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Vertebrate Endocrinology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Reabsorption

A
  • re-uptake of something that has been taken up before
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2
Q

Types of deiodinase enzyme

A
  1. Type 1 deiodinase
    - produced in the liver
    - located in the kidney and thyroid gland
    - converts T4 to T3 and provides negative feedback
  2. Type 2 deiodinase
    - expressed in thyroid, placenta, brain, pituitary gland skeletal and cardiac muscle
    - also in BAT (brown adipose tissue)
    - converts T3 to T2, which is biologically inactive (negative feedback)
  3. Type 3 deiodinase
    - in pregnant woman vital for communication with placenta
    - maintains placental thyroid hormone activity for developing fetus
    - in other words, placenta has their own deiodinase enzyme
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3
Q

Thyroid Hormone Function

A
  • functions to make thyroid hormone for:
    1. homeostasis
    2. to regulate energy expenditure
    3. to stimulate cell metabolism and cellular activity
  • primary function of TH is metabolism and energy
  • glucose lipid metabolism and energy
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4
Q

What happens when there is not enough T3 and T4 production?

A
  • TSH levels will increase, this will stimulate the production of T3 and T4
  • once there is an adequate amount of T3 and T4, TSH will stop
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5
Q

What do you need to have bioactive form of vitamin D

A
  • skin, liver, kidney and dietary
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6
Q

G alpha q and G alpha i function

A
  • detect levels of Calcium in blood stream

- when calcium binds to one of these will trigger either the release of PTH or inhibit the release of PTH

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7
Q

Steroid Hormones can be produced by

A
  • adrenal glands and gonads (androgens)
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8
Q

What is the bioactive form of Vitamin D

A
  • calcitrol
    1. SKIN
  • 7-dehydrocholesterol is converted to cholecalciferol (provitamin D) on the skin due to the presence of UV radiation
    2. LIVER
  • if not in the sun, can consume fish ooil and egg yolk for dietary supplement instead
  • from your diet you get Vitamin D2, or ergocalciferol
  • can consume plants/flowers and it will go to your lievr
  • Vitamin D2 will undergo bioactivation and become 25-hydroxyvitamin D3, or vitamin D3
    3. KIDNEY
  • 25-hydroxyvitamin D3 in the kidney
  • in the presence of PTH stimulating enzyme 1 alpha hydroxylase, Vitamin D3 will bind and convert to bioactive form
  • Vitamin D is released
    4. If calcium levels are high suppresses the production of 1 alpha hydroxylase
  • PTH stimulates production of 1 alpha hydroxylase
    5. Vitamin D will target 4 places when released to increase the blood level of calcium
    a. Skeleton to increase bone resorption
  • calcium released into blood stream and activate osteoclasts
    b. small intestine to increase calcium absorption
    c. kidney to increase calcium reabsorption
    d. Parathyroid gland to decrease parathyroid synthesis
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9
Q

Where does Thyroid hormone synthesis occur and where are thyroid hormones released?

A
  • thyroid hormone synthesis occurs on the apical side of follicle cells
  • thyroid hormones are released on the basolateral side of the follicle cells
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10
Q

Kidney PTH Function

A
  1. PTH binds to the PTH receptor G alpha s on the basolateral side of an epithelial cell located on the convoluted tubule of a nephron
  2. A calcium channel is inserted on the apical side of the epithelial cell
    - unidirectional, only goes one way
    - at the same time internalization of type 2 cells occur to be sent to lysozyme for destruction (down regulation of type 2)
  3. Calcium moves through the channel
  4. Protein-Calbindin (D28K)
    - a Vitamin D dependent protein, it is a binding protein
    - will bind to calcium and help move calcium to make it active
    - if not present calcium can move into the cell, but can not bind it is held there
  5. Type 1 and IIa are down regulated as well
  6. PTH inhibits renal reabsorption bc all of the channels were removed
    - decrease reabsorption or increase secretion of Calcium to blood stream in presence of PTH
  7. Calcium goes through the basolateral side into the blood vessel
    - if not secreted will go through Type II channel
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11
Q

Effects of Deficient and excess thyroid hormone in growth

A
  1. Deficient
    - leads to stunt in growth
  2. Excess
    - leads to osteoporosis
    - stimulates osteoclasts
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12
Q

How to check for thyroid function

A
  • measure the levels of T4

- want more levels of T4 to be present than T3

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13
Q

Adrenal Gland Components

A
  • one on each kidney (2)
  • medulla makes up 10% of adrenal gland
  • > derived from neural crest cells
  • > epinephrine and norepinephrine produced here
  • cortex has 3 layers
    1. zona glomerulosa
  • produces mineralocorticoids (aldosterone)
    2. Zona fasciculata
  • produces glucocorticoids (cortisol, androgens)
    3. Zona reticularis
  • produces glucocorticoids (androgens)
  • not fully mature until after birth (postnatally)
  • adrenal gland is an extension of the parasympathetic and sympathetic nervous system
  • > activated by fight or flight response
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14
Q

Parathyroid Hormone

A
  • synthesized as a prohormone
  • is metabolized by the kidney and liver
  • has a half life from 4-20 minutes
  • release and synthesis of PTH is continuous
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15
Q

What happens when glucocorticoids are released in very high amounts?

A
  • glucocorticoids are androgens and cortisol
  • if released in very high amounts are catabolic
  • lead to muscle wasting bc no longer in homeostasis
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16
Q

Regressed Thyroid Gland

A
  • is due to a decreased production of T3 or T4
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17
Q

Levels of T3 and T4 in blood stream

A
  • 40x more of T4 is released into the blood stream than T3
  • this is because T3 has a 100x higher binding affinity and is much more potent
  • In the periphery, as the structure moves towards the target tissue T4 will be converted to T3 by deiodinase enzyme
  • this process is called deiodinization
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18
Q

Thyroid hormone production steps

A
  1. TSH binds to the receptor G alpha s on the basolateral side of the follicular cell
  2. Sodium (Na+) and Iodide (I-) travel from the blood stream into the follicle cell through a sodium-iodide symporter using active transport
  3. Nucleus of the follicle cell secretes the protein thyroglobulin
  4. Next step is the oxidation of iodide (I-), iodide moves from the basolateral side to the apical side of the follicle cell and becomes molecular iodine (I2) in the presence of the enzyme thyroid peroxidase (TPO). It then moves into colloid region and binds to thyroglobulin
  5. As more TPO is input into the colloid region the thyroglobulin binds with the iodine and iodinization will occur. Forms T1(MIT), T2 (DIT), T3 (TIT), T4 (Thyroxine)
  6. The thyroid hormones in the colloid must return back to the blood stream to reach their target organs
  7. T3 and T4 are packaged into secretory vesicles and brought back into the follicle cell
  8. T1 and T2 have no biological activity and are endocytized back into the follicle cell
  9. will pull Iodine off of the thyroglobulin in the follicle cell and push it back into the colloid to start the process again
  10. T3 and T4 are exocytized from follicle cell into blood stream
    - T3 and T4 in the blood stream is 80-90% T4 and a much smaller percent of T3
    - T3 is very biologically active and very potent
    - T4 is not biologically active
    - can not go from T1-> T2->T3-> T4 unless in the colloid with the presence of TPO, but in the body deiodinization occurs and goes from T4->T3->T2
    - can take off iodines on thyroglobulin in periphery, but not put on
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19
Q

T3 Hormone receptor

A
  • T3 receptor is located in the nucleus
  • Heat Shock Protein (HSP) is dissociated from T4 and deiodinization will occur
  • T3 will then be translocated into the nucleus and bind to the promoter region inside of the nucleus
  • transcription of genes will occur and cause downstream effects
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20
Q

Thyroid Gland

A
  • is a plexus for massive blood supply with a lot of branching of blood vessels, provides many routes
  • > brings blood in and out
  • innervated by nerves that extend through the ganglia (collection of cell bodies in the PNS)
  • > comes from the cervical region (neck)
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21
Q

Mitochondria and the adrenal gland

A
  • mitochondria has an outer and inner layer
  • STAR (steroid acute regulatory protein) allows cholesterol to be translocated into the mitochondrial layers
  • in the presence of P45OSCC cholesterol is converted to pregnenolone
  • pregnenolone is then converted to progesterone (P4) and 17 alpha-hydroxypregnenolone
  • these will be converted to the adrenal glands final structures
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22
Q

