Sexually Transmitted Infections Flashcards

1
Q

What are the modes of transmission of HIV?

A

Sexual contact
Direct contact of broken skin with open sores, genital fluids or bloods of infected individuals
Sharing of needles
Mother –> child:
Pregnancy (placental), birth, breastfeeding
Infusion of infected blood

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2
Q

What are the goals of therapy of HIV ART?

A

To maintain CD4 cell count
Slow progression of HIV to AIDS
Reduce transmission of HIV

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3
Q

How are CD4 cell count and HIV viral load used in managing HIV pts on ART?

A

CD4 cell count
Normal: 500-1200 cells/mm^3
Most impt lab indicatior of immune fn in HIV infected pts. Strongest predictor of subseq disease progression & survival
Baseline before ini therapy
Q3-6mo after ini, Q12mo after adequate resp
Adequate response = increase by 50-150 cells/mm^3 in first 1y of therapy
Prophylaxis for pneumocystitis pneumonia when CD4<200 cells/mm^3

HIV viral load
To achieve viral load suppression of HIV
Most important indicator of response to antiretroviral thera
2-4 weeks after ini therapy (max 8 weeks) after treatment ini or modif
Q4-8 weeks until viral load is suppressed
Effective regimen generally achieved (undetectable HIV RNA level) by 8-24 weeks
Q3-6mo in stable & suppressed viral load (in practice Q1y)

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4
Q

Describe the benefits of early initiation of HIV ART.

A

Preserve CD4 T cell count
Reduce morbidity, mortality
Reduce risk of opportunistic conditions
Late initiation may not be able to recover CD4 T cell count
Reduce transmission of HIV

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5
Q

Describe the limitations of early initiation of HIV ART.

A

ADR, DDI
$$
Limited time to prepare pt for adherence needed
Non-adherence leading to drug resistance
Transmission of drug resistant virus in pts who do not maintain full virulogic suppression
Increased time on medication, w greater chance of treatment fatigue

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6
Q

List the classes of ART with named examples.

A
  1. Nucleoside Reverse Transcriptase Inhibitor (NRTI)
    Tenofovir, Emtricitabine, Abacavir, Lamivudine, Zidovudine
  2. Non-nucleoside Reverse Transcriptase Inhibitor (NNRTI)
    Raltegravir, Elvitegravir, Dolutegravir, Bictegravir
  3. Integrase Strand Transfer Inhibitor (ISTNI)
    Efavirenz, Rilpivirine
  4. Protease inhibitors
    Ritonavir, Lopinavir, Atazanavir, Darunavir, Fosamprenavir
  5. Fusion inhibitors
    Enfuvirtide
  6. CCR5 antagonist
    Maraviroc
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7
Q

List the recommended combination of ART for ART naive pts.

A

2 NRTI + 1 ISTNI:
Tenofovir + Emtricitabine + Bictegravir
Tenofovir + Emtricitabine + Dolutegravir
Abacavir + Lamivudine + Dolutegravir

1NRTI + 1ISTNI
Emtricitabine + Dolutegravir

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8
Q

What are the S/E & DDI for NRTIs?

A

Mitochondrial toxicity: lactic acidosis, hepatic steatosis, lipoatrophy (zidovudine > tenofovir = abacavir = lamivudine)
NV, diarrhoea

Tenofovir: + renal impairment, decrease bone mineral density
Abacavir: + MI
Zidovudine: + bone marrow suppression
Emtricitabine: + hyperpigmentation

Limited DDI (mainly renally cleared)

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9
Q

What are the S/E & DDI for ISTNIs?

A

NV
Diarrhoea
Wt gain
Headache
Depression Suicidal tendencies in pts already having psych conditions

B, D: increase SCr
R: pyrexia, increase CK (rhabdomyolysis)

Decrease F w polyvalent cations
B, D, E: CYP3A4 substrate

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10
Q

What are the S/E & DDI for NNRTIs?

A

Cutaneous reactions (rash, SJS)
QTc prolongation

Efavirenz: + hyperlipidemia, neuropsychiatric, hepatotoxicity
Rilpivirine: + depression, headache

CYP450 inducers and inhib

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11
Q

What are the S/E & DDI of protease inhibitors?

A

Metabolic complications (dyslipidemia, insulin resistance)
NV
Diarrhoea
Liperhypertrophy
Increase risk of osteopenia, osteoporosis

CYP3A4 inhib & substrates

Ritonavir: + CYP3A4 & 2D6 inhib, paresthesia, taste perversion
Darunavir: + skin rash, SJS, less lipid effects, good GI tolerability
Atazanavir: + hyperbilirubinemia, QTc prolongation, skin rash, good GI tolerability, less lipid effects

CI w PPI

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12
Q

What are the S/E & DDI of fusion inhibitors?

A

Infusion reactions: erythema, induration, nodules, cyst, pruritus, ecchymosis
Rare hypersensitivity
Increased bact pneumonia

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13
Q

What are the S/E & DDI of CCR5 antagonists?

A

Abdo pain
Dizziness
Musculoskeletal symptoms
Pyrexia
Rash
URTI
Cough
Hepatotoicity
Orthostatic hypotension

CYP3A4 substrate

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14
Q

What are the general modes of transmission for STI?

A

Sexual contact
Direct contact of broken skin with the open sores, genital fluid or blood from infected patients
Mother –> child: pregnancy (placental), childbirth, breastfeeding
Receiving contaminated blood (Sharing of needles, IV drugs use/abuse)

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15
Q

What are the general risk factors for STIs?

A

Sexual contact with mutliple sexual partners or with partners that have multiple sexual contacts
Illicit drug use
MSM
CSW
Immunocompromised
Unprotected sexual intercourse
Victims of sexual assault

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16
Q

Describe the general epidemiology for STIs.

A

Most common in 20-39y.o. (most sexually active)

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17
Q

Describe the prevention methods for STIs.

A

Abstinence
Sticking to mutually monogamous uninfected sexual partner
Pre exposure vacc (HPV, Hep B)
Post exposure prophylaxis
Barrier contraception
Avoid drug abuse, sharing needles

18
Q

What are the signs & symptoms of gonorrhea?

A

Male: purulent urethral discharge
Female: purulent vaginal discharge
Both: dysuria, urinary freq
Can infect var sites: urethritis, cervicitis, conjunctivitis, pharyngitis, proctitis, disseminated

19
Q

What are the signs and symptoms of chlamydia?

A

Male: purulent urethral discharge
Female: purulent vaginal discharge
Both: dysuria, urinary freq
Can infect var sites: urethritis, cervicitis, conjunctivitis, pharyngitis, proctitis, disseminated

20
Q

What are the signs and symptoms of syphilis?

A

Primary > Secondary > Early latent (<1y) > Late latent (>1y) > Tertiary

Neurosyphilis

21
Q

What diagnostic tests are used for gonorrhea?

A

Culture and gram stain of genital discharge
Nucleic acid amplification test (NAAT) ~ PCR

21
Q

What are the signs and symptoms of genital herpes?

A

Painful multivesicular, ulcerative lesions
Flu like symptoms (fever, malaise, headache) during first few days after appearance of lesions
Prodromal symptoms
Symptoms less severe w recurrence
Intermitttent viral shedding

22
Q

What diagnostic tests are used for chlamydia?

A

NAAT ~ PCR

22
Q

What diagnostic tests are used for syphilis?

A

Darkfield microscopy of exudates from lesions (less common)

Treponemal test (e.g. T. pallidium haemagglutinin amplification test [TPHA] or T. pallidium passive particle agglutination assay [TPPA])
Specific and sensitive for Treponema bact –> confirmatory. Unable to differentiate active and previous infection

Non-treponemal test (e.g. Venereal Disease Research Laboratory [VLDR] or Rapid plasma reagin [RPR] test)
+ve test indicates active infection. Quantitative tests indicates lowest dilution where Treponema bact is undetectable (e.g. 1:32 - lower dilution, lower viral load)

23
Q

What diagnostic tests are used for genital herpes?

A

NAAT ~ PCR (for HSV DNA)
Type specific serologic tests (takes 6-8 weeks to build up Ig)

24
Q

What is the recommended regimen for gonorrhea?

A

Treat concurrently w chlamydia unless tests exclude the diagnosis of one.

Ceftriaxone 500 mg / 1g IM single dose
Doxycycline 100 mg BD (for chlamydia) x7d

Alt:
Gentamicin 240 mg IM single dose
Azithromycin 2g single dose

25
Q

What is the recommended regimen for chlamydia?

A

Doxycycline 100 mg BD x7d

Alt:
Azithromycin 1g single dose
Levofloxacin 500 mg once daily x7d

26
Q

What is the recommended regimen for syphilis?

A

Primary, secondary, early latent (<1y):
IM benzathine pen G 2.4 million units single dose
Penicillin allergy: PO doxycycline 100 mg BD x14d

Late latent (>1y):
IM benzathine pen G 2.4 million units once a week x3 doses
Penicillin allergy: PO doxycycline 100 mg BD x 28d

Neurosyphilis:
IV crystalline pen G 3-4 million units Q4H x10-14d
IV crystalline pen G 18-24 million units daily as continuous infusion x10-14d
IM procaine pen G 2.4 million units AND probenecid 500 mg QID x10-14d
Penicillin allergy: IV/IM ceftriaxone 2g daily x10-14d

27
Q

What is the recommended regimen for genital herpes?

A

Acyclovir 400 mg TDS x7-10d
Valacyclovir 1g BD x7-10d

For severe
Acyclovir 5-10 mg/kg Q8H x 2-7d –> top up w PO for a total of 10d

28
Q

How do we manage sexual partners for gonorrhea?

A

Evaluate and treat sexual partners from the last 60d for S/S. If no sexual partners from the last 60d, evaluate and treat the most recent sexual partner.

Abstain from sexual intercourse for 7d after resolution of symptoms and completion of single dose regimen.

To prevent reinfection, abstain from sexual intercourse until sexual partner has also completed antimicrobial regimen.

29
Q

How do we manage sexual partners for chlamydia?

A

Evaluate and treat sexual partners from the last 60d for S/S. If no sexual partners from the last 60d, evaluate and treat the most recent sexual partner.

Abstain from sexual intercourse for 7d after resolution of symptoms and completion of single dose regimen.

To prevent reinfection, abstain from sexual intercourse until sexual partner has also completed antimicrobial regimen.

30
Q

How do we manage sexual partners for syphilis?

A

Monitor and evaluate sexual partners for signs and symptoms. Treat if necessary.

Abstain from sexual contact w new partners until syphilis lesions completely healed

Check w doctor if fully treated.

31
Q

How do we manage sexual partners for genital herpes?

A

Symptomatic sex partners shld be evaluated and treated. Asymptomatic sex partners of pts who have genital herpes shld be questioned concering Hx of neital lesions, encourages to examine themselves for lesions and seek medical attention early if lesions occur.

Order type specific serologic testing for HSV-2

Abstain from sexual intercourse w uninfected parteners when lesions or prodromal symptoms are present.

Encourage to inform current and future sex partners

32
Q

How do we monitor treatment for syphilis?

A

Jarshish Hexheimer rxn = acute febrile rxn within first 24h after any syphilis thera

Evaluate using non-treponemal test at 3, 6,12,18, 24 mo mark. At least 4 fold reduction in non-treponemal test.

For neurosyphilis, evaluate CSF fluid Q6mo till normal.

After 6mo if treatment fails, re-evaluate selected agents and re-evaluate for unrecognised neurosyphilis

33
Q

When do we use chronic suppressive therapy for recurrence of genital herpes?

A

Immunocompromised, comorbidities –> require continuous suppression
To reduce recurrences by 70-80% (>6/y)
Improve QoL
Long term safety and efficacy
Decrease transmission risk

Limitations
Concerns of adherence
Concerns of $$

34
Q

When do we use episodic therapy for recurrence of genital herpes?

A

More accepting of disease
Shorten duration and severity vs no antiviral
Concerns of adherence (better adherence)
Concerns of $$ (is cheaper)

Limitations
Req ini within 1d of symptom presentation or during prodromal stage
Does not improve viral shedding (risk of transmission)

35
Q

What is the recommended chronic suppressive therapy for recurrence of genital herpes?

A

Acyclovir 400 mg BD
Valacyclovir 500 mg once daily
Valacyclovir 1g once daily

36
Q

What is the recommended regimen for episodic therapy for recurrence of genital herpes?

A

Acyclovir 800 mg x 5d
Acyclovir 800 mg TDS x2d
Valacyclovir 500 mg BD x3d
Valacyclovir 1g once daily x5d

37
Q

What are the benefits of antiviral therapy in genital herpes?

A

Reduce symptoms of genital herpes by 2d
Reduces viral shedding by 4d

38
Q

Describe the non-pharmacological strategies in the management of genital herpes.

A

Warm saline bath
Symptomatic management (analgesia, anti-itch)
Good genital hygiene to prevent superinfection
Counselling regarding natural Hx of disease

39
Q

Describe the pathophysiology of HIV.

A

HIV infects CD4+ T cell of immune sys
Gp120 interacts w CCR5 or CXCR4 glycoproteins on the surface of CD4 cells –> triggers conformational change in Gp120
Gp41 unfolds and inserts its hydrophobic terminus in cell mem, draws virus closer to cell mem
Viral nucleocapsid enters host cell
Reverse transcriptase transcripes viral RNA –> viral DNA
Viral DNA integrated by DNA integrase into host cell genome (cleave dinucleotide from each 3’ end to form sticky ends)
Transcription of viral DNA –> transl of viral mRNA –> viral proteins, assembly of virus
Budding off
Loss of CD4+ T cells –> difficult for immune sys to fight infections