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Questions and Answers
Both hyperthyroidism and hypothyroidism cause a decreased production of GH.
Both hyperthyroidism and hypothyroidism cause a decreased production of GH.
False (B)
Insulin deficiency in childhood can lead to a delay in growth due to a lack of glucose.
Insulin deficiency in childhood can lead to a delay in growth due to a lack of glucose.
True (A)
Glucocorticoids have no effect on GH gene transcription at low doses.
Glucocorticoids have no effect on GH gene transcription at low doses.
False (B)
Acromegaly results from excessive GH production after epiphyseal closure.
Acromegaly results from excessive GH production after epiphyseal closure.
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Cretinism is caused by an excess of thyroid hormones during post-natal development.
Cretinism is caused by an excess of thyroid hormones during post-natal development.
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IGF has a 85% similarity with proinsulin in structure.
IGF has a 85% similarity with proinsulin in structure.
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IGF II is present in higher concentrations in the blood compared to IGF I.
IGF II is present in higher concentrations in the blood compared to IGF I.
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GH acts directly in all tissues during the growth process.
GH acts directly in all tissues during the growth process.
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Six types of IGF transporters exist in the blood.
Six types of IGF transporters exist in the blood.
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The main target organ of GH is the skin, where it predominantly promotes growth.
The main target organ of GH is the skin, where it predominantly promotes growth.
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Local IGFs can interact with organs to inhibit growth.
Local IGFs can interact with organs to inhibit growth.
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GH only affects protein metabolism and has no impact on lipid metabolism.
GH only affects protein metabolism and has no impact on lipid metabolism.
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The secretion of GH is regulated by the hypothalamus and hypophysis.
The secretion of GH is regulated by the hypothalamus and hypophysis.
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Hepatic ketogenesis is a metabolic effect caused directly by GH.
Hepatic ketogenesis is a metabolic effect caused directly by GH.
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Children with GH receptor deficiency showed better growth velocity when treated only with IGF-1 compared to those treated with both GH and IGF-1.
Children with GH receptor deficiency showed better growth velocity when treated only with IGF-1 compared to those treated with both GH and IGF-1.
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Mature chondrocytes undergo degradation during the growth stage from birth to puberty.
Mature chondrocytes undergo degradation during the growth stage from birth to puberty.
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Bone growth can continue after the pubertal closure of the epiphyseal plate.
Bone growth can continue after the pubertal closure of the epiphyseal plate.
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Growth hormone acts directly on bone tissues without the need for intermediates.
Growth hormone acts directly on bone tissues without the need for intermediates.
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The half-life of growth hormone is approximately 40 minutes.
The half-life of growth hormone is approximately 40 minutes.
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Acidophilic cells in the adenohypophysis are responsible for producing thyroid stimulating hormone.
Acidophilic cells in the adenohypophysis are responsible for producing thyroid stimulating hormone.
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The process of matrix calcification occurs from birth to puberty.
The process of matrix calcification occurs from birth to puberty.
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Growth hormone receptor dimerization leads to STAT activation that ultimately affects gene expression.
Growth hormone receptor dimerization leads to STAT activation that ultimately affects gene expression.
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Non-human growth hormone is effective in humans.
Non-human growth hormone is effective in humans.
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The developmental processes of chondrocytes are unaffected after puberty.
The developmental processes of chondrocytes are unaffected after puberty.
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Chromophobes in the adenohypophysis have minimal or no hormonal content.
Chromophobes in the adenohypophysis have minimal or no hormonal content.
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The hypothalamus produces growth hormone inhibiting factor (GHIF) which stimulates the hypophysis to release growth hormone.
The hypothalamus produces growth hormone inhibiting factor (GHIF) which stimulates the hypophysis to release growth hormone.
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Insulin can enhance the production of growth hormone.
Insulin can enhance the production of growth hormone.
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Growth hormone secretion is episodic due to various factors including muscular exercise and emotional stress.
Growth hormone secretion is episodic due to various factors including muscular exercise and emotional stress.
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An abrupt withdrawal of cortisol therapy can lead to dangerously low levels of cortisol in the body.
An abrupt withdrawal of cortisol therapy can lead to dangerously low levels of cortisol in the body.
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Cretinism is caused by an excess of thyroid hormones in the body.
Cretinism is caused by an excess of thyroid hormones in the body.
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Thyroid hormones have no effect on the amplitude and frequency of pulsatile secretion of growth hormone.
Thyroid hormones have no effect on the amplitude and frequency of pulsatile secretion of growth hormone.
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Glucose and fatty acids increase the release of growth hormone.
Glucose and fatty acids increase the release of growth hormone.
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Growth hormone production is enhanced by high doses of glucocorticoids.
Growth hormone production is enhanced by high doses of glucocorticoids.
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The pulsatile secretion of growth hormone is consistently high throughout a person's life.
The pulsatile secretion of growth hormone is consistently high throughout a person's life.
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Thyroid hormone is mandatory for differentiation during maturation.
Thyroid hormone is mandatory for differentiation during maturation.
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The primary hormone responsible for growth, growth hormone (GH), accounts for 30% of an individual's genetic potential for growth.
The primary hormone responsible for growth, growth hormone (GH), accounts for 30% of an individual's genetic potential for growth.
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The velocity of growth remains constant throughout the prenatal period, despite the absence of GH.
The velocity of growth remains constant throughout the prenatal period, despite the absence of GH.
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The epiphyseal plate, located between the diaphysis and epiphysis, is responsible for bone growth, with growth occurring from the epiphysis towards the diaphysis.
The epiphyseal plate, located between the diaphysis and epiphysis, is responsible for bone growth, with growth occurring from the epiphysis towards the diaphysis.
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Glucocorticoids are essential for growth in all stages of life, from prenatal to adolescence.
Glucocorticoids are essential for growth in all stages of life, from prenatal to adolescence.
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The cellular mechanisms underlying growth include hypertrophy, hyperplasia, differentiation, and matrix deposition, as well as remodelling.
The cellular mechanisms underlying growth include hypertrophy, hyperplasia, differentiation, and matrix deposition, as well as remodelling.
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The period of childhood growth, known as juvenile growth, is characterized by a significant increase in growth velocity.
The period of childhood growth, known as juvenile growth, is characterized by a significant increase in growth velocity.
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Final height is determined solely by the length of the spinal cord and long bones of the lower limbs.
Final height is determined solely by the length of the spinal cord and long bones of the lower limbs.
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The hormonal regulation of growth remains consistent throughout a person's life, with no significant changes in hormone levels or activity.
The hormonal regulation of growth remains consistent throughout a person's life, with no significant changes in hormone levels or activity.
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Flashcards
Growth Definition
Growth Definition
The sum of processes leading to an increase in body mass.
Factors Affecting Growth
Factors Affecting Growth
Heredity, nutrition, environment, and endocrine regulation influence growth.
Cellular Mechanisms of Growth
Cellular Mechanisms of Growth
Includes hypertrophy, hyperplasia, differentiation, matrix deposition, and remodeling.
Growth Hormone (GH)
Growth Hormone (GH)
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Growth Periods
Growth Periods
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Skeletal Growth Indicator
Skeletal Growth Indicator
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Epiphyseal Plate Role
Epiphyseal Plate Role
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Influence of Sex Hormones
Influence of Sex Hormones
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Chondrocytes
Chondrocytes
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Matrix calcification
Matrix calcification
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Osteoblasts
Osteoblasts
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Epiphyseal plate
Epiphyseal plate
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Somatomedins
Somatomedins
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Adenohypophysis
Adenohypophysis
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Chondrocyte degeneration
Chondrocyte degeneration
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Fusion of epiphyseal plate
Fusion of epiphyseal plate
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Insulin-like Growth Factor (IGF)
Insulin-like Growth Factor (IGF)
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Types of IGF
Types of IGF
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IGF and Growth Hormone (GH)
IGF and Growth Hormone (GH)
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IGF Transporters
IGF Transporters
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IGF Receptors
IGF Receptors
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Local IGF Action
Local IGF Action
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GH’s Role in Growth
GH’s Role in Growth
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Effects of GH on Metabolism
Effects of GH on Metabolism
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Tissue Effects of GH
Tissue Effects of GH
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Control of GH Secretion
Control of GH Secretion
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Insulin Deficiency
Insulin Deficiency
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Glucocorticoids
Glucocorticoids
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Panhypopituitarism
Panhypopituitarism
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Laron Dwarfism
Laron Dwarfism
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Cretinism
Cretinism
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GHRH
GHRH
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Negative feedback from IGFs
Negative feedback from IGFs
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Factors influencing GH
Factors influencing GH
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Regulation by hormones
Regulation by hormones
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Cortisol withdrawal
Cortisol withdrawal
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Episodic GH secretion
Episodic GH secretion
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Pulsatile GH secretion
Pulsatile GH secretion
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Thyroid hormone functions
Thyroid hormone functions
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Synergic actions of thyroid hormones
Synergic actions of thyroid hormones
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Study Notes
Growth
- Growth is the augmentation of body mass, specifically the addition of new tissue in humans, occurring from childhood to adulthood.
