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Pharma Flashcards

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1
Q

What are pharmacodynamics?

A

The actions of the drug on the body. Drug-Receptor interactions.

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2
Q

What is ADME?

A

Absorption, Distribution, Metabolism and Excretion (Elimination)

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3
Q

What do receptors do?

A

Determine the relationship between dose and effect.
Responsible for selectivity of drug response
Responsible for agonist and antagonist activity

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4
Q

What are the different types of receptors?

A

Ion channels, G Protein coupled receptors, enzyme linked receptors and steroid receptors

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5
Q

What does signal transduction and secondary messengers do?

A

Amplify the signal. But there must also be a way to turn off or desensitize the signal.

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6
Q

What are ion channel receptors?

A

A channel through the phospholipid bilayer that allows lipid insoluble molecules through to cause cellular polarization or depolarization. Opens when receptor is activated.
Nicotine activates a sodium ion channel. The influx of sodium depolarizes the cell. In the brain this leads to increased alertness.

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7
Q

What are G Protein coupled receptors?

A

Transmembrane receptor, quick
An agonist binds to a receptor on the G Protein which undergoes a change. GTP replaces GDP and then the GDP joins a subunit to go and power an effector protein.
There are many different types of effector proteins (ion channels, secondary messengers-Ca)
Can cause polarization, depolarization, protein phosphorylation, Ca release, etc.)
The biggest family of receptors, 60% of drugs work on this type of receptors. Morphine acts on this type to reduce pain

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8
Q

What does the G Protein subtype determine?

A

Determines the receptor effects.
Gs has a stimulatory effect by increasing cAMP.
Gi has an inhibitory effect by decreasing cAMP, increased K efflux. Both are activated by the pertussis bug.
Golf is for smelling and increases cAMP. Activated by cholera toxin

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9
Q

What are the types of enzyme linked receptors?

A

Guanylyl cyclase, tyrosine kinase receptors and tyrosine kinase associated receptors

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10
Q

How does guanylyl cyclase work?

A 
The drug (nitroglycerin) must pass through the cellular membrane in order to reach the receptor (intracellular). The interaction causes guanylyl cyclase to convert GTP to cGMP.
Activation causes vasodilation and relief of cardiac pain
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11
Q

How do tyrosine kinase receptors work?

A

Transmembrane. The drug (insulin) binds to the receptor on tyrosine kinase, which then phosphorylates proteins on tyrosine (Y) residues.

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12
Q

How do tyrosine kinase associated receptors work?

A

Transmembrane. A drug binds to a receptor that then activates a tyrosine kinase. An additional domain on the receptor, intermediate.
The immune system (cytokines) use this type of receptors.

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13
Q

What are steroid (nuclear) receptors?

A

The drug must pass through the cellular membrane and then pass through the nuclear pores into the nucleus of the cell. Binds to DNA and can turn a gene on and off to cause different protein synthesis (DNA transcription).
Hydrocortisone decreases cell proliferation.

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14
Q

How long do drug effects last?

A

The effects last as long as the drug is bound to the receptor. Depends drug-receptor affinities.

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15
Q

How do enantiomers affect carvedilol?

A

+ carvedilol is a selective beta-blocker. - carvedilol is selective for alpha receptors.

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16
Q

What is Kd?

A

The concentration that binds 50% of the available receptors.

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17
Q

What is affinity?

A

The degree of attraction between drug and receptor. Determines drug properties.
The dual arrows between D+R and DR

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18
Q

What is efficacy?

A

How good the response is to the drug. Used in clinical trials.
Effectiveness is used for the wider population.
Emax is the maximum possible efficacious.
The one way arrow between DR and response.
The y axis of a response vs. dose graph.

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19
Q

What is an agonist?

A

Drugs that bind to and activate the receptor.

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20
Q

What is a partial agonist?

A

Drugs that bind to the same receptors and activate them in the same way with a lower response.
Has affinity, but low efficacy.
Emax is not as high
Pindolol on heart rate

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21
Q

What is an antagonist?

A

Drugs that bind to a receptor, compete with and prevent the binding by other molecules. Blocks out response
Straight line on response vs. concentration graph

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22
Q

What is the law of mass action?

A

The drug receptor interaction is directly dependent upon the concentration of the drug and the concentration of the receptor.
More pronounced in the beginning.

