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Reproduction > Exam 3 lecture 1 > Flashcards

Exam 3 lecture 1 Flashcards

1
Q

Testes function

A

production of gametes and testosterone

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2
Q

duct system organs

A

(epididymis & vas deferens)

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3
Q

Duct system function

A

receive, mature and transport male gametes

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4
Q

accessory gland organs

A

prostate gland, bulbourethral gland and seminal vesicle

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5
Q

accessory gland function

A

secrete fluids that support sperm and generate the bulk of semen

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6
Q

penis function

A

transmit semen

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7
Q

what are the 3 stages of spermatogenesis?

A
  1. mitosis
  2. meiosis
  3. spermiogenesis
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8
Q

where do spematogenesis and spemiogenesis occur?

A

in the seminiferous tubules of testes

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9
Q

mitosis

A

spematogonia undergo mitosis to form primary spermatocytes (2N)

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10
Q

meiosis

A

primary spematocytes undergo meiosis to form secondary spermatocytes (2N) & then spermatids (1N) which are haploid

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11
Q

spermiogensis

A

spermatids mature into spematozoa with development of acrosome & flagella and with loff of most of cell cytoplam

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12
Q

what stage is mostly morphological changes?

A

spermiogenesis (condense chromosomes, elongate, lose cytoplasm, acrosome & flagella formed)

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13
Q

spermatozoa

A
  • are fully differentiated

- head(acrosomal cap) & tail (mitocondria)

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14
Q

how fast can spematozoa move?

A

1-4mm/min

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15
Q

How many sperm are produced/day

A

120 million sperm/day

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16
Q

how much sperm is in semen

A

120 million sperm/ml semen

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17
Q

what is the pH of semen?

A

7.5

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18
Q

what is the lifespan of sperm in the female?

A

24-48 hours

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19
Q

composition of semen

A

fluid & sperm from the vas deferens (10%), fluid from seminal vesicles (60%), fluid from prostate (30%) and small amounts of mucus from bulbourethral glands

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20
Q

what secretes testosterone?

A

leydig cells which are stimulated by LH

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21
Q

MOA of testosterone production

A
  • lipophilic (diffuses into cell)
  • most is converted into dihydrotestosterone (DHT) by 5lpha-reductase
  • DHT binds to androgen receptors in the cytoplasm
  • then enters the nucleus and binds to the hormone response element to induce gene transcriptions and protein synthesis
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22
Q

where are leydig cells located?

A

interstitial tissue in seminal vesicles

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23
Q

what is the more active form of testosterone?

A

DHT

3X greater affinity for androgen receptors than testosterone

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24
Q

what enzyme converts testosterone to DHT?

A

5 alpha-reductase

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25
Q

what else can testosterone be converted into?

A

estradiol via aromatase

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26
Q

what cells have aromatase to make estrogen to help with spematogenesis?

A

sertoli cells

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27
Q

functions of testosterone

A

development of 1* &2* sex characteristics, increased bone growth & Ca retention, increases RBC, increases basal metabolism

28
Q

what is the primary sex charcteristic?

A

enlargement of male sexual organs

29
Q

what are the secondary sex characteristics?

A

body hair (pubis, chest, abs, face, back), baldness, enlargement of larynx (lowering of voice), increased skin thickness & acne (increased sebaceous gland secretions) and increased protein production and muscle development

30
Q

where is gonadotropin-releasing hormone (GnRH) secreted?

A

hypothalamus

31
Q

what does GnRH do?

A

stimulate ant. pit. to secrete LH and FSH

32
Q

what stimulates sertoli cells to initiate spematogenesis?

A

FSH

33
Q

what stimulates leydig cells to secrete testosterone?

A

LH

34
Q

inhibin

A

secreted by sertoli cells and provides feedback to ant. pit.

35
Q

Where are PS impulses that lead to an erection generated?

A

sacral spinal cord

36
Q

an erection is achieved entirely by

A

resulting hemodynamic changes

37
Q

erectile tissue of the penis

A
  • 2 corpus cavernose

- corpus spongiosum

38
Q

erectile tissue is surrounded by

A

a dense collagenous sheath

39
Q

arterial inflow and venous outflow are balanced when?

A

in flaccid state

40
Q

arterial blood flow increases during

A

erection. Causes sinusoids of corposa to fill & leads to penile swelling and elongation

41
Q

PS impulses in an erection

A
  • dilate the arteries of the penis
  • generate nitric oxide (NO)-> incr. guanylate cyclase -> incr. cGMP-> decr,. intracellular Ca-> decr. SMC contraction-> vasodilation-> incr. blood flow-> expansion of the corpus cavernosum which squish veins & trap blood-> ERECTION
42
Q

Sympatheric impulses cause

A

emission and ejaculation

43
Q

emission

A

contraction of vas deferns, prostate gland & seminal vesicles which propel sperm & semen into urethra

44
Q

what stimulates ejaculation?

A

filling of the urethra with semen

45
Q

ejaculation

A

rhythmic, wavelike increases in pressure in the genital ducts and urethra which causes propulsion of the semen from the urethra

46
Q

resolution

A

sexual excitement disappears and erection ceases

47
Q

drugs that can cause ED

A

anticholinergics, DA antagonists, estrogens/antiandrogens, CNS depressants, agents that decr. penile blood flow (diuretics, BB, CNS sympatholytics)

48
Q

causes of ED

A
  • vascular problems: atherosclerosis, PVD, HTN
  • peripheral neuropathies, DM
  • endocrine- hypogonadism, inc. prolactin
  • psychogenic: depression, anxiety
  • drug induced
49
Q

cGMP cause

A

vasodilation of erectile tissue-> erection

50
Q

what degrades cGMP?

A

PDE5

51
Q

what drugs are PDEe inhibitors?

A

sildenafil, tadalafi and vardenafil HCL

- competitively &reversibly inhibit PDE5

52
Q

where else is PDE5 found?

A

peripheral vascular tissue, tracheal smooth muscle and platelets

53
Q

primary hypogonadism

A

< activity of testes-> decr. testosterone or other defect impairing male sexual function

  • starts with testicles
  • serum testosterone & sperm count are LOW and LH/FSH are HIGH
54
Q

secondary hypogonadism

A

improper GnRH signaling-> lack of LH-> lack of andogens.
also lack of FSH-> lack of sertoli cells in sufficient numbers
- ant. pit or hypothalamus
- testosterone & sperm LOW, FSH/LH LOW ot normal

55
Q

androgen insensitivity

A
  • lack of functional androgen receptors

- 5 alpha-reductase deficiency

56
Q

andropause

A
  • condition of reduced testosterone associated with diffuse sexual, physical and psychological symptoms
  • often called late-onset hypogonadism (LOH)
57
Q

can testosterone be given orally as a free drug?

A

no! shows rapid first pass metabolism

58
Q

common testosterone replacement theraoy

A
  • testosterone esters: more lipophilic; given IM
  • alkylated androgens: slower hepatic metabolism & can be given orally; less andogenic than testosterone; may cause hepatotoxicity
  • transdermal patch or gel: lipophilic; avoids first pass metabolism
59
Q

ADE of testosterone

A

acne, male pattern baldness, gynecomastia, reduced sperm production, aggressive behavior, Na retention, predispose to prostatic hyperplasia or cancer-> decreased urinary flow rate, increased Hct, sleep apnea, oral-hepatotoxicity

60
Q

gynecomastia

A

abnormal development of large mammary glands in males

61
Q

benign prostatic hyperplasia (BPH)

A

cell proliferation-> gland enlargement

- urinary urgency, frequency, straining, dribbling

62
Q

prostate cancer is treated with

A

androgen receptor agonists like flutamide

63
Q

what is the most common cause of death from cancer in men over 75?

A

prostate cancer

64
Q

most commonly used androgenic-anabolic steroids (AAS)

A

include testosterone esters- nandrolone, stanozolol, mathandienone, methenolol

65
Q

what are the effects of long term AAS use?

A

suppresses LH/FSH and inhibits testosterone production & spermatogenesis

  • associated with sexual dysfunction, infertility & depression
  • can cause dependence

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