biom3200 case study

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University of Guelph *

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3200

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Biology

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Feb 20, 2024

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Questions (10 marks) 1. What clues alerted Rose’s gynecologist that Rose was at risk for diabetes mellitus? (1 mark) Her gynecologist noticed Rose is overweight, has a family history (mother has diabetes), had gestational diabetes during her pregnancy and had a somewhat elevated fasting glucose. 2. How would the diet and exercise program suggested by the gynecologist have reduced Rose’s risk of diabetes? (1 mark) Both lifestyle changes can help to get rid of excess weight, improve insulin sensitivity and overall improve blood sugar control. Physical activity specifically helps muscle cells to use glucose and insulin more efficiently, since lack of exercise can cause muscle cells to lose their sensitivity to insulin, leading to insulin resistance. 3. What are the causes of polyuria, polydipsia, polyphagia, and weight loss in a person with diabetes mellitus? (2 marks) When there is a lack of or insufficient amount of insulin produced, blood sugar levels remain elevated in the bloodstream, instead of going into the body cells where they are needed for energy metabolism. Since the cells are deprived of glucose/energy, the body responds with an increase in hunger (polyphagia), however increased eating won’t resolve this but make matters worse by elevating the already elevated blood sugar. Since the body remains energy deprived in this scenario, it starts burning fat and muscle for energy instead, leading to weight loss. When blood sugar levels are normal, the kidney reuptakes all the solutes (including glucose) and directs it back to the blood. In hyperglycemia, the kidney can’t reuptake all the glucose that has been filtered since the amount filtered exceeds the amount reabsorbed because the transport proteins in the kidney tubules become saturated, so excess glucose ends up in the urine and exerts an osmotic effect that draws more water towards it, resulting in an increased output in urine volume. This is termed “osmotic diuresis.” The excess fluid excreted can lead to excessive thirst (polydipsia) due to dehydration and thus drinking more fluid to quench the thirst leads to more urination (polyuria). An increased glucose in the blood can trigger the kidneys to produce more urine in an effort to pass the glucose out the body. 4. How do metformin, the sulfonylureas, and the thiazolidinediones act to control diabetes mellitus? (1.5 marks) Metformin helps to restore/improve the body’s response to insulin by altering energy metabolism. It reduces hepatic gluconeogenesis and that the stomach/intestines absorb, improves GLP-1 and reduces glucagon function and to a lesser extent, increases glucose uptake in skeletal muscle. Sulfonylureas work by stimulating the beta cells to produce more insulin and improve the way insulin in used in the body. Thiazolidinediones reduce insulin resistance by increasing glucose utilization to lower glucose in the blood and by decreasing the output of glucose from the liver. Thiazolidinediones also modify gene transcription involved in glucose and lipid metabolism, ultimately increasing insulin sensitivity. 5. How is a glucose tolerance test performed, what are the normal and pathological result thresholds, and what do Rose’s results indicate? (2.5 marks)

Before the test is performed, the individual must be in a fasting state for a minimum of 8 hours, without consuming any food or water. After the allotted time has passed, a blood sample would be taken to measure the fasting blood glucose level. The person will then drink a solution (250- 300mL) containing glucose (around 75 grams). Blood glucose levels would then be checked after each hour-interval (1, 2 or 3) with 2 hours typically being the main allotted time to check. A normal glucose level would be equal to or less than 140 mg/dL (7.8 mmol/L), 140-199 mg/dL (7.8-11 mmol/L) would be considered prediabetes while 200 mg/dL (11.1 mmol/L) or higher would indicate a diabetes diagnosis. Rose results (which are >200 mg/dL) indicates a confirmed diagnosis for diabetes mellitus. 6. Should the doctor be concerned about Rose’s risk of developing diabetic ketoacidosis? Why or why not? (2 marks) The doctor should be concerned since Rose is presenting with a sudden loss of weight (which means fat is being burned for energy instead, producing ketones), polydipsia and polyuria which is caused by hyperglycemia that is confirmed >200 mg/dL from the glucose tolerance test. What is the function of the mitral valve, and when in the cardiac cycl e does it open and close? (2 marks) The mitral valve regulates blood flow from the left atrium to the left ventricle – it opens during ventricular diastole to allow for filling from the left atrium, into the left ventricle. It continues to remain open during atrial systole when the left atrium contracts to top up the blood in the left ventricle (end-diastolic volume). As soon as the pressure in the left ventricle exceeds the left atrium, the mitral valve closes shut which occurs during the phase of ventricular systole. 2. What happens to cardiac output due to mitral valve prolapse? (1 mark) A prolapsed mitral valve can potentially lead to mitral regurgitation where a leak/backflow occurs due to improper closing. Instead of the end-diastolic volume only being ejected from the left ventricle into the aorta, some of it backflows over to the left atrium, decreasing the cardiac output. 3. When in the cardiac cycle would blood regurgitate through a prolapsed mitral valve, and which way would the blood go, and why? (2 marks) A prolapsed mitral valve means that the valves are unable to close properly, between each beat of the heart. This can cause a leak or backflow into the left atrium which is referred to as “mitral valve regurgitation.” This specifically occurs when the left ventricle contracts which occurs during the ventricular systole phase of the cardiac cycle – in normal circumstances, the mitral valve would remain shut as pressure would increase in the left ventricle, but a prolapsed mitral valve would flop or bulge back into the left atrium. Due to this, blood may leak back to the left atrium, causing backflow. 4. What would be the effect of severe mitral regurgitation on the end-systolic volume of the left ventricle and left atrium? (3 marks)

