Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Pathophysiology > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

How many bones are in the human body?

A

206

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the axial skeleton comprised of?

A

Skull, vertebral column, and thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the appendicular skeleton comprised of?

A

Upper and lower extremities, shoulder girdle, pelvic girdle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Looking at an X-ray of a patient’s femur, what would the absence of a space between the epiphysis and metaphysis indicate?

A

The patient has stopped growing (post puberty)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens to the growth plate as children go through puberty?

A

Growth plate ossifies and becomes bone, also known as the epiphyseal plate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 components of the bone matrix?

A

1- Organic matrix/osteoid (25%)- mostly collagen fibers and proteoglycan which bind between collagen fibers. Glycoprotiens. Osteoblasts, osteoclasts, and osteocytes.
2- Inorganic mineral content (70%)- mineral salts; Ca and phosphorous called hydroxyapatite. They given bone its hard, rigid structure while serving as the body’s main reservoir for Ca and Phos.
3- Water (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the basic unit of compact bone?

A

Osteon or the harversion system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the harversian canal?

A

The haversian canal lies at the center of each osteon. It contains blood vessels, lymph vessels, and nerve fibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline the function of an osteoblast.

A

-Derived from the mesenchymal cells.
-Produce type I collagen
-Respond to PTH
-Produce osteocalcin
-Synthesize osteoid (non-mineralized bone matrix)
BONE BUILDING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline the function of an osteoclast.

A
  • The major RESORPTIVE cells of the bone
  • Large, multi-nucleated cells
  • Contain lysosomes filled with hydrolytic enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline the function of an osteocyte.

A
  • Transformed osteoblast surrounded in osteoid as it hardened from deposited minerals
  • The housekeeper- maintains bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the process of bone remodeling?

A

Bone remodeling is a lifelong process that can be thought of as ‘bone metabolism’. It is a three step process: Activation, Resorption, and Formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the RANK/RANKL relationship.

A

RANKL is produced by the osteoblasts to activate the RANK receptors on osteoclasts telling them to break down and resorb bone. Osteoblasts usually follow behind this process and build new bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is RANKL expression increased by?

A 
IL-1, IL-11, IL-17
TNF alpha
PTH
Prostaglandin E2
Glucocorticoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is RANKL decreased by?

A

IL-4
TGF beta
Estrogen (17beta-estradiol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is OPG’s role?

A

OPG is a glycoprotein also produced by the osteoblast that acts as a decoy or receptor antagonist for RANKL. OPG will fill the RANK receptor site so that RANKL cannot. This is how the body ‘turns off’ osteoclast bone resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is OPG production increased by?

A 
IL-1, IL-12, IL-18
TNF alpha
TGF beta, BMP-2
Estrogen (17beta-estradiol)
Leptin
Mechanical Strain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is OPG production decreased by?

A

PTH
Prostaglandin E2
Glucocorticoids
Cyclosporine A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of bone makes up the majority of the skeleton?

A

Compact bone (85%)

Spongy bone is 15%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the dense, double layered connective tissue covering bones?

A

Periosteum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a fracture?

A

A break in continuity of bone, an epiphyseal plate, or a cartilaginous joint surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe bone remodeling after a fracture.

A

1- Inflammation at the site of injury causes a hematoma to form around the bone. This creates an increase in blood supply
2-Soft Callous formation; cartilaginous (2-3wks)
3- Hard Callous (seen on Xray of newly healed bone-thicker)
4- Bone remodeling to normal

Adults casted for 8-12wks, children 4-6wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is a joint?

A

An articulation; point of contact between two bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why are the 3 types of joints?

A

1- Synarthrosis- Immovable
2- Amphiarthrosis- Slightly movable
3- Diarthrosis- Freely movable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the Synarthrosis Fibrous joints.

A

Bones united by fibrous tissue.
Ex:
-Sutures
-Syndesmoses- two bony surfaces that are united by ligament or membrane; permits very limited amount of movement
-Gomphoses- projection that fits into a complimentary socket and are held there by a ligament (our teeth in mandible/maxilla)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the Synarthrosis Cartilaginous joints.

