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Terms in this set (83)

*aka DJD
*biomechanical wear and tear, part of normal aging
*slow onset - joint stiffness, decreased range of motion, effusions
*thickened joint capsule with SYNOVIAL HYPERTROPHY
*narrowed joint space - loss of cartilage, osteoSCLEROSIS - brighter line under joint space
*subchondral CYSTS
*osteophytes - bony spurs
*joint fluid - mucin, few cells
*EBURNATION - polished, ebony look of bone
*accelerated by joint deformity or obesity
*pain IMPROVES with rest - noninflammatory picture

*type IV hypersensitivity reaction - autoimmune destruction of SYNOVIAL joints
*joints have "PANNUS" formation - membrane of granulation tissue creeps over articular surfaces of bone, destroying cartilage and underlying bone
*INCREASED synovial fluid "pockets"
*morning stiffness over 30 minutes, symmetric joint involvement
*pain improves with use
*boutonniere deformities of digits - forced flexion at PIP; DIP extension
*ulnar deviation of fingers
*swan neck deformity
*subluxation of MCP joints
*more likely to have BAKER'S CYST (popliteal fossa)
*HLA-DR4, +ESR, +inc gamma-globulin
*POSITIVE RF - IgM against Fc of IGG
+anti cyclic citrullinated peptide (more specific)
*joint fluid usually MUCIN POOR, + neutrophils

*MONOSODIUM URATE crystals precipitate into joints
*HYPERURICEMIA -genetic (Lesch-Nyhan syndrome), PRPP excess; increased cell turnover in cancer; von Gierke's disease; or decreased excretion of uric acid (more common - i.e. due to thiazides
*PODAGRA -MTP big toe
TOPHI - soft tissue - external ear, olecranon bursa, Achilles)
*asymmetric joint involvement
*recurrent acute flare-ups, over time become chronic picture
25% may develop uric acid RENAL STONES as well

4. SUPPURATIVE ARTHRITIS - "hot joint" = gonococcal, strep, staph - synovitis, tenosynovitis, dermatitis (pustules)
#1 overall = staph
(exc in people age 15-40)

5. PSORIATIC ARTHRITIS - no RF factor (dist from RA), also HLA-B27+
*asymmetric, patchy involvement
*classed as "seronegative"
*DACTYLITIS - Psausage fingers
PENCIL IN CUP deformity -Xray

*young men
*conjunctivitis, anterior UVEITIS
*triggered by INFECTION with CHLAMYIDIA or shigella

*peaks ages 1-3 years (toddler) in GIRLS
*acute febrile illness usually preceds -
*periarticular swelling, enlarged nodes, hepatosplenomegaly
PEMPHIGUS VULGARIS - potentially fatal - IgG against DESMOGLEIN 3 (part of desmosomes
IF: antibodies around epidermal cells in reticular or netlike* pattern
ACANTHOLYSIS - intra*epidermal bullae cause flaccid blisters in the SKIN and ORAL MUCOSA

*MMP = "cicatricial pemphigoid"
ORAL MUCOSA - most common
*eyes, genitalia, sinuses also
*IgG, C3 at BM - smooth line
*unzipping of epithelium -autoimmune attack on basement membrane
*NEGATIVE NIKOLSKY - dist. from Pemphigus Vulgaris

DERMATITIS HERPETIFORMIS - eruptions of clusters of pruritic papules, vesicles and bullae. Histology shows deposits of IgA at the tips of dermal papillae
*assoc with: CELIAC DISEASE

*TARGET LESIONS = multiple rings, dusky center
*macules, papules, and vesicles
*red, peeling lips
*many causes
*DRUG RXN - sulfas, B-lactams, phenytoin
*INFECTION - Mycoplasma pneumonia, HSv

STEVENS-JOHNSON - Fever, bulla formation and necrosis, and sloughing of skin involving 2 mucus membranes, including eye and lip . Usually caused by adverse drug reaction
*TOXIC EPIDERMAL NECROLYSIS - most esvere form - >30% of body surface area - very large bullae

BULLOUS PEMPHIGOID - IgG against HEMIDESMOSOMES - "bullous pemphigoid" is bullow - linear immunofluorescence
RED BULL - eosinophils (red) inside tense* blisters
*less severe than PV
*SPARES oral mucosa