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23
Q

What is EC50?

A

The effective concentration for 50% effectiveness.

Graph can be transformed by taking the log.

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24
Q

What is potency?

A

The concentration or dose of a drug required to produce maximum effect.
The x axis of a response vs dose graph

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25
What is an inverse agonist?
Binds to the receptor but does not cause a response. Lowers efficacy by creating a negative response
26
What happens when a partial agonist is administered in the presence of a full agonist?
The partial agonist will simply reduce the effects of the full agonist.
27
What happens when an antagonist is administer in the presence of a full or partial agonist?
It will reduce the effects of the agonist to a very low levels, less than just a partial agonist. Will be the same level no matter whether it is full or partial.
28
What are the types of antagonists?
Competitive reversible, irreversible, physiological, chemical and allosteric modulators.
29
How do competitive reversible antagonists work?
They compete with agonists for the receptors and make the site inactive when they bind. If the concentration of agonists is increased, the antagonists can be "bumped" out. The curves are shifted to the left (less potent) so EC50 is shifted to the right but Emax does not change.
30
How do irreversible antagonists work?
They covalently bond to the active site, making it inactive. They reduce efficacy by reducing the total number of receptors. Makes curve higher.
31
How do physiological antagonists work?
The effects of one agonist counteracts the effects of another agonist. Doesn't involve binding to a receptor Diminishes efficacy
32
How do chemical antagonists work?
A chemical interaction reduces the effect of the agonist. No receptors are involved
33
How do allosteric modulators work?
Bind to a site separate from the receptor. Don't compete with agonist for binding or interfere with agonist binding. Can increase or decrease agonist induced response
34
How does the Ca Phosphoinositide signaling pathway work?
A G protein stimulates PLC (phospholipase-C) which breaks down membrane bound PIP2 into 2 molecules (DAG and IP3) IP3 interacts with vesicles of Ca in the cell to create a cellular response. DAG becomes PK-C which helps a substrate become phosphorylated to create a cellular response.
35
How does desensitization and resesitization work?
When you continue to add an agonist over a long period of time, the receptor response wanes (desensitization). By leaving a period of rest in between administrations, you'll get a response of original magnitude (resensitization). The length of rest time depends on the receptor.
36
What is tachyphylaxis?
When tissue response to an agonist wanes over time.
37
What causes phosphorylation and dephosphorylation?
Kinases cause phosphorylation. Phosphatases cause dephosphorylation.
38
How does desensitization and resensitization work with G coupled proteins?
When a G coupled protein receptor is repeatedly administered an agonist, the beta-art will interact with the coated pit to promote endocytosis. The G Protein then leaves the membrane, surrounded by its membrane. This leaves less receptors to interact with the drug. The G Protein vesicle can then go back into the membrane or be broken down by lysozyme.
39
What is passive diffusion?
The movement of a drug from an area of high concentration to an area of low concentration through aqueous channels. Does not require ATP.
40
How does lipid diffusion work?
It does not require a channel. Depends on the pH (weak acids/weak bases) and lipid solubility (high) of the drug.
41
How do large molecules or those with low lipid solubility get into the cell?
Glucose, amino acids. Using transporters. | Transporter may be downgraded or damaged, causing not enough drug to get into the cell.
42
When is endo/exocytosis typically used?
During synaptic transmission
43
What is the Henderson-Hasselbach Equation?
pH=pKa+log(A/HA) | log(protonated/unprotonated)=pKa-pH
44
What parts of weak acids and bases can get into the cell?
HA (protonated acid) and B (uncharged base) can pass through the cell membrane. A (charged acid) and BH (protonated base) cannot pass through the cell membrane. We can get a drug to be in ionized or unionized form by changing the environment.
45
What is selectivity?
The affinity of a drug for a "desired" receptor/effector relative to other receptors/effectors. We want high selectivity. This will give less side effects and a higher potency.
46
What therapeutics categories have the most difficulty getting high selectivity for their drugs?
Chemotherapy and Mental Illness
47
What are TD50, ED50 and LD50?
The dose that gives clinically desired effective response, toxicity and lethal effects, respectively in 50% of the population who takes it.
48
What is the Therapeutic Index?
TD50/ED50 | The distance between the 2 curves is the therapeutic window. A bigger TI gives us more wiggle room (more safe).
49
What is a drug with a large TI and a drug with a small TI?
Penicillin has a large TI and Warfarin has a small TI
50
Why are patient responses to to an agonist variable among patients?
Variability in the plasma free drug concentration. | Variability of receptor sensitivity.
51
What is the volume of distribution (Vd)?
The measure of the apparent space in the body available to contain the drug. Calculated value How drug is distributed in body relative to plasma. High Vd means throughout large area of the body. Vd=Amount of drug in body (mg/kg)/Plasma concentration (mg/L)
52
What can you use volume of distribution for?
For determining clearance of a drug from the body and determining loading dose of a drug.
53
What is loading dose?
Loading dose=Vd(desired plasma concentration)/F | To get amount of drug in body into the therapeutic window rapidly. Then maintain it with a maintenance dose.
54
What can the body water be divided into?
Can be divided into 3 compartments; interstitial, intracellular and plasma. Most is intracellular. Can be used for metabolism, storage or non specific binding?
55
How does pKa affect where a drug will be in the body?
Acidic drugs are more likely in the blood. Basic drugs are more likely in the tissue.
56
What factors influence drug distribution in the body?
pKa of the compound and pH of the tissue compartment. Drug binding Specialized distrubution barriers (BBB, placenta)
57
What is clearance?
The measure of the ability of the body to eliminate the drug. Separate clearances of organs are added to get total clearance. The volume of plasma that would contain the amount of drug excreted per minute
58
What are the routes of excretion?
Liver (hepatic metabolism), gallbladder (bile) and kidney (urine)
59
What is the equation for clearance?
Cl=ke(Vd) | Cl=(0.693/t1/2)(Vd)
60
What are some factors that affect Vd? How do they affect t1/2?
Aging (decreased muscle) decreases t1/2 Obesity (increased adipose tissue) increases t1/2 Pathologic fluid increases t1/2
61
What are some factors that affect Cl? How do they affect t1/2?
Induction of Cyp450 decreases t1/2 Inhibition of Cyp450 increases t1/2 Organ failure increases t1/2
62
What is drug half life (t1/2)?
The time required to change the amount of drug in the body by one half during elimination t1/2(ke)=0.693 t1/2=(0.693*Vd)/Cl
63
What order is the pharmacokinetics of most drugs?
First order. Equal proportions of the drug is removed per unit time. Exponential decrease
64
What is drug accumulation?
It is inversely proportional to the dose that is lost. Opposite elimination. Accumulation factor=1/dose lost
65
What is bioavailability?
The fraction of unchanged drug reaching the reaching the systemic circulation following administration by any route. Measures the extent of absorption Bioavailability=(AUC admin route/AUC injected)(100) Referred to as F or fraction absorbed.
66
How is the rate of absorption found?
By seeing the time to peak concentration.
67
How is the extent of absorption found?
By seeing the peak concentration and the area under the plasma concentration vs. time curve
68
What are some limitations of drug absorption?
Tissue perfusion (blood flow), diffusion-limited absorption (partition coefficient) and first pass effect (distribution and metabolism)
69
What are some factors influencing drug absorption?
Drug formulation, water and lipid solubility, pKa, GI motility, gastric pH, posture and other drugs
70
How does being bound to proteins affect drug absorption?
Albumin is a protein that drugs most commonly are bound to. Can alter distribution times. Bound drugs are too big, so only unbound drugs can leave vessels.
71
What is the equation for dosing rate?
Dosing rate=Cl(Target concentration) | Amount/time
72
What is the equation for maintenance dose?
Maintenance dose=(dosing rate/F)(dosing interval) | F=fraction absorbed (bioavailability)
73
What are first order kinetics?
The amount of drug eliminated per unit time is proportional to concentration. Rate increases as drug concentration increases. Slope is -Kel(C)
74
What are zero order kinetics?
A constant amount of drug is eliminated per unit of time. Rate does not increases as drug concentration increases. Slope is -Kel
75
What is the equation for elimination constant?
Kel=-slope(2.303)
76
What are some advantages and disadvantages of an oral dosage form?
Advantages: Stability, safer (more room for error due to low bioavailability) Disadvantages: Less bioavailability,adherence issues, could be inactivated by stomach acid, must pass through liver metabolism before getting to systemic circulation.
77
How does renal elimination work?
Drugs with a low molecular weight enter the kidney via the renal artery into Bowman's capsule. (glomerular filtration) Lipid soluble, unionized drugs move back into the blood in the distal tubule (tubular reabsorption) while non-lipid soluble, polar and ionized drugs remain in the urine (tubular excretion)
78
What is creatinine clearance used for?
Used to assess renal impairment (kidney disease). Impaired creatinine clearance means that elimination is impaired so drugs will stay in the body longer, possibly more intensely.
79
What is enterohepatic cycling?
When drug is released by the liver as bile into the intestines, it may be reabsorbed by the blood to the liver. Drugs of higher MW favoured by bile elimination Reduces elimination and increases t1/2
80
How does metabolism factor into the life of drugs in the body?
Aids in the elimination of drugs from the body (increases clearance, decreased half life) Acts to limit absorption of orally administered drugs.
81
How does metabolism work?
Often removes biological activity but it can also result in active drug (pro-drug) Most follow first order kinetics Usually takes ~5 half lives to remove the drug from the body Drug metabolites are usually more polar than their parent compound. Molecular weight usually increases. The expression of drug metabolizing enzymes differs among tissue type. Ingestion of 2 or more drugs can affect the rate of metabolism in 1 or both drugs.
82
What is the first pass effect?
The rapid inactivation of oral drugs by the liver
83
What are some examples of Phase 1 drug metabolism reactions?
Phase 1: Oxidation, Reduction, Hydrolysis Most drugs go through phase 1 and phase 2 before being eliminated. Lipophilic (absorption) to hydrophilic (elimination)
84
What are some examples of Phase 2 drug metabolism reactions?
Phase 2: Glucuronidation, Sulfation, Acetylation | Interaction between polar and addition of new molecule. Now a conjugated derivative.
85
What are the therapeutic consequences of phase I and phase II metabolism?
Good: Accelerated renal excretion, drug inactivation, activation of prodrugs, decreased toxicity, increased therapeutic action Bad: Increased toxicity
86
What enzymes metabolize hepatic drugs?
Performed by the microsomal enzyme system (P450 system) Consists of 3 families that metabolize drugs (CYP1, 2, 3) and 9 families that metabolize steroids, fatty acids, etc. Has subcategories: MOA, esterases, proteases, amidases
87
What is the most popular CYP enzyme?
CYP 3A4/5
88
What are the critical parts of the P450 cycle for drug oxidation?
Two steps involved with an OH being added to the drug in the end. NADPH, O2, P450 reductase enzyme (flavoprotein) and P450 enzyme (hemoprotein) are critical for the reaction.
89
How do CYP inducers affect drugs?
Allows enzyme to change in response to dyanmic system that can respond to the environment. Increases clearance by the enzyme, making drugs using the enzyme less effective. Ex: Over time phenytoin causes an increased expression level for various CYP450 enzymes Rifampicin induces CYP450 Smoking Binding of a drug to a site on the gene encoding enzyme which turns on synthesis of more enzyme
90
What is a substrate, inducer and inhibitor of CYP3A4?
Substrate: Acetominophen, cocaine and testosterone Inducer: St. John's wort Inhibitor: Grapefruit juice
91
What are some examples of pro drugs?
Morphine, Minoxidil, Procainamide
92
How do enzyme inhibitor drug interactions work?
Drug A blocks the metabolism of drug B. Increases response and half life. Immediate effects. Ex: Cimetidine inhibits several different CYP450 enzymes. Interacts with warfarin, benzodiazepines, morphine, phenytoin. Causes decreased clearance, increased half life and response.
93
What food can reduce the rate of absorption?
Alcohol
94
What do genetic variations of the CYP gene family affect the enzyme?
Expression level, enzyme activity and enzyme induction
95
How do genetic variations of UDP glucoronosyl transferase affect the enzyme?
The activity
96
How do genetic variations of N-acetyl transferase affect the enzyme?
Expression level
97
Are there phenotypes for the CYP enzymes?
There are poor metabolizer (PM), extensive metabolizer (EM) and ultraextensive metabolizer (UM) phenotypes which can cause different types of responses.
98
What is the connection between race and the gentic variability of CYP2D6?
Caucasians have the highest frequency of the PM phenotype. Asians have the highest frequency of the IM phenotype. Africans have the highest frequency of the UM phenotype.
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