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Year 4 > Sexual health > Flashcards

Sexual health Flashcards

1
Q

Herpes simplex virus (HSV)

A

HSV-1 & HSV-2 infections generally manifest with oral, genital and ocular ulcers

seroprevalence for HSV is high with >90% of the population worldwide having detectable antibodies

NB HSV-1 usually oral, HSV-2 usually genital

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2
Q

transmission of Herpes simplex virus (HSV)

A

transmission via direct contact with mucosal tissue / secretions of infected individual or perinatal transmission (more common with HSV-2)

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3
Q

Presentation of Herpes labialis (cold sores)

A

prodrome (~24h) of tingling, burning or pain

recurring erythematous vesicles that turn into painful ulcerations on oral mucosa /lips

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4
Q

Presentation of genital herpes

A

painful genital ulceration ± dysuria & pruritis
usually presents as single/disseminated red bumps/white vesicles found around genitalia / anus
may have tender lymphadenopathy

NB primary infection is usually more severe and may present with systemic features such as fever, headache, malaise

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5
Q

Investigations for Herpes simplex virus (HSV) infection

A

cold sores are usually a clinical diagnosis

genital herpes usually requires nucleic acid amplification test (NAAT) or PCR

HSV serology may be used in asymptomatic pts, those with recurrent/atypical ulcers or to distinguish HSV types

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6
Q

Management of Cold sores

A

generally symptomatic management

consider topical choline salicylate gel or lidocaine or topical aciclovir (not recommended)

NB infection control is key e.g. don’t touch lesions, avoid kissing & oral sex

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7
Q

Management of genital herpes

A

Refer to GUM clinic

general:
saline bathing, analgesia, topical anaesthetics e.g. lidocaine

oral acyclovir/valaciclovir (within 5 days of symptom onset)

consider suppressive antiviral therapy with acyclovir daily if >6 attack per year)

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8
Q

Genital herpes in pregnancy

A

elective C-section if genital herpes at >28 weeks, & give suppressive therapy in the form of acyclovir if recurrent attacks

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9
Q

When to consider suppressive therapy for genital herpes

A

consider suppressive antiviral therapy with acyclovir daily if >6 attack per year)

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10
Q

Syphilis

A

A predominantly sexually transmitted infection caused by the spirochaete bacterium Treponema pallidum

more common in men especially those who have sex with men (MSM)

incubation period of 10-90 days

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11
Q

Window period for syphilis

A

12 weeks

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12
Q

Window period

A

the window period for a test designed to detect a specific disease (particularly infectious disease) is the time between first infection and when the test can reliably detect that infection. In antibody-based testing, the window period is dependent on the time taken for seroconversion.

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13
Q

Presentation of primary syphilis

A

local lesion at site of infection (NB often not seen in women as it may be on cervix)

small painless papule rapidly forms under and ulcer (the chancre), usually single, round/oval PAINLESS surrounded by bright red margins
resolves spontaneously within 3-6 weeks

may have regional (usually inguinal) non tender lymphadenopathy

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14
Q

Presentation of secondary syphilis

A

~6-10 weeks after primary infection

systemic symptoms of fever, malaise, lymphadenopathy, hight time headaches, aches

Rash: generalised polymorphic rash on palms/soles/trunk, reddish brown or copper colour, non pruritic

Buccal snail track ulcers

condylomata lata (board based, wart like smooth white papular erosions usually found in moist & warm areas e.g. genitalia)

NB rash on soles/palms = pathomemonic

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15
Q

Presentation of tertiary syphilis

A

3 distinct clinical syndromes that may co-exist

Cardiovascular syphilis:
characterised by aortitis (usually of aortic root), ascending aortic aneurysm
manifests with aortic regurgitation, angina & aortic aneurysms

Gummata:
chronic destructive granulomatous lesions with necrotic centres that tend to ulcerate, can occur in any organ
usually seen in skin/bones

Neurosyphilis:
dorsal column loss (tabes dorsalis = impaired proprioception, broad based gait, ataxia, absent reflexes), dementia (general paralysis of the insane), Argyll Robertson pupil (bilateral miosis, pupils accommodate but pupillary light reflex is absent)

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16
Q

Cardiovascular syphilis

A

characterised by aortitis (usually of aortic root), ascending aortic aneurysm
manifests with aortic regurgitation, angina & aortic aneurysms

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17
Q

Gummata

A

chronic destructive granulomatous lesions with necrotic centres that tend to ulcerate, can occur in any organ
usually seen in skin/bones

Tertiary syphilis

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18
Q

Neurosyphilis

A

CNS invasion causing inflammatory reaction of the meninges/cerebral parenchyma

dorsal column loss (tabes dorsalis = impaired proprioception, broad based gait, ataxia, absent reflexes)

dementia (general paralysis of the insane)

Argyll Robertson pupil (bilateral miosis, pupils accommodate but pupillary light reflex is absent)

managed with IM/IV benzathine pencillin for 10-14 days

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19
Q

Congenital syphilis presentation

A 
blunted upper incisors (hutchinson's teeth)
mulberry molars 
linear scars at angle of mouth
keratitis
saber shins
saddle nose
deafness
hepatomegaly 
jaundice
sensorineural hearing loss
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20
Q

Effects of in utero syphilis

A

miscarriage
stillbirth
hydrops fetalis

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21
Q

Investigating syphilis

A

Treponemal specific antibody tests:
e.g. treponema enzyme immune assay (EIA), T.pallidum particle agglutination test (TPPA), T.pallidum hem agglutination test (TPHA) etc
stay +ve after treatment

Non treponema specific:
anticardiolipin antibodies
-ve after treatment, insensitive for advanced syphilis

screen for other STIs

dark field microscopy (for T. pallidum)

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22
Q

Management of syphilis

A

1st line: single dose IM bezathine penicillin (alternatives = azithromycin / doxycycline)

Neurosyphilis = IM/IV benzathine pencillin for 10-14 days

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23
Q

Jarisch-Herxheimer reaction

A

ruction to treatment, after 1st dose

acute febrile illness with headache, myalgia, riggers, tachycardia

generally self resolved in 24h

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24
Q

Syphilis causative organism

A

spirochaete bacterium Treponema pallidum

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25
Q

Lymphogranuloma venereum

A

An STI caused by the L1/L2/L3 serovars of chlamydia trachomatis, its an infection of mononuclear phagocytes

generally endemic to the tropics but now appearing in local outbreaks in europe

NB majority of pts in the west are HIV +ve

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26
Q

Lymphogranuloma venereum causative organism

A

L1/L2/L3 serovars of chlamydia trachomatis

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27
Q

Lymphogranuloma venereum (LGV) vs Chlamydia causative organisms

A

LGV: L1/L2/L3 serovars of chlamydia trachomatis

Chlamydia: D-K serovars of chlamydia trachomatis

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28
Q

Risk factors for Lymphogranuloma venereum (LGV)

A

MSM
unprotected sex
receptive/insertive anal intercourse
multiple sexual partners

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29
Q

Presentation of Lymphogranuloma venereum (LGV)

A

Primary:
small painless genital pustules that form painless ulcers & heal in a couple of days

Secondary:
~3 weeks after exposure, painful inguinal/pelvic/perirectal lymphadenopathy (may form fistulating buboes)

Tertiary:
up to 20 yrs after infection, proctocolitis (anal itching, bloody mucopurulent anal discharge, rectal pain, constipation)
granuloma mucosa & enlarged nodes on DRE

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30
Q

Investigation of Lymphogranuloma venereum (LGV)

A

nuclear acid amplification tests (NAATs) with swabs from anogenital lesions/rectal mucosa/lymph node specimen

STI testing

colonoscopy/rectal biopsy may be needed for anal symptoms

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31
Q

Management of Lymphogranuloma venereum (LGV)

A

Doxycycline (100mg BD for 21 days)

Buboes may require surgical drainage)

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32
Q

Chlamydia

A

A common STI caused by chlamydia trachomatis servars D-K

refers to chlamydia genitourinary infections

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33
Q

Most prevalent STI in the UK

A

Chlamydia

most common in sexually active people <25y/o

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34
Q

Risk factors for chlamydia

A 
age <25
≥ 2 sexual partners in previous year
recent change in sexual partners
no barrier contraception 
infection with other STIs
poor socioeconomic status
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35
Q

Presentation of chlamydia in females

A

70% asymptomatic

cervicitis (discharge, bleeding)
deep dyspareunia, dysuria, vague lower abdo pain
intermenstrual/postcoital bleeding
friable inflamed cervix
pelvic adnexal tenderness & cervical excitation

NB always consider chlamydia asa cause of sterile pyuria

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36
Q

Presentation of chlamydia in males

A

50% asymptomatic

urethritis (dysuria, urethral discharge)
epididymo-orchitis (unilateral testicular pain ± swelling)
proctitis (perianal fullness)
fever

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37
Q

Investigating chlamydia

A

NAAT of vulvovaginal swab (women) or first void urine sample (men)

2 week window period

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38
Q

Window period for chlamydia

A

2 weeks

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39
Q

Complications of chlamydia

A

Reactive arhtirits (common cause of post STI reactive arthritis)
PID
Infertility (especially in females)
Fitz-Hugh-Curtis syndrome (Perihepatitis i.e. inflammation of the liver capsule, due to transabdominal spread of PID which presents with RUQ pain, nausea, vomiting)

