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ENRP II > Gynecological and Pregnancy Related Infections Part 3 > Flashcards

Gynecological and Pregnancy Related Infections Part 3 Flashcards

1
Q

focused exam of primary outbreak of gential herpes

primary outbreak is more severe than recurrent ones

A

bilateral scattered small shallow vesciles that are painful and bilateral lymphadenopathy with systemic symptoms

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2
Q

recurrent genital herpes

A

unilateral vesicles that can rupture and ulcerate, usually no systemic symptoms

all herpes vesicles can rupture and ulcerate, this is unilateral that is the difference

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3
Q

in herpes there is often associated ________-

A

lymphadenopathy

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4
Q

recurrent herpes infections are common due to the fact that the virus remains latent in the ?

A

sacral ganglia

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5
Q

herpes simplex is a double stranded _ virus that has lifelong peristency in the _

A

DNA

nerve root

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6
Q

HSV I involvement

A

orofacial

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7
Q

HSV II involvement

A

genital involvement

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8
Q

herpes can be transmitted to the infant via

A

vertical transmission

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9
Q

herpes cytology shows?

A

molding, multinucleation, margination

molding- nuclei conform the the shape of other nuclei
multinucleation- multiple nuclei form
margination- glass like quality of the nuclei due to viral particles present

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10
Q

genital herpes treatment specifically target?

A

DNA synthesis

Acyclovir (only one that can be given IV)
Famciclovir
Valacyclovir

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11
Q

for treatment of genital herpes it is most effective if started within _ hrs.

A

72

72 hrs from onset of lesions

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12
Q

MOA of acyclovir

A

it is adminsitered as a prodrug and targets herpes virus specific thymidine kinase and cellular kinases phosphoyrlate in order for it to be incorporated into viral DNA and stops the lengthening of DNA strands

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13
Q

how does viral herpes gain resistance to acylcovir?

A

there is a decreased production of thymidine kinase which prevents acyclovir from reaching its triphosphate active state and cannot be incorpoprated into viral DNA to stop synthesis

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14
Q

primary symphilis presentation

A

bump that is now a open wound and is painless with mild inguinal lymphadenopathy (later stage)

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15
Q

primary syphilis develops a _ chancre 6 weeks after contact

A

painless

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16
Q

_ weeks after a primary infection of syphilis what secondary syphilis presents and shows what

A

6 weeks

condyloma lata wart like lesion on the palms and soles (macular rash)

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17
Q

the macular rash in syphilis is on the palms and soles what other processes involve the palms and soles

A

rocky mountain spotted fever and toxic shock syndrome

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18
Q

secondary syphillis usually resolves in 2 months and will remain latent until becoming reactivated and forming tertiarry syphillis when?

A

6-40 years later

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19
Q

tertiary syphillis is characterized by involvement throughout the body and widespread _ formation

A

gumma

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20
Q

what are gummas?

A

lesions that involve skin, bones, soft tissue and other organs they show spirochete organisms with a area of central necrosis, paslama cells and histiocytes

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21
Q

tertirary syphillis can also cause _ with involvement of the vasa vasorum (small vessel that feeds the aorta)

A

thoracic aorta aneurysm/dilation

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22
Q

if tertiary syphillis involves the porerior columns of dorsal roots of the spinal cord there is loss of?

this is known as tabes doraslis

A

loss of position and vibration sense below the level of the lesion

patient will often fall with their eyes closed and fee together

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23
Q

if tertiary syphilis involves the midprain what happens

A

the pupils do not react to light but constrict in focusing with near object(argyll robertson pupils)

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24
Q

sphyillis is caused by?

microbiology

A

treponema pallidum which is a corckscrew spirocete with spinning motility

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25
Q

a key feature in both primary and secondary syphillis is the presence of?

A

plasma and lymphocytic infiltrarte termed lymphoplasmacytic infiltrate on histology

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26
Q

how do gummas in tertirary symphillis present hsitologically ?

A

they present with large areas of necrosis with histiocytes and plasma cells

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27
Q

what stain shows the spirochetal symphilis bacteria

A

silver stain

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28
Q

what are the nontrepnemal screening tests

A

VDRL, RPR, TRUST

nonspecific tests that checks the antibodies (screening test)

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29
Q

in syphilis _ is typically utilized to make the diagnosis

A

serology

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30
Q

after a nonspecific test more specific treponemal diagonostic tests check for antibodies against specific antigens: what are these tests?

A

FTA-ABS

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31
Q

if you have a direct tissue sample of syphillis you can use what to test it?

4 of them

A

PCR (most used- definitve and checks for DNA of syphillis)
Darkfield microscopy
fluroescent antibody testing
silver stain

32
Q

treatment for syphillis (primary/early/secondary/latent)

A

benzathine penicilin or doxycyline if allergic to penicillin

want to target treponema pallidum

33
Q

neurpsyphilis/ocular syphilis (tertiary) is treated with?

A

aqueous crystalline penicillin G

procain penicillin G and probenaecid

34
Q

what is benzathine penicillin

A

2 penicillin G molecules that react with diphenyethylene diamine that is given IM and contains a beta lactam ring

safe during pregnancy

35
Q

what does benzzathine penicillin cover

bacteria coverage

A

gram positive bacterio like beat hemolytic strep
gram negative bacteria like trepnema pallidum ( in syphillis)

36
Q

side effects of bezathine penicillin/ beta lactam antibiotics

A

allergic reactions and analphylactic shock

also penicillins and cephalosporins

37
Q

benzathine penicillin can cause a rare reaction when used to treat sphyillis which is termed?

A

Jarisch-herxheimer

38
Q

a chancroid is usually seen where?

location

A

in resource poor areas (africa, subsaharan, latin america)

39
Q

chancroid present with

A

multiple painful genital ulcers and inguinal lymphadenopathy

40
Q

chancroid is caused by?

A

gram negative bacillus haemophilus ducreyi

41
Q

is testing available for chancroid?

A

no, but rule out HSV and syphillis

42
Q

how do we treat chancroid

A

azithromycin, certriacoine, ciprofloxacin, erythromycin

43
Q

lymphogranuloma venerum (LGV) is found where

location

A

tropical/subtropical locations

44
Q

LGV presentation

A

one painless geninital ulcer that heals but then develops buboes which are painful unilateral inguinal lymphadenopathy

more common in men than women due to lymphatic drainage differences

45
Q

lymphogranuloma venerum is caused by

A

chlamydia trachomatic L1, L2, L3 serovars

a gram negative intracellular bacteria that relies on host ATP

46
Q

treatment of LVG

normal vs pregant

A

normal - doxycline
pregnant- macrolides (azithromycin)

47
Q

granuloma inguinale is found?

location

A

in india, papua new guinae, caribbean

48
Q

granuloma inguinale presentation

A

painless nodule that slowly enlarges that are beefy red can ulcerate and do NOT HAVE LYMPHADENOPETHY

49
Q

granuloma inguinale is caused by?

A

gram negative rod klebsiella granulomatosis

50
Q

biopsy of granuloma inguinale shows

A

donovan bodes which are collections of bacilli in cytoplasma of macrophages, monocytes, or histiocytes

51
Q

treatment of granuloma inguinale

A

azithromycin

52
Q

azithromycin is?

A

a macrolide, 50s subuint inhibitor that inhibits protein synthesis

53
Q

what are the macrolides?

A

erythromycin, azithromycin, clarithromycin

54
Q

toxic shock syndrome is characterized by the rapid onset of?

A

fever, erythematous rash on palms and soles, desquamation of skin 2 weeks after rash apperance, hypotension + systemic involvement indicationg shock

55
Q

TSS is caused by

A

staph aureus

can ocurr with MSSA and MRSA

usually in mentrual cases but doesnt have to be (high absorbent tampons)

56
Q

staph aureus is a ?

microbiology

A

gram positive, catalase positive, coagulase positive coccous that is found in clusters

57
Q

what is catalase

A

a enxyme that breaks down hydrogen peroxide

58
Q

what is coagulase

A

an enzyme that acitvates the formarion of a fibrin clot to help protect the baceria

59
Q

what are the virulence factors of staph aureus?

A

hyalurinidase (destroys CT)
staphylokinase (destroys clot)
lipase (destroys fat)

60
Q

staph aureus produces TSS by releasing what

A

toxic shock syndrome toxin 1 (TSST-1)

61
Q

what is the mechanism of action of TSST-1?

A

it acts as a super antigen to crosslink T cells and macrophages this binding releases cytokines that give systemic features like hypotension and fever (shock)

62
Q

how do we treat TSS

A

remove the foregin body or infection by surgical debriedment, care for the shock symptoms, and start empiric antibiotics

63
Q

what is the glycopeptide that is used to treat TSS

A

vancomycin

64
Q

vancomycin is used in TSS if the infection is _

A

suspected to have MRSA (methicillin resistant )

65
Q

what is the MOA of vancomycin?

A

it inhibits cell wall synthesis of bacateria by creating unstable cross links

66
Q

how has bacteria become vancomycin resistant ?

A

the resistant strains change from D-ala:D-Ala to D-ala:D-Lac/Ser

67
Q

what is a B-lactamase enxyme

A

this is an enxyme produced by some bacteria than give them resistance to Antibiotics like penacinllinase which helps it to degrade betalactam rings

68
Q

bacteria that produce extended spectrum b-lactamases are _ strains

A

multi drug resistant strains

69
Q

how do beta lactamase inhibitors work

A

they work by extending B-lactam spectrum of antibiotic activity to prevent resistant from betalactamases.

70
Q

what combination drug of betalactam is used to treat TSS

A

Piperacillin and Tazobactam (zosyn)

given IV, covers both gram positive and gram negative can be used to treat PID

71
Q

what cephalosporin can be used to treat TSS

A

Cefepime

4th generation, covers gram negative and gram positive, cell wall synthesis inhibitors

72
Q

cefepime when treating TSS is a fron tline agent when infection is with _

A

enterobacteriacea

73
Q

what carbapenems are used to treat TSS

A

meropenem and imipenem/clistatin

beta lactam antibiocs that are cell wall synthesis inhibitors

74
Q

meropenem has what side effects and resistance arise because?

A

side effects: clostridium difficile and allergic reactions
resistance: mutations in penicillin binding proteins

75
Q

is imepenem/cilastatin active against MRSA?

A

no

76
Q

imipenem is rapidly degraded by?

A

renal enzyme dehydropeptidase (DHP1)

77
Q

imipenem is coadmisnistered with?

A

cilastatin which is a DHP1 inhibitor and it prevents inactivation of imipenem

ENRP II (25 decks)

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