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Physiology (Costanzo) > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

What is the main function of the endocrine system?

A

Homeostasis

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2
Q

What functions does the endocrine system regulate?

A

Growth, development, reproduction, blood pressure, [ion/substance], behavior

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3
Q

Define a hormone.

A

Protein, steroid, amine transported through the blood to act on a distant target.

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4
Q

Name the twelve endocrine glands.

A

Hypothalamus, anterior and posterior pituitary, thyroid, parathyroid, adrenal cortex, adrenal medulla, kidney, GI tract, gonads, placenta, pancreas.

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5
Q

What hormones are released by the hypothalamus?

A

TRH, CRH, GnRH, GHRH, somatostatin, dopamine

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6
Q

What hormones are released by the anterior pituitary?

A

FSH, LH, ACTH, TH, MSH, GH Prolactin

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7
Q

What hormones are released by the posterior pituitary?

A

oxytocin, ADH

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8
Q

What hormones are released by the thyroid?

A

T3, T4, calcitonin

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9
Q

What hormones are released by the parathyroid?

A

PTH

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10
Q

What hormones are released by the pancreas?

A

insulin, glucagon

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11
Q

What hormones are released by the adrenal medulla?

A

NEpin., epin.

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12
Q

What hormones are released by the kidney?

A

renin, 1,25-dihydroxycholecalciferol

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13
Q

What hormones are released by the adrenal cortex?

A

cortisol, aldosterone, adrenal androgens

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14
Q

What hormones are released by the testes?

A

testosterone

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15
Q

What hormones are released by the ovaries?

A

estradiol, progesterone

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16
Q

What hormones are released by the corpus luteum?

A

estradiol, progesterone

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17
Q

What hormones are released by the placenta?

A

HCG, HPL, estriol, progesterone

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18
Q

From what parent molecule are peptide and protein hormones formed?

A

Amino acids

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19
Q

From what parent molecule are steroid hormones formed?

A

Cholesterol

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20
Q

From what parent molecule are amine hormones formed?

A

Tyrosine

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21
Q

What are the five steps in peptide/protein hormone formation?

A

DNA -> mRNA -> preprohormone -> prohormone -> hormone

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22
Q

Describe the tl of mRNA to preprohormone.

A

Translated on ribosome from N-terminal signal sequence. Moved to ER where translation is completed.

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23
Q

Describe the transition from preprohormone to prohormone.

A

Inside the ER the signal sequence is cleaved forming the prohormone. Sequences are removed that aided in protein folding.

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24
Q

Describe the transition from prohormone to hormone.

A

After transferring to the Golgi, and ultimately secretory vesicles, proteolytic enzymes cleave pieces of the protein to form the hormone.

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25
Q

Describe the release of the hormone.

A

Signal acts on the endocrine cell -> secretory vesicles release hormone ->physiologic action.

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26
Q

What organs/glands produce steroid hormones?

A

Adrenal cortex, gonads, corpus luteum, placenta

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27
Q

What are the seven steroid hormones?

A

Cortisol, aldosterone, estradiol, estriol, progesterone, testosterone, 1,25-dihydroxycholecalciferol

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28
Q

What three modifications happen to the cholesterol molecule to produce the various steroid hormones?

A

removal/addition of side chains
hydroxylation
aromatization

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29
Q

What are the two subcategories of amine hormones?

A

catecholamines

thyroid hormones

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30
Q

Name the three catecholamines.

A

NEpin., epin., dopamine

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31
Q

Name the two thyroid hormones.

A

T3, T4

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32
Q

Amine hormones are all derivatives of…

A

tyrosine.

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33
Q

Give an example of neural mechanisms affecting hormone secretion.

A

Sympathetic preganglionic neuron acting on adrenal medulla to release NEpin., Epin.

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34
Q

Give a biological definition of feedback.

A

A product of a biosynthetic pathway acts on its own pathway to enhance or suppress further secretion(/synthesis?).

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35
Q

Define negative feedback.

A

Some feature of hormone action, directly or indirectly, inhibits further secretion of the hormone.

