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Reproductive System > 6 > Flashcards

6 Flashcards

1
Q

Describe the epididymal maturation of sperm

A
  • on entry, spermatozoa is not capable of movement
  • once at the tail of the epididymis, they are capable of movement and have the potential to fertilize
  • addition of secretory products to surface of sperm
  • Maturation is dependent on support of the epididymis by androgens
  • look at chart on REPRO getting pregnant bb slide 6
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2
Q

What are the functions of semen?

A
  • nutrition source for spermatozoa
  • acts as a transport medium
  • neutralizes the acidic environment of the vagina
  • potentially a role for prostaglandins in stimulating muscular activity in the female tract
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3
Q

What does semen consist of?

A
  • spermatozoa (small portion)

- seminal plasma which is derived from accessory glands of the male reproductive tract

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4
Q

Describe what seminal plasma consists of and what glands contribute to it

A

Seminal vesicles

  • 60% of volume
  • alkaline fluid (neutralizes acid of male urethra and female reproductive tract)
  • fructose, prostaglandins, clotting factors (particularly semenogelin)
  • acts as a metabolic unit of the spermatozoa

Prostate gland

  • 25% volume
  • milky, slightly acidic fluid
  • proteolytic enzymes (breakdown clotting proteins, re-liquefying semen in 10-20 min)
  • citric acid, acid phosphorylate)

Bulbourethral glands (Cowper’s glands)

  • very small volume
  • alkaline fluid
  • a mucus that lubricates the end of penis and urethral lining
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5
Q

How do seminal vesicles and the prostate work together in regards to coagulation?

A
  • semen clots due to clotting factors from seminal vesicles

- prostate produces a substance with enzymes that can break down the coagulation that occurs

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6
Q

What are the normal values of semen analysis?

A 
Volume of ejaculate: 2-6mL
Viscosity: Liquefaction in 1hr
PH: 7-8
Count: >20 million/mL
Motility: >50%
Morphology: 60% normal
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7
Q

List and describe the four phases of the human sexual response

A
  • excitement phase: psychogenic and/or somatogenic stimuli
  • plateau phase: stimuli is maintained
  • orgasm phase: threshold is reached
  • resolution phase: return to haemodynamic norm followed by a refractory period only in males
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8
Q

What are the stimulants and efferents of the excitement phase (ejaculation)?

A

Stimulants

  • psychogenic
  • tactile (sensory afferents of penis and perineum) which travel up to a spinal reflex

Efferents

  • Somatic and autonomic efferents
  • pelvic nerve (Parasympathetic nervous system)
  • pudendal nerve (somatic nervous system)
  • leads to haemodynamic changes
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9
Q

Describe the physiological components of an erection

A
  • neuronal input causes sinusoids in corpus cavernosa to relax in order for arterial dilation to occur
  • venous compression also occurs even though there is increased blood flow, since there is tunica albuginea surrounding the corpus cavernosa
  • tunica albuginea is thick and not distended, very taught and rigid allowing for veins to stay compressed and erection to occur
  • corpus spongiosum is not completely compressed so that semen can leave urethra
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10
Q

Describe the parasympathetic innervation that causes an erection

A
  • sympathetic inhibited while parasympathetic stimulated via pelvic and cavernous nerve
  • lumbar and sacral spinal levels involved
  • pelvic nerve and pelvic plexus
  • cavernous nerve to corpora and vasculature
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11
Q

What is the important neurotransmitter in an erection and what is the neurophysiology behind it?

A
  • NITRIC OXIDE (NO)
  • inhibition of sympathetic arterial vasoconstrictor nerves
  • activation of PNS
  • activation of non-adrenergic, non-cholinergic, autonomic nerves to arteries
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12
Q

What is the role of NO in an erection?

A
  • post-ganglioic fibres release ACh
  • ACh bonds to M3 receptor on endothelial cells
  • rise in [Ca] via M3 receptors which causes activation of NOS and formation of NO
  • NO diffuses into vascular smooth muscle and causes relaxation (vasodilation)
  • NO also released directly from nerves
  • key mediator in this process is cGMP
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13
Q

What are some causes of erectile dysfunction?

