Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
169 Cards in this Set
- Front
- Back
Pathology of Osteoarthritis
1. gross level 2. microscopic level 3. biochemically |
1. - first, cartilage irregularities and splitting
- next, ulceration and loss of cartilage - next, bone on bone contact then eburnation (polished bone) 2. - fibrillation of cartilage 3. - decreased glycosaminoglycan content of cartilage, including less chondroitin sulfate, less keratin sulfate and less hyaluronic acid - increased MMP activity, which plays role in degradation of extracellular matrix of cartilage |
|
Pathogenesis: OA is primarIly a disease of ________ of joints.
|
hyaline cartilage
|
|
Pathogenesis: the initiating event in OA is ______ which results in _______.
|
mechanical stress, which results in change in chondrocyte metabolism - proteolytic enzyme production (MMPS)- disruption of cartilage matrix
|
|
In OA, mechanical stress means...
|
any compressional stress which too forcefully jams the 2 articulating surfaces of hyaline cartilage together.
|
|
As OA progresses, crystals of _______ are shed into the joint fluid and are commonly found in severe OA.
|
calcium phosphate
|
|
Clinical features of OA
|
-pain and stiffness of joint, worse with use, better with rest, or vv.
-morning stiffness <30 min -gelling -osteophytes impinging on dorsal roots &/or spinal cord - radicular sx in limbs:pain, numb, weak |
|
In OA, pain may be due to:
|
-inflammation of the periosteum (periostitis) at sites of bone remodeling
-subchondrial microfractures -irritation of synovial nerve endings by osteophytes -synovial inflammation from chemical junk |
|
On physicacal exam, OA presents:
|
-warmth and soft tissue swelling of joint is minimal
-tenderness and bony enlargement of joint -Crepitus from cartilage irregularities -possible locking due to a loose piece of cartilage -varus deformity of knee in 50% due to worse loss of cartilage |
|
In OA, classic enlargement occurs at which joints?
|
PIP joints (Bouchard's nodes) and DIP joints (Heberden's nodes)
|
|
Radiologic features of OA:
|
-asymmetric joint space narrowing due to cartilage loss
-subchondral bone sclerosis -subchondral bone cysts -osteophytes |
|
Labs of Osteoarthritis:
|
-Dx of OA is almost always by H&P and can be confirmed by XR
-WBC count in synovial fluid should be <200 cells per cubic mm |
|
Treatment of OA:
|
-exercise improves ROM & strength
-lose weight -therapeutic heat/massage -refer to OT or PT |
|
Treatment of OA:
|
-APAP, NSAIDS
-capsaicin cream (Zoxtrix) -oral chondroitin sulfate or glucosamine -intra-articular steroid injections -intra-articular injection of hyaluronic acid derivatives -arthroplasty (joint replacement) |
|
The most feared possibility when a patient presents with a joint which is red, hot, swollen, painful joints is:
|
Septic arthritis
|
|
Which form of arthritis is monoarticular?
|
Septic arthritis
|
|
Septic arthritis is caused by...
|
bacterial joint infection
|
|
Hydrolytic enzymes from neutrophils destroy joint fast by irreversible cartilage reabsorption possibly resulting in sepsis and death.
|
Septic arthritis
|
|
Bacterial access to joint occurs by...
|
-hematogenous spread (endocarditis, IV drug use)
-contiguous osteomyelitis -joint penetrating injury -prosthetic joint -joint injection |
|
SA in children is often linked to _____ because of _____.
|
osteomyelitis because of open epiphyses
|
|
SA in teens & adults is often linked to _______.
|
Neisseria gonorrheae infection
|
|
Labs of SA:
|
-of all causes of SA, blood culture is + in 50%
-synovial fluid constituents indicate decreased glucose, increased protein & lactate, WBC count >10,000/ul |
|
Treatment of SA:
|
-treat early with antibiotic
-Rocephin (ceftriaxone) or Nafcillin IV plus gentamicin IV |
|
Name 3 diseases that present with red, hot, swollen joints.
|
1. Septic arthritis
2. Gouty arthritis 3. Reiter's disease |
|
Clinical features of Lyme Disease
|
-rash in 50% of people
-if untreated, fatigue, fever, headache &/or arthralgias |
|
If Lyme Disease goes untreated, a minority develop the following complications:
|
-arthritis (knee)
-neorologic: headaches, meningeal signs (nuchal rigidity), cranial nerve dysfunction (facial nerve-bilateral Bell's Palsy) -Cardiac(AV block) |
|
ELISA detects replacement of IgM with IgG and is confirmed by Western Blot.
