Brainscape's Knowledge GenomeTM

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


See full index

2016 Endocrine > Test 1 Adrenocorticoids > Flashcards

Test 1 Adrenocorticoids Flashcards

1
Q

Starting molecule for all adrenocorticoids

A

Cholesterol

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

HPA axis

A
  • Circadian Rhythm
  • Stress (physical, emotional, and fever, hypoglycemia, and hypotension)

cause release of ACTH (peak in the morning) from HPA Axis

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

ACTH

A

(Adrenocorticotropin hormone) produced and released from the anterior pituitary and stimulates adrenal cortex to produce and release glucocorticoids (cortisol)

  • Proopiomelanocortin is the prohormone (precursor)
    • Produces ACTH, B-endorphin (important peptides that are cleaved from this big peptide)
  • Release is pulsatile & related to waking & meals
    • Cortisol is released after meals and when you wake up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Disorders related to ACTH and cortisol

A
  • Excess: Cushing’s syndrome
    • Hyperfunctioning of adrenal cortex
  • Insufficiency: Addison’s disease
    • Hypofunctioning of adrenal cortex
    • Symptoms: hyperpigmentation, weight loss, inability to maintain blood glucose in fast, hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adrenocortical Steriod Types

A

Adrenocortical hormones are steroid molecules produced and released by the adrenal cortex. Secretion of these hormones is controlled by the pituitary release of ACTH (Note: except aldosterone release which is controlled by angiotensin)

  • Glucocorticoid-intermediary effects on metabolism and immune function
    • Cortisol (humans)
  • Mineralocorticoid-salt retaining activity
    • Aldosterone
  • Androgens-having androgenic and estrogenic activity
    • DHEA: precursor to androstenedione(sense of well-being, vitality, cognition)
      • Low: difficult to think, low energy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hormones produced by:

adrenal medulla

and

andrenal cortex

A
  • Adrenal Medulla
    • Epinephrine and norepinephrine (catecholamines)
  • Adrenal Cortex
    • Cortisol (glucocorticoids)
    • Androgens
    • Aldosterone (mineralocortiocoids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Steroid Receptors

A
  • Steroids travel bound to binding globulin in blood this allows it to travel though the blood somewhat protected from degradation
  • Steroids are lipid-soluble, therefore use intracellular receptors in cytoplasma to form a dimeric-ligand bound receptor complex with hsp90 causing conformational change and loss of the heat shock proteins. The complex is then actively transported to the nucleus to bind GRE
    • Glucocorticoid Responsive Elements (GRE)
      • Mostly induces transcription
      • Also can decrease transcription (example: inhibits COX2 causing anti-inflammatory affects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mineralocorticoids

A
  • Aldosterone and others
    • Important for electrolyte balance, water balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Glucocorticoids

A
  • Most important: Cortisol
    • Influences the function of most cells in the body
    • Metabolic (dose related effects on carbohydrate, protein and fat metabolism)
    • Very potent anti-inflammatory agents (suppress inflammatory cytokines and chemokines)
    • Catabolic and anti-anabolic effects on bone, lymphoid and connective tissue, muscle, peripheral fat, and skin
      • Reducing growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Physiological effects of glucocorticoids

A

redistributes energy to fight infection/stress/etc

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

Physiological effects of glucocorticoids:

on carbohydrate & protein metabolism

A
  • Increases glucose synthesis, decrease peripheral glucose utilization.
    • Net effect of increase blood glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Physiological effects of glucocorticoids:

on lipid metabolism

A
  • Redistributes fat stores (increases insulin secretion which causes lipogenesis causing a net increase in fat deposition)
  • Lipolysis (increases free fatty acids and glycerol into circulation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Physiological effects of glucocorticoids:

on cardiovascular

A

• Primarily via mineralocorticoid action

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

Physiological effects of glucocorticoids:

on central nervous system

A
  • Mood (apathy, depression, psychosis) & memory
  • SE from synthetic steroids (mania, insomnia, anxiety)
  • Don’t take right before bed
  • Neurosteroids, CRH receptors in brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Physiological effects of glucocorticoids:

on skeletal muscle

A

• Muscle wasting due to protein metabolism (increases protein metabolism)

