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Stage 3 Case 1 > Non-opioids > Flashcards

Non-opioids Flashcards

1
Q

What is an NSAID?

A

NSAIDs are drugs that act to relieve inflammation but are not structurally related to the corticosteroids.

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2
Q

3 effects of NSAID

A
  • Analgesic
  • Antipyretic
  • Anti-inflammatory (at higher doses)
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3
Q

How do NSAID’s work?

A

Dampens the body’s inflammatory response by inhibiting COX-2 enzyme (COX-1 is inhibited as well)

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4
Q

Possible side effects of NSAID’s

A

Ulcers because of COX-1 inhibition, gastric haemorrhage, Reye’s syndrome in children (aspirin), ARF

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5
Q

How does paracetamol/acetaminophen work?

A

Activates cannabinoid receptors

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6
Q

What is COX?

A

An enzyme that is responsible for formation of prostanoids, including thromboxane and prostaglandins such as prostacyclin.

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7
Q

Where is COX-1 found?

A

Exists in the tissue as constitutive isoform

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8
Q

Where is COX-2 found?

A

At site of inflammation, cytokines stimulate the induction of the 2nd isoform

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9
Q

How is COX-2 inhibited

A

Anti-inflammatory actions of NSAIDs.

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10
Q

Prostaglandin synthesis pathway

A

Membrane phospholipid -> arachnoidid acid

Then Physiological regulation by COX-1 and Inflammatory response by newly expressed COX-2.

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11
Q

NSAID Analgesic effects

A

(CNS and peripheral effect) may involve non-
PG related effects
Not very strong

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12
Q

NSAID Antipyretic effects

A

(CNS effect) Reduce/increase body temperature

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13
Q

NSAID Anti-inflammatory effects

A 
(except acetaminophen) due mainly to 
 PG inhibition (particularly COX-2 inhibitors)
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14
Q

Uricosuric

A

Drugs that promote the excretion of uric acid

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15
Q

COX-2 central cytokine release

A
  1. COX-2 upregulation in dorsal horn neurones and supporting cells
  2. Prostogalndin production (also via COX-1)
  3. Action on PGE2 receptors on dorsal horn neurones
  4. Enhanced depolarisation of secondary neurones.
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16
Q

COX-2 peripheral inflammation

A
  1. COX-2 upregulation in inflammatory cells
  2. Prosogladin production
  3. Action of peripheral terminal PGE2 receptors
  4. Peripehral sensitization
17
Q

NSAIDs effect on peripheral inflammation?

A

Inhibit COX 2 so prostaglandins cannot be produced. Preventing development of peripheral sensitization

18
Q

NSAIDs effect on central cytokine release?

A

Inhibit COX 2 (and COX-1) so prostaglandins cannot be produced. Preventing enhanced depolarisation of secondary sensory neurones.

19
Q

Inhibition of COX-1 is responsible for their GIT toxicity.

A

Gastritis and peptic ulceration with bleeding and perforation (inhibition of PG + other effects).

20
Q

Effect on Respiration: triphasic (Aspirin)

A
  1. Low doses: uncoupling phosphorylation → ↑ CO2 → stimulates
    respiration.
  2. Direct stimulation of respiratory center → Hyperventilation → resp.
    alkalosis → renal compensation.
  3. Depression of respiratory center and cardiovascular center → ↓ BP,
    respiratory acidosis, no compensation + metabolic acidosis also.
21
Q

GI system (Aspirin)

A
  1. Dose dependent hepatitis.

2. Reye’s syndrome (liver and brain damage in children 9-12).

22
Q

Metabolic (Aspirin)

A
  1. Uncoupling of Oxidative Phosphorylation.

2. Hyperglycemia and depletion of muscle and hepatic glycogen.

23
Q

Endocrine: (Aspirin)

A

corticosteroids, thyroid.

24
Q

Cardiovascular (Aspirin)

A
  1. Platelets: Inhibition of platelet COX-1-derived TxA2with the net effect of
    increasing bleeding time (inhibition of platelet aggregation).
  2. Endothelial COX-2 derived PGI2can inhibit platelet aggregation (inhibition
    augments aggregation by TxA2).
  3. Aspirin (acetylsalicylic acid) covalently modifies and, irreversibly inhibits
    platelet COX. The enzyme is inhibited for the lifetime of the platelet (~8 -11
    days). Effect achieved at very low dose.
  4. Basis of therapeutic efficacy in stroke and MI (reduces mortality and
    prevents recurrent events).
25
Q

Additional Cardiovascular Considerations (Aspirin)

A
  1. Blood vessels/smooth muscle: COX-2 derived PGI2can antagonize
    catecholamine- and angiotensin II-induced vasoconstriction (NSAIDs can
    elevate bp).
  2. Atherosclerosis: Inhibition of COX-2 can destabilize atherosclerotic plaques
    (due to its anti-inflammatory actions).
26
Q

Renal (Aspirin)

A
  1. COX-1 and COX-2 – generated PGs (TxA2, PGF2, PGI2(glom), PGE2
    (medulla), powerful vasodilators) can both increase and decrease Na+
    retention (natriuresis predominates), usually in response to changes in
    tubular Cl-, extracellular tonicity or low bp.
  2. NSAIDs tend to promote Na+retention and can therefore increase bp. Can
    counteract effects of many anti-hypertensives (diuretics, ACE inhibitors and
    -AR antagonists).
  3. PGs have minimal impact on normal renal blood flow but become important
    in the compromised kidney. Patients (particularly elderly and volume
    depleted) are at risk of renal ischemia with NSAIDs.
27
Q

Gastrointestinal (Aspirin)

A

-PGs (generated via COX-1)
1) inhibit stomach acid secretion,
2) stimulate mucus and HCO3-secretion, vasodilation and therefore,
3) are cytoprotective for the gastric mucosa.
-Therefore, NSAIDs with COX-1 inhibitory activity will produce opposite
effects, leading to gastric distress, gastric bleeding, sudden acute
hemorrhage (effects are dose-dependent).

28
Q

Gestation (Aspirin)

A

-PGs (generated from COX-2) are involved in the initiation and progression
of labor and delivery. Therefore, inhibition of their production by NSAIDs
can prolong gestation.

29
Q

Analgesia (Paracetamol mechanism of action)

A

both centrally and peripherally
-associated with moderate anti-inflammatory actions.
-results from inhibition of PG synthesis in inflamed tissues.
-[PGs àlittle pain relief themselves, but potentiate the pain caused
by other mediators of inflammation (e.g., histamine, bradykinin).

30
Q

Anti-inflammatory action (Paracetamol mechanism of action)

A

PGs in inflammation àvasodilation and
increase vascular permeability.
-Inhibition of PGs by NSAIDs attenuates, not abolish, inflammation (NSAIDs
do not inhibit mediators of inflammation).
-Very modest relief from pain, stiffness, swelling for RA àoften prescribed
for their anti-inflammatory actions.

31
Q

Antipyretic actions (Paracetamol mechanism of action)

A

Fever, heat stroke, increase T°are hypothalamic
problems. So, NSAIDs do not decrease body T°.
-Fever àrelease of endogenous pyrogens (e.g., interleukin-1) released from
leucocytes àacts directly on the thermoregulatory centers in hypothalamus
àincrease body temperature.
-This is associated with increase in brain PGs (pyrogenic).
-Prevents the T°-rising effects of interleukin-1 by preventing the increase in
brain PGs.

Stage 3 Case 1 (12 decks)

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