Western Internal Medicine I WM510 Lecture 5 PDF

Western Internal Medicine I WM510 Taran Kermani MD, L.Ac 1 Rheumatology Taran Kermani MD. 2 Rheumatoid Arthritis Rheumatoid arthritis (RA) is a chronic systemic in ammatory disease whose major manifestation is synovitis of multiple joints. c A L. , D M i anat any age, but in 80% of begin Rheumatoid...

Western Internal Medicine I WM510 Taran Kermani MD, L.Ac 1 Rheumatology Taran Kermani MD. 2 Rheumatoid Arthritis Rheumatoid arthritis (RA) is a chronic systemic in ammatory disease whose major manifestation is synovitis of multiple joints. c A L. , D M i anat any age, but in 80% of begin Rheumatoid arthritis canm cases the age of onsetris between 35 and 50 years. e K not known (idiopathic). The cause is n a r in ammatory multi-systemic disease with RA isTaachronic the main target being the synovium. It has a prevalence of 1% and is more common in women than men ( : ratio of 3:1). The hallmark of RA is in ammatory synovitis that presents in a symmetric distribution. Taran Kermani MD. L.Ac 3 The intense joint in ammation that occurs has the potential to destroy cartilage and cause bone erosions and eventually deform the joint. rm e K n a r Ta , D M i an c A L. Synovium, also called the synovial membrane or stratum synoviale, is the soft tissue found around the joints. Speci cally it is around joint capsules, and synovial joints. Taran Kermani MD. L.Ac fl fl fl ♂︎ ♀︎ fl 4 Clinical ndings Diagnostic criteria—need 4 of the following diagnostic criteria. (1) Morning sti ness (>1hour) for 6 weeks (2) Swelling of wrists, MCPs, PIPs for 6 weeks c A L. , D (4) Symmetric joint swelling for 6 weeks M i (5) Rheumatoid Factor (RF) positive n (an autoantibody) a (6) CRP or ESR (blood tests indicating in ammation in body) m r enodules are not necessary for the diagnosis X-ray abnormalities and K of RA. n a r chronic a in ammatory symmetric arthropathy. There needs to RA is a T be involvement of multiple joints, but some joints are never involved (3) Swelling of 3 joints for 6 weeks in RA: DIPs Joints of the lower back Taran Kermani MD. L.Ac 5 Clinical ndings Because RA is a systemic disease, ~70% of patients present with constitutional symptoms before the onset of the arthritis: c A L. fatigue, anorexia, weight loss, generalized weakness. , D M Damage to the ligaments and tendons i nwith ulnar deviation of the a Radial deviation of the wrist digits rm e K (permanent exion of PIP) deformity Boutonnière n a r Swan-neck a deformity (permanent exion of DIP) T Rheumatoid nodules Extra-articular Manifestations In 20–30% of patients with RA usually occur in areas of mechanical stress (olecranon, occiput, Achilles tendon) Taran Kermani MD. L.Ac fl fl fl fl ff fi fi 6 rm e K n a r Ta , D M i an Rheumatoid nodules c A L. Ulnar deviation at MCP Boutonnière deformity Swan-neck deformity Taran Kermani MD. L.Ac 7 Diagnosis The diagnosis is based on the use of clinical criteria; there is no single test or nding that will diagnose RA. Rheumatoid factor (RF) is an autoantibody against the Fc portion of IgG. , D M i an Rheumatoid factors are found in approximately 70% of patients with RA. However, these antibodies are not speci c for RA and are found in 5% of healthy adults Treatment rm e K COX2-inhibitors (cardiac side e ects) n a r Glucocorticoids a (usually for short courses only) T Disease-modifying anti-rheumatic agents (DMARDs): NSAIDs (all have the same e ect) Antimalarials, gold, sulfasalazine, methotrexate (MTX), and tumor necrosis factor (TNF) receptor inhibitors (adalimumab, HUMIRA®) Taran Kermani MD. L.Ac ff ff 8 fi c A L. Systemic Lupus Erythematosus (SLE) Taran Kermani MD. L.Ac 9 Systemic Lupus Erythematosus (SLE) c A L. SLE is an in ammatory autoimmune disorder characterized by autoantibodies to nuclear antigens. , D M i n remission and The clinical course is marked byaspontaneous relapses. rm e The severity may varyKfrom a mild episodic disorder to a rapidly n fulminant, lif threatening illness. a r a of SLE should be suspected in patients having a T The diagnosis