BIOM3020 (2021) Exam SAQs Flashcards
In terms of evolution, the appearance of most of the components that we associate with a complete renin-angiotensin system coincides with the emergence of bony fish.
The genes for ACE/ACE2 appeared hundreds of millions of years earlier and are thought to
have had functions more closely related to
E) regulation of salt and water homeostasis.
Option E, regulation of salt and water homeostasis, is the most accurate choice, as ACE and ACE2 are known to be involved in the regulation of fluid balance, electrolyte levels, and blood pressure in various organisms, including mammals. This function is particularly important for maintaining osmotic balance in aquatic organisms like fish.
What is primary aldosterone and is it linked to hypokalaemia
Primary aldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands, leading to increased sodium retention and potassium excretion. Hypokalemia, which refers to low levels of potassium in the blood, is a common finding in patients with primary aldosteronism. In fact, it occurs in more than 60% of individuals with this condition.
Which TWO (2) nuclei in the middle zone of the hypothalamus have connections with the
neurohypophysis?
Supraoptic nucleus and
Paraventricular nucleus
Specify the nature of connection of the Supraoptic nucleus and Paraventricular nucleus, the hormones involved and their function.
The connection between these nuclei and the neurohypophysis is through the hypothalamo-hypophyseal tract, which is a bundle of axons. These axons originate from the supraoptic nucleus and the paraventricular nucleus and extend down to the posterior pituitary, which is the neurohypophysis. This tract serves as a pathway for the transport and release of hormones.
The hormones involved in this connection are vasopressin (antidiuretic hormone, ADH), produced by the supraoptic nucleus, and oxytocin, produced by the paraventricular nucleus
Briefly describe the anatomy of the adrenal gland, its developmental origin and its functional
sub-divisions
Anatomy of the adrenal gland:
The adrenal gland is located on top of each kidney. It consists of two main regions: the outer cortex and the inner medulla.
Developmental origin:
The adrenal cortex and adrenal medulla have different developmental origins. The adrenal cortex arises from mesoderm-derived cells, while the adrenal medulla originates from neural crest cells.
Functional sub-divisions:
The adrenal gland can be divided into three functional zones:
Zona glomerulosa: The outermost layer of the adrenal cortex. It produces mineralocorticoids, such as aldosterone, which regulate electrolyte and fluid balance.
Zona fasciculata: The middle layer of the adrenal cortex. It produces glucocorticoids, such as cortisol, which play a role in metabolism, immune response, and stress regulation.
Zona reticularis: The innermost layer of the adrenal cortex. It produces androgens, including dehydroepiandrosterone (DHEA), which serve as precursors for sex hormones.
The adrenal medulla, located in the inner region of the adrenal gland, is responsible for producing and releasing catecholamines, including adrenaline (epinephrine) and noradrenaline (norepinephrine). These hormones are involved in the body’s response to stress and regulation of various physiological processes.
Define precision medicine and state why this would be of benefit to people with type 2 diabetes
Precision medicine, also known as personalized medicine, is an approach to healthcare that considers individual variability in genes, environment, and lifestyle for each patient. It involves tailoring medical decisions and treatments to the specific characteristics of an individual, aiming to improve treatment effectiveness and minimize side effects.
Precision medicine would be beneficial to people with type 2 diabetes due to the following reasons:
precision medicine offers the opportunity to customize diabetes treatment based on individual characteristics, leading to more effective interventions, targeted therapies, improved prevention strategies, and better treatment outcomes for individuals with type 2 diabetes.
You have discovered a drug that increases the expression of FFAR2 (GPR43) receptors.
Explain how this drug can alter appetite regulation and whether or not its effects are altered by the
fibre content in the diet. Include in your answer whether the drug would be just as active in lean
people as in obese people and justify why this is the case.
The drug that increases the expression of FFAR2 (GPR43) receptors can potentially alter appetite regulation through the following mechanisms:
Increased Sensitivity to Short-Chain Fatty Acids (SCFAs): FFAR2 receptors are activated by SCFAs, which are produced by the fermentation of dietary fiber in the gut. By increasing the expression of FFAR2 receptors, the drug enhances the response to SCFAs. This activation can lead to the release of hormones that regulate appetite, such as peptide YY (PYY) and glucagon-like peptide-1 (GLP-1), which promote satiety and reduce food intake.
The effects of the drug may be influenced by the fiber content in the diet. A high-fiber diet provides more substrate for the production of SCFAs in the gut. Therefore, in individuals consuming a high-fiber diet, the drug’s ability to increase FFAR2 receptor expression would likely lead to greater activation of these receptors by SCFAs. This enhanced activation can further amplify the drug’s effects on appetite regulation.
The drug’s activity would be equally effective in lean people as in obese people. The drug’s mechanism of action involves increasing the expression of FFAR2 receptors, which are present on cells regardless of a person’s weight status. Therefore, the drug’s ability to alter appetite regulation through FFAR2 activation should be consistent across lean and obese individuals.
However, it’s important to note that the overall response to the drug’s effects on appetite regulation may still vary between individuals due to factors such as hormonal imbalances, gut microbiota composition, and other individual differences associated with obesity. These factors can influence appetite regulation independently of FFAR2 activation. Nevertheless, the drug’s ability to increase FFAR2 receptor expression and enhance sensitivity to SCFAs remains effective in both lean and obese individuals.
Define the word zeitgeber and list FIVE (5) examples of zeitgebers for peripheral clocks
Zeitgeber refers to external cues or environmental factors that help synchronize or entrain an organism’s biological rhythms or internal clocks to the 24-hour day-night cycle. Zeitgeber is a German word that translates to “time giver” or “time cue.”
Examples of zeitgebers for peripheral clocks (clocks located outside of the central nervous system) include:
Light: Light exposure, particularly natural daylight, is a potent zeitgeber. The presence or absence of light signals to the body’s circadian system, influencing various physiological processes and helping to regulate the sleep-wake cycle.
Meal Timing: The timing of meals, especially regular meal patterns, acts as a zeitgeber for peripheral clocks. Consistent meal timing helps synchronize metabolic processes, such as digestion, nutrient absorption, and energy metabolism, to specific times of the day.
Physical Activity: Regular exercise or physical activity can serve as a zeitgeber, affecting peripheral clocks. Engaging in physical activity during specific times of the day helps regulate energy expenditure, hormone release, and various physiological processes.
Social Interaction: Social cues and daily social routines can act as zeitgebers. Interacting with others, engaging in social activities, and following social schedules can influence peripheral clocks by influencing mood, stress levels, and behavioral patterns.
Temperature: Fluctuations in temperature, particularly the transition between warm and cool temperatures, can act as zeitgebers for peripheral clocks. Temperature changes help regulate physiological processes, including metabolic rate, thermoregulation, and sleep patterns.
These zeitgebers play a crucial role in entraining peripheral clocks and ensuring their synchronization with the external environment, allowing organisms to adapt to the daily rhythm and maintain optimal physiological functioning.
Discuss the TWO (2) major hormones produced by the testes. Include in your answer, the cell type producing each hormone, target tissues/cells and their major functions both inside and outside the reproductive tract
The two major hormones produced by the testes are testosterone and inhibin.
Testosterone:
Cell Type: Leydig cells, also known as interstitial cells, located in the connective tissue surrounding the seminiferous tubules.
Target Tissues/Cells: Throughout the body, including reproductive and non-reproductive tissues.
Major Functions:
Inside the Reproductive Tract: Testosterone is crucial for the development and maintenance of male reproductive organs, such as the testes, epididymis, seminal vesicles, and prostate gland. It promotes spermatogenesis (sperm production) in the seminiferous tubules of the testes.
Outside the Reproductive Tract: Testosterone plays various roles outside the reproductive tract, including:
Development and maintenance of secondary sexual characteristics in males, such as deepening of the voice, growth of facial and body hair, and increased muscle mass.
Stimulation of bone growth and maintenance of bone density.
Regulation of libido (sex drive) and sexual function.
Influence on mood, cognition, and behavior.
Modulation of protein synthesis, metabolism, and erythropoiesis (red blood cell production).
Inhibin:
Cell Type: Sertoli cells, located within the seminiferous tubules.
Target Tissues/Cells: The hypothalamus and anterior pituitary gland, providing negative feedback control.
Major Functions:
Inside the Reproductive Tract: Inhibin plays a role in regulating the secretion of follicle-stimulating hormone (FSH) from the anterior pituitary gland. It exerts negative feedback on the pituitary to inhibit excessive FSH release. By regulating FSH levels, inhibin helps modulate spermatogenesis in the seminiferous tubules.
Outside the Reproductive Tract: Inhibin is also involved in the modulation of other tissues and organs, including:
Regulation of the menstrual cycle in females by inhibiting follicular development.
Potential involvement in the regulation of bone density and bone turnover.
Possible effects on neurogenesis and neuroprotection in the brain.
Describe THREE (3) characteristics of peptide hormones and list TWO (2) examples
Three characteristics of peptide hormones are:
Peptide Structure: Peptide hormones are composed of amino acids linked together to form a peptide chain. They range in size from a few amino acids to larger polypeptides. Peptide hormones are water-soluble and are unable to pass through cell membranes.
