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Pathophysiology Endocrine > Module #3: Adrenal Cortex and Reproductive Hormones > Flashcards

Module #3: Adrenal Cortex and Reproductive Hormones Flashcards

1
Q

What is the role of the Adrenal Gland in the endocrine system?

A

Response to stress

Maintain water/salt equilibrium

Maintain BP

Sympathetic function = “extension of ANS”

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2
Q

What are the 2 regions of the adrenal gland?

A

Medulla

Cortex

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3
Q

What does the adrenal medulla do?

A

Release catecholamines –> epinephrine and norepinephrine

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4
Q

What does the adrenal cortex do?

A

Release aldosterone, cortisol, and dehydroepiandrosterone (DHEA)

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5
Q

What are the 3 layers of the adrenal cortex?

A

Zona glomerulosa = outer

Zona fasiculata = middle

Zona reticularis = inner

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6
Q

What does the zone glomerulosa do?

A

produce/secrete mineralcorticoids (ie aldosterone)

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7
Q

What does the zona fasiculata/zona reticularis do?

A

produce/secrete glucocorticoids (cortisol) and adrenal androgen (DHEA)

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8
Q

What is the first step of hormone synthesis in the adrenal cortex?

A

cholesterol –> pregnenolone

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9
Q

What is the enzyme that converts cholesterol to pregnenolone?

A

desmolase

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10
Q

What is the stimulus of the conversion of cholesterol to pregnenolone?

A

ACTH from anterior pituitary

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11
Q

What happens after cholesterol is converted to pregnenolone?

A

Pregnenolone can follow 3 pathways to form aldosterone, cortisol, or DHEA

will go to a different region to be converted to the different hormones (each region has specific enzymes for one of the pathways)

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12
Q

Which enzymes do the zona glomerulus (outer layer) contain?

A

enzymes to convert pregnenolone –> aldosterone

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13
Q

Which enzymes do the zona fasiculata (middle)/zona reticularis (inner) contain?

A

enzymes that will convert pregnenolone –> cortisol OR DHEA

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14
Q

What happens if there are deficiencies in the adrenal cortex enzymes?

A

Siginifcant adrenal pathology

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15
Q

How are adrenal cortex hormone production regulated?

A

Syntehsized @ rate of demand

NOT stored!

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16
Q

How do adrenal hormone levels fluctuate?

A

Follow Circadian Rhythm Pattern

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17
Q

What are the adrenal hormone stimulus signaling steps (start w/ hypothalamus)?

A

Hypothalamus releases CRH

CRH stimulates anterior pituitary to release ACTH

ACTH stimulates desmolase activity (cholesterol –> pregnenolone)

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18
Q

What is aldosterone influenced by?

A

Angiotensin II

ECF (extracellular fluid) K+ levels

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19
Q

What inhibits adrenal cortex hormone production?

A

Increased levels of cortisol inhibits release of ACTH and CRH = negative feed back loop

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20
Q

Where are glucocorticoids (cortisol) produced?

A

Zona Fasiculata

Zona Reticularis

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21
Q

What stimulates cortisol secretion?

A

ACTH from anterior pituitary

Normal Circadian Rhythm

Stress

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22
Q

What is the normal circadian rhythm of cortisol release?

A

Released between midnight and 8 am –> peak just before awakening

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23
Q

How does stress stimulate the release of cortisol?

A

Stimulates the release of ACTH

Alter normal circadian rhythm

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24
Q

What inhibits cortisol secretion?

A

Elevated levels of cortisol inhibits ACTH and CRH

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25
Q

What is the function of cortisol?

A

Acts as response to normal human stress:

Catabolic to produce/mobilize/store glucose

Maintains fluid volume

Modulates the immune system (anti-inflammatory response)

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26
Q

What are the target tissues of cortisol?

A

Bone

Adipose (fat) cells

Muscle

Tendon/Ligament/Connective Tissue

Immune System

CNS

Metabolism

Others

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27
Q

What is the action of cortisol on bones?

A

Stimulate osteoclasts/Ca2+ resorption –> decrease bone density

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28
Q

What is the action of cortisol on adipose cells?

A

Stimulate lypolysis –> mobilize FFA and glycerol for fuel and production of “new” glucose

Synergistic w/ glucagon, GH, catecholamines

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29
Q

What are the adverse results of cortisol stimulating lypolysis?

A

FFA are redistributed –> central obesity

Also leads to poor lipid profile

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30
Q

What is the action of cortisol on muscle?

A

Stimulates proteolysis –> mobilize amino acids for fuel and production of “new” glucose

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31
Q

What is the adverse result of cortisol on muscle?

A

Muscle wasting/weakness

Loss of lean body mass

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32
Q

What is the action of cortisol on tendon/ligaments/ connective tissue?

A

catabolic effect –> inhibits fibroblasts/collagen production

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33
Q

What is the adverse result of cortisol on tendon/ligaments/ connective tissue?

A

Ligament/Tendon failure

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34
Q

What is the beneficial action of cortisol on the immune system?

A

Anti-inflammatory –> decrease PGs, histamine, bradykinin, serotonin

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35
Q

What is the adverse action of cortisol on the immune system?

A

Poor wound healing/immune defenses –> impair T-lymphocytes, eosinophils, basophils, ILs, cell mediated immune response, antibody response, etc

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36
Q

What type of cortisol therapy is considered ok?

A

5 day taper

problem when its longer or high dose

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37
Q

What is the action of cortisol on the CNS?

A

Alters perception/mood

Negative feedback to hypothalamus (CRH)/anterior pituitary (ACTH)

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38
Q

What is the action of cortisol on metabolism?

A

Alters intermediary metabolism to produce, mobilize, store glucose

Liver = gluconeogenesis/glycogenesis

Optimizes/enhacnes effect of glucagon (lipolytic, impair glucose uptake) and catecholamines

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39
Q

Why does cortisol alter intermediary metabolism to produce/mobilze/store glucose?

A

Trying to save glucose for CNS survival –> stress response

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40
Q

What does gluconeogenesis do?

A

Uses FFA, glycerol and amino acis to form “new” glucose”

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41
Q

What is glycogenesis?

A

Glucose is stored as glycogen

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42
Q

What are the other effects of cortisol in the body?

A

Vasoconstriction/bronchodilation –> optimizes/enhances effect of caetcholamines

Fetal lungs –> surfactant production and lung development

Enhances bodes ability to tolerate stress –> cold, heat, trauma

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43
Q

Where are mineralcorticoids (aldosterone) produced?

A

Zona glomerulosa (outer)

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44
Q

What is the function of aldosterone?

A

Increase blood volume and BP by regulating renal sodium resorption = primary

Decrease plasma potassium

Increase plasma pH –> alkaline

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45
Q

How does aldosterone regulate renal sodium resorption?

A

Increases Na+ resorption in distal nephrone

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46
Q

What is the consequence of increasing Na+ resorption?

A

Increase H2O absorption (gradient follows Na+)

Facilitates K+ excretion –> decreases plasma K+

Facilitates H+ excretion –> increase plasma pH (more alkaline) and decreases urine pH (more acidic)

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47
Q

Describe the role that aldosterone has been suggested to play in vasoconstriction

A

Research suggests aldosterone is produce/secreted by non-Adrenal tissue and have paracrine effect –> aldosterone’s peripheral release contributes to vasoconstriction of blood vessels

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48
Q

What stimulates the release of aldosterone?

A

ACTH (not as influential as angiotensin II/K+ levels)

Angiotensin II

Hyperkalemia

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49
Q

Which system is angiotensin II involve in?

A

Renin-angiotensin system

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50
Q

What does the Renin-Angiontensin system do?

A

Slow hormonal system of BP regulation

Sensory cells in the kidneys monitor perfusion pressure and Na+ content of blood

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51
Q

What stimulates the release of renin from the kidney?

A

Decreased blood volume

Decreased Na+ concentration

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52
Q

Which cells release renin in the kidney?

