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PHYSL214 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is an endocrine gland?

A

Does not have a duct system.

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2
Q

What is an exocrine gland?

A

Has a duct system.

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3
Q

What is GnRH?

A

Gonadotropin-releasing hormone.

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4
Q

What is the source of GnRH?

A

Hypothalamus.

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5
Q

What is the major action of GnRH?

A

Increases secretions of FSH and LH.

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6
Q

What is CRH?

A

Corticotropin-releasing hormone.

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7
Q

What is the source of CRH?

A

Hypothalamus.

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8
Q

What is the major action of CRH?

A

Increases secretion of ACTH.

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9
Q

What is TRH?

A

Thyrotropin-releasing hormone.

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10
Q

What is the source of TRH?

A

Hypothalamus.

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11
Q

What is the major function of TRH?

A

Increases the secretion of TSH.

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12
Q

What is PIH?

A

Prolactin inhibiting hormone (dopamine)

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13
Q

What is the source of PIH?

A

Hypothalamus.

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14
Q

What is the major function of PIH?

A

Decreases secretion of PRL.

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15
Q

What is GHRH?

A

Growth hormone-releasing hormone.

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16
Q

What is the source of GHRH?

A

Hypothalamus.

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17
Q

What is the major function of GHRH?

A

Increases the secretion of GH.

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18
Q

What is SS?

A

Somatostatin.

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19
Q

What is the source of SS?

A

Hypothalamus.

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20
Q

What is the major function of SS?

A

Decreases the secretion of GH.

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21
Q

What hormones are secreted from the hypothalamus?

A 
GnRH
CRH
TRH
PIL
GHRH
SS
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22
Q

What is FSH?

A

Follicle-stimulating hormone

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23
Q

What is the source of FSH?

A

Anterior pituitary

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24
Q

What is the main action of FSH?

A

Stimulates follicle growth.

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25
Q

What is LH?

A

Luteinizing hormone.

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26
Q

What is the source of LH?

A

Anterior pituitary.

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27
Q

What is the main function of LH?

A

Causes ovulation, increases testosterone secretion.

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28
Q

What is ACTH?

A

Adrenocorticotropic hormone.

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29
Q

What is the source of ACTH?

A

Anterior pituitary.

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30
Q

What is the main function of ACTH?

A

Increases secretion of adrenal glucocorticosteroids.

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31
Q

What is TSH?

A

Thyroid stimulating hormone

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32
Q

What is the source of TSH?

A

Anterior pituitary

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33
Q

What is the main function of TSH?

A

Increase secretion of thyroid hormones T3/T4

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34
Q

What is PRL?

A

Prolactin

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35
Q

What is the source of PRL?

A

Anterior pituitary

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36
Q

What is the main function of PRL?

A

Increases production of milk

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37
Q

What is GH?

A

Growth hormone

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38
Q

What is the source of GH?

A

Anterior pituitary

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39
Q

What is the main function of GH?

A

Increases protein synthesis and increases growth.

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40
Q

What hormones are secreted by the anterior pituitary?

A 
FSH
LH
ACTH
TSH
PRL
GH
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41
Q

What is OXY?

A

Oxytocin

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42
Q

What is the source of OXY?

A

Posterior pituitary

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43
Q

What is the main function of OXY?

A

Expulsion of milk, contraction of uterus.

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44
Q

What is ADH?

A

Antidiuretic hormone (vasopressin)

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45
Q

What is the source of ADH?

A

Posterior pituitary

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46
Q

What is the main function of ADH?

A

Increases water reabsorption and decreases urine volume.

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47
Q

What hormones are secreted by the posterior pituitary?

A

Oxytocin and ADH.

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48
Q

What are the three forms of hormones?

A
  1. Protein (peptides, polypeptides, glycoproteins)
  2. Lipids (steroids, eicosanoids)
  3. Monoamines (catecholamines, thyroid hormones)
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49
Q

How are steroid hormones synthesized?

A
  1. Cholesterol
  2. Pregnenolone
  3. Progesterone (testosterone to estrogen)
  4. Aldosterone (or cortisol)
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50
Q

What is the mechanism of endocrine cells?

A

Release hormones from hormone producing cells into a vessel, which carries hormones to the target cell.

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51
Q

What is the mechanism of neuroendocrine cells?

A

Neurons release hormones or transmitters into blood stream, carried to target cell.

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52
Q

What is the mechanism of paracrine cells?

A

Hormone producing cells secrete hormones that diffuse hormones through ECF to nearby cells (local)

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53
Q

What is the mechanism of autocrine cells?

A

Hormone producing cell and target cell are the same.

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54
Q

What hormones bind to cell surface receptors?

A

Catecholamines and protein hormones.

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55
Q

What hormones bind to intracellular receptors?

A

Steroid hormones and thyroid hormones.

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56
Q

What are the two forms of cell surface receptors?

A

G-protein linked receptors, catalytic (tyrosine kinase) receptors.

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57
Q

What hormones act on G-protein coupled receptors?

A

Adrenaline, glucagon, FSH, LHM TSH, PTH

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58
Q

What hormones act on catalytic receptors?

A

Insulin and GH.

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59
Q

What is the solubility of protein (and catecholamine) hromones?

A

Water-soluble

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60
Q

What is the solubility of steroid hormones?

A

Lipid soluble.

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61
Q

What are protein steroid synthesized from?

A

Amino acids.

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62
Q

What are steroid hormones synthesized from?

A

Cholesterol

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63
Q

How are protein hormones stored?

A

In vesicles or by exocytosis.

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64
Q

How are steroid hormones stored?

A

Not stored, secreted by diffusion.

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65
Q

How are protein hormones transported?

A

Do not need special transport through blood.

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66
Q

How are steroid hormones transported?

A

Bound to plasma proteins in the blood

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67
Q

What is the time course of action for protein hormones?

A

Fast

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68
Q

What is the time course of action for steroid hormones?

A

Slow.

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69
Q

Describe the morphology of the pituitary:

A

Extends off the hypothalamus and upward from the mouth, contains two glands (anterior and pituitary) as well as a pituitary stalk and median eminence that divides the glands.

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70
Q

Where did the anterior pituitary stem from?

A

Mouth region.

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71
Q

Where did the posterior pituitary stem from?

A

Brain.

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72
Q

How does hormone communication occur in the anterior pituitary?

A

Neurodendocrine cells in the hypothalaus extend to the median eminence where they synapse on the primary plexus. Secreted hormones travel down through portal blood vessels into the anterior pituitary where they form the secondary plexus. Hormones close to the secondary plexus can be acted on by hormones that diffuse out of blood stream.

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73
Q

How does hormone communication occur in the posterior pituitary?

A

Neuroendocrine cells (SON and PVN) extend down into posterior pituitary where they synapse onto plexus.

74
Q

What class of hormones does the anterior pituitary house?

A

Protein hormones.

75
Q

What is the most abundant anterior pituitary hormone?

A

Growth hormone

76
Q

What kind of hormones are secreted from the hypothalamus? (Except PIH)

A

Peptides. PIH is catecholamine.

77
Q

What is the morphology of bones?

A

Epiphysis (top), epiphyseal plate (cartilage), diaphysis (shaft)

78
Q

How do bones grow? (What is the pathway?)

A

Progenitor cells (fibroblasts) differentiate into cartilage cells (chondrocytes) which proliferate into more cartilage cells. These cells then ossify into bone.

79
Q

What effect does gH have on fats?

A

Increase lipolysis to create more free fatty acids for energy use.

80
Q

What effect does gH have on carbohydrates?

A

Decreases glucose uptake into cells (hyperglycemia)

81
Q

What effect does gH have on proteins?

A

Increases amino acid uptake into cells
Increases protein synthesis
Increases cell size

82
Q

What is gH secretion increased by?

A 
GHRH
Hypoglycemia
High amino acid levels in blood
Deep sleep
Exercise
83
Q

What is gH secretion decreased by?

A 
Somatostatin
gH/IGF
Hyperglycemia
Increased fatty acid in blood
Ageing
84
Q

What is gigantism?

A

Caused by too much gH in childhood, increased linear growth.

85
Q

What is acromegaly?

A

Too much gH onset in adulthood, thickening of bones and distal features.

86
Q

What is dwarfism?

A

Too little gH in childhood, stunted growth.

87
Q

What is the major source of ADH (synthesis source)

A

Superoptic nucleus.

88
Q

What is the target for ADH?

A

Kidney and blood vessels

89
Q

What is the synthesis source of OXY?

A

Periventricular nucleus

90
Q

What class of hormones are secreted by the posterior pituitary?

A

Peptides

91
Q

What cells contain receptors for ADH?

A

Principle cells in the collecting duct of nephron tubules.

92
Q

Explain the mechanism of ADH on the nephron:

A
  1. ADH in blood binds to V2 receptor, activating Gs pathway.
  2. Vesicles containing water channels is activated and moved to duct lumen membrane to increase H20 uptake from filtrate.
93
Q

What triggers the release of ADH from the posterior pituitary?

A

Increase in osmotic pressure of ECF detected by osmoreceptors in the hypothalamus.

Decrease in volume of ECF (hemorrhage) detected by baroreceptors in the cardiovascular system.

94
Q

What two major effects does ADH have on ECF?

A

Increases volume of ECF and blood pressure, decreases osmolarity/osmotic pressure of ECF.

95
Q

What occurs with chronic hyperantidiuretic release?

A

Increased H20 retention, increased blood volume (SIADH)

96
Q

What occurs with chronic ADH under-release?

A

Central or neurogenic diabetes (lack of ADH release)

Nephrogenic diabetes insipidous (abnormal ADH release)

97
Q

What are the layers of the adrenal cortex from outermost to innermost?

A
  1. Zona glomerulosa.
  2. Zona fascicula.
  3. Zona reticulus.
98
Q

What hormone/hormone family is secreted from the zona glomerulosa?

A

Mineralocorticoids: Aldosterone

99
Q

What hormone/hormone family is secreted from the zona fasciculata?

A

Glucocorticoids: cortisol.

100
Q

What hormone/hormone family is secreted from the zona reticularis?

A

Androgens: DHEA and androstenedione.

101
Q

What is the function of aldosterone?

A

Control salt/electrolyte levels.

102
Q

What is the function of cortisol?

A

Regulate carbohydrate levels.

103
Q

What is the function of DHEA and androstenedione?

A

Regulate reproductive system.

104
Q

How are corticosteroids synthesized?

A

From cholesterol: pregnenolone: progesterone: cortisol, aldosterone or adrenal androgens.

105
Q

What are the major actions of aldosterone?

A
  1. Increases sodium reabsorption by the kidney.
  2. Increases water reabsorption via osmosis in the kidneys.
  3. Increased potassium secretion by the kidneys.
  4. Increases proton secretion by the kidneys.
106
Q

What is the mechanism of aldosterone on kidneys?

A
  1. Aldosterone diffuses into the principal cells of the collecting duct and binds to intracellular receptors.
  2. Na-H transporters, potassium gates, sodium gates, Na-K pumps, and proton gates are transcribed and transported to the lumen membrane.
107
Q

Describe the RAAS cascade:

A
  1. Decreased volume of ECF, BP, and plasma sodium concentration is detected and stimulates an increase in sympathetic output.
  2. Renin is activated and converts angiotensinogen to angiotensin I.
  3. Angiotensin I is converted to angiotensin II by ACE (in the lungs).
  4. Angiotensin II acts on the adrenal cortex to increase aldosterone secretion. Increased potassium concentrations in the plasma will also cause aldosterone secretion by the cortex.
  5. Angiotensin II will also directly cause constriction of blood vessels to raise BP.
  6. Aldosterone acts on collecting duct to increase Na/H20 and decrease K/H.
108
Q

What are the main functions of cortisol?

A
  1. Metabolism.
  2. Immunity.
  3. Others (GIT, Bones, Kidney,)
109
Q

How does cortisol affect metabolism?

A

Increases protein and fat breakdown, increases blood glucose and availability for CNS. Increases glycogen formation in liver.

110
Q

How does cortisol affect immunity?

A

Decreases lymph node size, lymphocyte number, humoral/cellular immunity, and production of inflammation.

111
Q

How is cortisol secretion controlled/regulated?

A
  1. Stress increases secretion of CRH from hypothalamus.
  2. CRH increases secretion of ACTH from anterior pituitary.
  3. ACTH increases cortisol secretion from adrenal cortex.

Cortisol has feedback inhibition on hypothalamus and anterior pituitary.

112
Q

How are adrenaline and noradrenaline synthesized?

A

Tyrosine: DOPA: dopamine : noradrenaline (20%) : adrenaline (80%)

113
Q

What is the result of too much aldosterone?

A

Conn’s syndrome: hypokalemia, metabolic alkalosis.

114
Q

What is the result of too little aldosterone?

A

Addison’s disease: hypotension, metabolic acidosis.

115
Q

What is the result of too much cortisol?

A

Cushing’s disease (muscle wasting, diabetes, decreased immunity)

116
Q

What is the result of too little cortisol?

A

Addison’s disease.

117
Q

What is the result of too much adrenal androgens?

A

Virilization in females.

118
Q

What is the result of too little adrenal androgens?

A

Lower secondary sex characteristics decreased libido.

119
Q

What are the major actions of catecholamines?

A
  1. Cardiovascular system.
  2. Smooth muscle.
  3. Metabolism.
120
Q

What effect do catecholamines have on the cardiovascular system?

A

Increased sympathetic response (fight or flight)

121
Q

What effect do catecholamines have on smooth muscle?

A

Breathe and sight (dilation of pupils, low GIT motility), bronchodilation

122
Q

What effect do catecholamines have on metabolism?

A

Increased breakdown of glucose and lipids for energy.

123
Q

What nerve controls catecholamine secretion from the adrenal medulla? What is the mechanism of release?

A

Splanchnic nerve (sympathetic preganglionic), synapses onto chromaffin cells and released Ach.

124
Q

How does the active thyroid follicle differ from the resting follicle?

A

Less colloid space in the active follicle due to hormonal secretion.

125
Q

What is the colloid?

A

Space in the thyroid follicle that contains hormones for secretion.

126
Q

What are C-cells?

A

Cells in the thyroid that secrete calcitonin.

127
Q

How are thyroid hormones synthesized?

A
  1. Tyrosine to MIT and DIT.

2. . DIT/MIT to T3 or T4.

128
Q

Describe the entire “lifetime” of thyroid hormones:

A
  1. Uptake of iodide from blood combines with thyroglobin.
  2. Iodinized TG couples with MIT and DIT.
  3. MIT+DIT = T3
    DIT +DIT = T4
  4. Storage in colloid.
  5. Endocytosis by colloid, release of thyroid hormones into blood.
  6. T4 is a prohormone that converts into T3, thyroid hormones typically bound during transport.
  7. Act on hormone receptors.
129
Q

What are the major effects of thyroid hormones?

A
  1. Metabolism.
  2. Growth and development.
  3. Other (cardio/repro/symp)
130
Q

What effect do thyroid hormones have on metabolism?

A

Catbolism and anabolism increased; increased metabolism and heat.

131
Q

What effect do thyroid hormones have on growth and development?

A

Tissue growth factors, increase protein synthesis and GH production.

132
Q

What effect do thyroid hormones have on other effects?

A

Increases sympathetic response, increased bone turnover.

133
Q

What does the overactivity of thyroid hormones cause?

A

Graves’ disease: increased metabolism.

134
Q

What does under activity of thyroid hormones cause?

A

Hashimoto’s thyroiditis: low metabolism, goitre, iodine deficiency.

135
Q

Where is the majority of calcium stored in the body?

A

Bones.

136
Q

Is calcium more present in ECF or ICF?

A

ICF.

137
Q

Is calcium more likely to be bound or free?

A

Bound.

138
Q

What are the three sources of calcium in the plasma?

A

Resorption from the bone.
Absorption from the small intestine.
Reabsorption from the kidneys.

139
Q

What are the main function of calcium?

A
  1. Structural roles in bone and teeth.
  2. Blood coagulation cascade.
  3. Intracellular messenger.
  4. Regulation of excitability.
140
Q

What is the main function of phosphate?

A
  1. Structural role.
  2. Metabolism.
  3. Buffer.
141
Q

What is the main target for PTH?

A

Bone.

142
Q

What is the main target for active vitamin D?

A

gatsrointestinal tract.

143
Q

What is the main target for calcitonin?

A

Kidneys.

144
Q

What is the cellular structure of bone?

A
  1. Caclified matrix that consists of collagen framework and calcum/phosphate coating.
  2. Bone cells.
145
Q

What are the three bone cells?

A

Osteoblasts, osteoclasts, osteocytes.

146
Q

What is the function of PTH?

A

Increases calcium and decreases phosphate in the plasma.

147
Q

What is the widely accepted theory of osteoclastic resorption?

A
  1. Osteoclast forms ruffled border with bone, releases enzymes that break down network of bone and release calcium and phosphates.
  2. Osteoclasts move away and osteroblasts move in to secrete osteoid and rebuilt network.
  3. Some osteoblasts are surrounded by osteoid and changed into osteocytes embedded within the framework.
148
Q

How is PTHsecretion regulated?

A

Negative feedback mechanism: inhibited when calcium levels in blood are high.

149
Q

How are calcium levels sensed?

A

Chief cells of parathyroid gland contain calcium receptors that are coupled to inhibitory and stimulatory G-proteins that increase or decrease PTH secretion.

150
Q

How is D3 synthesized?

A

Cholecalciferol (inactive D3): 25-OH cholecalciferol in liver (storage form): PTH secretion moved to kidneys and converted to D3.

151
Q

How is calcium absorbed by gut?

A

Enterocyte in duodenal cell stimulated by D3 collects calcium using calcium calbindin complex that allows calcium to be moved into blood.

152
Q

What is the inverse relationship between calcium and excitability?

A
  1. Low calcium favors opening of sodium channels and increased excitability.
  2. High calcium levels inhibits opening of sodium channels and decreased excitability.
153
Q

Where is D3 secreted from?

A

Proximal tubule of kidneys.

154
Q

What effect does D3 have on blood calcium/phosphate?

A

increases both.

155
Q

What effect does calcitonin have on blood phosphate/calcium?

A

Decreased both.

156
Q

What are the cell types in the pancreas?

A

Acinar and islet of langerhans.

157
Q

What is the function of the acinar cells?

A

Exocrine: secreted pancreatic juice to small intestine.

158
Q

Waht is the function of the islets of langerhans?

A

Endocrine function: contains alpha and beta cells that secrete different hormones.

159
Q

What islet cell does glucagon come from?

A

Alpha.

160
Q

What islet cell does insulin come from?

A

Beta.

161
Q

What islet cell does somatostatin come from?

A

Delta.

162
Q

What is the effect of insulin?

A

“Feasting” hormone: increases uptake of nutrients from the blood into various tissue. Decreases secretion of nutrients into the blood.
Anabolic effects in tissues.

163
Q

What is the effect of glucagon?

A

“Fasting” hormone: increases secretion of nutrients from various tissue into the blood, decreases uptake of nutrients into tissue.

164
Q

What kind of receptor does insulin act on?

A

Tyrosine kinase receptors; causes release of insulin receptor substrates (enzymes, transporters, gene expression)

165
Q

How is glucose transported?

A
  1. Secondary active: SGLT1 SGLT2 (sodium)

2. Facilitated transport: GLUT 1 GLUT 2

166
Q

What GLUT is insulin sensitive?

A

GLUT 4

167
Q

What is the mechanism of insulin on cells containing GLUT4?

A

Transportation of GLUT4 to membrane to take up glucose.

168
Q

What kind of receptor does glucagon act on?

A

G-couples receptors.

169
Q

Where does short-term glucose come from?

A

Shortly after a meal.

170
Q

Where does middle-term glucose come from?

A

Liver glycogen stores are broken down.

171
Q

Where does long-term glucose come from?

A

New glucose made from amino acids and fats.

172
Q

What are the actions of insulin in the liver?

A

Increased:

  • Glycogenesis.
  • Glycolysis.
  • Lipogenesis.
  • Protein synthesis

Decreased: breakdown

173
Q

What are the cations of glucagon?

A

Incrreased: breakdown
Decreased: build up

174
Q

What is the function of somatostatin?

A

Local effects in pancreas, inhibit release of insulin and glucagon.

175
Q

How are glucose levels detected?

A

Beta cell in islet takes in glucose, increases in ATP.

Potassium channels close as a result, causing depolarization; calcium channels open.

Calcium causes the movement of storage vesicles containing insulin to membrane.

176
Q

Why is glucagon secretion increased by amino acids?

A

Insulin is secreted in response to amino acids in blood, which lowers blood glucose even if the meal isnt rich in glucose. Therefore glucagon must counterract the effects of insulin to prevent hypoglycemia.

177
Q

What effect do GIT hormones have on insulin/glucagon?

A

Insulin: increases secretion.
Glucagon: depends.

178
Q

What effect do local islet hormones have in insulin/ glucagon?

A

SS decreases both.

The presence of glucagon activates insulin, but insult inhibits glucagon.

179
Q

What is the result of too much insulin?

A

Hypoglycemia; increased sympathetic activity and counter-regulatory hormone secretion via glucagon and cortisol.

180
Q

What is the result of too little insulin?

A

Diabetes mellitis:

Type 1: beta cells destroyed, absolute insulin deficiency.

Type 2: resistance to insulin, obesity.

PHYSL214 (5 decks)

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