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ID > ID test 4 part 2 > Flashcards

ID test 4 part 2 Flashcards

1
Q

Second most reported STD in the US

A

Gonorrhea

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2
Q

risk of ______ transmission is much higher than _____ in gonorrhea

A

male-to-female higher than female-to-male

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3
Q

gonorrhea symptoms

A

similar to UTI
males- profuse, purulent discharge
most females are asymptomatic

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4
Q

if gonorrhea is left untreated it can lead to

A

disseminated gonoccal infection- systemic; septic arthritis

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5
Q

most commonly reported STD in the US

A

chlamydia

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6
Q

1 cause worldwide of inocular blindness

A

chlamydia

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7
Q

stage 1 of syphillis

A

primary
chancre- PAINLESS lesion
highly contagious
resolves spontaneously in 3-6 weeks

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8
Q

Stage 2 of syphillis

A

secondary
mucocutaneous eruptions
non contagious except for mucosal lesions
if not treated, can appear 2-8 weeks after chancre

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9
Q

Stage 3 of syphillis

A

latent
asymptomatic w/ + serologic tests
early latent- 1 yr from onset- potentially contagious
late latent- non infectious

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10
Q

stage 4 of syphillis

A

tertiary
inflammation of any organ system
gummas- granulomatous lesions
2-3 yrs after initial infections

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11
Q

neurosyphilis

A

can occur at any stage

hemiplegia, hemiparesis, seizues

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12
Q

jarisch-herxheimer rxn

A

acute febrile rxn- fever, chills, myalgias, HA, tachycardia, >RR, > WBC, vasodilation
occurs w/in 2 hours of syphilis treatment
possibly due to toxin release or amplified immune response.

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13
Q

preferred treatment for syphilis is

A

PCN!

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14
Q

Herpes is a ____ virus

A

double-stranded DNA

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15
Q

primary HSV infection

A 
systemic symptoms- fever, HA, myalgia
can be asymptomatic
2-7 days after contract- genital lesions
painful ulcerations last 7-14 days
viral shedding 11-12 days
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16
Q

secondary HSV infection

A 
80% w/in first year
up to 4-8 times/yea
tingling, itching, burning 18-36 hours before lesion
heal faster & less vesicles (3-10 days)
viral shedding about lasts 4 days
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17
Q

effective treatment of HSV requires initiation of therapy within ___ of lesion onset

A

1 day

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18
Q

daily suppressive HSV therapy

A

recommended for pts with >6 episodes/yr

effective at decreasing transmission via asymptomatic viral shedding

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19
Q

gardisil

A

protects against 6, 11, 16 & 18- warts and cancer

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20
Q

cervarix

A

protects against 16 & 18- just cancer

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21
Q

bacterial vaginosis

A

gardnerella vaginalis- anaerobic bacteria

treat with metronidazole or clindamycin

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22
Q

trichomonisaisis

A

trichomonas vaginalis- anaerobic, flagellated protoanza

treat with metronidazole or tinidazole

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23
Q

vulvovaginal candidiasis

A

candida albicans-budding yeast

treat with azole

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24
Q

HIV-1

A

most cases

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25
Q

HIV-2

A

minority of cases, less virulent, concentrated in west Africa

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26
Q

HIV major genes

A

RNA retrovirus, viral genome (Gag, Pol, Env), reverse transcriptase

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27
Q

reverse transcriptase

A

RNA dependent DNA polymerase

makes ds-DNA from ss-RNA

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28
Q

tropisms

A

attraction of binding for a particular co-receptor in HIV

not static

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29
Q

CXCR5 co-receptor is more common on

A

T-helper cells

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30
Q

CCR5 co-receptor is common on

A

macrophages

more common form of initial attack

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31
Q

binding of GP120 to its receptors causes

A

a conformational change to the protein GP41

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32
Q

cellular protein found in some host immune cells that inhibits uncoating of HIV

A

receptor interacting molecule 5-alpha in T cells

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33
Q

lab tests to detect HIV

A

ELISA, western blot, virus isolation & culture, PCR

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34
Q

central concept of HIV

A

disease derives from toxic effects of HIV on host immune cells with decrease in CD4+ T cells as a main feature

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35
Q

goals of HIV therapy

A

suppress viral replication to <50 and preserve immune function

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36
Q

suggest that ___ drugs is the minimal # required for long-term suppression of HIV w/out developing resistance

A

3

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37
Q

genetic barrier

A

number of mutations required to become resistant to a treatment
low- bad\high-good

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38
Q

HIV prevention

A

possibly Truvada?-Emtricitabine & tenofovir

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39
Q

Nucleoside & nucleotide reverse transcriptase inhibitors (NRTIs)

A

competitive inhibitors of viral RT

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40
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

A

non-competitive inhibitors of viral RT in HIV-1 only!

generally low genetic barrier

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41
Q

Protease inhibitors (PI)

A

inhibit the post-translational, final activation step of viral polyproteins as the nascent viral particles are released
high genetic barrier

42
Q

fusion inhibitors (aka entry inhibitors) (FI)

A

block attachment and/or entry of the viral particle to cell

43
Q

CCR5 co-receptor Antagonists (CCR5I)

A

block attachment of certain strains of HIV to the R5 co-receptor & thus prevent entry & infection

44
Q

HIV integrase strand transfer inhibitors (ISTI)

A

inhibit the transfer & integration of the viral DNA into host cell DNA in the genome of infected cells
inhibit HIV-1 integrase
low genetic barrier

45
Q

many toxicities of NRTIs relate to

A

inhibition of mitochondriald DNA

46
Q

black box warning for NRTIs

A

lactic acidosis & liver damage

47
Q

NRTIs vs NNRTIs

A

both have good oral bioavailabilty
half-life: NNRTI>NRTI
NNRTI mostly hepatic
NRTI mostly tenal

48
Q

what NNRTIs are both inhibitors & inducers of P450?

A

Efavirenz & nevirapine

49
Q

inhibition

A

drug directly interacting with a molecule of p450 (direct interaction)

50
Q

induction

A

totally different process; binds to a nuclear receptor & travels to the nucleus of the cell & changes gene expression so that more of a particular p450 is made (change in gene expression)

51
Q

with PIs, viral particles are released, but

A

they are not mature and infectious

52
Q

HIV-1 protease is an

A

aspartyle protease

PIs cleave between PHE and PRO

53
Q

ritonavir is a PI drug with special uses as a

A

pharmacoenhancer or booster- given in combo
inhibits CYP3A4 so inhibits other HIV drug metabolism
inhibit PGP efflux sytsem

54
Q

fusion inhibitors-enfuvirtide MOA

A

binds to hydrophobic groove in GP41 & prevents membrane fusion
active on HIV-1 only!!

55
Q

viral load measures

A

the progression of the disease

56
Q

CD4+ count measures

A

current immune status & need for any prophylaxis

57
Q

Statins not metabolized through P450, so ok to use

A

pravastatin or rosuvastatin

58
Q

statins to avoid

A

DO NOT use atorvastatin, lovastatin, simvastatin

59
Q

NRTI’s(eg zidovudine, stavudine) serious ADRs

A

lactic acidosis & severe hepatomegaly with steatosis

60
Q

abacavir ADRs

A

hypersensitivity syndrome- HLA-B*5701 testing; increased MI risk

61
Q

didanosine & stavudine ADRs

A

peripheral neuropathy, pancreatitis

62
Q

maraviroc ADRs

A

hepatitis, allergic rxn

63
Q

zidovudine ADRs

A

neutropenia, severe anemia, granuloctyopenia

64
Q

atazanavir ADRss

A

kidney stones and gallstones

65
Q

most common life-threatening infection & second most common cause of lung disease

A

pneumocystis jirovencii pneuomonia aka PCP

66
Q

pneumocystis jirovencii pneumonia is

A

a fungus but has protozoal characteristics

67
Q

PCP presentation

A

a little different than normal pneumo

slow onset progressive dyspnea, non-productive cough, hypoxemia

68
Q

when to start PCP prophylaxis

A

all patients w/ AIDs or CD4<200

69
Q

PCP prophylaxis

A

Bactrim/ cotrimazole DS 1 tab daily; can also use SS 3x/wk

70
Q

when to stop PCP prophylaxis

A

when CD4>200 for 3 months

71
Q

PCP treatment

A

cotrimazole- high dose X21 days

add 21 days steroids in patients w/ significant hypoxia

72
Q

mucocutaneous candidiasis can be

A

oropharyngeal or esophageal

73
Q

oropharyngeal C. albicans presentation

A

white plaques on oral surfaces, may or may not be painful

74
Q

esophageal C.albicans presentation

A

burning pain, discomfort or difficulty swallowing

75
Q

primary prophylaxis for C.albicans

A

not recommended

76
Q

secondary prophylaxis for c. albicans

A

IF frequent occurrences or very severe cases

77
Q

treatment for oropharyngeal c.albicans

A

fluconazole 100mg PO QD

can use topicals

78
Q

treatment for esophageal c.albicans

A

fluconazole 100-400mg PO/IV QD

cannot use topicals

79
Q

what kind of infection is toxoplasma gondii encephalitis

A

protozoal infection

presentation- HA & CNS

80
Q

when to start primary prophylaxis for toxoplasma gondii encephalitis

A

all patients with CD4<100

81
Q

primary prophylaxis for toxoplasma gondii encephalitis

A

cotrimoxazole DS 1 tab QS

82
Q

stop primary prophylaxis toxoplasma gondii encephalitis

A

when CD4 >200 for 3 months

83
Q

secondary prophylaxis of toxoplasma gondii encephalitis

A

similar to treatment

84
Q

what kind of infection is cytomegalovirus retinitis

A

viral infection of the retina

aka CMV- can cause blindness

85
Q

at risk for CMV when

A

CD3<50

86
Q

primary prophylaxis for CMV

A

not recommended bc of drug toxicity

87
Q

secondary prophylaxis for CMV

A

recommended

ganciclovir, valganciclovir, foscarnet, cidofovir

88
Q

stop secondary prophylaxis for CMV

A

lifelong unless immune reconstitution occurs (CD4>100 for 3 months)

89
Q

start prophylaxis for MAC

A

when CD4<50

90
Q

prophylaxis for MAC

A

azithromycin 1200mg q week or clarithromycin 500mg BID

91
Q

stop MAC prophylaxis

A

when CD4 >100 for 3 months

92
Q

MAC treatment

A

clarithromycin or azithromycin + ethambutol + maybe rifabutin (min 12 months)

93
Q

immunizations in all HIV patients

A

hep B, flu, pneumonia

94
Q

immunization in pats who have risk of disease

A

hep A, HPV, menigococcaal, varicella

95
Q

Vaccine not recommended in HIV

A

varicella zoster

96
Q

HIV wasting definiation

A

> 10% weight loss + symptoms

97
Q

HIV wasting treatment

A

appetite stimulants- megesterol or dronabinol
anabolic agents- testosterone
anabolic steroids- cytokines

98
Q

AIDs-defining malignancies

A

kaposi’s sarcoma, non-hodgkin’s lymphoma, cervial cancer

99
Q

non-AIDs -defining malignancies

A

hodgkin’s disease

others- lung, anal, oropharngeal, liver, skin

100
Q

ART _____ initiated with cryptococcal meningitis

A

should not be

101
Q

IRIS

A

immune reconstitution inflammatory syndromes
w/in 4-8 weeks
usually worsening of symptoms
continue ART

102
Q

ART plays an important role in prevention & treatment of

A

opportunistic infections

ID (9 decks)

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