A
  • psychological (descending inhibition of spinal reflexes)
  • tears in fibrous tissue of corpora cavernosa
  • vascular (arterial and venous)
  • drugs
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14
Q

How can erectile dysfunction be treated?

A
  • must improve erection by increasing amounts of NO and cGMP

- viagra helps to slow rate at which cGMP is degraded which will results in vasodilation, leading to penile erection

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15
Q

Explain the emission and ejaculation phase

A

-both under sympathetic control

Emission

  • semen moved into prostatic urethra
  • smooth muscle contraction in prostate, vas deferens and seminal vesicles

Ejaculation

  • expulsion of semen
  • requires contraction of glands and ducts but also contraction of the internal sphincter (in bladder) to prevent retrograde ejaculation
  • rhythmic striata muscle contractions (pelvic floor, perineal muscles ischiocavernosus, bulbospongiosus)

Point Shoot

  • Point (erection requires Parasympathetic stimulation)
  • Shoot (ejaculation requires Sympathetic stimulation)
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16
Q

Describe the menstrual cycle changes

A
  • character of cervical mucus changes over the course of the menstrual cycle
  • Oestrogen provides thin and stretchy mucus which allows sperm to travel through female tract
  • Oestrogen and progesterone provides thick and sticky mucus which almost acts like a plug
  • this occurs right after fertilization to prevent entry of any further sperm
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17
Q

Where is sperm deposited and where is the site of fertilization?

A
  • site of sperm deposition: at external os of cervix, where it will be liquified so that the gametes can move up the tract
  • site of fertilization: ampulla of Fallopian tube
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18
Q

What is capacitation?

A
  • further maturation of sperm in female reproductive tract (6-8 hours)
  • sperm cell membrane changes to allow fusion with oocyte cell surface
  • tail movement changes from wave-like beat to whip-like action
  • now capable of undergoing of acrosome reaction
  • see diagram in REPRO getting pregnant bb slide 24
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19
Q

How long is the fertile window for?

A
  • Sperm can survive from 48-72 hours
  • oocyte can survive 6-24 hours (max)
  • fertile period: sperm can be deposited 3 days before ovulation for fertilization to be successful

Gamete transport

  • oocyte: beating cilia and peristalsis of uterine tube
  • sperm: own propulsion

Look at diagram on REPRO getting pregnant bb slide 25

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20
Q

What is the acrosome?

A
  • derived from the golgi region of developing spermatid
  • contains enzymes which help to remove the outer granulosa cels that surround the ovum
  • necessary for fertilization
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21
Q

What is the acrosome reaction?

A
  • sperm pushes through the corona radiata
  • binding of sperm surface receptor to ZP3 glycoproteins of zona pellucida
  • triggers acrosome reaction
  • digestion of zona pellucida
  • also consequent loss of outer membrane of sperm
  • allows single sperm to penetrate the ovum and fuse with membrane
  • see diagram on REPRO get pregnant bb slide 28
22
Q

What is the cortical reaction?

A
  • after fusion of the plasma membranes, cortical reaction occurs
  • blocks polyspermy
  • triggers meiosis 2 to finish
  • series of calcium waves are activated following fusion of oocyte and sperm membranes
  • resumption of meiosis 2 occurs
  • pronuclei move together
  • mitotic spindle forms leading to cleavage
  • look at diagram on REPRO getting pregnant bb slide 29-30
23
Q

What is a morula?

A
  • totipotent cells formed from multiple mitotic divisions

- right after fertilization

24
Q

How does fertilization work in assisted reproductive technology?

A
  • oocytes are fertilized in vitro and allowed to divide to the 4- or 8- cell stage
  • morula is then transferred into the uterus
  • PGD (pre-implantation genetic diagnosis)
  • cell can be safely removed from the morula and tested for serious heritable conditions prior to transfer of the embryo into the mother
25
Q

What is blastocyst and hatching?

A
  • first differentiation into inner and outer cell masses
  • formation of the blastocyst
  • blastocyst hatches from zona pellucida
  • no longer constrained —> now free to enlarge
  • can now interact with uterine surface to implant
26
Q

What occurs during implantation?

A
  • outer cell mass (trophoblast) interacts with endometrium
  • endometrium controls degree of invasion
  • ectopic implantation (at sites other than endometrium lined uterine cavity; invasion not controlled)
  • implantation in lower uterine segment can cause placenta praevia
  • look at diagram on REPRO getting pregnant bb slide 34
27
Q

What are the two ways of classifying reproductive infections?

A
  • sexually transmitted vs. Non-sexually transmitted

- based on presenting symptom

28
Q

What are some factors that affect genital tract infections?

A
  • age: 15-24 y/o are more likely
  • Ethnicity: black or black British have higher rates of STIs
  • low socio-economic status (access to education)
  • increased number of sexual partners
  • sexual orientation (ex. Homosexual men)
  • lack of immunization (Hep B, HPV)
  • lack of barrier contraception
  • “risky sexual behaviours “ such as multiple sexual partners, early age first intercourse, certain sexual practices (homosexual, anal)
29
Q

What is the most common STI in UK?

A

Chlamydia: chlamydia trachomatis

30
Q

How does Chlamydia trachomatis cause discharge in men? Describe it

A
  • chlamydia is an obligate intracellular bacterium
  • has a unique cell wall which inhibits phagolysosome fusion (virulence factor)
  • bacteria gets phagocytosed but inhibits fusion of phagosome and lysosome
  • without phagolysosome we cannot digest the bacteria and get ride of it
  • not a “true” gram-negative bacteria
  • typically asymptomatic in mean
  • but can cause mild urethritis, testicular pain, dysuria, or inflammation of other structures (eg. Epididymitis, prostatic is)
  • may have discharge
31
Q

How does gonorrhoea (caused by neisseria gonorrhoeal) cause discharge in men?

A
  • most common cause of urethral discharge
  • “gonococcus” is gram negative, diplodocus, unencapsulated and Pilated
  • pili on bacteria helps to adhere to mucosal membrane (i.e. urethra, cervix, pharynx, rectum)
  • 90% of men ARE symptomatic
  • causes yellow discharge and possibly dysuria (painful urination)
  • can cause epididymo-orchitis
  • treatment: ceftriaxone to treats gonorrhoea and azithromycin to “boost” effect of antibiotic
  • also helps to treat chlamydia as a common co-infection
32
Q

How does Non-gonococcal urethritis (NGU) cause discharge in men?

A
  • is a non-STI
  • inflammation of urethra with associated discharge
  • can possible be sexually transmitted (common):
  • chlamydia trichomatis
  • mycoplasma genitalium
  • trichomonas vaginalis
  • can be “pathogen negative” where you cannot find an organism but it is less common and occurs in older men
33
Q

What investigations can be done to detect STIs in men?

A

Urine sample

  • “first catch” urine for gonorrhoea/chlamydia
  • “mid-stream” urine for culture and sensitivities
  • gonorrhoea: microscopy and culture, NAATs (Nucleic Acid Amplification Test)
  • chlamydia: NAATs (most sensitive and specific)
  • urethritis: as above
  • excludes UTI as a cause of dysuria (more common in older men than younger men)

Urethral swab

  • gonorrhoea
  • should be done if pt. Is symptomatic

Men who have sex with men
-take rectal and pharyngeal sampling or swabs at an ulcer site

Blood tesT
-for syphilis and blood borne viruses

34
Q

What is the physiological discharge in women?

A
  • menstrual cycle
  • progesterone in the secretory phase (post-ovulation) which leads to thicker cervical mucus
  • features of this are:
  • cyclical
  • no other associated symptoms
  • clear
35
Q

How chlamydia cause discharge in women?

A
  • c. Trachomatis
  • most women are usually asymptomatic
  • can cause complication such PID and reactive arthritis
  • may cause discharge
  • may cause postcoital (bleeding after sex) or intermenstrual bleeding
  • may cause dyspareunia
  • can also cause infections (conjunctivitis) in neonates if patient is pregnant
  • treat with doxycycline or azithromycin
  • if pregnant use ezithromycin
36
Q

How does gonorrhoea cause discharge in women?

A
  • N. gonorrhoeae
  • typically asymptomatic but can cause vaginal discharge and lower abd pain
  • can cause PID
  • treat same as men
37
Q

How can trichomoniasis cause discharge in women?

A
  • bacteria: trichomonas vaginalis
  • Protozoa (flagellates)
  • presences of flagella (mobility) which help propel it through the reproductive tract
  • optimal growth is at pH 6.0 but vagina has pH 4
  • if there is increased alkalinity of vagina, then it will likely flourish
  • causes copious, yellow, odourous discharge
  • can cause irritation of vulva and vagina
  • typically diagnosed with swabs
  • treatment: metronidazole
38
Q

How does candidas cause discharge in women?

A
  • Candida albicans is a yeast in normal vagina
  • is activated in immunocompromised states (pregnancy, HIV), diabetes, antibiotics and oestrogen-containing oral contraceptives (COCP)
  • is VERY ITCHY
  • white non-offensive vaginal discharge with pruritis, pain and/or dyspareunia
  • investigated with high vaginal swabs and treated with oral and/or topical anoles
39
Q

How does bacterial vaginosis cause discharge in women?

A
  • non STI
  • caused by pH imbalance in vagina which allows growth of certain bacteria such as Gardeneralla vaginalis
  • thus normal bacteria (lactobacillus) is diminished
  • risk factors: practices that disrupt the vaginal flora such as washing it
  • increases risk of contracting STIs
  • presents with very offensive vaginal discharge, WITHOUT pruritis or pain
  • diagnosed by high vaginal swabs
  • treatment: metronidazole
40
Q

What investigations are done to check for STI in women?

A
  • urine samples are iNEFFECTIVE
  • chlamydia: Vulvo-vaginal swabs (VVS), endocervical (go with camera into cervix
  • gonorrhoea: VVS (if asymptomatic), endocervical
  • trichomoniasis: high vaginal swab (HVS) (posterior fornix)
  • BV: gram staining, KOH test (add KOH to sample and observe if there is a fishy smell)
  • Candida: HVS; Microscopy > culture
  • also consider ulcer swabs, rectal/pharyngeal swabs and serology
  • look at summary in Infections of the reproductive tract_student slide 24
41
Q

Describe Human Papillomavirus (HPV)

A
  • most common viral STI
  • most common cause of genital warts
  • warts typically regress without treatment, although topical treatments are available
  • DNA virus (non-enveloped)
  • many different types
  • types 6 and 11 cause 90% of genital infections
  • types 16 and 18 have the highest association with cervical cancer
  • can do PCR to identify high risk types (biopsy/swab)
  • can be vaccinated: gardasil (6,11, 16, 18) and cervarix (just 16 and 18)
42
Q

What is Herpes Simplex virus (HSV -1 and -2)

A
  • two strands: -1 and -2
  • HSV-1 can cause oral and genital herpes, also associated with “cold sores”
  • HSV-2 typically causes genital herpes and often leads to recurrent infection; can be particularly dangerous in pregnancy as vaginal delivery means the baby can develop complications of herpes; more likely to become infected with HIV
  • DNA virus (enveloped)
  • viral infection that lays dormant
  • lifelong infection: initial then recurrent infection
  • can be asymptomatic initially, or present with painful ulcers/blisters
  • can be accompanied by systemic symptoms such as fever, malaise and myalgia
  • should check all areas such as genitals, mouth, and anus
  • swabs: PCR and NAATs
  • Management: can use antivirals (eg. Aciclovir)
  • cannot eradicate the infection
  • reduce the severity and duration of the current episode
  • limited effect frequency/severity of repeated episodes
43
Q

What is syphilis (treponema pallidum)?

A
  • spirochete bacterium
  • transmission: direct contact, vertical transmission
  • not as common generally: 40% co-infected with HIV
  • prevalent among homosexuals (male) and 24-35 y/o men
  • can affect pregnant women and their babies

Primary Syphilis

  • typically painless ulcer(s) in the genitals, or other sites involved in sexual contact
  • initial infection
  • it is very infectious at this stage, but the lesion will usually disappear

Secondary Syphilis (25% of untreated cases)

  • 4 to 10 weeks after initial infection (more severe)
  • multi-system (occurs a few months later)
  • can enter a latent phase (can cause skin rashes)

Tertiary syphilis
-infection can remain latent and become reactivated late in life (ex. In pregnancy, which can lead to congenital syphilis)

  • Microscopy/PCR
  • serology (will usually do serology to see antibody effect)
  • management: penicillin-based antibiotics
44
Q

How can we manage STIs

A
  • co-infections are very common
  • similar route of transmission
  • may be asymptomatic
  • consider screening for others
  • consider presenting complaint
  • appropriate investigation and therapy
  • bacterial: can give multiple antibiotics (ex. Azithromycin and ceftriaxone)
  • targets different organisms
  • one antibiotic can augment the effect of the other
  • educate patients on safe sex and to avoid sex until course of treatment is completed
45
Q

What is PID?

A
  • infection of the uterus, Fallopian tubes, and ovaries
  • typically because of ascending infection:
  • chlamydia trachomatis
  • neisseria gonorrhoeae
  • gardnerella sp.
  • others eg. Mycoplasma genitalium
  • often polymicrobial
  • other sources of infection: intrauterine contraceptives (more to come), other uterine interventions
  • largest risk factor: infection
46
Q

What is endometritis?

A
  • inflammation of the endometrial lining of the uterus, and can be acute or chronic
  • affects uterus
47
Q

What is Salpingitis?

A
  • inflammation of Fallopian tubes
  • significant clinical complication when thinking about long-term damage to the ciliated epithelium of the Fallopian tubes
  • inflammatory exudate can cause the tubes to fill with pus, leading to adhesions and obstruction of the tube and can lead to turbo-ovarian abscess formation
  • typically stays within the Fallopian tube
48
Q

What are the risk factors of PID?

A
  • young age
  • multiple sexual partners
  • lack of barrier contraception
  • low socio-economic status
  • IUCD
49
Q

What are the signs and symptoms of PID?

A

Signs

  • Pyrexia (+/-)
  • pain on palpitation: abd, biannual vaginal exam
  • evidence of discharge/cervix it is (speculum)

Symptoms

  • lower abd pain
  • dyspareunia
  • pure lent discharge
  • abnormal uterine bleeding (ex. Intermenstrual or postcoital)
50
Q

What are some other causes of the symptoms of PID?

A
  • Constipation
  • ectopic pregnancy
  • appendicitis
  • UTI
  • endometriosis
  • ovarian cyst
  • postcoital/intermenstrual bleeding
51
Q

What are some complications of PID?

A
  • chronic pelvic pain
  • pelvic abscess (tube-ovarian)
  • can lead to subfertility:
  • adhesions from chronic inflammation will result in an increased risk of ectopic pregnancy since the tubes would be blocked by adhesions; reduces likelihood of successful fertilization
  • peritonitis
  • fitz-Hugh Curtis syndrome (peri-hepatitis)
52
Q

How can we manage PID?

A

Prevention > Cure

  • antibiotics
  • give if clinically suspected, dont delay because of investigations
  • negative swabs DO NOT exclude PID
  • broad spectrum
  • IV in more severe cases
  • analgesia
  • offer screening to sexual partner (Genital urinary medicine aka GUM)
  • in those who fail to respond to treatment, laparoscopy is essential to confirm the diagnosis or to make an alternative diagnosis

Reproductive System (11 decks)

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