Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHARMACOLOGY > 14-Drugs for inflammation > Flashcards

14-Drugs for inflammation Flashcards

1
Q

purpose of inflammation

A

contain damage associated w injury/ destroy foreign agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how often should IV sites be checked? why?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T/F: inflammation is a symptom not a disease

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

normally self-limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

topically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when does chronic inflammation occur?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute inflammation: general course and timeline

A

associated w injury, chemical damage, infection, antigens

normally lasts 8-10 days, then repair and healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

signs of inflamamiton:

A

pain, warmth, redness, swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

reasons inflammation may occur:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

name some of the chemical mediators of inflammation:

A

bradykinin, complement, histamine, leukotrienes, PGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is a cytokine? how are they produced?

A

mediate and regulate immune and inflammatory reactions

produced by macrophages, leukocytes, and dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

bradykinin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

complement

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

histamine

  • stored and released by
  • function
A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

leukotrienes

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PGs

  • released by
  • function
  • precursor for what
A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

cellular injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

COX 1 - PG - platelet agg

COX 2 - PG pain and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

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)

20
Q

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

A

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

21
Q

Thromboxane A2

A

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

22
Q

What is the role of lipoxygenase

A

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

23
Q

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

A

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

24
Q

goal of anti inflammatory drugs

A

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

25
Q

NSAIDs and glucocorticoids are:

A

anti-inflammatory drug classes

26
Q

NSAIDs

A

(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?
27
Q

adverse effects of NSAIDs

selective and non-selective

A

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

28
Q

contraindications for NSAIDs

A

pt.s w kidney failure

29
Q

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

A
  • present in all tissues
  • protects gastric mucosa, supports kidney function, promotes platelet agg
  • Undesirable: increases risk for GI bleeding and kidney failure
30
Q

COX 2: location, function, inhibition by medications

A

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

31
Q

Inhibition of COX 1 and COX 2 results in:

A

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

32
Q

Glucocorticoids

  • function
  • how are they administered
A 
used for severe or disabling inflammation (short-term control)
administered systemically (IV, IM, PO) or topically and intranasally
33
Q

mechanism of action of systemic glucocorticoid therapy:

A

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)

34
Q

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

A

pt.s have suppressed immune signs and symptoms

and don’t present the same clinically to infections, viruses, and bacteria

35
Q

adverse effects of glucocorticoids:

A

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

36
Q

antipyretics:

A

anti-fever!

defense mechanisms used to eradicate infection

37
Q

prolonged fevers can:

A

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

38
Q

antipyretics include:

A

NSAIDs

acetaminophen

39
Q

acetaminophen mechanism of action and cautions

A

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

40
Q

NSAIDs and Reye’s syndrome

A

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

41
Q

Antihistamines mechanism of action

A

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

42
Q

hyperactivity as a result of idiosyncratic CNS stimulation

A

administering benadryl for sedative effects, then hyperactivity!

43
Q

Anaphylaxis

A

hyper-immune and hyper-inflammatory response to an antigen

body releases massive amounts of histamine and other mediators of inflammation

44
Q

Anaphylaxis signs and symptoms

A

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

45
Q

Anaphylaxis multiple strata for med:

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

PHARMACOLOGY (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions