The Genitourinary System PT1 Flashcards

1
Q

Q: What are the main components of the urinary system?

A

The genitourinary system comprises the urinary system and the reproductive system.

The urinary system includes the kidneys, ureters, bladder, and urethra, responsible for filtering blood, producing urine, and excreting waste.

The reproductive system varies between sexes:

  • In males, it includes the testes, epididymis, vas deferens, seminal vesicles, prostate gland, and penis.
  • In females, it consists of the ovaries, fallopian tubes, uterus, cervix, and vagina.
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2
Q

Q: What are the differences between the male and female genitourinary systems?

A

Male:
-testes (which produce sperm and testosterone)
- the epididymis (for sperm storage and maturation)
- the vas deferens (sperm transport)
- seminal vesicles
- prostate gland (fluid production for semen)
- penis (for delivering sperm and urination).

Female:
- ovaries (which produce eggs and hormones)
- fallopian tubes (for egg transport and fertilization)
- the uterus (which houses and nourishes a fetus)
- the cervix (which allows passage between the uterus and vagina)
- the vagina (for receiving sperm and serving as a birth canal).

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3
Q

normal microbiota in this system

A
    • maintaining health by preventing the colonization of harmful pathogens
    • modulating the immune response
    • maintaining an acidic environment in the vagina to inhibit pathogen growth.

In females, lactobacilli are predominant in the vagina, producing lactic acid and hydrogen peroxide to create a protective barrier against infections.

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4
Q

Q: What characterizes the microbiome of the male genitourinary tract?

A

A:

Urine Flushing: Bladder and urethra are continuously flushed by urine.
=> The environment is generally drier and less hospitable to microbial growth compared to females.
==> Microbiota Levels: Very low number of normal microbiota in males.
Resident Microbes: Consists of skin microbes like Staphylococcus.

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5
Q

Q: What characterizes the microbiome of the female genitourinary tract?

A

A:
The reproductive tract has a moist environment, particularly the vagina
-> Complex and dynamic normal microbiota.
Dominant Species: Lower reproductive tract dominated by Lactobacillus species.
Defense Role: Provides non-specific defense through:
Low pH from lactic acid.
Production of bacteriocins.
Competition for nutrients and binding sites.

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6
Q

Q: What disease does Neisseria gonorrhoeae cause and what are its symptoms?

A

Neisseria gonorrhoeae
* Gram negative diplococci bacteria, can infect the urethra, cervix, throat, anus, and eyes
–> Obligate human pathogen (only replicate inside the cells of the human body)

Transmission = sexual contact with penis, vagina, mouth or anus OR from mother to child during vaginal childbirth
Disease: Gonorrhea
Symptoms: asymptomatic (female and male)
If appear ==

Men:
- penile discharge
- irritation or pain when
urinating
- anal discharge or discomfort
- conjunctivitis (pink eye)
- eye inflammation

Women:
- unusual Vaginal discharge
- pelvic pain
- intermenstrual bleeding (irregular vaginal bleeding)
- pain when urinating
- anal discharge or discomfort
- conjunctivitis (pink eye)
- eye inflammation

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7
Q

virulence mechanisms of Neisseria gonorrhoeae

A

What features it has, structure/function
1. Type IV pili on Neisseria gonorrhoeae
–> hair-like structures on the surface of this bacteria
= facilitate adhesion to host cells to establish infection
= Type IV pili can do Immune Evasion : can change surface proteins to avoid detection by the host immune system or switch expression of pili on and off to adapt to different environments within the host..
= pili facilitate the uptake of DNA from the environment, allowing genetic exchange and contributing to genetic diversity and adaptation, including antibiotic resistance.

