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Pharmacology > MCPHS PA Pharmacology NSAID practical Info Exam 3 > Flashcards

MCPHS PA Pharmacology NSAID practical Info Exam 3 Flashcards

1
Q

What are NSAIDs targeting to provide thier Analgesic, antipyretic, and anti-inflammatory effects?

A

They all target Cyclooxygenase.

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2
Q

Of all of the drugs we studied in the NSAID section of class which was not Anti-Inflammatory (therefore not an NSAID)?

A

APAP

Acetaminophen

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3
Q

What 3 products of Arachidonic Acid breakdown do NSAID and NSAID like drugs work on?

A

THromboxane A2 (TXA2)

(Platelets)

Prostaglandin E2 (PGE2)

(Leukocytes)

Prostacyclin (PGI2)

(Endothelial Cells)

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4
Q

What does PGE2 do?

A

Vasodilation; inflammation (redness, swelling, pain, attracts WBCs)

Sensitization of Nociceptors on Nerve endings

Central actions to mediate Pain perception

Thermoregulatory control of Temp

Increase mucas secretion in stomach

Increase Renal vasodilation and bloow flow (concern but not precaution)

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5
Q

What does TXA2 do?

A

Reduces platelet aggregation

Minimally promotes Vasodilation

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6
Q

What does PGI2 do?

A

Vasodilation and inhibition of platelet aggregation.

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7
Q

What two types of Cyclooxygenase (COX) did we look at?

A

COX 1 and COX 2

they are 60% identical

COX 3 is an unknown

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8
Q

What does COX 1 do?

A

Found in most tissues

Synthesizes prostaglandins involved in normal cell activity

Increased PGE2 (in most tissues) TXA2 (platelets), and PGI2 (vasculature)

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9
Q

What does COX 2 do?

A

Found in Kidneys and Brain

Inducible in areas of inflammation.

Produces prostaglandins at site of inflammation

Increased PGE2 (inflammed areas; kidney / brain), PGI2 (vasculature)

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10
Q

At what Dose is ASA COX 1 selective?

A

Less than 325 MG

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11
Q

Why is High dose ASA less desirable than non-selective COX inhibitors?

A

Salicylates (like in Acetyl Salacylate Acid) are a direct GI irritant and can lead to a GI bleed.

COX-1 inhibitors cause decrease in mucas secretion in stomach and can lead to stomach bleed.

High Dose ASA is both of the above, dual mechanism can cause higher risk of ulceration.

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12
Q

If stomach bleeds are a concern what NSAIDs might be recommended?

A

Celecoxib

Is a COX2 inhibitor which doesn’t inhibit COX1 and isn’t a Salicylate meaning it has no Stomach ADRs.

Meloxicam

Etodolac

Diclofenac

These are slightly more selective for COX2 and have been linked to less GI bleeds.

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13
Q

What are the adverse effects of non-selective COX inhibitors?

A

Less PGE2 in stomach (GI upset / ulceration / bleeding)

Less TXA2 in platelets (bleeding due to reduced platelet aggregation)

Less PGE2/PGI2 in Atherosclerotic Vessels (Increased BP, platelet aggregation, vasoconstriction = increased risk of MI/Stroke)

Less PGE2/PGI2 in renal vessels (kidney injury and increased BP less renal vasodilation and bloodflow = increased Na/H2O retention.)

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14
Q

Why is low dose ASA Cardioprotective?

A

At Low dose ASA inhibits TXA2 causing an irreversable anti-platelet effect (for 8-10 days) and inhibits only COX1 and not both COX1 and COX2 reducing the PGI2 decrease of inhibiting both.

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15
Q

WHy should you not use ASA on a PT < 19Y/O?

A

There is concern for development of Reye’s Syndrome which leads to liver failure and encephalopathy.

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16
Q

What are the GI ADRs for NSAIDS?

A

ABdominal Pain

Dysplasia

Nausea

Vomiting

Ulcers / Bleeding (rarely)

17
Q

What Hematologic ADRs do NSAIDs have?

A

Bleeding

THrombocytopehia (rare)

Neutropenia

Aplastic Anemia

18
Q

What Cardiovascular ADRs do NSAIDs have?

A

Fluid Retention (less Renal Vasodilation / bloodflow)

HTN

Edema

MI

CHF

19
Q

What Renal ADRs do NSAIDs have?

