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thyroid pgysiology Flashcards

1
Q

1. Where is the thyroid gland located?

A
  1. The thyroid gland is located in the anterior neck, just below the larynx.
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2
Q
  1. What is the structural and functional unit of the thyroid gland?
A
  1. The thyroid gland consists of thyroid follicles, and the structural and functional unit is made up of simple cuboidal epithelial cells called follicular cells.
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3
Q
  1. Where does the synthesis of the thyroid hormone begin?
A
  1. The synthesis begins in the paraventricular nuclei (PVN) inside the hypothalamus, which secretes thyrotropin-releasing hormone (TRH).
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4
Q
  1. What is the role of TRH in the hypothalamic-pituitary-thyroid axis?
A
  1. TRH stimulates thyrotropes in the adenohypophysis to secrete thyroid-stimulating hormone (TSH) into the bloodstream.
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5
Q
  1. Where does TSH go, and what is its role?
A
  1. TSH goes to the follicles of the thyroid gland, binding to receptors on the cell membrane, and activates a G stimulatory protein to stimulate adenylate cyclase.
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6
Q
  1. Why is iodine needed for thyroid hormone production?
A
  1. Iodine is needed to produce thyroid hormone and is ingested with different nutrients, often in the form of iodized salt.
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7
Q
  1. What is the form of iodine in the bloodstream, and how is it transported into follicular cells?
A
  1. Iodine circulates in the bloodstream as iodide (with a negative charge). It is transported from an area of low concentration (blood) to an area of high concentration (follicular cells) through secondary active transport using sodium (Na+). Pendrin, a specific protein, transports iodide from follicular cells into the luminal space.
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8
Q
  1. What is the enzyme in the luminal space of the thyroid gland, and what are its functions?
A
  1. The enzyme in the luminal space is thyroid peroxidase, and it has three functions: iodine oxidation, iodination, and coupling.
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9
Q
  1. Explain the process of iodine oxidation by thyroid peroxidase.
A
  1. Iodine oxidation involves converting iodide into iodine. In this process, iodide loses an electron, loses its negative charge, and becomes neutral.
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10
Q
  1. What is iodination, and what are the products of iodination in the thyroglobulin colloid?
A
  1. Iodination is the process of attaching 1 or 2 iodine molecules to the tyrosine amino acids in the thyroglobulin colloid. The products are monoiodotyrosine (MIT) with 1 iodine molecule and diiodotyrosine (DIT) with 2 iodine molecules.
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11
Q
  1. What is the role of coupling in the enzymatic activity of thyroid peroxidase?
A
  1. Coupling involves the thyroid peroxidase coupling iodinated tyrosine amino acids, such as MIT and DIT, into larger molecules, forming thyroid hormones like triiodothyronine (T3) and thyroxine (T4).
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12
Q
  1. What are the two main thyroid hormones, and how are they formed in the thyroid gland?
A
  1. The two main thyroid hormones are thyroxine (T4) and triiodothyronine (T3). T4 is created by coupling diiodotyrosine and diiodotyrosine (DIT+DIT), while T3 is created by coupling diiodotyrosine and monoiodotyrosine (DIT+MIT) with the help of thyroid peroxidase and other enzymes.
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13
Q
  1. What is the collective term for T3 and T4, and what enzyme is primarily involved in their synthesis?
A
  1. T3 and T4 collectively are known as the thyroid hormone (TH), and thyroid peroxidase is the primary enzyme involved in their synthesis.
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14
Q
  1. Describe the process of isolating T3 and T4 from iodinated thyroglobulin.
A
  1. Iodinated thyroglobulin goes inside follicular cells via endocytosis and ends up inside vesicles. These vesicles fuse with lysosomes, where lysosomal enzymes cut the thyroglobulin, isolating T3 and T4. The vesicles containing T3 and T4 then fuse with the cell membrane, releasing the thyroid hormones into the bloodstream.
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15
Q
  1. Why are T3 and T4 not water-soluble, and how are they transported in the blood?
A
  1. T3 and T4 are not water-soluble because the tyrosine amino acid in their structure contains a benzene ring. In the blood, T3 and T4 bind to a transporting protein called thyroxine binding globulin (TBG), which is synthesized by the liver.
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16
Q
  1. What is the major component of thyroid hormone circulating in the bloodstream, and how is it transported?
A
  1. The major component is T4 (Thyroxine), and it is transported bound to thyroxine binding globulin, a protein made by the liver.
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17
Q
  1. What enzyme converts T4 into the active form T3, and where does this conversion occur?
A
  1. The enzyme 5’-deiodinase converts T4 into the active form T3 by removing an iodine from the 5’-carbon atom. This conversion occurs inside the cell.
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18
Q
  1. What is the role of retinoic acid (RXR) in the action of T3 on the transcription factor?
A
  1. T3 binds to a transcription factor, and for its effects, it needs retinoic acid (RXR) to bind to the transcription factor as well. Both substances binding to the transcription factor activate it, move it inside the nucleus, and stimulate a specific gene sequence.
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19
Q
  1. What protein is synthesized as a result of the gene sequence activation, and what function does it perform?
A
  1. The protein synthesized is Sodium-potassium ATPase (Na+/K+-ATPase), which merges with the cell membrane and acts as a sodium-potassium pump. It pumps 3Na+ out of the cell and 2K+ inside the cell, requiring an ATP molecule for energy.
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20
Q
  1. How does increased expression of sodium-potassium pumps affect the cell’s energy requirements?
A
  1. Increased expression of sodium-potassium pumps leads to a higher demand for energy, requiring more macromolecules such as carbohydrates and fats.
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21
Q
  1. How does thyroid hormone affect the liver’s glycogenolysis process?
A
  1. Thyroid hormone stimulates the expression of proteins that promote glycogenolysis, the conversion of glycogen into glucose in the liver.
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22
Q
  1. What is gluconeogenesis, and how does thyroid hormone influence this process in the liver?
A
  1. Gluconeogenesis is the conversion of non-carbohydrates into glucose. Thyroid hormone stimulates the expression of proteins in the liver that facilitate gluconeogenesis from molecules like glycerol, amino acids, and lactate.
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23
Q
  1. What is the role of thyroid hormone in the expression of LDL receptors (LDL-R) in the liver?
A
  1. Thyroid hormone influences the expression of LDL receptors (LDL-R), which are involved in the uptake of low-density lipoproteins (LDL), often referred to as “bad cholesterol.”
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24
Q
  1. How does thyroid hormone affect cardiomyocytes?
A
  1. Thyroid hormone stimulates the expression of beta-1-adrenergic receptors in cardiomyocytes, which bind to epinephrine and norepinephrine.
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25
Q
  1. In non-contractile muscle cells of the SA node and the AV node, what does thyroid hormone stimulate?
A
  1. In non-contractile muscle cells of the SA node and the AV node, thyroid hormone stimulates the expression of beta-1-adrenergic receptors, which bind to epinephrine and norepinephrine.
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26
Q
  1. What are the three ways in which thyroid hormone affects the central nervous system (CNS)?
A
  1. Thyroid hormone increases dendrite formation, myelination, and the number of synapses in the CNS.
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27
Q
  1. What psychological effects can result from hyperthyroidism due to these CNS changes?
A
  1. Hyperthyroidism can lead to anxiety and irritability as a result of increased dendrite formation, myelination, and synapse formation in the CNS.
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28
Q
  1. What are the two important types of cells in bones, and what are their respective functions?
A
  1. Osteoblasts are responsible for bone deposition, while osteoclasts are responsible for bone resorption.
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29
Q
  1. How does thyroid hormone regulate bone remodeling, and what is the process called?
A
  1. Thyroid hormone maintains the balance between osteoblastic and osteoclastic activity, preventing excessive bone deposition or resorption. The process is called bone remodeling.
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30
Q
  1. How does thyroid hormone affect chondrocytes in the epiphyseal plates, and what is the result in terms of bone growth?
A
  1. Thyroid hormone affects chondrocytes by promoting proliferation, hypertrophy, and eventually ossification in the epiphyseal plates, causing bones to grow in length through interstitial growth.
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31
Q
  1. What type of ossification does thyroid hormone stimulate in the bones?
A
  1. Thyroid hormone stimulates endochondral ossification, the process of turning cartilage into bone.
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32
Q
  1. What process does thyroid hormone stimulate in adipose tissue, and what does this process involve?
A
  1. Thyroid hormone stimulates lipolysis in adipose tissue, which is the breakdown of triglycerides into fatty acids and glycerol by activating specific enzymes.
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33
Q
  1. What happens to the produced glycerol, and how is it further converted in the liver?
A
  1. The produced glycerol goes to the liver and is converted into glucose via gluconeogenesis.
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34
Q
  1. What is protein metabolism, and what are its two components?
A
  1. Protein metabolism is the sum total of catabolism (conversion of proteins to amino acids) and anabolism (conversion of amino acids into proteins).
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35
Q
  1. How does thyroid hormone regulate the activity of catabolism and anabolism in protein metabolism?
A
  1. Thyroid hormone regulates the activity of both catabolism and anabolism, keeping them balanced.
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36
Q
  1. What imbalance occurs in protein metabolism during hyperthyroidism, and what psychological state is explicitly mentioned?
A
  1. Hyperthyroidism causes a shift in the balance towards catabolism, and it is specifically noted not to be mistaken with lethargy.
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37
Q
