Endocrine System

Question 1

What are the two main physiological roles of oxytocin that I should know?

Answer 1

1. Maintainence of uterine contractions during labour.
2. Triggering of milk let-down during lactation.

Question 2

What is a goiter, and under what conditions related to thyroid hormone production might it develop? Explain the underlying mechanism.

Answer 2

A goiter is an enlargement of the thyroid gland. It may develop in both hypothyroidism (e.g. iodine deficiency) and hyperthyroidism (e.g. Grave’s disease). In hypothyroidism, low T3/T4 fails to inhibit TSH, leading to overstimulation of the gland.

Question 3

Name the three layers of the adrenal cortex and the main hormone each produces.

Answer 3

Glomerulosa: Aldosterone. Fasciculata: Cortisol. Reticularis: Androgens/oestrogens.

Question 4

Describe two factors that stimulate the release of growth hormone from the anterior pituitary.

Answer 4

Low blood glucose, exercise, sleep, or stress (via GHRH from hypothalamus).

Question 5

List three common signs and symptoms associated with hyperthyroidism. Briefly explain the physiological basis for each.

Answer 5

1. Weight loss – due to increased metabolic rate and energy expenditure.
2. Heat intolerance – from elevated heat production linked to enhanced metabolism.
3. Irritability – caused by increased sympathetic nervous system activity.

Question 6

What additional role do trophic hormones play besides stimulating hormone release?

Answer 6

Trophic hormones promote growth of target tissues via hyperplasia (more cells) or hypertrophy (larger cells).

Question 7

Why does growth hormone therapy not work in some patients with GH deficiency?

Answer 7

GH or GHRH receptor mutations prevent response to synthetic GH.

Question 8

Describe the two main regions of the adrenal gland and the general class of hormones produced by each.

Answer 8

Cortex: Steroid hormones (aldosterone, cortisol, androgens). Medulla: Catecholamines (adrenaline, noradrenaline).

Question 9

What is rickets and how does it relate to vitamin D deficiency?

Answer 9

↓ Vitamin D → ↓ Ca²⁺ absorption → ↑ PTH → poor bone mineralisation → deformities.

Question 10

Distinguish between paracrine and endocrine (hemocrine) signalling in hormonal communication, noting the route the hormone takes to reach its target.

Answer 10

• Paracrine hormones act on nearby cells without entering the bloodstream.
• Endocrine hormones travel via blood to distant targets.

Question 11

Why is calcitonin important in pregnancy?

Answer 11

Calcitonin helps protect maternal bone from being excessively broken down to supply foetal calcium. It inhibits osteoclasts, reducing bone resorption.

Question 12

How does PTH stimulate bone resorption?

Answer 12

Indirectly activates osteoclasts by binding to and stimulating osteoblasts. This causes an increase in the release of RANK ligand, which promotes osteoclast maturation and bone resorption.

Question 13

What are PTH’s effects on bone, kidney, and intestine?

Answer 13

↑ Bone resorption, ↑ renal Ca²⁺ reabsorption, ↑ intestinal absorption (via vitamin D).

Question 14

What is the cause of catecholamine hyperfunction and what hormone is mainly affected?

Answer 14

Cause: Pheochromocytoma (chromaffin cell tumour).
Hormone: Adrenaline.

Question 15

What are causes and symptoms of hypoparathyroidism?

Answer 15

Often due to inadvertent removal of parathyroid glands in thyroidectomy surgery.
Symptoms: hypocalcaemia → muscle spasms, tetany, paraesthesia.

Question 16

Briefly explain the dual nature of growth hormone’s effects on metabolism and growth.

Answer 16

Acute (metabolic): Increases protein synthesis, decreases glucose uptake.
Chronic (growth): Promotes cell hypertrophy, hyperplasia, and differentiation via IGF-1.

Question 17

Why does iodine deficiency result in goiter despite low levels of T3 and T4?

Answer 17

Low T3/T4 fails to inhibit TSH release via negative feedback, leading to persistently high TSH levels. TSH stimulates thyroglobulin production and cell growth, causing the gland to enlarge (goiter) even without TH synthesis.

Question 18

Explain how a clinical abnormality like diabetes insipidus can arise from incorrect hormone activity, specifically referencing the hormone involved.

Answer 18

Diabetes insipidus results from disrupted vasopressin (ADH) production, often due to pituitary tumours or head trauma, impairing water retention.

Question 19

Where is PTH produced and what triggers its release?

Answer 19

Parathyroid gland (chief cells); released when blood [Ca²⁺] falls.

Question 20

What is the role of IGF-1 in mediating the effects of growth hormone, and where is it primarily produced?

Answer 20

Promotes growth by stimulating cell division and differentiation; mainly produced in liver and local tissues.

Question 21

What mechanisms allow thyroid hormones to enter target cells and exert genomic effects?

Answer 21

T3 and T4 enter cells via diffusion and active transport. Inside the cytosol, T4 is converted to T3 by monodeiodinase. T3 then enters the nucleus and binds to thyroid hormone receptors (THR) on DNA promoter regions, modifying gene transcription.

Question 22

Describe two key metabolic effects of cortisol and how they contribute to the body’s response to stress.

Answer 22

Increases gluconeogenesis and lipolysis, ensuring energy availability.

Question 23

What are the three main mechanisms that control hormone release?

Answer 23

1. Negative feedback loops.
2. Stimulation by tropic hormones.
3. Neuronal control (e.g. adrenal medulla via sympathetic nerves).

Question 24

Where is calcitonin produced and what are its actions?

Answer 24

Thyroid C-cells; inhibits osteoclasts and renal Ca²⁺ reabsorption.

Question 25

What maintains calcium balance daily?

Answer 25

Dietary intake, excretion (faeces/urine), and exchange with bone.

Question 26

Describe at least three major physiological effects of thyroid hormones on the body. Provide a brief explanation for each effect.

Answer 26

1. Cardiovascular: Increases β1 adrenergic receptor expression → enhanced sensitivity to adrenaline. 2. Growth: Essential for normal growth and CNS development in early life. 3. Metabolism: Increases basal metabolic rate, stimulating glucose and lipid metabolism, and protein turnover.

Question 27

How does the posterior pituitary differ from the anterior pituitary in structure and hormone release?

Answer 27

**Structure:** Posterior is neural tissue, anterior is glandular. Hormone **Release:** Posterior releases hormones made in the hypothalamus via axonal transport; anterior responds to hypothalamic hormones via the hypophyseal portal system.

Question 28

How does the activity of the thyroid gland influence its morphology?

Answer 28

Increased thyroid activity leads to hypertrophy and hyperplasia of follicular cells, resulting in enlarged follicles with less colloid and more active epithelium. Inactive glands show flattened epithelium and abundant colloid.

Question 29

Describe the patterns of hormone release using cortisol and growth hormone as examples.

Answer 29

* Cortisol is released in a circadian rhythm (peaks in morning). * Growth hormone is released in a pulsatile manner, with larger pulses during sleep.

Question 30

What are some risks of growth hormone therapy in adults?

Answer 30

Diabetes, hypertension, possible increased cancer risk.

Question 31

What are the effects of thyroid hormones on the central nervous system during development?

Answer 31

Thyroid hormones are essential for CNS development, affecting the number of neurons and their myelination. Deficiency in late fetal or early neonatal life can cause irreversible neurological deficits.

Question 32

What dual role does TSH play in thyroid gland function?

Answer 32

TSH acts as both a tropic hormone, stimulating the synthesis and release of T3 and T4, and a trophic hormone, promoting growth of thyroid cells via increased size, number, and secretory activity.

Question 33

Explain the concept of a negative feedback loop in the context of hormonal regulation and give an example.

Answer 33

A hormone’s effect reduces its own production. Example: insulin lowers blood glucose, which in turn reduces insulin secretion.

Question 34

Describe the negative feedback mechanism that regulates thyroid hormone levels. How do high levels of T3 and T4 affect the secretion of TRH and TSH?

Answer 34

High levels of T3 and T4 exert negative feedback on both the hypothalamus and pituitary, suppressing TRH and TSH release, which reduces further TH production.

Question 35

Outline the initial precursor molecule in the synthesis of adrenal steroid hormones and where this process primarily occurs within the adrenal cells.

Answer 35

Precursor: Cholesterol. Location: Mitochondria and endoplasmic reticulum.

Question 36

List three common signs and symptoms associated with hypothyroidism. Briefly explain the physiological basis for each.

Answer 36

1. Fatigue – from reduced metabolic rate and impaired energy production. 2. Cold intolerance – due to decreased thermogenesis. 3. Weight gain – from slowed metabolism and reduced lipolysis.

Question 37

Contrast the clinical manifestations of excess growth hormone secretion in childhood versus adulthood.

Answer 37

Childhood: Gigantism (height increase). Adulthood: Acromegaly (soft tissue growth, insulin resistance).

Question 38

Briefly explain the cause and a major symptom of Cushing's Disease and Addison's Disease.

Answer 38

Cushing’s: Excess cortisol (e.g., tumour); symptom = upper body obesity. Addison’s: Cortisol deficiency (e.g., autoimmune); symptom = muscle weakness.

Question 39

Explain why some hormones require binding proteins for transport in the bloodstream and what additional function these proteins can serve.

Answer 39

Insoluble hormones need binding proteins for circulation; these proteins also extend hormone half-life by acting as reservoirs.

Question 40

What are key physiological roles of calcium besides bone structure?

Answer 40

Muscle contraction, neurotransmitter release, enzyme activity, blood clotting, hormone secretion, neuronal excitability.

Question 41

Which hormones regulate blood calcium, and when are they released?

Answer 41

PTH (low Ca²⁺), vitamin D (via PTH/low Ca²⁺), calcitonin (high Ca²⁺).

Question 42

Explain the steps involved in the synthesis of T3 and T4 within the thyroid gland, starting from iodide uptake to hormone release into the bloodstream.

