Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IDT Spring Term > Endocrine Pharmacology II - Leid > Flashcards

Endocrine Pharmacology II - Leid Flashcards

1
Q

What is produced in the hypothalamus that acts upon the anterior pituitary gland?

A 
Somatostatin (-)
GHRH (+)
GnRH
TRH
CRH
PRIH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is produced in the posterior pituitary gland?

A

Vasopressin/ ADH

Oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is produced in the anterior pituitary gland?

A 
GH
Prolactin
FSH
LH
ACTH
TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of cell produces growth hormone?

A

A somatotrope in the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of cell produces prolactin?

A

Lactotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which types of cells produce FSH and LH?

A

Gonadotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What type of cells produce ACTH?

A

Corticotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which type of cells produce TSH?

A

Thyrotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the most abundant type of cell in AP?

A

Somatotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What regulates GH release from somatotropes?

A

Somatostatin inhibits GH release and GHRH induces GH release. GHRH is constant, while somatostatin release is pulsatile. Therefore, GH release is pulsatile in reciprocal fashion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does GH-R signaling involve?

A

JAKS kinases and STAT proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the pathway of growth hormone?

A

Hypothalamus receives a signal to make and release GHRH. This enters the blood stream, and GH is produced from somatotropic cells. GH acts on the liver, and the liver releases IGF-1 and IGF-2, which are somatomedins that mediate GH growth-promoting effects. This is assuming that the person has functional IGF-1 and IGF-2 in the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the approved uses of GH?

A
  1. Treatment of kids in the 1st percentile (-2.25 SD)

2. Adult GH deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the differences between the two formulations of GH?

A

Somatrem has an N-terminal Met, while Somatropin is native GH and has an N-terminal Phe. They act the same.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does the use of GH compare to anabolic steroids?

A

Use of anabolic steroids such as Oxandrolone increases the rate of growth, but does not effect the extent (ends up the same height, just gets there sooner). GH, depending on the dose and frequency, can increase the height of a adolescent up to the 25th percentile.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are aromatase inhibitors?

A

They inhibit the conversion of testosterone to estradiol, which means that side effects associated with breast growth, voice changes etc. will not be experienced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What drives epiphyseal plate closure?

A

E2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the difference between acromegaly and gigantism?

A

Gigantism is where there is excessive GH secretion in a child, and their height is affected because the growth occurs before the epiphyseal plate closure. Acromegaly is excessive GH secretion in an adult, where flat bones grow and result in alterations to face, enlargement of hands and feet, sleep apnea, and carpal tunnel. Acromegaly can result in injury to the optic chiasm, optic nerve, and pituitary gland because of compression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What condition associated with GH can result in complications involving hypertension, accelerated CVD, DM, or increased risk in colon cancer?

A

Acromegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How can you treat gigantism or acromegaly?

A

Surgical
Pharmaceutically (Octreotide helps with 70% of people, bromocriptine/Cabergoline are DA, pegvisomant helps lower IGF-1 levels but does not shrink tumor)
Radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where is somatostatin located in the body?

A 
Hypothalamus
Brain stem
Cerebral cortex
GI tract
Pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does somatostatin regulate?

A 
Inhibits release of:
GH
Insulin
Glucagon
Gastrin
TSH
ACTH
Secretin
Pancreozymin
Cholecystokinin
Pepsin
Vasoactive intestinal peptide
Renin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is octreotide used for?

A

Inhibiting secretory events

It is more stable than somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Pasireotide used for?

A

It is another somatostatin analog that is selective for SSTR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What % of AP cells are lactotropes? What do they produce?

A

3-5% of AP cells

Prolactin, structurally related to growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When is prolactin produced in pregnancy?

A
  • Prolactin is produced starting in week 5 of pregnancy
  • High levels of estrogen and progesterone produced by the placenta suppress lactation
  • After parturition (birth) there is a sharp drop in estrogen and progesterone, and so prolactin exerts an effect on lactation
  • Prolactin is stimulated by suckling after the placenta is out of the body.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What negatively regulates prolactin?

A

The hypothalamus regulates prolactin with DA.

28
Q

What does hyperprolactinermia suppress?

A

The HPG axis (hypothalamic-pituitary-gonadal axis) is suppressed, which can disrupt the menstrual cycle about 50% of the time by inhibition of GnRH.

29
Q

The receptors for GH and Prl are very similar. DO they have actions at each other’s receptor?

A

GH can activate Prl R

Prl cannot activate GH R

30
Q

Is Prl R only found in the mammary glands?

