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Biology > Chapter 5 - Endocrine System > Flashcards

Chapter 5 - Endocrine System Flashcards

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1
Q

What can diabetes lead to if not controlled?

5

A 
Blindness
Kidney failure
Heart attack
Stroke
Amputation
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2
Q

What is it that hormones do?

A

They bind to receptions in the target tissue, inducing a change in gene expression or cellular functioning.

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3
Q

3 classifications of hormones by CHEMICAL structure

A
  1. Peptide hormones
  2. Steroid hormones
  3. Amino-Acid Derivative hormones
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4
Q

What are peptide hormones made from?

A

Derived from larger polypeptides that are cleaved during post translational modification.

They are made up of amino acids

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5
Q

How does a cell make peptide hormones?

A

Polypeptides are broken down

Smaller units go to the Golgi apparatus for modifications that ACTIVATE the hormone

Packages into vesicles and sent out of the cell via exocytosis

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6
Q

Can peptide hormones pass through the cell membrane?

Why / why not?

What are first / second messengers?

A

NO because they are charged.

They must hence bind to an exta cellular receptor. (Often a g-protein coupled receptor)

First messenger is the hormone - second messenger is within the cell. This is known as signaling cascade.

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7
Q

Examples of common second messengers?

A

Cyclic adenosine monophasphate (cAMP) – am regulated by enzyme called adenylate cyclase

Inositol triphosphate (IP3)

Calcium

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8
Q

Characteristics of peptide hormones:

Fast response?
Soluble?
Need carrier in bloodstream?

A

Fast response but short-lived (require constant stimulation of second messengers to continue the response)

Water-soluble

Do not need a carrier in the bloodstream

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9
Q

What are steroid hormones made from?

A

Cholesterol

Produced primarily by the gonads and adrenal cortex

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10
Q

Can steroid hormones pass through the cell membrane?

Why / why not?

A

Yes - because they are nonpolar

They don’t require an extra cellular receptor (receptor is intercellular, in cytosol or in the nucleus)

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11
Q

How does a steroid hormone communicate with target cell/tissue?

A

Crosses membrane

Binds to receptor inside the cell

Steroid hormone-receptor complex undergoes CONFORMATIONAL CHANGES

Receptor can then bind directly to DNA

Increases or decreases transcription of particular genes

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12
Q

Characteristics of steroid hormones:

Fast acting?
Soluble?
Carrier in bloodstream?

A

Slow acting but long-lasting (because they cause alterations in the amount of mRNA and protein present in the cell)

Non-soluble

Carried by proteins in the blood stream

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13
Q

Common carriers of steroid hormones:

A

Sex-hormone-binding globulin (specific)
Albumin (nonspecific)
Thyroxine-binding globulin (TBG)

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14
Q

What are amino-acid derivative hormones made from?

An example?

A

Made from one or two amino acids, usually with additional modifications

Eg: thyroid hormones are made from tyrosine with the additional of iodine atoms

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15
Q

What are common examples of amino-acid derivative hormones:
(4)
Long or short duration? Fast or slow?

A

Epinephrine
Norepinephrine
Triiodothyronine
Thyroxine

First two: think “adrenaline rush” fast onset but short lived
Last two: slow onset and longer duration (regulate metabolic rate over a long period of time)

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16
Q

What are catecholamines?

What do they bind to?

A

Epinephrine and norepinephrine

Bind to g-protein-couples receptors (like peptide hormones)

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17
Q

What do thyroid hormones bind to?

A

They bind intracellularly, like steroid hormones

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18
Q

Direct versus Tropic hormones?

A

DIRECT
Act directly on target tissue

TROPIC
Requires an intermediary
Usually originate in the brain and anterior pituitary gland

Eg: GnRH (gonadotropin-releasing hormone) and LH do not cause direct changes; they stimulate the production of another hormone by another endocrine gland.

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19
Q

What is the purpose of the endocrine system?

A

To use hormones and messengers to create changes in behavior and physiology to maintain homeostasis

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20
Q

High blood glucose can cause damage to which organs:

5

A

Retina of the eye (blindness)
Glomeruli of the kidneys (kidney failure)
Coronary vessels of the heart (heart attack)
Cerebral vessels of the brain (stroke)
Nerve damage in extremities (amputation)

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21
Q

Why are thyroid hormone levels higher in pregnant women?

A

Because high levels of estrogen and progesterone increase the production of TBG (thyroxine-binding globulin). Secretion of thyroid hormones is increased to compensate.

This is an example of a change in level of carrier protein (globulin increase) which sides a change in the level of the active hormone.

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22
Q

What systems does the hypothalamus connect?

What other endocrine gland(s) does it interact with? (2)

What else does the hypothalamus regulate? (2)

A

Connect nervous and endocrine systems. Located in the forebrain

Anterior pituitary
Posterior pituitary

Responds to increases in blood osmolarity, and regulated appetite/satiety

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23
Q

What is the suprachiasmatic nucleus?

A

A part of the hypothalamus

Received light input from the retinas, helps control sleep-wake cycles

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24
Q

What is the hypophyseal portal system?

A

A blood vessel system that directly connects the anterior pituitary and the hypothalamus.

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25
Q

Which hormones produced by the hypothalamus cause a response in secretions from the ANTERIOR PITUITARY? (5)

A
  1. GnRH - gonadotropin releasing hormone.
  2. GHRH - growth hormone releasing hormone (ALSO somatostatin, also affects GH)
  3. TRH - thyroid releasing hormone
  4. CRF - Corticotropin-releasing factor
  5. Dopamine aka PIF - prolactin inhibiting factor (this is the only one that causes a decrease in secretion from the pituitary)
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26
Q

What is an “axis” or three-organ system?

A

When the organs have receptors (ie cortisol receptors) to detect when high levels of cortisol in the blood have been obtained - cortisol can then inhibit the hypothalamus and Ant Pit from producing more hormones stimulating cortisol.

This is the Hypothalamic-pituitary-adrenal (HPA) axis

There is also the hypothalamic-pituitary-ovarian (HPO) axis, etc

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27
Q

How does the hypothalamus interact with the posterior pituitary?

What (2) hormones are release from the posterior pituitary (produced in the hypothalamus)?

A

Neurons in the hypothalamus send their axons down the pituitary stalk directly to the posterior pituitary.

  1. Oxytocin
  2. Antidiuretic hormone (ADH) aka Vasopressin
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28
Q

What is osmolarity?

A

Increased concentration of SOLUTES in the blood

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29
Q

Hormones secreted by the Anterior pituitary?

A

FLATPEG

FSH
LH
Adenocoeticotropic hormone ACTH
Thyroid stimulating hormone TSH
Prolactin
Endorphins
Growth hormone

FLAT are Tropic hormones
PEG are direct hormones

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30
Q

What does OXYTOCIN do?

A

Stimulates uterine contractions during labor
Stimulates milk letdown during lactation
May be involved in bonding behavior

*positive feedback mechanism

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31
Q

What does ANTIDIURETIC HORMONE (ADH) do?

A

Increases reabsorption of water in the kisney’s collecting duct (aka retain water in the body)
Constricts blood vessels
Responds to increased plasma osmolarity

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32
Q

What does PROLACTIN do?

How is it regulated?

A

Stimulates milk production in the mammary glands (in men: this is pathologic)

Dopamine from hypothalamus decreases production of prolactin in the Ant Pit. After placenta is removed, levels of estrogen, progesterone, and dopamine DROP and hence the block on prolactin release is lifted

33
Q

How does oxytocin contribute to milking?

What exactly does prolactin regulate?

A

Nipple stimulation
Oxytocin released from Post Pit
Breast muscle contract, milk ejected
Hypothalamus stops releasing Dopamine on Ant Pit
Allows prolactin release
Production and regulation of milk supply

34
Q

What are ENDORPHINS?

A

Secreted by Ant Pit

Decrease the perception of pain
Naturally occurring “Painkillers”

Morphine mimics this

35
Q

What is GROWTH HORMONE?

A

Secreted by Ant Pit. Promotes growth of bone and muscles

Bone growth occurs in the epiphyte all plate, which deal shut during puberty.

GH prevents glucose uptake in tissues that aren’t growing and stimulated breakdown of fatty acids.

36
Q

What can an excess or deficit of GH cause?

A

Excess or deficit BEFORE the epiphysial plate closes (ie during childhood)

Excess : gigantism
Deficit : dwarfism

During adulthood, GH primarily has an effect on the smaller bones instead.

Acromegaly (hands, feet, head)

37
Q

What does ADH do?

A

Secreted in response to low blood volume (detected by baroreceptors)
Or increased osmolarity (osmoreceptors)

Renal collecting duct permeability to water is increased.

Causes more water to be reabsorbed into the blood vessel

Increases blood volume and blood pressure

38
Q

What hormones does the posterior pituitary synthesize?

A

NONE

Oxytocin and ADH are both synthesized in the hypothalamus, the Post Pit simply releases them.

39
Q

What is the role of the thyroid?

What are the 3 hormones it releases?

A

Setting basal metabolic rate
Calcium homeostasis

T3 (triiodothyronine)
T4 (thyroxine)
Calcitonin

40
Q

T3 and T4 - where are they produced? What do they regulate and how?

A

Produced by tyrosine (amino acid) in the follicular cells

Make energy production more/less efficient
Direct the use of glucose/fatty acids

More T3 T4 = increased cellular respiration = higher protein and Attu acid turnover.

41
Q

What TYPE of hormone is T3 and T4?

Peptide, steroid, or amino-acid derivative

A

Amino acid derivative

42
Q

What is hypothyroidism?

What are some of its effects?

A

Deficiency in iodine, or inflammation of thyroid.

Thyroid hormones are secreted in insufficient amounts.

  • lethargy
  • decreased body temp
  • decreased respiratory rate
  • decreased heart rate
  • cold intolerance
  • weight gain
43
Q

What is hyperthyroidism?

What are some of its effects?

A

May result from a tumor or thyroid overstimulation.

  • heightened activity level
  • increased body temp
  • increased respiratory rate
  • increased heart rate
  • heat intolerance
  • weight loss
44
Q

What is CALCITONIN?

Where is it produced?

A

Produced in c-cells (parafollicular cells)

Decreases plasma calcium levels:

  1. Increase calcium excretion from the kidneys
  2. Decrease calcium absorption from the gut
  3. Increase storage of calcium in the bone
45
Q

What is PARATHYROID HORMONE?

What does it do?

A

Antagonistic hormone to CALCITONIN - increases blood calcium levels.

  1. Decreases excretion by the kidneys
  2. Increases “absorption of calcium in the gut” ie uptake from the gut into blood
  3. Increases bone resorption

**also affects PHOSPHORUS homeostasis by resorbing P from bone (increase P levels) and reducing reabsorption of P in the kidney (decrease P levels)

46
Q

What does Vit D have to do with PTH (parathyroid hormone)?

A

Vitamin D is required for the absorption of CALCIUM and PHOSPHATE in the gut.

It is activated by PTH!

Hence the absorption of Phosphorus in the gut (due to Vit C) cancels out the effect of reduced resorption in the kidney (due to PTH)

47
Q

What hormones does the adrenal cortex make?
(4)

What is each hormone controlled by?

What primary germ layer does adrenal cortex arise from?

A 
Cortisol  
   ACTH from Ant Pit
Cortisone
   Same
Antidiuretic hormone 
   Renin-Angiotensin-Aldosterone system 
Cortical sex hormones (androgens and estrogens)

**these are all steroid hormones!

Arises from MESODERM

48
Q

What are GLUCOCORTICOIDS and what do they do?

A

Regulate glucose levels, and affect protein metabolism. Also decrease inflammation (ie used to tx systemic
Inflammation)

Increase gluconeogenesis and decease protein synthesis, thereby RAISING blood glucose.

Cortisol and Cortisone

Cortisol is linked with STRESS, provides a source of fuel if the body has to react quickly to something.

**Cortisol also increases synthesis of catecholamines, resulting in increased catecholamines release.

49
Q

What are

MINERALOCORTICOIDS and what do they do?

A

Salt and water homeostasis.

Aldosterone

SODIUM IN, K and H OUT!

Increases sodium reabsorption (into the blood) in the kidney. Water follows, creating increase in blood volume and increase in blood pressure. PLASMA OSMOLARITY REMAINS UNCHANGED.

Also Aldosterone reduces potassium and hydrogen re absorption, promoting their excretion in urine.

50
Q

What is renin? What is it secreted by?

A

Renin is an enzyme that activates angiotensinogen (a plasma protein) into ANGIOTENSIN 1.

Renin is produced by the juxtaglomerular cells of the kidney.

51
Q

What is angiotensin-conveying enzyme and what does it do?

A

ACE

It converts angiotensin 1 to angiotensin 2 in the LUNGS.

(ACE inhibitors: tx of HBP!)

52
Q

What is angiotensin 2 and what does it do?

A

Angiotensin 2 is converted by ACE from angiotensin 1.

It stimulates the adrenal cortex to secrete aldosterone, which increases blood volume and blood pressure.

53
Q

Cortical sex hormones

Why does the adrenal cortex make sex hormones?

A

Androgens and estrogens

Females more sensitive to disorders of cortical sex hormones.

Excess cortical sex hormones in a female fetal development could mean that the baby is born with ambiguous or masculinized genitalia

Males can be affected similarly if the disorder leads to excessive estrogen production.

54
Q

Type 1 versus type 2 DM

A

Type 1 - autoimmune disease
Insulin-producing cells (b-cells) in the islets of Langerhan are destroyed. Require regular insulin injections.

Type 2 - acquired. Receptor-level resistance/insensitivity to the effects of insulin. Due to environmental factors such as high-carb diets and obesity. Certain drugs can help the body as it’s insulin more effectively. (Only require insulin when med intervention fails)

54
Q

What hormones are produced by the adrenal medulla?
(2)

What primary germ layer does adrenal medulla arise from?

A

Epinephrine
Norepinephrine

These are catecholamines. They are secreted directly into the blood stream.

Formed from the Ectoderm

55
Q

What do EPINEPHRINE / NOREPINEPHRINE do?

A

Fast-acting fight or flight response

EPINEPHRINE:
Increase breakdown of glycogen in liver and muscle
Increase basal metabolic rate

BOTH:
Increase heart rate
Dilate bronchi
Alter blood to supply correct systems

**stress response involves cortisol as well

56
Q

How much epinephrine vs norepinephrine is release in fight or flight response?

A 
80% epinephrine 
   Constricts small blood vessels
20% norepinephrine 
   Dilates large vessels
   Psychoactive drug (can tx depression)
58
Q

What hormones are produced by the pancreas?

3

A

Glucagon
Insulin
Somatostatin

59
Q

What is GLUCAGON?

Where is it produced?

A

Produced by alpha cells in the islets of Langerhan.

Secreted during times of fasting: stimulated degradation of protein and fat, conversion of glycogen to glucose, and gluconeogenesis.

*GI hormones such as CHOLECYSTOKININ and GASTRIN increase release of glucagon.

60
Q

What happens if there is too much insulin?

A

Hypoglycemia.

61
Q

How does hyperglycemia typically happen?

What are polyuria and polydipsia?

A

Underproduction, insufficient secretion, or insensitivity to insulin.

Too much glucose in the kidney will overwhelm the nephrons ability to reabsorb glucose, resulting in high glucose levels in urine, and increase in urine volume.

POLYURIA (incr freq of urination)
POLYDIPSIA (incr thirst)

62
Q

What is SOMATOSTATIN?

Where is it produced?

A

Produced in the delta-cells of the islets of Langerhan.

INHIBITS BOTH INSULIN AND GLUCAGON SECRETION.

Stimulated by high blood glucose and amino acid concentrations.

**also produced by the hypothalamus, where it decreases growth hormone secretion.

63
Q

What hormones affect blood glucose levels?

A

DECREASE:
Insulin

INCREASE:
Glucagon
Growth hormone
Glucocorticoids (cortisol)
Epinephrine

*COUNTER-REGULATORY hormones: ones that increase blood glucose levels

64
Q

What is TESTOSTERONE?

Where is is secreted?

A

Secreted by the testes (and adrenal
Cortex) in response to LH and FSH.

Causes sexual differentiation of he male: also secondary sex characteristics in males such as pubic hair, deep voice, muscle growth.

65
Q

What is ESTROGEN? Where is it produced?

A

Produced by the ovaries (and the adrenal cortex) in response to FSH

Thickening of the endometrium every month, promotes secondary sex characteristics such as breasts, pubic hair, body fat redistribution.

66
Q

What is PROGESTERONE? Where is it produced?

A

Produced in the ovaries (and adrenal cortex) in response to LH releases from ant pit.

Secreted by the corpus luteum.

Protects endometrium (estrogen established it)

67
Q

What is MELATONIN?

Where is it produced?

A

Secreted by the pineal gland (deep in the brain)

Causes overwhelming drowsiness.

Linked to circadian rhythms. Responds to light intensity by releasing melanin.

68
Q

What are ERYTHROPOETINS? Where are they produced?

A

Produced in the kidneys.

Stimulates bone marrow to increase production of red blood cells - secreted in response to low oxygen levels in the blood.

69
Q

What is ATRIAL NATRIURETIC PEPTIDE (ANP)?

Where is it secreted?

A

Secreted by the heart

Regulates salt and water balance

When cells in atria are stretched by excess blood volume, they release ANP which promotes the excretion of sodium and therefore increases urine volume.

ANTAGONOSTIC TO ALSOSTERONE as it lowers blood pressure and volume.

70
Q

What is THYMOSIN? Where is this secreted?

A

Release by the thymus (directly behind the sternum)

Important for t-cell development and differentiation. (Maturation)

The thymus atrophies by adulthood, and thymosin levels drop.

71
Q

What is INSULIN?

Where is it produced?

A

Insulin is produced by the beta cells of the islets of Langerhan in the pancreas.

Induced muscle and liver cells to take up glucose into glycogen. Stimulates anabolic processes such as fat and protein synthesis.

72
Q

What are 3 main functions of calcium?

What 3 different things does it play an important role in?

A
  1. Bone stricture / strength
  2. Regulate muscle contractions
  3. Blood clotting (cofactor)

Cell movement
Exocytosis
Neurotransmitter release

73
Q

What is ‘positive selection’ versus ‘negative selection’ when referring to T-cells?

A

Positive selection: only the T-cells that can recognize MHC survive (the rest undergo apoptosis)

Negative selection: cells that are self-reactive (react to organism’s own proteins) undergo apoptosis

74
Q

Do T-cells undergo clonal selection?

A

Yes, just like B-cells

Once exposed to an antigen, only the T-cells with the highest affinity for that given antigen can proliferate.

75
Q

What are the different types of T-cells?

4

A
  1. Helper T-cells
  2. Suppressor T-cells
  3. Cytotoxic T-cells

ALSO memory T-cells

76
Q

What are Helper T-cells?

What is another name for them?

A

Helper T-cells aka CD4+ t-cells

Secrete lymphokines (which recruit other immune cells: plasma cells, cytotoxic t-cells, macrophages: and increase their activity).

Respond to MHC-2 molecules. Most effective against bacterial, fungal, and parasitic infections (not viral: MHC-2 is exogenous, viral would be MHC-1)

Loss of CD4+ cells: Occurs in HIV
Prevents immune system from mounting proper response

77
Q

What are cytotoxic T-cells?

What else are they called?

A

Cytotoxic T-cell aka CD8+

Can directly kill VIRALLY infected cell. Injects toxic material into infected cell to promote apoptosis.

Responds to antigens presented on MHC-1 molecules, aka endogenous. Hence, most effective to viral, and intracelullar fungal or bacterial infections.

78
Q

What is a suppressor T-cell?

What else is it called?

A

Suppressor T-cell aka regulatory T-cell

Also presents CD4 BUT express a protein called Foxp3.

Helps to tone down immune response once infection has been contained.

Turns off self-reactive lymphocytes to create SELF-TOLERANCE.

*suppressor T-cells often were self-reactive and turned off. When it inactivated another T-cell, it either targets it for destruction or turns it into a suppressor t-cell

79
Q

What is a memory T-cell?

A

Similar to memory B-cell

Wait until exposure to the antigen for a second time.

Biology (11 decks)

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