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Unit 19 Flashcards

1
Q

how do stds spread

A

genitals, mouth, rectum, skin, placenta

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2
Q

viral/recurring stds

A

herpes, warts, aids

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3
Q

bact/elimanted stds

A

syph, clap, gonorhea, chancroid

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4
Q

high risk practice

A 
multi partners, unsafe/high risk sex practice
drug abuse
medically underserved
prior stds
non compliant std tx
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5
Q

low risk or no risk practice

A

monogomy

abstinence

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6
Q

genital herpes

A

recurrent, systemic, viral infc

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7
Q

what virus causes gential herpes

A

herpes simplex type 2

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8
Q

what virus causes cold sores

A

herpes simplex type 1

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9
Q

what type of microbe is herpes

A

neurotropic

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10
Q

neurotropic microbes

A

attack host cells ganglia

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11
Q

how does herpes spread

A

contact with shedding leisions or vaginal sec

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12
Q

incubation herpes

A

2-10 days

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13
Q

when do mnfts appear in herpes

A

3-7 days post contact with apperance of lesions

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14
Q

mnfts of herpes lesions

A

pain, burning at site (internal in women)

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15
Q

systemic mnfts of herpes

A

fever, m ache

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16
Q

when may a herpes virus become subclinical

A

if virus is latent

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17
Q

major problem with herpes

A

reoccurence

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18
Q

tx for herpes

A

no cure, symptom tx, anti viral for flare ups

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19
Q

which hpv strains have inc incidence in warts

A

6,11

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20
Q

characteristics of warts

A

beningn, neoplastic growth. short stock lesion with multi heads

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21
Q

incubation for warts

A

1-2 mo

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22
Q

cure for wart

A

no

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23
Q

tx for warts

A 
removal
topical drugs
sx
cryosx
monitor for ca
vaccine to prevent hpv?
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24
Q

what types of topical drugs are used in warts

A

cytotoxic or antimyotic

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25
what strains of hpv may cause ca
16 and 18
26
name of syph bact
treponema pallidum
27
how does syph spread
contact with leasions and across placenta at 16 wks gest
28
incuation syph
10-90 days
29
how does syph spread
microbe divides and spreads systemically
30
comp of syph
blindness, paralysis, hd, death
31
1 stage of syph
``` bact introduced. painless chancre (ulcrative bleeding) reginal lympahdenopathy ```
32
how long does it take for a painless chancre in 1st stage syph to heal
3-12 weeks
33
2nd stage of syph
appearance of further lesions
34
when does 2nd stage syph begin
6-8 weeks post infc
35
mnfts of 2nd stage syph
macupapular rashes (white, pimple like) on palms and soles white patches on mucous membs and tongue flat papules generalized and progressed lymphadenopathy fever and malaise latencyup to 50 yrs
36
when does 3rd stage of syph occur
1-35 years after primary infc
37
what happens in the 3rd stage of syph
irreversiable damage to bone, joints, cvs, ns,
38
what is important to remember about 3rd stage syph
we can eradicate syph bact but disease process is permanent. infc is systemic
39
tx for syph
long acting penicillin
40
why do we use long acting penicillin in syph
bact is spirochete shape - these bact have inc generation time of approx 30h. we need abx to last in system for duration of this time
41
bact name for clap
chlamyida trachomatis
42
characteristics of clap
gram -, tiny, hard to detect bacteria
43
what percent of clap is asymptomiatic
50
44
mnfts clap in male
white or clear urethral discharge mild dysuria rt pain in urethra testicular pain within scrotum rt inflm of epididymis
45
mnfts of clap in female
mucopurulent vaginal dc plus cervical mucous dysuria bleeding pelvic pain + PID
46
tx for clap
abx, doxycycline. azithromycin
47
bact name for gonorrhea
neisseria gonnorrhea
48
incubation of gono
3-8 days
49
mnfts of gono in female
purulent, vaginal dc | dysuria, genital irritation, late pelvic pain rt PID
50
mnfts of gono in male
urethral dc, dysuria
51
systemic mnfts of gono (m and f)
bacteremia pharygneal infc rt oral sex conjunctivitis rt contaminated hands touching eyes arthritis dermatits syndrome/ septic arthritis
52
mnfts of arthritis dermatis
swollen,painful joints
53
tx gono
``` 1st line: abx (cephalosporins) 2nd line: inc dose plus add another class of antibiotics ```
54
AIDS
infc rt HIV
55
incubation of HIV
varying
56
what does hiv target
IR and T helper cells
57
what happens when IR is targetted
inc immunesuppression -> opport infc, CA
58
2 forms of HIV
HIV 1 and HIV 2
59
how does HIV spread
sex, cont blood, maternal (in utero, LDR, lactation)
60
what is the risk of HIV for HCP1
0.3%
61
what does HIV infection by needle stick injury depend on
viral load of blood | depth and location of injury
62
3 phases of HIV infc
primary inf latent overt AIDS
63
primary infc
weeks-mo. introd + replication
64
window period
time req for dx test to detect microbe
65
what do we look for in the window period of HIV
looking for inc Ab in blood in response to Ag
66
how long may the window period be
up to 3 mo
67
what occurs in the primary infc
seroconversion | high viral load and dec cd4 count
68
seroconversion
formation of ab in blood
69
what is the relationship between viral load and CD4 count
inversely porportional to eachother
70
what classifies AIDS
cd4 count that falls below a certain number and stays down OR 2 infcs and/or Ca
71
latent periods AIDS
asymptomatic lymphatic tissue damage recurrent resp infc rt dec IR fatigue
72
when does overt aids occur
about 10 years after infc
73
what is targetted in overt aids
th cells, macrophages, b cells
74
what happens in overt aids
destrosy IR -> dec IR and defenses-> inc new infc + latent pathogens affects various organs
75
dx for aids
``` clinical progression ELISA western blot assay PCR CD4 count P24 Ag test NAT ```
76
what does ELISA measure
measures abs via ez linked reaction. measures ab against whole virus
77
western blot assay
measures virus spec ag. test with inc specifity
78
PCR
biochemical tests not typically done. Measures virus
79
CD4
measures number of t helper cells. (inc viral load - dec CD4)
80
P24 ag test
measures protein within viral vore. appears in serum of infctd individual.
81
NAT
nucleic acid testing. replaces PCR, detects virus by looking at its nucleic acid content
82
best early test for AIDS
p24 ag test
83
number one dx for AIDS
elisa
84
top 3 mfnts for aids
resp (TB/pnumonia) -> drug resistant TB GI NS (dementia, encephalopathy) -> extensive damage rt infc and toxins
85
why does oppurtunistic ca occur 2
malignant cells multiply because IR cannot control them -> neoplasia -> CA genetic mutation rt virus interruption to host cells
86
why does opportunistic infc occur
IR compromise and anatomic damage to IR
87
which oppurtunistic cas are most common in HIV
Kaposi sarcoma NHL cervical ca
88
kaposi sarcoma
cutaneous lesions visible on skin, mouth, lymph nodes. endothelial origin
89
tx AIDS/HIV
slow progression to AID | antiretrovirals

PAtho (31 decks)

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