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NUR 325 Funds of Pathopharm > Week 1 Pharm Principles > Flashcards

Week 1 Pharm Principles Flashcards

1
Q

Pharmaceutic Phase

A

Dissolution

All oral drugs must go through dissolution in order to be absorbed.

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2
Q

Pharmacokinetic Phase

A

Drug moving through the body and what the body does to the drug

Four processes
• Absorption, Distribution, Metabolism, Excretion

THINK –> GI tract -> blood -> liver -> bile
kidney -> urine

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3
Q

Pharmacodynamic Phase

A
  • What the drug does to the body
    • The action of the drug or mechanism of action (MOA)
    • The intended effect of the drug
    • The therapeutic action
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4
Q

The Phospholipid Layer

A
  • Cell membranes are composed of layers of cells
  • These cells are close together, drugs must pass to get to blood and site of action
  • Membrane structure is phospholipid
  • Drugs must be lipid soluble to pass membrane MOST COMMON
  • Water soluble drugs require passage through channels or pores
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5
Q

First Pass Effect

A
  • Metabolism of drug before systemic circulation
  • % of drug broken down in liver
  • Bioavailability is the amount of drug left after first pass
    * Bioavailability of PO varies (liver has to take some)
    * Bioavailability of IV is 100%
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6
Q

Enteral route

A
  • By way of GI tract (oral/gastric mucosa, small intestine, rectum)
    * EC intended to break down in small intestine NOT stomach
    * First pass effect
    * PO break down starts in stomach, absorbed in small intestine
    * First pass effect
    * SL, Buccal, Rectal all highly vascularized tissue
    * No first pass effect, by-passes liver

CANNOT MAKE PO DRUG RECTAL

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7
Q

Parenteral route

A
  • SQ, IM, IV, intrathecal (into spinal canal), epidural (the space around the spinal cord)
  • IV is the fastest (no barriers to absorption, often irreversible)
  • Does not go through first-pass effect
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8
Q

Topical (transdermal) route

A
  • Application of meds to body surfaces
    * Eyes, skin, ears, nose, lungs

Onset slower, don’t worry about first pass effect

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9
Q

Blood Brain Barrier (BBB)

A
  • Cells in the capillary wall in the brain with very tight junctions that prevent drug passages
  • Only drugs that have a transport system or are lipid-soluble can cross the BBB
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10
Q

What can cross the BBB?

A

Alcohol
Glucose

  • THIS IS NOT FULLY DEVELOPED IN INFANTS
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11
Q

Protein-Binding Effect

A

• Temp storage of drug molecule that allows drug to be available for a longer period
of time
• Drug ratio of bound to unbound (free) molecules varies
• Binding is reversible (a rapid process)

  • Goal: maintain a steady free drug concentration aka Steady State
  • Remember only unbound drug is active and free to exert effects
  • Albumin is the primary plasma protein
  • Drugs bind to protein [albumin]
  • Hypoalbuminemia (ie, malnutrition or liver disease)
    * More free drug is available for distribution to tissue site
    * Possibility of overdose and toxicity
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12
Q

Example: Protein-Binding

A
  • warfarin/Coumadin
    * Drug used to decrease coagulation (blood thinner)
    * Very highly protein bound (97 – 99%), leaves 1 – 3% free to exert effect

• A client with low albumin = less bound Coumadin (inactive) and more free
Coumadin (active)

  • More free Coumadin can exert effect
  • Increased risk of toxicity –> Increased bleeding
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13
Q

Metabolism

A
  • Method by which drugs are INACTIVATED or biotransformed
    * The new structure is called a metabolite
  • Liver is the major site for drug metabolism
    * Converts lipid-soluble drugs into water-soluble metabolites
    * Kidney can excrete these metabolites
    * Cytochrome P-450 enzymes
  • If liver isn’t working, drug can build up, increasing toxicity
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14
Q

Metabolism: CYP450

A

Clinical Significance
• Substrate – if a drug uses the CYP450 system for metabolism
• Pro-drug is a substrate that uses CYP450 to convert to an active form

 * Inducer – speeds up metabolism of the CYP450 system
      * Reduces the amount of drug in the body
      * Reduces therapeutic effect

 * Inhibitor – slows down metabolism of the CYP450 system
      * Increases the amount of drug in the body
      * Increases risk of toxicity
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15
Q

