Endocrine Block Answers

Question 1:

In addition to appetite regulation, what other physiological process is influenced by glucagon-like peptide-1 (GLP-1)?

a) Blood clotting

b) Bone density

c) Immune response

d) Insulin secretion

e) Memory formation

Answer 1:

d) Insulin secretion

Explanation:

D is correct due to GLP-1 not only regulates appetite but also enhances insulin secretion, which is important for blood glucose control.

a) Blood clotting: GLP-1 does not directly affect blood clotting. Blood clotting is mainly controlled by platelets, clotting factors, and other components of the circulatory system.

b) Bone density: GLP-1 is not involved in regulating bone density. Bone density is influenced by hormones like parathyroid hormone (PTH), vitamin D, and calcium levels.

c) Immune response: GLP-1 does not play a primary role in immune response. The immune system is regulated by various immune cells and signalling molecules, such as cytokines.

e) Memory formation: GLP-1 is not directly involved in memory formation. Memory formation is primarily associated with brain regions like the hippocampus and neurotransmitters like acetylcholine.

Question 2: 

Which of the following is NOT a component of a hormonal feedback loop?

a) Hormone

b) Receptor

c) Effector

d) Stimulus

e) Control centre

Answer 2: 

c) Effector

Explanation: 

A hormonal feedback loop typically includes a hormone, receptor, stimulus, and control center. The effector is not part of the feedback loop but is influenced by it.

a) Hormone: Incorrect. Hormones are chemical signals which are necessary components of feedback loops as they carry signals to target tissues to create a response.

b) Receptor: Incorrect. Receptors are key in feedback loops, as they detect changes in the environment and bind to hormones to initiate a response.

d) Stimulus: Incorrect. The stimulus triggers the feedback loop, such as a change in blood glucose levels, leading to hormone release.

e) Control Centre: Incorrect. The control centre (like the hypothalamus or pituitary gland) interprets the signal and controls hormone release, making it essential for the feedback loop.

Question 3: 

Which hormone is responsible for regulating calcium levels in the blood?

a) Insulin

b) Thyroxine

c) Parathyroid hormone

d) Cortisol

e) Growth hormone

Answer 3: 

c) Parathyroid hormone

Explanation: 

Parathyroid hormone is responsible for regulating calcium levels in the blood by stimulating calcium release from bones and increasing calcium absorption in the intestines which increases serum calcium.

a) Insulin: Incorrect. Insulin regulates blood glucose, not calcium.

b) Thyroxine: Incorrect. Thyroxine regulates metabolism, not calcium levels.

d) Cortisol: Incorrect. Cortisol is involved in stress response and metabolism, not calcium regulation.

e) Growth hormone: Incorrect. Growth hormone promotes growth and cell regeneration, not calcium regulation.

Question 4:

Which hormone is primarily produced by the stomach and plays a role in signalling hunger to the brain?

a) Leptin

b) Ghrelin

c) GLP-1

d) Thyroxine (T4)

e) Cortisol

Answer 4:

b) Ghrelin

Explanation:

Ghrelin is primarily produced by the stomach and serves as a hunger hormone, signalling the brain to stimulate appetite.

a) Leptin: Incorrect. Leptin is produced by fat cells and signals satiety (fullness), not hunger.

c) GLP-1: Incorrect. this is produced by L cells in small intestine and promotes insulin secretion and promotes satiety (fullness) 

d) Thyroxine (T4): Incorrect. Thyroxine regulates metabolism, not hunger signals.

e) Cortisol: Incorrect. Cortisol is involved in stress response and metabolism, not hunger regulation.

Question 5: 

Which hormone is released by the adrenal glands in response to stress and helps the body cope with it?

a) Insulin

b) Aldosterone

c) Epinephrine

d) Thyroid hormone

e) Parathyroid hormone

Answer 5: 

c) Epinephrine

Explanation: 

Epinephrine, also known as adrenaline, is released by the adrenal glands during the “fight or flight” response to stress, helping the body cope with immediate threats.

a) Insulin: Incorrect. Insulin which is released by the beta cells of the pancreas regulates blood sugar, not stress response.

b) Aldosterone: Incorrect. While Aldosterone is produced by the zona glomerulosa of the adrenal glands its function is to regulate blood pressure and fluid balance, not the immediate stress response.

d) Thyroid hormone: Incorrect. Thyroid hormones function to regulate metabolism but do not directly mediate the stress response.

e) Parathyroid hormone: Incorrect. Parathyroid hormone function to regulate calcium levels, not the stress response.

Question 6:

What is the primary function of glucagon-like peptide-1 (GLP-1) in appetite regulation?

a) Stimulating appetite and food intake

b) Enhancing insulin secretion

c) Increase blood concentration of glucose

d) Regulating blood pressure

e) Promoting fat storage

Answer 6:

b) Enhancing insulin secretion

Explanation:

GLP-1 is a hormone that enhances the secretion of insulin as it is an incretin and also suppresses appetite and promotes satiety by acting on receptors in the brain and gastrointestinal system.

a) Stimulating appetite and food intake: Incorrect. GLP-1 suppresses appetite, not stimulates it.

c) Increasing blood concentration of glucose: Incorrect. GLP-1 does the opposite by enhancing insulin secretion, which helps lower blood glucose.

d) Regulating blood pressure: Incorrect. GLP-1 is not primarily involved in blood pressure regulation.

e) Promoting fat storage: Incorrect. GLP-1 does not promote fat storage; it helps regulate blood glucose and reduces appetite.

Question 7:

What is the primary function of leptin in appetite regulation?

a) Stimulating hunger and food intake

b) Promoting fat storage

c) Suppressing appetite and increasing energy expenditure

d) Regulating blood glucose levels

e) Enhancing insulin sensitivity

Answer 7:

c) Suppressing appetite and increasing energy expenditure

Explanation:

Leptin is a hormone produced by fat cells that suppresses appetite and increases energy expenditure, helping to regulate body weight.

a) Stimulating hunger and food intake: Incorrect. Leptin suppresses hunger and decreases food intake, Ghrelin is what stimulates hunger and food intake. 

b) Promoting fat storage: Incorrect. Leptin signals to the brain that there is enough energy stored as fat, which decreases appetite, not promotes fat storage.

d) Regulating blood glucose levels: Incorrect. Leptin’s primary function is not to regulate blood glucose but to manage energy balance.

e) Enhancing insulin sensitivity: Incorrect. While leptin has some influence on metabolism, its main role is appetite suppression and energy expenditure, not directly enhancing insulin sensitivity.

Question 8: 

Which hormone is released by the thyroid gland and plays a crucial role in regulating the body’s metabolic rate?

a) Melatonin

b) Calcitonin 

c) Cortisol

d) Thyroxine

e) adrenaline

Answer 8: 

d) Thyroxine

Explanation: 

Thyroxine, also known as T4, is released by the follicular cells of the thyroid gland and is essential for regulating the body’s metabolic rate. 

a) Melatonin: Incorrect. Melatonin which is produced in the pineal gland regulates sleep-wake cycles, not metabolism.

b) Calcitonin: Incorrect.Whilst Calcitonin is released by the parafollicular cells of thyroid gland its function is for blood calcium regulation and not metabolism

c) Cortisol: Incorrect. Cortisol is produced by the zona fasciculata of the adrenal glands and manages stress and energy use, not overall metabolic rate.

e) Adrenaline: Incorrect. Adrenaline/epinephrine is produced by the adrenal glands medulla and functions to help the body respond to stress but does not regulate the metabolic rate long-term.

Question 9: 

What is the term for the underproduction or no production of insulin during childhood by the pancreas, leading to elevated blood glucose levels?

a) Diabetes insipidus

b) Type 1 diabetes mellitus

c) Type 2 diabetes mellitus

d) cushing’s syndrome

e) addison’s syndrome

Answer 9: 

b) Type 1 diabetes

Explanation: 

Type 1 diabetes is characterised by the underproduction of insulin by the pancreas, resulting in elevated blood glucose levels. The keyword in the Question is ‘Childhood’ Type 1 diabetes is an autoimmune disease which develops when you are young .

• a) Diabetes insipidus: Incorrect. Diabetes insipidus is a condition characterized by an imbalance of water in the body, often due to a lack of antidiuretic hormone (ADH) or a kidney response issue. It leads to excessive urination and thirst, but it is not related to insulin or blood glucose regulation.
• c) Type 2 diabetes mellitus: Incorrect. Type 2 diabetes typically develops later in life and is characterized by insulin resistance rather than a lack of insulin production. It is usually related to lifestyle factors and not commonly seen in children.
• d) Cushing’s syndrome: Incorrect. Cushing’s syndrome is caused by prolonged exposure to high levels of cortisol, not by insulin deficiency. It leads to symptoms like weight gain, high blood pressure, and high blood sugar, but it is unrelated to insulin production in the pancreas.
• e) Addison’s syndrome: Incorrect. Addison’s syndrome is a condition where the adrenal glands produce inadequate levels of cortisol and aldosterone. It is related to hormone deficiencies from the adrenal glands, not the pancreas, and does not involve insulin production or blood glucose regulation.

Question 10: 

Which hormone is responsible for promoting water reabsorption in the kidneys, thereby reducing urine output and conserving body fluids?

a) Thyroxine

b) Progesterone

c) Aldosterone

d) Renin

e) Glucagon

Answer 10: 

c) Aldosterone

Explanation: 

Aldosterone is produced by the adrenal glands and promotes water reabsorption in the kidneys, reducing urine output and conserving body fluids.Hence the more suited answer is Aldosterone as that directly impacts water reabsorption in kidneys.

a) Thyroxine: Incorrect. Thyroxine which is released by the follicular cells of the thyroid gland functions to regulate metabolism, not water reabsorption.

b) Progesterone: Incorrect. Progesterone is involved in reproductive processes, not water balance.

d) Renin: Incorrect. Renin is an enzyme which is produced by the juxtaglomerular cells of the kidney which initiates the RAAS by activating Angiotensin 1 to Allow the RAAS system to occur that will ultimately lead to the production of aldosterone.  However it does not directly cause water reabsorption. Aldosterone, produced as a result of the RAAS, is responsible for water retention.

e) Glucagon: Incorrect. Glucagon which is produced by the alpha cells of the pancreas regulates blood sugar levels, not water balance. → (when the glucose is GONe glucaGON is produced) 

Question 11: 

Which imaging modality is best suited for identifying the hypothalamus and pituitary gland on a sagittal plane?

a) Computed Tomography (CT)

b) Magnetic Resonance Imaging (MRI)

c) Ultrasound (US)

d) X-ray

e) Positron Emission Tomography (PET)

Answer 11: 

b) Magnetic Resonance Imaging (MRI)

Explanation: 

Magnetic Resonance Imaging (MRI) provides detailed images of soft tissues and is ideal for visualizing the hypothalamus and pituitary gland in a sagittal plane due to its excellent anatomical resolution.

a) Computed Tomography (CT): Incorrect. CT scans are useful for imaging bones and detecting acute conditions like haemorrhages, but they have lower resolution for soft tissues like the hypothalamus and pituitary gland compared to MRI.

c) Ultrasound (US): Incorrect. Ultrasound is good for imaging soft tissues and fluid-filled structures but is not suitable for visualising deep brain structures like the hypothalamus and pituitary gland.

d) X-ray: Incorrect. X-rays are primarily used for imaging bones and do not provide detailed images of soft tissues or brain structures like the hypothalamus and pituitary gland.

e) Positron Emission Tomography (PET): Incorrect. PET scans are used for assessing metabolic activity rather than providing detailed anatomical images. They are not ideal for imaging specific brain structures like the hypothalamus and pituitary gland.

Question 12: 

During embryological development, the thyroid gland descends from its initial position at the base of the tongue to its final location in the neck. What structure guides this descent ?

a) Thyroid cartilage

b) Cricothyroid

c) Thyroglossal duct

d) Cricoid

e) foramen caecum

Answer 12: 

c) Thyroglossal duct

Explanation: 

The thyroid gland’s descent is guided by the thyroglossal duct during embryological development, and thyroglossal cysts can form if remnants of this duct persist.

a) Thyroid cartilage: Incorrect. The thyroid cartilage is a part of the larynx and does not guide the descent of the thyroid gland during development.

b) Cricothyroid: Incorrect. The cricothyroid is a muscle associated with the larynx and does not play a role in the descent of the thyroid gland.

d) Cricoid: Incorrect. The cricoid cartilage is another component of the larynx and is unrelated to the thyroid gland’s descent.

e) Foramen caecum: Incorrect. The foramen caecum is an embryological remnant of the thyroglossal duct at the base of the tongue, marking the original location of the thyroid gland, but it does not guide its descent.

Question 13:

Which of the following is considered an endocrine tissue involved in regulating food intake?

a) Liver

b) Kidney

c) Large intestine

d) Adipose

e) small intestine

Answer 13:

d) Adipose

Explanation:

Fat tissue (adipose) is considered an endocrine organ that secretes hormones (leptin being one) involved in the regulation of food intake. Leptin suppresses hunger.

a) Liver: Incorrect. While the liver has some endocrine functions (e.g., producing glucose), it is not directly involved in regulating food intake.

b) Kidney: Incorrect. The kidneys play roles in regulating fluid balance and blood pressure, but they do not secrete hormones involved in regulating food intake.

c) Large intestine: Incorrect. The large intestine is involved in water absorption and waste formation but does not have a role in food intake regulation.

e) Small intestine: Incorrect. whilst the small intestine do release some hormones which regulate food intake e.g. GLP-1 its primary role is in nutrient absorption, not directly regulating food intake through endocrine signaling like adipose tissue does with leptin.

Question 14:

Which sex steroid is primarily responsible for maintaining the uterine lining during pregnancy?

a) Oestrogen

b) Progesterone

c) Luteinizing hormone (LH)

d) b-HCG

e) Follicle-stimulating hormone (FSH)

Answer 14:

b) Progesterone

Explanation:

Progesterone is the primary sex steroid responsible for maintaining the uterine lining during pregnancy, ensuring a suitable environment for the developing foetus.

a) Oestrogen: Incorrect. .Oestrogen is used to prepare the uterine lining for implantation of the fertilised egg  but is not primarily responsible for maintaining it during pregnancy.

c) Luteinizing hormone (LH): Incorrect. LH is involved in ovulation and the production of sex hormones but does not maintain the uterine lining during pregnancy.

d) b-HCG: Incorrect. b-HCG (human chorionic gonadotropin) produced by the syncytiotrophoblast cells of placenta  supports the corpus luteum, which in turn produces progesterone, but b-HCG itself does not directly maintain the uterine lining.

e) Follicle-stimulating hormone (FSH): Incorrect. FSH is involved in the development of ovarian follicles and does not maintain the uterine lining during pregnancy.

Question 15:

Which of the following conditions is characterized by excessive sex steroid production in the ovaries and can lead to symptoms like irregular menstruation and ovarian cysts?

a) Polycystic ovary syndrome (PCOS)

b) Hypogonadism

c) Menopause

d) Primary hyperparathyroidism

e) Adrenal insufficiency

Answer 15:

a) Polycystic ovary syndrome (PCOS)

Explanation:

Polycystic ovary syndrome (PCOS) is characterized by excessive sex steroid production in the ovaries, leading to symptoms such as irregular menstruation and the development of ovarian cysts.

b) Hypogonadism: Incorrect. Hypogonadism is characterized by low sex steroid production, not excessive production, and would not cause symptoms like ovarian cysts.

c) Menopause: Incorrect. Menopause is characterized by a decline in sex hormone levels, not excessive production, and is associated with the cessation of menstruation, not irregular menstruation and cysts.

d) Primary hyperparathyroidism: Incorrect. Primary hyperparathyroidism is related to excessive parathyroid hormone production, which affects calcium levels, not sex steroid production or ovarian function.

e) Adrenal insufficiency: Incorrect. Adrenal insufficiency involves insufficient production of adrenal hormones like cortisol, not excessive sex steroid production.

Question 16:

Which major endocrine gland is often referred to as the “master gland” because it controls the functions of other endocrine glands?

a) Hypothalamus

b) Thyroid gland

c) Parathyroid gland

d) Pituitary gland

e) Adrenal gland

Answer 16:

d) Pituitary gland

Explanation:

The pituitary gland is often called the “master gland” because it secretes hormones that regulate the functions of other endocrine glands in the body.

a) Hypothalamus: Incorrect. While the hypothalamus plays a crucial role in regulating the pituitary gland, it is not referred to as the “master gland” because it does not directly secrete hormones that control other endocrine glands.

b) Thyroid gland: Incorrect. The thyroid gland regulates metabolism, but it does not control the functions of other endocrine glands.

c) Parathyroid gland: Incorrect. The parathyroid glands regulate calcium levels but do not control other endocrine glands.

e) Adrenal gland: Incorrect. The adrenal glands secrete hormones like cortisol and adrenaline but are regulated by the pituitary gland rather than controlling other glands themselves.

Question 17:

How does the feedback loop between sex steroids and LH/FSH regulate the menstrual cycle?

a) High LH/FSH levels trigger menstruation.

b) Low sex steroid levels stimulate LH/FSH release.

c) Elevated sex steroid levels inhibit LH/FSH secretion.

d) LH/FSH have no influence on sex steroid levels.

e) LH/FSH levels remain constant throughout the cycle.

Answer 17:

c) Elevated sex steroid levels inhibit LH/FSH secretion.

Explanation:

Elevated sex steroid levels, particularly oestrogen and progesterone, inhibit LH/FSH secretion, helping to regulate the menstrual cycle.

a) High LH/FSH levels trigger menstruation: Incorrect. High LH/FSH levels trigger ovulation, not menstruation, furthermore they simulate sex steroid release

b) Low sex steroid levels stimulate LH/FSH release: Incorrect. Low levels of sex steroids can lead to the increased release of LH and FSH, but this is not the complete feedback loop that regulates the menstrual cycle.

d) LH/FSH have no influence on sex steroid levels: Incorrect. LH and FSH directly influence the production of sex steroids like oestrogen and progesterone.

e) LH/FSH levels remain constant throughout the cycle: Incorrect. LH and FSH levels fluctuate throughout the menstrual cycle, with a significant surge of LH triggering ovulation.

Question 18:

Which of the following hormones is primarily responsible for stimulating the production of androgens?

a) Follicle stimulating Hormone (FSH)

b) Thyroxine (T4)

c) Testosterone

d) Luteinizing hormone (LH)

e) Oestrogen

Answer 18:

d) Luteinizing hormone (LH)

Explanation:

Luteinizing hormone (LH) plays a crucial role in stimulating the production of androgens in theca cells. 

a) Follicle-stimulating hormone (FSH): Incorrect. FSH stimulates the development of ovarian follicles in females and spermatogenesis ((the production and maturation of sperm) in males, but it does not primarily stimulate androgen production.

b) Thyroxine (T4): Incorrect. Thyroxine regulates metabolism but does not influence androgen production.

c) Testosterone: Incorrect. Testosterone is an androgen itself, not a hormone that stimulates androgen production.

e) Oestrogen: Incorrect. Oestrogen is a sex hormone that influences female secondary sexual characteristics, but it does not stimulate androgen production.

Question 19:

What is a clinical example of hypogonadism?

a) Ovulation during the menstrual cycle

b) Puberty and growth spurts in adolescents

c) Elevated testosterone levels in males

d) Delayed or absent menstruation in females

e) High levels of LH and FSH in adults

Answer 19:

d) Delayed or absent menstruation in females

Explanation:

Hypogonadism in females can result in delayed or absent menstruation due to insufficient sex steroid production to carry out the menstrual cycle as it is very dependent on these hormones. 

a) Ovulation during the menstrual cycle: Incorrect. Ovulation is a sign of normal ovarian function, not hypogonadism.

b) Puberty and growth spurts in adolescents: Incorrect. Puberty is characterized by the normal onset of hormone production and does not indicate hypogonadism.

c) Elevated testosterone levels in males: Incorrect. Hypogonadism is associated with low levels of sex hormones, not elevated levels.

e) High levels of LH and FSH in adults: Incorrect. High levels of LH and FSH may indicate gonadal failure (as the body tries to stimulate hormone production), but this is not a direct example of hypogonadism itself.

Question 20:

Which of the following hormones is responsible for promoting uterine contractions during labour and milk ejection during breastfeeding?

a) Oxytocin

b) Oestrogen

c) Progesterone

d) Prolactin

e) hCG

Answer 20:

a) Oxytocin

Explanation:

Oxytocin is the hormone secreted by the posterior pituitary and responsible for promoting uterine contractions during labour and facilitating milk ejection during breastfeeding.

b) Oestrogen: Incorrect.This hormone helps regulate the menstrual cycle and prepares the uterus for pregnancy but does not directly cause contractions or milk ejection.

c) Progesterone: Incorrect. Progesterone maintains the uterine lining during pregnancy but does not promote labor contractions or milk ejection.

d) Prolactin: Incorrect. Prolactin produced by the anterior pituitary stimulates milk production, but it does not cause uterine contractions or milk ejection. → (p.s. Think proLACTin as in LACTATE)

e) hCG (human chorionic gonadotropin): Incorrect. hCG supports the early stages of pregnancy by stimulating the corpus luteum to produce progesterone until placenta takes over however it is unrelated to labor or milk ejection.

Question 21:

What hormone does the pancreas produce to raise blood glucose levels when they become too low?

a) GLP-1

b) Glucagon

c) Adrenaline

d) Insulin

e) Melatonin

Answer 21:

b) Glucagon

Explanation:

The pancreas alpha islet cells of Langerhans produce glucagon to raise blood glucose levels when they drop too low and this works in a feedback system with insulin. 

a) GLP-1:Incorrect. GLP-1 is a hormone produced by L cells of the small intestine that enhances insulin secretion and slows gastric emptying but does not directly raise blood glucose levels.

c) Adrenaline: Incorrect. Adrenaline (epinephrine) can raise blood glucose levels, but it is produced by the adrenal glands, not the pancreas.

d) Insulin:Incorrect. Insulin lowers blood glucose levels, doing the opposite of glucagon.

e) Melatonin:Incorrect. Melatonin which is released by the pineal gland regulates sleep-wake cycles and is not involved in glucose metabolism.

Question 22:

Which of the following is the main inhibitor for the release of vasopressin?

a) High blood osmolality

b) Low blood osmolality

c) Decreased blood volume

d) Aldosterone production

e) Sympathetic nervous system activation

Correct answer: b) Low blood osmolality

Explanation: Vasopressin, also known as antidiuretic hormone (ADH), is released by the posterior pituitary gland in response to increased blood osmolality (concentration of solutes in the blood). When blood osmolality is low, indicating a relatively dilute blood solution, there is no need for the body to conserve water. Therefore, the release of vasopressin is inhibited under conditions of low blood osmolality.

a) High blood osmolality:Incorrect. This stimulates (as you have alot of solutes in little blood), rather than inhibits, vasopressin release to conserve water.

c) Decreased blood volume:Incorrect. This triggers vasopressin release to help retain water and maintain blood pressure.

d) Aldosterone production:Incorrect. Aldosterone regulates sodium and water balance but does not directly inhibit vasopressin release.

e) Sympathetic nervous system activation:Incorrect. This can stimulate vasopressin release under stress, not inhibit it.

Question 23:

In the Renin-Angiotensin-Aldosterone System (RAAS), what is the primary function of angiotensin II?

a) Stimulating red blood cell production

b) Promoting sodium absorption in the kidneys

c) Increasing heart rate

d) Constricting blood vessels and raising blood pressure

e) Regulating calcium levels in the blood

Answer 23:

d) Constricting blood vessels and raising blood pressure

Explanation:

Angiotensin II primary function in the RAAS is to constrict blood vessels and raise blood pressure to maintain adequate perfusion to vital organs. This is one of its many potent effects as Angiotensin II has many effects at different levels to increase BP. 

a) Stimulating red blood cell production:Incorrect. Erythropoietin (produced by juxtaglomerular cells of the kidney), not angiotensin II, stimulates red blood cell production.

b) Promoting sodium absorption in the kidneys:Incorrect. This is primarily the function of aldosterone (it also promotes potassium excretion into urine), not angiotensin II.

c) Increasing heart rate:Incorrect. While angiotensin II affects blood pressure, heart rate regulation is primarily controlled by the autonomic nervous system.

e) Regulating calcium levels in the blood:Incorrect. This is managed by calcitonin , calcitriol and parathyroid hormone (PTH), not angiotensin II.

Question 24:

What hormone stimulates the production of red blood cells in response to low oxygen levels in the blood?

a) Cortisol from Adrenal Cortex

b) Erythropoietin from Liver

c) Cortisol from kidneys

d) Thyroxine from Thyroid gland

e) Erythropoietin from Kidneys

Answer 24:

e) Erythropoietin from Kidneys

Explanation:

Erythropoietin, produced by the kidneys, stimulates the production of red blood cells in response to low oxygen levels in the blood, a condition known as hypoxia.

1. a) Cortisol from Adrenal Cortex:Incorrect. Cortisol helps manage stress and metabolism but does not stimulate red blood cell production.
2. b) Erythropoietin from LiverIncorrect.: While the liver produces small amounts of erythropoietin, the kidneys are the main producers.
3. c) Cortisol from kidneys:Incorrect. Cortisol is produced in the adrenal cortex, not in the kidneys, and does not stimulate red blood cell production.
4. d) Thyroxine from Thyroid gland:Incorrect. Thyroxine regulates metabolism but does not influence red blood cell production directly.

Question 25:

Which of the following locations is GLUT5 primarily found?

a) Liver

b) Duodenum

c) Kidneys

d) Jejunum

e) Brain

Correct answer: d) Jejunum

Explanation: GLUT5 is a glucose transporter protein primarily found in the jejunum of the small intestine. It facilitates the transport of fructose from the intestinal lumen into enterocytes for absorption. While other organs and tissues may express GLUT5 to some extent, its predominant location is in the jejunum for the absorption of dietary fructose. 

a) Liver:Incorrect. The liver primarily expresses GLUT2 for glucose transport, not GLUT5.

b) Duodenum:Incorrect. While the duodenum is involved in nutrient absorption, it mainly expresses GLUT2, not GLUT5.

c) Kidneys:Incorrect. The kidneys predominantly use GLUT2 transporters, not GLUT5.

e) Brain:Incorrect. The brain relies on GLUT1 and GLUT3 for glucose transport, not GLUT5.

Question 26:

Which of the following characteristics best describes the GLUT1 transporter and what does this imply for its function?

a) GLUT1 is found in pancreas and liver.

b) GLUT1 displays cooperative binding kinetics.

c) GLUT1 exhibits a low Km value.

d) GLUT1 has a preference for fructose transport.

e) GLUT1 is primarily expressed in adipose tissue.

Correct answer: c) GLUT1 exhibits a low Km value.

Explanation: GLUT1 is a glucose transporter protein primarily found in the placenta and brain. Its low Km value signifies a high affinity for glucose, allowing efficient glucose transport even at low concentrations. This characteristic is crucial for tissues with high energy demands, like the brain, ensuring they receive a constant supply of glucose for energy production and metabolic processes.

• a) GLUT1 is found in pancreas and liver:Incorrect. GLUT1 is primarily found in the brain and placenta, not the pancreas or liver.
• b) GLUT1 displays cooperative binding kinetics:Incorrect. GLUT1 does not display cooperative binding; it operates independently of other glucose molecules.
• d) GLUT1 has a preference for fructose transport:Incorrect. GLUT1 transports glucose, not fructose. Fructose is transported by GLUT5.
• e) GLUT1 is primarily expressed in adipose tissue:Incorrect. GLUT4, not GLUT1, is the glucose transporter predominantly expressed in adipose tissue.

Question 27:

Which type of cell surface receptor is activated by insulin?

a) Ion channel receptor

b) G-protein coupled receptor

c) Tyrosine Kinase Receptor

d) Nuclear receptor

e) Steroid receptor

Answer 27:

c) Tyrosine Kinase Receptor

Explanation:

Insulin activates Tyrosine Kinase Receptor on the cell surface, initiating signalling pathways. Nuclear receptors are for steroid hormones which can pass through the cell phospholipid Bi-layer membrane. 

a) Ion channel receptor:Incorrect. These receptors control ion flow they are found commonly in postsynaptic neurons and certain neurotransmitters bind to them such as neurotransmitters such as glycine glutamate and GABA, not hormone signaling, and aren’t involved in insulin’s mechanism.

b) G-protein coupled receptor:Incorrect. These receptors are involved in signaling for many hormones e.g catecholamines (adrenaline and noradrenaline) and some neurotransmitters such as dopamine but not insulin, which uses a tyrosine kinase receptor.

d) Nuclear receptor:Incorrect. Nuclear receptors are for hormones that enter the cell, like steroid hormones, and do not interact with insulin.

e) Steroid receptor:Incorrect. Insulin is not a steroid hormone and does not interact with steroid receptors.

Question 28:

Which of the following hormones are primarily implicated in the aetiology of Addison’s disease?

a) Adrenaline and aldosterone

b) Adrenaline and noradrenaline

c) Thyroxine (T4) and cortisol

d) Cortisol and aldosterone

e) Cortisol and DHEA

Correct answer: d) Cortisol and aldosterone

Explanation: Addison’s disease, or primary adrenal insufficiency, is characterised by the insufficient production of cortisol and aldosterone by the adrenal glands. Cortisol, a glucocorticoid hormone, and aldosterone, a mineralocorticoid hormone, are both crucial for maintaining various physiological processes in the body. Insufficient production of these 

hormones lead to the symptoms associated with Addison’s disease.

a) Adrenaline and aldosterone:Incorrect. Adrenaline is produced by the adrenal medulla and is not directly involved in Addison’s disease, which affects cortisol and aldosterone production from the adrenal cortex.

b) Adrenaline and noradrenaline:Incorrect. These catecholamines are produced by the adrenal medulla, not the adrenal cortex, and are unrelated to Addison’s disease.

c) Thyroxine (T4) and cortisol:Incorrect. Thyroxine is produced by the thyroid gland, not the adrenal glands, and is unrelated to Addison’s disease.

e) Cortisol and DHEA:Incorrect. While cortisol is implicated in Addison’s disease, DHEA is less critical compared to aldosterone in the condition’s clinical symptoms.

Question 29:

Which intricate task do Sertoli cells primarily undertake within the testicular microenvironment?

a) Facilitation of testosterone synthesis

b) Orchestration of spermatogonia stem cell renewal

c) Provision of nourishment for Leydig cells

d) Mediation of spermatozoa transport

e) Maturation of sperm

Correct answer: e) Maturation of sperm

Explanation:

Sertoli cells play a crucial role in the process of spermatogenesis within the seminiferous tubules of the testes. Their intricate functions encompass the regulation and support of sperm maturation, ensuring the production of functional and motile spermatozoa. These cells provide physical support and create a microenvironment conducive to sperm development. They also secrete various factors essential for spermatogenesis, including growth factors, cytokines, and hormones.

a) Facilitation of testosterone synthesis:Incorrect. Leydig cells, not Sertoli cells, are responsible for testosterone synthesis.

b) Orchestration of spermatogonia stem cell renewal:Incorrect. While Sertoli cells provide support, they primarily focus on sperm maturation rather than directly orchestrating stem cell renewal.

c) Provision of nourishment for Leydig cells:Incorrect. Sertoli cells support spermatogenesis, not Leydig cells, which produce testosterone.

d) Mediation of spermatozoa transport:Incorrect. Sertoli cells are involved in the maturation process, but sperm transport is managed by other structures like the epididymis.

Question 30:

Which event typically occurs on day 14 of the menstrual cycle in women?

a) Maturation of a secondary follicle

b) Secretion of progesterone by the corpus luteum

c) Shedding of the endometrial lining

d) Follicular phase dominance

e) LH surge

Correct answer: e) LH surge

Explanation:

On day 14 of the menstrual cycle, an LH surge occurs. This surge in luteinizing hormone (LH) is a crucial event that triggers ovulation. The surge typically happens around mid-cycle and is characterized by a rapid increase in LH secretion from the anterior pituitary gland. This surge is essential for the final maturation and release of the dominant follicle (containing the mature egg) from the ovary. 

a) Maturation of a secondary follicle:Incorrect. This occurs earlier in the cycle during the follicular phase, not specifically on day 14.

b) Secretion of progesterone by the corpus luteum:Incorrect. This happens after ovulation, not on day 14 itself.

c) Shedding of the endometrial lining:Incorrect. This occurs during menstruation, at the start of the cycle, not on day 14.

d) Follicular phase dominance:Incorrect. The follicular phase leads up to ovulation, but the LH surge marks the transition to the luteal phase.

Question 31:

Which of the following neuropeptides is considered anorexigenic, meaning it suppresses appetite?

a) Neuropeptide Y (NPY)

b) Agouti-related peptide (AgRP)

c) Pro-opiomelanocortin (POMC)

d) Ghrelin

e) Orexin

Correct answer: c) Pro-opiomelanocortin (POMC)

Explanation: Pro-opiomelanocortin (POMC) is an anorexigenic neuropeptide, meaning it suppresses appetite and promotes satiety. When POMC neurons are activated, they release alpha-melanocyte-stimulating hormone (α-MSH), which acts on melanocortin receptors in the hypothalamus to reduce food intake.

a) Neuropeptide Y (NPY):Incorrect. NPY is orexigenic, meaning it stimulates appetite, the opposite of POMC’s function.

b) Agouti-related peptide (AgRP):Incorrect. AgRP is also orexigenic and works to increase appetite, not suppress it.

d) Ghrelin:Incorrect. Ghrelin is a hormone that stimulates hunger, not an anorexigenic peptide.

e) Orexin:Incorrect. Orexin increases wakefulness and appetite, so it does not suppress appetite.

Question 32:

Which of the following factors is known to increase insulin sensitivity?

a) Cortisol

b) thyroxine

c) Adiponectin

d) Growth hormone

e) Adrenaline

Correct answer: c) Adiponectin

Explanation: Adiponectin is a hormone secreted by adipose tissue that plays a crucial role in increasing insulin sensitivity. It enhances the body’s ability to respond to insulin, promoting glucose uptake by cells and contributing to better blood glucose regulation. Higher levels of adiponectin are associated with improved insulin sensitivity, which can help reduce the risk of insulin resistance and type 2 diabetes.

a) Cortisol:Incorrect. Cortisol increases blood sugar levels and can contribute to insulin resistance, reducing insulin sensitivity.

b) Thyroxine:Incorrect. Thyroxine primarily regulates metabolism and does not directly enhance insulin sensitivity; in some cases, hyperthyroidism can reduce insulin sensitivity.

d) Growth hormone:Incorrect. Growth hormone can actually reduce insulin sensitivity, especially when produced in excess.

e) Adrenaline:Incorrect. Adrenaline raises blood sugar levels and decreases insulin sensitivity during the fight-or-flight response.

Question 33:

How are the hypothalamus and the pituitary gland connected in terms of their anatomical relationship?

a) The hypothalamus is situated below the pituitary gland.

b) The hypothalamus and the pituitary gland are physically separated and do not have a direct connection.

c) The hypothalamus is located above and connected to the anterior pituitary via the hypothalamo-hypophyseal portal system.

d) The hypothalamus is located above and connected to the posterior pituitary via the hypothalamo-hypophyseal portal system.

e) The hypothalamus is part of the posterior pituitary.

Answer 33:

c) The hypothalamus is located above and connected to the anterior pituitary via the hypothalamo-hypophyseal portal system.

Explanation:

The hypothalamus is located above the pituitary gland and is connected to the anterior pituitary through a network of blood vessels known as the hypothalamo-hypophyseal portal system.

a) The hypothalamus is situated below the pituitary gland:Incorrect. This is anatomically incorrect; the hypothalamus is above the pituitary gland.

b) The hypothalamus and the pituitary gland are physically separated:Incorrect. The hypothalamus and pituitary gland are directly connected by both the portal system and nerve fibres.

d) The hypothalamus is connected to the posterior pituitary via the portal system:Incorrect. The posterior pituitary is connected to the hypothalamus via the hypothalamo-hypophyseal tract ( nervous connection between the hypothalamus and post pituitary). The portal system connects the hypothalamus to the anterior pituitary, not the posterior, 

e) The hypothalamus is part of the posterior pituitary:Incorrect. The hypothalamus and posterior pituitary are distinct structures, though connected via the pituitary stalk.

Question 34:

Which hormonal imbalance is commonly associated with pheochromocytoma?

a) Insulin overproduction

b) Thyroid hormone deficiency

c) Excess catecholamines

d) Elevated cortisol levels

e) excess mineralocorticoids 

Correct answer: c) Excess catecholamines

Explanation: Pheochromocytoma is a neuroendocrine tumour that typically arises from the chromaffin cells of the adrenal medulla. These tumours often lead to excessive secretion of catecholamines such as adrenaline (epinephrine) and noradrenaline (norepinephrine). The elevated levels of catecholamines can cause a variety of symptoms, including hypertension, palpitations, headaches, and sweating. Therefore, the hormonal imbalance commonly associated with pheochromocytoma is excess catecholamines.

a) Insulin overproduction:Incorrect. Pheochromocytoma affects catecholamine levels, not insulin production.

b) Thyroid hormone deficiency:Incorrect. Thyroid issues are unrelated to pheochromocytoma, which involves adrenal hormones.

d) Elevated cortisol levels:Incorrect. Cortisol is a glucocorticoid which is produced by the zona fasciculata of the adrenal cortex, but pheochromocytoma primarily affects the adrenal medulla, leading to excess catecholamines.

e) Excess mineralocorticoids:Incorrect. Mineralocorticoids like aldosterone are produced by the zona glomerulosa of the adrenal cortex, not the adrenal medulla, which is involved in pheochromocytoma.

Question 35:

What hormones are secreted by the posterior pituitary, and what is their primary function?

a) Oxytocin and antidiuretic hormone (ADH), regulating uterine contractions and water balance, respectively.

b) Thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH), controlling thyroid and adrenal gland functions, respectively.

c) Prolactin and growth hormone (GH), promoting milk production and growth, respectively.

d) Follicle-stimulating hormone (FSH) and luteinizing hormone (LH), regulating reproductive functions.

e) Cortisol and aldosterone, controlling stress response and electrolyte balance.

Answer 35:

a) Oxytocin and antidiuretic hormone (ADH), regulating uterine contractions and water balance, respectively.

Explanation:

The posterior pituitary secretes oxytocin, which is involved in uterine contractions during labour and milk ejection during breastfeeding, and antidiuretic hormone (ADH), which regulates water balance by controlling kidney function.

Incorrect 

b) TSH and ACTH:Incorrect. These hormones are secreted by the anterior pituitary, not the posterior.

c) Prolactin and growth hormone (GH):Incorrect. These hormones are also secreted by the anterior pituitary.

d) FSH and LH:Incorrect. These are anterior pituitary hormones that regulate reproductive functions, not posterior pituitary hormones.

e) Cortisol and aldosterone:Incorrect. These hormones are produced by the adrenal glands, not the pituitary.

Question 36:

Which hormones are produced by the anterior pituitary, and what are their primary functions?

a) Oxytocin and antidiuretic hormone (ADH), controlling uterine contractions and water balance.

b) Thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH), promoting thyroid and adrenal gland functions.

c) Prolactin and growth hormone (GH), regulating uterine lining and growth, respectively.

d) prolactin and luteinizing hormone (LH), regulate uterine lining and oversee reproductive functions.

e) Cortisol and aldosterone, managing stress response and electrolyte balance.

Answer 36:

b) Thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH), promoting thyroid and adrenal gland functions.

Explanation:

The anterior pituitary produces TSH, which stimulates the thyroid gland, and ACTH, which stimulates the adrenal cortex, both of which regulate thyroid and adrenal gland functions, respectively.

a) Oxytocin and ADH:Incorrect. These are secreted by the posterior pituitary, not the anterior pituitary.

c) Prolactin and growth hormone (GH):Incorrect. While these hormones are produced by the anterior pituitary, prolactin regulates milk production, not the uterine lining.

d) Prolactin and LH:Incorrect. While both these hormones are produced by the anterior pituitary, prolactin regulates milk production, not the uterine lining.

e) Cortisol and aldosterone:Incorrect. These hormones are produced by the adrenal glands, not the anterior pituitary.

Question 37:

 Which hormones are primarily released from the zona reticularis of the adrenal cortex?

a) glucocorticoids e.g. cortisol 

b) Epinephrine and norepinephrine

c) mineralocorticoids e.g. aldosterone 

d) Dehydroepiandrosterone (DHEA) and androstenedione

e) Corticosteroids

Correct answer: d) Dehydroepiandrosterone (DHEA) and androstenedione

Explanation: The zona reticularis is the innermost layer of the adrenal cortex. It primarily secretes weak androgens, including dehydroepiandrosterone (DHEA) and androstenedione. These hormones are precursors to more potent androgens such as testosterone and dihydrotestosterone. 

a) Glucocorticoids (e.g., cortisol):Incorrect. These are released from the zona fasciculata, not the zona reticularis.

b) Epinephrine and norepinephrine:Incorrect. These are produced by the adrenal medulla, not the cortex.

c) Mineralocorticoids (e.g., aldosterone):Incorrect. These are secreted by the zona glomerulosa, not the zona reticularis.

e) Corticosteroids:Incorrect. This is a broad term that includes both glucocorticoids and mineralocorticoids, which are produced in other zones of the adrenal cortex.

Question 38:

What is the primary function of adrenocorticotropic hormone (ACTH) produced by the anterior pituitary?

a) stimulating cortisol release from the liver 

b) Promoting growth and cell division

c) Stimulating cortisol release from the adrenal cortex

d) Controlling water balance in the body

e) Regulating blood calcium levels

Answer 38:

c) Stimulating cortisol release from the adrenal cortex

Explanation:

ACTH stimulates the adrenal cortex to release cortisol, a hormone involved in the body’s stress response and regulation of various metabolic processes.

a) Stimulating cortisol release from the liver:Incorrect. whilst ACTH stimulates Cortisol releasese, cortisol is produced by the adrenal cortex, not the liver.

b) Promoting growth and cell division:Incorrect. This is the function of growth hormone (GH), not ACTH.

d) Controlling water balance in the body:Incorrect. This is regulated by antidiuretic hormone (ADH), not ACTH.

e) Regulating blood calcium levels:Incorrect. This is controlled by parathyroid hormone (PTH), not ACTH.

Question 39:

Which ion is crucial for the biosynthesis of thyroxine (T4)?

a) Sodium (Na)

b) Calcium (Ca2+)

c) Iron (Fe2+)

d) Iodide (I-)

e) Potassium (K+)

Correct answer: d) Iodide (I-)

Explanation: Iodide ions (I-) are essential for the biosynthesis of thyroxine (T4) and triiodothyronine (T3), which are thyroid hormones. Iodide is actively transported into the thyroid follicular cells from the bloodstream, where it is incorporated into tyrosine residues on thyroglobulin (a protein synthesized by the thyroid gland). These iodinated tyrosine residues are then coupled together to form T4 and T3.

a) Sodium (Na):Incorrect. Sodium is important for many physiological processes, but it does not play a direct role in thyroxine (T4) biosynthesis.

b) Calcium (Ca2+):Incorrect. Calcium is involved in muscle contraction and bone health, but it is not involved in the production of thyroid hormones.

c) Iron (Fe2+):Incorrect. Iron is essential for oxygen transport in the blood but has no direct role in thyroid hormone synthesis.

e) Potassium (K+):Incorrect. Potassium is vital for nerve function and muscle contraction, but it is not involved in the production of thyroxine (T4).

Question 40:

Differentiate between the direct and indirect effects of growth hormone (GH).

a) Direct effects involve stimulating growth of target tissues, while indirect effects involve inhibiting growth.

b) Direct effects include increasing bone density, while indirect effects include promoting muscle growth.

c) Direct effects involve acting on target tissues, while indirect effects involve stimulating insulin production.

d) Direct effects involve GH binding to target cells, while indirect effects involve GH acting through insulin-like growth factor-1 (IGF-1).

e) Direct effects include promoting fat storage, while indirect effects involve increasing metabolism.

Answer 40:

d) Direct effects involve GH binding to target cells, while indirect effects involve GH acting through insulin-like growth factor-1 (IGF-1).

Explanation:

Direct effects of GH occur when it binds to target cells, stimulating growth. Indirect effects involve GH stimulating the production of IGF-1, which mediates many of GH’s growth-promoting actions.

a) Direct effects involve stimulating growth of target tissues, while indirect effects involve inhibiting growth: Incorrect, Indirect effects of GH do not involve inhibiting growth; instead, they promote growth through IGF-1.

b) Direct effects include increasing bone density, while indirect effects include promoting muscle growth: Incorrect, Both bone and muscle growth are influenced by both direct and indirect effects of GH, but the distinction lies in the involvement of IGF-1, not the tissue type.

c) Direct effects involve acting on target tissues, while indirect effects involve stimulating insulin production: Incorrect, GH indirectly affects growth via IGF-1, not by stimulating insulin production.

e) Direct effects include promoting fat storage, while indirect effects involve increasing metabolism: Incorrect, GH primarily promotes fat breakdown, not storage, and both direct and indirect effects can influence metabolism.

Question 41:

From which molecule are steroid hormones like cortisol and vitamin D derived?

a) Glucose

b) Amino acids

c) Fatty acids

d) Cholesterol

e) Glycogen

Correct answer: d) Cholesterol

Explanation: Steroid hormones, including cortisol, aldosterone, oestrogen, and testosterone, as well as vitamin D, are derived from cholesterol. Cholesterol serves as the precursor molecule for the synthesis of these hormones. Through enzymatic processes in various tissues, cholesterol is converted into different steroid hormones, each with distinct physiological functions.

a) Glucose:Incorrect. Glucose is the primary energy source for cells but is not involved in steroid hormone synthesis.

b) Amino acids:Incorrect. Amino acids are the building blocks of proteins, not steroid hormones.

c) Fatty acids:Incorrect. Fatty acids are used for energy storage and membrane formation but are not precursors for steroid hormones.

e) Glycogen:Incorrect. Glycogen is a storage form of glucose and is unrelated to the synthesis of steroid hormones.

Question 42:

What is the initial physiological event commonly observed in the development of type 2 diabetes mellitus?

a) Hyperglycaemia

b) Hyperinsulinemia

c) Hypoglycaemia 

d) Ketoacidosis

e) hyperproteinemia

Correct answer: b) Hyperinsulinemia

Explanation: In the early stages of type 2 diabetes mellitus, the body often compensates for insulin resistance by increasing insulin secretion from pancreatic beta cells. This results in hyperinsulinemia, where there are elevated levels of insulin in the bloodstream. The hyperinsulinemia aims to overcome the resistance of target tissues to insulin action and maintain normal blood glucose levels. However, over time, pancreatic beta cell function may decline, leading to decreased insulin secretion and eventually contributing to hyperglycemia characteristic of type 2 diabetes mellitus.

a) Hyperglycemia:Incorrect. Hyperglycemia (high blood sugar) occurs later in the progression of type 2 diabetes after insulin resistance worsens.

c) Hypoglycemia:Incorrect. Low blood sugar is not typically seen in the early stages of type 2 diabetes.

d) Ketoacidosis:Incorrect. Ketoacidosis is more commonly associated with type 1 diabetes and is a later-stage complication, not an initial event.

e) Hyperproteinemia:Incorrect. Elevated protein levels in the blood are not a characteristic event in the development of type 2 diabetes.

Question 43:

What is the primary function of calcitriol (1,25-dihydroxyvitamin D3)?

a)  Enhancement of calcium and phosphate absorption in the kidneys

b) Promotion of erythropoiesis

c) Maintenance of bone density

d) Enhancement of calcium and phosphate absorption in the small intestines

e) Regulation of blood pressure

Correct answer: d) Enhancement of calcium and phosphate absorption in the small intestines

Explanation: Calcitriol, the active form of vitamin D, plays a crucial role in calcium and phosphate homeostasis. One of its primary functions is to increase the absorption of calcium and phosphate from the small intestines. Calcitriol acts on the intestinal epithelial cells to enhance the expression of proteins involved in transporting calcium and phosphate across the intestinal lining into the bloodstream. This action helps maintain adequate levels of calcium and phosphate in the body, essential for various physiological processes, including bone health, muscle function, and nerve transmission.

a) Enhancement of calcium and phosphate absorption in the kidneys:Incorrect. While calcitriol does affect kidney function, its primary role is to enhance calcium and phosphate absorption in the intestines.

b) Promotion of erythropoiesis:Incorrect. Erythropoiesis (blood cell formation) is stimulated by erythropoietin, not calcitriol.

c) Maintenance of bone density:Incorrect. Calcitriol indirectly maintains bone density by increasing calcium absorption, but its primary action is in the intestines.

e) Regulation of blood pressure:Incorrect. Blood pressure regulation is controlled by different hormones, such as aldosterone and vasopressin, not calcitriol.

Question 44:

Which glucose transporter is primarily regulated by insulin?

a) GLUT1

b) GLUT2

c) GLUT3

d) GLUT4

e) GLUT5

Correct answer: d) GLUT4

Explanation: GLUT4 is the glucose transporter that is primarily regulated by insulin. In response to insulin signalling, GLUT4 is translocated from intracellular vesicles to the plasma membrane in insulin-sensitive tissues such as muscle and adipose tissue. This translocation increases the uptake of glucose into these cells, thereby lowering blood glucose levels.

a) GLUT1:Incorrect. GLUT1 is responsible for glucose transport in many tissues and is not regulated by insulin.

b) GLUT2:Incorrect. GLUT2 is found in the liver, pancreas, and kidneys and functions independently of insulin.

c) GLUT3:Incorrect. GLUT3 is primarily found in neurons and has a high affinity for glucose, but it is not insulin-regulated.

e) GLUT5:Incorrect. GLUT5 primarily transports fructose, not glucose, and is not regulated by insulin.

Question 45:

What is the key mechanism for regulating the secretion of growth hormone (GH) in the body?

a) Negative feedback by IGF-1

b) Positive feedback by thyroid hormones

c) Direct stimulation by cortisol

d) Inhibition by prolactin

e) Random fluctuations in GH production

Answer 45:

a) Negative feedback by IGF-1

Explanation:

The key mechanism for regulating GH secretion is negative feedback by insulin-like growth factor-1 (IGF-1), which inhibits further GH release when its levels are elevated.

b) Positive feedback by thyroid hormones:Incorrect. Thyroid hormones do not regulate GH through positive feedback; they have different regulatory mechanisms.

c) Direct stimulation by cortisol:Incorrect. Cortisol does not directly stimulate GH secretion; it is involved in stress responses.

d) Inhibition by prolactin:Incorrect. Prolactin primarily regulates lactation and does not inhibit GH secretion.

e) Random fluctuations in GH production:Incorrect. GH secretion is not random but is tightly regulated by negative feedback mechanisms involving IGF-1.

Question 46:

Which glucose transporter facilitates the entry of glucose into beta cells of the pancreatic islets of Langerhans?

a) GLUT1

b) GLUT2

c) GLUT3

d) GLUT4

e) GLUT5

Correct answer: b) GLUT2

Explanation: GLUT2 is the primary glucose transporter responsible for allowing glucose to enter beta cells in the pancreatic islets of Langerhans. This transporter plays a crucial role in sensing blood glucose levels and regulating insulin secretion by pancreatic beta cells. When blood glucose levels rise, GLUT2 facilitates the entry of glucose into beta cells, leading to insulin secretion and subsequent glucose uptake by peripheral tissues.

a) GLUT1 (Incorrect): GLUT1 is found in many tissues and is involved in basal glucose uptake, but it is not the primary transporter for glucose entry into pancreatic beta cells.

c) GLUT3 (Incorrect): GLUT3 is mainly found in neurons and does not play a role in glucose transport in pancreatic beta cells.

d) GLUT4 (Incorrect): GLUT4 is regulated by insulin and facilitates glucose uptake in muscle and fat cells, not pancreatic beta cells.

e) GLUT5 (Incorrect): GLUT5 primarily transports fructose, not glucose, and is not involved in glucose uptake in beta cells.

Question 47:

Which of the following glucose transporters is responsive to insulin and plays a crucial role in glucose uptake by muscle and fat cells?

a) GLUT-1

b) GLUT-2

c) GLUT-3

d) GLUT-4

e) GLUT-5

Answer 47:

d) GLUT-4

Explanation:

GLUT-4 is the glucose transporter responsive to insulin and is involved in facilitating glucose uptake by muscle and fat cells.

a) GLUT1 (Incorrect): GLUT1 is responsible for basal glucose uptake in many tissues and is not regulated by insulin.

b) GLUT2 (Incorrect): GLUT2 is involved in glucose sensing in the liver and pancreatic beta cells, but it is not insulin-responsive.

c) GLUT3 (Incorrect): GLUT3 is primarily found in neurons and is not insulin-regulated.

e) GLUT5 (Incorrect): GLUT5 is responsible for fructose transport, not glucose, and is not regulated by insulin.

Question 48:

What is the primary role of insulin in glucose level regulation?

a) Promoting glycogen breakdown

b) Stimulating gluconeogenesis

c) inhibiting glycogenesis 

d) Facilitating glucose uptake into cells

e) Inhibiting pancreatic alpha cells

Answer 48:

d) Facilitating glucose uptake into cells

Explanation:

Insulin promotes glucose uptake into cells, helping to lower blood glucose levels by facilitating its entry into tissues.

a) Promoting glycogen breakdown (Incorrect): Insulin promotes glycogen synthesis, not its breakdown. Glycogen breakdown is stimulated by glucagon.

b) Stimulating gluconeogenesis (Incorrect): Insulin inhibits gluconeogenesis. This process is stimulated by glucagon and other hormones during fasting.

c) Inhibiting glycogenesis (Incorrect): Insulin actually promotes glycogenesis, which is the storage of glucose as glycogen, not the inhibition of this process.

e) Inhibiting pancreatic alpha cells (Incorrect): Insulin does not primarily function by inhibiting alpha cells, which secrete glucagon. Its main role is to facilitate glucose uptake into cells.

Question 49:

In glucose metabolism, what is the primary role of glucagon?

a) Promoting glycogenesis

b) Increasing insulin secretion

c) Stimulating glucose uptake by cells

d) Raising blood glucose levels

e) Inhibiting liver function

Answer 49:

d) Raising blood glucose levels

Explanation:

Glucagon’s primary role is to raise blood glucose levels by stimulating the breakdown of glycogen and promoting gluconeogenesis.

a) Promoting glycogenesis (Incorrect): Glucagon promotes glycogen breakdown (glycogenolysis), not glycogenesis, which is the formation of glycogen from glucose.

b) Increasing insulin secretion (Incorrect): Glucagon raises blood glucose levels, while insulin lowers them; glucagon does not increase insulin secretion.

c) Stimulating glucose uptake by cells (Incorrect): Insulin, not glucagon, is responsible for stimulating glucose uptake by cells.

e) Inhibiting liver function (Incorrect): Glucagon actually stimulates liver function, particularly glycogen breakdown and gluconeogenesis, to raise blood glucose levels.

Question 50:

During fasting, which hormone plays a key role in stimulating the breakdown of stored glycogen in the liver?

a) Insulin

b) Cortisol

c) Glucagon

d) adrenaline

e) Growth hormone (GH)

Answer 50:

c) Glucagon

Explanation:

During fasting, glucagon stimulates the liver to break down glycogen and release glucose into the bloodstream to maintain blood glucose levels.

a) Insulin (Incorrect): Insulin promotes the storage of glucose as glycogen rather than its breakdown. During fasting, insulin levels decrease.

b) Cortisol (Incorrect): Cortisol helps mobilize energy stores during stress and prolonged fasting, but it does not directly stimulate glycogen breakdown in the liver.

d) Adrenaline (Incorrect): Adrenaline can stimulate glycogen breakdown in muscle and the liver during acute stress, but the primary hormone for this during fasting is glucagon.

e) Growth hormone (GH) (Incorrect): Growth hormone promotes fat utilization and protein conservation during fasting, but it is not the key hormone for glycogen breakdown.

Question 51:

What is the physiological stress response to hypoglycaemia?

a) Increased insulin secretion

b) Decreased glucagon secretion

c) Release of epinephrine and cortisol

d) Suppression of appetite

e) Activation of the parasympathetic nervous system

Answer 51:

c) Release of epinephrine and cortisol

Explanation:

Hypoglycaemia triggers the release of epinephrine and cortisol, which help raise blood glucose levels by promoting gluconeogenesis and glycogen breakdown.

a) Increased insulin secretion (Incorrect): Insulin secretion decreases during hypoglycemia to prevent further lowering of blood glucose levels.

b) Decreased glucagon secretion (Incorrect): Glucagon secretion actually increases during hypoglycemia to raise blood glucose levels.

d) Suppression of appetite (Incorrect): Hypoglycemia typically stimulates hunger to encourage glucose intake, not appetite suppression.

e) Activation of the parasympathetic nervous system (Incorrect): The sympathetic nervous system, not the parasympathetic system, is activated during hypoglycemia, leading to the release of stress hormones like epinephrine.

Question 52:

How would you define Type I diabetes?

a) A condition characterized by insulin resistance and obesity

b) A condition resulting from relative insulin deficiency

c) A simple deficiency state of insulin production

d) A condition caused by an autoimmune destruction of pancreatic beta cells

e) A disorder primarily associated with insulin hypersecretion

Answer 52:

d) A condition caused by an autoimmune destruction of pancreatic beta cells

Explanation:

Type I diabetes is defined as a condition in which pancreatic beta cells are destroyed by an autoimmune response, leading to a deficiency of insulin production.

a) A condition characterized by insulin resistance and obesity (Incorrect): This describes type 2 diabetes, not type 1, which is caused by autoimmune destruction of beta cells.

b) A condition resulting from relative insulin deficiency (Incorrect): Type 1 diabetes results from an absolute insulin deficiency due to the destruction of beta cells, not a relative deficiency.

c) A simple deficiency state of insulin production (Incorrect): While Type 1 diabetes involves a deficiency in insulin production, it is specifically caused by an autoimmune process, not just a simple deficiency.

e) A disorder primarily associated with insulin hypersecretion (Incorrect): Insulin hypersecretion is more related to the early stages of type 2 diabetes, not type 1 diabetes, which is characterized by a lack of insulin.

Question 53:

How does Type II diabetes develop insulin resistance?

a) It is characterised by insulin hypersecretion.

b) It is the result of obesity and decreased insulin sensitivity due to insulin hypersecretion for a prolonged period of time 

c) It is primarily caused by genetic factors.

d) It is characterised by high body weight and enhanced insulin sensitivity.

e) It is caused by insulin resistance without any association with obesity.

Answer 53:

b) It is the result of obesity and decreased insulin sensitivity due to insulin hypersecretion for a prolonged period of time. 

Explanation:

Type II diabetes is often associated with obesity and insulin resistance. Over time, beta cells may also become dysfunctional, leading to relative insulin deficiency

a) It is characterized by insulin hypersecretion (Incorrect): While insulin hypersecretion occurs initially, it leads to insulin resistance and is not the sole characteristic of type 2 diabetes.

c) It is primarily caused by genetic factors (Incorrect): Although genetic factors contribute, type 2 diabetes is primarily driven by lifestyle factors like obesity and physical inactivity.

d) It is characterized by high body weight and enhanced insulin sensitivity (Incorrect): Type 2 diabetes is characterized by insulin resistance and decreased insulin sensitivity, not enhanced insulin sensitivity.

e) It is caused by insulin resistance without any association with obesity (Incorrect): Obesity is a major risk factor for developing insulin resistance in type 2 diabetes, and the two are often closely linked.

Question 54:

What is the primary function of aromatase in the body?

a) Promoting muscle growth

b) Involved in converting oestrogen into progesterone 

c) Converting testosterone into oestrogen

d) Regulating LH and FSH secretion

e) Stimulating sperm production

Answer 54:

c) Converting testosterone into oestrogen

Explanation:

Aromatase is an enzyme responsible for converting testosterone into oestrogen, which is important for various physiological processes, including female reproductive function.

a) Promoting muscle growth (Incorrect): Aromatase does not promote muscle growth; it converts testosterone into oestrogen, which affects reproductive tissues, not muscle mass.

b) Involved in converting oestrogen into progesterone (Incorrect): Aromatase does not convert oestrogen into progesterone; it specifically converts androgens like testosterone into oestrogens.

d) Regulating LH and FSH secretion (Incorrect): Aromatase does not regulate luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. These are regulated by the hypothalamus and pituitary gland.

e) Stimulating sperm production (Incorrect): Aromatase is not involved in stimulating sperm production, which is primarily regulated by testosterone and FSH.

Question 55:

Which glucose transporter is primarily found in the liver and is essential for glucose uptake and release to regulate blood glucose levels?

a) GLUT-1

b) GLUT-2

c) GLUT-3

d) GLUT-4

e) GLUT-5

Answer 55:

b) GLUT-2

Explanation:

GLUT-2 is predominantly found in the liver and plays a crucial role in regulating glucose uptake and release to maintain blood glucose levels.

a) GLUT-1 (Incorrect): GLUT-1 is found in many tissues for basal glucose uptake, not primarily in the liver.

c) GLUT-3 (Incorrect): GLUT-3 is found mainly in the brain, not in the liver, and is involved in glucose uptake in neurons.

d) GLUT-4 (Incorrect): GLUT-4 is insulin-responsive and primarily found in muscle and fat tissues, not in the liver.

e) GLUT-5 (Incorrect): GLUT-5 is a transporter for fructose in the jejunum, not glucose, and is not involved in liver glucose regulation.

Question 56:

In addition to glucose regulation, what is another major function of insulin in the body?

a) Promoting protein breakdown

b) Increasing fat synthesis

c) Suppressing appetite

d) Regulating blood pressure

e) Stimulating cortisol release

Answer 56:

b) Increasing fat synthesis

Explanation:

Insulin not only regulates glucose levels but also promotes fat synthesis in adipose tissue.

a) Promoting protein breakdown (Incorrect): Insulin actually promotes protein synthesis, not breakdown.

c) Suppressing appetite (Incorrect): Insulin’s primary roles are in glucose regulation and fat synthesis, not directly suppressing appetite.

d) Regulating blood pressure (Incorrect): Insulin does not directly regulate blood pressure; this is more influenced by hormones like aldosterone and angiotensin 2.

e) Stimulating cortisol release (Incorrect): Insulin does not stimulate cortisol release; cortisol is stimulated by ACTH (produced and secreted by ant pituitary) and is regulated by the adrenal glands in response to stress.

Question 57:

What is the primary function of thyroid hormones in the body?

a) Regulating calcium balance

b) Promoting insulin secretion

c) Controlling blood pressure

d) Regulating metabolism

e) Enhancing blood clotting

Answer 57:

d) Regulating metabolism

Explanation:

Thyroid hormones play a crucial role in regulating metabolism, including the breakdown of nutrients and energy production in the body.

a) Regulating calcium balance (Incorrect): Calcium balance is primarily regulated by parathyroid hormone (PTH), calcitonin and vitamin D, not thyroid hormones.

b) Promoting insulin secretion (Incorrect): Thyroid hormones do not promote insulin secretion; insulin is secreted by the beta cells of the pancreas.

c) Controlling blood pressure (Incorrect): Thyroid hormones have some effect on heart rate and metabolism, but blood pressure is mainly controlled by the kidneys and cardiovascular system.

e) Enhancing blood clotting (Incorrect): Thyroid hormones do not play a direct role in blood clotting, which involves platelets and clotting factors.

Question 58:

In addition to calcium and phosphate regulation, what other physiological process is influenced by parathyroid hormone (PTH)?

a) Haemoglobin synthesis

b) Blood pressure regulation

c) regulating metabolism

d) Bone remodelling

e) Insulin secretion

Answer 58:

d) Bone remodelling

Explanation:

PTH plays a significant role in bone remodelling by regulating calcium release from bone tissue, affecting bone density and structure.

a) Haemoglobin synthesis (Incorrect): Haemoglobin synthesis is regulated by erythropoietin and iron, not by PTH.

b) Blood pressure regulation (Incorrect): PTH primarily affects calcium and phosphate metabolism, not blood pressure regulation.

c) Regulating metabolism (Incorrect): Metabolism is primarily regulated by thyroid hormones, not by PTH.

e) Insulin secretion (Incorrect): PTH does not regulate insulin secretion; insulin is regulated by blood glucose levels and other hormones e.g. GLP-1.

Question 59:

Which of the following is a common symptom of hypoparathyroidism?

a) Hypercalcemia

b) Muscle weakness 

c) Elevated phosphate levels

d) Increased bone density

e) Cardiac arrhythmias

Answer 59:

b) Muscle weakness and tetany

Explanation:

Hypoparathyroidism often leads to muscle weakness due to low calcium levels.

a) Hypercalcemia (Incorrect): Hypoparathyroidism leads to low calcium levels (hypocalcemia), not high calcium levels (hypercalcemia).

c) Elevated phosphate levels (Incorrect): Elevated phosphate levels can occur in hypoparathyroidism, but the primary symptom is muscle weakness due to low calcium.

d) Increased bone density (Incorrect): Hypoparathyroidism does not typically cause increased bone density; it more commonly leads to symptoms related to low calcium levels, so would lead to a low bone density.

e) Cardiac arrhythmias (Incorrect): While low calcium can cause arrhythmias, muscle weakness and tetany(muscle spasms) are more common symptoms of hypoparathyroidism.

Question 60:

How does parathyroid hormone (PTH) regulate vitamin D in the body?

a) PTH inhibits the activation of vitamin D.

b) PTH stimulates the activation of vitamin D.

c) PTH has no effect on vitamin D.

d) PTH promotes vitamin D breakdown.

e) PTH decreases vitamin D absorption.

Answer 60:

b) PTH stimulates the activation of vitamin D.

Explanation:

PTH stimulates the activation of vitamin D in the kidneys, leading to increased absorption of calcium and phosphate in the intestines.

a) PTH inhibits the activation of vitamin D (Incorrect): PTH stimulates, not inhibits, the activation of vitamin D in the kidneys.

c) PTH has no effect on vitamin D (Incorrect): PTH plays a crucial role in regulating vitamin D activation, so it definitely has an effect.

d) PTH promotes vitamin D breakdown (Incorrect): PTH does not promote vitamin D breakdown; it enhances its absorption and activation to increase calcium absorption.

e) PTH decreases vitamin D absorption (Incorrect): PTH increases the absorbtion and activation of vitamin D, which in turn increases calcium absorption from the intestines.

Question 61:

How do thyroid hormones influence growth and neuronal development in children?

a) By inhibiting bone growth and brain development

b) By reducing neuronal connections in the brain

c) By promoting growth of long bones and enhancing brain development

d) By slowing down growth and neuronal function

e) By impairing cognitive function

Answer 61:

c) By promoting growth of long bones and enhancing brain development

Explanation:

Thyroid hormones play a crucial role in promoting the growth of long bones and enhancing brain development in children, contributing to overall growth and cognitive function.

a) By inhibiting bone growth and brain development (Incorrect): Thyroid hormones promote, not inhibit, bone growth and brain development.

b) By reducing neuronal connections in the brain (Incorrect): Thyroid hormones enhance, not reduce, neuronal connections, which are vital for brain development.

d) By slowing down growth and neuronal function (Incorrect): Thyroid hormones accelerate growth and neuronal function, not slow them down.

e) By impairing cognitive function (Incorrect): A deficiency in thyroid hormones impairs cognitive function, but their normal function enhances brain development and cognition.

Question 62:

What is the result of T3/T4 deficiency in adults?

a) Increased metabolic rate and energy levels

b) weight gain and heat intolerance

c) Weight loss and muscle wasting

d) fatigue, weight gain, and cold intolerance

e) Heat intolerance, weight loss and anxiety 

Answer 62:

d) fatigue, weight gain, and cold intolerance

Explanation:

T3/T4 deficiency in adults can result in hypothyroidism, leading to symptoms such as fatigue, weight gain, and intolerance to cold due to decreased metabolic activity.

a) Increased metabolic rate and energy levels (Incorrect): T3/T4 deficiency decreases the metabolic rate, leading to fatigue, not increased energy levels.

b) Weight gain and heat intolerance (Incorrect): Weight gain occurs with T3/T4 deficiency, but heat intolerance is a symptom of hyperthyroidism, not hypothyroidism.

c) Weight loss and muscle wasting (Incorrect): T3/T4 deficiency typically leads to weight gain and muscle weakness, not weight loss and wasting.

e) Heat intolerance, weight loss, and anxiety (Incorrect): These symptoms are associated with hyperthyroidism, not T3/T4 deficiency, which leads to cold intolerance, weight gain, and fatigue.

Question 63:

What is the primary result of T3/T4 deficiency in children?

a) Increased growth and development

b) Increased cognitive function

c) Growth retardation and developmental delay

d) Hyperactivity and behavioural problems

e) Decreased athletic performance

Answer 63:

c) Growth retardation and developmental delay

Explanation:

T3/T4 deficiency in children can lead to growth retardation and developmental delay, as thyroid hormones are essential for normal growth and neuronal development during childhood.

a) Increased growth and development (Incorrect): T3/T4 deficiency actually leads to delayed growth and development, not increased growth.

b) Increased cognitive function (Incorrect): Cognitive function is impaired by T3/T4 deficiency, leading to developmental delays, not improvements.

d) Hyperactivity and behavioural problems (Incorrect): T3/T4 deficiency in children usually results in slowed development and lethargy, not hyperactivity.

e) Decreased athletic performance (Incorrect): While T3/T4 deficiency can affect performance, the primary concern is growth retardation and developmental delay.

Question 64:

What is the common cause of Addison’s disease?

a) Excessive cortisol production

b) Autoimmune destruction of the adrenal cortex

c) Overproduction of aldosterone

d) Pituitary adenoma

e) Insulin resistance

Answer 64:

b) Autoimmune destruction of the adrenal cortex

Explanation:

The most common cause of Addison’s disease is the autoimmune destruction of the adrenal cortex, leading to a deficiency of cortisol and aldosterone.

a) Excessive cortisol production (Incorrect): Addison’s disease is characterized by cortisol deficiency, not excessive production.

c) Overproduction of aldosterone (Incorrect): Addison’s disease involves low levels of aldosterone, not overproduction.

d) Pituitary adenoma (Incorrect): Pituitary adenomas can affect adrenal function, but Addison’s disease is primarily caused by autoimmune destruction of the adrenal cortex.

e) Insulin resistance (Incorrect): Insulin resistance is related to diabetes, not Addison’s disease, which involves adrenal hormone deficiency.

Question 65:

Conn’s syndrome is primarily associated with the overproduction of which hormone by the adrenal glands?

a) Glucocorticoids

b) Aldosterone

c) Androgens

d) Thyroxine (T4)

e) Epinephrine

Answer 65:

b) Aldosterone

Explanation:

Conn’s syndrome is characterised by the overproduction of aldosterone by the adrenal glands, leading to sodium retention and potassium loss.

a) Glucocorticoids (Incorrect): Conn’s syndrome is characterized by excess aldosterone, not glucocorticoids e.g. cortisol. 

c) Androgens (Incorrect): Androgens are not the primary hormone involved in Conn’s syndrome; aldosterone is.

d) Thyroxine (T4) (Incorrect): Thyroxine is a thyroid hormone, not related to Conn’s syndrome, which involves aldosterone overproduction.

e) Epinephrine (Incorrect): Epinephrine is produced by the adrenal medulla, but Conn’s syndrome is associated with aldosterone from the adrenal cortex.

Question 66:

What is the primary effect of thyroid hormones on heart rate and contractility?

a) Increasing heart rate and contractility

b) Decreasing heart rate and contractility

c) Having no effect on heart function

d) Slowing down heart rate while increasing contractility

e) Speeding up heart rate while decreasing contractility

Answer 66:

a) Increasing heart rate and contractility

Explanation:

Thyroid hormones have a stimulatory effect on the heart, increasing both heart rate and contractility.

b) Decreasing heart rate and contractility (Incorrect): Thyroid hormones actually increase heart rate and contractility, not decrease them.

c) Having no effect on heart function (Incorrect): Thyroid hormones do affect heart function by increasing both heart rate and contractility.

d) Slowing down heart rate while increasing contractility (Incorrect): Whilst thyroid hormones increase contractility it also speeds up heart rate, not decreases it.

e) Speeding up heart rate while decreasing contractility (Incorrect): whilst thyroid hormones increase heart rate, it also increases contractility, not decreases it.

Question 67:

How do glucocorticoids affect lipid metabolism?

a) Promoting fat breakdown and utilisation

b) Inhibiting fat absorption in the gut

c) Increasing fat storage in adipose tissue

d) Reducing cholesterol synthesis

e) Stimulating lipogenesis in the liver

Answer 67:

a) Promoting fat breakdown and utilization

Explanation:

Glucocorticoids promote the breakdown of fats (lipolysis) and their utilization for energy production.

b) Inhibiting fat absorption in the gut (Incorrect): Glucocorticoids e.g cortisol promote fat breakdown, not inhibit absorption in the gut.

c) Increasing fat storage in adipose tissue (Incorrect): While glucocorticoids can redistribute fat, their primary role in lipid metabolism is promoting fat breakdown.

d) Reducing cholesterol synthesis (Incorrect): Glucocorticoids do not primarily act on cholesterol synthesis; they promote fat breakdown for energy.

e) Stimulating lipogenesis in the liver (Incorrect): Glucocorticoids stimulate lipolysis (breakdown of fat), not lipogenesis, which is the formation of fats.

Question 68:

How does the adrenal gland respond to acute blood loss as an example of a stressor?

a) It releases insulin to lower blood glucose levels.

b) It promotes vasodilation to increase blood flow.

c) It secretes aldosterone to conserve sodium and water.

d) It releases glucocorticoids to increase blood glucose levels.

e) It stimulates the release of growth hormone.

Answer 68:

d) It releases glucocorticoids to increase blood glucose levels.

Explanation:

In response to acute blood loss and other stressors, the adrenal gland releases glucocorticoids, such as cortisol, to increase blood glucose levels and provide energy for the body’s needs.

a) It releases insulin to lower blood glucose levels (Incorrect): The adrenal gland releases glucocorticoids to raise blood glucose, not insulin to lower it.

b) It promotes vasodilation to increase blood flow (Incorrect): In response to blood loss, the body typically promotes vasoconstriction to maintain blood pressure, not vasodilation.

c) It secretes aldosterone to conserve sodium and water (Incorrect): While aldosterone helps with sodium and water retention, the primary response to acute blood loss is releasing glucocorticoids.

e) It stimulates the release of growth hormone (Incorrect): Growth hormone is not the primary response to acute blood loss; glucocorticoids are.

Question 69:

Which of the following hormones is primarily produced by the adrenal cortex and belongs to the class of glucocorticoids?

a) Epinephrine

b) Norepinephrine

c) Aldosterone

d) Cortisol

e) Testosterone

Answer 69:

d) Cortisol

Explanation:

Cortisol is a glucocorticoid hormone primarily produced by the adrenal cortex.

a) Epinephrine (Incorrect): Epinephrine is produced by the adrenal medulla, not the adrenal cortex, and it is a catecholamine, not a glucocorticoid.

b) Norepinephrine (Incorrect): Norepinephrine is also produced by the adrenal medulla and is a catecholamine, not a glucocorticoid.

c) Aldosterone (Incorrect): whilst Aldosterone is produced by the adrenal cortex it is a mineralocorticoid, not a glucocorticoid like cortisol.

e) Testosterone (Incorrect): whilst Testosterone is produced in small quantities by the adrenal cortex, it is an androgen and is not classified as a glucocorticoid.

Question 70:

What is the primary function of mineralocorticoids produced by the adrenal cortex?

a) Regulating blood glucose levels

b) Promoting bone growth

c) Controlling salt and water balance

d) Enhancing muscle contraction

e) Stimulating red blood cell production

Answer 70:

c) Controlling salt and water balance

Explanation:

Mineralocorticoids, such as aldosterone, play a crucial role in controlling salt and water balance in the body

a) Regulating blood glucose levels (Incorrect): Blood glucose levels are regulated by glucocorticoids like cortisol, not mineralocorticoids.

b) Promoting bone growth (Incorrect): Mineralocorticoids primarily control salt and water balance, not bone growth, this is controlled more by growth hormone, IGF-1 and thyroid hormones  .

d) Enhancing muscle contraction (Incorrect): Muscle contraction is not directly regulated by mineralocorticoids; they focus on salt and water balance.

e) Stimulating red blood cell production (Incorrect): Red blood cell production is regulated by erythropoietin, not mineralocorticoids like aldosterone.