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BIOM3200 > endocrine system - Feb 8th & 15th > Flashcards

endocrine system - Feb 8th & 15th Flashcards

1
Q

Who was Claude Bernard?

A
  • “father of modern physiology”
  • stated that our internal environment remains remarkably constant despite changes in the external milieu
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2
Q

Who was Walter Canon?

A

coined the term “homeostasis” to describe the relative stability of the internal environment

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3
Q

What does homeostatic control rely on?

A
  • sensor: constant monitoring
  • integrating centre: coordinates
  • response system: changes
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4
Q

Most systems operate in a ______ feedback manner

A

negative

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5
Q

Homeostasis is maintained largely in part by the ______ system

A

endocrine

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6
Q

What is the consequence of a hyper-function endocrine dysfunction?

A

Too much hormone

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7
Q

What is the consequence of a hypo-function endocrine dysfunction?

A

Too little hormone

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8
Q

What is the consequence of a resistance endocrine dysfunction?

A

hormone has too little effect

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9
Q

What is an endocrine gland?

A
  • a tissue that secretes a substance into the blood stream
  • substance then travels by the blood to influence a target cell
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10
Q

The Classic Minkowski experiment discovered _______

A

insulin

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11
Q

How did the Classic Minkowski experiment make its discovery?

A
  • surgical removal of the pancreas in a dog resulted in dog developing diabetes
  • implantation of pieces of pancreas under the skin of the dog resulted in prevention of symptoms of diabetes
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12
Q

What did Banting and Best discover?

A
  • insulin
  • identified antidiabetic substance in pancreatic extracts
  • injection of these extracts prevents symptoms of diabetes (prevents elevated blood glucose)
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13
Q

Describe the four properties of insulin:

A
  • peptide hormone produced by beta cells of pancreas
  • promotes absorption of glucose from blood to skeletal muscle and fat tissue
  • stored as hexamer, zinc ion and histadine residues in its inactive form
  • in its active form it is a monomer
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14
Q

What are the four types of hormones?

A
  1. protein and polypeptide hormones (<100 amino acids)
  2. steroid hormones (cholesterol derivatives)
  3. glycoprotein hormones
  4. amine hormones (catecholamines or thyroid)
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15
Q

What is autocrine signaling

A

A signaling molecule targets sites on the same cell that it is secreted from

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16
Q

What is paracrine signaling?

A

A Secretory cell secretes signaling molecules that affects another target cell in close proximity

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17
Q

What is endocrine signaling?

A

signaling molecule secreted into blood by endocrine gland

signaling molecule travels via blood to target molecule

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18
Q

Which type(s) of hormone(s) is/are synthesized in advance?

A
  • peptide
  • amine (cat & thyroid)
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19
Q

which type(s) of hormone(s) is/are synthesized on demand?

A

steroid

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20
Q

Peptide and amine hormones are stored in _______

A

secretory vesicles

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21
Q

Which type(s) of hormone(s) is/are released from cell via exocytosis?

A
  • peptide
  • amine (cat)
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22
Q

Which type(s) of hormone(s) is/are released from cell via diffusion?

A
  • steroid
  • amine (thyroid)
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23
Q

Which type(s) of hormone(s) is/are transported in the blood by being dissolved in the plasma?

A
  • peptide
  • amine (cat)
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24
Q

Which type(s) of hormone(s) is/are transported in the blood by being bound to carrier proteins?

A
  • steroid
  • amine (thyroid)
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25
Q

Which type(s) of hormone(s) has/have a short half-life?

A
  • peptide
  • amine (cat)
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26
Q

Which type(s) of hormone(s) has/have a long half-life?

A
  • steroid
  • amine (thyroid)
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27
Q

insulin is an example of a(n) _______ type of hormone

A

peptide

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28
Q

Estrogen / androgen are examples of _______ type of hormone

A

steroid

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29
Q

Epinephrine / norepinephrine are examples of ________ type of hormone

A

amine (cat)

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30
Q

Thyroxine (T4) is an example of a(n) _______ type of hormone

A

amine (thyroid)

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31
Q

hormones bind to ______ in target cells

A

receptors

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32
Q

Receptors have very high ______ for a particular hormone

A

specificity

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33
Q

What happens when “hormone overspill” occurs?

A

non-specific protein-receptor binding

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34
Q

Receptors for most hormones are found in the _______ of target cells

A

plasma membrane

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35
Q

Receptors for ____ and _____ hormones are inside the target cells

A
  • steroid
  • thyroid
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36
Q

How do transmembrane receptors work?

A
  • hormone binds to extracellular domain of receptor and activates one or more cytoplasmic signaling pathways
  • many of these pathways involve phosphorylation and enzyme activation
  • some pathways lead to DNA/mRNA/protein pathway response; other have local effect in target cell
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37
Q

What are the steps of the Adenylate Cyclase pathway?

A
  • hormone binds G protein coupled receptor, G-proteins dissociate
  • alpha subunit of G-protein activates adenylate cyclase (AC)
  • AC catalyzes product of cAMP
  • cAMP removes regulatory unit from PKA
  • active PKA activates other molecules (hormonal response)
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38
Q

What are the steps of the epinephrine - adenylate cyclase pathway

A
  • epinephrine binds to beta-adrenergic receptor on liver cell
  • G-proteins activated - subunit carrying GDP dissociates - GDP -> GTP
  • Subunit activated adenylyl cyclase which catalyzes ATP -> cAMP
  • cAMP activates PKA, which activates phosphorylase
  • Phosphorylase converts glycogen to glucose-6-phosphate
  • glucose-6-phosphate -> glucose (released from liver)
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39
Q

What did Robert Lefkowitz and Brian Kobilka do?

A
  • 2012 Nobel prize in Chem
  • how cells in our body sense their environments
  • focus on G protein coupled receptors
  • understanding how these proteins work crucial to unravelling complex network of signaling between cells
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40
Q

What are the steps of the phospholipase C-Ca2+ pathway?

A
  • Hormone binds GPCR, G-proteins dissociate
  • Phospholipase C (PLC) is activated
  • Active PLC causes breakdown of membrane phospholipid to IP3
  • IP3 binds to endoplasmic reticulum
  • Ca2+ released from ER into cytoplasm
  • Ca2+ activates other molecules (hormonal response)
41
Q

Alpha-adrenergic receptors activate ______

A

phospholipase C

42
Q

Beta-adrenergic receptors activate ______

A

adenylate cyclase

43
Q

Describe the mechanism by which steroid hormones carry out their functions

A
  • they are lipophilic so they move across the plasma membrane bound to a carrier protein
  • steroid hormone binds cell cytoplasm receptor
  • translocates to the nucleus, binds to DNA and acts as a transcription factor
  • stimulates gene transcription
  • protein products
  • response
44
Q

What is the general mechanism of action of the hypothalamic-anterior pituitary-peripheral target axes?

A

Hypothalamic neuroendocrine cells (hormone 1 - blood vessel) -> Anterior Pituitary cells (hormone 2 - general circulation) -> Target tissue (endocrine or non-endocrine) (hormone 3 - general circulation) -> Tissue response

45
Q

The pituitary gland is physically connected to the hypothalamus through a(n) ___________

A

infundibulum (stalk)

46
Q

The ____ pituitary is the endocrine gland

A

anterior / adenohypophysis

47
Q

The ____ pituitary is an extension of neural tissue

A

Posterior / neurhypophysis

48
Q

What are the 7 hypothalamic hormones / factors?

A
  1. Dopamine (PIH)
  2. Prolactin releasing hormone (PRH)
  3. Thyrotropin-releasing hormone (TRH)
  4. Corticotropin-releasing hromone (CRH)
  5. Somatostatin (GHIH)
  6. Growth hormone releasing hormone (GHRH)
  7. Gonadotropin-releasing hormone (GnRH)
49
Q

What is the function of dopamine (PIH)?

A

Inhibits prolactin secretion

50
Q

what is the function of prolactin releasing hormone (PRH)?

A

stimulates release of prolactin

51
Q

What is the function thyrotropin-releasing hormone (TRH)?

