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Phase 3a - Arun&Erin > Sexual & Genitourinary medicine > Flashcards

Sexual & Genitourinary medicine Flashcards

1
Q

What swabs are involved in sexual health testing?

A
  • Charcoal swabs
  • Nucleic acid amplification test (NAAT) swabs
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2
Q

What are charcoal swabs used for?

A
  • Allow for microscopy (w/ gram staining), culture & sensitivities
  • Swab with Amies transport medium at the end: contains chemical solution to keep microorganisms alive during transport
  • Can be used for endocervical swabs and high vaginal swabs
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3
Q

What are NAAT swabs used for?

A
  • Check directly for DNA or RNA of the organism
  • Specifically for chlamydia & Gonorrhoea
  • When gonorrhoea is suspected on NAAT test –> endocervical charcoal swab required for MC+S
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4
Q

How can NAAT swabs be taken for both men and women? (in order of preference)

A
  • Women: endocervical, vulvovaginal, then first-catch urine
  • Men: first-catch urine then urethral swab

Rectal & pharyngeal NAAT swabs - diagnose chlamydia in rectum & throat where anal or oral sex has occured

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5
Q

What are the ‘triple swabs’?

A
  • Endocervical - “ECS”
  • High Vaginal - “HVS”
  • Endocervical NAAT - “Chlamydia”
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6
Q

What does each swab test for in the triple swab?

A
  • ECS (charcoal): Gonorrhoea
  • HVS (charcoal): TB & BV, group B strep, candida
  • NAAT: Chlamydia & Gonorrhoea
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7
Q

What is the difference between double and triple swabs?

A

Double swabs:
* NAAT & HVS in charcoal

Triple swabs:
* NAAT & HVS in charcoal & ECS in charcoal

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8
Q

What is thrush?

(vaginal candidiasis)

A

Vaginal infection with a yeast of the candida family - MC is candida albicans

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9
Q

How does thrush come about?

A
  • Candida may colonise the vagina without causing symptoms
  • It then progresses to infection when the right environment occurs
  • e.g. during pregnancy, after Tx with broad-spectrum ABx that alter vaginal flora
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10
Q

What are 4 risk factors for developing thrush?

A
  • Increased oestrogen - e.g. in pregnancy (lower pre-puberty & post-menopause)
  • Poorly controlled diabetes
  • Immunosuppression - e.g. using corticosteroids
  • Broad-spectrum ABx
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11
Q

What are the symptoms of vaginal candidiasis (thrush)? (2)

A
  • Thick white discharge that does not typically smell
  • Vulval & vaginal itching, irritation or discomfort
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12
Q

What can more severe vaginal candidiasis infection lead to? (6)

A
  • Erythema
  • Fissures
  • Oedema
  • Dyspareunia (pain during sex)
  • Dysuria
  • Excoriation
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13
Q

What investigations can be done for vaginal candidiasis?

A
  • Testing vaginal pH using a swab and pH paper - to differentiate between BV/TV and candidiasis
  • Charcoal swab with microscopy can confirm Dx
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14
Q

What is the difference in pH between bacterial vaginosis/trichomonas and candidiasis?

A
  • BV/TV = pH > 4.5
  • Candidiasis = pH < 4.5
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15
Q

What are the treatment options for vaginal candidiasis (thrush)?

A
  • Antifungal cream: clotrimazole inserted into vagina
  • Antifungal pessary: clotrimazole
  • Oral antifungal tablets: fluconazole

AKA antifungal medications!!

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16
Q

What is the standard over-the-counter treatment for thrush?

A

Canesten Duo
* contains single fluconazole tablet & clotrimazole cream to use externally for vulval Sx

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17
Q

What is the most common STI in the UK?

A

Chlamydia

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18
Q

What kind of organism is Chlamydia trachomatis?

A

Gram negative bacteria
* Intracellular organism: enters & replicates within cells before rupturing the cell and spreading to others

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19
Q

What increases your risk of catching chlamydia?

A
  • Young
  • Sexually active
  • Multiple partners
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20
Q

What is the National Chlamydia Screening programme (NCSP)?

A
  • Aims to screen every sexually active person under 25 years for chlamydia
  • Annually or when they change their sexual partner
  • Everyone that tests positive should have a re-test 3 months after Tx (to make sure they have not contracted chlamydia again)
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21
Q

When a patient attends GUM clinic for STI screening, what is the minimum they are tested for?

A
  • Chlamydia
  • Gonorrhoea
  • Syphilis (blood test)
  • HIV (blood test)
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22
Q

What is the presentation of chlamydia in sexually active women?

A

75% cases asymptomatic
* Abnormal vaginal discharge
* Abnormal vaginal bleeding (intermenstrual/postcoital)
* Pelvic pain
* Dyspareunia
* Dysuria

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23
Q

What is the presentation of chlamydia in sexually active men?

A

50% asymptomatic
* Urethral discharge or discomfort
* Dysuria
* Epididymo-orchitis
* Reactive arthritis

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24
Q

What are the examination findings for chlamydia?

