1/13
Patho
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Compartment Syndrome:
Is a condition of increased pressure within a limited space (abdominal/limb compartments) that compromises the circulation and function of the tissues in the space.
Abdominal alters cardiovascular hemodynamics, respiratory mechanics, and renal function
Duration of pressure, elevation, metabolic rate of tissues, vascular tone, local BP all play a role
Less tissue pressure is required to stop circulation when hypotension or vasoconstriction is present
Clinical Manifestations:
Hallmark symptom of an acute compartment syndrome is severe pain that is out of proportion to the original injury or physical findings
Nerve compression may cause change in sensation, diminished reflexes, and eventually loss of motor function
Treatment:
Cast splitting/removal of restrictive dressings
Elevating extremity on pillows to reduce edema
Fasciotomy
6 “P” Signs of COMPARTMENT SYNDROME:
Pain
Paresthesia
Pallor
Pulselessness
Paralysis
Poikilothermia (inability to regulate your own body temp)
Hematogenous Osteomyelitis
Originates with infectious organisms that reach the bone through the bloodstream
Acute occurs predominantly in children
Chronic skin infections, chronic urinary infections, intravenous drug use (streptococcus pseudomonas) and staph
In children the infection usually affects the long bones of appendicular skeleton (metaphyseal to nutrient blood vessels)
In adults, vertebrae, sternoclavicular and sacroiliac joints, the symphysis pubis. Infection typically first involves subchondral bone then spread to joint space
Bacteremia:
Chills / fever / malaise
Local bone pain and tenderness
Treatment:
Blood and bone aspiration cultures
Antimicrobial agents are given first parenterally and then orally
IV antibiotics , surgery if needed
Contiguous Spread Osteomyelitis
Bacteria may be introduced directly into the bone by a penetrating wound, or open fracture, or a surgery.
Complications:
Pin tract infection in skeletal traction
Sepsis (infected) joints in joint replacement surgery
Wound infections after surgery (Staph / Strept)
Differs in that virtually any traumatized bone may be involved. Injury from local inflammation and trauma may devitalize bone and surrounding tissue, providing an inert matrix on which microorganisms introduced during trauma thrive.
Clinical Manifestations:
Persistent / Recurring Fever
Increased pain at operative trauma site
Continued wound drainage and wound separation
Joint pain / fever/ cutaneous drainage (prosthetic joint)
Treatment:
Surgical debridement of infected and necrotic tissue
Empiric IV antibiotics followed by targeted therapy
Address source control
Osteomyelitis with Vascular Insufficiency
Osteomyelitis may develop from a skin lesion; it’s most commonly associated with chronic or ischemic foot ulcers in people with long standing diabetes. Neuropathy causes a loss of protective reflexes, and impaired arterial circulation and repetitive trauma are the major contributors to skin fissure and ulcer formation.
Manifestations:
Often present with seemingly unrelated problems such as in grown toenails, cellulitis, or a perforating foot ulcer
Pain is often muted by peripheral neuropathy
Osteomyelitis is confirmed when bone is exposed in the ulcer bed or after debridement
Radiologic evidence is a late sign
Treatment:
Debridement and antibiotic therapy may benefit people who have good oxygen tension
Hyperbaric oxygen therapy may be used as an adjunctive treatment
Osteopenia: Characterized by a reduction in bone mass greater than expected for age, race, or sex that occurs because of a decrease in bone formation, inadequate bone mineralization, or excessive bone deossification.
Risk Factors:
Aging
Sedentary life style
Low calcium / Vit D
Smoking
Excessive Alcohol use
Corticosteroid Use
Low body weight / eating disorder
family history of osteopenia
Prevention:
Weight-bearing exercise
Avoid smoking and limit alcohol
Balanced diet
Bone density screening
Osteoporosis: Metabolic bone disease characterized by a loss of mineralized bone mass causing increased porosity of the skeleton and susceptibility to fractures
Risk Factors:
Poor nutrition or Age-related decrease in intestinal absorption of calcium because of deficient activation of Vit D
Postmenopausal women caused by estrogen deficiency
Long-term corticosteroid use, prolonged use of medications that increase calcium excretion like antacids, corticosteroids, anticonvulsants
Endocrine disorders (hyperthyroidism, hyperparathyroidism)
Cushing syndrome or diabetes mellitus
malignancies
Alcoholism (inhibit osteoblast)
Prevention:
Exercise may prevent or delay the onset of osteoporosis by increasing peak bone mineral density (BMD) during periods of growth
Medications for high risk individuals
Fall prevention strategies
Bone-strengthening
Nursing & Medical Interventions for Rhabdo:
1) Immediate Goals:
Prevent kidney damage
Correct electrolyte imbalances
2) Hydration:
Intravenous (IV) fluids are essential to flush out toxins and support kidney function
3) Medications:
Diuretics (in some cases) to increase urine output
Calcium, insulin / glucose to treat hyperkalemia - (more on this when we get to electrolytes imbalances)
4) Dialysis:
May be needed if kidney function severely deteriorates
5) Address Underlying Cause
Stop offending drugs or treat infections
Cite the primary features of ankylosing spondylitis (AS)
Eyes: Uveitis
Kyphosis (forward curvature) and extension of the neck
Enthesitis (inflammation and tendency for fibrosis and calcification at sites of muscle insertion) at shoulders, hips, knees, and heels
Enthesitis of costovertebral and costosternal junctions with flexion contraction of the diaphragm
Sacroilitis: inflammation in the sacroiliac joint
Progressive spinal fusion
Strongly associated with HLA-B27
Loss of lumbar lordosis occurs as disease progresses
Lower back pain (persistent/intermittent), becomes worse when resting
Lumbosacral pain
AS treatment
Is directed at controlling pain and maintaining mobility by suppressing inflammation
Therapeutic exercises, muscle-stretching exercises, maintaining ideal weight, quit smoking
Pharmacologic treatment includes use of NSAIDs to reduce inflammation, relieve pain, and reduce muscle spasms
Current practice is to use anti-TNF-ɑ therapies, including etanercept, infliximab, and adalimumab, which have demonstrated positive effects on disease activity
Reactive Arthropathies
Defined as sterile inflammatory joint disorders that are distant in time and place from the initial infective process.
May occur due to foreign substance in joint tissue
Has been seen in people with acquired immune deficiency
When cultured bacteria cannot be isolated even though there has been preceding infection, it’s no longer bacterial arthritis
Clinical Manifestation
Reiter Syndrome: may be accompanied by extra-articular symptoms like uveitis, bowel inflammation, and non-specific urethritis
Often develops in host after bacterial infection
Treatment:
Is largely symptomatic
NSAIDs are used in treating arthritic symptoms
Vigorous treatment of possible triggering infections is thought to prevent relapse of reactive arthritis
Psoriatic Arthritis
Is a seronegative inflammatory arthropathy that occurs in 7% of people with psoriasis. It’s a heterogeneous disease with features of the SpA in some people, RA in others, and features of both coexisting in others.
Etiology/Pathogenesis:
Genetic, environmental, and immunologic factors seem to play a role
Environmental factors that play a role in pathogenesis: infectious agents, and physical trauma
T-cell-mediated immune responses seem to play an important role in the skin and joint manifestations of the disease
Clinical Manifestations:
Evidence of skin or nail changes typical of psoriasis
5 subgroups of Psoriatic Arthritis:
(1) Asymmetric: about 35% of cases, often mild
(2) Spondylitis: pain & stiffness in the spine and neck
(3) Symmetric: about 50% of cases
(4) DIP: inflammation & stiffness near the ends of the fingers
(5) Mutilans: most severe, only about 5% of cases
Some with psoriatic arthritis have elevated serum of uric acid.
The abnormally elevated serum uric acid level is caused by the rapid skin turnover of psoriasis and the subsequent breakdown of nucleic acid followed by its metabolism to uric acid
Treatment:
Suppression of the skin disease may be important in controlling the arthritis
Often, affected joints are surprisingly functional and only minimally symptomatic
If there are musculoskeletal symptoms, NSAIDs may be used
DMARDs such as methotrexate, sulfasalazine, and leflunomide should be considered early in those with active disease
Gout:
Is a group of disorders characterized by increased serum uric acid and urate crystal deposits in the kidneys and joints
Pathogenesis:
Elevation of uric acid and the subsequent development of gout can result from overproduction of purines, decreased salvage of free purine bases, augmented breakdown of nucleic acids because of increased cell turnover, or decreased urinary excretion of uric acid
Clinical Manifestations:
Gout is characterized into 4 stages:
The asymptomatic hyperuricemia
Not symptoms may be present in the beginning
Acute gout arthritis
Is monoarticular and usually affects the first metatarsophalangeal joint
The tarsal joints, insteps, ankles, heels, knees, wrists, fingers, and elbows may also be initial sites of involvement
Often begins at night and may be precipitated by excessive exercise, certain medications or foods, alcohol, or dieting
Onset of pain is abrupt and redness and swelling is observed
Intercritical gout
In early stages of gout after initial attack has subsided, the person is asymptomatic, and joint abnormalities are not evident
Chronic tophaceous gout
After first attack, it may be months/years before another attack; because attach recur with increased frequency, joint changes occur and become permanent
Diagnosis:
Definitive diagnosis can only be made when monosodium urate crystals are in the synovial fluid or in tissue section of tophaceous deposits
Measurement of serum uric acid levels and collection of a 24-hour urine sample for determination of urate excretion in the urine is diagnostic (>7mg/dL in men, >6mg/dL in women)
Treatment:
Pharmacologic management of acute gout is directed toward reducing joint inflammation
Hyperuricemia and related problems of tophi, joint destruction, and renal problems are treated after the acute inflammatory process has subsided
NSAIDs, particularly indomethacin & ibuprofen are used for treating acute gouty arthritis; alternatives include colchicine and intra-articular deposition of corticosteroids
Education about disease and its management are fundamental to treatment
Ideal weight, moderation of alcohol consumption, smoking cessation, avoidance of purine-rich foods,
Describe the pathologic changes that may be found in the joint of a person with rheumatoid arthritis (RA).
Can be viewed as an aberrant immune response that leads to synovial inflammation and destruction of the joint architecture
Characteristic of RA is the development of an extensive network of new blood vessels (angiogenesis) in the synovial membrane that contributes to the attachment of rheumatoid synovitis
Neutrophils, macrophages, and lymphocytes are attracted to area and phagocytize the immune complexes, and release lysosomal enzymes capable of causing destructive changes in joint cartilage
Pannus is a feature of RA that differentiates it from other forms of inflammatory arthritis
Inflammatory cells found in the pannus have a destructive effect on the adjacent cartilage and bone
Erosion of articular cartilage due to pannus release proteolytic enzymes
Bone erosion (osteoclast activation)
Chronic joint changes and ankylosis (joint fusion)
Fibrosis and calcification of pannus may occur