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Pathophysiology & Pharmacology > Drugs For Treating Inflmmation > Flashcards

Drugs For Treating Inflmmation Flashcards

1
Q

Cardinal Signs of Inflammation

A
  • Remember that these are all caused by chemical mediators produced during inflammation.
    ~ Redness
    ~ Heat
    ~ Swelling
    ~ Pain
    ~ Functional Loss
  • Body’s reaction to:
    ~ Cell death
    ~ Cell injury
    ~ Exposure to allergen/pathogen
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2
Q

Effects of Bradykinin

A
  • Binds to the mast cells found in the connective tissues as well as basophils and platelets in the blood causing a release of histamine.
    ~ Allergen/Pathogen binding to mast
    cell receptors has the same effect.
  • Causes activation of the enzyme phospholipase A2.
    ~ Mobilizes arachidonic acid from cell
    membranes.
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3
Q

Metabolism of Arachidonic Acid

A
  • After being mobilized by phospholipase A2, arachidonic acid is metabolized within the cell.
  • 2 enzyme pathways metabolize arachidonic acid
    ~ Cyclooxygenase (COX) - produces
    prostaglandins and thromboxanes.
    ~ Lipoxygenase - produces
    leukotrienes.
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4
Q

Chemical Mediators of Inflammation

A
  • Bradykinin
    ~ Vasodilation/Increased Vessel
    Permeability
    > Contributes to Edema/Increased
    Heat/Redness
    ~ Stimulates Pain Receptors
  • Histamine
    ~ Vasodilation/Increased Vessel
    Permeability
    > Contributes to Edema/Increased
    Heat/Redness
    ~ Stimulates Pain Receptors
  • Prostaglandins
    ~ Vasodilation/Increased Vessel
    Permeability
    > Contributes to Edema/Increased
    Heat/Redness
    ~ Stimulates Pain Receptors
  • Leukotrienes
    ~ Vasodilation/Increased Vessel
    Permeability
    > Contributes to Edema/Increased
    Heat/Redness
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5
Q

NSAIDs and Aspirin

A
  • Both affect the COX pathway to exert their drug actions
  • COX-1 V. COX-2
    ~ Two different forms of COX enzyme.
    ~ Both have similar effects.
    > Result in the production of TXs &
    PGs
    > COX-1 - produced at a constant
    level in all cells to maintain
    normal levels of TXs & PGs.
    > COX-2 - also produced normally,
    but production increases in
    reaction to injury or infection.
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6
Q

NSAIDs Action

A
  • Inhibits/binds COX-1 and COX-2 enzymes
  • Effects of COX-1/COX-2 Inhibition/Binding
    ~ Reduces Pain
    > Decreased PG Production
    ~ Reduces Edema Formation
    > Decreased PG Production
    ~ Antipyretic/Reduces Fever
    > Decreases PGE2 Production
    > Aspirin not used for children
    recovering from viral infection as
    it can cause Reye’s Syndrome
    (abnormal fatty deposits in the
    brain: give Ibuprofen instead)
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7
Q

Why is Aspirin Separate from NSAIDs?

A
  • Aspirin is more selective for the COX-1 enzyme
    ~ Has all the same effects as the other
    NSAIDs, but is also an anti-platelet.
    > Interaction between PG-12 and
    TXs helps to determine whether
    a clot will form.
    • Because aspirin is more
    selective for COX-1 TX
    production is reduced while
    PG-12 production is
    maintained.
  • The binding of aspirin to the COX enzyme is irreversible
  • PG-I2 is a thinner and TX is a clotter and Aspirin shuts down TX production by inhibiting the COX-1 pathway
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8
Q

Is Inflammation fully controlled by inhibition COX-1 and COX-2?

A
  • No
    ~ Bradykinin still being formed.
    ~ Histamine is still being released.
    ~ COX-1 & COX-2 are incompletely
    inhibited.
    ~ Binding is reversible with NSAIDs.
    ~ The lipoxygenase pathway is still
    intact.
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9
Q

COX-2 Specific NSAIDs

A
  • Bextra (discontinued due to deaths)
  • Vioxx (discontinued due to deaths)
  • Celebrex (needs special approval)
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10
Q

Is inhibition of COX-2 a selectively good idea?

