Hormones Flashcards

1
Q

What are pheromones?

A

They are chemical signals that are released into the air and that communicate info from one individual to another and act through the olfactory system
Ex: synchronization of menstruation among human females living together in dorms; dogs (and other animals) marking territory by urination; mate attraction in arthropods

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2
Q

Simple Endocrine Pathway

A
  1. stimulus
  2. receptor protein
  3. endocrine cell
  4. blood vessel
  5. target effectors
  6. response
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3
Q

Simple Neuroendocrine Pathway

A
  1. stimulus
  2. sensory neuron
  3. hypothalamus/posterior pituitary
  4. neurosecretory cell
  5. blood vessel
  6. target effectors
  7. response
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4
Q

Hormone Cascade Pathway

A
  1. stimulus
  2. sensory neuron
  3. hypothalamus
  4. neurosecretory cell
  5. blood vessel
  6. endocrine cell
  7. blood vessel
  8. target effectors
  9. response
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5
Q

Pituitary gland is the…

A

“Master Gland”
-specifically posterior pituitary > hormones are synthesized in hypothalamus but released from nerve endings in posterior pituitary

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6
Q

Antidiuretic Hormon Pathway

A

-Homeostasis: blood osmolarity
-Stimulus: Increase in blood osmolarity (after sweating profusely)
-Osmoreceptors in hypothalamus trigger release of ADH
-Thirst AND kidney increases permeability
-Drinking water reduces blood osmolarity to set point and H2O reabsorption prevents further osmolarity increase
-Back to homeostasis

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7
Q

ADH is blocked by…

A

ETHANOL
-H2O cannot be reabsorbed
-leads to dehydration

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8
Q

What are tropic hormones?

A

Hormones that are released from the anterior pituitary that regulate the activity of other endocrine glands

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9
Q

What are non-tropic hormones?

A

Hormones that directly influence tissues that are not endocrine glands

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10
Q

AP hormones (tropic effects only)

A

-follicle-stimulating hormone (FSH) > testes/ovaries
-luteinizing hormone (LH) > testes/ovaries
-thyroid-stimulating hormone (TSH) > thyroid
-adrenocorticotropic hormone (ACTH) > adrenal cortex

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11
Q

AP hormones (non-tropic effects only)

A

-prolactin > mammary glands
-melanocyte-stimulating hormone > melanocytes
-endorphin > pain receptors in the brain

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12
Q

AP hormones (tropic and non-tropic effects)

A

growth hormone > liver and bones

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13
Q

Prolactin

A

-mammalian females: stimulates breast development and milk production
-mammalian males: helps regulate the level of testosterone secretion by the testes
-birds: regulates fat metabolism and reproduction
-amphibians: regulates metamorphosis
-fishes: regulates salt and water balance

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14
Q

Endorphins

A

-body’s natural opiates
-bind to pain receptors in brain and dull pain reception
-“runner’s high”
-morphine, opium, heroin are mimics of endorphins

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15
Q

Growth hormone (tropic and non-tropic effects)

A

-Tropic: liver cells > release of insulin-like growth factors (IGFs) > stimulation of bone and cartilage growth
-Non-tropic: all cells > amino acid uptake

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16
Q

Effect of underproduction of growth hormone in childhood

A

pituitary dwarfism

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17
Q

Effect of overproduction of growth hormone in childhood

A

gigantism

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18
Q

Thyroid, TRH, TSH, and thyroxine

A

-TRH = thyrotropin-releasing hormone; exposure to cold stimulates TRH
-TSH = thyroid-stimulating hormone aka thryotropin
-thyroxine: increases basal metabolic rate and turns off TRH production (negative feedback)
-Responses: upregulation of basal cell metabolism, stimulation of fat breakdown and protein synthesis, and heat

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19
Q

What are the two forms of thyroxine?

A

T3 and T4

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20
Q

What is the composition of T3 and T4?

