Muscu - Connective Tissue - Inflammatory Flashcards
(54 cards)
1
Q
Adhesive Capsulitis
A
- Fibroblastic proliferation, possibly secondary to inflammatin of the articular capsule of the shoulder leads to contraction of the capsule, adhesion formation and eventual loss of motion.
- Frozen shoulder
- Stiff shoulder
2
Q
Adhesive Capsulitis - History
A
- Data unknown but the incidence and prevalence may be disproportionately high in the diabetic population
- Most commonly presents between the ages of 40 and 60 years
- T1 DM is a common risk factor
- Other risk factors include:
- hypothyroidism
- dupuytren contracture
- cervical disk herniation
- Parkinson disease
- Cerebral hemorrhage
- tumors
3
Q
Adhesive Capsulitis - Presentation
A
- Progressive freezing of the joint with pain on attempted movement to a gradual thawing and gradual increase in range of motion
- The process can take from 6 months to 2 years
- Pain at the deltoid insertion
- Diffuse tenderness about the shoulder
4
Q
Adhesive Capsulitis - Diagnostic Testing
A
- Physical exam finds reduction (>50%) in range of motion and pain on motion
- MRI scan indicates a contracted capsule
- Radiographic studies, AP and axillary to rule out other destructive joint diseases
5
Q
Adhesive Capsulitis - treatment
A
- NSAIDs
- Nonnarcotic analgesics
- Moist heat
- Program of gentle stretching when appropriate
- Physical Therapy
6
Q
Bursitis
A
- Sterile inflammation of a bursa, which is a thin-walled sac lined with synovial membrane.
- Bursae are usually positioned between movable skeletal or muscular elements for protection.
7
Q
Bursitis - History
A
- Bursitis is classified by location and by etiology. Examples of regional bursitis are:
- prepatellar bursitis (housemaid’s knee)
- Ischial bursitis (weaver’s bottom)
- other locations for bursae include:
- olecranon bursa
- retrocalcaneal bursae
- subacromal bursae
- Trochanteric bursae
- Pes anserine bursae
- Examples of bursitis classified by etiology include:
- friction bursitis
- chemcial bursitis
- infective bursitis
8
Q
Bursitis - Pathogenesis
A
- Inflammation secondary to friction from overuse (repetitive motion) or trauma
- Inflammation associated with sysemic disease such as rheumatoid arthritis or gout
- Cause may not be apparent in some cases
9
Q
Bursitis - Presentation
A
- Of the different regional forms, only the knee will be presented as an example
- Initially pain only with activity or presure
- Localized swelling
10
Q
Bursitis - Diagnostic Testing
A
- Physical exam findings
- Radiographic studies, AP and lateral, to rule out destructive joint disease
- Aspiration should be preformed to rule out infection
11
Q
Bursitis - Treatment
A
- NDAIDs
- Ice
- activity modification
- Gentle stretching exercises when appropriate
- Corticosteroid use only in recalcitrant cases
12
Q
Epicondylitis
A
- Painful tissue swelling and inflammation associated with the epicondyles. Two important ones should be studied: lateral and medial epicondylitis of the elbow.
