Brainscape's Knowledge GenomeTM

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


See full index

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

Inflammation and Anti-Inflammatory Drugs Flashcards

1
Q

Inflammation

A

SHaRP

  • Swelling
  • Heat
  • Redness
  • Pain

and loss of function

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

Inflammation trigers

A

vasodilation

  • more blood flows to the area making it red, warm, and swollen
  • pressure causes pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

Purpose of Inflammatory Response

A
  • prevent the spread of pathogens
  • minimize further damage to tissues
  • promote repair and healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Neutrophils

A
  • first WBCs to arrive at injury site
  • infiltrates injured tissues
  • remove pathogens and damaged tissue through phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Macrophages

A
  • more long lived than neutrophils
  • phagocytose pathogens and cellular debris
  • engulf neutrophils during resolution of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Kinin Cascade

A

Bradykinin (and other kinins):

  • cause vasodilation
  • increase permeability of BV
  • lowers BP
  • stimulates pain receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PGE2

A

PGE2=inflammatory prostaglandin

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

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

Prostanoids

A

prostaglandins + thromboxanes

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

Eicosanoid Family

A
  • prostaglandins
  • thromboxanes
  • leukotrienes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Prostaglandin E2

A
  • signals creation of mucus to protect stomach lining
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Prostaglandin I2

A
  • in BV
  • inhibits platelet aggregation/blood clotting
  • promotes vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Thromboxane A2

A
  • in platelets
  • promotes platelet aggregation in the clotting process
  • vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

PGI2 and TXA2

A

COUNTERBALANCE eachother = homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Arachidonic Acid

A

substrate for ALL PROSTANOIDS

- prostaglandins and thromboxanes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

COX1 vs COX2

A

COX1: housekeeping; always on
COX2: inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Prostaglandin COX Binding

A
  • can technically bind COX1&2 but binds COX2 preferentially during times of inflammation because more COX2 is present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

The precise biological action of a given Prostaglandin is ______________

A

Tissue Dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

PGE2 stomach

PGE2 Injury site

A

stomach: protects stomach linin from erosion

injury site: plays central role in inflammation at the site of injury

27
Q

How does Prostaglandin act differently at different sites

A

TISSUE DEPENDENT

  • binds different prostaglandin receptors
  • dependent on the receptor type they interact with
28
Q

NSAIDS

A

Non-Steroidal Anti-Inflammatory Drugs
- provide analgesic, antipyretic, and anti-inflammatory effects

OTC NSAIDS include: Aspirin, ibuprofen, naproxen, diclofenac

29
Q

Aspirin

A

NSAID

30
Q

Ibuprofen

A

NSAID

31
Q

Naproxen

A

NSAID

32
Q

Diclofenac

A

NSAID

TOPICAL CREAM

33
Q

NSAIDs Effects

A
  • 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
Q

NSAIDs Side Effects

A
  • 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
Q

NSAIDs action

A
  • all similar actions: inhibit COX2
36
Q

COX1

A

housekeeping

37
Q

COX2

A

inflammatory

38
Q

NSAID side effects

- reduction COX1

A
  • GI discomfort
39
Q

NSAIDS contraindicated for

A

patients with:

  • peptic ulcers
  • aspirin hypersensitivity
  • coagulation defects
  • congestive heart failure
  • etc
40
Q

NSAIDS NOT recommended for people with

A
  • congestive heart failure

- kidney problems

41
Q

NSAIDs may induce

A

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
Q

Aspirin

A

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
Q

Selective COX2 Inhibitors

A
  • highly selective COX2>COX1 = selectively inhibiting production of pro-inflammatory PGE2
  • less risk of side-effects especially GI related
  • cardivascular side effects
44
Q

Celebrex

A

ONLY selective COX2 inhibitor on US market

45
Q

Selective COX2 inhibitors increase risk of ____

A

Thrombosis (which can lead to myocardial infarction and stroke)
- increases thromboxanes which messes with equilibrium (TXA2>PGI2)

46
Q

Aspirin can decrease _____ preventing _____

A
  • decrease risk of thrombosis
  • preventing coronary heart disease

BLOCKS COX1&2 equally (PGI2>TXA2)

47
Q

Acetaminophen is not

A

NSAID!

48
Q

Acetaminophen

A
  • anti-pyretic and analgesic
  • – NOT anti-inflammatory
  • mechanism unknown
  • narrow TI
49
Q

Acetaminophen Adverse Effects

A
  • most common cause of acute liver failure
  • ** worse in alcoholics***
  • causes NAPQI accumulation = toxic
50
Q

Acetaminophen overdose antidote

A
  • N-Acetylcysteine via IV
51
Q

Steroidal Anti-inflammatory Drugs

Glucocorticoids

A

(e. g. cortisol)
- produced by adrenal cortex
- effects:
- – inflammatory response, stress response, immune response
- – carbohydrate, protein, fat distribution
- – behavior

52
Q

Hydrocortisone

A

synthetic glucocorticoid

53
Q

Prednisolone

A

synthetic glucocorticoid

54
Q

Prednisone

A

synthetic glucocorticoid

55
Q

Dexamethasone

A

synthetic glucocorticoid

56
Q

Betamethason

A

synthetic glucocorticoid

57
Q

Glucocorticoids Anti-inflammatory effects

A
  • powerful anti-inflammatory effects by down-regulating the production of COX2 and inflammatory prostaglandin
58
Q

Immunosuppressive Effects of Glucocorticoids

A
  • reduce activity of immune cells including mast cells

- reduces the production of histamine and inflammatory activity, but also increases risk on infections

59
Q

Glucocorticoids for the Suppression of Inflammatory Responses

A

indicated for disorders with an inflammatory component

  • allergic reactions
  • asthma
  • arthritis
  • bursitis
  • cerebral edema
  • SLE
  • atopic dermatitis
60
Q

Adverse Effects of Glucocorticoid Therapy

A
  • NOT usually curative and can be dangerous

- USE AT MINIMALLY EFFECTIVE DOSES

61
Q

Metabolic Complications of Glucocorticoid Therapy

Carbohydrates

A
  • stimulate gluconeogenesis and inhibit glucose uptake by cells
    Net effect: increase plasma glucose levels, hyperglycemia, weight gain, diabetes
62
Q

Metabolic Complications of Glucocorticoid Therapy

Lipids

A
  • stimulate hormone-sensitive lipase -> ipolysis
    Net effect: increase fat redistribution to face, back of neck, etc.
    CUSHINGS
63
Q

Metabolic Complications of Glucocorticoid Therapy

Proteins

A
  • reduce protein synthesis

Net effect: muscle wasting and osteoporosis (major limitation on long-term therapy)

64
Q

Synthetic Glucocorticoid Drugs: Side Effects

A

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)

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