Anti-inflammatory Drugs Flashcards

1
Q

the 3 phases of inflammation of ______, subacute, and _____.

A

acute

chronic

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

the _____ phase lasts 1-3 days, and has 5 clinical signs: heat, redness, swelling, pain, impaired function

A

acute

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

the subacute phase lasts ___ - ___ days to about 1 month and corresponds to a cleaning phase. If it is not resolved, it becomes ______

A

3-4 days

chronic

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

prostaglandins in the hypothalamus stimulate the production of ________, which reset the temperature set to a higher point, and bone marrow to release more _______

A

cytokines

WBCs

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

step 3: biochemical messages are released to cause _______ and blood vessel ________, which allow WBCs to reach the site

A

vasodilation

blood vessel permeability

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

activation of local _______ in the tissues is step 2, which start to fight the infection until the _____ comes

A

macrophages

WBCS

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

in step 4, dendritic cells (phagocytic) present more information and samples from the invading organisms, so they specifically signal the _____

A

WBCs (T Helper cells)

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

in step 5, the main fighting force arrives. If a virus, _______ cells are recruited

A

cytotoxic CD8 cells

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

in step 5, ______ are recruited if it is bacterial

A

neutrophils

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

______ are specialized phagocytes that engulf the ____ - ____ bacterial

A

neutrophils

antibody-coated

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

things turn back to normal in step 6. Dead cells are ______, fibroblasts _____ the damaged site, involved cells return to _______

A

phagocytized
repair
circulation

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

_________ are the principle cells of chronic inflammation

A

macrophages

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

vascular changes, edema, and neutrophilic response are ____ inflammation, whereas good tissue destruction, scarring, and _______ are _____ inflammation

A

acute
angiogenesis
chronic

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

________ inflammation is a distintive pattern of chronic inflammation characterized by aggregates of activated _______ with scattered lymphocytes

A

granulomatous

macrophages

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

granulomas are attempting to ____-___ and isolate ____ ____ and debris

A

wall-off

foregin material

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

mycobacterium TB, T. pallidum, fungal infections may all cause ________ inflammation, which form in persistent T-cell responses, immune-mediated diseases, and foreign bodies (sutures/splinters)

A

granulomatous

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

inflammatory injury may occur if the reaction is ____ (severe infection), prolonged, or _______ (autoimmune)

A

strong

inappropriate

18
Q

pyrogens (and LPS) stimulate _______ in the vascular cells of the hypothalamus to produce ______

A

prostaglandins

fever

19
Q

C-reactive portein, _____, and _____ ____ are the 3 best known acute phase proteins. These are stimulated by cytokines

A

fibrinogen

serum amyloid A protein

20
Q

acute-phase proteins bind to microbial cell walls, to act as ________

21
Q

fibrinogen binds to ________ and causes them to form stacks (_______) that sediment more rapidly. This is why the ______ is a test for systemic inflammatory response

A

erythrocytes
roleaux
ESR

22
Q

prolonged infection stimulates the production of _____, which increase the bone marrow output of leukocytes, to compensate for the consumption of them in the inflammatory reaction

A

colony stimulating factors

23
Q

the body release ___ - ___ mg of cortisol daily. Half life is ___ to ___ minutes

A

10-20 mg

60 to 90 minutes

24
Q

glucocorticoids cause increase in gluconeogenesis, lipolysis, _____, ____ ____, and a decrease in inflammation and immune

A

proteolysis, insulin resistance

25
glucocorticoid injections caue changes in _____, resulting in mood changes (insomnia, euphoria, depression)
CNS changes
26
giving 5 mg of prednisone, is equivalent of giving _____ mg of cortisol (hydrocortisone). Range is 5-60mg.
20 mg
27
Prednisone (Deltasone) is primarily given in the ____ form
oral
28
if the condition came on fast and aggressive, treat with ____ initial doses, and taper ____
high initial | taper quickly
29
under treatment of prednisone will be more _______ than overtreatment
dangerous
30
prednisone inhibits ______
phospholipase
31
prednisone is activated by enzymes in the _____ to turn into _____ (used if there is liver toxicity/failure)
liver | prednisolone
32
2 weeks or longer on prednisone, you must ____
taper
33
GI disturbances are common (abdominal dissension, diarrhea) with _________
corticosteroid use
34
An ADR may cause _____ changes, rare risk of suicide
mood
35
if treatment extends over weeks to months, the patient should be given _______ therapy during additional stress or trauma
supplementary
36
it make take ___ to ___ for the HPA axis to function acceptably. Cortisol levels may not return to normal for another ___ to ___ months following taper
2-12 months | 6 to 9 months
37
withdrawal of prednisone will be fever, malaise, ______, and _____
arthralgia | myalgia
38
_______ of TB should be used in patients with latent TB if they are on prednisone
chemoprophylaxis
39
Prenisone 10mg #10 | take 1 tab PO q12 hours x 5 days
example
40
other inflammatory drugs include tetracyclines, _________ (inhibit cytokines and inflammatory pathways) , and metronidazole
macrolides (azithromycin) - protein synthesis inhibitors