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

Physiological effects of glucocorticoids:

on blood cells

A

• Decreased circulating lymphocytes, eosinophils, monocytes and basophils (decreases immune response)

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

Physiological effects of glucocorticoids:

on inflammation and immune system

A
  • Absolutely correlated with each other
  • Inhibition of leukocyte function
  • Decrease production of vasoactive and chemotractive factors (decreases inflammation)
  • Decrease expression of pro-inflammatory cytokines and COX2
  • Stress or infection activate HPA axis and increase ACTH & ultimately GC, which then suppress immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Major Therapeutic Concerns for Glucocorticoids:

Clinical Conditions

A
  • Addison’s disease
    • Hypofunctioning of adrenal cortex
    • Symptoms: hyperpigmentation, weight loss, inability to maintain blood glucose in fast, hypotension
  • Cushing’s disease (opposite of Addison’s disease)
    • Hyperfunctioning of adrenal cortex
    • Symptoms: central obesity (face, buffalo hump), hypertension, diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Major Therapeutic Concerns for Glucocorticoids:

Abrupt withdrawal from steroids

A
  • Can last several weeks to a year, depending
  • Acute adrenal insufficiency (can be fatal) – it takes the body a while to turn the system back on; glucocorticoids are essential for life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Major Therapeutic Concerns for Glucocorticoids:

Other concerns

A
  • Increased risk of infection
  • Fluid and electrolyte abnormalities
  • Hypertension
  • Hyperglycemia
  • Osteoporosis
  • Myopathy
  • Growth deficiency
  • Cataracts
  • Fat redistribution (fat around torso is bad)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Q: Cortisol is considered ______ in nature

a. Anabolic
b. Catabolic
c. Neutral

A

b. Catabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Q: Destruction of the adrenal cortex would result in compromised ability to synthesize:

a. Mineralocorticoids
b. Cortisol
c. ACTH
d. Sex hormones
e. Epinephrine

A

a. Mineralocorticoids
b. Cortisol
d. Sex hormones (some of them)

Note: ACTH made in anterior pituitary; epinephrine is made in adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Androgens

A
  • Androgens
    • Testosterone
      • Produced primarily in the Leydig cells (men)
      • Produced in the corpus luteum and adrenal cortex (women)
    • Men>>Women (500-700ng/dL, 30-50 ng/dL) very large difference between men and women
      • Naturally men’s levels decrease as he ages
    • Diurnal release with highest levels at waking (take level in the morning)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Androgen Mechanism of Action

A
  • Circulating androgens bound to sex hormone binding globulin
  • Androgen receptor in cytoplasm (intracellular)
  • Receptor-ligand complex dimerizes
  • In nucleus binds to Androgen Response Element
    • stimulates/suppresses gene expression
  • Dihydrotestosterone (DHT) has 5x affinity for androgen receptors vs. testosterone
    • Made from testosterone via 5a-reductase—enzyme that converts testosterone to DHT
    • More potent than testosterone
25
Q

Androgen Effects

A
  • Increase in sexual differentiation & maturation
  • Increases muscle mass (this is why men typically have a higher muscle concentration than women)
  • Bone growth
  • Erythropoiesis
  • Sex drive
  • Male pattern baldness (linked to DHT) – Too much testosterone
  • Prostatic hyperplasia (increase activity in the prostate – not ideal) – may cause cancer, difficult urination
26
Q

Androgen Replacement Therapy

A
  • Androgen-deficiency syndromes (hypogonadal state)
    • Intramuscular injections, transdermal patches, gels/creams, oral
    • Induce secondary male characteristics (facial hair, deepening of voice, increased libido)
27
Q

Side effects of androgen replacement therapy:

A
  • Priapism (erection lasting more than 4 hours)
  • Prostatic hyperplasia
  • Prostate cancer
  • Gynecomastia—WHY? Excess testosterone is broken down into estrogens
28
Q

Spermatogenesis and Male Contraception

A
  • Androgens inhibit LH/FSH secretion & decrease testosterone production
  • Testosterone is concentrated in the testes (100x circulating concentrations)
  • Attempts to manipulate spermatogenesis via hormones results in side effects
  • Lowering GnRH, LH/FSH = decreased testosterone levels
  • Molecular approach that inactivates a gene critical for sperm production (JQ1) – reversible
29
Q

