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MCAT > Endocrine > Flashcards

Endocrine Flashcards

1
Q

ADH Stimulus

A

low blood volume (want more water in blood)

high blood osmol (high [] particles in blood so you still want more water in the blood)

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2
Q

ADH Mechanism

A

peptide hormone so it binds to extracellular receptor which activates a secondary message and opens an aquaporon which allows water to flow through it

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3
Q

ADH Origin

A

Posterior Pituitary (osmol receptors)

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4
Q

ADH Result

A

increase water reabsorption across the collecting duct

bring water back into the body to maintain blood volume

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5
Q

Aldosterone Stimulus

A

low blood volume or high blood osmol

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6
Q

Aldosterone Mechanism

A

acts around distal convoluted tubule to activate sodium pumps

steroid hormone so it enters nucleus to activate transcription of sodium pumps

pumps more sodium into tissue

resulting osmotic pressure sucks fluid into tissue and concentrates urine

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7
Q

Aldosterone Origin

A

Adrenal Cortex

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8
Q

Aldosterone Result

A

increased water reabsorption

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9
Q

EPO Stimulus

A

low oxygen in blood

or

low blood volume

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10
Q

EPO Mechanism

A

released into blood

enters bone marrow

stimulates RBC production

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11
Q

Effect of low GFR on EPO?

A

cells sense low GFR, EPO increases

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12
Q

EPO Origin

A

Juxta-glomerulus cells

senses pressure in Bowman’s Capsule

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13
Q

What does GFR determine?

A

GFR determines how much filtrate is made.

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14
Q

The higher the hydrostatic pressure, the _______ GFR?

A

The higher the hydrostatic pressure, the higher GFR.

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15
Q

EPO Result

A

Increase in RBC production

Good: extra oxygen carrying, thicker blood moves slower

Bad: thicker blood can clot

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16
Q

Renin Stimulus

A

low blood volume or low blood pressure

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17
Q

Renin Origin

A

Juxta-glomerulus cells

(sense low GFR)

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18
Q

Renin Mechanism

A

3 Organ Hormone

  • secreted by kidney
  • travels to liver
  • in liver, renin activates angiotensinogen to angiotensinogen I
  • angio I travels to lungs
  • in lungs, angio 1 becomes angio 2 (effector molecule)
  • angio 2 activates adrenal cortex to make aldosterone (and arteriol constriction)
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19
Q

Renin Result

A

Increased Blood Pressure

(Increased Blood Volume)

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20
Q

How do you know a follicle is mature?

A

A mature follicle secretes estrogen.

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21
Q

2 Effects of Angiotensin 2

A
  • activates adrenal cortex to make aldosterone
  • constricts arterioles (to increase blood pressure)
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22
Q

Tmax

A

Kidney’s reabsorption receptors work at max rate (Tmax)

obeys saturation kinetics

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23
Q

What happens if you exceed the Tmax of glucose transporters in the kidney?

A

urinate glucose

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24
Q

Higher the Blood Pressure, the _______ time to reabsorb?

A

Higher the Blood Pressure, the less time to reabsorb.

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25
Q

The lower the Blood Pressure, the ______ time to reabsorb?

A

The lower the blood pressure, the more time to reabsorb.

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26
Q

High GFR, _______ Clearance

A

High GFR, Low Clearance

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27
Q

Clearance

A

how quickly the kidney gets rid of things

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28
Q

4 Hormones of Kidney

A

Aldosterone

ADH

EPO

Renin

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29
Q

What drives filtration?

A

Hydrostatic Pressure

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30
Q

What drives reabsorption?

A

ATP

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31
Q

What drives the concentration of urine?

A

Osmotic Pressure across the collecting duct

(osmotic pressure is created by the ascending loop of henle)

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32
Q

Angiogenesis

A

creation of blood vessels

increase in vascularization

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33
Q

ACTH Result

A

ACTH stimulates the adrenal cortex to secrete:

Sweet- cortisol and growth hormone

Salty- aldosterone

Sex- androgens

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34
Q

TSH Result

A

TSH stimulates thyroid to secrete TH.

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35
Q

Purpose of Growth Hormone.

A

Stress hormone that stimulates many metabolic pathways (anabolic and catabolic).

36
Q

2 Parts of Adrenal Gland

A

2 Parts of Adrenal Gland

  • Cortex
  • Medulla
37
Q

What does adrenal cortex produce?

A

Sweet Salty Sex

38
Q

What does the adrenal medulla produce?

A

Norepinephrine and Epinephrine

(both endocrine hormones and neurotransmitters)

39
Q

Peptide Hormone Mechanism

A

binds extracellular and activates secondary messenger

40
Q

Peptide Hormone Onset

A

Rapid

41
Q

Peptide Hormone Duration

A

Short Duration

42
Q

What effect does an antagonist have?

A

opposite effect

43
Q

What effect does an agonist have? Give an example.

A

same effect

Grave’s Disease

44
Q

What makes insulin?

A

Beta cells of pancreas

45
Q

Hormones of Anterior Pituitary

A

F FSH

L LH

A ACTH

T TSH

P Prolactins

E Endorphins

G Growth Hormone

FLAT PEG

46
Q

What makes glucagon?

A

Alpha cells of pancreas

47
Q

When is insulin secreted?

A

Insulin is secreted when blood glucose levels are high

48
Q

Insulin Mechanism

A
  • peptide hormone
  • binds extracellular
  • works on glute transporters to allow glucose to enter cell
49
Q

Aside from allowing glucose to enter the cell, what else does insulin do?

A

Insulin:

  • activates glycolysis
  • inhibits gluconeogenesis
  • activates fatty acid and protein synthesis
  • activates glyconeogenesis (making of glycogen- storage form of glucose)
50
Q

When is glucagon secreted?

A

low blood glucose levels

51
Q

What does glucagon do?

A

Glucagon:

  • activates gluconeogenesis (makes glucose from fats and proteins)
  • activates fatty acid degradation
  • breaks down proteins for Kreb’s
  • breaks down glycogen via glycogenolysis
52
Q

Glycogenolysis

A

breaking down of glycogen

53
Q

Beta Oxidation

A

Fatty Acid Degradation

54
Q

Hormones of Thyroid

A

Thyroxine (Thyroid Hormone)

Calcitonin

55
Q

Why is thyroid hormone secreted?

A

TH is secreted to increase metabolism.

56
Q

What stimulates the release of TH?

A

TH is stimulated by TSH from the anterior pituitary.

57
Q

Briefly describe the Tertiary Axis.

A

Hypothalamus (TRH) → Anterior Pituitary (TSH) → Thyroid (TH)

58
Q

Hyperthyroidism

A

making too much TH

59
Q

Primary Hyperthyroidism

A
  • Problem is with the thyroid gland
  • Making too much TH
  • Negative feedback will lower TRH and TSH but it won’t have any effect on TH levels
60
Q

Secondary Hyperthyroidism

A
  • too much TSH
  • problem with anterior pituitary
  • negative feedback will lower TRH
61
Q

Tertiary Hyperthyroidism

A
  • problem with hypothalamus
  • too much TRH
  • leads to too much TSH and TH
  • all 3 levels are up
62
Q

Primary Hypothyroidism

A
  • thyroid not working
  • low TH
  • upregulation of TRH and TSH
63
Q

Secondary Hypothyroidism

A
  • problem with anterior pituitary
  • low TSH leads to low TH
  • upregulate TRH
64
Q

3 Positive Feedback Examples

A
  • Oxytocin
  • Estrogen at high levels
  • Prolactin
65
Q

Posterior Pituitary Hormones

A

ADH and Oxytocin

66
Q

Oxytocin Stimulus

A

baby head on cervix

67
Q

Oxytocin Mechanism

A
  • positive feedback
  • electrical signal to posterior pituitary
68
Q

Oxytocin Origin

A

Posterior Pituitary

69
Q

Oxytocin Result

A

uterine contraction (and milk ejaculation as well)

70
Q

Calcitonin Result

A
  • builds bone
  • decrease levels of calcium in plasma
71
Q

Calcitonin Mechanism

A

activates osteoblasts to build bone (become osteocytes)

72
Q

Calcitonin Origin

A

thyroid

73
Q

Calcitonin Stimulus

A

high calcium levels in plasma

74
Q

Hormones of Parathyroid Gland

A

PTH

75
Q

Which hormone is an antagonist of calcitonin?

A

PTH

76
Q

PTH Mechanism

A

activates osteoclasts to break down bone (bone macrophages)

77
Q

PTH Origin

A

Parathyroid Gland

78
Q

PTH Stimulus

A

low levels of calcium in blood

79
Q

PTH Result

A

increased calcium levels in blood

80
Q

Exocrine

A

hormone released into duct

81
Q

Paracrine

A

released into interstitial fluid and acts locally

82
Q

Endocrine

A

released into blood

83
Q

Autocrine

A

acts on the same cell that released it

84
Q

What kind of a gland is the pancreas?

A

Endocrine- glucagon and insulin into blood

Exocrine- digestive juice into duct

85
Q

3 Stress Hormones

A

Growth Hormone

Glucagon

Cortisol

MCAT (7 decks)

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