- AKA - Tendinosis
13
Q
Epicondylitis - History
A
- Two common forms are:
- tennis elbow (lateral epicondylitis)
- golfer’s elbow (medial epicondylitis)
- Small tear in the dense connective tissue retinacula
- Tissue degeneration with fibroblast and microvascular hyperplasia
- Usually presents between 35 and 50 years of age
14
Q
Epicondylitis - Presentation
A
- Gradual onset of pain on th elateral side of the elbow during activities requiring wrist extension
- Gradual onset of pain on the medial side of the elbow during activities requiring wrist flexion
- Progressing severity of pain
- Occasionally the onset of pain can be related to a direct blow to the elbow or a powerful maximal contraction of the muscles
15
Q
Epicondylitis - Diagnostic testing (lateral epicondylitis)
A
- Physical exam findings of tenderness over the common origin of the extensor tendons just distal to the epicondyle
- Light tapping on the lateral epicondyle can be painful
- Pain on attempted lifting with the palm prone
- Can be mimicked by entrapment of the posterior interosseous (deep branch) nerve in the radial tunnel created by the attachment of the supinator
16
Q
Epicondylitis - Diagnostic Testing - Medial Epicondylitis
A
- Similar presentation except on the medial side
- Pain on the medial side of the elbow that radiates distally to the forearm
- Patients >35 and is less common than the lateral form
- Microtears and granulation in the attachments of the pronator teres and the flexor carpi radialis
- Differential diagnosis should include ulnar neuropathy at the elbow
17
Q
Epicondylitis - Treatment
A
- Modifying the activity to relieve the tendons of stress
- Rest
- Heat
- NSAIDs
- Rub-in anti-inflammatory creams
- Tennis elbow strap
- Corticosteroid injections for recalcitrant situations
- Surgery as a last resort
18
Q
Tendonitis
A
- The term tendonopathy is a recently coined description to be used to replace the terms tendonitis and tendinosis since both inflammatory and degenerative changes appear to be occuring in tendons with this disease.
AKA - Tendinitis (emphasizing possible inflammatory nature of the disease); Tendinosis (emphasizing the possible degenerative nature of the disease)
19
Q
Tendonitis - History
A
- Tendinitis (inflammation) occurs initially with swelling in the tendon sheath
- This leads to tendinosis (degeneration) in a chronic scenario
- Tendinitis is classified by region:
- Bicipital tendinitis
- Achillies tendinitis
- Posterior tibial tendon dysfunction
- Common form of tendinitis is bicepital tendinitis
20
Q
Tendonitis - Presentation
A
- Pain on movement of the associated muscle group and related joint
21
Q
Tendonitis - Diagnostic testing
A
- Physical exam
22
Q
Tendonitis - Treatment
A
- NSAIDs
- early use when inflammation is present
- Late use as an analgesic
- no proof that they facilitate healing
- Corticosteroid use is highly controversial
- no good evidence that it facilitates healing
- mild evidence of initial analgesic effects
- considerable evidence on the negative side effects
- Cryotherapy and therapeutic ultrasound techniques are used, but little supportive evidence exists
- Laser therapy has been tried but evidence is contradictory at best
- Manual techniques such as tissue mobilization are used but without supportive studies
- Eccentric training is under investigation, intiial studies are positive
23
Q
Tenosynovitis
A
- Inflammation of the thin inner synovial lining surrounding the tendons of the abductor policis longus and extensor policis brevis as they pass through a common sheath at the base of the thumb and distal end of the radius.
AKA - De Quervain’s tenosynovitis; Tenovaginitis stenosans
24
Q
Tenosynovitis - History
A
- Extremely common clinical disorder found mainly in manual workers
- Most common in women between 30 and 50 years of age
( De Quervain’s disease is stenosing tenosynovitis of the first dorsal compartment at the wrist (this compartment contains the tendons of the abductor pollicis longus and the extensor pollicis brevis)
25
Tenosynovitis - Presentation
* Pain and tenderness localized to the radial aspect of the wrist
* Pain worsens with thumb movement
26
Tenosynovitis - Diagnostic Testing
* Physical exam
27
Tenosynovitis - Treatment
* Rest with thumb and wrist immobilization
* Anti-inflammatory drugs systemically
* Corticosteroid injections
* Surgery to release the tendon in extreme cases
28
Giant Cell Arteritis
* Giant cell arteritis, a systemic vasculitis of medium- and large sized arteries, involves an immune reaction against a component of the vascular wall generating a ganulomatous inflammation. Giant cell arteritis is closely related to polymyalgia rheumatica and the two could represent two forms of the same disease.
