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Unit 4 > Pharmacokinetics/dynamic > Flashcards

Pharmacokinetics/dynamic Flashcards

1
Q

Simple definitions of pharmacokinetics and dynamic?

A

Kinetics—>what the body does to the drug

Dynamic—>what the drug does to the body

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2
Q

What are the 4 factors that determine a drug’s permeation?

A

Solubility/concentration/surface area/vascularity

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3
Q

What is pKa and which form of the drug can cross the membrane and which form is better excreted?

A 
pKa--->pH when the drug is 50% ionized and 50% nonionized
Nonionized form (uncharged) can cross membrane 
Ionized form (charged) is better excreted
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4
Q

Ionized and nonionized forms are water or lipid soluble?

A

Ionized—>water

Nonionized—>lipid

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5
Q

What are some examples of weak acid and base drugs?

A

Acid—>aspirin/loop and thiazide diuretics

Base—>local anesthetics/amphetamines/PCP

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6
Q

What pH environment would produced the most nonionized form of weak acid and base drugs?

A

Weak acid—>acidic

Weak base—>basic

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7
Q

Bound or unbound/ionized or unionized drugs are filtered through the kidney?

A

Unbound

Both ionized and nonionized are filtered (nonionized form undergo secretion and reabsorption)

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8
Q

What could you use to acidify the urine to increase renal excretion of weak base drugs?

A

NH4Cl

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9
Q

Weak acid and base drugs are better absorbed in the stomach or the small intestine?

A

Weak acid—>stomach

Weak base—>small intestine

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10
Q

What do we use lactulose to treat hepatic encephalopathy?

A

Hepatic encephalopathy—>increase ammonia/enlarged abdomen—>lactulose is converted to acidic acid—>acidify the guts—>convert NH3 (ammonia) to NH4+ (ammonium)—>increase ammonium excretion

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11
Q

If you keep increasing the drug dose and more is absorbed, and you keep doing that and no more is absorbed, what kind of transport is it for this drug?

A

Facilitated diffusion or active transport (saturable)—>the presence of ATP distinguish these two

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12
Q

Is IV a process of drug absorption?

A

No. Absorption is the entry of a drug from one compartment into the blood

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13
Q

Why should we be caution when taking warfarin and sulfonamide/UCB and sulfonamide at the same time?

A

They are both highly protein bound—>displace warfarin—>increase serum warfarin level
Kernicterus and bilirubin encephalopathy

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14
Q

What kind of drug can cross the blood brain barrier?

A

Lipid soluble or very small

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15
Q

What is the equation for Vd?

A

Vd=dose/plasma drug con.

Low plasma con. (drug leave plasma and goes into tissue)—>high Vd

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16
Q

A drug that is highly protein bound has a high or low Vd?

A

Low Vd (it stays in the plasma)

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17
Q

What is redistribution of a drug?

A

Drug goes to the target organ–>comes back out—>usually end up in fat (storage site)

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18
Q

What is an example of metabolizing an active drug into active metabolite?

A

Benzo

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19
Q

What are phase I and II drug metabolism?

A

Phase I—>reduction/oxidation/hydrolysis–>CYP450

Phase II—>Methylation/glucuronidation/acetylation/sulfation (More GAS) (transferases)

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20
Q

What are some common CY450 inducers?

A

Smoking and drinking in Barb’s Car Rifs her Phen

Smoking/drinking/Barbiturate/carbamazepine/rifampin/phenytoin

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21
Q

What are some common CY450 inhibitors?

A

COKE + grapefruit juice with your PI

Cimetidine/Omeprazole/ketoconazole/erythromycin/grapefruit juice/protease inhibitor

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22
Q

What is the most common drug that interacts with grapefruit juice?

A

Increase statins level

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23
Q

What drugs causes drug induces lupus and how?

A

Hydralazine/procainamide/isoniazid

with slow metabolizers (acetylators)

24
Q

How to distinguish between drug induced and regular lupus?

A

Drug induced has antihistone antibodies

25
Q

What does it mean when clearance of the drug is greater or smaller than GFR?

A

Cl greater than GFR—>secretion

Cl smaller than GFR—>reabsorption

26
Q

What is the definition of therapeutic window?

A

Dose between min effective and min toxic con.

27
Q

Does the time to steady state depends on the dose? if you increase dose, what will you see?

A

Nah brah

You will see a higher steady state drug con.

28
Q

Why do we use loading dose?

A

To achieve steady state faster (about 2x maintenance dose)

29
Q

What is the equation for half life/loading dose/maintenance dose?

A

Half life—>(0.7 x Vd)/Cl
Loading dose—>Cp x Vd
Maintenance dose—>Cp x Cl

30
Q

When will an antagonist has no affect on a receptor?

A

When there is no agonist existed for this receptor

31
Q

Under what situation can you compare the affinity of the 2 drugs? Left or right ward shift increase affinity?

A

When they are parallel to each other on the dose-response curve (meaning they work on the same receptor)
Left ward shift

32
Q

Define full and partial agonist in terms of efficacy

A

Full—>reach max efficacy

Partial—>well they don’t

33
Q

What happens if a partial agonist is in the presence of a full agonist? and what are some examples?

A

Partial agonist would compete with full agonist—>decrease the affect of full agonist—>thus partial agonist becomes an antagonist
Pindolo and tamoxifen—>when put in the body with natural full agonist (epi/norepi/estrogen)—>act as antagonists

34
Q

What if you keep adding partial agonist into full agonist?

A

Eventually you would only see the affect of partial agonists

35
Q

What does potentiation mean to a drug?

A

Increase potency

36
Q

What is physiologic antagonism?

A

2 opposing agonist against each other (like a vasodilator and a vasconstrictor)

37
Q

What is chemical antagonism?

A

One drug bind to another one to inhibit it

38
Q

What does therapeutic index mean?

A

E.g. TI=5

It means if you take 5x the normal dose of the drug—>you will get toxicity

39
Q

What are some common drugs with low TI?

A

Theophylline/digoxin/warfarin/Li+

40
Q

Beta receptors/alpha 2/M2/D2 are Gs or Gi coupled?

A

Beta—>all Gs

Alpha2/M2/D2—>Gi (MAD2)

41
Q

Gq coupled protein activates ___? and release ___ and ___?

A

Phospholipase C/IP3 (increase Ca) and DAG (activate PKC)

42
Q

What receptors are coupled with Gq protein?

A

M1/M3/alpha1

43
Q

Gs increase cAMP and then activate __?

A

PKA

44
Q

cGMP is 2nd messenger in what tissue?

A

Vascular smooth muscle

45
Q

What kind of receptors are for cytokines like EPO/interferon? and what does it activate?

A

JAKs?STATs

46
Q

What are the 4 phases of drug development?

A 
Phase I---->find out the safe dosage 
Phase II--->test for effectiveness 
Phase III---->test for side effects 
Approved by FDA
Phase IV--->look for long term side effect
47
Q

Which phase of the drug development does it usually fail?

A

Phase II

48
Q

What are the FDA classification of drugs for pregos?

A

A—>very safe
B—>safe
C—>may be safe (unknown drugs)
D/X—>harmful

49
Q

What cells in the stomach secretes gastrin?

A

Chief cell

50
Q

When is the best time to dose PPI and why?

A

Half an hour before breakfast/parietal cell needs to be turned on

51
Q

PPI is activated in basic or acidic environment?

A

Acidic

52
Q

How is the protective layer of the stomach formed?

A

Epithelial cell produces bicarb + mucus neck cell produces mucus

53
Q

What are some risk factors for peptic ulcers? and what can impair mucosal defense?

A

Smoking/stress/genetics

NSAIDs/H. pylori

54
Q

Bismuth salts need what kind of environment to work?

A

Acidic

55
Q

How is misoprostol used?

A

Prevent chronic NSAIDs induced peptic ulcer (inhibit prostaglandin production)

56
Q

How is H. pylori affect stomach lining?

A

It eats the lining—>decrease acid resistance—>predispose the pt with ulcers

Unit 4 (28 decks)

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