A

No, it is also found in hypothalamus (negative feedback), liver, testes, ovaries, prostate, and T cells

31
Q

Are there any drugs that utilize the Prl receptor? Where do drugs that have side effects of lactation work?

A

No drugs utilize the Prl receptor.
Dopamine antagonists (like antipsychotics) have an lactogenic effect.
Dopamine agonists, on the other hand, have an anti-lactogenic effect.

32
Q

If a person is lactating (either gender) and does not want to, what is often used?

A

Bromocriptine

33
Q

What role does HCS play in pregnancy, and how does the level change after delivery of a baby?

A

It is secreted by the placenta starting at 4 weeks, and increases to 1-2 g/day at term. Within 20 minutes of delivery, the levels drop to zero.

  • Deliver glucose to the fetus
  • 96% identical to GH, and has a small amount of activity at GHR to stimulate IGF2 secretion by the placenta to help the fetus grow.
  • Also stimulates lipolysis, gluconeogenesis and glycolysis
34
Q

What does over secretion of HCS possibly cause?

A

Gestational diabetes

35
Q

3-5% of Anterior pituitary cells are what type of cells?

A

Thyrotropes

36
Q

Where is the parathyroid gland located? What does it produce?

A

The parathyroid gland is located within the thyroid gland. It produces parathyroid hormone to regulate serum calcium levels, and therefore the amount of calcium in bone structures.

37
Q

What is the function of iodine in the thyroid?

A

It is necessary for T4/T3 production. Without it, a person would have hypothyroidism.

38
Q

What is cretinism?

A

Hypothyroidism during development. Causes preventable mental retardation.

39
Q

What are the components of a thyroid gland, and what is the function of each part?

A

Follicular cells - Target of TSH, synthesize TH after transporting thyroglobulin into the cell.

Parafollicular cells (C cells) - Secrete calcitonin in response to high serum calcium levels. Not part of HPT axis. Decreases osteoclast activity and increases Ca excretion. Antagonizes actions of parathyroid hormone and D3.

Colloid - Contains thyroglobulin, a precursor protein to T4

40
Q

Describe the pathway of iodine in thyroid hormone formation:

A
  • Iodide enters the follicular cell from the bloodstream, and then is transported to the colloid
  • Iodide is oxidized to iodine by the thyroid peroxidase
  • Iodine is condensed onto thyroglobulin at the 3 position of tyrosine to form MIT
  • More iodine is condensed onto MIT at the 5 position to form DIT
  • Later, 5’ deiodinase removes an iodine from T4 to form T3
41
Q

Describe the function of thyroid peroxidase:

A
  • Oxidizes iodide to iodine in the colloid
  • Condenses iodine onto thyroglobulin at the 3 tyrosine to form MIT
  • Re-iodinates MIT to DIT in the colloid
42
Q

What are the functions of TSH?

A
  • Stimulates iodide uptake into follicular cell and then transport into colloid in the thyroid
  • Stimulates oxidation by the thyroid peroxidase from iodide to iodine
  • Stimulation condensation of iodine onto thyroglobulin at the 3 tyrosine to form MIT
  • Stimulates re-iodination of MIT at the 5 tyrosine to form DIT
  • Stimulates condensation of two DIT molecules to form DIT-DIT
  • Stimulates proteolysis of thyroglobulin, and T4 is released into general circulation.
  • TSH also stimulates size and secretion of the gland in changing the follicular cells from cuboidal to columnar phenotype.
43
Q

Where does T4 get converted to T3, and where does T3 act?

A 
T4 is converted to T3 by the 5' deiodinase in the circulation (maybe at individual tissue levels)
T3 acts:
- negative feedback at pituitary for TSH
- Tissue action 
- Metabolism
- Fecal excretion
44
Q

If a person had high levels of TSH, what might that indicate? How about low levels of TSH?

A

High levels of TSH might indicate that the feedback inhibition is not working, and that there is low levels of T3. The person may be hypothyroid.
Low levels of TSH may indicate that the feedback inhibition is working too well, and that there are high levels of T3 to stimulate this. The person may be hyperthyroid.

45
Q

If a TFT comes back saying that T4 has been found highly protein bound to thyroxine binding globulin, albumin, and thransthyretin, what does that mean for the patient?

A

99% of T4 is protein bound, and so finding high levels bound is considered a normal finding. Only the 1% of free T4 is able to be converted into active T3. Usually high levels of T4 are found, and low levels of T3. Levels of TSH are more important for diagnosing thyroid conditions.