A
  • Leaves COX-1 intact to meet needs of body and reduce side effects
  • Addresses the specific enzyme responsible for the increases in PG that cause unwanted effects associated with inflammation
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11
Q

Problem with COX-2 Inhibitors

A
  • Interaction between PG-12 and TX determines whether a clot will form.
    ~ With inhibition of COX-2, PG-12
    production is inhibited.
    ~ Thromboxane is still produced since
    COX-1 is not being inhibited.
    > With TX able to dominate the
    interaction with PG-I2 the blood
    tends to clot more readily
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12
Q

Combination Aspirin Products: Buffered Aspirin

A
  • Aspirin + Buffering Agent
    ~ Buffering Agent
    > Neutralizes Stomach Acid
    • Decreases Aspirin Breakdown
    in Stomach
    • Decreases aspirin absorption
    into mucus lining of stomach.
    * Decreases stomach
    irritation.
    } When aspirin is
    absorbed PGs are
    inhibited which are a
    component of the
    mucus lining.
    } Aspirin forms an
    acid in the stomach
    tissues.
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13
Q

Combination Aspirin Products: Aspirin with Caffeine

A
  • Caffeine enhances the analgesic effects especially with headaches.
    ~ Constricts blood vessels
  • Elevates Mood
  • Common with people who have headaches
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14
Q

Aspirin Products Indications

A
  • Mild pain
  • Fever
  • History of Heart Disease
  • Inflammatory conditions
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15
Q

Aspirin Products Contraindications/Considerations

A
  • Not indicated for athletes with muscle or joint injuries. (especially acute due bleeding)
  • Presence of lower back pain. (May be due to kidneys = will result in worsening pain)
  • Preexisting blood or bleeding disorders (anemia, hemophilia)
  • History of ulcer, Gl bleeding or liver disease.
  • Do not use in combination with alcohol.
  • Do not use if pregnancy is suspected.
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16
Q

Aspirin Products Contraindications/Considerations: Asthma

A
  • Due to inhibition of COX pathway. (less PG)
    ~ Arachidonic acid enters the
    lipoxygenase pathway and produces
    leukotrienes.
    > LTs bind to receptors in the
    respiratory tract worsening
    Asthma symptoms
    • Increased bronchospasm
    and mucous production (2
    main things that block airway)
17
Q

Aspirin Side Effects

A
  • Gastrointestinal Effects
    ~ Ulceration
    ~ Gastritis
    ~ GI Bleeding
    ~ Causes
    > PG inhibition (affects lining)
    > Acid production (irritates lining)
  • Uncontrolled Bleeding
  • Nephrotoxicity - Kidney damage as a result of excess exposure to toxins.
    ~ Toxins come from the metabolization
    of Aspirin
  • Allergic Reactions
    ~ S&S
    > Hives - Raised, Swollen, Red, Itchy
    > Edema
    > Difficulty Breathing
    • Bronchospasm - Rare, but
    serous if present
    > Rhinitis
    > Shock
  • Reye’s Syndrome
    ~ Condition following viral infection d
    associated with aspirin use
    ~ Results in generalized brain and liver
    dysfunction due to abnormal fatty
    deposits
18
Q

NSAIDs Indications

A
  • Mild to Moderate Pain
  • Fever - use safely w/ children without risk of Reyes
  • Inflammatory Conditions
  • Not used for those with history of heart disease or stroke.
19
Q

NSAID Side Effects

A
  • Most less frequent than with aspirin.
  • Gastrointestinal Effects
    ~ All due to PG inhibition
    > Ulceration
    > Gastritis
    > GI Bleeding
  • Uncontrolled bleeding
  • Nephrotoxicity
  • Allergic Reactions
    ~ S&S
    > Hives - Raised, Swollen, Red, Itchy
    > Edema
    > Difficulty Breathing
    • Bronchospasm - Rare, but
    serous if present
    > Rhinitis
    > Shock
    ~ Individuals with Aspirin allergy often
    are allergic to NSAIDs
20
Q

NSAIDs Contraindications/Considerations

A
  • Presence of lower back pain.
  • Preexisting blood or bleeding disorders (anemia, hemophilia)
  • History of ulcer, Gl bleeding or liver disease.
  • Asthma
  • Caution when use in combination with other salicylates or NSAIDs
  • Do not use in combination with alcohol.
    ~ Deteriorates GI tract
21
Q

Corticosteroids

A
  • Hormones produced within the adrenal gland or produced in a laboratory.
    ~ Types
    > Mineralcorticoids
    > Glucocorticoids (decreases
    Inflammation)
  • Body naturally makes corticosteroids
22
Q

Corticosteroid Types

A
  • Mineralcorticoids
    ~ Affect mineral/fluid balance in body
    > Aldosterone causes the kidney to
    reabsorb sodium and excrete
    potassium.
    • Results in increased fluid
    retention.
  • Glucocorticoids
    ~ Supresses inflammation
    ~ Affect glucose and fatty acid levels in
    the body.
    > Mobilizes amino acids and fatty
    acids for energy metabolism.
  • Where are the stores for amino acids and fatty acids?
    ~ Proteins and triglycerides
  • Wherever there’s sodium there’s water = inflammation
23
Q

Glucocorticoid Anti-Inflammatory Mechanisms

A
  • Inhibits release of HT
  • Inhibits the enzyme that mobilizes arachidonic acid (phospholipase A2)
    ~ Effects of Inhibition of Phospholipase
    A2
    > Inhibits Cyclooxygenase Pathway
    > Inhibits Lipoxygenase Pathway
  • Inhibits PG, HT, and LT but leaves BK
24
Q

Corticosteroid Indications

A
  • Usually used when NSAIDs aren’t effective or when inflammation is a component of asthma
    ~ Skin diseases/infections
    ~ Nasal inflammation
    ~ Respiratory diseases
    ~ Orthopedic Injury/condition
  • If used to often, can break down cartilage and other structures
25
Q

Common Corticosteroid Types

A
  • All corticosteroids have mineralcorticosteroid and glucocorticoid effects
  • Those that exert mostly mineralcorticoid effects are mineralcorticoids and those that exert mostly glucocorticoid effects are glucocorticoids.
  • Ex. Cortisone has more equal mineralcorticoid and glucocorticoid effects while dexamethasone has 25 times stronger glucocorticoid effects and almost no mineralcorticoid effects.
  • Common Medications
    ~ Betamethasone
    ~ Cortisone
    ~ Dexamethasone
    ~ Prednisone
26
Q

Corticosteroid Side Effects

A
  • Much more common than NSAIDs and more serious
    ~ Inhibits Collagen/scar formation
    > No or reduced inflammation = no
    or reduced movement of cells and
    blood plasma into injured tissues
    • Reduced movement of plasma
    and cells limits materials
    necessary for collagen (scar)
    formation
  • Optic
    ~ Glaucoma (high pressure in eye)
    ~ Cataracts (abnormal protein deposits
    over lens of eye)
  • Gastrointestinal
  • Muscle weakness/wasting (frees up amino acids)
  • Increased blood pressure
    ~ Retains water causing it to go into
    circulation = increased BP
27
Q

Corticosteroid Contraindications/Considerations

A
  • Immune System Function
    ~ Suppresses the immune reaction
    ~ Mask symptoms of infection
  • Pregnancy
  • Corticosteroid use will decrease the amount of natural corticosteroid the body will make
28
Q

General Guidelines for Use

A
  • Use prior to activity if used for asthma.
  • Healing will be delayed.
    ~ Athletes receiving intra-articular
    injections should not stress the joint
    in the short term following the
    injection.
  • Withdraw from long term use must be tapered.
    ~ Prevent Flare Up
    ~ Restore Adrenal Function

Pathophysiology & Pharmacology (20 decks)

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