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Thyroid Gland Physiology Flashcards

1
Q

What are the hormones produced by the thyroid gland?

A

Pro-hormone Tetraiodothyronin (T4)

Tri-iodine-thyronine (T3)

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2
Q

What is the functional unit of the thyroid gland?

What odes it do?

A

Thyroid follicle

Synthesized thyroid hormones

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3
Q

How is the thyroid follicle organized?

A

Surrounded by single layer of epithelial cells that sit on a basal lamina

Follicular lumen - filled w/ colloid

Parafollicular cells

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4
Q

What will change the size and amount of colloid?

A

Activity

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5
Q

What do parafollicular cells secrete ?

When?

A

Calcitonin

When ca is high

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6
Q

What is contained in Colloid?

A

Newly synthesized thyroid hormones attached to TGB

Iodinated tyrosine of TBG

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7
Q

Where is iodine stored in thyroid gland?

How much? Allows for?

A

Stored in colloid as iodinated TGB

8000 ug total (600 ug in T4 and T3)

Allows to reservoir that could last body 2-3 mos. if iodine becomes deficient

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8
Q

How much hromone will the thyroid follicle cell secrete / day?

A

60 ug

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9
Q

What is T3 and T4 collectively called?

A

Iodothyronines

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10
Q

What is thyroxine?

What is Tri-iodothyronine?

A

T4 = 2 molecules of DIT

T3 = 1 DIT; 1 MIT

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11
Q

What is the major secretory product of the Thyroid follicle?

A

T4

T4 produced 10x more than T3

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12
Q

How is T4 converted to T3?

A

De-iodinated type 1 and type 2

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13
Q

How is T4 converted to Reverse T3 ?

What is different about reverse T3 from t3?

A

De-iodinase type 3

Reverse T3 = inactive

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14
Q

What is the function of peripherally converting T4 to T3?

A

Provides circulating T3 for uptake by other tissue where T3 supply is low

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15
Q

When would we want to reduce conversion of T4 —> T3?

A

Fasting

Medical & surgical stress

Catabolic disease

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16
Q

What can a deficiency in de-iodinated mimic?

Causing?

A

Mimics dietary iodine deficiency because MIT/DIT is not being recycled

Goiter

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17
Q

What is the driving force for the iodide trap?

A

Na-K+ pumps

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18
Q

What is the pathway for the synthesis of thyroid hormone?

A

Tyrosine —> Thyroglobulin (TG)

Thru rough Er, golgi out apical side into colloid

Iodide take up by trap — thru pendrin pump to apical membrane

Iodide —thyroid peroxidase (TPO)—> Iodine

iodine + TG —TPO—> iodinated TGB
(has MIT and DIT attached)

Iodinated TGB —TPO—> TGB w/ T3/T4
(Stored as colloid)

TSH stimulation —> TG w/ T3/T4 pinocytosed thru apical membrane

TG w/ T3/T4 —protease—> T3/T4 out basilar membrane

TG w/ MIT/DIT —intrathyroidal Deiodinase —> free TG and free iodide

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19
Q

What will be favored when iodide availability is restricted?

A

formation of T3

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20
Q

What is pendrin?

A

Chloride - iodide pump located on apical membrane of thyroid follicular cells

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21
Q

What is pendred syndrome?

Presents w/?

A

Mutation in pendrin gene (SLC26A4)

Causes defects in transport across apical membrane

Sensorineural hearing loss (affects cochlea)
HYPO-thyroidism w/ goiter

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22
Q

What can inhibit the uptake of iodide?

A

Perchlorate, thiocynate

Competes w/ NIS iodide trap to bind iodide

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23
Q

What steps in the synthesis of thyroid hormones will PTU affect?

A

PTU will inhibit Thyroid Peroxidase (TPO)

Blocking organification

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24
Q

What is organification in the synthesis of thyroid hormone pathway?

A

Thyroglobulin iodination

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25
Q

What is the Wolff-chaikoff effect?

A

Increased iodide will cause decreased T3/T4 production

Bc organification is inhibited

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26
Q

How can you assess the activity of the thyroid gland?

A

Asses by radioactive iodine uptake

If activity is high, then low amount of T3 resin uptake is seen

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27
Q

How are thyroid hormones transported in blood?

A

Mostly bound to plasma proteins (99%)

Some free (1%)

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28
Q

What is the equilibrium of thyroid hormones found in blood?

A

There is an equilibrium bw/

Free t3/t4 and bound T4/T3

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29
Q

What proteins are T3and T4 bound to in blood?

A

Thyroxine-binding globulin (TBG)-70%

Transthryretin

Albumin

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30
Q

Where is thyroxine-binding globulin synthesized?

What does it have a higher affinity for?

A

In liver

Higher affinity for T4

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31
Q

What is the half life of T4/T3?