A

Symphysis- Bone are united by a a pad or disk of fibrocartliage. Ex- symphysis pubis, intervertebral disks
Synchondrosis- Bones are united by hyaline cartilage. Ex- joints between the ribs and the sternum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What type of joints are Synovial Joints?

A

Diarthosis- allow for the most movement.

Synovial joints are designed to allow mobility. They are cover with a joint capsule, or synovial sheath. Movements happens due to contraction of the muscle-tendon unit and control is dependent on joint capsule and ligaments.
Synovial fluid is produced by fibroblast-like cells lining the joint capsule and is secreted into mobile joints to provide the lubrication necessary to reduce friction at articulating surfaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the synovial structure? (5)

A

1-Fibrous joint capsule
2-Joint cavity enclosed by a joint capsule
3-Synovial membrane that lines the inner surfaces of the capsule
4-Lubricating synovial fluid that coats joint surfaces
5-Hyaline cartilage that covers joint surfaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a Oblique Fracture?

A

Fracture resulting from rotational forces, the break is along an oblique course (45-degree angle) and does not rotate around the entire bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is an Occult Fracture?

A

A fracture in which there are clinical signs of a fracture but no radiographic evidence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is an Open Fracture?

A

A broken bone that is in communication through the skin with the environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is a Pathologic Fracture?

A

A fracture that develops secondary to an underlying issues. Ex- Osteoporosis, osteopenia, or tumor growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a Segmented Fracture?

A

Also called comminuted fractures; consist of more than one fracture line and more than two bone fragments. May be shattered or crush. Treatment issues arise from soft tissue damage and multiple bone fragments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a Spiral Fracture?

A

Fractures that result from rotational force and cause bone to separate in the form of an S around the bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a Transverse Fracture?

A

Fracture that occurs in a straight line at approximately a 90-degree angle to the longitudinal axis of the bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is a Greenstick Fracture?

A

An incomplete break in the bone with the intact side of the cortex flex. Most often seen in peds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is an Impacted Fracture?

A

Caused by excessive force that telescopes or drives one fragment into another.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the two most common options for fracture management?

A

Reduction-
Closed manipulation, traction, open reduction.
Immobilization-
Cast/splint, external fixation

39
Q

What happens during dislocation?

A

Temporary displacement of two bones; lost of contact between articular cartilage.

40
Q

What happens during a strain?

A

Injury to the muscle or tendon.

41
Q

What happens during a subluxation?

A

Partial loss of contact between articular surfaces.

common in the vertebra

42
Q

What happens during a sprain?

A

Injury to the ligament.

43
Q

What happens during an avulsion?

A

Small chunk of bone attached to a tendon or ligament is pulled away from the bone. (Ex-fracture of patella)

44
Q

What is articular cartilage?

A

(Hyaline Cartilage)

  • Smooth, shiny and white appearing.
  • Flexible, but stiff
  • Covers the end of bones in joint spaces.
  • Designed to withstand stress imposed by the movement of bony structures.
  • Provides cushion and takes on load/mechanical pressure.
  • Maintains some fluid and provides hydration/fluidity to decrease friction.
45
Q

Describe Osteoporosis

A

The loss of both compact and spongey bone. Bone resorption exceeds bone growth (unbalanced)

Definition: Bone mineral density that is 2.5 standard deviations or more below the mean peak bone mass. Presence of fragility fracture.

Types- Postmenopausal, Secondary (ex-to drugs), or Regional

46
Q

What are some causes of Osteoporosis?

A

Menopause
-Decreased Estrogen
-Increased Osteoclastic activity
Effects of Aging
-Decreased replicative activity of osteoprogenitor cells
-Decreased synthetic activity of osteoblasts
-Decreased biological activity of matrix bound growth factors
-Decreased physical activity

47
Q

What are some risk factors for Osteoporosis?

A 
Nonmodifiable
-Advanced age 
-Female gender
-European or Asian ancestry
-Family hx
Modifiable-
ETOH/tobacco/nutrition
Vitamin D deficiency 
Underweight/inactive
Endocrine dysfunction 
Certain meds (corticosteroids, anti-seizure meds)
48
Q

Describe Osteomalacia.

A

The softening of bones due to defective bone mineralization secondary to inadequate amounts of available Phos and Ca, or due to overactive resorption of Ca from the bone due to hyperparathyroidism.

49
Q

What are some causes of osteomalacia?

A
  • Nutrition deficiency
  • Hyperparathyroidism
  • Genetic abnormalities
  • Tumor inducing
  • Vitamin D deficiency- Malabsorption (bariatric surg), Liver disease, ESRD
50
Q

Describe the Pathophysiology of Osteomalacia.

A
  1. Vit D deficiency
  2. Plasma Ca concentrations drop
  3. Stimulates secretion of PTH
  4. Raises plasma Ca concentrations
    (Increased renal clearance of Phos)
  5. Concentrations of Ca and Phos remain too low
  6. Crystallization and ossification does not occur
51
Q

Describe Paget Disease.

A
  • Excessive resorption of spongy bone and accelerated formation of softened bone.
  • Disorganized, thickened, but soft bones
  • Most affects axial skeleton
  • Thickened bones can cause abnormal bone curvatures, brain compression, impaired motor function, deafness, atrophy of the optic nerve.
52
Q

Describe Osteoarthritis.

A

A non-inflammatory, degenerative joint disease; local areas of damage and loss of articular cartilage in joint space and formation of thick subchondral bone and new bone in joint margins.

Loss of proteoglycan from articular cartilage is the hallmark sign. Decreased water content of cartilage, cartilage degrades = wear’n tear

53
Q

Clinical manifestations of Osteoarthritis include:

A
  • Unilateral
  • Pain
  • Stiffness
  • Enlargement of joint
  • Tenderness
  • Limited motion
  • Deformity
  • Incidence increased with age (rare under 40)
54
Q

Describe rheumatoid arthritis.

A

A systemic, autoimmune inflammatory disease that affects the synovial joints. Type III hypersensitivity response (IgG, IgM systemic)

Eval includes 4 or more of the following:

  • Morning joint stiffness lasting at least 1 hour
  • Arthritis in three or more joint areas
  • Arthritis of the hand joints
  • Symmetric arthritis
  • Rheumatoid nodules
  • Abnormal amounts of serum rheumatoid factor
  • Radiographic changes
55
Q

How is JRA different than adult onset RA?

A

Pathophysiology of the two diseases are the same but..

-Three distinct forms of onset
Pauciarticular- involvement of 4 or fewer joints
Polyarthritis- involvement of more than 5 joints
Systemic disease- MOST COMMON
-Predominantly large joints
-Subluxation and ankylosis of spine is common
-Joint pain is NOT as severe as adult type
-Chronic uveitis is common
-Serologic tests often detect ANA
-Serologic tests seldom detect Rheumatoid Factor
-RA nodules are not limited to the subcutaneous-can be found in the heart, lungs, eyes, and other organs

56
Q

Describe Ankylosing Spondylitis (AS).

A
  • Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints
  • Systemic, immune inflammatory disease
  • Primary proposed site is the enthesis (sites where ligaments, tendons, and the joint capsule are insterted into the bone)
  • Begins with inflammation of fibrocartilage in the vertebra
  • Cause unknown but strong association with HLA-B27 antigen
57
Q

Signs and symptoms of ankylosing spondylitis include:

A
  • Low back pain/stiffness
  • Decreased ROM
  • Loss of normal curvature of vertebrae (hump on low back)
58
Q

Describe Gout.

A
  • Metabolic disorder that disrupts the body’s control of uric acid production and excretion. Manifests high levels of uric acid in the blood and other body fluids
  • Occurs when the uric acid concentration increased to high enough levels to crystallize.
  • Crystals deposit in connective tissues throughout the body
  • When these crystals occur in the synovial fluid, the inflammation is known as ‘gouty arthritis’
59
Q

Give examples of what may cause gout.

A
  • Diuretic therapy
  • Psoriasis
  • Advanced carcinoma
  • Renal disease
  • Multiple myeloma
60
Q

What is Genu varum and when is it abnormal?

A

Genu varum occurs in all newborns d/t intrauterine stress. It describes their bowleg appearance
Abnormal if persists longer than 2 1/2 years of age

61
Q

What is Genu Valgum and when is it abnormal?

A

Knock knees.

Peaks by 5-6 years and is abnormal if it persists past 6.

62
Q

What is syndactyly?

A

Webbing or fusion of the soft tissues of the fingers; may also involve fusion of the bone/nail.

63
Q

What are the two most common pediatric deformities of the foot?

A
  1. Metatarsus adductus (forefoot adduction)

2. Equinovarus deformity (clubfoot)

64
Q

What is developmental dysplasia of the hip?

A

Abnormality of the proximal femur, acetabulum, or both.

Risk Factors include: female, metatarsus adductus, torticollis, oligohydramnios, first pregnancy, and breech presentation

65
Q

Treatments for developmental dysplasia of the hip include:

A
  • Braces
  • Sequential casts
  • Surgery
66
Q

Describe Osteogenesis Imperfecta.

A
  • ‘Brittle bone disease’
  • Autosomal dominate
  • Defect in collagen production (def. in type I collagen which leads to bulky, brittle bones)
  • Results in osteoporosis, bowed and deformed limbs, short stature, spine curvature, and bluish sclera
  • Can be evident before birth (in utero fractures)
67
Q

Differentiate between severe osteogenesis imperfecta and mild/moderate forms.

A

Severe may result in stillborn or cause during or shortly after birth
Mild may not be picked up until the child begins to walk and develops fractures.

In Xray bones are almost transparent and the femur is often bowed.

68
Q

Describe Rickets.

A
  • Juvenile osteomalacia

- D/o causing mineralization failure, ‘soft’ bones, skeletal deformity

69
Q

What are some causes of Rickets?

A
  • Insufficient vit D
  • Insensitivity to vit D
  • Renal wasting of vit D
  • Inability to absorb Ca or vit D in the gut

**Correct dietary insufficiencies or will have significant bow-leggedness

70
Q

Describe osteomyelitis.

A

Severe infection of the bone and surrounding tissue that requires immediate treatment.

  1. Leukocytes enter initial site of infection
  2. Release lytic enzyme
  3. Pus spreads to impair local blood flow forming the sequestra
  4. Involucrum forms (new bone formed around abscess.
71
Q

Describe Exogenous osteomyelitis.

A
  • Spreads from adjacent soft tissue/bone
  • Chronically ill, diabetic, alcoholic, immunosuppressed
  • S. aureus (most common)
  • Pasteurella multicida
  • Ex- blow to the face
72
Q

Describe Endogenous osteomyelitis.

A
  • Also called hematogenous
  • Pathogens carried in blood
  • Common complication of sickle cell and low O2
  • Cutaneous, sinus, ear, dental, artificial joint infections
  • S. aureus (most common)
  • H. influenzae, Salmonella, and gram negative bacilli
73
Q

What are the contractile unit of myofibrils?

A

Sarcomere

74
Q

What do the mitochondria of the muscle do?

A

Supply energy.

75
Q

Describe the general steps in the initiation of a muscle contraction.

A
  1. An action potential travels down the axon to the motor end plate and synapses at the synaptic terminal
  2. ACh is released, binding to receptors
  3. Action potential reaches T-tubule
  4. Sarcoplasmic reticulum releases Ca
  5. Active-site exposure of actin , cross-bridge binding with myosin
  6. Contraction begins.
76
Q

Describe the general steps of the end of a muscle contraction.

A
  1. ACh is removed by AChE
  2. Sarcoplasmic reticulum recaptures Ca
  3. Active sites on actin are covered and there is no cross-bridge interaction with myosin
  4. Contraction ends
  5. Relaxation occurs, passive return to resting length
77
Q

Describe actin in myosin binding with respect to energy requirement.

A
  1. The active site on actin is exposed as Ca binds troponin
  2. The myosin head forms a cross-bridge with actin
  3. During the power stroke the myosin head bends, and ADP and phosphate are released
  4. A new molecule of ATP attaches to the myosin head, causing the cross-bridge to detach
  5. ATP hydrolyzes to ADP and phosphate which returns the myosin head to ‘cocked’ position.
78
Q

Which muscle fibers have high resistance to fatigue?

A

Red-Slow oxidative fibers

Ex-postural muscles

79
Q

What type of metabolism do slow oxidative fibers rely on?

A

Aerobic oxidation.

80
Q

Which muscle fibers work quickly but fatigue quickly?

A

White-Fast glycolytic fibers

Innervated by Type II motor neurons that allow for fast conduction, work quickly but fatigue quickly.
Ex- Ocular muscles.

81
Q

What type of metabolism do fast glycolytic fibers rely on?

A

Aerobic and high glycogen contents

82
Q

The greater the innervation ratio of a particular organ the great its _________ .

A

Endurance.

Ex- calf muscle- one motor neuron innervates 1.2 mil muscle fibers= greater endurance.

83
Q

What is Rhabdomyolysis.

A

(Myoglobinuria)
-Life threatening complication of severe muscle trauma with muscle cell loss.

Causes:

  • Crush syndrome
  • Compartment syndrome (swelling around the compartment in limb or muscle d/t trauma)
  • Malignant hyperthermia, infection, snakebite, cocaine, adverse effects of meds, long periods of immobility and unresponsiveness (elderly fall)
84
Q

Describe the pathophysiology of Rhabdomyolysis.

A

Limb compression
Local pressure
Local tamponade
Muscle/capillary necrosis
Edema
Rising compartment syndrome
Compartment tamponade =muscle ischemia and neural injury
Muscle infarction
=Myoglobinemia->renal failure
=ECF shift->Shock (->renal failure/cardiac dysrhythmia)
=Acidosis/hyperkalemia ->cardiac dysrhythmia

85
Q

Describe Duchenne Muscular Dystrophy.

A

-X-linked recessive inheritance (mostly males)- deletion of segment of DNA or single gene defect on short arm of the X chromosome.

86
Q

What does the Duchenne Muscular Dystrophy gene code for?

A

Encodes for the dystrophin protein. Dystrophin mediates the anchorage of the actin cytoskeleton of the skeletal muscle fiber to the basement membrane.
w/o this protein=degeneration of skeletal muscles and symmetric, progressive weakness and wasting of muscle. Dystrophin is replaced by fat

87
Q

What diagnostic studies confirm diagnosis?

A

CK (>10x normal)
EMG
Muscle biopsy

88
Q

What is a + Gower’s sign?

A

When child is on all fours and in order to get up they themselves up with their arms because they can’t plant feet on the ground and have greater strength in their upper extremities.

89
Q

What are the most common ages of advancement of Duchennes?

A
  • Age 2= s/s begin to advance

- Age 12-13= often lose the ability to walk and move towards developing restrictive lung disease.

90
Q

What are some s/s of Duchenne Muscular Dystrophy?

A
  • Shoulders and arms are held back awkwardly while walking
  • Sway back
  • Weak butt muscles (hip straightners)
  • Knees may bend back to take weight
  • Thick lower leg muscles (muscles are weak and mostly fat)
  • Tight heel cord (contractures), child may walk on toes
  • Weak muscles in front of leg cause foot drop and tip toe contractures
  • Poor balance, falls often
  • Thin, weak thighs
  • Belly sticks out due to weak belly muscles.
91
Q

Describe Myasthenia Gravis.

A

A chronic autoimmune disease affecting the neuromuscular function of voluntary muscles and characterized by profound muscle weakness and fatiguability.
ACh receptor antibodies are produced that destroy or block ACh receptors of the muscle end plate of the neuromuscular junction. These antibodies impair the transmission of ACh across the junction.
Resulting in muscle weakness and fatigability.

92
Q

Where does the weakness involved in myasthenia gravis commonly begin?

A
  • Ocular and cranial muscles

- Limb muscles can also be involved

93
Q

What is the treatment for myasthenia gravis?

A 
Anticholinesterase inhibitors (inhibit breakdown of ACh in neuromuscular synapse)
Corticosterioids, IVIG, plasmapheresis, and immunosuppressive drugs
Ventilation in severe cases

Advanced Pathophysiology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions