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MBM > Hormones 1 > Flashcards

Hormones 1 Flashcards

1
Q

How are micro and macronutrients related?

A

micronutrients involve metabolism of macronutrients

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2
Q

what are the three main macronutrients?

A
  1. carbohydrates (glucose)
  2. proteins (amino acids-synthesis of energy, ATP)
  3. fats (fatty acids)
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3
Q

How do macronutrients turn into energy?

A
  • we need to inhale oxygen so that macronutrients can be oxidized, convert into ATP, and then carbon molecule backbones being converted into carbon dioxide to exhale
  • waste turns into feces or urine
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4
Q

why do we talk about hormones at the beginning of metabolism?

A
  • hormonal regulation is involved in almost every aspect of metabolism
  • hormonal is systemic regulation
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5
Q

what is the endocrine system? how do cells communicate?

A
  • hormones- chemical signals, can travel long distances in blood to target cells
  • cell to cell communication (our bodies are symmetrical) -we are multi celled
  • endocrine gland or endocrine cells in an endocrine tissue synthesize and secrete small molecules and send them into the blood to carry to each and every cell
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6
Q

Why do some cells respond to a signal and others don’t even though they receive the same molecule?

A
  • one has the receptor and the other does not
  • only cells with receptors will respond
  • different hormones regulate different things
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7
Q

What are other forms of cell to cell communication besides hormones?

A
  • gap junctions- directly cell to cell, local
  • synaptic- across synaptic cleft, local
  • paracrine- by diffusion in interstitial fluid, local, need receptor
  • endocrine- by circulating body fluids, general, need receptors
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8
Q

What are the hormonal actions?

A
  1. Reproduction- testosterone, progesterone, estradiol, prolactin, androgen
  2. Growth and development- growth hormone, thyroid hormone, cortisol, prolactin
  3. Maintenance of internal environment- aldosterone, vasopressin, vitamin D, retinoic acid (vit A)
  4. Energy production, utilization, and storage- insulin, glucagon, epinephrine (Nor), cortisol, leptin
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9
Q

What is cortisol derived from? (6)

A
  • cholesterol
  • small molecules (hormones)
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10
Q

what are tyrosine derivatives? (6)

A
  • T3
  • T4
  • epinephrine
  • norepinephrine
  • amino acid can serve as precursor for hormone synthesis
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11
Q

What hormones are derived from peptides (various sizes)? (6)

A
  • TRH (thyrotropin-releasing hormone)
  • ACTH (adrenal corticotropin hormone)
  • these are small peptides
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12
Q

What are the two different groups of hormones? why is this important?

A
  • hydrophobic- fat soluble
  • hydrophilic- water soluble
  • this is important because they interact with cells, all cells have hydrophobic cell membranes
  • hydrophilic hormones interact with receptors on cell membrane (this is not as long lasting of an effect)-type 2
  • hydrophobic hormones can penetrate the cell membrane, sometimes nuclear membrane, to find receptors in cytosol (type 1)
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13
Q

How fast do hormones act?

A

slow but their effects last long

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14
Q

Where are steroid hormones derived from? what can they do?

A
  • cholesterol
  • hydrophobic- move through membranes
  • bind to intracellular receptors
  • affect transcription
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15
Q

how do steroid hormones affect gene expression?

A
  • steroid enters the cytosol and binds with a receptor to make a complex
  • it is transported from cytosol to nucleus
  • in the nucleus, it affects transcription and regulation of gene expression
  • these hormones are slow but long lasting, because transcription of mRNA affects the production of proteins
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16
Q

What are examples of steroid hormones?

A
  1. cortisol
  2. sex related:
    - testosterone
    - estrogen
    - water insoluble
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17
Q

What are the steps to steroid hormone formation from cholesterol?

A
  1. cholesterol
  2. pregnenolone
  3. glucocorticoids (cortisol)
    - mineralcorticoids (aldosterone)
    - testosterone goes to estradiol
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18
Q

What is the steroid family? where are they made? examples? function?

A
  • more than 50 corticosteroids from adrenal cortex
  • glucocorticoids (carb metabolism)
  • mineralcorticoids (electrolytes from blood)
  • sex hormones (testosterone-testes, estradiol- ovaries)
  • sometimes they have overlapping function because they are derived from the same path
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19
Q

What is the first step in hormone synthesis? steroid core structure?

A
  1. cholesterol side chain is cleaved off
  2. pregnenolone forms
  3. different hormones are derived but all have

4 ring structure

  • multi step process by specific enzymes with a common precursor
  • they have similar characteristics and properties
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20
Q

What gives us diversity as it pertains to steroid hormones?

A
  • we all have different concentrations of enzymes to synthesize different amounts of hormones, different regulations
  • hormones are important regulators
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21
Q

Where is cortisol synthesized? released? what is used for?

