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157 Cards in this Set
- Front
- Back
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Fibromyalgia is classified as what type of disorder and why?
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Affective disorder because there are psychological changes that accompany it
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Clinical features of fibromyalgia
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Wide spread pain esp. in the neck, trapezius, lower back and upper buttocks; chronic fatigue, stress, stiffness, and associated symptoms
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Most affected group for fibromylgia
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Women
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What is the pathophysiology of fibromyalgia
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Unknown but increasingly is pointing towards CNS mechanism
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What are the precipitating events of fibromyalgia?
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Usually after an infectious illness, or trauma
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What NT is associated with fibromyalgia?
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Increased levels of Substance P; however there is a poor correlation between Substance P and the degree of tenderness on physical exam
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Describe Substance P
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It is a NT specific for pain transmission in the doral horn of the spinal cord
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What is the situation with blood flow associated with Fibromyalgia?
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A decreased blood flow to the thalamus and caudate nucleus
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What is the function of the thalamus
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It is a relay station for all sensory input excluding olfactory
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What is the problem with sleeping for fibromyalgia patients?
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Stage 3-4 sleep is routinely interuppted by intrusions of alpha waves; alpha wave intrusion; however, studies have shown questionable differences
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How do you diagnosis fibromyalgia?
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only after you have ruled out everything else; also will see that 11 out of 18 trigger points are active
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What is the treatment for fibromyalgia?
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SSRI's, Muscle relaxant, tricyclic antidepressant, or combo of both
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What is not a good treatment for fibromyalgia and why?
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Steriods or NSAIDS; because it is not an inflammation and is a CNS mechanism
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What type of disease is Sarcoidosis?
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It is a granulomatous disease
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What is a granuloma?
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It is a localized,nodular, chronic inflammation
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What is the first step of Sarcoidosis?
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Macros arrive and are mad
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Second step of Sarcoidosis?
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Macros morph into squamous epitheloid cells that pack center of granuloma
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Third stage of Sarcoidosis?
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Lymphos arrive and squirt chemical junk onto macros which pisses of the macros even more so they bind together and form multinucleated giant cells
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Fourth stage of Sarcoidosis?
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Lymphos remain as collar but their squirting habits attract monocytes, more macros and fibroblasts
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Last stage of Sarcoidosis?
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The fibroblasts close the door and wall everything off.
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Where are the granulomas distributed in Sarcoidosis?
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The non-caseating granulomas are distributed in the lungs, lymph nodes, and liver
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Two immune features of Sarcoidosis?
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Depressed cellular immunity and heightened humoral immunity
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Clinical features of skin with Sarcoidosis
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Erythema nodosum (good prognosis) and lupus pernio (poor prognosis)
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Clinical features of the lungs with Sarcoidosis
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dyspnea, hemoptysis, bilateral hilar and mediastinal lymphadenopathy
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What is the incidental finding in a chest xray for Sarcoidosis?
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bilateral hilar and mediastinal lymphadenopathy
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Diagnosis for Sarcoidosis
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Transbronchial lung biopsy
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Helpful labs for diagnosis for Sarcoidosis
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ACE levels, hypercalcemia, and hypercaluria, Kveim Slitzbach test
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What is the Kveim Siltzbach test?
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Like a TB PPD. It is a suspension of spleen extract that is intradermally injected and will show a granulomatous reaction
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Treatment for Sarcoidosis (for asymptomatic hilar adenopathy, for arthritis, and for hypercalcemia)
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No tx for asymptomatic hilar adenopathy
Colchicine for arthritis Steroids for hypercalcemia |
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What should anyone on long term steroids do?
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Receive bisphosphonate and or Miacalcin
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If you need to stop or decrease steroids for Sarcoidosis what should you take?
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DMARD: Rheumatrex
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Sjogren's syndrome is what kind of disease?
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Immune mediated inflammatory disorder of exocrine glands
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Major symptoms and signs of Sjogren's syndrome?
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xerostomia, xerophthamia (anything dryness think Sjogren's syndrome)and mild joint pain
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What is primary Sjogren's syndome or sicca syndrome?
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It is when mucous membrane dryness and it's related effects occur in isolation.
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What is secondary Sjogren's syndrome?
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When it occurs with rheumatoid arthritis, SLE, and systemic sclerosis
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What type of pathology is there with Sjogren's syndrome?
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Emigration of CD4-T-lymphocytes that are in direct contact with ductal epithelial cells
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What are the Abs specific for Sjogren's syndrome?