A
  • Pelvic/abdominal tenderness
  • Cervical motion tenderness (cervical excitation)
  • Inflamed cervix (cervitis)
  • Purulent discharge
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25
Q

What is the first line treatment of uncomplicated chlamydia?

A

100mg doxycycline BD for 7 days

Abstain from sex for 7 days, notify sexual partners for contact tracing, consider safeguarding issues & sexual abuse

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26
Q

When is doxycycline contraindicated?

A

Pregnancy & breastfeeding
* Alternative options: azithromycin, erythromycin, amoxicillin

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27
Q

What are some complications of chlamydia?

A
  • Pelvic infalmmatory disease
  • Chronic pelvic pain
  • Infertility
  • Ectopic pregnancy
  • Epididymo-orchitis
  • Conjunctivitis
  • Lymphogranuloma venereum
  • Reactive arthritis
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28
Q

What are 5 pregnancy related complications of chlamydia?

A
  • Preterm delivery
  • PRoM
  • Low birthweight
  • Postpartum endometritis
  • Neonatal infection (conjunctivitis / Pneumonia)
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29
Q

What is lymphogranuloma venereum (LGV)?

A
  • Condition affecting lymphoid tissue around sit of infection with chlamydia
  • Most common in men who have sex with men (MSM)
  • Occurs in 3 stages: primary, secondary, tertiary
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30
Q

What happens in the 3 stages of LGV?

A

Primary
* Painless ulcer - on penis, vaginal wall or rectum

Secondary
* Lymphadenitis - swelling, inflammation, pain in lymph nodes infected with bacteria
* Inguinal or femoral lymoh nodes may be affected

Tertiary
* Inflammation of rectum (Proctitis) and anus
* Proctocolitis leads to anal pain, change in bowel habits, tenesmus and discharge

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31
Q

What is the treatment of lymphogranuloma venereum?

A

100mg doxycycline BD for 21 days

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32
Q

What is chlamydial conjunctivitis?

A

Usually result of sexual activity when genital fluid comes in contact with conjunctiva of eye (e.g. hand-to-eye spread)

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33
Q

How does chlamydial conjunctivitis present?

A
  • Chronic erythema
  • Irritation
  • Discharge
  • Unilateral
  • Lasting more than 2 weeks
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34
Q

What is bacterial vaginosis? (BV)

A

Overgrowth of anaerobic bacteria in the vagina
* It is NOT an STI

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35
Q

What causes bacterial vaginosis?

A
  • Lactobacilli = healthy vaginal bacterial flora
  • These produce lactic acid which keeps the vaginal pH low (< 4.5)
  • Acidic environment prevents other bacteria from overgrowing
  • Loss of lactobacilli = pH rises
  • This more alkaline environment enables anaerobic bacteria to multiply
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36
Q

What bacteria are associated with BV?

A
  • Gardnerella vaginalis (MC)
  • Mycoplasma hominis
  • Prevotella species
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37
Q

What are some risk factors for BV? (5)

A
  • Multiple sexual partners (although not sexually transmitted)
  • Excessive vaginal cleaning (douching, use of cleaning products & vaginal washes)
  • Recent ABx
  • Smoking
  • Copper coil
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38
Q

What is the presentation of BV?

A

50% ASx
* Fishy-smelling watery grey/white discharge

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39
Q

What investigations are done for BV?

A
  • Vaginal pH - swab and pH paper (normal 3.5-4.5, BV occurs > 4.5)
  • Charcoal vaginal swab - microscopy (can be HVS or self-taken low vaginal swab)
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40
Q

How does BV present on microscopy?

A

Clue cells
* epithelial cells from cervix that have bacteria stuck inside them, usually gardnerella vaginalis

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41
Q

What is the management of BV?

A

Metronidazole: ABx that targets anaerobic bacteria (given orally or vaginal gel)
* Alternative: clindamycin
* Advise about measures to reduce risk e.g. avoid vaginal irrigation/cleaning with soaps that disrupt natural flora
* Assess risk of other pelvic infections - Chlam & Gon swabs
* ASx doesn’t usually require Tx

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42
Q

What are the complications of BV?

A
  • Increases risk of catching STIs (Chl,Gon,HIV)

In pregnant women:
* Miscarriage
* Preterm delivery
* PRoM
* Chorioamnionitis
* Low birth weight
* Postpartum endometritis

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43
Q

What is trichomonas vaginalis?

A
  • Parasite spread through sexual intercourse & lives in urethra of men, and vagina & urethra of women
  • Classed as a protozoan: single-celled organism w/ flagella
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44
Q

What can trichomonas increase the risk of? (5)

A
  • Contracting HIV by damaging vaginal mucosa
  • BV
  • Cervical cancer
  • PID
  • Pregnancy-related Cx e.g. preterm delivery
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45
Q

How does trichomonas present?

A

Up to 50% ASx
* Typically frothy yellow-green vaginal discharge - may have fishy smell
* Itching
* Dysuria
* Dyspareunia
* Balanitis (inflammation to the glans penis)

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46
Q

What does examination of the cervix reveal in trichomonas?

A

“Strawberry cervix” (colpitis macularis)
* Caused by inflammation (cervicitis)
* Tiny haemorrhages across surface of cervix

Vaginal pH will be raised (> 4.5) like BV

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47
Q

How is a diagnosis of trichomonas made in women?

A

Charcoal swab with microscopy
* Swab taken from posterior fornix of vagina (alt. self-taken lower vag swab)

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48
Q

How is a diagnosis of trichomonas made in men?

A

Urethral swab or first-catch urine

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49
Q

What is the management of trichomonas?

A

Metronidazole
* Refer to GUM for contact tracing

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50
Q

What is Neisseria Gonorrhoea?

A
  • Gram negative diplococcus bacteria
  • Infects mucous membranes with a columnar epithelium
  • e.g. endocervix, urethra, rectum, conjunctiva and pharynx
  • Spreads via contact w/ mucous secretions from infected areas
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51
Q

What increases the risk of infection with gonorrhoea?

A
  • Young
  • Sexually active
  • Multiple partners
  • Having other STIs
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52
Q

What is the genital presentation of gonorrhoea in women?

A

50% symptomatic
* Odourless purulent discharge, possible green/yellow
* Dysuria
* Pelvic pain

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53
Q

What is the genital presentation of gonorrhoea in men?

A

90% symptomatic
* Odourless purulent discharge, possibly green/yellow
* Dysuria
* Epididymo-orchitis (testicular pain/swelling)

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54
Q

What are the other presentations of gonorhhoea - rectal, pharyngeal, prostatitis, conjunctivitis?

A

Rectal
* anal/rectal discomfort & discharge
* often ASx

Pharyngeal
* sore throat
* often ASx

Prostatitis
* perineal pain
* urinary Sx
* prostate tenderness on examination

Conjunctivitis
* erythema
* purulent discharge

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55
Q

How is a diagnosis of gonorrhoea made?

A
  • NAAT - detects RNA/DNA
  • Genital infection - swabs (EC, VV, urethral) or first-catch urine sample
  • Charcoal endocervical swab - Microscopy, Culture + ABx sensitivities (due to high rates of ABx resistance)
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56
Q

What is the management of uncomplicated gonorrhoea?

A
  • Single dose IM ceftriaxone (if sensitivities NOT known)
  • Single dose oral ciprofloxacin (if sensitivities ARE known)
  • Follow up “test of cure” with NAAT testing if ASx, or cultures if symptomatic
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57
Q

What is Disseminated gonococcal infection? (DGI)

A

Complication of untreated gonococcal infection, where bacteria spreads to skin & joints, causing:
* non-specific skin lesions
* polyarthralgia
* migratory polyarthritis
* tenosynovitis
* systemic Sx e.g. fever, fatigue

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58
Q

What are some complications of gonorrhoea?

A
  • PID
  • Chronic pelvic pain
  • Infertility
  • Epididymo-orchitis
  • Prostatitis
  • Gonococcal conjunctivitis (neonate) - medical emergency
  • Urethral strictures
  • Disseminated gonococcal infection
  • Skin lesions
  • Fitz-Hugh-Curtis syndrome
  • Septic arthritis
  • Endocarditis
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59
Q

What organism is responsible for cold sores and genital herpes?

A

Herpes simplex virus (HSV)
* Two strains: HSV-1 & HSV-2

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60
Q

What happens after the initial infection of HSV?

A

Virus becomes latent in the associated sensory nerve ganglia
* Cold sores: trigeminal nerve ganglion
* Genital herpes: sacral nerve ganglia

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61
Q

How is HSV spread?

A

Through direct contact with affected mucous membranes or viral shedding in mucous secretions
* Virus can be shed even when no Sx are present (i.e. can be contracted from asymptomatic individuals)

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62
Q

What are the 2 strains of HSV and what does each strain cause?

A
  • HSV-1: cold sores, often contracted in childhood & remains dormant in trigeminal nerve ganglion, reactivates as cold sores#
  • HSV-2: genital herpes, STI, can also cause lesions in mouth

HSV-1 can cause genital herpes usually contracted through oro-genital sex

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63
Q

What is the presentation of genital herpes?

A
  • Ulcers/ blistering lesions affecting genital area
  • Neuropathic pain (tingling/burning/shooting)
  • Flu-like Sx (e.g. fatigue, headache)
  • Dysuria
  • Inguinal lymphadenopathy
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64
Q

What other ways can HSV present (not genital)?

A
  • Aphthous ulcers (painful oral sores)
  • Herpes keratitis (cornea inflammation)
  • Herpetic whitlow (painful skin lesion on finger/thumb)
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65
Q

How is a diagnosis of genital herpes made?

A
  • Clinically made
  • Ask about sexual contacts inc. those w/ cold sores
  • Viral PCR swab from lesion can confirm Dx & causative organism
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66
Q

What is the management of genital herpes?

A
  • Aciclovir
  • Manage Sx: paracetamol, topical lidocaine (instillagel), avoid intercorse etc.
  • Refer to GUM
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67
Q

What issues can arise from having genital herpes when pregnant?

A
  • Risk of neonatal herpes simplex infection contracted during labour/delivery
  • Has high morbidity & mortality
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68
Q

What is the management of genital herpes in pregnancy?

A

Depends whether it is the first episode or recurrent
* Primary genital herpes: (contracted before 28 weeks) –> Aciclovir followed by prophylactic aciclovir
* Recurrent genital herpes: regular prophylactic aciclovir from 36 weeks gestation

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69
Q

What bacteria causes syphilis?

A

Treponema pallidum
* Spirochete - spiral-shaped bacteria

70
Q

How is syphilis transmitted?

A

Bacteria gets in through skin/mucous membranes, replicates then disseminates throughout body
* Mainly STI: oral, vaginal, anal sex
* Vertical transmission: mother–>baby
* IVDU
* Blood transfusions/transplants (rare)

71
Q

What are the stages of syphilis?

A

Primary
* Painless ulcer = “chancre” at original site of infection (usually genitals)

Secondary
* Systemic Sx (particularly skin & mucous membranes)

Latent
* Occurs after secondary stage where Sx disappear & Pt becomes ASx despite still being infected
* Early latent syphilis occurs within 2 years
* Late latent syphilis occurs from 2 years onwards

Tertiary
* Occurs many years after inital infection
* Can affect many organs
* Development of gummas, CVS & neuro Cx

72
Q

What is neurosyphilis?

A
  • occurs in infection involves CNS
  • presents w/ neurological Sx
73
Q

How does primary syphilis present?

A
  • Chancre: tends to resolve over 3-8 weeks
  • Local lymphadenopathy
74
Q

How does secondary syphilis present?

A
  • Maculopapular rash
  • Condylomata lata (grey wart-like lesions around genitals & anus)
  • Low-grade fever
  • Lymphadenopathy
  • Alopecia
  • Oral lesions
75
Q

How does tertiary syphilis present?

A
  • Gummatous lesions (gummas): granulomatous lesions that affect skin, organs, bones
  • Aortic aneurysms
  • Neurosyphilis
76
Q

How does neurosyphilis present?

A
  • Headache
  • Altered behavious
  • Dementia
  • Tabes dorsalis (demyelination affecting spinal cord posterior columns)
  • Ocular syphilis (affecting eyes)
  • Paralysis
  • Sensory impairment
  • Argyll-Robertson pupil: constricted pupil that accomodates when focusing on a near object but doesn’t react to light
77
Q

How is a diagnosis of syphilis made?

A
  • Antibody testing for antibodies to the T. pallidum bacteria
  • Presence of T. Pallidum can be confirmed with: dark field microscopy & PCR
  • Rapid plasma reagin (RPR) & Venereal disease research lab (VDRL) both test quantity of antibodies produced to syphilis - non-specific but sensitive tests (often produce false positives)
77
Q

What is the management of syphilis?

A
  • Single deep IM dose of benzathine benzylpenicillin
  • Alt: ceftriaxone, amoxilcillin, doxycycline
  • Full screening for other STIs
  • Contact tracing
  • Prevention of future infections
78
Q

What kind of virus is HPV?

A

Non-enveloped double-stranded circular DNA virus in the Papillomaviridae family

79
Q

How many types of HPV are there?

A

Over 150
* 40 affect anogenital area
* 15 are oncogenic

80
Q

What types of HPV cause genital warts?

A

HPV-6 and HPV-11

(low risk)

81
Q

How prevalent is HPV?

A
  • Extremely - nearly all men & women acquire HPV infection during their lifetime
  • almost 40% of women are infected with HPV during the first 2 years of sexual activity
  • High-risk HPV causes around 5% of cancers worldwide
82
Q

What cancers can HPV cause?

A
  • Cervical
  • Vulval
  • Vaginal
  • Anal
  • Penile
  • Head
  • Neck
83
Q

What are 2 important high risk HPV types?

A

HPV-16 and HPV-18 which can contribute to over 70% of cervical cancer

84
Q

What is the lifecyle of HPV?

A
  • HPV Entry: Microtrauma allows HPV to access basal keratinocytes via L1 & L2 capsid proteins and enter cells by endocytosis.
  • Infection Site: Virus establishes in basal layer for persistent infection, proliferating with basal cells.
  • Replication: Infected basal cells differentiate, triggering early gene expression and viral replication, releasing new virions.
  • Immune Response: Most infections clear in 12-14 months via Th1 pro-inflammatory, cell-mediated response.
  • Outcome: Immune system may clear or suppress virus, but 70-80% of cases don’t generate lasting antibodies, risking reinfection.
85
Q

How does HPV cause warts?

A

Hyperproliferation of infected epithelia

86
Q

How is HPV spread?

A
  • Skin-skin contact during sexual intercourse
  • Contact with contaminated surfaces
  • Oro-genital transmission
  • Perinatal vertical transmission
  • Autoinoculation
87
Q

What are some factors that increase the risk of HPV?

A
  • Early age of first sexual intercourse
  • High number of sexual partners
  • Condomless sexs
  • Immunosuppression (inc. HIV)
88
Q

How do HPV infections present?

A

70-90% asymptomatic: cleared within 12-14 months
* Warts: 2-5mm cauliflower-like growths (non-hairy skin = soft/non-keratinised, hairy skin = firm/keratinised)
* Pruritus / irritation around wart
* Pain/bleeding (due to local trauma)
* Haematuria & distortion of urinary flow (due to intra-meatal warts)

89
Q

What clinical examinations are done for HPV infections?

A
  • Examine anogenital area: ext genitalia, perineum, anus
  • Vaginal speculum exam
  • Meatoscopy: intrameatal warts
  • Proctoscopy: anal margin warts
  • Anoscopy: recurrent perianal warts
90
Q

What are some differentials for anogenital lesions?

A
  • Condyloma latum: moist whiteish papules w/ systemic Sx (fever, malaise, wt loss)
  • Molluscum contagiosum: flesh/pearly-coloured lesions w/ central dells
  • Pearly penile papules: 1-2mm flesh-coloured papules around corona/sulcus of penis glans
  • Skin tags: soft, skin-coloured, round pedunculated papilloma
  • Carcinoma in situ: multifocal/erythematous/pigmented lesions w/ smooth velvety surface
91
Q

What investigations should be done for genital warts?

A

Dx following clinical exam, swabs & blood tests not routinely performed, however offer full sexual health screen
* Urine sample
* Swabs of vagina, cervix, rectum, oropharynx for NAAT
* FBC, CRP, serology (HIV, syphilis, HBV, HCV)
* Biopsy: if wart is indurated, fixed, bleeding, ulcerated, pigmented

92
Q

What is the management of HPV infection?

A

No specific Tx
Aim = destroy/remove warts
* Self-administered Tx: topical treatment (podophyllotoxin, imiquimod & sinecathins)
* Specialist Tx: trichloroacetic acid / ablative methods (cryotherapy, excision, electrocautery)

93
Q

What are some side effects of podophyllotoxin, imiquimod & sinecathins?

A
  • Potential skin irritation
  • Imiquimod & sinecathins can weaken condoms
94
Q

How can HPV be prevented?

A
  • Condoms
  • Male circumcision
  • Vaccination: Gardasil (protects against strains 6,11,16,18)
  • Limiting number of sexual partners
95
Q

Who is eligible for the HPV vaccine?

A
  • Girls & boys aged 11-14
  • MSM 15-45 years
  • High risk individuals: transgender, sex workers
  • People living w/ HIV
96
Q

What kind of virus is HIV?

A

RNA retrovirus
2 types:
* HIV-1 (MC)
* HIV-2 (west africa)

97
Q

What is AIDS?

A

Acquired immunodeficiency syndrome
* Occurs when HIV is not treated, the disease progresses, person becomes immunocompromised
* Immunodeficiency leads to opportunistic infections & AIDS-defining illnesses

98
Q

How does HIV work?

A
  • Virus enters and destroys CD4 T-helper cells of immune system
  • An initial seroconversion flu-like illness occurs within a few weeks of infection
  • Infection is then ASx until condition progresses to immunodeficiency
  • Disease progression may occur years after initial infection
99
Q

How is HIV transmitted?

A
  • Unprotected sex (vaginal, anal, oral)
  • Vertical transmission (mother–>child)
  • Mucous memb/blood/open wound exposure to infected blood/bodily fluids (e.g. sharing needles, needle-stick injury)
100
Q

When do AIDS-defining illnesses occur?

A
  • Associated with end-stage HIV infection
  • Occur when CD4 count has dropped to a level that allows for unusual opportunistic infections & malignancies to appear
101
Q

Name some examples of AIDS-defining illnesses? (6)

A
  • Kaposi’s sarcoma
  • Pneumocystis jirovecii pneumonia (PCP)
  • Cytomegalovirus infection
  • Candidiasis (oesophageal/bronchial)
  • Lymphomas
  • Tuberculosis
102
Q

What are the 2 screening tests for HIV?

A
  • Fourth-generation lab test: HIV antibodies & p24 antigen (45 day window period)
  • Point-of-care tests: HIV antibodies (90 day window period)
103
Q

What is the normal range for CD4 count? And what is the range for someone with HIV?

A
  • Normal: 500-1200 cells/mm3
  • Under 200 cells/mm3: puts patient at high risk of opportunistic infections
104
Q

How else can you test for HIV? (to do with the blood)

A

Testing for HIV RNA per ml of blood indicates viral load
* An undetectable viral load means level is below recordable range (usually 20 copies/ml)
* Viral load can be in the hundreds of thousands in untreated HIV

105
Q

What is the management of HIV?

A

Combination of antiretroviral therapy (ART) medications
Aims to achieve normal CD4 count & undetectable viral load
* Usual starting regime is 2 NRTIs (e.g. tenofovir + emtricitabine) plus a third agent (e.g. bictegravir)

106
Q

Name 5 classes of antiretroviral therapy medications

A
  • Protease inhibitors (PI)
  • Integrase inhibitors (II)
  • Nucleoside reverse transcriptase inhibitors(NRTI)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTI)
  • Entry inhibitors (EI)
107
Q

What is given to HIV positive patients with a CD4 count under 200/mm3 to protect against pneumocystis jirovecii pneumonia?

A

Prophylactic co-trimoxazole

108
Q

What can HIV increase the risk of? And how can this be monitored?

A
  • CVD: monitor RF, blood lipids
  • HPV & cervical cancer: yearly cervical smears
109
Q

What vaccines should be avoided in patients with HIV?

A

Live vaccines: BCG and typhoid

110
Q

How can HIV transmission during birth be reduced?

A
  • If mother’s viral load< 50 copies/ml: normal vaginal delivery
  • If mother’s viral load> 50 copies/ml: consider pre-labour C section
  • If mother’s viral load> 400 copies/ml: pre-labour C section
  • If mother’s viral load unknown or > 1000 copies/ml: IV zidovudine given
111
Q

What prophylaxis is given to babies when mother has HIV?

A
  • Low-risk babies: zidovudine for 2-4 weeks
  • High-risk babies: zidovudine, lamivudine & nevirapine for 4 weeks
112
Q

What is PEP?

A

Post-exposure prophylaxis
* Must be commenced within 72 hours to reduce risk of HIV transmission
* Involves a combination of ART therapy: emtricitabine/tenofovir & raltegravir for 28 days

113
Q

What is PrEP?

A

Pre-exposure prophylaxis
* Taken before exposure to reduce risk of HIV transmission
* Usually emitricitabine/tenofovir

114
Q

What is contact tracing?

A

Process of telling your sexual partners that they may have been exposed to an STI to help them

115
Q

What is a paraphilia?

A

Experiencing recurring/intense sexual arousal to atypical objects, places, situations, fantasies, behaviours

116
Q

Name some examples of paraphilias

A
  • Voyeurism
  • Exhibitionism
  • Frotteurism: touching unconsenting person
  • Sexual masochism: being humiliated etc
  • Sexual sadism: suffering of another person
  • Paedophilia: sexual activity w/ prepubescent child
  • Fetishism e.g. somnophilia (unconscious), urophilia (urine)
  • Autogynaephilia (men aroused by visualising themselves as women)
  • Necrophilia
117
Q

What is the treatment for paraphilias?

A

Psychotherapy: CBT

118
Q

What is sexual aversion disorder?

A
  • Sexual disorder characterised by extreme avoidance of genital sexual contact with a sexual partner
  • More common in females
  • Accompanied by fear, revulsion, disgust, anxiety when faced with sexual situations
  • People with SAD may use strategies to avoid sexual contact: e.g falling asleep early, neglecting appearance, burying themselves in work
  • Can be helped with CBT
119
Q

What is hypoactive sexual desire disorder?

A
  • Sexual dysfunction that causes lack of sexual desire/interest and distress in relationships
  • Can be helped with hormone therapy (oestrogen), lifestyle changes & meds to boost libido
120
Q

What is female sexual arousal disorder?

A
  • Type of sexual dysfunction that makes it hard to get aroused and can affect a woman’s ability to reach orgasm
  • Can cause distress, low self-esteem, relationship problems
  • Can be helped with counselling & SSRIs
121
Q

What is erectile dysfunction?

A

An inability to obtain or maintain an erection sufficient for penetration and for the satisfaction of both sexual partners

122
Q

What are some causes of erectile dysfunction?

A
  • Vascular: HTN, atherosclerosis, hyperlipidemia, smoking
  • Neuro: Parkinson’s, MS, stroke, peripheral neuropathy, spinal cord injury
  • Hormonal: hypogonadism, hyperprolactinaemia, thyroid disease, Cushing’s
  • Drug induced: antihypertensives, BB, diuretics, antidepressants, antipsychotics, anticonvulsants, recreational drugs
  • Structural: pelvic/penile trauma, Peyronie’s disease
  • Systemic disease: DM, renal failure
  • Psychogenic: depression, anxiety, schizophrenia, performance anxiety
123
Q

What questions should you ask in an ED history?

A
  • Onset of sexual dysfunction (short vs gradual)
  • Duration of sexual dysfunction (lifetime vs acquired)
  • Difficulties with arousal
  • Rigidity of erections
  • Duration of sexual stimulation
  • Difficulties with ejaculation
  • Difficulties with orgasm
  • Presence/absence of morning erections
124
Q

What investigations are done for ED?

A

Based on the suspected cause of the ED e.g. vascular cause suspected –> tests to evaluate CVD risk
* FBC
* LFTs
* U&Es
* TFTs
* Lipid profile
* Fasting glucose and/or HbA1C
* Serum total testosterone

125
Q

In cases of complex or refractory ED, what specialised tests can be done?

A
  • Nocturnal penile tumescence testing (NPT): used to distinguish between organic vs psychogenic ED. Pt wears device overnight - measures number, tumescence & rigidity of erections
  • Duplex doppler imaging/angiography: if vascular cause suspected
126
Q

What is the management of ED?

A
  • Modify RF: stop smoking/drinking, wt loss
  • Phosphodiesterase-5 inhibitors (PDE-5 inhibitors): sildenafil, vardenafil, avanafil
  • Psychosexual councelling
  • Hormone therapy: e.g. low testosterone
  • Penile prosthesis: inflatable implants vs semirigid rods
127
Q

What can untreated ED lead to an increased risk of?

A

CVD

128
Q

What is female orgasmic disorder?

A

Difficulty/inability for a woman to reach orgasm during sexual stimulation

129
Q

What are the 4 types of orgasmic dysfunction?

A
  • Primary anorgasmia: never had an orgasm
  • Secondary anorgasmia: difficulty reaching orgasm, even tho had one before
  • Situational anorgasmia: MC, can only orgasm during specific situations e.g. oral sex, masturbation
  • General anorgasmia: inability to achieve orgasm under any circumstance, even when highly aroused
130
Q

What is the treatment for orgasmic dysfunction?

A
  • Treat underlying medical conditions
  • Switch antidepressant meds
  • CBT/ sex therapy
  • Oestrogen hormone therapy
131
Q

What is delayed ejaculation?

A

Condition where it takes a long period of sexual arousal to reach climax and release ejaculate.
Some people with DE can’t ejaculate at all

132
Q

How is delayed ejaculation classified?

A
  • Lifelong vs acquired: lifelong means present from time of sexual maturity, acquired means after a period of typical sexual functioning
  • Generalised vs situational: generalised isn’t limited to certain partners/kinds of arousal, situational happens only under certain conditions
133
Q

What are some psychological and medical causes of delayed ejaculation?

A
  • Depression/anxiety
  • Some antidepressants/antipsychotics
  • Other substances: antiHTN, diuretics, alcohol
  • Relationship problems
  • Performance anxiety/Poor body image
  • Cultural/religious taboos
134
Q

What are some physical causes of delayed ejaculation?

A
  • Birth defects that affect reproductive system
  • Injury to pelvic nerves that control orgasm
  • UTI
  • Prostate surgery
  • Diabetic neuropathy, stroke, spinal cord nerve damage
  • Hypothyroidism, hypogonadism (low testosterone)
  • Retrograde ejaculation
135
Q

What are some medications used to treat delayed ejaculation?

A
  • Amantadine (Parkinson’s)
  • Buspirone (anxiety)
  • Cyproheptadine (allergies)
136
Q

What is premature ejaculation?

A

Occurs when men ejaculate sooner than wanted during sex
* Always/nearly always ejaculate within 1-3 minutes of penetration
* Are not able to delay ejaculation all/nearly all the time

137
Q

What is the treatment for premature ejaculation?

A
  • Behavioural techniques: e.g. masturbate 1-2 hours before intercourse
  • Medications: e.g. topical lidocaine 10 mins before sex to reduce sensation and help delay ejaculation, SSRIs
  • Counselling
138
Q

What is retrograde ejaculation?

A

When semen enters bladder instead of emerging through penis during orgasm
* Still reach climax but ejaculate little/no semen = dry orgasm
* RE isn’t harmful but can cause male infertility

139
Q

What causes retrograde ejaculation?

A

Bladder neck muscle doesn’t tighten properly –> ejaculate enters bladder

140
Q

What increases your risk of having retrograde ejaculation?

A
  • DM, MS
  • Prostate/bladder surgery
  • Certain antiHTN drugs, antidepressants
  • Spinal cord injury
141
Q

What are some medications to treat retrograde ejaculation?

A
  • Imipramine (antidepressant)
  • Midodrine (constricts blood vessels)
  • Chlorpheniramine (antihistamine)

These help keep bladder neck muscle closed during ejaculation

142
Q

What is dyspareunia?

A

Pain during intercourse

143
Q

What are some possible causes of dyspareunia?

A
  • Vaginal dryness: from menopause, childbirth, breastfeeding, meds etc.
  • Skin disorders that cause ulcers, itching, burning etc.
  • UTIs
  • Vaginismus
  • Endometriosis
  • Pelvic Inflammatory Disease
  • Uterine fibroids
  • Stress
  • Self-image/body issues
  • Cancer, arthritis, diabetes, thyroid disease
144
Q

Who is at increased risk of dyspareunia?

A
  • More common in women
  • Take meds that cause vaginal dryness
  • Have viral/bacterial infection
  • Postmenopausal
145
Q

How is dyspareunia treated?

A

Treat underlying cause:
* ABs
* Antifungal meds
* Topical corticosteroids
* Oestrogen

146
Q

What is vaginismus?

A

Involuntary tensing of the vagina/pelvic floor muscles

147
Q

What causes are linked to vaginismus?

A
  • Past sexual abuse/ trauma
  • Past painful intercourse
  • Emotional factors
148
Q

What is the treatment of vaginismus?

A
  • Education & counselling
  • Pelvic floor exercises
  • Vaginal dilators
149
Q

What is vulvodynia?

A

Long-term pain in the vulva
* burning, irritation, stinging, rawness, soreness, sharp/knife-like

150
Q

What factors can contribute to vulvodynia?

A
  • Injury/irritation of nerves of the vulva
  • Past vaginal infections
  • Inflammation that affects vulva
  • Some genetic conditions
  • Allergies
  • Hormonal changes
151
Q

What investigations are done for vulvodynia?

A
  • Pelvic exam
  • Swabs
  • Biopsy
  • Bloods: hormone levels
152
Q

What medications are used to treat vulvodynia?

A
  • Antidepressants/anticonvulsants: ease long-term pain
  • Local anaesthetic: lidocaine before sex (short term pain relief)
  • Nerve blocks: given near to nerves that are sensitive to pain (long-standing pain that doesn’t respond to other Tx)
  • Hormone creams: oestrogen
  • Antihistamines: reduce itching
153
Q

What therapy is available to treat vulvodynia?

A
  • Pelvic floor therapy
  • CBT
  • Couples therapy
154
Q

What is Peyronie disease?

A

Condition that causes fibrous scar tissue to form in penis causing curved, painful erections

155
Q

What are the symptoms of Peyronie’s disease?

A
  • Swelling that later causes a hard lump to develop on shaft of penis
  • Curve in penis when erect
  • Painful erections: make sex difficult
  • Problems getting/keeping an erection
156
Q

What increases your risk of developing Peyronie’s disease?

A
  • Injury
  • DM
  • HTN
  • High cholesterol
  • CHD
  • Arteriosclerosis
  • Meds: BBs / antidepressants
157
Q

What are the treatment options for Peyronie’s disease?

A
  • Meds to slow down growth of hard area on penis / treat ED - verapamil and xiaflex
  • Sound waves to break down hard area
  • Surgery to straighten penis
158
Q

What is azoospermia?

A

No sperm found in ejaculate: can be obstructive or non-obstructive

159
Q

What are the types of azoospermia?

A

Pre-testicular
* imparied production of hormones responsible for creating sperm

Testicular
* abnormalities in structure/function of testicles

Post-testicular
* problems with ejaculation due to obstruction in reproductive tract

160
Q

What are some causes of non-obstructive azoospermia?

A
  • Genetic disorders/damage to hypothalamus & pituitary gland: hormone related azoospermia
  • Absence of testicles
  • Cryptorchidism (testicles haven’t dropped)
  • Sertoli cell-only syndrome (don’t produce sperm)
  • Tumours
  • Radiation
  • Diabetes
161
Q

What are some causes of obstructive azoospermia?

A
  • Missing connection somewhere: e.g epididymis / vas deferens tubes
  • Congenital: e.g. congenital bilateral absence of vas deferens (CBAVD)
  • Previous/current infection
  • Cysts, injury, vasectomy
162
Q

What is the treatment of azoospermia?

A
  • Obstructive: Surgery (reconnecting/reconstructing tubes that aren’t allowing sperm to flow)
  • Pre-testicular: hormonal Tx
  • Testicular: may not respond to medical Tx*

*Can still have biological children with IVF

163
Q

What is hypospadias?

A
  • Male birth defect where opening of penis is on underside rather than tip
  • Causes downward curve of penis & abnormal spraying during urination
164
Q

What are some risk factors for hypospadias?

A
  • FHx
  • Genetics
  • Maternal age > 35
165
Q

What is the treatment of hypospadias?

A

Surgery to reposition urethral opening (usually done between 6 -12 months)

166
Q

What is anejaculation?

A

Orgasm occurs but semen isn’t released from penis

167
Q

What are some causes of anejaculation?

A
  • Diabetes
  • Infections
  • Meds: antidepressants/alpha blockers to treat HTN/enlarged prostate
  • Nerve damage from bladder/prostate surgery
  • Parkinson’s/ MS
  • Spinal cord injury
  • Testicular cancer Tx
  • Anxiety/depression
168
Q

What is the treatment for anejaculation?

A
  • Psychotherapy
  • Sex therapy
  • Anxiety meds
169
Q

What is sexuality?

A

How you identify, how you experience sexual & romantic attraction, your interest in/preferences around sexual & romantic relationships & behaviour

170
Q

What is paraphimosis

A

Retraction of the foreskin but cant push it back - can lead to ischemia

Phase 3a - Arun&Erin (15 decks)

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