When to use androgen replacement therapy

A
  • low testosterone due to GnRH
30
Q

Anti-androgens and their clinical use

A

Clinical Use: BPH and prostate cancer

  • Androgen receptor antagonists (lipophilic drugs)
    • Flutamide
    • Bicalutamide
  • 5a-reductase inhibition (decrease amounts of DHT)
    • Finasteride
    • Dutasteride

Side Effects:Decreased libido, impotence, gynecomastia (some side effects may be relative to how much activity is being inhibited)

• Useful SE for finasteride: male pattern baldness (side effect is hair growth)

31
Q

Q: Androgens are generally considered

a. Anabolic
b. Catabolic
c. Neutral

A

a. Anabolic

32
Q

Which of the following is NOT a possible side effect of testosterone replacement therapy:

a. Increased sexual drive
b. Reversal of male pattern baldness
c. Increased red blood cell mass
d. Increased muscle mass

A

b. Reversal of male pattern baldness

33
Q

Gonadal Hormones

A

Estrogen

Progesterone

34
Q

Estrogens

A
  • Estradiol (E2)—ovaries (major active estrogen) from testosterone
    • Aromatase breaks down testosterone to make estrone and estradiol
  • Estrone (E1) – from fat - may correlate to levels of obesity
  • Estriol (E3) – made from estrone
35
Q

Progestins

A
  • Progesterone – building block for other sex hormones – steroid (often bound to a binding globulin)
    • Precursor for estrogen, androgen, and adrenocortical hormones
36
Q

Pharmacological Uses for Estrogens

A
  • Contraception
  • Hypogonadism
  • Hormone replacement post menopause
37
Q

Adverse Side Effects of Estrogens

A
  • Uterine bleeding
  • Cancer risks (breast cancer)
  • Nausea
  • Breast tenderness
  • Migraines and headaches
  • Gallbladder dysfunction
  • Hypertension
38
Q

Pharmacological Uses of Progestins

A
  • Hormone replacement post menopause
  • Contraception (only OR in combination)
  • Delay premature labor
  • Test estrogen secretion
    • Premenopausal woman: give supra-physiological dose of progesterone for several days then discontinu → progesterone withdraw should cause menstruation (if it doesn’t occur, this means that the endometrial lining is not building up because estrogen level is low)
39
Q

Adverse Side Effects of Progestins

A
  • May increase blood pressure
  • Can decrease HDL (not preferred)
  • Edema due to sodium retention
  • 3rd generation progestins have less androgenic activity compared to earlier generations
    • cause less facial hair growth, acne
40
Q

Q: Which of the following are associated with ESTROGEN?

a. Onset of menses
b. Increased risk of blood clotting
c. Increased risk of migraines
d. Proliferation of endometrium
e. Increased body temperature
f. Increased fat deposition
g. Sodium retention and bloating

A

b. Increased risk of blood clotting
c. Increased risk of migraines
d. Proliferation of endometrium

Note:

Onset of menses (progesterone level drop)

Increased body temperature (progesterone)

Increased fat deposition (progesterone)

Sodium retention and bloating (progesterone)

41
Q

Q: which of the following hormones could help to predict ovulation?

a. LH
b. FSH
c. Estrogen
d. Progesterone

A

a. LH
b. FSH
c. Estrogen

42
Q

Difference between Ovulation Predictor Kits and Fertility Monitors

A
  • Cost
    • Ovulation predictor kits are cheaper – only tracks rise in LH
    • Fertility monitor is more expensive – tracks LH and estrogen
  • Window of “opportunity”
    • Ovulation predictor kits – 24 – 36 hours
    • Fertility monitor – 2 – 4 days
43
Q

Role of progesterone during early pregnancy

A
  • Corpus luteum will continue to supplement progesterone (and estrogen) for about 10 weeks
    • Corpus luteum (where the follicle was released from) is kept healthy by hCG
  • Placenta takes over production and secretion of progesterone to maintain pregnancy
44
Q

Will extra estrogen and progesterone cause her to miscarry?

