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Jason's Cardiovascular Block > Hormonal/Lipid Mediators (Cardio) > Flashcards

Hormonal/Lipid Mediators (Cardio) Flashcards

1
Q

NSAID potency is paralled by:

A

Potency of prostaglandin inhibition

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2
Q

Arachidonic acid is a precursor for what?

A

biological active lipids

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3
Q

PUFA stands for? Comes from?

A

Poly-unsaturated fatty acids from our diet

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4
Q

How and Why would you want to store arachidonic acid?

A

Stored esterified in membrane phospholipids. Cause it’s POTENT once activated!

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5
Q

How do you RELEASE THE (arachidonic acid) KRAKKEN? (from the membrane?)

A

increase intracellular calcium

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6
Q

2 ways to metabolize arachidonic acid:

A
  1. COX1 (constitutive)- physiological PGs

2. COX2 (inducible) - gene induced by inflammatories like IL-1/TNF

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7
Q

COX-1 and COX-2 are expressed in which cells

A

ALL THE CELLS.

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8
Q

Features of Cyclic endoperoxides? what happens to them?

A

Highly unstable and converted to PGE, PGF, PGD

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9
Q

T/F Prostaglandins survive in the blood stream.

A

False. degraded by endothelial cells

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10
Q

PGE2 does what 5 things?

A
  1. Relaxes smooth muscle
  2. vasodilator
  3. hyperalgesic
  4. pyrogenic
  5. angiogenic
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11
Q

PGD2 and PGF2-alpha do what?

A

both bronchoconstrict

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12
Q

Main action of NSAIDs?

A

block cyclooxygenase

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13
Q

NSAID adverse effect?

A

gastric irritation/ulceration

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14
Q

Do NSAIDS influence cellular inflammation?

A

Nope. Mostly vascular.

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15
Q

Explain the synergy between PGE2 and BK

A

BK alone increases paina smidge, PGE alone only makes it red. Together they form a dynamic duo and BRING THE PAIN.

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16
Q

If PGE2 only acts locally, how does it get to the hypothalamus to cause fever

A

IL-1 travels from infection to hypothalamus, induces COX2 to produce PGE2 to turn the heat up.

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17
Q

PGE2 isn’t all bad, tell me 4 reasons why?

A
  1. Promotes blood flow
  2. promotes angiogenesis
  3. increases music secretion
  4. reduces gastric acid secretion
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18
Q

Is Thromboxane A2 a prostaglandin?

A

Nope. Missing the pentacyclin ring

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19
Q

What’s the half life of Prostacyclin?

A

3 minutes

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20
Q

Prostacyclin is our protector against coronary artery disease. 2 reasons why?

A
  1. reduce platelet activation

2. vasodilator

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21
Q

What is the half-life of Thromboxane A2?

A

30 seconds

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22
Q

What makes Thromboxane A2?

A

Platelets

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23
Q

Thromboxane A2 is prostacyclin’s evil twin brother. Two reasons why?

A
  1. increases platelet activation

2. vasoconstrictor

24
Q

Why is Aspirin so special?

A
  1. Promotes prostacyclin

2. Acetylation of COX

25
Q

What does Aspirin do to platelets?

A

irreversibly binds to them

26
Q

Platelet life span is how long?

A

8 days

27
Q

PGI2 aka….

A

Prostacyclin

28
Q

What are Aspirin triggered lipoxins?

A

Lipoxins involved in inflammation resolution.

29
Q

What happens if you convert linolenic acid to Eicosapentaenoic (EPA) instead of arachidonic acid?

A

Increase PGI3 instead of TxA3

30
Q

What does Increased PGI3/TxA3 ratio mean?

A

lower risk of heart disease

31
Q

5 Lipoxygenase does what? how is it activated? where is it found?

A

Inflames shit up. Activated by increased calcium via infection, allergic etc. ONLY found in inflammatory cells.

32
Q

We like to target 5 lipoxygenase with drugs. Why?

A

It’s ONLY found in inflammatory cells so we can minimize side effects

33
Q

Leukotriene B4 does shit to smooth muscle, so how does it cause inflammation?

A

attracts leukocytes

34
Q

What does montelukast do?

A

blocks CysLT1R (hay fever and asthma)

35
Q

Why is a local mediator only act locally?

A

Rapidly metabolized or ‘diluted’

36
Q

6 reasons why is the Mast Cell so Mighty:

A 
-Antigen via IgE
– Complement fragments C3a/C5a
– Neuropeptides
– Cytokines and chemokines
– Bacterial components
– Physical trauma
37
Q

Histamine interact with what kind of receptors?

A

G-Protein Coupled Receptors (H1-4)

38
Q

What’s Histamine’s Triple Response?

A
  1. Reddening: vasodilation at initiating site
  2. Swelling: increase vascular permeability
  3. Flare: response through sensory fibres
39
Q

What is Pruritus?

A

Itching

40
Q

Antihistamines target which receptor?

A

H1

41
Q

Name 2 sedative antihistamines

A

chlorpheniramine

promethazine

42
Q

Name 2 non-sedative antihistamine drugs. Why were they withdrawn from market?

A

terfenadine

astemizole

43
Q

Name two newer non-sedative agents?

A

Cetirizine

Loratidine

44
Q

Name two H2 receptor antagonists. What do they treat?

A

Cimetidine
Ranitidine
Both treat peptic ulcers

45
Q

Generally: Bradykinin is and does what?

A

Local peptide mediator for pain and inflam

46
Q

Bradykinin degrades into Kininase I and II, Kininase II is also known as:

A

Angiotensin Converting Enzyme

47
Q

Neural action of Bradykinin?

A

stimulate sensory nerve endings: Pain

48
Q

Other actions of Bradykinin?

A
  1. contract uterus, airways, gut

2. epithelial secretion in airways, gut

49
Q

Vascular actions of bradykinin?

A

Dilate arterioles and venules

Increase vascular permeability

50
Q

What is icatibant?

A

Selective B2 receptor antagonist for Rx of hereditary angioedema (too much BK)

51
Q

When the endothelium was removed from a vessel, what does Acetylcholine act like?

A

Vasodilator

52
Q

When the endothelium was intact from a vessel, what does Acetylcholine act like?

A

vasoconstrictor

53
Q

EDRF stand for?

A

endothelium-derived relaxant factor (ie. NO)

54
Q

EDHF stands for? does what?

A

endothelium-derived hyper polarizing factor, relaxes vessels

55
Q

Name the 3 isoforms of NOS

A

– nNOS (nerves, epithelial cells)
– iNOS (inducible- macrophages, smooth muscle)
– eNOS (endothelial cells)

56
Q

What is an L-NAME?

A

Inhibits NOS

57
Q

3 things that NOS does?

A
  1. inhibit platelet adhesion and aggregation
  2. Neurotransmitter
  3. Wasodilates in response to shear forces

Jason's Cardiovascular Block (15 decks)

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