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Book of Tables > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Study of drugs

A

Pharmacology

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2
Q

2 main areas of study in pharmacology

A

Pharmacokinetics

Pharmacodynamics

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3
Q

Pharmacokinetics is concerned with?

A

What the body does to the drug, in terms of absorption, distribution, metabolism, and elimination

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4
Q

Pharmacodynamics is concerned with?

A

What the drug does to the body, in terms of agonistic and antagonistic action

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5
Q

Different examples of entral administration

A

Enteral - via the alimentary canal

Orally
Sublingual
Rectal

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6
Q

Different examples of parenteral administration

A

Parenteral - not via the alimentary canal

Inhaled
Injected (intravenously, intraarterial, intramuscular, subcutaneous)
Topical or Transdermal

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7
Q

Medications bind to _____ as they are the most abundant serum protein, and is eventually processed at the ______.

A

Albumin; Liver

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8
Q

Percentage of the drug that reaches the bloodstream

A

Bioavailability

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9
Q

Main site of drug metabolism

A

Liver

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10
Q

Orally administered drugs need to pass through the _____ first.

A

Liver

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11
Q

The effect that describes the need for drugs to go through the liver first, before entering the bloodstream.

A

First pass effect

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12
Q

True or false. Upon reaching the liver, medications are always broken down by the liver enzymes.

A

False. Drugs may also be activated by the liver enzymes. An example is Prodrug, which is an inactive form of Acetaminophen, which only becomes active upon reaching the liver.

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13
Q

Explains why oral drug dosages are usually higher.

a. Bioavailability
b. First pass
c. Half life
d. Drug palatability

A

First pass. As some of the molecules of the drug is broken down, a larger dosage is required to maintain its potency.

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14
Q

Drugs, when stimulating or activating, are called _____. On the other hand, when drugs are blocking or deactivating, they are called _____.

A

Agonist drugs; Antagonist drugs

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15
Q

Main classes of GERD medications

A

Proton Pump Inhibitors
H2 Receptor blockers
Antacids

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16
Q

Inhibits the formation of gastric acid in the parietal cells.

A

Proton pump inhibitors. These medications inhibit the Hydrogen-Potassium-ATPase enzyme (proton pump).

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17
Q

Examples of Proton Pump Inhibitors.

A

-zole

Omeprazole, Pantoprazole, Lansoprazole

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18
Q

H2 Receptor blockers relieve GERD how?

A

Inhibition of H2 receptors decrease the stimulation of Parietal cells, and therefore the release of gastric acid

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19
Q

Examples of H2 Receptor blockers

A

-tidine

Limetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (Pepcid)

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20
Q

Antacids relieve GERD how? Examples of these medications are?

A

By binding to HCl, breaking it down and forming salt and water.

Calcium carbonate (Maalox)
Mylanta
Tums

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21
Q

General mechanism of action of anti-inflammatory drugs.

A

Inhibits Cyclooxygenase (COX).

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22
Q

COX is for the?

A

Protective lining of the stomach (COX1)
Inflammation and pain (COX2)
Pain (COX3)

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23
Q

Non-selective and Selective NSAIDs differ in action and side effects. What is inhibited by each, and what are these side effects?

A

Non-selective NSAIDs inhibit both COX1 and COX2, and side effects include gastric upset, ulceration, and bleeding.

Selective NSAIDs inhibit only COX2, and side effects include cardiac arrest and stroke.

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24
Q

Why are selective NSAIDs taken only as needed (when there is pain) and cannot be used as maintenance medications? Explain the physiology behind it.

A

Because of the more dangerous side effects of cardiac arrest and stroke.

COX2 contains PROSTACYCLINE, which is a vasodilator and anti-coagulant.

COX1 contains THROMBOXANE, which is a coagulant.

Non-selective NSAIDs only have gastric side effects because inhibition of both cause no net change in coagulation, and only result in damage to the lining of the stomach.

Selective NSAIDs, while preserving the lining of the stomach, have more serious side effects as there is increased coagulation. Inhibition of COX2 causes vasoconstriction and coagulation, while the unaffected COX1 also promotes coagulation.

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25
Q

Examples of selective and non-selective NSAIDs

A

Non-selective: Aspirin, Ibuprofen (Alaxan), Ketoprofen, Naproxen (Flanax and Skelan), Mefenamic acid (Advil and Ponstan)

Selective: Celecoxin (Celebrex), Rofecoxib (Arcoxia), Etodolac

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26
Q

Mechanism of corticosteroids.

A

Boosts the immune system by stimulating leukocytes and macrophages.

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27
Q

Endogenous steroids of the body

A

Aldosterone and Cortisol

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28
Q

Examples of corticosteriods

A

-one

Cortisone, Prednisone, Prednisolone

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29
Q

Side effects of corticosteriods

A

Brittle bones and cataracts

Brittle bones occur because of the decrease in vitamin D breakdown, which is essential for calcium uptake.

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30
Q

DMARDs are indicated for patients with?

A

Rheumatoid Arthritis

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31
Q

Mechanism of DMARDs

A

Immunosuppressant

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32
Q

Examples of DMARDs

A

Methotrexate, Azathioprine, Leflunomide, Anakinra

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33
Q

Side effects of DMARDs

A

Increased susceptibility to infections, distress, shortness of breath, nausea, vomiting

34
Q

Muscle relaxants are indicated for patients with?

A

Spasticity

35
Q

2 major categories of muscle relaxants. How are they different?

A

Centrally acting: acts at the level of the CNS

Peripherally acting: acts at the level of the muscle

36
Q

Examples and mechanisms of centrally acting muscle relaxants

A

Diazepam (Valium) stimulates GABA receptors in the brain and increases their inhibitory effect by causing an influx of Chloride ions, resulting in a hyperpolarized state.

Baclofen (Lioresal) inhibits the alpha motor neurons in the spinal cord, which innervate muscles.

37
Q

Examples and mechanisms of peripherally acting muscle relaxants

A

Dantrolene Sodium (Dantrium) inhibits the release of calcium in the sarcoplasmic reticulum

38
Q

General side effects of muscle relaxants

A

Muscle weakness and dizziness

39
Q

Opioid narcotics are only indicated in the presence of?

A

Severe pain

40
Q

Mechanism of Opioid narcotics

A

Stimulates opioid receptors, which release endorphins. Endorphins, in turn, suppresses physical and emotional pain.

41
Q

4 major classifications of opioid narcotics

A

Strong agonists
Mild to moderate agonists
Mixed agonist and antagonist
Antagonist

42
Q

Strong agonists have _____ affiliation to opioid receptors. Examples include?

A

High affinity

Morphine, Hydromorphone, Fentanyl, Meperidine (Demerol)

43
Q

Mild to moderate agonists do not have a strong affiliation to opioid receptors. Examples include?

A

Codeine
Hydrocodone
Oxycodone

44
Q

Mixed agonist and antagonist opioids are used to? Examples include?

A

Decreases dependency and addiction. They initially stimulate opioid receptors, and then block endorphins.

Pentazocine (Talwin)
Butorphanol (Stadol)
Nalbuphine (Nubain)

45
Q

Antagonist opioids are used to? Examples include?

A

Treat overdosage by blocking opioid receptors.

Nal-
Nalmefene
Naloxone
Naltrexone

46
Q

Side effects of Opioid narcotics

A

Euphoria, Dysphoria, Constipation

47
Q

Mechanism of Non-opioid narcotics

A

Inhibits COX3, which mediates pain.

48
Q

Non-opioid narcotics are indicated for?

A

Mild to moderate pain

49
Q

Examples of non-opioid narcotics

A

Prodrug (Phenacetin) - Acetaminophen
Tylenol
Paracetamol
Biogesic

50
Q

Anti-osteoporotic pharmacologic agents are called?

A

Bisphosphonates

51
Q

The mechanism of Bisphosphonates

A

Decreases osteoclast activity and increases the uptake of calcium.

52
Q

Examples of Bisphosponates

A

-dronate

Alendronate (Fosamax)
Residronate (Actonel)
Etidronate (Diaronel)

53
Q

Side effects of Bisphosphonates

A

Muscle weakness (increased Ca), gastric irritation, and esophageal lesions

54
Q

Mechanism of ACE inhibitors

A

Blocks the Angiotensin Converting Enzyme, thereby:

Decreasing Angiotensin II (potent vasoconstrictor)
Decreasing Aldosterone (anti-diuretic)
Breakdown of Bradykinin (vasodilator)

Results in decreased load to the hear via vasodilation and decreased peripheral resistance following a decrease in blood volume

55
Q

Examples of ACE inhibitors

A

-pril

Cunipril
Captopril
Phosinopril

56
Q

Mechanism of Digoxin (Digitalis, Lanoxin)

A

Causes an influx of sodium in the myocardium, increasing the strength of contraction.

Mainstay drug for CHF

57
Q

Mechanism of Diuretics

A

Adheres to the tubules of the kidneys and prevents water reabsorption. This decreases blood volume, and therefore blood pressure.

58
Q

Diuretics are also known as?

A

Water pills

59
Q

Examples of Diuretics

A

-ide

Thiazide
Furosemide (Lasix)
Bumetanide (Bumex)

60
Q

Mechanism of Calcium Channel Blockers

A

Inhibits the influx of calcium in the myocardium during phase 2, as well as influx in the blood vessels. Causes a decrease in HR and blood vessel tone (vasodilation)

Prevents arterial vasospasm and increases cellular metabolic rate, resulting in decreased myocardial oxygen demand and increased myocardial oxygen supply.

61
Q

Examples of Calcium Channel Blockers

A

-dipine

Amlodipine
Felodipine
Nisoldipine
Verapamil

62
Q

Location and action of Alpha and Beta receptors

A

Alpha receptors are located throughout the body in the blood vessels (action is more peripheral). Beta receptors are located in the heart and lungs (action is more central)

A1 is for vasoconstriction
A2 is for vasodilation

B1 is for increasing HR
B2 is for bronchodilation

63
Q

Which type of Beta-blocker cannot be given to patients with COPD

A

Non-selective

This is because these drugs block both B1 and B2 receptors. Inhibition of B2 results in bronchoconstriction, which is dangerous for patients with COPD. Severe DOB can result.

64
Q

Examples of non-selective beta blockers

A

-olol

Propanolol
Nadolol
Pembutolol

65
Q

Examples of selective beta blockers

A

-olol

Metoprolol
Atenolol

66
Q

Examples of alpha blockers

A

-zosin

Terazosin
Dexazosin
Prazosin
Teradexaneprazosin

67
Q

Alpha blockers inhibit which type of receptor?

A

Alpha 1 receptors for vasoconstriction, resulting in vasodilation and decreased blood pressure

68
Q

Mechanism of Anti-angina drugs

A

Stimulates nitric oxide and hemoglobin

Nitric oxide, being carried by hemoglobin, causes blood vessels to dilate as they pass through. Vasodilation reduces chest discomfort.

69
Q

2 types of Anti-angina drugs

A

Nitroglycerin and Isosorbide Dinitrates

70
Q

Nitroglycerins include?

A

Nitrates, Nitrostate, Nitrobid

71
Q

Isosorbide dinitrates include?

A

Isordyl, Isorbid

72
Q

General side effects of anti-hypertensives

A

Postural hypotension, dizziness

73
Q

General side effects of anti-angina medications

A

Postural hypotension, dizziness

74
Q

Difference in mechanism of anti-coagulant medications Warfarin (Coumadin) and Heparin (Carmin)

A

Warfarin is administered orally and acts as an antagonist to vitamin K, which is essential in the production of clotting factors 2, 7, 9, and 10

Heparin is administered intravenously and inhibits the clotting factors themselves.

75
Q

Name the human clotting factors

A 
1 - Fibrinogen
2 - Prothrombin
3 - Thromboplastin
4 - Calcium Ion
5 - Labile (Proaccelerin)
7 - Stable
8 - AHF-A (Classic)
9 - AHF-B (Christmas)
10 - Stuart
11 - AHF-C
12 - AHF-D (Hageman)
13 - Fibrin Stabilizing Factor
76
Q

Intrinsic (contact) pathway of clotting

A

Damage to blood vessels

Activates factors 12, then 11, then 10

Factor 10 acts with Factor 9 to activate Factor 2 (Prothrombin), then 1 (Fibrinogen), then 13

77
Q

Extrinsic (tissue) pathway of clotting

A

Damage to muscles and blood vessels

Activates factors 3, then 4, then 5, then 7, then 8, then 9

Factor 9 acts with Factor 10 to activate Factor 2 (Prothrombin), then 1 (Fibrinogen), then 13

78
Q

Examples of anti-platelet drugs

A

Aspirin
Ticlodipine
Ticlip
Clopidogrel (Flavix)

79
Q

Side effects of anti-coagulants and anti-platelets

A

Increased bleeding, hematuria, ecchymosis

80
Q

Aside from osteoporosis, what are the other significant side effects of prolonged corticosteroid use?

A

Muscle wasting, cataracts, increased BP (secondary to water and sodium retention), hyperglycemia, skin breakdown, and adrenocorticosuppression.

Book of Tables (14 decks)

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