A
  • adrenal glands on top of kidneys
  • synthesized in cortex of adrenal
  • medulla synthesizes epinephrine
  • used for glucose metabolism
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22
Q

What regulates the synthesis and secretion of cortisol?

A
  • regulated by the diurnal rhythm of ACTH (adrenocorticotropin hormone) from anterior pituitary
  • has a cycle, like circadian rhythm
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23
Q

What regulates ACTH?

A
  • CRH (corticotropin releasing hormone) from hypothalamus
  • hypothalamus releases CRH which regulates ACTH in the pituitary gland, which stimulates adrenal gland
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24
Q

What is the path from ACTH to the release of cortisol in the cell? (14)

A
  1. ACTH (cannot penetrate membrane) interacts with the G protein coupling receptors (biggest family of cell membrane receptors) on the surface of the cell membrane
  2. ATP converts to cAMP
  3. which regulates protein kinase A which regulates lipase to turn cholesterol ester(from LDL) into cholesterol
  4. cholesterol (too much is bad) goes into mitochondria where it is converted into progenelone
  5. progenelone leaves the mitochondria where it is converted into progesterone and 11-deoxycortisol
  6. deoxycortisol is transported back into the mitochondria where it is made into cortisol
  7. cortisol is then transported out of the cell
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25
Q

What part of the day is cortisol the highest? lowest? (14)

A
  • lowest in late afternoon and early evening
  • highest in the morning shortly after awakening to prepare for the day
26
Q

What does cortisol bind to in the bloodstream?

A

corticosteroid binding globulin (CBG)- carried in the bloodstream to target cells (alpha globulin)

  • also called transcortin
  • cortisol also binds albumin(highest concentration of carrier in blood)
27
Q

What is the path of a steroid hormone into the nucleus from extracellular space? function? (16)

A
  1. it is hydrophobic so it can pass through the cell membrane, into cytosol
  2. binds to receptor (GR) in cytosol
  3. makes receptor-hormone complex and transports into nucleus, through pore
  4. receptor interacts with hormone responsive element (HRE) on the promoter regions of its target genes, which is specific
  5. regulates transcription of target genes, gene expression by recruiting transcriptional coregulators and histone tail modifiers to increase or decreased expression
  6. mRNA is transported to cytosol for translation
    - cofactors are recruited
    - slow, long lasting
28
Q

What cells in the body have a cortisol receptor?

A

all tissues/cells in the body

29
Q

How does cortisol production help with low blood glucose? (17)

A
  1. hypothalamus senses low blood glucose levels
  2. it secretes CRH which regulates pituitary gland
  3. ACTH is released which goes into blood stream to reach the adrenal gland
  4. the adrenal cortex synthesizes cortisol
    - glucose levels increases
30
Q

What causes cushing syndrome? symptoms?

A
  • hypercortisol- too much
  • affects every tissue because cortisol receptors are in every cell in the body
  • bald head
  • acne on face, moonfaced
  • buffalo hump
  • hypertension- high blood pressure
  • skin thin
  • central obesity
  • bruising, blood clots affected
  • osteoporosis
  • overaccumulation of glucose and fat in central area
  • inhibits DNA, RNA, protein synthesis in peripheral tissues but enhances it in liver
  • enhancing catabolism of fat and muscle and increase hepatic gluconeogenesis, leads to hyperglycemia
31
Q

What causes hypercorticism?

A
  1. tumor in pituitary gland or hypothalamus overproducing ACTH or CRH which overstimulates adrenal gland (ACTH dependent)
  2. adrenal gland has tumor, generates a lot of cortisol from a little stimulation (ACTH independent)
  3. lung cancer ACTH released to stimulate adrenal gland (ACTH dependent)
  4. overtaking cortisol medication- overdose because of slow effect, person takes more to see an effect, adrenal gland shrinks or cushing syndrome occurs
32
Q

Feedback regulation in cortisol? HPA axis? (20)

A
  1. cortisol is secreted in response to stress (temperature, lack of sleep, pain, exercise, low glucose)
  2. CRH is upregulated in hypothalamus
  3. pituitary gland is stimulated to release ACTH
  4. adrenal gland synthesizes cortisol
  5. cortisol inhibits levels of ACTH and CRH
  6. which inhibits cortisol secretion further

hypothalamus->pituitary->adrenal axis (HPA axis)

33
Q

Where is thyroid hormone derived from?

A
  • tyrosine residues found in thyroglobulin (Tgb)
  • T3, T4 form in thyroid gland
34
Q

Where in the thyroid gland is thyroid hormone made?iodonation?

A
  • colloid (glycoprotein)
  • iodonation occurs here
  • follicular cells secrete thyroid hormone
  • C cells secrete calcitonin
  • T3= 3 iodines
  • T4= 4 iodines
35
Q

the importance of iodines in T3 and T4? (22)

A
  • number of iodines determines whether T3 or T4
  • T3 is more active and strong, more potent than T4
36
Q

What is the path of thyroid hormone synthesis? (23)

A
  1. TRH (thyrotropin releasing hormone) is released from hypothalamus
  2. TRH stimulates pituitary gland to release TSH (thyroid stimulating hormone)
  3. TSH is carried in blood stream to all cells in body, but only thyroid gland has receptor for TSH, it responds
  4. Thyroglobulin (TgB) is synthesized by ribosomes on the ER in thyroid follicular cells- this protein contains many tyrosine residues used to produce T3 and T4
  5. TgB is secreted by exocytosis into colloid (follicular lumen)
  6. iodination onto side chains of tyrosine residues attached to TgB
  7. coupling to make T3 or T4
  8. TgB containing T3/T4 is recycled by pinocytosis from colloid back to follicular cells
  9. TgB is digested by lysosomes
  10. T3 and T4 are released into the blood stream
  11. T3 and T4 have low water solubility, needs to be carried by TBG (thyroxine binding globulin), albumin in blood
37
Q

Function of thyroid hormone in the nucleus, transported from outside cell?

A
  1. hydrophobic- penetrates cell membrane, nuclear membrane (exert genomic and non genomic effects)
  2. thyroid hormone receptor (TR- type 1) is permanently bound on thyroid response element (TRE) in the form of homodimer or heterodimer, recruiting corepressors of the promoter region of target gene, represses transcription
  3. when thyroid hormone binds the TR, a complex forms, recruiting coactivators that promote histone acetylation which activates transcription of the target gene
    - slow but long lasting
    - nongenomic effects: bind to some membrane proteins and activate certain enzymes such as calcium, ATPase, adenylate cyclase, monomeric pyruvate kinase, MAP kinase
38
Q

Physiological effects of thyroid hormones?

A
  1. stimulates Na+/K+ ATPase (uses energy), increases basal metabolic rate by increasing O2 consumption, except in brain, spleen, testes
  2. increases fuel metabolism, especially liver, increasing glycolysis, cholesterol, bile salt synthesis
  3. generates heat- uses ATP
  4. amplifies epinephrine effects on lipolysis
  5. increases glucose uptake in muscle, increases protein synthesis and glycogenolysis
  6. increase cardiac output by enhancing heart rate and contractility
  7. increases sensitivity of cardio and skeletal muscle to catecholamine by increasing number of beta adrenergic receptors
  8. sensitizes pancreatic beta cells for optimum insulin secretion
39
Q

What is Graves disease? cause?

A
  • Hyperthyroidism
  • excessive sweating
  • weight loss -anxiety, stress
  • fast heart rate, palpitations
  • hypermetabolic state cause: antibody looks like TSH, binds receptor, overstimulates thyroid gland
40
Q

What is Hashimotos thyroiditis? cause?

A
  • Hypothyroidism
  • cold intolerance
  • fatigue
  • slow weight gain
  • slow heart rate, metabolism
  • hypometabolic state cause: autoimmune destructive antibodies, cannot generate enough hormone
41
Q

Feedback regulation in thyroid hormone axis (HPT)? (27)

A
  1. TRH (tri peptide) is synthesized and released by hypothalamus in pulsatile manner
  2. TRH stimulates TSH in pituitary
  3. TSH stimulates production of T3 and T4 in thyroid gland
  4. T3 and T4 are released into blood, go to liver
  5. in liver and other cells, T4 is converted to more T3 because T3 is 10x more potent
  6. T3 inhibits TSH and TRH
42
Q

Where does de-iodination of T4 occur?

A

liver, kidney, and spleen process T4 to T3

43
Q

Hyperthyroidism vs hypothyroidism? (T3 + T4, TSH, TRH levels)

A
  • Hypo: T3 + T4 decreased TSH increases TRH increases
  • Hyper: T3 + T4 increased TSH decreases TRH decreases
44
Q

Normal ranges of TRH? T3? total thyroxine? levels in hyper?

A
  • TRH (.49 - 4.67 mIU/L)
  • T3 (79 - 149 ng/dL)
  • thyroxine (4.5 - 12 ug/dL)
  • hyper: TRH below normal T3 above normal thyroxine above normal
45
Q

What are type 1 receptors?

A
  • nuclear receptors
  • reside intra cellularly and ligands (hormones) are hydrophobic
  • transcriptional factors, regulate target gene expression
  • example: thyroid, steroid hormones
46
Q

What are type 2 receptors?

A
  • on cell surface
  • protein hormones, catecholamines
  • bind to receptor, start a cascade of reactions to signal inside the cell
  • hydrophilic
47
Q

Where are receptors for peptide/protein hormones and epinephrine?

