arthritic making less space for the nerve roots. Spinal canal abnormality occurs in virtually every person as they age because the intervertebral discs become worn, and continued axial loading over the course of a lifetime leads to arthritis in the spine. The severity of symptoms will depend on the size of a person’s spinal canal and the degree of encroachment on the nerves.SymptomsIn spinal stenosis, leg pain is commonly greater than back pain and pain is characteristically worse with prolonged standing or walking and improved by rest. In more advanced cases, leg pain with weakness or numbness and tingling can be present.Key questions that can be very revealing in patients with suspected spinal stenosis include the following.When you go to the grocery store, do you find yourself leaning on the cart to minimize your pain?If you are standing in the kitchen doing dishes or cooking, do you lean on the counter for support?If you are walking in the mall, do you find yourself looking for places to sit frequently?- The preferred imaging to determine the degree of spinal canal narrowing and facet arthroplasty resulting in nerve impingement is an MRIDiscuss common characteristics (subjective and objective findings) of patients with lumbar spinal stenosisSubjectiveRadicular complaints in calves, buttocks, upper thighsPain w/ walking or prolonged standingVascular claudication – pain stops w/ restPsuedoclaudication – pain doesn’t stop immediately at restShort term relief by leaning forward/stoopingSometimes relief w/ sittingPain in back/leg when sleeping on back at nightPain w/ walking/standingObjectiveMuscle weaknessImpaired proprioception Diminished reflexesSensory changes (numbness/tingling)Bowel or bladder symptoms Sphincter tone decreasedDon’t confuse w/ prostate problems in older menIdentify the red flags associated with back and neck complaints which warrant further investigation “TUNA FISH”T- TraumaF- Fever U- Unexplained weight lossI – IV Drug UserN- Neurologic symptomsS – Steroid UseA- Age>50H – History of cancer (prostate, renal, breast, lung)Differentiate between DeQuervain’s Tenosynovitis and Carpal Tunnel SyndromeCarpal Tunnel Syndrome: Peripheral nerve compression of the medial nerve Caused by repetitive flexion and extension of the wrist or direct compression of medial nerve Pain and/or numbness are usual presenting symptomsBurning, tingling, or itching numbness of the hand and fingers, especially the thumb, middle, and index fingersMost often dominant hand – may be bilateralPain increases with wrist flexion or extensionParesthesia and numbness along thumb, index, long and radial half of ring fingersNighttime wakening of N/T in affected limbPositive Phalen’s test, Positive Tinel’s sign DiagnosticsMedian nerve conduction velocity study most usefulxray if limited wrist movement onlyTreatmentRest, splintingNSAIDS, NO CORTICOSTEROIDSVitamin B6, and management of concurrent diseasesOften resolves after pregnancy if symptoms relatedQuiz: Which of the following statements is true regarding the treatment of carpal tunnel syndrome? A) The goal of treatment is to prevent flexion and extension movements of the wrist.B) Splints are used in carpal tunnel syndrome because they allow for free movement of the fingers and thumb while maintaining the wrist in a neutral position.C) Corticosteroid injections are discouraged in the treatment of carpal tunnel syndrome because of the risks for median nerve damage, scarring, and infection.D) All of the aboveDeQuervain’s TenosynovitisInflammation involving the synovial sheaths and tendons of the abductor pollicis longus and extensor pollicis longus, and brevis tendons (snuff box)Pain at base of thumb or at the radial styloid process on abduction and extension of the thumb or on radial side of wrist with liftingGenerally seen in patients that perform pinch-grip activities like using hand tools, sewing, assemblyMore often middle-aged womenPhysical Exam Allen’s testPhalen’s test (negative)Tinel’s sign (negative)Confirmed by Finkelstein’s test (grasp the thumb in the palm while you deviate the wrist to the ulnar side)Xray only if history of traumaTreatmentRest, splinting for 3-6 weeksNSAIDSInjected corticosteroids Tendon release surgery. Describe how to perform a Phalen and Tinnel testA. Phalen test:Purpose: Assess for median nerve compressionProcedure: Have the patient maintain forced flexion of the wrist for 1 minute or more, with the dorsal surface of each hand pressed together. If the patient complains of numbness and paresthesia in the fingers =TEST IS POSTIVEB. Tinel test:Purpose: Assess for compression neuropathyProcedure: Percuss the median nerve at the wrist. If the patient complains of tingling in the digits (POSITIVE TINEL SIGN), compression at the site of percussion is likely.Differentiate between lateral and medial epicondylitis Lateral epicondylitis (AKA tennis elbow) is an overuse syndrome or tenosynovitis (inflammation involving synovial sheaths surrounding the tendon and the tendon) – typically from wrist extension and pronation and supination of the forearm. Presents with pain (worse with motion such as gripping) in elbow and forearm. Diagnosis made with PE. Xray can be used to r/o other causes of pain. MRI will show