Id Test #3

Front 1

This means to live on dead organic matter.

Back 1

Saprophytic

RM that's teh Dimorphic Fungi
B. dermatitidus
P. brasiliensis
C. immitus
H. capsulatum

Front 2

Yeast grow in ____ and molds grow in ________.

Back 2

hyphae (chains)

clusters of hyphae

Front 3

Dermatophytes are the ____ fungi.

Back 3

tinea

(RM 3 genus)

Front 4

Tinea manuum is on the ___, cruris on the ___, unguium on the ____, and corporis on the ___. `

Back 4

hands
groin
fingernails
body/torso

Front 5

This yeast is from pigeon droppings. What part of the body does it particularly disseminate?

Back 5

Cryptococcus neoformans

CNS (Cryptooccal meningitis = fatal if not quickly treated) --> RM the capsule gives it this ability

Front 6

How are dimorphic fungi spread? What is significant about these fungi?

Back 6

from contaminated dust

can afffect healthy and immunocomp ppl

Front 7

This fungus is inhaled in the lungs, mulitplies thru blood/lymph, and can present as bacterial pneumonia, TB, lung cancer, or ARDS.

Back 7

Blastomyces dermatitidus

(Dimoprhic Fungi)

Front 8

This fungus is primarly asymptomatic, can lay dormant for years, begins with painful mouth sores or hoarseness and may need therapy for 5 years.

Back 8

Paracoccidiodes brasiliensis

Front 9

This fungus is an endemic to SW U.S., brought about with dust storms & earthquakes, 50% asymptomatic, and can disseminate (fungal meningitis).

Back 9

Coccidioides immitus

Front 10

This fungus is from bird/bat dropings, is asymptomatic, has flu-like symptoms, and can disseminate in immunosupp.

Back 10

Histoplasma capsulatum

Front 11

Which pts are seen most with nosocomial aspergillosis?

Back 11

those with leukemia, organ or marrow transplants

(RM very fatal if dissemiantes to systemic system)

Front 12

In absence of ergosterol fungi will pick up ___ for cell walls.

Back 12

lanosterol

Front 13

Amp B and Nystatin distrub the ____ and can create ____.

Back 13

cell wall

NOS

Front 14

Which Amp B formulation is less toxic but more costly?

Back 14

Ambisome

Front 15

Amp B's cholesterol sequestration causes ____ and ____ toxicity.

Back 15

liver & kidney

(RM giving with other treatments like Aminoglycosides inc toxicity)

Front 16

Amp B is effective with ____ fungus(gi) and Nystatin is effective with ___ fungus(gi).

Back 16

Amp B = all

Nystatin = only Candida sp. (RM it's more toxic bc it changed the double bond scheme of Amp B)

Front 17

What do azole antifungals bind to in the CYP450-14alpha-demthylase?

Back 17

Heme

(RM bound covalently)

Front 18

Azoles are ___ more selective for fungi's 14alpha-demethylase; Squalene Epoxidase Inhibitors are ___ more selective for fungi than humans.

Back 18

1000x

100x

Front 19

Which 5 Azole antifungals can be used systemically?

(IK.FPV)

Back 19

Itraconazole
Ketoconazole
Fluconazole
Posaconazole
Voriconazole

Front 20

Which 2 CYP's metabolize and are thus tied up by Azole antifungals?

Back 20

3A4
2C9

(so drugs who need these will not be metabolized bc tied up on azoles)

Front 21

Warfarin & Phenytoin are metabolized by CYP___.

Back 21

2C9

Front 22

How is ketoconazole used with cyclosporin?

Back 22

it's used by the fact it blocks cyclosporin's metabolism (3A4) and thus now only have to get 20% of the dose

Front 23

What 2 ways have azoles become resistant?

Back 23

1. mutating the gene ERG11 - which encodes for C14alpha-demethylase

2. Increased azole efflux

Front 24

Which azole antifungal covers Pityrosporum ovale?

Back 24

Ketoconazole (Nizoral)

RM causes dandruff

Front 25

Which antifungal azole causes N/V and anorexia in 20%, is teratogenic, and causes sexual dysfunctions?

Back 25

Ketoconazole (Nizoral)

Front 26

What is the main difference Itraconazole has from Ketoconazole? What does this difference cause?

Back 26

it has a Triazole

this dec metabolism rate - less effects on mammaliam sterols and thus less SE's

(RM this is the one in a capsule?)

Front 27

What is the DOC for non-disseminating, dimorphic fungi?

Back 27

Oral caps of Itraconazole (Sporonox)

Front 28

Can Itraconazole be used to treat Aspergillus sp? In AIDs/immunocomp pts?

Back 28

yes

no - bc those pts have a higher (more basic pH) so they won't be able to absorb drug

RM can tell pt to eat with drug to enhance absorption

Front 29

T/F
Itraconazole oral solution is = to capsules.

Back 29

False

RM solution is indicated for Candidiasis (mouth infections)

Front 30

This agent causes a 20-fold increase in AUC of the HMG-CoA reductase inhibitors: lovastatin and simvastatin. This leads to rhabdomyolysis which leads to renal failure.

Back 30

Itraconazole (Sporonox)

Front 31

This agent is approved for prevention of invasive Aspergillus and Candida in immunocompromised patients (esp. hematopoietic stem cell transplant).

Back 31

Posaconazole (Noxafil)

This agents helps with growing problem of Candida resistance!

Front 32

What are 3 main differences Diflucan has compared to other antifungal azoles?

Back 32

1. Rapid and almost complete absorption from GI
2. Readily crosses the BBB
3. Metabolized by CYP450-2C9 (lesser degree by -3A4)

Front 33

What can help prevent diflucans Canidida resistance issue?

Back 33

Give vaginally and not orally

Front 34

This is the DOC for AIDS patients for maintenance of Cryptococcosis.

Back 34

Fluconazole (Diflucan)

Front 35

This is the DOC for Coccidioides immiuts induced meningitis.

Back 35

Fluconazole (Diflucan)

Front 36

Does Diflucan treat/cover Aspergillus sp? Does Vfend?

Back 36

No
(also Itraconazole is better in dimorphic and tinea infections)

Yes, V does (only difference btwn diflucan)

Front 37

What does Mycelex Troche treat? How?

Back 37

Oral Candida infections on mucous membranes

its a tablet that can be sucked - but not absorped bc of 1st pass

Front 38

Squalene Epoxidase Inhibitors treat mainly ___ infections.

Back 38

tinea

(bc they penetrate kartin precursor cells)

Front 39

5-FU mimics ____. And thus inhibits the production of ____.

Back 39

uracil

thymine

(RM this is the primary mech of 5-FU or Flucytosine)

Front 40

What 2ndary mechanism does Flucytosine have?

Back 40

phosphorylating to a Thymidylate synthetase inhibitor

phosphoarylating again and getting put into DNA causing a missense error --> apoptosis

Front 41

Why does Flucytosine not effect us?

Back 41

bc must be metabolized by Fungal Cytosine-Deaminase

We don't have

If fungus mutates this enzyme --> get resistance

Front 42

What two yeast is Ancobon good for?

Back 42

Cryptococcus neoformans
Candida sp.

Front 43

Griseofulvin is clinically limited to ___ infections. What does it affect (MOA)?

Back 43

tinea

microtubles

Front 44

What are the 3 echinocandins discussed? What do they inhibit?

Back 44

Capsofungin (Cancidas)
Anidulafungin (Eraxis)
Micfungin (Mycamine)

Fungal Cell Wall Synthesis

Front 45

Capsofungin is effective against ___ and ___ sp only. How is it admin?

Back 45

candida
aspergillus

IV only

(RM no SE's noted)

Front 46

Capsofungin + Voriconazole = ??

Back 46

synergy against aspergillus sp

Front 47

These antifungals also inhibit an enzyme call B-glucans synthase - so get permeability of cell wall?

Back 47

Echinocandins

Capsofungin (Cancidas)
Anidulafungin (Eraxis)
Micfungin (Mycamine)

Front 48

T/F
MAC (caused by Mycobacteria) is an opportunistic infection.

Back 48

True

(so it's everywhere & nonpathogenic in healthy people)

Front 49

What's the 1st sign of leprosy? What ultimately happens?

Back 49

1st sign - change in pigmentation

ultimately get muscle atrophy, resorption of small bones, and spontaneous amputation

Front 50

This is the most common bacterial opportunistic infection in AIDs pt's and is the 3rd most common opp infection altogether in AIDs pts.

Back 50

MAC

Front 51

Where does the TB turbercles expand to when it's a now secondary disease?

Back 51

Bronchi and URT

(RM these are formations in the lungs that have engulfed the bac – they clump together as a “sticky mess” and can be visual on x-rays)

Front 52

Who is in the category 2 positive PPD test?

Back 52

usually those from other countries who have high number TB

Front 53

Who is in the category 3 positive PPD test?

Back 53

"Everyone else"

typically healthy person who's been exposed

Front 54

Is extrapulmonary TB easily spread person-to-person?

Back 54

No

only if person has it with the pulmonary TB infection

Front 55

Which "R" ins RIPE is not approved by the FDA for TB treatment?

Back 55

Rifaximin

Front 56

RIPE?

Back 56

Antituberculosis Drugs

Rifampin, Rifapentine
Isoniazid
Pyrazinamide
Ethambutol

Front 57

Which 3 FQ's are used as 2nd line TB treatment?

Back 57

Levofloxacin
Moxifloxacin
Gatifloxacin

Front 58

This drug is bacterioSTATIC in resting TB bacilli and bacterioCIDAL for dividing one.

Back 58

Isoniazid

Front 59

What enzyme does Isoniazid need to become active?

Back 59

Catalase Peroxidase (katG)

(RM 3 species arise from this then acetylation creates 2 other species = active)

Front 60

MOA for Isoniazid?

Back 60

binds to inhA which then blocks fatty acid from binding and thus becoming mycolic acid

Front 61

Mutation on katG or inhA cause _____ resistance. If BOTH are mutated get _____ resistance.

Back 61

low-level
high-level

RM resistance is very profound - why TB pts need multiple therapy

Front 62

Do we have katG?

Back 62

no

this is why Isoniazid is very selective bc it's a prodrug and needs katG to get to active form

Front 63

Can Isoniazid be used alone as prophylaxis?

Back 63

Yes but not for treatment

Front 64

What must be given concurrently with Isoniazid? Why?

Back 64

B6 - Pyridoxine

bc isoniazid is dec's it and can cause peripheral neuritis (neuropathy)

RM DM and pregnant patients at higher risk - tho dose related

Front 65

Fast acetylators of Isoniazid have ____ NAT2 and slow acetylators have ___ NAT2? What does this affect?

Back 65

higher/lower

drug conc and t1/2

slow acetylators = more active form --> peri neuropathy
fast = more inactive metabolite --> this metabolite causes more hepatic toxicity

Front 66

What drug's metabolism can be affected by Isoniazid?

Back 66

PHY

(why PHY levels must be monitored while on drug)

Front 67

Is Rifampin good for MRSA?

Back 67

NO,

by yes for strept and spathy

Front 68

Is Rifampin good for N. meningitidis and H. influenzae?

Back 68

Yes

(RM good for most Gram + and Gram -)

Front 69

This drug is very lipophilic and increase the activity of Streptomycin or Isoniazid.

Back 69

Rifampin (Rimactane)

Front 70

Rifamycin inhibits the formation of _____ which is thus inhibits ____ production.

Back 70

mRNA
protein

(it only effects us when given in high doses)

Front 71

This drug causes orange pigmentation of body fluids, a 3A4/2C inducer, and has GI disturbances.

Back 71

Rifampin

Front 72

This drugs effects RT inhibitors, protease inhibitors, and OC.

Back 72

Rifampin (bc it's a potent 3A4/2C inducer)

Front 73

Does Rifabutin have better activity against MAC than Rifampin?

Back 73

yes

(RM doesn't induce CYP as much as rifampin)

Front 74

This drug can be given twice weekly during intese waves of Mycobacterium infections and weekly during continuous waves.

Back 74

Rifapentine

(RM much longer t1/2)

Front 75

What is Rifaximin indicated for?

Back 75

Traveler's diarrhea
Hepativ encephalopathy recurrence

(NOT TB!!!)

Rm given by oral route - but small amount absorbed

Front 76

What does Ethambutol block? What does this cause?

Back 76

ATF

blocked formation of arabinogalactans

(RM dispensed at + enantiomer)

Front 77

Resistance occurs for this drug if a single point mutation occurs in the embA gene which encodes for ATF.

Back 77

Ethambutol (Myambutol)

Front 78

What is the major SE of ehtambutol?

Back 78

optic neuritis

caused by chelation of Cu and Zn in retina and optic nerve --> this dec the amount going into mito e- transport chain

it's dose and duration dependent

Front 79

This drug exhibits antibac effects only at a slightly acidic pH, is dependent on Tuberculin P., but the target is unknown that inhibits mycolic acid synthesis?

Back 79

Pyraziamide

(RM tuberculin P. is what take prodrug into active acid)

Front 80

This drug is good for TB only and is used when all others have failed.

Back 80

Cycloserine

Front 81

What two things does Cycloserine inhibit? What CNS effects does it have?

Back 81

D-alanine racemase
D-alanine ligase

CNS: agonizes NMDA and decreases GABA syn (seizures!!!) --> also bad for depressed ppl by inc suicides

Front 82

What classifies TB as XDR (extensively drug resistant)? 4 things

Back 82

Resistant against:
Isoniazid
Rifampin
FQ's
(amikacin, kanamycin, or capreomycin)

Front 83

_____ recognizes cell surface sialic acid containing glycoproteins

Back 83

Hemagglutinin

Front 84

_____ cleaves sialic acid moieties, thereby releasing budding virions

Back 84

Neuraminidase

Front 85

___ are proteins associated with RNA core

Back 85

Nucleoproteins

Front 86

____ link the envelope to the core

Back 86

Matrix proteins (M1 and M2)

Front 87

___ are non-structural proteins

Back 87

NS

Front 88

This extent of the flu infections is based on ____.

Back 88

hemagglutinin

Front 89

People over the age of ___ seem to have degree of immunity to seasonal H1N1.

Back 89

60

33% over 65 have coverage somehow

Front 90

With flu vaccine there is a 1% chance of getting ______ and a 2% of getting it if get the flu altogether.

Back 90

Guillain-Barre syndrome
(causes paralysis)

Front 91

Which 2 drugs is the 2009 pandemic H1N1 resistant to? Which 2 is it sensitive to?

Back 91

Resistant to: Amantadine, Rimantadine

Sensitive to: Tamiflu and Relenza

Front 92

99.6% of the seasonal H1N1 isolates are resistant to ____

Back 92

Tamiflu

Front 93

This anti-influenzal is currently in P3 trails and would be an emergency use med by FDA standards.

Back 93

Peramivir

Front 94

T/F
Lots of info supporting resistance to Relenza.

Back 94

False

no isolates currently tested resistant

Front 95

T/F
More people die from pandemic flu than seasonal.

Back 95

False

more die from seasonal bc more get infected

Front 96

Amantadine covers with Influenza(s)?

Back 96

Type A only

(RM this mimics dopamine - gives SE's but can help with Parkinson's)

Front 97

Orthomyxoviruses is a ____ virus that causes ______.

Back 97

RNA
influenza

Front 98

Rubella Virus is a ____ virus that causes ____.

Back 98

RNA
German measles

Front 99

Adenovirus is a ____ virus that causes ____.

Back 99

DNA
the common cold (conjuctivitis and sore throat)

Front 100

Papillomaviruses is a _____ virus that causes ____.

Back 100

DNA
warts, Cervical cancer

Front 101

Herpesviruses is a ____ virus. While Picornavirus is a ____ virus.

Back 101

DNA
RNA

(RM pico causes common cold too - rhinovirus)

Front 102

Aman/Riman block the ___ channels and thus prohibit ____.

Back 102

M1 and M2
fusion

Front 103

Resistance of this drug occurs when there is an alteration on M1/M2 via mutation of their genes.

Back 103

Aman/Riman

Front 104

Resistance to Aman/Riman occurs by day ___ in 30% of ppl.

Back 104

5

Front 105

Anti-influenzal specificity is determined by different _______ forms.

Back 105

sialic acid

(reason why we don't pass H5N1 person to person)

Front 106

This drug is an analog of sialic acid and inhibits both Influenza A and B neuromamindase.

Back 106

Zanamivir (Relenza)

(RM also covers Riman/Aman resistant species)

Front 107

How is Zanamirivr admin?

Back 107

intranasal or dry powder inhalation

(bc only 5% oral bioavailability)

Front 108

At higher doses of Tamiflu and longer treatment times what 2 flu's can it be active against?

Back 108

H5N1
current pandemic H1N1

Front 109

Is Tamiflu readily absorbed in GI unlike Zanamivir?

Back 109

Yes
75% available after hepatic cleavage

Front 110

What can be given with Tamiflu to reduce elimination of agent - esp when there is a shortage?

Back 110

Probenicid

Front 111

What is Peramivir classified as tho unapproved?

Back 111

neuraminidase inhibitor

(SE:s N/V/D and nuetropenia)

Front 112

Epstein-Barr virus is HHV___ and CMV is HHV__.

Back 112

4
5

Front 113

Kaposi's Sacroma is HHV___

Back 113

8

(not one most ppl mid-aged have)

Front 114

These HHV's all target the mucoepithelia cell and lye latent in the neuron.

Back 114

1-3

Front 115

This HHV targets and lies latent in the B lymphocyte cells.

Back 115

CMV --> (HHV5)

Front 116

Where exactly does HHV3 lye latent?

Back 116

the spine

(RM causes great pain)

Front 117

HSV___ is the most common cause of viral meningitis. Is it more or less serious than bacterial meningitis?

Back 117

2

less; RM it's VE --> BM --> VM
(RM HSV1 or 2 can cause encephalitis or meningitis)

Front 118

What 3 things does the herpes virus severity depend on?

Back 118

age
site
immune status

(more AIDs pts with encephalitis)

Front 119

This agent is a guanine nuceloside analog.

Back 119

Acyclovir (Zovirax)

Front 120

Is Acyclovir an obligate chain terminator? What base does it replace?

Back 120

Yes
Guanine

(RM DNA needs a triphosphate nucleotide)

Front 121

What phosphorylates acyclovir the first time? The 2nd and 3rd?

Back 121

1: Herpes Virus Thymidine Kinase

2-3: Cellular GMP Kinase

Front 122

What kind of inhibition does Acyclovir cause?

Back 122

Competitive (with Guanine [dGTP])

Front 123

Where does the 1st phosphorylation occur for Acyclovir?

Back 123

in the infected cell - by Herpes TK
Acyclovir = 200X greater at Herpes TK

Front 124

What drug can help potentiate the effect of Acyclovir? How?

Back 124

Cellcept

By depleting the normal pools of dGTP (so now you've decreased competition)

Front 125

What is the most common mechanims of HSV resistance to Acyclovir?

Back 125

absent or decreased viral production of TK

Front 126

What one thing does Val-acyclovir give?

Back 126

higher blood volumes - so less of drug need

(RM both tho are nephotoxic)

Front 127

Acyclovir and Valacyclovir cover which HSV's? Valacyclovir covers which 2 alone?

Back 127

1-3 (both)

Val only: EMV & CMV

Front 128

Cidofovir is a ____ nucleotide analogue. What does it cover (3)?

Back 128

cytidine
Human Herp, Papilloma Virus, and Pox Virus (more monkey, less small)

Front 129

How can Cidofovir cover resistant (val)acyclovir strands?

Back 129

Bc not dependent on HSV TK for monophos --> already phos and gets diphos by host cell enzyme

Front 130

What does Cidofovir compete with? Is it an obligate terminator?

Back 130

dCTP
yes

(RM low oral so used mainly as topically or injectable)

Front 131

Adding _____ prevents nephrotoxicity of Cidofovir.

Back 131

Probenecid

Front 132

Cidofovir can treat CMV in _____. And is used for _____ (eye).

Back 132

AIDs pts
Keratitis (topically)

Front 133

Penciclovir is a _____ analogue and a _____ nucleoside mimic. Why is it useful if less potent then others?

Back 133

acyclovir / Guanosine

bc tho less potent get higher conc with a longer t1/2

Front 134

Is Penciclovir an obligate chain terminator? What does drug do?

Back 134

no

gets incorp --> causes a kink in chain --> DNA falls apart

Front 135

Famvir is the diacetyal ester prodrug of _____. What does this prodrug bring?

Back 135

Penciclovir

65-80% bioavailability

Front 136

Is Penciclovir/Famciclovir viral TK dependent?

Back 136

yes

so cross-resistance can occur

Front 137

What is Ganciclovir especially good against?

Back 137

HHV5

Front 138

Ganciclovir is monophos by ___ in HSV infections and by ____ in CMV infections.

Back 138

TK

CMV phosphotransferase

(both di and tripho by cellular kinases)

Front 139

Is Ganciclovir an obligate chain terminator?

Back 139

no

(RM this means causes kinks)

Front 140

This agent is indicated for CMV retinitis and HSV keratitis.

Back 140

Ganciclovir

(RM also used in conjunction with suicide gene therapy)

Front 141

Why is Idoxuridine and Trifluridine only good for DNA viruses?

Back 141

bc mimic thymidine

RNA doesn't use thymidine, it uses uracil

Front 142

This agent is used topically in treatment of HSV keratitis and keratconjuntivitis.

Back 142

Idoxuridine/Trifluridine

(RM there most potent in antiviral agnet --> very toxic to human cells like Ganciclovir)

Front 143

What is altered to make Idoxuridine/Trifluridine mimic Thymine?

Back 143

the -CH3 group at top
(not sugar like other antivirals)

this alters the H bonding - DNA now falls apart - so RM not a obligate chain terminator

Front 144

This agent is an adenosine analog with an arabinose instead of a ribose sugar.

Back 144

Vidarabine

(RM not a obligate chain term.)

Front 145

This agent inhibits HSV virion fusion and is a long-chain saturated aliphatic alcohol.

Back 145

Docosanol (Abreva)

Front 146

CD4+ are cells that express receptors for ____.

Back 146

glycoproteins

Front 147

What are the 3 main genes of the retrovirus?

Back 147

gag - encodes for Ncap
pol - encodes for 3 proteins that code for RT
env - encodes for gp120 and gp41 (which equals gp160 - together act like the ligands, where cd4+ is the receptor)

Front 148

What are the 3 very important proteins in the retrovirus?

Back 148

integrase
protease
reverse transcriptase

Front 149

What do we look for in a HIV saliva test?

Back 149

AB against p24

during latency body makes AB against p24

Front 150

What is p24?

Back 150

capsid associated with HIV
correlates with number of HIV copies in blood

Front 151

What causes a confirmational change in the CD4+ cell?

Back 151

binding of GP120

after this brings in chemokine receptors CCR5 or CXCR4 --> what causes virus to fuse with membrane

Front 152

Protein Inhibitors target the HIV _____.

Back 152

assembly

Front 153

HAART?

Back 153

highly active anti-retroviral therapy

controversy is to hit early or hard or to deferral

Front 154

The HIV RT lacks the ________ activity that is needed to correct transcription errors. What happens as a result?

Back 154

3'-exonuclease

mutations occur at every rep cycle - 100s of times a day
(why pt gets 6-8 differ combos)

Front 155

This was the 1st anti-retroviral. It mimcs thymidine and a potent inhibitor of HIV1 and HIV2.

Back 155

Zidovudine (Retrovir, AZT)

Front 156

Is AZT an obligate chain term? How is it phosphorylated?

Back 156

yes

mono, di, and tri by the host's thymidine kinase

(RM this drug competes with dTTP)

Front 157

Resistance for AZT occurs in 1/3 pt's after how long? What does large amounts of monophos AZT do?

Back 157

1 year

supresses bone marrow dna polymerase --> anemia or erhtroid stem cell toxicity

Front 158

How is Zerit better than Retrovir?

Back 158

it doesn't accumulate causing toxicity

(RM this is because it has less affinity for Thymidine kinase unlike AZT - why can't give them together)

Front 159

What does Lamivudine have affinity for? What is it not synergistic with?

Back 159

HIV1
HIV2
HBV

no synergy with emtricitabine

Front 160

This drug induces M184V mutations - which is good because decreases the virulence of disease.

Back 160

Lamivudine (Epivir) 3TC

Front 161

Why id Emtricitabine cross resistant to Lamivudine?

Back 161

bc of the same M184V effect

(RM potent inhibitor of HIV1 and 2)

Front 162

Didanosine is a competitor of ____, is a prodrug with a higher potency of AZT in treating:

Back 162

adenosine
(obligate term)

HIV1 and 2 in lymphocytes and monocytes

Front 163

Didanosine and Abacavir are ___ inhibitors.

Back 163

purine

Front 164

Abacavir mimcis which base? What usually occurs within 6 weeks of therapy?

Back 164

dGTP

HSR (death could occur - all pts must be counseled on it)

Front 165

What gene predisposes a patient to getting ABC HSR? What does this tell us?

Back 165

HLA-B*5701

that pt's genes can effect the pt's HIV progression

Front 166

What's the benefit of Tenofovir?

Back 166

only needs to 2 steps to get tri-pho

(RM this mimics adenosine)

Front 167

What's one distinguishing SE of Tenofovir?

Back 167

causes severe lactic acidosis --> leads to liver and kidney damage

Front 168

nNRT's are active only against HIV___, are not phosphorylated but are _____.

Back 168

1
metabolized by CYP450 isozymes

Front 169

What's the MOA for nNRTI's?

Back 169

bind to an allosteric site on RT
now cannot pick base so inhibits making viral DNA

Front 170

Nevirapine is a inducer of CYP___ and ___. What drugs are decreased when given together?

Back 170

3A and 2B6

Antivirals (not AZT or NRTIs which = synergy), OC's, Ketoconazole, and Clarithromycin

Front 171

What are the 2 specific sites of Nevirapine binding?

Back 171

103 and 181 (same with other nNRTIs)

RM if mutation occurs at either site = binding falls 100x

Front 172

What drug can restore AZT sensitivity to a once resistant strand?

Back 172

Delaviradine (Rescriptor)

Front 173

This HIV drug is good bc qd dosing, bad bc teratogenic, and causes CYP interactions lowering Protein Inhib and other nNRTI levels.

Back 173

Efavirenz (Sustiva)

Front 174

What 3 CYP's does Etravirine effect?

Back 174

3A4
2C9
2C19

Front 175

Rilpivirine has what benefit over Etravirine?

Back 175

longer t1/2 --> qd dosing

Front 176

Where does HIV protease cleave?

Back 176

PHE-PRO link

Front 177

What are all PI's substrates for?

Back 177

P-Glycoprotein efflux pumps

Front 178

Do resistance to one PI mean resistance for another?

Back 178

yes generally

Front 179

Which PI is the most potent CYP inhibitor? Least?

Back 179

Ritonavir

Saquinavir

Front 180

What are 2 SE's of PI's?

Back 180

Dylipidemia and glucose imbalances

see weight gain in girth

Front 181

This drug has a pharmacoinetic enhancer effect.And is potent against HIV1.

Back 181

Ritonavir (Norvir)

Front 182

This agent is a psuedo-pepitdomemetic inhibitor of HIV1 protease.

Back 182

Saquinavir (Invirase)

Front 183

Is Fos(amprenavir) active against HIV1 and HIV2?

Back 183

yes

Front 184

Name four PI's that are HIV1 and HIV2 active. (L,T,A,N)

Back 184

Lopinavir
Tipranavir
Atazanavir
Nelfinavir

Front 185

This PI has causes pronounced hyperlipidemic SE.

Back 185

Lopinavir

Front 186

This PI causes hyperlipidemia, hepatitis, and glucose imbalance.

Back 186

Tipranavir

Front 187

What's the benefit of Darunavir (Prezista)?

Back 187

has activity even in presence of multiple protease mutations

(RM this is 2nd gen --> covers HIV1 and 2)

Front 188

Enfuvirtide is only active against HIV__ and it's biomimetic peptide specifically binds to ____ which inhibis the fusion.

Back 188

1

GP41

(RM no cross resistance has been shown with other therapies - good thing BUT is very expensive)

Front 189

This agent is a CCR5 antagonist that is active against HIV1.

Back 189

Maraviroc

(RM get cough, cold and allergies symptoms because blocking the chemokine receptor)

Front 190

If taking Maraviroc with a CYP3A inhibitor dec dose by ____. If with a inducer increase dose by ___.

Back 190

dec by half
inc by doubling

(RM typical dose is 300 mg BID)

Front 191

Maracviroc has a black box warning for this...

Back 191

hepatotoxicity

(RM this drug is also CI with St. John's Warts and is a substrate for P-GP)

Front 192

This agent is the only Integrase Inhibitor.

Back 192

Raltegravir (Isentress)

Front 193

Name 3 good examples of CYP3A inhibitors. (PAC)

Back 193

PIs
Clarithromycin
Azole antifungals

Front 194

Name 5 good examples of CYP3A inducers. (ERPPC)

Back 194

Efavirenz
Rifampin
Carbamazepine
Phenobarbital
Phenytoin