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TT BL and DD Exam1 > Saturday Review > Flashcards

Saturday Review Flashcards

1
Q

Prostaglandins, Prostacyclin (PGI2), Thromboxane (TXA), and Leukotriene (LT) all are made from what precursor? What is that precursor converted into?

A

Arachadonic acid precursor -> Cyclooxygenase (PGG) -> Prostaglandins (PGE), Prostacyclins (PGI), Thromboxanes (TXA)

or AA -> 5’HPETE -> Leukotrienes

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2
Q

Leukotriene (LT) is made from what precursor? What is that precursor converted into?

A

Arachadonic acid -> 5-HPETE (lipoxygenase) -> LTA4 -> LTB4 or LTC4/D4/E4

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3
Q

Are Cox-1 constitutively expressed or induced?

A

Constitutively expressed (housekeeping-constantly occuring)

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4
Q

What are Cox-1 effects on the GI tract?

A
  • ↓ acid/pepsin secretion
    • ↑ mucous/bicarbonate production
    • ↑ contractions of smooth muscle
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5
Q

What are Cox-1 effects on platelets?

What happens if we use too much NSAIDS?

A

• Pro-aggregatory effect

Possibly bleed too much

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6
Q

What are Cox-1 effects on the kidneys?

A
  • ↑ Renal blood flow (makes for healthy kidney)

* Promote diuresis

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7
Q

What are Cox-1 effects on vascular smooth muscle?

A
  • [PGI2, PGE2] - vasodilation

* [TXA2] - vasoconstriction

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8
Q

What are Cox-1 effects on the bone?

A

• Stimulates bone formation and resorption

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9
Q

Are Cox-2 constitutively expressed or induced?

A

Induced by cytokines, shear stress, and growth factors

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10
Q

What inhibits COX-1 and 2? What is the distant substance gets inhibited?

A

NSAID use

inhibits prostaglandins, Thromboxanes, or prostacyclins down the line from AA

but we just need to get rid of COX to get therapeutic effects

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11
Q

What are COX-2 effects on areas of pain/inflammation?

A
  • Enhance edema formation
    • Enhance leukocyte infiltration via vasodilation
    • Potentiation of bradykinin pain-producing activity
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12
Q

What are COX-2 effects on the Hypothalamus/Fever?

A
  • ↑ Heat generation

* ↓ Heat loss

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13
Q

What are COX-2 effects on the kidneys?

A
  • Renal adaptation to stress via maintenance of RBF

* Present constitutively, but most important in elderly

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14
Q

What are COX-2 effects on endothelial cells?

A
  • Vasodilation

* Anti-aggregatory platelet effects

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15
Q

What are COX-2 effects on uterine smooth muscle?

A

• Labor contractions near parturition

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16
Q

What are COX-2 effects on the ductus arteriosus?

A

Maintenance of patent ductus arteriosus via vasodilatory effects

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17
Q

Effects on smooth muscle

PGE2 causes vaso______, TXA2 causes vaso______, PGI (prostacyclin) causes vaso_____

A

PGE2 causes vasodilation,
TXA2 causes vasoconstriction
PGI causes vasodilation

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18
Q

Effect of TXA2 on platelets?

A

TXA2 pro-aggregatory

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19
Q

Effect of PGE2/PGI2 on GI tract smooth muscle & secretory cells?

A

inhibit HCl secretion,
increase mucous secretion,
increase SM contraction

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20
Q

Effect of PGE2/PGI2 on kidney cells?

A

PGE2/PGI2 increase RBF, promotes diuresis

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21
Q

Effect of PGE2/PGF2 on uterine cells?

What happens when we use NSAIDS near term?

A

PGE2/PGF2 induces contractions near parturition

-use of NSAIDS may delay labor

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22
Q

PGE2 and PGI2 on Inflammatory cells

A

PGE2/PGI2 potentiate pain, edema, fever

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23
Q

4 Therapeutic uses of inhibition of COX. How strong of doses do the COX inhibitors have to be for each one?

A
  1. Analgesia - medium dose PRN
  2. Antipyretic - medium dose PRN
  3. Anti-inflammatory - high dose
  4. Antithrombotic - low but daily ie: aspirin
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24
Q

Inhibition of which COX (1 or 2) give antithrombotic effects in platelets?

A

Cox-1 inhibitor= antithrombotic

ie: aspirin

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25
Q

Inhibition of COX2 gives which therapeutic effect?

A
  1. Analgesia
  2. Antipyretic
  3. Anti-inflammatory
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26
Q

Side effects of COX-1 inhibition in gastric cells?

A

Gi ulceration, bleeding

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27
Q

Side effects of COX-1 inhibition in platelets?

A

Increased bleeding risk

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28
Q

Side effect of COX-1 and 2 inhibition in kidney cells?

A

Renal dysfunction

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29
Q

Side effect of COX 2 inhibition in uterine SM?

A

Delay labor

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30
Q

Side effect of COX2 inhibition in endothelial cells?

A

Increased thrombotic event

31
Q

What are the 4 main groups of NSAIDS

A
  1. aspirin
  2. traditional tNSAIDs
  3. Acetaminophen
  4. Celecoxib (COX-2 selective inhibitors)
32
Q

How do you distinguish the 4 main groups of NSAIDS?

A
  1. Selectivity for COX-1 vs COX-2

2. Reversible vs irreversible inhibition of COX enzyme

33
Q

Distinguish Aspirin using the 2 criteria needed for separating NSAIDS

A

irreversible inhibition of COX-1 and COX-2

34
Q

Distinguish tNSAIDs using the 2 criteria needed for separating NSAIDS

A

reversible inhibition of COX-1 and COX-2

35
Q

Distinguish Acetaminophen using the 2 criteria needed for separating NSAIDS

A

reversible inhibition of CNS COX-2

36
Q

Distinguish Celecoxib using the 2 criteria needed for separating NSAIDS

A

reversible selective inhibition of COX-2

37
Q

Which of the 4 main groups of NSAIDs is highest recommended? Why?

A

acetaminophen. tolerated better even though not as efficacious
-NO:
GI upset
bleeding
decreased renal function
labor effects.
increase in clotting

38
Q

Celecoxib increases or decreases clotting? Does it cause GI upset?

A

Celecoxib increases clotting

it does not cause GI upset

39
Q

Effects of leukotriene, LTB4 on inflammatory cell function and pulmonary / vascular smooth muscle.

A

Enhanced chemotaxis of neutrophils, aggregation, and transmigration through the endothelium

40
Q

Effects of leukotriene, LTC4/LTD4/LTE4 on inflammatory cell function and pulmonary / vascular smooth muscle.

A

Increased vascular permeability, bronchoconstriction, vasoconstriction

*imagine squishing a sponge

41
Q

Therapeutic uses of aspirin

A

analgesic (AG)
antipyretic(AP)
anti-inflammatory (AI)
antithrombotic (AT)

42
Q

Therapeutic uses of acetaminophen

A

analgesic (AG)

antipyretic(AP)

43
Q

Therapeutic uses of tNSAIDs

A

AG, AP, AI, AT

44
Q

Therapeutic uses of COX-2 selective inhibitors (Celecoxib)

A

AG, AP, AI

45
Q

Is a side effect of acetaminophen increase clotting?

A

No

only celecoxib is at risk for increase clotting

46
Q

How is low dose aspirin able to exert an anti-thrombotic / cardioprotective effect?

A

Secondary prevention of Myocardial infarction:

Active aspirin (ASA) concentrates in the hepatic portal vein –> concentration differential between endothelial surface and platelets –> selective effect on platelet COX1 and endothelial COX2

@ low dose aspirin: knocks out COX1 and COX2
- COX1 selective bc as soon as COX2 is knocked out, body starts making more faster -> gives you temporal advantage

-also platelets dont have nucleus -> cant make new enzymes

Larger circulating platelet COX1 means that COX1 on the platelets is preferentially inactivated relative to COX2 = anti-thrombotic effect (decrease clotting)

COX1 activated < COX2 activated= decreased clotting

47
Q

Potential cardiovascular toxicity associated with use of COX-2 selective agents.

