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Systemic Disease (Wolfe) > STIs > Flashcards

STIs Flashcards

1
Q

What is the #1 STD optometrists see in the US?

A

chlamydia, largely asymptomatic

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2
Q

What is the #1 symptom of an STD?

A

asymptomatic

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3
Q

How many people in the US have an STI?

A

1 in 5 people, 68 million in US

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4
Q

What is the #1 transmitted STD?

A

HPV, but there is a vaccine

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5
Q

What causes syphilis?

A

spirochete Treponema Pallidum, a helical bacteria 0.18 microns wide and 5-15 microns long

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6
Q

What barriers can syphilis cross?

A

placenta, blood brain, blood retinal

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7
Q

How is syphilis most often aquired?

A

via sexual intercourse, more rarely through blood contact or contact with chancre

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8
Q

How is a spirochete directly observed?

A

dark field microscopy

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9
Q

What are the stages of syphilis?

A

primary, secondary, latent, tertiary

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10
Q

What is true of primary syphilis?

A

all untreated primary will become secondary

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11
Q

How does secondary syphilis progress?

A

30% of untreated secondary becomes tertiary the rest remain latent, this is where you produce a rash

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12
Q

What happens with late syphilis?

A

can go back and forth between early and late latency

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13
Q

What is tertiary syphilis?

A

clinical neurosyphilis, cardiovascular syphilis and late benign dermatological involvement

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14
Q

When can asymptomatic CNS involvement occur in syphilis?

A

in all untreated cases in any phase of the disease; more likely than not it occurs during later stages

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15
Q

When will an optometrist detect syphilis?

A

when there is CNS involvement

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16
Q

What is a chancre?

A

ulcerative, painless active lesion in primary syphilis; upon direct contact enters lymphatics and blood stream and quickly disseminates

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17
Q

How long does it take between incubation and chancre?

A

3 weeks (range 3 days to 3 months)

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18
Q

How long does spontaneous healing of a chancre take?

A

2-8 weeks

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19
Q

When does secondary syphilis occur?

A

2-12 weeks after contact

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20
Q

What are s/s of secondary syphilis?

A

malaise, papular rash on trunk and extremities, palms of hands and soles of feet, uveitis (ocular involvement 5% of cases)

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21
Q

When is the greatest treponemal load?

A

secondary syphilis

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22
Q

What are clinical manifestations of syphilis?

A

rash 75-100% of the time and lymphadenopathy 50-86%; + malaise, mucous patches, condylomata lata (wart like), alopecia, liver and kidney involvement, splenomegaly

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23
Q

What is latent syphilis?

A

hot suppresses infection but no lesions are clinically apparent, only evidence is a positive serologic test

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24
Q

When may latent syphilis occur?

A

between primary and secondary stages, between secondary relapses, and after secondary stage

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25
Q

What is early latent?

A

<1 year duration

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26
Q

What is late latent?

A

> or equal to 1 year

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27
Q

What is tertiary syphilis?

A

30% get to tertiary, all organs and tissues of the body may become involved; gummas (granulomatous lesions) are found in cardiovascular and neurological systems

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28
Q

What are cardiovascular complications of tertiary syphilis?

A

lesions of the aorta and arteries of the CNS; arteritis, ischemia and aortic aneurysms

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29
Q

When does neurosyphilis occur?

A

at any stage, damage is caused by spirochetes actually damaging CNS

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30
Q

How can neurosyphilis be detected?

A

+CSF serology, increased protein and leukocytosis

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31
Q

What is syphilitic meningitis?

A

HA, nausea, stiff neck, confusion, CN palsies

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32
Q

When should you consider syphilitic cerebrovascular disease?

A

young patients with CV

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33
Q

T/F neurosyphilis is in almost half of individuals in secondary stage

A

true

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34
Q

What are s/s of neurosyphilis?

