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Human Bioscience II > Posterior Pituitary Hormones > Flashcards

Posterior Pituitary Hormones Flashcards

1
Q

What is ADH also known as?

A

Antidiuretic hormone and vasopresin

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2
Q

What does the hypothalamus control?

Through which types of signals does it control?

A

Posterior pituitary hormones

The posterior pituitary hormones are controlled by neuronal signals from the hypothalamus

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3
Q

Where is oxytocin synthesized?

Where is ADH synthesized?

A

In the cell body of the hypothalamus at the paraventricular nucleus

In the cell body of the hypothalamus at the supraoptic nucleus

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4
Q

What does ADH work on?

What is it packaged with in the posterior lobe of pituitary?

A

Works on kidney and blood vessels to promote action of water loss inhibition

Neurophysin (NPII)

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5
Q

What does oxytocin work on?

What is it packaged with in the posterior lobe of pituitary?

A

Works on breast and cervix

Neurophysin (NPI)

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6
Q

What are the two types of receptors for ADH?

What do V1 receptors do?

What do V2 receptors do? Where are they located?

A

V1 and V2

V1: Mediate vasoconstriction, increased ACTH secretion, and glycogenolysis

V2: Located in principle cells in distal convoluted tubule and collecting ducts in the kidney.
- They are coupled via G proteins to adenylate cyclase or phospholipase C

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7
Q

What differentiates ADH from oxytocin? How are they similar?

A

They are each made of 9 amino acids and differ by two amino acids

  • They differ at amino acid 3 and 8
    ADH= Phe & Arg
    Oxytocin= Ile & Leu
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8
Q

Which stimulatory factors affect ADH secretion?

A
  1. Increased serum osmolarity
  2. Decreased ECH volume
  • These increase ADH secretion because there is less water and more solute in the factors above
  • ADH keeps more water inside blood vessels
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9
Q

What is the function of ADH?

A

Regulation of body fluid osmolarity

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10
Q

What happens when deprived of water?

A
  1. Plasma osmolarity increases
  2. Osmoreceptors in anterior hypothalamus are stimulated
  3. Increase in ADH secretion from posterior pituitary
  4. Increase in water permeability of principal cells (late distal tubule and collecting duct)
  5. Water reabsorption increases
  6. Urine osmolarity increase and urine volume decreases
  7. Plasma osmolarity decreases toward normal
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11
Q

What happens when you drink water?

A
  1. Plasma osmolarity decreases
  2. Osmoreceptors in the anterior hypothalamus are inhibited
  3. Decrease in ADH secretion from posterior pituitary
  4. Decrease in water permeability of principal cells (late distal tubule and collecting duct)
  5. Water reabsorption decreases
  6. Urine osmolarity decreases and urine volume increases
  7. Plasma osmolarity increases toward normal
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12
Q

Which type of blood osmotic pressure stimulates hypothalamic osmoreceptors?

A

High blood osmotic pressure

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13
Q

What do osmoreceptors activate? What is secreted?

A

Hypothalamic neurosecretory cells are activated and ADH is released

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14
Q

From where is ADH secreted?

A

Nerve impulses liberate ADH from axon terminals in the posterior pituitary gland into the blood stream

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15
Q

Which body organ retains water?

What happens to urine secretion?

A

Kidneys retain water which decreases urine output

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16
Q

What occurs in sweat glands and arterioles when there is an increase in ADH?

A

Sweat glands decrease water loss via perspiration from the skin

Arterioles constrict which increases blood pressure

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17
Q

What is the effect of ADH on principal cells in the distal tubule?

A
  1. ADH receptor binds to V2 receptors
  2. Adenylyl cyclase signaling system is activated
  3. Aquaporin-2 expression on luminal membrane of principal cell increases
  4. Membrane water permeability increases
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18
Q

What is another way to increase ADH secretion?

What is decreased?

A

Hypovolemia which is volume contraction due to a hemorrhage

ECF (extracellular fluid) and blood pressure are decreased

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19
Q

What happens during a decrease in blood pressure?

A

The decrease in BP is sensed by the carotid and aortic baroreceptors and is transmitted via the vagus nerve to the hypothalamus which directs an increase in ADH secretion

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20
Q

What does ADH bind to during hypovolemia?
What is activated?
What is contracted in response?

A

ADH binds to V1 receptors on vascular smooth muscles.
Phospholipase C signaling system is activated
Vascular smooth muscle is contracted

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21
Q

What does the secretion in ADH do to body fluid?

A

There is a reduction in body fluid loss and an increase in total peripheral resistance (TPR) to increase blood pressure

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22
Q

What is the pathophysiology of ADH?

