Male Repro Flashcards

1
Q

Products of Sertoli cells

A

Inhibin: inhibits release of FSH
Activin: promotes release of FSH
AMH: ensure Wolffian duct will form
ABP: binds testosterone to keep it high in seminiferous tubules for the production of

Form blood testes barrier

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2
Q

Prostate Cancer

A

Prostate relies entirely on DHT
Therapies involve reducing the amount of testosterone produced:
-5alpha reductase (converts testosterone into DHT) when the tumor is androgen dependent
-GnRH agonist/antagonist
-Glucocorticoids
-CYP17 inhibitor
-AR antagonist
-estrogen treatment (to downregulate the pulse generator)

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3
Q

5 alpha reductase

A

Converts testosterone into potent DHT in peripheral tissues, specifically the external genitalia

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4
Q

DHT is more potent because

A

Has higher affinity for AR than testosterone

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5
Q

Function and location of Blood Testes Barrier

A

Made by tight junctions of adjoining Sertoli cells-below are spermatagonia and above are primary spermatocytes

  1. Prevent harmful substances from contaminating fluid around sperm
  2. Prevent sperm from entering blood stream (which could elicit an immune response)
  3. Maintain high testosterone locally
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6
Q

Significance of 17-HSD

A

Only found in Leydig cells

Serves to convert androstenedione into testosterone

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7
Q

Expression of CYP19 in males

A

Primarily found in Leydig cells and peripheral fat to convert androstenedione/testosterone into estrone/estradiol

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8
Q

Sperm stem cells

A

Spermatagonia

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9
Q

Kartagener’s Syndrome

A
  • immotile cilia syndrome
  • cilia lack dynein in order to function
  • males are sterile
  • also suffer chronic sinusitis and bronchitis
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10
Q

Effect of FSH

A
  • acts on seminiferous tubules to increase spermatogenesis

- acts on Leydig cells to increase their sensitivity to LH

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11
Q

Effect of LH

A

Stimulates Leydig to produce testosterone

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12
Q

Mechanisms for temperature regulation of testes

A
  1. Countercurrent heat exchange with papiniform plexus
  2. Dartos smooth muscle and cremaster skeletal muscle

Controlled by ANS

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13
Q

Pathway of testicular duct system

A

Seminiferous tubules–>straight tubules–>rete testis–>efferent ductule–>epidymis–>vas deferens–>ampulla (storage)–>ejaculatory duct
–>urethra

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14
Q

Epididymis

A

-where spermatozoa acquire motility

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15
Q

3 parts of the male urethra

A
  1. Prostatic
  2. Membranous
  3. Spongy
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16
Q

Seminal vesicles

A
  • Very coiled, but actually only one
  • Goblet cells
  • Produces majority of semen, include fructose needed to nourish sperm
17
Q

Benign prostate hyperplasia

A
  • enlargement of prostate due to an increase in the number of cells
  • linked to DHT formed by 5alpha-reductase
  • usually at the transition zone (around the urethra close to the ejaculatory ducts), which causes issues with urination
18
Q

Erection

A
  • ateriovenous anastomosis closed (these are normally open in a flaccid penis) so that erectile tissue can be filled
  • filling of veins
  • blood outflow reduced because of Buck’s fascia; raises penis to erect position
  • nitric oxide causes relaxation of smooth muscle of erectile tissues (this is the target of ED drugs…prolong the action of NO)
  • PARASYMPATHETIC
19
Q

Nervous System-Ejaculation

A

-SYMPATHETIC

20
Q

Capacitation

A

The process by which sperm are altered by the female reproduction system in order to be able to fertilize the egg

Involves removing sperm glycoprotein coat and proteins

21
Q

Kleinfelter’s

A

47, XXY
Elevated gonadotropes, low testosterone
Impaired spermatogenesis
Impaired male sexual development (small penis, weak muscle tone, sparse facial and torso hair)

22
Q

XX Male

A

Due to a fragment of SRY translocated onto the X chromosome
Presents like Kleinfelter’s
Duplicated SOX9

23
Q

Complete Androgen Resistance

A
46 XY
Genetically male, but phenotypically female 
Androgen receptor on X-chromosome 
No Wolffian duct formation
Regression of the Mullerian duct 
No DHT function
Testes still generating testosterone but receptors aren't working, so it is converted to E2
Male pseudeohermaphroditism
24
Q

Reifenstein’s Syndrome

A

Partial androgen resistance
Androgen receptor on X chromosome
Broad spectrum of secondary sex characteristics with ambiguous genitalia
Severity depends on the amount of resistance

25
Q

5alpha-reductase deficiency

A

Autosomal defect; would have to inherit two bad copies
Testosterone can work at Wolffian duct and AMH can regress Mullerian duct
Genetically male, but due to loss of DHT, secondary sex characteristics and genitalia are ambiguous

26
Q

Secondary Gonadotropin Deficiency

A

To due pathologies that negatively feedback on the GnRH pulse generator of FSH/LH

Examples: Cushing’s, exogenous glucocorticoid administration

27
Q

Primary gonadotropin deficiency

A

Due to GnRH receptor mutation, LH mutation, or FSH mutation

Caused by infarction, tumors, trauma, infection, radiation

Would likely lead to many pituitary-related problems