Lecture Exam 2

Secreted by the parathyroid gland

• Released when calcium level in blood is low (hypocalcemia)

  1. Stimulates osteoclasts to reabsorb bones

• This releases calcium into the circulation

2. Increases absorption of calcium into small intestine

• By promoting the activation of vitamin D in the kidney

3. Increases Ca2+ reabsorption in kidney

Reject, the thyroid gland is not directly involved

Accept

Reject, the target of PTH is osteoclasts

• PTH can speed up/slow down osteoclasts

Accept

Secreted by parafollicular cells of thyroid gland during hypercalcemia

When calcium levels in the blood excessive (hypercalcemia)

• But only when above 20%

• Affects are short-lived, rapid

• Inhibits osteoclasts and thus acts to accelerate bone deposition

Reject, calcitonin does not have an important role in homeostasis

Reject, calcium is homeostatically regulated, but bone metabolism is not

Accept

Generally between ages 25-35

Disease where bone resorption is greater than bone deposition to the point that bones become porous and lighter

“Pediatric disease with adult consequences”

• Normal composition, bone mass reduced

• Asymptomatic - x-rays are unable to pick up until 30-50% of bone mineral is lost

• Often undiagnosed until far advanced

• If current trends persist, 1 in every 2 American women will have postmenopausal osteoporosis

Accept

The osteoclasts

Parathyroid glands

Age 20

95%

-Leads to compression fractures in the vertebrae

Not breaking the “hip bone” - actually the femoral neck (which is 45% trabecular bone)

• Very dangerous - ¼ of people will die within 1 year of hip fractures

• Dietary calcium - raw material for making bone from osteoblast activity and vitamin D so that it can be absorbed

1000-1200 mg

500 IEUs

About 300 mg

Stress on the body → increases osteoblast activity → increases osteoid → building hydropaxities

Estrogen/testosterone restrain osteoclast activity (osteoclast inhibitors)

When menopause sets in → SHARP decline - hardly any/no estrogen is being produced

Decline is much less dramatic - steady decline throughout life

• As a result, most men do not show osteoporosis before age 60

Yes, but a ciliated source - the body can’t absorb it well - need 16 cups of broccoli per day

Accept

Only when 30-50% of bone mineral is already lost

Reject, it is asymptomatic and often doesn’t show up on an x-ray

Accept

Absence of menstrual period

12-15%

Not producing enough estrogen - estrogen is very low

Women 16-24 who have amenorrhea are already losing bone mass, and can have osteoporosis in their 20s!

Beneficial - some methods increase both estrogen/progesterone levels

• Some just progesterone - which can be problematic because it contributes to destroying the skeletal system

During menstruation

Smoking - contains several harmful chemicals that accelerate bone loss (like cadmium)

• Smoking causes a decline in estrogen and an increase in testosterone (deeper, raspy voice)

Causes calcium loss through the urine

Causes calcium leaching from the bones

Bone tissue formation

1. Intramembranous ossification

2. Endochondral (“in cartilage”)

Both occur after 8 weeks

Accept

Reject, cartilage and fibrous membranes are replaced by bone

Before 8 weeks

Skull, some facial bones (like the mandible), hyoid, and clavicle (all considered flat/irregular bones), but no long bones

Bone develops from a fibrous CT - producing membranous bones

1. Some fibrous CT cells become osteoblasts → forming an ossification center

2. Osteoblasts initiate formation of osteoid → mineralizes within a few days

3. Trapped osteoblasts become osteocytes

4. Other structural development occurs → formation of trabeculae (little beans) → spongy/compact bone, blood vessel network, bone marrow, periosteum

Bones that develop in unusual places

• Physical/chemical events can stimulate the development of osteoblasts in normal CT

Type of heterotropic bone

Deposition of bone around skeletal muscle

• Unknown trigger/cause

Bone growth outside of the skeletal system

• Can also be congenital (present at birth)

Hyaline cartilage is used for a model for bone construction - produces cartilage bones (that is broken down as ossification continues)

• Forms all other bones in the body

• At the site of bone formation, CT cells crowd together in the shape of the future bone

• These “Mesenchymal cells” develop into chondroblasts → to make a cartilage matrix

• This produces cartilage that continues to grow in length and thickness

Cartilage cells under the periosteum (surface of bone) specialize into osteoblasts

• Bone collar forms around the shaft (diaphysis) - encasing the cartilage

• Bone collar doesn’t start the process, it supports the process

Within the shaft, cartilage cells enlarge

• pH changes signal calcification (hardening) of the matrix

• Other chondrocytes are trapped and die - forming cavities

• But cartilage model is stabilized by bone collar

Periosteal bud invades the forming cavities in the 3rd month

• Osteoclasts erode the calcified cartilage

• Osteoblasts secrete osteoid

• Osteoid → produces bone covered cartilage trabeculae

Collection of vessels, nerve fibers, lymphatic, red marrow, osteoclasts, osteoblasts

Osteoclast break down new spongy bone → leads to formation of the medullary cavity

• Shortly before birth, secondary ossification centers appear in the epiphyses (ends of bone)

Next, the same process occurs in the epiphysis - except osteoclasts do not break down the new spongy bone

• Hence, no medullary cavity is formed

1. On the ends of bones where a junction/articulation is present with another bone (articular cartilage)

2. Between diaphysis and epiphysis (epiphyseal plates/growth plates)

Growth in the length of long bones

• Similar process to endochondral ossification

• Occurs at epiphyseal plate

Human growth hormone (hGH)

• Secreted from the anterior pituitary during infancy and childhood

Increase in testosterone and estrogen - provide for a “growth spurt”

• However, high levels of testosterone and estrogen later induce closure of epiphyseal plate (age 18 for women, age 21 for men)

• Growth occurs in thickness, especially to stress

Microscopic areas of bone are continuously broken down, reabsorbed, and then the area is reconstructed

How: Through “remodeling units” of adjacent osteoclasts/osteoblasts

Where: At periosteal/endosteal surfaces (both external and internal surfaces of the bone - internal = trabeculae, medullary cavity, volkmans canal)

Reject, bone remodeling is not uniform - some areas are replaced much more frequently than others

• Ex: distal end of the femur is replaced more than 2x per year!

Occurs at sites of high stress - not always good

• Rate of deposition increases where a bone is injured

• Ex: Plantar fascia - inflammation = bone spur growth = pain

Throughout the lifetime of an individual

• Rate of deposition increases when bone is injured - stress is placed on bone (weight-bearing exercise)

• Rate of resorption increases when bones are not stressed - (astronauts, atrophied bones of bedridden people)

• Bones will grow in circumference

• Where? From muscles pull on them - large, bony projections - occurs where heavy, active muscles attach

In response to mechanical and gravitational forces

• To maintain Ca2+ homeostasis in extracellular fluid

Giantism (hyper-hGH)

Dwarfism (hypo-hGH)

• Only effects epiphyseal plates of long bone - do not respond normally to hGH

• Head/torso are regular size, but limbs are shortened

Acromegaly

• Enlargement of bones, giantism, hands, tongue, oily skin (extra sebaceous glands), secondary diabetes, sleep apnea

Sending an electrical signal to something

Found in blood vessels, small/large intestines, walls of hollow organs

Very slow, but can be sustained

Ex: BP in blood vessels - continous process

Reject, cardiac muscle is only found in the heart

Smooth - expansion is not under conscious control

Skeletal - under voluntary contraction of muscle

Skeletal - conscious workload

Smooth

Smooth - not under voluntary control

Skeletal

Found only in the walls of the heart

Slow/moderate, steady rate

Under conscious control - skeletal muscle

Not under conscious control - smooth muscle, cardiac muscle

Obvious striations, multinucleate cells, long

Branching, striated, generally uninucleate cells, intercalated disks

Elongated cells, no striations, cells are arranged closely to form sheets

R, a signal causes contraction, but there is no signal that causes relaxation (lack of signal)

autonomic nervous system

Involuntary

• Has parasympathetic/sympathetic divisions

• Deals with cardiac and smooth muscle

• Conducts impulses from the CNS → muscles

Mobilizes the body systems during activity - speeding up

• “Fight or flight" response

• Sends excitatory signals → causes contraction

• Conserves energy - slows down

• Promotes functions during rest

• “Breed and feed”

• Sends inhibitory signals → inhibits contraction, maintains relaxation

• Voluntary control

• Deals with skeletal muscles

• Conducts impulses from CNS → skeletal muscles

Slow to fast

• Can contract rapidly

• Can exert tremendous power

• But tires/fails easily - must rest after activity

• Only involves one type of nerve fiber

• Nerve impulse = contraction, no nerve impulse = relaxation

Accept

“epi = covering”, “my” = muscle

Covering of dense irregular CT around a whole muscle

Direct, fleshy attachments

Indirect - all CT wrappings extend beyond muscle as a:

• Rope-like attachment

• Tough

• Can cross over rough bony projections - preventing wear/tear

Indirect - sheet like covering

1. Tendons

2. Aponeurosis