A
  1. Central diabetes insipidus
  2. Nephrogenic diabetes insipidus
  3. Syndrome of inappropriate ADH secretion (SIADH)
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23
Q

What occurs in central diabetes insipidus?
What is damaged?
How is it treated?

A
  • ADH deficiency due to hypothalamus/ posterior pituitary damage
  • Collecting ducts are less permeable to water… and produce large volumes of dilute urine -> excessive thirst
  • Tx: ADH analogue, dDAVP
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24
Q

What occurs in nephrogenic diabetes insipidus?

What is damaged?

How are the kidneys affected?

What is the overall change in ADH

A
  • Posterior pituitary is normal
  • V2 receptors, G protein or adenylyl cyclase in principal cells of the kidney are defective
  • Principal cells are unresponsive to ADH
  • Water reabsorption by kidney is reduced which produces large volumes of dilute urine
  • ADH levels are elevated
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25
Q

What occurs in SIADH?

How are the kidneys affected?

A
  • Excess circulating levels of ADH. ADH is secreted from abnormal sources (oat cell carcinoma of the lungs)
  • Excessive water reabsorption by the kidneys; small volume of concentrated urine is produced -> plasma osmolarity is reduced
  • Retention of fluid, headaches, and disorientation
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26
Q

What is the primary function of oxytocin?

A

Milk letdown aka ejection

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27
Q

What are the actions of oxytocin?

A
  1. Milk ejection: Oxytocin contracts the myoepithelial cells lining the mammary ducts
  2. Uterine contraction: Oxytocin is used to induce labor and to reduce postpartum bleeding
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28
Q

How is oxytocin secretion regulated?

A

Suckling of breast
Dilation of cervix
Conditioned responses

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29
Q

What do the CNS relays from the hypothalamus do?

What triggers the CNS relays?

A

Supraoptic and paraventricular nuclei cause a release of oxytocin from the posterior pituitary

  • Suckling and cervical stretch receptors
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30
Q

What are the effects of oxytocin on child birth?

A
  1. Head of fetus pushes against the cervix
  2. Nerve impulses from cervix are transmitted to brain
  3. Brain stimulates pituitary gland to secrete oxytocin
  4. Oxytocin is carried in bloodstream to uterus
  5. Oxytocin stimulates uterine contractions and pushes fetus toward cervix
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31
Q

What organ does hyperpituitarism affect?

What results in hyperpituitarism? Which is more common?

A

Anterior pituitary

  1. Adenomas (Benign)
  2. Pituitary carcinomas (rare)
  3. Pituitary hyperplasia
  4. Overstimulation by hypothalamus
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32
Q

What are the types of adenomas that result in hyperpituitarism?

What are the names of the specific types of anterior pituitary tumors?

A

Single or plurihormonal
Micro or macroadenomas

Somatotroph adenoma, corticotroph adenoma, Thyrotroph adenomas, Gonadotroph adenoma

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33
Q

What is the morphology of a hypersecreting adenoma?

A
  • Circumscribed lesions
  • Confined to sella turcica
  • Tumors are made of uniform cells with calcification and granule formation
  • Tumors lack reticulin (CT)
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34
Q

What can pituitary adenomas result in?

What do they impede on?

Which nasal fibers are affected?

What is the overall change in vision?

A

Breaking of blood vessels which poses a problem to vision
- Diplopia
- Ophtalmoplegia
- Optic Atrophy

Impedes on the optic chiasm from below

Inferior nasal retinal fibers are affected

Superior bitemporal vision loss

35
Q

How does vision loss correlate with field defects?

A

If the field defects are asymmetric then visual field loss is asymmetric

36
Q

What is ophthalmoplegia?

A

Paralysis of EOMs that control eye movements

37
Q

If you have optic atrophy will your vision recover?

A

NO, you would have to remove adenoma from pituitary and still have vision loss

38
Q

What results in hypopituitarism?

A
  1. Defects of hypothalamic or intrinsic pituitary deficit
  2. Destructive processes involving the anterior pituitary.
    - 75% of the pituitary parenchyma has to be involved
39
Q

Where is the thyroid gland located?

What is the structure?

What are the lobes made of?

A

Wrapped around the trachea below the Adam’s apple

Right and left lobes connected by isthmus

Thyroid follicles and parafollicular cells

40
Q

What occurs at the thyroid follicles?

What are thyroid follicles made of?

A

Thyroid hormone synthesis

Inner colloid has newly synthesized thyroid hormones attached to thyroglobulin

Outer layer has cells that produce glycoprotein: THYROGLOBULIN

41
Q

What do follicular cells have that make them specific?

What do they do?

A

Receptors for Thyroid stimulating hormone (TSH) -> initiate cascade for release of thyroid hormones into blood

42
Q

What is the biochemistry of thyroid hormone?

