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1st yr-Med 2022-2023 > GHM L10 > Flashcards

GHM L10 Flashcards

1
Q

Describe the purpose of meiosis

A
  • Cell division in sexually reproducing organisms
    -Reduces no. of chromosomes in gametes
    -in humans, somatic cells: DIPLOID (2 sets of chromosomes). GAMETES: HAPLOID (1 set of chromosomes)
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2
Q

Why are gametes haploid?

A

Organisms produced via sexual repdocution need correct number of chromosomes

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3
Q

Descibe the hypothalamic-pituitary-gonadal axis

A

GnRH secreted in hypothalamus (preoptic area)

In anterior pituitary, GnRH stimulates gonadotropes to release gonadotropins (LH, FSH)

LH, FSH in testes, ovaries,- stimulate testes + ovaries to secrete sex androgens, estrogens, progestins to the target cells

INHIBIN secreted by SERTOLI cells of testis - inhibit release of GnRH in hypothalamus and inhibit gonadotropes in anterior pituitary
Also ANDROGENS are involved in negative feedback and positive feedback
positive feedback (some stages in menstrual cycle)

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4
Q

Give an example of positive feedback in the hypothalamic-pituitary-gonadal axis

A

Menstrual cycle - hormonal surge
Androgens

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5
Q

Describe embryonic gonads

A

Precursors to somatic cells
Undifferentiated gonads
Consist of
-germ cells
-supporting cells
-steroidogenic ells
IDENTICAL

UNDERSTANDING:
-precursor to testes / ovaries
-depends on sex of individual
-RECOGNISE OVARY + TESTES on diagram

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6
Q

Describe the process of sex differntiation

A

FEMALE: (ovarian pathway)
-supporting cells differntiate into GRANULOSA cells (which enclose the oocytes to form follicles)
Steroidogenic cells differentiate into THECA cells

MALE: (testicular pathway)
-supporting cells differntiate into SERTOLI cells (encolose germ cells forming testicular cords
Steroidogenic cells differentiate into Leydic cells

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7
Q

Describe the process of gondal development in a male embryo

A
  1. 6th week of pregnancy (4 week embryo): migration of PRIMORDIaL (undifferentiated germ cells)
  2. Primordial germ cells have XY chromosomes
  3. XY primordial germ cells migrate to the medulla region of primordial gonad
  4. After these primordial cells collonise medulla of gonad, they proliferate by mitosis (for 2 weeks)
  5. PRIMORDIAL GERM CELLS develop into SPERMATOGONIA (immature sperm) - DIPLOID

all occurs before birth
6. Supporting sex cord cells form SERTOLI CELLS

Activation SRY protein locus (position) on Y chromosome - leads to formation of primitive testes (premature)

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8
Q

Describe the phenotrype sex differentiation of the male internal genitalia

A

Male + female internal genitalia derive from different duct systems
-Wolffian duct: MALE
-Mullerian duct: female

In male, MIS (Mullerian Inhibiting Substance) + AMH (anti-mullerian hormone) release - by SRY

SRY released by supporting cells (later SERTOLI)

Wolfian duct is triggered by testosterone to form Epidydymis, Vas deferens, (sperm duct) seminal vesicles

Mullerian duct - degenerates

Dihydrotestosterone - stimulates development of prostate gland (DHT) - type of androgen

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9
Q

Describe phenotypic sex differentiation of the male external genitlia

A

DHT needed for this process

early embryonic development: genitalia undifferentiated + form urogenital groove (8 weeks)

  1. DHT stimulates growth of prostate gland + fusion of genital folds, leads toformation of penis around urethra
  2. DHT stimulates formation of scrotum (formation of labioscrotal swelling, leading to formation of scrotum)
  3. Early fetal development, testes develop in abdomen, DHT descends them ABDOMEN -> SCROTUM (process important for normal testicular development + temp regulation for sperm production)
  4. hCG (human chronionic gonadotropin) produced by placenta - stimulates testosterone production in fetal testes
  5. Descent of testes from abdomen -> scrotum requires presence of hCG - if this process goes wrong, leads to CRYPTORCHIDISM - WHERE ONE / BOTH TESTES FAIL TO DESCEND PROPERLY INTO THE SCROTUM
  6. Exposure to DHT from 5th weekof development will lead to development of male external genitilia therefore, male phenotype
    if this goes wrong, leads to AIS - Androgen Insensitivy Syndrome - individuals with male sex chromosomes XY, have reduced / abscent response to androgens (including DHT) - therefore, despite the presence of the male XY chromosomes, external genitilia may not develop
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10
Q

