Male pathophysiology and Histology Flashcards

Week 12

1
Q

Effects of elevated temperature

A

Testicular atrophy

Spermatogenic cells atrophy

Leydig cell hyperplasia = increased risk of testicular cancer

Only Sertoli cells in SE

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2
Q

Why is T not high with Leydig cell hyperplasia?

A

androgen resistance (defect in receptor)

low functioning Leydig cells (if hypogonadism)

neg feedback

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3
Q

What are the two phases of testicular decent?

A

Transabdominal

Inguinoscrotal

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4
Q

When does transabdominal and inguniscortal decent occur?

A

T- first 3-6 months

IS= last trimester (6 months –> birth)

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5
Q

Hormones involved in Transabodminal testicular descent

A

INSL3 = Gubernaculum thickening

testosterone = degenerates cranial suspensory ligament.

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6
Q

Hormone action of Inguinoscrotal testicular descent

A

testosterone = shortening and contraction of gubernaculum

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7
Q

What is Cryptiochidism

A

incomplete descent of one or both testes

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8
Q

why is there an increased risk of Cryptorchidism in premature babies?

A

as the IS phase occurs from 6 months –> birth, the reaction of gubernaculum is not likely to be complete

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9
Q

What are the two treatments of Crytorchidism?

A

HCG
Acts on Leydig cells
Provides local, concentrated T

Early Surgery
Early to minimize time testes is in the body do reduce leydig proliferation

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10
Q

How does Cyrptochormism lead to infertility?

A

Leydig cell hyperplasia and spermatogenic cell atrophy = decreased sperm count

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11
Q

What is Varicocele and how does it lead to infertility?

A

Enlarged spermatic cord veins

Infertility
Reduced blood flow = reduced heat exchange = increased temp = infertility

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12
Q

causes of primary hypogonadism

A

Testicular dysfunction

Klinefelter’s Syndrome

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13
Q

Pathophysiology of Klinefelter’s syndrome

A

decreased T from Leydig cells = decreased responsiveness to LH

decreased inhibin = increased FSH

fibrosis of SE tubules = infetility

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14
Q

treatment of Pri Hypogonadism

A

T supplementation

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15
Q

Hormonal profile of pri vs sec hypogonadism

A

Pri = HYPERgonadotropic

Sec= HYPOgonadotrophic

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16
Q

Causes of sec hypogonadism and treatment

A

Pituitary/ hypothalamus dysfunction

Tumor or Kallmann’s syndrome

treatment
hCG supplementation

17
Q

causes of Hypergonasim

A

Androgen-secreting tumors

Adrenal adenomas

Leydig cell tumors

18
Q

clinical features of Hypergonadism

A

Precocious puberty

Excessive muscle mass

Mood swings

Unusual body hair growth

Acne

Gynecomastia

19
Q

Hormonal profile of Hypergonasims

A

Increased T

Decreased GnRH

20
Q

Features of a normal SE tubule

A

colonised by sertoliu ells and spermatogenic cell

small clusters of leydig cells

21
Q

Features of an atrophied SE tubule and what conditions would you see it in?

A

Collagen fibers
Missing cells

(Orchitis)
(Klinefelter’s Syndrome)

22
Q

Features of SE tubule esposed to high temps and what conditions would you see it in?

A

Cells in center of tubule
Leydig cell hyperplasia

(cryptorchidism)
(Klinefelter’s syndrome)

23
Q

features of Infant testis histology

A

Lower density of SE tubules

NO spermatogenic cells in tubules

24
Q

Epididymis features (histology)

A
  • pseudostratified cells with stereocilia
  • lumen filled with spermatozoa and proteins