A

Juxtaglomerular cells

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53
Q

What does renin do?

A

Trigger cascade that eventually produces angiotensin II

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54
Q

Where does the conversion of angiotensin to angiotensin II happen?

A

Blood stream

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55
Q

What is the enzyme that catalyzes the conversion of angiotensin to angiotensin II and where is it produced?

A

ACE = angiotensin- converting enzyme

produced in lungs

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56
Q

Clinically, what do ACE inhibitors do?

A

block the conversion of angiotensin –> angiotensin II –> lower BP

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57
Q

What does angiotensin II do?

A

Stimulate the production/secretion of aldosterone

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58
Q

What does hyperkalemia do?

A

Stimulates release of aldosterone from adrenal cortex

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59
Q

Does the K+ mechanism occur independently or dependently from the renin system?

A

Independently

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60
Q

What inhibits aldosterone secretion?

A

Hypernatremia = increased Na+ d/t overproduction or loss of H2O

ANP = atrial natriuretic peptide

Elevated ACTH levels (negative feedback)

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61
Q

Where does ANP come from?

A

Released in atria in response to increased BP

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62
Q

What does ANP do?

A

Inhibits renin release

Increases excretion of Na+/H2O –> opposite of aldosterone

Relaxes smooth muscles of smooth muscle vascular system –> dilation decreases TPR

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63
Q

What are the adrenal androgens?

A

DHEA = dihydroepiandrosterone

Androstenedione

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64
Q

Where are the adrenal androgens produced?

A

Zona Fasiculata (middle)

Zona Reticularis (inner)

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65
Q

What are androgens?

A

Sex hormones associated w/ the development/maintenance of male sexual characteristics –> deep voice, hair, baldness, etc

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66
Q

Are androgens only important in males?

A

No, also critical for females

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67
Q

What do androgens do in females?

A

Maintain muscle mass

Maintain bone density

Sexual desire

Sense of well being

Estrogen production

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68
Q

What happens when females have low androgen levels?

A

Low Libido

Muscle/bone mass loss

Fatigue

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69
Q

In males where are androgens produced?

A

Testes = testosterone

Adrenal cortex = DHEA/Androstenedione (later converted to testosterone)

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70
Q

In females where are androgens produced?

A

Ovaries = testosterone

Adrenal cortex = DHEA/Androstenedione (later converted to testosterone)

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71
Q

In females what happens to the majority of testosterone?

A

Converted to estrogen

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72
Q

Which adrenal gland androgen is produced in greater quantity?

A

DHEA

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73
Q

What happens to DHEA and androstenedione?

A

Converted to testosterone in periphery

74
Q

Which tissues are involved in DHEA and androstenedione conversion?

A

Gonads

Adipose tissue

Sebaceous glands

Hair follicles

Prostate

75
Q

In males does the conversion of DHEA and andostenedione contribute significantly to overall testosterone levels?

A

No

Most testosterone is produced in testes

76
Q

In females does the conversion of DHEA and androstenedione contribute significantly to overall testosterone levels?

A

Yes

Approximately 50% of circulating testosterone

77
Q

What is the most abundant circulating hormone in the body?

A

DHEA

78
Q

What kind of androgen is DHEA?

A

“Weak Androgen” –> poor binding affinity to androgen receptors in body

79
Q

What role does the adrenal gland androgens have in females?

A

Play role in axillary and pubic hair growth

80
Q

What role does the adrenal gland androgens have in males?

A

Not a significant role

Gonadal testosterone plays much bigger role in masculinization

81
Q

What happens in males if there is an excessive amount of adrenal androgens?

A

Adults = no effect

Pre-puberty = isosexual precocious puberty –> early puberty; definite as < 9 yo

82
Q

What happens in females if there is an excessive amount of adrenal androgens?

A

Adults = masculinization effects –> cystic acne, hirsutism, male type baldness, menstrual irregularities, infertility, and/or frank virilization

Pre-puberty = heterosexual precocious puberty –> girls develop secondary male characteristics; defined as < 8 yo

83
Q

What stimulates adrenal androgen secretion?