AKA - Temporal arteritis; cranial arteritis
29
Giant Cell Arteritis - Epidemiology
* Most common form of system vasculitis in adults
* Rarely presents before the age of 50
* More common in women than in men
* High incidence in the Nortic population, very rare in blacks
* Incidence rate of 6.9-32.8 per 100,000
* Often associated with polymyalgia rheumatica
30
Giant Cell Arteritis - Etiology
* Autoimmune in nature
| * Associted with HLA - DR4
31
Giant Cell Arteritis - Pathology
* Giant cell arteritis is a systemic disease, involvement extends from the aorta (giant cell aortitis) and vertebral arteries into the cranial arteries, especially the superficial temporal artery
* Nodular thickenings present in the artery wall
* Granulomatous inflammation of the inner media
* Fragmentation of the internal elastic membrane
* Mononuclear infiltrate with multinucleated giant cells and Langerhans cells
32
Giant Cell Arteritis - Presentation
* Vague, non-specific signs such as fever, anemia (of chronic disease), malaise, fatigue, and weight loss
* Headache is a prominent symptom
* Elevated ESR
* Pain, especially to palpation, often intense, along alongthe course of the temporal artery; the artery can be nodular
* Can present with blurred vision or blindness secondary to opthalmic artery involvement
* Can resent with pain in the mandible when chewing
* Can present with polymyalgia rheumatica: stiffness, aching pain in muscles of the axial spine and proximal limbs
33
Giant Cell Arteritis - Diagnostic Testing
* ESR, CBC, LFT and alkaline phoshatase levels, biopsy of temporal artery and histological confirmation
34
Giant Cell Arteritis - Treatment
* Glucocorticoid therapy
* Aspirin therapy to reduce the chance of ischemic events in the cranium
* Methotrexate as a glucocorticoid sparing agent
35
Giant Cell Arteritis - Management with complications
* Visual impairment due to opthalmic artery involvement
* Claudication in the extremities, strokes, myocardial infarctions and infarctions of visceral organs
* Increased risk of aortic aneurysm
36
Giant Cell Arteritis - Prevention
* Major goal is to prevent visual loss
| * Glucocorticoid toxicity
37
Microscopic Polyangitis
* Systemic necrotizing vasculitis of arterioles, capillaries, and venules with common involvement of the lung and kidney
AKA - microscopic polyarteritis; hypersensitivity vasculitis, leucocytoclastic vasculitis
38
Microscopic Polyangitis - History
* Age of onset is around 57
* Males more than females
* Associated with the presence of p-ANCA in 70% of patients
* Necrotizing glomeruonephritis and pulmonary capillaritis are predominant findings
* Involvement of skin, mucous membrane, lungs, brian, heart, gastrointestinal tract, kidneys and muscle
* Immune reaction to a drug or micro-organism
39
Microscopic Polyangitis - Presentation
* Initially fever, weight loss and muscle pain
* Rapidly progressing renal disease or failure
* Hemoptysis
* Mononeuritis multiplex
* Gastrointestinal and cutaneous vasculitis
* Arthralgias
* Abdominal pain
* Hematuria
* Proteinuria
* Hemorrhage
* Muscle pain or weakness
40
Microscopic Polyangitis - Diagnostic Testing
* ESR (elevated)
* CBC (anemia, leucocytosis and thrombocytosis)
* ANAC in 70% of patients (myeloperoxidase form)
* Biopsy of skin
41
Polyarteritis Nodosa
* A systemic necrotizing vasculitis of small and medium sized vessels with typical involvement of renal and visceral organs
AKA - PAN, Classic PAN
42
Polyarteritis Nodosa - History
* Incidence is about 3-4.5 per 100,000 individuals per year
* Lesion involve bifurcations and branch points
* Acutely, polymorphonuclear neutrophils infiltrate all layers of the vessel and perivascular areas
* Intimal proliferation and degeneration of the vascular wall
* Chronically, mononuclear cells infiltrate the vessel wall
* Fibroid necrosis, luminal compromise, thrombosis and infarction or hemorrhage of the vessel
