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Physiology 3 And Physiology For GE > Thyroid gland > Flashcards

Thyroid gland Flashcards

1
Q

Where is the thyroid gland located

A

Anterior part of the neck just below the larynx

It straddles the oesophagus

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2
Q

The two lobes of the thyroid gland are joined by

A

Ithmus

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3
Q

Lumen of follicles in the thyroid gland are surrounded by

A

Follicular cells

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4
Q

What produces calcitonin

A

The para follicular cells which are between the follicular cells

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5
Q

The lumen of the follicular cells contains

A

Colloid which contains thyroglobulins
Thyroglobulins are proteins which contains tyrosine.
Iodine attaches to the thyroglobulins which contains tyrosine to form the thyroid hormone( T4 - thyroxine and T3 -triiodothyronine collectively is the thyroid hormone)

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6
Q

Thyroglobulin is what kind of amino acid

A

Non essential amino acid

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7
Q

Even tho thyroglobulins is rich in the lumen it is still synthesized by the TSH(thyroid stimulating command) true or false

A

True

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8
Q

One thyroglobulin contains how many tyrosine

A

70

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9
Q

How is thyroid hormone synthesized and secreted

A

➢ Iodide trapping-Iodide( iodine in the blood is iodide)gets to the follicular cells by secondary active transport cuz as sodium is moving it provides iodide with energy to move into the follicular cells from the blood vessel
➢ Diffusion-Iodide moves into the lumen using simple diffusion
➢ Iodide Oxidation-Thyroid peroxidase which is located at the luminal border converts iodide to its active form. Thyroid peroxidase attaches the iodide to the tyrosine
➢organification or iodination of Thyroglobulin- when one of it attaches to the iodide it becomes mono iodothyroxine (MIT) and if two attaches to the iodide it becomes diiodothyroxine (DIT)
➢ Storage of Thyroglobulin- the thyroid hormones are stored on thyroglobulin in the lumen.
➢ Release of thyroid hormone-Iodinated thyroglobulins is engulfed and taken into the cell. Lysosomes in the cell contains protease which breaks off the MITS. Which are not coupled or not needed. Iodinase removes the iOdide from the tyrosine and both are recycled. T3 and T4 are lipid soluble so they diffuse into the blood

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10
Q

Can MIt couple with MIT?

A

No

MIT can only couple with DIt (Tri or T3) DIt can couple with DIT(tetra T4 thyroid hormone)

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11
Q

Iodide can only attach to the thyroglobulin if its in it’s active state true or false

A

True

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12
Q

What is BMR

A

Baseline Metabolism rate is the energy used by a cell when it’s at rest

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13
Q

Which hormone increases the protease activity

A

TSH

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14
Q

T3 and T4 are attached to the thyroid binding protein and albumin and circulated thru the blooodstream but not all are attached. Some are free. More of T3 are free or unbound. True or false

A

True

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15
Q

Why are T3 more potent although more of T4 is formed

A

Cuz more of the T3 is free than the T4

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16
Q

Thyroxine contains how many iodine atoms

A

Four

17
Q

What is Generally formed from T4 by cleaving

an iodine molecule

A

T3

18
Q

Thyroid hormones are stored in the form thyroglobulin in the follicles true or false

A

True and it’s for 2-3 months

19
Q

Concentration of T3 and T4

A

Concentration
●T4: T3 = 93% : 7%
●T4  T3
●Activity T3 = 5 T4

Concentration in plasma
●T3: 1.2 ~3.4 nmol/L
●T4: 85 ~142 nmol/L

20
Q

What’s timulates the release of thyroid hormones

A

The hypothalamus is stimulated by the TRH to stimulate the pituitary gland to produce TSH to act on the thyroid gland to produce thyroid hormones

21
Q

How are thyroid hormones transported in the blood

A

●Bound to plasma carrier proteins: T4 (slow release)
●Thyroxine-binding globulin ( TBG ): mainly
●Thyroxine-binding prealbumin
●Albumin
●Free: T3

22
Q

How does the thyroid hormones increase metabolic actions

A

Effects on metabolism

●Carbohydrate metabolism:  Uptake of glucose
● Glycolysis
● Gluconeogenesis
● Rate absorption of glucose
● Insulin secretion
●Fat metabolism: Lipid mobilization from the fat tissue
●Free fatty acid concentration in the plasma
●Oxidation of free fatty acid
●Protein metabolism: Protein synthesis (normal)
● Protein catabolism: so people with hyperthyroidism lose muscle tissue cuz the proteins are being broken down very fast since proteins are mostly found in the muscles it leads to loss of muscle tissues

●Elevation base metabolic rate: Calorigenic Action
 basal metabolic rate (BMR)
60 ~100%
(T3 increases the oxygen consumption and heat production in the body )

So if there’s hyperthyroidism you become heat intolerant cuz there’s too much heat being produced in your body
(BMR)

23
Q

How does the thyroid hormone affect growth

A

● Skeletal growth
●Growth and development of brain (fetus and baby)
●Tadpole  frog
●Cretinism:
young children with congenital thyroid deficiency

22
Effect on growth
●Physical Growth
  (Skeletal, Muscular and Visceral Growth)
●Mental Growth
●Thyroid hormone and growth
24
Q

Effect of thyroid on cardiovascular system

A

 Blood flow and cardiac output
● HR
● Heart strength
● Normal mean arterial pressure

●Thyroid hormones increases heart rate, cardiac contractility and cardiac output. They also promote vasodilation, which leads to enhanced blood flow to many organs.

25
Q

Effect of thyroid hormones on permissive actions

A

Thyroid hormone has permissive effects on catecholamines
●Upregulates beta-adrenergic receptors in many tissues (heart and nervous system)
●Potentiate (↑ the effect of being synergistic) actions of catecholamines
(i.e. hyperthyroid resemble symptoms of hypersecretion of E/NE)

26
Q

Effect of thyroid hormones on nervous system

A

Excitatory effects on the CNS
Too little thyroid hormone, the individual tends to feel mentally sluggish, while too much induces anxiety and nervousness.
e.g. Effect on sleep
●Constant tiredness (  T3,T4)
●Difficult to sleep (  T3,T4)
4. Effects of Thyroid Hormones on Specific Systems

26
●Effect on the function of the muscles
●Weakened (  T3,T4)
●Fine muscle tremor (  T3,T4)
●Sluggish(  T3,T4)
● Secretion of other endocrine glands
● Respiration
27
Q

How is thyroid hormone release regulated

A

1.Hypothalamus-adenohypophysis-thyroid axis
TRH — TSH — T3 、T4
Negative feedback- a.short feedback( TSH tells hypo that secretion is too much so stop) b. Long feedback(the thyroid hormones tell pituitary to stop and pituitary tells hypo to stop)
2.Auto-regulation
3.Iodide trapping mechanism

28
Q

Give three charact of TRH

A

Produced by Hypothalamus
●Downregulated by T4, T3
●Travels through portal venous system to adenohypophysis or pituitary Stimulates TSH formation

29
Q

Give three charact of TSH

A 
Produced by Adenohypophysis
●Upregulated by TRH
●Downregulated by T4, T3
●Stimulates several processes
●Iodine uptake: if iodine is low in the thyroid gland then T3 and T4 will also be low and will cause the TSH to increase and the thyroid gland to also increase 
●Growth of thyroid gland
30
Q

Name three thyroid disorders

A 
Grave’s disease- immunoglobulins behave likeTSH and bind to thyroid gland so thyroid hormones are produced . In this case there’ll be high thyroid hormone levels but low TSH since it’s not TSH that is producing the hormones but the immunoglobulins that are behaving like TSH. 
Cretinism
Goiter
Bulging eyes
Pseudo clubbing of fingers
31
Q

What is Graves’ disease or Basedow’s disease

A

An immune system disorder of the butterfly-shaped gland in the throat (thyroid).
The thyroid overproduces hormones. The condition is more common in women under the age of 40.

32
Q

Name five symptoms of Graves’ disease

A

Symptoms include anxiety, hand tremor, heat sensitivity, weight loss, puffy eyes and enlarged thyroid.
People may experience:
Whole body: excess sweating, fatigue, heat intolerance, or high blood pressure
Heart: fast heart rate, irregular heart rate, or palpitations
Mood: anxiety or nervousness
Eyes: abnormal protrusion of eyes or puffy eyes
Also common: alopecia, diarrhoea, goiter, hand tremor, insomnia, irritability, muscle weakness, no menses, thyroid dermopathy, or weight loss

33
Q

Treatment for Graves’ disease

A 
Radioactive iodine therapy. With this therapy, you take radioactive iodine (radioiodine) by mouth. ... 
Anti-thyroid medications. ... 
Beta blockers. ... 
Surgery. ... 
Treating Graves' ophthalmopathy. ...
34
Q

How to diagnose Graves’ disease

A

Blood tests. Blood tests can help your doctor determine your levels of thyroid-stimulating hormone (TSH) — the pituitary hormone that normally stimulates the thyroid gland — and your levels of thyroid hormones. People with Graves’ disease usually have lower than normal levels of TSH and higher levels of thyroid hormone
Your doctor may order another lab test to measure the levels of the antibody known to cause Graves’ disease. It’s usually not needed to diagnose the disease, but results that don’t show antibodies might suggest another cause of hyperthyroidism.

Radioactive iodine uptake. Your body needs iodine to make thyroid hormones. By giving you a small amount of radioactive iodine and later measuring the amount of it in your thyroid gland with a specialized scanning camera, your doctor can determine the rate at which your thyroid gland takes up iodine. The amount of radioactive iodine taken up by the thyroid gland helps determine if Graves’ disease or another condition is the cause of the hyperthyroidism. This test may be combined with a radioactive iodine scan to show a visual image of the uptake pattern.

Ultrasound. Ultrasound uses high-frequency sound waves to produce images of structures inside the body. It can show if the thyroid gland is enlarged. It’s most useful in people who can’t undergo radioactive iodine uptake, such as pregnant women.
Imaging tests. If the diagnosis of Graves’ disease isn’t clear from a clinical assessment, your doctor may order special imaging tests, such as a CT scan or MRI.

35
Q

What antibody is associated with Graves’ disease

A

The antibody associated with Graves’ disease — thyrotropin receptor antibody (TRAb) — acts like the regulatory pituitary hormone. That means that TRAb overrides the normal regulation of the thyroid, causing an overproduction of thyroid hormones (hyperthyroidism).

Thyrotropin-receptor antibody is an autoantibody to the thyroid cell receptor for thyroid-stimulating hormone. I

36
Q

What is the mechanism of Graves’ disease

A

autoimmune disease characterized by hyperthyroidism due to circulating autoantibodies. Thyroid-stimulating immunoglobulins (TSIs) bind to and activate thyrotropin receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone. which the body produces antibodies that are specific to a self-protein: the receptor for thyroid-stimulating hormone. (Antibodies to thyroglobulin and to the thyroid hormones T3 and T4 may also be produced.)

Graves’ disease is an autoimmune disease in which T lymphocytes become sensitized to antigens within the thyroid gland and stimulate B lymphocytes to synthesize antibodies, specifically thyrotropin receptor antibody (TRAb). These bind to the surface of thyroid cells.

37
Q

Difference between hyperthyroidism and thyrotoxicosis

A

Hyperthyroidism is characterised by increased thyroid hormone synthesis and secretion from the thyroid gland, whereas thyrotoxicosis refers to the clinical syndrome of excess circulating thyroid hormones, irrespective of the source.

38
Q

What are thyroid stimulating immunoglobulins

A

TSI stands for thyroid stimulating immunoglobulin. TSIs are antibodies that tell the thyroid gland to become more active and release excess amounts of thyroid hormone into the blood.

Physiology 3 And Physiology For GE (7 decks)

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