Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

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

Are Cox-1 constitutively expressed or induced?

A

Constitutively expressed (housekeeping-constantly occuring)

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

What are Cox-1 effects on the GI tract?

A
  • ↓ acid/pepsin secretion
    • ↑ mucous/bicarbonate production
    • ↑ contractions of smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

What are Cox-1 effects on the kidneys?

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

* Promote diuresis

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

What are Cox-1 effects on vascular smooth muscle?

A
  • [PGI2, PGE2] - vasodilation

* [TXA2] - vasoconstriction

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

What are Cox-1 effects on the bone?

A

• Stimulates bone formation and resorption

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

Are Cox-2 constitutively expressed or induced?

A

Induced by cytokines, shear stress, and growth factors

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

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

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

A
  • ↑ Heat generation

* ↓ Heat loss

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

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

What are COX-2 effects on endothelial cells?

A
  • Vasodilation

* Anti-aggregatory platelet effects

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

What are COX-2 effects on uterine smooth muscle?

A

• Labor contractions near parturition

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

What are COX-2 effects on the ductus arteriosus?

A

Maintenance of patent ductus arteriosus via vasodilatory effects

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

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

Effect of TXA2 on platelets?

A

TXA2 pro-aggregatory

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

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

A

inhibit HCl secretion,
increase mucous secretion,
increase SM contraction

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

Effect of PGE2/PGI2 on kidney cells?

A

PGE2/PGI2 increase RBF, promotes diuresis

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PGE2 and PGI2 on Inflammatory cells

A

PGE2/PGI2 potentiate pain, edema, fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

Cox-1 inhibitor= antithrombotic

ie: aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Inhibition of COX2 gives which therapeutic effect?
1. Analgesia 2. Antipyretic 3. Anti-inflammatory
26
Side effects of COX-1 inhibition in gastric cells?
Gi ulceration, bleeding
27
Side effects of COX-1 inhibition in platelets?
Increased bleeding risk
28
Side effect of COX-1 and 2 inhibition in kidney cells?
Renal dysfunction
29
Side effect of COX 2 inhibition in uterine SM?
Delay labor
30
Side effect of COX2 inhibition in endothelial cells?
Increased thrombotic event
31
What are the 4 main groups of NSAIDS
1. aspirin 2. traditional tNSAIDs 3. Acetaminophen 4. Celecoxib (COX-2 selective inhibitors)
32
How do you distinguish the 4 main groups of NSAIDS?
1. Selectivity for COX-1 vs COX-2 | 2. Reversible vs irreversible inhibition of COX enzyme
33
Distinguish Aspirin using the 2 criteria needed for separating NSAIDS
irreversible inhibition of COX-1 and COX-2
34
Distinguish tNSAIDs using the 2 criteria needed for separating NSAIDS
reversible inhibition of COX-1 and COX-2
35
Distinguish Acetaminophen using the 2 criteria needed for separating NSAIDS
reversible inhibition of CNS COX-2
36
Distinguish Celecoxib using the 2 criteria needed for separating NSAIDS
reversible selective inhibition of COX-2
37
Which of the 4 main groups of NSAIDs is highest recommended? Why?
acetaminophen. tolerated better even though not as efficacious -NO: GI upset bleeding decreased renal function labor effects. increase in clotting
38
Celecoxib increases or decreases clotting? Does it cause GI upset?
Celecoxib increases clotting | it does not cause GI upset
39
Effects of leukotriene, LTB4 on inflammatory cell function and pulmonary / vascular smooth muscle.
Enhanced chemotaxis of neutrophils, aggregation, and transmigration through the endothelium
40
Effects of leukotriene, LTC4/LTD4/LTE4 on inflammatory cell function and pulmonary / vascular smooth muscle.
Increased vascular permeability, bronchoconstriction, vasoconstriction *imagine squishing a sponge
41
Therapeutic uses of aspirin
analgesic (AG) antipyretic(AP) anti-inflammatory (AI) antithrombotic (AT)
42
Therapeutic uses of acetaminophen
analgesic (AG) | antipyretic(AP)
43
Therapeutic uses of tNSAIDs
AG, AP, AI, AT
44
Therapeutic uses of COX-2 selective inhibitors (Celecoxib)
AG, AP, AI
45
Is a side effect of acetaminophen increase clotting?
No only celecoxib is at risk for increase clotting
46
How is low dose aspirin able to exert an anti-thrombotic / cardioprotective effect?
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
Potential cardiovascular toxicity associated with use of COX-2 selective agents.
* COX-2 is constitutively expressed to prevent clotting | * Inhibiting COX-2 intravascularly allows COX-1's pro-aggregatory effects to increase thrombus formation
48
DDI w/ Celicoxib
warfarin (increased risk of bleeding)
49
DDI w/ Aspirin
phenytoin, warfarin, EtoH, Lithium
50
DDI w/ acetaminophen
alcohol -> hepatotoxicity
51
Contraindication of Aspirin, Ibuprofen/naproxen/ketorolac, Celicoxib?
Pregnancy - all but acetaminophen decreases labor
52
Aspirin and acetaminophen use Phase I or Phase II metabolism?
Phase II
53
Which NSAIDS has antithrombotic properties?
Aspirin * only one - note: acetaminophen is the only one w/ AI effects
54
DDI of aspirin
phenytoin warfarin ETOH lithium
55
DDI of acetominophen
alcohol -> hepatotoxicity
56
DDI of celecoxib
warfarin
57
list which Metabolism each drug uses: phase I or II: 1. Aspirin 2. Acetominophen 3. tNSAIDs 4. Celecoxib
1. Aspirin: Phase 2 2. Acetominophen: Phase 2 3. tNSAIDs: Phase I 4. Celecoxib: Phase I
58
Which drugs use Renal excretion methods: 1. Aspirin 2. Acetominophen 3. tNSAIDs 4. Celecoxib
1. Aspirin: Phase 2 3. tNSAIDs: Phase I 4. Celecoxib: Phase I
59
Mineralocorticoid Effects (aldosterone):
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
What is the most potent anti-inflammatory agent
decamethasone (decadron)
61
What drug has the greatest suppression of ACTH secretion at pituitary
decamethasone (decadron)
62
Hypercoagulability can be increased due to which two diseases?
a. Ie: factor V Leiden: makes clotting harder to turn off Ie: disseminated cancer: makes you more likely to clot
63
Most common type of embolus
Thromboembolus
64
Shock: what is it? what are 3 types?
cant perfuse tissue w/ enough blood 1. Cardiogenic shock: 2. Hypovolemic shock: 3. septic shock
65
What is Cardiogenic shock and Hypovolemic shock?
1. Cardiogenic shock: a. Heart not pumping well enough 2. Hypovolemic shock: a. Not enough blood volume
66
Red infarctions are also considered which: hemorrhagic or anemic? arterial or venous blockage?
Hemorrhagic | Venous
67
White infarctions are also considered which: hemorrhagic or anemic? arterial or venous blockage?
Anemic | Arterial
68
What is a DIC?
clotting and bleeding at the same time
69
Metaplasia
change from 1 benign, differentiated cell type to another preceding event to cancer if not properly controlled
70
Dysplasia
disordered growth: § Loss of cytologic uniformity § Loss of normal histologic maturation § Loss of architectural orientation
71
what is the hallmark of early pre-malignant neoplasia?
dysplasia
72
Neoplasia
progressive unchecked increase in cell number
73
what is tumor synonymous with?
neoplasia

TT BL and DD Exam1 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions