Physio Exam II

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You just got a job with Bones-Are-Us, a major biotech firm. And, you have been assigned to work on a tissue engineering therapy for bone. Your therapy must take into consideration the critical components for any generalized tissue engineered therapy. Select two and BRIEFLY describe your therapy based on them.

Answers will vary widely but each should discuss two of the following: Cells, Extracellular Matrix Hormones, Angiogenesis. Examples include using a fibrin foam scaffold which contains adult bone marrow mesenchymal cells or BMP-2 to promote osteogenesis of host invading cells. You answer must state one of the four components AND site an example application.

Compare antagonism, additive effects, synergism, and permissiveness as they relate to hormone interactions

Compare antagonism, additive effects, synergism, and permissiveness as they relate to hormone interactions. Now, as an example, give me an example from the central nervous system where hormones can be antagonistic.

Antagonism is when one hormone inhibits the action of another hormone. An Additive effect is when the positive effect of two or more individual hormones is equal to the sum of their individual effects. A synergism effect is when the positive effect of two or more individual hormones exceed the sum of their individual effects. Permissiveness is the interaction between hormones such that a hormone has no stimulatory or inhibitory effect upon its own but in some what prepares cells to receive another hormone or hormones with a greater response then without this "pretreatment." Antagonistic hormones with the central nervous system can involve interactions and feedback for the hypothalamus and/or anterior pituitary; by example hypothalamus derived GHRH and somatostatin have antagonistic effects on GH secretion from the anterior pituitary. Another example is GH or other anterior pituitary hormones have an antagonistic effect upon subsequent hypothalamus hormone secretion.

Differentiate between the anterior and posterior pituitary in regard to the hypothalamus regulation of hormonal secretion. Also, provide one example of a hormone from each pituitary lobe.

Anterior pituitary synthesizes and releases hormones via positive and negative regulation from hormones released from hypothalamus which travel to anterior pituitary via blood. Posterior pituitary serves as a depot for release of hypothalamus synthesized hormones Anterior- GH, FSH, LH, TSH, ACTH, prolactin Posterior- Oxytocin, ADH

Differentiate between the anterior and posterior pituitary in regard to the hypothalamus regulation of hormonal secretion. Also, provide one example of a hormone from each pituitary lobe.

Differentiate between a BRU for cancellous and cortical bone. Oh, don't forget to define BRU. Hold on there, you are not done. First, what is the most important regulator of BRUs? AND, how do osteoblasts, osteoclasts and YES, osteocytes fit into this?

BRU (bone structural unit) represents the end result of a remodeling cycle- cortical bone- a haversian system or cortical osteon [advancing tunnel with a "cutting cone" or resorption and a " closing cone" of forming new bone. Cancellous bone- a wall or packet of bone or trabecular osteon, resorbs and forms bone in a disk-like semilunar structure on the surface of trabeculae Frequency Osteblasts- build bone so, lay down osteoid following the removal of "old bone" by osteoclasts. Osteocytes since mechanical forces being applied to bone so therefore can regulate BRU frequency.

Rigor mortis is the phenomenon that occurs after death whereby an individual's muscles become fully contracted or "stiff." Based on your extensive familiarity with how muscle contraction works please explain this phenomenon. Hint: Once your dead your cells no longer can generate new ATP.

Because ATP is required to pump calcium into the sarcoplasmic reticulum (SR), calcium will diffuse into the sarcoplasm (cytoplasm of the myofiber) and not be returned to the SR. The increased intracellular calcium levels will causes troponin to pull tropomyosin off the myosin binding sites on actin. This will allow crossbidge cycling to occur. The crossbridges will have been "energized" by the splitting of the last intact APT molecules insid the cell. Each energized crossbridge will undergo one last powerstroke. The resulting force production is what causes the muscles to "stiffen." The crossbridges cannot detach from actin without additional intact ATP molecules. Because the supply of ATP is depleted, the muscles remain in the contracted state.

Harry's glucocorticoid levels are very elevated. His blood ACTH and glucocorticoid binding protein levels are normal. He also has abnormally elevated epinephrine levels. He is a little stressed right now. What is his likely problem?

Because his ACTH is normal his anterior pituitary and hypothalamus are functioning normally. Because the binding proteins are normal the problem is not with clearance. The elevated epinephrine levels suggest the adrenal medulla is putting out too much epinephrine, although the hypothalamus is likely normal. As both medulla and cortex (source of glucocorticoids) are putting out too much or their respective hormones there may be a tumor in the adrenal glands affecting both.

Gary is 13, suffered a bad infection and following routine follow up physical exam, underwent a glucose tolerance test and found his glucose levels greatly elevated compared to normal. Not knowing any other diagnostics outline the possible pathology(s) he may be suffering from. What would be the next set of diagnostics to perform? Treatment?

He may have Type 1 (insulin dependent diabetes mellitus- IDDM, or juvenile onset diabetes. This means his pancreatic beta islet cells may have been destroyed resulting in no insulin production. Test for blood insulin to confirm. He could also be suffering from Type II or non-insulin-dependent diabetes mellitus- NIDDM or mature onset diabetes. If his blood insulin levels are more or less normal AND he is extremely overweight he may be suffering from Type II which results from unresponsive insulin-receptors due to the constant overload to his glucose regulatory system. For Type I insulin administration. For Type II diet and exercise.

Mildred the ostrich was fabled for her sprinting skills. She laughed at the lumbering slow butsteady running gate of Herriot the hippopotamus. Mildred challenged Herriot to a race. Herriot quickly agreed but insisted on a marathon race across 20 miles of the Serengeti Plain. Chuck the Lion was asked to judge the race and for his troubles he would get to eat the loser. Who did Chuck get to eat? Relate your answer to peak activity levels during the Marathon race, muscle fibers, anaerobic threshold & ATP.

Chuck ate Mildred. Because Mildred is a sprinter, she has predominately fast glycolytic fibers. These "white fibers" are capable of rapidly producing large amounts of tension, but only for short duration because of their dependence on glycolysis for energy (ATP) production. Harry therefore was the early leader in this long distance Marathon, but because ATP production via glycolysis could not keep up with ATP demands. Therefore she rapidly exceeded anaerobic threshold. He was forced to rest for relatively long periods to build up her glycolysis ATP stores. Herriot on the other hand has predominately slow oxidative fibers. These "red fibers" are found in muscles specializing in maintaining low-intensity contractions for long periods of time without fatigue. These fibers enabled Herriot's endurance because her energy demands did not exceed his anaerobic threshold, therefore insuring her of sufficient ATP for the slow pace she used during the race.

Differentiate between direct and indirect bone formation? Which is critical for long bone growth?

Indirect bone formation requires the formation of cartilage, its mineralization and replacement with bone, thus secondary or indirect. Direct bone formation does not include cartilage as an intermediary. Indirect bone formation is critical for long bone growth thus the primary determinate for overall growth.

A scientist studying the limitations to maximum running speed in humans, states that her hypothesis is as follows: Maximum running speed is limited by the on-off timing of the muscles involved. More specifically, maximum running speed is limited by the time taken to deactivate the muscle cells used to produce movements of the limbs. Using your knowledge of muscle physiology, state by this is a reasonable hypothesis?

Looking at an individual muscle twitch, the time then for relaxation is a least two times the length of the period of contraction. Contraction occurs more quickly than relaxation because diffusion of calcium form the SR into the sarcoplasm is very rapid, whereas the active transport of calcium back into the SR is much slower. Therefore, the ability of a muscle cell to complete a contraction is limited by the time it takes to completely relax the muscle before the next contraction occurs.

Describe the interplay between erosion rate, matrix apposition rate and mineral apposition rate during bone remodeling. AND, how this interplay is affected when say as a result of a tumor in the anterior pituitary substantially increasing TSH secretion.

Erosion rate occurs during bone erosion and is driven by osteoclast resorption. Erosion precedes formation. Matrix and mineral apposition rates occur during bone formation. Matrix apposition rate is driven by osteoid secretion by osteoblasts, whereas mineralization rate occurs AFTER matrix apposition and not via osteoblast secretion. With an anterior pituitary tumor with increased TSH an increase in thyroid hormone production by the thyroid gland results. This results in hyperthyroidism with an increase in metabolic activity. This increases rates of all processes, erosion rate, matrix and mineral apposition rates. Whereas overall the extent of erosion is relatively unchanged the matrix deposited and subsequent mineralization is decreased. This is because matrix deposition and subsequent mineralization take time which is not allowed during increased metabolic activity.

Why does muscle fatigue occur?

Exceed anaerobic threshold

One theory states that maximum running speed is limited by the time taken to deactivate the muscle cells used to produce movements of the limbs. Using your knowledge of muscle physiology, state why this is a reasonable hypothesis.

Looking back at an individual muscle twitch, we see that the time taken for relaxation is at least two times the length of the period of contraction. Contraction occurs more quickly than relaxation because diffusion of calcium from the SR into the sarcoplasm is very rapid, whereas the active transport of calcium back into the SR is a much slower process. Therefore, the ability of a muscle cell to complete a contraction is limited by the time it takes to completely relax the muscle before the next contraction occurs.

Your are asked to mediate a disagreement between two of your friends. One says that muscle contraction rate is the primary limiting factor which determines running speed. The other says that is not. Who is correct and why? Don't worry about being diplomatic here.

Would you expect the concentration of ACTHRH in a systemic venous blood sample to be higher, lower, or the same as the concentration ACTHRH in a sample of hypothalamic-hypophyseal portal blood? Why?

Lower, much lower. Because ACTHRH are meant for "local" between the hypothalamus and anterior pituitary therefore in the circulation beyond the hypothalamic-hypophyseal portal blood compartment they would become rapidly diluted in the large blood volume.

Takeo goes to his physician for a checkup prior to starting his freshman year at University. He is diagnosed with very elevated blood sugar. It has nothing (not directly anyway) to do with the 2 dozen Krispy Kreme donuts he had for breakfast hours ago. Not knowing anything else about Takeo please suggest possible problem(s) and how you would diagnose, discuss all possible data involved.

He has insulin dependent diabetes mellitus or type I diabetes. Check his blood insulin level if low despite high glucose this would suggest this disease. He has type two or insulin independent diabetes. If his blood insulin level is high along with the high glucose this would suggest this disease. This is not typically disease of the young. Also check to see if he has a history of obesity during his childhood.

Would you expect the concentration of FSHRH in a systemic venous blood sample to be higher, lower, or the same as the concentration FSHRH in a sample of hypothalamic-hypophyseal portal blood? Why?

Lower, much lower. Because FSHRH are meant for "local" between the hypothalamus and anterior pituitary therefore in the circulation beyond the hypothalamic-hypophyseal portal blood compartment they would become rapidly diluted in the large blood volume.

Would you expect the concentration of TSHRH in a systemic venous blood sample to be higher, lower, or the same as the concentration TSHRH in a sample of hypothalamic-hypophyseal portal blood? Why?

Lower, much lower. Because TSHRH are meant for "local" between the hypothalamus and anterior pituitary therefore in the circulation beyond the hypothalamic-hypophyseal portal blood compartment they would become rapidly diluted in the large blood volume.

Margie falls and breaks her right femur. She was just walking and tripped on a piece of cracked cement, a fracture would not have occurred under normal circumstances. Not knowing anything else about Margie please provide two theories (based on age) you would consider looking into to explain why she fractured her femur.

Margie is over 50, post-menopausal and suffering from osteoporosis that has resulted in weakened bone. Margie is under 50 and not suffering from osteoporosis but from some Ca metabolic bone disorder that resulted in weakened bone OR bone remodeling is out of balance due to over working osteoclasts and/or underworking osteoblasts possibly due to drastic increase in activation frequency.

How does signaling to muscle change as load resistance is increased? Will this always result in change in muscle length?

Motor unit recruitment is increased....the size principle. More larger units are recruited as load increases. However if resistance exceeds tensile force developed then muscle cannot shorten.

Describe how oxidative muscle fibers differ from glycolytic fibers, and explain how each of these factors relates to the ability of a fiber to resist fatigue.

Oxidative fibers are smaller in diameter, have more myoglobin, less sarcoplasmic reticulum, fewer glycolytic enzymes, more mitochondria, and a greater capillary density than glycolytic fibers. This enables them to be much more resistant to fatigue than glycolytic fibers because they have a greater supply of oxygen (increased capillary) and fuel to the cells, as well as a greater ability to use cellular respiration (more mitochondria) as opposed to glycolysis (fewer glycolytic enzymes) as their primary metabolic pathway. This decrease the amount of lactic acid produced. Lactic acid accumulations associated with development of fatigue by a muscle cell.

Osteoporosis can occur in men although it is most prevalent in women. For each of the physiological conditions below, what will be the likely affect upon bone loss? Your answer will be either positive, negative or no effect. (in other words if the condition increases bone loss it is positive) Pharmacological delivery of calcitonin Staying inside and not consuming any dietary supplements for Vit D3 Balanced exercise regimen Estrogen therapy increase in soda consumption surgical removal of parathyroid gland

Pharmacological delivery of calcitonin negative Staying inside and not consuming any dietary supplements for Vit D3 positive Balanced exercise regimen negative Estrogen therapy negative Increase in soda pop consumption no effect Surgical removal of the parathyroid gland negative

Jennifer is 30 years old and has abnormally low estrogen levels. Her hypothalamus, anterior pituitary and ovaries are functioning normally representing normal estrogen production for her age. What is a likely explanation for her condition?

She likely has abnormally low estrogen binding proteins in the blood. Because estrogen is a steroid hormone it is transported in the blood via specific binding proteins. If those proteins are diminished for whatever reason that means that estrogen will be cleared much more rapidly than normal. Since estrogen production is normal the increased clearance rate will mean a reduction in blood estrogen.

Define the sliding filament model of muscle contraction. Use words and/or diagrams. In your answer CLEARLY state whether the Z disc, I band, H zone, and A band change in length during contraction. Make sure you define the interactions between the two primary responsible filaments.

Sliding filament model is based on the contraction of sarcomeres within myofibrils via the sliding of actin filaments across myosin filaments thus shortening sarcomeric length. A sarcomere contracts when myosin heads bind to specific sites on actin resulting in the actin filament sliding along the myosin filament toward the M-line or center of the sarcomere. When a sarcomere shortens- The A band represents the myosin filament and does not change in length. The H zone represents the distance between actin filaments within a sarcomere and gets shorter as the actin filaments in the same plane get closer. The I band represents the distance between myosin filaments between two sarcomeres and gets shorter. The Z disc disk/line represents the connection point between actin filaments between sarcomeres and does not change.

What the heck does the sarcoplasmic reticulum have to do with the county coroner determining time of a murder victim's death?

Soon after death, within hours, sarcoplasmic reticulum degrades releasing calcium which results in muscle contraction. But because there is no way to remove this calcium, muscle relaxation cannot occur. Therefore rigor mortus occurs. However, hours longer in this process the myofibrils eventually degrade as well with a loss of contraction and muscle relaxation, body limpness, occurs.

As you age, motor units within your body become larger. What are the consequences for motor control?

The ability to finely control muscle actions depends largely on the sizes of the motor units making up an individual muscle. As motor units become larger this means more muscle fibers are innervated by each individual motor neuron. Having many small motor units allows for more precise, controlled movements. If, with age the motor units become large, this means that fine, motor movements will become much more difficult to perform because of the loss of small motor units.

Please refer to question 3, muscle contraction scaled from those sliding filaments mentioned above. Now the problem is how do you get a cell surface signal from the afferent neuron that stimulates a muscle cell, deep into that cell to regulate contraction within the cell? As you think on the events that occur as a result of that action potential signaling from the presynaptic axonal terminus through to the end of contraction and muscle fibril relaxation. Describe those events. Focus your answer on the involvement of Ca++ in this process. Lastly, what happens if you were to run out of ATP during contraction?

The action potential arrives at the terminal axonal buds resulting in an influx of Ca++ ions via voltage-regulated Ca++ gates. Synaptic vesicles containing acetycholine (AcH) release AcH into the synaptic cleft. Upon binding to AcH receptors on sarcolemma of the motor end plate Na+ channels are opened. This initiates an action potential that travels along the sarcolemma then down the T tubule. These triggers Ca++ release from the terminal cistenae of the sarcoplasmic reticulum. Ca++ binds to troponin resulting in a conformational change that removes tropomyosin from blocking myosin binding sites on actin filaments. Contraction occurs when myosin cross bridging to actin results in the powerstroke with sliding of actin filaments along the myosin filaments. ATPases are also activated. At conclusion of action potential, Ca++ is actively transported back into the sarcoplasmic reticulum. The myosin heads recock with expenditure of ATP. Tropomyosin reblocks myosin binding sites on actin and relaxation occurs. If you run out of ATP during contraction, the contracted muscle will not be able to relax because Ca cannot be pumped back into the sacroplasmic reticulum.

Explain the phenomenon of twitch summation and tetanus; and isotonic and isometric contraction.

When individual muscle twitches (contractions) occur with increasing frequency that does not allow for complete relaxation. When twitch frequency is increased to the point where contraction tension is maintained (no relaxation of tension between individual twitches thus fused or complete) tetanus results Isotonic contraction results in a shortening of the muscle while isometric contraction does not result in a change in overall muscle length.

Harry at the age of 18 was diagnosed with gigantism due to a pituitary tumor. His condition was treated by surgical removal of an aspect of his pituitary gland. What hormonal replacement therapy do you think Harry's physician prescribed following this procedure?

The aspect of the pituitary removed was the anterior pituitary therefore the hormones needing to be replaced would be growth hormone, ACTH, thyroxine stimulating hormone, FSH, LH, and Prolactin maybe.

During pregnancy the liver increases production (and thus the plasma concentration) of the major plasma binding protein for the thyroid hormones (TH). This causes feedback that result in an increase in the plasma concentration of TH, but no evidence of hyperthyroidism. Describe what happens.

The increased concentration of binding protein causes more TH to be bound, lowering the plasma concentration of free TH. This causes less negative feedback inhibition of thyroid stimulating hormone (TSH) secretion by the anterior pituitary. The increased TSH causes the thyroid to secrete more TH until the free concentration returns to normal levels. The end result is an increased total plasma TH but normal free TH levels. There is no hyperthyroidism because it's only the free concentration that exerts effects on TH's target cells.

What is the interrelationship between matrix and mineral appositional rates during bone remodeling.

The matrix appositional rate is the rate of new osteoid (not required in answer but non-mineralized extracellular matrix) deposition laid down by the newly differentiated osteoblasts following the erosion period. Mineral appositional rate is the rate that the osteoid becomes mineralized due to the deposition of hydroxyapatite within it. New bone formation requires both to occur with matrix apposition obviously preceding mineralization.

Due to an automobile accident, Henry has been in a manual wheelchair for the past 5 years. Based on Wolff's law, what has happened to the long bones in Henry's legs and arms?

Wolff's law states that bone grows in response to the stresses placed upon it. Since Henry's legs have gone unused since his accident, the bones will grow thinner and weaker over time. After 5 years, even if Henry were suddenly healed, his leg bones would not be able to support his weight properly, and major physical therapy would be necessary to allow him to walk again. Assuming Henry has had full use of his arms, they would not be adversely affected by his wheelchair-bound status. It is possible that the extra exercise Henry's arms are getting could possibly result in increased bone density to compensate for the stresses placed upon them. Also, the pattern of density would likely change, because the process of pushing the wheels places more stress on the ulna (the smaller bone in the forearm) than would normally occur in day to day life.

As I discussed in class numerous times, it is not possible to clearly delineate between physiological systems with clear separations of black and white. The endocrine and nervous systems are no exception. Provide one example of how the endocrine system exerts control over the nervous system and then conversely one example how the nervous system exerts control over the endocrine system.

endocrine system exerts control over the nervous system. The anterior pituitary is a neurosecretory gland in the brain which upon hormonal stimulation secretes hormones. nervous system exerts control over the endocrine system The hypothalamus is a neurosecretory gland in the brain which upon nervous stimulation secretes hormones. The hypothalamus upon receiving stress stimuli sends nerve impulses to the adrenal medulla which secretes catecholamines (epinephrine/norepinephrine).

Define bone remodeling. What cells are involved? What is the most important single aspect impacting bone remodeling and bone mechanical integrity. Why is bone remodeling important? (The question involves 4 physiological processes which we have discussed. I require 3 out of the 4 processes.)

(2 pt) Bone remodeling is the lifelong renewal of the skeleton via resorption and re-deposition of bone. (1 pt) Osteoclasts are responsible for bone resorption via degradation of both inorganic an organic components. (1 pt) Osteoblasts are responsible for bone re-deposition via laying down of osteoid which subsequently becomes mineralized. (1 pt) Activation frequency (3 pt) Bone remodeling is critical to store and release Ca++ in the regulation of blood Ca++. Bone remodeling is critical for skeletal adaptation according to Wolfe's Law. Bone remodeling is critical for bone repair and regeneration. Bone remodeling is critical for bone growth.

Define bone remodeling. What cells are involved? What is the most important single aspect impacting bone remodeling and bone mechanical integrity. How is bone remodeling associated with Wolff's Law?

(2 pt) Bone remodeling is the lifelong renewal of the skeleton via resorption and re-deposition of bone. (1 pt) Osteoclasts are responsible for bone resorption via degradation of both inorganic an organic components. (1 pt) Osteoblasts are responsible for bone re-deposition via laying down of osteoid which subsequently becomes mineralized. (1 pt) Activation frequency (2 pt) If stress forces are remove from bone, the net effect of remodeling will be a loss of bone thus focus on resorption; whereas, if there is an increase in forces applied there will be a net gain of bone mass thus focus on osteoblasts.

In respect to the sliding filament model, what happens to the sarcomere during a contraction? What aspects of the sarcomere change in length and which do not? Finally, why do they change or not change. Pretty pictures are fine too (with labels of course).

-During contraction of the sarcomere, the actin or thin filaments slide along the -myosin or thick filaments, thus it gets shorter. -The A band does not change because neither the actin or myosin filament length changes. -The I band gets shorter because it is the represents the distance between two neighboring actin filaments between two sarcomeres. When the actin filaments slide along the myosin filaments the actin filaments get closer because of their staggered placement. -The H zone gets shorter because it is the distance between two actin filaments in the same plan within a sarcomere, thus when the actin filaments slide toward the middle of the sarcomere they come closer to one another.

Tell me please how the smallest functional unit within a myofiber works. Pretty pictures are fine too (with labels of course).

What is the role of the sarcoplasmic reticulum during a muscle twitch? Your answer will be longer than a simple sentence.

A muscle twitch consists of basically contraction and relaxation elements. To initiate contraction, stored Ca is released from the sarcoplasmic reticulum via voltage gated Ca channels which then interacts with the troponin complex allowing the myosin heads to engage the actin resulting in sarcomere shortening and overall muscle contraction. To induce relaxation, Ca must be physically pumped via active transport back into the sarcoplasmic reticulum thereby removing the Ca from the troponin complex with the result that actin and myosin disengage. This results in re-lengthening of the sarcomere and relaxation of the muscle.

Define cancer. Is it contagious (justify your answer)? And, reconcile the monoclonal theory of cancer with the multi-hit theory of cancer.

A population of abnormal cells showing temporally unrestricted growth preference (continually increasing numbers of cells in the population) over their normal counterparts. It is not contagious because cancer represents somatic mutations not genomic mutations. A single mutation is required that initiates cancer. However additional mutations must occur for a cancer to result. One additional or more subsequent mutations are required for cancer progression from benign to metastasis forms.

A drug that blocks the action of acetylcholine is injected directly into the hypothalamus of an animal. The secretion rates of several anterior pituitary hormones are observed to change. How is this possible, since we do not think of acetylcholine is a hypophysiotropic hormone (that is- controlling the release of hypothalamus hormones)? HINT-HINT. This question refers to stimuli which govern hormone secretion. How could GH be impacted by this event? One last question, could this injection directly into the hypothalamus have any impact on the adrenal gland?

Acetylcholine and many other neurotransmitters are released by neurons that terminate on the hypothalamic neurons that secrete the hypophysiotropic hormones. Therefore, manipulation of these neurotransmitters will alter secretion of the hypophysiotropic hormones and thereby the anterior pituitary hormones. GH could be increased, decreased or not affected, depending on the relative release of GHRH and somatostatin. If GHRH is stimulated then GH increases, if somatostatin is stimulated then GH decreases, and if both are stimulated then GH does not change. YES. It could impact both the medulla and cortex. It could stimulate ACTHRH from the hypothalamus which increases ACTH which goes to adrenal cortex to increase glucocorticoid release. It could also stimulate the hypothamic neurons which are involved in the innervation circuit to the adrenal medulla resulting in an increase in secretion of epinephrine/norepinephrine.

We see science fiction becoming reality every day. Sometime in the not too distant future therapeutic gene therapy becomes a clinical reality. For Mirim this should have been a boon but instead it may become a potential nightmare. Her therapy resulted in an endocrine mixup such that the physical location of her ACTH receptors became switched with her PTH receptors. Everything else remains the same downstream of the receptors, meaning that if a hormone binds to its respective receptor a normal biological response will ensue. Your question is this, what changes occur in ACTH and PTH responses for Mirim after this unfortunate accident?

Actually both ACTH and PTH are protein based hormones thus both have receptors on the cell surface. Therefore there was not a significant location change that resulted in any expected change in function. Mirim will be ok.

How does the adrenal medulla and cortex differ in their regulation of the body's response to stress? Stop. Don't start writing paragraphs....Answer these two specific sub-questions. What are the respective stimulatory pathways regulating the medulla and cortex? Why is this important in respect to how the medulla and cortex each respond to a stress?

Adrenal medulla is directly innervated to the central nervous system whereby neural signals from the central nervous system induce the secretion of catecholamines (epinephrine and norepinephrine). For adrenal cortex, the hypothalamus secretes ACTH releasing hormone which via the blood induces secretion of ACTH from the anterior pituitary, which via the blood induces release of glucocorticoids from the adrenal cortex. The medulla pathway permits rapid-short term response to stress while the cortex enables slower, long-term response to stress

Define bone remodeling its relationship to bone balance throughout life. What happens to the balance equation upon the initiation of menopause? Why? What happens if the matrix apposition rate is increased? Why?

Bone remodeling is the life long renewal of the skeleton via resorption and re-deposition of bone. When in balance bone resorption equals bone replacement thus not net bone mass change. During the childhood the balance is shifted to net bone gain, which continues to mid-30s after which the balance shifts to net loss of bone. At the initiation of menopause and the loss of estrogens, rate of bone loss increases. The bone balance due to an increase in matrix apposition rate will depend on if the mineral apposition rate parallels it. If it does not there will not necessarily be a shift to more bone as bone represents mineralized matrix.

Differentiate between compact and cancellous bone; woven and lamellar bone; the lamellar patterns in a cortical osteon (Haversian canal) and a cancellous osteon.

Differentiate between compact and cancellous bone; woven and lamellar bone; the lamellar patterns in a cortical osteon and a cancellous osteon

Differentiate between compact and cancellous bone; woven and lamellar bone; the lamellar patterns in a cortical osteon (Haversian canal) and a cancellous osteon; and an osteoblast and an osteocyte.

Compact is the denser bone along the external aspects of bone providing mechanical strength and having porosity via canniculi interconnecting entrapped osteocytes. Woven bone is the first bone formed either by direct or indirect bone formation and is unorganized. Upon remodeling it becomes organized into lamellar bone with significant increase in strength. Cortical osteon has concentric rings of lamellar bone with a central hole containing blood vessels and nerve. A cancellous osteon has layers of lamellar bone being laid down sequentially upon the "flat" surface. An osteoblast is a bone forming cell upon the surface of bone laying down osteoid which is later mineralized. The osteocyte is an osteoblast that becomes surrounded by osteoid thus subsequently entrapped in bone, but maintains communication with other cells via canniculi and acts as mechaniosensor for bone.

An individual muscle can vary in its ability to perform work, say lift loads. This can be simplified to the contraction capacity of the muscle. Briefly explain the various aspects of contraction that impact its work. Focus on force, velocity and duration.

Contractile force is impacted by changing the number of muscle fibers activated, the size of muscle fibers, stretching of the series-elastic elements via titanic contraction, and extending muscle sarcomere length beyond resting length. Contractile velocity is a impacted by smaller loads and predominance of fast glycolytic fibers Contractile duration is impacted by smaller loads and predominance of slow oxidative fibers

Describe for me the anatomy of cortical bone?

Cortical, dense or compact bone typically resides toward the outside of an individual bone. The periosteum (fibrous membrane) directly attaches to the surface of cortical bone via Sharpey's fibers and blood vessels can enter cortical bone from this outer bone surface. Cortical bone is not simply dense without perforations but comprised of series of overlapping osteons or Haversian systems each containing a central or Haversian canal which contains blood vessels and nerve. Circles of Lamellae radiate out from the central canal. Within this lamellae reside osteocytes within lacuna which are interconnected to other lacuna via canacliculi. Neighboring lamellae comprise collagen fibers that run in opposite directs providing resistance to torsional force. Trabecular, spongy or cancellous bone connects to the inner surface of cortical bone. OR a pretty picture with labels.

Cancer represents somatic mutations thus it is typically not considered to be directly transmittable from one individual to another. There are exceptions however. Please discuss how cancer can be considered a contagious disease? Now aside from a certain bad tempered animal, you also have to discuss one other situation where cancer can also be transmitted from one individual to another.

Facial tumors in Tasmanian devils. Due to the behavior of these animals, tumor cells are transmitted from one individual to another due to scratching and biting around the face. The tumor remains benign but can go to such an extent that animals cannot eat. 3 pts The other is if cancer cells are physically injected or surgically transferred from one individual to another.

Please clarify the truth or provide counter opinion to the following statement....osteoblasts secrete bone. (I want more than true or false in your answer).

False. Osteoblasts can only secrete osteoid or non-mineralized extracellular matrix. The extracellular osteoid then becomes mineralized due to the deposition of hydroxyapatite within it creating new bone. Thus this new bone formation requires osteoid deposition to precede mineralization.

We see science fiction becoming reality every day. Sometime in the not too distant future therapeutic gene therapy becomes a clinical reality. For Charlie this should have been a boon but instead it may become a potential nightmare. His therapy resulted in an endocrine mixup between his adrenal medulla and adrenal cortex. When that aspect of the brain that controls the medulla is engaged the adrenal cortex is signalled and visa versa for when the hypothalamus initiates signaling to the cortex it signals to the medulla. What would this mean to Charlie? There is more than one answer possible.

First option. Although brain stimulates the cortex via neuron there is no efferent medulla equilivant cells to respond so not response occurs. Same for hypothalamus. It secretes ACTHRH to anterior pituitary that secretes ACTH to signal the medulla now, but not efferent down stream parts in the medulla to act on ACTH. Overall not functional communication for either system. Second option. Assuming that medulla and cortex do respond to the mixed up signaling. Then when the brain NOW signals the cortex it releases glucocorticoids and aldosterone and when the hypothalamus releases ACTHRH it signals release of catecholamines from medulla. This would mean a mix up in dealing with short term and long term stress. In other words you would not have a functional flight or fight syndrome response.

Would you expect the concentration of ACTHRH in blood sampled from your adrenal gland to differ from a sample taken between your hypothalamus and posterior pituitary? Why?

First this is a non-relevant question. There is not blood supply between the hypothalamus and posterior pituitary only between the hypothalamus and anterior pituitary. Second ACTHRH communicates between the hypothalamus and the anterior pituitary.

Would you expect the concentration of TSHRH in blood sampled from your thyroid gland to differ from a sample taken between your hypothalamus and posterior pituitary? Why?

First this is a non-relevant question. There is not blood supply between the hypothalamus and posterior pituitary only between the hypothalamus and anterior pituitary. Second TSHRH communicates between the hypothalamus and the anterior pituitary.

John goes to his Endocrinologist with the following symptoms- elevated metabolic rate, he is always nervous and remains very slim despite eating 5 meals a day. He is also a bit "bug-eyed" as well. Please detail the sequence of clinical blood work the Endocrinologist would do to COMPLETELY diagnose John's condition.

First, the Endocrinologist would test of blood thyroid hormone (also can put T3 and/or T4). If high then likely has Grave's disease. Second series of tests is to determine why. The Endocrinologist would also test for TSH and for TSHRH. If TSH is elevated and TSHRH is not then likely the problem is in the anterior pituitary. If TSHRH is also elevated then likely the hypothalamus.

Harvey, a 6 ft invisible rabbit and essentially human (he used to pal around with the late Jimmy Stuart) has been feeling rather poorly. He has no energy and is lethargic. He is really off his mental game. And, his ankles appear swollen and he scratches a lot (no is isn't fleas). Oh, he is getting plenty to eat. Please detail possible clinical blood work to be done to diagnose Harvey's condition. Now knowing the problem what would be the clinical therapy most likely to be used to correct Harvey's problem?

First, would test of blood thyroid hormone (also can put T3 and/or T4). If low then Harvey likely has Myxedema. Second series of tests is to determine why. The Endocrinologist would also test for TSH and for TSHRH. If TSH is suppressed and TSHRH is not then likely the problem is in the anterior pituitary. If TSHRH is also supressed, then likely the hypothalamus. Give exogenous T3/T4.

There are many factors that govern the magnitude of response to a hormone. Please discuss them in the context of juvenile and mature onset diabetes.

For juvenile diabetes it is simply that insulin is not produced so the hormone concentration is the limiting factor. For mature onset diabetes it is more complex representing a loss in sensitivity to insulin. This can be a result of multiple causes including loss of functional receptors, change in receptor affinity for insulin, some change in post receptor amplification and/or a change in effector molecules.

Now, as an example, tell me what type of hormone interaction, if any, occurs between the following hormone pairs. Oh, and tell me what physiological outcome is being controlled with each pair. GHRH and Somatostatin Insulin and glucagon PTH and TSH

GHRH and Somatostatin Antagonism—GH and growth Insulin and glucagon Antagonism—blood glucose PTH and TSH No direct interaction—No answer for this part required but if you said PTH-blood Ca+ and TSJ-metabolism your ok.

Kumar is a type 1 diabetic who has been taking insulin for years. Now all of a sudden for some unknown reason it not only is he having to administer more insulin but even then he cannot control his blood sugar as he once could. In general terms what is possibly happening to insulin ability to control blood sugar? Hint, hint, there are more than one answer.

He could have had a loss in hormone (insulin) sensitivity and/or a loss of hormone (insulin) responsiveness.

Consider the following clinical situations and define the most likely endocrine explanation for each situation. Conrad is 25 years old and abnormally tall, 8 ft 5 in. His blood IGF-I, GH and GHRH are all abnormally high. Which endocrine tissue is most likely the principal cause of this situation AND how long has this situation likely to have been ongoing?

Hypothalmus, because going upstream...IGF-I governed by GH which is governed by GHRH. GHRH is produced by hypothalamus. Likely cause is a tumor in the hypothalamus that developed during childhood because abnormal growth dictates long bone growth which must occur prior to growth plate closure.

Kumar displays symptoms of excess blood cortisol concentration. What factors could be measured in a blood sample to determine whether the condition is caused by a defect at the hypothalamic/anterior pituitary level or the adrenal cortex level? No, no, no, you're not done yet! What may be impacted if all that blood work comes back normal?

If ACTHRH and/or ACTH is elevated in accompaniment with the excess cortisol secretion, the condition is secondary to the defect at the hypothalamic/anterior pituitary level. If ACTHRH and ACTH levels are below normal in accompaniment with excess cortisol secretion, the condition is due to a primary defect at the adrenal cortex level, with the excess cortisol inhibiting the hypothalamus and anterior pituitary in negative-feedback fashion.

Charlie displays symptoms of excess blood cortisol concentration. What factors could be measured in a blood sample to determine whether the condition is caused by a defect at the hypothalamic/anterior pituitary level or the adrenal cortex level? No, no, no, you're not done yet! What may be impacted if all that blood work comes back normal?

Consider isotonic and isometric contraction. How is the muscle shortening velocity affected between these two types of contraction? Is the peak muscle tension always greater for isotonic than for isometric contraction?

In isotonic contraction, muscle shortening velocity is affected by the load. The greater the load the more reduced the shortening velocity. For isometric contraction, as the load exceeds the tensile force of the muscle no muscle shortening occurs. No, because for isometric contraction, load exceeds muscle contractile force whereas for isotonic load is less than contractile force the isometric contraction tensile load essentially always exceeds isotonic contraction tensile force.

Consider a gallon of milk (milk fat content irrelevant here). When you go to lift it from the table, how is your biceps muscle shortening velocity affected between when you first open the milk container and when it is empty? Now compare the peak muscle tension and muscle shortening velocity between lifting a full gallon of milk and lifting your roommate (one hand only please). How would you classify the differences in contraction if they exist?

In isotonic contraction, muscle shortening velocity is affected by the load. The greater the load the more reduced the shortening velocity. So, after first opening it is heaviest so reduced shortening velocity compared to when it is empty. Compared to your roommate, the milk develops peack muscle tension to contract muscle and overcome resistance of milk so you pick it up with one hand. Since your roommate is not "TinkerBell" when you attempt to one hand lift him/her although you develop greater muscle tension you never overcome the resistance load of their weight so the muscle does not shorten. Isotonic for lifting the full gallon of milk and isometric contraction for your roommate.

Describe the relationship between contraction and action potential frequency in skeletal muscle.

In skeletal muscle, as action potential frequency increases, successive twitches begin to fuse with each other and contractile force rises. Eventually, when action potentials are delivered in very close succession, fused tetanus occurs and maximum occurs and maximum isometric force is reached (seen as a plateau region in the graph).

As you may know, the probability of mutation of cells can be increased many fold when a person is exposed to certain chemical, physical or biological factors. Discuss three factors that can increase the probability of cancer and how mutations of the cells occur.

Ionizing radiation, such as (1)x-rays, gamma rays, and particle radiations can predispose individuals to cancer. Ions formed in tissue cells under the influence of radiation are highly reactive and can rupture DNA strands therefore causing mutations. 3 pts Chemical substances of certain types have a high probability of causing mutations. Chemical substances that are known to cause cancer are called carcinogens. The carcinogens that currently cause cancer by far the greatest number of deaths are those in cigarette smoke. 3 pts Physical irritants can lead to cancer for instance, continued abrasion of the linings of the intestinal tract by some types of food. The damage to the tissues leads to rapid mitotic replacement of cells. The more rapid the mitosis, the greater the chance for mutation

What is just as important as bone loss to fracture risk?

Issues related to increased risk of falling (trauma event)

ou go onto the internet and buy online a new "drug", silly you. If more "silly" you take it. It results in you seriously retaining water (ie. Your urine output is greatly curtailed because you have elevated ADH levels) and you're starting to show signs of acromegaly. Yeah I know I purposely did not give you a time line. Let's just say its long enough for these clinical changes. What tissue/organ did the drug target? Please explain your answer.

It is most likely the hypothalamus because an increase in ADH would be attributable to the posterior pituitary but due to release of ADH from there but synthesized in the hypothalamus. The acromegaly would be due to increased growth hormone which taken together with the increase in ADH likely represent increased GHRH production from the hypothalamus.

List the phases of muscle twitch, AND then explain the mechanisms underlying each phase. Make sure in your explanation you relate signaling from the afferent neuron to the sarcomere, interaction between the myosin and actin molecules, and role of Ca++.

Latent period- muscle has been excited by neuron, but no contractile force has yet been developed. An action potential prior arrived to the afferent neuron signaling Ca influx and release of neurotransmitter which initiates an efferent potential on the surface of the muscle cell. The surface action potential proceeds to the T tubules and enters the muscle cell to stimulate release of Ca from sarcoplasmic reticulum. The Ca is now in the sarcoplasm. Contraction has not yet been initiated. Period of contraction- The increase in sarcoplasmic Ca results in Ca binding on the troponin complex which results in exposure of the myosin binding sites on the actin, the binding of myosin to actin and a power stroke sliding the actin along the myosin filaments, which shortens the sarcomere and the muscle. Maximum tensile force is reached during this period. Period of relaxation- The period when tensile force declines because Ca is pumped back into the sarcoplasmic reticulum and myosin and actin are unbound and the sacromeres return to pre-contraction length.

What would happen to Wolff's Law if your osteocytes stopped functioning?

Likely that the remodeling balance would be lost because osteocytes are the mechanosensors for bone. The bone would not be able to sense change in load to bone and correct for changes in load.

You get into a bet with your loud mouthed, know-it-all cousin. He argues that the rate that neurons activate muscles to contract alone determines your maximum sprinting speed. It's all about contraction "baby." You get great satisfaction in correcting him. What did you say?

Maximum running speed is limited by the on-off timing of the muscles involved. More specifically, maximum running speed is limited by the time taken to deactivate the muscle cells used to produce movements of the limbs. Looking at an individual muscle twitch, the time then for relaxation is a least two times the length of the period of contraction. Contraction occurs more quickly than relaxation because diffusion of calcium from the SR into the sarcoplasm is very rapid, whereas the active transport of calcium back into the SR is much slower. Therefore, the ability of a muscle cell to complete a contraction is limited by the time it takes to completely relax the muscle before the next contraction occurs.

The endocrine and nervous systems are intimately intertwined. A perfect example of this can be found in the adrenal gland. How do these systems intersect in the adrenal gland and what is the advantage of this arrangement?

Medulla- Neural. Direct nerve connection to the hypothalamus to induce release of epinephrine and norepinephrine. Cortex- Hormonal. ACTHRH is released from the hypothalamus which travels via blood to the anterior pituitary stimulating the release of ACTH. ACTH travels via the blood to the cortex to simulate which stimulates release of mineralocorticoids and glucocorticoids. For medulla the nerve connection permits very rapid response to stress, while the blood pathways for the cortex permit long-term sustained response to stress

Describe the process of metastasis. Provide two reasons why this is an inefficient process.

Metastasis is the release of cells from the primary tumor site, the dissemination of those cells via lymphatic, blood vessels or body cavities, the arrest of those cells, usually in small blood vessels, the extravasation penetration of those cells through vessel walls and into the surrounding tissues, and the survival and growth of cells at the secondary site. Any 2 of the following- Mechanical stress imposed by circulation Poor nutrition Toxicity due to high oxygen concentrations Immunological effect such as provided by T-lymphocytes, polymorphs, macrophages and natural-killer cells

You have an afferent neuron innervating two efferent cells, another neuron and a muscle fiber. How does each cell respond to this afferent neuron signaling?

Neuron to neuron signal conduction results in signal transmission down the length of the efferent neuron axon as an action potential. The primary difference is related to cell size. Neurons are typical mononuclear cells and signal transduction is a plasma membrane surface phenomenon. Whereas muscle cells represent fused precursor cells and are correspondingly much more massive and the constitutive sarcomere regulation must be integrated. Neuron to muscle begins as an action potential along the plasma membrane in the muscle cell but ALSO proceeds down the T tubules of the muscle cell and triggers Ca2+ release from the sarcoplasmic reticulum. Ca2+binds to troponin on actin filaments; tropomyosin physically moves aside to uncover cross-bridge binding sites on actin. Myosin cross bridges attach to actin and bend, pulling actin filaments toward sarcomere (powered by ATP). Muscle cell contraction results.

What is the interrelationship between osteoid and "bone" during bone remodeling.

New osteoid or non-mineralized extracellular matrix is laid down by the newly differentiated osteoblasts following the erosion period. The extracellular osteoid then becomes mineralized due to the deposition of hydroxyapatite within it creating new bone. Thus this new bone formation requires osteoid deposition to precede mineralization.

A drug that blocks the action of norepinephrine (which directly impacts neurons) is injected directly into the hypothalamus of an animal. The secretion rates of several anterior pituitary hormones are observed to change. How is this possible, since we do not think of norephinephrine is a hypophysiotropic hormone (example- it does not behave like say growth hormone stimulatory hormone or somatostatin)? HINT-HINT. This question refers to stimuli which govern hormone secretion.

Norepinephrine and many other neurotransmitters are released by neurons that terminate on the hypothalamic neurons that secrete the hypophysiotropic hormones. Therefore, manipulation of these neurotransmitters will alter secretion of the hypophysiotropic hormones and thereby the anterior pituitary hormones.

By now you know that Ca++ is important for many physiological functions, therefore its humoral concentrations are tightly regulated. Discuss this regulation in respect to the governing hormones, making sure you mention their source and how they regulate Ca++.

PTH (parathyroid hormone) is produced by the parathyroid gland which resided in the thyroid gland. When Ca++ levels drop below preset then PTH is released going to the kidney to induce activation of VitD3 which goes to the small intestine to increase adsorption of dietary Ca++ and PTH goes to the bones to induce resorption and release of Ca++. Calcitonin is produced by the thyroid gland. When humoral Ca++ becomes elevated calcitonin is released and induces Ca++ incorporation into bone.

George stops growing at an early age of 10 years. His primary care physician does the necessary bloodwork and determines that his growth hormone releasing factor and growth hormone levels are normal. She is stumped. She calls you for an endocrinology consult. What additional blood work would you recommend if any? Explain your answer. Are there any other possible explanations?

Request determination of blood (serum or plasma) IGF-I because growth hormone stimulates its production by the liver as well as in other tissues. Therefore if blood IGF-I concentration is low could indicate that liver is not secreting it normally. Other explanations can include non-functional or disrupted functionality of IGF-I receptors. Also, thyroid hormone levels could be low and this could also in part explain the lack of growth. SPECIAL NOTE!!!! If you put down somatostatin for blood work you are wrong because if these levels are high there would be a clear decrease in GH levels. Nor are receptor changes acceptable for blood work as this is not blood work, but this is acceptable rot other possible explanations

Percy stops growing at an early age of 8 years. His primary care physician does the necessary bloodwork and determines that his growth hormone releasing factor and growth hormone levels are normal. She is stumped. She calls you for an endocrinology consult. What additional blood work would you recommend if any? Explain your answer. Are there any other possible explanations?

Request determination of blood (serum or plasma) IGF-I because growth hormone stimulates its production by the liver as well as in other tissues. Therefore if blood IGF-I concentration is low could indicate that liver is not secreting it normally. Other explanations can include non-functional or disrupted functionality of IGF-I receptors. Also, thyroid hormone levels could be low and this could also in part explain the lack of growth. SPECIAL NOTE!!!! Many of your put down somatostatin. I gave you credit this time although this is wrong...If somatostatin levels are high there would be a clear decrease in GH levels. Second I as asked for blood work for the first question, but gave credit for receptor related answers although they would not be part of blood assays.

Laura stops growing at an early age. Her pediatric endocrinologist does bloodwork and determines that her growth hormone and IGF-I are within normal limits. Oh, and during the office visit the endocrinologist noted some behavioral issues and referred Laura to a developmental psychologist who noted severe developmental delays in cognitive function. Putting all this together what other bloodwork should be considered and why?

Request determination of blood (serum or plasma) thyroid hormone, because if below normal levels for her age, she could be suffering from hypothyroidism also called creatinism.

Sandeep tripped, fell and broke his wrist. His visit to the ER and fixation of his broken wrist led to a series of clinical evaluations. The resulting diagnosis was he had a form of osteoporosis. He could not understand how this could be his problem as he was only 25, he takes plenty of Ca++ dietary supplements, he is physically active and his osteoblasts functioned within normal tolerances. Despite this his blood Ca++ was well below normal. Provide a possible explanation(s) for Sandeep's dilemma. Justify your explanation(s) suggesting additional clinical tests.

Several possible explanations exist, possibly multiple explanations resulting in a lack of Ca++ for bone mineralization. His parathyroid gland has ceased to produce PTH; determine blood PTH levels. PTH levels are normal but he has inadequate VitD3 production or is not taking as supplement. Check blood VitD3. If VitD3 is normal, the kidney may not be processing to active VitD3. Check for activated VitD3. Intestine is not functioning properly. Assuming PIT and VitD3 pathways are normal look for intestinal function. Lastly, and you get 1 pt special credit if you give this is that despite PTH/VitD3 pathways are normal he could have Osteogenesis Imperfecta, an inheritable disorder.

You may or may not have seen the Star Trek reruns (I don't care which version). In all versions one of the primary means of personal transportation was teleportation. Let's assume teleportation is currently available and Charlie teleports, but a mistake occurs. In the process for some unfathomable reason his testosterone receptors are switched with his growth hormone receptors. Everything else remains the same downstream of the receptors, meaning that if a hormone binds to its respective receptor a normal biological response will ensue. Your question is this, what changes occur in testosterone and growth hormone responses for Charlie after this unfortunate accident?

Testosterone receptors are now on the cell surface not in the cytoplasm which poses no problem in testosterone gaining access to its receptor. It is irrelevant for testosterone here that it is a steroid. Growth hormone is a protein therefore insoluble through the plasma membrane. With growth hormone receptors now internalized within the cell it cannot bind to its receptor. The effect of this on Charlie will depend on how old he is, is he still growing or done.

Now, using what you know about bone formation, apply to this question concerning bone repair. You are riding your bike on Fifth during the 5 pm rush hour. You're sideswiped by a PAT bus, no not a direct hit but only enough contact to send you onto the sidewalk. Obviously, it hurt. You have sustained "road rash" and skeletal injuries. You break your left femur and a narrow bolt from your bike is driven into your humerus creating a 2 mm diameter hole. Obviously, you get the best medical intervention. Please explain the process involved in the repair of these skeletal injuries.

The femoral fracture is biomechanically unstable so will heal by endochondral bone formation. This will include the formation of a cartilage based callus from the initial hematoma. This callus will eventually be replaced by a bony callus. This will biomechanically stabilize the fracture sight such that the cast which was initially used to insure that the reduced fracture remained intact can now be removed. Over months remodeling will remove the callus and the healed bone will approach that of the pre-fracture bone. The humerus repair being a simple hole is biomechanically stable. No further clinical intervention beyond insuring that infection does not occur is necessary. This hole will heal by direct bone formation without intervening cartilage or callus formation. Osteoblastic precursor cells will populate the area and eventually replace the hematoma with woven bone which will eventually become remodeled to lamellar bone. The remodeling process will take many months.

Now, using what you know about bone formation, apply to this question concerning bone repair. You are riding your bike on Fifth during the 5 pm rush hour. You're sideswiped by a PAT bus, no not a direct hit but only enough contact to send you onto the sidewalk. Obviously, it hurt. You have sustained "road rash" and skeletal injuries. You break your left femur and right humerus. For whatever reason they put your femur in a cast, leaving a little mechanical play, and used a rigid fixation plate, with complete mechanical stabilty, to repair your humerus. Please explain the processes involved in the repair of these skeletal injuries.

The femoral fracture is biomechanically unstable so will heal by endochondral bone formation. This will include the formation of a cartilage based callus from the initial hematoma. This callus will eventually be replaced by a bony callus. This will biomechanically stabilize the fracture sight such that the cast which was initially used to insure that the reduced fracture remained intact can now be removed. Over months remodeling will remove the callus and the healed bone will approach that of the pre-fracture bone. The humerus repair is biomechanically stable. This fracture will heal by direct bone formation without intervening cartilage or callus formation. Osteoblastic precursor cells will populate the area and eventually replace the hematoma with woven bone which will eventually become remodeled to lamellar bone. The remodeling process will take many months.

Please differentiate between a marathon runner and a sprinter. Focus your answers on differences in muscle fiber type in reference to the muscles in their legs.

The leg muscles of the sprinter runner are predominately fast glycolytic fibers. These fibers are capable of rapidly producing large amounts of tension, but only for short duration because of their dependence on glycolysis for energy (ATP) production. This enables for rapid but flying for only brief periods. Say to get into a tree or fly away from a predator. This is because these fiber types rapidly exceeded anaerobic threshold and thus the turkey is forced to rest from flying for relatively long periods to rebuild up glycolysis ATP stores. The leg muscles of the marathon runner are predominately slow oxidative fibers. These fibers are found in muscles specializing in maintaining low-intensity contractions for long periods of time without fatigue. These fibers enable flying endurance because her energy demands did not exceed his anaerobic threshold, therefore insuring that the goose has sufficient ATP to maintain long distance flight migrations.

1. What is the interrelationship between matrix and mineral appositional rates during bone remodeling.

Julie Jumpsohigh is waiting impatiently for the physician to finish removing the cast from his leg, which she broke the last day of school six weeks ago at the track and field meet. Summer vacation is half over, and she hasn't been able to swim, high jump, or participate in any of her favorite sports. When the cast is finally off, Julie's excitement is replaces with concern when she sees that the injured limb is noticeably smaller in diameter than her normal leg. What is the explanation for this reduction in size? How can the leg be restored to its normal size and functional ability? What is the basic concept extensible from what you know about bone physiology that applies to her situation? Oh, paraphrase that concept as well (ie. define it simply).

The muscles in the immobilized leg have undergone disuse atrophy. The physician or physical therapist can prescribe regular resistance-type exercises that specifically use the atrophied muscles to help restore them to their normal size. Wolfe's Law-use it or loose it.

How does post synaptic signal transduction differ between neuron to neuron signal conduction and neuron to muscle cell signal conduction?

The primary difference is related to cell size. Neurons are typical mononuclear cells and signal transduction is a plasma membrane surface phenomenon. Whereas muscle cells represent fused precursor cells and are correspondingly much more massive and the constitutive sarcomere regulation must be integrated. Neuron to neuron signal conduction results in signal transmission down the length of the efferent neuron axon as an action potential. Neuron to muscle begins as an action potential along the plasma membrane in the muscle cell but ALSO proceeds down the T tubules of the muscle cell and triggers Ca2+ release from the sarcoplasmic reticulum. Ca2+binds to troponin on actin filaments; tropomyosin physically moves aside to uncover cross-bridge binding sites on actin. Myosin cross bridges attach to actin and bend, pulling actin filaments toward sarcomere (powered by ATP). Muscle cell contraction results.

As a muscle cell undergoes hypertrophy (it grows bigger) by fusion with additional pre-muscle cells (satellite cells) it adds myofibrils. Why would it be important that the ratio of myofibrils to sarcoplasm volume remain constant? Your answer will involve the sarcoplasmic reticulum AND sarcomere function. To help you in this quest, tell me what would happen if the sarcoplasm volume increased disproportionately greater than the number of myofibrils?

The sarcoplasmic reticulum stores the Ca that is released into sarcoplasm to initiate contraction by binding to the troponin complex. As more myofibrils are added the increase in sarcoplasmic volume must be matched to maintain the same myofibril to sarcoplasmic volume ratio. If there is a disproportionate increase in sarcoplasm then when Ca is released into it from the sarcoplasmic reticulum then it would be diluted compared to when ratio is maintained. This would reduce rate of contraction or even block contraction due to dilution effect on Ca concentration in sarcoplasm. For relaxation it would take longer to pump Ca back into sarcoplasmic reticulum also because of dilution effect.

Explain the size principle and how it relates to the amount of tension developed by a skeletal muscle. BUT, hold there, you're not done yet. Interestingly as individual age, motor units within the body become larger. What would you expect the consequences for motor control would be when this occurs?