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Anti SS-A Ab (anti-Rs Ab)
Anti SS-B Ab (anti-La Ab) |
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Diagnosis of Sjogren's syndrome?
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Dry anything with mild joint pain and Schirmers Test, rose Bengal test, Whole Saliva Sialometry
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What is a Schirmers Test?
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Office measure of the amount of tears secreted in five minutes
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What is the Rose Bengal test?
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Corneal abrasion is the palpebral fissure
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What is the Whole Saliva Sialometry?
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patient sucks on a peice of hard candy for three minutes and expectorates. If saliva content is decreasted then biopsy should be done
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What type of disease is polymyositis/dermatomyositis
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It is an autoimmune disease with idiopathic inflammatory myopathy
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Four main categories of clinical features for polymyositis/dermatomyositis?
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Muscle weakness, muscle enzymes, electromyography of myopathy, muscle inflammation
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Course of onset of polymyositis
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3-6 months without idenfiable event
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Proximal muscle weakness associated with polymyositis?
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Stairs and chairs, lifting head off pillows (neck, limbs, and trunk), dysphonia
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Serum muscle enzymes evidence of polymyositis?
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Increased serum CPK-MM, Aldolase, ALT, AST, LDH
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Chemical assays for polymyositis?
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Increased sed rate, urine dip is positive for hemoglobin due to muscle breakdown (rhabdomyolysis)
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Immunopathology of polymyositis?
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T-cells and macros surround non-necrotic muscle fibers and ANTI-JO-1 ABS
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What is the fifth clinical feature of polymyositis?
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Dermatomyositis
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Dermatomyositis takes the form of: (six things)
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Gottron's sign, Heliotrope rash, Shawl sign, V sign, Periungual telanectasias
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What is Gottron's sign?
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It is gottron's papules in the joints
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What is Shawl sign?
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Macules over shoulders, arms and upper back
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What is periungual telanectasias?
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Dilated vessels of the skin surround the fingernails
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Treatment of polymyositis and dermatomyositis
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CPK-MM monitoring, DMARDS (methotrexate or azathioprine)
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What is polymyalgia rheumatica?
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It is not an autoimmune disease by a myalgia disease affecting proximal muscle groups (neck, limbs, trunk)
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What type of population does polymyalgia rheumatica affect mostly?
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White females over the age of 50
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Clinical features of polymyalgia rheumatica
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Slow onset without an identifiable precipitating event; difficulty climbing stairs and getting out of bed and chairs
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What else do some people with polymyalgia rheumatica also develop?
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Temporal arthritis
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Lab diagnosis of polymyalgia rheumatica?
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ESR of 50-100 mm/hr
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Clinical diagnosis of polymyalgia rheumatica?
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Muscle pain, stiffness, response to steroids
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What is temporal arthritis?
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headache, increased sed rate, permanent blindness
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What is treatment for polymyalgia rheumatica?
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Steroids (low dose for polymyalgia rheumatica and high dose for temporal arthritis)
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What kind of disease of osteoporosis?
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It is a demineralizing bone disease.
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Common injuries associated with osteoporosis?
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Fx of the vertebrae, pelvis, femur, femoral neck, distal radius
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What causes fractures in osteoporosis?
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Decreased bone mass
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What are pathological fractures?
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Fractures that can otherwise withstand compressional and shear stresses
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Signs and symptoms of osteoporosis?
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Osteopenia, pathological fractures, crush fractures of lumbar vertebrae, severe back ache due to bone fragments on spinal cord and or dorsal roots, radiculopathy
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What is primary osteoporosis?
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Mainly postmenopausal OP or Senile OP
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What is secondary osteoporosis?
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Endocrine, neoplasia, gastrointestinal, drugs, miscellaneous
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Bone loss in osteoporosis is most dramatic in where?
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Areas with abundent trabeculae
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What are the age related factors of osteoporosis?
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Less osteoblastic activity
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Hormonal factors of osteoporosis?
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Low estrogen and a little bit of testosterone deficiency
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Complications of osteoporosis?
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Back pain, radiculopathy, immoilization, pneumonia, DVT/pulmonary embolism
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Lab findings of osteoporosis?
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DEXA scan
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Treatment for osteoporosis?
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Selective estrogen receptor modulator (SERM), Bisphosphonates (Fosamax), Miacalcin
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SERM does not cause:
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Breast soreness or cancer, endometrial hyperplasia, uterine bleeding or cancer
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SERM does not reduce:
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hot flashes, vaginal dryness, risk of thromboembolism
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Best way to prevent OP in postmenopausal women?