Male Reproductive Anatomy

A

Organs

  • Gonads - in males, this is testes - produce gametes, secrete hormones
  • Ducts: transport, store gametes - vas deferens - sperm duct
    -Accessory sex glands: support gametes (prostate gland)

Testes

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11
Q

State 3 functions of the penis

A
  • Urination
  • Erection
  • Ejaculation
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12
Q

Describe the function of the scrotum

A
  • Supports testes
    -Temp regulation
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13
Q

ANATOMY OF TESTES

A

TUNICA VAGINALIS - outer capsule layer

TUNICA ALBUGINEA inner capsule layer

SEPTUM

SEMINIFEROUS TUBULE

RETE TESTIS

EFFERENT DUCTULES

HEAD OF EPIDYDYMES

BODY EPIDYDYME

TAIL OF EPIDYDYMIS

VAS DEFERENS

-lies inside tuniva vaginalis together with epididymis
-site of SPERMATOGENESIS + androgen production

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14
Q

State the ducts found in the male reproductive system

A
  • Urethra

-Spermatic cord - blood, autonomic nerves + lymph vessels, vas deferens

-Epididymis - spermatozoa (sperm cells) complete maturation (2 week)

-Vas deferens - fushion of epidydymis, stores mature sperm

-Rete testis -carries sperm from seminiferous tubules to epididymis, fusion of seminiferious tubules

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15
Q

Describe spermatogenesis

A

Conversion of DIPLOID spermatogonia into haploid spermatozoa

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16
Q

Describe spermiogenesis

A

Converstion of HAPLOID spermatid -> HAPLOID spematozoa

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17
Q

Describe sertoli cells

A

SUSTENTACULAR CELLS “nurse cells” - provide physical + nutritional support to sperm cells in maturation process

Found in seminiferous tubules

Activated by FSH (produced by pituitary gland)

Sertoli cells connected to each other via TIGHT JUNCTIONS, forms blood-tesits barrier (separates testicular environment from bloodstream)

SECRETE AMH: Anti-mullerian hormone, inhibin (regulates FSH production), ABP (androgen binding protein - binds to androgens, testosterone)
Oestradiol (directs spermatogenesis)

18
Q

Describe the location and function of the prostate gland

A

Location - surrounds + opens into urethra where it leaves the bladder

Secretes: SLIGHTLY ALKALINE FLUID - activates sperm + prevents them from sticking together

PROSTATE - problems are common in males over 40

19
Q

Describe the location and function of bulbourethral gland

A

Cowper’s gland

Paired galdns, beneath prostate gland

Exocrine glands (secrete fluids)

Secretes alkaline mucous into urethra

Wash residual urine out of urethra when ejaculating semen, raises pH, neutralises acidity of urine

20
Q

Describe the process of penile erection

A
  1. Physiological response to sexual stimulation
  2. Dilation of cavernous arteries in erectile tissue
  3. Mediated by release of NO in response to sexual stimulation
  4. No activates enzyme guanylate cyclase, increases cGMP, which leads to smooth muscle in erectile tissue to relax, allowing dilation of cavernous arteries - they can fill with blood, leads to erection
21
Q

Describe the 3 columns of erectile tissue

A
  1. 2 x corpora cavernosa
    1 x corpous spongiosum
22
Q

State organs involved in ejaculation

A

Brain
Spinal cord
Peripheral Genital organs

23
Q

Desribe the composition of semen

A

SEMINAL FLUID: thick, yellow, alkaline

-mucus
-fructose
-coagulating enzyme
-prostaglandins

24
Q

State 3 accessory glands

A
  • Seminal vesicle
    -Prostate gland
    -Bulbourethral gland
25
Q

Describe the process of capacitation

A

SPERM MATURATION

Ejaculated sperm cannot fertilise, sperm undergo CAPACITATION in female reproductive tract

Capacitation destabalises sperm”
-removal of glycoproteins from surface of sperm
-exposes other proteins which bind to zona pellucida (protective layer around egg)
-increase in intracellular calcium in sperm
-activation of membrane lipases + protein kinases - makes sperm more fluid, increase mobility + better penetration of egg
-increase membrane fluidity

26
Q

Describe the journey the sperm cell undertakes to fertlise the egg

A

Seminiferous tubules (in testes) to fallopian tubes

27
Q

Describe the production of testosterone in males

A

H Y P O T H A L A M U S

GnRh

ANTERIOR P I T U I T A R Y

LH FSH

L E Y D I G CELLS SERTOLI

testosterone inhibin
spematogensis

28
Q

Describe the production and function of androgens in the body

A

Androgens produced by adrenal glands, include testosterone, DHEA (weak precursor to testosterone)

29
Q

Why are the androgens released from adrenals considered as “weak” precursors?

A

Weaker effects than testosterone

30
Q

Describe how weaker precursors are converted into more potent androgens

A

By secondary endocrine glands, gonads - testes, ovaries

DHEA / other weak precursors further metabolised, converted to more potent androgens e.g. testosterone

31
Q

Where are androgens produced in larger quantities? Adrenals or Gonadal tissues

A

GONADAL TISSUES

32
Q

Describe male hormone control

A

FSH + LH only released during puberty

FSH released by pituitary gland stimulates sertili cells in testes to facilitate spermatogenesis (production of sperm)

RELEASE OF FSH REGULATED BY NEGATIVE FEEDBACK MECHANISM. As spermatogenesis progresses, testosterone levels increase, causing sertoli cells to release INHUBIN - sends negative feedback signal to pituitary gland surpresssing FSH release

LH, released by pituitary gland, stimulates Leydig cells to produce testosterone

33
Q

State where Leydig cells are found

A

Testes

34
Q

Describe characteristics of male puberty

A

9-14

Puberty initiated by release of GnRH
Stimulates anterior pituitary to release LH, FSH
Stimulates testosterone release

LEPTIN - produced by fat cells, involved

Physical changes:
-Adult body odor, increased sebum
-Testicular enlargement
-Penis growth
-Foreskin retraction
-Pubic hair
-Male pattern musculature
-More frequent erections
-Body, facial hair growth
-Adam’s apple more prominent
-Voice change - due to growth of larynx

35
Q

Describe precocious puberty

A
  1. Incomplete (peripheral) precocious puberty: early activation in gonads (testes boys, ovaries girls) or adrenal glands. Production of sex hormones at early age
  2. True (complete precocity) precocious puberty: activation of HPG axis, regulates production of sex hormones. In this one, level of gonadotropins (LH, FSH) higher than expected for individual ages
  3. Isosexual preocity: precocious puberty where development of secondary sexual characteristics is consistent with the individual’s biological sex. Boys develop masculine secondary sexual characteristics prematurely
  4. Contrasexual (heterosexual) precocity: development of secondary sexual characteristics that are not consistent with individual’s biological sex - girls experience virilization, boys experience femiziation
  5. Gonadotropin-dependent-precocious puberty: when precocious puberty left untreated. This condition leads to premature closure of growth plates in long bones, resulting in limited height potential and short stature
36
Q

Describe the treatment of true precocious puberty

A

This is caused mainly by abnomarlties in CNS

Treated by GnRH blockers

Surpress release of gonadotropins, slowing down / delaying puberty

37
Q

Describe the causes of precocious puberty

A

GONADOTROPIN INDEPENDENT cause
Can be endogenous or exogenous
Endogenous: testicular source: Testicular tumor, LH excess: HCG producing tumor
Adrenal source: adrenal tumor
Exogenous: Testosterone cream

38
Q

Describe Complete AIS, its symptoms and causes

A

COMPLETE ANDROGEN INSENSITIVITY SYNDROME

  1. Male has typical male chromosome pattern - 46, XY
  2. Born phenotypically female - born with external genitalia which appear female - body unable to respond to androgens (male sex hormones), so incomplete masculinisation of external genatalia during fetal development
  3. Presents at puberty - abscent menarche (menstrual period in female) - individuals have no uterus - other changes including breast development occur at puberty (due to converstion of androgens to estrogens in the periphery)

4.Gonads not ovaries but testes: despite apperance of external female genatalia. Testes in abdomen instead of scrotum

  1. No uterus, no menstrual cycle, amenorrhea
39
Q

Describe the causes and symptoms of amenorrhea

A

Due to complete AIS
Absence of uterus
Therefore, absence of menstrual cycle - amenorrhea

40
Q

Describe the symptoms and causes of cryptorchidism

A

Absence of one / both testicls from scrotum

Because testes develop in abdomen during fetal development, fail to descend into scrotum

(most cryptochid testes descend into scrotum without any intervension, within first few months)

if not descended by 6 months ORCHIOPEXY: if testes not descended into scrotum by 6 months, orchiopexy type of surgery

RISKS

-reduced fertility in males with prev orchiopexy
-testicular cancer - men who have history of cryptorchiddism, but testes have descended, are at risk

41
Q

Describe the causes and symptoms of testicular cancer

A

Malignant
90% germ cell cancer (90% of testicular cancers are germ cell tumours) - unlike ovarian cancers which are of epithelial origin)

RISK FACTORS:
-cryptochidism
-white european
-maternal DES

1st yr-Med 2022-2023 (57 decks)

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