- Growth is not a homeostatic (self-regulating) process, but rather occurs in defined periods.
- Factors driving growth include: heredity, nutrition, environmental influences, and endocrine regulation.
- Cellular mechanisms underlying growth include: hypertrophy (increase cell size), hyperplasia (increase cell number), differentiation, matrix deposition, and remodeling.
Endocrine Control of Growth
- Growth hormone (GH) is the primary hormone, accounting for about 30% of an individual's genetic potential for growth.
- Secondary hormones influencing growth include thyroid hormones, glucocorticoids, and sexual hormones.
- Hormonal regulation varies across life stages: prenatal, infantile, juvenile, and adolescence. Insulin and IGFs are present throughout these periods.
- GH production begins in the infantile period and continues through adolescence, while thyroid hormones start in the infantile period. Sexual hormones significantly impact growth only during adolescence.
- Prenatal: Growth is consistent; GH is not a major factor.
- Infantile: Shows a growth peak shortly after birth, boosted by thyroid hormone.
- Juvenile: Growth slows.
- Adolescence: Exhibits another growth peak, primarily fueled by sex hormones.
Skeletal Growth
- Height is a key indicator of skeletal growth.
- Final height depends on the length of the spinal cord and long bones, especially in the lower limbs.
- Epiphyseal plates are crucial to bone growth; these plates are located at the ends of long bones and enable lengthwise growth. Growth occurs from the diaphysis (shaft) toward the epiphysis (end).
- Epiphyseal plates undergo changes throughout development.
- From birth to puberty: mature chondrocytes produce extracellular matrix, mature chondrocytes hypertrophy and degrade, matrix calcification, osteoblasts and blood vessels migrate, and bone formation.
- Puberty and post-puberty: thinning of epiphyseal plates, cessation of new cell generation in the plate, chondrocytes degenerate, and fusion of the plates with the diaphysis and epiphyses occurs.
Adenohypophysis and GH Action
- The adenohypophysis (anterior pituitary) contains cells producing various hormones, including glycoprotein hormones (somatotropes produce Growth Hormone; lactotropes produce prolactin) and others like thyrotropes, gonadotropes and corticotropes.
- Growth hormone (GH) receptor activation leads to downstream signaling cascades involving JAKs and STATs, culminating in cellular effects.
Insulin-like Growth Factors (IGFs)
- IGFs are necessary intermediaries for GH's bone growth effects.
- These growth factors share structural similarity with insulin.
- Blood levels of IGFs typically follow the same growth pattern as GH, with a peak in adolescence.
- IGFs are produced primarily in the liver.
- IGFs act directly on various tissues including bone.
Thyroid Hormone
- Thyroid hormones modulate GH production, with an impact on both amplitude and frequency of GH secretion pulses.
- Thyroid hormones play a pivotal role in development, especially of the nervous system.
- Deficiency in thyroid hormones leads to cretinism, characterized by delays in neurological and physical development.
Glucocorticoids
- Glucocorticoids have effects on growth as well as tissue functionality.
- They can have either a permissive or inhibitory effect on growth depending on doses.
- Low doses sometimes accelerate GH action while high doses can inhibit growth.
- Excessive levels can result in a decrease in weight.
GH Secretion Modality
- GH secretion follows episodic and pulsatile patterns.
- Episodic secretion is triggered by factors like amino acid levels, exercise, temperature, and stress.
- Pulsatile secretion is correlated with growth periods, and levels tend to be higher in adolescence.
Clinical Points
- Imbalances in growth hormones (insufficient or excessive production) can lead to conditions like dwarfism, gigantism, and acromegaly.
- Cretinism is also linked to a deficiency in thyroid hormones.
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Description
Explore the intricate processes of human growth from childhood to adulthood. This quiz covers the physiological aspects of growth, including hormonal regulation and cellular mechanisms. Understand the factors influencing growth, such as heredity and nutrition.
