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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
What does it mean when clearance of the drug is greater or smaller than GFR?
Cl greater than GFR--->secretion | Cl smaller than GFR--->reabsorption
26
What is the definition of therapeutic window?
Dose between min effective and min toxic con.
27
Does the time to steady state depends on the dose? if you increase dose, what will you see?
Nah brah | You will see a higher steady state drug con.
28
Why do we use loading dose?
To achieve steady state faster (about 2x maintenance dose)
29
What is the equation for half life/loading dose/maintenance dose?
Half life--->(0.7 x Vd)/Cl Loading dose--->Cp x Vd Maintenance dose--->Cp x Cl
30
When will an antagonist has no affect on a receptor?
When there is no agonist existed for this receptor
31
Under what situation can you compare the affinity of the 2 drugs? Left or right ward shift increase affinity?
When they are parallel to each other on the dose-response curve (meaning they work on the same receptor) Left ward shift
32
Define full and partial agonist in terms of efficacy
Full--->reach max efficacy | Partial--->well they don't
33
What happens if a partial agonist is in the presence of a full agonist? and what are some examples?
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
What if you keep adding partial agonist into full agonist?
Eventually you would only see the affect of partial agonists
35
What does potentiation mean to a drug?
Increase potency
36
What is physiologic antagonism?
2 opposing agonist against each other (like a vasodilator and a vasconstrictor)
37
What is chemical antagonism?
One drug bind to another one to inhibit it
38
What does therapeutic index mean?
E.g. TI=5 | It means if you take 5x the normal dose of the drug--->you will get toxicity
39
What are some common drugs with low TI?
Theophylline/digoxin/warfarin/Li+
40
Beta receptors/alpha 2/M2/D2 are Gs or Gi coupled?
Beta--->all Gs | Alpha2/M2/D2--->Gi (MAD2)
41
Gq coupled protein activates ___? and release ___ and ___?
Phospholipase C/IP3 (increase Ca) and DAG (activate PKC)
42
What receptors are coupled with Gq protein?
M1/M3/alpha1
43
Gs increase cAMP and then activate __?
PKA
44
cGMP is 2nd messenger in what tissue?
Vascular smooth muscle
45
What kind of receptors are for cytokines like EPO/interferon? and what does it activate?
JAKs?STATs
46
What are the 4 phases of drug development?
``` 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
Which phase of the drug development does it usually fail?
Phase II
48
What are the FDA classification of drugs for pregos?
A--->very safe B--->safe C--->may be safe (unknown drugs) D/X--->harmful
49
What cells in the stomach secretes gastrin?
Chief cell
50
When is the best time to dose PPI and why?
Half an hour before breakfast/parietal cell needs to be turned on
51
PPI is activated in basic or acidic environment?
Acidic
52
How is the protective layer of the stomach formed?
Epithelial cell produces bicarb + mucus neck cell produces mucus
53
What are some risk factors for peptic ulcers? and what can impair mucosal defense?
Smoking/stress/genetics | NSAIDs/H. pylori
54
Bismuth salts need what kind of environment to work?
Acidic
55
How is misoprostol used?
Prevent chronic NSAIDs induced peptic ulcer (inhibit prostaglandin production)
56
How is H. pylori affect stomach lining?
It eats the lining--->decrease acid resistance--->predispose the pt with ulcers

Unit 4 (28 decks)

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