A
  • COX-2 is constitutively expressed to prevent clotting

* Inhibiting COX-2 intravascularly allows COX-1’s pro-aggregatory effects to increase thrombus formation

48
Q

DDI w/ Celicoxib

A

warfarin (increased risk of bleeding)

49
Q

DDI w/ Aspirin

A

phenytoin, warfarin, EtoH, Lithium

50
Q

DDI w/ acetaminophen

A

alcohol -> hepatotoxicity

51
Q

Contraindication of Aspirin, Ibuprofen/naproxen/ketorolac, Celicoxib?

A

Pregnancy

  • all but acetaminophen decreases labor
52
Q

Aspirin and acetaminophen use Phase I or Phase II metabolism?

A

Phase II

53
Q

Which NSAIDS has antithrombotic properties?

A

Aspirin

  • only one
  • note: acetaminophen is the only one w/ AI effects
54
Q

DDI of aspirin

A

phenytoin
warfarin
ETOH
lithium

55
Q

DDI of acetominophen

A

alcohol -> hepatotoxicity

56
Q

DDI of celecoxib

A

warfarin

57
Q

list which Metabolism each drug uses: phase I or II:

  1. Aspirin
  2. Acetominophen
  3. tNSAIDs
  4. Celecoxib
A
  1. Aspirin: Phase 2
  2. Acetominophen: Phase 2
  3. tNSAIDs: Phase I
  4. Celecoxib: Phase I
58
Q

Which drugs use Renal excretion methods:

  1. Aspirin
  2. Acetominophen
  3. tNSAIDs
  4. Celecoxib
A
  1. Aspirin: Phase 2
  2. tNSAIDs: Phase I
  3. Celecoxib: Phase I
59
Q

Mineralocorticoid Effects (aldosterone):

A

Physiologic:­ Na+ reabsorption at kidney -> ­ blood volume and BP (loosely coupled to ­ K+ and H+ secretion)

Pharmacologic: Excess -> fluid retention (edema), hypertension, hypokalemia, metabolic alkalosis

60
Q

What is the most potent anti-inflammatory agent

A

decamethasone (decadron)

61
Q

What drug has the greatest suppression of ACTH secretion at pituitary

A

decamethasone (decadron)

62
Q

Hypercoagulability can be increased due to which two diseases?

A

a. Ie: factor V Leiden: makes clotting harder to turn off

Ie: disseminated cancer: makes you more likely to clot

63
Q

Most common type of embolus

A

Thromboembolus

64
Q

Shock:
what is it?
what are 3 types?

A

cant perfuse tissue w/ enough blood

  1. Cardiogenic shock:
  2. Hypovolemic shock:
  3. septic shock
65
Q

What is Cardiogenic shock and Hypovolemic shock?

A
  1. Cardiogenic shock:
    a. Heart not pumping well enough
    1. Hypovolemic shock:
      a. Not enough blood volume
66
Q

Red infarctions are also considered which:
hemorrhagic or anemic?
arterial or venous blockage?

A

Hemorrhagic

Venous

67
Q

White infarctions are also considered which:
hemorrhagic or anemic?
arterial or venous blockage?

A

Anemic

Arterial

68
Q

What is a DIC?

A

clotting and bleeding at the same time

69
Q

Metaplasia

A

change from 1 benign, differentiated cell type to another

preceding event to cancer if not properly controlled

70
Q

Dysplasia

A

disordered growth:
§ Loss of cytologic uniformity
§ Loss of normal histologic maturation
§ Loss of architectural orientation

71
Q

what is the hallmark of early pre-malignant neoplasia?

A

dysplasia

72
Q

Neoplasia

A

progressive unchecked increase in cell number

73
Q

what is tumor synonymous with?

A

neoplasia

TT BL and DD Exam1 (23 decks)

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