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Pharm Exam 1 > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

DEA regulating how NPs prescribe vs state

A

DEA tells us about controlled substances
- what schedule the drug belongs to

STATE- regulates medications and who can prescribe within the state

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2
Q

Clinical trial process

A
  • process of making a new drug
  • has to be approved by FDA

Preclinical: testing on animals (monitor toxic effects, efficacy, reactions)
-after data collected in animals, then application sent tonFDA for approval to continue to clinical trials
Clinical trials:
-phase 1: 20-100 healthy people- testing absorption, distribution, metabolism and elimination. Most effect dose and routes are determined- focuses on safety
-phase 2: hundreds of patients with disease get drug and test same as phase 1
-phase 3: DFA approval needed then double blinded study with thousands of people
-phase 4: post market DFA approves drug (monitor long term effects. Compare to similar drugs on market)

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3
Q

Imp qualities for a conscientious prescriber?

A

Trust, open communication, polypharmacy, vitamins, holistic assessment, allergies, pregnant

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4
Q

Pros vs cons prescribing medications vis EMR vs paper

A

EMR:
Pros- ready at pharmacy, easy to read, catches drug interactions, present normal dosages to pick from
Cons- call if mess up, need script for schedule 2

Paper:
Cons- handwriting, lose it, wait at pharmacy, can’t track

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5
Q

Side effect vs adverse effect

A

Side effect: expected, secondary unwanted effect occurs d/t drug therapy. Ex/N/V

Adverse effect: unintended pharmacological effect when medication administered correctly
Ex: anaphylactic, rash

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6
Q

Pharmacodynamics

A

What the drug does to the body

A set of processes by which drugs produce specific biochemical or physiologic changes in the body

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7
Q

Can a drug create an effect?

A

No. It can speed up and slow down something that is already occurring in the body

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8
Q

What can effect pharmacodynamics?

A 
Age
Gender
Ethnicity 
Weight
Potency of drug
Liver/kidney fnc
Genetics
Nutrition
Diet
Route
Pharmacogenomics
Disease
Drug-drug competition
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9
Q

Ligand

A

Any chemical, endogenous or exogenous, that interacts/ binds to a receptor

Exogenous (purely drugs- body doesn’t make them)
Ex: medications, hormones

Endogenous (exist in the body)
Ex: hormones, neurotransmitters

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10
Q

Agonist vs antagonist

A

Agonist: binds to receptor, memetic effect, affinity and efficacy

Antagonist : binds to receptor with affinity but no efficacy

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11
Q

Full agonist
Partial agonist
Inverse agonist

A

Full: maximum effect with a few receptors activated ex albuterol

Partial: produce submaximal effect- all receptors are activated but not getting full effect
Ex: subaxone decrease pain but not getting high

Inverse: binds to the same receptor sites but gives opposite effect

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12
Q

Antagonist types

A

Antagonist: has affinity but no efficacy ( binding but no affect)
Ex: beta blockers

Chemical antagonist; drug forms with a bond with a second drug making it unavailable for interaction

Competitive: both ligands go to the active site- one will have more affinity and therefore bind to the receptor leaving more free drug of the other less affinity

Non competitive (allosteric): binds to a different site other than the active site, changing the active site and not allowing the effect

Physiologic: drug produces opposite affect through different pathways

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13
Q

Synergism

A

Taking two drugs to make a greater effect. Important because we can prescribe two drugs together that can lead to positive or negative effect

Ex: oxycodone and Tylenol
Ex: aspirin and Coumadin

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14
Q

Four types of receptors

A

1) G-protein coupled
2) Gated ion channel
3) enzyme linked receptors
4) intracellular receptors

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15
Q

G-protein coupled receptors

A

-most common
-requires second messenger
-transmembranous
-interact with a Ligand and receptor to produce conformational change in the function of the cell
Ex: beta blockers

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16
Q

Gated ion channel receptors

A
  • Bind to generate an action potential,
  • open and close to allow certain ions to pass through (effect pos/ meg charges)
  • only first messenger

Ex: lidocaine

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17
Q

Enzyme linked receptors

A
  • cytokines, tyrosine kinase activated
  • transmembranous
  • substrate binds to receptor which binds to enzyme causing action
  • limited by down regulation

Ex: insulin

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18
Q

Intracellular receptors

A

-second messenger
- goes through membrane to attach
-lipid soluble
Ex sex hormones, glucocorticoids

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19
Q

Affinity

A

Binding strength to receptor

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20
Q

Efficacy

A

Max affect the drug will have on the body

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21
Q

Potency

A

Amount of drug needed for an effect, more morphine than diluadid to reach same effect
-concentration of drug you need minimal 60% of dose reach effect

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22
Q

Which ligand has affinity but no efficacy?

A

Antagonist

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23
Q

Selectivity vs specificity

A

Selectivity : ligand will have more affinity toward a receptor (ex alpha and beta receptors)

Specificity : lock and key, receptor can only accept certain ligands

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24
Q

How would you order the steps for signal transduction?

A

1) a ligand binds to the cell surface receptor
2) the receptor activates a protein at the cell membrane
3) the second messenger molecule is released
4) final target causes response

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25
First messenger
Starts the signal process from the Cell surface- passes a message to the second messenger
26
Second messenger
-don’t always use one - message is sent to the cell and causes the movement and signal to do the work on the inside of the cell- amplify the signal Ex: cyclic AMP, calcium ions
27
Are second messengers usually required for hydrophilic it lipophilic ligands ?
Hydrophilic
28
Therapeutic index
Related the dose of a drug require to produce a desired effect to that which produces an undesired effect
29
Drug has a low therapeutic index
You need to watch closely, Increased risk for toxicity and adverse effects Ex Coumadin INR between 2-3
30
Drug has high therapeutic index
Safer drug. More room for error, less monitoring
31
Upregulation
Cell receives a weak signal from repeated administration of drug “Famine” not enough insulin for the amount of receptors, receptors working hard, call in help (add more receptors)
32
Down regulation
Body will absorb receptors because they aren’t doing anything. Causes harder time finding receptors, more breakthrough pain meds causing drug tolerance, reduces sensitivity to a message Plenty of ligand available to receptor, so receptors get lazy and decrease
33
What happens if you stop a beta blocker?
Upregulation and rebound hypertension
34
Pharmacokinetics
- what the body is doing to the drug - absorbed> distributed and metabolized > excreted - factors affecting pharmacokinetics: age, pregnancy, hepatic/renal diseases, drug interaction, nutritional status
35
Four pharmacokinetic processss
Absorption Distribution Metabolism Elimination/excretion
36
Absorption
-rate at which drug leaves a site of administration and passes to systemic circulation
37
Distribution
How the compound is distributed around the body and it’s propensity to accumulate in certain tissues and organs
38
Metabolism
How the body breaks down the compound by the liver (in first pass) Key issues: drug-drug interactions and effects of metabolites on other chemicals
39
Excretion
The rate and process through which the compound exits the body
40
Bioavailability
Amount of drug that gets into the bloodstream by absorption (fraction of unchanged drug) If it is metabolized proportion to bloodstream then there is no drug that will work on your body
41
First pass
Oral medication does to the liver and then it gets to side of action The amount that is still not metabolized to work on the body after first pass (goes through liver) Enteral and some suppositories
42
How is bioavailability impacted by route of administration?
PO has decreased amount that is available IM, sub q, subinguinal, iv, intranasal less breakdown before working
43
Suppository
Doesn’t go right into bloodstream- no guarantee it doesn’t go through first pass effect- depends on how far up the suppository goes If asked what bypasses first pass don’t include rectal!
44
What are the characteristics of a drug that would make it easier to pass through the cell membrane into the cell?
Weak acid/weak base/ non ionized | Lipophilic
45
What are the characteristics of a drug that would make it more difficult to pass through the cell membrane into the cell?
Size, ionized, hydrophilic
46
Passive diffusion
No energetic used to go from area of higher concentration to area of lower concentration
47
Active transport
Energy needed to go from area of lower concentration to area of higher concentration
48
Drug trapping
when a patient overdoses, you can trap the drug in the urine. If it’s acidic you trap with a base (HCO3). If it’s a base, you trap with an acid (ammonium)
49
Properties of a drug that has a large volume of distribution
Predict where drugs go, dose based on disease state The drug will concentrate in the tissues with large volume of distribution ( lipophilic, small molecular weight, absorb well)
50
Properties of a drug that has a small volume of distribution
The drug will concentrate in the plasma with small volume of distribution
51
How does renal and liver disease impact volume of distribution?
Renal: decrease ability to metabolize the drug so drug is accumulated in tissues, increase fluid with disease Liver: more active free drug, decreased albumin, increase toxicity
52
Albumin
Major protein in the body that drugs bind to. Take a drug and it is absorbed, the proteins carry it around, not all of it will work at once because the body needs to maintain homeostasis. Drug binds to the protein to transport across the body and is stored by protein until it is needed. 95% protein bound means 5% of drug is actually having and affect in the body.
53
What may Halle. If you give a patient two drugs that are highly protein bound?
Drug A 95% protein bound, drug b 98%- drug b has higher affinity for that receptor so drug a will be more effective and more toxic Because you have more free drug If both drugs are same % protein bound then nothing will change in the drugs and they will work normally
54
What Medication routes avoid first pass?
Everything besides oral and suppository
55
Phase 1
CYP 450 Where the drug is converted to a drug that is more easily to excrete/water soluble Induction and inhibition
56
Induction
Decreases the effect the of the substrate Drug A substrate Drug B inducer drug A will decrease effect
57
Inhibition
Increases the effect of the substrate | Drug A substrate Drug B inhibitior drug A will increase effect
58
Prodrug
When an inactive drug becomes active when reacting with phase one enzyme CYP 450 Ex codeine to morphine
59
What organs are involved with excretion?
``` #1 kidney Stool, skin, bile, lungs, sweat, salivary glands, hair ```
60
Characteristic of a drug that makes it easier to excrete?
Hydrophilic drug You can’t excrete protein bound drugs- the drug stays attached to the protein so it travels and stays in the body
61
What can occur as the drug goes through the proximal tubule, loop of henle, and distal tubule?
Reabsorbed, excreted and site of effect by diuretics
62
Clearance
Is the final element in the elimination process!! Most imp factor in determining drug concentration b/c everyone absorbs medication differently If you aren’t clearing the drug, you can become toxic
63
Half-life
Time it takes the body to get rid of 50% of drug under normal circumstances
64
Things that can impact half life
Disease Weight Metabolism
65
How many half life’s does it take to get to steady state?
5
66
How many half lives to no longer have a therapeutic benefit of a drug once d/c?
5
67
Steady state
Dose= clearance | OptimAl state of medication in the blood
68
Slow metabolizer
Your body takes a longer time for certain enzymes to process the drug so you need a lower dose than a normal(extensive) metabolizer
69
Ultra-rapid metabolizer
Your body metabolized the medication quicker so you need to increase the dose or frequency, or change the medication
70
Schedule 1
High abuse potential Not FDA approved Not prescribed Ex marijuana, ecstasy, lsd, heroin
71
Schedule 2
DEA #, hard copy, no refills, high potential for abuse Narcotics and stimulants Morphine, fentanyl, oxy, methadone, hydro morphone, amphetamine, adderall
72
Schedule 3
Tylenol with codeine, less abuse risk
73
Schedule 4
Benzos (lorazepam, tranadol)
74
Schedule 5
Low potential | Robuttussin with Codie e
75
You prescribe a medication for a patient that is typically highly protein bound. The patients albumin is 2.5. In terms of drug availability , what would you do?
Decrease the dose of the medication Low albumin won’t bind to the drug which will cause a toxic effect, lowering the drug dose will decrease the risk for toxicity
76
T/f a high degree of plasma binding can result in restricted drug distribution.
True Only unbound portion of drug is distributed
77
When drugs have been metabolized and each the kidney tubule. If the drug is ionized and lipophobic, the drug will tend to
Be passively eliminated in urine
78
What info do you need to calculate creatine clearance?
Age, sex. Weight, serum creatine
79
Generic name vs trade name
Generic: not capitalized ex acetaminophen Trade: capital ex Tylenol
80
Volume of distribution
The measure of the apparent space in the body available to contain a drug Predicts concentrations, absorption, and accumulation Larger -tissues Smaller- plasma
81
Grapefruit juice
Inhibitor
82
What do you give if acidic overdose
Sodium bicarbonate
83
What do you give if basic overdose
Ammonium chloride
84
T/F lipophilic will pass easily through the blood brain barrier
True
85
Generic vs trade name
Generic: not capitalized ex acetaminophen Trade: capitalized ex Tylenol

Pharm Exam 1 (1 decks)

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