Physio Exam 2
Mildred the ostrich was fabled for her sprinting skills. She laughed at the lumbering slow but steady 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 and 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.
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 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
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
How does signaling to muscle change as load resistance increases?
Motor unit recruitment is increased (size principle). More, larger units are recruited as load increases. However, if resistance exceeds tensile force developed, then muscle cannot shorten (cannot pick the thing up).
How does gaining to muscle chance as load resistance increases? Will this always result in change in muscle length?
Motoro unit recruitment is increased according to the size principle. more, larger units are recruited as load increases. however, if resistance exceeds tensile force developed, then muscle cannot shorten.
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)
Thyroid gland becomes non-functional: positive (loss of calcitonin) Petite skeletal frame, routinely exercise, maintain adequate Ca++ intake: negative Block osteoclast function: negative Chronic Glucocorticoids for pain: positive Increase in sparkling water consumption: nothing Lose kidney, need dialysis: positive (lack of VitD3 processing)
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.
Turkey: predominantly fast glycolytic fibers "white fibers" are capable of rapidly producing large amounts of tension, but only for short duration because of the dependence on glycolysis for ATP. Enables rapid, but short flying periods. Typically, fiber type is rapidly exceeding the anaerobic threshold --> forced to rest for long periods of time to rebuild glycolysis ATP stores Goose: muscles are primarily slow oxidative fibers "red fibers" specializing in low-intensity for long periods of time without fatigue enables flying endurance because energy demands does not exceed anaerobic threshold ensures goose has enough ATP for long D
Relationship: SR & time of death?
after death, SR degrades => release Ca2+ supply => muscle contraction no way to remove Ca (requires ATP) => muscle cannot relax hours later, myofibrils degrade => body limpness
Bobby: menial physical work for 20 years in right arm. Effect? Why?
Wolff's Law: "Use It or Lose It" Right arm will increase in diameter & thickness + increased muscle mass (more bone development) Upon Retirement: right arm will slowly lose bone + muscle mass to resemble the left arm advantages from endurance training will also reverse
How muscle functios
contraction of sarcomere => the actin filaments slide along the myosin filaments A-band: length does not change I-band (represents the distance between two actin filaments in different sarcomeres) gets shorter H-zone (represents the distance between two actin filaments in the SAME sarcomere) gets shorter as actin filaments get pulled towards center of sarcomere
Erosion rate, matrix & mineral apposition rate, & interplay between those with result of a tumor in the anterior pituitary (substantially increasing TSH)
erosion rate: during bone erosion, driven by osteoclasts (resorption phase that precedes formation) Matrix/Mineral rate: - Matrix: how fast osteoid is secreted (osteoblast dependent) - Mineralization: how quickly the osteoid mineralizes Anterior pitarui hormone (increased TSH) => increased thyroid hormone production - hyperthyroidism => increase all metabolic rates - matrix deposition & mineralization rates decrease (not enough time because of increased metabolic rate)
Osteoblasts secrete bone. True or False.
false, they can only secrete osteoid. the osteoid will then mineralize (due to deposition of hydroxyapatite) which will create new bone.
What determines max running speed?
limited by the on-off timing of muscles limited by the time it takes to relax the muscle cells used to produce movement
What is the interrelationship between osteoid and "bone" during bone remodeling.
new osteoid is laid down by the osteoblasts (following erosion process) extraceulluar osteoid then mineralizes, due to the deposition of hydroxyapatite within it creating new bone new bone formation requires osteoid deposition to precede mineralization
Define cancer. Contagious? How is cancer multiple mutations?
population of cells that show unrestricted growth not contagious because cancer cells are somatic mutations (not genomic) first mutation ≠ cancer, must be a series of mutations (Rb gene must be knocked out to prevent the gatekeeper from prohibited further replication of cancerous cells)
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?
3 pts 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.
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.
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, she will be fine both ACTH and PTH are protein based hormones that have receptors on the cell surface excess presence of cortical binding proteins in blood -> maintain high levels of cortisol in the blood
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. 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?
