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year 3 > Sex Ed > Flashcards

Sex Ed Flashcards

1
Q

What bacteria is responsible in maintaining the pH of the vagina

A

Doderlein Lactobacilli

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2
Q

How does Doderlein Lactobacilli maintain the pH of the vagina

A

Glucose -> lactic acid

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3
Q

What is the normal pH of the vagina and why

A

4.5, prevents growth of bacteria

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4
Q

Symptoms of vulvovaginitieg

A
  1. Change in colour/volume/smell of discharge
  2. Itching
  3. Burning
  4. Irritation
  5. Dyspareunia
  6. Dysuria
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5
Q

Non-infectious causes of vulvovaginitieg

A
  1. Atrophic Vaginitis (post-menopause)
  2. Retained Foreign objects (condoms, tampons).

Needs to be examined by speculum

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6
Q

Examination findings in atrophic vaginitis

A
  1. Smooth, Shiny Vaginal Epithelium and strpophy
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7
Q

What causes atrophic vaginities

A
  1. Lack of oestrogen to maintain uterus wall causes thinning and inflammation
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8
Q

RF for atrophic vaginitis

A
  1. Smoking

2. Breastfeeding

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9
Q

Treatment of atrophic vaginitis

A

Local Oestorgen creams

Lubricants

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10
Q

Three types of infectious vulvovagiitis

A
  1. Bacterial Vaginosis
  2. Candida Vulvovaginitis

^ imbalance in normal flora

  1. Trichomoniasis

^ STD

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11
Q

What STDs cause cervicitis rather than vulvovaginitis

A
  1. Gonnorheoa
  2. Chlamidyia
  3. Mycoplasma

Vaginitis is rare

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12
Q

What is bacteria vaginosis

A

When number of lactobacilli decrease = increase in pH

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13
Q

What bacterial species will proliferate in when there is a lack of lactobacilli

A
  1. Gardnerella vaginalis
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14
Q

RF for bacterial vaginosis

A
  1. New sex partenr
  2. Multiple partners
  3. Douches
  4. Antibiotics
  5. IUD

NOT A STD as it doesn’t colonise the male reproductive tract

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15
Q

5 Characteristics of discharge in bacterial vaginosis

A
  1. Thin
  2. Homogenous
  3. Grey
  4. Foul Smell that gets WORST when having sex
  5. NO VULVAL INVOLVEMENTR
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16
Q

Consequence of other symptoms of bacterial vaginosis that were not mentioned in the previous card

A

Signs of mixed infection

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17
Q

Criteria for Bacterial Vaginosis

A

AMSEL CRITERIA

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18
Q

What is the Amsel Criteria

A

3 of 4 must be met:

  1. Thin Grey Vaginal Discharge
  2. Vaginal pH> 4,5
  3. Positive WHIFF-AMINE TEST
  4. SALINE WET MOUNT FOR CLUE CELLS
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19
Q

What is the WHIFF-AMINE TEST

A
  1. Discharge placed on slide and 10% KOH added

causes a fishy odour

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20
Q

What are clue cells

A
  1. Vaginal epithelial cells with coccobacilli (stippled borders)
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21
Q

Treatment of bacterial vaginosis

A
  1. Oral Metronidazole (500mg 2x daily for 7 days)

OR

Vaginal Creams (2% CLindamycin)

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22
Q

What topical antiboitic should not be used with condoms

A
  1. CLINDAMYCIN (makes them less effective)
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23
Q

What species of candida causes candida vulvovaginitis

A

Candida albicans (normally present in low numbers)

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24
Q

RF for candidiasis

A
  1. Immunosuppressions (glucocorticoids)
  2. DM
  3. Antiboitics
  4. Increased oestrogen levels (pregnancy, contraception and COCP)
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25
Q

Symptoms of candidiasis

A
  1. Intense itching
  2. Thick, White ‘cottage cheese’, odourless vaginal discharge
  3. Vulva is also flamed
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26
Q

Symptoms specific to vulva inflammation

A
  1. Dyspareunia

2. Dysuria

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27
Q

Screening for candidiasis

A
  1. Saline wet mount (10% KOH to destroy cellular elements)

2. Vaginal Culture if no pathogens seen on microscopy or recurrent symptoms or non-albicans species

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28
Q

What would be seen under a saline wet mount for candidiasis

A
  1. Yeast or hyphae form
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29
Q

What is uncomplicated candidiasis

A
  • Otherwise healthy, immunocompetent, non-pregnancy females
  • <3 Episodes in the past year with MILD to MODERATE SYMPTOMS
  • Confirmed albicans species
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30
Q

