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95 Cards in this Set
- Front
- Back
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MMMM
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Mixing and Matching of mucous membranes
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Acute STD manifestations
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Vaginitis, Cervicitis, Genital Ulcers, Vesicular lesions, Vaginitis
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Chronic STD manifestations
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Recurrent Herpes, genital warts, PID, Tertiary syph, Immunodeficiency
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Sequele
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Infertility, Ectopic pregnancy, cervical cancer, opportunistic infections, vertical transmission
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Treponema pallidum
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Spirochete, self-coating antigenic masking with fibronectin, motile, slow division, no successful culture = SYPHILIS
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Spread of treponema pallidum
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Congenital and sexual, usually between contact with active lesions
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Key pathogenic mechanism of syph
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Adhesion during initial contact. If it can't attach, it will die
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Virulence factors of treponema
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Produces hyaluronidase, survives intracellularly
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Response needed to control syph
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TH1. Antibody adhesion causes an immune complex (Type III) reaction
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Primary syph
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Painless chancre, generally single with no exudate
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Stage flow of treponema infection
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Primary, secondary, early latent, late latent, tertiary -- ALL stages can be stopped with antibiotics
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Differential of primary syphilis
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Herpes and chanchroid disease, both similar appearance.
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Diagnosis of primary syph
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Darkfield appearance of spirochetes from lesion.
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Secondary syph
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"Great Imitator" Rash, mucous membrane lesions, same basic constitutional symptoms, asymptomatic CNS involvement
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Diagnosis of secondary syph
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Same darkfield as primary, but in this case the serology will be 100% positive
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3 manifestations of tertiary syph
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1. Neuro - meningeal destruction, cortex involvement, imbalance and nerve damage
2. Cardio - aortitis 3. Gumma - nonspecific granulatomous lesion, local tissue destruction in skeletal system and skin |
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Congenital syph
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4th month gestational infection, stillbirth and late abortion. If the fetus lives, will have snuffles/rash/facial osteochondritis, organ involvement
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2 serologic tests for syph
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RPR: tests antilipid antibodies
VDRL: tests antitreponemal antibodies |
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Serologic procedure for syph testing
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RPR: if pos, likelihood of syph but can also detect other lipid antigens. If neg, syph is not likely
VDRL: If pos with pos RPR, diagnose and treat for syphilis. If neg, the RPR test was most likely a false positive |
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Do anti-lipid antibodies remain high throughout syphilis progression? Do anti-treponemal?
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No. Yes. You would then think, why not just go to the VDRL first? Because the VDRL cannot detect a current syph infection, only that one has existed at some point. The RPR indicates current infection if positive.
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CSF RPR testing
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If pos, presence of neurosyphilis. There should be no antilipid antibodies in the CSF under normal circumstances
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If mom has syph . . .
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. . . you have to assume the baby has it too.
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Treatment of syph
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Benzathiane Penicillin G. If they're allergic, you go to tetracycline, third gen ceph, or z-pack
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Herpesviridiae
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Cause latent neuronal infection in hosts. Which explains why they all reactivate (HSV, VZV et al)
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HSV-1
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Associated with non-genital infections
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HSV-2
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Associated with genital herpes
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Replication of Herpes
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Is via lytic infection. Binding to heparan sulfate, fuses, replicates in nucleus, makes RNA and builds structural components in cytoplasm. They come back into the nucleus, bud through the NUCLEAR membrane. They essentially kill the cell
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Lesion of herpes
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Thin-walled vesicle on an inflammatory base. Coupled with lymphadenopathy, lesions will ulcerate and hurt a lot. Lesions last several weeks.
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3 ways Herpes interferes with immune response
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1. Blocks interferon
2. Blocks MHC-I presentation 3. Binds Fc portion and complement (inactivated) |
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Does Herpes lyse neurons?
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No, it rests there.
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When HSV is reactivated. . .
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it returns to the site of initial infection. Lesions are often in the same place.
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Opthamalogical effects of Herpes
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Conjunctivitis, Blepharitis, Keratitis
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Reoccurence of genital herpes
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Once every 3 months, incidence can be exacerbated.
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Therapy for genital herpes
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Acyclovir
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Complications of herpes infection
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1. HIV-1 can cause fatal sporadic encephalitis (travel through facial neurons into brain) lesions in temporal lobe
2. Neonatal transmission 3. Immunocompromised |
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Diagnosis of Herpes
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1. Serology
2. Histo staining to show giant cells as well as chromatin margination 3. Culture 4. PCR |
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Disease caused by Haemophilus Decreyi (gram neg)
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Chancroid lesion disease with cocommittant lymphadenopathy. The chancre erodes to ulcer, very painful, often asymptomatic in women
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How do you diagnose Chanchroid disease?
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Basically rule out HSV and syph
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Epidemiological problem with chancroid disease?
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Ulcerating lesions? You do the math on how easy it would be to transmit HIV.
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Therapy for chancroid disease
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Azithromycin, 3rd gen ceph, cipro, erythromycin
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Molluscum contagiosum
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Poxviridae--firm umbilicated papules, occur on lower abdomen and genitalia, can spontaneously resolve in up to a year
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Diagnosis of molluscum contagion
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Appearance of molluscum bodies in cytoplasm. You cannot culture it.
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Treatment of molluscum contagiosum
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Remove them
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2 distinctive types of HPV
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1. Cutaneous -- infect keratinizing epi
2. Genital -- infect nonkeratinizing epi |
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What's key to remember about HPV?
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It is directly linked to increased risk and development of cervical cancer.
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Regions of HPV genome that correlate with oncogenesis
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E5, E6, and E7
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When do the genital warts of HPV appear?
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3-4 months after inoculation
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Koilocyte
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An HPV cell effect where the nucleus shrinks and the nucleus is eaten by a vacuole . . . can you tell I'm tired of STDs by now?
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When does HPV cause cancer?
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When the viral genome becomes integrated into host genome.
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HPV types most likely to be integrated into cellular DNA?
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Serotypes 16, 18
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What is the specific role of E6 and E7 in oncogenesis with HPV?
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Will block or alter tumor suppression genes of host cell
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Can you clear an HPV infection without treatment?
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Yes, most young women do.
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Are the cutaneous HPV subtypes (1-4) associated with cancer?
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Yes, but mostly in immunocompromised patients
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Continuum of progressive HPV related changes
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Mild cervical neoplasia, moderate neoplasia, severe dysplasia, carcinoma in situ . . . and then begin standard cancer staging
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Serotypes of oral papilloma
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6, 11
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Diagnostic tool for HPV infection
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The PAP smear - demonstrates the koilicytic changes and other unusual cellular changes on cervix.
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Serotypes of HPV in Gardasil vaccine
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6,11,16, 18
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Neisseria Gonorrhoae
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Aerobic, gram neg, paired cocci, grows on chocolate Thayer-Martin agar, needs CO2
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Virulence factors of Gonorrhea
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1. Pilin, Por, and Opa: Antigenically variant attachment and phagosome fusion resistance proteins
2. LOS - Endotoxin 3. IgA protease |
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Where does N. Gonorrhea attach? What's special about this site?
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Nonciliated mucosal cells. The bug will induce nonphagocytic cells to uptake for translocation purposes.
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N. Gonorrhea infects . . .
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subepi spaces. Loves it.
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Pathogenesis of infection once N. Gonorrhea gets into subepi spaces
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1. Kills epi
2. Microabscesses 3. PUS PUS PUS |
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Men and gonorrhea
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They give it to women more frequently than women return the favor
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Clinical gonorrhea in men
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Urethritis with dysuria and pus discharge. Ascending: epididymitis
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Clinical gonorrhea in women
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Endocervical with pus discharge, dysuria, and bleeding. Ascending: PID and infertility
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PID
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Sequelae of acute gonorrheal infection. Endometritis, fallopian tube involvement.
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Disseminated gonorrhea
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Septic arthritis
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Neonatal gonorrhea
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Most commonly opthalmia neonatorum-- an ugly conjunctivitis
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Diagnosis of gonorrhea
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1. Thayer-martin culture
2. Gram stain of exudate - men 3. PCR probe |
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Treatment for gonorrhea
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1. Penicillin (resistant)
2. Quinolone (resistant) 3. 3rd gen ceph **Also treat with macrolides or doxy for presumed chlamydial infection |
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Chlamydia Trachomatis
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Small, energy parasitic obligate intracellular bacteria. Sole purpose is to infect cells with elementary bodies, divide and divide, then lyse the cell releasing hundreds more elementary bodies.
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Special effect of chlamydia invasion
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It will stimulate phagocytosis in columnar epi.
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Cause of chlamydial acute disease
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Cell rupture from binary fission.
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Immune response to chlamydia
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Initially neutrophils (pus causing) to site of cell destruction, then macrophages, then lymphoid formation, then scarring.
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Serovars A-C of Chlamydia
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Eye infection. D-K handle every other kind of infection.
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Major outcome of Trachomars
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Blindness
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Clinical chlamydia in a man
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Discharge, itching, dysuria. Ascending: epididymitis
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Does chlamydia cause arthritis?
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Yes
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Clinical chlamydia in a woman
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Identical to gonorrhea, except that the urethral inflammation mimics a UTI
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Oculogenital infxn of clam
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Keratitis, inclusion conjunctivitis (~80%)
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Lymphogranuloma Venereum
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Multisystem chlamydia infxn (in macrophages). causes severe regional lymphadenopathy - necrotic, persistant infection with scarring.
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Diagnosis of chlamydia
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1. Cell scrapings, inoculate McCoy, you should see tiny cocci in 72 hours
2. Cytostaining 3. Direct antibody or ELISA 4. PCR |
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Is serology useful for chlamydia?
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Not particularly, except for LGV
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Treatment of chlamydia
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Doxy or Azithromycin
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The plasma STDs - myco and urea.
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They look like everyone, or no one, require antibiotics that do not require a cell wall. Macrolides or Doxy
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3 major causes of vaginitis
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1. Trich
2. Candida 3. Unspecified bacterial vaginosis |
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Pathogenesis of trich
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Small flagellate attracts PMNs, activates alternate complement pathway. Usually sexually transmitted. Causes LBW and birth difficulties
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Treatment of Trich
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Metro (it's a protozoa)
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Do I really need to make a card on yeast infections?
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No, sorry guys.
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Cause of bacterial vaginosis
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Change from lactobacilli to anaerobes
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Is bacterial vaginosis an STD?
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No.
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Effects of bacterial vaginosis
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LBW, preterm delivery
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Treatment of vaginosis
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Azoles, clindamycin
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What's a clue cell and when do you find it?
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A cell surrounded by Gardnerella and Mobiluncus, when a vag is infected with anaerobes
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Difference between scabies and crabs?
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Scabies burrow and cause track lesions, eczema. Crabs attach to hair shaft and cause secondary bacterial infections. Both are treated with Permethrin
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