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Pharmacology Test 2 > Inflammation and Anti-Inflammatory Drugs > Flashcards

Inflammation and Anti-Inflammatory Drugs Flashcards

(64 cards)

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1
Q

Inflammation

A

SHaRP

  • Swelling
  • Heat
  • Redness
  • Pain

and loss of function

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2
Q

Inflammation trigers

A

vasodilation

  • more blood flows to the area making it red, warm, and swollen
  • pressure causes pain
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3
Q

3 Key Processes in the Inflammatory Response

A

1) Vasodilation: resulting in increased blood flow
2) Increased Vascular Permeability: plasma leaks from blood vessels into the damaged area
3) migration of neutrophils and other leucocytes from blood into damaged area

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4
Q

Purpose of Inflammatory Response

A
  • prevent the spread of pathogens
  • minimize further damage to tissues
  • promote repair and healing
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5
Q

Neutrophils

A
  • first WBCs to arrive at injury site
  • infiltrates injured tissues
  • remove pathogens and damaged tissue through phagocytosis
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6
Q

Macrophages

A
  • more long lived than neutrophils
  • phagocytose pathogens and cellular debris
  • engulf neutrophils during resolution of inflammation
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7
Q

Mast Cells

A
  • part of immune system
  • mediate wound healing and defense against pathogens
  • release HISTAMINE, a MAJOR vasodilator (helps make gaps for passage)
  • major role in allergy, eczema, and anaphylaxis
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8
Q

Inflammatory Response Order

A

1) Neutrophils 2) Macrophages

  • BV dilates
  • packed endothelial cells become leaky
  • – this allows WBCs to reach the damaged area
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9
Q

Kinin Cascade

A

Bradykinin (and other kinins):

  • cause vasodilation
  • increase permeability of BV
  • lowers BP
  • stimulates pain receptors
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10
Q

PGE2

A

PGE2=inflammatory prostaglandin

- released by macrophages and mast cells in the injured region to enhance the action of bradykinin

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11
Q

Prostaglandins

A

ALL come from ARACHIDONIC acid

  • found in all tissues of the body
  • belong to the EICOSANOID family
  • – includes: prostaglandins, thromboxanes, and leukotrienes
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12
Q

Prostanoids

A

prostaglandins + thromboxanes

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13
Q

Eicosanoid Family

A
  • prostaglandins
  • thromboxanes
  • leukotrienes
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14
Q

Prostaglandin E2

A
  • signals creation of mucus to protect stomach lining
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15
Q

Prostaglandin I2

A
  • in BV
  • inhibits platelet aggregation/blood clotting
  • promotes vasodilation
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16
Q

Thromboxane A2

A
  • in platelets
  • promotes platelet aggregation in the clotting process
  • vasoconstriction
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17
Q

PGI2 and TXA2

A

COUNTERBALANCE eachother = homeostasis

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18
Q

Prostaglandin E2 results in

PGE2

A
  • vasodilation
  • increased vascular permeability
  • increased sensitivity of pain receptors to bradykinin
  • pain neuromodulation in dorsal horn of spinal cord
  • pyresis (fever)
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19
Q

Prosanoids in Inflammation

A
  • mast cells and macrophages produce large amounts of PGE2 that is released in the inflamed region of the body
  • Arachidonic acid released from cell membrane loses P group and becomes acting -> interacts with COX2 => PGE2
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20
Q

Arachidonic Acid

A

substrate for ALL PROSTANOIDS

- prostaglandins and thromboxanes

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21
Q

COX1 vs COX2

A

COX1: housekeeping; always on
COX2: inflammation

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22
Q

Prostaglandin Synthesis

A

membrane phospholipid -1-> arachidonic acid (FA) -2-> cyclic endoperoxides -3-> prostaglandins

1) Phospholipase A2
2) Cyclo-oxygenase (COX)
3) Prostaglandin synthases

  • can technically bind COX1&2 but binds COX2 preferentially during times of inflammation because more COX2 is present
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23
Q

Prostaglandin COX Binding

A
  • can technically bind COX1&2 but binds COX2 preferentially during times of inflammation because more COX2 is present
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24
Q

Inflammatory Prostaglandin Synthesis

A

membrane phospholipid -1-> arachidonic acid (FA) -2-> cyclic endoperoxides -3-> prostaglandins

