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ZOOL461 > Habibi Lectures > Flashcards

Habibi Lectures Flashcards

1
Q

what are the different means of delivery by hormones?

A

endocrine, neuroendocrine, paracrine, autocrine, neurocrine, or pheromonal route

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2
Q

endocrine

A

the hormone is released into the circulation and is transported to the target cell by blood vessels (gonadotropin secreted from pituitary to target testis/ovary)

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3
Q

neuroendocrine

A

the hormone is released by nerve cells into the circulation and is transported to the target cells (vasopressin secreted by hypothalamic neurons via posterior pituitary to target kidney and vascular smooth muscle)

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4
Q

paracrine

A

hormone is released and diffuses to its target ell through the immediate extracellular fluid (epidermal growth factor-1)

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5
Q

autocrine

A

target of the secreted hormone is the same cell that released it (prostaglandins and some growth factors)

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6
Q

neurocrine

A

neurons secrete the hormone in the immediate vicinity of the target cell (neurotransmitters such as norepinephrine and dopamine)

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7
Q

pheromone

A

hormone is released into the environment to induce a biological response in another animal, usually species specific and may also be called exocrine action (reproductive pheromones in mammals, fish, insects)

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8
Q

what are 4 different types of molecules involved in information transfer?

A

peptides/proteins, steroids (androgens, estrogens, progestogens, corticosteroids), amino acids/amino acid derivatives (iodothyronines, catecholamines), eicosanoids (prostaglandins, prostacyclins)

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9
Q

what is the antagonist to the present agonist: testosterone?

A

cyproterone acetate (anti-androgen)

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10
Q

what is the antagonist to the present agonist: 17-beta-estradiol?

A

tamoxifen (anti-estrogen)

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11
Q

what is the antagonist to the present agonist: progesterone?

A

RU486 (anti-progestogen)

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12
Q

what are the units of the association rate constant, K+1?

A

M^-1 sec^-1

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13
Q

what are the units of the dissociation rate constant, K+1?

A

sec^-1

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14
Q

how do you calculate equilibrium association constant Ka, (M^ -1)?

A

K+1/K-1

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15
Q

what is analogous to the equilibrium association constant ?

A

affinity of hormone-receptor interaction

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16
Q

how do you calculate equilibrium dissociation constant Ka, (M)?

A

1/Ka

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17
Q

what is analogous to the equilibrium dissociation constant ?

A

hormone potency (ED50)

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18
Q

affinity of hormone-receptor interaction determines:

A

potency of hormone (ED50)

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19
Q

the number of receptors determines:

A

the capacity for effect/maximum responsiveness

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20
Q

what does the affinity of hormone-receptor interactions depend on?

A

changes in receptor structure

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21
Q

intracellular receptors can respond to hormones such as:

A

steroids (diffusion) and iodothyronines (active transport), peroxisome proliferator-activator (PPAR) (lipophilic) - receptor can act as a ligand-activated transcription factor

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22
Q

plasma membrane receptors can respond to hormones such as:

A

peptides, proteins, and catecholamines (adrenaline, noradrenaline) (hydrophilic)

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23
Q

what are the two domains that comprise receptors?

A

binding domain and activation domain

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24
Q

what are the three domains that comprise intracellular receptors that can act as transcription factors?

A

Hormone binding (conformational change when bound to hormone to allow DNA binding), DNA binding, activation domains (initiates transcription when bound to DNA)

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25
Q

what is the name of the DNA sequence that the activated hormone-receptor complex interacts with?

A

hormone response element (present in promoter)

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26
Q

tyrosine kinase receptor is stimulated by:

A

EGF, insulin

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27
Q

what is an example of a ligand-gated sodium channel?

A

nicotinic acetylcholine receptor (2 alpha, beta, gamma, delta subunits) - requires 2 ACh to activate and open Na channel

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28
Q

what binds to alpha subunit of binding domain of ACh receptor (nACH-R) irreversibly?

A

alpha-bungarotoxin (snake venom), kills instantly

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29
Q

what inhibits phosphodiesterases?

A

methylxanthines (theophylline, caffeine, amenophylline)

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30
Q

phosphodiesterase 5 (PDE 5) causes:

A

cGMP hydrolysis in smooth muscle, thus causes smooth muscle contraction (terminates relaxation)

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31
Q

what does sildenafil citrate (Viagra) inhibit?

A

PDE 5 (potent, reversible, selective inhibitor), blocks cGMP hydrolysis effectively

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32
Q

what are the 5 types of cells in the anterior pituitary lobe?

A

gonadotrophs (FSH, LH), lactotrophs (PRL), somatotrophs (GH), corticotrophs (ACTH), thyrotrophs (TSH)

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33
Q

what are the 3 classes of hormones of the adenohypophysis?

A

Family I: peptides (GH, PRL)
Family II: glycoprotein (FSH, LH, TSH, choronic gonadotropin)
Family III; derived from pro-opiomelanocortin (POMC) (ACTH, alpha/beta melanocyte stimulating hormone, beta-endorphin, beta-lipotropic hormone)

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34
Q

what enzymes do POMC derived peptide hormones require?

A

prohormone covertases

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35
Q

which hormone is produced by the intermediate lobe?

A

alpha-melanocyte stimulating hormone (a-MSH), if intermedial lobe absent, produced in the anterior pituitary

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36
Q

what factors inhibit PRL release?

A

PRL-inhibiting factor (dopamine, DA)

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37
Q

what factors promote PRL release?

A

cholecytokinin (CCK), PGE1

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38
Q

what are the reproductive actions of PRL in males?

A

increase and maintain LH receptors in testis, sustain testosterone levels, increase sperm motility

39
Q

what are the reproductive actions of PRL in females?

A

increase progesterone synthesis, stimulates lactation, stimulates synthesis of casein (major milk protein) and fatty acids, stimulated migration of IgA lymphoblasts to the mammary gland, osmoregulatory function in uterus

40
Q

how does GH exert its action of somatic growth (of skeletal and soft tissue)?

A

directly at the target cell (anti-insulin actions: increased lipolysis, increased blood sugar) or indirectly through production of growth factors (IGF-I or IGF-II acts on skeletal & extraskeletal)

41
Q

GH release is stimulated by:

A

GnRH, hypoglycemia, high protein meal

42
Q

GH release is inhibited by:

A

somatostatin (SRIF: somatotropin-release-inhibitory-factor), IGF-I, fatty acids

43
Q

what are the 3 main actions of GH?

A

body growth (linear), lipolysis, increase glucose availability (hyperglycemia)

44
Q

hyperplasia

A

increase in cell number (proliferation, duplication, growth)

45
Q

why does linear growth stop at puberty?

A

high gonado-steroids causes apoptosis of cells in chondrocytes layer of epiphysis

46
Q

what is the effect of IGF-I on bone growth?

A

increased differentiation and proliferation of chondrocytes in the epiphysis

47
Q

Laran dwarfism

A

caused by lack of receptors to GH, cannot treat this condition (unless CRISPR gene therapy before puberty)

48
Q

GH synergizes with what other hormone?

A

thyroid hormone (T4)

49
Q

can T4 stimulate growth in hypophysectomized rats? can GH stimulate growth in thyroidectomized rats?

A

T4 cannot stimulate growth, but GH can stimulate growth (linear growth, but still abnormal development)

50
Q

TSH release is stimulated by?

A

TRH (thyroid releasing hormone - Glu-His-Pro-Nh2)

51
Q

TSH release is inhibited by?

A

T3, T4

52
Q

what are the functions of TSH?

A

stimulate Thyroglobulin (Tg) synthesis inside follicular cells of thyroid gland, stimulates synthesis of T3 and T4

53
Q

what causes goiter?

A

low T3, T4 (iodine deficiency), high TSH stimulates thyroid gland and causes hyperplasia/enlargement

54
Q

tetraiodothyronine

A

T4 is the main secretion of the thyroid gland, but is deiodenated in peripheral tissue

55
Q

triiodothyronine

A

T3 is what activates intracellular receptors (active transport into cells)

56
Q

which iodine do diodenases remove from T4?

A

5’ (if a different iodine is removed, reverse T3 is produced and is inactive)

57
Q

what are some of the functions of thyroid hormones (T4, T3)?

A
  1. metamorphosis
  2. growth effects
  3. stimulation of nerve growth factor production for development of nervous system (brain size, number of neurons, myelin formation)
  4. metabolic functions (oxygen consumption, thermogenesis): maintains BMR and functions to provide long-term adaptation
  5. metabolic functions: increase protein synthesis, growth rate, and results in net positive nitrogen balance
  6. metabolic functions: favours lipolysis, increases fatty acid levels in blood
58
Q

what is the effect of opiates on GnRH release?

A

inhibits GnRH release

59
Q

what is the effect of Kiss peptin on GnRH release?

A

stimulates GnRH release (Kiss peptin is stimulated by estrogen)

60
Q

what is the effect of GABA on GnRH release?

A

increase (also inhibits DA)

61
Q

what is the effect of DA on GnRH release?

A

inhibits GnRH release and inhibits gonadotropes in anterior pituitary

62
Q

what is the effect of estrogens produced by the gonads on the brain?

A

increases GnRH release by stimulating kiss peptins

63
Q

what is the effect of estrogen and progesterone combined on the brain?

A

inhibits GnRH release

64
Q

what is the effect of androgens (in males) on the brain?

A

inhibits GnRH (hypothalamus) and LH/FSH release (hypothalamus)

65
Q

what are the 2 gonadal peptides?

A

inhibin and activin: present in female ovary and male testis, belong to the transforming growth factor-beta superfamily (TGF-B)

66
Q

inhibin

A

inhibits secretion of FSH without effecting LH

67
Q

activin

A

stimulates secretion of FSH independent of GnRH (no change in LH) in addition to other actions

68
Q

what process do most follicles undergo?

A

atresia: degeneration that includes loss of the oocyte

69
Q

what are the stages of ovarian development and oogenesis?

A
  1. maturing egg (finite # of germ cells/primoridal follicles)
  2. primary follicle (have receptors for gonadotropins and leave resting pool)
  3. secondary follicle (theca and granulosa cells become more numerous)
  4. tertiary follicle (follicular fluid filled spaces merge to form a single large cavity: the antrum)
  5. preovulatory (Graafian) follicle (oocyte attaches to cumulus granulosa cells, arrest in Prophase I until ovulation)
  6. can undergo atresia or ovulation (stop at Metaphase II unless fertilized)
70
Q

general effects of estrogens:

A
  1. enlargement and maintenance of varinga, uterus, uterine tubes, ovaries, external reproductive organs
  2. development of breasts and ductile system of mammary glands
  3. increased deposition of adipose tissue in various subcutaneous layers, particularly breasts, thighs, buttocks
  4. influence skin texture and vascularization, skeletal growth, hair distribution, electrolyte balance, feedback action on pituitary and brain, stops linear growth (fusion of epiphysis), calcium uptake
71
Q

general effects of progestogens:

A
  1. promote secretory changes in the endometrium, prepares uterus for implantation of the fertilized ovum
  2. reduced uterine contraction and prevents expulsion of the implanted ovum
  3. promotes secretion of nutrients by cells lining the fallopian tube
  4. promotes development and secretion and alveolar tissue, and general swelling due to secretory development in breast tissue
72
Q

what are the 2 functions of testis?

A

provide spermatozoa and secrete hormones (androgen, estrogen, peptides)

73
Q

what are some effects of androgens?

A
  • control development of primary and secondary male sexual characteristics
  • stimulates spermatogenesis
  • act on CNS to increase sexual activity (libido)
  • regulate gonadotropin secretion and release
  • exerts anabolic effect and growth
  • aggressive behaviour
74
Q

testosterone is converted to:

A

dihydrotestosterone (DHT) by 5-alpha reductase (present in males only)

75
Q

what are the gonadosteroid levels during menopause?

A

0 estrogen and progesterone, high GnRH

76
Q

effects of insulin

A

released by beta Islet of Langerhans cells: MAIN HYPOGLYCEMIC HORMONE

  • increases glucose transport into insulin sensitive cells (via GLUT4 transporters) (does not affect glucose transport in renal tubules, RBC, intestinal mucous, liver and brain)
  • enhances cellular utilization and storage of glucose (enhances glucose oxidation in adipose tissue to produce ATP)
  • enhances utilization of amino acids (muscle synthesis)
  • promotes fat synthesis (increase activity of lipoprotein lipases)
  • increase glycogenesis (primarily in muscles: increase hepatic glucokinase activity to phosphorylate glucose, increase glycogen synthase activity)
77
Q

effects of glucagon

A

released by alpha Islet of Langerhans cells:
ONE OF THE HYPERGLYCEMIC ANTI-INSULIN HORMONES
-increase glycogenolysis in liver (glucagon and epinephrine GPCR = cAMP activates cAMP-dependent protein kinases)
-increase gluconeogenesis
-increase lipolysis (FFA can be converted to glucose)

78
Q

what is secretion of insulin affected by?

A
  1. increased glucose (+)
  2. increased amino acid (+)
  3. GI hormones (gastrin, secretin, cholecytokinin) (+)
  4. sympathetic activity (catecholamines like NE inhibits)
79
Q

norepinephrine acts of adrenergic receptors which have 2 subtypes, what are the 2 subtypes and where are they found?

A

alpha sub-type: insulin-secreting beta pancreatic cells

beta sub-type: glucagon-secreting alpha pancreatic cells

80
Q

which hormones oppose insulin action? (7)

A
  1. glucagon (increases blood glucose levels, stimulated by catecholamines like NE)
  2. cortisol (long-term control)
  3. adrenaline (PNS)
  4. GH (increases blood glucose to mobilize energy)
  5. thyroid hormones (T3, T4)
  6. PRL (pregnancy)
  7. estrogen
81
Q

what are the hormones produced by the adrenal medulla?

A

chromaffin tissue secretes catecholamines:

  • epinephrine (E) or adrenaline
  • norepinerphine (NE) or noradrenaline
  • dopamine (DA)
82
Q

what are the hormones produced by the adrenal cortex?

A
  • glucocorticoids

- mineralocorticoids

83
Q

stereogenic capabilities

A

possesses specific enzymes that allow production of steroid hormones (e.g. adrenal cortex)

84
Q

what are the layers of the adrenal cortex (from outside in)

A
  • cortex
  • zona glomerulosa (mineralocorticoids-aldosterone)
  • zona fasciculata (glucocorticoids-cortisol)
  • zona reticularis (gonadocorticoids-androgens)
85
Q

what enzyme does adrenal medulla contain that allows synthesis of E from NE?

A

phenylethanolamine-N-methyltransferase (PNMT)

86
Q

outline the synthesis of catecholamines

A
  1. phenylalanine to tyrosine (phenylalanine hydroxylase)
  2. tyrosine to dihydroxyphenylalanine DOPA (tyrosine hydroxylase - RATE LIMITING ENZYME)
  3. DOPA to dopamine (DOPA decarboxylase)
  4. dopamine to norepinephrine (dopamine beta-hydroxylase)
  5. norepinephrine to epinephrine (phenylethanolamine-N-methyltransferase, PNMT)
87
Q

what is the effect of epinephrine?

A
  • increase circulating glucose level
  • increase cardiac output
  • elicits a redistribution of the blood supply (restriction to parts of body not involved in muscular activity, skeletal muscle blood flow is increased)
  • stimulates pulmonary ventilation by dilation of bronchioles
88
Q

what is the effect of adrenaline:

A

HYPERGLYCEMIA:

  • stimulation of hepatic glycogenolysis
  • stimulation of hepatic gluconeogenesis
  • inhibition of insulin release (alpha adrenergic receptor)
  • stimulation of glucagon release (beta adrenergic receptor)
  • stimulation of ACTH release (increases cortisol release by adrenal cortex)
89
Q

which hormone are alpha adrenergic receptors more sensitive to? and what are its effects?

A 
NE
Increase in:
-gluconeogenesis
-dilation of pupils
-sweating
-GH secretion
-arterial constriction (renal/cutaneous)
-muscle contraction (gastrointestinal/urinary sphincters)

Decrease in:
-insulin secretion

90
Q

which hormone are beta adrenergic receptors more sensitive to? and what are its effects?

A 
E
Increase in:
-glycogenolysis
-lipolysis
-arteriolar dilation
-cardiac contractility (B1 receptor)
-heart rate (B1)
-muscle relaxation (GI, bronchial, urinary) (B2)
-glucagon secretion
-thyroid hormone secretion
-renin secretion (B2)

Decrease in:
-glucose utilization (in select tissues)

91
Q

what are the effects of glucocorticoids?

A

increases glucose availability:

  • increase gluconeogensis
  • inhibit uptake of glucose and amino acids by certain cells (includes adipose tissue)
  • catabolic effects in skeletal muscle and adipose tissue (allows for conversion by gluconeogenesis in liver)
92
Q

exophtalmus

A

increased hypertrophy and hyperplasia in eyes, eyeballs appear to bulge, symptom of hyperthyroidism

93
Q

Hashimoto’s disease

A

autoimmune disease where antibodies result in low T3 and T4 secretion (attack thyroid glands)

94
Q

what is the mechanism of Grave’s disease?

A

antibodies activate TSH receptors to produce increased T3 and T4 (negative feedback = decreased TSH), an autoimmune disease

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