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Repro > Male Repro > Flashcards

Male Repro Flashcards

1
Q

FSH in males

A

to Sertoli cells

make sperm

diploid to haploid

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2
Q

emission mechanism

A

sympathetic T10-L2

contraction of seminal vesicles and prostate

expulsion of sperm/seminal fluid into posterior urethra

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3
Q

erect penis mechanism

A

parasympathetic

  • smooth muscle relaxation, blood flow into corpus cavernosa, sinusoidal spaces fill, veins that enable outflow forced shut and trapped
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4
Q

what area of prostate gets bigger in nodular hyperplasia

A

transition zone

L: small transition zone younger person (blue)

R: can see much larger transition zone, taking up 90% of prostate

Causes partial urinary obstruction

So passing urine gets harder in older men- incomplete emptying of bladder

Stroma form small nodules– net effect is to block urethra

Effects: incomplete emptying of bladder leading to nocturia

Causes bladder to hypertrophy and thicken muscle

Predisposition to bacterial infection bc don’t empty bladder totally

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5
Q

flaccid penis mechanism

A

sympathetic

  • , constant suppress to penis so remain flaccid – flaccid by smooth muscle contraction
    • flaccid: 2 corpus cavernosa w low blood flow
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6
Q

5ARI

A

prevent t to DHT (potent in prostate!)

decrease prostate volume

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7
Q

intracavernosal injection

A
  • has to go into corpora cavernosa
  • pure prostaglandin
  • pain with erection (more than pain with injection)
  • highly effective – mimics natural physiology
  • do it with Doppler evalulation
  • disadvantages –
    • can hit vein and bruise
    • pain at injection site
    • cumbersome if poor dexterity
    • can be sensitive to small doses
    • some people are tired of using it all the time
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8
Q

T and prostate cancer?

A

most show no association

treamtent MAy stim growith in previously undaignosed tmros

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9
Q

neurotransmitters in ejaculation

A

serotonin

dopamine

oxytocin

GABA

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10
Q

3 types of intratesticular ducts

A
  1. straight tubules
  2. rete testes
  3. efferent ductules
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11
Q

epithelium of glans

A

•Glans of penis, as compared to rest of penile urethra, is lined by a stratified squamous epithelium compared to the vast majority of the penile urethra which is a pseudo-stratified columnar epithelium

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12
Q

DHT inhibitors for BPH

A

DHT inhibitor– GH inhibitor to debulk prostate

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13
Q

PDE5 inhibitors

A
  • increase intracellular Ca – erection: cell relaxed by sequestration of Ca à drive Ca into ER (relax)
  • reset: phosphodiesterase 5 – breaks down cAMP, GMP – turn off event
  • if inhib PDE 5 – perpetuates cycle for longer
  • need all of the first things!! sexual stimualation etc
  • enable smooth muscle relaxation in the cells of the penis (upstream stuff has to work)
  • all side effects from other PDE in the body
  • Cialis – in body for longer
  • look like cGMP – binde PDE5 – prevents PDE from binding cGMP, does work for a longer time!!
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14
Q

leydig cells

A

secrete T under LH

  • LH stimulates Leydig
  • FSH stimulates Sertoli
  • Then negative-feedback loop to hypothalamus
  • As androgen-binding proteins rise, the Sertoli cells secrete inhibin which goes back to cause inhibition of FSH from anterior pituitary
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15
Q

male hormonal changes with age

A

decreased total and free T

increased SHBG

increased FSH, LH

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16
Q

clomid

A

increase FSH and LH centrally

won’t work if testicles failed

no neg impact on sperm making - use for decreased sperm cunt for hormonal reasons and fertility

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17
Q

what kind of cancer is on the penis

A
  • Squamous cell carcinoma:
  • etiology (HPV), growth,
  • Spread (inguinal nodes)
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18
Q

black arrow

A

•Would find spermatogonia right up against basal part (black arrow)

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19
Q

adverse events with transdermal gel

A

risk for transfer to partner and kids

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20
Q
A
  • Flat line cells that would be straight tubules (black arrow)
  • At the top you can see scalloped appearance (blue arrow)
  • As well as development of smooth muscles in tunica propria
  • This is beginning of efferent ductules
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21
Q

what hormones to check in hypogonadism patients

A

FSH

LH

Estradiol (T conversion in periphery - obese)

DHEA

prolactin (inhibits GnRH)

thyroid

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22
Q

How does T travel in the blood?