A

general paresis, tabes dorsalis, argyll robertson pupils and cranial nerve involvement

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35
Q

What is the natural history of syphilis?

A

government paid to have individuals with syphilis and had them deny treatment to those patients to study the course/progression of the disease

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36
Q

What is the order of progression for syphilis?

A

inoculation, incubation period (1 week), development of primary syphilis and chancre that resolves in 1-6 weeks, early latent period, secondary period with development of rash, late latent phase, tertiary with gummas

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37
Q

Statistics for syphilis

A

100% of people inoculated from dirty toilet will get primary syphilis; 100% of untx syphilis develops into secondary; 75% of secondary syphilis becomes latent while 30% gets stuck in loop of secondary and latent; 45% with latent develop permanent latency; 30% with permanent latency develop tertiary; 20% with tertiary are incapacitated and 10% die

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38
Q

How is congenital syphilis contracted?

A

in utero or during passage through birth canal

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39
Q

What are s/s of congenital syphilis?

A

rhinitis, skin rash, liver infection, interstitial keratitis, hutchinson’s teeth, frontal bossing (square cranium), saddle nose

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40
Q

What is hutchinson’s triad for congenital syphilis?

A

teeth, interstitial keratitis, CN 8 deafness

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41
Q

What do non-treponemal tests look for?

A

reagin looks for inflammatory markers of a spirochete found in the body

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42
Q

What are non-treponemal tests?

A

rapid plasma reagin and venereal disease research laboratory VDRL

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43
Q

What are treponemal specific tests?

A

specific to the treponemal spirochete; FTA-ABS, MHA-TP, HATTS, TPHA-TP

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44
Q

What is the rapid plasma reagin?

A

non-specific syphilis associated antibody; low specificity, high sensitivity aka high false positives

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45
Q

What are the multiple antigens for rapid plasma reagin?

A

cardiolipin, lecithin, cholesterol

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46
Q

What can cause biological false positives for RPR?

A

infectious mononucleosis, malaria, pregnancy, lupus, RA, drug use

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47
Q

What are RPR results for primary, secondary, and latent/tertiarty syphilis?

A

(+)titer 4-6 weeks, (+++)titer with highest load almost 100% sensitive, and decreasing titers/sensitivity respectively

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48
Q

What will an adequate treatment of syphilis show?

A

(-) titer; 4x reduction in titer

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49
Q

What is FTA-ABS?

A

immunofluorescent assay technique, +/- cross-reactivity with Lyme disease, highly sensitive and specific

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50
Q

T/F FTA-ABS remains positive after treatment

A

true

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51
Q

Testing interpretation + RPR +FTA-ABS

A

active syphilis

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52
Q

Testing interpretation - RPR +FTA-ABS

A

adequately treated or latent/late neurosyphilis

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53
Q

Testing interpretation + RPR - FTA-ABS

A

biologic false positive

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54
Q

Testing interpretation - RPR - FTA-ABS

A

no exposure of very recent

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55
Q

When is CSF examination indicated for syphilis?

A

patients with syphilis who demonstrate any of the following criteria: neurologic or ophthalmic s/s, evidence of active tertiary syphilis, treatment failure, HIV infection with CD4 <350 and/or nontreponemal serologic test titer of > 1:32

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56
Q

T/F any ocular involvement is considered neurosyphilis

A

true

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57
Q

What is CSF testing in syphilis?

A

no gold standard, CDC recommends CSF-VDRL

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58
Q

What is the neurosyphilis equation?

A

CSF leukocytosis + elevated protein + neurological symptoms > 1 year = neurosyphilis

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59
Q

What is a common syphilis treatment?

A

penicillin G

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60
Q

When do ocular manifestations of syphilis occur?

A

secondary or tertiary

61
Q

What are ocular manifestations of syphilis?