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36
Q

Describe how testosterone secretion acts as a negative feedback mechanism.

A

Hypoth -> ant. pit -> testis -> testosterone

testosterone acts on ant.pit and hypoth. to inhibit secretion of GnRH or LH.

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37
Q

Define long and short feedback loops.

A

Long feedback loop: hormone or product acting back on hypothalamic-pituitary axis (or other).

Short feedback loop: product acting within hypothalamic-pituitary axis.

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38
Q

Give an abstract definition of negative feedback.

A

Level is judged as adequate or high, further action is inhibited.

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39
Q

Give a non-hormonal example of (-)fb.

A

High blood glucose stimulates beta cell of pancreas to release insulin. Insulin causes uptake of blood glucose; insulin inhibits its own release from beta cells in pancreas.

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40
Q

Define positive feedback.

A

Some feature of hormone action causes more secretion. Leads to explosive events.

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41
Q

Give a non-hormonal example of (+)fb.

A

Depolarization of axon membrane opens V(Na+) channels. Na+ moves into axon causing further depolorization. This causes even more V(Na+) channels to open.

Result: explosive upstroke

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42
Q

Describe (+)fb during the midpoint of the menstrual cycle.

A

Ovaries release estrogen. Estrogen acts on anterior pituitary to release FSH, LH. FSH, LH act on ovaries to release more estrogen.

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43
Q

Describe (+)fb during parturition.

A

Cervical dilation sends neural impulse to hypothalamus which stimulates oxytocin release from posterior pituitary. Oxytocin release acts on cervix to cause further dilation.

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44
Q

How is the response of a hormone regulated?

A

[hormone], (+) or (-) fb, presence/absence of receptor on tissue

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45
Q

Define sensitivity in the context of hormones.

A

The concentration of hormone necessary to produce 50% of the maximal response.

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46
Q

How does sensitivity change?

A

The number of receptors.

The affinity of the receptor for a ligand.

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47
Q

What is the cellular mechanism of down-regulation?

A

Decrease synthesis, increase degradation, or inactivate receptors.

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48
Q

What is the cellular mechanism of up-regulation?

A

Increase synthesis, decrease degradation, or activate receptors.

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49
Q

Why is down-regulation necessary?

A

A high [hormone] can have its effects reduced so as not to stray too far from homeostasis.

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50
Q

Give an example of down-regulation with respect to progesterone.

A

Progesterone leads to a down-regulation of its own receptor AND estrogen receptors.

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51
Q

Give an example of down-regulation with respect to T3.

A

T3 down-regulates TRH receptors in anterior pituitary, therefore chronically high T3 levels decrease hypoth.-ant.pit. response.

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52
Q

Give an example of up-regulation with respect to prolactin. Give an example of up-regulation with respect to GH.

A

Prolactin increases its own receptors in the breast. GH up-regulates its own receptors in skeletal muscle and liver.

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53
Q

Give an example of up-regulation with respect to estrogen.

A

Estrogen up-regulates its own receptors and LH receptors in ovaries.

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54
Q

What are the five typical/well-known mechanisms of signal transduction?

A

adenylate cyclase, phospholipase C, steroid hormone, tyrosine kinase, guanylate cyclase

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55
Q

Describe the structure of G-proteins.

A

receptor domain, linked to 7TM domain, linked to intracellular domain that is associated with alpha, beta, gamma subunits.

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56
Q

What proteins increase G-alpha activity? What proteins decrease G-alpha activity?

A

GAPs (GTPase-activating proteins) increase GTP hydrolysis thus deactivating G-alpha.

GEFs (guanine-nucleotide exchange factors) increase exchange of GDP for GTP, thereby activating G-alpha.

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57
Q

Describe the seven steps in the adenylyl cyclase mechanism.

A
  1. hormone binds
  2. G-alpha-s-GTP dissociates
  3. G-alpha-s-GTP associates with adenylate cyclase
  4. AC converts ATP to cAMP
  5. cAMP is either inactivated by PDE or activates PKA
  6. PKA phosphorylates targets
  7. physiologic response
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58
Q

Describe the seven steps in the phospholipase C mechanism.

