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Physiology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Endocrine system basics

A

Series of messenger systems with hormonal feedback loops
Hormones regulate distant target organs

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2
Q

Hormones

A

Regulate metabolism, growth, development, tissue function, sexual function, reproduction, sleep and mood, etc…

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3
Q

Control center of the endocrine system

A

Hypothalamus

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4
Q

Endocrine

A

Chemical signals secreted into the blood and transported to target tissues

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5
Q

Exocrine

A

Secrete substances into ductal system leading to an epithelial surface (internal or external)
Sweat glands, salivary glands, etc…

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6
Q

Paracrine

A

Cell to cell communication via chemical signals (short distance!)
Within a neuron, AP from cell body to axon terminal, triggers NT release, downstream cell is then influenced by paracrine NT and undergoes change/continues AP

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7
Q

Autocrine

A

Chemical signals which act upon the cell which created them (super super short)
Cell recognizing a change in its environment and telling itself to change/adapt to the new environment

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8
Q

Endocrine vs Paracrine vs Autocrine vs Exocrine

A
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9
Q

Hypothalamus

A

Located in the diencephalon and plays a crucial role in homeostasis and hormone production/release
Regulates body temp
Maintain physiological cycles
Controlling appetite
Managing sexual behavior
Regulating emotional responses
Regulates metabolism

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10
Q

How does the hypothalamus regulate the body

A

Feedback loops
Can increase or decrease production of releasing or inhibiting hormones based on circulating levels or changes in physiologic need

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11
Q

Pituitary gland

A

Base of the brain under the hypothalamus
Can produce and release hormones as indicated by the hypothalamus (stimulated with inhibiting or releasing hormones)

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12
Q

Connection of hypothalamus to pituitary gland

A

Anterior: Vascular portal system
Posterior: Neurons

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13
Q

Parts of the pituitary

A

Anterior and posterior

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14
Q

Anterior pituitary

A

Produces and releases many of the hormones within the endocrine system

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15
Q

How the anterior pituitary is connected to the hypothalamus

A

Hypothalamo-hypophseal portal system

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16
Q

Hormones synthesized by the anterior pituitary

A

Growth hormone (GH)
Thyroid- stimulating hormone (TSH)
Adrenocorticotropic hormone (ACTH)
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Prolactin (PRL)

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17
Q

Chart of anterior pituitary hormones from hypothalamus to effects

A
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18
Q

Posterior pituitary

A

Doesn’t make hormones, able to store hormones made by the hypothalamus in vesicles and then releases when needed, can releases a large amount very quickly, don’t need to synthesize the hormone

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19
Q

Advantage of posterior pituitary

A

When secreting ADH and oxytocin, usually you want them very quickly (bleeding out or labor) and want a lot. Since they are already made and just stored, when stimulated a lot can be released at once into the body

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20
Q

Hormones secreted by the posterior pituitary

A

Antidiuretic hormone
Oxytocin

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21
Q

Posterior pituitary chart hypothalamus to effects

A
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22
Q

How posterior pituitary is connected to the hypothalamus

A

Infundibulum/pituitary stalk which is comprised of axons

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23
Q

Pineal gland

A

Releases melatonin which controls circadian rhythms

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24
Q

Thyroid overview

A

Releases T3/T4 and regulates metabolism
Also releases calcitonin which acts to lower calcium levels in the blood

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25
Q

Parathyroid overview

A

Releases parathyroid hormone (PTH) which acts to increases serum calcium and decreases serum phosphorus levels in the blood

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26
Q

Pancreas

A

Releases insulin which lowers blood sugar
Releases glucagon which raises blood sugar

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27
Q

Insulin

A

Lowers blood sugar

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28
Q

Glucagon

A

Raises blood sugar

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29
Q

Exo pancreas

A

Digestion

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30
Q

Endo pancreas

A

Insulin and glucagon release

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31
Q

Adrenal cortex releases

A

Aldosterone and cortisol

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32
Q

Aldosterone

A

Released by the adrenal cortex and helps to regulate blood volume

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33
Q

Cortisol

A

Released by the adrenal cortex and has catabolic and anti-inflammatory effects

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34
Q

Adrenal medulla

A

Releases catecholamines

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35
Q

Ovaries

A

Releases estrogen for XX characteristics

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36
Q

Testes

A

Releases testosterone hormone for XY characteristics

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37
Q

Chart of Hypothalamus - Pituitary axis

A
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38
Q

Types of hormones

A

Peptide
Steroid
Tyrosine derivaties

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39
Q

Peptide hormones

A

Bind to receptors on the cell for 2nd messenger, unable to get into the cell since H20 soluble
Pit/hypo make
Insulin/glucagon
PTH (parathyroid hormone)