Answer 42

1. Follicular cells synthesise thyroglobulin and enzymes. 2. Iodide is co-transported with sodium into the cell and into the colloid. 3. Iodine is added to thyroglobulin, forming T3 and T4. 4. Iodinated thyroglobulin is taken back into the follicular cell. 5. Enzymes cleave T3 and T4 from thyroglobulin. 6. Free T3 and T4 enter the bloodstream.

Question 43

Detail the hypothalamic-pituitary-thyroid axis. Explain how TRH and TSH influence thyroid hormone secretion.

Answer 43

The hypothalamus releases TRH, which stimulates the anterior pituitary to release TSH. TSH acts on thyroid follicular cells, promoting the synthesis and release of T3 and T4, as well as iodine uptake, protein synthesis, and thyroid cell growth.

Question 44

Describe the anatomical relationship between the hypothalamus and the anterior pituitary gland and how hormones from the hypothalamus reach the anterior pituitary.

Answer 44

Hypothalamic neuroendocrine cells secrete hormones into the hypophyseal portal system, a direct vascular link to the anterior pituitary.

Question 45

What is the primary function of tropic hormones? Give an example of a hypothalamic hormone that acts as a tropic hormone.

Answer 45

Tropic hormones stimulate other endocrine glands to release hormones. TRH is a hypothalamic tropic hormone that stimulates TSH release.

Question 46

What are the four types of local hormone signalling, and how do they differ from endocrine signalling?

Answer 46

1. Autocrine (acts on the same cell). 2. Solinocrine (within gland lumen). 3. Paracrine (nearby cells). 4. Neurocrine (neuronal version of paracrine). Unlike endocrine signalling, they do not travel through the bloodstream.

Question 47

Outline the crucial role of iodide in thyroid hormone synthesis. From where does the body obtain this essential element?

Answer 47

Iodide is essential for the synthesis of thyroid hormones. Each T3 molecule contains 3 iodide atoms, and each T4 contains 4 iodide atoms. The body obtains iodide solely from the diet.

Question 48

What are the differences between primary and secondary hyperparathyroidism?

Answer 48

- Primary: Caused by parathyroid gland overactivity leading to increased bone resorption, hypercalcaemia and decreased bone density, increasing the risk of fractures. Secondary: Caused by chronic kidney disease. Impaired kidney function = ↓ Ca2+ retention, ↓ production of active vitamin D, leading to hypocalcemia. This stimulates excessive PTH secretion, which attempts to raise Ca2+levels by increasing bone resorption, further weakening bones.

Question 49

What does active vitamin D do?

Answer 49

Increases intestinal Ca²⁺ absorption via calcium channels, calbindin, and ATPases.

Question 50

Describe the follicular structure of the thyroid gland. What is contained within these follicles, and what is its significance?

Answer 50

The thyroid gland consists of follicles lined by cuboidal epithelial cells. These follicles contain colloid, which stores thyroglobulin, a large protein that contains tyrosine residues essential for thyroid hormone synthesis.

Question 51

Outline the two main stimuli that trigger the release of vasopressin (a.k.a. ADH) from the posterior pituitary.

Answer 51

Increased plasma osmolarity and decreased plasma volume.

Question 52

How do thyroid hormones exert their effects at the cellular level? Include how T3 enters cells, interacts with nuclear receptors, and affects gene transcription.

Answer 52

T3 and T4 enter cells by diffusion or active transport. Inside the cell, T4 is converted to T3, which binds to nuclear thyroid hormone receptors (THRs). These receptors are part of a hormone-receptor complex that binds to thyroid response elements on DNA, initiating gene transcription and protein synthesis, leading to physiological effects.

Question 53

Describe two key characteristics that distinguish peptide hormones from steroid hormones in terms of their mechanism of action on target cells.

Answer 53

**Mechanism of Action:** * Peptide hormones bind to cell surface receptors triggering second messengers. * Steroid hormones diffuse through membranes to bind cytosolic or nuclear receptors. **Speed of Effect:** * Peptide hormone effects are rapid. * Steroid hormones have slower, gene-level effects.

Question 54

Explain how the hypothalamic-pituitary axis controls the secretion of cortisol, including the hormones involved.

Answer 54

Hypothalamus releases CRH → anterior pituitary releases ACTH → adrenal cortex secretes cortisol.

Question 55

What is the role of ghrelin in growth hormone regulation?

Answer 55

Stimulates GH release directly and indirectly via GHRH stimulation.

Question 56

What is Hashimoto’s disease, and how does it affect thyroid hormone production?

Answer 56

Hashimoto’s disease is an autoimmune disorder in which the immune system attacks and destroys thyroid follicular cells. This impairs the gland’s ability to produce T3 and T4, leading to hypothyroidism.

Question 57

How is calcium distributed in the body and ECF?

Answer 57

99% in bone; cytosol has very little. In ECF: 50% ionised (active), 45% protein-bound, 5% in salts.

Question 58

Explain how negative feedback mechanisms regulate the secretion of growth hormone.

Answer 58

GH and IGF-1 inhibit GHRH release and stimulate somatostatin, reducing GH secretion.

Question 59

How is growth hormone secretion patterned throughout the day?

Answer 59

Pulsatile and diurnal: Small daytime pulses, larger pulses during sleep.