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Adv Patho > Musculoskeletal System-Exam 2: Ch. 46, 46 > Flashcards

Musculoskeletal System-Exam 2: Ch. 46, 46 Flashcards

1
Q

What is an osteoblast

A
  • Bone formingcells

- Theirprimaryfunctionistolaydownnewbone.

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2
Q

What is an osteocyte

A
  • mostabundantcells inbone
  • located in lacunae spaces and in canals of the canaliculi
  • bone maintenance
  • mature bone cells
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3
Q

What is an osteoclast

A
  • *responsible for bone resorption and remodeling
  • resorbbonebysecretionofhydrochloricacid,acidproteasesandmatrix metalloproteinases(MMPs)thathelpdigestcollagen,alongwiththeactionof cytokines.
  • cells that degrade bone to initiate normal bone remodeling and mediate bone loss in pathologic conditions by increasing their resorptive activity.
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4
Q

What is bone tissue made out of

A

Bone matrix: collagen, proteoglycans and hdroxapatites, and bone cells

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5
Q

Quiescence

A

Site where cells remain dormant until the next cycle

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6
Q

Describe structure of a young, long bone

A

1: Periosteum: outer bone surface; double layered connective tissue
2. Endosteum: lines bone cavities
3. Diaphysis: shaft and compact bone
4. Epiphysis: end of the bone and cancellous bone
5. Epiphyseal plate: growth plate
6. Red Marrow: new blood cells

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7
Q

Describe the structure of a mature, long bone.

A
  1. Medullary cavity: red and yellow marrow
  2. Epiphyseal line: bone stops growing in length
  3. Periosteum: outer bone surface
  4. Endosteum: lines bone cavities
  5. Bone marrow: about 4% of adult weight; blood cells and fat (yellow marrow)
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8
Q

Describe the structure of a cortical/compact bone.

A

Haversian System

  1. haverisan cannal-central canal
  2. lamellae-concentric layers of bone matrix
  3. lacunae-the space housing the osteocytes in bones and chondrocytes in cartilage.
  4. osteocytes-to reside in lacunae; respond to mechanical strain and to send signals of bone formation or bone resorption to the bone surface, to modify their microenvironment, and to regulate both local and systemic mineral homeostasis.
  5. canaliculi- microscopic canals between the lacunae of ossified bone.
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9
Q

Explain two types of ossification.

A
  1. Intramembranous ossification-formstheflatbonesoftheskull,face,jaw,andcenterof clavicle.
  2. Endochondral ossification-anessentialprocesses during fetaldevelopment. Cartilage is present and forms most bones in the body, most long bones, and replace cartilage with bone.
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10
Q

What are the 5 bone cells

A
  1. osteoblasts
  2. osteocytes
  3. osteoclasts
  4. mesenchymal stem cell and osteochondral progenitor
  5. hematopoietic stems cells
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11
Q

Describe the role of nutrition and different hormones in bone growth.

A
  1. Vitamin D- absorbs calcium from intestines; insufficient causes rickets and osteomalacia; get from sunlight
  2. Vitamin C- necessary for collagen synthesis by
    osteoblasts; deficiency results in scurvy
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12
Q

Explain the consequences of vitamin D deficiency.

A

causes rickets and osteomalacia and bone loss

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13
Q

Differentiate the factors affecting bone resorption and formation.

A
  • menopause- associated hormonal changes
  • age related factors
  • changes in physical activity
  • drugs
  • secondary disease that lead to development of various bone d/o
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14
Q

What is spondylitis

A

Inflammatory disease

  • fibrosis, ossification, fusion of spine, sacroiliac joints due to uncontrolled bone formation
  • genetic association-HLA
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15
Q

What is osteoarthritis

A

loss and damage of weight bearing synovial joints; especially articular cartilage and joint capsule of central and peripheral joints

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16
Q

What is rheumatoid arthritis

A

autoimmune, inflammatory disease; results in joint swelling, tenderness, synovial joint destruction

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17
Q

Explain the etiology, clinical manifestations and pathophysiology of ankylosis spondylitis.