severe tenosynovitis but not necessary. Treated with rest, ice, NSAIDS, PT, and possible corticosteroid injections and splinting. Medial epicondylitis (AKA golfer’s elbow) is less common. Overuse syndrome of wrist flexion. Pain on medial epicondyle worsens with wrist flexion. Treated same as lateral epicondylitis. Imaging: Usually unnecessary, but it may be useful if needed to rule out alternative diagnoses.Identify at least 3 physical exam maneuvers to assess the knee1. Diagnosing ACL injury: Lachman’s test () ; anterior drawer test ()2. Diagnosing meniscal tears: McMurray () and Apley () 3. Diagnosing PCL injury: posterior drawer test () and Thumb sign4. Diagnosing collateral (MCL and LCL) injury: Valgus and Varus stress test () see above Q#8EndocrineHyperthyroidHyperthyroidism, a common clinical condition, includes a heterogeneous group of conditions characterized by the excessive secretion and synthesis of one or both of the thyroid hormones: thyroxine (T4) and triiodothyronine (T3). The clinical manifestations of hyperthyroidism result from the effects of excessive thyroid hormone on body tissue, resulting in alterations in growth, metabolism, and development. These manifestations are sometimes mistaken for signs of psychiatric illnesses. The long-term effects of inadequately treated overt hyperthyroidism are heart disease, osteoporosis (in postmenopausal women), mental illness, and infertility.Patients may be asymptomatic in the presence of mild elevations of thyroid hormones; they are more likely to remain asymptomatic at increasing levels if the increased secretion has been gradual.Graves’ diseaseToxic nodular goiterSubacute thyroiditisThyrotoxicosis factitiaJod-Basedow phenomenonAutoimmune diseaseUnknown development of nodules that progress from nontoxic to toxic over timeThought to be caused by viral infectionExcessive ingestion of exogenous thyroid hormonesLarge intake of iodine in diet in a person with thyroid diseaseHyperthyroidism is characterized by the excessive secretion and synthesis of one or both of the thyroid hormones, T3 and T4. Hyperthyroidism can be classified into subclinical or overt.Subclinical—This is where the TSH is low or undetectable, but the FT4 and thyroid antibodies are normal. It is prudent to monitor patients regarding this situation if they are over 65 as the likelihood that conversion to overt hyperthyroidism can occur. Asymptomatic patients under 65 with a TSH of less than 0.1 or between 0.1 and 0.4 should also be monitored for conversion.Overt—Clear evidence that a low/undetectable TSH with high levels of FT4 and/or T3 exist.?Common forms of hyperthyroid include the following.Graves’ disease—This is an autoimmune disorder characterized by agonist antibodies that cause an overproduction of thyroid hormone. Graves’ disease accounts for 80–90% of hyperthyroid cases.Subacute thyroiditis—This is glandular inflammation and follicular cell destruction, frequently found after a viral infection.Toxic multinodular goiter—This is a complication of chronic, inactive nodule goiter, typically due to iodine deficiency.Toxic adenomaQuiz: Which of the following laboratory findings should the clinician expect in a patient with untreated Graves' disease? A) Elevated thyroid-stimulating hormone (TSH), B) Elevated T4, C) Elevated TRH, D) All of the above **from dunphy typo? A is not correct as it would be low TSH in hyperthyroidism?History and PhysicalThe clinical presentation of hyperthyroidism depends on the duration, the amount of excessive thyroid hormone secreted, and the organ system affected. So, like hypothyroidism, the differential diagnosis will depend upon the presenting complaint.?HistoryPhysicalFatigueMuscle atrophyWeight lossTremorsIncreased appetiteWarm, flushed, moist skinDiaphoresisHyperpigmentationHeat intoleranceFine and silky hairDiarrheaThinning hairBlurred visionDermopathy of legsIncreased tearingIncreased liver functionPhotophobiaExopthalmosPalpitationsLid lag and edemaExertional dyspneaCorneal ulcerationMenstrual irregularitiesHyperactive reflexesIncreased neck sizeSinus tachycardia?Elevated BP?AFibAnxiety/nervousnessSymptoms of CHFInsomniaGynecomastiaIrritabilityProximal muscle weaknessEmotional labilityLoss of muscle toneRestlessnessOsteoporosis?Hypercalcemia?Potassium wastingThere are three approaches to hyperthyroidism.Radioactive iodine (RAI)—This essentially destroys thyroid tissue and creates hypothyroidism in the patient. It is contraindicated in pregnancy, lactation, or in women seeing pregnancy within the next 6 months.Anti-thyroid drugs (ATD)—There are two main drugs used here in the United States; before initiating these medications, it is important to obtain a CBC and LFTs because they can cause rashes, elevated LFTs, agranulocytosis, and hepatotoxicity.Methimazole (MMI): Usually started at 10 mg daily unless FT4 levels are more than twice normalPropylthiouracil (PTU): Starting doses of 50–150 mg TIDBeta blockers can be used as an adjunct for patient with symptomatic tachycardia over 90 bpm and/or with CVD.Thyroidectomy—this is a surgical procedure that is a definitive cure and used primarily in individuals who have failed ATDs or are not candidates for ATDs.?Recommendations for the type of therapy related to a specific condition can be found in Table 5 of the ATA Guidelines.?Most cases of hyperthyroidism will need at least one consultation with an endocrinologist. Hyperthyroidism is a situation where the course of progression is often hyperthyroidism initially and then, as the thyroid “burns out,” it becomes hypothyroid. Pregnant or lactating women or women seeking pregnancy within the next 6 months should be managed by an endocrinologist.Thyroid testingThere are differing opinions on whether to screen for thyroid disorders in asymptomatic adults.Recommendations of 6 Organizations Regarding Screening ofAsymptomatic Adults for Thyroid DysfunctionOrganizationRecommendationAmerican Thyroid AssociationWomen and men > 35 years old should be screened every 5 years.American Association of Clinical EndocrinologistsOlder patients, especially women, should be screened.Academy of American Family PhysiciansPatients?>?60 years old should be screened.American College of PhysiciansWomen > 50 years with an incidental finding suggestive of symptomatic disease should be evaluated.U.S. Preventative Services Task ForceThere is insufficient evidence for or against screening.Royal College of Physicians of LondonScreening of the healthy adult population is unjustified.Adapted from the ATA/AACE Clinical Practice Guidelines for Hypothyroidism in Adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocrine Practice, 18(6).?Although there is no consensus about population screening in healthy individuals, there is evidence to support screening in the following at-risk populations, including those withautoimmune disorders;pernicious anemia;first-degree relative with AI thyroid disease;history of neck radiation;history of prior thyroid surgery or dysfunction;abnormal thyroid examination; andpsychiatric disorders.?Additional diagnoses that support thyroid screening are listed in Table 9 of the ATA/AACE Clinical Practice Guidelines.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. It identifies areas of increased and decreased thyroid function, often termed hot and cold 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 noduleA 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’ diseaseGraves’ diseaseGraves’ 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.-Graves’ disease—This is an autoimmune disorder characterized by agonist antibodies that cause an overproduction of thyroid hormone. Graves’ disease accounts for 80–90% of hyperthyroid cases.- Thyroperoxidase antibodies (TPO Abs)—Useful in detecting autoimmune thyroiditis (Graves’ or Hashimoto’s)- Thyroglobulin antibodies?(TBG Abs)—Useful in confirming or differentiating between autoimmune thyroiditis types (Graves’ or Hashimoto’s)Toxic multinodular goiter- Toxic multinodular goiter—This is a complication of chronic, inactive nodule goiter, typically due to iodine deficiency.A 70-year-old patient presents with a complaint of difficulty swallowing, tachycardia, sweating, and unintentional weight loss. Upon physical exam, the patient is found to have an enlarged thyroid that has an abnormal contour. Without any further testing, what diagnosis would you say is the most likely? Overt hypothyroidism Hashimoto’s thyroiditis Subclinical hyperthyroidism Nodular goiterToxic 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 hyperthyroidismThis 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.Subacute thyroiditis- Subacute thyroiditis—This is glandular inflammation and follicular cell destruction, frequently found after a viral infection.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.Thus, 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 tendeSubacute 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.ThyroidtoxicosisThe 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. An excess of dietary iodine may also precipitate symptoms of hyperthyroidism.Although thyroid hormones are required to regulate normal growth and development, excessiverelease of T4 and T3 from the thyroid into the circulation upregulates metabolism, leading to an increase in total body heat production, heart rate and contractility, and vasodilation. This explains the clinical manifestations of thyrotoxicosis, which include palpitations, diaphoresis, heat intolerance, and anxiety.T3 is normally 20 to 100 times more biologically active than T4, which is converted to T3 in peripheral tissues. Interestingly, the degree of symptomatology does not consistently correlate with the extent of thyroid hormone overproduction. In general, younger patients tend to have symptoms more reflective of sympathetic activation (tremors, anxiety, and hyperactivity), whereas older patients manifest more cardiovascular symptoms, including atrial fibrillation and dyspnea, as well as weight loss.DrugIndicationsAdverse Reactions and Prescribing Considerationspropylthiouracil (PTU)HyperthyroidismCommon: Pruritus, drowsiness, allergic dermatitis, nausea, vomiting, arthralgiaRare: AgranulocytosisNote: Onset of drug action is 1 week, peaking in 4–10 weeks with a duration of 1–4 weeks.methimazole (MM) (Tapazole)HyperthyroidismCommon: Pruritus, drowsiness, allergic dermatitis, nausea, parotitis, arthralgiaRare: AgranulocytosisNote: Onset of drug action is 1 week, peaking in 4–10 weeks with a duration of 36–72 hours.