The end-systolic volume would ultimately decrease – when the left ventricle contracts, blood is ejected not only in the aorta but also a portion of it goes back into the left atrium, increasing volume and pressure within that compartment, due to the prolapse. This leads to chain effects such as an increase in the preload or end-diastolic volume in the left ventricle. Less blood is also going out into systemic circulation due to the backflow which means reduced afterload. To compensate, the heart works harder to eject a larger volume into the aorta and due to the increased end- diastolic volume 5.) Atrial fibrillation is a type of arrythmia which refers to an abnormal or irregular heartbeat; this makes the atrium out of sync with the ventricle and as a result, blood doesn’t flow properly from the atrium, into the ventricle. When the heart isn’t pumping as efficiently, it compromises the amount of oxygenated blood delivered into systemic circulation. The lack of blood supply can cause symptoms like tiredness, and may explain Eve’s fatigue. 1. In detail, describe how ACh stimulates the production of action potentials in skeletal muscle fibers. (3 marks) It all starts in the neuromuscular junction, which refers to the interface between a motor neuron and a skeletal muscle fiber. When a motor neuron approaches a muscle, it branches out several extensions called synaptic boutons that can release neurotransmitters. They’re situated over a specific region of the muscle called the end plate. The synaptic cleft, which is essentially a space, separates the boutons from the end plate. The end plate under each bouton contains several ridges called junctional folds, which contain high number of ligand-gated ion channels for acetylcholine. These channels are specifically located on the post-synaptic membrane. When a nerve signal reaches the end of the axon, the axon terminal will release acetylcholine into the synaptic cleft, where it’ll bind to ligand-gated ion channels, which causes conformational changes in the protein. The protein would then act as an ion channel, allowing sodium ions to enter and potassium ions to leave (however not equally). Sodium will largely cross the membrane via these channels, which would cause depolarization to occur since the cell would increasingly become positive. This leads to a cascade effect, triggering neighboring channels to open, causing more sodium ions to enter, following the electrochemical gradient. Once a specific threshold voltage is met, this would create an action potential – sodium would then be able to diffuse into the cell, anywhere along the membrane. . 2. How do the ACh receptor antibodies inhibit the production of action potentials in skeletal muscle? (2 marks) The ACh receptor antibodies inhibit the production of action potentials by targeting (in different ways) the acetylcholine receptors on the post-synaptic membrane, which decreases the availability of functional acetylcholine receptors (AChRs) present. This subsequently leads to a decreased end-plate depolarization, and overall decreased action potentials in the skeletal muscle. 3. How did the drugs that inhibit AChE improve Sana’s muscle function? (2 marks)

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Acetylcholinesterase (AChE) is an enzyme found in the synaptic cleft that breaks down acetylcholine. Drugs which inhibit the enzyme stop the breakdown of the neurotransmitter from occuring, increasing the concentration of acetylcholine present at the neuromuscular junction, to help muscle activation and contraction. This can be helpful when there is limited functional AChR population as in the case of myasthenia gravis. 4. What is a myasthenic crisis? (1 mark) A potential exacerbation for individuals with myasthenia gravis that can potentially be life-threatening. It’s categorized as a worsening of respiratory and bulbar muscular weakness that can lead to upper airway obstruction or dysphagia, thus requiring ventilation or intubation. 5. Following Sanas diagnosis, her md ordered a ct scan to image the thymus. Why is this performed in pts with her condition? The thymus, which is a gland apart of the immune system is believed to produce the ACh receptor antibodies that block acetylcholine in myasthenia gravis. As adults age, the thymus gland gets smaller however it’s typically bigger than usual in individuals with myasthenia gravis. Uncommonly, some people with this diagnosis also get tumors in the thymus which can potentially become cancerous. The CT scan would be able to detect any abnormalities in Sana’s thymus. 6. In 2018, Health Canada approved the use of ecluzimab for the treatment of myasthenia gravis and in 2020, CADTH recommended reimbursement of the drug for this indication. What is the mechanism of action of ecluzimab? (1 mark) Ecluzimab is a specialized type of immunosuppressant or antibody that specifically targets and neutralizes C5 complement protein , which is responsible for deploying a complex group of proteins called the membrane attack complex (MAC). This complex is a defense mechanism of the complement system and by preventing this mechanism from occurring, it protects the neuromuscular junction from damage at the end plate region in patients with myasthenia gravis. Questions (10 marks) 1. Describe the normal hormonal fluctuations that occur in FSH, LH, estradiol, and progesterone during the ovarian menstrual cycle. (4 marks) The menstrual cycle can be primarily divided into the Follicular phase (Day 0-14) and the Luteal Phase (Day 14-28). FSH: Initially, in the beginning of the menstrual cycle there is an increase in GnRH secreted by the hypothalamus because it’s the start of the menstrual cycle. This should cause a steady increase in FSH and LH, but instead we see a different pattern. There is a slight increase in FSH followed by a slow drop. At the same time, there is a steady amount of LH being released, with no apparent fluctuations. So once FSH is released (initial rise) in the follicular phase, it will enter the ovaries and cause “follicular maturation” of the primary follicles; some of which will mature into a secondary follicle. The maturing of the follicles produces “oestrogen,” which has a negative feedback on the pituitary gland in the first 10 days of the menstrual cycle. At low

concentrations, oestrogen inhibits the release of LH which explains its steady release. Another interaction is that FSH is secreted primarily in low concentrations of oestrogen, So as oestrogen progressively increases, FSH decreases, which explains its drop from its initial increase. After 10 days of the menstrual cycle, as oestrogen levels rise, it will have a positive feedback and stimulate the release of LH. With increases in GnRH alongside oestrogen, there is a massive spike in LH concentration that triggers ovulation of the most mature follicle in the ovary, or oocyte (14-day mark). FSH also has a small surge due to the LH spike. Post-ovulation, LH will drop back down, and GnRH will also slowly drop. This also marks the start of the Luteal phase . Oestrogen levels will slowly decrease (somewhat) and progesterone levels would start to increase at the start of the luteal phase. After the follicle ovulates, the follicle will turn into a “corpus luteum,” and it will eventually slowly degrade and release 3 hormones – oestrogen, inhibin and progesterone. Inhibin will inhibit secretion of FSH. At the 21-day mark, progesterone is increasing and oestregon is still detectable. Progesterone would feedback negatively to the hypothalamus, inhibiting release of GnRH, which will affect in turn decrease FSH and LH during luteal phase. Progesterone would also stimulate endometrial growth. The corpus luteum would eventually degenerate, allowing new set of follicles to mature; as it degenerates, oestrogen, inhibin and progesterone will decrease. This will mean progesterone would no longer inhibit GnRH, so GnRH would increase leading to a new cycle. 2. Why was progesterone administration followed by progesterone withdrawal effective in causing a menses? (2 marks) 3. How can basal body temperature be used to track patterns in the menstrual cycle, and what does the absence of a temperature changes indicate? (2 marks) 4. What is the likely pathophysiological cause f_o_r_ _A_m_a_n_d_a_’s_ _h_i_r_s_u_t_i_s_m_?_ _(_1 mark) 5. W_h_a_t_ _a_r_e_ _t_h_e_ _p_o_s_s_i_b_l_e_ _s_o_u_r_c_e_s_ _o_f_ _A_m_a_n_d_a_’s_ _e_s_t_r_o_g_e_n_?_ _(_1 mark)

biom3200 case study

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