Receptor Activation: Peptide hormones bind to specific receptors on the surface of target cells. This binding triggers a cascade of intracellular signaling events, usually involving second messengers, which ultimately mediate the cellular response to the hormone.
Rapid Action and Short Half-Life: Peptide hormones generally act quickly once they bind to their receptors, initiating rapid cellular responses. Due to their hydrophilic nature, peptide hormones are rapidly degraded by enzymes, resulting in a relatively short half-life in the bloodstream.
Two examples of peptide hormones are:
Insulin: Insulin is a peptide hormone produced by beta cells in the pancreas. It plays a crucial role in regulating blood glucose levels by promoting the uptake of glucose into cells, particularly in muscle and adipose tissue. Insulin also stimulates glycogen synthesis and inhibits gluconeogenesis in the liver.
Growth Hormone (GH): Growth hormone is a peptide hormone produced by the anterior pituitary gland. It stimulates growth, particularly during childhood and adolescence, by promoting cell division, protein synthesis, and the uptake of nutrients. GH also influences metabolism, promoting the breakdown of fats for energy and inhibiting glucose uptake by cells.
Progesterone is a critical steroid hormone in female reproduction, with multiple functions and sites of action throughout the reproductive tract and the body. If the nuclear progesterone receptor (PGR), which mediates the effects of progesterone, was inhibited or knocked out, what would be the morphological and functional effect of this:
a) in the ovary?
b) in the mammary gland?
c) in the cycling uterus (human)?
d) in the pregnant uterus?
a) In the ovary: Inhibiting or knocking out the nuclear progesterone receptor (PGR) in the ovary would likely disrupt several processes. Progesterone plays a crucial role in the regulation of the menstrual cycle and ovulation. Without the PGR, follicular development and ovulation might be impaired, potentially leading to irregular or absent menstrual cycles and reduced fertility.
b) In the mammary gland: Progesterone is essential for mammary gland development and function. Inhibiting or knocking out the PGR would likely result in impaired mammary gland growth and differentiation. This could lead to underdeveloped mammary glands and hinder the ability to produce milk during lactation.
c) In the cycling uterus (human): Progesterone is involved in preparing and maintaining the endometrium (the lining of the uterus) for implantation of a fertilized egg. If the PGR is inhibited or knocked out, the endometrium may not undergo the necessary changes to support implantation. This could lead to difficulties in achieving and maintaining pregnancy.
d) In the pregnant uterus: Progesterone is crucial for maintaining pregnancy by supporting the growth and development of the uterine lining and preventing contractions that could lead to premature labor. Inhibiting or knocking out the PGR in the pregnant uterus could result in uterine contractions, leading to preterm labor and potential pregnancy loss.
a) Describe the molecular mechanisms involved in oestrogen-driven uterine epithelial
proliferation in the rodent uterus.
b) How does subsequent progesterone counteract the actions of oestrogen?
a) Molecular mechanisms involved in estrogen-driven uterine epithelial proliferation in the rodent uterus:
Estrogen binds to estrogen receptors (ERs) present in uterine epithelial cells. This binding activates ERs, which act as transcription factors. Activated ERs bind to estrogen response elements (EREs) in the promoter regions of target genes, leading to gene transcription. This results in the synthesis of proteins involved in cell proliferation, such as growth factors and cell cycle regulators. Estrogen also induces the production and release of growth factors, which bind to their receptors and activate downstream signaling pathways that promote cell proliferation.
b) Progesterone counteracts the actions of estrogen in the following ways:
Modulation of Estrogen Receptor Activity: Progesterone inhibits estrogen-driven gene transcription by interfering with estrogen receptor (ER) binding to estrogen response elements (EREs) in the promoter regions of target genes. This suppresses the expression of genes involved in cell proliferation.
Changes in Co-regulator Proteins: Progesterone alters the recruitment of co-regulator proteins that interact with ERs. These co-regulators can enhance or inhibit the transcriptional activity of ERs, ultimately affecting the balance between estrogen- and progesterone-driven gene expression. Progesterone promotes the recruitment of co-regulators that inhibit estrogen-driven gene expression.
Induction of Differentiation: Progesterone promotes the differentiation of uterine epithelial cells, leading to changes in cellular morphology and secretory function. This counteracts the proliferative effects of estrogen and promotes the development of a receptive endometrium.
Name FOUR (4) factors that contribute to worsening of asthma during pregnancy.
Four factors that contribute to worsening of asthma during pregnancy are:
- Hormonal Changes: Pregnancy is associated with hormonal fluctuations, including increased levels of estrogen and progesterone. These hormonal changes can affect the airways and contribute to increased bronchial hyperresponsiveness, leading to worsening asthma symptoms.
- Increased Blood Volume and Cardiac Output: During pregnancy, there is an increase in blood volume and cardiac output to support the growing fetus. This increased circulation can affect lung function and exacerbate asthma symptoms.
- Immune System Changes: The immune system undergoes modifications during pregnancy to accommodate the developing fetus. These changes can alter the inflammatory response in the airways and make pregnant women with asthma more susceptible to exacerbations triggered by allergens or respiratory infections.
- Non-Optimal Asthma Management: Poorly controlled asthma before or during pregnancy can significantly impact asthma outcomes during pregnancy. Inadequate asthma management, including underuse of controller medications, lack of asthma action plans, or insufficient follow-up with healthcare providers, can contribute to worsening asthma symptoms during pregnancy.
It is essential for pregnant women with asthma to work closely with their healthcare providers to optimize asthma management and ensure adequate control of symptoms throughout pregnancy.
Describe the inflammatory mechanisms proposed to be involved in worsening of asthma during pregnancy.
The inflammatory mechanisms proposed to be involved in worsening of asthma during pregnancy include:
Increased Th2-Type Inflammation: Pregnancy is associated with a shift towards a Th2-type immune response, characterized by increased production of cytokines such as interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13). This Th2-type inflammation promotes eosinophilic inflammation, airway remodeling, and increased bronchial hyperresponsiveness, leading to worsening asthma symptoms.
Hormonal Influences on Inflammation: Hormonal changes during pregnancy, such as increased levels of estrogen and progesterone, can impact the immune response and inflammation in the airways. Estrogen has been shown to enhance Th2-type immune responses and promote inflammation, while progesterone has been associated with anti-inflammatory effects. The balance between these hormonal influences can affect the overall inflammatory state and contribute to asthma exacerbations.
Altered Immune Tolerance: During pregnancy, the maternal immune system undergoes changes to promote immune tolerance towards the developing fetus. This altered immune tolerance can result in a reduced ability to suppress pro-inflammatory responses in the airways, leading to an exacerbation of asthma symptoms.
Interactions with Respiratory Infections and Allergens: Pregnant women with asthma may be more susceptible to respiratory infections and have increased airway responsiveness to allergens. These interactions can trigger inflammatory responses, exacerbating asthma symptoms during pregnancy.
These inflammatory mechanisms contribute to the worsening of asthma during pregnancy. It is important for pregnant women with asthma to work closely with their healthcare providers to manage and control inflammation effectively to minimize the impact on maternal and fetal health.
Apart from its actions in stimulating red blood production, erythropoietin is increasingly being used to treat a range of other conditions. Discuss two ‘non-classical’ actions of erythropoietin, including its mechanism of action.
Two non-classical actions of erythropoietin (EPO) are tissue protection and neuroprotection.
Tissue Protection:
EPO has been shown to have tissue-protective effects in various organs. It acts as an anti-apoptotic and anti-inflammatory agent, promoting cell survival and reducing tissue damage in different pathological conditions. EPO binds to its receptor (EPOR) on target cells, initiating downstream signaling pathways that mediate tissue protection.
Mechanism of Action: EPO binding to EPOR activates intracellular signaling pathways, including the JAK2/STAT5 pathway, which leads to the activation of anti-apoptotic genes and the inhibition of pro-apoptotic factors. EPO also modulates inflammatory responses by suppressing the production of pro-inflammatory cytokines and promoting the release of anti-inflammatory cytokines, thereby reducing tissue inflammation and damage.
Neuroprotection:
EPO has shown neuroprotective effects in various neurological conditions, including stroke, traumatic brain injury, and neurodegenerative diseases. It promotes cell survival, enhances neuronal regeneration, and modulates inflammatory responses in the brain.
Mechanism of Action: EPO exerts its neuroprotective effects by binding to EPOR on neurons and glial cells in the central nervous system. This binding activates several intracellular signaling pathways, including the PI3K/Akt and MAPK pathways, which promote neuronal survival, inhibit apoptosis, and enhance neuronal plasticity. EPO also stimulates angiogenesis, which improves blood flow to the brain, and reduces inflammation by suppressing pro-inflammatory cytokines.
In summary, the non-classical actions of EPO involve tissue protection and neuroprotection. EPO acts as an anti-apoptotic and anti-inflammatory agent, promoting cell survival and reducing tissue damage in various organs. In the brain, EPO exhibits neuroprotective effects by enhancing neuronal survival, inhibiting apoptosis, and modulating inflammatory responses. These actions are mediated through the binding of EPO to its receptor, leading to the activation of signaling pathways that promote tissue and neuroprotection.