A

conjunctivitis, scleritis, interstitial keratitis, granulomatous uveitis, chorioretinits, retinal vasculitis, arterial occlusion

62
Q

Diagnosis of ocular syphilis

A

prompt diagnosis to avoid treatable irreversible vision loss, consider CSF testing, evaluate any anterior uveitis or CN palsy with coincident skin rash

63
Q

T/F in all cases of syphilis, the possibility of coinfection w/ HIV must be ruled out

A

true

64
Q

What is the most common HIV transmission?

A

unprotected sex with HIV infected partner, also infected blood/breast milk/semen/vaginal fluid coming in contact with mucous membrane or damaged tissue

65
Q

What are risky behaviors for HIV?

A

sharing needles

66
Q

Can HIV be transmitted from mother to child?

A

yes

67
Q

HIV 1 vs 2

A

1 identified in 1985, 2 predominantly found in W Africa with slower progression and milder immunodeficiency

68
Q

What does the HIV virus do?

A

retrovirus binds to CD4 glycoprotein molecules (chemokine receptor) on the surface of the target host cells

69
Q

What is viral load?

A

ongoing viral replication; higher load correlated with more rapid progression to AIDs

70
Q

What is CD4 count?

A

assessment of health of your system; normally 1000 cells/cubic mm (600-1500)

71
Q

When do CD4 counts drop?

A

drop progressively in HIV infection, provides an estimate of immunity, cell mediated immunity is critical for protection agains infectious process, involves memory CD4 cells unable to recognize specific pathogen

72
Q

What characterizes AIDs?

A

CD4 <200 cells/cubic mm = AIDs

73
Q

What is the average time for progression to AIDs without therapy?

A

10-11 years

74
Q

What is the average time to death following AIDs?

A

3.7 years

75
Q

What is the initial/early phase of HIV?

A

newly infected with no symptoms, acute retroviral syndrome flu-like illness 2-3 weeks following infection with recovery in weeks

76
Q

What occurs in initial HIV infection?

A

body mounts immune response by producing antibodies= HIV+ status; seroconversion in 6 weeks to 6 months to develop in 95% of those infected

77
Q

How are mutations involved in HIV?

A

during process of viral replication, many mutations are formed which confuses killer T cells CD 8; antibody titers are not sufficient to destroy the replicating virus

78
Q

What is the chronic phase of HIV?

A

10-11 years “latent” period, relatively health: progressive deterioration of immune system and viral replication; minor immune dysfunction, abnormal blood studies, minor constitutional problems

79
Q

When is antiretroviral therapy given?

A

day 1 of diagnosis, ART patients may live with clinical latency for several decades

80
Q

What is the crisis phase of HIV?

A

systemic diagnosis of AIDs, manifestation of an indicator disease + HIV confirmation; CD4 < 200 cells/mm3 with or without an indicator disease

81
Q

What percent of individuals with AIDs have ocular involvment?

A

75-100%

82
Q

When can you detect antibodies for HIV?

A

6 weeks to 6 months after exposure

83
Q

What is the viral lode test?

A

measures # of HIV RNA molecules per mililiter of plasma (want low to reduce progression and transmission)

84
Q

What is the chance of causing disease progression in 60 months for 20,000 and 200,000 respectively?

A

1% and 24%

85
Q

What is the goal for viral load?

A

as low as possible aka below limit of quantification, typically <25-50

86
Q

What can a PCR detect?

A

down to 50 copies of HIV RNA

87
Q

What are 3 AIDs defining malignancies?

A

kaposi’s sarcoma, burkitt’s lymphoma, primary CNS lymphoma

88
Q

What is ART (HAART) therapy?

A

cocktail of 2 nucleoside reverse transcriptase inhibitors and 1 non-nucleoside reverse transcriptase inhibitor or integrase strand transfer inhibitor or protease inhibitor

89
Q

What is a NRTI?

A

nucleoside reverse transcriptase inhibitor; prevents elongation of viral DNA, prevents replication by blocking reverse transcriptase from binding

90
Q

What is a NNRTI?

A

non-nucleoside reverse transcriptase inhibitor; bind to a specific area adjacent to the site of the reverse transcriptase enzyme

91
Q

What is INSTI?

A

integrase strand transfer inhibitor; blocks HIV’s DNA incorporation into CD4 cell’s DNA

92
Q

What is PI?

A

protease inhibitor; case premature release of immature, non-infectious viral particles

93
Q

What are the names of common ART options?

A

Biktarvy, Triumeq, Atripla, Genvoya, Complera

94
Q

What is prophylactic HIV treatment?

A

pre exposure and post

95
Q

What is PrEP?

A

pre-exposure, for high risk groups, once daily med (Truvada and Descovy) aka combo of 2 HIV meds (tenofovir NRTI and emtricitabine NRTI)

96
Q

What is PEP?

A

post-exposure, begin within 72 hours, different cocktail

97
Q

What is oral thrush/candidias?

A

yeast infection of the mucus membrane lining the mouth and tongue, normal component in oral microbiota –> opportunistic infection in HIV patients

98
Q

When can you get opportunistic infections?

A

CD4 500-200 cells/mm3 or ratio of CD4 to lymphocytes less than 30%

99
Q

What opportunistic infections do you get with 500-200 cells?

A

thrush, herpes zoster, and hairy leukoplakia

100
Q

What is hairy leukoplakia?

A

Epstein Barr, white patch on the side of the tongue

101
Q

What infection can you get with CD4 200-100?

A

pneumocystis carinii pneumonia

102
Q

What is the most significant HIV/AIDs complication?

A

pneumocystis pneumonia a fungal infection of the lungs

103
Q

What infections are possible with CD4 less than 100 cells/mm3?

A

cyptococcosis and cryptosporidiosis

104
Q

T/F there is CSF involvement with infection and CD4 less than 100

A

true

105
Q

What is cyptococcosis?

A

fungal infection, wound/cutaneous, pulmonary or meninigitis

106
Q

What is cryptosporidiosis?

A

parasitic, intestine to diarrhea, need fluid rehydration and electrolytes

107
Q

What infections are possible with CD4 less than 50 cells?

A

mycobacterium avium complex, progressive multifocal leukocephalopathy or primary central nervous system lymphoma

108
Q

What is mycobacterium avium complex?

A

group of bacteria related to TB; found in soil, food, and water; can infect lungs, bones or intestines and can spread through out body

109
Q

What is progressive multifocal leukocephalopathy?

A

secondary to immune suppression as side effect of biologic med for psoriatic arthritis; infection that damages myelin of white matter, fatal

110
Q

What is conjunctival microvasculopathy?

A

perilimbal injection, comma shaped vesicles, sludging of the blood columns due to HIV

111
Q

What are adnexal ocular manifestations of HIV?

A

molluscum, HZO, primary non-hodgkin

112
Q

What is immune recovery uveitis?

A

occurring after onset of ART, in patients with history of inactive CMV

113
Q

What is HIV retinopathy?

A

CWS, intraretinal hemes, microaneurysms, IRMA; see a patient back in 3 months

114
Q

What is ischemic maculopathy?

A

enlargement of FAZ

115
Q

What is CMV retinitis?

A

most common sight threatening opportunistic infection, can lose vision in 48 hours

116
Q

What is CD4 with CMV?

A

less than 50

117
Q

What is acute retinal necrosis syndrome?

A

peripheral retinitis tx with IV acyclovir

118
Q

What is progressive outer retinal necrosis syndrome?

A

posterior pole retinal necrosis leading to NLP

119
Q

What is ocular toxoplasmosis?

A

parasitic infection, focal or diffuse, prophylaxis in seropositive patients with low CD4 counts (pyrimethamine-sulfamethoxazole)

120
Q

What are examples of fungal infections from HIV?

A

pneumocystic choroidopathy, candidal chorioretinitis, cryptococcus chorioretinits, histopasma chorioretinits

121
Q

What are bacterial infections with HIV?

A

syphilis¯_(ツ)_/¯ endogenous bacterial retinitis, mycobacterium TB

122
Q

When do cranial nerves get involved with neuro-ophthalmic HIV?

A

50% due to cyptococcal meningitis

123
Q

What are appropriate disinfectants for HIV?

A

3% hydrogen peroxide, 70% ethanol, 10% bleach/water solution

124
Q

What organism is chlamydia?

A

obligate intracellular parasite

125
Q

Trachoma and Inclusion Conjunctivitis serotypes

A

A-C and D-K respectively

126
Q

What does trachoma produce?

A

chronic conjunctivitis causing blindness

127
Q

What is transmission of trachoma?

A

flies, eye to eye

128
Q

What are signs of trachoma?

A

follicular conjunctivitis, Arlt’s line, trichiasis, corneal opacity

129
Q

What is treatment of trachoma?

A

SAFE– surgery for entropion, antibiotic zithromax, facial hygiene and environment change

130
Q

What are urogenital symptoms of chlamydia?

A

pain areas in lower abdomen, and urogenital system, pain during sex or urination, abnormal discharge or bleeding

131
Q

What is adult inclusion conjunctivits?

A

oculogenital disease of conj and genitals, acute follicular conjunctivitis, preauricular lymphadenopathy

132
Q

What is chlamydial testing?

A

conj or urethra swab, polymerase chain reaction, urine specimen (gold standard)

133
Q

What is chlamydia treatment?

A

azithromycin 1 g single dose, oral doxy, erythromycin, ofloxacin, levofloxacin

134
Q

What meds are appropriate for chlamydia during pregnancy?

A

erythromycin and amoxicillin

135
Q

T/F you must report chlamydia to the health department

A

true, requires name of individuals who test positive; TN promotes expedited partner delivered therapy

136
Q

What are signs of ophthalmia neonatorum?

A

redness, mucopurulent discharge, swelling of lids, conjunctival chemosis, bilateral symptoms

137
Q

Why do infants lack follicles?

A

they have not developed lymphoid tissue

138
Q

What is ophthalmia neonatorum prophylaxis?

A

erythromycin ung, povidine-iodine, 1% silver nitrate

139
Q

What are risk factors for gonorrhea?

A

25 year old, hx of STI, inconsistent condom use, new or multiple sex partners, substance abuse

140
Q

What bacteria causes gonorrhea?

A

neisseria gonorrhea, gram negative diplococcus

141
Q

How does gonorrhea cause infertility?

A

leading cause of infertility due to infected women developing pelvic inflammatory disease

142
Q

What are clinical presentations of gonorrhea?

A

urethritis, cervicitis, proctitis, and conjunctivitis

143
Q

What can severe gonorrhea cause?

A

endocarditis, menigitis, myocarditis

144
Q

What is polyarticular tenosynovitis?

A

joint inflammation following dissemination of gonorrhea in wrists, ankles, hands, and feet

145
Q

What is the test of choice for diagnosis of gonorrhea?

A

culture, nucleic acid amplification test, PCR, or transcription mediated amplification assay

146
Q

What are ocular signs of gonnococcal keratoconjunctivitis?

A

marked lid edema, conj hyperemia, copious purulent exudate, preauricular lymphadenopathy, conj membrane

147
Q

Why must a patient be hospitalized with a corneal ulcer from gonorrhea?

A

it can penetrate the cornea in 24 hours leading to perforation and endophthalmitis

148
Q

What is management of gonorrhea?

A

gentamicin, tobramycin or bacitracin; if corneal involvement then ceftriaxone

149
Q

What is the ALLOW method?

A

ask, legitimize, limitations, open up further discussion, work together to develop treatment plan

Systemic Disease (Wolfe) (10 decks)

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