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 (131I; 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 orallyWomen 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.Subclinical hypothyroidSubclinical 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 nonspecificThe 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. Primary hypothyroidMore 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, precocious puberty, in addition to growth retardation. Growth retardation is treatable with hormone replacement therapy, but mental retardation persists.The sensitive thyrotropin assay is the most specific test for diagnosing primary hypothyroidism. A rise in the TSH will precede any other abnormality of thyroid function as the first evidence of primary hypothyroidism. Hypothyroidism caused by primary thyroid failure can be confirmed by a concomitant finding of a decrease in serum FT4. Patients in an early stage of hypothyroidism may present with an increase in serum TSH together with a normal or low-normal serum FT4.By radioimmunoassay, primary hypothyroidism is associated with low FT4 with an elevated TSH level. The normal range of TSH is 0.35 to 2.5 mIU/L.There is general agreement that a TSH level above 10 mIU/L should be treated in patients with primary hypothyroidism. Levels of 4.5 to 10 mIU/L have varied recommendations. The goal of thyroid hormone replacement in primary hypothyroidism is to normalize, not suppress, the TSH. Suppressed TSH, particularly in postmenopausal women or individuals with levothyroxine overreplacement, causes decreased bone mineral density after several years, leading to osteoporosis.Quiz: A patient is diagnosed with hypothyroidism. Which of the following electrocardiogram (ECG) changes should the clinician expect as a manifestation of the disease? Sinus bradycardiaQuiz: After 6 months of synthroid therapy, the clinician should expect which of the following in the repeat thyroid studies? Normal TSHSecondary hypothyroidMore specifically, secondary hypothyroidism refers to the failure of the pituitary gland to secrete adequate amounts of TSH.Referral to an endocrinologist is necessary if the patient has cardiac disease, symptoms of myxedema, or central (secondary or tertiary) hypothyroidism. After starting hormone replacement therapy, if signs or symptoms of myxedema, chest pain, or thyrotoxicosis occur, the endocrinologist should be consulted.Drugs Commonly Prescribed 16.2 Hypothyroidism: Lifelong Pharmaceutical TreatmentDrugIndicationsAdverse Reactions and Prescribing ConsiderationsSyntheticL-thyroxine*T4 (Levothroid, Levoxyl, Synthroid)Patients with increased TSH level, usually three times the upper limit of the assay. Overt hypothyroidism, lifelong pharmaceutical treatment.Goal: To give enough thyroid supplement orally to result in normal free T4 and TSH levels.Monitor antihyperglycemics, oral anticoagulants, and potential sympathomimetics.Wait 4–5 hours after cholestyramine ingestion.Not to be prescribed for obesity.Use with caution in patients with cardiovascular disease, diabetes, adrenal insufficiency.Increased sensitivity in myxedema and severe hypothyroidism.Start with the lowest dose and increase by 0.025 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. Discuss at least 3 vital body functions which thyroid hormones regulateBody FunctionHyperthyroidismHypothyroidismMetabolicIncreased appetite (Polyphagia), Weight Loss, hypercalcemia, K wasting, increased alkaline phosphataseDecreased appetite, Weight GainGeneralFatigue, Muscle Atrophy, TremorsFatigue, decreased libido, hypersomnia, periorbital puffinessIntegumentaryDiaphoresis, Heat Intolerance, thinning hair, pruritus, onycholysisHair loss, ankle swelling, cold intolerance, dry cool rough skin, alopecia, dry course thick hairGIDiarrhea, Increase in BMConstipation, nausea, hypoactive bowel sounds, ascites, enlarged tongueEyeBlurred vision, tearing, double vision, decreased visual acuity, photophobia, increased orbital pressure, lid lag, exophthalmos, corneal ulcerN/ANeurologicalTremors in hands, hyperactive reflexesMemory deficits, personality changes, hyporeflexia, bradykinesiaCardiopulmonaryPalpitations, SOBOE, tachycardia, HTN, CHF, A-FibExercise intolerance, bradycardia, cardiac enlargement, pleural effusionGUDecreased menstrual flow, gynecomastiaIrregular menses, decreased fertilityHead & NeckIncreased neck size, enlarged thyroid glandEnlarged neck, enlarged tongue (late), hoarsenessPsychosocialAnxiety, nervousness, insomnia, irritability, restlessness, emotional lability, Increase in HR, RR, and BPDepression, slowing of mental processesMusculoskeletalWeakness, loss of muscle tone, Osteoporosis in womenMuscle weakness and crampingHematologicalFatigue, normochromic normocytic anemiaDescribe a goiter and the type of thyroid dysfunction that can be associated with itA goiter is the hypertrophy and hyperplasia of the thyroid gland in response to TSH levels. Most commonly seen with Hashimoto’s thyroiditis (hypothyroidism) in the United States. Toxic multinodular goiter (hyperthyroidism) in iodine deficiency. Grave’s Disease (hyperthyroidism) has a firm goiter. Differentiate between overt hypothyroidism and subclinical hypothyroidismFor synthroid Rx TSH 4–8 = 25 mcgTSH 8–12 50 mcgTSH >12 = 75 mcgOvert hypothyroidismTSH above 10 and FT4 is decreased. In overt hypothyroidism, both the TSH and the FT4 will be abnormal—TSH will be high and FT4 will be low.Too little hormone is being produced, and the pituitary is attempting to get the thyroid to produce more Low FT4 and high TSHSubclinical hypothyroidismTSH levels are increased, but the FT4 is within rangeSome have symptoms, others do notDifferentiate between Hashimoto’s thyroiditis and Grave’s diseaseBoth are autoimmune, attacking thyroid cells. Graves – overproduction of thyroid leading to hyperthyroidism- 90% of hyperthyroidism casesHashimoto’s – underproduction of thyroid leading to hypothyroidism-Identified via TPO and TBG Abs in bloodIdentify the roles of TSH, FT4, TT3, and TPO Abs in determining thyroid functionThyroid Stimulating Hormone (TSH)—Pituitary “messenger” to thyroid to increase or decrease thyroid hormone production. used to diagnose hypothyroidism. TSH and FT4 should be used to follow treatment. If the TSH is low or insufficiently elevated in the presence of low T4, central hypothyroidism caused by hypothalamic or pituitary disease should be excluded before starting replacement therapy. Free T4 (FT4)—Circulating unbound thyroid hormone produced by the thyroid, replaced by levothyroxine medication, useful for the diagnosis of hypothyroidism both overt and subclinical*Primary or overt hypothyroidism is associated with a low FT4 and elevated TSH*Subclinical hypothyroidism is a mildly increased TSH with a normal FT4Total T3 (TT3)—Circulating unbound thyroid hormone that has been converted from T4. T3 is not routinely used as a diagnostic tool because it isn’t sensitive or specific to the hypothyroidism. T3 levels may be normal in early disease, and may not fall until late in the disease. Thyroperoxidase antibodies (TPO Abs)—Useful in detecting autoimmune thyroiditis (Graves’ or Hashimoto’s) Diagnostic for Hashimoto’s thyroiditis when found in high titers (1:400). Higher levels TPO = more thyroid destruction = more severe hypothyroidism No universal screening recommendations for thyroid disease. ATA recommends screening for Baseline at 35Pregnant women Women older than 60Individuals with autoimmune disease.Thyroid Stimulating Hormone (TSH)—Pituitary “messenger” to thyroid to increase or decrease thyroid hormone productionFree T4 (FT4)—Circulating unbound thyroid hormone produced by the thyroid, replaced by levothyroxine medication, useful for the diagnosis of hypothyroidism both overt and subclinicalTotal T3?(TT3)—Circulating unbound thyroid hormone that has been converted from T4, useful for the diagnosis of hyperthyroidismThyroperoxidase antibodies (TPO Abs)—Useful in detecting autoimmune thyroiditis (Graves’ or Hashimoto’s)Thyroglobulin antibodies?(TBG Abs)—Useful in confirming or differentiating between autoimmune thyroiditis types (Graves’ or Hashimoto’s)Identify at least one “at-risk” population who should be considered for thyroid screening-Pregnant women-Women older than 60 years-Persons with other autoimmune diseases-Persons with pernicious anemia-Persons with a family history (1st degree relative) of thyroid disease-Persons with a history of prior thyroid surgery or dysfunction or neck radiation-Persons with Abnormal thyroid exam-Persons with psychiatric disorders(Dunphy, p. 847 & 859 and “Thyroid Disorders” Lecture)Discuss one physical characteristic seen in a hyperthyroid patient-Smooth, velvety skin-Soft, thin hair-Skin with increased pigmentation, spider angiomas, and vitiligo-Onycholysis (splitting and spooning of the nails)-Exophthalmos (buldging eyes)(Dunphy, p. 851 & Hollier, p. 231)Muscle atrophy, tremors, hyperpigmentation, warm flushed moist skin, fine silky hair, thin hair, increased LFT, Exopthalamos, lid lag and edema, corneal ulceration, sinus tach, elevated BP, A.Fib, symptoms of CHF, gynecomastia, osteoporosis, hypercalcemia, potassium wastingObesityIdentify the categories of obesity based on the BMIOverweight BMI is 25-29.9; relative weight is 100%-120%Obesity BMI is 30-40 140%-200% Severe (morbid) obesity BMI is greater than 40 greater than 200%Identify treatment options for obesity based on BMI and comorbid conditionsBMI >25: Diet, exercise and behavior modificationBMI >27 with comorbidity or >30 with or without comorbidity: MedicationBMI >35 with comorbidity or BMI>40 with or without comorbidity: SurgeryComorbidity is defined as HTN, dyslipidemia, T2DM, OSATreatment options: lifestyle changes (diet, exercise- 45-60 minutes/day), managing behavior (i.e. H.A.L.T. – hungry, angry, lonely, tired, behavior modification), reduce caloric intake, drugs (i.e. fenfluramine/Fen Phen, dexfenfluramine/Redux, phentermine, diethylopropion, orlistat). Surgical intervention (vertical-banded (mason) gastroplasty and roux-en-Y bypass) for BMI over 40 OR over 35 with comorbitiesA structured weight loss diet is most effective. Encourage formal programs or weight loss groups (WW, etc.). Diet goals should include a program with1200–1500 calories per day for women and 1500–1800 calories per day for men;500–750 calorie deficit per day;low CHO diet, increased fiber, and decreased saturated fats; andless than 800 calories per day in certain circumstances under medical supervision.Identify at least 3 risks associated with obesitydiabetes,CVD, Afib, HTN, NSTEMI, varicositiescancer, skin infectionsarthritisgallbladder disease, GERD, acute pancreatitis, NAFLDstress incontinence, infertilityOSAIdentify at least 3 causes of obesityCalorie excess—either overeating or high intake of carbohydratesFood insecurity—eating from a fear of potential hunger or past experience with poor availability of food on a regular basisGenetic predisposition with familial history—influences of ghrelin and leptin levelsMedication influences—antidepressants, anti-seizure, steroids, insulin, oral contraceptivesPsychological factors—self-soothing, large CHO intake = increased serotoninDisease states—hypothyroidism, insulin resistance, PCOS, Cushing’sQuiz: How often should the clinician examine the feet of a person with diabetes? At every visitHIV/AIDSHIV testing- The CDC and the United States Preventive Task Force recommend screening the following for HIV.?Adolescents and adults aged 15 to 65 years?Younger adolescents and older adults who are at increased risk (see populations at risk)?All pregnant women, including those who present in labor who are untested and whose HIV status is unknownDescribe at least one at-risk population that is recommended to have HIV screening.Population at risk: Very high risk: men who have sex with men (MSM) and active injection drug High risk: individuals who engage in unprotected vaginal or anal intercourse with individuals of unknown serostatus; those having sexual partners who are HIV-infected, bisexual, or injection drug users; individuals exchanging sex for drugs or money; or those who have acquired or have requested testing for other sexually transmitted infections (STIs) to be at high risk for contracting HIV.Persons who are not sexually active, those who are sexually active in exclusive monogamous relationships with uninfected partners, and those who do not fall into any of the high-risk or very high-risk categories are not considered at increased risk for HIV infection.Once the infection is established, HIV preferentially targets CD4+ T cells. This leads to progressive CD4+ T cell decline, consequent immunodeficiency, and chronic inflammation.About 10% to 60% of individuals with acute HIV infection will not experience any symptoms. Additionally, many individuals who develop a symptom or sign of acute HIV infection report a mild, short-lived, nonspecific symptom during the first 4 weeks of the infection. Quiz: Most patients with acute HIV infection will exhibit signs and symptoms associated with acute retroviral syndrome. FALSEIn patients who have acute symptomatic infection, the usual time from HIV exposure to the development of symptoms is 2–4 weeks.The most cost-effective screening test to determine HIV status is which of the following? ELISAIt should be noted that reestablishment of complete suppression of the virus to below the detection limit of established viral load assays should remain the primary goal of ARV therapyQuiz: The current goal of treatment for a patient with HIV infection is which of the following? Viral suppression of HIV to undetectable levels in the peripheral bloodThe differential diagnosis of acute HIV infection includes the following.?Mononucleosis due to Epstein-Barr virus (EBV)?Cytomegalovirus (CMV)?Toxoplasmosis?Rubella?Syphilis?Disseminated gonococcal infection?Viral infections?Autoimmune diseasesQuiz: HIV differential diagnosis includes _____.You Answered syphilis, rubella, and varicella Correct Answer influenza, hepatitis, and cytomegalovirus toxoplasmosis, rheumatoid arthritis, and hypothyroidism strep, lupus, and chancrePost-exposure prophylaxis (PEP) - PEP meds must be started within 72 hours (3 days) after possible exposure to HIV. The sooner, the better. If prescribed PEP for HIV, the medicine must be taken everyday for 28 days.Three-drug combination regimens lasting 1 month are recommended in all cases of occupational exposure. In contrast to prior guidelines, two-drug regimens are no longer recommended, unless in consultation with an HIV specialist.Preferred regimen:?Integrase inhibitor PLUS 2-NRTI backbone? Raltegravir (Isentress, RAL) 400 mg twice daily PLUS Truvada (tenofovir DF 300 mg + emtricitabine 200 mg) 1 tablet once daily? Contraindicated in PEP: nevirapine (hepatotoxicity, rhabdomyolysis, hypersensitivity).Begin PEP promptly, as quickly as possible, preferably within hours, rather than days, after exposure, according to the regimens listed above.Quiz: Knowing that the current Health and Human Services Guidelines on the Treatment of HIV in Adults recommends to start HIV treatment immediately after the diagnosis, you proceed to _____. refer your patient to an HIV medicine specialist or an infectious disease specialistDiscuss common symptoms of acute retroviral syndrome.Symptoms and signs associated with acute symptomatic HIV infection, known as acute retroviral syndrome, include?fever;?lymphadenopathy;?sore throat;?rash;?myalgia/arthralgia;?diarrhea;?weight loss; andNone of these findings is specific for acute HIV infection, but prolonged duration of symptoms and the presence of mucocutaneous ulcers are suggestive of the diagnosis.Discuss an intervention to prevent HIV and HIV-associated behaviors.*safe sex practices - latex condoms *needle exchange programs*universal testing of donated blood products *education to HIV positive women of childbearing age about c-sections, arv drugs for mother and baby*voluntary HIV testing a routine part of medical care*new models for HIV diagnosing outside medical setting *prevent new infection by working with HIV infected and their partners to minimize riskIdentify physical exam findings in the patient with HIV.fever, sore throat, myalgia, headaches, cervical lymphadenopathy, night sweats, majority are asymptomaticflu-like sumptoms 6 days to 6 weeks after viral transmissiondark purple colored spots (karposi's sarcoma)hairy leukoplakia: condition that is characterised by irregular white patches on the side of the tongue and occasionally elsewhere on the tongue or in the mouth.?non-productive cough, SOB, and fever for several weeks pulmonary symptoms: pcp pneumonia, tb, bacterial pneumonialocalized candida infectionsother STD'sweight loss anemia, leukopenia, and/or thrombocytopeniaAnemia1. Types of anemia and RBC indices on a CBCNormal values (general)Hgb 13-18 g/dLHct 37-55 %Reticulocytes 0.4-1.5 %To diagnose anemia first you have to understand causes, can be caused by destruction (bleeding, hemolysis) or decreased production (kidney problem, marrow problem)First look at reticulocytes (normal 0.4-1.5)Reticulocyte high-> due to destruction BleedingHemolysis:- jaundice, increase bilirubin, bilirubin gallstone- Increased LDH (lactic acid dehydrogenase, normal 100-230)- decreased haptoglobin (normal 30-200)- abnormal RBC morphologyReticulocyte low or normal ->due to decreased production, next step look at MCV (normal 78-93)Low MCV (microcytic): think 1st iron deficiency anemia, could also be due to a genetic disorder like Thalassemia, inflammation disorder, sideroblastic anemia, etc.High MCV (macrocytic): classified as megaloblastic->decreased folate, decreased B12 or non-megaloblastic->?marrow a/hypo plasiaNormal MCV (normocytic): classified as myelophthisic->marrow invasion, leukemia, granulomas, cancer or most common non-myelophthisic-> renal failure, inflammation, ?marrow a/hypo-plastic & VertigoParkinson’sParkinson's disease is a progressive neurologic disorder with four hallmark signs.Resting tremorCogwheel rigidityBradykinesiaPostural instability?Other characteristics include the following.Facial maskingDifficulty standing from the chairTendency to freeze when initiating movement/ambulatingFestinating gait: This gait is a quick, short stride with head down and flexed at the waist. It may appear that the patient cannot stop themselves and may fall forward.Reduced arm swing on the affected sideShort, shuffling strides that way require multiple steps to turn.?The resting tremor associated with PD is often asymmetric involving the upper extremities. It can also involve the lower extremities or the tongue.Keep in mind that there is a group of Parkinsonian syndromes that present similarly: progressive supranuclear palsy, multiple system atrophy, and vascular or ischemic Parkinson’s disease.?Resting tremor may also be medication induced. Certain medications can cause extrapyramidal side effects similar to Parkinson's disease. Antipsychotics are the most common offending agent. Metaclopromide (Reglan) and phenothiazines such as Compazine can also cause Parkinsonian features, including a resting tremor.Quiz: Sam, aged 65, is started on L-dopa for his Parkinson's disease (PD). He asks why this is necessary. You tell him: "The primary goal of therapy is to replace depleted stores of dopamine."Intention, Postural & Resting tremorsResting tremor occurs when a body is at complete rest against gravity or sitting still with arms resting in the lap. The most common conditions that are associated with resting tremor are Parkinson's disease and medication tremors.Wilson's disease is another condition that is associated with resting tremor. This is a very rare genetic disorder associated with copper toxicity. Patients who are affected may have extrapyramidal symptoms [similar to Parkinson's] with a slow and progressive course. There may be symptoms of incoordination in the hands, dysarthria, and gait disorder, bradykinesia, rigidity, and ophthalmologic changes. The work up for Wilson’s includes serum ceruloplasmin and copper. Diagnosis is confirmed with liver biopsy, which identifies the copper toxicity. Treatment is aimed at lowering copper levels. Postural tremor can be seen when the patient is asked to extend their arms in front on them. The most common type would be essential tremor. This is the most common form of all movement disorders. This tremor is seen in the hands, and at times the head, and there are cases where the voice may be involved. The tremor is bilateral and generally symmetric. There is often a positive family history of similar tremor and drinking alcohol often reduces it. Postural tremors can also be medication induced. Signs and symptoms of drug-induced tremors depend on the drug used and the patient’s predisposition to its side effects.Medications such as steroids, caffeine, anti-epileptics, antidepressants, and asthma medications