Exam 1, ch. 1 review

Question 1

Father of western/modern medicine

Answer 1

Hippocrates

Question 2

First recorded physician? Where?

Answer 2

Imhotep, in ancient egypt

Question 3

First Medical textbook

Answer 3

Materia Medica

Question 4

Who is paracelsus? What is their famous quote?

Answer 4

Father of toxicology; The dose makes the poison

Question 5

Pharmocodynamics

Answer 5

What the drug does to the body

Question 6

Pharmacogenomics

Answer 6

Looks at genetic profile, how you’ll respond to the drug, some drugs require genomic testing. E.g. her-2 positive

Question 7

Toxicology

Answer 7

Poisons and toxins and how they affect your body

Question 8

Pharmacokinetics

Answer 8

What the body does to the drug i.e. What organ metabolizes it, half-life, how it crosses barriers

Question 9

Define the following terms: agonist, antagonist, allosteric, orthosteric

Answer 9

• Agonist: Will bind to receptor (receptor is on cell surface)
• Antagonist: Blocks the receptors from receiving/functioning, prevents it from happening or dampers it
• Allosteric: binds somewhere outside active site
• Orthosteric: Binds at active site

Question 10

State the difference between toxins and poisons

Answer 10

• Poisons are non-biologic, arsenic or lead.
• Toxins are biological substances that are from living organisms like pufferfish, mushrooms, etc.

Question 11

List the different types of drugs, and what causes them to interact with their receptor

Answer 11

Solid, liquid or gas. The causes are similar to a lock and key analogy, molecular weight, and types of bonds.

Question 12

Describe the relative bond strengths

Answer 12

Covalent is the strongest, then electrostatic, and the weakest is hydrophobic because there isn’t a charge. The stronger the bond, the less the specificity, and the weaker the bond, the more specific it is.

Question 13

Define racemic mixtures, and correlate stereoisomerism and differences in drug effects

Answer 13

Racemic mixtures are 2 different optical isomers. They can be the same molecular formula but create different effects/results.

Question 14

Define and describe the terms receptor and receptor site.

Answer 14

Receptor is mostly on the outside of the cell and is where a drug can bind to the receptor to be transported inside the cells. A receptor site is the specific site the drug binds to, and there are multiple kinds of sites. You have orthosteric and allosteric sites. Some are active and competing, some aren’t.

Question 15

Analyze drug response curves to determine Bmax, Emax, Kd, and EC50

Answer 15

study graphs!

Question 16

EC50

Answer 16

When 50% of the desired effect is achieved. i.e. when propranolol drops the heart rate from 120 to 60

Question 17

Kd

Answer 17

Kd is when 50% of the receptors are bound, does NOT equal EC50

Question 18

Emax

Answer 18

Emax is the the drug concentration needed to achieve full maximum effect of the drug.

Question 19

Bmax

Answer 19

The highest concentration needed to achieve 100% receptor-bound drug.

Question 20

Distinguish between a competitive inhibitor and an allosteric inhibitor.

Answer 20

A competitive inhibitor will compete with the active site and block other drugs from binding and starting a reaction. An allosteric inhibitor is non competing and bonds to the receptor outside the active site, and since its non-competing, it is more effective.

Question 21

Describe physiologic antagonism.

Answer 21

When 2 different types of receptors that are doing opposite tasks. It’s when drugs act at different receptors to squelch effects of other drugs. I.e. acetylcholine agonizes Muscarinic receptors to lower heart rate while norepinephrine is agonizing beta receptors to raise heart rate.

Question 22

Differentiate potency and efficacy. Compare the efficacy and the potency of 2 drugs on
the basis of their graded dose-response curves

Answer 22

Potency is the concentration of the drug required to produce 50% of the maximal effect.

Efficacy is greatest possible response a drug can deliver, and must take into account toxicity.

Question 23

Describe the following terms: partial agonist, inverse agonist

Answer 23

Partial agonist is an agonist when acting alone, but becomes an antagonist when in presence of a full agonist

Inverse agonist in practice is an antagonist, but they are agonizing a receptor in order to block effects. It works by shutting down downstream response.

Question 24

Evaluate haw a partial agonist can also be an antagonist

Answer 24

It’s an antagonist when a full agonist is present. It bonds to the receptor and keeps the full agonist from binding, which in turns weakens the reaction, becoming an antagonist.

Question 25

Describe the role of drug carriers, and list the most common ones in the blood.

Answer 25

Bind to drug but do not affect the body. BOUND drug cant cross barriers. Albumin binds to acidic drugs, alpha-1 acid glycoprotein bind to basic drugs, and lipoproteins bind to neutral drugs.

Question 26

What happens if albumin is low?

Answer 26

Less of the drug is bound to albumin, therefore the drug becomes more toxic in its free form.

Question 27

Does albumin cross barriers easily?

Answer 27

No, albumin bound with drugs do not cross barriers easily. Drugs in free form cross much easier.

Question 28

What happens if the patient receives multiple drugs that bind to albumin?

Answer 28

They compete for albumin receptor sites, resulting in a higher concentration of free form drugs, increasing the effect of the drug on the body.

Question 29

Calculate the therapeutic index of an unknown drug

Answer 29

For animals: LD50 divided by ED50

For humans: TD50 divided by ED50

Question 30

Predict the charge on a drug based on its pH and pKa

Answer 30

If the ph < pKa, then it is protonated (hydrogen ion attached). If it is a weak acid, its uncharged. If its a weak base, its charged.

If the pH > pKa, then it is unprotonated (no hydrogen ion attached). A weak acid is charged, and the base is uncharged.

Question 31

Correlate the Henderson Hasselbach equation with the charge on acidic and basic drugs.

Answer 31

It relates pKa to pH. pKa tells us at what pH you’ll have charged and non-charged at equilibrium.

Question 32

Discuss the four main causes of drug variation

Answer 32

1. Alteration in concentration of drug that actually reaches the receptor (Rate, age, weight, sex, disease state, genetics, illness)
2. Variation in concentration of endogenous receptor ligand (everyone has different amount of receptors on cell surface, can be affected by health status)
3. Alteration in number of FUNCTIONAL receptors (may be blocked unknowningly)
4. MOST IMPORTANT Changes in components of response distal to receptor. i.e. post receptor process, bodies natural ability to compensate.

Question 33

In order to cross barriers, drugs need to be

Answer 33

Uncharged.

Question 34

Define monoclonal antibodies and how they are produced

Answer 34

Drugs created by living organisms, may be direct or modified in lab. They are extracted from living systems (blood, transplants, microbiota) and produced by Recombinant DNA technology. They are produced by clones of a single parent cell.

Question 35

Draw the basic structure of a monoclonal antibody

Answer 35

Slide 75 of lecture 1 notes

Question 36

Appreciate the naming conventions in monoclonal antibodies

Answer 36

Prefix is the variable (target system for body, and source e.g. mice) with -mab as the suffix.

Question 37

List uses for monoclonal antibodies in pathologic conditions

Answer 37

Extremely specific to targeted cells, therefore resulting in less side effects and increase in efficacy. Can cause cell death by various mechanisms, such as for cancer cells.

Question 38

Describe the role of the FDA

Answer 38

They oversee development process of drugs in US, and demand that drug must be safe AND effective (vitamins dont have to be effective).

Question 39

List the difference in regulation between prescription and OTC drugs

Answer 39

Rx: only available by authorization of health professional, viewed as “more effective” by public. (Safety does not always equal efficacy).

OTC: freely available to public, low risk for harm/abuse, does NOT equate to safe.

Question 40

Define steps to bring a prescription drug to market.

Answer 40

vitro/animal testing for 4 years, apply for IND (investigative new drug)

Broken into 4 phases.

Phase 1: 20-100 healthy volunteers for dosing, safety, and may include patients IF they are high risk.

Phase 2: 100-200 patients, double blind study, testing efficacy. This does include patients with the actual disease the drug is treating.

Phase 3: 1000s of patients, market formulation, route.

NDA: new drug application

Phase 4: finally make money back, drug is on the market. patent expires after 20 years.