A

free T is very low - bind AR, activate, go to nucleus

falls apart easily –> hard to measure - const disappearing

free T

albumin-bound (liver)

sex hormone binding globulin (liver)

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23
Q

What if High T, low FSH + low LH

A

exogenous - taking illicit steroids –> infertile don’t want to come off steroids

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24
Q

treaments for hypogonadism

A

oral (not in US - first pass to liver) - but can give clomid (increase FSH and LH = won’t work if tests fail, no neg impact in sperm making, give form sperm making!)

transdermal - patch and gel

injectable

long term

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25
Q

serum PSA

A

marker for prostate carcinma

found in serum

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26
Q

type b spermatogonia

A
  • Starts by having those spermatogonia, at the time of puberty when testosterone levels reach the right number, divide mitotically
  • Will undergo a number of mitotic divisions giving rise to two types of spermatogonia that, histologically, you cannot tell the difference:
  • Type A spermatogonia: remain always associated with basal lamina and always remain as germ cells to give rise to the next wave

•Type B spermatogonia: These enter and continue the process to develop into spermatozoa

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27
Q

Prostatic Intraepithelial Neoplasia (PIN

A
  • Benign glands (stratified epithelium) containing atypical cells [nucleoli]
  • Precursor lesion
  • Increased risk for development of prostate cancer
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28
Q

marker of testes tumor

A
  • Most common cancer in men: 25-40 yrs old
  • Presents with painless enlargement of testis or with metastasis
  • Wide spectrum of cellular differentiation – complex classification

•Characteristic marker : oncogenes duplicated on short arm of chromosome 12 (= isochromosome 12p = i12p)

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29
Q

When do you check T levels?

A

AM - T levels highest (AM erection phenomenon

lost n poor sleepers, night workers

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30
Q

3 parts of spermiogenesis

A
  • Golgi phase: Golgi produces granules that coalesce to eventually produce acrosome
  • Acrosome phase: Acrosome becomes fairly complete, mitochondria being to move to mid piece, and centrioles move to opposite pole you get the developing complex that will give rise to the spermatozoa
  • Enveloping sertoli cell phagocytosizes excess cytoplasm, or residual body, in maturation phase.
  • When released, this is called spermiation
  • The acrosome contain a number of hydrolytic enzymes
  • Not clear if sole function is to get through zona pellucida or whether there is mechanical shearing in addition
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31
Q

primary hypogonadism

A

testicular failure (viral, klinefelters)

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32
Q
A
  • At higher magnification can get an appreciation of highs and lows of epithelium (black arrow)
  • This will lead into epididymis on the bottom (blue arrow)
  • Round, see stereo-cilia projecting up into the lumen
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33
Q

nodular hyperplasia of the prostate

A

“BPH”

glandular and stromal hyperplasia

high proportion of men by 80s

diffuse and nodular enlargement, compression of urethra

glandular areas and stromal tissue increases

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34
Q

contraindications for T therapy

A

prostate cancer (acutally prbably safe)

breast cancer

BPH

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35
Q

What are the two cell types in the seminiferous tubules?

A

sertoli cells and spermatogonia

  • Between the tubules there are clumps of cells = interstitial cells of Leydig
  • They don’t sit in the seminiferous tubules
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36
Q

Do you give T for fertility?

