14-Drugs for inflammation Flashcards
purpose of inflammation
contain damage associated w injury/ destroy foreign agent
how often should IV sites be checked? why?
q1h - IV needle results in tissue damage, can lead to inflammation
T/F: inflammation is a symptom not a disease
T
why should we consider non-pharmacological methods w inflammation first?
normally self-limiting
what is the best route for anti-inflammatories to be administered?
topically
when does chronic inflammation occur?
if body is not able to contain/neutralize agent causing initial inflammation
leads to tissue damage
Acute inflammation: general course and timeline
associated w injury, chemical damage, infection, antigens
normally lasts 8-10 days, then repair and healing
signs of inflamamiton:
pain, warmth, redness, swelling
reasons inflammation may occur:
physical injury, chemical trauma, infection, cell death, extreme heat
name some of the chemical mediators of inflammation:
bradykinin, complement, histamine, leukotrienes, PGs
what is a cytokine? how are they produced?
mediate and regulate immune and inflammatory reactions
produced by macrophages, leukocytes, and dendritic cells
bradykinin
A chemical mediator of inflammation
inactive form in plasma (stored and released by mast cells)
vasodilator + pain
complement
chemical mediator of inflammation
series of 20+ proteins that neutralize/destroy proteins
stimulates histamine release by mast cells
initiate immune response
histamine
- stored and released by
- function
chemical mediator of inflammation
stored and released by mast cells
cause dilation of BV, SM constriction, swelling, and itching
leukotrienes
- released by
- function
- what does it contribute to?
chemical mediator of inflammation
stored and released by mast cells
similar effects to histamine
contribute to asthma and allergy symptoms
PGs
- released by
- function
- precursor for what
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
Mast cells release chemical mediators: histamine, bradykinin, complement, leukotrienes, and PGs in response to:
cellular injury
in response to tissue damage, arachidonic acid (AA) is released. COX 1 and Cox 2 (cyclooxygenase 1 and 2) then convert AA into:
COX 1 - PG - platelet agg
COX 2 - PG pain and inflammation
what 2 drugs can inhibit the conversion of AA into PGs? how do they differ?
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)
T/F arachidonic acid is always present in cell cytoplasm?
F - arachidonyl esters are present in the plasma membrane and is converted into AA by phospholipase A2 when cells are punctured
Thromboxane A2
it stimulates activation of new platelets and increases platelet aggregation (most potent)
PG precursor
What is the role of lipoxygenase
converts AA into leukotrienes (phagocyte activation, neutrophil chemotaxis, bronchoconstriction)
Explain the consequence of ASA in inflammation as it relates to inhibiting COX 1 and 2
AA is now free floating (not being converted into PGs) and available for lipoxygenase to be converted into leukotrienes
goal of anti inflammatory drugs
to prevent or decrease intensity of inflammatory response and reduce fever, if present
NSAIDs and glucocorticoids are:
anti-inflammatory drug classes
NSAIDs
(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?
adverse effects of NSAIDs
selective and non-selective
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
contraindications for NSAIDs
pt.s w kidney failure
COX 1: Location, function, inhibition by medications, undersirable outcomes
- present in all tissues
- protects gastric mucosa, supports kidney function, promotes platelet agg
- Undesirable: increases risk for GI bleeding and kidney failure
COX 2: location, function, inhibition by medications
at sites of tissue injury
mediates inflammation, sensitizes pain receptors, mediates fever in brain
desirable: results in suppression of inflammation
Inhibition of COX 1 and COX 2 results in:
reduction of inflammation and fever
inhibition of formation of gastric mucosa
increased gastric acid secretion
inhibition of platelet agg
Glucocorticoids
- function
- how are they administered
used for severe or disabling inflammation (short-term control) administered systemically (IV, IM, PO) or topically and intranasally
mechanism of action of systemic glucocorticoid therapy:
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)
what is a consideration to have when diagnosing individuals on glucocorticoid therapy?
pt.s have suppressed immune signs and symptoms
and don’t present the same clinically to infections, viruses, and bacteria
adverse effects of glucocorticoids:
adrenal insufficiency (wean!), hyperglycemia, mood changes, osteoporosis, immunosuppression
antipyretics:
anti-fever!
defense mechanisms used to eradicate infection
prolonged fevers can:
induce febrile seizures (especially in children), tissue damage, reduce mental acuity, cause delirium, or coma
antipyretics include:
NSAIDs
acetaminophen
acetaminophen mechanism of action and cautions
direct action of hippocampus and vasodilation (sweating and dissipation of heat)
not anti-inflammatory
*caution in pt.s w liver disease
NSAIDs and Reye’s syndrome
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
Antihistamines mechanism of action
block actions of histamine at H1 receptor (treatment of allergic rhinitis)
induce sedative effects
- relieve runny nose, sneezing, itchy eyes and throat
hyperactivity as a result of idiosyncratic CNS stimulation
administering benadryl for sedative effects, then hyperactivity!
Anaphylaxis
hyper-immune and hyper-inflammatory response to an antigen
body releases massive amounts of histamine and other mediators of inflammation
Anaphylaxis signs and symptoms
itching, hives in throat and chest
cough caused by swelling larynx
rapid fall in BP, reflex tachycardia, bronchoconstriction(SOB)
SHOCK LIKE
Anaphylaxis multiple strata for med:
- adrenergic agonist (epi, alpha 1, beta 1 (increase CO) and 2)
- antihistamine (benadryl/Diphenhydramine)
- beta2 adrenergic agonists (ventolin)
- systemic glucocorticoids (hydrocortisone)
