Female Repro L4: STI Flashcards

1
Q

Etiology of vaginitis

A
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2
Q

GENITAL HERPES SIMPLEX

A

**Pathophysiology **

  • Initial viral replication takes place in the epidermis and dermis at the site of viral entry
    • – Incubation period is 2-7 days but can be longer
  • Immunoglobulin IgM to type 2 virus develop within 21 days of exposure in 85% of patients
  • Fetal infection
    • – Transplacental infection seen in 50% of cases of maternal primary lesion
    • – Complications include spontaneous abortion, symmetric IUGR, microcephaly, and cerebral calcifications
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3
Q

SYPHILIS

A
  • Transmission of syphilis
    • – Direct contact with an infectious moist lesion
    • – Transplacental transfer to a fetus from an infected mother
  • Associated with a high rate of co-infection with HIV

Pathophysiology

  • Resolution of chancre in 1-5 weeks
  • Secondary syphilis occurs 2 weeks to 6 months after the primary lesion
    • – A generalized cutaneous eruptions at sites of metastatic foci (heals within 2-6 weeks)
    • – Generalized, non-tender, lymph node enlargement observed in patients with secondary syphilis (85%)
  • Tertiary syphilis is characterized by the presence of gummas
  • Treponemal organism cross the placenta at every stage of pregnancy

Sx

Primary

  • Firm, painless, genital sore (labia, vulva, vagina, cervix, anus, lips, nipples)
  • Painless, rubbery, regional lymph node enlargement
  • Generalized lymph node enlargement 3-6 weeks after exposure
  • Spirochetes found on dark-field microscopy of moist lesions
  • Positive serology in 70% within 1-4 weeks after the development of primary chancre

Secondary

  • Generalized, symmetric, extragenital papulosquamous eruptions
  • Condyloma latum, mucous patches
  • Positive dark-field findings in moist lesions
  • Positive serologic tests for syphilis
  • Lymphadenopathy

Latent

  • Positive serologic tests for syphilis
  • Absence of clinical manifestation
  • Normal CSF examination

Tertiary

  • Neurologic (general paresis, tabes dorsalis)
  • Cardiovascular (asymptomatic aortitis, aortic aneurysm and regurgitation)
  • Skin and mucous membrane (perforation of the nasal septum, indolent skin ulcers)
  • Ophthalmic (blindness)
  • ENT (sensorineural deafness)
  • Bone (osteitis)
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4
Q

CONGENITAL SYPHILIS

A
  • History of maternal syphilis
  • Positive serologic tests for syphilis
  • Manifestation of early congenital syphilis
    • – Non-immune hydrops
    • – Macerated skin
    • – Anemia
    • – Thrombocytopenia
    • – Hepatosplenomegaly
    • – Jaundice
  • Stillborn (50%) or premature
  • Large and edematous placenta
  • Other findings appear later (2 years) (Hutchison teeth, interstitial keratitis, eighth nerve deafness, saddle nose, saber shin, etc.)
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5
Q

GENITAL CHLAMYDIAL INFECTION

A

C. trachomatis has tropism for columnar and transitional epithelium

Infection does not confer lasting immunity

Pathogenesis

  • C. trachomatis serovars B and D through K
    • – Attach only to columnar epithelial cells
    • – No deep tissue invasion
    • – Features of infection: discharge, swelling, erythema and pain are localized
    • – Systemic manifestation of clinical infection may not be apparent
  • Incubation period of symptomatic disease is 7 to 14 days
  • Mechanism for pathogenesis of chlamydial diseases is immune-mediated response (lymphocytes and mononuclear cells )
  • Major outer membrane protein (MOMP) plays a role in pathogenesis
  • MOMP triggers cytokine release which promotes an inflammatory response
  • Molecular mimicry is believed to exist between chlamydial antigen and ciliated epithelium of endosalpingeal cells
  • Adverse sequelae are related to chronic inflammatory changes as well as fibrosis

Sx

CERVICITIS

  • The most common chlamydial syndrome
  • More than 50% are asymptomatic
  • Symptoms, when present, include
    • – Mucopurulent discharge
    • – Intermenstrual bleeding
    • – Post-coital bleeding
    • – Lower abdominal pain
    • – Cervical edema/ulceration

URETHRAL SYNDROME

  • Results from urethritis
  • Associated with frequency, dysuria and lower abdominal pains

PID

  • Ascending infection of upper genital tract
  • Seen in 30% of patients
  • Clinicalfeaturesinclude – Lower abdominal pains
    • – Vaginal discharge
    • – Dysuria
    • – Constitutional symptoms - fever, chills
  • Less acutely symptomatic than PID due to GC
  • Higher rates of infertility than GC
  • Significant risk of ectopic pregnancy

REITER’S SYNDROME: Associated with HLA-B27

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6
Q

Gonorrhea

A

Pathophysiology (partial)

  • Mechanisms of evading the immune system
    • – Inactivation of mucosal IgA1 by bacterial proteases
    • – Blocking antigen by the binding of antibodies to a reduction modifiable protein (rmp)
    • – Antigenic and phase variation o fOpa, Pil, and lipooligosaccharide (LOS)
    • – Masking of gonococcal antigen (sialytion of LOS) which prevents phagocytosis

**Sx: **​Similar clinical syndromes as C. trachomatis

DISSEMINATED INFECTION

  • A clinical syndrome seen in asymptomatic carriers
  • Consists of a triad of polyarthralgia, tenosynovitis and dermatitis ± septicemia
  • Endocarditis and meningitis have been described

VULVOVAGINITIS IN CHILDREN

  • Non-keratinized vaginal epithelium in children is particularly vulnerable to gonococcal infection
  • Infection results in severe vulvovaginitis
  • Genital mucous membrane is red and swollen
  • Should raise suspicion of sexual abuse
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7
Q

HIV INFECTION

A

An acute mononucleosis-like illness seen in 45-90% of patients in first few months of infection

**Pathophysiology: MATERNAL-TO-CHILD-TRANSMISSION (MTCT) OF HIV **

  • Contact with infected genital secretion at time of vaginal delivery (most cases)
  • Crossing the placenta or maternofetal transfusion during prenatal period
  • Penetrating gut mucosa during breastfeeding , especially in a setting of inflammation
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8
Q

HPV

A

HPV is a small, non-enveloped, double- stranded DNA virus

Pathogenesis

  • E7 binds to and phosphorylates the Rb portion of E2F/Rb complex
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