14-Drugs for inflammation

Question 1

purpose of inflammation

Answer 1

contain damage associated w injury/ destroy foreign agent

Question 2

how often should IV sites be checked? why?

Answer 2

q1h - IV needle results in tissue damage, can lead to inflammation

Question 3

T/F: inflammation is a symptom not a disease

Answer 3

T

Question 4

why should we consider non-pharmacological methods w inflammation first?

Answer 4

normally self-limiting

Question 5

what is the best route for anti-inflammatories to be administered?

Answer 5

topically

Question 6

when does chronic inflammation occur?

Answer 6

if body is not able to contain/neutralize agent causing initial inflammation
leads to tissue damage

Question 7

Acute inflammation: general course and timeline

Answer 7

associated w injury, chemical damage, infection, antigens

normally lasts 8-10 days, then repair and healing

Question 8

signs of inflamamiton:

Answer 8

pain, warmth, redness, swelling

Question 9

reasons inflammation may occur:

Answer 9

physical injury, chemical trauma, infection, cell death, extreme heat

Question 10

name some of the chemical mediators of inflammation:

Answer 10

bradykinin, complement, histamine, leukotrienes, PGs

Question 11

what is a cytokine? how are they produced?

Answer 11

mediate and regulate immune and inflammatory reactions

produced by macrophages, leukocytes, and dendritic cells

Question 12

bradykinin

Answer 12

A chemical mediator of inflammation
inactive form in plasma (stored and released by mast cells)
vasodilator + pain

Question 13

complement

Answer 13

chemical mediator of inflammation
series of 20+ proteins that neutralize/destroy proteins
stimulates histamine release by mast cells
initiate immune response

Question 14

histamine

• stored and released by
• function

Answer 14

chemical mediator of inflammation
stored and released by mast cells
cause dilation of BV, SM constriction, swelling, and itching

Question 15

leukotrienes

• released by
• function
• what does it contribute to?

Answer 15

chemical mediator of inflammation
stored and released by mast cells
similar effects to histamine
contribute to asthma and allergy symptoms

Question 16

PGs

• released by
• function
• precursor for what

Answer 16

in most tissues and stored and released by mast cells
increase cap. permeability, attract WBCs, and pain
gastric cytoprotection, decrease gastric acid secretion
Thromboxane A2 - precursor

Question 17

Mast cells release chemical mediators: histamine, bradykinin, complement, leukotrienes, and PGs in response to:

Answer 17

cellular injury

Question 18

in response to tissue damage, arachidonic acid (AA) is released. COX 1 and Cox 2 (cyclooxygenase 1 and 2) then convert AA into:

Answer 18

COX 1 - PG - platelet agg

COX 2 - PG pain and inflammation

Question 19

what 2 drugs can inhibit the conversion of AA into PGs? how do they differ?

Answer 19

Selective COX 2 inhibitors (only block conversion of COX 2 into PG for pain and inflammation)
Non-selective COX inhibitors (block conversion of AA into COX 1 and 2 - no PGs)

Question 20

T/F arachidonic acid is always present in cell cytoplasm?

Answer 20

F - arachidonyl esters are present in the plasma membrane and is converted into AA by phospholipase A2 when cells are punctured

Question 21

Thromboxane A2

Answer 21

it stimulates activation of new platelets and increases platelet aggregation (most potent)
PG precursor

Question 22

What is the role of lipoxygenase

Answer 22

converts AA into leukotrienes (phagocyte activation, neutrophil chemotaxis, bronchoconstriction)

Question 23

Explain the consequence of ASA in inflammation as it relates to inhibiting COX 1 and 2

Answer 23

AA is now free floating (not being converted into PGs) and available for lipoxygenase to be converted into leukotrienes

Question 24

goal of anti inflammatory drugs

Answer 24

to prevent or decrease intensity of inflammatory response and reduce fever, if present

Question 25

NSAIDs and glucocorticoids are:

Answer 25

anti-inflammatory drug classes

Question 26

NSAIDs

Answer 26

(non-steroidal anti-inflammatory drugs) - treat mild to moderate pain and fever by inhibiting COX 1 and/or 2 - 2 classes: selective COX 2 inhibitors, and ibuprofen and similar agents?

Question 27

adverse effects of NSAIDs | selective and non-selective

Answer 27

non-selective: increased risk of GI bleed (second leading cause of peptic ulcer disease in Canada*) selective COX 2: high risk of MI, stroke, and asymptomatic hypertension (only used w pt.s not at risk of cardiovascular disease) Reye's Syndrome (4-14) --> ASA

Question 28

contraindications for NSAIDs

Answer 28

pt.s w kidney failure

Question 29

COX 1: Location, function, inhibition by medications, undersirable outcomes

Answer 29

- present in all tissues - protects gastric mucosa, supports kidney function, promotes platelet agg - Undesirable: increases risk for GI bleeding and kidney failure

Question 30

COX 2: location, function, inhibition by medications

Answer 30

at sites of tissue injury mediates inflammation, sensitizes pain receptors, mediates fever in brain desirable: results in suppression of inflammation

Question 31

Inhibition of COX 1 and COX 2 results in:

Answer 31

reduction of inflammation and fever inhibition of formation of gastric mucosa increased gastric acid secretion inhibition of platelet agg

Question 32

Glucocorticoids - function - how are they administered

Answer 32

``` used for severe or disabling inflammation (short-term control) administered systemically (IV, IM, PO) or topically and intranasally ```

Question 33

mechanism of action of systemic glucocorticoid therapy:

Answer 33

inhibit the release of histamine block activity of phospholipase A2 and COX 2 enzymes inhibit immune response (suppress phagocytic/lymphocytic activity, interleukin-2 and 3, platelet agg factor)

Question 34

what is a consideration to have when diagnosing individuals on glucocorticoid therapy?

Answer 34

pt.s have suppressed immune signs and symptoms | and don't present the same clinically to infections, viruses, and bacteria

Question 35

adverse effects of glucocorticoids:

Answer 35

adrenal insufficiency (wean!), hyperglycemia, mood changes, osteoporosis, immunosuppression

Question 36

antipyretics:

Answer 36

anti-fever! | defense mechanisms used to eradicate infection

Question 37

prolonged fevers can:

Answer 37

induce febrile seizures (especially in children), tissue damage, reduce mental acuity, cause delirium, or coma

Question 38

antipyretics include:

Answer 38

NSAIDs | acetaminophen

Question 39

acetaminophen mechanism of action and cautions

Answer 39

direct action of hippocampus and vasodilation (sweating and dissipation of heat) not anti-inflammatory *caution in pt.s w liver disease

Question 40

NSAIDs and Reye's syndrome

Answer 40

common in 4-14 don't use ASA in children "use Tylenol" (can also use Ibuprofen) - associated w previous viral illnesses and use of aspirin that can cause brain inflammation, fatty deposits in liver, death within days

Question 41

Antihistamines mechanism of action

Answer 41

block actions of histamine at H1 receptor (treatment of allergic rhinitis) induce sedative effects - relieve runny nose, sneezing, itchy eyes and throat

Question 42

hyperactivity as a result of idiosyncratic CNS stimulation

Answer 42

administering benadryl for sedative effects, then hyperactivity!

Question 43

Anaphylaxis

Answer 43

hyper-immune and hyper-inflammatory response to an antigen | body releases massive amounts of histamine and other mediators of inflammation

Question 44

Anaphylaxis signs and symptoms

Answer 44

itching, hives in throat and chest cough caused by swelling larynx rapid fall in BP, reflex tachycardia, bronchoconstriction(SOB) SHOCK LIKE

Question 45

Anaphylaxis multiple strata for med:

Answer 45

- adrenergic agonist (epi, alpha 1, beta 1 (increase CO) and 2) - antihistamine (benadryl/Diphenhydramine) - beta2 adrenergic agonists (ventolin) - systemic glucocorticoids (hydrocortisone)