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
Lymphogranuloma venereum
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
26
Lymphogranuloma venereum causative organism
L1/L2/L3 serovars of chlamydia trachomatis
27
Lymphogranuloma venereum (LGV) vs Chlamydia causative organisms
LGV: L1/L2/L3 serovars of chlamydia trachomatis Chlamydia: D-K serovars of chlamydia trachomatis
28
Risk factors for Lymphogranuloma venereum (LGV)
MSM unprotected sex receptive/insertive anal intercourse multiple sexual partners
29
Presentation of Lymphogranuloma venereum (LGV)
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
30
Investigation of Lymphogranuloma venereum (LGV)
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
31
Management of Lymphogranuloma venereum (LGV)
Doxycycline (100mg BD for 21 days) | Buboes may require surgical drainage)
32
Chlamydia
A common STI caused by chlamydia trachomatis servars D-K refers to chlamydia genitourinary infections
33
Most prevalent STI in the UK
Chlamydia most common in sexually active people <25y/o
34
Risk factors for chlamydia
``` age <25 ≥ 2 sexual partners in previous year recent change in sexual partners no barrier contraception infection with other STIs poor socioeconomic status ```
35
Presentation of chlamydia in females
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
36
Presentation of chlamydia in males
50% asymptomatic urethritis (dysuria, urethral discharge) epididymo-orchitis (unilateral testicular pain ± swelling) proctitis (perianal fullness) fever
37
Investigating chlamydia
NAAT of vulvovaginal swab (women) or first void urine sample (men) 2 week window period
38
Window period for chlamydia
2 weeks
39
Complications of chlamydia
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)
40
Human papillomavirus (HPV) (focus on genital warts)
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
41
Human papillomavirus (HPV) serotypes causing warts
6 & 11
42
Fitz-Hugh-Curtis syndrome
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
43
Most common viral STI in UK
Human papillomavirus (HPV)
44
Risk factors for genital warts
``` 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
45
Presentation of Genital warts (HPV)
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
46
Investigations for genital warts (HPV)
speculum exam in women proctoscopy (if unreceptive sex) biopsy & viral testing (if uncertain diagnosis or treatment resistance)
47
Genital warts in children
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
48
Prevention of HPV
HPV vaccination with Gardasil (quadrivalent covering type 6,11,16,18) given to all boys & girls aged 11-13
49
Management of genital warts (HPV)
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%
50
Genital warts in children
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
51
Prevention of HPV
HPV vaccination with Gardasil (quadrivalent covering type 6,11,16,18) given to all boys & girls aged 11-13
52
Treatment of genital warts in pregnancy
Treatment of choice = cryotherapy Imiquimod & Podophyllotoxin = contraindicated in pregnancy
53
Molluscum contagiosum
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
54
Presentation of Molluscum contagiosum
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)
55
Investigation of Molluscum contagiosum
usually clinical diagnosis consider HIV testing if widespread/facial/lesions in adults
56
Management of Molluscum contagiosum
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
57
Scabies
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
58
Risk factors for scabies
``` overcrowding poverty poor nutritional status homelessness poor personal hygiene institutionalisation dementia sexual contact immunosuppression children ```
59
Presentation of scabies
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
60
Investigations for scabies
largely clinical diagnosis histological examination of skin scrapping = confirmatory
61
Management of scabies
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
62
Crusted (Norwegian) scabies
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
63
Gonorrhoea
An STI caused by the bacteria Neisseria gonorrhoea that leads to genitourinary tract infections such as urethritis, cervicitis, PID, epididymitis
64
Gonorrhoea
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
65
Window period for gonorrhoea
2 weeks
66
Risk factors for gonorrhoea
``` young age history of previous STI new/,multiple partners recent sexual activity abroad history of drug use commercial sex work MSM ```
67
Presentation of gonorrhoea in women
endocervical (asymptomatic or PV discharge ± lower abdo pain) urethral (dysuria but no frequency) Rectal (asymptomatic) pharyngeal (asymptomatic)
68
Presentation of gonorrhoea in men
urethritis (discharge ± dysuria) Rectal (usually asymptomatic or discharge ± perianal pain & pruritis) pharyngeal (asymptomatic) epididymal (unilateral scrotal pain & swelling)
69
Investigations for gonorrhoea
NAAT (endocervical smear in women, first pass urine in men) 2 week window period other STI screen & GUM
70
Management of gonorrhoea
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)
71
Complications of gonorrhoea
``` PID infertility Fitz-Hugh-Curtis syndrome septic arthritis (most common cause of optic arthritis in young sexual active people) Disseminated gonococcal infection ```
72
Disseminated gonococcal infection (DGI)
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
73
Vaginal candida (thrush)
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
74
Causative organism for thrush
~80% are caused by candida albicans
75
Risk factors for thrush
``` pregnancy diabetes mellitus vaginal foreign body immunosuppression (e.g. HIV) imbalance of local flora e.g. from Abs use steroid use ```
76
Presentation of thrush
``` erythematous vuvla & vagina pruritis vulvae vulval soreness white, crumbly, sticky vaginal discharge (like cottage cheese), typically non offensive / odourless superficial dyspareunia dysuria ```
77
Investigations for thrush
``` clinical examination / no swabs required vaginal pH (normal, i.e. <4.5) ``` NB if complicated infection then take swabs for culture/sensitivity/microscopy
78
Management fo thrush
1st line: clotrimazole pessary 2nd line: oral itraconazole / fluconazole NB in pregnancy only local treatment (creams/pessaries) may be used
79
Management of recurrent vaginal candidiasis
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
80
Vaginal candidiasis in pregnancy
Oral Treatments e.g. oral itraconazole / fluconazole are contraindicated only pessaries or creams e.g. clotrimazole pessary may be used
81
Trichomonas vaginalis
a very common STI caused by trichomonad vaginalis, a flagellated protozoa parasite in adults its almost exclusively sexually transmitted MOST common curable STI worldwide
82
Presentation of trichomonas vaginalis in women
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)
83
Presentation of trichomonas vaginalis in men
usually asymptomatic common cause of non-gonoccocal urethritis dysuria & discharge
84
Investigations for trichomonas vaginalis
``` 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) ```
85
Management of trichomonas vaginalis
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
86
Bacterial vaginosis (BV)
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)
87
Risk factors for Bacterial vaginosis (BV)
``` sexual activity new sexual partner previous STIs afro-carribbean women use of IUD vaginal douching bubble baths receptie oral sex smoking ```
88
Presentation of Bacterial vaginosis (BV)
often asymptomatic offensive, fishy smelling vaginal discharge, usually are/milky clear pruritus & pain = uncommon
89
Protective factors for Bacterial vaginosis (BV)
circumcised partner condom use COCP (oestrogen encourages lactobacilli)
90
Investigations for Bacterial vaginosis (BV)
``` 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
91
Management of Bacterial vaginosis (BV)
advice on vaginal hygiene e.g. avoid douching if asymptomatic: no treatment unless pregnant if symptomatic: PO metronidazole for 5-7 days
92
Bacterial vaginosis (BV) in pregnancy
↑ risk of preterm labour, low birth weight, chorioamnionitis, later miscarriage use oral metronidazole for 5-7 days even if asymptomatic
93
Amsel criteria
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
94
Non gonococcal urethritis (NGU)
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
95
Causative organism for Non gonococcal urethritis (NGU)
chlamydia trachomatis (most common) myelopsama genitalium trichomonas vaginalis
96
Most common form of urethritis
Non gonococcal urethritis (NGU)
97
Presentation of urethritis
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
98
Investigations for urethritis
first pass urine or urethral smear/swab NAAT consider urine dipstick to exclude UTI STI screening
99
Management of urethritis
NGU: doxycycline BD for 5-7 days or 1g azithromycin stat Gonococcal urethritis: IM ceftriaxone ± azithromycin PO
100
Complications of urethritis
epididymitis/orchitis prostatitis systemic dissemination of gonorrhoea reactive arthritis
101
Epididymo-orchitis
an infection/inflammation of the epididymis & the testes usually caused by local spread of a genitourinary tract infection or bladder infections
102
Aetiology of Epididymo-orchitis
Men <35yrs: STI e.g. chlamydia & gonorrhoea Men >35yrs: UTIs e.g. E. coli & pseudomonas Unvaccinated children: mumps
103
Presentation of Epididymo-orchitis
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
104
Important differential for Epididymo-orchitis
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
105
Investigations for Epididymo-orchitis
exclude STI (first pass urine NAAT) if mumps suspected = IgG/IgM serology urine MC&S scrotal USS
106
Management of Epididymo-orchitis
If organism as per organism e.g. ceftriaxone for gonorrhoea or doxycycline for chlamydia if unknown organism: 500mg ceftriaxone IM + 100mg doxycycline PO
107
Chancroid
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
108
Causative organism of chancroid
Haemophilus ducreyi
109
Presentation of chancroid
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)
110
Distinguishing chancroid from syphilis chancre
chancre in syphilis = not painful chancroid = painful
111
Investigating chancroid
usually clinical diagnosis gram stain / culture of ulcer swabs
112
Management of chancroid
azithromycin or ceftriaxone
113
Pelvic inflammatory disease (PID)
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
114
Aetiology of pelvic inflammatory disease
often polymicrobial most common causes include chlamydia trachomatis & Neisseria gonorrhoea other causes include gardenella vaginalus, mycoplasma hominis
115
Risk factors for pelvic inflammatory disease
``` multiple sexual partners unprotected sex history of previous STIs IUD termination of pregnancy ```