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40
Q

Steroid hormones

A

Precursor is cholesterol, lipid based
Fat soluble so can go through the plasma bind in cell or nucleus
Ex: Aldosterone, cortisol, estrogen, testosterone

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41
Q

Tyrosine derivatives

A

Amino acid base
T3/T4
Catecholamines
Prolactin inhibiting factor

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42
Q

Hormone receptor types

A

Cell membrane receptors
Cell cytoplasm receptors
Cell nuclear receptors

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43
Q

Types of hormones that bind to cell membrane receptors

A

Proteins, peptides, catacholamines

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44
Q

Types of hormones that bind to cell cytoplasm receptors

A

Steroid hormones

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45
Q

Types of hormones that bind to cell nuclear receptors

A

Thyroid hormones

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46
Q
A
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47
Q

Down regulation of receptors

A

Decrease in number because of overstimulation
Decrease the tissue sensitivity

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48
Q

Up regulation of receptors

A

Increase in number often due to hormone deficit
Increases sensitivity of tissue to hormone

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49
Q

Protein bound hormones

A

Steroid
T3/T4

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50
Q

Proteins that dissolve in plasma and are H20 soluble

A

Peptide hormones

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51
Q

Thyroid axis

A

TRH in hypothalamus to anterior pituitary to release TSH which then goes systemically to increase release of T3/T4

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52
Q

ADH axis

A

Osmoreceptors detect salt concentration
When osmolarity is high ADH is increase (sucks in water)
PTH released when serum calcium is low

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53
Q

Osmoreceptors

A

Measure internal salt concentration

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54
Q

Location of pituitary and impact with growth

A

Sits on the “turkish saddle” and right below optic chiasm
If there is tumor growth it presses on the optic chiasm and results in bitemporal hemianopsia

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55
Q

Primary endocrine disorder

A

Due to the downstream organ
Thyroid or adrenal gland has an issue with their hormone secretion

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56
Q

Secondary endocrine disorder

A

Due to problems with the pituitary (anterior)

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57
Q

Tertiary endocrine disorder

A

Problem with the hypothalamus

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58
Q

Thyroid

A

Located on the front of the trachea and is the largest purely endocrine gland in the body
Right and letf lobe with parathyroid glands on each “peak”

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59
Q

Thyroid hormones main controls

A

Metabolism
Growth and development
Cellular and body functions
Mood
Metabolize cholesterol

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60
Q

Two thyroid hormones

A

Triiodothyronine (T3, 3 iodine’s)
Thyroxine/tetraiodothyronine (T4, 4 iodine’s)

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61
Q

Hypothalamic - Pituitary - Thyroid Axis

A

Hypothalamus releases TRH (thyrotropin releasing hormone) into the pituitary, which then releases TSH (thyroid stimulating hormone) to the thyroid, which then secretes T3 and T4 and works as a negative feedback loop

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62
Q

Iodine

A

Trace element absorbed by the small intestine
Integral part of T3 and T4

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63
Q

Hypothyroidism

A

Underactive thyroid gland, decrease in T3 and T4
Bradycardia
Cold intolerance
Constipation
Fatigue
Weight gain
Myxedema coma

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64
Q

Hyperthyroidism

A

Increase in thyroid gland function, increase in T3/T4
Weight loss
Exophthalmos
Heat intolerance
Diarrhea
Tremors
Muscle weakness
Thyroid storm

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65
Q

Cells of the thyroid

A

Two primary cells
Follicular cells and parafollicular cells (C cells)

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66
Q

Parafollicular cells

A

Neuroendocrine cells that make calcitonin, which lowers calcium concentrations

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67
Q

Calcitonin

A

Lowers serum calcium concentrations (decrease for less muscle contraction, increase for more)
Secreted by parafollicular cells in the thyroid

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68
Q

Follicular cells

A

Synthesize thyroid hormones
Arranged in follicles with colloid center (storage center)
Produces thyroglobulin which stores hormones until needed
Contain receptor that TSH acts on

