Unit 4 Musculoskeletal System Flashcards
1
Q
List 5 Systemic Autoimmune Rheumatic Diseases
A
- Rheumatoid arthritis
- Systemic lupus erythematosus
- Systemic sclerosis/scleroderma
- Polymyositis
- Dermatomyositis
2
Q
What is Rheumatoid arthritis (etiology and pathogenesis)?
A
is a systemic autoimmune disease that causes chronic inflammation of connective tissue, primarily in the joints (and systemic involvement)
Etiology
genetic
- HLA DR4
- T cell-mediated immune response
? environmental
- ? bacterial and viral pathogens initiate the reaction
Pathophysiology/Pathogenesis
- antigen antibody reaction
- formation of immune complexes
- release of cytokines, tumor necrosis factors
- release of enzymes and prostaglandins
- attack synovial membrane and cartilages
- destruction of articular cartilages and subchondral bone erosion
3
Q
Describe in detail the process that leads to the formation of rhuematic arthritis.
A
4
Q
What are the clinical manifestations and the results of rheumatoid arthritis
A
Clinical Manifestations
Joint Manifestations
- Morning joint stiffness lasting at least 1 hour
- Arthritis of three or more joint areas
- Arthritis of the hand joints
- Symmetric arthritis
- (nodules, ulnar bone, ulnar drift)
Extra-articular Manifestations
- Vasculitis
- Eye lesions
- Pleuritis, pericarditis
Results
- May lead to subluxation (dislocation of the joint, resulting in misalignment of the bone ends)
- Instability of the joint
- Limitation of movement
5
Q
Descrive Seronegative spondyloarthropathies
A
Inflammation and involvement of the peripheral joints with an absence of rheumatoid factor
- Ankylosing spondylitis
- Juvenile ankylosing spondylitis
- Reactive arthritis, enteropathic arthritis (i.e., inflammatory bowel disease)
- Psoriatic arthritis
6
Q
Describe ankylosing spondylitis
A
- is a chronic, inflammatory joint disease characterized by stiffening and fusion (ankylosis) of the spine and sacroiliac joints
- systemic immune inflammatory disease
Etiology/risk factors
- Unknown - but there is a strong association with HLA-B27 antigen
- Men:women = 3:1
http://postimg.org/image/441vvk6yp/Pathogenesis
- Increased susceptibility to infections or environmental agents – linked with HLA B27
- Autoimmune phenomena
Joint manifestations
- Low back pain
- Early morning stiffness
Extra-articular manifestations
- Acute anterior uveitis
- Aortitis
- Respiratory function involvement
- Weight loss, fever
7
Q
Describe osteoarthritis (etiology and pathogenesis).
A
- Degenerative joint disease
- Primary OA
- Secondary OA has a known underlying cause such
- Congenital or acquired defects of joint structures, trauma, metabolic disorders, or inflammatory diseases
Etiology
- Men>women – in younger age group
- Women>men – middle age group
- Obesity
- Occupation
Pathogenesis
- mechanical injury – release of cyokines – release of protease enzymes – that leads to
- loss of articular cartilage
- leaving the underlying bone unprotective
- erosion of subchondral bone
- new bone formation – osteophytes
- irritation of the synovial membrane
- synovitis and joint effusion
8
Q
What are osteoarthritis-induced joint changes?
A
Progression
- A progressive loss of articular cartilage
- Synovitis
- Osteophytes
- Bone spurs
Manifestations
- Joint pain
- Stiffness
- Limitation of motion
- Joint instability
- Deformity
9
Q
Compare RA, AS and OA in terms of risk factors, pathogenesis, joint involvements and clinical manifestations (test questions).
A
10
Q
List three categories of joint disorders/rheumatic disorders
A
- Systemic Autoimmune Rheumatic diseases
- Seronegative spondyloarthropathies
- Osteoarthritis syndrome
11
Q
What are metabolic bone disorders?
A
are characterized by abnormal bone structure that is caused by altered or inadequate bone remodeling, which may be attributable to genetics, diet or hormones.
- Osteopenia
- Osteoporosis
12
Q
What is Osteopenia?
A
Definition
- Reduction in bone mass greater than expected for age, race, or sex
Causes
- Decrease in bone formation
- Inadequate bone mineralization
- Excessive bone deossification
13
Q
What is Osteoporosis (etiology)?
A
- Porous bone
- Characterized by decreased bone mass
- WHO defines osteoporosis based on the bone density:
- normal > 833 mg/cm2
- osteoporosis < 648 mg/cm2
Etiology
Primary causes
- Senile > 50 years
- Women > men
- Environmental (risk) factors
- Decreased physical activity
- Smoking / drinking
- Low calcium diet
- Immobilization
- Family History
Secondary causes
- Endocrine
- Hyperparathyroidism
- Cushing’s syndrome
- Acromegaly
- Neoplasia
- Intestinal malabsorption
14
Q
Describe the pathogenesis of osteoporosis. Describe the interaction between peak bone mass and occurence of osteoporosis.
A
Pathogenesis
- the remodeling cycle – the process of bone resorption and bone formation is disrupted
- increase in the rate of resorption
- delay in the rate of bone formation
Peak bone mass (after the age of 30)
- depends on heredity
- (blacks have greater peak bone mass than whites or asians)
- sex steroid deficiency
- dietary factors
- inadequate calcium and vitamin D
15
Q
Describe the clinical manifestations of osteoporosis.
A
Clinical Manifestations
Low back pain
Fractures
- Greater loss of spongy bone than compact bone
- Thus – crush fractures of vertebrae, fractures of the neck of femur, distal end of radius
Diagnosis
- Clinical history
- BMD assessment
- Dual-energy x-ray absorptiometry (DXA) of the spine and hip
16
Q
What diseases involve Softening of the Bones
A
Osteomalacia
- A generalized bone condition in which inadequate mineralization of bone results from a calcium or phosphate deficiency, or both
Rickets
- A disorder of vitamin D deficiency, inadequate calcium absorption, and impaired mineralization of bone in children
17
Q
What are fractures? Describe how they are classified.
A
- Occur when stress is placed on the bone than is able to absorb
Classification (http://postimg.org/image/lq8bwcx35/)
By cause
- Sudden injury
- Stress fractures
- Pathologic fractures
Location
- Proximal, midshaft, distal
Types
- Open or closed
Pattern of fracture line
- Comminuted, compression, greenstick
Special names
- Colle’s: The term Colles fracture is classically used to describe a fracture at the distal end of the radius, at its cortico-cancellous junction. However, now the term tends to be used loosely to describe any fracture of the distal radius, with or without involvement of the ulna, that has dorsal displacement of the fracture fragments. Colles himself described it as a fracture that “takes place at about an inch and a half (38mm) above the carpal extremity of the radius” and “the carpus and the base of metacarpus appears to be thrown backward
- Pott’s: An example of Pott’s fracture would be in a sports tackling injury. The player receives a blow to the outside of the ankle, causing the ankle to roll inwards (so that the sole of the foot faces laterally).
18
Q
Describe the pathophysiology of a bone fracture.
A
Pathophysiology
- When a bone is broken – the periosteum and blood vessels are disrupted
- bleeding – followed by hematoma formation
- bone tissue adjacent to the fracture dies
- dead tissue stimulates inflammation
Clinical Manifestations
- Pain
- Swelling
- Loss of function
- Deformity of the affected part
- Abnormal mobility
Stages of Fracture Healing
- Hematoma formation
- Fibrocartilaginous callus formation
- Bony callus formation
- Remodelling
- Review page 1412-1413
19
Q
How can one promot bone healing?
