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Pharm 2 > exam 3 > Flashcards

exam 3 Flashcards

1
Q

echinocandins

A

candida
aspergillus

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2
Q

polyenes

A

candida
aspergillus
histoplasma
blastomyces
coccidioides

broadest!

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3
Q

Broadest spectrum of all antiFUNGAL drugs; rough side effects

A

polyenes

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4
Q

azoles

A

candida (most)
aspergillus (most)

some:
cryptococcus
histoplasma
blastomyces

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5
Q

flucytosine

A

candida
cryptococcus

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6
Q

antifungal target:

cell wall synthesis

A

echinocandins

“itching to cross the wall”

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7
Q

antifungal target:

cell membrane pores alteration

A

polyenes

“Pores=Polyenes”

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8
Q

antifungal target:

Ergosterol (Cell Membrane) Synthesis

A

azoles

“azOLes = ergosterOL”

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9
Q

antifungal target:

Nucleic Acid Synthesis

A

5-flucytosine

“cytosine”

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10
Q

MOA

INHIBIT (1, 3) β-D-glucan synthase, which synthesizes B (1, 3) glucan fibrils, which are essential to the _____ _____

A

echinocandins

cell wall

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11
Q

__________fungin

A

echinocandins

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12
Q

what is the biggest disadvantage of echinocandins

A

IV administration only

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13
Q

MOA

Amphipathic compounds, bind to ergosterol in the cell membrane  create pores, pores change the membrane permeability and allow increased leakage of intracellular components  death of fungi occurs

A

polyenes

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14
Q

amphotericin B
nystatin

A

polyenes

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15
Q

Drug of choice for the treatment of life-threatening invasive/systemic fungal infections

NOT affected by renal or hepatic function!

A

amphotericin B

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16
Q

3 main adverse effects of amph B

A

infusion reaction
(cytokine =IgG); premedicate!

nephrotoxicity (permanent!)

anemia (reversible!)

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17
Q

antifungal

  • Monitor kidney function, electrolytes, CBC

decreases K and mag

A

amph B

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18
Q

what 3 drugs are used to premedicate with amph B

A

tylonel
benadryl
hydrocortisone

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19
Q

lipid formulations
amph B

benefits and drawbacks

A

Slowly releases AmphB; reduced risk of nephrotoxicity

Reduced incidence of infusion reactions

20-50x more expensive*

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20
Q

2 examples of lipid form of amph B

A

abelcet (complex)

ambisome (vehicle/pod)
cmax is higher!

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21
Q

polyenes
antagonistic with _________*

A

azoles

“A=A”

Azoles eliminate ergosterol, but this is the target of polyenes (amph B)

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22
Q

polyenes
synergistic with _________ + _____________*

A

echinocandins
flucytosine

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23
Q

Inhibit fungal 14 a-demethylase (CYP450-CYP51)  reduction in ergosterol levels  cell membrane permeability issues

Levels of squalene and lanosterol go up  increased toxicity

A

azoles

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24
Q

All systemic AZOLE antifungals are ____azoles; except for ketoconazole, which is an imidazole*

A

TRIazoles (3 nitrogens)

except for ketoconazole (2 nitrogens)

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25
Q

Fungistatic=low dose

fungicidal=high dose

A

azoles

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26
Q

which azole is oral only

A

itraconazole

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27
Q

which azole IS the only one that is RENALLY eliminated*

which 2 azoles have the vehicle (renal toxic)

A

fluconazole

posaconazole, voriconazole

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28
Q

which azole does NOT cause QT prolongation***

A

isavuconazole, “isabella”

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29
Q

which azole has significant safety concerns regarding ORAL tablets

A

Ketoconazole “Killer”

severe liver injuries
adrenal insufficiency
QT prolong
lots of drug-drug interactions

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30
Q

which drug means you should NOT give AZOLES

A

warfarin

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31
Q

which 2 azoles require acidity “take with a coke”

A

ITRAconazole

VORIconazole

“itra + vori are acidic hoes”

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32
Q

which azole is contraindicated in CHF

A

ITRAconazole

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33
Q

can cause photosensitivity and visual disturbances*

azole

A

VORIconazole

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34
Q

what part of the azole causes nephrotoxicity*

A

the VEHICLE it is in

cresemba is a prodrug that does NOT have this vehicle

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35
Q
  • MOA

Fluorinated analog of the nucleobase cytosine

related to 5 FU (an anticancer drug); can impact both DNA and RNA synthesis; fungal cells have cytosine permease (an enzyme) that brings flucytosine (5-FC) into the cell  gets converted to 5-FU (by cytosine deaminase)  gets converted into nucleotides  get incorporated into RNA and DNA

A

flucytosine

inhibits RNA/protein + DNA synthesis

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36
Q

which 2 enzymes are involved with flucytosine

A

permease: brings it into the cell

deaminase: converts to 5-FU

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37
Q

true or false

2 enzymes permease and deaminase make flucytosine SELECTIVE since they do not exist in humans

A

true

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38
Q

which antifungal is NEVER used alone

A

flucytosine

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39
Q

which antifungal class is the ONLY one that causes QT prolongation

A

azoles (triazoles)

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40
Q

true or false

all viruses depend on host to replicate

A

true

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41
Q

what is the ONLY antiVIRAL that is CIDAL*

A

hep C drugs

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42
Q

what type of ssRNA is similar to our RNA

A

positive ssRNA

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43
Q

where are most antiviral targets

A

nucleic acid replication

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44
Q

what does mimicking mean for antivirals*

A

Mimicking means you bypass the 1st step of phosphorylation (which is often rate limiting)  you already start with a monophosphate

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45
Q

true or false

once a person is infected with HERPES, they are infected for life

A

true

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46
Q

patients with renal dysfunction (2)

A

decrease dose

extend dosing interval

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47
Q

MOA
o NucleoSIDE analog, inhibits viral DNA synthesis - blocks viral DNA polymerase
 Activated by a viral kinase (the virus has their own kinase*)
o Only the infected cells will activate/phosphorylate the drug into triphosphate

A

acyclovir + ganciclovir

herpes

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48
Q

which antiVIRAL is good for solid organ transplant
HIV patients*

A

ganciclovir

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49
Q

o Inhibits spermatogenesis → USE CONTRACEPTION
o Bone marrow suppression
o Carcinogenic
o Teratogenic

A

ganciclovir

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50
Q

what are the 2 drugs that are good for CMV, HSV (herpes) RESISTANT antivirals

A

cidofovir (mimics monophosphate = bypasses 1st step of phosphorylation*)

foscarnet (keeps triphosphate from binding, NO phosphorylation)

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51
Q

what is the most common form of herpes resistance

A

mutations in viral kinases

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52
Q

what are the 2 newest herpes antivirals

A

letermovir (bone marrow transplant)

maribavir

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53
Q

Current treatments are NOT curative

Disease IS preventable with a vaccine

A

hep B

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54
Q

all HBV (hep B) antiviral agents inhibit HBV ________________

A

polymerase

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55
Q

Lactic acidosis, severe hepatomegaly

Can cause HIV resistance in patients with unrecognized or untreated HIV

A

hep B (HBV) antivirals

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56
Q

which HBV antiviral is

active against HIV, but is NOT approved to use with HIV*

A

adefovir

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57
Q

what 3 drugs can be used for HBV or HIV

A

tenofovir disoproxil
tenofovir alafenamide
epivir

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58
Q

what drug is the BEST for HIV or HBV

A

tenofovir ALAFENAMIDE

(less in the plasma, less nephrotoxicity/bone toxicity)

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59
Q

no vaccine

treatment can eliminate it

A

hep C

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60
Q

what is the most common genotype of hep C

A

1B

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61
Q

what is the direct acting antiviral targets (DAA) for

A

hep C HCV

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62
Q

antiviral

________buvir*

A

NS5B polymerase (blue) inhibitors

HCV hep C

“B= Buvir”

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63
Q

antiviral

__________asvir*

A

NS5A cofactor (orange) inhibitors

HCV hep C

“A= Asvir”

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64
Q

antiviral
__________previr*

A

NS3/4A protease (green) inhibitors

HCV hep C

“Previr=Protease”

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65
Q

true or false

NON-nucleoside (nucleotide) does NOT need to be phosphorylated

A

true

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66
Q

true or false

hep C drugs are often combined (hitting at 2 targets)

A

true

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67
Q

which drugs are
contraindicated with strong INDUCERS of Pgp/CYP3A4

means it will DECREASE levels

A

DAA (hep C)

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68
Q

antacids, H2, PPIs (absorption reduced)

amiodarone (bradycardia)

CYP3A4 inducers

A

DAA drugs (hep C)

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69
Q

what are the 4 main HIV drugs involved in blocking* 1) attachment
2) interaction
or
3) fusion

“entry inhibitors”

A

fostemsavir
maraviroc
ibalizumab
fuzeon

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70
Q

MOA

inhibit the reverse transcriptase inhibitor, preventing formation of DNA from HIV RNA

A

reverse transcriptase inhibitors

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71
Q

nucleoside/tide require _______________ (competitively inhibit RT)

NON-nucleoside/tide do NOT require _________________
(non-competitive binding to RT)

A

phosphorylation

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72
Q

Class Boxed Warning:
lactice acidosis with hepatomegaly with steatosis

A

NRTIs (nucleoside/tide RT inhibitors)

for HIV

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73
Q

hypersensitivity reactions, test for HLA-B1507

A

Abacavir (does NOT require renal dosing)

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74
Q

which HIV drug is good for labor/childbirth

A

Zidovudine

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75
Q

which 2 HIV classes have CYP450 interactions

A

NNRTIs (NON nucleoside/tide RT inhibitors)

protease inhibitors

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76
Q

MOA

Prevent the covalent insertion/integration of HIV + prevent formation of HIV provirus

A

integraase inhibitors

“____________tegravir”

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77
Q

Due to extensive first pass metabolism (and Pgp transport), administer with a PK Booster!

what are the 2 boosters* they INHIBIT CYP3A4, protect from metabolism

A

Protease inhibitors (PIs)

ritonavir
cobicstat

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78
Q

MOA

Competitively inhibit the cleavage of non-functional viral precursor proteins into functional proteins

A

protease inhibitors

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79
Q

antiviral

adverse effects include

insulin resistance
hyperlipidemia

A

protease inhibitors

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80
Q

what combos of drugs are used for pre-exposure prophylaxis for HIV

A
  • Tenofovir alafenamide + emtricitabine (Descovy)
  • Tenofovir disoproxil + emtricitabine (Truvada)
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81
Q

what are most common flu types

A

A, B

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82
Q

MOA

Blockage of the neuraminidase enzyme that normally cleaves the virus that is tethered to the host cell  now the virus is PERMANENTLY tethered to the infected host cell

A

tamiflu, relenza,
rapivab (IV ONLY)

(flu)

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83
Q

inhibits endonuclease activity of RNA polymerase, prevents cap-snatching (normally, the flu virus “steals” the cap from our mRNA to replicate)

A

xofluza

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84
Q

which antifungal causes bone marrow suppression*

A

flucytosine

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85
Q

which antifungal binds to ergosterol

A

amph B (polyenes)

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86
Q

which antifungal reduces cell membrane integrity by blocking synthesis of ergosterol

A

azoles

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87
Q

which antifungals cause histamine reactions

A

echinocandins

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88
Q

which adjunctive measure is used to LESSEN nephrotoxicity for amph B

A

normal saline infusion (not benadryl!)

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89
Q

A patient in the ICU on IV fentanyl (CYP3A4) started on IV VORICONAZOLE***(inhibitor CYP3A4) should be monitored for:

A

resp depression and sedation

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90
Q

Which of the following are true regarding the azole antifungals? 3

A

hepatotoxic
teratogenic
affect metabolism of other drugs

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91
Q

Which PK booster has protease inhibitory activity

A

rotonivir

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92
Q

someone is infected with a HSV-2 strain that LACKS thymidine kinase activity and should be treated with

A

cidofovir
foscarnet

(herpes resistant drugs)

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93
Q

Which one of the following is an anti-HSV agent that is dependent on viral thymidine kinase phosphorylation

A

acyclovir

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94
Q

which herpes antiviral does NOT require phosphorylation in order to inhibit viral DNA sysnthesis

A

foscarnet

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95
Q

ganciclovir resistant CMV strain responds to cidofovir suggesting that ganciclovir resistance is LIKELY due to

A

mutation in KINASE

96
Q

absorption of this antiviral is REDUCED with polvalent cations (chelation)

A

integrase inhibitors

97
Q

Which anti-HIV drug class is associated with rashes

A

Non-nucleoside/tide reverse transcriptase inhibitors

98
Q

___________irine

does NOT require phosphorylation

antiviral

A

NON-nucleotide/side RT inhibitors (NNRTIs)

99
Q

ESTER-linked is

C=O with ?

A

O

“Queen Ester with Boobs”

100
Q

AMIDE-linked is

C=O with ?

A

N

101
Q

LA’s

metabolism: plasma esterases, shorter acting, less stable

A

ESTER-linked

102
Q

LA’s

metabolism: P450 enzymes, longer acting, more stable

A

AMIDE-linked

103
Q

LA’s

allergy more likely (PABA)

A

ESTER-linked

104
Q

what type of subunit is involved in LA’s sodium channel

A

alpha subunit
(4 domains)

105
Q

Voltage sensor component of the sodium channel

A

S4+ segment

106
Q

When the S4+ Segment senses a voltage change, the formation of the ______ changes

A

pore

107
Q

what part does the LA bind to

A

inactivation region (H/P)

108
Q

protonation =

A

ionization (when it works on the sodium channel)

109
Q

what is the only LA that does not have to be protonated to work

(does NOT have an amine group)

A

benzacaine

110
Q

4 parts of the LA

A

aromatic ring

ester/amide “link”

hydrocarbon chain

amiNe group (ionizable region)

111
Q

what is the most common aromatic ring

A

benzine (6 figure)

112
Q

increasing the size of the ___ group will increase lipophilicity

A

R group

113
Q

longer R group/longer chain means _______ potent

A

more potent!

114
Q

true or false

the MORE acidic the pH, the LESS likely the LA will work (due to the HIGHER concentration of protons)

A

true

more likely to be ionized/protonated and be unable to cross the membrane

115
Q

what are the 2 things that affect binding to sodium channel

A

pKa
pH

116
Q

a ________ pKa results in FASTER onset of action

A

LOWER pKa

117
Q

what does frequency dependence depend on

A

rate of dissociation

LAs prefer to target RAPIDLY depolarizing tissues

118
Q

__________, ____________ drugs dissociate more rapidly

A

smaller, lipophilic

119
Q

Overall Effectiveness of LAs
* Depends on:
(4)

A

o Hydrophobic/lipophilic character
o Ability to ionize
o Overall affinity (kd) for binding site
o Frequency of channel opening

120
Q

how do lipid emulsion infusions work

A

lipophilic version of the LA will be trapped inside the lipid molecule  the free plasma concentration begins to drop  the plasma concentration goes down  the drug leaves the neuron  goes into the droplet  metabolizes  eliminated

121
Q

EUTECTIC mixture of local anesthetic

___________ the melting point

A

lidocaine + prilocaine

LOWERS the melting point

122
Q

what are the main receptors for
vestibular

A

M1!!

H1?

123
Q

what are the main receptors for
CTZ

A

D2
5HT3

chemoreceptors
NK receptors?

124
Q

what are the main receptors for
vomiting center

A

H1
M1
5HT3

125
Q

what are the 2 types of drug that works centrally and peripherally for NAUSEA

A

5HT3 (zofran)

cannabinoids (agonists)

126
Q

true or false

antihistamines work on the H1 + M1 receptors

A

true

antimuscarinic effects (dry mouth, urinary retention)

127
Q

example of antimuscarinic motion sickness drugs

A

scopolamine

antihistamine as well:
antivert
dramamine
benadryl

128
Q

which 5HT3 has the highest risk for QT prolongation

(dont give prophylactically)

A

dolasetron

129
Q

what are the 3 drugs that are great for DELAYED emesis*

A

palonosetron

netupitant

akynzeo (combo of both!)

130
Q

examples of NK1 antagonists (N/V)

A

fosaprepitant
aprepitant
netupitant*
cinvanti
akynzeo

P450 enzyme interactions

131
Q

block D2 + M1 + H1

A

compazine
phenergen
reglan
olanzapine (antipsychotic)
amisulpride

EPS symptoms

132
Q

which D2 antagonist is associated with QT prolongation

A

amisulpride (D2 + D3)

133
Q

N/V

low level ____
moderate level ____
high level ____

A

2
3
4

134
Q

what are considered N/V supplements

A

D2 receptor (phenergen, olanzapine)

benzos

135
Q

what is a contraindication for laxatives

A

bowel obstruction

136
Q

surfactant laxatives are stool ____________

A

softeners

docusate

137
Q

what is the most abused class of laxatives

A

stimulants

138
Q

what are the 3 antimotility/antisecretory agents for diarrhea

A

lomotil (diphenoxylate has abuse potential, so combined with atropine)
pepto bismol
imodium

139
Q

what are good antimicrobial agents for diarrhea

A

fluoroquinolones (____floxacin)

azithromycin

parasites = flagyl

140
Q

what drugs have very low systemic absorption

A

IBS drugs

141
Q

which IBS drug is a sodium/hydrogen transport exchange inhibitor

A

IBS-Rella (ibsrella)

NHE3 inhibitor

142
Q
  • Used to “reset” microflora
    o Activity against anaerobic and gram-negative bacteria, including c-diff
A

rifaximin

143
Q

what 2 drugs for IBS have RESTRICTED use*

A

lotrenex (black box ischemic colitis)

zelnorm

144
Q

disease

ANY portion of the GI tract

intermittent-transmural lesions

A

Crohn’s

145
Q

disease

COLON/distal intestine

continuous-superficial lesions

A

ulcerative colitis

146
Q

modified aspirin, cleaved into 2 parts
(sulfa + 5ASA)

___________zine

DEPENDENT ON ACTIVATION OFTEN

A

salicylates

147
Q

_____ cells stimulate parietal (proton pump) cells

A

ECL cells

148
Q

what are 4 ways to limit acid production

A

vagus nerve (Ach)

histamine

gastrin/CCK

blocking proton pump/parietal

149
Q

pH of parietal cell =
pH of lumen =

A

pH of parietal cell = 7
pH of lumen = 2

150
Q

why do PPIs have long lasting effects

A

irreversibly bind

MUST be systemically absorbed to work (enteric coating)

151
Q

PPIs interact with CYP2C19, resulting in Plavix dose being __________***

A

reduced! risk of clotting/restenosis

152
Q

which H2 is off the market for neuro issues

A

Zantac

Tagamat has sex issues

153
Q

these drugs are good for aspiration prophylaxis

A

H2 antagonists

154
Q

what is a drug-drug interaction with sucralfate (coating agent)

A

quinolone abx (ciprofloxacin)

155
Q

pepto bismol can cause _____________ of the stool

A

darkening (benign)

156
Q

what is a PGE-1 analog that is category x for pregnancy and helps prevent NSAID gastric ulcers*

A

misoprostol

157
Q

what is the standard therapy for peptic ulcer disease*

A

clarithromycin
amoxicillin

if allergy: flagyl

158
Q

PGP INHIBITOR! for pamora (movantik) opioid drugs would cause what

A

decrease in analgesia
or
a central effect

159
Q

which drug exerts its pharmacological effects by directly inhibiting leukocyte extravascular migration

A

natalizumab

160
Q

which drug exerts its pharmacological effect by directly promoting ion movement from the gastrointestinal epithelial cell into the lumen of the GI tract

A

lubiprostone

161
Q

what drug is good for the proximal small intestine

A

mesalamine (5ASA)

162
Q

what are the 2 M phase drugs**

A

vinca
taxanes

both involved in microtubules
neurotoxicity, NMB issues

163
Q

true or false

doxorubicin is cell cycle NON specific

A

true

164
Q

cell cycle NON specific are ______ dependent

A

dose

165
Q

cell cycle specific are ______ dependent

A

schedule/time

166
Q

chemo drugs

 Vesicants
emetogenic

given on intermittent schedule (monitor for neutropenia)

A

alkylating agents

167
Q

what chemo drugs have a highly toxic compound (acrolein) what drug should be given + what should be done**

A

mesna
+
hydration

nitrogen mustards (cyclophosphamide)

168
Q

what are 3 effects of cisplatin **

A

electrolyte disturbances (HYPOmagnesemia)

NMB issues

emetogenesis

169
Q

anthracycline CHEMO drugs

___________rubicin

what is the broadest activity + HIGHEST CARDIOTOXICITY risks?

A

DOXOrubicin (treatment=iron chelating agent= dexrazoxane)

very high doses
CHF NOT responsive to digoxin

170
Q

MOAs of CHEMO drug class

1) DNA intercalator
* Sit in the middle of DNA/penetrating DNA, cause disruption

2) Inhibit Topoisomerase II
* Helps unwind DNA strands; inhibiting DNA synthesis

3) Generate Reactive Oxygen Species (ROS)
* Can cause significant tissue damage; cardiac toxicity

A

Anthracyclines

171
Q

what are 2 adverse effects of anthracyclines

A

cardiotoxicity

radiation recall reaction

172
Q

MOA chemo drugs*

 Interferes with the synthesis of normal DNA/RNA bases and/or the incorporation of these bases into DNA/RNA

A

anti-metabolites

173
Q

MOA chemo drugs*

Inhibits the enzyme DHFR (which is normally used for one-carbon-transfer reactions)

Inhibits dTMP synthesis  cannot make thiamine  inhibition of DNA synthesis

A

methotrexate (MTX)

174
Q

what is the rescuer for MTX chemo drug

A

leucovorin

175
Q

what are the adverse effects of anti-metabolites (MTX)

A

GI tract issues
thrombocytopenia

176
Q

“central” regimen chemo drugs

A

taxanes

______taxel

177
Q

hypersensitivity reactions with taxanes can be reduced with what*

____________ P450 metabolism

A

liposomal formulation

“saturable” = strict dosing regimen

178
Q

which chemo drug has a risk of pulm toxicity with HIGH O2 flows and cutaneous toxicity*

A

bleomycin

the enyzme bleomycin hydrolase is NOT found in these locations

179
Q

MOA chemo drug
 Molecule has a DNA-binding region + iron-binding domain at opposite ends
 By forming a complex with iron, the drug “shunts” the passage of electrons to molecular oxygen
 Results in the formation of ROS aka FREE RADICALS

A

bleomycin

180
Q

Which of the following CHEMO drugs is associated with alterations in serum electrolytes, which may require dosage changes of neuromuscular blocking agents?

A

cisplatin (hypomagnesium)

181
Q

Renal toxicity due to which of the following drugs can usually be circumvented or diminished by MESNA administration?

A

cyclophosphamide

182
Q

MOA
o Inhibit COX-1 and COX-2, which inhibits prostaglandins

o Different Types of Prostaglandins:

PGI2: normally causes vasodilation + inhibits clotting
* This is the good guy!

TXA: normally causes vasoconstriction + promotes clotting
* This is the target!

A

NSAIDs

183
Q

steroids inhibit __________________

A

phospholipase

184
Q

which COX is

constitutively expressed/stays constant

organ issues

A

1

185
Q

which COX is

inducible (10-18x)

more involved in PAIN

A

2

186
Q

what are the 2 black box warnings of NSAIDs
(NON-aspirin!)

A

CV risks

GI risks

187
Q

what are the 3 different combos for patients with GI risks for NSAIDs

A

Celebrex!!

NSAID + PG analog (misoprostol)

NSAID + PPI

188
Q

NSAIDs ___________ sodium water retention

A

increase

189
Q

what can lead to incrased risk of BLEEDING with NSAIDs

A

SSRIs
SNRIs
glucocorticoids
anticoags, platelet inhibitors

190
Q

what 2 drugs can lead to increased risk of renal toxicity with NSAIDs*

A

ACE inhibitors (_______pril)
ARBs (_______sartans)

191
Q

baby aspirin inhibits COX __

full dose aspirin inhibits COX __ + __

A

COX 1 only =baby dose

COX 1+ 2= full dose, other NSAIDs

192
Q

who is at high risk of pseudo-allergy with NSAIDs (NOT celebrex)

A

asthma
nasal polyps

193
Q

what is a treatment for salicylism

A

sodium bicarb
activated charcoal
glucose, K

194
Q

should you take aspirin or other NSAID first

A

take aspirin first

space out the drugs

195
Q

which NSAID shouldnt be used for chronic therapy or intraop due to bleeding risk

A

ketorolac

196
Q

which NSAID has sulfa risk

A

celebrex (lasix is worse)

197
Q

can tylonel cause renal damage

A

yes

198
Q

MOA

o 1) DECREASE calcium (channel INHIBITION) influx =  excitatory NT release
o 2) INCREASE potassium (channel ACTIVATION) efflux = hyperpolarizing neuron

A

opioids

199
Q

what are the 4 serotonergic drugs for opioids**

can cause serotonin syndrome!!!

A

meperidine
methadone
fentanyl
tramadol

200
Q

which opioid blocks NMDA and monoamines

A

methadone

201
Q

Highest risk of unintentional OD death from resp depression

A

methadone

202
Q

Which opioid blocks 5HT + NE

A

tramadol

203
Q

What 2 opioids are activated by 2D6**

A

tramadol
codeine

INHIBITOR of 2D6= no helpful analgesia, but you would still have serotonin effects!

204
Q

what 2 drugs are good for opioid use disorder

A

buprenex
methadone

205
Q

tylonel

Normally, the toxic metabolite is immediately taken care of by GLUTHATHIONE; with large doses, this enzyme is depleted

A

N-acetylcysteine

206
Q

___ cells recognize particular epitopes

A

B cells

207
Q

“________ ________” occurs to check for self-recognition  B-cell is eliminated

this is where autoimmune diseases start

A

Check Process

208
Q

“_________ ______________”: critical step in activation*
 When the B cell encounters the antigen, it requires coactivation by a helper T-cell

A

Linked Recognition

209
Q

PRIMARY immune response 1st Ig___**
2nd Ig___

A

1st: IgM
2nd: IgG

210
Q

SECONDARY immune response

A

IgG!!!

211
Q

Each antibody can bind to ___ identical antigens

A

2

212
Q

what are the 5 main antibody classes based on

A

structure of the CONSTANT/Fc domain

213
Q

antibody:

bound to surface of B cells, main first type

A

IgD

214
Q

antibody:

gland secretions

A

IgA

215
Q

antibody:

basophils/mast cells

A

IgE

216
Q

antibody:

first to be secrete in response to antigen

A

IgM

(immune complexes)

217
Q

antibody:

largest/most diverse class

A

IgG

218
Q

___ cells bind to MHC I or II

A

T cells

219
Q

cytotoxic or memory T cell

A

CD8

220
Q

helpter T cell

A

CD4

221
Q

CD8/cytotoxic/memory T cells binds to what

A

infected, NON immune cells

MHC I

222
Q

CD4/helper T cells binds to what

A

antigen-presenting cells
immune cells

MHC II

223
Q

What stimulates the shift from IgD  IgG, IgM, IgE, etc

A

T helper cells (CD4) secreting cytokines

224
Q

hypersensitivity reactions*

IgE mediated
mast cells
omalizumab
drug-induced

A

Type I

225
Q

hypersensitivity reactions*

IgG

CD8/cytotoxic

complement activation

ADCC (antibody dependent cell-mediated cytotoxicity)

A

Type II

226
Q

hypersensitivity reactions*

IgM
immune complex

complement activation

neutrophils

A

Type III

227
Q

hypersensitivity reactions*

cell mediated (no antibody)

T helper cells, activated macrophages

A

Type IV

228
Q

hypersensitivity reactions*

blood transfusion reactions

A

II

229
Q

hypersensitivity reactions*

rheumatoid arthritis
lupus

A

III

230
Q

hypersensitivity reactions*

poison ivy
sulfa drugs (bactrim)
contact derm

A

IV

231
Q

what are the 3 common drugs that cause drug-hypersensitivity

A

penicillin
cephalosporins
local anesthetics

232
Q

specificity of antibodies is due to the presence of

A

hypervariable regions

233
Q

what type of T cell is involved in linked recognition

A

CD4 helper

234
Q

what is released from mast cells

A

cytokines, leukotrienes, histamine, heparin

235
Q

pH of 7.5 = what form?
pH of 8.5 = what form?

A

the LOWER the pH, the MORE ionized

Pharm 2 (3 decks)

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