may cause a postural tremor. Eliminating the offending agent is often the treatment of choice. Intention or kinetic tremor is characterized by an increase in amplitude when the patient attempts voluntary movement. It can be assessed by having the patient perform the finger-to-nose movement. Intention tremor may be associated with medications, alcohol or drug abuse, multiple sclerosis, stroke, or a mass affecting the cerebellum. Because intention tremor is a symptom of one of these disorders, it cannot be treated, per se. Coping mechanisms such as occupational therapy can be offered.Identify at least three laboratory tests to rule out systemic causes of tremor.???Electrolyte/ABGs (metabolic imbalances, drugs, caffeine, physiological fatigue)???Serum glucose (hypoglycemia)???Toxicology screen/drug levels (toxic conditions, antipsychotic drugs, caffeine)To rule out systemic causes of tremor, basic laboratory tests should be ordered. Thyroid function tests should be done to rule out hyperthyroidism as well as CMP to rule out hypoglycemia, electrolyte imbalance, and liver disease. Additional testing may be considered based on the suspected etiology. For example, an MRI would be indicated if patient exhibited cerebellar dysfunction during the examination.Describe at least one pharmacologic treatment option for tremor.primidone (Mysoline)-anticonvulstantbeta blocker- propranolol (Inderal), lopressorbenzodiazepine- (Ativan, Klonopin, Valium, and Xanax)Dosages are gradually increased to achieve optimal response. If monotherapy is ineffective, a neurology referral is appropriate. If the tremor is medication induced, that agent may be reduced or eliminated. Parkinson’s disease may be treated with a dopamine agonist or dopamine replacement.Describe a medication commonly associated with tremorsExtrapyramidal side effects similar to Parkinson's disease. Antipsychotics are the most common offending agent. Metoclopramide (Reglan) Phenothiazine -Compazine SteroidsCaffeineAnti-epilepticsAntidepressants (SSRI-celexa, Lexapro, Prozac, Zoloft) or Tricyclic (Elavil, etc)Asthma medications Vertigo classificationQuiz: Dizziness may be defined as _____. instablity. feeling faint. lightheadedness. all of the above.?Peripheral vestibular disease?CNS disorders?Systemic disorders Peripheral Vestibular Disease accounts for 40–50% of all cases of vertigo and dizziness. This class falls into my vertigo category, which is where the patient reports a feeling of internal or external movement. For example, the patient might say, “When I sit up, the room feels like it is spinning around me.” Peripheral vertigo occurs when there is dysfunction of the vestibular nerve or in the labyrinth of the middle ear (semicircular canals and cochlea). Potential etiologies could include inner ear inflammation or infection, tumor, and otoliths (which are small calcium particles in the labyrinth).There are three types of peripheral vestibular disease, which include BPPV, labyrinthitis, and vestibular neuritis. Benign paroxysmal peripheral vertigo condition is often benign and self-limiting.LabyrinthitisLabyrinthitis may produce the same symptoms as vestibular neuritis but the patient will complain of tinnitus and/or hearing loss.Hearing loss may be associated with labyrinthitis but not vestibular neuritis. No specific tests exist to diagnose vestibular neuritis or labyrinthitis. Therefore, a process of elimination is often necessary to diagnose the condition. The differentiating symptom between the two conditions is hearing—labyrinthitis can affect hearing whereas neuritis does not.Vestibular neuritisVestibular neuritis is a disorder resulting from an infection that inflames the inner ear or the nerves connecting the inner ear to the brain. This inflammation disrupts the transmission of sensory information from the ear to the brain. Symptoms are usually acute in onset and will resolve within days and also tend to worsen with movements. Symptoms can be mild or severe, ranging from subtle dizziness to a violent spinning sensation (vertigo). They can also include nausea, vomiting, unsteadiness and imbalance, difficulty with vision, and impaired concentration. There is no hearing loss or tinnitus. Nystagmus is often seen on exam. Identify three central nervous system (CNS) disorders that can be associated with S disorders that disrupt the pathway between the vestibular apparatus and the brain can cause central vertigo or dizziness. Acute onset of symptoms can occur from injury to the brainstem or cerebellum. Common etiologies would include stroke, TIA, vertebrobasilar insufficiency, basilar migraine, cerebellar hemorrhage, and the onset of multiple sclerosis. Central vertigo can be accompanied by brainstem symptoms such as blurred vision, double vision, numbness, weakness, loss of balance, slurred speech, swallowing problems, hoarseness, or Horner syndrome. In the primary care setting, patients with acute vertigo accompanied by headache and brainstem symptoms should be immediately sent to the ER to rule out stroke or hemorrhage. Symptoms that have been present for days and without neurological impairment should undergo further work-up with MRI. ................
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