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MSII Unit 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Pharmcodynmaics

A

Giving people drugs and looking for responses

focus on effect

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2
Q

Therapeutics

A

The dosage and the frequency that you give the drug to the patient
therapeutic effect—>normal dosing of a drug—>desired effect

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3
Q

Toxicology

A

Toxicity of drugs and environmental substances

Toxic effect—>patient takes toxic amount of dosage

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4
Q

Drug action

A

Molecular action—>invisible
can produce different effect when exposing to different tissues (ex. caffeine)
2 different actions can produce similar effect on certain tissue

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5
Q

Drug effect

A

pharmacologic effect—>visible response

a summation of all molecular actions

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6
Q

Secondary effect of drugs

A

usually side effect—>sometimes it is desired like caffeine for asthma patients (increase respiration)

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7
Q

1 mole equal to

A

6.022 x 10^23 molecules

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8
Q

Drug receptors

A

macromolecules that are usually interact with endogenous compounds
many drug receptor interactions (augment/inhibit) —>change in function of the cell—>pharmacologic response

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9
Q

Emax

A

max effective dose to illicit max effect from a tissue

can be picked during the development of the drug to avoid secondary effect

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10
Q

Reversible drug-receptor bond

A

ionic/van der waals/hydrogen

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11
Q

Irreversible drug-receptor bond

A

covalent

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12
Q

G protein couple function

A

Drug and receptor interaction is short
G protein amplifies drug-receptor interaction into a longer effecting time
The function of G protein (cleavage into alpha and beta/gamma subunits) depends on ATP level of the cell

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13
Q

The making of drugs

A

Find the endogenous compound—>make a drug that is similar to it—>the more similar the better
Stereoisomer—>one would fit and the other would block or do nothing

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14
Q

Dose response relationship

A

The amount of drug to take to reach certain state (like how much alcohol to drink to get tipsy)

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15
Q

EC50

check page 12 for log dose response curve

A

the amount of drug that induce a response halfway between the baseline and Emax or the amount of drug needed to induce a response for 50% of the population

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16
Q

Spare receptors

refer to page 13 for the graph

A

For certain agonist—>you dont have to occupy all the receptor to illicit the maximal response
sometime drugs has to occupy all spare receptors to achieve Emax (low intrinsic activity)

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17
Q

Intrinsic activity

A

ability to stimulate the receptor once bound

drugs with best intrinsic activity—>bring it to Emax

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18
Q

Secondary receptor

A

outside target tissues—>may cause side effects

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19
Q

What could happen if you keep giving a patient an agonist?

A

Receptors got overstimulated by drugs over time—>homeostasis—>desensitize the receptors (by decrease the number of it/decrease sensitivity)
Give the cell a break—>get full response again

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20
Q

What could happen if you abruptly stop an antagonist drug?

A

Hypersensitivity through homeostasis trying to compensate for the low level of activity of certain tissues

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21
Q

Antagonist

A

Bind to receptor but does not produce effect—>block agonist from binding it

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22
Q

Would the good agonist have more or less molecules (high or low doses) present at the cell?

A

Less (and low dose), since it doesnt take much for it to reach Emax, but it will take the not so good agonist more molecules to achieve it

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23
Q

What happen if the weak agonist has the same intrinsic activity as the strong one?

A

You need higher dose for the weak one to achieve Emax

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24
Q

What are the two ways to quantify agonist?

refer to page 19 for the graph

A

Efficacy—>intrinsic activity (verrical relation on the log dose curve)
Potency—>the amount of drug that is needed to reach Emax (horizontal relation on the curve)

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25
Q

What is competitive antagonist?

A

Molecule that binds to the site where the agonist binds to but has a different structure as the agonist thus produces no effect

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26
Q

How can you overcome competitive antagonist?

A

Increase the dose of agonist

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27
Q

What are the 2 mechanism of noncompetitive antagonist?

A
  1. Change the effector—>agonist still binds but no effect

2. Change the effector site—>agonist cannot bind

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28
Q

What kind of drugs can do passive simple diffusion?

A

Lipid soluble/small/no charge down to its concentration gradient

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29
Q

What does a facilitated diffusion require?

A

Carrier protein

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30
Q

What drives filtration through membrane?

A

Hydrostatic pressure/drug must be small

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31
Q

What is the similarity between active transport and micropinocytosis?

