Gynae - Chronic STIs Flashcards

1
Q

HIV (Human Immunodeficiency Virus)

Pathophysiology
Transmission and At-Risk Groups
Clinical Features

A

1.) Pathophysiology - single-stranded RNA retrovirus that infects and replicates with CD4 cells (Th cells)
- reverse transcriptase converts ssRNA into dsDNA
- seroconversion: primary infection where the body starts producing detectable levels of HIV antibodies
- ↓CD4 in response to initial, rapid replication of HIV, this is where the patient is extremely infectious
- over the next months-years, infection can become latent with ↓CD4 and ↑viral load, eventually, it becomes sx and develops into AIDS (avg 10 years)

2.) Transmission and At-Risk Groups
- UPSI (inc oral): MSM, high prevalence areas, UPSI with a partner who has lived/travelled in Africa
- needle-sharing: IV drug users
- vertical: during utero, childbirth or breastfeeding (can have a vaginal delivery if undetectable viral load)
- medical procedures: blood products, skin grafts, organ donation and artificial insemination

3.) Clinical Features
- seroconversion illness (2-6wks post-exposure): fever, malaise, muscle aches, lymphadenopathy, pharyngitis, maculopapular rash
- latent phase: often just asymptomatic
- symptomatic HIV: weight loss, fevers, diarrhoea,
frequent minor opportunistic infections (HZV, thrush)
- AIDS-defining conditions: TB, CMV infection, pneumocystis jiroveci pneumonia (PCP), non-Hodgkin’s lymphoma, Kaposi’s sarcoma

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2
Q

Management of HIV

Investigations
Highly Active Antiretroviral Therapy (HAART)
Monitoring
Additional Management

A

1.) Investigations
- ELISA tests: test for serum/salivary HIV antibodies and p24 antigen, reliable 4-6wks after exposure but can take up to 3 months to develop antibodies
- rapid home-testing kits can give results in 30 mins, but have ↓accuracy and need confirming w/ ELISA
- contact tracing to help identify those at risk

2.) Highly Active Antiretroviral Therapy (HAART)
- the aim is to have an undetectable viral load (<50) and normal CD4 count (500-1200), this has an excellent prognosis with a low risk of transmission
- classes: reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, entry inhibitors
- these are combined into 1 tablet to be taken daily: Atripla, Stribild, Eviplera, Triumeq
- drugs are taken life-long, non-adherence to HAART can lead to resistant mutations, making Tx difficult

3.) Baseline Investigations
- diagnostic HIV test, CD4 count, HIV viral load
- HIV resistance profile, HLA B*5701 status
- FBC, U+Es, LFTs, bone profile, lipid profile
- serology: syphilis, hep B/C/A, Schistosoma (in Africa)
- IgG levels: toxoplasma, measles, varicella, rubella

4.) Additional Management
- CD4 <200: prophylactic PO Co-trimoxazole OD against PCP
- CD4 <50 : PO Azithromycin once weekly to prevent TB (MAI)
- CD4 <50: regular ophthalmology review to assess for CMV retinitis
- monitoring of cardiovascular risk factors and blood lipids due to increased risk of cardiovascular disease
- yearly cervical smears for women (instead of every 3 years)
- vaccinations: influenza, pneumococcal, hepA+B, polio/diphtheria/tetanus, avoid live vaccines

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3
Q

Preventing Transmission of HIV

Post-Exposure Prophylaxis
Preventing Transmission During Birth
Breastfeeding

A

1.) Post-Exposure Prophylaxis
- taken if suspicious of exposure w/in last 72hrs
- course lasts 1 month: Truvada (OD), Raltegravir (BD)
- given to babies depending on mother’s viral load:
- <50: zidovudine for 4 weeks
- >50: zidovudine, lamivudine, nevirapine for 4 weeks

2.) Preventing Transmission During Birth
- viral load <50: normal vaginal delivery
- viral load >50: consider C-section esp if >400
- unknown viral load or >10,000: IV zidovudine should be given during the caesarean

3.) Breastfeeding
- not recommended for mothers with HIV even with an undetectable viral load

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4
Q

Stages of Syphilis (Treponema pallidum)

Primary Syphilis
Secondary Syphilis
Tertiary Syphilis
Neurosyphilis

A

1.) Primary Syphilis - the presence of chancres
- papule appears before ulcerating into a chancre 9-90 days post-infection on a genital site
- chancres are painless, non-itchy, hard, singular
- typically heal within 3-10wks w/ or w/o symptoms
- atypical chancres can appear at other sites, be multiple and painful

2.) Secondary Syphilis - develops 3 months post-infection
- skin rash: on hands and soles (not painful or itchy)
- fever, malaise, arthralgia, weight loss, headaches, painless lymphadenopathy
- condylomata lata: elevated plaques at moist areas of skin e.g. inner thighs, anogenital region, axillae
- silvery-grey lesions: oral, pharyngeal, genital
- disease then enters the asymptomatic latent phase

3.) Tertiary Syphilis - presents after many years
- gummatous: granulomas that can affect the skin, organs and bones, non-infectious at this stage
- cardiovascular: aortic aneurysms, angina +others
- neurosyphilis

4.) Neurosyphilis
- headaches, altered behaviour, dementia, paralysis, sensory impairment
- Tabes dorsalis: demyelination affecting the SC posterior columns,
- Argyll Robertson pupil: pupil is constricted and unreactive to light, but reacts to accommodation

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5
Q

Pathophysiology and Management of Syphilis

Pathophysiology
Investigations
Management

A

1.) Pathophysiology - g-ve spirochete bacterium
- primary syphilis: enters through a break in the skin or through intact mucous membranes to form an infectious hard ulcer (chancre) at the site of contact
- If untreated, can cause systemic damage via obliterating arteritis causing ischaemia
- incubation period is 2-3 weeks
- risk factors: UPSI, multiple partners, MSM, HIV
- can also have vertical transmission

2.) Investigations
- antibody testing as a screening test, if positive, refer to a specialist GUM centre for further testing:
- dark ground microscopy of chancre fluid, PCR swabs
- serology: treponemal tests, non-treponemal tests
- LP: CSF antibody tests in neurosyphilis

3.) Management - via a specialist service e.g. GUM
- 1 dose of IM of benzathine penicillin (benzylpenicillin) is the standard treatment for syphilis
- other types of penicillin are used in other scenarios e.g. late syphilis and neurosyphilis: Ceft, Amoxi, Doxy
- full screening for other STIs
- avoid sexual activity until treated
- contact tracing, prevention of future infections

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6
Q

Genital Warts

Pathophysiology
Clinical Features
Differential Diagnoses
HPV Vaccination

A

1.) Pathophysiology - HPV infection of keratinocytes causing their rapid growth manifesting as lesions
- HPV 6 and 11 responsible for roughly 90% of cases
- transmission: skin-skin contact during sex, penetration is not necessary, condoms aren’t fully protective
- rarely passed on during oral and vertical
risk factors: early first sexual intercourse, multiple partners, immunosuppression, smoking, diabetes

2.) Clinical Features - most are asymptomatic and resolve spontaneously, some sx include:
- genital warts can appear weeks to years after the initial infection, they can affect the penis, scrotum, vulva, vagina, cervix, perianal skin or inside the anus
- warts are usually painless, fleshy growths that can be soft or hard and can be singular or multiple
- warts may cause irritation or become inflamed

3.) Differential Diagnoses
- vestibular papillomatosis: small, shiny, skin-coloured growths on the vulva, non-viral, non-STI
- molluscum contagiosum: viral infection causing small firm raised papules on the skin

4.) HPV Vaccination - offered to all girls aged 12-13
- Gardasil contains protection against HPV 16/18/6/11
- best if administered before first sexual contact

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7
Q

Management of Genital Warts

Investigations
Topical Treatments
Physical Ablation

A

1.) Investigations
- diagnosis is usually made on examination, small lesions may require magnification using a colposcope
- proctoscopy if there are warts around the anal margin or there are sx such as irritation and bleeding
- speculum to check for internal warts in women
- biopsy may be required for atypical lesions and suspected intraepithelial neoplastic lesions
- offer a full STI screen due to risk of co-infection

2.) Topical Treatments
- podophyllotoxin: small warts, non-keratinised
- imiquimod: larger warts, particularly keratinised warts
- catephen and trichloroacetic acid not used in the UK
- may weaken latex condoms, cause local inflammation
- contraindicated in pregnancy/breastfeeding
- change in therapy if <50% response after 4-5wks

3.) Physical Ablation
- cryotherapy: used for multiple warts or pregnancy
- excision: large warts or accessible small hard warts
- electrosurgery: excision + removal of remains using an electric current, used for large warts failing topical tx
- laser surgery: for difficult to access warts (e.g. in anus)

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8
Q

Genital Herpes

Pathophysiology
Primary Infection Symptoms
Secondary/Recurrent Infection Symptoms
Differential Diagnoses

A

1.) Pathophysiology - HSV remains dormant in the nearest nerve ganglion (trigeminal in cold sores, sacral in genital herpes) where it cannot be reached by the immune system, can then be reactivated
- HSV1: cold sores, but can cause genital herpes
- HSV2: mainly causes genital herpes
- asymptomatic shedding is where you can shed and transmit the virus (infectious) without any sx
- risk factors: UPSI (can spread w/ contraception), multiple partners, oral sex w/ partner w/ cold sores, immunosuppression (recurrent outbreaks)

2.) Primary Infection Symptoms - you can be asymptomatic for years after the initial infection but some can get primary sx instantly:
- painful small red blisters around the genitals that are can form open sores, males (penis, thigh, anus, buttocks), females (vulva, clitoris, buttocks, anus)
- neuropathic pain: tingling, burning or shooting
- vaginal or penile discharge, dysuria, itchy genitals
- flu-like symptoms: fever, muscle aches, etc.
- inguinal lymphadenopathy
- sx last up to 3 weeks including ulcers

3.) Secondary/Recurrent Infections - occurs when HSV becomes reactivated to cause outbreaks
- overtime outbreaks reduce in severity and length due to improved antibody recognition and response
- sx: painful red blisters around the genitals with burning and or itching sensation present

4.) Differential Diagnoses - genital ulceration
- aphthous ulcers, varicella-zoster virus, trauma and other vesiculobullous disorders
- consider underlying HIV if very recurrent (>5/yr)

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9
Q

Management of Genital Herpes

Investigations
Management
Herpes in Pregnancy

A

1.) Investigations - best diagnosed during primary infection at a GUM clinic or GP surgery
- 1°NAAT (PCR) swabs: now considered superior to viral culture
- HSV serology may be useful in certain situations such as recurrent genital ulceration of unknown cause
- consider screening for other STIs

2.) Management
- PO Aciclovir 400mg TDS for 5 days + (helps to reduce severity)
- daily aciclovir as suppressive treatment if outbreaks are very frequent (>6/yr), or severe
- simple analgesics, petroleum jelly and ice packs to reduce the pain and discomfort of an infection
- avoid all sexual contact during an outbreak
- full STI screen and safe sex advice, advised informing their recent and current sexual partners

3.) Herpes in Pregnancy
- pre-existing herpes: baby has protection due to having antibodies from the mother, vaginal births are still recommended even if recurrent lesions at the time
- new-onset herpes: esp in T3 is more dangerous due to lack of antibodies, a C-section is recommended
- 3 types of neonatal herpes: skin, eyes and mouth (SEM) herpes, disseminated (DIS) herpes affecting the internal organs, and CNS herpes (can –> encephalitis)
- antivirals are usually sufficient for SEM but mortality is much higher for DIS and CNS herpes

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