A
  1. hormone binds
  2. G-alpha-q-GTP dissociates
  3. G-alpha-q-GTP associates with PLC
  4. PLC converts PIP2 to DAG and IP3
  5. IP3 stimulates Ca2+ release from ER/SR
  6. Ca2+ and DAG stimulate PKC
  7. physiologic response
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59
Q

Give two examples of the guanylyl cyclase mechanism.

A

ANP (atrial natriuretic peptide) and NO

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60
Q

Describe ANP (artrial natriuretic peptide) signalling.

A

ANP binds receptor. Causes activation of GC. GC converts GTP to cGMP. cGMP activates cGMP-dependent kinase. Physiologic response.

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61
Q

Describe NO signalling.

A

NO synthase cleaves arginine into citrulline and NO. NO diffuses to nearby cells and activates cytosolic GC. GC converts GTP to cGMP. Cause relaxation of vascular smooth muscle.

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62
Q

Give four examples of serine/threonine kinases.

A

PKA, PKC, Ca2+-calmodulin dependent protein (CaMK), mitogen-activated protein kinase (MAPK).

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63
Q

Describe the activation of monomeric tyrosine kinases.

A

ligand binds monomer, monomer dimerizes, dimers intrinsically phosphorylate themselves and targets.

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64
Q

Give two examples of representative monomeric type Tyr-kinases.

A

NGFs, EGFs

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65
Q

Describe the activation of dimeric tyrosine kinases.

A

ligand binds to dimer, activates intrinsic Tyr-kinase domain, phosphorylates itself and targets.

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66
Q

Describe the activation of tyrosine kinase-associated receptors.

A

ligand binds, receptors dimerize, activates associate JAK, JAK phosphorylates itself, the receptor, and targets.

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67
Q

What is a well known target of JAK?

A

STAT (signal transducer and activator of transcription)

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68
Q

What is an example of a dimeric tyrosine kinase?

A

IGFs

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69
Q

Temporally, how does steroid signalling compare to peptide/protein signalling?

A

Steroid (hours)

Peptide/protein (minutes)

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70
Q

Describe the seven steps of the steroid signalling mechanism.

A
  1. steroid diffuses into cell
  2. binds cytoplasmic (nuclear) receptor
  3. receptors dimerize and bind SREs
      1. cause transcription and translation of genes
  5. physiologic response
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71
Q

What effect does 1,25-dihydroxycholecalciferol have on the intestine?

A

Causes Ca2+ absorption in the intestine.

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72
Q

What effect does aldosterone have?

A

Causes Na+-channel synthesis in renal distal tubule and collecting duct.

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73
Q

Describe the anatomical relationship of the hypothalamus to the posterior and anterior pituitary.

A

Hypothalamus projects neurons to the posterior pituitary. Hypothalamus is connected to the anterior pituitary by hypothalamic-hypophyseal portal system.

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74
Q

The posterior pituitary is differentiated ______

A

Neural tissue.

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75
Q

Since the post. pit. consists of the axonal projections of the hypothalamus; ADH and oxytocin are really…

A

Neuropeptides.

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76
Q

Where is ADH primarily synthesized?

A

Supraoptic nuclei of hypothalamus.

77
Q

Where is oxytocin primarily synthesized?

A

Paraventricular nuclei of hypothalamus.

78
Q

Describe the synthesis and release of posterior pituitary hormones.

A

ADH and oxytocin are synthesized in their respective nuclei of the hypothalamus and transported in vesicles down axons into the post. pituitary. Stimuli causes release from post. pituitary into bloodstream.

79
Q

From what tissue is the anterior pituitary derived?

A

Endocrine tissue.

80
Q

What two factors are unique to the hypothalamic-hypophyseal portal system?

A

Direct delivery of a high [hormone]

Hormones secreted into the portal do not appear in the general circulation.