46
Q

What are the thyroid receptor subtypes, and what is their function?

A

Tissue-dependent
Alpha- Deleterious (rapid heart rate, arrhythmia, heart failure, muscle wasting, bone loss)
Beta - Beneficial (Reduced LDL, fat loss)

47
Q

If there was a company developing a drug that targeted nonspecific thyroid receptors, what would you be worried about?

A

Cardiovascular effects, such as arrhythmias, fat heart rate, heart failure, bone loss, muscle wasting.

48
Q

Auto-immune disorder characterized by anti-TSH receptor antibodies. What do these antibodies do, and what disorder is this?

A

The antibodies attack the TSH receptor and keep it constantly stimulated, which produces an effect of hyperthyroidism.
- Grave’s Disease

49
Q

What options are there to treat hyperthyroidism?

A
  1. Drug therapy:
    - Inhibit peroxidase (methimazole or propylthiouracil)
    - Block I- transport with thiocyanate
    - Iodide (high levels inhibit proteolysis and therefore T4 secretion) - not sure how
    - Radioactive iodine (131 used therapeutically to reduce size of thyroid gland - ends up concentrating in salivary glands and destroying parenchyma. 123 used for imaging)
  2. Surgery (resect thyroid)
  3. Adjuvant therapy (Ca channel blockers, beta-AR antagonists to block myocardial effects, glucocorticoids to repress 5’- deiodinase)
50
Q

If you give a corticosteroid to a hyperthyroid person, what will happen?

A

It regulates 5’-deiodinase, so it can repress its action to slow down production of T3

51
Q

What would you want to give to block increased heart rate caused by hypothyroidism?

A

A beta AR antagonist

52
Q

Hashimoto’s Disease

A

Hypothyroid condition

  • Autoimmune disease
  • severe adult form is myxedema
53
Q

What do perchlorate, goiter, TR mutations, and cretinism have in common?

A

They are all implicated in hypothyroidism:

  • Perchlorate may cause hypothyroidism
  • hypothyroid patients develop goiter
  • thyroid resistance may be due to TR mutations
  • Cretinism is hypothyroidism in the womb
54
Q

What type of thyroid hormone do the following formulations contain?

  • Levothyroxine
  • Armour thyroid
  • Cytomel
  • Liotrix
  • Triostat
A 
Levothyroxine is T4
Armour thyroid is a random mix of T3 and T4
Cytomel is T3
Liotrix is T3 and T4 (less T3 though)
Triostat is injectable T3
55
Q

What is the dosing for levothyroxine, and how long does it take to get to steady state?
How do you monitor effectiveness of T4?

A

1.6 ug/kg/day
Takes 5-6 weeks to reach steady state (7 day t1/2)
Take TFT - look at TSH. It should go down after T4 is converted into T3 and the negative feedback loop is activated.

56
Q

What about the structure of amiodarone causes it to interact with the thyroid hormone production?

A

There are two iodine molecules in the structure of amiodarone. These cause it to interfere with the uptake of T4, block the conversion of T4 to T3, and even inhibit the reception of T3. This acutely increases T4, decreases T3, and increases TSH. For most people, this creates a hypothyroid situation. For others, the iodine can stimulate the production of more T4 and there becomes a hyperthyroid issue.

57
Q

What happens after about 3 months of amiodarone use?

A

The HPT axis tends to normalize. However, because the iodine dose has been about 100x the daily dose, levels of iodine in the body will be elevated for about 9 months (long half life)

58
Q

What drug was previously used for nocturnal enuresis?

A

Vasopressin

59
Q

What does rhizopus nigrans do?

A

Add an 11 alpha -OH

60
Q

What does Arthrobacter simplex do?

A

Adds a 1-2 double bond

61
Q

What does chemical oxidation and reduction do from diosgenin to prednisolone?

A

It changes the 11 alpha -OH to a double bonded O, then to an 11 beta -OH for cortisol to prednisolone.

62
Q

What disease is this?

Excessive ACTH and cortisol.

A

Cushing’s Disease

63
Q

What disease is this?
Insufficient cortisol.
Diuresis, hyponatremia/hyperkalemia

A

Primary Addison’s disease

64
Q

What disease is this?

Insufficient ACTH, hypopituitarism

A

Secondary Addison’s disease

65
Q

What disease is this?

Excessive ACTH release, 21-hydroxylase deficiency

A

Congenital adrenal hyperplasia

IDT Spring Term (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions