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ATTH 5100 > Drugs & Pharmacology In Sport > Flashcards

Drugs & Pharmacology In Sport Flashcards

1
Q

Why shouldn’t you give anti-inflammatory ex in the first 24 hours after a significant sprain?

A

Anti-inflammatory works in brain for pain, but decreases inflammation and decreases fever. Anti-inflammatories affects platelets because it will decrease clotting.

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2
Q

Name some problems that can come up when using supplements.

A
  • can be contaminated
  • can be wrong dose if not regulated
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3
Q

Why are platelets essential post injury?

A

Bleeding creates a cast around the injury, but we tend to over bleed. The body needs to get rid of this.

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4
Q

4 different ways that drugs are named:

A
  • chemical
  • generic (ex. Acetaminophen, ibuprofin)
  • trade names (ex. Tylenol, Motrin, Advil)
  • generic drug (has something in front of generic name ex. Apo-doxycycline)
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5
Q

3 ways to classify drugs:

A
  • chemical structure
  • mechanism of action (ex. Beta blockers)
  • legal classification of drugs (OTC vs prescription vs controlled substances)
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6
Q

What is the Food and Drugs Act (2020)?

A
  • overarching legislation for food, drugs, cosmetics, and therapeutic devices (including general rules and advertising)
  • part 1: food, drugs, cosmetics and devices
  • part 2: administration and enforcement
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7
Q

What are the steps for drug approval?

A
  1. Preclinical testing (animals)
  2. Phase 1: clinical trial (healthy humans)
  3. Phase 2: clinical trial (test efficacy, side effects)
  4. Phase 3: clinical trial (efficacy, safety)
  5. Health Canada Process
  6. Phase 4: Clinical trial (post market surveillance)
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8
Q

What schedule drugs are now deleted due to change in legislation?

A
  • schedule 5: propylhexedrine (stimulant)
  • schedule 7: cannabis over 3 kg
  • schedule 8: cannabis small amounts
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9
Q

What are schedule 1 drugs?

A
  • narcotics
  • cocaine
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10
Q

What are schedule 2 drugs?

A

Cannabis related

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11
Q

What are schedule 3 drugs?

A
  • narcotic-like
  • LSD
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12
Q

What are schedule 4 drugs?

A

Barbiturates

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13
Q

What are schedule 6 drugs?

A

Precursors

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14
Q

What are schedule 9 drugs?

A

Device to make pills or other medication

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15
Q

Define pharmacodynamics.

A
  • effects of drug on the body
  • mechanism of action (eg. Activation or blockage of cellular receptors)
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16
Q

Name some examples of mechanisms of action for drugs.

A
  • inhibiting uptake, synthesis, storage
  • increasing release
  • blocking transmitter inactivation
  • inhibiting enzymes
  • inhibiting transport processes
  • activating (agonist) or blocking (antagonist) receptors
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17
Q

What is the dose-response curve?

A

As we increase dose, the response increases until the response can’t go any higher. This is the case for almost every drug.

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18
Q

Define placebo.

A
  • a therapeutic or adverse reaction that is not due to a pharmacological effect of the drug
  • may be due to physiological reaction in anticipation (eg. Hormone release)
  • commonly only subjective symptom response
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19
Q

Name and describe 3 multiple drug effects:

A
  • additive (eg. 2 hypertensive medications)
  • synergistic (effect is greater than additive, ex. 10+10 = 30)
  • antagonistic (effect produces less of an effect - ex. Naloxone)
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20
Q

Name 4 Adverse Drug Reactions (ADRs):

A
  • side effects/sensitivities (not the same as allergies)
  • overdose toxicity (taking a drug above its therapeutic range)
  • allergic reactions
  • drug interactions
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21
Q

Describe organ adverse reaction.

A
  • usually issue around cytotoxicity
  • liver (ex. acetaminophen)
  • kidney (NSAIDs)
  • liver, gut, heart (alcohol)
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22
Q

Why do some athletes need to be careful about taking anti-inflammatory ex around weigh in time?

A

They may retain water if they are using it for the first time

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23
Q

Define pharmacokinetics.

A
  • how the body deals with the drug
  • study of the time course of a drug and its metabolites in the body after administration by any route
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24
Q

What are the 4 steps of pharmacokinetics?

A
  1. Absorption
  2. Distribution
  3. Biotransformation
  4. Excretion
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25
Q

Describe drug absorption.

A

Process of drug movement from the administration site to the systemic circulation

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26
Q

Name some different routes of administration.

A
  • oral (swallowed, sublingual, buccal)
  • topical (eyes, ears, nose, skin (transdermal))
  • vaginal, rectal
  • injection (IV, IM, SQ, intra-articular, intra-cardiac)
  • inhaled
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27
Q

Why would you not want to take some drugs orally?

A

Some drugs taken orally will be completely broken down in stomach, needs to be taken otherwise.

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28
Q

When would you use intravenous (IV) injection for a drug?

A
  • want a big drug to work fast
  • often done in the hospital setting
  • risk of infection
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29
Q

What can you do if an oral drug cannot be taken because they are not awake?

A

Can be given rectally

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30
Q

Pros and cons of oral route of administration.

A
  • convenient
  • not in a rush
  • can have side effects more than other routes
  • may need increased doses vs other routes
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31
Q

When would you take a drugs sublingually?

A
  • small dose/pill that is absorbed very quickly
  • ex. Ativan to calm someone down
  • membranes are very thin under the tongue
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32
Q

Name some factors that can affect absorption.

A
  • solubility, particle size
  • concentration
  • circulation to the site of administration (increased with movement)
  • surface area at the site of administration (determined by the route of administration)
  • exercise - decreases gut blood flow, increases blood flow to muscle and skin
  • ice (slow down) vs massage (speed up) of area where drug is applied
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33
Q

Name some factors that affect oral absorption of a drug.

A
  • formulation (tablet, liquid, delayed release)
  • stability to acid and enzymes
  • motility of gut
  • food in stomach (can delay or stop absorption)
  • degree of first-pass metabolism
  • lipid solubility
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34
Q

Why can taking anti-inflammatories continuously cause ulcers?

A

Anti-inflammatories stop mucus production so that the lining is not protected.

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35
Q

Define bioavailability.

A

Extent to which - and sometimes rate at which - the active moiety (drug or metabolite) enters systemic circulation, thereby gaining access to the site of action. How the blood gets to where it can be used.

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36
Q

What is the first pass effect?

A

Drugs taken orally that are subjected to hepatic clearance before entering the systemic circulation.

37
Q

Describe the 6 steps of the first-pass effect.

A
  1. Drug is taken orally.
  2. Drug enters GI tract.
  3. Active drug is absorbed from stomach and small intestines.
  4. High blood concentration of drug is in hepatic portal vein.
  5. Low blood levels after passing through liver (drug metabolized in liver).
  6. Drug goes to inferior vena cava, right side of the heart, then lungs, left side of heart, then aorta, then to the rest of the body.
38
Q

How does exercise effect oral absorption?

A
  • heavy exercises decreases gastric emptying.
  • If drug is absorbed in duodenum, it will not get absorbed well.
  • light exercises increases gastric emptying
  • exercise decreases blood flow to the gut because the blood goes to the muscles. Decreased absortion of drug in gut if taken before exercise.
39
Q

After administration, the drug is distributed via what fluids?

A
  • interstitial fluids
  • cellular fluids
  • if you don’t have blood supply to the area you need the drug, you won’t get the drug.
40
Q

Describe how distribution of drugs depend on the type of tissue.

A
  • first minute: heart, kidney, brain (biggest distribution of blood unless shunting due to exercise)
  • several minutes to hours: muscle, skin, fat, other internal organs
41
Q

What is the limiting factor in distribution of drugs?

A

Pattern of blood flow

42
Q

Describe 2 physiological factors affecting drug distribution.

A
  • cardiac output (poor SV, slow HR = slower distribution)
  • local blood flow (blood-brain barrier, local capillary structure, placenta - lipid soluble drugs cross more readily)
43
Q

Name 4 physiochemical factors affecting distribution.

A
  • permeability
  • lipid solubility
  • binding to plasma proteins
  • accumulation in tissues (ex. Marijuana, THC in fat)
44
Q

Describe bound vs free drugs.

A
  • drugs that are bound to albumin cannot leave the blood vessel and go where it needs to go.
  • free drugs are able to go out of the blood vessel.
45
Q

What is biotransformation?

A
  • metabolism, process of how we get rid of drugs
  • conversion by enzymes to more polar (less lipid soluble) forms
  • occurs in the smooth endoplasmic reticulum of cells in the liver (can occur in kidney and intestine)
46
Q

Describe phase 1 reaction in biotransformation.

A
  • conversion to polar metabolite through oxidation, reduction, and hydrolysis
  • effects are: inactivation, reduction of activity, or increased activity (rare)
47
Q

Name an example of a drug converted into a more active form.

A

Codeine (less effective) converted to morphine (more effective).

48
Q

Describe phase 2 reaction in biotransformation.

A
  • conjugation: coupling of drug (or its polar metabolite) with an endogenous substance
  • effects: same as phase I (inactive, partial inactivate, increase)
49
Q

Name 3 factors affecting biotransformation:

A
  • genetic (mutation leading to gene deletion)
  • environmental (drug interactions)
  • physiological (ex. Liver disease / cirrhosis)
50
Q

Name one common drug interaction.

A

Grapefruit juice and birth control: takes away hormones faster than you want, may affect how effective birth control is.

51
Q

Describe drug excretion.

A
  • unchanged drug or polar metabolites
  • urine, feces, bile, sweat, exhalation
  • primary mechanism via urine/kidneys
  • exercise - decreases blood flow to kidneys and gut, decreased urine output resulting in decreased renal clearance - drugs may have a longer effect
52
Q

How does exercise effect renal excretion?

A
  • decreases renal blood flow
  • increases urinary pH
  • decreases renal clearance
  • change in reabsorption of drugs
  • transient proteinuria, hemoglobinuria (high intensity) - some people have blood in pee after marathons
53
Q

Why are elimination kinetics important?

A

Because drugs need to be dosed at the right time and right amount

54
Q

What is zero order of elimination kinetics?

A

A constant amount of drug is eliminated per unit of time (saturation occurs)

55
Q

What is 1st order of elimination kinetics?

A

A constant fraction of the drug is eliminated per unit of time

56
Q

What is 2nd order or multi-exponential elimination kinetics?

A

May vary with time and dose (not specific zero or 1st order)

57
Q

Define pharmacogenetics.

A
  • Genes and the body : drug interaction
  • different people metabolize drugs differently, perhaps at different rates
58
Q

Define clinical pharmacokinetics.

A

The specific quantitative pharmacokinetic properties of a drug determine its dosing schedule, dose and means of administration

59
Q

Dosing schedule depends on what 2 factors?

A
  • therapeutic window
  • kinetics
60
Q

What is the lower and upper limit of the therapeutic range (window)?

A
  • lower limit: concentration that produces half the greatest possible effect - needs to be greater than 5% of patients
  • upper limit: no more than 5-10% of patients experience a harmful side effect
61
Q

Why is dosing schedule important with anti-inflammatories?

A

Giving a second dose before it hits subtherapeutic range to have a constant amount of the drug is important because if inflammation comes back in between, it will do nothing for the inflammation.

62
Q

What is IC50?

A

Half maximal inhibitory concentration

63
Q

MTD/MTC stands for:

A

Minimum toxic dose

64
Q

MED/MEC stands for:

A

Minimum effective dose

65
Q

Name 2 drugs with narrow therapeutic windows.

A
  • coumadin
  • lithium
66
Q

Name 2 drugs with wide therapeutic windows.

A
  • some antibiotics (Penicillin)
  • some anti-inflammatories (ibuprofen)
67
Q

Rate of input =

A

Rate of loss

68
Q

Dosing and frequency is related to what 3 factors?

A
  • bioavailability
  • clearance
  • volume of distribution
69
Q

What is drug half life (t 1/2)?

A
  • time required for the plasma concentration of the drug to be reduced by half
  • generally drugs that are given intermittently are given at the t 1/2 interval. Too soon = side effects. Too late = subtherapeutic.
  • steady state occurs in approximately 3 doses
70
Q

What is tolerance?

A
  • diminished response to drug overtime
  • must increase dose to get the same effect
  • develops slowly
  • cross tolerance with other agents in same class
71
Q

How does tolerance develop?

A
  • enzyme induction: increase enzyme quantity vs increase rate of metabolism
  • change in # of receptors (up regulated)
  • change in affinity of the receptor for the drug
  • decreased responsiveness at the receptor
72
Q

What is the difference between tolerance and addiction?

A
  • tolerance is physiological, diminished action of the drug.
  • addiction is a bio psychological process that results in repeated use of drug/behaviour despite harm to oneself and/or others
73
Q

What are reasons for patient non adherence with drugs?

A
  • cost
  • forgetfulness
  • inconvenient (4x/day vs 2x/day)
  • poor patient education (some people aren’t told that some drugs don’t work without regular dosing)
74
Q

Why does dosage change with age?

A
  • physiology changes with age
  • child cannot metabolize drugs as quickly
  • elderly may have sensitivity. May need dosing changes for organ changes (liver, kidney function)
75
Q

Describe the absorption of alcohol.

A
  • occurs in GI track by simple diffusion (small size)
  • 70-80% in duodenum and jejunum
  • delayed if food in stomach
76
Q

Describe the distribution of alcohol.

A
  • areas with high blood flow rapidly reach equilibrium (brain, heart (toxic), lungs, liver)
  • 4% into fatty tissues
  • volume of distribution less for women than for men (depends on % body fat)
77
Q

How is alcohol eliminated?

A
  • principle elimination is by oxidation to CO2 and H2O
  • <1% in urine
  • 1-3% in lungs
  • 90-95% in liver oxidation
78
Q

How is alcohol metabolized?

A
  • ethanol converted to acetaldehyde with ADH (alcohol dehydrogenase)
  • metabolized in the liver (cytosol)
  • first pass effect
79
Q

Describe alcohol oxidation.

A
  • acetaldehyde converted to acetate with ALDH (Aldehyde dehydrogenase)
  • oxidation occurs in mitochondria
  • acetate released to blood - oxidized to CO2
  • since enzymes are involved, there is potential for genetic variation
80
Q

Describe the clinical effects of alcohol.

A
  • CNS depressant
  • diuretic
  • toxic effects on muscle, heart, brain (cerebellum), liver
81
Q

50-100 mg/dl of alcohol causes what effect?

A

Incoordination

82
Q

150-200 mg/dl of alcohol causes what effect?

A

Increase reaction time

83
Q

200-300 mg/dl of alcohol causes what effect?

A

Nausea/vomit/ataxia

84
Q

> 400 mg/dl of alcohol causes what effect?

A

Coma/respiratory failure/death

85
Q

Alcohol dehydrogenase operates 5x normal in what populations? What effects are seen?

A
  • 85% Asian populations, 5-10% English, 20% Swiss
  • acetaldehyde accumulates resulting in vasodilation, facial flushing, bronchospasm and tachycardia.
86
Q

Aldehyde dehydrogenase-2 deficiency occurs in what populations? What effects are seen?

A
  • 50% Asian populations
  • increase acetaldehyde - stops the conversion to acetate (facial flushing, tachycardia, diaphoresis, muscle weakness)
87
Q

What is the difference when prescribing pills for codeine and morphine?

A
  • dosing: 14-45 mg q 6 hours for codeine. 5-15 mg q 4 hours for morphine.
  • time to effect: 30+ minutes for codeine. 15+ minutes for morphine.
  • duration: 4-8 hours for codeine. 3-6 hours for morphine.
88
Q

Dosing issues with codeine:

A
  • up to 10% of caucasians are rapid metabolisers (faster action, increase dose systemically)
  • up to 10% of Caucasians are poor metabolisers
89
Q

Symptoms of opioid intoxication and overdose:

A
  • slurred speech, drowsy, confusion
  • pinpoint pupils
  • breathing problems, apnea
  • cyanosis
  • cold, clammy skin
  • slowing heart beat
  • unconscious
  • vomit, seizures

ATTH 5100 (13 decks)

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