A

NO T treatment suppresses spermatogenesis - has a low T but giving T will make it worse

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37
Q

3 effects of nodular hyperplasia

A

Effects: incomplete emptying of bladder leading to nocturia

Causes bladder to hypertrophy and thicken muscle

Predisposition to bacterial infection bc don’t empty bladder totally

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38
Q

secondary hypogonadism

A

hypothalamic or pituitary dysfunction

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39
Q

spermiation

A

spermatozoa are released inot the lumen after spermatogenesis

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40
Q
A

•Another picture of a prostatic concretion and nicely showing the pseudo-stratified columnar epithelium that makes up this gland

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41
Q

torsion of the testes

A

twisting of vascularsupply

infarction

swollen dusky scrotum - extremely painful

predisposing causes - incomplete descent, atrophy, trauma

immediate surgery

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42
Q

Kallman’s syndrome

A

prob of cranial development

can’t smell

pituitary and hypthaamaus not connected

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43
Q
A

•Higher power showing penile urethra (black arrow) and glands of Letray (blue arrow) and connective tissue

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44
Q

definition of hypogonadism

A

signs and symtoms

total T checked in AM less than 350

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45
Q

hormonal causes of ED

A
  • obesity
  • diabetes
  • prior injury to testes
  • secondary – thyroid, anabolic steroids
46
Q

cryptorchidism

A

undescended testis

do not descend into scrotal sac

can stop anywhere

not due to hormonal disorders

  • Histologic changes occur after 2 years –recommended to perform surgical correction by 2 yrs
  • Risk of trauma, infertility and 5-10 x increase in risk of tumor development
47
Q
A
  • Seminal vesicles on top left (black arrow) with finger-like projections
  • Prostate gland (yellow arrow) and prostatic urethra (blue arrow)
  • What is unique about the prostate gland is that it is a fibromuscular organ loaded with elastic tissue and a LOT of smooth muscle
  • It is called tubular alveolar because it doesn’t have a single duct
  • When it contracts forcefully the fluid is sprayed into the urethra through a number of different ducts
  • Analogy: squeeze a wet sponge -> water will spray everywhere and not just in one place
48
Q
A

prostate

Prostate

Folded medium sized glands

Several layers line it

Concretions (debris in lumen)

49
Q

hypospadias

A

A condition in which the opening of the penis is on the underside rather than the tip.

50
Q

Side effects of SSRIs

A

drowsiness, dizziness, insomnia, nausea, sexual dysfunction

51
Q

epispadias

A

An epispadias is a rare type of malformation of the penis in which the urethra ends in an opening on the upper aspect (the dorsum) of the penis. It can also develop in females when the urethra develops too far anteriorly.

52
Q
A

vas deferens

  • Here is a tubular organ that is very muscular:
  • 3 layers of smooth muscle = inner longitudinal layer, circular layer and outer longitudinal layer
  • How to distinguish this from ureter?
  • Epithelium!
  • This is pseudo-stratified columnar epithelium, it would be transitional in ureter
53
Q

spermiogenesis

A

•Haploid spermatids undergo spermiogenesis and develop into spermatozoa. Three specific phases can be found:

•Golgi phase: Golgi apparatus begins to produce granules that will bleb off the trans-golgi, fuse with one another and turn into the acrosome

•Acrosomal phase: Fusions of granules continue and spread over anterior surface of what will be the condensed nucleus. Centrioles will also migrate to the OPPOSITE pole as the acrosome because from centrioles will come flagella

•Chromatin will begin to condense and mitochondria begin process of moving towards neck region

•Maturation phase: Acrosome is fully formed, flagella is fully formed, mitochondria are wound around mid-piece and there’s an awful lot of cytoplasm that has to be blebbed off and thrown away

  • That bleb is called the residual bodies
  • At the end of the maturation phase, spermatozoa is ready to be released into the lumen to move onto next phase
  • Sperm that finish in the seminiferous tubules during this process of development are incapable of fertilizing an egg. Look fine, but still need to be tuned up in epididymis
54
Q

ejection mechanism

A

sympathetic (and somatic)

S2-S4

bladder neck closes

relaxation of external (striated) urinary sphincter

rhythic contraction of bulbospongiosus/pelvic floor muscles

55
Q

neurogenic causes of ED

A
  • diabetes
  • radical pelvic surgery (prostatectomy) – chance to regain erection function at 2 years
56
Q

PCA3

A
  • Prostate CAncer gene 3 – non-coding RNA
  • Urinary biomarker
  • Determined in urine collected after rectal exam (prostate massage)
  • Supplements PSA – low sensitivity, higher specificity
  • With PSA -Reduces number of unneeded biopsies
57
Q

mechanism of penile smooth muscle relaxation

A

smooth muscle cells of sinusoids/arteries

increase intracellular Ca – erection

  • cell relaxed by sequestration of Ca à drive Ca into ER
  • reset: phosphodiesterase 5 – breaks down cAMP, GMP – turn off event
    *
58
Q

seminoma

A

most common testicular tumor

solid, pale, hemotgenous

lobules of uniform round clear cells surrounded by fibrous septa containing lymphocytes

59
Q

embryonal carcinoma

A

testicular tumor

  • Peak age = 30 years
  • Macro: Varied appearance, hemorrhage & necrosis
  • Micro: Sheets, papillary or glandular patterns, marked anaplasia (variation in nuclear size and shape)
  • Keratin expression + (immunohistochemistry) [neg in seminoma]
60
Q

efferent ductules

A
  • Connection between mediastinum of testes and epididymis is called efferent ductules
  • Easy to see efferent ductules because they have scalloped appearance (highs and lows, highs and lows)
  • Epithelium covering this is made up of alternating cuboidal cells and tall columnar ciliated cells

Function of these cells is to sweep and move things “downhill”

61
Q

What cells phagocytose residual bodies of sperm?

A

Sertoli Cells

62
Q

spermatocytogenesis

A

first phase of spermatogenesis

  • Starts by having those spermatogonia, at the time of puberty when testosterone levels reach the right number, divide mitotically
  • Will undergo a number of mitotic divisions giving rise to two types of spermatogonia that, histologically, you cannot tell the difference:
  • Type A spermatogonia: remain always associated with basal lamina and always remain as germ cells to give rise to the next wave
  • Type B spermatogonia: These enter and continue the process to develop into spermatozoa
  • During spermatocytogenesis, spermatogonia undergo a number of divisions eventually giving rise to a primary spermatocyte
63
Q

what if all hormones are low and prolactin is high

A

pituitary adenoma or other CNS lesion (brain)

64
Q

What if Low T, high FSH + high LH

A

testis failure

i.e. klinefelters

testicles don’t work and trying to compensate

65
Q

treatment for prostate cancer

A

Over treating prostate (indolent cancer)

Gleason 6 is considered indolent- wont metastasize and won’t die form it

So treat Gleason 7-10 but NOT Gleason 6

For Gleason 6– active surveillance – rebiospy every 6 months for 3 years and if changes score (biopsy different region not progression of disease) then offer surgery

For higher scores:

surgery - radical

radiation - pellets in prostate and external beam

hormonal than chemo if metastatic

66
Q

intraurethral alprostadil

A
  • suppository – put it an inch into the penis
  • corpus spongeosum has own blood supply
  • pellet falls out and comes out and is absorbed
  • erection can be really really sore – prostaglandins from pain
  • for people who have spinal cord injury and can’t feel anything
67
Q

what if low T, high E

A

obesity

T to E in periph

68
Q

TURP

A

Minimally invasive surgery– tunnel out pieces of prostate using scope up the urthera

TRUP- trans-urtehral R of prostate

69
Q

What do Sertoli Cells secrete

A

Androgen Binding Protein (ABP) - binds T (from Leydig cells) to keep concentration high in tubules for spermatogenesis

•MIF to cause degradation of mullerian ducts

70
Q

what part of the penis does the urethra run through?