* Healing involves collagen deposition and aneurismal formation
* Multiple organ systems involved; notable lack of pulmonary system involvement
* Renal involvement features arteritis without glomerulonephritis
* Strong association with Hep B antigen
43
Polyarteritis Nodosa - Presentation
* Non-specific signs and symptoms such as fever, weight loss, and malaise
* Initially, weakness, malaise, headache, abdominal pain, myalgias
* Organ specific complaints follow based on the organs affected
* Hypertension, renal insufficiency, or hemorrhage
44
Polyarteritis Nodosa - Diagnostic Testing
* No specific test avialable
* ESR (invariably elevated)
* CBC (elevated leukocyte count, anemia of chronic disease)
* Hypergammaglobulinemia and positive Hep B surface antigens in 30% of patients
* Biopsy of the involved organs
45
Takayasu Arteritis
* Involves a wide spread granulomatous inflammatory reaction, most likely of autoimmune etiology and leading to stenosis in the walls of medium and large-sized vessels, typically involving the aortic arch and its branches
AKA - Aortic Arc syndrome; Pulseless disease
46
Takayasu Arteritis - Epidemiology
* Presents predominately in women under 40 years of age
* The est. annual incidence is 2.6 cases per 1,000,000 population (100 fold lower than incidence in japan)
* Most common in asia
* Predominately in women under 40
47
Takayasu Arteritis - Etiology
* Thought to be autoimmune process
48
Takayasu Arteritis - Pathology
* Panarteritis with mononuclear cell infiltrates and multinucleated giant cells
* Intimal proliferation and fibrosis
* Narrowing of the lumen of the aorta in its arch and virtual obliteration of the distal portions of the branches of the arch
* Pulmonary trunk can also be involved
* Disease can progress rapidly, initially, then halt after 102 years, permitting long term survival
49
Takayasu Arteritis - Presentation
* Generalized signs include fever, malaise, night sweats, arthralgias, anorexia, and weight loss
* Ocular disturbance such as visual loss including total blindness
* Retinal hemorrhages
* Weakening of the pulse in the upper extremity
* Coldness and numbness in the hands and fingers
* Hypertension
* Specific presentation often depends on the arteries involved
50
Takayasu Arteritis - Diagnostic Testing
* Arteriography is the gold standard
| * Biopsy when possible
51
Wegeners granulomatosis
* necrotizing vasculitis most commonly affecting the respiratory and renal systems
52
Wegeners granulomatosis - History
* rarely encountered in clinical practice, incidence unknown
* Prevalence is 3/100,000
* Average age is about 40
* Triad:
- Acute necrotizing granulomas of the mucosa in the upper and lower respiratory tract
- Necrotizing granulomatous vasculitis affecting small to medium sized vessels
- Focal necrotizing renal disease involving cresentic glomerulitis
* Other organs involved include eyes, skin, and heart
* Thought to be autoimmune disease, possibly triggered b an environmental pathogen
* c-ANCA antibodies present in 95% of cases
* Unbalance Th1 cytokine production
53
Wegeners granulomatosis - Presentation
* Non-specific signs such as fever, malasie, weakness, arthralgias, anorexia, and weight loss
* Persistent pneumonia with bilateral cavitating nodules with infiltrates
* Chronic sinusitis
* Mucosal ulcersations of the nasopharynx
* Nasal septum perforation and saddle nose deformity
* Serous otitis media
* Cough, hemoptysis, dyspnea, and chest pain
* Renal disease
* Other features can include:
- skin rashes
- muscle and jont pain
- mononeuritis or polyneuritis
54
Wegeners granulomatosis - Diagnostic Testing
* ESR elevated
* CBC (mild anemia and leukocytosis)
* mild hypergammaglobulinemia
* mildly elevated rheumatoid factor
* c-ANCA antibody levels (also important to monitor treatment)
* tissue biopsy