81
Q

Describe how hypothalamic hormones induce anterior pituitary hormone release into the general circulation.

A

Hypothalamic hormone travels down hypoth. neuron where it is released into capillary plexus.

Travels through capillary plexus into ant. pit. causing hormone release or inhibition.

Ant. pit. hormone is released into general circulation.

82
Q

Describe, in detail, how TRH causes thyroid hormone secretion.

A 
TRH synth. in hypoth. neurons.
Secreted into median eminence.
Release into capillary plexus.
Reaches ant. pit., stimulates release of TSH.
TSH travels in gen. circ. to thyroid.
Increase in thyroid hormone secretion.
83
Q

What cell types release FSH, LH, ACTH, TSH, Prolactin, and GH?

A 
thyrotrophs (TSH)
gonadotrophs (FSH, LH)
corticotrophs (ACTH)
lactotrophs (Prolactin)
somatotrophs (GH)
84
Q

How are the ant. pit. hormones grouped into families?

A

Based on structural and functional homology:
(FSH, LH, TSH)
(ACTH)
(GH, prolactin)

85
Q

Describe why FSH, LH, TSH are grouped into a family.

A

They share the same alpha-subunit, but different beta-subunits.

86
Q

What other hormone is similar to the (FSH,LH,TSH) family?

A

human chorionic gonadotropin (HCG)

87
Q

What is the common precursor of the ACTH family?

A

pro-opiomelanocortin (POMC)

88
Q

What four hormones/peptides are formed from cleavage of POMC? What cleaves POMC?

A

ACTH, gamma-lipotropin, beta-endorphin, MSH.

Endopeptidases.

89
Q

Describe the normal feedback loop of glucocorticoids on the hypoth.-ant.pit.

A

Glucocorticoids inhibit hypothalamic-release of CRH, and ant.pit-release of ACTH.

90
Q

How is the feedback of glucocorticoids altered in Addison’s disease?

A

Insufficient(or absent) secretion of glucocorticoids fails to inhibit release of CRH and therefore ACTH.

91
Q

What is the effect of removing this (-)fb loop?

A

increase in ACTH levels, and increase in alpha, beta, gamma-MSH levels causing increased skin pigmentation.

92
Q

What are the causes of Addison’s disease (primary adrenal insufficiency)?

A 
adrenal dysgenesis (improper development)
impaired steroidogenesis (unable to biochemically produce cortisol)
adrenal destruction (disease processes leading to gland damage)
93
Q

What are the effects of GH biochemically?

A

Increased protein, carb, fat metabolism.

94
Q

What family is GH in?

A

(GH, prolactin, HPL)

95
Q

Describe the levels of GH throughout life.

A

Steady increase from birth to childhood.
Spike in puberty (from estrogen or testosterone).
Decrease to a steady level in adulthood.
Steady decrease until lowest levels in senescence.

96
Q

Draw the regulation diagram of GH, including the hypothalamus, anterior pituitary, and target tissues.

A

Draw.

97
Q

What cell type does GHRH act on in the anterior pituitary?

A

Somatotrophs to stimulate synth. and secre. of GH.

98
Q

What cell type does somatostatin (SRIF) act on in the anterior pituitary?

A

Somatotrophs to inhibit GH secre.

99
Q

What are the target tissues of GH?

A

Liver, muscle, adipose tissue, bone, virtually every organ.

100
Q

What are the three actions of GH?

A

Diabetogenic effect.
Increased protein synth. and organ growth.
Increased linear growth.

101
Q

How does GH cause a diabetogenic effect?

A

GH causes insulin resistance and decreased glucose uptake and utilization.
Therefore, increased blood [glucose], also increased lipolysis in adipose tissue.

102
Q

How does GH cause increased protein synthesis and organ growth?

A

GH causes increase in uptake of amino acids and stimulates synthesis of DNA, RNA, and protein.
Therefore increase in lean body mass and organ size.

103
Q

How does GH cause an increase in linear growth?

A

GH alters every aspect of cartilage metabolism (DNA, RNA, protein).
Therefore growing bones have epiphyseal plate widening, more bone laid down on end of long bones, and increase in metabolism of cartilage-forming cells and proliferation of chondrocytes.

104
Q

What are the symptoms of GH deficiency?

A

failure to grow, short stature, mild obesity, delayed puberty.

105
Q

What are the four causes of GH deficiency?

A

Decreased secre. of GHRH (hypoth. dysfunction).
Primary deficiency of ant. pit.
Failure to generate somatomedins in liver.
Deficiency of receptors in target tissues.

106
Q

What is the Tx for GH deficiency in children?

A

hGH

107
Q

What is the effect of GH excess before puberty?

A

Gigantism

108
Q

What is the effect of GH excess after puberty?

A

Increase in periosteal bone growth, increase organ size, increases hand/foot size, increase tongue size, insulin resistance and glucose intolerance.

109
Q

What is acromegaly most often due to?

A

Pituitary adenoma.

110
Q

What is the Tx for GH excess?

A

Somatostatin analogue (octreotide).

111
Q

What hypothalamic hormone stimulates release of prolactin?

A

TRH

112
Q

Draw the regulation diagram of prolactin.

A

Draw.

113
Q

Describe how breast-feeding stimulates prolactin production.

A

Mechanical stimulation of nipple (suckling) sends message through afferent fibers to hypothalamus inhibiting dopamine release. Inhibition of the inhibitor (dopamine) increases prolactin release.

114
Q

What are the three actions of prolactin?

A

Breast development
Lactogenesis
Inhibition of Ovulation

115
Q

Describe the effect of prolactin+estrogen+progesterone during puberty in females.

A

The three act together to stimulate branching of the mammary ducts.

116
Q

Describe the effect of prolactin+estrogen+progesterone during pregnancy in females.

A

The three act together to stimulate growth and development of mammary alveoli (which produce milk after parturition).

117
Q

Describe prolactin’s effect on lactogenesis.

A

Stimulates production of lactose, casein, and lipids.

118
Q

How do estrogen and progesterone inhibit lactation during pregnancy?

A

They down-regulate prolactin receptors in breast tissue.

119
Q

How does prolactin inhibit ovulation?

A

Prolactin inhibits synth. and release of GnRH. Therefore decrease in fertility while breast-feeding.

120
Q

How does a prolactinoma affect men?

A

Increase in prolactin (from the tumor) inhibits GnRH release, decreases spermatogenesis, therefore decrease in fertility.

121
Q

What are the causes of prolactin deficiency?

A

Destruction of entire ant. pit., destruction of lactotrophs in ant. pit., therefore no lactation.

122
Q

What are the causes of prolactin excess?

A

Destruction of hypothalamus, interruption of portal lead to loss of dopamine inhibition.

Prolactinomas.

123
Q

What are the symptoms of prolactin excess?

A

Galactorrhea and infertility.

124
Q

What is the Tx for prolactin excess?

A

Bromocriptine (dopamine agonist).

125
Q

Name the posterior pituitary hormones.

A

ADH/vasopressin

oxytocin

126
Q

Describe how post. pit. hormones are synthesized and secreted.

A

tl in hypothalamus as prepropressophysin and prepro-oxyphysin. Golgi cleaves signal peptide and propressophysin and pro-oxyphysin are packaged in secretory vesicles. En route to post. pit., neurophysins are cleaved from each and ADH and oxytocin are stored in secre. vesicles until stimulus reaches hypothalamus.

127
Q

How large is ADH and oxytocin?

A

They are both nonapeptides differing in two amino acids.

128
Q

Describe how hypothalamic APs signal secretion of ADH and oxytocin.

A

AP travels down hypoth. axon to cause opening of VCa2+ channels. Ca2+ enters causing vesicular fusion. ADH and oxytocin are released and enter nearby fenestrated capillaries.

129
Q

Describe how increased serum osmolarity is affected by ADH.