A
- Reduction of the fracture
- Closed manipulation or surgical reduction
- Immobilization
- Immobilization through the use of external devices
- Preservation and restoration of the function
- Therapy
20
Q
What is a displacement fracture?
A
Displaced fracture. In this type of fracture, the bone fragments on each side of the break are not aligned. A displaced fracture may require surgery to realign the bones properly.
21
Q
What are complications of fractures?
A
Complications
- Loss of skeletal continuity
- Injury from bone fragments
- Pressure from swelling and hemorrhage
- Fracture blisters, compartment syndrome
- Involvement of nerve fibers (complex regional pain syndrome)
- Reflex sympathetic dystrophy and causalgia
- Development of fat emboli
22
Q
What is compartment syndrome?
A
Description
- A condition of increased pressure within a limited space
- Compartment syndrome is a limb- and life-threatening condition which occurs after an injury,
- when there is not a sufficient amount of blood to supply the muscles and nerves with oxygen and nutrients
- raised pressure within the compartment such as the arm, leg or any enclosed space within the body and leads to nerve damage because of the lack of blood supply.
- The severity of compartment syndrome can be divided into acute, subacute, and chronic compartment syndrome.
Pathophysiology
- an increase in compartment contents or reduction in a compartment’s volume
- pressure is elevated, capillary blood flow is compromised.
- Edema of the soft tissue within the compartment further raises the intra-compartment pressure, which compromises venous and lymphatic drainage of the injured area.
- Pressure, if further increased in a reinforcing vicious circle, can compromise arteriole perfusion, leading to further tissue ischemia.
- Untreated compartment syndrome-mediated ischemia of the muscles and nerves leads to eventual irreversible damage and death of the tissues within the compartment.
- There are three main mechanisms that are hypothesized to cause compartment syndrome. One idea is the increase in arterial pressure (due to increased blood flow due to trauma or excessive exercise) causes the arteries to spasm and this causes the pressures in the muscle to increase even further. Second, obstruction of the microcirculatory system is hypothesized. Finally, there is the idea of arterial or venous collapse due to transmural pressure.
Clinical Manifestations
- There are classically 6 “Ps” associated with compartment syndrome —
- pain out of proportion to what is expected based on the physical exam findings,
- paresthesia,
- pallor,
- paralysis,
- pulselessness,
- and pressure.
The first signs of compartment syndrome are numbness, tingling and paresthesia.[8][9]
Loss of function, and decreased pulses or pulselessness however,are late signs.
23
Q
Describe the pathophysiology of compartment syndrome us this diagram.
24
Q
Describe the general structure of bones.
A
Types of Bone
http://lyceum.algonquincollege.com/lts/AandPResources/module5-2.htm?sectionID=5
Bone Stucture
25
Types of bone cells:
* osteoclasts, which destroy bones
* osteoblasts, which create bones
* osteocytes, which hold the bone together
* osteogenic cells
**Osteoclasts**
* large multinucleate cells that are responsible for the breakdown of bones.
* The breakdown of bone is very important in bone health because it allows for bone remodeling.
* Osteoclasts are formed by the conjoining of many different cells created from the bone marrow that travel in the circulatory system.
* Osteoclasts are usually found in the small pits on bones called resorptive pits. The pits are formed by
* Osteoclasts resorb the bones by first latching onto the bone. After latching on to the site of the bone where it is suppose to resorb it, it releases a number of enzymes which breakdown the bone tissue.
* The final product of the resorption of the bone is calcium and phosphorus ions. This reabsorption process can sometimes take up to weeks for the Osteoclast to complete.
* The breakdown of bones is controlled by hormones in the bloodstream which instruct the osteoclasts when and where to break down bone tissue.
**Osteoblasts**
* bone cells that are responsible for the formation of new bone.
* Unlike the much larger osteoclasts, osteoblasts are much smaller; they only have one nucleus.
* Osteoblasts also work in groups to form new bone.
* Osteoblasts are important because it allows the bones to be made, remodeled, and repaired.