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40
Q

Human papillomavirus (HPV) (focus on genital warts)

A

Genital warts are the most common form of viral genital mucosal lesions and are caused by infection with HPV type 6 / 11

most common viral STI in UK

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41
Q

Human papillomavirus (HPV) serotypes causing warts

A

6 & 11

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42
Q

Fitz-Hugh-Curtis syndrome

A

Perihepatitis i.e. inflammation of the liver capsule, due to transabdominal spread of PID

violin string like adhesions from peritoneum to liver

presents with RUQ pain, nausea, vomiting
pain may refer to R shoulder

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43
Q

Most common viral STI in UK

A

Human papillomavirus (HPV)

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44
Q

Risk factors for genital warts

A 
smoking
multiple sexual partners
history of STIs (20% of pts with warts have other STIs)
unprotected intercourse
immunosuppression

NB: consistent condom usage majorly ↓ risk fo warts

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45
Q

Presentation of Genital warts (HPV)

A

single or multiple lesions which may forma confluent mass
usually 1-5mm discrete smooth exophytic papillomas which may be slightly pigmented (broad based or pedunculated)
may bleed or itch

usually found in vulva/anal/cervical region in women
usually found around foreskin/glans/shaft/urethral/anal regions in men

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46
Q

Investigations for genital warts (HPV)

A

speculum exam in women
proctoscopy (if unreceptive sex)

biopsy & viral testing (if uncertain diagnosis or treatment resistance)

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47
Q

Genital warts in children

A

discovery of genital warts in children should prompt consideration of sexual abuse unless clear evidence of mother-to-child transmission at birth / non sexual transmission from another household memeber

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48
Q

Prevention of HPV

A

HPV vaccination with Gardasil (quadrivalent covering type 6,11,16,18)

given to all boys & girls aged 11-13

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49
Q

Management of genital warts (HPV)

A

education & STI screening
assess current partner + all partners in previous 6 months

1st line: Podophyllotoxin (topical) or cryotherapy
2nd line: topical imiquimod 5%

majority clear without treatment in 1-2 yrs
recurrence common, in 20-30%

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50
Q

Genital warts in children

A

discovery of genital warts in children should prompt consideration of sexual abuse unless clear evidence of mother-to-child transmission at birth / non sexual transmission from another household member

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51
Q

Prevention of HPV

A

HPV vaccination with Gardasil (quadrivalent covering type 6,11,16,18)

given to all boys & girls aged 11-13

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52
Q

Treatment of genital warts in pregnancy

A

Treatment of choice = cryotherapy

Imiquimod & Podophyllotoxin = contraindicated in pregnancy

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53
Q

Molluscum contagiosum

A

a common localised viral infection caused by the molluscum contagiosum virus a member of the poxviridae family

most often seen in children but if seen in adults often due to sexual contacts

spreads via close personal contact or indirectly via formites e.g. contaminated towel

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54
Q

Presentation of Molluscum contagiosum

A

characteristic pinkish/pearly white papule with a central umbilication, usually found in clusters (anywhere on body except palms & soles)

if sexually transmitted often seen in genitalia/pubis/thighs/lower abdomen

lesions on face/eyelids/oral mucosa rare (usually seen with immunosuppressed pts)

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55
Q

Investigation of Molluscum contagiosum

A

usually clinical diagnosis

consider HIV testing if widespread/facial/lesions in adults

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56
Q

Management of Molluscum contagiosum

A

generally no treatment needed, self limiting, usually resolves within 18month

self care advice ie.e. avoid scratching, don’t share towels, use condoms if genital lesions

if troublesome symptoms = imiquimod 5% or cryotherapy

refer to specialist if HIV+ve, widespread lesions, or if eyelid/occular infection

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57
Q

Scabies

A

a parasite skin infestation caused by sarcoptes scabiei mites which is primarily spread by close ski to skin contact

outbreaks are known to occur in hospitals, prisons, residential/nursing hoes

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58
Q

Risk factors for scabies

A 
overcrowding 
poverty
poor nutritional status
homelessness
poor personal hygiene 
institutionalisation 
dementia
sexual contact 
immunosuppression
children
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59
Q

Presentation of scabies

A

Infected contacts may be asymptomatic for 3-4weeks

intense widespread pruritis:
worse at night, may have history of itch in close contacts
excortication (scratching) marks are common

greyish/silvery linear burrow on side of fingers / interdigital webs / flexor aspects of wrist
± erythematous papules / vesicular lesions

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60
Q

Investigations for scabies

A

largely clinical diagnosis

histological examination of skin scrapping = confirmatory

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61
Q

Management of scabies

A

treat whole household & close physical contacts at same time even if asymptomatic
1st line: permethrin 5%
2nd line: malathion 0.5%

General:
avoid close with contacts with others until treatment complete
launder/iron/wash clothing/bedding to kill mites

NB pruritis may persist for 4-6 weeks post treatment

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62
Q

Crusted (Norwegian) scabies

A

hyper infestation with thousands of mites seen in those with immunosuppression e.g. HIV

presents with hyperkeratotic crusted lesions on hands/feet/scalp/nails ± lymphadenopathy

treatment of choice = Ivermectin & isolation of individual

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63
Q

Gonorrhoea

A

An STI caused by the bacteria Neisseria gonorrhoea that leads to genitourinary tract infections such as urethritis, cervicitis, PID, epididymitis

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64
Q

Gonorrhoea

A

An STI caused by the Gram-negative diplococcus Neisseria gonorrhoea that leads to genitourinary tract infections such as urethritis, cervicitis, PID, epididymitis

transmission is via direct inoculation of infected secretions from one mucous membrane to another usually via sexual contact

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65
Q

Window period for gonorrhoea

A

2 weeks

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66
Q

Risk factors for gonorrhoea

A 
young age
history of previous STI
new/,multiple partners 
recent sexual activity abroad
history of drug use
commercial sex work 
MSM
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67
Q

Presentation of gonorrhoea in women

A

endocervical (asymptomatic or PV discharge ± lower abdo pain)
urethral (dysuria but no frequency)
Rectal (asymptomatic)
pharyngeal (asymptomatic)

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68
Q

Presentation of gonorrhoea in men

A

urethritis (discharge ± dysuria)
Rectal (usually asymptomatic or discharge ± perianal pain & pruritis)
pharyngeal (asymptomatic)
epididymal (unilateral scrotal pain & swelling)

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69
Q

Investigations for gonorrhoea

A

NAAT (endocervical smear in women, first pass urine in men)
2 week window period

other STI screen & GUM

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70
Q

Management of gonorrhoea

A

1st line: IM ceftriaxone 1g single dose

2nd line: 500mg ceftriaxone IM + oral azithromycin (NB this is 1st line inpregancy) or 400mg PO cefixine + azithromycin 2g (e.g. if needle phobic)

test of cure (NAAT) at 2 weeks post treatment + partner notification (STI screen + empirical Abx)

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71
Q

Complications of gonorrhoea

A 
PID
infertility 
Fitz-Hugh-Curtis syndrome
septic arthritis (most common cause of optic arthritis in young sexual active people)
Disseminated gonococcal infection
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72
Q

Disseminated gonococcal infection (DGI)

A

due to haematogenous spread of infection
rare (~1%)

characterised by tenosynovitis, migratory polyarthritis, dermatitis (maculopapular/vesicular rash on trunk & extremities), fever

later endocarditis, perihepatitis, septic arthritis

IV ceftriaxone for 7 days is treatment of choice

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73
Q

Vaginal candida (thrush)

A

A very common yeast infection of the lower female reproductive tract, ~80% are caused by candida albicans

peak incidence age 20-40

~80% of women have candida vulvovaginitis at some point in their life

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74
Q

Causative organism for thrush

A

~80% are caused by candida albicans

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75
Q

Risk factors for thrush

A 
pregnancy 
diabetes mellitus 
vaginal foreign body
immunosuppression (e.g. HIV)
imbalance of local flora e.g. from Abs use
steroid use
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76
Q

Presentation of thrush

A 
erythematous vuvla & vagina 
pruritis vulvae
vulval soreness 
white, crumbly, sticky vaginal discharge (like cottage cheese), typically non offensive / odourless
superficial dyspareunia 
dysuria
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77
Q

Investigations for thrush

A 
clinical examination / no swabs required
vaginal pH (normal, i.e. <4.5)

NB if complicated infection then take swabs for culture/sensitivity/microscopy

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78
Q

Management fo thrush

A

1st line: clotrimazole pessary
2nd line: oral itraconazole / fluconazole

NB in pregnancy only local treatment (creams/pessaries) may be used

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79
Q

Management of recurrent vaginal candidiasis

A

i.e. if ≥4 episodes in a year

high vaginal swab to confirm diagnosis with MC&S
check for diabetes

consider maintenance treatment e.g. PO fluconazole

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80
Q

Vaginal candidiasis in pregnancy

A

Oral Treatments e.g. oral itraconazole / fluconazole are contraindicated

only pessaries or creams e.g. clotrimazole pessary may be used

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81
Q

Trichomonas vaginalis

A

a very common STI caused by trichomonad vaginalis, a flagellated protozoa parasite

in adults its almost exclusively sexually transmitted

MOST common curable STI worldwide

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82
Q

Presentation of trichomonas vaginalis in women

A

foul smelling frothy yellow/green purulent discharge with offensive odour
vulval pruritis
dysuria
offensive odour PV
lower abdo pain
cervicitis (strawberry cervix i.e. erythematous mucosa with petechiae)

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83
Q

Presentation of trichomonas vaginalis in men

A

usually asymptomatic
common cause of non-gonoccocal urethritis
dysuria & discharge

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84
Q

Investigations for trichomonas vaginalis

A 
vaginal pH (↑, pH >4.5)
high vaginal swab (NAAT if available = test of choice otherwise saline wet mount = mobile trophozoites & multiple flagella, if wet mount inconclusive = culture)
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85
Q

Management of trichomonas vaginalis

A

contact tracing & further STI screening

1st line: PO metronidazole for 5-7 days
2nd line: single dose PO metronidazole

NB treat both sexual partners at same time & avoid intercourse until 1 week after treatment

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86
Q

Bacterial vaginosis (BV)

A

describes an overgrowth of predominantly aerobic organisms such as Gardnerella vaginalis leading to a consequent fall in lactic acid producing lactobacilli leading to ↑ vaginal pH

almost exclusively seen in sexually active women (but not and STI, only sexually associated)

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87
Q

Risk factors for Bacterial vaginosis (BV)

A 
sexual activity
new sexual partner
previous STIs
afro-carribbean women
use of IUD
vaginal douching
bubble baths
receptie oral sex
smoking
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88
Q

Presentation of Bacterial vaginosis (BV)

A

often asymptomatic

offensive, fishy smelling vaginal discharge, usually are/milky clear
pruritus & pain = uncommon

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89
Q

Protective factors for Bacterial vaginosis (BV)

A

circumcised partner
condom use
COCP (oestrogen encourages lactobacilli)

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90
Q

Investigations for Bacterial vaginosis (BV)

A 
vaginal pH (↑, pH>4.5)
whiff test (addition of KOH = fishy odour)
microscopy of discharge (clue cells - epithelia cells with stippled appearance)

Amsel criteria for diagnosis (3/4 of the following)

  • thin white homogenous discharge
  • vaginal pH >4.5
  • positive whiff test (addition of potassium hydroxide = fishy odour)
  • clue cells in microscopy
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91
Q

Management of Bacterial vaginosis (BV)

A

advice on vaginal hygiene e.g. avoid douching

if asymptomatic:
no treatment unless pregnant

if symptomatic:
PO metronidazole for 5-7 days

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92
Q

Bacterial vaginosis (BV) in pregnancy

A

↑ risk of preterm labour, low birth weight, chorioamnionitis, later miscarriage

use oral metronidazole for 5-7 days even if asymptomatic

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93
Q

Amsel criteria

A

For diagnosis of bacterial vaginosis

3/4 of the following

  • thin white homogenous discharge
  • vaginal pH >4.5
  • positive whiff test (addition of potassium hydroxide = fishy odour)
  • clue cells in microscopy
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94
Q

Non gonococcal urethritis (NGU)

A

inflammation of urethral mucosa the can be caused by carious pathogens, this term is reserved for men

usually an STI

this is used to describe the presence of urethritis in the absence of gonococcal bacteria on the first swab

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95
Q

Causative organism for Non gonococcal urethritis (NGU)

A

chlamydia trachomatis (most common)
myelopsama genitalium
trichomonas vaginalis

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96
Q

Most common form of urethritis

A

Non gonococcal urethritis (NGU)

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97
Q

Presentation of urethritis

A

usually asymptomatic if gooccocal

mucopurulent discharge ± blood, urethral pruritus, dysuria, penile discomfort
burning/itching of urethral meatus

NB generalised symptoms are rare and should rase suspicions

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98
Q

Investigations for urethritis

A

first pass urine or urethral smear/swab NAAT

consider urine dipstick to exclude UTI

STI screening

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99
Q

Management of urethritis

A

NGU:
doxycycline BD for 5-7 days or 1g azithromycin stat

Gonococcal urethritis:
IM ceftriaxone ± azithromycin PO

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100
Q

Complications of urethritis

A

epididymitis/orchitis
prostatitis
systemic dissemination of gonorrhoea
reactive arthritis

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101
Q

Epididymo-orchitis

A

an infection/inflammation of the epididymis & the testes usually caused by local spread of a genitourinary tract infection or bladder infections

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102
Q

Aetiology of Epididymo-orchitis

A

Men <35yrs:
STI e.g. chlamydia & gonorrhoea

Men >35yrs:
UTIs e.g. E. coli & pseudomonas

Unvaccinated children:
mumps

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103
Q

Presentation of Epididymo-orchitis

A

unilateral scrotal pain & swelling
pain radiating to ipsilateral flank
if STI related may have urethritis or urethral discharge

NB mumps usually presents with headache, fever, unilateral/bilateral parotid swelling

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104
Q

Important differential for Epididymo-orchitis

A

Testicular torsion:
usually acute, severe unilateral testicular pain & swelling., absent cremaster reflex
usually pts <20y/o
treat Epididymo-orchitis as testicular torsion until proven otherwise

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105
Q

Investigations for Epididymo-orchitis

A

exclude STI (first pass urine NAAT)
if mumps suspected = IgG/IgM serology
urine MC&S
scrotal USS

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106
Q

Management of Epididymo-orchitis

A

If organism as per organism
e.g. ceftriaxone for gonorrhoea or doxycycline for chlamydia

if unknown organism:
500mg ceftriaxone IM + 100mg doxycycline PO

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107
Q

Chancroid

A

primarily sexually transmitted infection caused by fastidious gram-negative coccobacilus Haemophilus ducreyi, generally a tropical disease &more common in men

important co factor for HIV transmission

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108
Q

Causative organism of chancroid

A

Haemophilus ducreyi

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109
Q

Presentation of chancroid

A

4-10 days incubation period
small (1-2cm) painful, shapely demarcated genital ulcers with ragged, undermined edges & a greyish necrotic base
unilateral lymphadenopathy (usually inguinal)

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110
Q

Distinguishing chancroid from syphilis chancre

A

chancre in syphilis = not painful

chancroid = painful

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111
Q

Investigating chancroid

A

usually clinical diagnosis

gram stain / culture of ulcer swabs

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112
Q

Management of chancroid

A

azithromycin or ceftriaxone

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113
Q

Pelvic inflammatory disease (PID)

A

compromises a spectrum of inflammation & infection of the upper female genital tract including the uterus, fallopian tubes, ovaries, surrounding tissue

usually secondary to ascending infection from the endocervix

most common cause of infertility

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114
Q

Aetiology of pelvic inflammatory disease

A

often polymicrobial

most common causes include chlamydia trachomatis & Neisseria gonorrhoea

other causes include gardenella vaginalus, mycoplasma hominis

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115
Q

Risk factors for pelvic inflammatory disease

A 
multiple sexual partners
unprotected sex
history of previous STIs
IUD
termination of pregnancy
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116
Q

Presentation of pelvic inflammatory disease

A 
lower abdo pain
deep dyspareunia
cervical excitation
dysuria
menstrual irregularities 
vaginal discharge
fever
adnexal / cervical motion tenderness
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117
Q

Investigating pelvic inflammatory disease

A

pregnancy test to exclude ectopic pregnancy
high vaginal / cervical swab
Chlamydia & Gonorrhoea screen
ESR/CRP (↑)

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118
Q

Management of pelvic inflammatory disease

A

Oral ofloxacin + metronidazole / IM ceftriaxone + metronidazole

consider IUD removal

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119
Q

Complications of pelvic inflammatory disease

A

Perihepatitis (Fitz-Hugh-Curtis syndrome)
infertility
ectopic pregnancy

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120
Q

Infectious mononucleosis (glandular fever)

A

a usually self limiting infection caused by Epstein-Barr virus (EBV) which is a human herpes virus (HHV 4)

most frequently seen in teenagers & young adults

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121
Q

Presentation of Infectious mononucleosis

A

Classic triad of sore throat, pyrexia, lymphadenopathy (in anterior/posterior neck triangles)

malaise, headache, splenomegaly, hepatitis, lymphocytosis, haemolytic anaemia

maculopapular pruritic rash (in 99% of pts taking ampicillin/amoxicillin whilst having the disease)

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122
Q

Investigating Infectious mononucleosis

A

monospot antibody test (+ve, specific for EBV antibodies)
FBC (lymphocytosis, atypical lymphocytosis)
LFTs (AST & ALT ↑)
heterophiles antibody test (+ve)

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123
Q

Management of infectious mononucleosis

A

avoid contact sports for 8 weeks to ↓ risk of splenic rupture
simple analgesia e.g. paracetamol
avoid alcohol

generally self limiting in 2-4 weeks

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124
Q

Fraser competency

A

The Fraser guidelines are used to assess if patient who has not yet reached 16 years of age is competent to consent to treatment, for example with respect to contraception

The following points should be fulfilled:

1) the young person understands the professional’s advice
2) the young person cannot be persuaded to inform their parents or allow the professional to contact them on their behalf
3) the young person is likely to begin, or continue having, sexual intercourse with or without contraceptive treatment
4) unless the young person receives contraceptive treatment, their physical or mental health, or both, is likely to suffer
5) the young person’s best interests require them to receive contraceptive advice or treatment with or without parental consent

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125
Q

Important points about Fraser competency

A

its a legal obligation to discuss the value of parental support

children under the age of 13 are considered to be unable to consent for sexual intercourse & hence a consultation regarding this age group should automatically trigger child protection measures

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126
Q

Child <13y/o & contraception

A

children under the age of 13 are considered to be unable to consent for sexual intercourse & hence a consultation regarding this age group should automatically trigger child protection measures

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127
Q

Contraceptive of choice in young people

A

Progesterone only implant (Nexplanon)

128
Q

Aims of partner notification

A

treatment of those infected / screening those at risk
↓ re-infection in your pt
preventing onward transmission (i.e. breaking chain of infection)
preventing complications of untreated infections
opportunity to educate & discuss behavioural change

129
Q

Type of partner notification

A

Patient referral:
pt contacts partners themselves

Provider referral:
partner is contacted by clinic (usually health advisor), source pt is not identified

Contractual referral:
in complex situations there may be a mutual agreement of a timeline i.e. if the pt has not unformed the partner by a set date then the clinic will

130
Q

Follow up after partner notification

A

generally pt & partner contacted 1-2 weeks later ti check if treatment was complete, sex has been abstained from, all contact have been accounted for

131
Q

Look back period for partner notification

A

look back period generally 3-6 months
may be longer e.g. secondary syphilis

all contacts in look back period should be informed regardless of condom use

132
Q

Hormone replacement therapy (HRT)

A

the use of low dose oestrogen + progesterone (in a women with a uterus) to alleviate menopausal symptoms

133
Q

Indications for HRT

A

vasomotor symptoms e.g. flushing/insomnia/headaches

premature menopause (continue unti age 50, main aim to prevent osteoporosis)

134
Q

Types of HRT

A

in women with uterus = oestrogen + progestogen
in women without uterus = only oestrogen

give continuous combined regime if amenorrhoea >12 months/sequential HRT received for >12 months
give sequential combined regimes if amenorrhoea <12 months

135
Q

Compounds used in HRT

A

natural oestrogens e.g. estradiol / estrone are used over synthetic oestrogens e.g. ethinylestradiol

synthetic progesterones e.g. levonogestrel are generally used

136
Q

Adverse effects of HRT

A

↑ Risk of breast cancer (further ↑ risk if taking progesterone)

↑ Risk of endometrial cancer (give progesterone in addition to oestrogen in women with a uterus to reduce this risk)

↑ risk of VTE (Transdermal route does not ↑ risk of VTE)

↑ risk of stroke

↑ risk of IHD (if taken >10yrs after menopause)

137
Q

Side effects of HRT

A

nausea
breast tenderness
fluit retention
weight gain

138
Q

Emergency contraception

A

forms of contraception that can be administered within a specific time period after unprotected sexual intercourse (UPSI) to prevent pregnancy

139
Q

Intrauterine device / copper coil as emergency contraception

A

insert within 5 days of UPSI (or if >5 days post UPSI may be inserted up to 5 days after likely ovulation date)

can be left in for longer contraception, but if removal is wanted then wait until next menstrual period

140
Q

Time window after UPSI the intrauterine device can be used as emergency contraception

A

insert within 5 days of UPSI

or if >5 days post UPSI may be inserted up to 5 days after likely ovulation date

141
Q

Levornogestrel (Levonelle) emergency contraception

A

effective up to 72h post UPSI

single dose 1.5mg (double if BMI>26 / weight >70kg)

repeat dose if vomiting within 3h

can be used >1x per menstrual cycle

can commence hormonal contraception immediately after use

142
Q

Time window after UPSI Levornogestrel (Levonelle) can be used as emergency contraception

A

effective up to 72h post UPSI

143
Q

Ulipristal (EllaOne) emergency contraception

A

effective up to 120h post UPSI

single 30mg dose

may ↓ effectiveness of hormonal contraception (start/restart hormonal contraception 5 days after taking EllaOne)

repeat dose possible in same menstrual cycle

144
Q

Time window after UPSI Ulipristal (EllaOne) can be used as emergency contraception

A

effective up to 120h post UPSI

145
Q

Combined oral contraceptive pill (COCP)

A

Examples: Microgynon, Logynon, Qlaira and Zoely

MOA: inhibits ovulation

Risks include: ↑ VTE/stroke risk, ↑ risk of breast cancer, ↑ risk of cervical cancer

Advantages include: ↓risk of endometrial cancer, ↓ risk of ovarian cancer, ↓ risk of colorectal cancer

generally taken for 21 days then 7 day pill free window with withdrawal bleed but can tricycle i.e. take packets back to back to avoid bleeding

146
Q

Combined oral contraceptive pill (COCP) contraindications

A 
>35y/o + smoking >15 cigarettes/day
migraine with aura
breastfeeding <6 weeks postpartum
current breast cancer
previous VTE/thrombogenic mutation
147
Q

starting the Combined oral contraceptive pill (COCP)

A

start within 5 days of start of cycle = no extra precautions needed

if started later in cycle = use additional contraception for 7 days

148
Q

Missed pills Combined oral contraceptive pill (COCP)

A

1 pill missed:
take missed pill i.e. 2 pills in 1 day and continue as normal

≥ 2 pill missed:
take last missed pill i.e. 2 at the same time then continue as normal
missing pill in:
Week 1: consider emergency contraception if unprotected sex in pill free break/week 1
Week 2: no need for emergency contraception
Week 3: finish current packet & omit pill free window

149
Q

Combined oral contraceptive pill (COCP) and surgery

A

discontinue 4 weeks before elective surgery, offer progestogen only contraceptive as alternative

NB does not apply to minor surgery

150
Q

Advantages of Combined oral contraceptive pill (COCP)

A

↓risk of endometrial cancer
↓ risk of ovarian cancer
↓ risk of colorectal cancer

151
Q

Disadvantages of Combined oral contraceptive pill (COCP)

A

↑ VTE/stroke risk
↑ risk of breast cancer
↑ risk of cervical cancer

152
Q

Progesterone only pill (POP)

A

Examples: Desogestrel, Norethisterone

MOA: thickens cervical mucous (desogestrel also inhibits ovulation)

should be taken at same time everyday (>3h late = missed pill), no pill free interval

irregular vaginal bleeding = most common side effect

153
Q

Starting Progesterone only pill (POP)

A

immediate protection if commenced within 5 days of starting cycle

if started after day 5 of cycle take 2 days of additional contraception

154
Q

Missed pills Progesterone only pill (POP)

A

Missed pill = pill >3h late (>12h for Desogestrel)

if pill missed = take pill ASAP (i.e. 2 in one day) & continue with rest of packet, use additional contraception until regular pill taking reestablished for 48h

155
Q

Injectable contraceptive

A

Examples: depo provera

MOA: inhibits ovulation & thickens cervical mucous

duration: 12 weeks (cannot be reversed once given)
contraindications: current breast cancer

side effects include irregular bleeding, ↑ weight*, ↑ risk of osteoporosis

156
Q

Contraceptive method proven to cause weight gain

A

Injectable contraceptive (depo provera)

157
Q

Implantable contraceptive

A

Examples: Implanon, Nexplanon

MOA: inhibits ovulation & thickens cervical mucous

Duration: 3 years

contraindications: current breast cancer

side effects: irregular bleeding or heavy bleeding

158
Q

Implantable contraceptive implant site

A

subdermal implantation into proximal non-dominant arm just overlying the triceps

159
Q

Intrauterine device (IUD)

A

Copper coil

MOA: prevent fertilisation & toxic to sperm (spermicidal)

Duration: 5-10 years (depends on type)

effective immediately after insertion

side effects: periods tend to be heavier, longer & more painful, ↑ risk of PID, expulsion

160
Q

Intrauterine system (IUS)

A

Examples: Mirena coil, Jaydess, Kyleena

MOA: inhibits implantation & prevents endometrial proliferation

Duration: 5 years (Jaydess = 3 years)

effective 7 days after insertion

many pts have infrequent bleeding & spotting early on before menses becomes lighter or absent

NB can be used as endometrial protection (progesterone component) of HRT

161
Q

Combined contraceptive patch

A

Examples: Evra patch

similar to COCP, 4 week cycle, wear patch every day for first 3 weeks and change weekly, then no patch during 4th week leading to withdrawal bleed

If patch changed delayed at end of week 1/2
if <48h: put on new patch immediately and continue
if >48h: change patch immediately + 7 days of barrier contraception, consider emergency contraception if sex during window where patch wasn’t changed or in last 5 days

forgetting patch at end of patch free week = 7 days of additional contraception

162
Q

Post partum contraception time window

A

women require contraception from 21 days post partum

163
Q

Lactational amenorhoea

A

contraceptive method in post partum period

if women fully breastfeed (no supplementary feeds), amenorrhoeic & <6 months post partum

164
Q

Types of post partum contraception

A

Lactational amenorhoea

POP (can bed started any time post partum even if breastfeeding)

COCP (contraindicated in breast feeding & <6 weeks post partum)

IUD/IUS ( can be inserted within 48h of birth or at 4 weeks postpartum)

165
Q

Epilepsy & contraception

A

UKMEC 3 for COCP & POP is people taking lamotrigine, phenytoin, carbamazepine, barbiturates, topiramate

166
Q

Contraception in women aged >40

A

No method of contraception is solely contraindicated by age

167
Q

Women aged <50yrs & contraception

A

Hormonal contraception can be continued till age 50

non hormonal contraception methods can be stopped after 2 yrs amenorrhoea

168
Q

Women aged >50yrs & contraception

A

non hormonal methods can be stopped after 1yr of amenorrhoea

COCP (switch to non-hormonal or progestogen only contraceptive)

Depo-provera (switch to non hormonal method, stop after 2 yrs of amenorrhoea, or switch to progestogen only contraceptive)

Implant/POP/IUS (continue use, if amenorrhoeic check FSH & stop 1 year after if FSH ≥30u/L or stop at age 55)

169
Q

Hepatits A virus (HAV)

A

virus spread by faecal oral route, may be sexually transmitted in MSM or seen in IVDU

2-4 week incubation period

Most common form of acute hepatitis

170
Q

Presentation of Hep A

A

prodrome:
mild flu like symptoms (fever, malaise, joint pain) ± RUQ pain, tender hepatomegaly

Icteric phase:
jaundice, pruritus, dark urine, pale stools, abdo pain

171
Q

Investigations for Hep A virus (HAV)

A

IgM antibody to HAV (+ve from symptoms onset to 3-6 months after)
IgG antibody to HAV (+ve for several years, if only IgG = post infection or vaccination)
LFTs (↑ AST, ↑ALT, ↑ALP)
Bilirubin (↑)

172
Q

Management of Hep A

A

usually self limiting, only needing supportive care

Vaccination available for high risk individuals e.g. MSM or IVDU

173
Q

Hepatits B virus (HBV)

A

viral infection spread by sexual contact, parentally or perinatally

incubation period 6-20 weeks

most common cause of hepatitis world wide

174
Q

Presentation of Hep B

A

acute infection often subclinical with flu like symptoms

symptomatic hepatitis: fever, skin rash, nausea, jaundice, RUQ pain

chronic help B:
detectable surface antigen (HBsAg) >6 months
nausea, fatigue, poor ppetute, non specific abdo pain, ↑ risk of hepatocellular carcinoma

175
Q

Hep B serology

A 
Surface antigen (HBsAg):
implies acute disease (present 1-6 months)
Anti-HBs:
implies immunity (either due to exposure or chronic infection)

Anti-HBc:
previous / current infection (i.e. negative if immunised)

HBeAg:
marker if HBV replication & infectivity

176
Q

Management of Hep B

A

notify health protection unit
1st line: pegylated interferon

Prevention:
Hep B vaccination at 2,3 & 4 months of age + at risk groups e.g. IVDU/healthcare workers/sex workers

177
Q

Hep B & pregnancy

A

Hep B routinely screened for

if chronic/acute infection in mother = full vaccination course + Hep B immunoglobulin for Baby

178
Q

Immunisation of Hep B on serology

A

anti-HBs +ve only

179
Q

Previous Hep B infection but not carrier on serology

A

anti HBc +ve

HBsAg -ve

180
Q

Previous Hep B infection now carrier on serology

A

anti HBc +ve

HBsAg +ve

181
Q

Acute Hep B infection on serology

A

anti-HBc +ve (especially IgM kind)

182
Q

Hepatitis C virus (HCV)

A

virus that may be transmitted via sexual intercourse, especially high risk of HIV confection

incidence rising in UK

no vaccine available

183
Q

Hep C presentation

A

acute infection generally asymptomatic

chronic disease generally mild & unspecific but ↑ risk of HCC, cirrhosis, cryglobulinaemia

184
Q

Hep C investigations

A

HCV RNA test (gold standard)
NB if +ve for >6months = chronic Hep C

anti-HCV antibodies to check for previous infection

185
Q

Hep C management

A

combination of protease inhibitors ± ribavirin

186
Q

Human Immunodeficiency virus (HIV)

A

a retrovirus that targets & destroys CD4 T cells and is the etiological agent of acquired immunodeficiency syndrome (AIDS)

Types:
HIV 1 (responsible for global epidemic)
HIV 2 (restricted to africa)
187
Q

Epidemiology of HIV

A

HIV diagnosis peaked in 2014 in UK, has been declining since

affects ~38million people globally

188
Q

Routes of transmission of HIV

A

sexual (~80% of infections worldwide)

parenteral

vertical transmission from mother to child (during birth/breastfeeding)

189
Q

Risk factors for HIV infection

A 
needle sharing for IVDU
unprotected receptive anal intercourse
unprotected receptive penile-vagnial intercourse 
needle stick injury
high maternal vial loads
MSM
190
Q

Pathophysiology of HIV infection

A

HIV enters body & attaches to CD4 receptors on target cells with its gp120 glycoprotein

viral envelop fuses with host cell using coreceptor CCR5/CXCR4

viral RNA is transcribed into dsDNA by viral reverse transcriptase & then integrated into the DNA by viral integrase

genomic RNA is used to replicate virus

viron repurposes part of cell membrane as envelope & lead cell = cell death & release of virons to infect more cells

191
Q

Window period for acute HIV infection

A

4 weeks

192
Q

Acute primary HIV infection (seroconversion illness)

A

1-6 weeks post infection

presents with fever, malaise, myalgia, pharyngitis, headaches, diarrhoea, neuralgia, neuropathy, lymphadenopathy, fatigue
maculopapular rash

NB antibody test generally negative but viral P24 antigen & HIV RNA ↑

193
Q

Time between infection with HIV & seroconversion illness

A

1-6 weeks

194
Q

tests for HIV seroconversion illness

A

HIV antibody test -ve
Viral p24 antigen ↑
HIV RNA ↑

195
Q

Clinical latency stage of HIV

A

asymptomatic stage after acute seroconversion illness
generally low viral loads & normal CD4/CD8 count

may persist for 8-10 yrs

196
Q

Symptomatic HIV stage (latency stage)

A

non specific constitutional symptoms e.g. fever, night sweats, diarrhoea, weight loss

Non-AIDS defining conditions (CD4 count <500cells/mm3)
e.g. chronic subfebrile temperature, persistent generalised lymphadenopathy, chronic diarrhoea (>1 month)

localised opportunistic infection e.g. oral candida, oral hairy leukoplakia, HPV related lesion (warts, SCC of anus), tine infections

197
Q

Acquired immunodeficiency syndrome (AIDS)

A

a person developing serious opportunistic infections or disease as a result their damaged immune system from advanced symptomatic HIV (stage 3)

severe immunodeficiency

CD4 count generally <200 cell/μL

198
Q

Persistent generalised lymphadenopathy

A

enlargement of ≥2 non contigous lymph node groups for >6 months usually non tender

sign of symptomatic HIV infection

199
Q

Oral candida

A

may be a sign of symptomatic HIV infection

creamy white patches in the mouth that can be scrapped off, may be tender, erythematous
pt may have cotton feeling in mouth
redness, soreness, fissuring may occur at angle of mouth

managed with topical solutions or oral fluconazole

200
Q

Oral hair leukoplakia

A

may be a sign of symptomatic HIV infection

triggered by EBV, similar to oral candida, creamy white patches in mouth but unlike candida they cannot be scrapped off

201
Q

CDC classification of HIV

A

1993 CDC classification of HIV in adults stages according to CD4 count & clinical category

CD4 count:
normal: 500-1500 cells/mm3
category 1: ≥500 cells/mm3
category 2: 200-499 cells/mm3
category 3: <200 cells/mm3

Clinical category
Category A: asymptomatic infection, persistent generalised lymphadenopathy (PGL) or acute HIV infection

Category B: symptomatic HIV i.e. HIV indicator conditions

Category C: AIDS defining conditions

NB categories A3,B3,C1,C2,C3 has AIDS

202
Q

Category A of CDC classification of HIV

A

asymptomatic infection, persistent generalised lymphadenopathy (PGL) or acute HIV infection

203
Q

Category B of CDC classification of HIV

A

symptomatic HIV i.e. HIV indicator conditions e.g. oral candida/ oral hairy leukoplakia, chronic diarrhoea

204
Q

Category C of CDC classification of HIV

A

AIDS defining conditions e.g. oesophageal candidiasis, Kaposi sarcoma etc

205
Q

CD4 count ranges for CDC classification of HIV

A

normal: 500-1500 cells/mm3
category 1: ≥500 cells/mm3
category 2: 200-499 cells/mm3
category 3: <200 cells/mm3

206
Q

AIDS defining conditions

A
  • Candidiasis of the esophagus, bronchi, trachea, or lungs
  • Cervical cancer, invasive
  • Coccidioidomycosis, disseminated or extrapulmonary
  • Cryptococcosis, extrapulmonary
  • Cryptosporidiosis, chronic intestinal (greater than one month’s duration)
  • Cytomegalovirus disease or CMV (other than liver, spleen, or nodes)
  • Cytomegalovirus retinitis (with loss of vision)
  • Encephalopathy, HIV related
  • Herpes simplex: chronic ulcer(s) (more than 1 month in -duration); or bronchitis, pneumonitis, or esophagitis
  • Histoplasmosis, disseminated or extrapulmonary
  • Isosporiasis, chronic intestinal (more than 1 month in duration)
  • Kaposi sarcoma
  • Lymphoma, Burkitt’s (or equivalent term)
  • Lymphoma, immunoblastic (or equivalent term)
  • Lymphoma, primary, of brain
  • Mycobacterium avium complex or M kansasii, disseminated or extrapulmonary
  • Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary)
  • Mycobacterium, other species or unidentified species, disseminated or extrapulmonary
  • Pneumocystis pneumonia (PCP)
  • Pneumonia, recurrent
  • Progressive multifocal leukoencephalopathy
  • Salmonella septicemia, recurrent
  • Toxoplasmosis of brain
  • Wasting syndrome due to HIV
207
Q

Investigations for HIV

A

HIV antibody detection (ELISA)
FBC (anaemia, thrombocytopenia, lymphocytopenia, ↓CD4 count)
check other infections (TB/Hep B/CMV/toxoplasma/syphillis/varicella)
STI screening
baseline CXR
cervical smear

208
Q

Diagnosis of HIV

A

based on anti-HIV antibodies in serum (IgG/IgM antibodies against HIV virus)
should be positive

209
Q

Diagnosis fo acute HIV infection

A

anti-HIV antibodies may not be present

HIV PCR & p24 antigen tests are used, these are positive before appearance of HIV antibodies

210
Q

Testing recommendations for HIV

A

Test people at ↑ risk of HIV:
MSM, female partners of MSM, black african, people who inject drugs, sex workers, prisoner, trans women, people form countries with high HIV seroprevelance + their sexual partners

test people attending health services who’s users have associated risk of HIV:
e.g. GUM/TB/hepatitis/lymphoma clinics, antenatal clinics, TOP services, addiction/substance misuse services

all people with symptoms and/or signs consistent with HIV indicator conditions

people accessing healthcare in areas with high seroprevalence (>5/1000)

211
Q

Oesophageal candidiasis

A

AIDS defining condition

resents with dysphagia, odynophagia of solids & fluids, retrosternal pain
often also concomitant oral candidiasis

diagnosed via endoscopy

management = 14-21 days of oral fluconazole (if severe IV fluconazole or IV echinocandin)

212
Q

Systemic candidiasis (candidaemia / disseminated candidiasis)

A

live threatening (up to 40% mortality)

presents similar to bacterial sepsis i.e. fever, chills, fatigue, headache, myalgia, end organs infection e.g. pneumonia, meningitis or endocarditis

investigated with blood cultures, serology, imaging

Managed with IV fluconazole/echinocandia

213
Q

Pneumocystis pneumonia (PCP)

A

Pneumocystis jirovecii penumonia is an infection of the lung caused by the fungal organism pneumocystis jirovecii

leading AIDS defining illness, in ~50% of pts PCP is the first manifestation of AIDS

most common opportunistic infection of AIDS

214
Q

Risk factors for Pneumocystis pneumonia (PCP)

A

CD4 count <200 cells/mm3
other AIDS defining illnesses
poor compliance with PCP prophylaxis / retrovirals
malnutrition

215
Q

Presentation of Pneumocystis pneumonia (PCP)

A

dyspnoea (especially exertional)
non productive cough
tachypnoea
low grade fever, malaise, fatigue, chills, weight loss

Very few chest sign on examination (often normal respiratory exam, may have ↓ sats at rest)

NB if extra pulmonary disease (rare) = hepatomegaly, lymphadenopathy, ocular disease

216
Q

Investigating Pneumocystis pneumonia (PCP)

A

Induced sputum / bronchoscopy & bronchoalveolar lavage (+ve for pneumocystis, NB sputum is often negative)

Chest X-ray (bilateral interstitial pulmonary infiltrates, may show pneumothorax or bilateral perihilar shadowing)

LDH (↑)
ABG (↓O2)
CD4 count (<200cells/mm3)

217
Q

Management of Pneumocystis pneumonia (PCP)

A

1st line: Co-trimoxazole

2nd line: IV pentamidine (severe cases)

NB Co-trimoxazole = trimethoprim + sulfamethoxazole

218
Q

Prevention of Pneumocystis pneumonia (PCP)

A

PCP prophylaxis is given to all HIV pts with CD4 count <200cells/mm3

prophylaxis with oral co-trimoxazole

219
Q

Common complication of Pneumocystis pneumonia (PCP)

A

pneumothorax

220
Q

Cryptococcosis

A

opportunistic fungal infection with cryptococcus neoformans, common cause of HIV related meningitis

AIDS defining illness, associated with bird droppings (especially pigeons)

most often seen in pts with CD4 count <100cells/mm3

221
Q

Presentation of Cryptococcosis

A

meningitis/menigoencephalitis:
headache, confusion, altered mental state, coma, seizures,
neurological signs (diplopia, ataxia, aphasia, signs of ↑ ICP)
Meningism (neck stiffness, photophobia, headache)

222
Q

Investigations for Cryptococcosis

A

CSF/blood/urine cultures

cryptococcus antigen titres (from CSF/serum)

MRI brain (soap bubble lesions in brain, hydrocephalus, cysts)

223
Q

Management of Cryptococcosis

A

Induction:
amphotericin B + flucytosine

consolidation:
PO fluconazole

Maintenance:
low dose fluconazole for several months

224
Q

Cryptosporidosis

A

AIDS defining protozoal infection with cryptosporidium hominis & cryptosporidium pavuum

presents as water diarrhoea, abdo cramps, low grade fever, nausea lasting up to a month)

generally seen in CD4 count 200-500cells/mm3 but may be severe if CD4 count <50cells/mm3 (i.e. more chronic)

diagnosis with cryptosporidium oocytes (acid fast cysts) & +ve cryptosporidium antigen test

managed with HAART (as hard to eradicate if CD4 count<200cells/mm3) + nitazoxamide/paromocyin

225
Q

Toxoplasmosis

A

AIDS defining infection caused by protozoal parasite toxoplasma gondii, one of the most common human parasites, leading to encephalitis

often seen if CD4 count <200cells/mm3

cerebral toxoplasmosis = most common neurological AIDS defining condition

226
Q

Toxoplasmosis presentation

A

generally asymptomatic if immunocompetent

cerebral toxoplasmosis (toxoplasmosis encephalitis):
fever, headache, seizures, focal neurological deficits, mental state changes, cerebellar sign
usually a reactivation 
ocular toxoplasmosis (chorioretinitis)
yellow-white retinal lesions, marked vitreous retraction, visual field deficits, ↓ visual acuity 
usually cute infection
227
Q

Toxoplasmosis investigations

A

serology (anti-toxoplasmosis IgM/IgG

contrast CT/MRI brain (multiple ring enhancing lesions = brain abscesses, often in basal ganglia)

228
Q

Toxoplasmosis management

A

pyrimethamine +sulfadiazine + folinic acid

prevention with dapsone + pyrimethamine

229
Q

Cytomegalovirus (CMV)

A

A member of the herpes virus family that will infect the majority of human, after primary infection establishes lifelong latency

HIV pts with CD4 count <50/mm3 are at risk of reactivation

230
Q

Presentation of cytomegalovirus (CMV)

A

CMV retinitis:
most common CMV manifestation in HIV pts
floaters, photopsia, visual field deficits, painless visual loss
usually unilateral
yellow, white areas with perivascular exudates & haemorrhages on ophthalmoscopy

NB other presentations include CMV pneumonia (interstitial pneumonitis) & GI manifestations

231
Q

Investigations for cytomegalovirus (CMV)

A

histopathology:
owls eye appearance, due to large intranuclear inclusion body

serology:
anti-CMV IgG/IgM (not useful if immunosuppressed)

PCR for CMV DNA

232
Q

Management of cytomegalovirus (CMV)

A

treatment:
valganciclovir / ganciclovir / foscarnet
Cidofivir if resistant CMV

+ optimise antiretroviral therapy

Prophylaxis:
valganciclovir or ganciclovir

233
Q

Tuberculosis in HIV

A

infection caused by mycobacterium tuberculosis, may occur at any CD4 count

↑ chance of extra pulmonary TB or atypical presentation

often due to reactivation of latent TB

234
Q

TB in HIV presentation

A

generally disseminated TB with chest involvement & generalised lymph node involvement

fever, fatigue, night sweats, weight loss
productive cough, haemoptysis, SOB, pleuritic chest pain
lymphadenitis i.e. generalised lymphadenopathy with firm enlarged nodes
sterile pyuria
potential CNS involvement

235
Q

Investigations for TB

A

CXR (usually apical lesion or millet seed like profile of biliary TB)

Sputum smear (acid fast bacilli on Ziehl-Nielsen stain)

sputum culture

236
Q

Management of TB in HIV

A

Treatment:
2 months of Rifampicin + Isoniazid + Pyrazinamide + Ethambutol
Then 4 months of Rifampicin + Isoniazid

Prophylaxis:
isoniazid prophylaxis recommended for at risk HIV pts

NB drug resistant TB is an issue with HIV pts

237
Q

Myobacterium avian complex (MAC) / Myobacterium avian intracellulare (MAI)

A

opportunistic infection of immunocompromised individuals usually with CD4 count <50cells/mm3

seen in up to 40% of AIDS pts

238
Q

Presentation of Myobacterium avian complex (MAC)

A

3 syndromes: disseminated MAC, Pulmonary MAC, MAC lymphadenitis

Disseminated MAC*: (most commonly seen in HIV)
diarrhoea, malaise, fever, significant weight loss, wasting, fever, sweats, pallor, tender hepatosplenomegaly, generalised lymphadenopathy

Pulmonary MAC: cough, ↑sputum production, dyspnoea, haemoptysis, fever, night sweats

MAC lymphadenitis: cervicofacial lymphadenopathy

239
Q

Investigations for Myobacterium avian complex (MAC)

A

FBC (↓Hb, ↓CD4) albumin (↓)

sputum/blood/bone marrow culture (+ve for MAC growth)

CT/USS abdo (lymphadenopathy + hepatosplenomegaly)

CT chest (thin walled cavitary lesions of upper lobes)

240
Q

Management of Myobacterium avian complex (MAC)

A

Treatment:
12 months course of Abx (clarithromycin/erythromycin + ethambutol + rifabutin)

Prophylaxis:
macrolide (azithromycin / clarithromycin) until CD4 count >100cells/mm3

241
Q

Microsporidiosis

A

caused by microsporidium (in HIV pts)

presents with low volume diarrhoea

diagnosed on immunofluorescent staining of stool

managed with HAART, erythromycin

242
Q

Isosporiasis

A

caused by isosporiasis belli

causes watery diarrhoea, abdo pain, fatigue, weight loss

treat with co-trimoxazole

243
Q

Aspergillosis

A

uncommon in HIV unless CD4 count <30

presents with cough, fever, dyspnoea

Cavitating lesions on CXR

treated with amphoteracin B or itraconazole

244
Q

HIV wasting syndrome

A

unintentional weight loss ≥10%, fatigue, fever, diarrhoea

due to variety of factors

245
Q

Histoplasmosis

A

infection caused by histoplasmosis capsulate, in HIV usually a reactivation of latent disease

usually seen in CD4 count <200

246
Q

Histoplasmosis presentation

A

fever, weight loss, erythema nodosum, lymphadenopathy, hepatosplenomegaly, non productive cough, pleuritic chest pain, ulcerative oral lesions

247
Q

Investigation & management of Histoplasmosis

A

CXR (diffuse nodular density, focal infiltrate/cavity)
fungal blood cultures

managed with itraconazole

248
Q

Bacterial pneumonia in HIV

A

common causes include

  • strep pneumoniae (characterised by rusty sputum, but can be prevent with pneumovax)
  • H.influenzae
  • mycoplasma pneumoniae
  • Staph aureus (especially in IVDU/advanced HIV, may cause cavitating lesions)

presentation is often atypical
CXR often shows diffuse infiltrates

249
Q

At what CD4 counts do vaccinations become ineffective

A

CD4 count <200 makes many vaccines ineffective

250
Q

Progressive multifocal leukoencephalopathy (PML)

A

progressive demyelinating condition caused by Joh Cunningham virus (JC virus) due to oligodendrocytes being infected with JC virus

presents with seizures, behavioural change, speech/motor/visual impairment, other focal neurological deficits, impaired vigilance

MRI shows disseminated non enhancing white matter lesions without mass effect, scalloping at grey-white matter interface), CSF (+ve for JC virus DNA on PCR)

no treatment available

251
Q

HIV associated neurocognitive disorders (HAND)

A

due to HIV virus directly infection nervous system i.e. AIDS dementia, typically seen in untreated pts with advanced HIV infections

leads to subcortical dementia presenting with memory loss, depression, movement disorders, bradykinesia, impaired vigilance, aphasia, gait disturbance

investigated with MRI/CT (cortical/subcortical atrophy + multiple subcortical non enchaining lesions)

managed with early use of antiretroviral therapy

252
Q

Herpes simplex virus & HIV

A

usually atypical presentations in HIV pts

e.g. chronic oral/genital ulcers (>1 month) or may cause encephalitis or herpes simplex keratitis (blurry vision, painful watery eyes, dendritic corneal ulcer)

management with aciclovir

NB chronic mucocutaneous herpes (>4 weeks) = AIDS defining

253
Q

Molluscum contagiosum & HIV

A

common skin infection causing pinkish/pearly white papules with central umbilication,

lesions on face/eyes indicate immunosuppression and may be seen in HIV pts

treatment is imiquimod

254
Q

Human papilloma virus & HIV

A

HIV +ve women are advised to have yearly cervical cytology due to ↑ risk of developing cervical cancer

invasive cervical cancer = HIV defining diagnosis

presents as postcoital/intramenstrual/postmenopausal bleeding, vaginal discharge

255
Q

Kaposi sarcoma

A

connective tissue cancer caused by human herpes virus 8 (HHV-8) also known as Kaposi’s sarcoma associated herpes virus (KSHV)

characterised by neoplastic cells & abnormally growing blood vessels

256
Q

Presentation of kaposi sarcoma

A

multiple visceral / cutaneous elevated tumours with rapid growth

initial stage:
painless, non pruritic violet/red/brown/black papules or nodules on skin/mucosa usually moth/nose/throat/face/chest

lesions may also involve internal organs e.g. lungs (dyspnoea, haemoptysis, pleural effusion), GI tract (can cause fatal bleed)

257
Q

Investigations of Kaposi sarcoma

A 
skin biopsy (spindle cells*, angiogenesis, leukocyte infiltration)
CXR/Abdo USS/bronchoscopy/endoscopy 
consider HHV-8 serology
258
Q

Management of Kaposi sarcoma

A

HAART = vital (lesions may spontaneously resolve after immune reconstitution)
radio/chemo/cryotherapy

259
Q

Non-Hodgkins lymphoma in HIV

A

high grade B cell lymphomas are common in HIV population

presents as rapidly growing, bulky, painless lymphadenopathy, easy bruising, hepatosplenomegaly, fever, night sweat, weight loss

FBC (thrombocytopenia, pancytopenia, lymphocytosis), blood smear (nucleated RBCs), lymph node/bone marrow biopsy (monomorphous lymphocytic proliferation)

treated with chemo & opportunistic infection prophylaxis as CD4 count will drop

260
Q

Primary CNS lymphoma in HIV

A

extra nodes non Hodgkins lymphoma associated with EBV infection, usually seen with CD4 count <100

presents with symptoms of ↑ICP (seizures, papilloedema, headache), lethargy, focal neurological deficits, personality changes, confusion

CT contrast shows (solitary solid enhancing lesion with homogenous enhancement)
Thalium SPECT (+ve), CSF (+ve for EBV DNA)

managed with wholegrain radiotherapy, dexamethasone (↓ tumour size)

even treated the survival is <1 year

261
Q

Primary CNS lymphoma vs toxoplasmosis

A

Toxoplasmosis = multiple enhancing lesions on contrast CT & negative Thalium SPECT

Primary CNS lymphoma = single enhancing lesions on contrast CT & positive Thalium SPECT

262
Q

HIV peripheral neuropathy

A

can occur at any stage of HIV infection but more common in advanced disease, due to direct infection of nerves by HIV

presents as symmetrical distal numbness & pain in lower limbs, usually strength is preserved, reflexes are absent or ↓, pain & temp sensation is impaired

may also cause autonomic symptoms such as postural hypotension, impotence, bladder dysfunction or diarrhoea

managed with gabapentin for neuropathic pain

263
Q

HIV assoicated nephropathy (HIVAN)

A

classically a collapsing focal segmental glomerulosclerosis due to direct infection of kidneys with HIV

usually seen in pts with CD4 count<200 & detectable viral loads

causes nephrotic syndrome (Proteinuria (> 3g/24hr), Hypoalbuminaemia (< 30g/L), Oedema) & progressive kidney failure (↓ eGFR)

managed with HAART or transplant

NB black individuals with HIV are more commonly effected

264
Q

Nucleoside reverse transcriptase inhibitors (NRTIs) examples

A 
emtricitabine (FTC)
Lamivudine (3TC)
abacavir 
zidovudine (AZT)
Stavudine (d4T)
didanosine (ddI)
tenofivir

NB Tenofivir alafenamide (TAF) = tenofivir pro drug

265
Q

Class of drugs for emtricitabine (FTC), Lamivudine (3TC), abacavir , zodofivir (AZT), Stavudine (d4T), didanosine (ddI), tenofivir

A

Nucleoside reverse transcriptase inhibitors (NRTIs)

266
Q

MOA of Nucleoside reverse transcriptase inhibitors (NRTIs)

A

act as nucleoside analogues = competitive blockage of nucleoside binding to reverse transcriptase leading too termination of the viral DNA chain and preventing viral RNA being transcribed into DNA

267
Q

Zidovudine (NRTI) side effects

A 
bone marrow suppression (anaemia, neutropenia)
lipoatrophy
peripheral neuropathy 
skin/nail pigmentation
lactic acidosis
hepatic stenosis
268
Q

Stavudine (NRTI) side effects

A 
lipoatrophy
peripheral neuropathy 
pancreatitis 
lactic acidosis
hepatic stenosis
269
Q

Didanosine (NRTI) side effects

A

peripheral neuropathy

pancreatitis

270
Q

Rarely used NRTIs in HIV

A

Zidovudine, stavudine, didanosine

271
Q

Emtricitabine (NRTI) side effects

A

reversible skin pigmentations

272
Q

Abacavir (NRTI) side effects

A

~5% of pts have life threatening hypersensitivity reaction associated with HLA-B5701

273
Q

Tenofivir (NRTI) side effects

A 
renal dysfunction (glycosuria, subnephrotic proteinuria, ↑ creatinine)
↓ bone mineral density

NB the prodrug TAF has ↓ nephrotoxicity

274
Q

antiretroviral causing life threatening hypersensitivity reaction

A

Abacavir (NRTI)

~5% of pts have life threatening hypersensitivity reaction associated with HLA-B5701

275
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs) examples

A 
nevirapine
efavirenz
etravarine
rilpivirine 
doravirine
276
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs) MOA

A

noncompetitive inhibitors of viral reverse transcriptase that bind at separate location to NRTIs

277
Q

Nevirapine (NNRTI) side effects

A

rash (potentially SJS)

hepatotoxicity (contraindicated in Hep B/C confection)

278
Q

Efavirenz (NNRTI) side effects

A 
CNS toxicity (confusion, vivid/disturbing dream/somnolence)
teratogenic
279
Q

Antiretroviral contraindicated in Hep B/C coinfection

A

Nevirapine as it is hepatotoxic

280
Q

Protease inhibitors (PI) examples

A 
darunavir
atazanavir 
lopinavir 
ritonavir
tipranavir

NB ritonavir, tipranavir are now rarely used

281
Q

Protease inhibitors (PI) MOA

A

inhibition of viral HIV-1 protease =inability to cleave viral mRNA into functional units = synthesis of impaired viral proteins = production of immature (non-infective) visions

282
Q

Protease inhibitors (PI) administration

A

PIs are always given with low dose ritonavir (as it inhibits cytochrome P450) to ↑ intracellular concentration of the drug

known as boosted PI

283
Q

Fusion inhibitors examples

A

Enfuvirtide (T-20) (given BD via SC injection)

NB fusion inhibitors are reserved for those with highly drug resistant HIV

284
Q

Fusion inhibitors MOA

A

competitively binds to viral protein gp41 & thereby prevents fusion with cells

285
Q

Fusion inhibitors side effects

A

skin irritation at injection site (enfuvirtide)

286
Q

Integrase inhibitors examples

A

raltegravir
elvitegravir
dolutegravir
bictegravir

287
Q

Integrase inhibitors MOA

A

inhibit viral integers = blockade of viral DNA integration into hosts DNA = inhibition of viral replication

288
Q

Integrase inhibitors side effects

A

↑ creatine kinase

raltegravir (muscle pain, rhabdomyolysis)

dolutegravir (mood/sleep disturbances)

289
Q

Co-receptor antagonists examples (ART)

A

Maraviroc (CCR5)

290
Q

Co-receptor antagonists MOA

A

blocks CCR5 co-receptor onT-cells & monocytes that is essential for cell infection = inhibits gp120 interaction = prevents irons docking to cell

291
Q

Co-receptor antagonists side effects

A

hepatotoxicity

allergic reaction

292
Q

Weight gain on antiretroviral therapy

A

Agents such as Tenofivir alafenamide (TAF)

293
Q

Weight gain on antiretroviral therapy

A

Agents such as Tenofivir alafenamide (TAF) is more associated with weight gain that tenofivir

integers inhibitors especially raltegravir are associated with weight gain

294
Q

Indications for anti retroviral therapy

A

all persons with HIV regardless of CD4 count should be started on ART

prioritise ART if:
CD4 count <350
high viral load
presence of AIDS defining illness

295
Q

antiretroviral therapy regimes

A

2 NRTIs plus 1 ritonavir boosted PI / 1 NNRTI / 1 integrase inhibitors

296
Q

Switching antiretroviral therapy

A

deterioration of condition may require switching of therapy or adding a further ART

virological failure = persistently detectable HIV viral load on ART

new regime should be guided by HIV resistance testing & previous ART

297
Q

Drug interactions of Protease inhibitors

A

inhibit P450

298
Q

Drug interactions of Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

A

potent liver enzyme inducer = ↓ levels of other drugs

299
Q

Drug interactions of Nucleoside reverse transcriptase inhibitors (NRTIs)

A

exacerbate cytopenic effect of chemo

300
Q

Indications for post exposure prophylaxis (PEP)

A
  • needle stick injury especially with HIV contaminated instrument / needles
  • contamination of open wound / mucous membrane with HIV contaminated fluid e.g. bites
  • unprotected sexual activity with a known / potentially HIV infected person
  • sexual assault (↑ risk of HIV transmission)
301
Q

Timing of post exposure prophylaxis (PEP)

A

ASAP / within 1-2h of exposure = ideal

> 72h after exposure = ineffective / ↓effectivity

NB for non occupational exposure the timing is usually later (~23h)

302
Q

When post exposure prophylaxis (PEP) is needed

A

receptive / insertive vaginal & anal sex
fellatio with ejaculation
splash of semen into eye with HIV +ve individual
receptive anal sex with a person of unknown status from a group with high HIV prevalence

NB PEP is not needed if fellatio without ejaculation or cunilingus even with HIV +ve individual

303
Q

post exposure prophylaxis (PEP) follow up

A

HIV tests at 3 & 6 months post exposure
repeat Hep B/C & syphilis serology
monitor for drug toxicity (FBC/U&Es/LFTs)

Important to facilitate completion of PEP regime

304
Q

Treatment as prevention (TAsP)

A

when HIV +ve individual pt takes ART it ↓ their oral load
when pt with undetectable viral load for >6months = virus cannot be passed on unisexual encounters

if undetectable viral load = untransmissable = TAsP

i.e,. treating pt with ART to reduce viral loads & ↓ rate of new HIV infections (essentially TAsP is too protect others)

305
Q

Pre exposure prophylaxis (PrEP) eligibility

A

negative HIV test result & no signs/symptoms of acute HIB infection

normal renal function

indications met for PrEP

306
Q

Pre exposure prophylaxis (PrEP) indications

A

MSM:
condomless anal sex in last 6 months / sex with HIV +ve partner (unless partner on TAsP)

heterosexual men & women:
sexually active with HIV +ve partner, inconsistent / no condom use with one/more sexual partners of unknown HIV status

MSM & heterosexual men & women who had STI in last 6 months

IVDU with high risk needle behaviour (e.g. needle sharing) or HIV +ve injection partner

307
Q

Pre exposure prophylaxis (PrEP) indications

A

MSM:
condomless anal sex in last 6 months / sex with HIV +ve partner (unless partner on TAsP)

heterosexual men & women:
sexually active with HIV +ve partner, inconsistent / no condom use with one/more sexual partners of unknown HIV status

MSM & heterosexual men & women who had STI in last 6 months

IVDU with high risk needle behaviour (e.g. needle sharing) or HIV +ve injection partner

308
Q

Pre exposure prophylaxis (PrEP) follow up

A

HIV test every 3 months
STI screening every 3 months
renal assessment at baseline & every 6 months
counselling on adherence & risk reduction

309
Q

HIV & pregnancy

A

due to ↑ incidence of HIV infection amongst heterosexual population there are ↑ number of HIV +ve women giving birth

aim of treating pregnant HIV +ve women is to minimise harm to both mother & baby + ↓chance of vertical transmission

310
Q

Interventions to reduce transmission of HIV in pregnancy

A

early HIV diagnosis (via testing at antenatal screening)

HAART to ↓ viral load during pregnancy (offered to all women regardless if they have taken it previously)

continue HAART after delivery

infant feeding (bottle feeding)

delivery via elective C-section at 38 weeks

AZT (zidovudine) monotherapy for 4 weeks post term for baby

AZT infusion started 4h before C-section

exclusive formula feeding (breastfeeding contraindicated)

311
Q

HIV transmission in pregnancy

A

usually occurs late in pregnancy at time of deliver or via breastfeeding

without intervention mother-to-child transmission rate is 15-20%

312
Q

Delaying planned C-section in HIV +ve pregnancies

A

preplanned C section should be delayed to 39 weeks if maternal viral loads <50 copies/ml to ↓ risk of Transient Tachypnea of the Newborn (TTN)

313
Q

HIV mother-to-child transmission rate with intervention

A

rate is <1%

314
Q

Considering vaginal delivery in HIV +ve pregnancy

A

if maternal viral load is <50 copies/ml at 36 weeks but the preferred method is still C-section

315
Q

Pubic lice (crabs)

A

crab’-shaped, grey-brown in colour,and about 2 mm in length which transmitted by close body contact

presents as finding of lice / eggs, itchy red papules, itching usually worse at night

managed with two applications of malathion 0.5% aqueous lotion or permethrin 5% dermal cream, seven days apart.

Year 4 (12 decks)

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