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157 Cards in this Set

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