A

Regulates secretion of thyroid stimulating hormone (TSH)

52
Q

What is the function of corticotropin-releasing hormone (CRH)?

A

regulates secretion of adrenocorticotropic hormone (ACTH)

53
Q

What is the function of somatostatin (GHIH)?

A

inhibits secretion of growth hormone (GH)

54
Q

What is the function of growth hormone releasing hormone (GHRH)?

A

stimulates secretion of growth hormone

55
Q

What is the function of Gonadotropin-releasing hormone (GnRH)?

A

regulates secretion of gonadotropin-releasing hormones, lutenizing hormone (LH) and follicle stimulating hormone (FSH)

56
Q

CRH is produced by ________ within the ________

A

parvocellular neuroendocrine cells ; hypothalamus

57
Q

blood vessels carry the CRH peptides to the ____ where they stimulate ____ to secrete ______

A

anterior pituitary ; corticotropes ; adrenocorticotropic hormone (ACTH)

58
Q

ACTH is in the ____ family

A

Proopiomelanocortin (POMC)

59
Q

What are convertases?

A
  • enzymes that cleave POMC
  • Different convertases give rise to different products
60
Q

What are the two tissues that make up the adrenal glands?

A
  • adrenal cortex
  • adrenal medulla
61
Q

What is the function of the adrenal cortex?

A

Secretion of steroids (corticosteroids):
* Glucocorticoids (eg:cortisol)
* Mineralcorticoids (eg: aldosterone)
* Sex steroids (eg: testosterone)

62
Q

What is the function of the adrenal medulla?

A
  • secretes catecholamines (eg: epinephrine)
  • (modified sympathetic ganglia)
63
Q

Glucocortinoids are controlled by ______

A

ACTH

64
Q

Mineralcorticoids are controlled by ________

A

Reninangiotensin system

65
Q

Sex steroids are controlled by _____

A

ACTH

66
Q

What are the three layers of the adrenal glands from innermost to outermost?

A
  1. Zona reticularis
  2. Zona fasciculata
  3. Zona glomerulosa
67
Q

mineralocorticoids are found in the ____ layer of the adrenal glands

A

Zona Glomerulosa

68
Q

Glucocorticoids are found in the ____ layer of the adrenal glands

A

zona fasciculata

69
Q

Androgens are found in the ____ layer of the adrenal glands

A

Zona reticularis

70
Q

Epinephrine is found in the ____ layer of the adrenal glands

A

medulla

71
Q

Why is cortisol essential for life?

A
  • protects against hypoglycemia (low blood sugar)
  • promotes gluconeogenesis (increases blood sugar)
  • plays a role in immune system (suppression of immune system, regulation of inflammatory response)
  • causes breakdown of skeletal muscle for gluconeogenesis
  • causes bone catabolism
  • affects brain function (mood, memory, learning)
72
Q

What is Cushing’s Syndrome **

A
  • Primary hypercortisolism
  • high blood corticosteroids (prolonged exposure to high cortisol levels)
  • caused by glucocorticoid drugs or diseases that result in excess cortisol, ACTH or CRH
  • changes in carb and protein metabolism, hyperglycemia, hypertension, muscular weakness
  • puffy appearance, CNS disorders
73
Q

What is Cushing’s Disease ?

A
  • Secondary hypercortisolism
  • high blood corticosteroids (prolonged exposure to high cortisol levels)
  • pituitary-dependent (ie: tumour in pituitary gland produces large amounts of ACTH resulting in adrenals production of excess cortisol)
  • ACTH levels are LOWER in Cushing’s SYNDROME
74
Q

What is Addison’s Disease?

A
  • Primary hypercortisolism
  • low blood cortisol
  • adrenal insufficiency
  • cause by genetics, autoimmune dysfunction etc.
  • can be acquired if high-dose steroids are taken for longer than one week (because of CRH and ACTH suppressions which suppresses adrenal glands
75
Q

Describe the rhythm of adrenal cortisol secretion

A

Continuous, pulsatile, circadian release

76
Q

What is pituitary pars intermedia dysfunction? (PPID)?