A

They all require ATP

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32
Q

Can protein bound drug cross the capillary membrane?

refer to page 27

A

No

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33
Q

Does the stomach favor the absorption of weak acid/base drugs?

A

Weak acid drug (refer to page29)

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34
Q

How do we administer weak base drugs?

A

IV or IM

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35
Q

What is the enteral route of drug administration?

A

Through the GI tract—>rectal/oral (use suspension of chewy if can’t swallow)—>treat chronic condition/sublingal

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36
Q

What influences the route of drug administration?

A

Setting/rapidity/target organ

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37
Q

What is first pass metabolism?

page 31

A

The drug is going through the liver first and then get metabolized. Less amount of drug enters the circulation system after.

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38
Q

When to use rectal route?

A

When oral is not an option (coma pt/old pt)/children with seizure

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39
Q

When to use sublingual route?

A

Area under the tongue has thin mucosal membrane and high blood flow/use for cardiac med and vomiting/must absorb quickly

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40
Q

Characteristics of IV route?

A

Bypass liver/treat acute condition/rapid side effect/danger of administering too rapid

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41
Q

When do you use intraarterial?

A

For IV contrast/dye/thrombolytic drugs

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42
Q

When do you use intramuscular?

A

Slower absorption/2nd most common route after IV/contraceptive medication (hormone therapy)/antipyschotic

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43
Q

When do you use subcutaneous?

A

Inject into the fat underneath the skin/insulin is most common

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44
Q

When do you use intrathecal?

A

Injection into the spinal fluid/for cancer chemo therapy/anesthesia/when you need to cross the blood brain barrier

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45
Q

Can you use topical route for both local and systemic effect?

A

Yes

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46
Q

Characteristics of inhalation route?

A

Rapid absorption for systemic effect (nicotine)/local effect on lungs (albuterol)

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47
Q

Bioavailibilities of drugs

A

Not all drugs will be absorbed. Some will get metabolized via first pass metabolism. AUC of oral/AUC of IV = fraction of dose available for action

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48
Q

How to predict plasma concentration?

A

(Fraction absorbed x dose) = Cp (plasma con.) x Vd (volume needed to achieve the desired blood con. of a drug)
Dissolution is often the limiting step (drug might be packed too tight)
Vd = Dose/Cp

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49
Q

What do we need to be aware of for generic drugs?

A

AUC might be lower for generic drugs, meaning its bioavailability will be lower, meaning more dose is needed compare to name brand.

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50
Q

What factors affect the absorption of enteral route?

A

Food might interfere with the absorption of the drug (sometimes use food to protect the lining of the stomach from the drug)/blood flow in the GI is essential

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51
Q

What factors affect the absorption of parental route?

A

Blood flow is the key/use heat or cold to manipulate the blood flow/also muscle movement if it’s IM/can put drugs in different form to manipulate the release of the drugs

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52
Q

How to predict Vd?

A 
Vd = dose/Cp
Vd = liters/kg (weight for patient/body surface area is safer to use to dose)
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53
Q

What is the 2 compartment model?

page 47

A

The volume of drugs are in equilibrium between plasma and total Vd
Drug elimination occur in plasma (2nd half life), the initial half life occur during distribution to Vd (1st half life)

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54
Q

What is the concept of redistribution?

A

Drug will go to high blood flow organs first (brain/lungs/kidneys/heart) and the redistribute other organ. So if the target organ is the high blood flow organs then the drug will wear out pretty quickly

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55
Q

What are the bad affect for fetus caused by drugs?

A 
Teratogenic effects (abnormal tissues differentiation)/toxic effect (chronic or acute condition e.g. low birth weight/addiction/respiratory depression) 
Use A/B safety rating drugs
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56
Q

What kind of drugs can enter blood brain barrier?

A

BBB prevent drugs from freely entering the brain (tight junction)
Drugs need to be lipid soluble and be transported by a carrier mechanism
Might need higher dose for drugs that need to cross BBB
Might need to use lipid soluble precursors (since the drug itself is charged and can’t pass)

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57
Q

How to treat over dose with weak electrolyte drugs?

A

Weak acid drugs—>give bicarbonate to alkylate the plasma

Weak base drugs—>decrease plasma pH with HCl

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58
Q

What are the characteristics of protein binding drugs?

