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Pharmaco Yr 2 Term 2 > 1st Generation nonselective NSAIDs > Flashcards

1st Generation nonselective NSAIDs Flashcards

1
Q

What does NSAIDs stand for?

A

Nonsteroidal Anti-Inflammatory Drugs

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2
Q

What are 1st generation NSAIDs?

A

Nonselective NSAIDs, that have analgesic and anti-inflammatory properties. They are used for mild-moderate pain that is associated with inflammation (acute causes)

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3
Q

What are the 5 cardinals signs of the acute inflammatory response?

A 
Rubor (Redness)
Tumor (Swelling)
Calor (Heating)
Dolor (Pain)
Functio Laesa (Loss of function)
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4
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage.

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5
Q

What is the pain pathway?

A
  1. Nociception - process of detecting and signalling the presence of a noxious stimulus to the CNS
  2. Transmission - Opiods interfere here
  3. Interpretation - subjective experience by the brain
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6
Q

How is inflammation protective?

A
  • increase blood flow
  • increase leakiness of blood vessels (WBCs can go out to fight the infection)
  • triggers wound healing (cascade)
  • pain –> protect our body by reflexes to prevent further damage
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7
Q

What are the signals of tissue damage (actual/potential)?

A
  • bradykinin (peptide formed when proteases act on protein fragments)
  • cytokines
  • histamines
  • K+ –> increase concentration inside vs outside hence causes damage to cell as it goes out of cell
  • ATP –> ATP goes out of cell
  • Prostanoids: Prostaglandin, Prostacyclin, Thromboxane
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8
Q

How do cell membrane phospholipids form eicosanoids?

A

Phospholipids are acted on by phospholipase A2 to produce arachidonic acid (AA).
Arachidonic acid (AA) is acted on by:
1. 15-Lipoxygenase to form Lipoxins
2. Cyclooxygenase (COX) to form Prostanoids –> Prostaglandins
3. 5 Lipoxygenase to form Leukotrienes

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9
Q

How do Steroids work?

A

They mimic endogenous cortisol to act on glucocorticoid receptors to change the expression of gene, causing reduced production of Phospholipase A2, hence inhibiting production of all eicosanoids

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10
Q

What is the most serious adverse reaction of Steroids?

A

Immunosuppression due to inhibition of leukotrienes

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11
Q

What do NSAIDs target?

A

Cycloxygenase -> inhibits production of prostanoids eg. prostaglandin

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12
Q

What are the 3 types of prostanoids? What do they do?

A

Prostacyclin:

  • vasodilation
  • Inhibits platelet aggregation

Classical Prostaglandin:

  • increases vascular permeability
  • pain

Thromboxane:

  • vasoconstriction
  • platelet aggregation
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13
Q

How do you determine which effect dominates (prostacyclin vs thromboxane)?

A

depends on:

  • cell type
  • nature of injury (close wound - prostacyclin, open wound - thromboxane)
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14
Q

What is Aspirin?

A

An Old NSAID with anti-inflammatory, analgesic and anti-pyretic (anti fever) properties)

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15
Q

What do typical NSAIDs block?

A
  • vasodilation - heating, swelling, redness
  • increased vascular permeability - swelling
  • pain - inflammation
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16
Q

How is Aspirin analgesic?

A

Typical NSAIDs block the production of the prostaglandins, which sensitise the nociception fibres to stimulation by other inflammatory mediators.

17
Q

What is analgesic ceiling? What is it caused by?

A

When an increase in dosage does not result in an increase in analgesia
This is caused due to the presence of Bradykinin and Leukotrienes which is not blocked by NSAIDs (only prostaglandin is).

18
Q

Do NSAIDs alter the normal body temperature?

A

No.

19
Q

What is proof that NSAIDs cross the BBB to the brain?

A

It is antipyretic

20
Q

What do prostaglandins do?

A

They act as the body’s thermostat to regulate the body’s temperature when it is too high.

21
Q

Why do we get fever during infections?

A

Fever increases the temperature of our body to make it a less conducive environment for infection (viral, bacteria)

22
Q

How is Aspirin an effective Antiplatelet?

A

Aspirin is an irreversible COX inhibitor - very potent effect on platelets because platelets are fragments of megakaryocytes which are not full cells and have no nucleus and hence have no apparatus to make new proteins/enzymes and hence cannot synthesize new COX enzymes.

Platelets:
The production of thromboxane (from COX 1) which promotes platelet aggregation can only be restored by formation of new platelets.
Hence the effect lasts 1-2 weeks (long lasting)

vs

Endothelial cells:
The production of prostacyclin (from COX 2) which inhibits platelet aggregation can be restored by synthesis of new enzymes
This effect only lasts a few hours

23
Q

What is baby aspirin?

A

Blood thinnner
Low doses of aspirin of 8mg/day (vs analgesic dose of 500-1000mg every 4-6 hours) for patients at risk of thrombotic effects.

24
Q

What are the adverse effects of Aspirin?

A

DOSE DEPENDENT

NSAID toxicity:

  • Gastric Intolerance
  • bleeding
  • hypersensitivity

Salicylate Chemical Structure induced toxicity:

  • tinnitus
  • uricosuric (increase secretion of uric acid)
  • central hyperventilation
  • respiratory alkalosis
  • fever
  • dehydration
  • metabolic acidosis
  • respiratory acidosis
  • Hyperprothrombinaemia (excessive lack of thrombosis increases risk of bleeding)
  • Vasomotor Collapse
  • Renal and respiratory failure
  • Coma
25
Q

What are the clinical effects of Aspirin

A
  • Antiplatelet
  • Analgesic
  • Anti Inflammatory
  • Antipyretic
26
Q

Why is Aspirin majorly contraindicated in children?

A

It causes Reye’s Syndrome
Rare but life threatening condition causing swelling of brain (encephalitis) and liver due to the accumulation of lipids

Symptoms:
vomiting
personality changes
listelessness
delirium
convulsions
loss of consciousness
death (if pressure is not alleviated)

Risk is higher in children with viral infections
Exception: Kawasaki syndrome - inflammation with increased thrombosis

27
Q

What are some examples of NSAIDs?

A

Naproxen
Indomethacin
Diclofenac

28
Q

What is Naproxen used for?

A

Dysmenorrhoea

  • more effective in women (free fraction 40% higher) but it can still be used in men
  • half life of 12-14 hours (long and hence convenient)
29
Q

What is Indomethacin used for?

A

Strong inflammatory conditions only!
Eg. Rheumatoid Arthritis, Gout
- stronger anti-inflammatory due to additional steroid-like phospholipase A2 inhibition
- CNS adverse effects: 15-25% report confusion or depression. Psychosis and hallucinations also occur

30
Q

What is Diclofenac used for?

A

Inflammatory joint disease
Eg. Rheumatoid Arthritis/Osteoarthritis (Arthritis conditions)
Oral/Topical: cream for joints
- short plasma half-life (<2hrs) therefore low GI risk
- longer half-life in synovial fluid

Pharmaco Yr 2 Term 2 (11 decks)

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