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PCL201 Finals review > PCL201TT1 > Flashcards

PCL201TT1 Flashcards

1
Q

What routes of administration are included within Enteral?

A
  1. Oral 2. Rectal 3. Sublingual (Beneath the tongue)
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2
Q

What is the definition of bioavailability

A
  1. Proportion of administered drugs that is absorbed from site of administration and reaches systemic circulation UNCHANGED
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3
Q

What factors determines absorption in Oral administration?

A
  1. pKa of drug and pH of GI
  2. Solubility
  3. Gastric emptying rate
  4. Intestinal motility
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4
Q

Why are drugs taken with foods, good and bad

A
  1. Food can protect stomach from irritant drugs
  2. Some drugs form complexes with food
  3. Bioavailiability is increased with food due to delayed gastric emptying
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5
Q

What is the 2 formulations for oral drugs

A
  1. Enteric coating release in the small intestine, (not in stomach)
  2. Extended/Controlled release
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6
Q

What are the benefits of controlled release?

A

Decrease frequency of dosing, therefore increasing compliance

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7
Q

Advantages of oral admin.

A
  1. Really cheap
  2. Very convenient
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8
Q

What are the major disadvantages for oral admin

A
  1. First-pass effect
  2. Subject to degredation in stomach
  3. Irritant to stomach mucosa
  4. Slow onset of actions, and some patients may be unconcious/can’t take orally
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9
Q

Advantages and disadvantages of rectal admin

A

ADVANTAGES: No first pass, larger dose is good, can be administered if vomiting/unconscious
DISADVANTAGES: Poor compliance, absorption is not regular, irritant to mucosa

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10
Q

Sublingual admin advantages and disadvantages

A

ADVANTAGES: No first pass, very rapid onset
DISADVANTAGES: Very few drugs can penetrate the oral mucosa, which may not be convenient for large doses

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11
Q

IV advantages and disadvantages

A

AD: Controlled concentrations in blood, and accurate dosing is possible. large dosing is okay
DIS: Toxicity is easy; need to disinfect area readily, more expensive

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12
Q

2 types of IV injection

A

Slow infusion - Slow IV injection like IV drip
Bolus injection - For emergencies for fast onset, drug is pumped into the blood at a very fast rate

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13
Q

What are the 3 L’s for transdermal patch

A

Lipophilic, low dose, low molecular weight

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14
Q

How small does a drug have to be for passive diffusion?

A

Below 150~200 Da

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15
Q

What is partition coefficient

A

It is the Pow of the drug
The higher Pow, the more lipophilic, so more absorbed

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16
Q

What’s a feature of facilitated diffusion at a very high conc

A

At a very high solute concentration it is likely to max out the speed, due to saturation of protein

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17
Q

What individuals have more water?

A

Leaner males that are younger

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18
Q

Volume of distribution formula

A

Vd = Dose/Initial concentration

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19
Q

How does larger Vd affect half life of drug?

A

Larger Vd -> less elimination (less in plasma to eliminate) -> increase half-life

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20
Q

Where is potency on the drug response curve

A

EC50, half way to Emax

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21
Q

Therapeutic index

A

TD50/ED50

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22
Q

Affect on D-R curve for partial agonist

A

Less efficacy as drug will never produce max response

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23
Q

Which type of transport is SLC transporters involved in?

A

Facilitated and secondary active transport

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24
Q

How can multi drug resistance form?

A

Existence of wide variety of efflux transporters that can bind to variety of drugs

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25
Structure of p-gp transporter
12 TM domains and 2 ATP binding domains
26
Major family of enzymes that contribute to phase I biotransformation
1. Monooxygenase 2. Oxidases and dehydrogenases 3. Reductase 4. Hydrolases
27
What is one key thing for phase I reactions
Almost all of them insert a single oxygen molecule
28
Steps for P450 oxygen cycle
1. P450 with ferric (3+) binds to drug 2. Electron from reductase reduces iron to ferrous (2+) *Only ferrous can bind to oxygen 3. Ferrous binds to oxygen 4. 2nd electron from reductase is added on to O2 5. Causes activation of oxygen 6. Oxygen is split, 1 goes into water 7. Hydrogen is pulled from RH (drug) to form OH group, producing carbocation (radical) 8. OH group on iron transferred onto drug 9. Ferric is regenerated
29
Where is POR located (NADPH p450 reductase) and which domain links it
Cytosolic side, N domain links it
30
Which is the most abundant P450 enzyme in liver and small intestine and which % of drugs does it metabolise
CYP3A4, 50% of all drugs
31
CYP1A2 And 1A1 location and what is it induced by
CYP1A2 is located in liver, induced by PAH's CYP1A1 is located ouside
32
What drug and its reaction reaction does CYP2C9 do?
Hydroxylation of tolbutamide Phenytoin Warfarin
33
Which P450 is highly polymorphic in humans
CYP2D6
34
Where is CYP2C19?
Mainly in the liver
35
Where is CYP2C9 located in
Main 2C enzyme in the liver
36
Function of CYP2E1
Ethanol metabolism and small toxicants
37
Where is CYP2E1
Liver, Kidney and some other tissues
38
How is quinone/doxorubicin metabolised? which phase and type of reaction is it, How can it cause toxicity?
Quinone → Hydroquinone via NADH/NADPH reductase But if Quinone converted to Semiquinone via POR, it has chance to turn into OH radical
39
How is expoxide metabolised?
Epoxide → Dihydrodiol via Epoxide Hydrolase
40
All phase 2 reactions
1. Glucuronidation 2. Glutathione conjugation 3. Sulfation 4. Acetylation 5. Methylation
41
What is the glucuronidation enzyme and its cofactor and its possible substrate
Enzyme: UGT Substrates: Hydroxyl, carboxyl, amine, thiol Cofactor: UDPGA (Uridine diphosphate glucuronic acid)
42
What effects does genetic deficiency in glucuronidation affect the body?
Gilbert's syndrome, usually survivable, may cause jaundince Crigler-Najjar syndrome, very severe, causes jaundice
43
Glutathione Conjugation Enzymes, Substrates, and Cofactors
Enzymes: GST (Glutathione-s-Transferase) Substrates: Epoxides, Nitro groups and hydroxylamines (Highly electrophilic groups) Cofactor: GSH (remember SH - thiol group)
44
Sulfation enzymes, substrates, and cofactors
Enzyme: SULT Substrates: Phenols, aliphatic alcohols Cofactor: PAPS (SO3-)
45
How can metabolism of acetaminophen cause liver cell death?
1. If glucuronidation or sulfation pathways are saturated too much (too much drug) 2.If converted by CYP2E1 or CYP3A4, then it forms NAPQI 3. NAPQI is a radical and it can bind to proteins, causing cell death
46
Acetylation enzymes, substrates, cofactors
Enzyme: NAT (N-acetyltransferase) Substrates: Aromatic amines, hydrazines Cofactor: Acetyl CoA
47
Methylation enzymes, substrates, cofactors
Enzyme: MT (Methyltransferase) Substrates: Phenol, catechol. aliphatic and aromatic amine, N-heterocyclic, thiol Cofactors: SAM
48
Explain induction
Induction is when certain compounds boost the transcription of P450 enzymes This causes rapid degredation of drug molecules, causing less therapeutic effects (in most cases)
49
How does the aryl hydrocarbon receptor work (AHR)
1. Inducer binds to AHR, along with a bunch of other proteins forming a complex 2. This complex moves into the nucleus, boosting transcription of P450 enzymes 3. This increases biotransformation
50
Which enzymes/reactions/P450 does AHR effect
Phase I: CYP1A1, 1A2, 1B1, 2S1 Phase II: GST, UGT
51
How does St.John's wort effect biotransformation
CYP3A4 is induced, increasing its transcription rate and therefore decreasing drugs that are metabolised by it
52
how can induction be a potential benefit, what p450
Cabbage induces CYP1A2, reducing the levels of 17B-estradiol (Bad estrogen)
53
How did seldane (Terfenadine) get banned?
If taken with ketoconazole erythromycin, it can inhibit CYP3A4 (normal pathway) This causes build up of terfenadine, leading to arrhythmia
54
How can grapefruit be bad?
It inhibits CYP3A4 so it inhibits metabolism for CYP3A4 drugs
55
How do you test for P450 inhibition?
Get a cDNA sample to express the enzyme Put it together with various chemicals
56
Which P450 should pharmaceutical companies avoid?
CYP3A4 - Too busy since it metabolises majority of drugs CYP2D6 - High polymorphism in humans
57
What drugs use OATPs?
Digoxin Fexofenadine
58
What drugs use OATs
Antivirals Penicillin NSAIDS Diuretics
59
How is panadol biotransformed?
Sulfation pathway SULT Glucuronidation pathway UGT
60
What does cyclophosphamide turn into after biotransformation
Phosphoramide mustard
61
How is propafenone metabolised?
Metabolised into 2 products, one (5-hydroxypropafenone) is also anti-arrhythmic drug, so its metabolism also replaces its drug
62
What is diethylstilbestrol?
Teratogen, causing rare vaginal cervial cancer and other effects in both males and females

PCL201 Finals review (7 decks)

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