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Pharm Exam 1 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

Steps of the drug use process

A
  1. Assessment
  2. Select the the optimal regimen for the patient
  3. Dispense and counsel
  4. Administration of the drug
  5. Monitor and follow up the patient
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2
Q

What is medication reconciliation?

A
  • The process of comparing the patient’s medication orders all medications the patient has been taking
  • Prescription, over-the-counter, and dietary supplements
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3
Q

What is the purpose of medication reconciliation?

A

Avoid medication errors

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4
Q

What is the cause of more than 40% of medication errors?

A

Inadequate medication reconciliation

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5
Q

What is evidence-based pharmacotherapy?

A

An approach to decision-making that relies on appraisal of scientific evidence and its strength

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6
Q

What is first level evidence-based pharmacotherapy?

A

Reviews of evidence-based practice guidelines or current textbooks with evidence links

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7
Q

What is second level of evidence -based pharmacotherapy?

A

Consultation of electronic databases of systematic reviews and/or meta-analyses

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8
Q

What is third level evidence-based pharmacotherapy?

A

Literature searches using electronic database

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9
Q

What is a medication error (ME)?

A

Any mistake in the medication process regardless of outcome

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10
Q

What is an adverse drug event (ADE)?

A

Harm resulting from the use of the medication

  • Some ADEs are the result of MEs
  • Some ADEs are not the result of MEs (not due to error)
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11
Q

What is an adverse drug reaction (ADR)?

A

And ADE that is not preventable (not caused by error)

  • ADRs represent reactions to a normal pharmacological intervention
  • A side effect is not an ADR unless it causes harm
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12
Q

Is the difference between an adverse drug event and an adverse drug reaction? ADE vs ADR

A
  • ADE: Sometimes preventable, sometimes not

- ADR: Not preventable, normal reaction to medication

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13
Q

What are some examples of electronic guidelines for pharmacotherapy?

A
  • UpToDate
  • National guideline clearing House
  • Medscape
  • BMJ clinical evidence
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14
Q

What are some examples of textbooks/reviews available electronically with updates for pharmacotherapy?

A
  • Goodman and Gilman’s pharmacological basis of therapy

- Scientific American medicine online

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15
Q

What are some examples of regular textbooks for pharmacotherapy?

A

Pharmacotherapy: principles and practice (Chisolm-Burns)

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16
Q

What are the two main operational concepts of pharmacology?

A
  1. Pharmacodynamics

2. Pharmacokinetics

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17
Q

What is pharmacodynamics?

A
  • Sites of action for drug at a molecular level
  • Attributes of drugs at the sites
  • Effects of drugs, through these sites, on normal and relevant pathologic states
    “The effect of a drug on the body”
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18
Q

What is pharmacokinetics?

A
  • Absorption: How the body breaks the drug down
  • Distribution: How the body brings the drug to different tissues
  • Elimination: How the body processes and excretes the drug
    “The fate of a drug following its administration”
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19
Q

To what does the “intended” effect of a drug refer?

A
  • “On-target” effects

- Therapeutic use of drug

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20
Q

To what does the “adverse” effect of a drug refer?

A
  • “On-“ or “off-target” effects
  • Lifestyle use of a drug
  • Either licit or illicit
  • Licit: Caffeine to help stay awake
  • Illicit: Opiates for a high instead instead of for pain
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21
Q

What is an “on-target” effect of a drug?

A
  • Effects caused by the drug acting on its intended receptor in the body
  • i.e. Antihistamine acting on H1 receptor to reduce itching (intended) or sedation (adverse)
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22
Q

Is an “off-target” effect of a drug?

A
  • Effects caused by the drug acting on UNINTENDED receptor in the body
  • i.e. Antihistamine acting on muscarinic receptor causing dehydration and drying (adverse)
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23
Q

What are the 6 major targets of drug action in the body?

A
  1. G protein-coupled receptors (GPCRs)
  2. Ion channels
  3. Enzyme-linked receptors
  4. Nuclear receptors
  5. Transporters
  6. Enzymes
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24
Q

Describe how G protein-coupled receptors work

A
  1. A ligand, or agonist, binds to the G protein-coupled receptor embedded in the cell surface membrane
  2. The receptor undergoes a conformational change
  3. GDP in the G protein is exchanged for GTP, causing the alpha subunit to disassociate from the beta-gamma dimer
  4. Both subunits can work on in effector
  5. Sometimes it’s an activation of the effector, sometimes its inhibition of the effector
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25
Q

What are the proximal targets for G proteins and what are their effects?

A
  • Gs = increase in adenylyl cyclase (increase cAMP)
  • Gi = decrease in adenylyl cyclase (decrease cAMP, stimulate potassium channels)
  • Gq = increase in PLC-B (increase in calcium)
  • G12 = increase in rho (contractility, shape, etc.)
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26
Q

How do prostaglandin’s work on neurons to incite pain?

A
  • Prostaglandins are released from damaged tissue
  • Prostaglandins bind with prostanoid receptors to stimulate Gs proteins, or excitatory proteins, and increase cAMP, which is pro-excitatory in a neuron
  • The neuron depolarizes and propagates a nerve stimulus along an axon
  • This causes the release of neurotransmitters and causes pain
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27
Q

How do opiates work to reduce pain?

A
  • Opiates find to opiate receptors, which in turn activate potassium channels
  • Potassium reflux hyperpolarizes the neuron and inhibits transmission of pain stimuli
28
Q

How do bradykinins work on on neurons to incite pain?

A
  • Bradykinins are released from damaged tissue
  • Bradykinins bind with B2 receptors to stimulate Gq proteins, or excitatory proteins, and increase calcium in the cell
  • The neuron depolarizes and propagates a nerve stimulus along an axon
  • This causes the release of neurotransmitters and causes pain
29
Q

What are the roles of ion channels?

A
  • Sit below the cell surface

- Conduct ions from one side of the membrane to the other (i.e. sodium, potassium, calcium)

30
Q

Describe membrane potential

A
  • Voltage is the potential across any membrane
  • How was it generated?There’s a lot of potassium on the inside, and a lot of sodium, calcium, and chloride on the outside
  • At rest, inside of cell is more negatively charged than outside of cell, causing a negative action potential
31
Q

How does an action potential work?

A
  • The resting membrane potential of a cell is a voltage of about -65
  • Sodium potassium channels help keep the inside more negative and outside more positive (for every 2 Ks transported into the cell, 3 Nas are transported out)
  • An outside stimulus will cause sodium ion channels to let sodium into the cell, decreasing the voltage of the membrane potential
  • Once the voltage hits a certain threshold, around -35 or 40, voltage-gated sodium and calcium channels are activated, causing sodium and calcium to flood into the cell, depolarizing the membrane
  • The signal is propagated along the axon by stimulating adjacent sodium channels to open. The refractory period helps move the stimulus forward.
  • Potassium channels open, allowing the the potassium out of the cell to help re-polarize the membrane
  • Sodium potassium channels help bring the membrane potential back to resting state
32
Q

What are the two types of ligand-gated ion channels?

A

Excitatory and inhibitory

33
Q

How do excitatory ligand gated channels work?

A

Use cations (sodium, potassium) to cause depolarization

34
Q

What ligands do excitatory ligand gated ion channels recognize?

A

Glutamate, acetylcholine (nicotinic receptors), and purines

35
Q

How do in inhibitory ligand gated channels work?

A

Use anion chlorine to cause hyperpolarization

36
Q

What ligands do inhibitory ligand gated ion channels recognize?

A

Gamma-aminobutyric acid (GABA) and glycine

37
Q

What is the relationship between ligand gated and the voltage gated ion channels?

A

Ligand gated channels can activate voltage gated channels

38
Q

What are enzyme-linked receptors?

A

Receptors that, when activated by agonist, exhibit:

  1. a capacity to phosphorylate other proteins, usually tyrosine residues either
    - Intrinsically, i.e. they are protein kinases or
    - Extrinsically, through association with protein kinases
  2. and sometimes a scaffolding functionality -> signal transduction
  3. Important for cell growth, how immunologically cells communicate with each other (cancer, inflammatory diseases)
39
Q

How do enzyme-linked receptors work?

A
  1. Ligand binds with receptor
  2. Kinases used P on receptors to phsphorylate proteins
  3. When phosphorylated, these proteins cause signal cascades
40
Q

What are some common drug act on enzyme-liked preceptors?

A

Insulin, cancer treatment

41
Q

In what types of cells are nuclear receptors found?

A

Genes

42
Q

What is the purpose of nuclear receptors?

A

Regular transcription of genes and gene activity

43
Q

What types of drugs commonly act on nuclear receptors?

A
  • Steroids

- Sex hormones

44
Q

What types of drugs commonly act of voltage gated ion channels?

A
  • Local anesthetics
  • Antiepileptics
  • Antidysrhythmics
  • Antihypertensives
45
Q

What types of drugs commonly act on ligand gated ion channels?

A
  • Muscle relaxants
  • Anesthetics
  • Sedatives
46
Q

Name the different types of transporters

A
  1. Passive transport, facilitated diffusion: Ions moving down their concentration gradient, No energy required
  2. Primary active transport: Uses hydrolysis of ATP to transport against a concentration gradient
  3. Secondary active transport: Uses passive energy of an ion moving down its concentration gradient to bring another ion against its concentration gradient
    - Symport: Moves in the same direction as the passive ion
    - Antiport: Moves in the opposite direction as the passive ion
47
Q

What types of drugs commonly act on transporters?

A
  • Antidepressants
  • Amphetamines
  • PPIs
  • Diuretics
  • Cardiac glycosides
48
Q

What are the two most common sites of drug action?

A
  1. G protein coupled receptors

2. Enzymes

49
Q

How do drug act on enzymes?

A

Drugs inhibit an enzymatic activity

50
Q

What are the two types of the inhibition of enzymatic activity?

A
  1. Reversible inhibition

2. Irreversible inhibition

51
Q

Describe reversible inhibition of enzymatic activity

A
  • It is usually competitive, i.e. Drug and substrate compete for the same site
  • For example, statins, which have a much higher affinity for binding site, compete with HCG CoA enzyme to inhibit cholesterol production/distribution
52
Q

Describe irreversible inhibition of enzymatic activity

A
  • Always based on stable covalent linkage between the drug and enzyme
  • Drug attaches to enzyme permanently
  • For example, Aspirin inhibits COX1 and COX2 by permanently covalently bonding to the binding site
53
Q

Define agonist

A
  • A macromolecular entity, endogenous (natural) or synthetic, that activates the receptor to which it is directed
  • Can be classified as full or partial agonists
  • Partial agonist cannot activate all receptors or pathways, while full agonists can
  • High enough levels of weak partial agonists can compete with substrates and act as antagonists, i.e. Chantix competes with nicotine to help stop smoking
  • Binds reversibly, along with antagonists, at orthosteric site, main binding site
54
Q

Define antagonist

A
  • A macromolecular entity, almost always synthetic, that prevents the actions of another ligand (i.e. agonist) At the receptor to which it is directed
  • Can be classified as neutral (or pure) antagonists or inverse agonists
  • Neutral antagonists bind directly binding site, or orthsteric site, to stop activation
  • Inverse agonists bind to active receptors to lower the activity of the receptors themselves (all receptors have some level of activity and can even activate alone sometimes)
  • Binds reversibly, along with agonists, at orthosteric site, main binding site
55
Q

What is the difference between occupation activation?

A
  • Occupation is governed by infinity, or how tightly a drug binds to a receptor
  • Activation is governed by efficacy
  • Binding does not necessarily cost activation, binding may not cause a response because there is no efficacy even if there is high affinity
56
Q

What is the relationship between occupation and concentration of drug?

A
  • With few ligands, there is higher affinity because the receptors want to bind the ligands
  • With high levels of ligand, there is no affinity because receptors have bound enough ligands
57
Q

Describe the three phases of drug response

A
  • Phase 1: Very little drug causes very little in terms of response
  • Phase 2: More drug gives a great deal more response
  • Phase 3: Emax - more drug will not create more response, max effect
58
Q

What is the difference between potency efficacy?

A
  1. Potency: Concentration or dose of drug required to achieve a certain effect
    - Usually referenced to EC50 or ED50 (50% refers to drug’s own Emax), or the dose of drug that gives us half maximum effect
    - The lower the EC50 or ED50, the greater the potency (i.e. If we only need a small amount to get to 50% of Emax, very potent. If we need a boat load of drug to get to 50% of Emax, not very potent.
  2. Efficacy: Magnitude of the drug action at the limit of its concentration or dose (Emax)
    - The greater the Emax, the greater the efficacy
59
Q

What is the relationship between dose therapeutic response and dose adverse response?

A

How an increased concentration of a drug is related to adverse effects

60
Q

What is the minimal useful effect of a drug?

A

The smallest dose that actually works with the least amount of side effects

61
Q

What is the maximum tolerated adverse effect of a drug?

A

The dose at which the patient cannot tolerate the adverse effect any longer, the problem of the adverse effect is too significant

62
Q

What is the therapeutic window?

A

The difference between the therapeutic effect, or when the drug begins to work, and toxic effect

63
Q

What is duration of action of a drug?

A

Begins when drug starts working and ends when drug stops working

64
Q

Describe the quantal dose response curve

A
  • Quantal is based on population
  • ED50 is % of human population that needs a certain dose have therapeutic response
  • LD50 is the percent of people dead at a certain dose
65
Q

What is the therapeutic index?

A

Toxic dose of the drug for 50% of the population divided by an effective dose for 50% of the population

  • Therapeutic index = TD50/ED50
  • The higher the therapeutic index, safer the drug
  • Low therapeutic index means we need to monitor the person more
66
Q

How do drug-drug interactions play out at a pharmacodynamic level?

A
  • Drugs may compete for the same binding site, i.e. albuterol and beta blockers for B2 receptors
  • Drugs may affect membrane potentials that impact efficacy of the other drugs, i.e. diuretics and dig both depend on K levels, diuretics lower K and cause dig tox
  • Drugs works synergistically to potentiate side effects, i.e. antihistamines and alcohol work together at H1 receptors to cause excessive sedation

Pharm Exam 1 (4 decks)

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