VII- Viral STI HPV and HSV Flashcards

1
Q

clinical pres of genital HSV

A

lesions in sex organ areas
-painful grouped macules > papules > vesicles > pustules > ulcers + fever, inguinal adenopathy, malaise

will recur more discreetly and cause vulvar irritation, tingling, pain

more severe in women

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2
Q

clinical pres of neonatal HSV

A
  1. lesions localized to skin, eyes, mouth 10-11 days after birth + recur often in first 6 mo
    -if untreated then blindness, microcephaly, spastic quadriplegia
  2. encephalitis with or without lesions so poor feeding, seizures, lethargy, bulging fontanel
  3. disseminated lesions in viscera and skin so respir distress, jaundice, shock, DIC, pneumonitis
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3
Q

transmission of HSV

A
  1. direct contact with lesions
  2. saliva
  3. sexual transmission for genital

HSV-1 more oral lesions, 2 for genital

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4
Q

HSV prevention

A
  1. for neonates: physical exam, C sections, ward precautions if staff has herpetic whitlow or orolabial lesions
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5
Q

HSV treatment

A
  1. for neonates: IV admin of antivirals for all cases
  2. oral lesions self limit and not need antiviral
  3. genital herpes: oral antiviral for primary + long term if recurrent
  4. ocular: topical AV
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6
Q

herpesvirus antiviral mechanism

A

phosphoylation of viral thymidine kinase leads to inhibiting viral DNA polymerase
-acyclovir, famciclovir, valacyclovir

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7
Q

common mutations in acyclovir resistant infections HSV

A

thymidine kinase so resistant virus are TK-

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8
Q

treating acyclovir resistant HSV

A

use foscarnet bc no HSV phosphorylation needed > still inhibits viral DNA polymerase
-nonnucleoside inhibitor

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9
Q

latent vs lytic HSV

A

latent if virus in sensory neuron ganglia (sacral for genital or trigeminal for cold sores)
-can have spontaneous reactivation to lytic

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10
Q

HPV mechanism in cervical cancer

A

shifts from genome amplification and virus production to genome integration and cancer cells via in E6 and E7 expression

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11
Q

HPV E6

A

will inhibit p53 so impact apoptosis and cellular senscence

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12
Q

HPV E7

A

will inhibit Rb so impact cell cycle progression into replication phase (G1 to S)

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13
Q

common HPV types in genital warts

A

either high risk: HPV 16, 18, 31, 33
or low risk: HPV 6, 11

for mucosal specifically

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14
Q

common HPV in laryngeal papillomas

A

HPV 6, 11
same as low risk genital

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15
Q

common HPVs in cervical cancer

A

majority HPV 16 > 18 > 31, 33, 45

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16
Q

transmission of HPV genital warts

A

sexually transmit via cuts and abrasions for entry
-incubate for 3-4 months

17
Q

diagnosing HPV genital warts

A

clinical appearance sufficient
-histological markers of hyperkeratosis and koilocytes
-PCR for detecting high risk strains

18
Q

treating HPV genital warts

A
  1. self admin- podophyllotoxin, sinecatechins, imiquimod
  2. clinician admin - cryotherapy, surgery, laser, interferon

if low grade = cauterize, cryo, laser, surgery loop excision
if high grade = radiation, chemo, hysterectomy

19
Q

HPV vaccine guidelines

A

-routine for kids 11-12, 2 doses
-catch up for indivs up to 26 not previously vac, 3 doses for age 15-26
-consider for 27-45 based on risks

20
Q

how HPV vaccine generated

A

made in yeast
-from viral capsid protein L1

21
Q

pres of genital warts HPV

A

hyperkeratotic, firm, exophytic papules + itching/pain/burning

if cervical then can be exophitic, endophytic, or flat