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69
Q

Thyroglobulin

A

Produced by follicular cells
Stores T3/4 until needed by combing with them

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70
Q

Production of thyroid hormone

A

Iodine trapped by thyroid and combined with tyrosine via TPO to make MIT and DIT which then combine to make T3/T4 (DIT + DIT = T4… MIT + DIT = T3)
Combines with thyroglobulin in colloid for storage
Thyroglobulin complex broken down once back in the follicle and then secreted into the blood

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71
Q

Thyroid peroxidase enzyme (TPO)

A

Combines iodine and tyrosine to make MIT and DIT which then combines to make T3/T4

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72
Q

How follicle cells trap iodine

A

Extracellular Na/iodine symporter uses gradient to move into the cell
(Na takes iodine with it into the colloid)

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73
Q

Thyroid stimulating hormone (TSH)

A

Up regulates sodium - iodide symporter
Stimulates proteolysis of iodinated thyroglobulin to T4 and T3 and secretes across membrane into circulation

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74
Q

How T3 and T4 travel systemically

A

Bound to thyroxine binding globulin protein and in inactive state
Need to be unbound to be active
Then converted from T4 to T3 in tissues to act

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75
Q

The body can only use T3 or T4

A

T3
So must be converted to T3 in the organ by removing a molecule of iodine

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76
Q

T4 binding to intranuclear receptor

A

Activates genes for increasing metabolic rate and thermogenesis
Increase O2 and energy consumption

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77
Q

Physiological functions of T3

A

Increase metabolic rate
Lipolysis or lipid synthesis
Stimulate metabolism of carbs
Anabolism of proteins (or catabolism in high doses)
Increase potency of catecholamines

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78
Q

Cardiovascular effects of T4

A

Converted to T3 in tissues
Increases metabolism, causes skin arterial dilation to “blow off” excess heat
Decreases afterload and increases CO
Increased expression of Beta 1 receptors to increase HR, SV, and CO
MAP stays the same

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79
Q

Thyroid hormones in children

A

Brain development in peri-natal period
Act synergistically with growth hormone to stimulate bone growth

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80
Q

Grave’s disease

A

Hyperthyroidism
B cells create antibodies that bind to TSHR to secrete T3 and T4
No negative feedback loop

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81
Q

Hashimoto’s thyroiditis

A

B cell antibodies attack TPO enzyme which is what makes T3 and T4 from MIT/DIT
Can be fatal or cause heart failure

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82
Q

Hypothyroidism

A
83
Q
A
84
Q

Hypothalamus Anterior Pituitary Target organ chart

A
85
Q

Growth hormone target site

A

Whole body is the target but mainly musculoskeletal

86
Q

Growth hormone releasing hormone causes

A

Target organ to release insulin like IGF-2 which acts to induce growth

87
Q

Feedback for GHRH

A

IGF-1 acts as negative feedback

88
Q

Hypothalamus Pituitary Growth hormone axis

A
89
Q

Causes of growth hormone releasing hormone secretion

A

Hypoglycemia
Starvation
Trauma/stress/excitement
Exercise
Sex hormones
Deep sleep

90
Q

Inhibitors of growth hormone releasing hormone

A

Hyperglycemia
Elevated growth hormone (from negative feedback)
GHIH (somatostatin)
Age
Obesity

91
Q

Metabolic effects of GH

A

Shifts metabolism to burning fat instead of sugars, so starts lipolysis which provides fatty acids and glycerol for energy metabolism

92
Q

Impacts of GH on the body

A

Metabolizes fat (lipolysis)
Gluconeogenesis (produce glucose form non-carbs)
Increase serum cholesterol (for fat breakdown)
Antagonizes insulin’s action (increase serum glucose)

93
Q

Hypoglycemia and GHRH

A

Decrease in glucose stimulates growth hormone

94
Q

Hyperglycemia and GHRH

A

Increase in glucose inhibits growth hormone

95
Q

Gluconeogenesis

A

Production of glucose from non-carbohydrate substrates
Stimulated by GH

96
Q

GH impact on serum cholesterol

A

Increases cholesterol
Which increases fat breakdown

97
Q

GH on the ehart

A

Increases sodium and water retention
Increases BP

98
Q

Negative feedback loops of GH

A

GH negatively feeds back to the hypothalamus
IGF-1 negatively feeds back to the pituitary

99
Q

Effects of IGF-1

A

Bone/cartilage grows and thickens
- Osteoblast activation
- Increased bone length prior to adulthood
- Increased bone thickness