A
  • Penis has erectile tissue, deep artery in the center of the corpus cavernosum
  • Urethra runs through corpus spongiosum
71
Q

alpha blockers for BPH

A

Alpha blockers– relax smooth muscle, open up urethra

72
Q

klinefelters

A

nondisjunction - poor fertility

73
Q

blue arrow

A
  • If you see a dividing cells (blue arrow), it’s probably a primary spermatocyte
  • The secondary ones go quickly to spermatids
74
Q

what brain receptors integrate sexual responses?

A

5HT-1 enhances seuxal response (can be hypersensitive in PE)

5HT-2 inhibits sexual response

75
Q

Promescent

A

FDA approved

OTC

topical lidocaine

only deep nerves for ejaculation not sensory nerves

76
Q

acute prostatitis

A

cause: UTI bacteria (E coli, gram neg)

neutro[hils

symp: dysuria, frequency, lower back pain
diagnosis: fractionated urine (after palpation of prostate see if there are more neutrophils)
treat: abx

77
Q

rete testes

A
  • Following straight tubules you get to rete testis.
  • Rete testis have cuboidal cells lining the ducts
  • These cells, along with sertoli cells, have one major function to absorb fluid from cohort of sperm that have been shed into duct
78
Q

straight tubules

A

straight from seminiferous tubules

  • Seminiferous tubules are blind ended ducts that begin and end at the mediastinum of testes
  • As you get to the end of ducts, the germinal epithelium goes and your left with sertoli cells that form the walls of the next intratesticular ducts which are called your straight tubules
79
Q

3 stages of spermatogenesis

A
  1. spermatocytogeneis = spermatogonia to primary spermatocytes
  2. meiosis = Primary spermatocyte that are formed now undergoes a process called meiosis and you end up with haploid cells
  3. spermiogeness - golgi phase, acrosome phase, maturation phase to become spermatozoa
  4. spermiation -•Sperm are released into the lumen
80
Q

Gleason grading system

A

1 + 2 are benign

3 - glands

4 - cords

5 - solid sheets

find the top 2 patterns and add the numbers together

5 diagrams (scores)

Heterogeneous disease – so look at most common cancer pattern then the second

Take the patterns and add those 2 numbers and get the Gleason score out of 10

Closer to 10 predicts worse

1 and 2 found to be benign though so really looking at 3-5

3à start to form singular glands

4à start to form cords of glands

5à they form sheets of glands

81
Q

Sertoli Cells

A
  • Sertoli cells are cells with triangular shaped nucleus with a prominent nucleolus
  • The cytoplasmic reaches of sertoli cells are intimately associated into EVERY single one of the various developing cohort of sperm

•Sertoli cells attach very tightly (via tight junctions with the basal lamina) and form the blood-testes barrier

•NOTHING gets through that barrier because the spermatogonia that existed at the beginning is recognized by immune system as self, but everything else would be recognized as non-self

•Sertoli cells set off 2 different compartments

•Spermatogonia = basal compartment

•Rest of the compartment = adluminal compartment

  • Something occurs when you get at type B spermatogonia that will continue this process of spermatogenesis to allow it to squeeze through that tight junction and then it seals right behind it
  • 2 entirely different environments created by sertoli cells
  • Sertoli cells are there to nourish, feed and care for the cohort
  • Because of tight junctions, nothing is getting through (ex. Nutrients, oxygen, and etc.)