A

cell membrane

48
Q

Where are receptors for steroid hormones?

A
  • cytosol
  • complex translocates to nucleus and affects transcription
49
Q

Where are receptors for thyroid hormones?

A
  • nucleus
  • complex affects transcription
50
Q

Steroid receptor family?

A
  • Glucocorticoid receptors (GR)
  • Mineralcorticoid receptors (MR)
  • Androgen receptors (AR)
  • Estrogen receptors (ER)
  • Progesterone receptors (PR)
51
Q

Thyroid receptor family?

A
  • Thyroid receptor (TR)
  • Retinoic acid receptor (RAR, RXR)
  • Vitamin D receptor (VDR)
  • Peroxisome proliferator activated receptor (PPAR)
52
Q

Orphan receptor family?

A

receptors with non identified ligand

53
Q

Classes of steroid hormones?

A
  • Progestins (progesterone)- regulate events during pregnancy and serve as precursor for other classes of hormones
  • Glucocorticoids (cortisol, corticosterone)- promote gluconeogenesis and suppress inflammation in pharmacological doses
  • Mineralcorticoids (aldosterone)- regulate ion balance by promoting reabsorption of K+, Na+, Cl-, HCO3- in kidneys
  • Androgens (androstenedione, testosterone)- promote male sexual development and maintain male sex characteristics
  • Estrogens (estrone, estradiol)- female sex hormones which support female characteristics
  • Vitamin D- receptors in intestine, bone and kidney, Vit D stimulates dietary Calcium and Pi absorption into bloodstream, reabsorption in renal tubule and mineralization of bone
54
Q

Effects of Cortisol?

A
  • inhibits synthesis of DNA, RNA, proteins in peripheral tissues
  • enhances catabolism in muscles, adipose tissue, bone, connective tissues and lymphatic tissues
55
Q

Effects of Glucocorticoids?

A
  • present in all tissues so effects are universal
  • RNA, protein synthesis stimulated in liver
  • antagonistic to insulin, agonistic to glucagon
  • increase gluconeogenesis
  • increase protein catabolism in tissues
  • increase hepatic uptake of amino acids
  • inhibit utilization of glucose in extra hepatic tissues
56
Q

Addison’s disease? causes?

A
  • hypoglucocorticoids
  • deficient in production of cortisol- adrenocortical insufficiency caused by dysfunction of adrenal cortex
  • caused by autoimmune disease (most), TB, HIV/Aids, adrenal cancer, glucocorticoid therapy, tumors on pituitary and hypothalamus (secondary)
  • symptoms:
  • weakness, weight loss, fatigue, anorexia, nausea, vomiting, hypotension, hyponatremia, hypoglycemia
  • aldosterone synthesis regular is normal b/c it is not regulated by ACTH
  • hyperpigmentation due to absence of feedback inhibit which leads to elevated ACTH (primary)- increases in accentuated over pressure areas (knuckles, knees)
  • Treatment:
  • administer glucocorticoids in water soluble form hydrocortisone hemisuccinate or phosphate
57
Q

What is TBG?

A
  • thyroxine binding globulin
  • transports thyroid hormones through circulation
  • TBG levels are affected by estrogens, androgen, glucocorticoid therapy, certain liver diseases, inherited factors
58
Q

Hypothyroidism? symptoms? causes? treatments?

A
  • deficient in thyroid hormone
  • in children, severe growth and developmental defects, physically and mentally
  • in adults, low basal metabolic rate and cold intolerance
  • causes:
  • gland fails to produce sufficient amount of hormone
  • dietary iodine deficiency or dysfunctional gland
  • inherited defects
  • pituitary and hypothalamic deficiency lead to secondary hyperthyroidism, is rare
  • treatment: T4 administration
59
Q

Hyperthyroidism? symptoms? causes? treatment?

A
  • palpitation, nervousness, easy fatigue, hyperkinesia, diarrhea, excessive sweating, heat intolerance, weight loss with good appetite
  • Graves disease is most prominent- auto antibodies which mimic action of TSH
  • treatment:
  • antithyroid drug
  • surgery
  • radioactive iodine therapy
60
Q

View page 19 of hormone 1 pdf.

A

hi

61
Q

Clinical implications of vitamin D?

A
  • Rickets- deficiency in Vit D in children, bone remodeling is defective
  • Osteomalacia- deficiency of Vit D in adults, pain, partial bone fractures, muscle weakness, calcification of bone matrix is deficient
  • Chronic renal failure- results in lack of calcitrol production and may cause rickets of osteomalacia
  • Cancers:
  • cancers with metastasis causing bone destruction, hypercalcemia
  • adenoma- functional benign tumor, hyperparathyroid causing hypercalcemia and phosphaturia, hypercalcuria which leads to renal stones
  • extensive bone reabsorption (hypercalcemia)

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