|
Lyme Disease
|
|
Treatment of Lyme Disease
|
-Prevention: tick repellants
-Antibiotics: rash/arthritis - po Vibramycin (doxycycline) or Amox (amoxicillin); carditis/meningitis - IV Rocephin (ceftriaxone) |
|
Arthritis which occurs after genitourinary, gastrointestinal and possibly respiratory infection.
|
Reiter's Syndrome aka Reactive Arthritis
|
|
Originally referred to as the clinical triad of arthritis, conjunctivitis, and nonconococcal urethritis.
|
Reiter's Syndrome aka Reactive Arthritis
|
|
Considered one of the seronegative spondyloarthropathies (SNSA)
|
Reiter's Syndrome aka Reactive Arthritis
|
|
SNSA
|
seronegative spondyloarthropathies
|
|
The SNSAs are:
|
-Reactive Arthritis
-Lyme Arthritis -Psoriatic Arthritis -Gouty Arthritis -Osteoarthritis -Septic Arthritis |
|
Seronegative denotes absence of _________.
|
rheumatoid factor
|
|
Nongonococcal urethritis with C.trachomatus is frequently the trigger for _________.
|
Reiter's Syndrome
|
|
Clinical features of Reiter's Syndrome
|
-typically begins 2-4 weeks post gastroenteritis or venereal infx.
-nongonococcal urethritis -conjunctivitis usually accompanies or follows urethritis -articular manifestations typically appear last -extraarticular manifestations |
|
-dactylitis or sausage digits
-asymmetric oligoarthritis of lower extremities -enthesopathy |
articular manifestations of Reiter's Syndrome aka Reactive arthritis
|
|
entheses
|
attachment sites of tendons to ligaments
|
|
-Circinate balanitis
-Keratodermal blennorrhagica |
Extra-articular manifestations of Reiter's Syndrome aka Reactive arthritis
|
|
Circinate balanitis
|
shallow ulcer of glans or shaft of penis
|
|
Kertodermal blennorrhagica
|
papulosquamous rash most often on palms or soles.
|
|
Immunohistochemical studies of synovium reveal antigenic material from infecting organisms but no viable organisms.
|
Reiter's Syndrome aka Reactive arthritis
|
|
-increased sed rate & C-reactive protein
-synovial fluid: turbid,WBC count >5000/ul,low viscosity |
Labs for Reiter's Syndrome aka Reactive arthritis
|
|
Consider Reactive arthritis when:
|
-asymmetric oligoarthritis esp. in young person
-extra-articular manifestations -h/o prior infections supports Dx |
|
Treatment of Reactive arthritis
|
-NSAIDs & exercise until arthritis remits
-rarely, systemic or intra-articular steroids -DMARDs if no response to NSAIDs |
|
DMARDs
|
Disease Modifying Anti-Rheumatic Drugs
|
|
-increased epidermal cell turnover leading to acanthosis (thickening)
-pink-to-salmon plaques covered with silver scales -nail changes (oil slick discoloration,pitting,thickening,oncholysis) -Auspitz sign -Koebner phenomenon |
The skin condition Psoriasis
|
|
Auspitz Sign
|
multiple small bleeding points on skin when scrape gently or lift scales due to dilated tortuous capillaries under plaque
|
|
Koebner Phenomenon
|
psoriatic lesion develops at the site of minor skin trauma, surgical suture lines, etc.
|
|
T/F: Psoriatic Arthritis is a seronegative spondyloarthropathy.
|
True.
|
|
T/F: Psoriatic Arthritis appears in psoriasis patients who have extensive skin leasions.
|
True.
|
|
___________ arthritis may really be another form of Reactive Arthritis, ie. reactive to Staph and Strep antigens in ____________.
|
Psoriatic Arthritis...psoriatic skin lesions.
