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Advanced Patho Test 1 > TEST 4: Musculoskeletal > Flashcards

TEST 4: Musculoskeletal Flashcards

1
Q

Bone cells
(Lecture, p.1402)

A

Bone cells enable bone to grow repair itself, change shaped and synthesize new bone tissue and reabsorb old tissue

  1. Osteoblasts: responsible for bone formation through ossification and osteogenesis

Osteoid = no mineralized bone matrix

  1. Osteocytes= mature bone cells
    -“bone in maintenance”
    -Lacunae: spaces
    -Canaliculi: canals
  2. Osteoclasts: responsible for bone reabsorption and remodeling
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2
Q

Bone matrix
What is it?
Composition?
(Lecture, p.1405)

A

-Is made of the extracellular elements of bone tissue, specifically collagen fibers, structural proteins, carbohydrate- protein complexes, ground substance, and minerals

-Is 35% collagen and proteoglycan
-Like rebar, flexible strength
-If this is missing bone is brittle

-Is 65% mineralized bone (hydroxyapatite)
-The cement, weight bearing strength
-If missing bone is too flexible

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3
Q

Phases of Bone remodeling
(Lecture, p. 1407, AO)

A
  1. Quiescent: resting state, restored bone, stays like this until a stimulus
  2. activation: phase 1, osteoblasts and osteocytes signal to form osteoclasts, active remodeling phase
  3. resorption: osteoclasts eat away old bone, active breakdown and resorption of old/ damaged bone tissue
  4. formation: osteoblasts mature and help make new bone
  5. mineralization: involves deposition of calcium and phosphorus (hydroxyapatite) into the osteoid transforming it to mature bone
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4
Q

Factors that affect bone growth
(Lecture)

A

Nutrition:
-Vitamin D is needed for the absorption of calcium from the intestines (insufficiency results in the softening of bones)
-Ie Ricketts (children) osteomalacia (adults)
-Vitamin C is needed for collagen synthesis by osteoblasts (insufficiency results in scurvy)

Hormones:
-Growth hormone, thyroid hormone, estrogen, and testosterone

-Exercise and weight training

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5
Q

Factors that regulate bone remodeling
(Lecture, p. 1409)

A

-Is a balance between bone reabsorption (osteoclasts) with bone formation (osteoclasts)
-There must be a balance to maintain stable bone mass

The process can be altered by:
-Menopause related hormone changes
-Age related factors
-Changes in physical activity
-Drugs (steroids)
-Secondary diseases (renal)

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6
Q

3 types of Arthritis
(Lecture, p. 1452)

A

Spondylitis: inflammatory process that results in fibrosis, ossification
-The fusion of spine and and sacroiliac joints due to uncontrolled bone formation
-Genetic association with HLA

Osteoarthritis: loss, damage of weight bearing synovial joints
-Articular cartilage and joint capsule of central and peripheral joints

Rheumatoid arthritis: inflammatory, joint swelling and tenderness
-Synovial joint destruction
-Autoimmune

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7
Q

Ankylosing Spondylitis (AS)
What is it
Risk factors
Symptoms
Patho
(Lecture, p. 1459, AO)

A

-Chronic inflammatory disease of the axial spine (arthritis of the spine).

-Chronic inflammation leading to pain, stiffness, and eventual joint fusion.

-Risk factors: genetic (HLA-B27), more common in men than women, onset is 20-40 years old, more common in African American

-Manifestations: pain, stiffness in neck and lower back

-Patho: immune mediated inflammation
(Fibrocartilage is inflamed, damage to fibrocartilaginous tissue occurs, scar tissue forms, calcification occurs and joints can fuse “bamboo spine”)

-Develop boney protuberances and erode the disc space—> Can result in fusion of vertebrae in spine

GEM HLA-B27 antigen

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8
Q

Osteoarthritis
(Lecture, p. 1452, AO)

A

-Characterized by degenerative, pathological changes in cartilage, bone, synovium, ligament, muscle, and periarticular fat.

-Most common form of age related joint disease involving synovial joints

-Chronic inflammation

-Risk factors: age, previous injury, obesity

-Manifestations: gradual pain aggravated by activity, stiffness lasting <30 mins after awakening or activity, occasional joint swelling

-Patho: synovial joint experiences local areas of damage to articular cartilage, new bone formation of joint margins, bone hypertrophy, bone thickening of the joint capsule

-Cartilage is worn down

HALLMARK OF OA: degeneration of articular (joint) cartilage that cushions the ends of a bone in a joint

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9
Q

Rheumatoid Arthritis
(Lecture, p. 1455)

A

-A chronic, systemic inflammatory autoimmune disease distinguished by joint swelling, tenderness, and destruction of synovial joints leading to disability.

-Risks: genetics, T cell abnormalities, autoantibody formation (IgG and IgM), more common in women, diagnosed between 35-50 years old

-Manifestations: symmetric joint swelling in hands/ wrists and large joints, pain unrelated to rest or use (improves over the course of the day)

-Patho: cytokine related inflammation (arginine—> citrulline) of synovial membranes —> articular cartilage, joint capsule, ligaments, and tendons—> thickening of articular membrane—> vascular changes (increased enzyme destruction)—> fibrin deposition

GEM— citrulline is considered an antibody and CAN be tested for to diagnose this, also test for rheumatoid factor and ANA

Double GEM- genetic factor of HLA-DR4 is involved (Type IV hypersensitivity)

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10
Q

Osteoporosis
Characteristics
Risks
Manifestations
Normal bone mass
(Lecture, p. 1437, AO)

A

-Characterized by low bone mineral density caused by altered bone microstructure that leads to an increased risk of fractures (an imbalance between bone resorption and bone formation)

-Risk: post menopausal, dietary changes that decrease calcium and vitamin D, decreased level of activity, low BMI, hormones (PTH, thyroid, cortisol, GH), medicines, alcohol, tobacco

-Post menopausal= decreased estrogen, increase ROS—> clasts—> blasts

-Manifestations: bone aches, weakness/ deformities, usually diagnosed with fractures, bone mass <648mg/cm2 measured with dual energy xray absorptiometry (DXA)

-Normal bone mass= 833 mg/cm2

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11
Q

Technical Mechanisms of osteoporosis?
(Lecture, p.1439)
we need a video on this, explained poorly

A

Bone destruction:
-RANKL (protein produced by osteoblasts): plays a role osteoclast formation, function, and survival

-RANK (receptor that RANKL will find) located on osteoclast precursors and mature osteoclasts

Bone protection:
-Osteoprotegerin (OPG): produced by osteoblasts, binds to and inhibits RANKL, protects against bone loss

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12
Q

Scoliosis
Definition
Classifications
Patho
Grading
(Lecture, p.1484, AO)

A

Is a rotational (lateral) curvature of the spine

Classified as either—>
-Non structural: cause other than the actual spine (ie posture, leg length discrepancy, pain)

-Structural: associated with vertebral rotation

Can be: congenital, neuromuscular, trauma, bone and joint disorders, idiopathic (70%)

Patho: CNS abnormality involving balance (reticular system), curve increases most rapidly during period of growth

-Severity of curvature:
< 20 degrees= monitor, regular checkup
20-30 degrees= more frequent monitor
30- 40 degrees = risk of progression is small, treated with a brace
45-50 degrees = spine is biochemically unstable, considered severe, require surgical correction, can cause decrease in pulmonary function

GEM— this is mainly a kid problem having to do with rapid growth spurts

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13
Q

Motor units for contraction
(Lecture, p.1414)

A

-Are comprised of multiple fibers innervated by a single motor neuron

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14
Q

Muscle patho
(Lecture)

A

Atrophy: a decrease in size or cell of tissue
-results from disuse, severing the nerve supplying the muscle
-Myofibrils will decrease in size (bones don’t atrophy but the density may decrease?

Strain: a trauma to muscle or tension when stretched beyond limit (may involved a tear/ rupture—> inflammation—> pain/ swelling)

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15
Q

Muscular dystrophy overview
Definition
Patho
(Lecture)

A

-Disease associated with progressive loss of muscle function
-Many types with distinct features
-Typically genetic in origin (mutation of muscle specific genes)
-Usually limited treatment options

Underlying patho of all dystrophies:
-Dystrophin anchors actin cytoskeleton to basement membrane of skeletal muscle fibers
-The absence of dystrophin results in poorly anchored fibers torn apart during muscle contraction—> calcium enters the cells—> cell death, fiber necrosis—> degeneration of muscles

GEM- mutation is in the dystrophin gene on the X chromosome-

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16
Q

Duchenne Muscular Dystrophy
(Lecture, p. 1491)

A

-Most common form of dystrophy, genetic disorder associated with mutation of dystrophin protein leading to comprised muscle fiber integrity
-This results in muscle fiber damage, calcium overload, cell death and a cycle of inflammation, regeneration, fibrosis, and fatty infiltration
-X linked genetic disorder (1:2,500 male live births)
-Onset 2-6
-SEVERE FORM characterized by progressive muscle degeneration and weakness

-Manifestations: falling, difficulty rising and walking, weakness in hips and legs (waddling gait) muscle enlargement, elevated CK levels (progressive leads to respiratory and cardiac defects)

-Patho: mutation of dystrophin gene
-Neuromuscular junction is functional but the muscle fibers are affected (voluntary muscle fibers first)

-No good treatment

17
Q

Aging and sarcopenia
(Lecture, p. 1424)

A

Sarcopenia: decline of skeletal muscle mass (size, number, and quality) and function with age

-One of the most important causes of functional decline and loss of independence in older adults
-Less muscle strength creates potential for many other chronic problems
-Usually presents to PCP with weakness

18
Q

Sarcopenia etiology
(Lecture)

A

-Nutrition status (insufficient calories/ protein intake)
-hormone levels (low levels of estrogen, testosterone and GH)
-immunologic (chronic low grade inflammation in the elderly)
-metabolic (insulin resistance as we age)

-Results in: decreased motor units, decreased muscle fibers, atrophy—> decreases muscle mass and strength

-Huge problem in the elderly that leads to loss of independence

HALLMARK- decreased muscle strength

19
Q

Patho of sarcopenia
(Lecture)

A

-Inactivity, inflammation, aging, endocrine factors, neuro degeneration, anorexia

-No effective treatment- resistance exercise to prevent, small amounts of protein throughout the day, Vitamin D

20
Q

Effects of aging on bones
(Lecture)

A

-Bone matrix/ mass decrease
-Increased bone fractures
-Bone loss causes deformity, loss of height, pain, and stiffness (ie stopped posture, loss of teeth)
-Joints with rigid, fragile and/or calcified cartilage
-Muscle mass decreases

21
Q

Osteoblasts
(AO)

A

-Function to form bone through ossification or osteogenesis
-Are derived from mesenchymal stem cells
-Are primarily responsible for the synthesis and mineralization of bone
-Produce the ECM (composed of type 1 collagen, ground substance, protein)
-Can be detected by alkaline phosphates levels and osteocalcin
-Once they become encased in the bone matrix, they mature into osteocytes

22
Q

Osteocytes
(AO)

A

-Derived from osteoblasts that have become surrounded by mineralized bone matrix during the process of osteogenesis
-Are the most abundant cell in mature bone tissues and occupy small spaces in the matrix with projections that connect other osteoblasts and osteocytes
-Play a critical role in maintaining bone tissue (contribute to bone remodeling)
-Secrete signaling molecular like sclerostin and RANKL that play roles in osteoclast differentiation

23
Q

Osteoclasts
(AO)

A

-Are responsible for breakdown of bone tissue (aka bone reabsorption)
-Are crucial for the normal remodeling of bone
-Several factors regulate their differentiation and activity (ie RANKL, and osteoprotegerin)

24
Q

RANK/RANKL/OPG overview
(AO)

A

-Is a critical regulatory pathway in bone metabolism, influencing osteoclasts differentiation and activity

-The interplay between this system ensures proper bone remodeling and maintenance of bone density it

25
Q

RANK
(Receptor activator of nuclear factor kappa-B)
What is it?
What does it do?
(AO)

A

-RANK is a receptor expressed on the surface of osteoclasts
-When it binds to RANKL (on a type of osteoblast), it triggers a signaling cascade that promotes the differentiation of osteoclast precursors cells into active osteoclasts
-When activated this stimulates bone resorption by increasing the number and activity of osteoclasts (osteoclasts break down bone tissue by releasing calcium and minerals into the blood)

26
Q

RANKL
(Receptor activators of nuclear factor kappa-b ligand)
(AO)

A

-Is a protein produced by osteoblasts and osteocytes
-Is a key factor in regulation of osteoclast development and activity
-RANKL binds to RANK on osteoclast precursors, activating them and initiating differentiation into mature osteoclasts (enhances the survival and activity of mature osteoclasts)

27
Q

OPG
(Osteoprotegerin)
(AO)

A

-OPG is a soluble receptor and a decoy receptor for RANKL, produced by osteoblasts
-Main role is to INHIBIT RANKLS’s ability to activate RANK, thus reducing osteoclastogenesis (formation of osteoclasts)

28
Q

Components of the bone matrix
(AO)

A
  1. Organic components (35%):

-Type 1 collagen:
-most abundant protein in the matrix, provides tensile strength and flexibility (allows bones to withstand stretching/ bending forces)
-Collagen molecules form a triple helix structure that assembles into fibrils

-Proteoglycans:
-Large molecules made up of a core protein where GAG chains are attached
-Help retain water to hydrate the matrix
-Regulate the processes of bone remodeling and mineralization
-Involved in cell signaling

  1. Inorganic components (65%)
    -Hydroxyapatite:
    -A crystalline calcium phosphate mineral that provides rigidity and hardness of bone
    -Crystals are deposited within the collagen to assist with strength
    -Also serves as a reservoir for Calcium and phosphate ions
29
Q

The role of Vitamin D
(AO)

A

In bone growth:
-Essential for intestinal absorption of calcium and phosphate
-Enhances the efficiency of calcium absorption from food in the intestines
-Plays a role in regulating bone remodeling by Influencing activity of osteoblasts and osteoclasts

Deficiency:
-Rickets in children
-Osteomalacia in adults

30
Q

Role of Vitamin C
(AO)

A

In bone growth:
-Crucial for collagen synthesis
-Facilitates hydoxylation of proline and lysine residues in collagen that stabilize the matrix
-Acts as an antioxidant

Deficiency:
-Scurvy

31
Q

Lordosis vs Kyphosis
(AO)

A

-Usually a result of spondylitis

Lordosis (Loss of normal lumbar curve):
-Flatter lumbar regions
-Can affect posture and spinal alignment

Kyphosis (Increased concavity of upper spine):
-Thoracic region becomes more concave
-Results in a forward curvature of the upper spine contributing to a stooped appearance

32
Q

Estrogen and bone remodeling
(AO)

A

-Estrogen plays a crucial role in maintaining bone health, affecting the activity and lifespan of both osteoblasts and osteoclasts and is particularly significant in regulating apoptosis

-Normally, estrogen helps balance the number of osteoblasts and osteoclasts and healthy levels promote apoptosis in osteoclasts
-If apoptosis is not adequate, this leads to an increased number of active osteoclasts leading to disproportionate bone loss compared to bone formation (ie more bone is resorbed than made which results in net loss of bone density)

-This is why post menopausal women are at risk for osteoporosis

33
Q

In which patients is Scoliosis more likely to manifest?
(AO)

A

More likely to develop in people with:

-Muscular dystrophy
-Cerebral Palsy

-Would be considered a secondary complication to those diseases

34
Q

What is dystrophin?
(AO)

A

-A large protein that plays a critical role in maintaining the structural integrity of skeletal muscle fibers, acting as an anchor connecting the cytoskeleton muscle fibers to the ECM

35
Q

Becker muscular dystrophy
(P.1491)

A

-More modest mutation with residual dystrophin expression (both caused by dystrophin deficiency)
-Onset of symptoms is seen later than in Duchennes
-Have more CARDIAC manifestations in this one

36
Q

Gout
What is it
Patho
Symptoms
Diagnosis
Treatment
(P. 1460)

A

-A systemic disease of uric acid disturbance that results from deposition of monosodium urate crystals.

-Increased serum uric acid above a specific threshold leads to MSU crystal formation in and around joints, forming precipitates (deposited in connective tissue throughout body)

-Patho: crystallization in synovial fluid triggers TNF-a causing painful inflammation of the joint

-Manifestations: acute onset joint pain, (first joint involved is usually first metatarsophalangeal joint)

-diagnosis: gold standard MSU crystal identification for diagnosis,ESR, CRP, hyperuricemia

-Treatment: NSAIDS, colchicine, glucocorticoids
Maintenance: allopurinol

Advanced Patho Test 1 (20 decks)

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