Bone remodeling: lifelong renewal of skeleton via resorption and re-deposition of bone Osteoclasts: responsible for bone resorption via degradation of both inorganic and organic components Osteoblasts: responsible for bone re-deposition (laying down osteoid) Activation frequency is most important aspect impacting bone remodeling. If stress forces are removed from bone, the net effect of will be a loss of bone -> focus on resorption if there is in increase in forces applied --> net gain of bone mass thus focus on osteoblasts (formation)
Differentiate between compact and cancellous bone; woven and lamellar bone; the lamellar patterns in a cortical osteon (Haversian canal) and a cancellous osteon.
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 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
Metabolism rate stuck on high? Endocrinologist.
First, test blood thyroid hormone (T3/T4). If high => Grave's disease Test TSH & TSHRH: High [TSH] & Normal [TSHRH] => anterior pituitary problem High [TSH] & High [TSHRH] ===> hypothalamus
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.
Symptoms of excess [Blood cortisol]. How can we tell if this is an issue with the {hypothalamus + anterior pituitary} or the {adrenal cortex}?What about if blood work is normal?
If ACTHRH and/or ACTH are elevated => hypothalamus/anterior pituitary if ACTHRH and/or ACTH are LOW => adrenal cortex issue
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?
Isotonic contraction: muscle shortening velocity is affected by the load. great there load, the more reduced the shortening velocity Isometric contraction as the load exceeds the tensile force of the muscle, no 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. ???
You 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.
Describe the process of metastasis. Provide two reasons why this is an inefficient process.
Metastasis: - release of cells from primary tumor site - spread of those cells via lymph, blood vessels, or body cavities - settling of those cells - penetration of those cells through vessel walls into tissue - survival and growth of cells at the new site 2 reasons: - mechanical stress imposed by circulation - poor nutrition - toxicity due to high oxygen levels - immune system
Communication: Nerve -> Muscle vs. Nerve -> Nerve
N->N: results in signal transmission down the length of the efferent neuron axon as an action potential N->M: begins as an AP, along plasma membrane, down T-tubule, triggers Ca2+ release, Ca2+ bind to troponin, myosin attaches to actin and pulls actin filament toward sarcomere (ATP) => contraction Cell Size difference: N: mono nucleated, small, surface transmission of signal M: larger cells, must get through the entire z-axis of the muscle (not just at surface, must penetrate -> T-tubule)
Explain feedback control in blood glucose regulation: 1.) Just eaten donuts 2.) Giving birth
Normally, negative feedback regulates glucose levels (blood glucose goes up, release insulin, blood glucose should go back down, inhibit further release of insulin) Giving birth: changing from one physiological state to another (positive feedback)
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.
25-year old, normal osteoblasts, physically active, Ca2+ supplements. But he has osteoporosis. Explain why.
PTH gland has ceased producing PTH => determine PTH levels or Inadequate VitD3 levels => check blood VitD3 or Inherited from parents (osteogenesis imperfecta)
Describe cortical bone.
Resides on outside of individual bone periosteum (fibrous membrane) attaches to surface of bone (made up of Sharpey's fibers, blood vessels enter here) Compromise of series of Haversian systems: - each has a canal for nerves + blood vessels - circles of lamellae radiate out - in each lamellae, lie osteocytes within lacuna (interconnected to other lacuna via caniculi) - Neighboring lamellae comprise collagen fibers that run in opposite directions to add resistance to torsional forces (- spongy bone on inside)
Balance between myofibril and sarcoplasmic volume
Sarcoplasmic Reticulum stores the Ca2+ that is needed to initiate sarcomere contraction if disproportionate, Ca2+ would be diluted => reduce rate of contraction also, relaxation would take longer to bring Ca2+ back because of the dilution
Diagnose high blood sugar levels.
Type-1 diabetes: insulin dependent diabetes mellitus - low insulin & high glucose blood levels Type-2 diabetes: high insulin & high glucose blood levels - check obesity history
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.