What is the essential element?

Can it cross the cell? Why?

A

They are Amines made from tyrosine

Iodine, you need it to make thyroid hormones

Yes, they can cross because they are hydrophobic.

43
Q

What are the subtypes of thyroid hormone?

Which are functional?

Which has higher affinity?

Which is used predominantly? What happens with it?

Which is biologically active?

A

T3, T4, rT3

T3, T4

T3

T4 and made more than T3. T4 crosses and is converted into T3 in the cells via 5’- iodenase

T3

44
Q

What are the mechanisms of action of thyroid hormone?

A
  1. Hydrophobic molecule thus it can cross into any cell
  2. Modifies the activity of target tissue by binding to nuclear receptors thus it activates nearly every tissue in the body
45
Q

Where is thyroglobulin synthesized? Where does it then go?

A

Thyroglobulin is synthesized by rough ER and secreted into the colloidal lumen via exocytosis

46
Q

Where is iodide transported? How?

Which type of transportation is used?

A

Iodide is actively transported from the blood into the follicular epithelial cells across the basolateral membrane. Pump activity is inhibited by perchlorate and thiocyanate

Active Na transportation

47
Q

Does iodide get into the cell? What happens once it enters?

How is activity blocked?

A

Iodide traverses the cell to the apical membrane and into the colloidal lumen where it is oxidized to iodine in the lumen by the enzyme thyroid peroxidase.

Thyroid peroxidase activity can be blocked by propylthiouracil

48
Q

What is iodinated? Which enzyme is used?
What is this process called?

A

Tyrosine residues of thryoglobulin are iodinated to form monoiiodotyrosine (MIT) and Diiodotyrosine (DIT)

Enzyme: Thryoid peroxidase

AKA: Organification of thyroglobulin

49
Q

What do coupling reaction occur between?
What is created?
Which enzyme is used?
Which reaction is faster?

A

Coupling reactions occur between MIT/DIT or between DIT/DIT
T3 & T4 created
Enzyme: Thyroid peroxidase
The 2nd rxn is faster thus there is more T4

50
Q

What happens to the follicular cells when stimulated?

What are they stimulated by?

A

Stimulant: TSH

Thyroglobulin complex is endocytosed by follicular epithelial cells

51
Q

What is cleaved by the thyroglobulin complex?
Which type of mechanism is used?
Where is it secreted?

A

T3, T3, MIT, DIT are cleaved
Proteolytic mechanism
Secretion into the blood

52
Q

What is deiodinated?
Where does deionation occur?
Which enzyme is used?
Where is it recycled to?

A

MIT/DIT deiodinated
Occurs in follicular cells
Enzyme: Thyroid deiodinase
Recycled into intracellular pool

53
Q

What is thyroid hormone bound to?

If it is bound what happens?

A

Bound to plasma proteins (Thyroxine binding globulin- TBG)

It is inactive when bound thus it can’t cross membrane

54
Q

What alters free thyroid hormone levels?

Which state reduces thyroid hormone levels?
Which state increases thyroid hormone levels?

A

Changes in blood levels of TBG alter free thyroid hormone levels

Hepatic disease- TBG reduces and total thyroid hormone levels reduce because it was high before

Pregnancy: TBG increase and total thyroid hormone level increases because it was low before

55
Q

What is the free unbound state?

A

T3 & T4

56
Q

What happen when T4 is activated?

Which is most active?

Which is produced more?

A

When activated T3 is converted to T3 via 5’-iodinase in target tissue

T3 is most active

T4 is produced in abundance 10x more

57
Q

What is special about thyroid hormone in relation to thyroid gland?

A

Thyroid hormones synthesize and store TH in glands for future use

58
Q

What does TSH regulate?

Which type of effect is seen?

What does overstimulation of thyroid gland lead to?

A

Growth of thyroid gland

Trophic effect

Overstimulation of thyroid gland -> thyroid hypertrophy and hyperplasia

59
Q

Which receptors does TSH activate?
What is the receptor also activated by?

A

TSH activates a receptor coupled to G protein and adenylate cyclase

Receptor also activated by thyroid stimulating immunoglobulins which are antibodies to TSH receptor

60
Q

What does hyperthyroidism result from?

What is this disease known as?

A

Hyperthyroidism results from increased thyroid-stimulating immunoglobulin which leads to an increase in T3/T4

Graves disease

61
Q

How are TSH levels in Grave’s disease?

Which type of feedback mechanism is displayed here?

A

TSH levels are low due to high circulating levels of thyroid hormones inhibiting TSH secretion

Negative feedback

62
Q

How is negative feedback displayed?

What does negative feedback work directly on?

Which hormone is in abundance? What state is it in?

A

Free T3 mediates the negative feedback effect by downregulating the expression of TRH receptors on thyrotropes

Hypothalamus

T3 in free state

63
Q

What do thyroid stimulating immunoglobulins activate?

A

Activate TSH receptors -> T3/ T4 production

64
Q

What are thyrotrophes?

A

Endocrine cells in the anterior pituitary that produce TSH in response to thyrotropin releasing hormone

65
Q

What does the hypothalamus do in thyroid hormone regulation ?

A

Releases TRH (Thyrotropin Releasing hormone) to the anterior pituitary

66
Q

What does the anterior pituitary do in thyroid hormone regulation?

A

Releases TSH to the thyroid gland

67
Q

What does the thyroid gland do in thyroid hormone regulation?

A

Releases T3/T4

68
Q

What happens if there is too much T3/T4?

A

Negative feedback inhibition by downregulating TRH receptors on the anterior pituitary or directly on the thalamus

69
Q

What are the actions of thyroid hormone?

A
  1. Growth
  2. CNS
  3. BMR- Basal metabolic rate
  4. Metabolism
  5. Cardiovascular
70
Q

What is the role of thyroid hormone on BMR?

Which enzyme is used?

A

Increase in sodium/potassium pump
Increase in oxygen consumption
Increase in heat production
Increase in BMR

ATPase

71
Q

What is the role of thyroid hormone on metabolism?

What do thyroid hormones increase?

A

Increase in protein synthesis and degradation
Lipolysis- Triglycerides breakdown into fatty acids and glycerol

Increase glucose absorption form GI tract

72
Q

What is the role of thyroid hormone on cardiovascular system?

What is induced?

A

Increase in cardiac output of heart rate & contractility and ventilation

Myosin, B1-adrenergic receptors, Ca2+ ATPase are induced

73
Q

What is the cardiac output equation?

A

Cardiac output= heart rate x stroke volume

74
Q

What is hyperthyroidism?
What is hyperthyroidism also known as?

What are the causes?

A

Hypermetabolic state caused by elevated T4/T3
Thyrotoxicosis

Causes:
- Pituitary adenomas
- Thyroid adenoma (rare)
- Graves disease
- Thyroid carcinomas
- Neonatal thyrotoxicosis
- Excessive thyroid hormone therapy for hypothyroidism

75
Q

Why is the effect of a pituitary adenoma on TSH?

A

The tumor on the pituitary causes too much TSH which leads to an increase in T4. Normally negative feedback would occur but since there is a tumor the result is too much TSH

76
Q

What are the symptoms of hyperthyroidism?

A
  1. Increase BMR
  2. Weight Loss
  3. Increased thermogenesis and sweating
  4. Increased cardiac output and cardio issues
  5. Goiter: Graves disease
  6. Multiple ocular manifestations in Grave’s disease
77
Q

What is treatment for hyperthyroidism?

A
  1. Propylthiouracyl: Blocks thyroid peroxidase
  2. Thyroidectomy: Removes thyroid
  3. Radiolabeled iodine: Kills thyroid tissue
  4. B- adrenergic blockers: Cardiovascular complications that inhibit epinephrine
78
Q

What are the ocular manifestations in Graves disease?

A

Exophthalmos
Lagophthalmos
Bulbar conjunctiva injected
Corneal Dryness
Ocular misalignment
Diplopia
Compressive Optic atrophy -> visual defects

79
Q

What are treatments for ocular symptoms of Graves disease?

A
  1. Restore normal thyroid status “Euthyroid”
  2. Sodium/ H2O restriction to reduce edema
  3. Surgical lid retraction repair
  4. Prisms or occlusion therapy
  5. Strabismus surgery
  6. Orbital decompression
  7. Eye lubricants
  8. Steroids
80
Q

What is a common autoimmune disease that causes hypothyroidism?

What is the best treatment?

A

Hashimoto’s Thyroiditis

Destroy the thyroid gland

81
Q

What is hypothyroidism?

A

Reduced action of thyroid hormone

82
Q

What are the causes of hypothyroidism?

A
  1. Genetic defect
  2. Post- ablative
  3. Autoimmune disease
  4. Iodine deficiency
  5. Pituitary failure- No TSH= no T3/T4
  6. Hypothalamic failure
  7. Thyroid stimulating hormone resistance- receptor not working
83
Q

What are the symptoms of hypothyroidism?

A

Decreased BMR
Weight gain
Decreased thermogenesis and cold sensitivity
Decreased cardiac output
Droopy eyelids
Goiter
Myxedema: specific form of cutaneous and dermal edema

84
Q

What is the treatment for hypothyroidism?

A

Hormone replacement surgery

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