A

No, the pills contain progesterone, which is needed to maintain pregnancy

45
Q

Emergency Contraception (the “Morning After” pill): MOA

A
  • MOA—Inhibits ovulation
    • Could (theoretically) prevent implantation
    • Has never been shown
      • Not believed to be the main MOA
46
Q

Types of emergency contraception pills

A
  • Progestin-only pills (levonorgestrel)
  • Combination oral birth control pills
    • Dose and schedule of appropriate pills can be found at www.ec.princeton.edu/questions/dose.html#dose
  • Ulipristal acetate (Ella®)
    • Slightly different MOA—selective progesterone receptor modulator; partial agonist at PG receptors

NOTE: Bleeding post pill caused by progesterone withdrawal

47
Q

Mifepristone (RU846)

A
  • progesterone receptor antagonist
    • Clinical use: abortion
    • Used in conjunction with prostaglandin to induce abortion – about 48 hours after mifepristone
48
Q

Q: For emergency contraceptives: the menses (bleeding) that occurs after their use is caused by:

a. Drop in estrogen levels
b. Drop in progesterone levels
c. Abortion/rejection of fertilized embryo
d. Sheer willpower to not have a baby

A

b. Drop in progesterone levels

49
Q

Hormonal Oral Contraception:

Combined estrogen and progestin

A
  • Allows lower doses of both
    • MOA
      • Inhibits ovulation (main MOA)
      • Increases viscosity of cervical mucus – makes it harder for sperm to navigate to the uterus
      • Decreases formation of the endometrium
      • Decreases flow through the fallopian tubes
50
Q

Hormonal Oral Contraception:

Progestin only

A
  • Usually continuous dosage – must be taken every 24 hours
    • Oral, injectable, subcutaneous
  • MOA
    • Inhibits ovulation (not always – minipill)
    • Increases viscosity of cervical mucus – make it harder for sperm to navigate
    • Decreases endometrium build up
    • Decreases flow through fallopian tubes
51
Q

Return to Normal Cycling on Discontinuation of Oral Contraception

A

Combination pills may show faster return to normal cycling than progestin only formulations

52
Q

Adverse Effects of Oral Contraceptives

A
  • Older formulations vs. newer “low dose”
  • Cardiovascular
    • Hypertension
    • Clots (myocardial infarction, stroke, DVT) – increased risk in smokers
  • Increased risk of cancer
    • Estrogen/progesterone combo→ breast cancer
    • cervical cancer (linked to HPV – should not be hormonally driven)
  • Endocrine & Metabolic
    • Fluid retention (from progesterone component)
    • Cholesterol (increase LDL, decrease HDL)
    • Glucose (small subset of women)
    • Acne/hirsutism(hair growth in woman)
  • Migraines/headaches (E), nausea (E), break through bleeding (E), edema (P), mood effects (E/P), weight gain (controversial)
53
Q

Contraindications for Contraceptives (you should know if concern is for combination and/or progestin only)

A
  • Clotting history or predisposition (due to estrogen)
  • Uncontrolled cholesterol or hypertension
  • Pregnancy
  • Estrogen positive cancer history (personal or family) – shouldn’t take combo
  • Smokers…especially older (should not take combined)
  • Migraine sufferers (should not take combined)
  • Gallbladder (?)
54
Q

Q: A 40 year old smoker approaches you because her doctor suggested that she shouldn’t use combined BC pills… why?

A

Estrogen component

55
Q

Selective Estrogen Receptor Modulators (SERMs)

A
  • Clinical Uses: osteoporosis, breast cancer
  • Act as estrogen agonist in some tissues, antagonists in other tissues
    • Tamoxifen
    • Raloxifene
    • Clomiphene
56
Q

Tamoxifen

A
  • primarily an estrogen antagonist in breast, estrogen agonist in bone and endometrium
    • Used in estrogen (+) breast cancer
57
Q

Raloxifene

A
  • primarily an estrogen agonist in bone, estrogen antagonist in breast (and endometrium?)
    • Used in osteoporosis
58
Q

Clomiphene

A
  • MOA—Estrogen partial agonist (increases amplitude of LH & FSH pulses)
    • Induction of ovulation
    • May result in multiple follicles developing and being released à may produce multiple births

2016 Endocrine (19 decks)

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