  1. Has IgA Protease
    –> an enzyme that specifically targets and cleaves immunoglobulin A (IgA) antibodies.
    = Immune Evasion: By cleaving IgA antibodies, directly neutralizes a key component of the immune defense.
    ==> reduces the ability of the host to clear the infection, allowing the bacteria to invade tissues more effectively.
    = Tissue Invasion: The breakdown of IgA facilitates deeper penetration and invasion into mucosal tissues.
  2. PorB (Outer Membrane Protein B)
    –> major outer membrane protein that plays a role in nutrient uptake and interacts with host cell membranes.
    = Immune Evasion: PorB can interfere with the host’s immune system
    ==> helps suppress host cell apoptosis and modulates immune signaling pathways, aids in bacterial survival within the host.
    = Membrane Invasion: PorB facilitates bacterial entry into epithelial cells, promoting bacterial colonization and persistence.
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8
Q

Neisseria gonorrhoeae its impact on HIV susceptibility

A
  1. Gonorrhea causes inflammation in the urogenital tract
    ==> leading to the recruitment of immune cells, including CD4+ T cells (T helper cells/ target cells for HIV)
    => increased presence of these cells at the infection site can enhance the likelihood of HIV transmission.
  2. The damage to mucosal surfaces caused by gonorrhea can compromise the physical barriers that protect against pathogens, including HIV
    ==> making it easier for the virus to enter the bloodstream.
  3. infection stimulates the production of cytokines and chemokines
    => increase the activation and proliferation of HIV target cells, facilitating viral entry and replication.
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9
Q

Q: What disease does Chlamydia trachomatis cause and what are its symptoms?

A

Gram-negative obligate intracellular bacterial parasite, only found in humans
Transmission : Sexually transmitted, can also be transmitted from mother to child during vaginal childbirth

Intracellular bacteria are those that live and replicate inside the cells of their host.
= can evade certain components of the host’s immune system, such as antibodies and some phagocytic cells that target pathogens outside cells

An obligate intracellular bacterium cannot survive or reproduce outside of its host cell. It relies entirely on the host cell’s environment for nutrients and energy, as it often lacks the necessary machinery to perform these functions independently.

Disease: Causes chlamydia.

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10
Q

Q: What disease does Treponema pallidum cause and what are its symptoms?

A

Gram-negative bacteria, distinct spiral cell
shape, motile
Sexually transmitted, can also be transmitted
from mother to child during pregnancy and
vaginal childbirth (congenital syphilis)

Disease: Syphilis
4 stages and their Symptoms: primary, secondary,
latent, tertiary (neurologic & psychological)
3. latent stage = the hidden stage, where there are no visible signs or symptoms.
Can last for years, during which the disease remains in the body without causing noticeable symptoms

  1. tertiary stage = Can affect multiple organ systems
    - Neurologic Effects: Neurosyphilis, which can cause headaches, altered behavior, movement problems, paralysis, and dementia.
    - Cardiovascular Effects: Cardiovascular syphilis can result in aortic aneurysms or heart valve disease.
    - Psychological Effects: Can lead to severe psychological issues, including cognitive decline and personality changes
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11
Q

Flashcard 4: Trichomonas vaginalis

Q: What disease does Trichomonas vaginalis cause and what are its symptoms?

A

protozoan parasite, meaning it is a single-celled eukaryotic organism// only found in humans, with no animal reservoirs.

Disease: Trichomoniasis

Symptoms:
Women: Itching, burning, redness, and soreness of the genitals; discomfort with urination; a thin discharge with an unusual smell.
Men: Often asymptomatic, but can cause irritation inside the penis, mild discharge, or slight burning after urination or ejaculation.

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12
Q

Why Are Many Gonorrhea Cases Asymptomatic?

A

Stealth Entry with Antigenic Variation: Neisseria gonorrhoeae can change the proteins on its surface, making it difficult for the immune system to detect and respond to the infection.

Hiding Inside Cells – Particularly in Epithelial Cells: The bacteria can invade and live inside epithelial cells, evading detection by the immune system.

Location, Location, Location: Gonorrhea often infects areas that do not produce strong immune responses, such as the cervical canal in women and the urethra in men.

Higher Tolerance: Mucosal Surfaces: These surfaces are adapted to withstand constant exposure to microorganisms and are less likely to mount a robust inflammatory response.

More Noticeable Response: Inflammatory Response: When symptoms do appear, they are often due to the body’s inflammatory response to the infection, which can lead to pain and discharge.

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13
Q

Treatment Options for Neisseria gonorrhoeae (ANTIBIOTIC RESISTANCE)

A

Penicillin, Tetracycline, Cefixime, Ceftriaxone: These antibiotics inhibit bacterial cell wall synthesis, causing the bacteria to burst and die.

Ciprofloxacin: This antibiotic inhibits DNA replication, preventing the bacteria from multiplying.

Azithromycin: This antibiotic inhibits protein synthesis by binding to the 50S ribosomal subunit, preventing the bacteria from producing essential proteins.

ANTIBIOTIC RESISTANCE:
1. Genetic Variability and Horizontal Gene Transfer
==> Neisseria gonorrhoeae can rapidly acquire and exchange genetic material, including resistance genes, through horizontal gene transfer.
==> can undergo genetic mutations that confer resistance to antibiotics,

  1. Host Behavior: Misuse and Overuse of Antibiotics
    => Incorrect use of antibiotics, such as not completing prescribed courses or using antibiotics without medical supervision, can promote the development of resistant strains.
    => High rates of reinfection due to unprotected sexual activity and lack of partner notification and treatment can lead to the spread of resistant strains.
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14
Q

Chlamydia trachomatis Virulence Mechanisms

A
  1. Type III Secretion System (T3SS)
    ==> specialized protein delivery system used by Chlamydia trachomatis to inject effector proteins (bacterial proteins that alter host cell functions) directly into the host cell.
    ==> allows the bacteria to manipulate host cellular processes, facilitating bacterial entry, survival, and replication within the host cells.
    => can create a more favorable environment for bacteria own survival and reproduction.
  2. TARP (Translocated Actin-Recruiting Phosphoprotein)
    => one of the effector proteins
    - induces the reorganization of the host cell’s actin cytoskeleton
    ==> aiding in bacterial entry and the formation of an inclusion body where the bacteria can replicate safely.
    - supports bacterial survival and protects it from immune detection.
  3. Pgp3 (Plasmid Glycoprotein 3)
    -> a protein associated with immune evasion.
    - helps suppress the host immune response,
    => reducing the ability of the host to clear the infection.
    - can interfere with normal immune signaling pathways
    => allowing the bacteria to persist within the host for extended periods.
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15
Q

Treatment Options Chlamydia infections

A

typically be cured with antibiotics that inhibit bacterial protein synthesis
=> target either the 50S or 30S ribosomal subunits
=> effectively halting protein production necessary for bacterial growth.

– Antimicrobial resistance in Chlamydia trachomatis is not common but is a growing concern.

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16
Q

Virulence Mechanisms of Treponema pallidum

A
  1. Shape and Movement
    - The spiral or corkscrew shape of Treponema pallidum
    ==> allows it to move through viscous environments like mucus and penetrate tissues effectively.
    - highly motile
    ==> enabling them to spread throughout the body.
  2. Outer Membrane Sheath
    - helps the bacteria evade the host’s immune system by masking itself from immune detection
    => the bacteria can persist in the host for extended periods.
  3. TprK (Treponemal repeat protein K)
    - a surface protein involved in attachment to host cells and tissues.
    –> undergoes antigenic variation, changing its surface antigens
    ==> evade the immune system continuously
    ==> makes it difficult for the host to mount an effective and lasting immune response.
17
Q

treatment options for syphillis

A

antibiotics, most notably benzathine benzylpenicillin.
==> This antibiotic inhibits bacterial cell wall synthesis, leading to the death of the bacteria.

global shortage : Recent shortages of benzathine benzylpenicillin have contributed to a rise in syphilis incidence, as timely treatment becomes difficult.

Antimicrobial Resistance: Although not common, resistance is gradually increasing, necessitating careful monitoring and the development of alternative treatments.

18
Q

Trichomonas vaginalis virulence mechanisms

A
  1. Adherence and Immune Evasion
    - AP65, AP51, AP33:
    => involved in adherence to host cells
    => help the parasite evade the immune system through molecular mimicry.
    ==> mimic host molecules, allowing the parasite to avoid detection by the immune system.
  2. Tissue Damage
    CP65 (Cysteine Protease) enzyme that breaks down host tissues
    => facilitating invasion and causing damage
    ==> Contributes to the destruction of epithelial cells, leading to inflammation and symptomatic infection.
  3. Dysbiosis
    The parasite can disrupt the normal vaginal microbiota ==> phagocytizing Lactobacillus species, which are protective bacteria that help maintain a healthy vaginal environment.
    -> This disruption can lead to an imbalance (dysbiosis), making the host more susceptible to infection and inflammation.
19
Q

treatment of Trichomonas vaginalis

A

Metronidazole: typically resolved after a single dose.
- works by interacting with the DNA of the parasite
=> inhibiting protein synthesis.
=> a loss of helical DNA structure and induces strand breakage, ultimately leading to cell death.

Antimicrobial Resistance: Although not common, resistance to metronidazole is gradually increasing, necessitating monitoring and alternative treatments.

20
Q

Human immunodeficiency virus’s disease

A

Disease = Acquired immunodeficiency (AIDS)

21
Q

Human papillomavirus (200+ strains, 40 responsible for STIs) and its disease

A

Disease = Genital warts or cervical cancer (also vaginal, anal, vulvar and penile
cancers)
* Vaccine available to protect against strains 6, 11, 16 and 18

22
Q
  • Herpes Simplex -1 and -2
A

HSV is part of this large family of DNA viruses.
==> Alphaherpesvirus Subfamily: This subfamily includes HSV-1, HSV-2, and Varicella Zoster Virus (VZV).

Types:

HSV-1: Typically associated with oral infections (cold sores).
HSV-2: More commonly associated with genital infections.
Genome: Both HSV-1 and HSV-2 are double-stranded DNA viruses with high genomic homology, meaning they share a significant portion of their genetic material.

23
Q

HSV pathogenesis Primary infection

A
  1. The virus enters the body through breaks in the skin or mucous membranes.
    => typically infects epithelial cells of the oral or genital mucosa.
  2. Replication:
    Once inside the host cell, the viral genome is transported to the nucleus where replication begins.
    ==> The virus uses the host cell machinery to transcribe and translate its DNA into viral proteins.
  3. Virus Assembly and Release:
    New virus particles are assembled in the host cell and released either through cell lysis or exocytosis.
    => Released virus particles infect nearby cells and can access sensory nerve endings.
  4. Spread to Nervous System:
    Virus travels via sensory neurons to the regional ganglia (trigeminal ganglia for oral HSV, sacral ganglia for genital HSV).
    The virus establishes latency in these ganglia.
24
Q

Pathogenesis of HSV
latent infection

A

Latency:
* The viral genome remains in a non-replicating state within the sensory neurons.
–> No viral proteins or particles are produced during this time, rendering the virus hidden from the immune system.

  • The virus remains dormant in the ganglia for the host’s lifetime.
    => During latency, the viral DNA is maintained as an episome in the nucleus of neurons.
25
Q

Pathogenesis of HSV recurrent Infection

A

The latent virus can reactivate, typically triggered by stress, illness, immune suppression, or other unknown factors.
==> the virus resumes replication within the neuron and travels back to the original site of infection.
==> The virus remains in neurons where the immune response is less active, allowing it to evade detection.

Doesnt cause harm in latent phase// becomes problematic when reactivated, leading to symptomatic outbreaks and potential transmission. {cause symptoms and increase the risk of transmission to sexual partners}

Symptoms:
- leads to recurrent lesions at the site of initial infection (cold sores or genital lesions).
causes cell lysis and the release of new virions, leading to symptomatic outbreaks.

26
Q

describe how genital herpes is transmitted

A

primarily transmitted through direct skin-to-skin contact during vaginal, anal, or oral sex with an infected partner.

  1. HSV-1, commonly associated with oral herpes (cold sores), can cause genital herpes through oral-genital contact, such as oral sex/ kissing
  2. HSV-2, more commonly associated with genital herpes, is transmitted during these activities.
  3. Asymptomatic Shedding
    - the virus reactivates and begins replicating
    - travels from nerve cells to the surface of the skin or mucous membranes, where it can be shed
    - virus particles are present on the skin or in bodily fluids like saliva or genital secretions.

Touching someone’s skin in areas where there are no sores or where the virus is not shedding does not usually result in transmission.
==> is unlikely to transmit the virus unless there is direct contact with the infected area when the virus is active.
Symptoms : Painful blisters or sore/ Pain, Itching, and Burning
HIV risk == genital lesions from herpes increases the risk of acquiring and transmitting HIV. The open sores provide an entry point for the virus, and inflammation can attract immune cells that are target cells for HIV.

==> more commonly diagnosed in females, suggesting that the female genital tract may be more susceptible to HSV infection. Factors such as the larger surface area of mucous membranes and hormonal influences may contribute to this increased susceptibility.

27
Q

Prevention and controlling of STIs

A

Best to prevent initial infection ;
* Comprehensive education about STI
* Counseling and support particularly for at risk populations
* Promotion of barrier protection – use of condoms
* Development of vaccines – currently no vaccine for any bacterial or protozoan STIs

Easy to control these pathogens after infection, however;
* MUST have de-stigmatization of STIs
* Education about symptoms and importance of early diagnosis & control of spread to
sexual partners
* Access to health care and timely and effective treatment

28
Q

Q: What are the structural and environmental differences between the male and female genitourinary systems?

A

A:

Male System: Includes the urethra, which is longer and serves dual functions (urination and ejaculation). The external location of the testes allows for a cooler environment for sperm production.
Female System: Features a shorter urethra, making it more susceptible to UTIs. The vagina is a moist environment with a complex microbiome that helps protect against infections. Internal reproductive organs are maintained at body temperature.

29
Q

Q: How do the microbiomes of the lower and upper female reproductive systems differ?

A

A:

Lower Reproductive System (Vagina): Dominated by Lactobacillus species, which maintain a low pH and protect against pathogens.
Upper Reproductive System (Uterus and Fallopian Tubes): Generally sterile, with the cervix acting as a barrier to prevent bacterial invasion and maintain sterility.

30
Q

Q: How does the immune response differ in controlling bacterial, protozoan, and viral infections in the genitourinary system?

A

A:

Bacterial Infections: Involve innate responses like phagocytosis and adaptive responses such as antibody production.
Protozoan Infections: Trigger innate responses including phagocyte activation and adaptive responses like Th1-mediated immunity.
Viral Infections: Involve interferon production, NK cell activity, and adaptive immunity through cytotoxic T cells and neutralizing antibodies.

31
Q

Q: What is an advantage of viruses traveling along neuronal pathways rather than spreading throughout the body in the blood?

A

A:

Latency: Viruses like HSV can establish latency in neurons, avoiding immune detection and persistence in the host.
Selective Localization: Neurons have reduced immune responses, allowing viruses to avoid detection.
Rapid Reactivation: Allows quick reactivation and transport to the original infection site, enabling recurrent infections without systemic spread.

32
Q

Q: Why is the minimum window period for HSV antibody detection two to six weeks after exposure?

A

A:

Immune Response Timing: It takes time for the immune system to recognize the virus and produce detectable antibodies.
Antibody Production: Specific antibodies (IgM and IgG) develop within two to six weeks.
Prior Infection Influence: Previous infections may lead to a faster immune response upon re-exposure, shortening the window period.