|
|
-oligoarthritis most comm. spread through small joints (PIP,DIP, MCP), sausage digits
-Arthritis mutilans -Extra-articular involvement (psoriatic skin lesions, nail changes, sausage digits, enthesopathy) |
Psoriatic Arthritis
|
|
-pencil in cup deformity at phalanges
-acro-osteolysis=resorption of distal bone tuft of distal phalanx -joint space loss |
Radiologic features of Psoriatic arthritis
|
|
Treatment of Psoriasis (Skin Disease)
|
-topical steroids (kenalog cream)
-topical coal tar preps (Psorigel) -Vit. D derivatives (Dovonex) -Vit. A derivatives(Soriatane) -PUVA=pulsed UVA light -Rheumatrex (methotrexate) -Enbrel (etanercept) |
|
Treatment of Psoriatic Arthritis
|
-NSAIDs
-intra-articular steroid injections -Enbrel -DMARDs (Rheumatrex, Azulfidine) |
|
A metabolic disease; hyperuricemia in the blood, which has musculoskeletal consequences
|
Gouty Arthritis
|
|
Uric acid comes from the breakdown of _______, _______ & ________.
|
purines, adenosine & guanosine
|
|
Patients with Gout
|
-mostly men, peak in 40s
-hyperuricemia -at higher plasma concentrations of urate, monosodium urate crystals precipitate out of solution into cooler peripheral joints (ankles, toes) and tissues (ears & fingers) |
|
Clinical Presentation of Gout
|
-abrupt: usually one joint(MTP,ankle,knee). Pt often well at bedtime, awakes w/podagra. exquisitely painful.
-attack resolves in days to weeks despite crystals still in joint |
|
Factors which precipitate acute attack of Gout
|
-start of uric acid therapy (allpurinol)
-start of diuretic therapy -surgery/trauma, severe illness, stroke, acute myocardial infarction -alcohol binges |
|
Clinical Presentation of Gout
1. Intercritical Phase 2. Subsequent Attacks 3. If untreated |
1. all quiet, but most have recurrence w/in 2 years of 1st attack
2. often worse: high fever & chills suggesting septic joint;more likely to involve upper extremity joints &/or multiple joints 3. shorter intercritical phases & progressive joint destruction;urate crystals in soft tissue |
|
gouty tophi
|
urate crystals in soft tissue
(ear pinnae,olecranon bursa,fingers & toes, achilles tendon) |
|
Diagnosis of Gout
|
-Pt presents with abrupt onset mono or oligoarthritis of lower extremity
-Hyperuricemia >6-7mg/dl -aspiration of fluid shows needle-shaped, negatively bifringent, monosodium urate crystals |
|
Treatment for Acute Attack of Gouty Arthritis
|
-NSAIDS:Indocin(indomethacin),Advil(Ibuprofen),Anaprox(naproxen)
-Cochicine-90% get relief and this supports dx of gout -Steroids-if can't use above |
|
_______ is contraindicated for treatment of Gout because in small doses it may worsen hyperuricemia.
|
Aspirin
|
|
Prophylaxis and Uric Acid Lowering TX of Gout
|
-lose weight and lose the boose
-avoid dehydration and diuretics -get serum urate below 5mg/dl |
|
In a condition called ______, calcium pyrophosphate crystals are at fault. These crystals are ____________ bifringent.
|
Pseudogout, positively
|
|
Diagnosis of Pseudogout
|
-patient presents with abrupt onset mono or oligoarthitis
-serum urate level NOT elevated -aspiration of joint fluid shows: calcium pyrophosphate crystals and NO bacteria |
|
Treatment of Pseudogout
|
-urate lowering drugs are irrelevant
-NSAIDS -Cochicine(may or may not be beneficial for acute attack but given prophylactically it decreases the # & duration of attacks -intra-articular steroids will terminate attacks in resistant cases |
|
A chronic inflammatory systemic disease dominated by joint destruction
|
Rheumatoid Arthritis
|
|
________ arthritis is considered a symmetric polyarthritis
|
Rheumatoid
|
|
symmetric polyarthritis
|
arthritis that affects homologous joints on both sides of the body
|
|
Joints commonly affected in RA are:
|
-MCP and PIP joints
-carpal bones and wrist -Knees and MTP joints |
|
-synovial microvasculature
-hyperplasia of Type A & B synoviocytes -early T cell emigration & infiltration into synovial tissue -proliferation of blood vessels and of synovial fibroblasts (hypertrophic synovium) -hypertrophied synovium grows over articular cartilage to form a pannus -pannus(synovium) grows, invades & destroys the cartilage and subchondral bone |
Earliest changes of Rheumatoid arthritis
|
|
Pathogenesis: Joint damage in ______ arthritis is of immune origin, ie. an autoimmune disease, in genetically disposed individuals.
