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Muscu - Connective Tissue - Inflammatory > Muscu - Connective Tissue - Inflammatory > Flashcards

Muscu - Connective Tissue - Inflammatory Flashcards

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
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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
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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
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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
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5
Q

Adhesive Capsulitis - treatment

A
  • NSAIDs
  • Nonnarcotic analgesics
  • Moist heat
  • Program of gentle stretching when appropriate
  • Physical Therapy
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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.
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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
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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
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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
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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
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11
Q

Bursitis - Treatment

A
  • NDAIDs
  • Ice
  • activity modification
  • Gentle stretching exercises when appropriate
  • Corticosteroid use only in recalcitrant cases
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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
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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
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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
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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
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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
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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
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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)

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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
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20
Q

Tendonitis - Presentation

A
  • Pain on movement of the associated muscle group and related joint
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21
Q

Tendonitis - Diagnostic testing

A
  • Physical exam
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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
Q

Tenosynovitis - Presentation

A
  • Pain and tenderness localized to the radial aspect of the wrist
  • Pain worsens with thumb movement
26
Q

Tenosynovitis - Diagnostic Testing

A
  • Physical exam
27
Q

Tenosynovitis - Treatment

A
  • Rest with thumb and wrist immobilization
  • Anti-inflammatory drugs systemically
  • Corticosteroid injections
  • Surgery to release the tendon in extreme cases
28
Q

Giant Cell Arteritis

A
  • 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
Q

Giant Cell Arteritis - Epidemiology

A
  • 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
Q

Giant Cell Arteritis - Etiology

A
  • Autoimmune in nature

* Associted with HLA - DR4

31
Q

Giant Cell Arteritis - Pathology

A
  • 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
Q

Giant Cell Arteritis - Presentation

A
  • 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
Q

Giant Cell Arteritis - Diagnostic Testing

A
  • ESR, CBC, LFT and alkaline phoshatase levels, biopsy of temporal artery and histological confirmation
34
Q

Giant Cell Arteritis - Treatment

A
  • Glucocorticoid therapy
  • Aspirin therapy to reduce the chance of ischemic events in the cranium
  • Methotrexate as a glucocorticoid sparing agent
35
Q

Giant Cell Arteritis - Management with complications

A
  • 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
Q

Giant Cell Arteritis - Prevention

A
  • Major goal is to prevent visual loss

* Glucocorticoid toxicity

37
Q

Microscopic Polyangitis

A
  • Systemic necrotizing vasculitis of arterioles, capillaries, and venules with common involvement of the lung and kidney

AKA - microscopic polyarteritis; hypersensitivity vasculitis, leucocytoclastic vasculitis

38
Q

Microscopic Polyangitis - History

A
  • 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
Q

Microscopic Polyangitis - Presentation

A
  • 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
Q

Microscopic Polyangitis - Diagnostic Testing

A
  • ESR (elevated)
  • CBC (anemia, leucocytosis and thrombocytosis)
  • ANAC in 70% of patients (myeloperoxidase form)
  • Biopsy of skin
41
Q

Polyarteritis Nodosa

A
  • A systemic necrotizing vasculitis of small and medium sized vessels with typical involvement of renal and visceral organs

AKA - PAN, Classic PAN

42
Q

Polyarteritis Nodosa - History

A
  • 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
Q

Polyarteritis Nodosa - Presentation

A
  • 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
Q

Polyarteritis Nodosa - Diagnostic Testing

A
  • 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
Q

Takayasu Arteritis

A
  • 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
Q

Takayasu Arteritis - Epidemiology

A
  • 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
Q

Takayasu Arteritis - Etiology

A
  • Thought to be autoimmune process
48
Q

Takayasu Arteritis - Pathology

A
  • 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
Q

Takayasu Arteritis - Presentation

A
  • 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
Q

Takayasu Arteritis - Diagnostic Testing

A
  • Arteriography is the gold standard

* Biopsy when possible

51
Q

Wegeners granulomatosis

A
  • necrotizing vasculitis most commonly affecting the respiratory and renal systems
52
Q

Wegeners granulomatosis - History

A
  • 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
Q

Wegeners granulomatosis - Presentation

A
  • 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
Q

Wegeners granulomatosis - Diagnostic Testing

A
  • ESR elevated
  • CBC (mild anemia and leukocytosis)
  • mild hypergammaglobulinemia
  • mildly elevated rheumatoid factor
  • c-ANCA antibody levels (also important to monitor treatment)
  • tissue biopsy

Muscu - Connective Tissue - Inflammatory (1 decks)

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