  1. What are the layers of the skin, specifically in the epidermis and dermis?
A
  1. The layers of the skin include the epidermis with the Stratum Corneum, Stratum Lucidum (found only in thick skin), Stratum Granulosum, Stratum Spinosum, and Stratum Basale. The dermis contains blood vessels that provide nutrition.
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38
Q
  1. How does thyroid hormone affect the metabolic rate, and how does the body respond to regulate it?
A
  1. Thyroid hormone increases the metabolic rate, leading to the dilation of blood vessels and increased blood flow. The skin may appear soft and flushed, and heat is radiated. Apocrine and merocrine sweat glands produce sweat, with increased sensitivity to catecholamines such as epinephrine and norepinephrine.
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39
Q
  1. What are the effects of hypothyroidism on the integumentary system, specifically nails and hair?
A
  1. Hypothyroidism causes brittle nails and thin hair.
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40
Q
  1. Conversely, what effects on hair are noted in the context of hyperthyroidism?
A
  1. Hyperthyroidism causes thick hair.
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41
Q
  1. What secretions in the GI tract does thyroid hormone stimulate?
A
  1. Thyroid hormone stimulates the secretions of the entire GI tract, including alkaline fluid, intestinal fluid, etc.
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42
Q
  1. How does thyroid hormone influence the motility of the GI tract?
A
  1. Thyroid hormone enhances the motility of the entire GI tract by stimulating the contractions of the smooth muscle cells.
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43
Q
  1. What gastrointestinal symptom is associated with hyperthyroidism?
A
  1. Hyperthyroidism causes diarrhea.
    peeing out of your butt hole
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44
Q
  1. Conversely, what gastrointestinal symptom is associated with hypothyroidism?
A
  1. Hypothyroidism causes constipation. Thik stuck stole
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45
Q
  1. What releases thyrotropin-releasing hormone (TRH), and where is it released?
A
  1. Specific neurons in the paraventricular nucleus (PVN) of the hypothalamus release thyrotropin-releasing hormone (TRH).
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46
Q
  1. How does TRH reach the anterior pituitary, and what cells does it stimulate there?
A
  1. TRH goes through the hypophyseal portal system, the vascular connection between the hypothalamus and the anterior pituitary. TRH stimulates specific cells called thyrotropes in the anterior pituitary, which secrete thyroid-stimulating hormone (TSH).
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47
Q
  1. What is the overall effect in the thyroid gland, and what is the collective name for the hormones produced?
A
  1. In the thyroid gland, the overall effect is the production of T3 and T4, collectively forming the thyroid hormone (TH). TH is transported through the blood with the help of thyroxine-binding globulin (TBG), a protein produced by the liver.
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48
Q
  1. How does the negative feedback mechanism work in the regulation of TH when levels are high?
A
  1. High levels of TH exert a negative feedback mechanism that inhibits the paraventricular nucleus from producing TRH.
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49
Q
  1. Conversely, what happens in terms of negative feedback when TH levels are low?
A
  1. Low levels of TH exert a negative feedback mechanism that stimulates the paraventricular nucleus to release excessive amounts of TRH.
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50
Q
  1. How does TH affect basal metabolic rate in cells, and what process is increased?
A
  1. TH increases basal metabolic rate in cells by enhancing sodium-potassium ATPase activity. It stimulates lipolysis, glycolysis, and gluconeogenesis, raising blood glucose levels, making it a hyperglycemic hormone. It also increases the uptake of low-density lipoproteins (LDL) in the liver.
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51
Q
  1. What are the effects of TH on bones?
A
  1. TH promotes normal bone growth and maturation.
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52
Q
  1. How does TH influence muscles?
A
  1. TH promotes normal muscular function and development.
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53
Q
  1. What effects does TH have on the heart?
A
  1. TH promotes normal cardiac output.
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54
Q
  1. What impact does TH have on the brain?
A
  1. TH promotes normal nerve development, increases the number of synapses, myelination, and the number of dendrites in the brain.
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55
Q
  1. What are the effects of TH on the GI tract?
A
  1. TH promotes normal motility and secretion of the GI tract.
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56
Q
  1. How does TH impact the skin?
A
  1. TH promotes normal hydration of the skin tissue.
57
Q
  1. Which hormone is produced by the anterior pituitary gland?
A
  1. b) TSH
58
Q
  1. Which cells are stimulated by TRH?
A
  1. c) Thyrotropes
59
Q
  1. Which two substances collectively form TH?
A
  1. c) Diiodotyrosine and monoiodotyrosine
60
Q
  1. Which substance binds TH in the bloodstream?
A
  1. b) Thyroxine binding globulin
61
Q
  1. What is NOT correct about the effects of T3 on the cell?
A
  1. b) ↑ the cellular ATP levels
62
Q
  1. What is WRONG about the effects of TH on the CNS?
A
  1. b) ↑ dendrite formation
63
Q
  1. Where is the thyroid gland located?
A

