Brainscape's Knowledge GenomeTM

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


See full index

LSM3211 > L17 & L18 > Flashcards

L17 & L18 Flashcards

1
Q

Name three 1st generation anti-histamines

A
  1. Chlorpheniramine
  2. Diphenhydramine
  3. Promethazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name three 2nd generation anti-histamines

A
  1. Cetirizine
  2. Fexofenadine
  3. Loratadine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of drugs are antihistamines?

A

Inverse agonists

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

Histamine stabilizes H1-receptors in _____ form
Antihistamines stabilize H1-receptors in _____ form

A

Active
Inactive

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

Clinical use of 2nd Gen Antihistamines

A

Preferred for mild-moderate allergy disorders

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

Clinical use of 1st Gen Antihistamines

A

Commonly used for non-allergic conditions

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

Main advantages of 2nd gen antihistamines

A

Non-sedating or Less-sedating antihistamines
High H1-receptor specificity

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

5 cardinal signs of inflammation

A

heating, redness, swelling, pain, loss of function

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

Describe the Arachidonic Acid Cascade

A
  1. Arachidonic acid is a polyunsaturated fatty acid present in cell membranes.
  2. When cells are stimulated by various factors (e.g., hormones, inflammatory mediators), arachidonic acid is released from cell membranes by the action of phospholipase A2 (PKC can also activate PLA2)
  3. Released arachidonic acid is then metabolized by different enzyme pathways, primarily the cyclooxygenase (COX) and lipoxygenase (LOX) pathways, leading to the formation of various eicosanoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the Synthesis of Prostanoids

A
  1. COX-1 or COX-2 cyclooxygenase action: AA → PGG2
  2. COX-1 or COX-2 peroxidase action: PGG2 → PGH2
  3. PGH2 converted into prostanoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name 5 main prostanoids

A

classical prostaglandins (PGE2, PGF2a, PGD2), PGI2 (prostacyclin), TXA2 (thromboxane)

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

What type of receptors are prostanoid receptors

A

GPCRs

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

PGI2 biological function

A

Vasodilatation
Inhibition of platelet aggregation
Renin release
Natriuresis

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

PGD2 biological function

A

Vasodilatation
Inhibition of platelet aggregation
Bronchoconstriction

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

PGF2α biological function

A

Vasoconstriction
Bronchoconstriction
Uterine contraction

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

PGE2 biological function

A

Vasodilatation
Inhibition of gastric acid secretion
Promotion of gastric cytoprotection
Bronchodilation / bronchoconstriction

16
Q

TXA2 biological function

A

Vasoconstriction
Promotion of platelet aggregation
Bronchoconstriction

17
Q

Mechanism of action of traditional NSAIDs

A

Inhibits cyclooxygenase (COX-1/2) and blocks prostanoid production

18
Q

Which NSAID irreversibly acetylates (COX-1/2) by forming covalent bonds with serine residue

A

Aspirin

19
Q

Describe the MOA of aspirin

A

Irreversibly acetylates (COX-1/2) by forming covalent bonds with serine residue → AA access obstructed by acetyl grp in aspirin-modified COX → block prostanoid production

20
Q

Describe the MOA of other NSAIDs besides aspirin

A

Inhibit COX by reversible steric hindrance, blocking the hydrophobic tunnel via hydrogen bonding

21
Q

Three Main actions of NSAIDs in inflammation

A

Anti-inflammatory, Analgesic, Antipyretic

22
Q

MAO of NSAIDs As Anti-inflammatory Drugs

A

Block formation of PGI2, PGE2, PGD2

23
Q

Effect of NSAIDs As Anti-inflammatory Drugs

A

→ Vasodilatation, which contributes to redness, heating and edema
→ Increased vascular permeability, which contributes to swelling (edema)
→ Pain associated with inflammation

24
Q

MAO of NSAIDs As Analgesic Drugs

A

Block PGE2 sensitization of peripheral nociceptive fibres → Reduced sensitization of pain signal transmission via the norciceptors

