Sexual Health Flashcards

1
Q

Definition of recurrent candidiasis

A

4 or more symptomatic episodes- x2 lab- confirmed, in 12 months

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2
Q

Treatment of recurrent candidiasis

A

Fluconazole 150mg stat q72h for 3 doses + maintenance 150mg weekly for 6 months

Or

Clotrimazole 2% nocte for 3 days, repeat monthly for 6 months

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3
Q

Apart from gonorrhoea and chlamydia, what other organisms can cause PID

A

Mycoplasma
Gardnerella
Bacteroides
Trichimonas
GBS

Chronic PID- actinomyces, TB

No organism isolated in 20% of cases

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4
Q

Syphilis classification

A

Early (<2 years):
- primary
- secondary
- early latent

Late (>2 years):
- late latent
- tertiary

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5
Q

Primary syphilis

A

Presents 9- 90 days following exposure.
Solitary painless purple papule. Inflammatory changes lead to necrosis, ulcerates (highly infective) then turn into a chancre.

Chancre is a 1-2cm moist base, well- defined margin, found in mucosal surfaces (genital or extra- genital)
Associated non- tender and rubbery inguinal lymphadenopathy

Resolves in 3-8 weeks

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6
Q

Secondary syphilis

A

Develops after 1-6 months of exposure

Systemic illness- lethargy, malaise, fever, anorexia, headache

Skin changes:
- generalised lesions affecting skin + mucous membranes
- symmetrical + non- itchy lesions- can be macular, papular, and rarely pustular
- condylomata lata- warty lesions on moist areas (that are smooth and moist)
- alopecia

Other:
- lymphadenopathy
- hep
- glomerulonephritis
- meningitis
- iritis
- optic neuritis
- ocular nerve palsy
- sensory- neural deafness

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7
Q

Latent syphilis

A

Asymptomatic
All untreated individuals become asymptomatic in 12- 24 months
No longer infectious after 24 months but women may still pass on infection to unborn fetus (vertical transmission)

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8
Q

Tertiary syphilis

A

Gummatous syphilis- necrotic nodules or plaques which develop 3-12 years after primary infection

Neurosyphilis- occurs 10-20 years after primary infection

Cardiovascular syphilis- aortic regurgitation, angina, aneurysm, 10- 40 years after infection

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9
Q

Syphilis serology

A

Progression: positive IgM -> IgG -> TPPA -> VDRL

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10
Q

Diagnosis of syphilis

A

T pallidum enzyme immunoassay (EIA)

Then TPPA or TPHA if positive EIA to confirm infection

Can also perform RPR for confirmation. Positive 3-5 weeks after infection

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11
Q

Treatment for syphilis

A

Primary + secondary: long acting Benzathine Penicillin G 2.4 MU IM x1 dose

Latent: 3 doses at 1- weekly intervals

If penicillin allergy: doxycycline

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12
Q

Repeat serology after treatment of syphilis

A

Repeat in 3, 6, 12 months

Serological cure- 4-fold drop in RPR titre
Reinfection- 4- fold rise in RPR titre
Inadequate treatment- if not reached 4- fold drop in RPR titre

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13
Q

Pathophysiology of HIV

A

HIV attaches to CD4 molecules on T cells and inhibit lymphocyte growth and enhances apoptosis

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14
Q

Copper IUD MOA

A

Inhibits fertilisation due to effect of copper on sperm and egg
Alteration in copper content of cervical mucus inhibits sperm penetration
Endometrial inflammatory reaction prevents implantation

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15
Q

COCP MOA

A

Inhibition of ovulation by providing high levels of synthetic oestrogen and progestogen so exerts negative feedback on pituitary to stop release of LH and FSH

Thickens cervical mucus which prevents sperm penetration

Thins endometrium which reduces receptiveness to implantation

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16
Q

POP MOA

A

Causes cervical mucuos to be viscous and hostile, preventing penetration of sper
Thins the endometrium inhibiting implantation

Cerazette inhibits ovulation

17
Q

Risk of VTE among users of Drospirenone- containing oral contraceptive pills

A

Oestrogen interfere with the renin- angiotensin- aldosterone system which regulates body fluids and BP.

Oestrogen’s effect on RAAS leads to fluid retention, weight gain and a small increase in BP.

Ethinylestradiol increases plasma concentration of factors II, VII, VIII, X, XII and fibrinogen

Progesterone has a high affinity for the mineralocorticoid receptor and is an antagonist of aldosterone. Aldosterone is involved in haemostasis, leading to a decrease in coagulability.

Drospirenone has a high affinity for the progesterone and mineralocorticoid receptors. It promotes natriuresis (haemoconcentration) and counteracts the effect of ethinyloestradiol (hence weight gain, HTN and fluid retention less common with Drospirenone).
Drospirenone’s anti- mineralocorticoid properties in turn lead to a hypercoagulable state, creating a possible mechanism for the increased risk of VTE with the use of Drospirenone- containing OC’s

18
Q

Mechanism of lactational amenorrhea for contraception

A

Suckling and the resultant hyperprolactinaemia disrupts pulsatile GnRH release. Sufficient FH is produced to stimulate folliculogenesis but insufficient LH hence preventing ovulation