116
Presentation of pelvic inflammatory disease
``` lower abdo pain deep dyspareunia cervical excitation dysuria menstrual irregularities vaginal discharge fever adnexal / cervical motion tenderness ```
117
Investigating pelvic inflammatory disease
pregnancy test to exclude ectopic pregnancy high vaginal / cervical swab Chlamydia & Gonorrhoea screen ESR/CRP (↑)
118
Management of pelvic inflammatory disease
Oral ofloxacin + metronidazole / IM ceftriaxone + metronidazole consider IUD removal
119
Complications of pelvic inflammatory disease
Perihepatitis (Fitz-Hugh-Curtis syndrome) infertility ectopic pregnancy
120
Infectious mononucleosis (glandular fever)
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
121
Presentation of Infectious mononucleosis
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)
122
Investigating Infectious mononucleosis
monospot antibody test (+ve, specific for EBV antibodies) FBC (lymphocytosis, atypical lymphocytosis) LFTs (AST & ALT ↑) heterophiles antibody test (+ve)
123
Management of infectious mononucleosis
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
124
Fraser competency
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
125
Important points about Fraser competency
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
126
Child <13y/o & contraception
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
127
Contraceptive of choice in young people
Progesterone only implant (Nexplanon)
128
Aims of partner notification
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
Type of partner notification
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
Follow up after partner notification
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
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Look back period for partner notification
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
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Hormone replacement therapy (HRT)
the use of low dose oestrogen + progesterone (in a women with a uterus) to alleviate menopausal symptoms
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Indications for HRT
vasomotor symptoms e.g. flushing/insomnia/headaches premature menopause (continue unti age 50, main aim to prevent osteoporosis)
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Types of HRT
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
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Compounds used in HRT
natural oestrogens e.g. estradiol / estrone are used over synthetic oestrogens e.g. ethinylestradiol synthetic progesterones e.g. levonogestrel are generally used
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Adverse effects of HRT
↑ 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)
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Side effects of HRT
nausea breast tenderness fluit retention weight gain
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Emergency contraception
forms of contraception that can be administered within a specific time period after unprotected sexual intercourse (UPSI) to prevent pregnancy
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Intrauterine device / copper coil as emergency contraception
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
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Time window after UPSI the intrauterine device can be used as emergency contraception
insert within 5 days of UPSI or if >5 days post UPSI may be inserted up to 5 days after likely ovulation date
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Levornogestrel (Levonelle) emergency contraception
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
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Time window after UPSI Levornogestrel (Levonelle) can be used as emergency contraception
effective up to 72h post UPSI
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Ulipristal (EllaOne) emergency contraception
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
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Time window after UPSI Ulipristal (EllaOne) can be used as emergency contraception
effective up to 120h post UPSI
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Combined oral contraceptive pill (COCP)
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
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Combined oral contraceptive pill (COCP) contraindications
``` >35y/o + smoking >15 cigarettes/day migraine with aura breastfeeding <6 weeks postpartum current breast cancer previous VTE/thrombogenic mutation ```
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starting the Combined oral contraceptive pill (COCP)
start within 5 days of start of cycle = no extra precautions needed if started later in cycle = use additional contraception for 7 days
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Missed pills Combined oral contraceptive pill (COCP)
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
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Combined oral contraceptive pill (COCP) and surgery
discontinue 4 weeks before elective surgery, offer progestogen only contraceptive as alternative NB does not apply to minor surgery
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Advantages of Combined oral contraceptive pill (COCP)
↓risk of endometrial cancer ↓ risk of ovarian cancer ↓ risk of colorectal cancer
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Disadvantages of Combined oral contraceptive pill (COCP)
↑ VTE/stroke risk ↑ risk of breast cancer ↑ risk of cervical cancer
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Progesterone only pill (POP)
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
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Starting Progesterone only pill (POP)
immediate protection if commenced within 5 days of starting cycle if started after day 5 of cycle take 2 days of additional contraception
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Missed pills Progesterone only pill (POP)
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
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Injectable contraceptive
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
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Contraceptive method proven to cause weight gain
Injectable contraceptive (depo provera)
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Implantable contraceptive
Examples: Implanon, Nexplanon MOA: inhibits ovulation & thickens cervical mucous Duration: 3 years contraindications: current breast cancer side effects: irregular bleeding or heavy bleeding
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Implantable contraceptive implant site
subdermal implantation into proximal non-dominant arm just overlying the triceps
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Intrauterine device (IUD)
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
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Intrauterine system (IUS)
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
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Combined contraceptive patch
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
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Post partum contraception time window
women require contraception from 21 days post partum
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Lactational amenorhoea
contraceptive method in post partum period if women fully breastfeed (no supplementary feeds), amenorrhoeic & <6 months post partum
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Types of post partum contraception
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)
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Epilepsy & contraception
UKMEC 3 for COCP & POP is people taking lamotrigine, phenytoin, carbamazepine, barbiturates, topiramate
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Contraception in women aged >40
No method of contraception is solely contraindicated by age
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Women aged <50yrs & contraception
Hormonal contraception can be continued till age 50 non hormonal contraception methods can be stopped after 2 yrs amenorrhoea
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Women aged >50yrs & contraception
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)
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Hepatits A virus (HAV)
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
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Presentation of Hep A
prodrome: mild flu like symptoms (fever, malaise, joint pain) ± RUQ pain, tender hepatomegaly Icteric phase: jaundice, pruritus, dark urine, pale stools, abdo pain
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Investigations for Hep A virus (HAV)
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 (↑)
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Management of Hep A
usually self limiting, only needing supportive care Vaccination available for high risk individuals e.g. MSM or IVDU
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Hepatits B virus (HBV)
viral infection spread by sexual contact, parentally or perinatally incubation period 6-20 weeks most common cause of hepatitis world wide
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Presentation of Hep B
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
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Hep B serology
``` 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
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Management of Hep B
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
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Hep B & pregnancy
Hep B routinely screened for if chronic/acute infection in mother = full vaccination course + Hep B immunoglobulin for Baby
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Immunisation of Hep B on serology
anti-HBs +ve only
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Previous Hep B infection but not carrier on serology
anti HBc +ve | HBsAg -ve
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Previous Hep B infection now carrier on serology
anti HBc +ve | HBsAg +ve
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Acute Hep B infection on serology
anti-HBc +ve (especially IgM kind)
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Hepatitis C virus (HCV)
virus that may be transmitted via sexual intercourse, especially high risk of HIV confection incidence rising in UK no vaccine available
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Hep C presentation
acute infection generally asymptomatic chronic disease generally mild & unspecific but ↑ risk of HCC, cirrhosis, cryglobulinaemia
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Hep C investigations
HCV RNA test (gold standard) NB if +ve for >6months = chronic Hep C anti-HCV antibodies to check for previous infection
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Hep C management
combination of protease inhibitors ± ribavirin
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Human Immunodeficiency virus (HIV)
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) ```
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Epidemiology of HIV
HIV diagnosis peaked in 2014 in UK, has been declining since affects ~38million people globally
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Routes of transmission of HIV
sexual (~80% of infections worldwide) parenteral vertical transmission from mother to child (during birth/breastfeeding)
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Risk factors for HIV infection
``` needle sharing for IVDU unprotected receptive anal intercourse unprotected receptive penile-vagnial intercourse needle stick injury high maternal vial loads MSM ```
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Pathophysiology of HIV infection
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
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Window period for acute HIV infection
4 weeks
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Acute primary HIV infection (seroconversion illness)
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 ↑
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Time between infection with HIV & seroconversion illness
1-6 weeks
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tests for HIV seroconversion illness
HIV antibody test -ve Viral p24 antigen ↑ HIV RNA ↑
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Clinical latency stage of HIV
asymptomatic stage after acute seroconversion illness generally low viral loads & normal CD4/CD8 count may persist for 8-10 yrs
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Symptomatic HIV stage (latency stage)
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
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Acquired immunodeficiency syndrome (AIDS)
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
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Persistent generalised lymphadenopathy
enlargement of ≥2 non contigous lymph node groups for >6 months usually non tender sign of symptomatic HIV infection
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Oral candida
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
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Oral hair leukoplakia
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
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CDC classification of HIV
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
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Category A of CDC classification of HIV
asymptomatic infection, persistent generalised lymphadenopathy (PGL) or acute HIV infection
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Category B of CDC classification of HIV
symptomatic HIV i.e. HIV indicator conditions e.g. oral candida/ oral hairy leukoplakia, chronic diarrhoea
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Category C of CDC classification of HIV
AIDS defining conditions e.g. oesophageal candidiasis, Kaposi sarcoma etc
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CD4 count ranges for CDC classification of HIV
normal: 500-1500 cells/mm3 category 1: ≥500 cells/mm3 category 2: 200-499 cells/mm3 category 3: <200 cells/mm3
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AIDS defining conditions
- 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
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Investigations for HIV
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
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Diagnosis of HIV
based on anti-HIV antibodies in serum (IgG/IgM antibodies against HIV virus) should be positive
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Diagnosis fo acute HIV infection
anti-HIV antibodies may not be present HIV PCR & p24 antigen tests are used, these are positive before appearance of HIV antibodies
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Testing recommendations for HIV
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)
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Oesophageal candidiasis
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)
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Systemic candidiasis (candidaemia / disseminated candidiasis)
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
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Pneumocystis pneumonia (PCP)
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
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Risk factors for Pneumocystis pneumonia (PCP)
CD4 count <200 cells/mm3 other AIDS defining illnesses poor compliance with PCP prophylaxis / retrovirals malnutrition
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Presentation of Pneumocystis pneumonia (PCP)
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
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Investigating Pneumocystis pneumonia (PCP)
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)
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Management of Pneumocystis pneumonia (PCP)
1st line: Co-trimoxazole 2nd line: IV pentamidine (severe cases) NB Co-trimoxazole = trimethoprim + sulfamethoxazole
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Prevention of Pneumocystis pneumonia (PCP)
PCP prophylaxis is given to all HIV pts with CD4 count <200cells/mm3 prophylaxis with oral co-trimoxazole
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Common complication of Pneumocystis pneumonia (PCP)
pneumothorax
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Cryptococcosis
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
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Presentation of Cryptococcosis
meningitis/menigoencephalitis: headache, confusion, altered mental state, coma, seizures, neurological signs (diplopia, ataxia, aphasia, signs of ↑ ICP) Meningism (neck stiffness, photophobia, headache)
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Investigations for Cryptococcosis
CSF/blood/urine cultures cryptococcus antigen titres (from CSF/serum) MRI brain (soap bubble lesions in brain, hydrocephalus, cysts)
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Management of Cryptococcosis
Induction: amphotericin B + flucytosine consolidation: PO fluconazole Maintenance: low dose fluconazole for several months
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Cryptosporidosis
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
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Toxoplasmosis
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
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Toxoplasmosis presentation
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 ```
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Toxoplasmosis investigations
serology (anti-toxoplasmosis IgM/IgG contrast CT/MRI brain (multiple ring enhancing lesions = brain abscesses, often in basal ganglia)
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Toxoplasmosis management
pyrimethamine +sulfadiazine + folinic acid prevention with dapsone + pyrimethamine
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Cytomegalovirus (CMV)
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
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Presentation of cytomegalovirus (CMV)
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
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Investigations for cytomegalovirus (CMV)
histopathology: owls eye appearance, due to large intranuclear inclusion body serology: anti-CMV IgG/IgM (not useful if immunosuppressed) PCR for CMV DNA
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Management of cytomegalovirus (CMV)
treatment: valganciclovir / ganciclovir / foscarnet Cidofivir if resistant CMV + optimise antiretroviral therapy Prophylaxis: valganciclovir or ganciclovir
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Tuberculosis in HIV
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
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TB in HIV presentation
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
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Investigations for TB
CXR (usually apical lesion or millet seed like profile of biliary TB) Sputum smear (acid fast bacilli on Ziehl-Nielsen stain) sputum culture
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Management of TB in HIV
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
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Myobacterium avian complex (MAC) / Myobacterium avian intracellulare (MAI)
opportunistic infection of immunocompromised individuals usually with CD4 count <50cells/mm3 seen in up to 40% of AIDS pts
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Presentation of Myobacterium avian complex (MAC)
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
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Investigations for Myobacterium avian complex (MAC)
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)
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Management of Myobacterium avian complex (MAC)
Treatment: 12 months course of Abx (clarithromycin/erythromycin + ethambutol + rifabutin) Prophylaxis: macrolide (azithromycin / clarithromycin) until CD4 count >100cells/mm3
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Microsporidiosis
caused by microsporidium (in HIV pts) presents with low volume diarrhoea diagnosed on immunofluorescent staining of stool managed with HAART, erythromycin
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Isosporiasis
caused by isosporiasis belli causes watery diarrhoea, abdo pain, fatigue, weight loss treat with co-trimoxazole
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Aspergillosis
uncommon in HIV unless CD4 count <30 presents with cough, fever, dyspnoea Cavitating lesions on CXR treated with amphoteracin B or itraconazole
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HIV wasting syndrome
unintentional weight loss ≥10%, fatigue, fever, diarrhoea | due to variety of factors
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Histoplasmosis
infection caused by histoplasmosis capsulate, in HIV usually a reactivation of latent disease usually seen in CD4 count <200
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Histoplasmosis presentation
fever, weight loss, erythema nodosum, lymphadenopathy, hepatosplenomegaly, non productive cough, pleuritic chest pain, ulcerative oral lesions
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Investigation & management of Histoplasmosis
CXR (diffuse nodular density, focal infiltrate/cavity) fungal blood cultures managed with itraconazole
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Bacterial pneumonia in HIV
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
At what CD4 counts do vaccinations become ineffective
CD4 count <200 makes many vaccines ineffective
250
Progressive multifocal leukoencephalopathy (PML)
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
HIV associated neurocognitive disorders (HAND)
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
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Herpes simplex virus & HIV
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
Molluscum contagiosum & HIV
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
Human papilloma virus & HIV
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
Kaposi sarcoma
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
Presentation of kaposi sarcoma
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
Investigations of Kaposi sarcoma
``` skin biopsy (spindle cells*, angiogenesis, leukocyte infiltration) CXR/Abdo USS/bronchoscopy/endoscopy consider HHV-8 serology ```
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Management of Kaposi sarcoma
HAART = vital (lesions may spontaneously resolve after immune reconstitution) radio/chemo/cryotherapy
259
Non-Hodgkins lymphoma in HIV
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
Primary CNS lymphoma in HIV
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
Primary CNS lymphoma vs toxoplasmosis
Toxoplasmosis = multiple enhancing lesions on contrast CT & negative Thalium SPECT Primary CNS lymphoma = single enhancing lesions on contrast CT & positive Thalium SPECT
262
HIV peripheral neuropathy
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
HIV assoicated nephropathy (HIVAN)
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
Nucleoside reverse transcriptase inhibitors (NRTIs) examples
``` emtricitabine (FTC) Lamivudine (3TC) abacavir zidovudine (AZT) Stavudine (d4T) didanosine (ddI) tenofivir ``` NB Tenofivir alafenamide (TAF) = tenofivir pro drug
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Class of drugs for emtricitabine (FTC), Lamivudine (3TC), abacavir , zodofivir (AZT), Stavudine (d4T), didanosine (ddI), tenofivir
Nucleoside reverse transcriptase inhibitors (NRTIs)
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MOA of Nucleoside reverse transcriptase inhibitors (NRTIs)
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
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Zidovudine (NRTI) side effects
``` bone marrow suppression (anaemia, neutropenia) lipoatrophy peripheral neuropathy skin/nail pigmentation lactic acidosis hepatic stenosis ```
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Stavudine (NRTI) side effects
``` lipoatrophy peripheral neuropathy pancreatitis lactic acidosis hepatic stenosis ```
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Didanosine (NRTI) side effects
peripheral neuropathy | pancreatitis
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Rarely used NRTIs in HIV
Zidovudine, stavudine, didanosine
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Emtricitabine (NRTI) side effects
reversible skin pigmentations
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Abacavir (NRTI) side effects
~5% of pts have life threatening hypersensitivity reaction associated with HLA-B5701
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Tenofivir (NRTI) side effects
``` renal dysfunction (glycosuria, subnephrotic proteinuria, ↑ creatinine) ↓ bone mineral density ``` NB the prodrug TAF has ↓ nephrotoxicity
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antiretroviral causing life threatening hypersensitivity reaction
Abacavir (NRTI) ~5% of pts have life threatening hypersensitivity reaction associated with HLA-B5701
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Non-nucleoside reverse transcriptase inhibitors (NNRTIs) examples
``` nevirapine efavirenz etravarine rilpivirine doravirine ```
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Non-nucleoside reverse transcriptase inhibitors (NNRTIs) MOA
noncompetitive inhibitors of viral reverse transcriptase that bind at separate location to NRTIs
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Nevirapine (NNRTI) side effects
rash (potentially SJS) | hepatotoxicity (contraindicated in Hep B/C confection)
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Efavirenz (NNRTI) side effects
``` CNS toxicity (confusion, vivid/disturbing dream/somnolence) teratogenic ```
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Antiretroviral contraindicated in Hep B/C coinfection
Nevirapine as it is hepatotoxic
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Protease inhibitors (PI) examples
``` darunavir atazanavir lopinavir ritonavir tipranavir ``` NB ritonavir, tipranavir are now rarely used
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Protease inhibitors (PI) MOA
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
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Protease inhibitors (PI) administration
PIs are always given with low dose ritonavir (as it inhibits cytochrome P450) to ↑ intracellular concentration of the drug known as boosted PI
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Fusion inhibitors examples
Enfuvirtide (T-20) (given BD via SC injection) NB fusion inhibitors are reserved for those with highly drug resistant HIV
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Fusion inhibitors MOA
competitively binds to viral protein gp41 & thereby prevents fusion with cells
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Fusion inhibitors side effects
skin irritation at injection site (enfuvirtide)
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Integrase inhibitors examples
raltegravir elvitegravir dolutegravir bictegravir
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Integrase inhibitors MOA
inhibit viral integers = blockade of viral DNA integration into hosts DNA = inhibition of viral replication
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Integrase inhibitors side effects
↑ creatine kinase raltegravir (muscle pain, rhabdomyolysis) dolutegravir (mood/sleep disturbances)
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Co-receptor antagonists examples (ART)
Maraviroc (CCR5)
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Co-receptor antagonists MOA
blocks CCR5 co-receptor onT-cells & monocytes that is essential for cell infection = inhibits gp120 interaction = prevents irons docking to cell
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Co-receptor antagonists side effects
hepatotoxicity | allergic reaction
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Weight gain on antiretroviral therapy
Agents such as Tenofivir alafenamide (TAF)
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Weight gain on antiretroviral therapy
Agents such as Tenofivir alafenamide (TAF) is more associated with weight gain that tenofivir integers inhibitors especially raltegravir are associated with weight gain
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Indications for anti retroviral therapy
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
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antiretroviral therapy regimes
2 NRTIs plus 1 ritonavir boosted PI / 1 NNRTI / 1 integrase inhibitors
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Switching antiretroviral therapy
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
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Drug interactions of Protease inhibitors
inhibit P450
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Drug interactions of Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
potent liver enzyme inducer = ↓ levels of other drugs
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Drug interactions of Nucleoside reverse transcriptase inhibitors (NRTIs)
exacerbate cytopenic effect of chemo
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Indications for post exposure prophylaxis (PEP)
- 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)
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Timing of post exposure prophylaxis (PEP)
ASAP / within 1-2h of exposure = ideal > 72h after exposure = ineffective / ↓effectivity NB for non occupational exposure the timing is usually later (~23h)
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When post exposure prophylaxis (PEP) is needed
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
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post exposure prophylaxis (PEP) follow up
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
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Treatment as prevention (TAsP)
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)
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Pre exposure prophylaxis (PrEP) eligibility
negative HIV test result & no signs/symptoms of acute HIB infection normal renal function indications met for PrEP
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Pre exposure prophylaxis (PrEP) indications
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
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Pre exposure prophylaxis (PrEP) indications
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
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Pre exposure prophylaxis (PrEP) follow up
HIV test every 3 months STI screening every 3 months renal assessment at baseline & every 6 months counselling on adherence & risk reduction
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HIV & pregnancy
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
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Interventions to reduce transmission of HIV in pregnancy
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)
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HIV transmission in pregnancy
usually occurs late in pregnancy at time of deliver or via breastfeeding without intervention mother-to-child transmission rate is 15-20%
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Delaying planned C-section in HIV +ve pregnancies
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)
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HIV mother-to-child transmission rate with intervention
rate is <1%
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Considering vaginal delivery in HIV +ve pregnancy
if maternal viral load is <50 copies/ml at 36 weeks but the preferred method is still C-section
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Pubic lice (crabs)
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.