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Nonliner (Dose Dependent Pharmacokinetics) > Thyroid Orjala > Flashcards

Thyroid Orjala Flashcards

1
Q

Which organ is the only organ that contains Iodine?

A

Thyroid

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2
Q

Why is the thyroid very well vascularized?

A

It has one of the highest rates of blood flow per gram

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3
Q

What is a Goiter?

A

Abnormal growth of the thyroid

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4
Q

What is one of the treatments for a goiter?

A

burnt seaweed

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5
Q

What is Professor Theodor Kocher of Bern known for?

A

Awarded the nobel prize in physiology of medicine 1909. Got the death rate of the thyroid gland from surgery to be less than 5 percent

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6
Q

What is the functional unit of the thyroid?

A

Thyroid follicle

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7
Q

What are follicles?

A

Single layer epithelial cells that surround an empty colloid

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8
Q

How do you make T3 from T4?

A

Deiodinization

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9
Q

What amino acid are T3 and T4 biosynthesized from?

A

L-tyrosine

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10
Q

What isomer are all natural thyroid hormones in?

A

L isomer

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11
Q

Why are thyroid hormones important?

A

Regulation of metabolism, growth, development, and maintaining homeostasis.

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12
Q

Describe the molecule of the Thyroid Hormone in terms of rotation and bonds

A

Free rotation around the phenyl either bond is restricted. Phenyl and tyrosyl rings are at at a 90 degree confirmation relative to each other

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13
Q

Why is keeping the tyrosine hormone in a lock conformation important?

A

The molecule must be in a lock confirmation to bind with the target site. It has to be 90 degrees to be effective

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14
Q

What is the oxygen bridge and is it important?

A

The role of the oxygen bridge is to keep the orientation of the iodophenyl substituents. It isn’t essential for the molecule and can be substituted by S or CH2

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15
Q

What is responsible for most of the mass of thyroid hormones?

A

iodine

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16
Q

For T3, what is the % ionized at pH 7.4?

A

10%

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17
Q

Fro T4, what is the % ionized at pH 7.4?

A

80%

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18
Q

What is the active form of the thyroid hormone?

A

T3

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19
Q

Is T3 or T4 less ionized at pH of 7.4? And what does this mean?

A

T3. It means it has more hydrogen bonding which is essential because it binds to nuclear receptors to a greater extent than T4

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20
Q

What kind of bonding does T4 have?

A

More ionic bonding than hydrogen bonding

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21
Q

What kind of hormone is T4?

A

prohormone

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22
Q

Where is T4 deiodinated?

A

Peripheral tissues and target cells such as the kidney and liver

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23
Q

Which thyroid hormone circulates the most in the body?

A

T4

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24
Q

Which thyroid hormone is more potent?

A

T3

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25
Q

What is the treatment for hypothyroidism?

A

Give T4, because it has a longer half life and is cheaper. You only need to give less dose, because its less potent than T3

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26
Q

Where are the thyroid hormone stored and secreted?

A

In the Follicle Lumen

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27
Q

Where are Thyroglobulin made?

A

ER

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28
Q

What must happen to I- before it can attach to tyrosine moeties on Thyroglobulin?

A

It must be oxidized

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29
Q

How does T3 + T4 get released into the bloodstream?

A

Proteolysis of Thyroglobulin + I

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30
Q

Where does I- get oxidized in the body?

A

The apical membrane

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31
Q

What form of Iodine is mainly found in the body?

A

I- , Iodide

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32
Q

What is all Iodine consumed and absorbed as?

A

I-

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33
Q

What is the recommended daily intake of iodine?

A

150 microgram/day for adults

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34
Q

What food contains Iodine?

A

Cereals, fish, eggs, bread, meat and poultry

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35
Q

What channel help transport I- into the thyroid follicular cell?

A

Na+/I- symporter. 2 Na+ and 1 I- goes in. Does not require energy

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36
Q

Is Na+ higher inside or outside the cell?

A

Outside

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37
Q

What is the net charge into thyroid follicular cell?

A

Negative

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38
Q

Is I- concentration in the blood high or low?

A

low

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39
Q

Where does transport of I- occur?

A

Basal membrane of follicular cells

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40
Q

What can the transport of I- across the basal membrane be inhibited by?

A

Perchlorate (ClO4-) and Thiocynate (SCN-)

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41
Q

What hormone is the NAS (Na+, I- symporter) regulated by

A

TSH

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42
Q

What are the steps for the production and secretion of T3 and T4 hormones

A
  1. I- comes into the cell via NAS
  2. I- gets oxidized at the follicle colloid
  3. I- attaches to TYR residues (Iodination) TPO
  4. Conjugation
  5. Endocytosis of thyroglobulin into the cell
  6. Proteolysis of hormone to release T3 +T4
43
Q

Where does I- get oxidized and by what?

A

TPO at the apical membrane

44
Q

What enzyme catalyzes coupling reaction?

45
Q

What reaction is a target for antithyroid drugs and high dose Iodine treatment

A

Coupling reaction

46
Q

What happens when there is an increase of TSH

A
  1. turn on endocytosis to release T3+ T4
  2. Increase release of T4 + T3
  3. Increase Iodide uptake
47
Q

What proteins doe thyroid hormones bind to?

A
  1. TBG
  2. Transthyretin
  3. Albumin
48
Q

How is T3 different than T4?

A
  1. Lower binding
  2. Shorter half life
  3. rapid action
  4. Lower binding affinity
49
Q

How does T4 convert to T3?

A

Idothyronin deiodinases (D) . Removes an I from the outer ring

50
Q

What can the conversion of T4 to T3 be inhibited by?

A

Propylthiouracil. An anti-thyroid drug to treat hypertension

51
Q

What is the function of rT3?

A

It his no function. It is when D removes I from the inner ring.

52
Q

What confirmation does T3 have to be in to be active?

A

Skewed confirmation (Lock confirmation). This will allow it to bind to the receptor

53
Q

What is the Anti-skewed conformation?

A

rT3. D remove the I- from the inner ring. Not lock and there is free rotation. Unable to bind to receptor

54
Q

What conformation must T3 be to interact with a receptor

A

skewed confirmation

55
Q

What is Type 1 deiodination

A

Converts T3 –> T4 for circulation. Present in liver, kidney and thyroid

56
Q

What type of deiodination can PTU inhibit?

A

Type I. It lowers T3 circulation

57
Q

What is Type II deionination?

A

Present in target cells

58
Q

How is Type I different from Type II?

A

Converts T4 to T3 but lowers the amount of T3 circulating

59
Q

What is Type III?

A

Present in almost all tissues. The bodies way to get rid of T3 to make it to rT3 or T2.

60
Q

What is Type II 5D regulated by?

A

Ubitquitination

61
Q

Why would you want to regulate Type II 5D

A

Don’t want too much T3

62
Q

Describe regulation of Type II 5D by ubiquitination

A

5D, removes I to expose lysine group. This will let uniquitin to recognize lysine and attach to it. Marking it for the proteasome to be degraded. Goes to the Blood then the liver and kidney.

63
Q

What is the main way for T3 to be excreted

A

inner ring deioniation and conjugation

64
Q

How does conjugation metabolize T3?

A

Increases water solubility for excretion in urine or bile

65
Q

Describe the regulation of thyroid hormone synthesis

A

TRH–>TSH–> TH

66
Q

What AA are attached to TRH?

A

Glu, His, Pro

67
Q

Why are there AA attached to TRH?

A
  1. To get it into circulations
  2. Prevent them from getting rapidly degraded
  3. Inhibit amino peptidase because there is no carboxyl group. It does not get cleaved
  4. Increases half life
68
Q

Where are TRH produced

A

hypothalamus

69
Q

Describe the process of turing on the transcription of TSH

A
  1. TRH binds to TRHR in the pituitary gland
  2. Activation of phospholipase C to release Ca2+
  3. Ca2+ is transported to the nucleus and turns on the transcription of TSH
70
Q

What is TSH down regulated by

A

TH gives negative feedback

71
Q

What is TSH

A
  1. Thyroid stimulation hormones
  2. Glycoprotein
  3. Has two subunits alpha and beta
  4. GPCR
72
Q

What is TSHR

A

Thyrotropin receptor
7 transmembrane domain
intracellularly coupled to GPCR

73
Q

Via the TSH how is TH made and released

A
  1. TSH binds to TSHR
  2. GDP to GTP
  3. Activates two pathwyas
    - main, adenlayte cyanate
    - Phospholipase C
74
Q

Where does T4 convert to T3?

A

target cells

75
Q

Wh y is T3 more reactive?

A

Hydrogen Bonding

76
Q

What are the forms of THR that exist?

A

Alpha and Beta

77
Q

How are the alpha and beta form of THR distinguished?

A
  1. Sequence
  2. Chromosomal location
  3. Different subforms
78
Q

What is homodimerization of the THr

79
Q

Where do THR bind on DNA?

A

Binds to the TRE on DNA. THR has a dna binding domain and an ligand binding domain

80
Q

What is palindrome

A

same sequence when you read in different directions

81
Q

What is direct repeat

A

repetition of dna fragments with bases in between

82
Q

When HDAC is present can dna be transcribed?

83
Q

What activates HDAC?

A

When there is no T3, which recruits corepressors and activates HDAC. The histones are deacetylated

84
Q

What does HAC do when T3 is present?

A

It unwinds the histones so you can a change to transcribe. ALSO recruits rna polymerase which is a transcription enzyme

85
Q

Which thyroid disorder is the most common?

A

Hypothyroidism

86
Q

What are the causes of hypothyroidism?

A

Iodine deficiency

t3+t4 not being produced

87
Q

What are the treatment for hypothyroidism?

A

thyroid extract + T4 (Levothyroxine)

88
Q

What is Hashimoto’s Disease?

A

an autoimmune disease that attacks the thyroid.

no thyroid hormone

89
Q

What is hyperthyroidism?

A

Over production of thyroid hormone

90
Q

What are the treatments for Hyperthyroidism?

A
  1. Surgery
  2. I 131 radiation
  3. Block thyroid production
    - complex anions
    - PTU + MMI
91
Q

What is Graves disease?

A

hyperthyroidism. Over productions of TH. No TH negative feedback

92
Q

Describe the antibodies and the TSH receptor in terms with graves disease

A

body develops agonist antibodies for over productions of TH.

93
Q

What two ways do Beta particles kill cells?

A
  1. Direct: breaks double C=C bind which splits the back bone of DNA that blocks DNA synthesis.
  2. Indirect, creates free radicals. OH form water. This creates oxidative damage to the DNA and other cellular targets.
94
Q

What do you do if you have radiation induced thyroid cancer?

A

Administer KIO3 (potassium iodate) or KI (potassium iodide). They will compete for the NAI pump with the radioactive I. You pee the excess I out.

95
Q

What is use to block thyroid hormone production?

A 
Iodine
-lugol's solution 
Complex Anions (compete with I for NIS)
-ClO4
-SCN
-TcO4
96
Q

How does high concentration of iodine block thyroid hormone production?

A

Inhibit NIS
inhibit TPO
inhibit TH release

97
Q

What is the drug class of PTU?

A

Thioamides

98
Q

What is the mechanism of action of thioamides and PTU?

A

Inhibits Type I deionitation
Inhibits TPO
prevents I from attaching to tyrosine residues and coupling reactions
Local affect. Traps it inside the thyroid gland. Only inhibits the new synthesis of TH not the stored ones.

99
Q

What is required for PTU/ Thioamides to have the mechanism of action it has?

A
  • AT C2 be thioketo or Thioenol

- propyl at C6

100
Q

What are the properties of PTU

A

Rapidly absorbed
Short plasma half life (1.5)
acts locally by being trapped
glucoronide major metabolite

101
Q

What is the MAO of methimazole (MMI)

A

Inhibits TPO only

102
Q

What is the differences between PTU and MMI?

A

MMI is more potent

103
Q

What is carbimazole?

A

Prodrug for MMI. Makes MMI tastes better

also decrease the rate of release for MMI

Nonliner (Dose Dependent Pharmacokinetics) (4 decks)

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