QUIZ 5 SBI4U

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1. The goal of the furnace and thermostat system is to maintain the inside of the home at a constant, comfortable temperature despite changes in the temperature outside. Similarly, the body has systems in place to maintain a steady state of its internal environment such as the body’s temperature. The ability to maintain a constant internal environment in response to environmental changes is called homeostasis. All homeostatic control systems start with a stimulus, have three functional components - a receptor, coordinating centre and regulator, and end with a response. In the case of the furnace and thermostat system, A sensor, such as a thermocouple, serves as the receptor to detect the house's temperature, which is the stimulus. and sends the information to the thermostat (the coordinating centre of the system). The thermostat compares this temperature to the temperature set by the resident. If the temperature in the room is too low, the thermostat sends a signal to the furnace (the effector of the system) to turn on. Similarly, in the human body, receptors in the skin detect the temperature change. They send the information by nerve impulses to temperature centers in the hypothalamus. The hypothalamus, which is the coordinating centre of the system, integrates the information and sends nerve impulses to the capillaries in the skin and the sweat glands, which are the effectors of the body. b. This is a negative feedback system because the response causes the opposite effect of the original stimulus. 2. Positive feedback involves a response that reinforces the change detected. A common example is labour/childbirth. In childbirth, when the fetus’s head presses up against the cervix, it stimulates nerves that tell the brain to stimulate the pituitary gland, which then produces oxytocin. Oxytocin causes the uterus to contract. This moves the fetus even closer to the cervix, which causes more oxytocin to be produced until childbirth occurs and the baby leaves the womb. 3. There are three steps of urine formation. The first step in urine formation is called filtration. It occurs in the glomerulus and Bowman’s capsule. Blood that is about to be filtered enters a glomerulus, which is a tuft of blood capillaries (the smallest of blood vessels). These capillaries act as semi-permeable membranes (filters) so that larger molecules, like plasma protein, blood cells, and platelets, cannot pass through their walls, whereas smaller molecules and wastes can pass through. The resulting filtrate is collected in Bowman’s capsule and then flows into the proximal tubule which begins the second step. The second step in urine formation is a multi-step process known as reabsorption. As the filtrate moves through the proximal tubule, glucose and amino acids are removed and returned to the blood. The filtrate then passes through the loop of Henle. As the descending section of the loop of Henle is permeable to water, water is drawn out by osmosis because the surrounding medulla has a high sodium concentration. This water then moves through the capillary membranes back into the blood. Sodium ions are actively transported out of the filtrate in the ascending section of the loop of Henle, which creates a salt gradient throughout the medulla. Nutrients from the filtrate are selectively reabsorbed into the blood through active and passive transport. The process continues

until the threshold level of a substance is reached so that no more movement across membranes occurs. Secretion, the third step in urine formation occurs in the distal tubule. excess H+ ions from the blood are selectively reabsorbed into the nephron through active transport. The distal tubule helps to regulate potassium (K+) and salt (NaCl) concentration in body fluids. As in the proximal tubule, pH is controlled by the tubular secretion of hydrogen ions (H+) and the reabsorption of bicarbonate ions. The end product of all these processes is urine, which is essentially a collection of substances that have not been reabsorbed during glomerular filtration or tubular reabsorption. 4. 5. The pancreas has a key role in maintaining normal blood glucose levels by secreting the blood sugar-lowering hormone insulin and its opponent glucagon. When blood sugar levels are high, the pancreatic beta cells release insulin, which causes the muscles, liver, and other organs' cells to take up glucose from the circulation. When blood levels are low, the islets of Langerhans' alpha cells release glucagon, which facilitates the transformation of glycogen to glucose, which is then released into the blood and raises blood sugar levels.

6. 7. A reflex arc is a simple neural circuit that runs through the spinal cord. Its components are receptors, afferent neurons, interneurons, efferent neurons and effectors. A reflex arc begins with a stimulus, for example when the fingers come in contact with a hot stove. When the finger touches a hot stove, the heat on your finger triggers a sensory receptor in the skin. The sensory receptor sends the stimulus to the spinal cord. Interneurons in the spinal cord receive the information and immediately send a signal to the motor neurons. The motor neurons activate an effector organ in this case a muscle. The effector organ causes an immediate response i.e. contracting and pulling the hand away from the hot stove. 8. Action potential occurs in the formation of a nerve impulse. It is the voltage difference across a nerve cell membrane when the nerve is excited. When the nerve is excited by a stimulus, a section of the cell membrane becomes more permeable to sodium than potassium as such the gates of the sodium channel open and the gates of the potassium channel close. Sodium ions rush into the nerve cell because of the electrochemical gradient. The rapid influx of sodium ions causes a charge reversal known as depolarization. Once the charge on the inside becomes positive, the sodium gates close, stopping the influx of sodium. Depolarization does not last long. As soon as the inside of the cell becomes positive, the sodium-potassium pump in the cell membrane starts up again to push sodium out and pull potassium in. The sodium-potassium pump restores the condition of the resting membrane by transporting sodium ions out of the neuron while moving potassium ions into the neuron, at a ratio of 3 Na+ to 2 K+ ions. The energy for the pump comes from ATP, and the process of restoring the original polarity of the nerve membrane is called repolarization. During synaptic transmission, a neurotransmitter travels through the synaptic cleft (the gap between neurons) and binds to a receptor on the post-membrane. This results in the nerve impulse being transmitted down to the next neuron.

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9. Homeostasis Case Study: Central Diabetes Insipidus Synopsis of the patient’s life for four months leading to the doctor’s visit For the past four months, Mrs. Darcy Johnson, 44, has been suffering from an ailment that causes her to frequently feel thirsty and urinate a lot. Her father has Type 2 Diabetes, according to her family history. There was not a single family member with diabetes insipidus, deafness, vision loss, or any kind of neurological or renal problem. In addition to not drinking alcohol, the patient had never smoked. Her medical history did not include any history of radiation therapy, brain surgery, cerebrovascular illness, or brain tumour. When she reached 40 years old, her body weight—which had been roughly 56 kg in her 20s—gradually grew to 75 kg; at that point, she experienced excessive thirst, frequent, abnormal urination and polyuria. After two months of these symptoms, the patient visited her primary doctor whom performed a blood test . A blood test indicated fasting plasma glucose and HbA1c levels of 105 mg/dL and 6.7%, respectively, while a urine glucose test came back negative. She was initially assumed to have a bladder condition, therefore oral solifenacin succinate (5 mg/day) was administered. However, because of the persistence of her symptoms, more laboratory testing was recommended. Test Results Upon physical examination, her height was 150 cm, her weight was 67 kg, her blood pressure was 140/63 mmHg, her pulse rate was 69 beats per minute, and her body temperature was 36.7°C. She produced 6.3 litres of pee per day. She had a parched mouth. The results of laboratory testing showed low urine osmolality (Uosm; 125 mOsm/kg), high plasma osmolality (Posm; 321 mOsm/kg), and high serum sodium (158

mEq/L) and chloride (121 mEq/L). The amount of AVP in plasma was 0.6 pg/mL, which is quite low. These findings revealed that the kidneys' incapacity to concentrate urine and preserve bodily water led to hypertonic dehydration and hypotonic polyuria. Diabetes insipidus was taken into consideration (Ohara et al., 2022) . When the doctors ran the vasopressin administration test, two hours after intravenous vasopressin was administered, the results showed a sharp increase in Uosm from 73 to 509 mOsm/kg and a decrease in urine volume from 140 to 15 mL/30 min. Nephrogenic diabetes insipidus was ruled out and CDI was diagnosed as a result of the notable increase in Uosm by up to 100% (Ohara et al., 2022). Questions on Central Diabetes Inspidus 1. What is Central Diabetes Inspidus Central diabetes insipidus (CDI) is a rare and treatable condition in which the body doesn’t have enough antidiuretic hormone, which leads to extreme water loss through your urine ( Cleveland Clinic, n.d) . Central diabetes insipidus is the most common type of diabetes insipidus. 2. What causes Central Diabetes Inspidus? Central diabetes insipidus is caused by the body's inability to produce enough antidiuretic hormone (ADH) also known as vasopressin. The hypothalamus is responsible for the production of ADH. The pituitary gland subsequently stores and releases ADH. ADH helps regulate the water balance in the body by controlling the amount of water the kidneys reabsorb while they filter wastes out of the blood. The body normally produces and releases more ADH when we are dehydrated or losing blood pressure. The increase in ADH tells the kidneys to hold onto more water instead of releasing it in pee. In central diabetes insipidus, the hypothalamus isn’t making enough ADH and/or the pituitary gland isn’t releasing enough ADH. This causes frequent and

excessive water loss through urine ( Central Diabetes Insipidus: MedlinePlus Medical Encyclopedia , n.d.). Specific causes include damage to the hypothalamus or pituitary gland, tumours, or an inherited gene mutation on chromosome 20. 3. What are the primary symptoms of Central Diabetes Inspidus? Symptoms of central diabetes insipidus include Increased urine production, Excessive thirst, Confusion and changes in alertness due to dehydration and higher than normal sodium levels in the body, if the person is unable to drink. 4. How is Central Diabetes Inspidus diagnosed? Various tests are done to diagnose Central Diabetes Inspidus. This is because the symptoms of central diabetes insipidus are similar to those of other conditions, including type 1 diabetes and type 2 diabetes. The first set of tests done is to confirm diabetes inspidus. This is commonly done with a blood test which measures sodium levels and the amount of certain substances in your blood. A Water deprivation test is conducted to diagnose diabetes insipidus and identify its cause. The test involves not drinking any liquids for several hours. A healthcare professional will measure how much urine the patient passes, check their weight, and monitor changes in their blood and urine. In some cases, the health care professional may give them a man-made version of vasopressin or other medicines during the test. The water deprivation and vasopressin test help differentiate Central Diabetes Inspidus from other forms of Diabetes Inspidus through serum and urine osmolality. 5. What are the other types of Diabetes Inspidus? There are 3 other types of Diabetes Inspidus: Nephrogenic diabetes insipidus, Dipsogenic diabetes insipidus and Gestational diabetes insipidus.

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Nephrogenic diabetes insipidus occurs when the body produces enough vasopressin but the kidneys do not respond properly to the hormone. Consequently, the urine becomes overly diluted. It is brought on by inadequate calcium, excessive potassium, or a clogged urinary tract. Dipsogenic diabetes insipidus occurs when an issue in the hypothalamus leads individuals to become thirsty and drink more fluids. Consequently, they might need to urinate frequently.It is brought on by hypothalamic damage from surgery, infections, inflammations, tumours, or head traumas. Gestational diabetes insipidus is an uncommon and transient disease that can arise during pregnancy. This kind of diabetes insipidus develops when the mother's placenta produces an excess of an enzyme that degrades her vasopressin. Given their increased placental tissue, women carrying multiple babies are more susceptible to developing the disease. ( Diabetes Insipidus , 2022) 6. How does Diabetes Inspidus differ from Diabetes Mellitus? Diabetes mellitus is characterized by an abnormally high level of glucose in the blood, generally known as blood sugar. The kidneys attempt to eliminate the excess glucose by excreting it in urine. Blood glucose levels are normal in diabetes insipidus, but urine cannot be adequately concentrated by the kidneys. 7. How do healthcare professionals treat central diabetes insipidus? Doctors most frequently use desmopressin, a synthetic hormone, to treat central diabetes insipidus. This hormone substitutes the vasopressin the body isn't producing. This medication is available as an injection, tablet, or nasal spray. 8. How do eating, diet, and nutrition affect central diabetes insipidus?

Nutrition, diet, and eating habits have not been linked to the development or prevention of diabetes insipidus. Doctors could advise patients to follow a low-protein, low-sodium diet to help their kidneys produce less urine to alleviate discomfort. Sometimes these adjustments by themselves can manage the symptoms, however, this is not often the cause of symptoms of central diabetes insipidus. 9. What are the risk factors of Central Diabetes Inspidus? Risk factors for developing CDI include Brain surgery, Family history of diabetes insipidus and/or Wolfram syndrome, Head injury, and Infection of the brain. Unfortunately, most occurrences of central diabetic inspidus (CDI) cannot be avoided. 10. How common is Central Diabetes Inspidus? Central Diabetes insipidus is rare, affecting about 1 in 25,000 people worldwide. ( Diabetes Insipidus , 2022). REFERENCES Central diabetes insipidus: MedlinePlus Medical Encyclopedia . (n.d.). https://medlineplus.gov/ency/article/000460.htm Diabetes insipidus . (2022, August 29). National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/kidney-disease/diabetes- insipidus#:~:text=Water%20deprivation%20test.,in%20your%20blood%20and%20urine. Professional, C. C. M. (n.d.). Central Diabetes Insipidus (CDI) . Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/23515-central-diabetes-insipidus-cdi Ohara, N., Takada, T., Seki, Y., Akiyama, K., & Yoneoka, Y. (2022). A 75-Year-Old Woman with a 5-Year History of Controlled Type 2 Diabetes Mellitus Presenting with

Polydipsia and Polyuria and a Diagnosis of Central Diabetes Insipidus. American Journal of Case Reports , 24 . https://doi.org/10.12659/ajcr.938482

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QUIZ 5 SBI4U

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