A

T3: tyrosine and 3 iodine atoms
T4: tyrosine and 4 iodine atoms

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21
Q

What does the thyroid produce mostly? T3 or T4?

A

T4

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22
Q

What happens to thyroxine when there’s iodine deficiency?

A

Leads to production of inactive thyroxine, which cannot turn off production of TRH by negative feedback > thyroid cannot stop making inactive thyroxine and works too hard and swells

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23
Q

What happens when the thyroid cannot stop making inactive thyroxine?

A

-called Hypothyroidism
-symptoms: goiter (thyroid swells and neck has bulge), low metabolism, intolerance of cold, general physical and mental sluggishness
-children: hypothyroidism causes cretinism

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24
Q

What causes the thyroid to produce too much active thyroxine?

A

-aka Hyperthyroidism
-Negative feedback mechanism fails even though blood levels of thyroxine are high
-Graves’ Disease: an autoimmune disease in which an antibody to the TSH receptor is produced that activates the secretion of thyroxine (agonist to receptor)

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25
Q

What is the effect of hyperthyroidism?

A

Thyroid remains maximally active and. grows larger
-symptoms: nervous, jumpy, hot, fat buildup behind eyeballs

26
Q

What are the adrenal glands composed of?

A

Adrenal Medulla and Cortex

27
Q

Medulla

A

-produces epinephrine and norepinephrine
-develops from nervous system and remains under its direct control

28
Q

Cortex

A

-produces cortisol and is under hormonal control (mainly by ACTH from anterior pituitary)

29
Q

Fight or Flight

A

Adrenal medulla produces epinephrine (aka adrenaline) in response to stress, initiating fight or flight reactions (increased HR and breathing rates, elevated BP, glycogen breakdown, increased metabolism, and changes in blood flow patterns)

30
Q

Epinephrine and norepinephrine pathway

A
  1. tyrosine > tyrosine beta-hydroxylase
  2. L-dopa > Dopa decarboxylase
  3. Dopamine > Dopamine beta-hydroxylase
  4. Norepinephrine > phenylethanolamine N-methyl transferase
  5. Epinephrine (adrenaline)
31
Q

Receptors for epinephrine and norepinephrine

A

Epinephrine: alpha-adrenergic and beta-adrenergic
Norepinephrine: alpha-adrenergic

32
Q

What are beta blockers?

A

Drugs that inactivate only beta-adrenergic GPCR receptors and can be used to reduce fight-or-flight responses to epinephrine.

33
Q

What do beta blockers do?

A

They prevent the activation of adenylyl cyclase that leads to cAMP production and the fight-or-flight responses but leave the alpha receptors available to norepinephrine and its regulatory functions

34
Q

What is a common prescribed beta blocker?

A

Propranolol: reduces performance anxiety

35
Q

Adrenal Cortex

A

use cholesterol to produce steroid hormones, including the main glucocorticod, cortisol, that mediates the body’s response

36
Q

Mechanism for steroids and cytoplasmic receptors

A
  1. Signal (outside of cell)
  2. Ligand binds to cortisol receptor/chaperone protein complex (inside the cell)
  3. Once bound, chaperone protein releases from receptor
  4. steroid and cortisol receptor molecule move into nucleus
37
Q

Regulation of cortisol release

A
  1. Stimulus: fright or stress
  2. Release of corticotropin RH from hypothalamus
  3. Release of tropic hormone adrenocorticotropin (ACTH) from anterior pituitary
  4. Release of cortisol from adrenal cortex
  5. Cortisol stimulates cells that are not critical to the emergency to decrease use of glucose
38
Q

Why is cortisol helpful?

A

Can help reduce inflammation and allergies

39
Q

Why is long-term stress and high levels of cortisol dangerous?

A

-blocks the immune system
-high levels of stress and cortisol can make us more susceptible to infections and disease

40
Q

Short-term stress responses

A

Effects of epinephrine and norepinephrine:
1. glycogen broken down to glucose; increased blood glucose
2. increased BP
3. increased breathing rate
4. increased metabolic rate
5. Change in blood flow patterns (increased alertness, decreased digestive and kidney activity)

41
Q

Long-term stress responses

A

Effects of glucocorticoids:
1. proteins and fats broken down and converted to glucose > increased blood glucose
2. immune system may be suppressed

42
Q

What produces sex steroids and what are they?

A

WHAT PRODUCES: gonads (testes and ovaries)
WHAT ARE THE STEROIDS: androgens/testosterone (males) and estrogen/progesterone (females)

43
Q

Male Sex Steroid Pathway

A
  1. Hypothalamus
  2. GnRH (gonadotropin releasing hormone)
  3. anterior pituitary
  4. LH & FSH
  5. testes
  6. testosterone
  7. sperm (secondary sex characteristics)
    NEGATIVE FEEDBACK
44
Q

Female Sex Steroid Pathway

A
  1. Hypothalamus
  2. GnRH
  3. Anterior pituitary
  4. LH & FSH
  5. Ovaries
  6. Estrogen
  7. eggs (secondary sex characteristics)
    NEGATIVE and POSITIVE FEEDBACK
45
Q

Up until what week can an embryo develop into either gender?

A

7th week

46
Q

What does the Y chromosome cause?

A

Causes the gonads to produce androgens, male reproductive system develops

47
Q

If androgens are absent, what reproductive system develops?

A

Female reproductive system (they are the default)

48
Q

What is the difference between mammal and bird gender development?

A

Mammals: females are default
Birds: males are default (and estrogens trigger female development)

49
Q

What is Klinefelter’s Syndrome?

A

When biological males have an extra X chromosome and have more feminine features
-small testicular size leads to reduced fertility and increased sterility

50
Q

What is Castrato?

A

When males are castrated before puberty and therefore cannot produce the right sex steroids, leading them to stay pubescent and retain their high operatic voices

51
Q

Control of Glucose Levels in the Blood

A

PANCREAS:
1. Stimulus: rising blood glucose level
2. Beta cells produce and secrete insulin into blood
3. Liver takes up glucose and stores it as GLYCOGEN/body cells take up more glucose
4. Blood glucose declines to homeostasis

  1. Stimulus: dropping blood glucose level
  2. Alpha cells produce and secrete glucagon into blood
  3. Liver breaks down glycogen and releases glucose into blood
  4. Blood glucose levels rise back to homeostasis
52
Q

Type I Diabetes

A

Lack of protein hormone insulin

53
Q

Type II Diabetes

A

Lack of insulin receptor activity on target cells

54
Q

What happens to cells in Type I Diabetes?

A

They do not take up glucose and use fat and protein for fuel, resulting in body’s wasting away and tissue and organ damage

55
Q

Melatonin (rhythmic hormone)

A

-produced by pineal gland in brain
-release occurs in the dark
-inhibition is triggered by light

56
Q

Melatonin and Effect of Seasons

A

Changes in day length changes melatonin profiles, and these changes elicit other changes in the plant or animal that are seasonally appropriate (white Siberian hamsters in winter and darker in summer)

57
Q

Melatonin and Seasonality on Reproductive Behavior

A

-sheep and deer breed in autumn
-small rodents breed in spring
-reproductive organs are often seasonally controlled (by melatonin), such as testicle size in Syrian hamsters (long days/spring = reproductively active; short days/autumn = inactive)

58
Q

What is the “period” gene?

A

Originally discovered in flies, but the period gene regulates how fast our biological clock runs

59
Q

Termination of Hormonal Signals

A
  1. Intracellular termination (signal transduction lecture)
  2. Extracellular clearance of hormones
60
Q

Types of Extracellular Clearance of Hormones

A
  1. Degradation of hormone by ENZYMES in the liver, blood, or lymph (or conversion to inactive form)
  2. Removal of hormones from blood by kidneys and subsequent excretion > why we can detect hormones in urine test