Muscoskeletal part 1 Flashcards
Sudden injury fractures
Could be compression, shearing and tension. Human bones have low tolerance for tension.
Complete vs incomplete fracture
Complete is all the way through bone
Potts fracture
Ankle-distal fibula
Colles fracture
Wrist-distal radius
How are joint disorders categorized
Inflammatory or non
Non = no synovial membrane inflammation or system S&S
Osteoarthritis
Non-inflammatory degenerative with loss of articular cartilage in synovial joints
The most common joint disease
Types of osetoarthritis
Primary with an unknown etiology, age is a factor and maybe wear and tear
Secondary from congenital defects, trauma, or inflammation
Pathophysiology of osteoarthritis
Articular cartilage erodes, bone underneath thickens, spurs form and it mainly affects weight bearing joints
Clinical manifestations of OA
Hip, knee, foot, hand, lumbar and C-spine affected commonly
Aching, diffuse pain exacerbated by USE
Stiffness, reduced mobility, crepitus, swelling, deformed joints.
New bone formation causes areas of enlargement in OA to feel hard, in RA they feel soft
Two nodes in OA
Heberden (distal interphalangeal joint)
Bouchard’s (middle joint)
RA definition
Rheumatism is an disease process or condition involving joints and connective tissue
Arthritis is joint swelling (a descriptive term not a diagnosis)
RA overview
A chronic, systemic autoimmune disease which causes connective tissue inflammation (mainly joints) with no known cause
Family predisposition
RA etiology
Autoimmune mediated
70-80% have RF factor (self produced antibody IgRF)
Activation of T-cells by a microbial agent, from a genetic predisposition and environmental trigger
RA pathogenisis
Begins as synovitis, immune system has inflammatory response which destroys surrounding joint structures.
Normal inflammation mechanisms lead to tissue destruction (phagocytes, lysosomal enzymes, vasodilation, increased vascular permeability)
Chronic inflammation causes hyperplasia of synovial cells and surrounding tissue
RA pathogenesis part 2
Extensive angiogenesis within synovium
New granulated vessel tissue (pannus) extends between cartilage and subchondral bone
Inflammatory cells within Pannus have a destructive effect on the cartilage and bone
Local clinical manifestation of RA
5 cardinal signs of inflammation
Rheumatoid nodules - granulomatous lesions that develop around small blood vessels, usually over pressure points
Systemic clinical manifestations of RA
Immune mediated fatigue, weakness, weight loss, anorexia, fever
Generalized aching and stiffness
Exacerbations and remissions
Common RA joints
Fingies, hands, wrists, knees and feetsies
Infectious arthritis
Results from spread of pathogens during sepsis from adjacent bone infections
From surgery or removing joint fluid, most commonly lyme disease
Pathophysiology of arthritis
Knee or other weight bearing joints
Transient exudation of fluid into joint cavity
S&S of synovitis
Gout overview
A group of diseases called Gout syndrome
We focus on acute gouty arthritis, men over 40 most common
Gout physiology
Problem with uric acid production or excretion, too much of it means it is deposited in joint cavaties where it crystallizes
90% in big toe
Gout classifications
Primary gout:
Genetic defect leading to abrnomal purine metabolism or decreased excretion of uric acid
Secondary gout:
From an underlying condition like a tumor elevating nucleic acid breakdown or renal disease leading to decreased exretion
Gout pathogensis
Uric acid (from purines -A/G) crystallizes as monosodium urate. Decreased temp increases crystals Crystals set off inflammatory response
Gout patho 2
Microtophi (nodes of MU crystals) have chemotactic properties
The inflammation destroys joint tissue
Repeat attacks will eventually build up tophi (larger versions)
Leukocytosis
elevated WBC
Clinical manifestations of acute gout
Usually one joint, decreased temp increases risk.
Swelling, hyperemic, warm, painful
Fever, leukocytosis, tachy cardia, exhaustion
Clinical manifestations of chronic gout
Less inflammation, more deformities
Sub q deposits in ears, arms and patella
25% have renal failure
Ankylosing Spondylitis definition
Ankylosis - stiffening of joint
Spondylitis - vertebrae inflammation
Classified as spondyloarthropathy (RF factor generally not seen)
Ankylosing spondylitis overiew
A chronic inflammatory joint disease with thickening of the spine and SI joints (males) and peripheral joints (females)
Onset is 20-30 years old
Marked by remission and exacerbation
Etiology of ankylosing spondylitis
System inflammatory response, with genetic predisposition and environmental trigger
Pathogenesis
Immune mediated, inflammatory erosion of sites where tendons and ligaments attach to bone
Begins in SI joints and travels up
Vertebral inflammation leads to fibrosis, ossification, and fusion of joints
Clinical manifestations of ankylosing spondylitis
Kyphosis, osteoporosis, hip and back pain (exacerbated by REST)
may restrict chest wall movement because of costovertebral joint involvement
Similar systemic S&S of RA
Characters of muscular disorders
Weakness (can't contract) Fatigue (can't sustain contraction) Spasm (myotonus) Fibrillation Myalgia (pain)
Neurogenic atrophy
Denervation causes muscle cells to fibrilliate, atrophy, and eventually be replaced with fibrous tissue
Neurogenic atrophy from upper motor neuron
Located in central cortex f brain, can be caused by injury to CNS, CVA, head injury, ALS, spinal cord trauma
Neurogenic atrophy lower motor neurons
Injury to peripheral nerves from intervertebral disk rupture, ankylosing spondylitis, knife wounds, ischema (the beeties)
Axons regrow at 1-2mm/weel
Myasthenia (muscle weakness) Gravis (potent) etiology
Autoimmune mediated, believed to be caused by sensitizes helper T cells which leads to attack on ACH receptors in NMJ
Often associated with lupius, RA)
Myasthenia Gravis pathophysiology
Post synaptic ACH receptors not recognized as self, so they are destroyed by helper T cells
Myasthenia Gravis cranial nerves which can be involved
9, 10, 11, 12
Clinical manifestation of myasthenia gravis
Begins with fatigue after exercise, recurrent upper resp track infections, facial weakness, airway and swallowing problems, weak resp muscles, and eventually quadriparesis
Fibromyalgia
10:1 ratio to women, widespread joint and muscle pain with fatigue and tender points plus nonrestorative sleep
Noninflammatory
Can co exist with other muscular disorders
Characterized by pain in all areas, especially ‘tender points’ <3 months
Fibromyalgia tender points
Occiput, traps, dimples, outer lower glute
Anterior: C5-C7, second rib, elbows, knee
Precipitating fibromyalgia factors
Flu-like viral illnes, chronic fatigue syndrome, HIV, lime disease, trauma (physical/emotional) steroid withdrawal
Clinical manifestations of fibromyalgia
Diffuse and chronic, gnawing or burning pain.
Fatigue without relief by sleep
Headache, IBS, excess sensitivity to cold
Chronic fatigue syndrome
Pronounced fatigue with sudden onset, debilitating tiredness >6months and may worsen with physical and mental activity
CFS etiology
Unknown, neurological, psychatric and biological underpinnings
Possibly secondary to viral infection
4:1 M:F ratio
CFS pathogenesis
Low brain stem perfusion, CNS abnormalities, immune dysfunction, increased inflammatory cytokines
CFS clinical manifestations
6 months of symptoms Fatigue worsened by effort Muscle and joint pain Headaches Flu like symptoms with tender lymph nodes Various neurocognitive symptoms
Muscular Dystrophies
All are marked by degeneration of skeletal muscle with
Genetic defect
Primary muscle cell pathology
Progress S&S related to muscle wasting
Pathophysiology of muscular dystrophies
Abnormality in intracellular metabolism of muscle fibers, deficiency of dytrophin ( a muscle cell protein membrane which binds actin to cell membrane and part of NMJ)
The deficiency leads to degeneration and necrosis of cell, replacement of fiber with fat and other CT, and release of CK enzymes
Duchenne’s MD
x-linked recessive (more common in males)
Most common MD
Usually die before 21
First noted at 3 (clumsy/falls)
Slow motor development, progressive weakness, muscle wasting, waddling gait, walk on toes, kyphoscoliosis
1 in 3 retarded
Die from resp insufficiency
Beckers MD
Mild form of Duchenne’s
S&S later in life and milder, live to be 35
Myotonic MD
Second most common, chromosome 19 autosomal (M and F equally)
S&S appear in adulthood with slow progression
Insulin resistance in muscle cells is common
Myotonic MD 2
Mental and muscle deterioration, myotonia (muscles can contract by not relax) Facial weakness (hatchet face appearance)
Cerebral palsy
Highly variable presentaiton some degree of motor impairement
Non progressive
S&S change with growth and maturation
Etiology of CP
Caused by ischemia, pre peri or immediately postnatal
Also caused by genetic mutations, infections or metabolic disorders in utero.
Patho of CP
Brain atrophy specific to motor function, atrophy not limited to areas of motor control
Clinical manifestations of CP
Quads, diplegia Spastic hyperreflexia/paralysis Loss of motor control Ataxic gait Loss of balance Intellectual, speech and vision problems Seizures
Subluxation
Incomplete or partial disolocation of joint or organ
Rhabdomyolysis
Or myoglobinuria
Excessive muscle damage releases intercellular protein Myoglobin after cell destrction
Commonly found first in urine
Etiology of rhabdo
Direct trauma or crush injury Infections Hyperthermia Excessive exertion Electrocution Burns NM blocking agents CNS depressants Inflammation Acidosis
Pathogenesis of rhabdo
Injury causes ischemia, edema, compartment pressure and tamponade so muscle infarcts A limp extremity can cause rhabdo Cell contents released: Myoglobin CK Phosphate Potassium Calcium
Compartment vs crush syndrome
Rhabdo in local scale or global
Rhabdo clinical manifestations
Significant amounts of myoglobin, CK in urine with red/brown pee
Renal failure
Shock/acidosis
Lyte issues