1) Phospholipase A2
2) Cyclo-oxygenase (COX2)
3) Prostaglandin synthases

Produced at site of injury

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25
The precise biological action of a given Prostaglandin is ______________
Tissue Dependent
26
PGE2 stomach | PGE2 Injury site
stomach: protects stomach linin from erosion injury site: plays central role in inflammation at the site of injury
27
How does Prostaglandin act differently at different sites
TISSUE DEPENDENT - binds different prostaglandin receptors - dependent on the receptor type they interact with
28
NSAIDS
Non-Steroidal Anti-Inflammatory Drugs - provide analgesic, antipyretic, and anti-inflammatory effects OTC NSAIDS include: Aspirin, ibuprofen, naproxen, diclofenac
29
Aspirin
NSAID
30
Ibuprofen
NSAID
31
Naproxen
NSAID
32
Diclofenac
NSAID TOPICAL CREAM
33
NSAIDs Effects
- reduce the production of inflammatory grostaglandin E2 (PGE2) and so they attenuate inflammatory effects - reduce swelling - attenuate bradykinin-induced pain - reduce allodynia (tenderness of skin) - reduce fever
34
NSAIDs Side Effects
- due to binding COX1 instead of COX2 (bind both equally) - Inflammatory PGE2 levels reduced (good); housekeeping PGEs produced by COX1 also reduced (bad) - -- stomach issues
35
NSAIDs action
- all similar actions: inhibit COX2
36
COX1
housekeeping
37
COX2
inflammatory
38
NSAID side effects | - reduction COX1
- GI discomfort
39
NSAIDS contraindicated for
patients with: - peptic ulcers - aspirin hypersensitivity - coagulation defects - congestive heart failure - etc
40
NSAIDS NOT recommended for people with
- congestive heart failure | - kidney problems
41
NSAIDs may induce
Asthma Attacks! Anaphylactic Shock - b/c decrease in COX, arachidonic acid not converted into cyclic endoperoxides - INSTEAD arachidonic acid is created into cysteinyl leukotrienes = bad - -- 5-lipoxygenase
42
Aspirin
NSAID - Unique among NSAIDS, aspirin binds COVALENTLY (irreversibly) to the COX1&2 Enzymes - net effect => anti-platelet drug - -- clot inhibitors - binding of COX1 => GI effects
43
Selective COX2 Inhibitors
- highly selective COX2>COX1 = selectively inhibiting production of pro-inflammatory PGE2 - less risk of side-effects especially GI related - cardivascular side effects
44
Celebrex
ONLY selective COX2 inhibitor on US market
45
Selective COX2 inhibitors increase risk of ____
Thrombosis (which can lead to myocardial infarction and stroke) - increases thromboxanes which messes with equilibrium (TXA2>PGI2)
46
Aspirin can decrease _____ preventing _____
- decrease risk of thrombosis - preventing coronary heart disease BLOCKS COX1&2 equally (PGI2>TXA2)
47
Acetaminophen is not
NSAID!
48
Acetaminophen
- anti-pyretic and analgesic - -- NOT anti-inflammatory - mechanism unknown - narrow TI
49
Acetaminophen Adverse Effects
- most common cause of acute liver failure * ** worse in alcoholics*** - causes NAPQI accumulation = toxic
50
Acetaminophen overdose antidote
- N-Acetylcysteine via IV
51
Steroidal Anti-inflammatory Drugs | Glucocorticoids
(e. g. cortisol) - produced by adrenal cortex - effects: - -- inflammatory response, stress response, immune response - -- carbohydrate, protein, fat distribution - -- behavior
52
Hydrocortisone
synthetic glucocorticoid
53
Prednisolone
synthetic glucocorticoid
54
Prednisone
synthetic glucocorticoid
55
Dexamethasone
synthetic glucocorticoid
56
Betamethason
synthetic glucocorticoid
57
Glucocorticoids Anti-inflammatory effects
- powerful anti-inflammatory effects by down-regulating the production of COX2 and inflammatory prostaglandin
58
Immunosuppressive Effects of Glucocorticoids
- reduce activity of immune cells including mast cells | - reduces the production of histamine and inflammatory activity, but also increases risk on infections
59
Glucocorticoids for the Suppression of Inflammatory Responses
indicated for disorders with an inflammatory component - allergic reactions - asthma - arthritis - bursitis - cerebral edema - SLE - atopic dermatitis
60
Adverse Effects of Glucocorticoid Therapy
- NOT usually curative and can be dangerous | - USE AT MINIMALLY EFFECTIVE DOSES
61
Metabolic Complications of Glucocorticoid Therapy | Carbohydrates
- stimulate gluconeogenesis and inhibit glucose uptake by cells Net effect: increase plasma glucose levels, hyperglycemia, weight gain, diabetes
62
Metabolic Complications of Glucocorticoid Therapy | Lipids
- stimulate hormone-sensitive lipase -> ipolysis Net effect: increase fat redistribution to face, back of neck, etc. CUSHINGS
63
Metabolic Complications of Glucocorticoid Therapy | Proteins
- reduce protein synthesis | Net effect: muscle wasting and osteoporosis (major limitation on long-term therapy)
64
Synthetic Glucocorticoid Drugs: Side Effects
adverse effects of steroids from immunosuppressive drugs that reduce protein synthesis: - suppression of injury response - suppression of response to infection - suppression of endogenous corticosteroids - muscle wasting - osteoporosis - bacterial and opportunistic infections - fluid retention - fat redistribution: CUSHINGOID symptoms: "moon facies", buffalo hump CUSHING'S Syndrome

Pharmacology Test 2 (8 decks)

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