|
Rheumatoid
|
|
The autoimmune response of this disease is due partly to Type 3 Hypersensitivity , ie. immune complex-mediated tissue injury. 80% of pts have RFs, which result in the attraction of WBC causing inflammation.
|
Rheumatoid arthritis.
|
|
RFs
|
Rheumatoid factors - autoantibodies to the Fc portion of IgG in the serum and synovial fluid.
|
|
Essential for Diagnosis of RA
|
documentation of inflammatory synovitis
-by synovial fluid leukocytosis (WBC >2000) -typical erosions on XR |
|
-RF found in 80% of patients
-increased ESR and C-reactive protein (CRP) -anemia of chronic disease |
Labs of RA
|
|
Synovial hypertrophy and pannus formation may cause peripheral nerve entrapment in selected joints.
|
Rheumatoid Arthritis
|
|
morning stiffness greater than 2 hours
|
Rheumatoid Arthritis
|
|
morning stiffness less than 30 minutes
|
Osteoarthritis
|
|
-frozen shoulder (adhesive capsulitis)
-ulnar nerve entrapment-paresthesias of 4th/5th digi -Baker's Cyst(post.herniation of joint capsule) -Tarsal Tunnel Syndrome-entrapment of post.tibial nerve-parethesias of sole -MTP Subluxations -Valgus deformities |
Rheumatoid Arthritis
|
|
Deformed hands:
-MCP and PIP joints involved -nodules in finger tendons (locking) -tendon rupture-Swan Neck & Boutonniere Deformity -Opera Glass hands-ulnar deviation at MCP joints, radial deviation at wrists |
Rheumatoid Arthritis
|
|
Extraarticular Manifestations of Rheumatoid Arthritis
|
-Skin: nodules in skin,bursae,tendons &/or over pressure points
-Ocular: Keratoconjunctivitis sicca -Respiratory: interstitial fibrosis, pluerisy/pleural effusion -Heart: pericardial effusion, restrictive pericarditis w/sns of RHF -GI: gastritis & peptic ulcer dz from NSAID tx -Blood: anemia of chronic dz |
|
-NSAIDS (Advil,Arthrotec, Daypro,Alleve)
-Corticosteroids(glucocorticoids) -DMARDS |
Treatment for RA
|
|
DMARDS
|
Disease Modifying Anti-Rheumatic Drugs
-Rheumatrex(methotrexate) -Imuran(azathioprine) |
|
The prototype of autoimmune diseases, characterized by production of antibodies to components of cells in the nucleus.
|
Systemic Lupus Erythematosus (SLE)
|
|
Dominated by:
-severe fatigue -arthralgias/arthritis -some permutation of its many systemic effects, many of which are vasculitic |
SLE
|
|
Used to be called connective tissue diseases or collagen vascular disease because of the prominence of effects in connective tissue and in blood vessels themselves
|
SLE and other autoimmune diseases
|
|
central disturbance is rampant production of auto-antibodies to a variety of self antigens in/on the cell surface, cytoplasm or nucleus
|
SLE
|
|
In SLE, auto-antibody production is due to immune cell abnormalities of the _____
|
B cells, T cells and monocytes
|
|
In SLE, abnormalities to immune cells cause:
|
-B cell hyperactivity leading to hyperglobulinemia
-Increased # of Ab producing cells -Heightened responses to both foreign and self Ags |
|
Immuno complex (IC) deposition results in inflammation and vasculitis of various organs and tissues
|
SLE
|
|
Anti-nuclear antibodies bind to self-antigenic components of _____, _____, _____, _____
|
DNA, RNA, nuclear proteins, protein-nucleic acid complexes
|
|
Labs:
-generic ANAs -anti-dsDNA Abs -anti-Smith Abs -C reactive protein is low even when sed rate is high |
SLE
|
|
_____ Abs in a lupus patient may fluctuate over time but _____ Abs remain more constant.
|
anti-dsDNA, anti-Smith
|
|
Skin manifestations:
-malar, butterfly rash -general erythema, often photosensitive -discoid lesions=red papules or plaques with thick scale and hypopigmented center -alopecia -mucus membrane lesions -Raynaud's Phenomenon |
Skin Manifestations of SLE
|
|
Musculoskeletal manifestations:
-arthralgias & arthritis -arthritis similar to RA but not erosive -myalgias -fibromyalgia |
Musculoskeletal Manifestations of SLE
|
|
Manifestations of Renal Dysfunction:
-glomerulonephritis, nephrotic syndrome, renal failure |
Renal Manifestations of SLE
|
|
Neuropsychiatric Manifestations:
-CNS problems, cranial and peripheral neuropathies, psychiatric problems: intractable headaches, seizures,chorea,CVA,cranial neuropathies,peripheral neuropathies,organic brain syndrome |
Neuropsychiatric Manifestations of SLE
|
|
Serositis:
-Pleurisy -Pericarditis |
serositis of SLE
|
|
GI Manifestations:
-abdominal pain, nausea/vomiting, anorexia due to diffuse peritonitis, pancreatitis, IBD, mesenteric vasculitis |
GI Manifestations of SLE
|
|
Pulmonary Manifestations:
-pneumonitis -pulmonary hemmorhage due to pulmonary vasculitis -pulmonary hypertension |
Pulmonary Manifestations of SLE
|
|
Cardiac Manifestations:
-pericarditis -myocarditis -- CHF -endocarditis -coronary vasculitis -atherosclerosis leading to AMI |
Cardiac Manifestations of SLE
|
|
Vascular Manifestions
-acute necrotizing vasculitis |
Vascular Manifestions of SLE
|
|
Reticuloendothelial System
-splenomegaly -lymphadenopathy, at single or multiple sites, nodes soft & tender |
Reticuloendothelial Manifestions of SLE
|
|
Hematologic Manifestations
-increased sed rate -cytopenias |
Hematologic Manifestations of SLE
|
|
Treatment for SLE
|
-avoid sun
-NSAIDs & steroids -DMARDs |
|
Clinical course of SLE
|
-usually relapsing-remitting
-some have downhill course to death in months -10 year survival = 70% |
|
Dominated by fibrotic and degenerative skin changes.
|
Scleroderma
|
|
Includes the changes of scleroderma plus systemic fibrosis and systemic vascular injury.
|
Systemic Sclerosis
|
|
Scleroderma is aka ____.
Systemic Sclerosis is aka ____. |
Limited Scleroderma
Diffuse Scleroderma |
|
CREST comprises most of the manifestations of ________ and it stands for_______.
|
-Limited Scleroderma
-Calcinosis, Raynaud's Phenomenon, Esophageal Dysmotility, Sclerodactyly, Telangectasias |
|
Calcinonis
|
subcutaneous tissues develop calcifications that are either palpable, visible as radio-opacities on Xray or both. Fingertips most often.
|
|
Raynaud's Phenomenon
|
Painful, triphasic color change in acral areas, ie. fingers, toes, nose, ears. In response to cold exposure or stress, the acral arterioles constrict (ischemia-white). Next the area becomes cyanotic (blue) probably because the arterioles redilate slightly and perfusion is so minimal that blood releases oxygen. Next, arterioles dilate greatly (reactive hyperemia -very red)
|
|
Esophageal Dysmotility
|
atrophy and fibrosis of the esophagus causes:
-dysphagia -LESD which causes GERD, Barrett's esophagus (metaplasia of epithelial cells of lower esophagus leading to precancerous lesion) from chronic GERD |
|
Sclerodactyly
|
-first manifestation to occur in crest is diffuse edema of fingers and hands later replaced by skin thickening and tightness
-eventually, claw-like hand w/tapered fingers w/tight, shiny skin -skin change later affects face, pulling into a tight mask with bared teeth |
|
Telangectasias
|
-most commonly result from alcohol abuse
-permanently dilated blood vessels of the nose and cheeks -in Scleroderma, it is more widespread and occurs w/o alcohol |
|
anti-centromere antibodies
|
Limited Scleroderma
|
|
SCL-70 antibodies
|
Diffuse Scleroderma aka Systemic Scleroderma
|
|
Fibrotic and vascular changes that originally affected only the hands, esophagus and face intensify in those areas and cause problems in other systems
|
Diffuse Scleroderma aka Systemic Scleroderma
|
|
Skin Manifestations of Systemic (Diffuse) Scleroderma
|
-skin changes spread to arms, legs, trunk
-scattered hyperpigmentation of skin creates S&P appearance -involved skin loses sweat glands and hair follicles -hand skin becomes so tight that finger motility is impaired -mouth becomes so tight that eating & oral hygiene become difficult -ischemia of the fingers causes skin ulcers, necrosis and then loss at the tips |