A

ETIOLOGY: reduced flexibility of spine over time and vertebrae can fuse; inflammatory disease

CLINICAL MANIFESTATION: hunched forward posture; pain in back and joints

PATHO: high association with the histocompatibility antigen human leukocyte antigen (HLA-B27). There is a misfolding of HLA-B27 in the endoplasmic reticulum which causes the misfolded proteins to accumulate. This results in a stress response by the ER and increased production of IL-23 which can act on T-helper cells.

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18
Q

Explain the etiology, clinical manifestations and pathophysiology of osteoarthritis.

A

ETIOLOGY: chronic arthropathy characterized by disruption and potential loss of joint cartilage along with joint changes, including bone hypertrophy

CLINICAL MANIFESTATION: stiffness after waking up or inactivity, joint swelling

PATHO: very little friction in the synovial joints; wear and tear; as we age we have fewer proteoglycas in cartilage; cartilage flakes and thins; loss of cartilage means bones are not protected and cysts develop and break through the joint cavity. Osteophytes grow outward and alter bone and joint anatomy. Associated with inflammation and decreased bone strength

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19
Q

Explain the etiology, clinical manifestations and pathophysiology of rheumatoid arthritis.

A

ETIOLOGY: autoimmune disease in which body attacks joints

CLINICAL MANIFESTATION: inflammation that causes the tissue that lines the inside of joints (the synovium) to thicken, resulting in swelling and pain in and around the joint

PATHO: Immune complexes produced by synovial lining cells and inflamed blood vessels. Plasma cells produce antibodies. Macrophages and lymphocytes produce pro inflammatory cytokines and chemokines. Released inflammatory mediators and various enzymes contribute to the systemic and joint manifestations.

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20
Q

What is osteoperosis

A
  • a progressive metabolic bone disease that decreases bone density (bone mass per unit volume) with deterioration of bone structure
  • main issue is that old bone is being resorbed faster than new bone being made therefore bone increasingly thin, porous, less dense
  • imbalance of osteoblast and osteoclasts
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21
Q

What factors affect osteoperosis

A
  • Primary cause: post menopausal
  • Secondary causes: sequela of other diseases, medicines, alcohol, tobacco, decreased dietary and/or absorption of calcium and vitamin D, decreased exercise, family hx, and low BMI
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22
Q

How does estrogen decrease in aging result in osteoporosis?

A
  • decrease in estrogen lead to increased ROS (oxidative stress)&raquo_space; high turnover of clasts into blasts&raquo_space; pro-inflammatory cytokines&raquo_space; decreased osteoprotegerin and insulin like growth factor
  • thus in menopause, estrogen decreases&raquo_space; increase RANKL&raquo_space; RANK&raquo_space; increased formation of clasts and decrease in clast apoptosis + estrogen needed for extracellular kinases (ERKs) to decrease apoptosis blasts and increase apoptosis clasts not balanced

**accelerates the effects of aging on bone by decreasing defense against oxidative stress (OS). Estrogen protects the adult skeleton against bone loss by slowing the rate of bone remodeling and by maintaining a focal balance between bone formation and resorption

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23
Q

Describe anatomy of skeletal muscle

A

Organization of cylindrical skeletal muscle fibers in a muscle that is attached to bones by tendons

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24
Q

How do motor neurons control muscle contraction?

A

Alpha motor neurons (also called lower motor neurons) innervate skeletal muscle and cause the muscle contractions that generate movement. Motor neurons release the neurotransmitter acetylcholine at a synapse called the neuromuscular junction.

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25
Q

Describe process of excitation-contraction coupling in skeletal muscle

A

Step 1: Action potential spread along the sarcolemma to the T-tubules (transverse tubules)
Step 2: Calcium is released into the sarcoplasmic reticulum (S.R.)
Step 3: Calcium binds to actin and the blocking action of the tropomyosin is removed
Step 4: Myosin heads attach to begin contraction
Step 5: Calcium is removed and the binding sites on actin become blocked again by tropomyosin
Step 6: muscle relaxes

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26
Q

Identify the striated muscle cell proteins in muscular dystrophy

A

Dystrophin-glycoprotein complex (DGC)

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27
Q

Describe the etiology, manifestations and pathology of Duchene Muscular dystrophy.

A

ETIOLOGY: An inherited disorder of progressive muscular weakness, typically in boys.

CLINICAL MANIFESTATION:falling, difficulty rising, waddling, muscle enlargement, CK blood levels; progressive and can lead to respiratory and cardiac defects; mostly males; x linked inheritance; onset age 2-6

PATHO: mutations in dystrophin; early myonecrosis which triggers inflammation. Which leads to fibrosis that permeates muscle and causes stiffness and contractures, major cause of disability in DMD. Lost muscle is replaced by fat.

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28
Q

Differentiate the severity in DMD, BMD and LGMD.

A

DMD (Duchenne MD)-mutation in dystrophin

BMD (Becker MD)- less severed than DMD

LGMD (limb-girdle MD)-mutation in sarcoglycoprotein; progressive weakness from hips moving to shoulders; onset in adolescence or early adulthood

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29
Q

Define sacropenia

A

is a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength and it is strictly correlated with physical disability, poor quality of life and death. Risk factors for sarcopenia include age, gender and level of physical activity.

30
Q

Describe the factors contributing to and the pathophysiology of sarcopenia.

A

age related changes: central and peripheral nervous system innervations, hormonal status, inflammatory effects, caloric and protein intake

31
Q

Explain how to reverse sarcopenia.

A
  • resistance exercise
  • nutritional interventions
  • pharmacological interventions
  • combination of above
32
Q

Summarize the effects of aging on the musculoskeletal system.

A
  1. bone matrix decreases
  2. bone mass decreases
  3. increased bone fractures
  4. bone loss causes deformity, loss of height, pain, and stiffness (stooped postures, loss of teeth, occurs in both sexes)
  5. some prednisone risk factors (alcohol, menopause/andropause, smoking, steroids)
33
Q

What are the 5 bone cells

A
  1. osteoblasts
  2. osteocytes
  3. osteoclasts
  4. mesenchymal stem cell and osteochondral progenitor-become osteoblast
  5. hematopoietic stems cells-become osteoclast
34
Q

What is rahabdomyolysis

A

the presence of large amounts of muscle protein (myoglobin) in the urine. It usually occurs after major muscle trauma, especially a muscle crush injury. Long distance running, certain severe infections, and exposure to electrical shock can cause extensive muscle damage and excessive release of myoglobin. Rhabdo may cause renal failure if they myoglobin gets trapped in the delicate capillaries or tubules of the kidney, interfering with renal blood flow.

35
Q

What is dsytrophin

A

protein needed to anchor actin in cytoskeleton to basement membrane of skeletal muscle fibers. Absence of dsytrophin results in poorly anchored fibers torn apart due to muscle contraction which leads to calcium entering cells which leads to cell death, fiber necrosis and degeneration of muscle

36
Q

Treatment for MD

A
  1. gene therapy: to deliver coding regions of the gene encoding dystrophin using specialized delivery vehicles (vectors)
  2. stem cell research: multiple stem cell populations, both of adult or embryonic origin, or fresh isolation satellite cells
37
Q

What are the 5 phases of bone remodeling

A
  1. activation
  2. resorption
  3. reversal
  4. formation
  5. Queisence
38
Q

What happens in activation during bone remodeling?

A
  1. Pre-osteclasts are attracted to the remodeling sites

2. Pre-osteoclasts fuse to form multinuclateated osteoclasts

39
Q

What happens in resorption during bone remodeling?

A
  1. Osteoclasts dig out a cavity, called a resorption pit, in spongy bone or burrow a tunnel in compact bone
  2. calcium can be released into the blood for use in various body functions
  3. osteoclasts disappear
40
Q

What happens in reversal during bone remodeling?

A
  1. mesnchymal stem cells, pre-cursors to osteoblasts, appear along the burrow or pit where they..
  2. proliferate and differentiate into pre-osteoblasts, then.
41
Q

What happens in formation during bone remodeling?

A
  1. pre-osteoblasts mature into osteoblasts at the surface of the burrow or pit and
  2. release osteoid at the site, forming a new soft non-mineralized matrix
42
Q

What happens in quiesecence during bond remodeling?

A
  1. site, with reseting, lining cells, remain dormant until the next cycle
43
Q

Threshold potential voltage

A

-55 mv opens activation gate which allows more sodium to come and causing cell to become more positive

44
Q

Resting voltage

A

-90mv

45
Q

Peak voltage point

A

+30mv; depolarization which produces the action potential

46
Q

Inactivation gate

A

when peak potential is reach (+30m) and close the sodium channel so no more sodium can come in

47
Q

depolarization

A

produces action potential

flow of positive charges due to sodium ions moving across cell membrane

48
Q

transverse tubule or T tubule

A

invagination of sarcolemma

49
Q

sarcolemma

A

plasma membrane of the muscle cell

50
Q

dihydropyridine receptor

A

located on membrane of t tubule; pulls on to ryanodine receptor to allow calcium ions open up and allows calcium out

51
Q

sarcoplasmic reticulum

A

rich in calcium; tubes that surround t tubules

52
Q

triad

A

2 sacroplasmic reticulums and T tubule

53
Q

what does calcium bind to

A

troponin

54
Q

potassium ion efflux

A
  • repolarization

- potassium leaves the cell until it reaches its equilibrium which is -90mv aka the resting membrane potential

55
Q

sodium ion influx

A
  • depolarization

- cells becoming more positive as sodium keeps coming in

56
Q

Atrophy

A

decrease in size of cell or tissue. Muscle atrophy may results from muscle disuse or severing of the nerve supplying the muscle. With muscular atrophy, the size and the myofibrils is reduce. Although bones do not atrophy, bone density can decrease with disuse or metabolic deficiencies or disease

57
Q

Strain

A

trauma to a muscle or tendon, usually occurring when the muscle or tendon is stretched beyond its normal limit. Strains may involve tissue tears or ruptures. Inflammation occurs with injury to muscles or tendons, leading to pain and swelling of tissue. Healing may take several weeks.

58
Q

Osteoid

A

nonmineralized bone matrix

59
Q

What happens if mineral (hydroxyapatite) is removed?

A

bone is too flexible

60
Q

What happens if collagen in removed

A

bone is too brittle

61
Q

Osteogenesis Imperfecta

A

is caused by defective genes. These genes affect how the body makes collagen, a protein that helps strengthen bones.The condition can be mild, with only a few fractures during a person’s lifetime. In more severe cases, it can involve hundreds of fractures that occur without any apparent cause.

62
Q

Where can you get vit D2 and vit D3

A

vit D2-plants
vit D3-animal based food and UV light

vit D3>vit D2

63
Q

Disorders of bone remodeling:

A
  • Osteoporosis
  • Primary Menopause associated
  • Age related
Secondary:
Glucocorticoid induced 
Immobilization induced 
Renal osteodystrophy 
Rickets
64
Q

What type of joints are affected in OA?

A

synovial

65
Q

Who are affected more by RA?

A

women

66
Q

What part of the bone becomes thinner in osteoperosis?

A

cortical bone

67
Q

What is a side effect of steroids on bones?

A

lead to bone loss, osteoporosis, and broken bones because they have an effect on Vit D and bone

68
Q

What bones does osteoporosis affect the most as we age?

A

spine, femoral neck in both men and women

69
Q

Cause of secondary osteoporosis in men

A

steroids, immunosuppressive drugs, low testosterone, smoking, alcohol, COPD/asthma, GI disease, RA, immobilization, thyrotoxicosis

70
Q

Factors affecting bone growth:

A
  1. nutrition
    - vit D: important for calcium absorption in intestines
    - vit C: important for collagen synthesis by osteoblasts; deficiency results in scurvy
  2. hormones
    - growth hormone from anterior pituitary
    - thyroid hormone required for growth of all tissues
    - sex hormones as estrogen and testosterone

Adv Patho (23 decks)

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