Lecture Exam 2

Parathyroid hormone (PTH)

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

A or R: The thyroid gland is directly involved in the parathyroid gland

Reject, the thyroid gland is not directly involved

A or R: PTH is the most important hormone in bone metabolism

Accept

Accept or R: The target of the PTH is the osteoblasts/osteoids

Reject, the target of PTH is osteoclasts

• PTH can speed up/slow down osteoclasts

A or R: Parathyroid activates vitamin D to become vitamin D3, used in small intestine

Accept

Calcitonin

Secreted by parafollicular cells of thyroid gland during hypercalcemia

When is calcitonin released?

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

A or R: Calcitonin has an important role in Ca2+ homeostasis?

Reject, calcitonin does not have an important role in homeostasis

A or R: Bone metabolism is homeostatically regulated

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

A or R: PTH is an efferent pathway

Accept

When is peak bone mass?

Generally between ages 25-35

Osteoporosis

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

Characteristics of osteoporosis

“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

A or R: All people will have normal bone mass loss throughout life. However, this is 27% higher for a woman

Accept

What is the affector in the PTH?

The osteoclasts

What is the effector in the PTH pathway?

Parathyroid glands

What age does trabecular bone loss begin?

Age 20

How much of the vertebral bodies are composed of trabecular bone?

95%

-Leads to compression fractures in the vertebrae

Hip fracture

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

What is most important for prevention of osteoporosis while still in peak bone mass area?

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

How much calcium do you need per day?

1000-1200 mg

How much vitamin D do you need per day?

500 IEUs

How much calcium is in 1 8 ounce cup milk?

About 300 mg

What is the benefit of exercise for preventing osteoporosis?

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

What is also important for prevention of osteoporosis during peak bone mass?

Estrogen/testosterone restrain osteoclast activity (osteoclast inhibitors)

Estrogen production thoughout life

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

Testosterone progression throughout life

Decline is much less dramatic - steady decline throughout life

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

Is broccoli a source of calcium?

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

A or R: 1 in every 2 American women will have postmenopausal osteoporosis

Accept

When are x-rays able to pick up on bone loss?

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

A or R: Osteoporosis is symptomatic

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

A or R: With osteoporosis, the bone mass is reduced by the composition of bone is normal

Accept

Amenorrhea

Absence of menstrual period

% of body fat when cycling/menstruation stops

12-15%

Side effects of amenorrhea

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!

Birth control - role in prevention of osteoporosis caused by lack of estrogen

Beneficial - some methods increase both estrogen/progesterone levels

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

When do peak estrogen levels occur?

During menstruation

Impact of smoking on bones

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)

Impact of excessive protein intake on bones

Causes calcium loss through the urine

Impact of sodium chloride (salt) on the bones

Causes calcium leaching from the bones

Ossification

Bone tissue formation

Two types of ossification

1. Intramembranous ossification

2. Endochondral (“in cartilage”)

Both occur after 8 weeks

A or R: Most of the human skeleton is initially made up of cartilage and fibrous membranes

Accept

A or R: Cartilage and fibrous membranes become bone

Reject, cartilage and fibrous membranes are replaced by bone

How long is an embryo’s skeleton composed of fibrous membranes and cartilage?

Before 8 weeks

What does intramembranous ossification form?

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

Intramembranous ossification

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

Heterotropic bones

Bones that develop in unusual places

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

Myositis ossifications

Type of heterotropic bone

Deposition of bone around skeletal muscle

• Unknown trigger/cause

Fibrodysplasia ossificans progressiva

Bone growth outside of the skeletal system

• Can also be congenital (present at birth)

Endochondral Ossification

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

Stage 1 (EO)

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

Stage 2 (EO)

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

Stage 3 (EO)

Periosteal bud invades the forming cavities in the 3rd month

• Osteoclasts erode the calcified cartilage

• Osteoblasts secrete osteoid

• Osteoid → produces bone covered cartilage trabeculae

Periosteal bud

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

Stage 4 (EO)

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)

Stage 5 (EO)

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

• Hence, no medullary cavity is formed

Where does hyaline cartilage remain at the end of ossification?

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)

Bone growth AFTER birth

Growth in the length of long bones

• Similar process to endochondral ossification

• Occurs at epiphyseal plate

Most important and major influence on bone growth after birth

Human growth hormone (hGH)

• Secreted from the anterior pituitary during infancy and childhood

Secondary influence on bone growth after birth

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

Bone Remodeling

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)

A or R: Bone remodeling is uniform

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!

Extra bone growth

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

When does bone remodeling take place?

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

Why does bone remodeling occur?

In response to mechanical and gravitational forces

• To maintain Ca2+ homeostasis in extracellular fluid

What is the result of abnormally high secretion of hGH before puberty?

Giantism (hyper-hGH)

What is the result of abnormally low secretion of hGH before puberty?

Dwarfism (hypo-hGH)

Achondroplastic (genetic dwarfism)

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

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

What is the result of hypersecretion of hGH that just occurred after puberty?

Acromegaly

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

Innervation

Sending an electrical signal to something

Smooth muscle location

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

Smooth muscle contractions

Very slow, but can be sustained

Ex: BP in blood vessels - continous process

A or R: Cardiac muscle is found in the blood vessels

Reject, cardiac muscle is only found in the heart

Tissue type in wall of urinary bladder

Smooth - expansion is not under conscious control

Tissue type in the wall of the opening out of the urinary bladder

Skeletal - under voluntary contraction of muscle

Tissue type in the body of biceps brachii

Skeletal - conscious workload

Tissue type in the wall of a large artery in biceps brachii

Smooth

Tissue type in the iris of the eye (opens/closes the pupil)

Smooth - not under voluntary control

Tissue type in the diaphragm (muscle in breathing):

Skeletal

Cardiac muscle location

Found only in the walls of the heart

Cardiac muscle contraction

Slow/moderate, steady rate

Voluntary muscles

Under conscious control - skeletal muscle

Involuntary muscle

Not under conscious control - smooth muscle, cardiac muscle

Characteristics of skeletal muscle

Obvious striations, multinucleate cells, long

Characteristics of cardiac muscle

Branching, striated, generally uninucleate cells, intercalated disks

Characteristics of smooth muscle

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

A or R: For skeletal muscle, a signal causes both contraction and relaxation

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

Both smooth and cardiac muscle are innervated (motor control) by the ________

autonomic nervous system

Autonomic nervous system (ANS)

Involuntary

• Has parasympathetic/sympathetic divisions

• Deals with cardiac and smooth muscle

• Conducts impulses from the CNS → muscles

Sympathetic divison

Mobilizes the body systems during activity - speeding up

• “Fight or flight" response

• Sends excitatory signals → causes contraction

Parasympathetic division

• Conserves energy - slows down

• Promotes functions during rest

• “Breed and feed”

• Sends inhibitory signals → inhibits contraction, maintains relaxation

Somatic nervous system

• Voluntary control

• Deals with skeletal muscles

• Conducts impulses from CNS → skeletal muscles

Skeletal muscle contraction

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

A or R: Each skeletal muscle is an organ

Accept

Epimysium

“epi = covering”, “my” = muscle

Covering of dense irregular CT around a whole muscle

Epimysium fused to periosteum

Direct, fleshy attachments

Tendons

Indirect - all CT wrappings extend beyond muscle as a:

• Rope-like attachment

• Tough

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

Aponerosis

Indirect - sheet like covering

Indirect attachment

1. Tendons

2. Aponeurosis