A

Increased serum osmolarity is sensed by osmoreceptors in the anterior hypoth. causing APs to travel down ADH neurons. APs propagate to post. pit. causing release of ADH. ADH acts on distal tubule and coll.ducts to increase H2O absorption.

130
Q

Describe how hypovolemia is handled by the post. pit.

A

Decrease of ~10%ECF causes decrease in arterial BP. Sensed by baroreceptors of left atrium, carotid, and aortic arch. Signal sent via vagus nerve (CN X) to hypothalamus…

131
Q

What are four stimuli of ADH release?

A

Pain, nausea, nicotine, opiates

132
Q

What are three inhibitors of ADH release?

A

Ethanol, alpha-adrenergic agonists, ANP

133
Q

What are the two actions of ADH?

A

Increase water permeability.

Contraction of vascular smooth muscle.

134
Q

How does ADH increase water permeability?

A

ADH binds receptor in distal tubule and coll.duct.
Signals via Gs to A.C.
cAMP directs insertion of aquaporin-2 (AQP2) channels in luminal membrane causing water reabsorption and concentration of urine.

135
Q

How does ADH affect vascular smooth muscle?

A

ADH binds to vascular smooth muscle receptor. Signals via Gq to PLC. IP3/Ca2+ produces contraction of vasc. smooth muscle, constric. of arterioles, and increase total peripheral resistance.

136
Q

What are three conditions caused by dysregulated ADH?

A

Central diabetes insipidus.
Nephrogenic diabetes insipidus.
Syndrome of Inappropriate ADH (SIADH).

137
Q

Describe the pathophys of central diabetes insipidus.

A

Failure of post. pit. to secrete ADH. Therefore:
low circulating ADH, coll.ducts impermeable to water, large volume of concentrated urine, increased serum osmolarity, increased [Na+] serum.

138
Q

What is the treatment for central diabetes insipidus?

A

dDAVP (an ADH analogue)

139
Q

Describe the pathophys of nephrogenic diabetes insipidus.

A

Coll.duct receptors are unresponsive to ADH. Therefore:
Coll.ducts impermeable to water, large volume of concentrated urine, increased serum osmolarity, increased [Na+] serum. Notably, high serum ADH.

140
Q

What is the Tx for nephrogenic diabetes insipidus? How does it work?

A

Thiazide.
inhibits Na+ reabsorp. in early distal tubule therefore less dilute urine.
decreased GFR, less water filtered, less water excreted.
secondary volume contraction, therefore proximal solute and water reabsorp. => less water excreted.

141
Q

Describe the pathophys of SIADH.

A

Autonomous secretion of ADH (i.e. tumor), excess water reabsorption dilutes body fluids, urine is inappropriately concentrated

142
Q

What is the Tx for SIADH?

A

Demeclocycline (ADH antagonist), or water restriction.

143
Q

What is the target tissue and effect of oxytocin?

A

Stimulates contraction of myoepithelial cells of milk ducts.

144
Q

What are four stimuli of oxytocin secretion?

A

Suckling, (sight, smell, sound) of infant, cervical dilation, orgasm

145
Q

What are inhibitors of oxytocin secretion?

A

Opioids

146
Q

Describe how suckling causes oxytocin secretion in detail.

A

Nipple sensory receptors send impulse via afferent neurons to spinal cord.
Ascends spinothalamic tract to brain stem, then PVN of hypothalamus.
Within seconds oxytocin is released from post. pit.

147
Q

What conditioned responses lead to oxytocin release?

How does orgasm result in oxytocin release?

A

Sight, sound, smell of infant.

Cervical dilation during orgasm.

148
Q

What are the two actions of oxytocin?

A

Milk ejection

Uterine contraction

149
Q

Describe how oxytocin causes milk ejection.

A

Prolactin stimulates lactogenesis, milk is stored in milk ducts of mammary alveoli.
Oxytocin causes contraction of myoepithelial cells lining the milk ducts.

150
Q

What hormone used for inducing labor? What other problems does it treat?

A

Oxytocin is used to induce labor. It also can be used to reduce postpartem bleeding.

151
Q

What is the more active thyroid hormone? What is the major secreted product of the thyroid?

A

T3 is the active form, T4 is secreted and converted by target tissues to T3.

152
Q

Define the colloid of the thyroid.

A

The colloid consists of iodinated moieties including thyroid hormones (MIT, DIT, T3, T4) attached to thyroglobulins.

153
Q

Describe thyroglobulin.

A

A polysaccharide with many tyrosine residues.

154
Q

What are three unusual features of thyroid hormone synthesis?

A

Dietary iodine must be supplied.
Synthesis is partially intracellular and partially extracellular.
T4 is the major product although T3 is the more active form.

155
Q

Describe the first four steps of thyroid hormone synthesis (up to formation of MIT, DIT)

A
  1. TG synthesis on rER, transported to Golgi, fuses w/apical membrane facing lumen.
  2. Na+/I- cotransport on basal membrane
  3. Oxidation of I- to I2 by thyroid peroxidase
  4. I2 + Tyr(TG) -> MIT, DIT on TG
156
Q

What chemical inhibits thyroid peroxidase?

A

Propylthiouracil

157
Q

Describe the last four steps of thyroid hormone synthesis (from the coupling rxn to deiodination).

A
  1. 2 DITs form T4 (faster rxn), DIT+MIT forms T3 (slower).
  2. TG+(MIT, DIT, T3, T4) is endocytosed into follicular cells.
  3. TG is hydrolyzed, releasing T3, T4 which enter capillaries, MIT and DIT remain in follicular cell.
  4. MIT, DIT are deiodinated to recycle I- and Tyr residues.
158
Q

What problem in biochemical synthesis mimics dietary iodine deficiency?

A

Deficient thyroid deiodinase (less I- recycled from DIT, MIT)

159
Q

How does free and TBG-bound T3, T4 act physiologically?

A

Free T3, T4 is physiologically active.

TBG-bound T3, T4 acts as a resorvoir of thyroid hormones.

160
Q

Describe how hepatic failure affects thyroid hormone synthesis.

A

Decrease in hepatic protein synthesis leads to decreased TBG synthesis. This leads to an increase in free T3, T4 leading to a (-)fb on thyroid hormone synthesis.

161
Q

Describe how pregnancy affects thyroid hormone synthesis.

A

Increase in estrogen leads to decrease in TBG breakdown. This leads to high TBG levels, less free T3, T4, and an overall increase in thyroid hormone synthesis.

162
Q

How would pregnancy present with respect to blood levels of thyroid hormones?

A

Increased total thyroid hormone, normal free thyroid hormones.

163
Q

How is T4 converted to T3 in target tissues?

A

2 T4’s are deiodinated giving 2 T3’s and an I2

164
Q

Describe how starvation affects skeletal muscle and brain with respect to thyroid hormones.

A

Skeletal muscle 5’-deiodinase is inhibited (lower O2 consumption, decreased metabolic rate); while brain 5’-deiodinase is not affected (keeping brain metabolism normal).

165
Q

Draw the regulatory diagram of thyroid hormone release (from hypothalamus to the gland itself).

A

Draw.

166
Q

Describe where TRH is synthesized, what cell types it acts on, and what hormone is secreted.

A

PVN of the hypothalamus secrete TRH which acts on thyrotrophs of the ant.pit. stimulating tc/tl of TSH and secretion.

167
Q

How does TSH affect the thyroid gland?

A

TSH has a trophic effect on the thyroid gland as well as stimulating each step of the biosynthetic pathway of thyroid hormones.

168
Q

What is the effect of prolonged elevated TSH levels on the thyroid gland?

A

Hypertrophy and hyperplasia.

169
Q

What other molecules stimulate thyroid cells?

A

Thyroid-stimulating immunoglobulins (IgG) are the antibody to the TSH receptor.

170
Q

What ratio do target tissues form T3 and rT3 from T4? What conditions cause an increase in rT3:T3? What conditions cause a decrease?