|
GI Manifestations of Systemic (Diffuse) Scleroderma
|
-anywhere from mouth to rectum
-fibrosis of small bowel leading to hypomotility, cramping, bloating -colon develops wide-mouth saccular diverticuli |
|
Cardiac Manifestations of Systemic (Diffuse) Scleroderma
|
-pericardial effusion may impair ventricular filling
-coronary vasospasm leads to left ventricular dysfunction -systemic hypertension leading to left ventricular hypertrophy and failure -pulmonary fibrosis leading to pulmonary hypertension and right ventricular hypertrophy and failure |
|
Pulmonary Manifestations of Systemic (Diffuse) Scleroderma
|
-pulmonary fibrosis (restrictive lung disease & right ventricular failure)
-fibrosis causes decreased alveolar oxygen uptake |
|
Kidney Manifestations of Systemic (Diffuse) Scleroderma
|
-marked sclerosis of arteries -->decreased GFR--> progressive azotemia and increased renin secretion--> malignant hypertension
|
|
Musculoskeletal Manifestations of Systemic (Diffuse) Scleroderma
|
-joint pain and stiffness due to skin tightness and tendon involvement
-friction rubs/crepitus of large joint (knee) due to fibrosis of synovium -flexion contractures of fingers, wrist and elbow from fibrosis of synovium and periarticular structures |
|
Clinical Course of Systemic (Diffuse) Scleroderma
|
-unpredictable, generally slowly progressive
-CREST syndrome may remain nonprogressive for long periods -prognosis is poor if cardiac, pulmonary or renal involvement |
|
Treatment for Systemic (Diffuse) Scleroderma
|
-no cure and nothing alters course of disease for long. Therefore, treatment is symptomatic.(Treat individual manifestations)Also, steroids provide no benefit in this time of inflammation.
|
|
Treatment for:
-Raynaud's -GERD -Hypertension |
-calcium channel blockers, angiotensin II receptor blockers
-antacids, anti-histamines (H2 blockers), proton pump inhibitors -ACE-inhibitors |
|
Immune-mediated inflammatory disorder of exocrine glands dominated by salivary and lacrimal gland dysfunction (dryness).
|
Sjogren's Syndrome
|
|
Primary Sjogren's Syndrome
|
when mucous membrane dryness and its related effects occur in isolation, it is called ______.
|
|
Secondary Sjogren's Syndrome
|
When other autoimmune diseases, notable RA, SLE and Systemic Sclerosis, may themselves cause similar exocrine gland degeneration and dysfuntion, it is known as ________.
|
|
Clinical Features of Sjogren's Syndrome
|
Dysfunction of:
1. Lacrimal Gland - dry, irritated eyes with foreign body sensation; corneal abrasions 2. Salivary Gland - dry mouth, oral sores and dental caries;lingual and labial fissures, dysphagia and GERD, parotid and/or submandibular gland swelling and tenderness 3. other mucous membrane - dry vaginal membranes (dyspareunia);recurrent or persistent sinusitis, dry tracheobronchial membrances leading to URI (pneumonia);pancreatic dysfn leading to nutrient malabsorption |
|
anti-SS-A Ab aka anti-Ro Ab
anti-SS-B Ab aka anti-La Ab |
Sjogren's Syndrome
|
|
Pathology: Emigration of CD4 T-lymphocytes come in direct contact with ductal epithelial cells, causing cell mediated gland destruction
|
Sjogren's Syndrome
|
|
Diagnosis of Sjogren's Syndrome
|
-suspect SS if patient presents with chronically dry eys and mouth, esp. with mild joint pain
-ROSE BENGAL TEST=staining of cornea for abrasion -Whole Saliva Sialometry=patient sucks on sugarless candy for 3 min. and spits watching for decreased secretions. -SCHIRMER's Test=measure of the quant. of tears secreted in 5 min. in response to irritation by a strip of Schirmer's filter paper under each lower eyelid. -young moisten 15mm, 1/3 of elderly moisten 10mm, SS will moisten <5mm |
|
Labs:
-salivary gland biopsy -70% have elevated ESR |
Labs for Sjogren's Syndrome
|
|
Treatment for Sjogren's Syndrome
|
-avoid meds w/anticholinergic effects since much exocrine gland function is cholinergic
-treat Keratoconjunctivitis sicca, Xerostomia, dyspareunia, nephritis, pneumonitis, neueropathy, etc. |
|
Treatment for Keratoconjunctivitis sicca
|
-hypotears (artificial tears)
-HydroEye caps = blend of omega-6 fatty acids and mucin |
|
Treatment for Xerostomia
|
-stimulate saliva (sugarless gum, chewing paraffin or sucking on fruit pit, oral pilocarpine)
-Evoxac(cevimeline)=cholinergic agonist-salivation -Fluoride treatment against caries in absence of saliva |
|
Inflammatory disease of muscle.
|
Polymyositis
|
|
Inflammatory disease of muscle with a variety of dermatologic manifestations.
|
Dermatomyositis
|
|
four main categories of clinical features of PM & DM
|
1. Proximal muscle weakness
2. Elevated serum levels of skeletal muscle enzymes 3. Electromyographic evidence of myopathy 4. Biopsy evidence of muscle inflammation 5. Skin rash - permits the Dx of Dermatomyositis |
|
slow onset over 3 to 6 months without an identifiable precipitating event
|
Polymyositis/Dermatomyositis
|
|
3 main components of Acute Inflammation
|
1. Local Hyperemia:from local arteriolar vasodilation-inc'd flow volume but dec'd flow velocity-neutros & RBC to site
2. Vascular Permeability:leakage of water,plasma proteins and neutrophils into tissue-swelling & pain 3.Leukocyte Emigration:accumulation, leakage & subsequent movement of neutrophils into the tissue by dec'd laminar flow |
|
Histamine, Bradykinin, Leukotrienes, IL-1, TNF
|
chemical mediators of inflammation aggravate leakiness
|
|
after moving into the tissues, the neutros move toward the site of injury along gradients of _____.
|
chemotactic factors (chemical junk)
|
|
Vasoactive amines
|
chiefly histamine, found in mast cells adjacent to capillaries and venules, and in circulating basophils and platelets.
|
|
Histamine causes _____, _____ and therefore ______.
|
arteriolar dilation, venular leakage, edema.
|
|
Eicosanoids
|
the prostaglandins and leukotrienes
|
|
Prostaglandins and Leukotrienes lead to:
|
fever, pain, edema, vasodilation, bronchospasm
|
|
Which pathway do NSAIDs block?
|
cyclooxygenase pathway
|
|
Which pathway do steroids block?
|
phospholipid-induced production of arachidonic acid
|
|
a) Leukotriene receptor antagonists
b)5-lipoxygenase inhibitor |
a) Accolate (zafirlukast)
Singulair (montelukast) b) Zyflo (zileuton) - off market |
|
Acute phase reactions associated with injury or infection and induced by IL-1,IL-6, and TNF
|
-fever,lethargy,dec'd appetite,inc'd neutrophil count,ACTH release leading to corticosteroid release,hepatic synthesis of various proteins (acute phase reactants)
|
|
acute phase reactants
|
-fibrinogen
-C-reactive protein -complement |
|
In inflammation, the increased levels of _____ in the blood cause the sed rate to increase significantly.
|
fibrinogen
|
|
What role does Nitric Oxide play in the inflammation process?
|
vasodilation
|
|
Lysosomal enzymes
|
-elastase
-alpha1-antitrypisin: counteracts elastase |
|
Outcomes of Acute Inflammation (4)
|
1. Complete resolution
2. Scarring 3. Abscess formation: occurs when injury is due to pyogenic bacteria 4. Progression to chronic inflammation |
|
Chronic inflammation is seen in what 4 settings?
|
1. persistent infection
2. prolonged exposure to toxic agents 3. autoimmune disease 4. sarcoidosis |
|
Chronic inflammatory cells
|
macrophages, lymphocytes, plasma cells
|
|
Granulomatous Inflammation
|
distinctive form of chronic inflammation, characterized by aggregation of activated macros that develop a squamous "epitheloid" appearance. It may also become surrounded with fibroblasts and connective tissue
|
|
The role of the lympatics:
|
to remove inflammatory fluid and debris from the interstitial space
|
|
To prevent the normal net leakage of plasma proteins into the brain, and to prevent exposure to drugs, toxins or hormones that may enter the body, brain capillaries have:
|
blood brain barrier - tighter endothelial cell junctions
|
|
_______ allows penetration of the BBB by antibiotics, which is typically very selective.
|
Vascular permeability caused by inflammation
|
|
Morphologic Patters in Acute and Chronic Inflammation (4)
|
1. Serous Inflammation
2. Fibrinous Inflammation 3. Suppurative Inflammation 4. Ulceration - necrosis and erosion |