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infec y3s1 > IC18 STI > Flashcards

IC18 STI Flashcards

1
Q

HIV: mode of transmission

A

via specific body fluids
Blood, semen, genital fluids, breast milk

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2
Q

HIV: Risk factors
(who to conduct testing for)

A

IV drug users
Person who have unprotected sex with multiple partners
Man who have sex with man
Commercial sex workers
Persons treated for STDs ⇒ increased risk of HIV
Recipients of multiple blood transfusion
Persons who have been sexually assaulted
Pregnant women

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3
Q

HIV: clinical presentation
(1) acute (primary) infection

A

Occurs soon after contracting HIV
Flu-like illness: swollen lymph nodes, fever, malaise & rash ⇒ lasts 2-3 weeks

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4
Q

HIV: clinical presentation
(2) asymptomatic

A

No signs & symptoms
Persists for many years

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5
Q

HIV: clinical presentation
(3) persistent generalised lymphadenopathy

A

Persistent unexplained lymph node enlargement in neck, underarms & groin
More than 3 months of symptoms

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6
Q

HIV: clinical presentation
(4) AIDS & related conditions

diagnostic criteria & symptoms (organs involved & systemic s)

A

Requirements for AIDS diagnosis:
* AIDS = CD4 <200 cells /mm3 or presence of AIDS-defining diseases
Healthy individuals: CD4 500-1200 cells /mm3
* Immune system too weak to fight against invading virus & bacteria
* Person succumb to Opportunistic infections

Organs involved: lung, eyes, GIT, nervous system & skin

Systemic symptoms: fevers, unexplained weight loss, diarrhoea

Rare cancers

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7
Q

Goals of anti-retroviral therapy

A
  • Reduce HIV-associated morbidity & mortality
  • Prolong duration & quality of survival
  • Restore & preserve immunologic function
    To avoid reaching state of being immunocompromised; maintain CD4 T cell count
  • Maximally & durably suppress plasma HIV viral load to undetectable levels
  • Prevent HIV transmission
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8
Q

Surrogate markers of HIV

A
  1. CD4 Cell count
  2. Viral load
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9
Q

Surrogate markers of HIV: CD4 count
what it indicates

A

Normal individuals: 500-1200 cells/ mm3
Indicator of immune function
strongest predictor of subsequent disease progression + survival

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10
Q

Surrogate markers of HIV: CD4 count
purpose

A

To determine urgency for initiating antiretroviral therapy
* Note: current → to start treatment when patient is infected with virus to prevent CD4 cell count from decreasing
* Late start to treatment = unlikely recovery of CD4 cell count to normal levels

To assess response to antiretroviral therapy (compare with initial diagnosis)
(1) assessed at baseline, (2) every 3 to 6 months after treatment initiation & (3) every 12 months after adequate response

To assess need for initiating/ discontinuing prophylaxis for opportunistic infections

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11
Q

Surrogate markers of HIV: CD4 count
effective treatment definition

A

increase in CD4 count in the range of 50 to 150 cells/mm3 during the first year of therapy

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12
Q

Surrogate markers of HIV: Viral load
indication

A

Amount of virus in plasma
Most important indicator of response to antiretroviral therapy
Help with predicting clinical progression

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13
Q

Surrogate markers of HIV: Viral load
Assessment timeline

A
  • Before initiation of therapy
  • Within 2-4 weeks after treatment initiation OR modification (no later than 8 weeks)
  • Every 4-8 weeks until viral load suppressed
  • Those on stable regime & suppressed viral load ⇒ every 3-6 months
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14
Q

Surrogate markers of HIV: Viral load
effects of treatment

A

achieve viral suppression by 8-24 weeks
* No longer have detectable HIV RNA levels

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15
Q

earlier ART initiation

indication & requirements

A

For all HIV-patients regardless of CD4 cell count

adherence: Require at least 95%, if not have risk of resistance

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16
Q

earlier ART initiation: benefits

A
  • Maintenance of higher CD4 count & prevention of potentially irreversible damage to immune system
  • Decreased risk for HIV-associated complications
  • Decrease risk of non-opportunistic conditions
    CVD, renal disease, liver disease & non-AIDS-associated malignancies and infection
  • Decreased risk of HIV transmission ⇒ positive public health implications
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17
Q

earlier ART initiation: limitations

A
  • Development of treatment-related SE & toxicities
  • Development of drug resistance
    Due to incomplete viral suppression; especially non-adherence
    Loss of future treatment options
  • Transmission of drug-resistant virus for those without full virologic suppression
    Important to check for resistance pattern of virus before initiating treatment
  • Lesser time for patient to understand HIV and its treatment + preparation for need of adherence
  • Increased total time on medications → greater treatment fatigue
  • Increased costs
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18
Q

Recommended combinations (patients naive to ART)

A

2 NRTIs + 1 INSTI [First line]
1 NRTIs + 1 INSTI

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19
Q

Recommended combinations: 1 NRTI & 1 INSTI requirements

A
  • HIV RNA >500k copies/ mL (extremely high)
  • HBV coinfection
    HBV → requires 2 AV against HepB virus (tenofovir, emtricitabine, lamivudine)
  • Starting on ART before results of HIV genotypic resistance testing/ HBV testing
    Must confirm that patient does not have co-infection of HBV & resistance against drug before treatment
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20
Q

ART drug classes

A
  1. NRTI
  2. INSTI
  3. NNRTI
  4. PI
  5. fusion inhibitor
  6. CCR5 antagonist
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21
Q

(1) NRTI: drugs

A

lamvudine
abacavir
zidovudine
emtricitabine
tenofovir

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22
Q

(1) NRTI: Advantages

A

Established in combination ART
Renal elimination → fewer DDI

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23
Q

(1) NRTI: disadvantages

A

AE related to mitochondrial toxicity → rare but serious
* Lactic acidosis & hepatic steatosis (fatty infiltration)
* Morphologic complication ⇒ Lipoatrophy (lost of fat)
* Zidovudine>Tenofovir=Abacavir=Lamivudine

Requires dose adjustment in renally impaired patients (except abacavir)

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24
Q

(1) NRTI: Adverse effects

lamvudine, tenofovir, emtricitabine

A

lamvudine
Minimal toxicity; N/V/D

tenofovir
Minimal toxicity; hyperpigmentation, N/D

emtricitabine
* N/V/D
* Possible renal impairment
* Decrease in bone mineral density ⇒ increased risk of osteoporosis & osteopenia

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25
Q

(1) NRTI: Adverse effects

zidovudine, abacavir

A

Abacavir
* N/V/D
* Hypersensitivity reaction in patients with HLA-B*5701
Discontinue if occurs & do not rechallenge
Require testing for HLA-B5701 before initiation

  • Association with MI ⇒ avoid in high CVD risk patients

zidovudine
* N/V/D
* Myopathy
* Bone marrow suppression ⇒ causes anemia/ neutropenia
(To monitor FBC)

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26
Q

(2) INSTI: drugs

A

bictegravir
raltegravir
elvitegravir
dolutegravir

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27
Q

(2) INSTI: Advantages

B&D

A

Bictegravir & dolutegravir ⇒ good virologic effectiveness
High genetic barrier to resistance [B&D > R&E]
Generally well tolerated

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28
Q

(2) INSTI: Disadvantages

bioavailability, DDI

A

Bioavailability lowered by concurrent administration of polyvalent cations
Bictegravir, dolutegravir & elvitegravir ⇒ CYP 3A4 substrates

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29
Q

(2) INSTI: Adverse effects

common ones

A

weight gain, diarrhoea, nausea & headache

Depression & suicidality in those with pre-existing psychiatric conditions

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30
Q

(2) INSTI: Adverse effects

bictegravir & elvitegravir

A

increase SCr
Inhibits tubular secretion of creatinine

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31
Q

(2) INSTI: Adverse effects

raltegravir

A

Pyrexia
Elevation of CK ⇒ rhabdomyolysis

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32
Q

(3) NNRTI: drugs

A

efavirenz
Rilpivirine

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33
Q

(3) NNRTI: Advantages

A
  • Long t1/2 ⇒ OD dosing
  • Less metabolic toxicities than with some PIs
    Hyperlipidemia, insulin resistance
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34
Q

(3) NNRTI: Disadvantages

GB, CR, DDI, S, Q

A
  • Low genetic barrier for resistance
  • Cross resistance among approved NNRTIs
  • Skin rash, SJS [R < E]
  • Potential for CYP450 drug interactions → inducers & inhibitors
    Efavirenz: CYP3A4 substrate, CYP2B6 and 2C19 inducer
    Rilpivirine: CYP3A4 substrate, oral absorption is reduced with increased gastric pH; use with PPIs is contraindicated.
  • QTc prolongation
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35
Q

(3) NNRTI: AE

Efavirenz, Rilpivirine

A

Efavirenz
* Rash
* Hyperlipidemia: increased LDL-C & TG
* Neuropsychiatric SE: dizziness, depression, insomnia, abnormal dreams, hallucination
* Hepatotoxicity

Rilpirivine
CNS: Depression & headache

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36
Q

(4) protease inhibitor: drugs

A

Liponavir
Azatanavir
Darunavir
Fosamprenavir
Ritonavir

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37
Q

(4) protease inhibitor: Advantages

A

High genetic barrier to resistance

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38
Q

(4) protease inhibitor: Disadvantages

A
  • Metabolic complications → dyslipidemia, insulin resistance
  • GI SE → N/V/D
  • Liver toxicity (especially with chronic hepatitis B or C)
  • CYP3A4 inhibitors & substrates: potential for DDI
  • Morphologic Complications → Fat maldistribution (Lipohypertrophy)
  • Increased risk of osteopenia/osteoporosis
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39
Q

(4) protease inhibitor: characteristics

ritonavir

A
  • Potent CYP3A4, 2D6 inhibitor
  • PK enhancer → combined with other PI [Lopinavir/ritonavir] to increase the other PI concentration levels

SE: paresthesia (numbness of extremities) & taste perversion

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40
Q

(4) protease inhibitor: characteristics

azatanavir

A

(+) Good GI tolerability & less lipid effects
* Absorption depends on low pH
Contraindication with PPIs

SE: hyperbilirubinemia, prolong QT interval, skin rash

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41
Q

(4) protease inhibitor: characteristics

darunavir

A

(+) Good GI tolerability & less lipid effects
(-) Skin rash & concern for SJS
Due to sulfonamide component

42
Q

(5) fusion inhibitor: drug & characteristics

administration & DDI

A

Enfuvirtide

SC injection BD
no DDI

43
Q

(5) fusion inhibitor: AE

A
  • Injection site reaction→ erythema/ induration, nodules/ cyst, pruritis, ecchymosis
  • Rare hypersensitivity → fever, chills, decrease BP, rash
  • Increased bacterial pneumonia
44
Q

(6) CCR5 antagonist: drug

A

maraviroc

45
Q

(6) CCR5 antagonist: requirement

A

Only for those with strains of HIV using CCR5 receptor to enter CD4 cells
* Need co-receptor tropism assay before initiation (to check which receptor HIV uses to enter cells)
* Must be CCR5 predominant

46
Q

(6) CCR5 antagonist: potential DDI & AE

A

Potential DDI: CYP3A4 substrate
ADR:
Abdominal pain, cough, dizziness, musculoskeletal symptoms, pyrexia, rash, upper respiratory tract infections, hepatotoxicity, orthostatic hypotension

47
Q

STI caused by bacteria

A

Syphilis: Treponema pallidum
Gonorrhoea: Neisseria gonorrhoeae
Non-gonococcal urethritis
Chlamydia

48
Q

STI caused by virus

A

herpes simplex virus (HSV)
HIV

49
Q

Mode of transmission for STIs

A
  • Mainly by sexual contact with infected person
  • Direct contact of broken skin with open sores, blood or genital discharge
    Must be deep/ big
  • Receiving contaminated blood
    Important to start on post-exposure prophylaxis
    Usually screened to ensure no STI in blood
  • From infected mother to child
    During pregnancy → ie: syphilis, HIV
    During childbirth → ie: chlamydia, gonorrhoea, HSV
    Breastfeeding → ie: HIV
50
Q

RF for STIs

A
  • Unprotected sexual intercourse
  • Number of sexual partner
    Those with multiple sexual partners→ more likely to acquire & transmit STI
    Those with sexual contact with people who have multiple sexual partners
  • MSM
  • Prostitution (CSW) → covers first 2 points
  • Illicit drug use → ie sharing of needle by IV drug users
51
Q

individual prevention methods of STI

A
  • Abstinence & reduction of number of sexual partners
    long-term, mutually monogamous relationship with an uninfected partner
  • Barrier contraceptive methods
    male latex condoms when used consistently & correctly
  • Avoid drug abuse & sharing needles
  • Pre-exposure vaccination
    HPV (Human papillomavirus), Hepatitis B
  • Pre- and Post-exposure prophylaxis → HIV
    Pre: if viral load is not suppressed, partner is at risk of infection → to take AV pills continuously
    Post: after possible exposure to virus
52
Q

(B) Gonorrhoea: causative organism

A

Neisseria gonorrhoeae

53
Q

(B) Gonorrhoea [&chlamydia] : transmission

A

sexual contact, mother-to-child during childbirth

54
Q

(B) Gonorrhoea: diagnostic method

A

gram-stain of genital discharge, culture, NAAT

55
Q

(B) Gonorrhoea [&chlamdymia] : possible infection to other sites

A

Urethritis → urethra; Cervicitis → cervix; Proctitis → rectal area; Pharyngitis → throat; Conjunctivitis

Disseminated → throughout the body

56
Q

(B) Gonorrhoea [&chlamdymia] : clinical presentation (uncomplicated)

male & female

A

both
Dysuria
Urinary frequency
Male
Purulent urethral discharge
female
Mucopurulent vaginal discharge

57
Q

(B) Gonorrhoea [&chlamdymia] : clinical presentation (complicated)

male & female

A

both
disseminated disease
male
Epididymitis
Prostatitis
urethral stricture

female
Pelvic inflammatory disease
Ectopic pregnancy, infertility

58
Q

(B) Gonorrhoea: pharmacological management

first line & alternative

A

First line
Ceftriaxone:
* 500 mg IM single dose for those <150kg
* 1g IM single dose for those ≥150kg

Alternative (if ceftriaxone unavailable)
* Gentamicin 240 mg IM in single dose AND
* Azithromycin 2g PO in single dose

PO doxycycline 100 mg BD x7 days if chlamydia infection not excluded

59
Q

(B) Chlamdymia: causative organism

A

Chlamydia trachomatis

60
Q

(B) Chlamdymia: diagnostic test

A

NAAT

61
Q

(B) Chlamdymia: pharmacological management

first line & alternative

A

First line
PO Doxycycline 100 mg BD x7 days

Alternative (if ceftriaxone unavailable)
PO Azithromycin 1g in single dose
OR
PO levofloxacin 500 mg OD x7 days

Possible to use azithromycin as first line if adherence is of concern

62
Q

(B) Chlamdymia: requirements for testing of cure

A

pregnancy, non-adherence or symptoms persist
* Need to check for possibility of reinfection

63
Q

(B) gonorrhea & Chlamdymia: management of sex partners

A
  • Sex partners in last 60 days should be evaluated & treated
    If last sexual exposure >60 days, to treat most recent partner
  • Abstain from sexual activity for 7 days after treatment to minimise disease transmission
  • Abstain from sexual intercourse until all sex partners are treated to minimise risk of reinfection
64
Q

(B) syphilis: causative organism

A

Treponema pallidum

65
Q

(B) syphilis: transmission

A

sexual contact, mother-to-child (transplacental during pregnancy)

66
Q

(B) syphilis: diagnosis

A

Darkfield microscopy of exudates from lesions
2 serological tests ⇒ more common

67
Q

(B) syphilis: diagnosis
serological tests

A
  1. trepenomal test
  2. non-trepenomal test
68
Q

(B) syphilis: trepenomal test

how it works, what it tells, limitation

A
  • Use treponemal Ag to detect treponemal Ab (produced during infection)
  • More sensitive & specific than non-treponemal test ⇒ used as confirmatory test
  • May remain active for life → not for monitoring response to treatment
    Ab remains present in body; not necessarily indicate current infection
69
Q

(B) syphilis: non-trepenomal test

what it tells, how it works

A
  • To determine if infection is CURRENT or PAST
  • Use nontreponemal Ag (cardiolipin) to detect treponemal Ab
  • Positive tests → presence of any stage of syphilis
  • Result reported in quantitative VDRL/ RPR test = most dilute serum concentration with positive reaction
    Result of 1:16 positive ⇒ 1:32 no reaction seen (no Ab at that dilution)
  • Higher VDRL/ RPR = greater bacteria presence (more Ab produced)
    Ab titre correlate with disease activity ⇒ used to monitor response to treatment
  • Non-treponemal test titres usually declines after treatment; becomes non-reactive with time
70
Q

(B) syphilis: pharmacological management
primary/ secondary/ early latent (<1 year)

regimen & penicillin allergy (+ counselling)

A

IM Benzathine penicillin G 2.4 million units x1 dose

penicillin allergy
PO doxycycline 100 mg BD x14 days
Counselling
* Take with food to reduce GI upset
* Take with glass of water & maintain upright at least 30 mins to prevent heartburn
* Do not take with milk, Ca or Fe ⇒ take 2 hours apart

SE
GI, photosensitivity

71
Q

(B) syphilis: pharmacological management
tertiary/ unknown duration/ late latent (>1 year)

regimen & penicillin allergy

A

IM Benzathine penicillin G 2.4 million units once a week x3 dose

penicillin allergy
PO doxycycline 100 mg BD x28 days

72
Q

(B) syphilis: pharmacological management
neurosyphilis

regimen & penicillin allergy

A

IV crystalline (benzyl) penicillin G 3-4 million units q4h or 18-24 million units q24h x10-14 days
OR
IM procaine penicillin G 2.4 million units OD + PO probenecid 500 mg QID x10-14 days

penicillin allergy
IV/ IM ceftriaxone 2 g OD x10-14 days

Concerns for cross-sensitivity
* Skin prick test to confirm penicillin allergy
* To desensitise if necessary
(1) Daily low level of exposure of allergen (penicillin) → build up to therapeutic dose
(2) Continue at therapeutic dose → if miss dose, should restart low dose again

73
Q

(B) syphilis: formulation
PenG

IM benzathine, IM procaine, IV crystalline

A

IM benzathine ⇒ released over a week (slower)
High sensitivity of syphilis from penG ⇒ low concentration of drug required

IM procaine ⇒ releases over a day + IV crystalline ⇒ high dose
Bacteria entering CSF → require high dose of penicillin G to reach CSF concentration

74
Q

(B) syphilis: formulation
probenecid

purpose

A

reduces secretion of penicillin ⇒ increases concentration of penicillin in systemic circulation
* Cannot give IM procaine alone in neurosyphilis; unable to achieve high enough CSF concentration

75
Q

(B) syphilis: response upon treatment

A

Jarisch-Herxheimer reaction = acute febrile reaction, frequently accompanied by headache, myalgia, and other symptoms that usually occur **within the first 24 hours after any therapy **for syphilis
* Antipyretics will help but not prevent

76
Q

(B) syphilis: monitoring of response

syphilis & neurosyphilis, duration of tests

A

Primary / secondary/ Latent syphilis: Quantitative VDRL/ RPR at 3, 6, 12, 18 & 24 months (using blood)
* treatment success = decrease of VDRL or RPR titre by at least fourfold (ie: 1:64 to 1:16)

Neurosyphilis: CSF examination (Quantitative VDRL/ RPR) every 6 month until CSF normal

77
Q

(B) syphilis: indication of treatment failure

A
  • show sign & symptoms of disease
  • Failure to decrease VDRL/ RPR titre by fourfold OR VDRL/ RPR titre increase
    ie 1:16 to 1:64
  • Retreat & re-evaluate for unrecognised neurosyphilis
78
Q

(B) syphilis: management of partners

A
  • All at risk sexual partners should be evaluated for STIs & treat if test positive
  • Persons receiving syphilis treatment must abstain from sexual contact with new partners until the syphilis lesions are completely healed
79
Q

(V) Genital herpes: causative agent

A

HSV2 mainly

80
Q

(V) Genital herpes: transmission

A

transfer of body fluids and intimate skin-to-skin contact

81
Q

(V) Genital herpes: infection timeline

development & healing of vesicles, viral shedding

A

Vesicles develop over 7-10 days; heal in 2-4 weeks
* Reactivation of virus → will have shorter healing time

Intermittent viral shedding from epithelial cells
* Possible even when person is asymptomatic
* Transmission can occur even without presence of vesicles

82
Q

(V) Genital herpes: diagnosis methods

A
  1. patient hx
  2. virologic testing
  3. type-specific serologic test
83
Q

(V) Genital herpes: diagnosis
patient hx

A

Previous lesions
Sexual contact with similar lesions at genitals

84
Q

(V) Genital herpes: virologic test

A

NAAT (PCR) for HSV DNA from genital lesions

85
Q

(V) Genital herpes: type specific serologic test

what is tested, problem for first-episode serology

A

Testing for Ab

  • Ab to HSV develop during the first several weeks after infection & persist indefinitely
  • Serology is not useful for first episode infection → takes between 6 & 8 weeks for serological detection following a first episode
    Requires time for buildup of Ab to sufficient concentration for detection

Presence of HSV-2 antibody ⇒ anogenital infection

86
Q

(V) Genital herpes: clinical presentation

first infection

A
  • classical painful multiple vesicular or ulcerative lesions (When vesicles break)
  • local itching, pain, tender inguinal lymphadenopathy (lymph at inguinal)
  • Flu-like symptoms (ie: fever, headache, malaise) during first few days after the appearance of lesions
87
Q

(V) Genital herpes: clinical presentation

recurrent

A
  • Prodromal symptoms → mild burning, itching or tingling
  • Symptoms less severe → less lesions, heal faster, milder symptoms
    Due to previous immunity; presence of Ab reduces severity
88
Q

(V) Genital herpes: supportive care & counselling

A
  • Warm saline bath → relief discomfort
  • Analgesia & anti-itch → symptomatic relief
  • Good genital hygiene → prevent superinfection of bacteria
  • Counselling about natural history
    Inform that infection is lifelong + possible transmission even without vesicles; triggers for vesicles + reactivation is possible
89
Q

(V) Genital herpes: drug choice

MOA, clinical effects, when to start

A

acyclovir & valacyclovir

Mechanism of action: inhibit viral DNA polymerase → inhibit DNA synthesis & replication
Clinical effects:
* Reduce viral shedding by 7 days
* Reduce duration of symptoms by 2 days
* Reduce time to healing of 1st episode by 4 days

Starting
Maximum benefit ⇒ initiate at earliest stage of disease (within 72 hours)

90
Q

(V) Genital herpes: first episode
acyclovir

dose, F, t1/2, counselling points, SE

A
  • PO 400 mg TDS x7-10 days
  • IV 5-10 mg/kg q8h x2-7 days + PO for 10 days
    For severe disease/ complications requiring hospitalisation/ herpes encephalitis
    Usually for immunocompromised (will have higher viral load)

F = 10-20%; t1/2 ~3 hours

Counselling
* Take with/ without food
After food if have GI upset
* Maintain adequate hydration ⇒ prevent crystallisation in renal tubules

SE (general, non-specific)
Malaise, headache, N/V/D

91
Q

(V) Genital herpes: first episode
valacyclovir

dose, F, t1/2, counselling points, SE

A

PO 1g BD x7-10 days

L-valine ester of acyclovir (prodrug)
Rapidly & almost completely converted to acyclovir & valine

F = 55%; t1/2 ~3 hours
* Can give higher dose & less frequently

Counselling: similar to acyclovir including hydration

SE: mainly headache

92
Q

(V) Genital herpes: recurrent

definition

A

Median = 4 recurrences the year after first symptomatic episode

93
Q

(V) Genital herpes: recurrent therapies

A
  1. chronic suppressive therapy
  2. episodic therapy
94
Q

(V) Genital herpes: [1] chronic suppressive therapy

drug & dosing

A

PO Acyclovir 400 mg BD
PO valacyclovir 1 g OD

95
Q

(V) Genital herpes: [1] chronic suppressive therapy

indications

A
  • patients who have many recurrences
  • Patients with complicated disease course (ie disseminated disease)
  • immunocompromised hosts → may have severe disease state during reactivation of HSV
96
Q

(V) Genital herpes: [1] chronic suppressive therapy

advantages

A
  • reduces the frequency of recurrences by 70%–80% in patients who have frequent recurrences (ie: >6 recurrences per year)
  • Most will have no symptomatic outbreaks ⇒ improved QOL
  • decreased risk of transmission
    in combination with consistent condom use & abstinence during recurrences
    Reduction in chance of viral shedding + barrier method
97
Q

(V) Genital herpes: [1] chronic suppressive therapy

disadvantages

A

Cost → daily dosing
Compliance → continuous dosing

98
Q

(V) Genital herpes: [2] episodic therapy

when to start

A

when patient have prodromal symptoms OR vesicles present

99
Q

(V) Genital herpes: [2] episodic therapy

drug & dose

A

Either one of the following:
* PO Acyclovir 800 mg
BD x5 days OR TDS x2 days
* PO valacyclovir 500 mg BD x3 days
* PO valacyclovir 1 g OD x5 days

100
Q

(V) Genital herpes: [2] episodic therapy

advantage

A
  • Shorten duration & severity of symptoms
  • Less costly compared to chronic suppression
  • Patient more likely to be compliant
101
Q

(V) Genital herpes: [2] episodic therapy

disadvantage

A
  • Requires initiation of therapy within 1 day of lesion onset or during the prodrome that precedes some outbreaks
  • Does not reduce risk of transmission
    Once patient is off AV → can shed virus & transmit HSV
102
Q

(V) Genital herpes: management of sexual partners

A
  • Symptomatic sex partners: evaluated & treated in the same manner as patients who have genital lesions.
  • Asymptomatic sex partners of patients who have genital herpes should be questioned concerning histories of genital lesions, encouraged to examine themselves for lesions and seek medical attention early if lesions occur.

infec y3s1 (7 decks)

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