Practice 5 structured short- and long-answer medical questions on Weekly Year 2: Physiology Exam - May 15, 2026 (Sections B & C). Review model answers for ex...
Answer: When blood pressure drops, leading to decreased renal perfusion, the juxtaglomerular apparatus responds in several ways. Firstly, macula densa cells detect reduced sodium and chloride delivery to the distal tubule and signal the juxtaglomerular cells. Secondly, reduced stretch of the afferent arteriole directly stimulates juxtaglomerular cells. These cells release renin. Renin initiates the renin-angiotensin-aldosterone system (RAAS). Angiotensin II, a potent vasoconstrictor, constricts both afferent and efferent arterioles, but more so the efferent arteriole. This helps to maintain glomerular hydrostatic pressure and thus GFR. Angiotensin II also stimulates aldosterone release, which promotes sodium reabsorption in the distal tubule and collecting duct, increasing blood volume and further supporting GFR. Therefore, the juxtaglomerular apparatus plays a crucial role in preventing a drastic fall in GFR during hypotension.
Answer: Plasma calcium concentration is primarily regulated by parathyroid hormone (PTH) and calcitonin, acting on bone, kidneys, and the gastrointestinal tract. When plasma calcium levels fall, the parathyroid glands release PTH. PTH acts on bone to increase osteoclast activity, releasing calcium and phosphate into the blood. In the kidneys, PTH increases calcium reabsorption in the distal tubules and collecting ducts, reducing calcium excretion. PTH also stimulates the conversion of calcidiol to calcitriol (active vitamin D) in the kidneys. Calcitriol then enhances calcium absorption from the small intestine. Conversely, when plasma calcium levels rise, calcitonin, released from the thyroid C-cells, acts to lower them. Calcitonin inhibits osteoclast activity, reducing calcium release from bone, and may have some minor effects on renal calcium excretion. This intricate interplay ensures adequate calcium for physiological functions and prevents hypercalcemia.
Answer: Inspiration during quiet breathing is an active process. The primary inspiratory muscles are the diaphragm and the external intercostal muscles. When stimulated by the phrenic nerve, the diaphragm contracts and flattens, increasing the vertical dimension of the thoracic cavity. Simultaneously, the external intercostal muscles contract, lifting the ribs upwards and outwards, increasing the anteroposterior and lateral dimensions of the thoracic cavity. These combined actions increase the volume of the thoracic cavity. As the thoracic cavity expands, the visceral pleura and parietal pleura are pulled apart, leading to an increase in lung volume due to the elastic recoil of the lungs and chest wall. According to Boyle's Law (P1V1 = P2V2), as lung volume increases, the intrapulmonary pressure (pressure within the alveoli) decreases, becoming lower than atmospheric pressure. This pressure gradient drives air from the atmosphere into the lungs until intrapulmonary pressure equals atmospheric pressure.
Answer: Synaptic transmission at a chemical synapse begins when an action potential arrives at the presynaptic terminal. This depolarization opens voltage-gated calcium channels, allowing calcium ions (Ca2+) to influx into the presynaptic terminal. The influx of Ca2+ triggers the fusion of synaptic vesicles, containing neurotransmitters, with the presynaptic membrane. This process, exocytosis, releases neurotransmitters into the synaptic cleft. Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane. This binding causes a conformational change in the receptor, leading to the opening or closing of ion channels. If cation channels open (e.g., Na+ influx), the postsynaptic membrane depolarizes, creating an excitatory postsynaptic potential (EPSP), bringing the neuron closer to its firing threshold. If anion channels open (e.g., Cl- influx) or cation channels close, the postsynaptic membrane hyperpolarizes, creating an inhibitory postsynaptic potential (IPSP), moving the neuron further from its firing threshold. Summation of EPSPs and IPSPs determines whether the postsynaptic neuron will fire an action potential.
Answer: Blood glucose homeostasis is a critical process primarily regulated by the interplay of insulin and glucagon, produced by the pancreatic islets of Langerhans. The normal fasting blood glucose range is typically 70-100 mg/dL. **Hormonal Regulation:** * **Insulin:** Released by beta cells of the islets of Langerhans in response to hyperglycemia (e.g., after a meal). Insulin's main actions are to lower blood glucose by: * Promoting glucose uptake into peripheral tissues (muscle, adipose tissue) via GLUT4 transporters. * Stimulating glycogenesis (conversion of glucose to glycogen) in the liver and muscles. * Inhibiting gluconeogenesis (synthesis of glucose from non-carbohydrate precursors) and glycogenolysis (breakdown of glycogen) in the liver. * Promoting fat synthesis and inhibiting fat breakdown. * **Glucagon:** Released by alpha cells of the islets of Langerhans in response to hypoglycemia (e.g., during fasting). * Primarily acts on the liver to increase blood glucose by stimulating glycogenolysis and gluconeogenesis. * Inhibits glycogenesis and promotes lipolysis. * **Other Hormones:** Cortisol and growth hormone can increase blood glucose by promoting gluconeogenesis and reducing glucose utilization. Epinephrine also raises blood glucose by stimulating glycogenolysis. **Organ Involvement:** * **Pancreas:** Produces insulin and glucagon. * **Liver:** Acts as a glucose reservoir. It stores glucose as glycogen (glycogenesis) and releases glucose into the blood by breaking down glycogen (glycogenolysis) or synthesizing new glucose (gluconeogenesis). * **Muscles:** Store glucose as glycogen and use glucose for energy. Insulin promotes glucose uptake via GLUT4. * **Adipose Tissue:** Takes up glucose in response to insulin (via GLUT4) and stores it as fat. Insulin also inhibits lipolysis. **Cellular Mechanisms:** * **GLUT4 Transporters:** Insulin-dependent glucose transporters found in muscle and adipose tissue. Insulin signaling leads to their translocation to the cell membrane, facilitating glucose uptake. * **Enzymatic Pathways:** Regulation of key enzymes involved in glycolysis, glycogenesis, glycogenolysis, and gluconeogenesis. **Response to a High Carbohydrate Meal:** 1. **Hyperglycemia:** Ingested carbohydrates are digested into glucose, leading to increased blood glucose levels. 2. **Insulin Release:** High blood glucose stimulates pancreatic beta cells to release insulin. 3. **Glucose Uptake and Storage:** Insulin promotes glucose uptake into muscle and adipose tissue (GLUT4). In the liver and muscles, insulin stimulates glycogenesis, storing excess glucose as glycogen. In adipose tissue, glucose is converted to fatty acids. 4. **Inhibition of Glucose Production:** Insulin suppresses hepatic gluconeogenesis and glycogenolysis. 5. **Result:** Blood glucose levels return to the normal fasting range. **Response to Prolonged Fasting:** 1. **Hypoglycemia:** Blood glucose levels begin to fall as glucose is utilized by tissues. 2. **Glucagon Release:** Low blood glucose stimulates pancreatic alpha cells to release glucagon. 3. **Glucose Production:** Glucagon acts on the liver to stimulate glycogenolysis (releasing stored glucose) and gluconeogenesis (synthesizing new glucose from amino acids, lactate, and glycerol). 4. **Inhibition of Glucose Uptake:** Insulin levels decrease, reducing glucose uptake by peripheral tissues. Adipose tissue starts lipolysis, releasing fatty acids for energy, sparing glucose for the brain. 5. **Other Hormonal Influence:** Increased levels of cortisol and growth hormone further support gluconeogenesis and reduce glucose utilization by peripheral tissues. 6. **Result:** Blood glucose levels are maintained within a functional range to supply the brain and other vital organs. In summary, blood glucose homeostasis is a dynamic process involving a negative feedback system that relies on precise hormonal control, the metabolic capabilities of key organs, and specific cellular signaling pathways to prevent potentially damaging excursions in blood glucose levels.