Brainscape's Knowledge GenomeTM

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


See full index

AU 15 - Pharm Final > Endocrine #2 > Flashcards

Endocrine #2 Flashcards

1
Q

Osteoblasts

A

Bone generating cells

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

Osteocytes

A

Mature bone cells
Spider shaped
Maintain bone tissue

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

Osteoclasts

A

Bone destroying cells

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

Bone formation

A

The process by which osteoblasts synthesize bone

Osteoblasts function in groups of connected cells

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

Osteons

A

Group of organized osteoblasts together that make bone

Individual osteoblasts cannot synthesize bone by themselves

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

Bone resorption

A

The process by which osteoclasts break down bone and release the minerals, resulting in a transfer of calcium from bone fluid to the blood

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

Bone homeostasis

A

The balance between bone formation and bone resorption

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

If the body is low on Ca, what occurs?

A

Parathyroid hormone (PTH) will be released and

1) bone resorption will increase
2) Ca elimination by the kidney will decrease
3) Ca absorption increases in the gut

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

Parathyroid hormone

A

88 aa protein, only the first 34 are required for activity

T1/2 in plasma ~4 minutes

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

What are the parathyroid receptors?

A

PTHR1

PTHR2

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

PTHR1

A

Located in bone and kidneys
Activation leads to expression of RANK ligand (RANKL) - leading to bingin and activation of osteoclasts and bone resorption

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

PTHR2

A

Located in CNS, pancreas, testis, placenta

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

What effects does PTH have on the kidney?

A

Maximize Ca resorption
Decrease PO4 resorption
Enhance vitamin D production

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

PTH effect on vitamin D

A

PTH enhances the production of calcitrol (active form of vitamin D)
This enhances the absorption of Ca from the gut

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

Calcitrol

A

Plays a complex role in the Ca homeostasis

  • Increases Ca absorption in the gut (main one)
  • decrease Ca excretion in kidney
  • increase bone resorption and mineralization
  • increase osteoclasts development
  • decrease PTH secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F - Vitamin D is only related to Calcium

A

False - Most cells have vitamin D receptors

There are hundreds of vitamin D responsive genes

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

Calcitonin

A

Released by parafollicular cells of the thyroid in response to high serum Ca concentrations
Counteracts the effect of PTH

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

What are the effects of Calcitonin

A

Increases bone formation
Decreased kidney resorption of Ca
Decreases Ca absorption by the gut

19
Q

Bisphosphonates

A

A class of drugs that prevent the loss of bone mass
Used to treat osteoporosis and similar diseases
Most commonly prescribed drugs to treat osteoporosis

20
Q

Bisphosphate effects

A

Inhibit bone resorption and osteoclast activity
Restore bone density
Mechanism is not totally understood

21
Q

Where do androgens (Testosterone) come from?

A

95% come form Leydig cells of the tests (some come from ovary)
5% from the adrenal gland

22
Q

What stimulates testosterone synthesis and release?

A

LH

23
Q

Theraputic use of Androgen

A

Androgen deficiency (low T, etc)

24
Q

What are the major types of Estrogen?

A

Estradiol (E2)
Estrone (E1)
Estriol (E3)

25
Q

Estradiol (E2)

A

Major secretory product of ovary

26
Q

Estrone (E1) and Estriol (E3)

A

Made in liver from estradiol

27
Q

Natrual estrogens

A

From which synthetic estrogens were derived (estradiol, estrone, estriol)

28
Q

Synthetic estrogens

A

Most commonly used in oral contraceptives

29
Q

Synthetic nonsteroidal compounds with estrogenic activity

A

Have also been used clinically

30
Q

What are the major clinical uses of Estrogen?

A

Primary hypogonadism
Postmenopausal hormonal therapy
Other uses

31
Q

How is estrogen used to help treat hypogonadism

A

For replacement therapy in estrogen-deficiencies due to underdeveloped ovaries, premature menopause, castration, or menopause
Attempts to mimic physiology of puberty

32
Q

How is estrogen used to help treat postmenopausal hormonal therapy

A

Prevent hot flashes and osteoporosis

Use only the lowest possible doses because of increased risks for breast and endometrial cancer

33
Q

Estrogen receptor and treatment of breast cancer

A

If the breast cancer cells are estrogen receptor positive, estrogen is likely to be driving cell proliferation
The drug tamoxifen antagonizes the effect of estrogens in breast cancer cells and blocks proliferation

34
Q

Class 1 Nuclear Receptor Molecular Biology

A

1) Binding of agonists (eg estradiol to estrogen receptor) produces a conformational change that exposes AF-2 region of the receptor
2) Co-activator proteins such as SRC-1 can only bind to the receptor if AF-2 is exposed. Thus, the co-activators only bind to the receptor if agonist is bound
3) Antagonists bind perfectly well to the receptor, but their binding does not lead to exposure of AT-2. Therefore, the antagonist receptor binds to the DNA, but does not bind co-activators, and the antagonist does not activate transcription

35
Q

Tamoxifen

A

It’s a SERM (selective estrogen receptor modultor)
Acts as an antagonist in some tissues but acts as an agonist in other tissues
It is speculated that things like availability of co-activators determines if it acts as an agonist or antagonist

36
Q

Where are progestins synthesized?

A

Corpus luteum
Placenta
Adrenal cortex

37
Q

Progestins are the precursors to what?

A

Androgens
Estrogens
Adrenocortical hormones

38
Q

Progestins play a biological role in what?

A

Menstrual cycle and pregnancy
side note: males have progesterone receptors too, but it’s not tremendously understood what effects they have on male sexuality

39
Q

What is required during menstrual cycle for follicle development, ovulation, and pregnancy?

A

Coordinated pattern of FSH and LH secretion

40
Q

What are the clinical uses of Progesterone?

A 
Hormonal replacement therapy
Contraception
Diagnosis: estrogen secretion
Dysmenorrhea
Endometriosis
41
Q

What effect do Estrogen + Progesterone oral contraceptives have?

A

Block LH and FSH release from the pituitary

42
Q

What effect do Progesterone oral contraceptives have?

A

Thickening of cervical mucus (blocks sperm from contacting egg)
Block release of eggs from the ovary

43
Q

What are the types of emergency oral contraceptive pills?

A

1) Higher doses of progesterone alone, or progesterone plus estrogen

2) RU486 (mifepristone) - a low efficacy progesterone partial antagonist
- lower dose: emergency oral contraceptive
- higher dose: abortifacient (first several months)

AU 15 - Pharm Final (7 decks)

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