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Flashcards in STIs Deck (49)
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1
Q

Most common STI

A

Chlamydia

2
Q

Impact of STI highest in

A

Heterosexuals under 25
MSM
Black ethnic minorities

3
Q

Largest STI diagnosis increase in MSM

A

Syphilis up 20%

Gonorrhoea up 22%

4
Q

Chlamydia Trachomatis

A

Obligate intracellular pathogen

Asymptomatic infection common

5
Q

Serovar

A

Distinct variation within species of bacteria or virus

6
Q

Chlamydia Serovars D-K

A

Most UTIs
Males- urethritis, epididymitis, prostatitis
Females- Cervicitis, PID, Fitz-Hugh Curtis
Neonate- conjunctivitis and pneumonia

7
Q

Chlamydia Servars L1-3

A

Lymphogranuloma venerum

–> buboes, proctitis (inflammation of lining of rectum)

8
Q

Chlamydia trachomatis complications

A

Reactive arthritis

Infertility

9
Q

Chlamydia trachomatis treatment

A

Doxycyline

Azithromycin

10
Q

Neisseria gonorrhoea- Males

A
Urethritis
Proctitis
Sore throat
Epididymitis
Prostatitis
11
Q

Neisseria gonorrhoea- Females

A

Cervicitis
PID
Peri-hepatitis
Septic abortion

12
Q

Neisseria gonorrhoea- Neonates

A

Conjunctivitis

13
Q

Neisseria gonorrhoea- complications

A

Septic arthritis
Blindness
Infertility
Septicaemia

14
Q

Neisseria gonorrhoea- management

A

Ceftriaxone

–> drug resistance increasing

15
Q

Genital warts

A

HPV
90% asymptomatic
Multiple sites
Some associated with carcinoma (16,18,31,33)
Increasing incidence ano-genital and oropharyngeal carcinoma
Vaccination

16
Q

Genital warts management

A

Topical podophyllotoxon
Imiquimod
Cryotherapy

17
Q

Herpes Simplex Virus 1 + 2

A
HSV-1 = Oral
HSV-2 = Genital
Primary infection
Latency
Reactivation
18
Q

Herpes simplex virus 1+2- management

A

Aciclovir
Famciclovir
Valaciclovir

19
Q

Syphilis bacteria

A

Treponema pallidum

Gram negative spirochete bacterium

20
Q

Treponema pallidum

A

Primary, secondary, latent, tertiary, congenital
Often asymptomatic in early stages
Diagnosis depends on serology

21
Q

Syphilis treatment

A

Penicillin

Doxycycline

22
Q

Primary Syphilis

A
Chancre (sore) usually single, painless
Dark ground positive
Lymphadenopathy
Serology may be negative
Infectious ++
23
Q

Secondary Syphilis

A
Rash
Fever
Lymphadenopathy
Condyloma lata
Serology positive
Infectious ++
24
Q

HIV Routine testing

A

GUM, Ante-natal, TOP, DDU

New registrations in GP and medical admissions in areas where high prevalence

25
Q

HIV Opportunistic testing of individuals at high risk

A
STI
MSM
HIV + partner
IDU
High prevalence country
26
Q

HIV Diagnostic testing with indicator clinical conditions

A

TB/lymphoma

27
Q

Primary HIV infection

A

Acute retroviral syndrome
75% patients develop symptoms within 2-6 weeks of infection
Wide differential diagnosis- glandular fever, flu
Increased viral replication
Decreased CD4 count
Time of high risk of transmission
May be HIV antibody negative

28
Q

HIV antibody

A

Primary HIV infection may be HIV antibody negative
HIV RNA/p24 antigen positive
HIV antibody can take up to 3 months to become positive

29
Q

Primary HIV 1 infection Common features

A
Headache
Lymphadenopathy
Pharyngitis
Nausea
Oral/genital ulceration on occasion
Rash
Myalgia
Fever
Fatigue
Weight loss
Night sweats
30
Q

HIV causing disease

A

Infects CD4+ cells, macrophages and dendritic cells
Acute (primary) HIV infection leads to massive CD4+ cell loss
Chronic HIV infection associated with on-going CD4+ cell loss, decline in immune function and progressive immunosuppression

31
Q

HIV-associated disease- Direct HIV effect

A

Wasting
Diarrhoea
Neurological problems

32
Q

HIV-associated disease- Opportunistic infections

A
Viral
Fungal
Bacterial
Mycobacterial
Parasitic
INFECTIONS
33
Q

HIV-associated disease- Malignancies

A

Kaposi’s sarcoma- affects lining of blood vessels, often appears as skin lesions
Lymphoma
Carcinoma cervix

34
Q

CD4 count >500

A

Low risk HIV-related disease

35
Q

CD4 count 350-500

A

Symptomatic HIV disease possible

36
Q

CD4 count <200

A

Risk PCP, gut infections

37
Q

CD4 count <100

A

CMV, MAI, crypto, toxo, KS

38
Q

Aims of antiretroviral therapy

A

Suppression of HIV replication –>
CD4 count recovery –>
Immune reconstitution –>
Long term reduced risk of morbidity and mortality

39
Q

Antiretroviral Therapy Principles

A

HAART= highly active antiretroviral therapy
6 classes of ARV drugs available
Act during viral replication cycle to prevent production of new HIV particles
Combination antiretroviral therapy always
At least 3 drugs from at least two classes –> usually 2 NRTIS + NNRTI or PI
Lifelong treatment
Adherence vital for success –> resistance can develop quickly, and can be transmitted

40
Q

Antiretroviral therapy Drugs

A

At least 3 drugs from at least 2 classes

Usually 2 NRTIS + NNRTI or PI

41
Q

NRTI

A

Nucleoside Reverse transcriptase inhibitors
Lamivudine
Stops RNA synthesis

42
Q

NNRTI

A

Non-nucleoside reverse transcriptase inhibitors
Nevirapine
Stops RNA synthesis

43
Q

PI

A

Protease inhibitors
Ritonavir
Stops virus protein being cut up

44
Q

Types of antiretroviral drugs

A
Fusion inhibitor
Co-receptor antagonist
Nucleoside reverse transcriptase inhibitor
Non-nucleoside RT inhibitor
Integrase inhibitor
Protease inhibitor
45
Q

Short term SEs HAART

A
Nausea/vomiting/headache
Sleep disturbance (efavirenz)
46
Q

Long term SEs HAART

A
Lipodystrophy (NRTIs + PIs)
Renal dysfunction (tenofovir)
Peripheral neuropathy (d4T, AZT, DDI)
Lactic acidosis- may be fatal (d4T, DDI)
47
Q

Problems with HAART

A

Long + short term side effects
IRIS- paradoxical inflammatory reaction to pathogen
Drug interactions
Complex regimens/polypharmacy

48
Q

PEP/ PEPSE + PrEP

A
Indications
--> High risk sexual exposure <72 hours
--> Needlestick
Available via virology/GUM/A+E
PrEP- safe and efficacious
49
Q

HIV management pregnancy

A

Early HIV screening
ARVT for mother- immediate + continued if low CD4, 2nd trimester + discontinued if high CD4
Elective C section- vaginal delivery possible if undetectable HIV load
ARVT for infant
No breastfeeding
–> Reduced risk of transmission from 25 to less than 1%