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HRT
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What is the general progression of Paget's disease?
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Intense osteoclastic activity and hypervascularity with resultant bone resorption followed by intense abnormal osteoblastic activity and resulting in abnormal bone formation.
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Signs and symptoms of Paget's disease?
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Boen pain, bone hypervascularitiy, warmth of overlying skin, enlarged soft bones
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What is the primary osteolytic phase of Paget's disease??
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Highly vascular CT replaces marrow and osteoclasts resorb bone
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What is the mixed phase of Paget's disease?
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Bone absorption and new bone formation together
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What is the osteosclerotic phase of Paget's disease??
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New bone formation and thickening of bone but lacks lamellar structure and causes a mosaic pattern
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Most likely effect in the body of Paget's disease?
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Chalkstick fracture
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Laboratory findings of Paget's disease?
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Alkaline phosphatase elvated, urine calcium elevated, and urine hydroxyproline elevated
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X-ray findings of Paget's disease?
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Bones are thicker, more radiopaque with multiple fissure fractures
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Complications of bone hypervascularitiy in Paget's disease?
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Increased CO, with high output of CHF, ischemic neurologic events from subclavian steal phenomena
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Complications in vertebrae from Paget's disease?
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Vertebral crush fx and back pain and radiculopathy
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Complications in cranial nerve foramina in Paget's disease?
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Narrow foramina which causes entrapment of CN and causes cranial neuropathy
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Treatment for Paget's disease?
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Bisphosphonate (fosamax)
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What dominates scleroderma?
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Fibrotic and degenerative skin changes
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What does systemic scleroderma entail?
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systemic fibrosis and systemic vascular injury
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What is the manifestations of limited scleroderma?
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CREST (calcinosis, Raynauds phenomenon, esophageal dysmotility, sclerodactyly, telangectasias
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Describe the calcinosis in limited scleroderma?
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tissues develop calcifications in fingertips
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What is Raynauds phenomenon?
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Color changes in acral areas that go from white to blue to very red
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What is the esophageal dysmotility in limited scleroderma?
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Dysphagia, Lower esophageal sphincter dysfunction, Gerds, barretts esophagus
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What is barretts esophagus?
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Pre cancerous lesion
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Describe sclerodactyly in limited scleroderma
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First manifestation is diffuse edema of fingers and hands which turn into claw like and then the face is affected into a tight mask
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Describe telangectasias in limited scleroderma?
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Permanently dilated blood vessls of the cheek and nose
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Describe the T-cell activation in limited scleroderma?
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T-Cells activate B-cell activation (AUTO Abs), Fibroblasts (Fibrosis), Injured Endothelial cells (Ischemia), Inflammatory WBC (Inflammatory chemical junk)
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What are the specific antibodies unique to limited scleroderma?
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Anti-centromere Abs
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What are the specific antibodies unique to diffuse scleroderma?
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SCL-70 Abs
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Scleroderma also other Abs besides the two maines ones...
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generic anti-nuclear Abs and RF
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What is the clinical effects on the skin in diffuse scleroderma?
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Skin changes in arms, legs, trunks, S&P appearance, Loses sweat glands and hair follicles, finger mobility impaired,mouth becomes tight and eating and oral hygeine is difficult
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Effect on fingers in diffuse scleroderma?
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ISchemia of fingers causes skin ulcers which leads to necrosis and finger loss
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Effect on GI tract in diffuse scleroderma?
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Small bowel is effected and hypomotility occurs and colon develops saccular diverticuli
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Effect on heart in diffuse scleroderma?
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Pericardial effusion, coronary vasospasm, systemic hypertension, pulmonary hypertension
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Effect on lungs in diffuse scleroderma?
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Pulmonary fibrosis, restrictive lung disease and right ventricular failure, decreased alveolar oxygen uptake
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Effect on kidneys in diffuse scleroderma?
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Decreased GFR which leads to azotemia, increased renin secretion and malignant hypertension
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Effects on musculoskeltal system in diffuse scleroderma?
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Joint pain and stiffness, frction rubs/crepitus, flexion contractures
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What is acute inflammation?
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When neutrophils infiltrate the tissue
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What is chronic inflammatin
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lymphocytes and macrophages enter the tissue
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How is the tissue repaired in chronic inflammation?
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By fibrosis and neovascularization
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Three main components of acute inflammation
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Local hyperemia, vascular permeability, leukocyte emigration
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What causes hyperemia in acute inflammation?
