PSL300 > Growth > Flashcards

Growth Flashcards

(54 cards)

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1
Q

Posterior Pituitary

A

Neural tissue
Vasopressin (ADH), Oxytocin

stores & releases neurohormones made by hypothalamus.

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2
Q

Anterior Pituitary

A

Endocrine tissue
Prolactin, TSH, ACTH, GH, FSH, LH

Produces its own hormones, stimulated by hypothalamic tropic hormones via the hypothalamo–hypophyseal portal system.

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3
Q

What connects the hypothalamus and pituitary gland?

A

The infundibulum.

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4
Q

What are the two parts of the pituitary gland?

A

Posterior pituitary (neural tissue) and anterior pituitary (endocrine tissue).

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5
Q

What hormones are secreted by the posterior pituitary?

A

Oxytocin and Vasopressin (ADH) — both made in the hypothalamus.

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6
Q

How does the hypothalamus control the anterior pituitary?

A

Via tropic neurohormones traveling through the hypothalamic–hypophyseal portal system

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7
Q

What type of hormone is GH? aka Growth Hormone

A

Peptide hormone (191 amino acids).

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8
Q

Where is GH produced?

A

Anterior pituitary (somatotrophs).

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9
Q

What stimulates GH release?

A

GHRH, sleep, fasting, exercise, stress, hypoglycemia, ghrelin.

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10
Q

What inhibits GH release?

A

Somatostatin, high glucose, obesity, aging, high IGF-1 (negative feedback).

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11
Q

What is the main target organ for GH?

A

The liver, which releases IGF-1 (Insulin-like Growth Factor 1).

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12
Q

Describe the GH–IGF-1 pathway.

A

Hypothalamus → GHRH → Anterior Pituitary → GH → Liver → IGF-1 → Bone & tissue growth.

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13
Q

What is IGF-1?

A

A peptide hormone with insulin-like structure that mediates GH’s growth effects.

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14
Q

What type of feedback does IGF-1 exert?

A

Negative feedback on both the hypothalamus and anterior pituitary.

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15
Q

What cells are responsible for cartilage production in bone growth?

A

Chondrocytes.

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16
Q

How does GH promote bone growth?

A

Indirectly via IGF-1, which increases chondrocyte recruitment, proliferation, and matrix production.

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17
Q

What happens to growth plates at puberty?

A

Epiphyseal plates close, ending bone length growth.

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18
Q

When does GH peak during the day?

A

Early night, during deep sleep (slow-wave sleep).

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19
Q

Why does GH peak at night?

A

Because GHRH increases and somatostatin decreases during early sleep.

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20
Q

How does fasting affect GH?

A

Fasting increases GH secretion to spare muscle and promote fat metabolism.

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21
Q

What causes gigantism?

A

Excess GH before epiphyseal plate closure → excessive bone length.

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22
Q

What causes acromegaly?

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A

Excess GH after epiphyseal plate closure → bone thickening (jaw, hands, feet).

23
Q

What is the most likely cause of GH excess?

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A

Pituitary adenoma (tumor).

24
Q

GH excess leads to…

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A

↑ Chondrocytes, ↑ IGF-1, ↓ GHRH (feedback inhibition).

25
Where are thyroid hormones produced?
In thyroid follicles — follicular cells surround colloid.
26
What is the role of iodine?
Iodide is added to thyroglobulin to form MIT and DIT, precursors to T₃ and T₄.
27
What forms T₃ and T₄?
T₃ = MIT + DIT (active form) T₄ = DIT + DIT (prohormone)
28
Which hormone is more active?
T₃ (3–5× more potent).2
29
How are T₃ and T₄ released?
Thyroglobulin is reabsorbed, cleaved, and T₃/T₄ enter circulation.
30
What stimulates TSH release?
TRH from the hypothalamus.
31
What does TSH do?
Stimulates T₃/T₄ synthesis and thyroid growth via a G-protein–cAMP pathway.
32
What regulates thyroid hormone levels?
Negative feedback — high T₃/T₄ inhibit TRH and TSH release.
33
Metabolic
↑ BMR, ↑ O₂ use, ↑ heat production, ↑ protein turnover
34
Nervous
↑ Reflexes, alertness, brain development
35
Growth
Works with GH/IGF-1 for bone and tissue growth
36
Cardiovascular
↑ HR, contractility, β-adrenergic receptors
37
Muscular
Maintains tone; excess = weakness
38
What causes hyperthyroidism?
Excess thyroid hormone, often due to Graves’ disease or tumors.
39
Mechanism of Graves’ disease?
Autoantibodies (TSI) bind to and activate TSH receptors, → ↑ T₃/T₄, ↓ TSH.
40
Graves’ disease symptoms?
Goiter, weight loss, anxiety, exophthalmos, tachycardia, heat intolerance.
41
What causes hypothyroidism?
Iodine deficiency or underactive thyroid.
42
Symptoms of hypothyroidism?
Fatigue, cold intolerance, weight gain, bradycardia, goiter.
43
Why goiter in iodine deficiency?
↓ T₃/T₄ → ↑ TRH, ↑ TSH → thyroid growth (no hormone output).
44
TRH, TSH, and TH levels in iodine deficiency?
↑ TRH, ↑ TSH, ↓ T₃/T₄.
45
Chondrocytes
Divide and lay down new cartilage at the growth plate
46
Old chondrocytes
Disintegrate as they move deeper into the bone
47
Osteoblasts
Replace dead chondrocytes by laying down ossified bone (brown in diagrams)
48
What Happens at Puberty?
- The epiphyseal plates gradually ossify (turn into bone). - Once fully fused, no more lengthening is possible. - This marks the end of vertical bone growth in adulthood.
49
How is bone growth regulated?
First we have the hypothalamus that stimulates growth hormone releasing hormone to be released (GHRH) This is going to travel to the anterior pituitary where growth hormone is actually released GH will travel to various target tissues but the main one is the liver The liver is going to produce insulin like growth factor which is important for cartilage growth This is a negative feedback as insulin like growth hormone regulates GH from the anterior pituitary Somatostatin inhibits growth hormone release
50
Growth Hormone (GH) and Circadian Rhythm
GH secretion is pulsatile — it’s released in bursts rather than continuously. Pattern: Major GH peak: occurs shortly after sleep onset, especially during deep sleep (slow-wave sleep). Smaller pulses: happen throughout the day, but the night pulse is the largest. Why this matters: Sleep triggers GH release via hypothalamic GHRH (growth hormone–releasing hormone). Somatostatin, which inhibits GH, is low during early sleep, allowing the big GH pulse. This timing supports tissue repair, growth, and protein synthesis during rest.
51
Fasting and Growth Hormone
Fasting significantly influences GH secretion. Short-term fasting (12–24 hrs): ↑ GH secretion (more frequent pulses, larger amplitude). Purpose: to spare muscle protein and promote fat utilization. GH helps maintain blood glucose indirectly by reducing glucose uptake in tissues and increasing lipolysis. Longer fasting (days): GH remains elevated, while insulin decreases and cortisol may increase → promoting fat breakdown and ketone production. So fasting enhances GH as a survival adaptation to preserve lean mass while shifting to fat metabolism.
52
Thyroid Gland Structure
- Made of thyroid follicles - Each follicle has: Follicular cells (purple) around the edge Colloid (sticky protein-rich center) - Also contains C-cells → secrete calcitonin (regulates calcium)
53
How Thyroid Hormones Are Made
- Follicular cells make thyroglobulin (a large protein precursor) - Iodine from the blood is converted to iodide - Iodide is transported into the follicular cells - Thyroglobulin + iodide are secreted into the colloid - Enzymes in the colloid attach iodide to tyrosine residues on thyroglobulin - MIT (Monoiodotyrosine) = 1 iodide - DIT (Diiodotyrosine) = 2 iodides - These combine to form: - T₃ (Triiodothyronine) = MIT + DIT → active - T₄ (Thyroxine) = DIT + DIT → less active - Modified thyroglobulin is taken back into follicular cells via vesicles - Enzymes cleave off T₃ and T₄ - T₃ and T₄ enter the bloodstream
54
What are the functions of thyroid hormones?
Metabolic (metabolic rate, oxygen consumption, heat production, protein degradation, lipolysis) Nervous system (enhances speech, thinking, reflexes) Growth and development (essential in children, works with GH) Cardiovascular (enhances heart rate and contractility; peripheral blood flow, works in part by increasing numbers of Beta adrenergic receptors + other proteins) Muscular (too much causes muscle weakness)
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