Endocrine System Flashcards

1
Q

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

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

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

A

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.

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3
Q

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

A

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

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4
Q

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

A

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

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5
Q

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

A
  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.
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6
Q

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

A

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

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7
Q

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

A

GH or GHRH receptor mutations prevent response to synthetic GH.

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8
Q

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

A

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

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9
Q

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

A

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

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10
Q

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

A
  • Paracrine hormones act on nearby cells without entering the bloodstream.
  • Endocrine hormones travel via blood to distant targets.
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11
Q

Why is calcitonin important in pregnancy?

A

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

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12
Q

How does PTH stimulate bone resorption?

A

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.

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13
Q

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

A

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

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14
Q

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

A

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

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15
Q

What are causes and symptoms of hypoparathyroidism?

A

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

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16
Q

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

A

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

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17
Q

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

A

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.

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18
Q

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

A

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

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19
Q

Where is PTH produced and what triggers its release?

A

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

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20
Q

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

A

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

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21
Q

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

A

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.

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22
Q

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

A

Increases gluconeogenesis and lipolysis, ensuring energy availability.

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23
Q

What are the three main mechanisms that control hormone release?

A
  1. Negative feedback loops.
  2. Stimulation by tropic hormones.
  3. Neuronal control (e.g. adrenal medulla via sympathetic nerves).
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24
Q

Where is calcitonin produced and what are its actions?

A

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

25
Q

What maintains calcium balance daily?

A

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

26
Q

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

A
  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.
27
Q

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

A

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.

28
Q

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

A

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.

29
Q

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

A
  • Cortisol is released in a circadian rhythm (peaks in morning).
  • Growth hormone is released in a pulsatile manner, with larger pulses during sleep.
30
Q

What are some risks of growth hormone therapy in adults?

A

Diabetes, hypertension, possible increased cancer risk.

31
Q

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

A

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.

32
Q

What dual role does TSH play in thyroid gland function?

A

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.

33
Q

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

A

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

34
Q

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?

A

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.

35
Q

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

A

Precursor: Cholesterol. Location: Mitochondria and endoplasmic reticulum.

36
Q

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

A
  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.
37
Q

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

A

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

38
Q

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

A

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

39
Q

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

A

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

40
Q

What are key physiological roles of calcium besides bone structure?

A

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

41
Q

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

A

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

42
Q

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.

A
  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.
43
Q

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

A

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.

44
Q

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

A

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

45
Q

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

A

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

46
Q

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

A
  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.
47
Q

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

A

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.

48
Q

What are the differences between primary and secondary hyperparathyroidism?

A
  • 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.
49
Q

What does active vitamin D do?

A

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

50
Q

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

A

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.

51
Q

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

A

Increased plasma osmolarity and decreased plasma volume.

52
Q

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

A

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.

53
Q

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

A

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.

54
Q

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

A

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

55
Q

What is the role of ghrelin in growth hormone regulation?

A

Stimulates GH release directly and indirectly via GHRH stimulation.

56
Q

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

A

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.

57
Q

How is calcium distributed in the body and ECF?

A

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

58
Q

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

A

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

59
Q

How is growth hormone secretion patterned throughout the day?

A

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