STD's Flashcards

1
Q

List the sexually transmitted diseases

A
Chlamydia
Ghonnorhea
Trichinomas vaginalis
PID
Genital herpes
Genital warts
HIV
Syphillis
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2
Q

What causes genital herpes

A

Herpes simplex virus.

transmitted via skin-to-skin contact -vaginal, anal or oral sex

virus can lie dormant until it recurs later in life causing recurrent outbreaks.

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3
Q

Pathophysiology behind genital herpes

A

Two types of HSV
HSV1: Genital & Oral herpes
HSV2: Genital herpes

HSV enters the body through small cracks in the skin or through the mucous membranes of mouth, vagina, rectum, urethra or under the foreskin.

After infecting the surface, the virus travels up the nearest nerve to the ganglion and remains there.

Remains dormant for long, as here it cannot be reached by the immune system.

During the reactivation of the virus, it travels back down the nerve onto the surface of the genitals once again to cause a symptomatic outbreak.

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4
Q

How does HSV spread even when people are unaware of infection

A

Asymptomatic shedding

When the virus multiplies and becomes transmissible without stimulating an immune response from the host and thus no symptoms are present

HSV is notorious for this and up to 1/3 of all transmissions occur this way

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5
Q

Risk Factors for genital herpes

A

multiple sexual partners

oral sex with a partner suffering from cold sores

Barrier contraception reduces risk but transmission is still possible especially by areas not covered by condoms e.g. THIGHS

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6
Q

Sx of genital herpes

A

Primary infection symptoms

Secondary (recurrent) infection symptoms

Cold sores

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7
Q

Primary infection symptoms of herpes

A

1)Small red blisters around the genitals that are very painful and can form open sores
HEAL AFTER 20 DAYS
-F: vulva, clitoris, buttocks and anus
-M: penis n same
2) Vaginal or penile discharge
3) Flu-like symptoms, fever, muscle aches
4) Itchy genitals

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8
Q

Secondary (recurrent) infection symptoms of herpes

A

recurrent outbreaks are shorter and less severe and over time outbreaks usually reduce in severity and length.

due to antibody production increasing recognition of the virus and increasing the effectiveness of response.

1) Burning and itching around the genitals
2) Painful red blisters around the genitals

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9
Q

Cold sores

A

They are mainly caused by HSV-1 and can be occasionally caused by HSV-2.

painful lesions around the mouth and nose that last between [[7-10 days]].

usually dormant with outbreaks occurring up to a few times a year.

If someone suffering from cold sores gives oral sex to a partner, the partner is at risk of contracting genital herpes as a result.

The dormant aspect of the infection means people may contract herpes from a partner without knowing. As a result this can make a diagnosis of genital herpes quite shocking and very difficult for a patient.

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10
Q

Dx of genital herpes

A

Genital ulcer sx

1) aphthous ulcers
2) varicella-zoster virus
3) trauma

[[more than 5 outbreaks]] of genital herpes in one year

indicate a weakened immune system and therefore an underlying diagnosis of HIV.

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11
Q

Dg of herpes

A

History
– sexual partners,
- history of cold sores
- history of any other STIs.

Swab from the open sore –

  • This swab will be tested for the presence of HSV and - -PCR can differentiate between type 1 and 2.
  • Even if this swab is negative, the diagnosis of herpes can still be made later on if flare-ups persist.

Other Sti
- screen for other possible std’s especially if history is suggestive

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12
Q

Management of genital herpes

A

Primary infection

1) Aciclovir:: reducing the number and size of the lesions caused by HSV
2) sexual health advice
- no sex during outbreaks
- disclose it to recent/ current partners

Recurrent outbreaks

1) [[Episodic rx]] w/ aciclovir whenever outbreaks occur
2) Over the counter painkillers, petroleum jelly and ice packs

Over 5 outbreaks a year // Severe outbreaks
-Suppressive rx : daily doses of aciclovir to prevent new outbreaks.

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13
Q

What happens to a woman with Genital herpes who gets pregnant

A

The mother should maintain rx w/ Aciclovir but the baby should be protected from acquiring the infection due to the antibodies she will pass to the foetus through the placenta.

c/S can be offered as the risk of the baby acquiring HSV transvaginally is 0-3%

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14
Q

What happens if a mother contracts Herpes herself in the last trimester of pregnancy

A

more dangerous for the baby as the mother has not produced antibodies to pass onto the growing foetus.

baby is a lot more likely to contract herpes during vaginal birth (2/5 chance) and so a caesarean section is recommended in this circumstance.

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15
Q

3 Forms of neonatal herpes

A

1) SEM:=skin, eyes and mouth herpes
2) DIS= disseminated herpes affecting the internal organs!
3) CNS herpes = affecting the nervous system and the brain and can lead to !!encephalitis!!

Aciclovir is sufficient for SEM herpes but mortality is estimated to be much higher for DIS and CNS herpes, especially if undiagnosed for some time.

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16
Q

What are genital warts

A

benign epithelial or mucosal outgrowths caused by DNA human papilloma virus (HPV).

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17
Q

How many types of HPV are there

A

over 100 types of the human papilloma virus, responsible for different types of warts.

More than 40 types of HPV have been associated with anogenital warts (condyloma acuminatum)

however HPV6 and HPV11 are responsible for roughly 90% of cases.

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18
Q

Pathophysiology of genital warts

A

spread through skin-to-skin contact during vaginal and anal sexual intercourse,

however penetrative sex is not necessary for transmission!!
——In rare cases it can be passed on from the hand to genitals, during oral sex and to the neonate during delivery.

It is important to note that condoms do not fully protect against HPV as not all skin is covered e.g. the inner thighs just like herpes

virus penetrates the epithelial barrier and !!infects basal keratinocytes!!!.

Within the keratinocyte the virus replicates resulting in multiplication of the keratinocyte and this rapid growth manifests as lesions.

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19
Q

Risk Factors for genital warts

Sim to other std’s and cervical cancer

A
Early age at first sexual intercourse
Multiple partners
Immunosuppression
Smoking
Diabetes associated with persistence of warts
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20
Q

Clinical Features of genital warts

A

Onset of weeks to years
painless, fleshy growths that can be soft or hard and can be singular or multiple.

Can also cause extragenital lesions in oral cavity, larynx, conjunctivae and the nasal cavity.

Most are assyx and spontaneously resolve

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21
Q

Dx of genital warts

A

Vestibular papillomatosis:
-projections of the vestibular epithelium or labia minora
Dx sx: non-viral and not sexually transmitted
Dx dg: Application of acetic acid does not change their colour – HPV lesions turn whitish.

Molluscum contagiosum: viral infection causing small firm raised papules on the skin.

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22
Q

What is vestibular papilomatosis

A

https://www.healthline.com/health/vestibular-papillomatosis

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23
Q

Dg work up of genital warts

A

Colposcopy and biopsy IF neoplasms suggested

Vaginal speculum

Proctoscopy - Anal lesions

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24
Q

Rx of genital warts

A

Lesion usually resolve especially postpartum

2 types: Topical rx & Physical ablation

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25
Q

Topical rx

A

Podophyllotoxin:
twice daily for 3 days followed by 4 days rest (4-5 cycles)
Clusters of small warts, better for non-keratinised lesions

Imiquimod:
3 times weekly and wash off after 6-10 hours (up to 16 wks)
Larger warts, particularly keratinised warts

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26
Q

C.I on topical rx of warts

A

Topical treatments may weaken latex condoms.

They are also contraindicated in pregnancy and breastfeeding, and may cause local inflammation.

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27
Q

Physical ablation for rx of warts

A

Excision: Pedunculated/large warts or small hard warts
-surgical removal under local anaesthetic

Cryotherapy: Multiple small warts
-freezing using liquid nitrogen usually repeated weekly (consider alternative treatment if no response after 4 weeks)

Electrosurgery: Large warts that have failed to respond to topical treatment
-excision removes the majority of the wart and then an electric current is passed through a metal loop pressed against the wart to remove any remaining part

Laser surgery: Difficult to access warts e.g. inside the anus
-a laser is used to burn the warts under local or general anaesthetic.

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28
Q

Vaccination against HPV

A

HPV vaccine is offered to all girls aged 12-13. This was introduced in 2008 and the vaccine originally protected against the high risk HPV types 16 and 18, however since 2012 the vaccine Gardasil® additionally protects against the most common types HPV 6 and 11.

The vaccine is most beneficial if administered before first sexual contact.

It is argued that only immunising females will not necessarily protect males and herd immunity will not apply to men who have sex with men.

In some countries, Gardasil is administered to both males and females.

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29
Q

How does HPV affect pregnancy

A

HPV is not associated with miscarriage, premature birth or other pregnancy complications.

due to the hormonal changes associated with pregnancy, genital warts may multiply or enlarge.

Treatment is to reduce the burden of lesions so that during childbirth the neonate’s exposure is reduced.
physical ablation methods are preferred during pregnancy .

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30
Q

Can HPV be transmitted to the baby

A

The risk of transmission to the neonate during birth is extremely low

If transmission does occur then the immune system will usually clear the virus

in rare cases the baby may develop
respiratory papillomatosis!!!
where genital warts develop in the throat.

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31
Q

What is HIV

A

human immunodeficiency virus (HIV).
a single stranded RNA retrovirus that infects and replicates within the human immune system using
host [[CD4]] cells.

Without treatment, destruction of the immune system can lead to acquired immune deficiency syndrome (AIDS).

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32
Q

Pathophysiology of HIV

A

penetrates the host CD4 cell and empties its contents.

viral RNA are converted into double stranded DNA by reverse transcriptase, and combined with the host DNA using the enzyme integrase.

The viral DNA is read, creating viral protein chains and the immature virus pushes out of the cell [retaining some cell membrane]

virus becomes mature when the protease cuts the viral protein chains, to create a working virus.
The t helper cell is destroyed during this process.

33
Q

What changes viral RNA. To DNA in Host CD4 cells

A

reverse transcriptase

34
Q

What enzyme integrates viral DNA into host DNA after conversion

A

enzyme integrase.

35
Q

What enzyme causes the maturation of the HIV virus

A

Protease during the cleavage of viral proteins and subsequent death of CD4 cells

36
Q

How do CD4 levels change in response to HIV

A normal range for CD4 cells is about 500-1,500.

A

Initial phase
-CD4 levels fall in response to the initial, rapid replication of HIV – and at this stage a person is extremely infectious. This is marked by flu like symptoms d/2 seroconversion

Latent phase begins after months- years
-patientinitially be asymptomatic, but with CD4 levels falling and viral load increasing, they may become more susceptible to infections and can later become symptomatic

AIDS

  • over an average of 10 years,
  • CD4 drops to below 200
37
Q

What are the four ways HIV is transmitted

A

Unprotected sexual contact – vaginal, anal or oral.

Sharing of injecting equipment.

Medical procedures – blood products, skin grafts, organ donation and artificial insemination.

Vertical transmission – from mother to child in utero, during childbirth or breast feeding.

38
Q

Risk groups for HIV

A

Men who have sex with men
Intravenous drug users
Those in high prevalence areas
Those who have had unprotected sex with a partner who has lived or travelled in Africa

39
Q

Classification of Sx of HIV

A

Seroconversion Illness

Symptomatic HIV

AIDS sx

40
Q

List the seroconversion illness sx

A

2-6 weeks after exposure, patients may experience a non-specific, flu-like illness. Features include:

Fever
Muscle aches
Malaise
Lymphadenopathy
Maculopapular rash
Pharyngitis

Latent phase follows

41
Q

List the sx of symptomatic HIV

A

After the latent phase

Weight loss
High temperatures
Diarrhoea
Frequent minor opportunistic infections, e.g. herpes zoster or candidiasis

42
Q

AIDS defining illnesses

A

pnuemocystis jiroveci pnuemonia,
non-Hodgkin’s lymphoma,
TB.

43
Q

Dg work up of HIV

A

ELISA
test for serum/salivary HIV antibodies and p24 antigen.
give reliable results 4-6 weeks after exposure.

44
Q

Rx of HIV

A

Highly active antiretroviral therapy (HAART)

  • does not cure HIV, but aims to reduce the viral load to undetectable levels in the serum.
  • patient must keep taking the drugs for the rest of their lives. Non-adherence to HAART can result in resistance mutations which make treatment difficult or impossible.

Combination drugs classes combine to 1x/day tablets:
nucleoside reverse transcriptase inhibitors (NRTIs)
protease inhibitors (PIs)
non-nucleoside reverse transcriptase inhibitors (NNRTIs)
integrase strand transfer inhibitors (InSTIs)

Psychological support

Regular monitoring

POST EXPOSURE PROPHYLAXIS

45
Q

Which regular tests are included in HIV monitoring

A
CD4 count
HIV viral load
FBC
Urinalysis
ALT, AST and bilirubin
Patients may also require pregnancy testing, and in treatment failure, resistance testing.
46
Q

What is post exposure prophylaxis

A

Rx for when a pt has as suspects exposure to the HIV within the last 72 hrs to lower the risk of becoming infected.

1 month course of
Truvada (one tablet daily) + Raltegravir (one tablet twice daily)

47
Q

Can HIV be transmitted to the baby ?

A

Yes.
It can be transmitted in utero
Can be transmitted during delivery and transmitted during through breastfeeding.

48
Q

How is HIV transmission to the baby prevented

A

Antenatal antiretroviral therapy during pregnancy and delivery

Avoidance of breastfeeding

Neonatal post-exposure prophylaxis

49
Q

Can HIV mothers deliver transvaginally

A

yes if the serum load is undetectable in the mother

50
Q

what is the risk of transission to the baby w/ and w/o rx

A

w/ rx adherance: <1%.

w/o rx: greater than 1 in 4

51
Q

what is syphillis

A

exually transmitted infection caused by the spirochete gram-negative bacterium Treponema pallidum subspecies pallidum.

52
Q

types of syphillis

A

Other subspecies of Treponemes are responsible for non-sexually transmitted diseases such as Bejel, a chronic skin and tissue disease, Yaws, a disease of the bones and joints, and Pinta, a skin disease. Unlike syphilis, these diseases are transmitted by any close contact (sexual or not) and do not pass from mother to fetus.

53
Q

pathophys of syphillis

A

1)primary syphilis occurs when
-motile Treponema pallidum enters through a break in the skin or through intact mucous membranes.
The bacteria divide and an infectious hard ulcer (CHANCRE) subsequently forms at the site of contact after an incubation period of 2-3 weeks. This is the first stage of acquired symptomatic syphilis:.

If left untreated, T. pallidum can persist and cause systemic damage via OBLITERATING ARTERITIS
This is where endothelial cells of the vessels excessively proliferate causing the lumen of the vessels to become narrowed. This can then result in ischaemia at the tissues supplied by these arteries which leads to the symptoms associated with syphilis.

54
Q

sx of syphillis classification

A

congenital

acquired : early (up to 2 years) / late

  • assyx(latent)
  • sxxx
    1) primary
    2) secondary
    3) tertiary
55
Q

dg of syphillis

A

Dark ground microscopy of chancre fluid- detects spirochaete in primary syphilis

PCR testing of swab from active lesion

Serology:

1) Treponemal tests – assess for exposure to treponemes necessarily syphilis)
- Treponemal ELISA (IgG/IgM) – remains positive for life
- TPPA or TPHA – remain positive for life

2) Non-treponemal tests:
- RPR/VDRL: rises in early disease; falling titres indicate successful treatment or progression to late disease. False positives can occur in inflammatory conditions or during pregnancy.
- Lumbar puncture: CSF antibody tests in neurosyphilis

56
Q

rx of syphillis

A

Penicillin is the treatment of choice.

others

  • avoid sexual contact of any kind, or exposure of other people to active lesions until the condition has been successfully treated
  • Contact tracing (ppl recently contacted)
  • Screening for other STIs
  • Follow-up serology to determine response to treatment
57
Q

what is Jarisch Herxheimer reaction!!!!

A

inflammatory response secondary to death of treponemes, and results in a flu-like illness within 24 hours of treatment

supportive measures suff

neuro/cardivascular syph: oral steroids

58
Q

preg of syphillis

A

antenatal syphillis screening should be done as it can be transferred to the fetus causing

  1. miscarriage
  2. stillbirth
  3. pre-term labour
  4. Congenital syphilis
59
Q

spread of syphillis

A

sexual transmission, the infection can also be transmitted from mother to fetus via the placenta (congenital syphilis) and through infected blood products.

60
Q

rf of syphillis

A

Engaging in unprotected sex – especially with high risk partners.
Multiple sexual partners.
Men who have sex with men (MSM).
HIV infection.

61
Q

primary syphillis

A

1) papule (slightly elevated lesion with no fluid) will appear before ulcerating into a CHANCRE at the site of inoculation
- a painless singular, hard and non-itchy ulcer
- typically develops 9-90 days post infection on a genital site e.g. penis, scrotum, anus, rectum, labia or cervix.

However, chancres may be atypical in that they can appear at other sites e.g. oral, be multiple and painful. Classically chancres

62
Q

when does a chancre heal

A

heal within 3-10 weeks with or without symptoms but may persist during secondary syphilis.

63
Q

when does Secondary syphilis occur

A

develops 3 months post infection

64
Q

sx of Secondary syphilis

A

Skin rash – hands and soles of the feet (not usually itchy or painful)
Fever
Malaise
Arthralgia
Weight loss
Headaches
Condylomata lata- elevated plaques like warts at moist areas of skin e.g. inner thighs, anogenital region, axillae
Painless lymphadenopathy
Silvery-gray mucous membrane lesions – oral, pharyngeal, genital

65
Q

what phase comes immediatley after secondary syphillis

A

LATENT PHASE comes after secondary phase

66
Q

Tertiary syphilis

3 subtypes

A

gummatous syphilis,
neurosyphilis
cardiovascular syphilis

67
Q

what is Gummatous syphilis

A

Granulomas can form in bone, skin, mucous membranes of the upper respiratory tract, mouth and viscera or connective tissue e.g. lung, liver, testis.

Patients at this stage are non-infectious.

68
Q

what is Neurosyphilis

A

Tabes dorsalis
– ataxia, numb legs, absence of deep tendon reflexes, lightning pains,
loss of pain and temperature sensation,
skin and joint damage.

Dementia – cognitive impairment, mood alterations, psychosis.

Meningovascular complications
– cranial nerve palsies, stroke, cerebral gummas.

Argyll Robertson pupil
– pupil is constricted and unreactive to light, but reacts to accommodation.

69
Q

what is Cardiovascular syphilis:

A

Aortic regurgitation due to aortic valvulitis (diastolic murmur), also aortic root dilatation.

Angina due to stenosis of the coronary ostia.

Dilation and calcification of the ascending aorta.

70
Q

how do you treat syphillis in pts w/ peniccilin allergy

A

advise penicillin desensitisation

71
Q

rx for early syph

A

Benzathine penicillin 2.4 MU IM single dose.

72
Q

rx for late syph

A

Benzathine penicillin 2.4 MU IM 3 doses at weekly intervals

73
Q

rx for neurosyphillis

A

Procaine penicillin or Benzylpenicillin

74
Q

what is the presentation of Congenital syphillis

A

saddle nose, rashes, fever and failure to gain weight.

75
Q

list the non treponemal tests

A

VDRL: rises in early disease; falling titres indicate successful treatment or progression to late disease. False positives can occur in inflammatory conditions or during pregnancy.

-Lumbar puncture: CSF antibody tests in neurosyphilis

76
Q

what is the venereal disease research laboratory (VDRL) test

A

checks for the antibodies your body makes in response to antigens produced by cells damaged by the bacteria

77
Q

What is a rapid plasma reagin (RPR) test?

A

detecting the nonspecific antibodies that your body produces while fighting the infection

78
Q

what is the Treponema pallidum particle agglutination assay (TPPA test)

A

indirect agglutination assay used for detection and titration of antibodies against the causative agent of syphilis,