100
Q

GH and IGF-1 cascade chart

A
101
Q

GH pathologies

A

Pituitary dwarfism
Gigantism
Acromegaly

102
Q

Pituitary dwarfism

A

Normal body proportions but decreased rate of development
IGF-1 deficiency

103
Q

Giantism

A

Pre-adolescent elevated GH
Often develops diabetes becomes tumor is blind to hyperglycemia

104
Q

Acromegaly

A

Post-adolescent GH elevation
Growth of bone thickness but not length because epiphyseal plate has closed

105
Q

Prolactin

A

Under hypothalamic inhibition via dopamine
Increased levels of prolactin doesn’t necessarily decrease PRH release from the hypothalamus

106
Q

Prolactin actions

A

Increase milk production
Decreases GnRH
Decreases LH/FSH

107
Q

Prolactin is a ________ feedback loop

A

Positive
As more milk production, stimulates more milk production
When suckling stops dopamine increases and inhibits prolactin

108
Q

Dopamine and prolactin

A

Dopamine is always on and you need to inhibit it to turn on prolactin

109
Q

Hyperprolactinemia

A

XY: Infertility and decreased sex drive
XX: Infertility and decreased sex drive

110
Q

Most common anterior pituitary tumor

A

Prolactinoma

111
Q

Prolactinoma

A

Hyperprolactinemia symptoms plus
- Headache
- Bitemporal hemianopsia

112
Q

Posterior pituitary releases

A

ADH and oxytocin

113
Q

ADH main function

A

Regulate sodium concentration within the blood via osmoreceptors
When highly concentrated, more ADH to dilate

114
Q

Where does ADH act

A

Distal convoluted tubule of the kidneys which reabsorbs water back into the blood via aquaporins

115
Q

ADH axis chart

A
116
Q

Aquaporins

A

On the collecting duct and only permeable to water
Allows the kidneys to reabsorb water

117
Q

Things that increase ADH

A

Nicotine
Opiates
Nausea
Increased osmolarity
Decreased IV volume

118
Q

Things that decrease ADH

A

Alcohol
Cortisol

119
Q

Things that stimulate thirst

A

ADH secretion
Angiotensin II
Increased osmolality
Decreased IV volume

120
Q

Diabetes insipidus

A

ADH deficit or defect
Can’t reabsorb water from the collecting duct which means peeing more water and causes dehydration

121
Q

Causes of DI

A

Neurologic/Central: Low or abnormal ADH from head injury, hypothalamic destruction, post pituitary destruction
Nephrogenic: Normal or high ADH from abnormal ADH receptor in kidney

122
Q

SIADH

A

Inappropriate ADH secretion, means too much ADH that is secondary to another disease process elsewhere in the body
Retaining too much water

123
Q

Treatment for SIADH

A

Withhold water but not food

124
Q

Oxytocin

A

Causes uterine contractions and milk ejection

125
Q

Oxytocin feedback loop

A

Positive feedback loop

126
Q

Secretion of oxytocin causes

A

Vaginal stretch - Labor or intercourse
Suckling infant

127
Q

Inhibition of oxytocin

A

Lack of secretory stimuli

128
Q

Layers of the adrenal gland way to remember

A

GFR
Salt
Sugar
Sex

129
Q

Layers of the adrenal gland

A

Cortex: zona glomerulosa, zona fasciculata, zona reticularis
Medulla

130
Q

Hormones made in the Zona glomerulosa

A

Mineralocorticoids - aldosterone

131
Q

Mineralocorticoids - adrenal

A

Mineral base that influences salts and absorption
Aldosterone

132
Q

Glucocorticoids - adrenal

A

Glucose, increase in glucose
Cortisol

133
Q

Androgens - adrenal

A

Sex hormones
Estrogen and testosterone

134
Q

Aldosterone main effects

A

Increase sodium and water retention, prevent hyperkalemia
Activates sodium potassium exchangers in kidneys so it absorbs Na (water follows Na) and kicks K into the urine

135
Q

Chemoreceptors - aldosterone

A

Release aldosterone in response to elevated levels of K

136
Q

Secondary actions of aldosterone

A

Vasoconstriction
Vascular stiffness
Cardiac inflammation

137
Q

Renin - angiotensin - aldosterone - system (RAAS)

A

Baroreceptors detect decrease in BV and BP and trigger release of renin
This cleaves angiotensinogen into angiotensin I
This is converted into angiotensin II in the lungs via ACE
Angiotensin II then leads to cardiac and vascular effects (vasoconstriction leads to increase in BV and BP)

138
Q

AngII

A

Potent vasoconstrictor which increases BP
Triggers aldosterone
ACTH secretion that causes thirst sensation

139
Q

Stimuli to release aldosterone

A

Increased K+ in the body
Ang II
Decreased arterial blood volume

140
Q

Hormones made in zona fasciculata

A

Glucocorticoids - cortisol

141
Q

Cortisol feedback loop

A

Cortisol is the primary negative feedback to the hypothalamus for CRH regulation

142
Q

Cortisol axis

A

Hypothalamus releases CRH to pituitary
Pituitary releases ACTH to the adrenal cortex
Adrenal gland releases cortisol

143
Q

Glucocorticoids involved in

A

Glucose metabolism

144
Q

Cortisol effects

A

Gluconeogenesis - increases blood glucose
Inhibits tissue building and promotes catabolism of stored nutrients - increase cholesterol
Impair wound healing
Increased blood pressure
CNS stimulant
Bone reabsorption for increased serum calcium

145
Q

Anabolism

A

Set of metabolic pathways that construct molecules from smaller units

146
Q

Catabolsim

A

Breaking down molecules into smaller units

147
Q

Short term cortisol stimulation

A

Nerve impulses from sympathetic fibers that trigger the adrenal medulla to secrete catecholamines

148
Q

Cushing’s syndrome

A

Adrenal cortex overproduces cortisol

149
Q

Cushing’s disease

A

Pituitay produces increased ACTH, usually a tumor

150
Q

Zona reticularis

A

Produces sex hormones like angrogen
Regulated by ACTH

151
Q

Hypothalamic - pituitary - gonadal axis

A

Hypothalamus - GnRH - Anterior pit - LH, FSH - Gonads - Sex hormones

152
Q

General function of cortex of adrenal gland

A

Hormonal/endocrine
Regulated and slow

153
Q

General function of medulla of adrenal gland

A

Autonomic nervous system, fast
Receives sympathetic input and releases catecholamines

154
Q

Functions of the pancreas

A

Exocrine to help in digestion
Endocrine to help regulate blood sugar (via insulin and glucagon)

155
Q

Endocrine pancreas

A

Regulates blood sugar in the whole body via insulin and glucagon

156
Q

Exocrine pancreas

A

Ductal network, releasing lipase and amylase to help in digestion

157
Q

Anatomy of the pancreas

A

95% is exocrine tissue that produces pancreatic enzymes for digestion
Remaining is endocrine cells called islets of Langerhans

158
Q

Islets of Langerhans

A

Produce hormones that regulate blood sugar
Alpha and beta cells

159
Q

Alpha vs beta islet of langerhans

A

Alpha produces glucagon (25%)
Beta produces insulin (60%)

160
Q

Glycolysis

A

Breakdown of glucose into ATP and pyruvate

161
Q

Gluconeogenesis

A

Making glucose from things that aren’t carbs
Building up sugars
Occurs mainly in the liver

162
Q

Glycogen

A

Stored in the form of glucose
Glycogen molecule may contain 30,000 glucose units
Stored in the liver and skeletal muscle

163
Q

Glycogenolysis

A

Breakdown of glycogen to release glucose for energy production

164
Q

Glycogenesis

A

Formation of glycogen from glucose

165
Q

Insulin derived from

A

Prohormone molecule called proinsulin which is a peptide hormone

166
Q

Structure of insulin

A

Protein that is composed of two chains
A chain and B chain linked by sulfur atoms

167
Q

How to activate insulin

A

Cleave the c-peptide chain that is attached to the A and B chains

168
Q

C-peptide

A

This is cleaved off of insulin to make it active
Can measure the amount in the blood and can determine cause of hypoglycemia

169
Q

Insulin

A

Peptide hormone that promotes glucose uptake, glycogenesis, lipogenesis, and protein synthesis

170
Q

Trigger for insulin release

A

Hyperglycemia - stores glucose as glycogen
Promotes

171
Q

What increases secretion of insulin

A

Elevated glucose
Elevated cortisol or glucagon
Rest and digest

172
Q

What decreases secretion of insulin

A

Low glucose/fasting
GH

173
Q

Glucagon

A

When blood sugar levels are too low this is released by the pancreas to increase blood glucose from stores (glycogen)
Glycogenolysis
Gluconeogenesis