* The osteoblasts come from the differentiation of osteogenic cells in the tissue that covers the outside of the bone, or the periosteum and the bone marrow.
* The osteoblast creates and repairs new bone by actually building around its self. First, the osteoblast puts up collagen fibers. These collagen fibers are used as a framework for the osteoblasts work.
* The osteoblast then deposits calcium phosphate which is hardened by hydroxide and bicarbonate ions.
* The brand new bone created by the osteoblast is called osteoid.
* Once the osteoblast is finished working it is actually traped inside of the bone once it hardens.
* When the osteoblast becomes trapped, it becomes known as a osteocyte.[6] Other osteoblasts remain on the top of the new bone and are used to protect the underlying bone, these become known as lining cells.
**Osteocytes**
* are osteoblasts which have become trapped inside of the bone matrix.
* Once a osteoblasts creates the new bone around itself, it is trapped and can no longer move or form bone; this is how a osteocyte is created.
* When the osteoblast is transformed into an osteocyte, the transformation causes the osteocyte to loose a majority of its organelles. What replaces these organelles are large quantities of microfilaments.
* Osteocytes develop long branches which allow them to contact each other and also contact the bone lining cells. The osteocyte lies within a small chamber called a lacuna, which is within the bone matrix.[7] Osteocytes remain in contact with each other cells in the bone through gap junction - coupled cell process, which pass through small channels in the bone matrix called the canaliculi.[8]
* The osteocyte is still a mysterious cell, in the way that biologists still have not figured out the true function of the osteocyte. Even though the function of the osteocyte is still under investigation, there are some ideas on what they might do.
* One function of the osteocyte might be the remodeling of the bone through growths of new arms on the cell. It is also known that osteocytes can secrete growth factors which activate lining cells or stimulate osteoblasts.
* Finally, it is believed that the osteocyte might compensate for he strain on the bone due to their many arms which extend out to other osteoc
26
What is the role of RANK L in bone remodelling (test question)?
* RANKL + RANK(receptor) = allow for differentiation of osteoblast to osteoclast
* OPG can block RANK(receptor), decreasing osteoclast production
* Thereby decreasing osteoclast activity
* Estrogen increases the level of OPG, resulting in minimized osteoclast activity
* Low estrogen leves decrease amount of available OPG, allowing more differentation of osteoclasts
* Results in increased breakdown of bone by osteoclasts.
[http://postimg.org/image/s8qk8a8d5/](http://postimg.org/image/s8qk8a8d5/)
27
Descrive hormonal control of bone remodelling (test question).
* Actions of Parathyroid Hormone
* Actions of Calcitonin
* Actions of Vitamin D
[http://postimg.org/image/dp7ar0pil/](http://postimg.org/image/dp7ar0pil/)
28
What are the major influences on bone tissue equilibrium?
* Mechanical stress
* Calcium and phosphate levels in the extracellular fluid (inorganic elements for minerlization)
* Bone cells and matrix proteins (organic elements)
* Hormones and local growth factors
* Cytokines
29
Describe bone remodelling and factors that affect it.
* Bone resorption by osteoclasts
* Bone formation by osteoblasts
* Controlled by:
* Cytokines
* Growth factors
* Interaction with RANKL, the RANK receptor and
30
What are metabolic bone diseases?
are characterized by abnormal bone structure that is caused by altered or inadequate bone remodeling, which may be attributable to genetics, diet or hormones.
31
Compare Osteoporosis and Osteomalacia (TQ).
32
What are the different types of bone fractures (TQ)
33
Describe the process of fracture healing (TQ).
34
What are complications of fractures and how do you monitor for them (TQ)?
Monitoring
* progressive unrelieved pain
* parathesia (tingling/numbness)
* coolness/pale
* slow capillary refill
* sensation of tightness
35
What are the difference between o. arthiritis and a.spondilitus (TQ)?
36