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vasodilation
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What causes the site to be red and warm in acute inflammation?
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The vasodilation
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Vasodilation causes
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increase in flow volume and decrease in flow velocity
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What causes the site to be swollen and painful in acute inflammation
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Vascular permeability
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What contributes to endothelilal cell leakiness?
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Release of histamine by the mast cells
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What is released following damage to tissues?
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Histamine, bradyknin, leukotrines, Il-1, TNF
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How do the neutrophils enter tissues?
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Because laminar flow decreases there is increased contact of neutorphils with endothelial cells and they can diapedesis into tissue
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What does leukocytes activate?
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Arachidonic acid, prostaglandins and leukotrienes
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Where is histamine found?
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Mast cells
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What does histamine cause?
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Arteriolar dilation, venular leakage and edema
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What are eicosanoids?
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prostaglandins and leukotrienes
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How are the eicosanoids produced?
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The membrane phospholipids are broken down by phospholipases and arachdonic acid is produced. arachodonic acid is processed in two pathways: cycloxygenase which makes prosta and lipoxygenase which makes leuko
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Leukotrienes are several thousand times more potent then histamine doing
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vascular permeability and bronchospasm
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How do NSAIDs work?
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They block the cycloxygenase pathway and some of the block phospholipase-inducted production of AA
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What induces the systemic inflammatory effects or acute phase reactions
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IL-1, IL-6 and TNF
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Two important acute phase reactants
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Fibrinogen and C-reactive protein
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How does inflammation effect ESR?
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The fibrinogen proteins are increased so that the sed rate is increased significantly.
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How is the C-reactive protein used diagnostically?
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It increases rapidly in viral meningitis and even higher in bacterial meningitis
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Role of nitric oxide in inflammation?
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It vasodilates and has a role in the hypotensive effects of septic shock
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When do abscess formation occurs in acute inflammation?
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When there is pyogenic bacteria such as Staph, Strep, Pneomococi, meningococci, and h. influenza
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Describe the lysosomal enzyme Elastase in the acute inflammation
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It is counteracte by Alpha1-antitrypsin. Elastase causes emphysema
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What causes emphysema in ppl who do not smoke?
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Homozygotic alpha1-antitrypsin deficiency
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How is chronic inflammation resolved?
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Fibrosis and neovascularization
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what are the chronic inflammatory cells?
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Monocytes,T and B lymphocytes, plasma cells (terminally differentiated B cells) and eosinophils
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Where are eosinophils found in chronic inflammation?
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Parasites or IgE mediated reactions such as allergies and asthma
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What is granulomatous inflammation?
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When activated macros form a epitheloid aggregation and surrounded by fibroblasts
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Function of the lymphatic system?
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To take up the net fluid loss from the tissues and dump it back into the venous system
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Where does the lymphatic system dump contents from L side of body?
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by the thoracic duct at L internal jugular vein and L subclavian vein
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Where does lymph. system dump contents from R side of body?
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R lymph duct at right internal jugular vein and right subclavian vein
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What is serous inflammation?
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Outpouring of watery stuff such as with a skin flister
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What is fibrinous inflammation?
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Fibrinogen leaks out and results in fibrin meshwork of find threads
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What is suppurative inflammation
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Pus forms abscesses which is caused by pyogenic organisms
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What is a type 1 hypersensitivity reaction?
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Develop within minutes of exposure to allergin and histamine is released from mast cells; IgE mediated reactions or allergy and anaphylaxis
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What is a Type 4-delayed hypersensitivity reaction?
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T-lymphocytes and macrophages come to area of infection and it takes week
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Reiters syndrome is also called
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reactive arthritis
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Reactive arthritis occurs when?
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After genitourinary, gastrointestinal and poss. respiratory infection
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Reactive arthritis is considered
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seronegative spondyloarthropathies
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What bacteria causes gastroenteritis infection of Reiters syndrome
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Salmonella, Shigella, Yersinia, Campylobacter
C. diff |
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Venereal causes of Reisters syndrome
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Chlamydia trachomatis
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what is usually the trigger for Reiters syndrome
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Chlamydia and nongonococcal urethritis
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What are the manifestations of Reisters syndrome
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Sausage digits, asymmetric oligoarthritis, enthesopathy (achilles tendon pain, circinate balanitis, kertodermal blennorrhagica (rash)
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What are the laboratory findings for Reiters syndeome
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Increased sed rate and CRP and abnormal synovial fluid
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Treatment for Reiters
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NSAIDS, DMARDS, and steriods
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