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Phsyiology 210 B > Endocrine 1 > Flashcards

Endocrine 1 Flashcards

1
Q

Major Hormones of the hypothalamus

A
  • GnRH —> inc LH and FSH
  • CRH (corticotropin rh) —> inc ACTH
  • TRH (thyrotropin rh) —> inc TSH
  • PIH (prolactin Ih) —> dec PRL
  • GHRH (GH rh) —>inc GH
  • GHIH (GH ih or SS) / somatostatin —> dec GH
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2
Q

Major hormones of the anterior pituitary

A
  • FSH —> stimulate follicle growth
  • LH (luteinizing hormone) —> spermatogensis
  • ACTH (adrenocorticotropic hormone) —>inc testosterone sec
  • TSH (thyroid stimulating hormone) —> inc adrenal steroid sec (T3 and T4)
  • PRL (prolactin) —> produce milk
  • GH —> inc protein synthesis
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3
Q

Major hormones of the posterior pituitary

A
  • oxytocin (OXY) —> expulsion of milk

- ADH —> increases H2O reabsorption, decrease urine volume.

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4
Q

Major hormones of the adrenal cortex

A
  • glucocorticoids (cortisol) —>
  • Mineralocortoids (aldosterone) —> effects metabolism and increases Na+ reabsoption in nephron

(Counter regulatory)

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5
Q

Major hormones of the thyroid hormone

A
  • T3 —> metabolism and growth
  • T4 —> metabolism and growth
  • calcitonin —> decrease blood Ca+
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6
Q

Major hormones of the parathyroid glands

A
  • parathyroid hormone (PTH) —> increases blood Ca+
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7
Q

Major hormones of the pancreas

A
  • insulin —> lowers blood glucose
  • glucagon —> raises blood glucose

(Counter regulatory)

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8
Q

Classifications of hormones based on structure?

A

1) proteins
2) lipid
3) monamines

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9
Q

Types of protein hormones

A

1) small peptide (TRH, oxytocin, ADH)
2) polypeptides (insulin, glucagon, GH)
3) glycoproteins (FSH, LH and TSH)

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10
Q

Types of lipid hormones

A

1) steroids (cortisol, aldosterone, sex hormones)

2) eicosanoids (prostaglandin, leukotriens)

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11
Q

Types of monamine hormones

A

1) catecholamines ( dopamine, noradrenaline, adrenaline)

2) thyroid hormone ( T3 and T4)

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12
Q

What are steroid hormones made form ? And what is the pathway?

A

Cholesterol.

Cholosterol —> pregnenolone —> progesterone —> aldosterone, cortisol and (testosterone —> estrogen)

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13
Q

What are eicosanoids made form?

A

Form arachidonic acid

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14
Q

What are catecholamines made form?

A

From tyrosine

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15
Q

What are thyroid made form?

A

From Tyrosine

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16
Q

The four types of ways hormones reach their target

A

1) endocrine (via blood to distant target)
2) paracrine (via blood to Nearby target)
3) neuroendocrine (AP = stimulates nerve to sec hormone, moves via blood and stored in cell terminal of nerve cell)
4) autocrine (self stimulating, act on itself)

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17
Q

Types of hormone receptors

A

1) cell surface receptors

2) intercellular receptors

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18
Q

What kind of hormones bind to cell surface receptors ?

A

Proteins which bind protein hormones and to catecholamines

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19
Q

What kind of hormones bind to cell intracellular receptors ?

A

Proteins which bind to steroid hormones, and to Thyroid hormones, t3 and T4

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20
Q

Protein hormones are soluble where and not soluble where?

A
  • soluble in aqueous environment

- insoluble in lipid environments

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21
Q

Lipid hormones are soluble where and not soluble where?

A
  • soluble in lipid environments

- insoluble in aqueous environments

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22
Q

Why are surface receptors not inside the cell?

A

Because they are insoluble in lipid/fat env and cant pass through cell membrane = stay outside

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23
Q

Why are intracellular receptors inside the cell and not outside

A

They are insoluble in aqueous env but soluble in lipid/fat env, so they can pass through the cell memb

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24
Q

Types of cell surface receptors

A

1) G-protein receptor: G protein regulate second messenger
- (receptors for adrenaline and glucagon)

2) Catalytic receptors: reactors have enzymatic activity (tyrosine kinase),or closely associated with enzyme after binding to ligand
- (receptors for insulin and GH)

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25
Q

Role of second messenger

A

Hormone binds to surface receptor = change receptor conformation = G protein change conformation = inc/dec enzyme inside cell = produces second messenger (cAMP) = acts on protein kinase (PKA) = phophsorylation of protein = respond of target cell.

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26
Q

Types of intracellular receptors (3X)

A

1) mainly in cytoplasm (receptors for steroid hormones)
2) mainly in nucleus (receptors for sex steroids)
3) bound to DNA in the nucleus (thyroid hormones, T3 and T4)

All these receptors end up i the nucleus as transcription factors

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27
Q

Where do all intraceullar receptors end up?

A

All intraceullar receptors end up in the nucleus as transcription factors

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28
Q

What’s the pathway for intracellular receptor pathways

A

Steroid hormone passes through cell memb to bind to receptor either in the cytoplasm or nucleus, either why end up in a receptor in nucleus to act as transcription factor to porduce protein that act on the target cell.

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29
Q

What happens to hormones bind to plasma proteins

A

It solublizes it / becomes bound and inactive, balance between bound (inactive) and unbound (active) hormones regulate hormone amount

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30
Q

Catecholamines come from the

A

adrenal medulla.

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31
Q

Proteins hormone (& catecholamines)

1) solubility
2) synthesis
3) storage/Secretion
4) transport
5) hormone receptors
6) mechanism of action
7) time course

A

1) solubility : water soluble
2) synthesis : from amino acids (from tyrosine)
3) storage/Secretion : in granule / exocytosis
4) transport : doesn’t need solubilization in blood
5) hormone receptors : surface receptor
6) mechanism of action : intracellular signalling pathways
7) time course : FAST

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32
Q

Steroid hormone ( & T3 and T4)

1) solubility
2) synthesis
3) storage/Secretion
4) transport
5) hormone receptors
6) mechanism of action
7) time course

A

1) solubility: lipid soluble
2) synthesis: from cholesterol (from tyrosine)
3) storage/Secretion: not stored / diffusion
4) transport: bound to plasma proteins
5) hormone receptors: intracellular
6) mechanism of action: gene regulation
7) time course: SLOW

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33
Q

Examples of protein and catecholamine hormones

A

Most hormones of the hypothalamus, pituitary, pancreas, parathyroid, GI tract, adrenal medulla

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34
Q

Examples of steroid and thyroid hormones

A

Most hormones form the adrenal cortex, ovaries and tests and thyroid gland.

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35
Q

The hypothalamus-pituitary unit is composed of

A

composed of the:

  • anterior pituitary (up growth to mouth)
  • posterior pituitary (downstream growth)
  • connected by the pituitary stalk
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36
Q

Is the blood supply to ant pit direct or indirect? Explain pathway

A

Indirect.

(Blood comes in) Artery —> primary plexus —> Portal blood vessel —> secondary plexus (inside the ant pit) —> vein in anterior (blood leaving)

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37
Q

The two nucleus within hypothalamus that communicate with pituitary glands are:

A
  • Supraoptic nucleus (SON)
  • Paraventricular nucleus (PVN)

These are the regions where there are cells bodies which communicate with the posterior pituitary

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38
Q

• Supraoptic nucleus (SON) and the Paraventricular nucleus (PVN) produce 2 different hormones, they both travel down the

A

nerve axon and into the posterior pituitary which are then stored in the terminals and will be released for a AP or stimulus.
Then the vein carries these hormones away.

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39
Q

Is the blood supply to the post pit direct or indirect? What’s the pathway

A

Direct.

(Blood come in) artery —> SON/PVN axons reach all the way down to the and insert their hormones —> vien (blood leaving) exits with the hormones from the SON/PVN

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40
Q

Where are hormones stored in the SON / PVN?

A

In the nerve terminus within the post pit.

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41
Q

How does the ant pit receive hormones and where

A

They receive hormones within the secondary plexus via anterior glands

42
Q

Neurons in hypothalamus produce hormones via

A

cell bodies.

43
Q

Main regions of the bone

A
  • epiphysis (round-head end of bone)
  • Epiphyseal plate (cartilage)
  • Diaphysis (shaft)
44
Q

When is the epiphyseal plate present? what does being open mean?

A

In bones of children who are growing.

Being open means when its responsive to hormones and it can cause bone to grow LONGER.

45
Q

When we stop growing in height, its due to the

A

cartilage/ephyiseal plate isn’t no longer able to contribute to that growth and so it said to be in a CLOSED state.

46
Q

Progenitor cells (Fibroblasts)

A

able to differentiate into cartilage cells.

47
Q

Cartilage cells (chondrocytes)

A

Can perform proliferation (cell division) and ossification (bone formation)

48
Q

Where are progenitor cells (fibroblasts) located in the bone?

A

Within the epiphyseal plate

49
Q

If this child has a deficiency in GH and is much smaller then average.
Take growth hormone and inject it in vivo. Then the child will grow.

If you took a sample of bone cartilage and put in in vitro (in a test tube or beaker), you

A

wont see any growth.

50
Q

Does GH work in VIVO or in VITRO or both? Why?

A

It works only in vivo (inside body).

Because inside body it require insulin light growth factor (IGF) in order to work. Outside the body IGF isn’t present and therefore GH wont work.

51
Q

Where is IGF produced?

A

In the liver

52
Q

In vitro, insulin light growth factor isn’t produced and is missing, therefore there is

A

NO GROWTH.

53
Q

Effects of GH on metabolism

1) fats
2) carbohydrates
3) proteins

A

1) fats: increases lipolysis, increases free fatty acids for E.
2) carbohydrates: decrease glucose uptake = hyperglycaemia (“diabetogenic”)
3) proteins: increases protein uptake, synthesis and cell size.

54
Q

Growth hormone secretion is

increased by:

A
  • GHRH
  • Ghrelin
  • hypoglycaemia (low glucose in blood)
  • increase in amino acids
  • deep sleep
55
Q

Growth hormone decreased by

A
  • somatostatin (GHIH)
  • GH
  • IGF
  • hyperglycaemia
  • increase fatty acids
  • aging
56
Q

Too much GH can lead to what conditions

A

1) gigantism: in children, increased linear growth. Keep on growing.
2) acromegaly: in adults, thickening of bones, large hands and feet, jaw.

57
Q

Too little GH can lead to what conditions ?

A

1) dwarfism: in children, stunted growth due to low GHRH, low GH, low IGF, low receptor #

58
Q

Post pit hormone secretions form which neurons ?

A

SON: ADH —> kidney and blood vessels

PVN: oxytocin —> uterus and mammary glands

59
Q

Where is ADH produced and what is its target cells

A

Produced in the post pit and targets the principle cell within the kidneys.

60
Q

How does ADH function, what’s its mechanisms?

A

ADH in blood binds to cell G-protein surface receptors = cAMP second messenger acts on vesicle with inactive water channels = activates AQP2 channels = water passes through APQ2 from lumen to the blood = less volume of urine, more volume in blood. Hence antdieretic effect

61
Q

What kind of receptor does ADH increase to increase water reabsorption in principle cells within the kidney?

A

Increases AQP2 receptors

62
Q

What are the 2 factors effecting secretion of ADH? Which is more effective ?

A

1) increase osmotic pressure detected by osmoreceptors in hypothalamus (dehydration) [more effect stimuli]
2) decrease blood volume detected by baroreceptors in cardiovascular sys.

63
Q

• An increase in osmotic pressure and decrease in volume = release of.

A

ADH

64
Q

Too much ADH

A

Syndrome of inappropriate ADH secretion (SAIDH):

  • Increased H2O retention
  • increased blood volume
65
Q

Too little ADH

A

1) central or neurogenic diabetes insipidus (lack of ADH, large volumes of dilute urine)
2) nephrogenic diabetes insipidus (abnormal ADH receptors in kidney; large volumes of dilute urine)

66
Q

• Central diabetes insipidus:

A

due to lack of ADH (abnormal production)

67
Q

• Neurogenic dramatic insipidus:

A

problem in the kidney, so ADH is produced just not able to do its function. Could be due to lack of ADH receptors or to much urine

68
Q

Factors effecting oxytocin secretion

A

1) Partition: giving birth

2) lactation: release of milk

69
Q

Actions of oxytocin in partition

A

Baby’s head puts pressure on the uterus opening = uterine stretch of smooth muscle cells = signals hypothalamus = post pit releases OXY = contraction of uterus = baby exits

(+) feedback system, prevents blood loss as muscles stretch.

70
Q

Actions of oxytocin during action

A

As baby suckles, sends single to hypothalamus = posterior pituitary releases oxytocin = milk ejection reflex

71
Q

Is oxytocin responsible for production of milk?

A

The production of milk is NOT dependant on the production of oxytocin, prolactin is responsible for the production of milk. Oxytocin only is reasonable for the release of milk.

72
Q

Structure of adrenal gland is composed of what 3 main sections

A

1) zona glomerulosa
(outer most, thinnest layer)

2) zona fasciculata
(middle, thickest layer)

3) Zona Reticularis
(Innermost, thin layer)

Each produce hormones

73
Q

Where is the adrenal gland located?

A

On top of both kidneys

74
Q

What kind of cell are within the medulla of the adrenal gland?

A

Chromatin cells of adrenal medulla

75
Q

Hormones of the adrenal cortex

A

1) zona glomerulosa: aldosterone (mineralocorticoid)
—-> control electrolyte / salt levels

2) zona fasciculata: cortisol (gluco-corticoids)
—> control sugar

3) Zona Reticularis: DHEA and andro-stenedione (androgens)
—> regulate sex

76
Q

How are corticosteroids made?

A

From cholesterol —> pregnenolone —> progesterone —-> (cortisol, aldosterone, adrenal androgens)

77
Q

Major actions of aldosterone

A

1) increased Na+ reabsorption by kidney (primary action)

2) increased H2O retention by kidney
(Secondary)

3) increased H+ secretion by kidney
(loss of H+ in urine)

4) increased K+ secretion by kidney
(loss of K+ in urine)

78
Q

What cells does aldosterone act on?

A

Principle and intercalated cells that form the lining of the lumen, where fluid flows to become urine.

79
Q

Mechanism of action for aldosterone

A

Aldosterone is a steroid hormone that can pass through the cell membrane to bind to the receptor in the nucleus, act as a transition factor to regulate Protein synthesis.

These proteins assist in regulating the transport channels of ions, causing the movement of H+ and K+ towards the urine (duct lumen), and Na+ towards the blood. As Na+ moved in the blood, so does H2O = increasing water reabsorption = increasing blood volume.