A

Most hydrophilic drugs bind to albumin and hydrophobic ones bind to alpa and beta proteins
Protein binding can change apparent Vd (smaller if tissue bind/bigger if plasma protein bind)

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59
Q

What is the unexpected toxicity related to protein binding drugs?

A

Drug 1 binds to protein in plasma, and then drug 2 comes in who has a higher affinity for protein binding then displace drug 1, drug 1 then go on having effects

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60
Q

What is loading dose?

A

Only free drug can exert effect so certain amount of drugs are needed to tie up all plasma binding site first

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61
Q

What is biotransformation of drugs?

A

Clearing drugs from the plasma mainly via liver

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62
Q

What are the steps of biotransformation?

A

Change the structure of the drugs first (unable it to work as before)
And then reverse the characteristics that made the drug easy to absorb—>make it bigger/water soluble/charged

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63
Q

Where in liver does the biotransformation take place?

A

Smooth endoplasmic reticulum (has lipid bilayer to attract lipid soluble drugs)/cytoplasm/mitochondria

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64
Q

What are the two phases of biotransformation?

A

Phase I—>oxidate/reduce/hydrolyze to convert the drug to primary product (some of them are water soluble enough to excrete)
Phase II—>further process the primary products that are not ready to excrete (conjugation)
The whole process make the drug from lipophilic to hydrophilic

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65
Q

What is the hepatic microsmal drug metabolizing system?

A

Referring to phase I and II in SER in the liver:
Induction—>drugs can induce their own (or other drug) metabolism (increase first pass metabolism)
Inhibition—>the enzymes in the SER can be inhibited by drugs or by the interaction of 2 drugs—>one drug will not be metabolized—>toxicity
Induction is possible here because there’s feedback between the enzyme system and the sites where the enzymes are produced—>so more enzymes can be called to metabolized the increase dose of certain drug (no induction in non microsomal system)

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66
Q

How does competitive antagonist shift the log dose curve?

A

Horizontally

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67
Q

How does the non competitive antagonist shift the log dose curve?

A

Vertically. It lowers the Emax

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68
Q

How to calculate the amount of drug excreted by kidneys?

A

Amount excreted = amount filtered at kidneys - amount reabsorbed
Amount excreted = (glomerular filtration + active tubular secretion) - (pass and active reabsorption)

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69
Q

Can protein bound drugs be filtered?

A

No only free drugs

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70
Q

What does the amount filtered depends on?

A

Glomerular blood flow and free drug con.

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71
Q

What is active tubular secretion?

A

enzyme transport compound into the nephron against its con. gradient.
Can be competitively inhibited (used to maintain drug dosage over time)
Can be saturated (1st order and zero order)

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72
Q

What is passive reabsorption?

A

Con. of drugs in nephron is higher than that of plasma—>drug diffuse back to the plasma from the nephron

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73
Q

Can lipid soluble drugs diffuse back from the proximal tubule to plasma? Can water soluble drugs do?

A

Lipid soluble drugs can diffuse back (tubular reabsorption) but not water soluble ones

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74
Q

How does pH trapping works?

A

Give bicarb to alkalize the blood—>prompt the drugs to stay in ionized form—>bicarb is dumped to urine to maintain pH—>urine pH goes up—>prompt the drugs to stay in ionized form so they can’t diffuse back to plasma

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75
Q

How does the drug enter bile for excretion?

A

Secretion (water soluble drugs)/pass diffusion (small molecules and lipid soluble drugs)

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76
Q

What is enterohepatic cycling?

A

Drugs goes from liver to small intestine and back, so it doesn’t get excreted. Can use activated charcoal to bind lipid soluble drugs in guts to prevent cycling

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77
Q

What is the definition of clearance?

A

Clearance total = clearance metabolic (biotransformation) + clearance renal (renal excretion)

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78
Q

What are the biphasic of elimination?

A

Alpa distribution and beta elimination

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79
Q

What are Ka and Ke?

A

Ka—>absorption rate constant (we determine this)

Ke—>elimination rate constant (rate limiting step either biotransformation or renal excretion)

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80
Q

Tell me about zero order rate of absorption kinetics

A 
It tells us how much dose to give
It is a fixed amount absorbed per unit time
Ct=Ka x t
e.g. IV infusion/transcutaneous patch 
Ka is the slope and it is a constant
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81
Q

First order absorption kinetics?

A

It is a proportion per unit time, it is responsive to dosage. The more dosage, the more absorbed.
E.g. oral drugs

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82
Q

Zero order elimination kinetics?

A

Help us to now how often to give a drug.
It is a fixed amount eliminated per unit time (Vmax)
Insensitive to drug con.
Ct = Co (initial con.) - Ke x t
E.g. ethanol (saturate all enzymes responsible to eliminate it) phenytoin.

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83
Q

First order elimination kinetics?

A

It is a proportion eliminated per unit time (98% of drugs)
Use log graph to produce a straight line
Half life (t1/2) is only for 1st order kinetics
You can saturate a 1st order to change it into zero order
t1/2 = 0.693/Ke
t1/2 = 0.693Vd/Cl

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84
Q

What is steady state?

A

When rate of absorption equals to rate of elimination
The time requires to achieve SS con. is dependent on t1/2
Time to SS is independent of dosage
It takes 4 half life to achieve SS

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85
Q

What happens when the dose interval is much greater than t1/2?

A

It is single dose—>no SS is achieved cuz drug wears off

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86
Q

How to achieve SS with single doses?

A

repeated single dose. The dose interval is equal or within t1/2.

87
Q

Does the dose affect the time it takes to achieve SS?

A

No. same dose per unit given in a different ways yield the same Css average

88
Q

Cp at 1st t1/2 = ? during approaching the SS and what about during elimination?

A

50% of Css. 50% of drugs has been eliminated. It also takes about 4 t1/2 (93%) to eliminate all the drugs

89
Q

What happens if a drugs has fast elimination rate?

A

achieve SS faster

90
Q

What is loading dose regarding dosing?

A

It is used to achieve certain plasma con. of drugs to control an immediate problem. It does not shorten the time it takes to reach SS. Continuous dose (maintenance dose) is needed to reach SS

91
Q

Does neonate has higher or lower apparent Vd?

page 97

A

Higher, because neonates has higher percent of volume in body—>loading dose needs to be higher in neonate

92
Q

What carries out the phase I oxidation for drug metabolism?

page 59

A

Oxidation—>add O2 or change the proportion of O2 in the molecule
Mixed function oxidase system is responsible for oxidation—>system consists of p450 and p450 reductase (10 p450 surrounding 1 reductase)

93
Q

What are the characteristics of p450?

A

Low specificity (many drugs can bind). Do mainly oxidation, some reduction

94
Q

What is so special about CYP2D6?

A

Largest degree of identified genetic variation. Metabolize about 65 common drugs. Since many drugs can bind—>some drugs don’t get metabolized—>toxicity

95
Q

What is phase I reduction and hydrolysis of drug metabolism?

A

Reduction—>add H2 or change the proportion of H2

Hydrolysis—>cleave a molecule by adding a water

96
Q

How do we use the phase I reaction in our favor?

A

Pro drug can be turned into active component. E.g. T4 is given as pro drug, it is metabolized into T3 in the liver and becomes active

97
Q

What are first and zero order of metabolism kinetics?

A

v (velocity of metabolism) = (Vmax x D (drug con.))/(Km + D)
If Km is larger than D, then the enzyme system is efficient and it is first order
If D is larger than Km, then the enzyme system is saturated and it is zero order (e.g. alcohol)

98
Q

What can be mistaken as acute mastitis?

A

Inflammatory carcinoma of DCIS

99
Q

What kind of DCIS does carrier of BRCA1 pt has risk for?

A

Medullary

100
Q

Why does LCIS often detected accidentally?

A

LCIS produces no mass and no calcification.

It also lacks E-cadherin (so cells are not bound to each other)

101
Q

Why does invasive lobular carcinoma invade in a single file?

A

Cuz they are British. It’s actually because they lack E-cadherin

102
Q

What drug do you use to treat ER/PR + breast cancer?

A

Tamoxifen

103
Q

What do you use to treat HER2 + breast cancer?

A

Trastuzumab

104
Q

What population is more susceptible for triple negative breast cancer?

A

Black

105
Q

What does BRCA1 mutation associated with?

A

Breast and ovarian carcinoma

106
Q

What is associated with male breast cancer?

A

BRCA2 mutation and Klinefelter syndrome

usually invasive ductal carcinoma

107
Q

What kind of cells invade the synovial membrane in RA?

A

CD4+ cell

108
Q

How does pannus form in RA?

A

Activated macrophages secrete TNF-alpha and IL-1—>activate synovial fibroblast—>leads to release of metalloproteinases—>bone and cartilage degradation

109
Q

What is the mechanism of glucocorticoids for the treatment of RA?

A
  1. It inhibits phospholipase A2 which then inhibit the formation of prostaglandin
  2. It inhibits the production of numerous cytokine—>prevent the induction of COX-2
110
Q

What does antimalarial drugs inhibiting for the treatment of RA?

A

Reduce T cell activation and chemotaxis

111
Q

Which DMARD acts more quickly than the others?

A

Sulfasalazine (inhibit cytokine release)

112
Q

What does low dose of MXT does for RA?

A

Inhibit AICAR transformylase and cause adenosine accumulation (inhibitor of inflammation)

113
Q

What does leflunomide inhibit for RA?

A

DHODH—>reduce T and B cell population

114
Q

What does biologic response modifiers do for RA?

A

Inhibit cytokines like TNF-alpha and IL-1—>target either cytokine or the receptors

115
Q

What are the monoclonal antibodies anti-TNF-alpha drugs for RA?

A

Etanercept/Infliximab/Adalimumab (fully human antibody—>non-antigenic) /Golimumab/Certolizumab

116
Q

What are the IL-1/6 antagonist drug for RA?

A

Anakinra/Tocilizumab

117
Q

Which drug is anti-B cell for RA?

A

Rituximab (anti-CD20)

118
Q

Which drug is anti-T cell for RA?

A

Abatacept

119
Q

What is the current approach on treatment for RA?

A

Be more aggressive

120
Q

Most uric acid is secreted or reabsorbed?

A

Reabsorbed

121
Q

Which gout drug prevent tubulin polymerization that leads to inhibition of leukocyte migration?

A

Colchicine (like a cancer drug)

122
Q

What is the pathophsyiology of gout?

A

Synoviocyte eats urate crystals—>attract PMN and MNP—>inflammation

123
Q

Allopurinol inhibits which enzyme?

A

Competitively inhibits xanthine oxidase—>metabolize to alloxanthine which is a non-competitive inhibitor for XO

124
Q

Which drug inhibit urate reabsorption?

A

Probenecid

125
Q

What is the newer version of allopurinol?

A

Febuxostat (non-competitive inhibitor)

126
Q

Why do we need higher con of Tamoxifen than estrogen to treat breast cancer?

A

Cuz estrogen has a higher binding affinity to its receptor than that of Tamoxifen

127
Q

Which isomer of Clomiphene do we use to induce ovulation?

A

Trans isomer (cis isomer is a weak estrogen agonist)

128
Q

Why use progestin in HRT?

A

To counter the endometrial stimulatory effects of estrogen—>reduce risk of endometrial cancer

129
Q

What are the risks associated with progesterone?

A

Thrombosis and pul embolism/atrophic effect on endometrium (dont use for prego)

130
Q

When to use progestin only contraceptive?

A

When pt is contraindicated for estrogen/does produce irregular menstrual cycle

131
Q

What is tumor heterogeneity?

A

Clone cells from the original tumor cell change—>become more aggressive/metastatic—>hard to treat

132
Q

What is the progression of cell cycle?

A

G1—>S (DNA replication) —>G2—>M (cell division)

133
Q

What does kinase do?

A

Phosphorylate protein

134
Q

How does cyclin and Cdks control cell cycle?

A

They form a dimer—>cyclin determines which protein to phosphorylate—>different dimer formation function in different phases of cell cycle

135
Q

Which phase of the cell cycle does Rb control?

A

Cyclin/Cdk complex has to phosphorylate Rb to get E2F to pass from G1 to S phase

136
Q

Cell arrest in G1 or G2 involves?

A

DNA damage

137
Q

Absence G1/G2 arrest is associated with the mutation of?

A

p53

138
Q

What are the two major apoptotic pathways?

A

Death receptor dependent pathway (extrinsic, at cell surface)/mitochondrial pathway (intrinsic)

139
Q

What is the intrinsic resistance to anti cancer drug?

A

Inactivation of apoptotic promoting protein/gene or survival of anti-apoptotic protein/gene

140
Q

What is the acquired resistance to anti cancer drug?

A
  1. (during chemotherapy) Anticancer drug induce DNA damage—>cancer cells learn to repair DNA damage
  2. Amplification of gene that makes drugs ineffective
  3. Efflux pump (require energy) that eject drugs
  4. Protein that facilitate drug transport inside of the cell stop working
  5. Blocking drug activation
  6. Inactivate drugs
141
Q

What kind of cells are anticancer drugs toxic to?

A

Rapidly dividing cells like bone marrow and intestinal epithelium/hair/reproductive system

142
Q

What is used to shorten leukopenia period from cancer drugs?

A

G-CSF

143
Q

What are the targets for delayed toxicities from cancer drug?

A

Major organs

144
Q

Anticancer drugs follows ____ order kinetics?

A

First order

145
Q

What kind of tumor does cell cycle nonspecific drug kill?

A

Slow growth tumor (solid tumor) and high growth tumor

146
Q

What is the mechanism of alkylating agent?

A

(electrophiles) Transfer an alkyl group to DNA (N7 guanine)—>promote cross linking of DNA—>DNA damage

147
Q

What drug do we give Leucovorin with?

A

MXT and 5-FU

148
Q

What is the mechanism of Cytarabine?

A

Ara-C is converted to Ara-CMP—->Ara CTP—->premature DNA chain termination

149
Q

What is the first line treatment for pancreatic carcinoma?

A

Gemcitabine

150
Q

What drug interacts with allopurinol?

A

6-mercaptopurine—>degraded by XO—>allopurinol inhibits XO—>increase 6-MP—>toxicity
If use allopurinol—>reduce dose of 6-MP

151
Q

What are DNA intercalating agents derived from?

A

Microbe Streptomyces

152
Q

What does Dexraoxane do?

A

Iron chelating agent that blocks the formation of free radicals and protect against cardiotoxicity

153
Q

What phase of cell cycle does microtubule inhibitors (natural product) work?

A

M phase

154
Q

What kinds of resistance does Vinca alkaloid has?

A

Amp of P-glycoprotein (cell surface—>efflux)/mutation of tubulin—>drug can’t bind

155
Q

What does Topoisomerase do?

A

They relieve torsional strain caused by unwinding of DNA during replication. Topo I break and reseal ssDNA and Topo II dsDNA

156
Q

What is the mechanism of Topoisomerase inhibitor?

A

Inhibit resealing of the nicked strands of DNA

157
Q

What drug group is used to treat lymphoma and leukemia?

A

Glucocorticoids

158
Q

What does androgen ablation therapy consist of?

A

GnRH analogs and AR blockers

159
Q

Which drug inhibit drug transporter (out of the cell)?

A

Verapamil

160
Q

Decreased expression of HGPRT is associated with the resistance of which drug?

A

6-MP—>since it needs HGPRT to convert to active form (TIMP)

161
Q

Most non-receptor kinases are?

A

Serine/threonine kinase

162
Q

Chronic myeloid leukemia (CML) is characterized by which chromosome?

A

Philadelphia chromosome (Ph) that involves a 9:22 translocation

163
Q

What is the consequence of 9;22 translocation in CML?

A

Bcr-Abl fusion—>Abl is constitutively active—>usually only activated when required

164
Q

Bcr-Abl protein needs ___ to phosphorylate other proteins?

A

ATP

165
Q

What is hematologic/cytogenetic/molecular responses regarding CML treatment?

A

Normalization of blood count (no immature cells)/low or no Ph level/no or low Bcr-Abl mRNA

166
Q

Nilotinib and Dasatinib are ineffective against?

A

T315I mutation

167
Q

Which drug is effective against T315I mutation?

A

Ponatinib

168
Q

BRAF gene encodes what kind of kinase?

A

Serine/threonine kinase

169
Q

What is the only drug that is approved to treat malignant melanoma?

A

Dacarbazine

170
Q

Is there ligand binding for ErbB2?

A

Nein

171
Q

What are the ligands for ErbB1?

A

TGF-alpha and EGF

172
Q

Which p450 metabolize Erlotinib?

A

CYP3A4

173
Q

What kind of drugs will inhibit the absorption of Erlotinib?

A

Proton pump inhibitors

174
Q

What kind of antibody is Trastuzumab?

A

Humanized

175
Q

Why give Taxanes in addition to Trastuzumab?

A

Trastuzumab inhibits proliferation and Taxanes induce cell death

176
Q

What is Ado-trastuzumab conjugate to?

A

Microtubule inhibitor DM1 (antibody-drug conjugate)

177
Q

What cells are antibody dependent cellular toxicity attracts on top of the antibody (e.g. Rituximab)

A

Monocyte/macrophages

178
Q

What does P450 do?

A

Oxidation (lose an e- and increase in oxidation state) and reduction (gain an e- and decrease in oxidation state)—>phase I

179
Q

What is the goal for P450 metabolism?

A

Make the drug more water soluble

180
Q

Where are the majority of the P450?

A

Bound to lipid membranes of SER in liver

181
Q

Codeine (prodrug) is converted to active drug in liver to?

A

Morphine via CYP2D6

182
Q

What does induction in drug metabolism mean?

A

Speed up CYP—>up prodrug activity or elimination

183
Q

What does inhibition in drug metabolism mean?

A

Inhibit CYP—>up bioavailability of the drug (decrease elimnation) or decrease activity of the drug

184
Q

What does polymorphism in drug metabolism mean?

A

CYP can be really slow or fast or not working at all

185
Q

What is Phenytoin?

A

Anticonvulsion/seizure drug

186
Q

Which CYP metabolize Warfarin and Phenytoin?

A

CYP2C9

187
Q

Explain the example of inducer-smoking and substrate theophyllin

A

If a pt smokes—->his CYP1A2 metabolize theophyllin faster—>he needs more theophyllin

188
Q

What is an inducer of CYP2C9?

A

St John’s wort (treat depression)

189
Q

What do you use Verapamil to treat?

A

High BP and HR

190
Q

What is an inducer for CYP2D6?

A

Rifampin (TB)

191
Q

What is the polymorphism of CYP2C9/2C19?

A

Poor metabolizer

192
Q

What is the polymorphism of CYP2D6?

A

Poor and rapid metabolizer

193
Q

What is the percentage for Black/Asian for 2C19 polymorphism?

A

20/15-20%

194
Q

What is the percentage for White for 2D6 poor metabolizer polymorphism?

A

5-10%

195
Q

What is the percentage for Ethiopian/Souther European for 2D6 ultra fast metabolizer polymorphism?

A

30/10%

196
Q

What is pharmacogenetics?

A

Study of genes and their alleles in relation to drug response in a given pt

197
Q

What is pharmacogenomics?

A

Us the knowledge from pharmacogenetics to develop new drugs

198
Q

Clinical trials look for?

A

+ response for majority of ppl and few ADR

199
Q

How many CYP variants metabolize 90% of the common drugs?

A

6

200
Q

Can some CYP metabolize the same drugs?

A

Yes

201
Q

CYP2D6 genotype refere to page 226

A

Poor/intermediate/extensive (normal)/ultra

202
Q

Clopidogrel CYP2C19 alleles

A

1 (normal) /2 and 3 (poor metabolizer)/17 (ultra)

203
Q

What does G6PD do?

A

Antioxidant

204
Q

What should be avoided from pt with G6PD deficiency?

A

Fava bean and oxidant drug

205
Q

What is malignant hyperthermia (RYR1 mutation)?

A
  • response to inhalation anesthetics—>uncontrolled Ca release—>fever/muscle contraction/metabolic acidosis
206
Q

What kind of food is high in Vitamin K?

A

Leafy green like broccoli and kale

207
Q

What are the genes responsible for Warfarin variation?

A

CYP2C9 and VKORC1

208
Q

What is the mechanism of Leflunomide?

A

Inhibit DHODH/anti T cell and B cell autoantibody production

209
Q

What is the prodrug for Mecaptopurine?

A

Azathioprine

210
Q

If a pt smokes, has heart problem, HTN, hepatic disease. endometrial/breast cancer, pregnant, which kind of contraceptive you shouldnt give?

A

Estrogen

211
Q

Micronized form of progesterone is compounded with?

A

Peanut oil

212
Q

What is mini-pill best used for?

A

Lactating women and pt with venous thrombosis

213
Q

What is the translocation in APL?

A

15;17

MSII Unit 1 (7 decks)

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