•Sertoli cells are long-lived

•They don’t divide, they are resistant to things that would kill most other things (X-ray)

•In addition to their role as protecting/nourishing cohort of developing sperm, they also have other functions:

•Secrete MIF to cause degradation of mullerian ducts

•Secrete androgen-binding proteins under influence of FSH

  • Process of spermatogenesis is based on presence of testosterone
  • To keep testosterone levels high enough, sertoli cells secrete androgen-binding proteins which bind testosterone and allow spermatogenesis to occur
82
Q

blue arrow

A

•Prominent nucleolus of Sertoli cell (blue arrow)

83
Q

visual appearance of prostate adenocarcinoma

A

arise in periophery (unlike BPH)

macro - firm, hard to see

micro - simple glands, crowded, looks like prostate but simpler

NO BASAL CELLS

•Rules of “2s”

– “2” many; 2 crowded; 2 small; 2 simple; 2 large nucleoli (glands)

• Monoclonal = Lumenal cell (no basal cells)

84
Q
A
  • Basal lamina (blue arrow)
  • Spermatogonia (black arrow)
  • Sertoli nucleus (yellow arrow)
  • Primary spermatocyte (green arrow)
  • Early spermatid (bolded red arrow)
  • Late spermatid (orange arrow on top)
85
Q

vas deferens

A
  • Vas deferens is thick, fibrous tubular organ with an enormous amount of smooth muscle
  • All of these parts have enormous amount of smooth muscle because sympathetics are responsible for ejaculation from L1 and L2
  • Similar to cross section of ureter
  • Penile urethra also covered by pseudo-stratified cells
86
Q

chronic prostatitis

A

cause: bacterial and apacterial

asymptomatic - no pain

tx: longer duration of abx and NSAIDs (antiinflam)

87
Q

Treatments of PE

A

Serotonin Reuptake Inhibitors (for depression) - start at very low doses

EMLA cream (lidocaine) - 20-30 min pre intercourse

Promescent - FDA approved, OTC - topical lidocaine that only hits deep nerves for ejaculation NOT sensory nerves from intercourse

88
Q

spermatogenesis

A
  • The spermatogonia develop into sperm via spermatogenesis
  • Going from germ cell to a spermatozoa
  • The process moves in an orderly fashion from basal lamina to the lumen
  • Earliest form of sperm, spermatogonia, is sitting right up against the basal lamina
  • Latest form that is shed into lumen, spermatozoa, are going to be furthest away because they are most developed
  • Takes about 64 days to go through this process of spermatogenesis

From spermatogonia to spermatozoa

89
Q

criteria for PE

A

ejaculation w min stimulation, before the man wishes, causes distress

90
Q

What are the two compartments made by the Sertoli cells?

A
  • Sertoli cells attach very tightly (via tight junctions with the basal lamina) and form the blood-testes barrier
  • NOTHING gets through that barrier because the spermatogonia that existed at the beginning is recognized by immune system as self, but everything else would be recognized as non-self
  • Sertoli cells set off 2 different compartments

•Spermatogonia = basal compartment

•Rest of the compartment = adluminal compartment

91
Q

treatment for testis tumor

A
  1. remove tumor and see if it’s seminoma or non seminoma
  2. seminoma - radiation
  3. NSGCT - dissection of lymph nodes

all tumors: chemo if stage II or III

92
Q

vascular causes of ED

A
  • hypertensive
  • poorly controlled lipids
  • diabetes
  • CAD
  • ED is a predictor of CAD/stroke – same factor as smoker or family history, if poor blood flow into their penis also poor blood flow in other places
    • study to send to cardiologist – overall shows health
93
Q

cause of nodular hyperplasia of prostate

A

incrase estrogen with age –> increase DHT Receptor –> increase T efect on zone

Due to: increase in estrogen receptors

94
Q

side effects of PDE inhibitors

A
  • catastrophic lowering of BP – heart attack, give NO, die
    • only dangerous if combine with NO
  • headache
  • flushing
  • back pain
  • visual disturbances
  • be careful with angina
  • non-arteritic anterior ischemic optic neuropathy – optic nerve loses blood flow, incredibly rare – NAION
  • tachyphylaxis – body gets used to drug and it stops working
    • very rare in this – likely signifies progression of disease state – TAKE SERIOUSLY!
  • PDEI failure
    • 70% discontinue in 1 year – drug doesn’t work, underlying disease need to work up
95
Q

Risks of T therapy

A

hepatotoxicity

infertility

edema

gynecomasita

apnea

CVD?

96
Q
A
  • At higher power:
  • Scalloped appearance at bottom of image are efferent ductules (black arrow)
  • Epididymis on top, basal cells, pseudo-stratified columnar epithelium (blue arrow)
  • At luminal surface you can see stereo-cilia (red arrow)
  • Continue down into part of vas deferens
97
Q

adverse events with IM T

A

polycythemia - opp of anemia

mostly in weekly injectins

98
Q

signs and symptoms of hypogonadism

A

sexual dysfunction (libdo, erectile anejaculation

low energy,concentration, mood, strength

ospteopenia, decreased insulin sensitivty, truncal obesity, metabolic syndrome

99
Q

likely metastasis of prostate cancer

A

bone

Metastasis of prostate cancer

Has great predisposition to go to bone

Will present with lumbar bone metastasize before the prostate cancer found

Bone thickens and collapses

Cytokines released by cancer in the bone marrow released and cause this

100
Q

penile implant surgery

A
  • if drugs fail or blood flow shot
  • inflatable
  • mechanical malfunction under 10 years – have to replace if it dies (can keep in if don’t want to be sexually active)
  • may not like it
  • may not like size
101
Q

spermatogonia

A
  • Primordial germ cells that go up dorsal mesentery to populate the gonadal ridge sit there quiescently until the right time
  • The spermatogonia develop into sperm via spermatogenesis
  • Going from germ cell to a spermatozoa
102
Q

what is the most common cancer in males?

A

prostate cancer

103
Q

type A spermatogonia

A
  • Starts by having those spermatogonia, at the time of puberty when testosterone levels reach the right number, divide mitotically
  • Will undergo a number of mitotic divisions giving rise to two types of spermatogonia that, histologically, you cannot tell the difference:

•Type A spermatogonia: remain always associated with basal lamina and always remain as germ cells to give rise to the next wave

104
Q

orgasm mechanism

A

sensory experience

can occur independently of erection, emission, ejection

105
Q

transitional zone ofprostate

A

small in kids and enlarges in adults

most predisposed to cancer

106
Q
A
  • Leydig cells sit in interstitial space (black arrow)
  • Under influence of LH, group of Leydig cells begin to secrete testosterone
  • This group of Leydig cells are inactive
107
Q
A
  • As you move up, you get these things with a unique appearance (yellow arrow)
  • These are early spermatids
  • They are going to develop through process talked about to the terminal, late spermatids (bolded red arrow)
  • Still have nucleus pushing into the Sertoli cells
108
Q

corpus cavernosa

A
  • Corpus cavernosa are just erectile tissue
  • Corpus cavernosa (middle top image) can see cavernous spaces
  • Top right image has arrow pointing to one of the helicine arteries
109
Q

three types of excretory ducts

A
  1. epididymus
  2. vas deferens
  3. penile urethra
110
Q
A
  • Higher power image showing pseudo-stratified columnar epithelium
  • Seminal fluid nicely sitting in the valleys (black arrow)
  • Easy to distinguish seminal vesicles from gallbladder as seminal vesicles have much higher projections that flop
111
Q

epididymus

A
  • Epididymis: has multiple parts – head and tail
  • Takes 12 days to make transit from head to tail
  • Physiologically: sperm removed from tail of epididymis can fertilize egg
  • Developmental process occurring during transit
  • Composed of a pseudo-stratified columnar epithelium (common in male reproductive system - will see this all the way down to the urethra)
  • From the surface of the pseudo-stratified cells are long cilia-looking things that are actually stereo-cilia
  • Stereo-cilia increase surface area for absorption of liquids and ingestion of residual bodies as it makes its way down

Repro (6 decks)

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