The size principle is a description of motor unit recruitment in skeletal muscle. It says that the smallest motor units are recruited first, followed by successively larger motor units a more force is required by the muscle as a whole. When maximum force is require, all available motor units are recruited. The ability to finely control muscle actions depends largely on the sized of the motor units making up an individual muscle. Having many small motor units allows for more precise, controlled movements. Having fewer large motor units allows for a large development of force, but much less control over gradation in force Therefore if motor units become large with age, this means that fine motor movements will become much more difficult to perform.

Paul stayed up all night studying and wanted to stay for his upcoming Physiology exam. He thus consumed a one-pound bag of candy shortly prior to the exam with the hopes that the "sugar high" would keep him functioning at maximum efficiency. The opposite occurred. Using your knowledge of the hormonal control of blood glucose, describe why an individual, after eating an entire one-pound bag of candy, will become lethargic and sleepy shortly thereafter.

The sugar in the candy is broken down into glucose and the glucose is absorbed into the bloodstream. When an individual eats this much sugar in one sitting, this results in a drastic increase in blood glucose levels that stimulates the release of large amounts of insulin from the pancreas. Insulin stimulates the uptake of glucose into muscle cells, liver cells, and adipose cells. The large amount of insulin released in response to the spike in blood glucose levels can cause a precipitous fall in plasma glucose levels such that they become much lower than normal homeostatic levels. This decrease in blood glucose means that the brain, which runs almost exclusively on glucose, is not getting enough fuel to perform optimally. The result is sluggishness.

Please differentiate between a Canadian goose that migrates north/south with the seasons compared to a turkey that can fly but for the most part walks for a living. Focus your answers on differences in muscle fiber type in reference to the pectoral muscles ("breast") muscles.

The turkey breast muscles are predominately fast glycolytic fibers. These "white fibers" are capable of rapidly producing large amounts of tension, but only for short duration because of their dependence on glycolysis for energy (ATP) production. This enables for rapid but flying for only brief periods. Say to get into a tree or fly away from a predator. This is because these fiber types rapidly exceeded anaerobic threshold and thus the turkey is forced to rest from flying for relatively long periods to rebuild up glycolysis ATP stores. The Canadian goose breast muscles on the other hand are predominately slow oxidative fibers. These "red fibers" are found in muscles specializing in maintaining low-intensity contractions for long periods of time without fatigue. These fibers enable flying endurance because her energy demands did not exceed his anaerobic threshold, therefore insuring that the goose has sufficient ATP to maintain long distance flight migrations.

Your Bohemian grandmother is a hard drinking, cigarette smoking woman who abhors dairy products of any kind. Although a small, seemingly frail woman of 65 years, at one time she competed in track and field in her college days. What is your advice to her regarding her recently diagnosed osteoporosis? What can she do and what can she not do to reduce the possibility of a fractured bone.

Whereas presently there is nothing she can do to reverse her bone loss she can take steps to reduce the rate of bone loss, possibly even stop it altogether. First she should stop drinking in excess, give up the cigs, and either learn to consume dairy products, eat TUMS or other calcium source. She once performed active exercise, she should consider doing this again after consulting with her physician and modifying her exercise to her current age and medical condition. Wolff's law will help maintain her bone mass. There is nothing she can do about her body type although getting into shape will help add muscle mass. Physical activity will help her maintain her balance too. Anabolic hormones are a possibility such as estrogen, PTH related peptide, etc. BUT they have associated risks.

You have a friend that has just taken an oral glucose tolerance test. This means that she has had to fast 8-14 hours prior to drinking a glucose solution. Blood glucose levels were recorded after 2 hours. Her fasting glucose level was 175 mg/dl and her 2 hr reading was 400 mg/dl. Normal measures should be <110 mg/dl for fasting and <140 mg/dl after 2 hrs. Should she be concerned? If she should be concerned, what is likely wrong with her? In your answer please include how glucose would be normally regulated under such a test as this and how that it may be disrupted with your friend. What are her clinical options to correct her glucose response levels?

Yes She likely has diabetes type 1. She could have type 2 but she is within normal body size range is your age. (if you talked about type 2 you will not per say miss it either) Normally, blood glucose is highly regulated, such that when blood glucose levels become elevated the pancreas responds by secreting insulin which acts on essentially every cell in the body to internalize glucose thus reducing circulating glucose concentrations.

For this question I refer you to a recent TV commercial from Fruit Roll-ups Double Dares. The commercial begins with two boys (about 12 years of age) where one boy double dares the other to jump on one leg until he is told to stop. The boy who is dared starts jumping on his right leg. Time flashes forward about 10 years. The boy, now a man—though stupid man—is still jumping on that same leg. It's visually obvious that the right leg is noticeably larger than the left—its huge people. Otherwise everything is physically normal for him. Is this possible or just a TV fantasy? If it is possible, how are the bones and the muscles of the right leg impacted by this 10 years of constant jumping (yeah I know he sleeps sometime, but otherwise he is jumping)? In your answer please discuss not only biomechanical interactions but also from the standpoint of endurance training. Now final question, the idiot finally realizes what a fool he has been and stops jumping on the right leg, returning to normal standing and walking behavior, what happens to the right leg?

Yes. 3 pts Biomechanically Wolff's law dictates that both the bone and muscles in the right leg will grow to compensate for the increased mechanical loads being placed on them. In short "use it or lose it." This means the leg bones will increase in overall diameter and be thicker. The muscle mass will also increase placing more stresses on muscle bone attachment sites further increasing bone growth to resist this. 3 pts The constant effort of repeatedly jumping up and down will represent endurance training for the boy/man. This means he will increase his ability of the exercised muscles to stay in aerobic condition utilizing oxidative phosphorylation for ATP production reducing his lactic acid production and increasing alternative energy sources to provide energy. Bone is not involved in endurance training specifically here. 2 pts When he returns to normal behavior the right leg will gradually return to normal, eventually it will resemble the left leg, with the bones and muscles of the right leg reducing in mass and size. The advantages of the endurance training will also gradually reverse as well.

Why does muscle fatigue occur (Keep your answer at its simplest, you can answer in just 4 words). In applying this concept how does exercise training modify fatigue response? Specifically, compare how training for downhill skiing athletes (fast and short duration) to cross-country skiers (steady and long duration) affect resistance to fatigue in muscles?

You exceed anaerobic threshold. Regular bouts of anaerobic, short-duration, high-intensity resistance training would be recommended for competitive downhill skiing. By promoting hypertrophy of the fast glycolytic fibers, such exercise better adapts the muscles to activities that require intense strength for brief periods, such as a swift, powerful descent downhill. In contrast, regular aerobic exercise would be more beneficial for competitive cross-country skiers. Aerobic exercise induces metabolic changes within the oxidative fibers that enable the muscles to useO2 more efficiently. These changes, which include an increase in mitochondria and capillaries within the oxidative fibers, adapt the muscles to better endure the prolonged activity of cross-country skiing without fatiguing.

How would the following situations impact bone balance...how will each situation alter your body's gain of bone overall? answer will be positive, negative, no effect Your thyroid gland secretions are greatly reduced Your index finger and thumb overlap...a lot...so in 50 years in future this will impact bone gain how You take bisphosphonate drugs which block osteoclast function You stay inside and don't take vit 3 supplements Increase in sparkling water consumption You lose your kidneys and are maintained on dialysis without additional therap You take a trip to space station and decide to stay there. You focus on the new fad diet with each meal consisting of 2 dozen Krispy Kreme donuts with 2 large milkshakes and frozen yogurt for desert.

Your thyroid gland secretions are greatly reduced positive Your index finger and thumb overlap...a lot...so in 50 years in future this will impact bone gain how negative You take bisphosphonate drugs which block osteoclast function positive You stay inside and don't take vit 3 supplements negative Increase in sparkling water consumption no effect You lose your kidneys and are maintained on dialysis without additional therapy positive (due to no VitD3 processing) You take a trip to space station and decide to stay there. negative You focus on the new fad diet with each meal consisting of 2 dozen Krispy Kreme donuts with 2 large milkshakes and frozen yogurt for desert. positive

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