A

ACTH

84
Q

What inhibits adrenal androgen release?

A

Cortisol

85
Q

What are some clinical diseases of the adrenal cortex?

A

Addison’s Disease

Hyperadrenalism = Cushing’s Syndrome or Cushing’s Disease

Primary Hyperaldosteronism = Conn’s Syndrome

85
Q

What is Addison’s Disease?

A

Adrenalcortical insufficiency

Desruction of adrenal cortex –> loss of ALL adrenal cortex hormones

85
Q

What will the labs of a pt with Addison’s look like?

A

Elevated ACTH (trying to stimulate adrenal cortex)

Decreased levels of adrenal hormones

85
Q

What will the labs of a pt with Addison’s look like?

A

Elevated ACTH (trying to stimulate adrenal cortex)

Decreased levels of adrenal hormones

86
Q

What are some clinical diseases of the adrenal cortex?

A

Addison’s Disease

Hyperadrenalism = Cushing’s Syndrome or Cushing’s Disease

Primary Hyperaldosteronism = Conn’s Syndrome

87
Q

What is the effect of Addison’s on the zona glomerulosa?

A

Decreased mineralcorticoids (aldosterone) secretion

87
Q

In addition to dehydration and polyuria what else do you see in pts w/ excessive excretion of Na+ and H2O?

A

Hypotension

Hyponatremia (Na+ levels)

Decreased blood volume –> circulatory failure

87
Q

What happens in the body w/ increased K+ and H+ retention?

A

Hyperkalemia

Metabolic acidosis

87
Q

What is the effect of Addison’s on the zona reticularis and zona fasiculata?

A

Decreased glucocorticoids (cortisol) secretion

Decreased adrenal androgens

87
Q

What are the consequences of decreased glucocorticoid secretion?

A

Hypoglycemia

Fatigue

Loss of appetite

87
Q

What are the consequences of decreased adrenal androgens?

A

Female = decreased axilla/pubic hair

Hperpigmentation –> elevated ACTH –> elevated MSH

Weakness

Anorexia

Weight loss

Nausea

87
Q

What are the 2 conditions of hyperadrenalism (excessive adrenocortical hormones)

A

Cushing’s Syndrome

Cushing’s Disease

87
Q

What is Cushing’s Syndrome?

A

Excess cortisol of any pathology

87
Q

What are some of the causes of Cushing’s Syndrome?

A

Tumor Secreting Glucocorticoids

Prolonged pharmaceutical usage of glucocorticoids

Effects = primarily elevated cortisol levels

87
Q

What is Cushing’s Disease?

A

Excessive ACTH –> excess cortisol

87
Q

What is a cause of Cushing’s Disease?

A

Tumor in pituitary –> excessive/elevated ACTH

87
Q

Besides elevated cortisol what else can be elevated in pts w/ Cushing’s Disease?

A

Mineralcorticoids

Adrogenic Effects

87
Q

What are the effects of increased glucocorticoids?

A

Poor would healing = decreased immune function

Hyperglycemia (d/t increased cortisol) –> glycosuria

Muscle wasting (d/t increased protein catabolism)

Osteoporosis (d/t increased cortisol)

Central Obesity (face/trunk = round, Buffalo Hump)

87
Q

What are the effects of increased mineralcorticoids?

A

Hypertension (d/t elevated aldosterone and cortisol)

87
Q

What are the effects of increased adrenal androgens?

A

Females:

Virilizition

Menstrual Disorders

87
Q

What causes primary hyperaldosteronism aka Conn’s Syndrome?

A

Tumor of adrenal cortex that secretes aldosterone?

87
Q

What are the results of Conn’s Syndrome?

A

Hypertension (increased ECF volume) –> increase Na+ and H2O reabsorption in kidneys

Hypokalemia –> increase K+ secretion in kidneys

Metabolic alkalosis –> increased H+ secretion in kidneys

87
Q

What determines fetal sexual differentiation?

A

Sex Chromosomes:

Males = XY

Females = XX

88
Q

Describe fetal male genitalial differentiation

A

Y chromosome secretes SRY antigin –> gonads into testes

Testes secrete testosterone:

Wolffian Duct –> epididymis, vas deferens, seminal vesicle

Sertoli Cells –> MIH (Mullerian-inhibitng factor) prevents Mullerian Duct from becoming female

Prostate converts Testeserone to DHT (dihydrotestosterone) –> scrotum, penis, prostate gland

89
Q

Describe fetal female genetalial differentiation

A

NO SRY antigen –> glands into ovaries

No male hormones:

MIH not release –> Mullerian duct becomes fallopian tubes, uterus, vagina

Wolffian duct DOESN’T become epididymus , vas deferens, and seminal vesicle

89
Q

What are the primary male sex organs?

A

Testes

90
Q

What does the testes do?

A

Produce testosterone

Produce spermatogenisis –> spermatozoa

91
Q

What are the consequences of decreased aldosterone secretion?

A

Excessive excretion of Na+ and H2O in Urine –> dehydration and polyuria

Excessive retention of K+ and H+

92
Q

What are the 2 hormones that are required to produce spermatozoa?

A

Testosterone

FSH

93
Q

Where is testosterone synthesized in the testes?

A

Interstitial Cells of Leydig

94
Q

What are the physiological effects of testosterone?

A

Anabolic Effects

Androgenic Effects

95
Q

What are the anabolic effects of testosterone?

A

Stimulate GH secretion –> IGF-1 release

@ End of puberty promotes mineralization (closure) of growth plates

Stimulates protein synthesis in muscles

96
Q

What are the androgenic effects of testosterone?

A

Regulate development and maintenance of male accessory sex organs

Plays role in differentiation of male productive tract and brain

@ Puberty = development of secondary males sexual characteristics

Plays role in libido/potency (spermatogenesis)

97
Q

What are the secondary male sex characteristics developed @ puberty?

A

Laryngeal changes = deep voice

Growth of facial, pubic, axillary hair

Receding hair pattern @ temples

Increase muscle mass (protein anabolism)

Stimulate growth spurt

Influence sex drive

Influence sexual behavior

Increased sebaceous gland excretion –> acne

98
Q

What happens to testosterone when adults age?

A

Gradually decreases (slow and steady)

100
Q

What does GnRH do?

A

Stimulates LH and FSH release from anterior pituitary

101
Q

What does LH (leutinizing hormone) do?

A

Stimulates the synthesis and secretion of testosterone from testes

102
Q

What inhibits LH?

A

Increased blood levels of testosterone (negative feedback loop)

103
Q

What does FSH do?

A

Stimulates spermatogenesis (sertoli cells)

Stimulates release of Inhibin from testes

105
Q

Approximately when does male puberty occur?

A

13 - 16

120
Q

What are the hormones that regulate testes and testosterone?

A

GnRH:

LH

FSH

125
Q

What does inhibin do?

A

Inhibits anterior pituitary from releasing FSH –> spermatogenesis

127
Q

What does the hypothalamus do during male puberty?

A

Secretes GnRH in bursts

128
Q

What does GnRH stimulate in the anterior pituitary during puberty?

A

Increased Release of FSH and LH

129
Q

In males what does increased LH do?

A

Stimulates testes to produce and release testosterone

130
Q

In males what does the increased testosterone do during puberty?

A

Stimulates androgenic/anabolic changess

Increased blood levels of testosterone inhibit release of GnRH from anterior pituitary (negative feedback)

131
Q

In males during puberty what does increased FSH do?

A

Initiates spermatogenesis

Stimulates secretion of inhibit (cells of sertoli) –> inhibits FSH release from anterior pituitary (negative feedback)

132
Q

What happens if there is atrophy of the testes @ the time of normal puberty?

A

Sex organs remain small

Secondary sex characteristics fail to develop

133
Q

What happens if there is atrophy of the testes after puberty?

A

Sterility –> no spermatogenesis

Testosterone production decreases –> atrophy of secondary sex organs (penis, scrotum, prostate)

134
Q

What are the female primary sex organs?

A

Ovaries

135
Q

What do the ovaries do?

A

Oogenesis –> production of female germ cells (ova)

Produce: estrogen and progesterone

136
Q

What is estrogen involved in?

A

Menstrual Cycle

Fertilization

Puberty

Bone Metabolism ((+) effect on bone density)

Blood Chemistry

CNS Responses

137
Q

What does estrogen do during the menstral cycle?

A

Accelerates the maturation of ovarian follicles right before ovulation

Thickens Endometrium

Increases Uterine Muscle Contraction

Changes properties of vagina to assist in fertilization

Prepares mucous plug of the cervical os to allow sperm to enter the uterus

138
Q

What is the role of estrogen during fertilization?

A

Prepare the sperm to penetrate/fertilize ovum

Regulate the speed that the ovum travels in Fallopian tube

139
Q

What does estrogen do to females during puberty?

A

Stimulate ductal development in breast

Induces changes in the vagina

Changes in subucatenous fat distribution

Synergistic w/ adrenal androgens –> axillary/pubic hair

Accelerate epiphyseal plate closure

Regulate development and maintenance of female secondary sex characteristics

140
Q

What are the female secondary sex characteristics?

A

Narrow Shoulders

Wide Pelvis

Wide Carrying Angle

Etc

141
Q

What are functions of estrogen on bone density?

A

Accelerate epiphyseal plate closure @ puberty

Increase Ca2+ retention in the kidney

Increase osteoblastic activity

142
Q

What is estrogens role in blood chemistry?

A

Positive effect on blood cholesterol (increase HDL/VLDL; decrease LDL)

Increase coagulation –> increase risk of thrombosis w/ excessive levels

Increase Na+ and H2O retention in kidneys

143
Q

What does estrogen do in the CNS?

A

Influence sexual response, sexual behavior, mood

144
Q

What are the major functions of progesterone?

A

Prepare female genitalia for implantation/maturation of fertilized ovum

Maintain pregnancy

145
Q

What is the target tissue of progesterone?

A

Uterus

146
Q

What does progesterone do in the uterus?

A

Stimulates the growth of uterine muscles (myometrium)

Increase blood supply to the endrometrium

Promotes implantation by decreasing uterine muscle activity

Narrows cervical os and changes mucous plug to prevent sperm from entering uterus

Increases basal body temperature (metabolic)

147
Q

When is progesterone given as birth control?

A

During follicular phase

148
Q

How does progesterone work as a contraceptive?

A

Inhibits LH –> inhibit ovulation

Inhibit the effects on cervical os and mucous plug

149
Q

When given in combination, what does progesterone and estrogen do?

A

Prevent LH/FSH release

21 days on; 5-7 off = menstrual flow

150
Q

What are the effects of high doses of progesterone?

A

Anesthetic effect on CNS

Increases susceptibility to epileptic episodes

Increase basal body temperature

151
Q

When do you observe a decrease in progesterone?

A

Postpartum

Luteal Phase

152
Q

Clinically what is decreased levels of progesterone suspected to be involved in?

A

Postpartum depression

PMS

153
Q

What is the general overview of the Menstrual cycle beginning w/ Day 1 as the start of menstruation?

A

Day 1 - 14 = Follicular Phase

Day 14 = Ovulation

Days 14 - 28 = Luteal Phase

154
Q

How long does a normal mentruation last?

A

2 - 6 days

155
Q

What happens during the follicular phase?

A

Endrometrium thickens

Approximately 20 follicles mature (FSH) –> 1 becomes dominant and others degenerate

Days 12 - 13 estrogen levels increase (+ feedback on LH) –> stimulate surge of LH

156
Q

What happens during ovulation?

A

Surge of LH –> ovum release from follicle

Cervical mucous has thinned (spinnbarkeit)

Cervical Os opens slightly (allow sperm to enter uterus)

157
Q

What happens during the luteal phase?

A

Follicle = corpus luetum

Corpus Luetum –> increased progesterone/estrogen

Progesterone releaxes uterine muscle activity –> implantation if ovum is fertilized

No fertilization –> estrogen/progesterone fall –> decrease blood flow to endrometrium

Ischemia of endometrium –> menses (break down of uterine lining and bleeding)

158
Q

Hormonally what is happening during the early follicular phase?

A

GnRH = released from hypothalamus

GnRH stimulates release of FSH/LH from anterior pituitary

LH/FSH stimulate production of estrogens

Estrogens enter blood stream –> (+) feedback on FSH receptors in follicles

159
Q

What is the specific role of LH in the production of estrogens?

A

Stimulates production of androgens (androstenedione/testosterone) in the ovaries
(internal cells of the follicles)

160
Q

What is the specific role of LH in the production of estrogens?

A

Stimulates production of aromatase in ovary (grandulosa cells of the follicles) –> converts androgens to estrogens

161
Q

Hormonally what is happening during the mid-follicular phase?

A

Dominant follicle emerges continues to produce estrogen ( (+) feedback)

Apoptosis of non-dominant follicles

162
Q

Hormonally what is happening during late-follicular phase?

A

Estrogen levels increase –> ( (+) feedback on release of LH)

Surge of LH

163
Q

What happens if there is a slow surge of LH or no surge of LH?

A

Ovulation doesn’t occur

164
Q

Hormonally what is happening during the Luteal Phase of the Menstral Cycle?

A

Ovum released –> Corpus Luetum

Corpus Luetum secretes progesterone and estrogen

Progesterone/estrogen INHIBIT release of FSH/LH ( (-) feedback) –> decrease in progesterone/estrogen as luteal phase progresses

Low levels of progesterone/estrogen –> constriction of blood flow to endometrium –> menses –> new cycle

165
Q

What happens if fertilization occurs?

A

Progesterone/estrogen levels stay elevated

166
Q

Where are the pregnancy hormones produced?

A

Placenta

hCG produced from syncytioltrophoblast until placenta is fully developed

167
Q

What is hCG?

A

Human Chorionic Gonadotropin

168
Q

What is the function of hCG?

A

Maintains production of estrogen/progesterone in corpus luetum until placenta takes over

Suppresses follicle maturation in maternal ovaries

169
Q

What can hCG be used for?

A

Pregnancy Test

Measurable 6 - 8 days after conception

170
Q

Which hormones does the placenta produce?

A

Progesterone

Estrogen

Corticotropin Releasing Hormone (CRH)

Human Placental Lactogens (hPLs)

171
Q

What does CRH do?

A

Plays role in regulation of birth

172
Q

What happens to the concentration of CRH during pregnancy?

A

Increases

173
Q

What is the rate of concentration of CRH critical for?

A

Timing of birth

174
Q

What happens if there is an increased rate of CRH?

A

Contributes to premature birth

175
Q

What happens if there is a decreased rate of CRH?

A

Contributes to delayed birth

176
Q

What does hPL do?

A

Plays role in lactation and physical growth

177
Q

When does menopause typically occur?

A

45 - 55

178
Q

What happens during menopause?

A

Ovarian tissue gradually ceases to respond to FSH/LH

Decreased levels of estrogen/progesterone

179
Q

What happens to the menstrual cycle when the ovaries stop responding to FSH/LH?

A

Irregular Cycles

Gradually Stop Cycle

180
Q

What happens during menopause when estrogen/progesterone levels decrease?

A

Regression of secondary sex characteristics

Atrophy of breast tissue

Thinning of pubic/axillary hair

Accessory sex organ Atrophy:
          Fallopian tubes shrink
          Vaginal epithelium thins (decreases  
          secretions)
          Exteneral genitalia shrinks

Mood changes

Increase risk of osteoporosis –> loss of estrogen

Increased Cardiovascular risks –> loss of estrogen

Pathophysiology Endocrine (3 decks)

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