multi-system disease with a positive test for ant -nuclear SLE is a systemic disease in which tissues and multiple organs are damaged by pathogenic autoantibodies and immune complexes. antibodies (ANA, are antibodies that have the capability of binding to certain structures within the nucleus of the cells). Taran Kermani MD. L.Ac e­ fl 10 Epidemiology/Pathogenesis SLE is of unknown etiology. The incidence of SLE is in uenced by many factors, including sex, race, and genetic inheritance. c A L. , D M i nsex distribution is more equal. Among older individuals, the a SLE occurs in 1:1000 white Race is also a factor,rasm e women but in 1:250 black women. K Familial occu rence of SLE has been repeatedly n a r documented. a T The abnormal immune response probably depends on About 85% of patients are women. Sex hormones appear to play some role, most cases develop after menarche and before men pause. interactions between a susceptible host and environmental factors. Ultraviolet (UV)-B light is the only environmental factor known to cause ares. Taran Kermani MD. L.Ac 11 Criteria for the classi cation of SLE (pleuritis or pericarditis) rm e K n a r Ta , D M i an c A L. * A patient is classi ed as having SLE if any 4 or more of 11 criteria are met. Taran Kermani MD. L.Ac o­ fl fl fi fi r­ 12 c A L. The systemic features include fever, anorexia, malaise, and weight loss. , D some time; the Most patients have skin lesionsiatM characteristic "butter y" (malar) n rash a ects less than half a of patients. m r e Other cutaneousKmanifestations are discoid lupus, typical ngertip lesions, nail fold infarcts, and spli ter n a r Alopecia is common. hemorrhages. a T Raynaud phenomenon, present in about 20% of patients, Skin involvement often before other features of the disease. Taran Kermani MD. L.Ac 13 Malar Rash Fingertip lesions Discoid Rash Taran Kermani MD. L.Ac n­ 14 ff Splinter Hemorrhage fl fi Sign and Symptoms c A occur in Joint symptoms, with or without active synovitis,. L over 90% of patients and are often the earliest , D manifestation. M i The arthritis can lead to reversible swan-neck defo mities, n a never noted on but erosive changes are almost m radiographs r e K is a ected in the majority of patients. The pericardium n a failure ar may result from myocarditis and hypertension. Heart T Cardiac arrhythmias are common. Taran Kermani MD. L.Ac 15 Lab Findings SLE is characterized by the pr duction of many di erent autoantibodies. Antinuclear antibody (ANA) tests are nearly 100% sensitive for SLE but not speci c: c A L. , D Positive in low titer in up to 20% of healthy adults M i In many patients with non-lupus conditions such as n a thyroid disease, rheumatoid arthritis, autoimmune m scler derma, and Sjögren r syndrome. e K DNA (anti-dsDNA) and to Antibodies tondouble-stranded a Smith (anti-Sm) are speci c for SLE but not sensitive, r a sinceT they are present in only 60% and 30% of patients, respectively. In medical diagnosis, test sensitivity is the ability of a test to correctly identify those with the disease (true positive rate), whereas test speci city is the ability of the test to correctly identify those without the disease (true negative rate). Taran Kermani MD. L.Ac fi fi o­ fi ff ⚕︎ 16 o­ ⚕︎ ⚕︎ Sign and Symptoms ANA immuno uorescence patterns (a) homogeneous, (b) speckled, (c) nuclear dots, (d) nucleolar, (e) centromeres, (f) nuclear membranes, (g) cytoplasmic, (h) negative and unspeci c Taran Kermani MD. L.Ac 17 Treatment Since there is no cure for SLE, treatment is aimed at controlling symptoms. Belimumab is an IgG monoclonal antibody given intravenously to prevent B-cell activation. c A NSAIDs are used to treat arthritis and pleurisy.. L , skin rashes. Corticosteroid creams are used to treat D M and oral Anti-malaria drugs (hydroxychloroquine) i corticosteroids may also a ben used for skin and arthritic symptoms. rm e (azathioprine, etc) are used for patients Cytotoxic drugs K n with severe symptoms, along with corticosteroids. a r a should be advised to wear protective clothing, All patients T sunglasses, and sunscreen when in the sun. Taran Kermani MD. L.Ac fi fl 18 Prognosis c A. The prognosis of patients with SLE has improved L signi cantly in recent years with a 10 year ,survival rate D >85%. M i n a of the CNS, kidney, heart, People with severe involvement m and lungs have a worse r prognosis in terms of overall e survival and disability. K n a r nephritis is probably the most common cause Lupus a T overall of disability in patients with SLE. Taran Kermani MD. L.Ac 19 Raynaud Phenomenon c A Raynaud phenomenon is de ned as episodesLof. pallor or cyanosis in response to cold or emotional,stimuli. D M of blood vessels The pallor is caused by vasoconstriction i n in reduced blood ow. (arteries and arterioles) thata results rm the blood ow will rebound After rewarming theehands, (hyperemia) and K the skin will appear reddened or blushed. n a for patients with Raynaud phenomenon to It is common r a complain of cold sensitivity and to have other areas of the T skin involved, including the ears, nose, and lower extremities. Taran Kermani MD. L.Ac fl fi fi 20 Taran Kermani MD. L.Ac 21 , D M i an c A L. rm e K The initial phase of RP, mediated by excessive n a r consists of well-demarcated digital vasoconstriction, a pallorTor cy nosis the subsequent (recovery) phase of RP, caused by vasodilation, leads to intense hyperemia and rubor. Taran Kermani MD. L.Ac 22 a­ Raynaud Phenomenon c A.often L Episodes come as sudden attacks and are most , triggered by rapid changes in ambient temperature. D Mbut typically involve Attacks may begin in one or twoningers all ngers and/or toes symmetrically and bilaterally. a rm (Raynaud disease) denotes Primary Raynaud phenomenon e K a patient without an associated underlying disease. n a r Raynaud phenomenon is used to describe Secondary a Twith a de ned secondary or associated disease patients (e.g., scleroderma, SLE). Taran Kermani MD. L.Ac 23 One test that allows the di erentiation between primary and secondary Raynaud is the nail-fold capillaroscopy test c A L. Done by placing a drop of oil on the patient’s nail-fold at the base of the ngernail. , D Examination of this area under a microscope is then M conducted to look for any capillary changes. i n a rm e K n a r Ta Normal Raynaud’s Scleroderma Taran Kermani MD. L.Ac fi ff fi fi fi 24 (A) Raynaud phenomenon a ecting the patient’s ngers (pallor phase). (B) Nail-fold capillaroscopy showing dilated capillary loops. (C) Normal appearance of the patient’s tongue. (D) Blanched white tongue during an episode of lingual Raynaud phenomenon. Taran Kermani MD. L.Ac 25 About 5% of the general population has symptoms and signs consistent with Raynaud phenomenon. It is more common among young women, about 30% have a rst-degree relative with Raynaud, and most have primary Raynaud phenomenon without any de ned cause or associated systemic disease. c A L. , D M Treatment i n a or mittens whenever outside in Patients should wear gloves temperatures that precipitate rm attacks. Keeping the body e warm is also a cornerstone of initial therapy. K n surgical therapy should be considered in Medicalaorra patients who have severe symptoms or are experiencing T tissue injury from digital ischemia. Calcium channel blockers are rst-line of therapy for RP. Taran Kermani MD. L.Ac fi fi ff fi 26 Scleroderma (Systemic sclerosis) c A L. Systemic sclerosis (SSc) is a chronic multi-system disease characterized clinically , D by accumulation of by thickening of the skin causedM connective tissue, and i n by involvement of visceralaorgans (GI, lungs, kidneys). m r Symptoms usually appear in the 3rd to 5th decades, and e K women are a ected 2-3 times as frequently as men. n a r Two forms a of scleroderma are generally recognized: T Limited (80% of patients, CREST) Di use (20%) Taran Kermani MD. L.Ac 27 Clinical Findings CREST syndrome, a variant of scleroderma, is now called limited scleroderma. c A. The acronym CREST represents the hallmarks,ofLthe disease: Calcinosis, Raynaud, EsophagealD dysfunction, Sclerodactyly, and Telangiectasia. M i n a rm Calcinosis is a condition e in which calcium deposits K n occur in soft tissues usually a r in the ngers (especially a T PIP joints), knees, and elbows. These deposits occur near the skin surface and may ulcerate and become infected. Taran Kermani MD. L.Ac ff fi ff 28 Sclerodactyly refers to skin thickening, primarily a ecting the ngers and toes. , D M i Telangiectasia widened venules n a cause threadlike red linesm or r patterns on the skin. e K n Raynaud phenomenon a All patients have r Tathickening. and skin c A L. → The Raynaud phenomenon occurs because of vascular damage and diminished blood ow to the extremities. Taran Kermani MD. L.Ac 29 Clinical Findings (Di use) GI features include c A L. Esophageal → dysmotility (also in limited) The scleroderma renal crisis in which malignant hypertension develops and causes acute renal failure. Small intestine → hypomotility , D M i n a Pulmonary features include rmrestrictive lung disease. Pulmonary brosisewith K is now the leading cause of Pulmonaryninvolvement a death in SSc. r a Tfeatures include Renal Large intestine → bacterial overgrowth, malabsorption, and dilatation, with formation of large diverticula. Taran Kermani MD. L.Ac fl ff ff 30 fi fi Clinical Findings Clinical Findings Patients with limited scleroderma generally have skin involvement that does not extend above the elbow or above the knee. Rarely in some patients, the face may be a ected. , D M i an Limited disease generally progresses slowly compared to the di use form of scleroderma, which is more likely to a ect internal organs. c A L. rm e SSc. K There is no cure for n skin d-penicillamine may be used. For the a ramanifestations, T Raynaud phenomenon, calcium-channel For severe Treatment blockers, speci cally nifedipine For hypertension, ACE inhibitors are the drugs of choice Taran Kermani MD. L.Ac 31 Sjögren Syndrome c A L. Sjögren syndrome is a systemic autoimmune disorder, clinical presentation is usually dominated by dryness of the eyes and mouth due to immune-mediated dy function of the lacrimal and salivary glands. , D M i seen in women, with a ratio n The disorder is predominantly a of 9:1 m r e between the ages of 40 and 60 years. Most cases develop K n can occur in isolation ("primary" Sjögren a Sjögren syndrome r a or in association with another rheumatic disease. sy drome) T It is most frequently associated with rhe matoid arthritis but also occurs with SLE, scleroderma, Hashimoto th roiditis, and etc. Taran Kermani MD. L.Ac u­ ff fi ff n­ 32 Clinical Findings Keratoconjunctivitis sicca (dryness of the eyes) c A. of the L caused by lymphocyte and plasma cell in ltration , lacrimal glands. D M Burning, itching, and Ocular symptoms are usually mild. i n body or a grain of sand the sensation of having a foreign a in the eye occur commonly. rm e K the For some patients, n initial manifestation is the a r inability a to tolerate wearing T contact lenses. inadequate tear pr duction Taran Kermani MD. L.Ac 33 Clinical Findings For most patients, symptoms of dryness of the mouth (xerostomia) dominate those of dry eyes. c A L.have A few patients have such severe xerostomia that, they di culty speaking. D Persi tent xerostomia results ofteni M n in rampant dental caries. a m by Some patients are mostrtroubled e loss of taste and smell. K n which Parotid enlargement, a r may be a chronic or relapsing, T develops in 1/3 of patients. Patients frequently complain of a "cotton mouth" sensation and di culty swallowing foods, esp cially dry food. Taran Kermani MD. L.Ac fi e­ o­ s­ ffi ffi 34 Clinical Findings Systemic manifestations include c A L. Dysphagia , D Pleuritis M i Obstructive airways disease and interstitial lung n a disease (in the absence of smoking) m r e Peripheral neuropathies K n Pancreatitis a r Ta against SS-A and SS-B (also called Ro and La, Antibodies Small vessel vasculitis respectively) are often present in primary Sjögren syndrome. Taran Kermani MD. L.Ac 35 Treatment Treatment of sicca symptoms is symptomatic and suppor ive. Severe systemic in ammatory manifestations are treated with prednisone or various immunosuppressive medications. Arti cial tears applied frequently will relieve ocular symptoms. c A L. The mouth should be kept well lubr cated. Sipping water frequently or using sugar-free gums and hard candies usually relieves dry mouth symptoms. , D M decrease salivary secretions i Atropinic drugs and decongestants n and should be avoided. a rmmay compromise patient’s quality Although Sjögren syndrome e of life signi cantly,K the disease is usually consistent with a n normal life span. a r a are in uenced mainly by the presence of T Poor prognoses systemic features associated with underlying disorders. Taran Kermani MD. L.Ac i­ fl fl fi fi 36 Taran Kermani MD. L.Ac 37 Fibromyalgia Taran Kermani MD. L.Ac 38 Fibromyalgia c A L. Fibromyalgia is a common syndrome, a ecting 3-10% of the general population. , D A disorder characterized by M i Chronic widespread musculoskeletal pain, aching, sti ness, n paresthesia a m Disturbed sleep er along with multiple tender points Easy fatigabilityK n isaunknown, more common in women than in men. r The cause a T Diagnosis is made clinically, evaluation reveals soft tissue tender points but no objective joint abnormalities by exam, laboratory, or radiograph. Taran Kermani MD. L.Ac 39 Clinical Findings The patient complains of chronic aching pain and sti ness, frequently involving the entire body but with prominence of pain around the neck, shoulders, low back, and hips. Fatigue, sleep disorders, , D M i an c A L. rm e K chronic headaches, n a r and Tairritable bowel symptoms are common. subjective numbness, Even minor exertion aggravates pain and increases fatigue. Taran Kermani MD. L.Ac ff ff 40 Clinical Findings Physical examination is normal except for "trigger points" of pain produced by palpation of various areas such as the trapezius, the medial fat pad of the knee, and the lateral epicondyle of the elbow. rm e K n a r Ta , D M i an c A L. Taran Kermani MD. L.Ac 41 Treatment Patient education is essential. Patients can be comforted that they have a diagnosable syndrome treatable by speci c though imperfect therapies and that the course is not progressive. Cognitive behavioral therapy, including programs that emphasize mindfulness meditation, is often helpful. c A L. , D antidepressants. Less There is modest e cacy in using tricyclic than 50% of the patients experienceia M sustained improvement. ancial. bene Exercise programs are alsom re tive. e NSAIDs are generally ine K Tramadol and acetaminophen combinations have ameliorated n a symptoms modestly r in short-term trials. a T Op oids and corticosteroids are ine ective and should not be used to treat bromyalgia. ➡ Acupuncture is also ine ective (Current medical diagnosis and treatment). 😡 Taran Kermani MD. L.Ac ff fi c­ ff ff ffi fi i­ 42 Chronic fatigue syndrome c Myalgic encephalomyelitis/chronic fatigue syndrome (ME/ A. CFS) is a disabling and complex illness. , L D able to do their usual People with ME/CFS are often not M activities, may become con nedito bed, have n overwhelming fatigue that isanot improved by rest. m r e worse after any activity, whether it’s ME/CFS may getK physical or mental. Known as post-exertional malaise n (PEM) ra a T Other symptoms can include problems with sleep, thinking and concentrating, pain, and dizziness. People with ME/CFS may not look ill Taran Kermani MD. L.Ac 43 Anyone can get ME/CFS: Most common in people between 40 and 60 years old c A L. A ects children, adolescents, and adults of all ages , D Mthan other races White persons are diagnosed imore n and ethnicities a mME/CFS have not been rwith About 90% of people e diagnosed. Some Kof the reasons: n schools in the US do not have ME/CFS a Most medical r a of their physician training as part T The illness is often misunderstood and might not be Women are a ected more often than men taken seriously by some healthcare providers. Taran Kermani MD. L.Ac fi ff ff 44 The causes ME/CFS is not yet found, and there are no speci c laboratory tests to diagnose ME/CFS directly. The diagnosis of ME/CFS is based on in-depth evaluation of a person’s symptoms and medical history. rm e K n a r Ta , D M i an c A L. https://www.cdc.gov/me-cfs/pdfs/interagency/What-are-MECFS-Symptoms_508.pdf 45 Fatigue vs CFS c A L. Fatigue, as an isolated symptom, accounts for 1–3% of visits to generalists. , D The symptom of fatigue is often poorly described and less M associated with well de ned by patients than symptoms i n speci c dysfunction of organasystems. the closely related complaints of rm Fatigue or lassitude and e weakness, tiredness, and lethargy are often attributed to K n overexertion, poor physical conditioning, sleep disturbance, ra obesity,aundernutrition, and emotional problems. T A history of the patient’s daily living and working habits may obviate the need for extensive and unproductive diagnostic studies. Taran Kermani MD. L.Ac fi fi fi 46 The diagnosis of CFS remains hotly debated because of the lack of a gold standard. Persons with CFS report a greater frequency of childhood trauma and psychopathology and demonstrate higher levels of emotional instability and selfreported stress. rm e been Sleep disorders haveK n reported in 40–80% of a r patients with Ta CFS. A study found that atopy is associated with chronic fatigue syndrome. Taran Kermani MD. L.Ac 47 Clinical nding of Fatigue Clinically relevant fatigue is composed of 3 major components: c A L. , D Easy fatigability (di culty in completing M activities) i nconcentration and Mental fatigue (di culty with a memory) rm e Kthat can cause fatigue include: Important diseases n a and hypothyroidism, Heart failure, hyperthyroidism r a infections, COPD, sleep apnea, anemia, autoimmune T disorders, MS, IBS, Parkinson disease, CVA, and Generalized weakness (di culty in initiating activities) cancer. Taran Kermani MD. L.Ac ffi ffi ffi 48 fi , D M i an c A L. Alcohol use disorder, side e ects from medications, and psychological conditions (insomnia, depression, anxiety, etc) may be the cause. c A L. , D M i with other These conditions are usuallyaassociated n characteristic signs, but patients may emphasize fatigue rmsymptoms unless directly and not reveal their e other K asked. n a r The lifetime prevalence of signi cant fatigue (present for a T 2 weeks) is about 25%. at least Common outpatient infectious causes include mononucleosis and sinusitis. Although frequently associated with Lyme disease, severe fatigue as a long-term sequela is rare. Taran Kermani MD. L.Ac 49 Clinical nding of Chronic Fatigue syndrome (CFS) There is no single pathogenic mechanism and no physical nding or laboratory test can be used to con rm the diagnosis. c A. L The evaluation of chronic fatigue syndrome includes , D A thorough history and physical examination M i CBC, ESR n serum electrolytes, a creatinine, Blood chemistries: BUN, rm glucose, calcium e K tests Liver function n a function tests r Thyroid a T Urinalysis Tuberculin skin test (PPD) Screening questionnaires for psychiatric disorders Taran Kermani MD. L.Ac fi fi ff fi 50 fi fi Clinical nding of Fatigue Other tests to be performed as clinically indicated: Serum cortisol ANA RF Immunoglobulin levels , D M i an rm e K HIV antibody n a r a testing is usually More extensive T unhelpful. Lyme serology in endemic areas 51 52 c A L. Treatment of Fatigue Management of fatigue involves identi cation and treatment of conditions that contribute to fatigue, such as cancer, pain, depression, disordered sleep, weight loss, and anemia. c A L. , D M Resistance training and aerobic iexercise ninconsistent results in a Psycho-stimulants have shown randomized trials of treatment rm of cancer-related fatigue. e K to raise levels from moderately low therapy Testosteronen to mid-normal in men 65 years or older had no bene t for a r vitality a Tor walking distance. Vitamin D treatment signi cantly improved fatigue in otherwise healthy persons with vitamin D de ciency. Taran Kermani MD. L.Ac 53 Treatment of CFS A variety of agents and modalities have been tried for the treatment of chronic fatigue syndrome. c A L. Acyclovir, IVIG, nystatin, clonidine, etc do not improve symptoms. , D M i At present, cognitive-behavioral therapy and graded exercise are n a with chronic fatigue the treatments of choice for patients m syndrome. r e K therapy, a form of non-pharmacologic Cognitive-behavioral n treatment emphasizing self-help and aiming to change a r perceptions and behaviors that may perpetuate symptoms and a T disability, is helpful. There is very limited evidence that dietary modi cation is bene cial. Chronic fatigue syndrome is not associated with increased allcause mortality, but one study showed a substantial increased risk of completed suicide. Taran Kermani MD. L.Ac fi fi fi 54 Polymyalgia Rheumatica Giant cell arteritisAc. L , D M Both a ect the same population (patients i over the age of 50) n aincreases with each decade of life. the incidence of the disease m r e for the same HLA haplotypes, and show Both show preference K similar patterns of cytokines in blood and arteries. n a r (also called temporal arteritis) is a systemic a arteritis Giant cell T panarteritis a ecting medium-sized and large vessels. Probably represent a spectrum of one disease: Polymyalgia rheumatica and giant cell arteritis also frequently coexist. Taran Kermani MD. L.Ac 55 Polymyalgia Rheumatica c A L. Polymyalgia rheumatica is a clinical diagnosis based on pain and sti ness of the shoulder and pelvic girdle areas, frequently in association with fever, malaise, and weight loss. , D occurs in the In approximately 2/3 of cases, polymyalgia M absence of giant cell arteritis. i n a in the shoulders, hips, and pain Because of the sti ness and m r trouble combing their hair, putting lower back, patients have e on a coat, or risingK from a chair. n rheumatica does not cause muscular weakness a Polymyalgia r a primary muscle in ammation or secondary to either through T nerve infarction. A few patients have joint swelling, particularly of the knees, wrists, and sternoclavicular joints. Taran Kermani MD. L.Ac fl ff ff ff ff 56 57 Giant cell arteritis c A L. The mean age at onset is approximately 79 years. , D M i n is unknown, While the cause of giant cellaarteritis varicella-zoster antigen m is found in nearly 75% of the r temporal arteries of e a ected patients (compared to 22% K of controls). n a r symptoms are headache, scalp tenderness, The classic a Tsymptoms (particularly *amaurosis fugax or visual About 50% of patients with giant cell arteritis also have polymyalgia rheumatica. diplopia), jaw claudication (highest positive predictive value), or throat pain. *transient loss of vision in one or both eyes ff 58 Taran Kermani MD. L.Ac The temporal artery is usually normal on physical examination but may be nodular, enlarged, tender, or pulseless. rm e K n a r Ta , D M i an c A L. Taran Kermani MD. L.Ac 59 60 Lab ndings in Polymyalgia Rheumatica c A L. Anemia and elevated acute phase reactants (markedly elevated ESR) are present in the most cases , D M i n Lab ndings in Giant cell arteritis a m have high ESRs and CRPs rarteritis Patients with giant cell e K Most patients also have a mild normochromic, normocytic n a r thrombocytosis. anemiaaand T The alkaline phosphatase (liver source) is elevated in 20% but cases of polymyalgia rheumatica occurring with normal acute phase reactants are well documented. of patients with giant cell arteritis. Taran Kermani MD. L.Ac 61 Treatment of Polymyalgia Rheumatica Patients with isolated polymyalgia rheumatica (ie, those not having “above the neck” symptoms) are treated with prednisone, 10–20 mg/day orally. If the patient does not experience a dramatic improvement within 72 hours, the diagnosis should be revisited. , D M i an c A L. rm e K diagnosis and treatment in giant cell The urgency of early n arteritis relates to the prevention of blindness. Once a r blindness a develops, it is usually permanent. T Therapy with high dose of prednisone should be initiated Treatment of Giant cell arteritis immediately and a temporal artery biopsy performed promptly thereafter. Taran Kermani MD. L.Ac fi fi 62