174
Q

Glycogenolysis vs gluconeogenesis

A

Lysis is catabolic
Genesis is anabolic
Glycogenolysis: Breakdown of glycogen to free the stored glucose chains
Gluconeogenesis: Forms glucose from non-glucose sources

175
Q

Hypoglycemia immediate action

A

Glucagon secretion
Sympathetic stimulation

176
Q

Hypoglycemia delayed reaction

A

Growth hormone increases serum glucose by increasing fatty acid metabolism
Cortisol increases serum glucose

177
Q

Hyperglycemia immediate action

A

Insulin secretion

178
Q

Insulin resistance

A

Increased exposure to insulin decreases (down regulates) the amount of insulin receptors

179
Q

Transport protein for glucose

A

Glut4

180
Q

Glut4

A

Glucose transport protein that is stimulated by insulin
When insulin binds, glut4 incorporates into the plasma

181
Q

Incretin

A

When there is glucose present in the lumen of your small intestine, incretins are released
Incretins enhance the glucose - dependent insulin secretion resulting in stimulation of pancreatic B cells

182
Q

Types of incretins

A

GIP and GLP-1

183
Q

DPP4 enzyme

A

Responsible for the degradation of incretins such as GLP-1
- Increased levels result in less incretin and less insulin release and higher blood glucose

184
Q

Parathyroid glands

A

Regulate the calcium and phosphorus levels in our body via the release of PTH (parathyroid hormone)

185
Q

Chemoreceptors parathyroid glands

A

Detect calcium concentration in the blood
When low levels of calcium are detected, chief cells secrete PTH to increase serum calcium levels

186
Q

Downstream effects of detecting low calcium levels

A

Parathyroid release PTH onto the kidneys and the bones
Kidneys increase vitamin D to increase Ca and Pi absorption in the gut
Kidney’s cause increase in Ca reabsorption from the urine and Pi excretion into the urine
Bones have increased osteoclast activity and creases Ca release into the blood

187
Q

Hydroxyapatite

A

Ion salt formed between calcium and phosphorus
Can deposit in the vasculature and tendons
Also found in the kidney stones

188
Q

Ca/P relationship

A

Calcium has an inverse relationship to phosphorus
Therefore when phosphorus in the blood rises, levels of calcium in the blood fall
Because phosphorous binds to calcium reducing free calcium

189
Q

Exception to Ca/P relationship

A

Vitamin D in the gut causes an increase in both Ca and Pi

190
Q

FLAT PG

A

Pituitary gland hormones
Follicle stimulating hormone
Leutanizing hormone
ACTH
TSH
Prolactin releasing hormone
Growth hormone

191
Q

Bone deposition

A

Depositing or creating new bone matrix by the osteoblasts

192
Q

Bone reabsorption

A

Osteoclasts break down the tissue in bones and release minerals to the blood

193
Q

PTH

A

Increases amount of Ca by reabsorbing from the urine
Decreases the amount of phosphate by increasing the amount of secretion into the urine

194
Q

Increase calcium and AP

A

Increased Ca blocks sodium channels
Makes the threshold potential less negative, so harder to reach threshold
Hypoexcitable
Negative bathmotropic effect

195
Q

Negative bathmotropic effect

A

Increase in calcium makes it harder for Na to go into the cell and harder to depolarize

196
Q

Decreased calcium and AP

A

Low calcium releases sodium channels so more sodium enters the cell decreasing the threshold potential
Hyperexcitable
Positive bathmotropic effect

197
Q

Positive bathmotropic effect

A

Decrease in Ca makes it easier for Na into the cell
Hyperexcitable

198
Q

PTH regulating serum Ca

A

Low serum calcium will increase PTH and increase Ca
High serum calcium will decrease PTH and decrease calcium

199
Q

PTH on organ systems

A

Increase bone reabsorption
In kidneys decrease phosphate reabsorption and increase Ca reabsorption
In intestines increase calcium reabsorption

200
Q

1 alpha-hydroxylase

A

Activates Vitamin D and is increased by PTH and produced in the kidneys

201
Q

Vitamin D

A

Increase Ca and Pi absorption in the intestines
Increases kidney reabsorption of Ca from the urine

202
Q

Calcitonin

A

Thyroid hormone that is released by C cells
Decreases Ca levels by inhibiting osteoclast activity and increases renal excretion of calcium

203
Q
A

Physiology (5 decks)

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