A

55% rT3, 45% T3
Increase: pregnancy, fasting, stress, hepatic or renal failure, beta-adrenergic blocking agents
Decrease: obesity

171
Q

What six effects do thyroid hormones have?

A
  1. Increased BMR
  2. Metabolism
  3. Cardiovascular and respiratory
  4. Growth
  5. CNS
  6. ANS
172
Q

How do thyroid hormones affect BMR?

A

Increase glucose absorption in GI tract and potentiate other hormone effects on gluconeogenesis, proteolysis, and lipolysis.
Overall catabolic with respect to protein.

173
Q

How do thyroid hormones affect the cardiovascular system and respiration?

A

Increase O2 consumption causing high demand.
T3, T4 increase synthesis of beta-adrenergic receptors in the heart so heart it:
more sensitive to sympathetic NS stimuli and heart rate and contractility are increased.

174
Q

How do thyroid hormones affect growth?

A

Thyroid hormones are required for growth to normal adult stature. Act synergistically with GH and somatomedins. T3, T4 promote ossification and fusion of bone plates.

175
Q

What is one way to tell hypothyroidism from bone age?

A

Bone age < chronological age

176
Q

How do thyroid hormones affect CNS?

A

In perinatal period T3, T4 are essential for normal CNS maturation (hypothyroidism screening in infants).
In adults hypothyroidism leads to: listlessness, somnolence, impaired memory, decreased mental capacity. Hyperthyroidism leads to: hyperexcitability, hyperreflexia, irritability.

177
Q

How do thyroid hormones affect ANS?

A

Not very well understood. T3, T4 act synergistically with catecholamines on beta-adrenergic receptors; therefore one hyperthyroidism treatment is propanolol.

178
Q

Describe the pathophysiology of Graves’ disease.

A

Increased circulating levels of thyroid-stimulating Ig, these increase synthesis of T3, T4 and cause thyroid hypertrophy from the Ig (NOT from TSH!!).

179
Q

What causes of hyperthyroidism decrease TSH levels? What causes increase TSH levels?

A

Decrease: Graves’ disease, thyroid neoplasm, exogenous application of T3.
Increase: Disorder of the hypothalamus or anterior pituitary.

180
Q

How does hyperthyroidism decrease levels of TSH?

A

(-)fb from T3 acting on ant.pit.

181
Q

What is the most common cause of hypothyroidism? What are three other causes?

A

Most common thyroiditis (autoimmune destruction of the gland, or blockage of T3, T4 synthesis).
Other causes: surgical removal of thyroid (from hyperthyroidism), hypothalamic or ant.pit. failure, iodine deficiency.

182
Q

How is hypothyroidism diagnosed with respect to levels of TSH?

A 
Low T3, T4 from bloodwork.
High TSH (defect in thyroid)
Low TSH (defect in hypoth. or ant.pit.)
183
Q

What are the symptoms of hypothyroidism?

A

Low BMR, weight gain w/o change in diet, decrease in body temp (cold intolerance), decreased HR, slow movement, slurred speech, slowed mental activity, lethargy, somnolence, periorbital puffiness, constipation, hair loss, menstrual dysfunction.

184
Q

What is myxedema? What causes it?

A

Myxedema: lower leg (pretibial) or behind the eyes (exopthalmos) swelling.
Accumulation of mucopolysaccharides in interstitial fluids pulls water from capillaries into tissues leading to swelling.

185
Q

How can hypothyroidism cause goiter?

A

Low T3, T4 release (-)fb on ant.pit., leads to increase in TSH which has a trophic effect on the thyroid gland.

186
Q

Define cretinism.

A

Untreated perinatal hypothyroidism leading to irreversible growth and mental retardation.

187
Q

What is the treatment for hypothyroidism?

A

Thyroid hormone replacement therapy (T4)

188
Q

What thyroid pathologies discussed lead to goiter? Which do not?

A

Goiter: Graves’, TSH-secreting tumor, autoimmune thyroiditis, iodine deficiency
No goiter: Ingestion of T4, Ant.Pit. failure

Physiology (Costanzo) (2 decks)

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