a. In the anterior neck, below the larynx.

64
Q
  1. Where are the parathyroid glands located?
A

b. In the posterior aspect of the thyroid gland. In the past, during thyroidectomies, they would be removed alongside the thyroid gland because their location was unknown. Generally, there are four parathyroid glands.

65
Q
  1. What are the two types of cells in the parathyroid glands?
A

c. (i) Oxyphil cells (still under research, believed to play a role in stimulating other cells to produce parathyroid hormone, and believed to produce parathyroid hormone-related protein and vitamin D), (ii) Chief cells (primarily responsible for secreting parathyroid hormone - PTH).

66
Q

. What is the initial step in parathyroid hormone synthesis?

A

a. Specific genes are expressed in the nucleus. These genes are transcribed by an RNA-polymerase type 2, producing mRNA.

67
Q
  1. How is mRNA translated into a functional protein in parathyroid hormone synthesis?
A

b. The mRNA goes into the cytoplasm, where ribosomes translate it into a preform of parathyroid hormone. The protein undergoes specific modifications and cleavage processes within the rough ER and Golgi apparatus, turning into parathyroid hormone packaged into vesicles.

68
Q
  1. What is the primary stimulus for PTH release?
A

c. Low blood Ca++ levels (hypocalcaemia). On chief cells, there are seven pass transmembrane receptors highly sensitive to Ca++. When Ca++ levels are high, calcium binds to these receptors, triggering processes that inhibit PTH release. If Ca++ levels are low, vesicles containing PTH merge with the cell membrane, releasing PTH into the bloodstream.

69
Q
  1. What stimulates the production of PTH in terms of humoral stimuli?
A

d. Ions, such as Ca++, nutrients, chemicals, etc. Hormonal stimuli, which involve stimulation by hormones, and neural stimuli, which involve stimulation by neural tissue, are the other types of stimul

70
Q
  1. What is the main structural unit of the thyroid gland?
A

a. The follicle, made up of follicular cells.

71
Q
  1. What is the function of parafollicular cells (C-cells) in the thyroid gland?
A

b. Parafollicular cells (C-cells) regulate calcium and are stimulated by high calcium blood levels.

72
Q
  1. What is the overall stimulus for calcitonin release?
A

c. High blood Ca++ levels (hypercalcemia).

73
Q
  1. What are the steps in calcitonin synthesis?
A

d. Specific genes expressed in the nucleus, transcribed to produce mRNA, which goes into the cytoplasm. Ribosomes translate it into a preform of calcitonin. The protein undergoes modifications and cleavage processes in the rough ER and Golgi apparatus, turning into calcitonin packaged into vesicles. High blood calcium levels stimulate the vesicles to fuse with the cell membrane, releasing calcitonin into the bloodstream.

74
Q
  1. What are the two types of cells in the bones that regulate bone remodeling?
A

a. Osteoclasts (responsible for bone resorption) and osteoblasts (responsible for bone deposition).

75
Q
  1. What is the role of PTH on osteoblasts?
A

b. PTH binds to receptors on osteoblasts, stimulating them to secrete RANK ligand.

76
Q
  1. How does PTH affect osteoclasts?
A

c. RANK ligand, secreted by osteoblasts in response to PTH, binds to RANK receptors on osteoclasts, making them very active and releasing chemicals that break down components of bones.

77
Q
  1. What is the outcome of the breakdown of bone components induced by PTH?
A

d. A lot of Ca++ and PO4^(3-) are accumulated and released into the blood.

78
Q
  1. What cells in the kidneys does PTH affect?
A

a. Cells of the distal convoluted tubule (DCT) in the nephron.

79
Q
  1. What is the signaling pathway activated by PTH in the kidneys?
A

b. PTH activates a G stimulatory protein, which goes to an effector enzyme on the cell membrane - Adenylate cyclase. The activated effector enzyme increases cAMP levels, activating protein kinase A (pkA).

80
Q
  1. What do the activated pKA and specific genes stimulate in the kidneys?
A

c. They stimulate the synthesis of specific proteins, called calcium transport proteins, which embed into the cellular membrane and allow Ca++ in the lumen of the DCT to flow into the cell. This is a process that is normally impermeable to ions like sodium, chlorine, water, and calcium.

81
Q
  1. What is the primary function of sodium-potassium ATPases embedded in the membrane?
A

a. They move against the gradient, pumping 3Na+ outside the cell and 2K+ inside the cell, using ATP in primary active transport.

82
Q
  1. How does the buildup of Na+ in the extracellular space contribute to secondary active transport?
A

b. When there is a buildup of Na+ in the extracellular space, it enters the cell down the concentration gradient without using energy. This process helps Ca++ get out of the blood against its concentration gradient, leading to an increase in calcium concentration in the blood.

83
Q
  1. What is the outcome of secondary active transport induced by PTH?
A

c. Phosphates are excreted in the form of PO4^3- or HPO4^2-, contributing to the phosphate buffer system.

84
Q
  1. What is the inactive precursor of vitamin D found in the skin?
A

a. 7-dehydrocholesterol.

85
Q
  1. What happens to 7-dehydrocholesterol when exposed to UV light?
A

b. It is converted into cholecalciferol (CCF).

86
Q
  1. What is the role of 25-hydroxylase in the liver?
A

c. It puts a hydroxyl group on the 25th carbon atom of cholecalciferol, producing 25-hydroxycholecalciferol.