25
Q

Why is there an “Analgesic Ceiling” for NSAIDs

A

NSAIDs are able to suppress mild-moderate pain because it does not directly block nociceptive activation

26
Q

MAO of NSAIDs As Antipyretic

A

Block formation of PGE2 in the hypothalamus

27
Q

Effect of NSAIDs As Antipyretic

A

By reducing PGE2 levels, NSAIDs lower the set point temperature in the thermoregulatory center, allowing the body to dissipate heat more effectively and reduce the elevated body temp associated with fever

28
Q

Role of Aspirin beyond inflammation

A

As an anti-platelet drug or “blood thinner”

29
Q

Why does Aspirin block more TXA2 than PGI2

A
  • platelets lack a nucleus and the ability to synthesize new proteins → when aspirin irreversibly inhibits the COX1 in platelets, the platelets cannot produce new COX enzymes during their lifespan
  • endothelial cells have nucleus and can synthesize new proteins, including COX1 → when aspirin inhibits the COX1, they can synthesize new COX1 to replace the inactivated ones
30
Q

Adverse Effects of Traditional NSAIDs
- GI Tract: N&V, gastric upset, and gastric ulceration, mainly due to ___________________
- ____________ reaction: skin rash, nasal congestion, anaphylactic shock
- _________ due to blood thinning by aspirin (Type A ADR)
- All non-aspirin NSAIDs have increased risks of heart attack/stroke
- Aspirin-linked __________ in children with viral infection
- Aspirin-induced asthma in susceptible asthmatics, associated with viral URTI
– COX inhibition increases the availability of AA to be broken down by _____________
- Kidney: __________, hypernatremia, H2O retention, edema, ________, ↓glomerular filtration rate (GFR) (Type C ADR)
- ________ toxicity
- High dose: __________, deafness, tinnitus

A

Adverse Effects of Traditional NSAIDs
- GI Tract: N&V, gastric upset, and gastric ulceration, mainly due to COX-1 inhibition: ↓PGE2
- Pseudo-allergic reaction: skin rash, nasal congestion, anaphylactic shock
- Bleeding due to blood thinning by aspirin (Type A ADR)
- All non-aspirin NSAIDs have increased risks of heart attack/stroke
- Aspirin-linked Reye’s Syndrome in children with viral infection
- Aspirin-induced asthma in susceptible asthmatics, associated with viral URTI
– COX inhibition increases the availability of AA to be broken down by LOX into leukotrienes
- Kidney: acute renal failure, hypernatremia, H2O retention, edema, hyperkalemia, ↓glomerular filtration rate (GFR) (Type C ADR)
- Pregnancy toxicity
- High dose: Dizziness, deafness, tinnitus

31
Q

Name a COX-2 Selective Inhibitor (Coxibs)

A

Celecoxib

32
Q

Limitations of Coxibs
- Expectation of _____________ with COX-2 selective inhibitors not realized (still have GI issues, but reduced)
- ____________due to constitutive expression of both COX-1 & COX-2 in the kidney
- ___________ in pregnancy
- Relative increase in _______ favors _________, which may increase the risk of _________ (heart attack and stroke).
- impair ______and hence may exacerbate ulcers - healing requires ______and ________

A

Limitations of Coxibs
- Expectation of complete GI tract sparing with COX-2 selective inhibitors not realized (still have GI issues, but reduced)
- Renal toxicity due to constitutive expression of both COX-1 & COX-2 in the kidney
- contraindicated in pregnancy
- Relative increase in TXA2 favors platelet aggregation, which may increase the risk of thrombosis (heart attack and stroke).
- impair wound healing and hence may exacerbate ulcers - healing requires COX-2 and PGE2

33
Q

Name a CNS-selective COX (may be COX-3) inhibitor

A

Paracetamol (Acetaminophen)

34
Q

Main features of Paracetamol

A

Good analgesic, Potent antipyretic, but weak anti-inflammatory effect

LSM3211 (2 decks)

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