CYP450 Inhibitor Example

A

Grapefruit juice is a known CYP450 inhibitor
“It will stop breakdown of other meds”

 • Taking grapefruit juice with another drug that uses this system increases the 
    amount of drug in body
 • Can lead to toxicity

Teaching point
• Don’t take medications with grapefruit juice
• Avoid eating grapefruit or drinking the juice for 2-4 hours after taking meds

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16
Q

Excretion

A
  • Elimination of drug from the body
    • Generally only hydrophilic (water soluble) drugs can be excreted effectively
  • Kidney is the major site of excretion
    • Through glomerular filtration
    • Tubular secretion
    • Tubular reabsorption
  • Reabsorption and Secretion
    • Some of the drug is secreted, some is reabsorbed

• Important in maintaining a steady state
• Example: 90% of Penicillin G is excreted through the kidney so very little is
reabsorbed so the drug would need to be given more frequently to maintain
steady state

17
Q

Excretion LABS

A

Renal labs

- blood urea nitrogen (BUN) 
- creatinine
18
Q

glomerular filtration rate (GFR)

A
  • Best measure of kidney function
  • Calculated from the creatinine level, age, body size, and gender
  • GFR of drugs is related to free drug concentration in plasma

“Want to look at this first”

19
Q

Half-Life

A

• Serum half-life (T ½) is time required for the serum concentration of a drug to
decrease by 50%

• Takes 5 half-lives for 97% of drug to be eliminated

  • T ½ varies from drug to drug
    * Can be minutes, hours, days, weeks or more
  • Example:
    • Patient is taking a drug with T ½ of 1 week and stops taking
    • It will take about 5 weeks for drug to be gone from system
20
Q

Half-Life: Steady State

A
  • Takes about 4-5 half-lives for “steady state” to occur
    • Goal is steady state
  • Steady state occurs when intake of drug equals amount metabolized/excreted
  • T ½ determines dosing interval, ie QD, QID
21
Q

Half-Life Example

A

• A one time dose of morphine 10 mg is given at 12:00

  • T ½ of morphine is 3 hours
    • At 15:00, 5 mg of morphine is left in body
    • At 18:00, 2.5 mg is left
    • At 21:00, 1.25 mg is left
    • At 24:00, 0.625 mg is left
    • At 03:00, 0.313 mg is left
  • Note after 5 half-lives most of the drug has been eliminated
  • Patient will start feeling pain again about 18:00
22
Q

Around the Clock Dosing (ATC)

A

• Goal is to maintain 50% concentration in body

• Example: Morphine 10 mg given every 3 hours (ATC)
• After about 4 doses there would be a constant level or “steady state” of 5 mg at
all times
• Serum concentration maintained at 50%

  • Used to treat chronic pain
  • PRN ordered for “break through” pain
23
Q

Onset, Peak & Duration definitions

A

Onset – time it takes for drug to elicit therapeutic response (latent period)

Peak – time it takes for drug to reach its maximum therapeutic effect

Duration – time drug concentration is sufficient to elicit a therapeutic response

24
Q

Multiple Effects: Example

A
  • Drug name: metaproterenol
  • MOA: broncho dilator
  • Uses: Acute asthma attack or COPD
  • Adverse Effects: Tachycardia and/or palpitations
  • Multiple Effects:
    • Desired: dilates bronchial passage
    • Not Desired: tachycardia or palpitations
25
Q

Receptors

A

Proteins located on cell surfaces

Chemicals in the body interact with drugs to produce effects
Ex. Hormones, neurotransmitters

These chemicals BIND with the drug = drug-receptor complex

Complex initiates a physiochemical reaction
AGONIST= stimulates/activates
ANTAGONIST= inhibits/blocks

26
Q
A

• A drug that has the ability to INITIATE a desired therapeutic effect by BINDING to a
receptor.

• Example: isoproterenol= beta1 adrenergic AGONIST

• Binds to beta receptors and
causes vasodilation lowering
peripheral vascular resistance

27
Q
A

• A drug that has the ability to INITIATE a desired therapeutic effect by BINDING to a
receptor.

• Example: isoproterenol= beta1 adrenergic AGONIST
• Binds to beta receptors and causes vasodilation lowering peripheral vascular
resistance

WHAT WE WANT TO HAPPEN

28
Q

Antagonist

A

• A drug that produces its action NOT by stimulating receptors but PREVENTING or
BLOCKING or INHIBITING other natural substances (ligands) from binding and
causing a response

  • Examples:
    • ranitidine/Zantac, an H2 ANTAGONIST
      • Blocks release of gastric acid
    • diphenhydramine/Benadryl, an H1 ANTAGONIST
      • Blocks action of histamine
    • propanolol/Inderal, a Beta 1 adrenergic ANTAGONIST
      • Blocks action of epinephrine

BLOCKS

29
Q

Receptor-Less Activation

A

• Not all drug responses involve receptors

• Some drugs act through simple physical or chemical interactions with small
molecules

• Examples:
• Antacids work by neutralizing gastric acidity through DIRECT chemical
interaction
• Magnesium Sulfate works as a powerful laxative by retaining water in the
intestinal lumen through the osmotic effect

30
Q

Narrow therapeutic index [NTI]

A

• NTI have a ratio of lowest concentration at which clinical toxicity commonly occurs

• Therapeutic levels checked to ensure the medication is dosed effectively but avoid
toxicity

• Examples: theophyllin, digoxin, phenobarbital, lithium, coumadin

31
Q

What is a Black Box Warning?

A
  • Required by the FDA for drugs that are especially DANGEROUS
  • Is the strongest safety warning a drug can carry and still remain on the market
  • The boxed warning must appear prominently:
    • On the package insert
    • On the product label
    • On any magazine or other advertising
32
Q

JUST THE FACTS

A

Med errors are the 3rd leading cause of death

33
Q

Processes to Prevent Errors

A
  1. Restrict high-alert drugs and medication routes
  2. Practice drug differentiation. Use of “tall-man” lettering for look-alike drug names. Ex. “HePARin”
  3. Use computerized systems for adm meds
  4. Make patient information readily accesible
  5. Standardize and simplify
  6. Apply reminders
  7. Include the patient in therapy
  8. Don’t use trailing zeros (1 mg)
  9. Use leading zeros (0.25 mg)
34
Q

High Alert Medications

A

In 1995 the Institute for Safe Medication Practices (ISMP) identified these drugs to most likely cause serious harm and death
• Insulin (antidiabetic)
• Heparin (anticoagulant)
• Opioids (pain mgt)
• Injectable potassium chloride (IV KCL)
• Neuromuscular blocking agents
• Chemotherapy drugs

35
Q

How do drug interactions occur?

A
  • Drug- DRUG (CYP450)
    - May be intended
    - May be unintended
    - Increased risk w/ polypharm & NARROW THERAPEUTIC INDEX DRUGS (NTI)
  • Drug- FOOD (grapefruit juice)
  • Drug- HERB
  • Drug- DISEASE (kidneys or liver not working)
36
Q

Drug Interactions that INCREASE Therapeutic Effects

A
  • Additive effects: 2 drugs taken with similar MOA
    • Ex. 2 antibiotics given to treat a complicated infection

• Synergism/Potentiation: 2 drugs with DIFFERENT MOA but result in a combined
drug effect greater than that of either drug alone
• Ex. Coumadin and Aspirin

• Activation of drug-metabolizing enzymes in the liver –> decreases metabolism rate
of the drug (CYP450 system)

• Displacement: Displacement of one drug from plasma protein-binding sties by a
second drug –> increases effect of displaced drug

37
Q

Drug Interactions that DECREASE Therapeutic Effects

A
  • Antidote: drug given to ANTAGONIZE the toxic effects of another drug
    • Ex. naloxone antidote for opioid overdoses

• Intestinal Absorption -> applied to PO medications

  • Activation of drug-metabolizing enzymes in the liver –> enzyme inducers
    • Increased metabolism rate of the drug [quicker out of system]
    • CYP450 system
38
Q

Older Adults and Pharmacokinetic Consequences

A

HEPATIC CHANGES: drugs metabolized more slowly

CARDIAC & CIRCULATORY CHANGES: impaired circulation = decrease distribution
of drugs

Decreased Production of CYP 450 enzymes increased risk for drug interactions can decrease up to 30% in elderly!

RENAL CHANGES: drugs excreted less completely

GASTROINTESTINAL CHANGES: decreased absorption of oral drugs

NUR 325 Funds of Pathopharm (10 decks)

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