exam deck 3 Flashcards

1
Q

What regulates the release of growth hormone (GH)?

A

GH release is regulated by Growth Hormone-Releasing Hormone (GHRH) and Growth Hormone-Inhibiting Hormone (GHIH, or somatostatin).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the release pattern of GH.

A

GH is released in pulses, following a circadian rhythm, with peak levels during sleep, childhood, and adolescence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does GH promote bone growth?

A

GH stimulates precursor cells in bone to differentiate into chondrocytes, which produce IGF-1; IGF-1 then stimulates chondrocytes to proliferate, forming new cartilage and bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What role does IGF-1 play in GH effects?

A

IGF-1 mediates many of GH’s growth-promoting effects, including cell division and protein synthesis, acting both locally (auto/paracrine) and as a circulating hormone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the metabolic effects of GH?

A

GH promotes amino acid uptake for protein synthesis, breaks down fats for energy, and conserves glucose (anti-insulin effect).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does IGF-1 contribute to GH’s metabolic effects?

A

IGF-1 enhances amino acid and glucose uptake into cells, providing energy and substrates for growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does insulin interact with GH?

A

Insulin is required for growth, enhancing protein synthesis, and promoting glucose uptake into cells, which complements GH’s effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why are thyroid hormones essential for GH function?

A

Thyroid hormones stimulate GH receptor expression, enabling GH to effectively stimulate growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What effect do sex hormones have on growth?

A

They coordinate the pubertal growth spurt, stimulate GH/IGF-1 production, and induce epiphyseal plate closure to stop growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is cortisol’s role in growth?

A

at high levels, cortisol inhibits GH and protein synthesis, promoting protein breakdown instead, often as part of a stress response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes pituitary dwarfism?

A

GH deficiency in childhood leads to short stature; it can be treated with hGH before epiphyseal plates close.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is gigantism, and what causes it?

A

Excess GH in childhood, often due to a pituitary tumor, causing extreme height due to excessive bone growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is acromegaly?

A

Acromegaly is caused by excess GH after epiphyseal plates have closed, leading to thickening of bones in the hands, feet, and face.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is the thyroid gland located, and what are its components?

A

The thyroid gland is located at the base of the throat, containing follicular cells that produce thyroid hormones and clear (C) cells that produce calcitonin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the two main thyroid hormones, and what is their precursor?

A

The main thyroid hormones are T3 and T4, both derived from tyrosine and containing iodine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are T3 and T4 transported in the blood?

A

Being lipophilic, T3 and T4 require plasma-binding proteins, primarily thyroid-binding globulin (TBG), for transport.

17
Q

What are the main functions of thyroid hormones?

A

Thyroid hormones increase metabolic rate, generate heat, stimulate protein and enzyme synthesis, are critical for growth, and are essential for fetal brain development.

18
Q

How do thyroid hormones influence growth?

A

They are anabolic, supporting protein synthesis and growth by increasing GH receptor expression.

19
Q

What is hyperthyroidism, and what are its symptoms?

A

Hyperthyroidism is an overproduction of thyroid hormones, leading to increased metabolic rate, heat intolerance, weight loss, muscle weakness, and increased heart rate.

20
Q

What is Graves’ disease?

A

Graves’ disease is an autoimmune disorder where antibodies stimulate the thyroid, leading to hyperthyroidism and potentially causing a goiter and eye bulging (exophthalmos).

21
Q

How is hyperthyroidism treated?

A

Treatments include surgical removal of part of the gland, radioactive iodine, and thyrostatic drugs (e.g., propylthiouracil).

21
Q

What causes hypothyroidism, and what are its symptoms?

A

Caused by iodine deficiency or autoimmune destruction of the thyroid, symptoms include cold intolerance, weight gain, fatigue, and slow heart rate.

22
Q

How is hypothyroidism treated?

A

With oral thyroxine (T4) supplements or iodine-enriched foods.

22
Q

What is a goiter, and what causes it?

A

A goiter is an enlarged thyroid gland, often caused by TSH stimulation when iodine deficiency prevents adequate thyroid hormone production.

23
Q

What system primarily controls aldosterone secretion?

A

The renin-angiotensin system.

24
Q

What triggers renin release from kidney cells?

A

Low blood volume (e.g., from hemorrhage or dehydration) and low sodium levels, detected by sensor cells in the kidney.

25
Q

How does renin lead to aldosterone production?

A

Renin release initiates angiotensin II production, which binds to receptors on zona glomerulosa cells in the adrenal cortex, stimulating aldosterone synthesis.

26
Q
A
27
Q

What is hypercortisolism?

A

A condition where there is excess cortisol in the blood, also known as Cushing’s syndrome.

28
Q

List some symptoms of Cushing’s syndrome.

A

Hyperglycemia (high blood glucose), muscle and tissue wasting, fat redistribution to the trunk and face (moon face), mood disorders, immunosuppression, and skin breakdown leading to abdominal striations.

29
Q

What are the three main causes of hypercortisolism?

A

Primary Hypercortisolism: Caused by an adrenal tumor producing excess cortisol.
Secondary Hypercortisolism (Cushing’s Disease): Due to a pituitary tumor secreting excess ACTH, overstimulating cortisol production.
Iatrogenic Hypercortisolism: Caused by long-term glucocorticoid therapy for other conditions.

30
Q

How is hypercortisolism treated?

A

Treatment includes surgical removal of the tumor or gradual withdrawal of glucocorticoid therapy to allow the HPA axis to adjust.

31
Q

What is hypocortisolism, and what is another name for this condition?

A

Hypocortisolism is low cortisol in the blood, also known as Addison’s disease or adrenal insufficiency.

32
Q

List some symptoms of Addison’s disease.

A

Hypoglycemia, low blood pressure, loss of salt balance (risk of dehydration), mood disorders, weakness, and lethargy.

33
Q
A
34
Q

Describe the two main causes of hypocortisolism.

A

Primary Adrenal Insufficiency: Caused by direct adrenal damage (e.g., tuberculosis, tumors, autoimmune attack), leading to a loss of cortisol and aldosterone production.
Secondary Adrenal Insufficiency: Caused by pituitary disease leading to ACTH deficiency, resulting in cortisol insufficiency but not affecting aldosterone.

35
Q

What is Addison’s crisis, and why is it dangerous?

A

Addison’s crisis is a severe drop in cortisol levels during stress or illness, leading to profound hypoglycemia and potential fatality.

36
Q

How is Addison’s disease treated?

A

Daily oral glucocorticoids and mineralocorticoids, dietary and fluid management, and treatment of the underlying cause.