80
Q

Control of aldosterone secretion

A

Decrease in volume of ECF / decrease blood pressure / decrease in Na+
= activate the sympathetic nerve.
= stimulate the release of renin from kidney.
= renin (enzyme) converts angiotensinogen to angiotensin I (inactive peptide).
= ACE (enzyme) converts angiotensin I to angiotensin II (active peptide).
= angiotensin II increases blood pressure and acts on the adrenal gland to secrete aldosterone
= aldosterone from adrenal gland increases Na+ and H2O reabsorption into the blood
= increase blood volume, Na+, blood pressure, volume of ECF, and a decrease in K+

81
Q

Major actions of cortisol

1) metabolism
2) on immune system

A

1) metabolism:
- increase protein breakdown
- increase fat break down
- increase glucose formation in liver
- increase glycogen (hyperglycaemia)
- increase glucose available for CNS
- decrease glucose utilization by peripheral tissue

2) on immune system
- Decrease lymph node size
- Decrease lymphocyte number
- Decrease humoral/cellular immunity
- Decreaseproduction of inflammatory substances
- Increase infections

82
Q

Effects of cortisol on metabolism

A

Glucose is secreted from the blood and effects 4 different sites.

1) LIVER —> cortisol increases uptake of glucose form liver to the blood. glycogen (storage form) leaves liver and enter blood, Gluconeogenesis occur at the liver. Amino acids from Proteins and glycerol+FFA form adipose tissue both come to liver to increase glycogen.
2) ADIPOSE TISSUE: uptake of glucose is decreased by cortisol, release glycerol+FFA=E
3) muscle, bone, skin: uptake of glucose is decreased by cortisol, releases amino acids.
4) CNS: uptake of glucose is increased by cortisol.

83
Q

What does cortisol do to glucose in the blood

A

It increases it

84
Q

Control of cortisol secretion

A

Stress = activates hypothalamus = releases CRH (corticotropin releasing hormone = activate ant pit - release of ACTH blood = activate adrenal cortex = released of CORTISOL

85
Q

Cortisol has why kind of feedback system, and on what?

A

(-) feedback on both the hypothalamus and Ant Pit.

86
Q

Catecholamines synthesis

A

Tyrosine = DOPA = dopamine = noradrenaline (noradrenaline) = adrenaline (epinephrine)

87
Q

Too much aldosterone

A

Conns syndrome —>

  • increased vol of ECF
  • increased blood pressure
  • hypokalemia
  • metabolic alkalosis
88
Q

Too little aldosterone

A

Addison’s disease —>

  • hypotension
  • metabolic acidosis
  • hyperkalemia
89
Q

Too much cortisol

A

Cushing’s disease —>

  • increase blood glucose
  • muscle wasting
  • moon face
  • decrease resistance to infection
90
Q

Too little cortisol

A

Addison’s disease —>

  • decrease blood glucose
  • increase skin pigmentation
91
Q

To much adrenal androgens

A
  • verilization in females (look more masculine)
92
Q

Too little adrenal androgen

A
  • decrease sexual hair growth

- decrease libido in female

93
Q

Major actions of catecholamines (adrenaline and noradrenaline)

1) cardiovascular system:
2) smooth muscle
3) metabolism

A

1) cardiovascular system:
- increase heart rate
- increase force of contraction
- increase cardia output
- redistribution of blood flow

2) smooth muscle:
- dilation of pupils
- bronchodilatation
- decrease GIT motility

3) metabolism:
- increase glygonenolysis (skeletal muscle and liver)
- increase lipolysis
- increase gluconeogensis

94
Q

Control of catecholamines secretion

A

Stimulation of the splanchnic nerve = releases Ach = stimulates the chromaffin cells inside adrenal cortex = release of catecholamines = increase in adrenaline and noradrenaline

95
Q

Glycolysis

A

Conversion of glucose to pyruvate acid

96
Q

Glycogenesis

A

Synthesis of glycogen from glucose

97
Q

Glycogenolysis

A

Breakdown of glycogen to glucose

98
Q

Gluconeogenesis

A

Synthesis of glucose from amino acids

99
Q

Lipogenesis

A

Synthesis of fats

100
Q

Lipolysis

A

Breakdown of fats

101
Q

Ketogenesis

A

Formation of keytone body from break down of fatty acids

102
Q

Anabolism and catabolism

A

Anabolism = formation of new mol.

Catabolism = breakdown of mol.

Phsyiology 210 B (24 decks)

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