BEHCET'S DISEASE: immune mediated systemic VASCULITIS - GI (bloating, tenderness, pain), pulmonary (hemoptysis), musculoskeletal (arthralgia), C/V (aneurysms, PERICARDITIS ) and neuro (optic nerve), skin (erythema nodosum) - "silk road disease"
*UVEITIS (hypopyon)

Note: various "jxn" proteins go in order of TAD-GH (apical to basal)
*T = tight junction (zonula occludens; claudins + occludins)
*A = adherens junction (zonula adherens - cadherins)
*D= demosomes (macula adherens) - keratin
*G = gap junctions - connexons - channels
H= hemidesmosome - connects keratin in basal cells to underlying basement membrane
I = postemenopausal - increased - increased bone resorption due to decreased estrogen
femoral neck fx - weight bearing* bones
*distal radius (colles) fx
II - SENILE - affects men and women >70 yrs - can be treated with SERMs, calcitonin, bisphosphonates, pulsatile PTH, steroids C/I
*prophylaxis = regular weight bearing exercise
Labs are normal - Ca2+, phos, ALP, PTH - just decreased bone mass*
*ALL BONES affected equally
*thinned cortices, enlarged medullary spaces on Xray

OSTEOPETROSIS - "marble bones" - defective osteoclasts due to CARBONIC ANHYDRASE ii and other mutations that can't make acidic environment - bone resorption doesn't occur normally. Thickened, dense bones; occluded marrow spaces, "bone in bone." Children tend to have RECESSIVE form, adults AUTOSOMAL DOMINANT.
*PANCYTOPENIA - triggers extramedullary hematopoiesis - death in children due to infections and ANEMIA
*CRANIAL NERVE PALSY - impingement - deafness, blindness, HYDROCEPHALUS
*FRACTURES - brittle
Tx: BMT - donor monocytes become osteoclasts
LABS: LOW serum Ca2+, INC alk phos

OSTEOMALACIA/RICKETS = vit D def - defective calcification of osteoid material - soft bones "bow out." Increase PTH secretion to compensate for decreased serum calcium leads to decreased phosphate. Hyperactivity of osteoblasts (need alk environment)
LABS: dec Ca2+, dec phosphate, inc alk phos, inc PTH

PAGET'S DISEASE - aka "osteitis deformans" - fairly common - localized disorder of bone remodeling caused by INCREASED OSTEOBLAST AND CLAST activity. Excess bone resorption (initial osteolytic phase) is followed by replacement with soft, poorly mineralized matrix (osteoblastic phase). characteristic "woven" or "mosaic" bone pattern. Most affected = SKULL, PELVIS, FEMUR, VERTEBRAE. Inc hat size, dentures, HEARING LOSS (auditory foramen narrows). Fractures and pain can result.
LABS: ALK PHOS - really elevated
*HIGH OUTPUT HEART FAILURE - inc AV shunting - hypervascularity, overlying SKIN feels warm
*LONG BONES - "chalk-stick" fractures

OSTEITIS FIBROSA CYSTICA - pseudohyperparathyroidism or primary hyper-PTH- kidney wastes Ca2+ and phosphate is increased, triggering PTH release - marrow replaced by cystic spaces with fibrous tissue (BROWN TUMORS).

HYPERTROPHIC OSTEOARTHROPATHY - idiopathic, painful swelling of wrists, fingers, ankles, knees or elbows due to periosteal inflammation and new bone formation at the ends of long bones, metacarpals and metatarsals. Can be caused by CYANOTIC congenital heart disease, IBD or INTRATHORACIC CARCINOMA. Will regress when underlying disease is treated.

OSTEOGENESIS IMPERFECTA - variable inheritance pattern, defect in type I collagen leads to fragile bones, blue sclera, and lax ligaments. Several subtypes.

OSTEOMA - benign, often involves skull - dense normal bone
HYPEROSTOSIS FRONTALIS INTERNA - osteoma extends into orbit* or sinuses
Dislocation of the elbow joint caused by a sudden pull on the extended pronated arm, such as by an adult tugging on an uncooperative child or by swinging the child by the arms during play. The technical term for the injury is radial head subluxation.[2]

n radial head subluxation, there is little complaint of pain, and the patient generally reports pain in the proximal forearm. Radial head subluxation is a common pediatric presentation generally occurring between the ages of 1 and 3 years, although it can happen anytime between 6 months of age and 7 years. After age 3, children's joints and ligaments gradually grow stronger, making radial head subluxation less likely to occur. The pathologic lesion is generally a tear in the attachment of the annular ligament to the periosteum of the radial neck, with the detached portion becoming trapped between the head of the radius and the capitellum. The older child will usually point to the dorsal aspect of the proximal forearm when asked where it hurts. This may mislead one to suspect a buckle fracture of the proximal radius.

This injury has also been reported in infants younger than six months and in older children up to the preteen years. There is a slight predilection for this injury to occur in girls and in the left arm. The classic mechanism of injury is longitudinal traction on the arm with the wrist in pronation, as occurs when the child is lifted up by the wrist. There is no support for the common assumption that a relatively small head of the radius as compared to the neck of the radius predisposes the young to this injury.

The forearm contains two bones: the radius and the ulna. These bones are attached to each other both at the proximal, or elbow, end and also at the distal, or wrist, end. Among other movements, the forearm is capable of pronation and supination, which is to say rotation about the long axis of the forearm. In this movement the ulna, which is connected to the humerus by a simple hinge-joint, remains stationary, while the radius rotates, carrying the wrist and hand with it. To allow this rotation, the proximal (elbow) end of the radius is held in proximity to the ulna by a ligament known as the annular ligament. This is a circular ligamentous structure within which the radius is free, with constraints existing elsewhere in the forearm, to rotate.The proximal end of the radius in young children is conical, with the wider end of the cone nearest the elbow. With the passage of time the shape of this bone changes, becoming more cylindrical but with the proximal end being widened.

If the forearm of a young child is pulled, it is possible for this traction to pull the radius into the annular ligament with enough force to cause it to be jammed therein. This causes significant pain, partial limitation of flexion/extension of the elbow and total loss of pronation/supination in the affected arm. The situation is rare in adults, or in older children, because the changing shape of the radius associated with growth prevents it.
HANGMAN - Most common C-spine fracture. Mechanism of the injury is forcible hyperextension of the head, usually with distraction of the neck. Traditionally this would occur during judicial hanging, when the noose was placed below the condemned subject's chin. When the subject was dropped, the head would be forced into hyperextension by the full weight of the body, a sufficient force to cause the fracture. However, despite its long association with judicial hangings, one study of a series of such hangings showed that only a small minority of hangings produced a hangman's fracture.[7]

Apart from hangings, the mechanism of injury - a sudden forceful hyperextension centered just under the chin - occurs mainly with deceleration injuries in which the victim's face or chin strike an unyielding object with the neck in extension. The most common scenario would be a frontal motor vehicle accident with an unrestrained passenger or driver, with the person striking the dashboard or windshield with their face or chin. Other scenarios would include falls, diving injuries, and collisions between players in contact sports.

Although a hangman's fracture is unstable, survival from this fracture is relatively common, as the fracture itself tends to expand the spinal canal at the C2 level. It is not unusual for patients to walk in for treatment and have such a fracture discovered on X-rays. Only if the force of the injury is severe enough that the vertebral body of C2 is severely subluxed from C3 does the spinal cord become crushed, usually between the vertebral body of C3 and the posterior elements of C1 and C2.

*JEFFerson fracture - "burst" - C1 - compression = bilateral anterior and posterior breaks

Ankylosing spondylitis (AS) is a systemic rheumatic disease, meaning it affects the entire body. Approximately 90% of AS patients express the HLA-B27 genotype, meaning there is a strong genetic association. However, only 5% of individuals with the HLA-B27 genotype contract the disease.[18] Tumor necrosis factor-alpha (TNF α) and IL-1 are also implicated in ankylosing spondylitis. Autoantibodies specific for AS have not been identified. Antineutrophil cytoplasmic antibodies ANCA are associated with AS, but do not correlate with disease severity.[citation needed] In a study of 40 patients with AS, ANCA was an infrequent finding, being present in only six patients.[19]

The association of AS with HLA-B27 suggests the condition involves CD8 T cells, which interact with HLA-B.[citation needed] This interaction is not proven to involve a self antigen, and at least in the related Reiter's syndrome (reactive arthritis), which follows infections, the antigens involved are likely to be derived from intracellular microorganisms.[citation needed] There is, however, a possibility that CD4 T cells are involved.

Symptoms appear gradually, usually around 23 years of age.[24] Initial symptoms are typically chronic pain and stiffness in the middle part of the spine or the entire spine, often with pain referred to one or other buttock or the back of thigh from the sacroiliac joint. Since the initial signs and symptoms are not specific for ankylosing spondylitis, there is a lag-time between onset of disease and diagnosis, which averages between 8.5 years to 11.4 years.[24]

About 40 percent of AS patients experience inflammation in the anterior chamber of the eye (uveitis), causing redness, eye pain, vision loss, floaters and photophobia. This is thought to be due to the association that both AS and uveitis have with the inheritance of the HLA-B27 antigen. Other common symptoms of AS include: generalized fatigue and sometimes nausea. Less commonly, aortitis, aortic valve insufficiency, apical lung fibrosis and ectasia of the sacral nerve root sheaths may occur.

When the condition presents before the age of 18, it is relatively likely to cause pain and swelling of large limb joints, particularly the knee. In prepubescent cases, pain and swelling may also manifest in the ankles and feet, where calcaneal spurs may also develop.

Pain is often severe at rest, but improves with physical activity. However, many experience inflammation and pain to varying degrees regardless of rest and movement.[citation needed]

Ankylosing spondylitis is one of a cluster of conditions known as seronegative spondyloarthropathies, in which rheumatoid factor tests are negative and the characteristic pathological lesion is an inflammation of the enthesis (the insertion of tensile connective tissue into bone).
Due to injured SUPERIOR GLUTEAL nerve - when pt stands on injured leg, opposite hip drops
*injured ABDUCTOR muscles of thigh - gluteus minimus and medius

Trendelenburg's sign is found in people with weak or paralyzed abductor muscles of the hip, namely gluteus medius and minimus. It is named after the German surgeon Friedrich Trendelenburg.

The gluteus medius is very important during the stance phase of the gait cycle to maintain both hips at the same level. Moreover, one leg stance accounts for about 60% of the gait cycle. Furthermore, during the stance phase of the gait cycle, there is approximately three times the body weight transmitted to the hip joint.[citation needed] The hip abductors' action accounts for two thirds of that body weight. The Trendelenburg sign is said to be positive if, when standing on one leg, the pelvis drops on the side opposite to the stance leg to reduce the load by decreasing the lever arm. By reducing the lever arm, this decreases the work load on the hip abductors. The muscle weakness is present on the side of the stance leg. A Trendelenburg sign can occur when there is presence of a muscular dysfunction (weakness of the gluteus medius or minimus) or when someone is experiencing pain. The body is not able to maintain the center of gravity on the side of the stance leg. Normally, the body shifts the weight to the stance leg, allowing the shift of the center of gravity and consequently stabilizing or balancing the body. However, in this scenario, when the patient/person lifts the opposing leg, the shift is not created and the patient/person cannot maintain balance leading to instability
The Trendelenburg gait pattern (or gluteus medius lurch) is an abnormal gait (as with walking) caused by weakness of the abductor muscles of the lower limb, gluteus medius and gluteus minimus. People with a lesion of superior gluteal nerve have weakness of abducting the thigh at the hip.

This type of gait may also be seen in L5 radiculopathy and after poliomyelitis, but is then usually seen in combination with foot drop.

During the stance phase, the weakened abductor muscles allow the pelvis to tilt down on the opposite side. To compensate, the trunk lurches to the weakened side to attempt to maintain a level pelvis throughout the gait cycle. The pelvis sags on the opposite side of the lesioned superior gluteal nerve.

This gait is precipitated by strain to the gluteus maximus and gluteus minimus. Sufferers frequently complain that an overly strenuous session at the gym, particularly with glute-isolating equipment, result in this awkward gait, or worse.[citation needed]

This gait may be caused by cleidocranial dysostosis.

Biofeedback and physical therapy have been used in treatment.[1]

When the hip abductor muscles (gluteus medius and minimus) are weak, the stabilizing effect of these muscles during gait is lost.

E.g., Stand on right leg -- if left hip drops, then it's a + right Trendelenburg (the contralateral side drops because the ipsilateral hip abductors do not stabilize the pelvis to prevent the droop).

"When the patient walks, if he swings his body to the right to compensate for left hip drop, he will present with a compensated Trendelenburg gait; the patient exhibits an excessive lateral lean in which the thorax is thrust laterally to keep the center of gravity over the stance leg