How is uncomplicated candidiasis treated

A

Single 150 mg ORAL FLUCONAZOLE

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31
Q

What is complicated candidiasis

A
  1. Pregnant/DM/Immunosupressed
  2. Severe Symptoms
  3. History of >3 episodes in one year
  4. Non-Albicans
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32
Q

Treatment of complicated candidiasis

A
  1. 2/3 doses of 150mg Fluconazole (72 hours apart)

2. Intravaginal Boric Acid

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33
Q

Symptoms of Trichomoniasis infection 1

A
  1. THIN, Purluent vaginal discharge
  2. Burning and Itching
  3. Dysuria
  4. Urinary frequency
  5. Lower abdomen pain
  6. Dyspareunia
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34
Q

Diagnosis of trichomoniasis

A
  1. Erythema of cultus and vaginal mucosa
  2. MOTILE Trichomonads on saline wet mount
  3. GOLD” nucleic Acid Amplification Test (NAAT) for DNA
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35
Q

Treatment of trichomoniasis

A
  1. 2g oral Metronidazole (or Tinidazole but not for pregnancies)
  2. Screen all partners.
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36
Q

Characteristics of Treponema Pallidum

A
  1. Gram-Negative, Spirochetes.

2. Obligate Parasite

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37
Q

What is an obligate parasite

A

Cannot survive outside the host

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38
Q

Adapation of a spirochete

A
  1. Spiral shape contains endoflagella to move them about by spinning
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39
Q

Two ways syphilis can be transmitted

A
  1. Acquired syphilis: enters through bodily fluid

2. Congenital Syphilis

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40
Q

Passages of acquired syphilis

A
  1. Cuts/breaks in skin or mucous membranes of the external genitalia and mouth
  2. Sexual Contact (oral, anal or vaginal)
  3. Contaimated needles
  4. direct contacts with skin lesions containing spirochetes
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41
Q

What is congenital syphilis

A
  1. Mother has syphilis and t.pallidum infects baby during vaginal delivery.
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42
Q

Four stages of infection in acquired syphilis

A
  1. Primary, early localised stage (week 1-3):

Spirochetes destroys the skin and soft tissue where they enter the body - painless CHANCRES that heal on their own

  1. Secondary, dissemination stage (week 6-12)

Spirochetes invade the lymph nodes causing lymphadenopathy -> lymph -> blood

Spirochetes enter the blood (spriochetaemia), causing generalised lymphadenopathy.

Spirochetes attach to endothelial cells and capillaries on surface = non-itchy maculopapular rash

Either pustular or papulosquamous (scaly and hard).

Resolves in a few weeks

  1. Latent phase

Disease enters a dormant phase, spirochetes found in capillaries of organs and tissues

Early sub-phase:

During the first year of infection, spirochetes re-enter the blood. Can still be found circulating in the blood, causing secondary stage symptoms

Late sub-phase:

After the first year of infection.

Tertiary Phase:
Overall, capitally infection causes a severe immune response.

Type IV hypersensitivity reaction:

T-cells recruit macrophages and release TNF and IL-1 and IL-6

Swelling, oedema, redness and warmth, fever.

Plasma cells produce antibodies against t/ pallidum antigens and stick to them to form Gumma

These gummy form organ damage:

Cardiovascular syphilis, neurosyphilis

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43
Q

Three characteristics of Chancres

A
  1. Raised Border
  2. Hard Base
  3. Fluid Rich in Spirochetes that spread to other parts of the body and individuals

Look at where the primary chancre originated from to see how it was transmitted.

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44
Q

When might a primary chancre not be seen in syphilis

A
  1. BLOOD TRANSFUSION
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45
Q

How does the maculopapular rash in stage 2 of acquired syphilis spread

A

Trunks -> arms and legs, genitalia -> palms and soles

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46
Q

Three types of rashes found in stage 2 syphilis

A
  1. Pustular
  2. Papulosquamous
  3. Condyloma Lata (white painless rash found in moist regions)
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47
Q

Most infectious stage of syphilis

A
  1. Stage 2, secondary.
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48
Q

Three main antigens of t. palladium

A
  1. Group specific antigen
    Species specific antigen

Cardiolipin

Plasma cells produce antibodies against these antigens

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49
Q

Structure of a gamma

A
  1. Immune cell complex, surrounded by fibroblasts.

Inside is coagulative necrotic

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50
Q

What is cardiovascular syphilis

A
  1. Endarteritis (vaso vasorum inflammation which supplies the blood vessels)

Can cause aortic aneurysms

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51
Q

What is neurosyphilis

A
  1. Spirochetes sit in the capillaries supplyingg the posterior spinal cord = Tabes Dorsalis
  2. Destroys protective sheath of spinal cord nerves: Loss of vibration sense and proprioception.

Sometimes, they invade the anterior spinal cord: General Paresis (loss of sensation and weakness).

  1. Invade into brain: Slurred speech, beavhiour, memory loss, difficulty coordinating and paralysis
  2. Invade into the eyes
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52
Q

Sign of eye invasion of syphilis

A
  1. Argyll Robertson Pupil
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53
Q

What is Argyll Robertson Pupil

A
  1. Pupil loses light reflex but has accommodation reflex, which means it constricts with a nearby object but no response to light
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54
Q

Two ways a baby can be infected with syphilis

A
  1. Placenta

2. Childbirth

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55
Q

Symptoms of early disease of syphilis in babies

A
  1. Snuffles
  2. Maculopapular rash
  3. Hepatosplenomegaly from organ damage
  4. Optic neuritis
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56
Q

Symptoms of late disease of syphilis in babies

A
  1. Saddle Nose
  2. Saber Shins
  3. Hutchinson Teeth
  4. Hearing Loss
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57
Q

Diagnosis of syphilis

A
  1. Non-Treponemal Tests:

Rapid Plasma Reagin test
2. Venereal Disease Research Lab Test

to detect anti-cardiolipin (REAGIN)

  1. Trependemal Tests:

T.pallidum particle agglutination
2. Fluorescent treponema antibody absorbed. Detect antibodies specifically targeting t pallidum.

58
Q

Diagnosing congenital syphilis

A
  1. If baby has four times higher the non-treponema serological titer
  2. CSF fluid: VDRL, cell count and protein
  3. Long Bone X-rAYS
  4. Eye exam
  5. Hearing test s
59
Q

Treatment of syphilis

A
  1. IM Penecillin G Benzathine

IV in neurosyphilis

  1. Doxycyclin
60
Q

What is the Jarisch-Herxheimer Reaction

A
  1. Spirochetes die and release lots of antigens together.

Causes severe IMMUNE REACTION.

Lasts for a few days.

61
Q

Types of hypersensitivity reactions

A

I: IgE mediated (exposure to external antigens/allergies)
II: Antibody-mediated cytotoxic reaction (IgG or IgM) (antibodies binding to antigens in host tissues)
III: Immune complex-mediated (SLE, glomerulonephritis, RA)
IV: Cell-mediated, delayed.

62
Q

Type 1 vs Type 2 herpes simplex virus

A

Type 1: NO ANTIBODIES to HSV

Painful vesicles on erythematous base
Pruritus
Dysuria
Inguinal Lymphadenopathy

Systemic Symptoms

Type 2: Antiboidies

NON-PRIMARY INFECTION

Less severe

GENERALLY, HSV-1 is above the waist infection, while HSV-2 is below the waist

63
Q

Two characteristics of HSV-1 strains

A

Envelope, double stranded DNA

64
Q

How can Herpes spread

A
  1. Most contagious when virus-filled lesions are present 2. Spread by asymptomatic shedding (ie., Saliva and Genital secretions)

Usually moves into the body through small cracks in the skin or mucosa. Binds to epithelial cells receptors and get abosrbed

65
Q

What is the lytic cycle

A
  1. Where the viral DNA is transcribed and Translate by cells, forming new viral proteins = new herpes viruses that invade neighbouring epithelial cells.
66
Q

Where do HSV strains remain dormant in the body

A

HSV-1: Trigeminal Ganglia

HSV-2: Sacral Ganglia (genitalia neurons)

FOR LIFE

67
Q

When HSV re-activates in the neurones, how do symptoms present

A

Trigeminal and Sacral ganglions serve only one side of the face and body:

Ulcers form on the ipsilateral side as the ganglion ove

68
Q

Triggers for HSV

A
  1. Stress
  2. Skin Damage
  3. Viral Illness

Recurrent episodes are less severe

69
Q

Symptoms of HSV

A
  1. Prodrome: Tingling or Burning before ipsilateral blisters appear.

Primary Infection is asymptomatic except in children: Gums, palate, tongue, lips

Fever and Enlarged Lymph Nodes.

Pharyngitis

  1. GENITALS:

Form at the lbaia majora, mons pubis, vaginal mucosa and cervix in women

Shaft of penis in men.

  1. Keratoconjuctivitis

Pain, Redness, Tearing, Light sensitivity

Corneal involvement:
Blurry Vision, Branching Dendritic Lesions (CLASSIC)

  1. NEuro:

Meningiitis or Encephalitis from Temporal lobe infection

Commonly happens during reactivation

Requirews a lumbar puncture

70
Q

Characteristics of HSV lesions

A

Small, painful fluid filled blisters that ulcerate and heal in a few weeks.

71
Q

Where do HSV blisters form

A

The Vermilion border (border of the lip).

72
Q

What is Herpetic Whitlow

A

Infection of HSV at the finger tips

Easy to get carrie to to other parts of the body (auto inoculation)

73
Q

What is Herpes Gladiatorum

A
  1. Infection of trunk, extremities and head from skin to skin contacts (common among wrestlers).
74
Q

What is Eczema Herpeticum

A

HSV infection from Atopic Dermatitis

75
Q

What does a lumbar puncture show for HSV

A
  1. Increased RBC, EBCs and protein levels
76
Q

Symptoms of Neonatal HSV

A
  1. Skin, Eye and Mucous membrane infection (at site of damaged skin)
  2. CNS infection (lethargy, irritability, seizures)

Requires lumbar puncture, CT, MRI and EEG

2-3 weeks after delivery
3. Disseminated infection: Sepsis and organ failure.

77
Q

Diagnosis of HSV

A
  1. PCVR
  2. Antibody responses
  3. Viral culture
78
Q

Treatment of HSV

A
  1. Often resolves its own

2. Acyclovir at start of prodrome

79
Q

Symptoms of Acutec PID

A
  1. Lower abode pain that WORSENS during sexual intercourse or sudden movement
  2. Post-coital bleeding
  3. Intermenstrual bleeding
80
Q

Symptoms of Chronic PID

A
  1. Weight loss, abdominal pain

2. Fever gradually increases

81
Q

Investigations for STDs

A
  1. First-Void Urine
  2. Nucleic Acid Amplification Test
  3. Urethral and endocervical swabs
  4. HIV testing
82
Q

First line treatment for Chlamidyia

A
  1. Doxycycline (100mg twice daily for 7 days)

2. Azithromycin if not tolerated

83
Q

Symptoms of Chlamidyia

A
  1. Increased Vaginal Discharge
  2. Post coital bleeding
  3. Prupulent vaginal dischagre
  4. Dysuria
  5. Pelvic pain

Remember, asymptomatic in 70% of women

84
Q

What other parts of the body may chlamidyia present

A
  1. Lymphogranuloma centrum: tenesmus, anorectal discharge, diarrhoea
  2. Rectal chalmidyia (anal discharge)
  3. Adult conjunctivitis
  4. Oropharyngeal infection
85
Q

What is Reactive Arthritis

A

Triad:

  1. Conjunctivitis
  2. Nongonoccoccal urethritis
  3. ASYMETRIC OLIGOARTHRITIS

Can’t see, can’t pee, can’t climb a tree

Also keratoderma blennorhagica, achilles tenditis.

86
Q

What STD causes reactive arthritis

A

Chlamidyia

87
Q

RF for reactive arthritis

A
  1. Male
  2. 20-40 years olf
  3. White (as they more likely carry HLA-B27 gene)
88
Q

Diagnosis of Syphilis

A
  1. Dark-field microscopy
  2. PCR
  3. TPPA
  4. VDRL
89
Q

Hep A: Chronic or Acute

A

Acute

90
Q

Where is Hep A contracted

A

Food and Water

91
Q

How does the Immune system tackle Hep A

A

Anti- HAV IgM is raised over 6 weejs

Anti- HAV IgG rises slowly during this time and after (persist for life)

So if someone has IgG but no IgM, they were vaccinated but not infected or had a prior infection

92
Q

Treatment of Hep A

A

Fluids

93
Q

Hep E, acute or chronic

A

Acute mainly but can be chronic in immunocompromised

94
Q

Hep E transmission

A

Food and water

Pregnancy (vertical transmission) - can cause acute liver failure

95
Q

Diagnosis of Hep E

A

Stool culture and blood tests to check for HEV RNA

96
Q

Treatment of Hep E

A
  1. Liver transplant

2. Ribavirin

97
Q

Transmission of Hep B

A
  1. Acute AND Chronic

2. Blood, body fluids and vertical transmission

98
Q

Serology of Hep B

A
  1. HesAg and Anti-Hbs

If one is positive, the other is negative

99
Q

What is the exception to having no HBsAG or Anti-Hbs

A
  1. Cleared infection (anti-has has not rise enough to be detected)
  2. Never exposed
100
Q

Hep B infection serology in chronic or acute infection vs vaccinated or recovered

A
  1. HbsAg positive, but Anti-HBs negative

2. HBsAg negative, but Anti-HBs positive

101
Q

Antibodies found in Hep B

A
  1. Antibodies AGAINST HBcAg

IgM-anti-HBc and total anti-HBc

Total Anti-HBc remains high but the former decreases

HBeAg: positive = highly infectious

Sign of replication

HBV DNA PCR: Mirrors HBeAg

Shows virus is replicating

102
Q

Complication of Hep B

A

Cirrhorsis - Hepatocellular carcinoma

103
Q

Treatment of chronic Hep B

A
  1. Pegylated Interferron SC

2. Tenofovir

104
Q

Transmission of Hep D

A

Body fluids and Blood

105
Q

What’s interesting about Hep D

A

Has a HBsAg outer envelope (HBV), so requires prior HBV virus to infect: CO-INFECTION

They infect each other at the same time or during a chronic Hep B infection

106
Q

Testing for Hep D

A
  1. Hep B confirmation test
  2. HDV IgM
  3. Total HDV antibodies
  4. HDV RNA
  5. HDag
107
Q

Treatment of Hep D

A
  1. Peg-INF alpha-2a (HDV RNA elevated) or 2b (AST and ALT elevated)
108
Q

Transmission of Hep C

A
  1. Blood or body fluids
109
Q

Extrahepatic manifestations of hep c

A
  1. Cryoglobulinemia
  2. Membranoproliferative glomerulonephritis
  3. Prophyria Cutanea Tarda (blisters)
110
Q

Microscopic findings for gonnorhoea

A

Gram negative, diplococci

111
Q

Prevalence of symptoms in gonorrhoea vs chlamidyia

A

G - 90%

C - 10%

112
Q

Treatment of Chlamidyia

A

Doxycycline

113
Q

Treatment of Gonnorheoa

A

IM Ceftriaxone - GOLD STANDARD

114
Q

What causes Lymphogranuloma centrum

A

C. Trachematis

115
Q

LGV vs Syphilis

A

Syphilis is a indurated lesion with one swollen inguinal ligament.

This is Groove Sign

116
Q

What is a main cause for a painful genital lesion that bleeds on contact

A

Chancroids (haemophilus Ducreyi infection)

117
Q

Treatment of Chancroids

A

Ciprofloxacin and Ceftriaxone

118
Q

What is the GODL standard diagnostic for HIV

A

HIV antibody AND HIV antigen testing

119
Q

What forms part of post-exposure prophylaxis in HIV

A

Raltegrivir and Truvada

120
Q

When is cART indicated for HIV

A

CD4 + < 200

AIDS diagnosis

Or if HIV is already diagnosed and CD4 starts to fall below 350

121
Q

VDRL vs TPPA as markers for syphilis

A

VDRL is released immediately after infection and then go away

TPPA are present for the rest of your life, as a marker for a previous syphilis infection

122
Q

Appearance of non-malicious penile ulcers

A

Smooth lesions around the coronal margin of the glans

Re-assure and discharge

123
Q

First Line treatment for pneumocystis pneumonia

A

Co-Trimoxazole

124
Q

What is the first line contraceptive in under 18s for controlling painful, heavy periods

A

COCP

125
Q

Appearance of trichomoniasis

A

Motile PROTOZOA

126
Q

What is the most effective treatment for Kaposi’s sarcoma

A

Starting cART

127
Q

Most common cause of epididymis-orchitis in older guys

A

E.COli

128
Q

What long-term contraception can be given to women with fibroids

A

IUS! Controls heavy bleeding from fibroids

129
Q

What is the initial screening tool for Syphilis

A

EIA

130
Q

What serum levels are monitored for Syphilis treatment

A

RPR

131
Q

What condition can result in increased CA-125

A

PID

132
Q

After prescribing antibiotics to a pregnant woman for UTIs, what should be the next management step

A

Urine Culture

133
Q

Main treatment of cellulitis

A

Clarithromycin

134
Q

Most common cause for viral meningitis in adults

A

Coxsackie B

135
Q

Management of necrotising Fasciitis

A

Surgical Debridement

136
Q

How long should someone with infectious mononucleosis avoid contact sports for

A

8 weeks after having glandular fever

137
Q

What does lymphogranuloma venerum associate with that isn’t seen in Syphillis

A

Proctocollitis and rectal bleeding

138
Q

What is diagnostic for HIV in the early stages of infection (3-12 weeks)

A

HIV p24 antigen testing

139
Q

How often should valaciclovir be used to treat herpes

A

Twice daily for 10 days

140
Q

How often is Metronidazole given to women for

A

5-7 days

year 3 (25 decks)

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