A
  • in horses
  • impaired pituitary (hyperplasia and hypertrophy of pars intermedia
  • increases secretion of cortisol by adrenal glands
  • high blood glucose and suppression of immune system
77
Q

the ____ is the largest purely endocrine gland

A

thyroid

78
Q

The thryoid gland is ____ lobes connected by _____

A

2 ; isthmus

79
Q

thyroid ____ take up ____ from the blood

A

follicles ; iodide

80
Q

in the ____ of the thyroid, ____ enzyme helps attach ____ to ____ in thyroglobulin

A

colloid ; thyroid peroxidase enzyme (TPO) ; iodide ; tyrosine residue

81
Q

Thyroglobulin is made by _____

A

follicular cells

82
Q

iodide is brought into follicular cells by _____

A

sodium-iodide transporter

83
Q

After iodide is brought into the follicular cells it is brought into colloid by _____

A

pendrin transporter

84
Q

____ removes an electron from iodide in the colloid to produce iodine

A

thyroid peroxidase enzyme (TPO)

85
Q

What are the two possible outcomes of iodine binding tyrosine residues in thyroglobulin?

A
  1. one iodine on a tyrosine ring produces monoiodotyrosine (MIT)
  2. two iodines on a tyrosine ring produces diiodotyrosine (DIT)
86
Q

Enzymes in the colloid modify the structures of MIT and DIT, joining them together to produce ____ or ______

A
  • Triiodothyronine T3 (MIT + DIT)
  • Tetraiodothyronine T4 (DIT + DIT)
87
Q

Describe the steps of thyroid hormone synthesis after the formation of T3 and T4

A
  • T3 and T4 still attached to thyroglobuline backbone
  • thyroglobulin taken back up by follicular cells and cut, separating T3 and T4 upon stimulation by TSH
  • T3 and T4 secreted out to bloodstream bound to carrier protein
88
Q

Most thyroid hormones in blood circulation are bound to plasma carrier protein called _______

A

Thyroxin-binding globuline (TBG)

89
Q

True or false: Thyroid hormones that are still bound to their carrier protein are active

A

False: hormones have to lose the carrier protein to be active

90
Q

Is T4 or T3 more biologically active?

A

T3

91
Q

What are the physiological actions of thyroid hormones

A
  • elevate basal metabolic rate
  • needed for normal gonadal development and function
  • needed for normal embryonic/fetal development (CNS developments)
92
Q

Is production of thyroid hormone typically higher in younger or older people

A

Younger

93
Q

What are the consequences of Hypothyroidism?

A
  • abnormally low BMR
  • weight gain
  • lethargy
  • intolerance to cold
94
Q

What are the consequences of hyperthyroidism?

A
  • Increased BMR
  • weight loss
  • muscular weakness
  • nervousness
  • protruding eyes
95
Q

What is Cretinism?

A
  • congenital thyroid hormone deficiency (arising from maternal hypothyroidism or iodine deficiency)
  • reduced physical growth and developmental delays
  • Treatment with T4 soon after birth can restore mental development by age 5
96
Q

What are goiters?

A
  • abnormal thyroid growth due to hypothyroidism
  • low iodide intake results in low thyroid hormone production
  • low plasma thyroid hormones result in high TRH
  • high TRH results in high plasma TSH
  • High plasma TSH stimulates excess growth of thyroid
97
Q

What is Graves Disease?

A
  • due to hyperthyroidism
  • autoimmune antibodies activate thyroid gland leading to high T3 and T4
  • high thyroid hormone concentration leads to low TRH and low plasma TSH
  • causes exophthalmia (protruding eyes)
98
Q

Synthetic thyroid hormone medications contain only ____, this can be an issue because:

A
  • T4
  • T4 must be converted to T3 for it to work; conversion is done by de-iodinase and in some people this enzyme is deficient or not working; some providers might add Cytomel (T3) in addition to Synthroid (T4)
  • Synthetic T3 and T4 still lacks T2 and T1 and calcitonin

BIOM3200 (12 decks)

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