87
Q
  1. What is the active form of vitamin D produced in the kidneys?
A

d. 1,25-hydroxycholecalciferol (calcitriol).

88
Q
  1. What is the function of calcium channel proteins in the duodenum?
A

e. They help absorb more calcium from the gut lumen, releasing it into the blood.

89
Q
  1. What is the primary target of calcitonin?
A

a. Bones.

90
Q
  1. What is the function of calcitonin on osteoclasts?
A

b. Calcitonin binds directly to osteoclasts’ receptors, inhibiting them and favoring osteoblastic activity.

91
Q
  1. What substances are secreted by osteoblasts under the influence of calcitonin for bone deposition?
A

c. Proteoglycans, collagen type 1, hydroxyapatite, etc.

92
Q
  1. Which cells are responsible for parathyroid hormone secretion?
A

a. Oxyphil cells.

93
Q
  1. What is the primary stimulus for PTH release?
A

c. Hypocalcemia.

94
Q
  1. What is the main stimulus for calcitonin release?
A

b. Hypercalcemia.

95
Q
  1. What is the function of osteoblasts?
A

b. Bone deposition.

96
Q
  1. What is the enzyme GTPase responsible for?
A

a. Cutting GTP and turning it into GDP.

97
Q
  1. Which of the following is the inactive precursor of vitamin D?
A

b. 7-dehydrocholecalciferol.

98
Q
  1. What is going to have a negative effect on vitamin D synthesis?
A

c. High blood Calcitonin levels.

99
Q
  1. What is the active form of vitamin D?
A

a. Calcitriol.

100
Q
  1. What does calcitonin inhibit?
A

b. Osteoclasts.

101
Q
  1. Which cells are responsible for calcitonin secretion?
A

d. Parafollicular cells.

102
Q
  1. What stimulates the anterior pituitary to produce TSH?
A

Hypothalamus produces TRH.

103
Q
  1. What is activated with the conversion of GTP to GDP in the thyroid hormone secretion pathway?
A

G proteins.

104
Q
  1. What does cAMP do in the synthesis of thyroid hormones?
A

Increases production and release of T3 and T4.

105
Q
  1. When T3 and T4 are released, where do they bind to exert their effects on target cells?
A

Receptor in target cells.

106
Q
  1. What is the major biologically active thyroid hormone at the cellular level?
A

T3 (Triiodothyronine).

107
Q
  1. What process occurs when T3 and T4 bind to receptors in target cells?
A

Translocation to the nucleus, binding to thyroid response elements, and stimulation of gene transcription, leading to an increase in BMR.

108
Q
  1. How do T3 and T4 complete the negative feedback loop?
A

By suppressing the production of TRH and TSH by the hypothalamus and anterior pituitary.

109
Q
  1. What is synthesized by the follicular cells in the thyroid gland?
A

Thyroglobulin.

110
Q
  1. What is the function of the parafollicular cells in the thyroid gland?
A

Contain calcitonin-secreting C-cells, which regulate calcium levels.

111
Q
  1. In the synthesis of thyroid hormones, what happens when iodine moves into the colloid?
A

It attaches to tyrosine residues on thyroglobulin to form DIT and MIT, which couple together to form T3 and T4.

112
Q
  1. Which thyroid hormone is a prohormone and converted to T3 by the liver and kidney?
A

T4 (Thyroxine).

113
Q
  1. What percentage of T4 and T3 is bound to thyroxine binding globulin (TBG) in plasma?
A

More than 99%.

114
Q
  1. Name the three hormone-binding proteins that bind T4 and T3 in the plasma and their respective percentages.
A
  • Thyroxine binding globulin (70%)<br></br> - Thyroxine binding pre-albumin (20%)<br></br> - Albumin (5%)
115
Q
  1. How is T3 binding to serum proteins compared to T4?
A

T3 is not bound very strongly to serum proteins compared to T4.

116
Q
  1. What type of hormones will enter cells, and why?
A

Only unbound hormones will enter cells (<1%) because they are free to do so.

117
Q
  1. What correlates more closely with the metabolic state in the plasma, free or total concentration of thyroid hormones?
A

The free concentration of thyroid hormones.

118
Q
  1. Why might alterations in TBG levels result in confusing total T4 levels?
A

Because many drugs and factors affect TBG levels.

119
Q
  1. Provide examples of states that increase TBG levels.
A

Pregnancy, OCP (oral contraceptive pills), chronic active hepatitis, and biliary cirrhosis.

120
Q
  1. Provide examples of states that decrease TBG levels.
A

Androgens, Cushing’s syndrome, severe systemic illness, and chronic liver disease.

121
Q
  1. What is the primary effect of thyroid hormones on all cells, especially neurons?
A

Increase metabolic rate and increased glucose uptake.

122
Q
  1. In liver tissue, what are the effects of thyroid hormones on glycogenolysis, gluconeogenesis, and glycogenesis?
A

Increased glycogenolysis and gluconeogenesis, and decreased glycogenesis.

123
Q
  1. What are the effects of thyroid hormones on adipose connective tissue regarding lipolysis and lipogenesis?
A

Increased lipolysis and decreased lipogenesis.

124
Q
  1. How do thyroid hormones affect the lungs, and how does it contribute to meeting increased O2 demand?
A

Increased breathing rate, contributing to increased O2 demand.

125
Q
  1. In the heart, what are the effects of thyroid hormones on heart rate and force of contraction?
A

Increased heart rate and increased force of contraction.

126
Q
  1. What is the relationship between thyroid hormones and basal metabolic rate?
A

Thyroid hormones increase basal metabolic rate.

127
Q
  1. How do thyroid hormones contribute to thermogenesis?
A

Thyroid hormones increase thermogenesis, accounting for about 30% of temperature regulation.

128
Q
  1. What are the metabolic effects of thyroid hormones on carbohydrate metabolism?
A

Increased blood glucose due to stimulation of glycogenolysis and gluconeogenesis, and increased insulin-dependent glucose uptake into cells.

129
Q
  1. How do thyroid hormones affect lipid metabolism?
A

Mobilize fats from adipose tissues and increase fatty acid oxidation in tissues.

130
Q
  1. What is the impact of thyroid hormones on protein metabolism?
A

Increased protein synthesis.

131
Q
  1. What role do thyroid hormones play in growth, particularly related to growth hormone releasing hormone (GHRH)?
A

GHRH production and secretion, as well as GH/somatomedines, require thyroid hormones for activity.

132
Q
  1. Why are thyroid hormones essential for the development of the fetal and neonatal brain?
A

Myelinogenesis and axonal growth require thyroid hormones.

133
Q
  1. How do thyroid hormones influence normal CNS activity, and what are the effects of hypothyroidism and hyperthyroidism?
A

Thyroid hormones are crucial for normal CNS activity. Hypothyroidism leads to slow intellectual functions, while hyperthyroidism causes nervousness, hyperkinesis, and emotional lability.

134
Q
  1. What is the permissive sympathomimetic action of thyroid hormones?
A

Thyroid hormones increase the responsiveness of adrenaline and noradrenaline by increasing the number of receptors. This effect also enhances cardiovascular responsiveness.

135
Q
  1. What are the key enzymes involved in the degradation of thyroid hormones?
A

De-iodinases.

136
Q
  1. Where is Type I deiodinase (D1) found, and what is its role in thyroid hormone degradation?
A

Found in the liver and kidney.

137
Q
  1. Where is Type II deiodinase (D2) found, and what tissues does it affect?
A

Found in the heart, skeletal muscle, fat, thyroid, and pituitary.

138
Q
  1. Where is Type III deiodinase (D3) found, and what is its role in the degradation of T3 and T4?
A

Found in fetal tissue, placenta, and brain (except the pituitary). It breaks down the majority of T3 into inactive T2 and T4 into inactive reverse T3.

Endocrine system (12 decks)

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