Endo 4 Flashcards

1
Q

Where is the thyroid gland located?

A
  • thyroid cartilage (adam’s apple)
  • sits just in front of trachea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the structure of the thyroid gland?

A

-right and left lobe joined by isthmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A
  • single layer of cuboidal cells- follicular cells (make thyroid hormone and colloid)
  • parafollicular cells- important for calcium homeostasis because they release calcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the colloid?

A
  • jelly substance in thyroid follicle
  • thyroid hormone stored here
  • one of the only endocrine cells in the body that stores its hormone outside of the cell in a depot then releases it from there when needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the blood supply to the thyroid gland?

A
  • internal carotid gives rise to the superior thyroid artery
  • subclavian gives off inferior thyroid artery
  • superior, middle, and inferior thyroid vein drain into internal jugular vein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What structures are at risk when doing a thyroid surgery?

A
  • internal jugular vein, internal carotid artery, and vagus nerve
  • laryngeal nerve; sends motor instructions to the vocal chords (speak in low raspy voice if this gets cut because you can’t put tension on the vocal chords)
  • all run long neck on left and right side
  • hard to access the thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the actions of thyroid hormone?

A
  • increases BMR (utilize fuel, oxygen, and generating heat)
  • stimulates protein synthesis, importantly sodium-potassium ATPase which improves neuroconduction because you can reset resting membrane potential quickly and maintain Na and K concentrations
  • as a byproduct, this process also generates heat known as calorigeneic effect (break down ATP and release energy which generates heat)
  • regulates metabolism; synthesis of proteins (growth-works with insulin and hGH), stimulates breakdown of glycogen (glycogenolysis- sends glucose to tissues for energy) and fats (lipolysis) for ATP production
  • stimulates hepatic excretion of cholesterol (LDL) (hepatocytes take excess cholesterol and put it into bile and be excreted)
  • upregulates beta receptors for catecholamines (in lungs- help them to relax to have better ventilation to get more oxygen to make ATP and makes heart beat faster and stronger which helps deliver blood to tissues that are more metabolically active because of the thyroid hormone)
  • permissive with most aspects of growth working with insulin and hGH getting energy into the cells (essential for mental development and cognitive skills, necessary for maintaining reproductive health)
  • turns everything up! applicable everywhere in body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the types of thyroid hormones?

A
  • tri-iodothyronine or T3
  • made of tyrosine (amino acid) and benzene ring which makes it lipid soluble
  • tetra-iodothyronine or thyroxine or T4
  • thyroid makes a lot of T4 but T3 is more potent in stimulating cells
  • T4 is hard to breakdown and has long half life
  • when T4 gets to tissues, it can get converted at tissues into T3 and stimulate and have potent effects (peripheral conversion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is thyroid hormone regulated?

A
  • low blood levels of T3 and T4 or low metabolic rate stimulate the release of TRH (sensed by hypothalamus-thermoreceptors detect drop in temperature to indiate lower metabolic rate)
  • TRH goes down hypophyseal portal vein system to anterior pituitary and get release of TSH in blood
  • TSH has an effect on thyroid gland and in particular the thyroid follicular cells
  • follicular cells produce TH and store in colloid/release it in blood
  • stimulates tissue via nuclear receptors
  • when levels get too high, feeds back on hypothalamus and anterior pituitary to shut off release of TRH and TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is thyroid hormone synthesized?

A
  • need to produce colloid first (TGB)
  • colloid has amino acids and some are tyrosine
  • iodide comes from diet and ends up in bloodstream- transporters on follicular cells to transport iodide inside the cell (Na-iodide co transporter)
  • oxidize iodide done by TPO enzyme which forms elemental iodine which is highly reactive with tyrosine
  • I2 binds to benzene rings and forms T1 and T2
  • T1 and T2 together get T3, T2 and T2 get a T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Once synthesized, how is thyroid hormone released from colloid?

A
  • follicular cell brings some colloid in (endocytosis)
  • use enzymes in lysosome and combine with endosome which gives you digestion of the colloid
  • this releases TH from the rest of the protein
  • TH diffuses out into the blood
  • blood is made out of water so TH has to be bound to a protein carrier
  • thyroid binding globulin made by liver and just allows TH to move around body
  • follicular cells control this under signal of TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe iodination of tyrosine

A
  • thyroglobulin is a proteoglycan containing many tyrosine residues
  • each residue is capable of binding with 2 iodide ions
  • negatively charged iodide ions cannot bind tyrosine directly, they must first be oxidized to I2=iodine catalyzed by TPO
  • not all tyrosine residues are bound with iodine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What pathology can happen with thyroperoxidase?

A
  • sometimes is the target of immune attack
  • autoimmune disorder known as Hashimoto’s thyroiditis
  • when protein is being attacked in the follicular cells, they die and disappear
  • unable to make TH and become hypothyroidal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What occurs with iodine deficiency?

A
  • thyroid gland can’t make thyroid hormone (low T4 levels) which feeds back on anterior pituitary and hypothalamus
  • TRH and TSH levels rise
  • if you keep stimulating thyroid gland, follicular cells create more follicles to create more TH “factories” because there is no iodide to make TH
  • overall gland starts to grow and you get a goiter
  • hyperplasia: process of increasing number of follicular cells
  • hypertrophy of gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When can hyperthyroidism arise?

A
  • overstimulation of thyroid gland to produce thyroid hormone (excessive TRH and TSH release/production)
  • often TSH release from functional adenoma on anterior pituitary *high TSH
  • production of auto-antibodies that bind to and stimulate the TSH receptor and acts like TSH which causes thyroid gland to grow (Graves’ disease) *low TSH and high T3/T4
  • overproduction of TH by the thyroid gland (thyroid adenoma or toxic nodule) *would expect low TSH here because you have a lot of TH being produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the effects of hyperthyroidism?

A
  • increased BMR with a tendency to lose weight
  • poor tolerance of hot environment and hyperhidrosis
  • tendency to fatigue due to muscle wasting as muscle proteins are broken down
  • abnormally fast heart rate or palpitations
  • abnormally acute alertness making individual irritable, tense, anxious (like a sympathetic response all the time)
  • hyperreflexia
  • exopthalmos: edema in the eyes (eyes may become dry because eyelids can’t close completely) and smooth muscle in eyes is sympathetically activated so looks like they are staring at you
  • thyroid hypertrophy
  • goiter may or may not be present
17
Q

Why does hypothyroidism occur?

A
  • failure of thyroid gland to produce TH
  • deficiency of TRH or TSH release or production
  • inadequate intake of iodine which is required for thyroid hormone production
  • loss of thyroid follicular cells as in Hashimoto’s thyroiditis
  • goiter or normal sized thyroid gland
18
Q

What are the effects of hypothyroidism?

A
  • reduced BMR with a tendency to gain weight
  • poor tolerance of cold temperatures
  • tendency to fatigue due to insufficient muscle strength and nutrient metabolism
  • elevated blood cholesterol levels due to reduced hepatic excretion
  • bradycardia, weak pulse, and potentially hypotension
  • hyporeflexia and decreased alertness
  • puffiness particularly in the face, hands, and feet called myxedema caused by accumulation of mucoproteins (GAGs) and fluid in connective tissues
19
Q

Where are the parathyroid glands?

A
  • dorsal aspect of thyroid often at vascular poles
  • middle and inferior cervical ganglia, recurrent laryngeal nerve could be damaged
20
Q
A

chief cell: releases parathyroid hormone

21
Q

What is the thyroid’s role in calcium homeostasis? What is the parathyroid’s role?

A
  • parafollicular cells around the thyroid follicle release calcitonin
  • calcitonin takes calcium out of blood and puts it on bone to ossify it
  • parathyroid gland releases PTH which takes calcium out of bone and putting it in circulation
22
Q

Why does calcium need to be regulated?

A

-neurons need calcium and muscles need calcium to contract

23
Q

How does calcium exist in the body?

A
  • calcium exists as Ca2+ (ionized)
  • some exists bound to albumin in blood
  • most is found in depot in bones as hydroxyapatite which needs to be mobilized to get into blood stream
24
Q

How is calcium regulated?

A
  • excess of Ca in blood (can cause heart tetanic contractions or heart arrhythmias) stimulates release of calcitonin from thyroid gland C cells
  • calcitonin stimulates osteoblasts to bring Ca into bone
  • Ca levels will drop which stimulates parathyroid gland to release PTH
  • PTH promotes release of Ca from bone into blood by stimulating osteoblasts to activate the osteoclasts to remove calcium from bone
  • PTH also talks with kidneys and causes calcitriol (vitamin D)
  • calcitriol goes to intestine and tells proximal part to take up the calcium and increase blood Ca levels
  • hypothalamus and pituitary not needed here
25
Q

What is the endocrine control over bone density?

A
  • hGH, androgens, and estrogens control bone length
  • long bones have protein that gives them tensile strength and calcium salts that give the bone compression strength
  • calcitonin is important during early growth to maximize calcium salts in the bone
  • PTH modulates serum calcium later in life to control amount of calcium salt
  • androgens and estrogens increase the protein matrix and cells that create bone to increase bone strength which leads to closure of growth plates