A

T4 = 6 days

T3 = 1 day

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32
Q

How will levels of T4 and T3 resin uptake change in

Hyperthyroidism?

A

Increase in T4

High T3 resin reuptake bc no open spots on TBG

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33
Q

How will levels of T4 and T3 resin uptake change in

HYPOthyroidism?

A

Low T4

Low T3 resin reuptaken (bc more was able to bind TBG)

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34
Q

How will levels of T4 and T3 resin uptake change in

HIGH TBG?

A

Increase T4

Low levels of T3 resin reuptaken (bc so much TBG it can bind to)

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35
Q

How will levels of T4 and T3 resin uptake change in

LOW TBG?

A

low T4 (not enough TBG for it to bind to)

High T3 resin reuptaken (bc not enough TBG for it to bind to)

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36
Q

How will levels of T4 and T3 resin uptake change in

Hepatic failure?

A

Low TBG (bc synthesized in liver)

High T3 resin reuptaken (bc not enough TBG for it to bind to)

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37
Q

How will levels of T4 and T3 resin uptake change in

Pregnancy?

A

High estrogen —> high TBG

LOW T3 resin reuptaken
bc so much TBG for it to bind to

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38
Q

How does hepatic failure and its resultant change in TBG level alter reaction of free thyroid hormones?

A

Will cause transient increase in level of FREE t3,t4

Followed by INHIBITION of SYNTHESIS of T3,T4 (negative feedback)

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39
Q

How does pregnancy and its resultant change in TBG level (increased) alter reaction of free thyroid hormones?

What is the term for this clinically?

A

Increase in bound T3, T4
Transient decrease in free T3, T4 (causes increase in synthesis and secretion of T3, T4)

Increase in total levels of T3 and T4 but now free and bound are back in equilibrium
==clinically EUthyroid

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40
Q

What hypothalamic hormones will be secreted in the HP-thyroid axis?

A

Thyrotropin releasing hormone (TRH)

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41
Q

What pituitary hormones will be secreted in the HP-Thyroid axis?

A

Thyroid stimulating hormone (TSH)

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42
Q

What regulates the HP-Thyroid axis?

A

T3 acts back on pituitary and hypothalmus to inhibit

Long loop negative feedback

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43
Q

What is the role of thyroid stimulating hormone?

A

◦ Regulate growth of Thryoid gland
‣ Trophic effect
◦ secretion of thyroid hormones

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44
Q

What is TSH regulated by?

A

TRH and T3

45
Q

What is the second messenger system used by TSH?

A

Adenylate cyclase (cAMP)

46
Q

What characterizes the release of TSH?

A

Constant

Unlike GH which was pulsatile

47
Q

What are the factors that will stimulate thyroid hormone secretion?

A

Thyroid stimulating hormone

Thyroid-stimulating immunoglobulins

Increased TBG levels in pregnancy

48
Q

What are the factors that will inhibit thyroid hormone secretion?

A 
Iodide deficiency
Deiodinase deficiency
Excessive I- intake (Wolff Chaikoff effect) 
Perchlorate, thiocynate 
			◦ Inhibits Na+/I- cotrnasport 
            (= no iodide)
Decreased TBG levels
				◦ Liver disease 
Free T3
49
Q

What is the function of Thryoid hormones?

A

Acts at Thryoid hormone receptor at DNA and influences gene transcription

Thus influences synthesis of proteins

50
Q

How does TSH change during primary HYPOthyroidism?

A

Increased levels (no t3 to act back)

51
Q

How do TSH levels change during secondary/tertiary Hypothyroidism?

A

Decreased levels

52
Q

How do TSH levels change during primary HYPERthyroidism?

A

Decreased (lots of T3 to act back on it)

53
Q

How do TSH levels change during secondary/tertiary hyperthyroidism?

A

Increased TSH levels

Will see goiter

54
Q

What are thyroid stimulating immunoglobulins?

A

Stimulatory factors that will stimulate TSH R. In absence of TSH hormone

55
Q

What effect will thyroid stimulating immunoglobulins have on the HP-Thyroid axis?

A

Will increase levels of Thyroid hormones = HYPER thyroidism

Decrease TSH levels

Could cause Graves’ disease

56
Q

What charaterizes HYPER thyroidism?

A
  • Increased BMR
    * Weight loss
    * Negative nitrogen balance
    * increased heat production
    * Sweating
    * Increased cardiac output
    * Displeasure
    * Tremor, msucle weakness
    * Exophthalmos
    * Goiter (depends)
57
Q

What proteins will thyroid hormones produce?

A 
◦ Proteins: 
		‣ Na-K ATPase
		‣ Transport proteins
		‣ B1-adrenergic receptors
		‣ Lysosomal enzymes
		‣ Proteolytic proteins
		‣ Structural proteins
◦ Proteins in Cardiac Msucle cells
		‣ Mysosin 
		‣ B-1 adrenergic receptors
		‣ Ca ATPase
◦ Proteins in Liver and Adipose tissue
		‣ Key metabolic enzyme
58
Q

What are the functions of thyroid hormones?

A 
‣ Growth 
‣ CNS maturation
‣ Increase Basal Metabolic Rate
‣ Increase Metabolsim 
‣ Increase Cardiac output
	• Due to upregulation of B1 adrenergic Rs.
59
Q

How do thyroid hormones increase Basal Metabolic Rate (BMR)?

A

◦ Increase in Na-K ATPase —> increases Metabolic rate

‣ Leads to increased O2 consumption and heat production

60
Q

What characterizes the increase in BMR produced by a single dose of T4?

A

Takes several hours to occur

But has long lasting effect (>30 days)

61
Q

How does thyroid hormones increase lipid metabolism?

Effect on plasma concentration of cholesterol and triglycerides?

A

‣ Stimulates fat mobilization —> increases [FAs] in plasma
‣ Enhanced oxidation of FA

‣ LOW plasma concentration of cholesterol and triglycerides

62
Q

What conversion needs thyroid hormones?

A

Carotene —> Vitamin A

63
Q

How does thyroid hormones increase carbohydrate metabolism?

A

‣ Increase in gluconeogenesis and glycogenolysis
• Generates free glucose

‣ enhances insulin dependent entry of glucose into cell

64
Q

How do thyroid hormones act on the cardiovascular system?

How?

A

Increase cardiac output

Stimulates Cardiac Beta1 adrenergic receptors

Increases number of B1 receptors (=more sensitive to stimulation by sympathetic nervous system) (increased cardiac chronotropy and ionotropy - speed and force)

65
Q

How do thyroid hormones increase growth?

A

◦ Act w/ Growth hromone and Somatomedins to promote bone formation

66
Q

How does Thyroid hormone cause CNS maturation?

A

Increases development of synapses, dendritic brnach in ad myelination

67
Q

What happens if thyroid hormones are deificient during perinatal period?

A

‣ Abnormal development of synapses
‣ Decreased dendritic branching and myelination

Irreversible neural changes that could lead to Congenital hypothyroidism if not treated after birth (cretinism)

68
Q

What are the steps from T3 —> increased cardiac output?

A

T3–> increased tissue thermogenesis

Heat —> decreases systemic vascular resistance

Decr. SVR —> decr. BP —> decr. After load

Decr. After load —> increase speed and force of cardio —> increased cardiac output

Decr. BP—>Renin-angio-aldo axis —> increases preload—> increased cardiac output

69
Q

How does HYPOthyroidism affect metabolism?

A

Low BMR
Weight gain
Cold intolerance
High blood cholesterol concentration
‣ Bc fat is not being mobilized by thyroid hormones
blindness & yellowing of skin
‣ Bc carotene is not being converted to vitamin A (need thyroid hormones for this)

70
Q

How does hypothyroidism affect bone?

A

‣ Stunted growth

• Bc THs no longer working with GH to promote bone formation

71
Q

How does HYPOthyroidism affect the CNS?

A 
‣ Cretinism 
		‣ Listlessness
		‣ Slowed movemnt
		‣ Somnolence
		‣ Impaired memroy
		‣ Decreased mental capacity
72
Q

How does HYPOthyroidism affect the skin?

A

Myxedema

73
Q

How does HYPO-thyroidism affect the CV system?

A

‣ Bradycardia
‣ Decreased contractility
‣ Decreased cardiac output
‣ Heart failure

74
Q

How does HYPO-thyroidism affect the intestine?

A

Constipation

75
Q

How does HYPER-thyroidism affect metabolism?

A

‣ High BMR
• More thyroid hormones ==> increased Na-K ATPase synthesis ==> increased metabolic rate
‣ Heat intolerance
‣ Weight loss

76
Q

How does HYPER-thyroidism affect bones?

A

Osteoporosis

77
Q

How does HYPER-thyroidism affect the CNS?

A

‣ Agitation
‣ Anxiety
‣ Difficulty concentrating
‣ Hyper reflexia!!!!!!!!!

78
Q

How does HYPERthyroidism affect skin?

A

Sweating

79
Q

How does HYPERthyroidsim affect the CV system?

A

‣ Tachycardia
‣ Atrial fibrillation
‣ Palpitation
‣ High output heart failure

80
Q

How does HYPERthryoidisim affect the GI system?

A

Diarrhea

81
Q

What is congenital hypothyroidism (Cretinism)?

A

deficient Thyroid hormones during perinatal period
◦ Have major effect on CNS
◦ Mental and physical deficits

82
Q

What could cause congenital hypothyroidism (Cretinism)

A

‣ Iodide deficiency
‣ Maternal intake of anti-thyroid medication
‣ Impaired development of thyroid gland
‣ Inherent deficit in the synthesis of thyroid hormones

83
Q

What are the SXs associated with Congenital HYPOthyroidism (Cretinism) ?

A 
‣ Feeding problems
		‣ Respiratory difficulty
		‣ Protruding tongue
		‣ Curse facial features
		‣ Growth retardation
		‣ Mental retardation
		‣ Jaundice
		‣ Dry skin
		‣ Hypotonia
84
Q

What is primary HYPERthyroidism also called?

A

Graves’ disease

85
Q

What can cause SEcondary hyperthyroidism?

A

TSH-secreting PITUITARY tumor

86
Q

What is the treatment for hyperthyroidism?

A

Thyroidectomy

Propylthiouacil (PTU) - inhbits TPO

87
Q

What is Graves’ disease?

Caused by ?

A

Primary HYPERthyroidism

Stimulation of TSH R. By thyroid stimulating IMMUNOGLOBULINS

88
Q

How will TSH levels appear in primary hyperthyroidism?

A

Low bc high T3 feedbacks and inhibits it

89
Q

What is a characteristic sign of Grave’s disease?

Caused by?

A

‣ Exophthalmos
• Abnormal protrusion of eyeball and periorbital edema

◦ Due to recognition by anti-TSH abs within orbital cells

90
Q

How will levels of TSH, TSI and T3,T4 present in Graves’ disease?

A

T3,T4 = high

Thyroid stimulating immunoglobulins = high

TSH = low

91
Q

Will a Goiter be present in Graves’ disease?

A

Yes

Bc TSI is still over stimulating the thyroid gland

(But TSH is low)

92
Q

What is primary HYPOthyroidism?

A

Low T3,T4 secreted by thyroid gland

93
Q

What is Hashimoto thyroiditis?

What will this present with?

A

Common cause of HYPOthyroidism in iodine sufficient parts of world

THs synthetics impaired by TG or TPO ABs

Will have low T3,t4 but HIGH TSH

=goiter

94
Q

What could cause PRIMARY HYPOthyroidism?

A

Gland destruction via surgery, irradiation, autoimmune diseases, idiopathic atrophy

Hashimoto’s thyroiditis

Iodine deficiency, enzyme defects

Transient low t3,t4 bc of postpartum, thyroiditis, therapeutic radiation

Agenesis of gland

95
Q

What can cause secondary/tertiary HYPOthyroidism?

A

Hypothalamic disease

Pituitary disease (Sheehan syndrome)

Resistance to Thyroid hormones

96
Q

How can you treat HYPOthyroidism?

A

Replacement doses of T4

Younger patients need more bc they have faster metabolism of it and it has shorter half life

97
Q

What are the risks of administering T4 to women beyond menopause?

A

Can cause osteoporosis

98
Q

What are the sympoms of HYPOthyroidsim?

A

Fatigue
Weight gain
Cold intolerance

99
Q

Will grave’s disease have goiter?

Due to what?

A

Yes

Due to overstimulation of thyroid gland by Thyroid Stimulating Immunoglobulins

100
Q

Will TSH secreting tumors present with a goiter?

Why?

A

Yes

Bc TSH is constantly stimulating the thyroid gland

101
Q

Will ingestion of T4 cause a goiter?

Why?

A

No

Does not cause growth of thyroid gland

102
Q

What is another name for Hashimoto’s thyroiditis?

A

Autoimmune thyroiditis

103
Q

Will Hashimoto’s thyroiditis cause a goiter?

Why?

A

Yes

Bc thyroid hormones are not being synthesized due to TG or TPO abs

But low levels of T3,T4 cause HIGH TSH
—> Goiter

104
Q

Will TSH deficiency cause a goiter?

A

No

Idiots

105
Q

Will iodide deficiency present with a goiter?

Why?

A

Yes

Bc no iodide = no T3, T4

Elevates TSH —> overstimulates gland —>

GOITER

106
Q

When could a patient with iodide deficiency present as asymptomatic and euthyroid?

A

If gland can maintain normal blood levels of thyroid hormones

(Pregnancy)

107
Q

When could Iodide deficiency cause a patient to be hypothyroidic?

A

If gland cannot maintain normal levels of thyroid hormones

108
Q

What is Sheehan syndrome?

Sxs?

Goiter?

A

HYPO-pituitarism due to necrosis of pituitary gland

Seen after pregnancy 
		• Agalactorrhea 
		• Difficulties in lactation 
		• Amenorrhea common
		• Hypothyroidism sometimes present

NO goiter bc pituitary is damaged = no TSH to stimulate thyroid gland

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