Precursor of adrenal gland and end products

A
  1. Precursor
    - Cholesterol
    - building blocks in adrenal gland cortex to convert to other structures
  2. End products
    - aldosterone
    - androgens
    - cortisol
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23
Q

What factors affect PTH and calcium levels

A
  1. Vitamin D
  2. Magnesium
  3. Phosphate
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24
Q

DHEA

A
  • an intermediate
  • has biological activity
  • claims that it is linked to an inc of immune function, inc mood, inc energy, inc skeletal muscle strength, inc sex drive, DEC aging process
  • peaks in mid 20s and decreases w age
  • synthetic DHEA popular over the counter stimulants
  • naturally occurs in yams, sweet potato and soy products (high in fiber and gas in these)
  • produced mostly in the adrenal gland, but can be produced in reproductive glands
  • DHEA can be converted to testosterone and estrogen(estradiol)
  • all over body effects
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25
Q

Wolff-Chaikoff Effect

A
  • there is a peak in iodide in the blood stream

- the thyroid gland auto-regulates to fix it

26
Q

How to determine where adrenal androgens are coming from

A
  • adrenal androgens (gonadal and adrenal glands derived) are regulated by ACTH
  • measure intermediate of DHEA to determine if androgens are coming from gonads or adrenal glands
27
Q

Resorption

A
  • bone releases calcium under stimulation of osteoclast activity
  • the process under which something is reabsorbed
28
Q

Right Lobe vs Left Lobe of Thyroid Gland

A
  • the right lobe of the thyroid gland is more vascularized than the left
  • receives a large blood supply
  • this is why it is larger than the left lobe
29
Q

Osteoclast

A
  • breaks down bony matrix
  • apoptosis
  • autophagy (when osteoblast breaks down to an osteoclast)
30
Q

Euthyroid sick syndrome

A
  • patient appears to have a thyroid disorder, but nothing is wrong with the thyroid gland
  • patient is severely malnourished and anorexic
  • it is a result of other issues of the body
31
Q

Aldosterone

A
  • targets the kidney
  • specifically the distal convoluted tubule and collecting duct of the nephron
  • Na+, K+ and water homeostasis!
  • aids in the reabsorption of sodium and water
  • potassium is secreted
  • blood pressure and volume increases
  • also has an effect on the juxta and glomerular cells
32
Q

Cortisol

A
  • stress related
  • negative feedback at the level of the hypothalamus and anterior pituitary gland
  • suppresses CRH (corticotropin RH) at hypothalamus and ACTH(adrenocorticotropic hormone) at anterior pituitary
  • is lipophilic in free form and can fuse through membranes, but if has a protein associated with it can not freely fuse through
    Level Regulation
  • to dec cortisol levels laughing, yoga, massage therapy
  • to increase cortisol levels sleep deprivation, burnout, stress, anorexia, caffeine
    Functions
  • cortisol increases blood sugar, inc metabolism of fat, protein and carbs, DEC bone formation (stim osteoclasts), potent in aiding anti-inflammatory pathways, DEC IL-2 on helper B cells which support antibody production, dec allergy prevention, DEC immune functions
  • increases metabolism, inc gluconeogenesis, inc glycogenolysis, inc proteolysis, inc lipolysis
  • at the level of cardiovascular tissue function will inc myocardial contractility (HR), inc cardiac output, inc catecholamine effect (fight or flight)
33
Q

Enlarged Thyroid Gland

A
  • is called a Goiter

- due to an over production of T3 or T4 (Thyroxine)

34
Q

Thyroiditis

A
  • inflammation of the thyroid gland
  • caused by different underlying factors
    ex: Infection, fever, etc
35
Q

Addison’s Disease

A
  • adrenal gland does not produce enough cortisol
  • leads to fatigue, muscle weakness, weight loss, loss of appetite and abdominal pain
  • measure cortisol level using a stress test
  • treat with exogenous forms of cortisol
36
Q

Thyroid Gland Components

A
  • consists of thyroid follicles and “c cells”
  • “c cells” (parafollicular cells) secrete calcitonin
  • thyroid follicles are made up of individual follicle cells connected via proteins
  • the apical side of the follicle cells face the colloid, or middle region of the thyroid follicle
  • TSH binds to the G alpha s subunit on the basolateral side of the follicle cells and regulate the process
37
Q

Aldosterone excess

A
  1. Primary diagnosis is CONN SYNDROME
    - benign tumor on adrenal gland hyper-secretes aldosterone and leads to hypertension
  2. Secondary Diagnosis is HYPERALDOSTERONISM
    - continued stimulation of renin-angiotensin-aldosterone cascade (RAA)
    - steady decrease in blood volume
  3. Tertiary Diagnosis is BARTER SYNDROME
    - waste sodium chloride
    - constantly lost through urine
    - as a result turn RAA on (renin-angiotensin-aldosterone cascade)
38
Q

Parathyroid Hormone Targets

A
  1. targets bone to increase osteoclast activity
    - > osteocyte is an intermediate, mature bone cell (aid in bone structure)
    - > osteoclast breaks down deposition as moves away from bone (bone is broken down releasing calcium ions into the blood stream)
  2. targets the kidney to increase vitamin D
    - > vitamin D aids in calcium reabsorption
  3. targets the small intestine
39
Q

Thyroid Hormone affect on bone

A
  • thyroid hormone targets bone and activates osteoblast and osteoclast activity
  • osteoblasts are responsible for building bone and increasing bone density
  • osteoclasts are responsible for breaking down the bony matrix
  • thyroid hormone is very important for bone growth, especially in children
40
Q

4 Names for follicle cells

A
  • comprise the outer region of a thyroid follicle
    1. Follicle cells
    2. Follicular cells
    3. Epithelial cells
    4. thyroid cell
41
Q

Sodium Phosphate transporters for PTH

A
  • aid in movement of phosphate and sodium across the membrane
    1. Type I
  • renal proximal convoluted tubule apical
    2. Type II
  • renal proximal convoluted tubule basolateral
    3. Type IIa
  • renal proximal convoluted tubule apical
    4. Type IIb
  • small intestine
42
Q

Abnormality in iodine metabolism

A
  • iodine converts to iodide
  • environmental factors can affect this
  • perchlorate (inc levels of solvent in dry clean industry)
  • low levels of perchlorate are found in drinking water
  • in fetal development if there is a lack of iodide, its fine
  • BUT if mother is lacking iodide fetus can have hyperthyroidism or hypothyroidism
43
Q

Reuptake of Calcium with Vitamin D

A
  • regulate amount of reabsorption using Vitamin D
  • Vitamin D increases intestinal reabsorption of calcium
  • increases renal reabsorption of calcium
44
Q

Parathyroid Gland

A
  • 4 glands, 2 are superior and 2 are anterior on thyroid gland
  • chief cells (tightly packed)
  • VITAL for calcium regulation
  • have calcium sensors
  • plasma calcium levels regulate whether Parathyroid Hormone (PTH) is released
  • > high and low levels of calcium
45
Q

Disease of PTH

A
  1. Hypoparathyroidism
    - when individual loses some, all or most of PTG
  2. Hyperparathyroidism
    - tumor at the Parathyroid gland
    - causes renal failure
    - can not regulate Vitamin D and calcium
    - if have a mutated receptor entire system shuts down
46
Q

Cushing’s Disease

A
  • 2 types
    1. Corticotropin Dependent
  • elevated glucocorticoids caused by elevated ACTH
  • tumor at the level of pituitary gland
    2. Corticotropin Independent
  • abnormal level of cortisol, regardless of ACTH levels
  • caused by abnormality at level of the adrenal gland
  • symptoms for both are the same
  • > rounded face, muscle wasting, enlarged dorsocervical fat pad
47
Q

Calcium and the Kidney

A
  • at the level of the kidney, almost all of calcium is reabsorbed due to PTH (proximal convoluted tubule)
  • 40% conv tubule and 30% absorbed through food
  • increase the amount of Vitamin D, increase amount of calcium that can be reabsorbed
48
Q

Hypothalamic Pituitary Thyroid Signaling Mechanism

A
  • TRH (thyroid releasing hormone) is released from PVN and binds to G alpha q on thyrotroph
  • releases TSH which binds to G alpha s on basolateral side of follicle cell
  • negative feedback system
49
Q

Parafollicular, or “c cells”

A
  • produce calcitonin
  • regulates calcium levels in the blood stream while working in opposite effects to PTH
  • calcitonin is bone sparring
  • > stimulates osteoblasts to regulate blood level of calcium
  • there is no limit to how much calcium in bone
  • > aids in density, structure and strength
  • inc levels of calcium in bone is good
  • dec levels of calcium in bone leads to osteoporosis, weak, brittle bones
  • Calcitonin moves calcium from the blood stream to the bone and PTH moves calcium from the bone to the blood stream
  • > dec plasma level of calcium
50
Q

Final Products Released from adrenal cortex

A
  1. Aldosterone
  2. Cortisol
  3. Androgens
51
Q

What can you do for a patient with a defective thyroid gland?

A
  • give T4 or T3 as an exogenous thyroid hormone

- but if patient has a mutated receptor, nothing will occur

52
Q

Diseases of the Thyroid Gland

A
  • both autoimmune diseases
    1. Graves
  • hyperthyroidism
  • overactive thyroid gland, causes weight loss
  • increased basal metabolism
  • antibodies bind to the TSH receptor and act as an agonist with very high binding affinity
  • drives TSH to continue producing excess T3 and T4
  • leads to increased size of thyroid gland
  • can cause bulging eyes, eyelids will retract and eyes protrude out
    2. Hashimoto
  • hypothyroidism
  • TG is not active enough, causes weight gain
  • does not produce enough Thyroid Hormones
  • > administer exogenous T3 and T4 to level out the thyroid
  • more common in women
  • a patient lacks Thyroglobulin, Thyroid Peroxidase and the products for production of TSH
  • if occurs in utero (for dev fetus) can cause severe mental retardation and decreased development
53
Q

If adrenal cortex is chronically stressed what happens to hormone levels

A
  • cortisol increases and DHEA dec
54
Q

Steps for final adrenal gland product

A
  1. cholesterol is converted to pregnenolone by P45OSCC enzyme
  2. produces progesterone(P4) and 17alpha-hydroxypregnenolone
  3. progesterone final products are cortisol and androgens
  4. 17alpha-hydroxypregnenolone final products are cortisol and estrogen
55
Q

Aldosterone Steps

A
  1. Kidney produces renin
  2. liver produces angiotensinogen which is converted by renin to angiotensin 1
  3. endothelial cells that line the blood vessel produces ACE (angiotensin converting enzyme)
  4. ACE converts angiotensin 1 to angiotensin 2
  5. Angiotensin 2 targets the adrenal cortex to produce aldosterone and it is carried to the blood stream
  6. aldosterone then targets the kidney
  7. RAA- renin-angiotensin-aldosterone cascade
  8. aldosterone is metabolized in the liver and excreted in urine
  • aldosterone is vital for homeostasis and survival
  • angiotensin 2 stimulates aldosterone release, but abnormal levels of potassium will also cause this release
56
Q

What triggers the start of STAR and P45SOCC

A
  • ACTH(adrenocorticotropic hormone) binds to G alpha s on adrenocortical cells
57
Q

Thyroid Hormones

A
  • T3 (TIT)

- T4 (Thyroxine)

58
Q

Brown Adipose Tissue

A
  • common in young mammalian species
  • as we age BAT becomes WAT
  • hibernating animals have more BAT even as adults
  • aids in body temperature regulation (lipid droplets in adipose tissue)
  • contains more iron and mitochondria
  • mitochondrial respiration vital in lipid glucose metabolism
59
Q

What regulates calcium levels in the blood stream?

A
  1. Parathyroid Hormone
  2. Calcitonin
  3. Vitamin D - aids in absorption of calcium
60
Q

Thyroid hormone in cardiovascular system

A
  • targets cardiac muscle
  • inotropic (modify strength of contraction)
  • chronotropic (modify speed of contraction)
  • effects the amount of blood being moved
  • effects cardiac output
61
Q

Deiodinization of thyroid hormones in periphery

A
  • T4 in periphery is converted to T3 which causes a downstream affect
  • T3 will deiodinize to T2 which is biologically inactive
62
Q

Estrogen effect on osteoblast and osteoclast activity

A
  • causes an increase in osteoblast activity and a decrease in osteoclast activity
  • effects receptors for vitamin D and PTH
  • as you age and estrogen levels dec, osteoporosis becomes an issue (osteoclast inc, osteoblast dec)
  • > growth hormone stimulates osteoblast

Vertebrate Endocrinology (4 decks)

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