A

Renal Insufficiency

Renal Failure

20
Q

What Pregnancy ADRs do NSAIDs have?

A

Constriction / Premature closure of PDA in preterm infant (3rd trimester)

(Ibuprofen / Lysine / Indomethacin in infant to promote closure)

21
Q

What Pulmonary / Skin ADRs do NSAIDs have?

A

Hypersensativity concerns

May be solved by switching subclass.

22
Q

What are Leukotrienes?

A

They are a metabolite of Arachidonic Acid that facilitate T-Cell Proliferation and act as Chemo-attractants.

23
Q

How can Leukotrienes lead to NSAID hypersensativity?

A

When COX functions are inhibited more Leukotrienes will be produced as they are an alternative pathway for AA metabolization.

Lareg Chronic doses can lead to the following,

T-Cell proliferation

Chemo-attractant properties,

Asthmatic airway constriction

24
Q

What can be done in a NSAID Hypersensativity situation if a PT still needs NSAIDs?

A

They can attempt to use a different subclass.

25
Q

Why do COX 2 inhibitors lead to an increase in CV events?

A

With COX 1 PGI2 is inhibited which is bad (as inhibiting it causes platelet aggregation / vasocontriction), but TXA2 is inhibited which is good (as inhibiting it reduces platelet aggregation) evening out the effect somwhat.

COX2 inhibits PGI2 but not TXA2, which means there will be platelet aggregation, with no reduction to even it out.

26
Q

Why is Celecoxib the only COX2 inhibitor we are currently using?

A

It was found that the more COX2 Selective something is the More CV risk there is.

27
Q

Can NSAIDs be combined with Low Dose ASA to reduce CV risk?

A

NSAID’s Combined with low Dose ASA see reduced (cardio protective) efficacy, but there may be some benefits to combining Low Dose ASA with COX2 inhibitors.

28
Q

How do Cos inhibitors effect GFR and BP?

A

COX inhibitors constrict the afferent Arteriole due to inhibition of vasodilatory prostaglandins. This increases BP and reduces GFR.

29
Q

What is the “Triple Whammy”?

A

Use of a COX inhibitor, ACEI / ARB, and Diuretic at the same time.

COX inhibitors constrict afferent arteriole.

ACEI/ARBs reduce GFR by dilating the Efferent Arteriole

Diuretics reduce blood flow through glomerulus by reducing blood volume

Combined this leads to large reduction of GFR

Not uncommon to see PT on all 3, but avoid Chronic use of COX inhibitor.

30
Q

Can you use an ACEI/ARB, COX inhibitor, and Diuretic at the sam time?

A

Yes, but the PT will need to be closely monitored for at least 30 days.

31
Q

How does the “Triple Whammy” stop Renal compensatory functions?

A

Normally Renin secretions would lead to Angiotensin II or Aldosterone maintaining Volume / BP, but ACEI/ARB prevent this.

Also PG synthesis would allow for dilation of the Afferent Arteriole increasing GFR, but this is blocked by COX inhibitors.

32
Q

What are the Clinical concerns for COminations of ACEI/ARB with COX inhibitors with Diuretics?

A

COX-inhibitor + ACEI/ARB

Normally body compensates for drug effects by normal volume status (some concern for AKI at the start of ACEI/ARB)

Cox Inhibitor + Diuretic

(Body usually able to maintain GFR with help of ANgiotensin II)

Diuretic + ACEI/ARB

(Body usually able to compemsate via PG synthesis; rarely a concern commonly used together)

33
Q

Which NSAID or NSAID like medication is safest for use in Children?

A

Acetaminophen

34
Q

Which NSAID or NSAID like medication has the least numebr of side effects?

A

Acetaminophen

35
Q

What is the primary concern when using APAP?

A

Ensuring that the max daily dose is not exceeded as it is the #1 cause of liver failure in the world.

36
Q

What is the Danger of Large Doses of APAP?

A

APAP forms NAPQI which is normally detoxified with Glutathione, but to large a dose of APAP leads to to large an amount of NAPQI which will deplete Glutathione and cause cellular necrosis in the liver.

37
Q

What is the max dose of Acetaminophen a day?

A

Approx 4g/day; however in a PT with alcohol abuse history or liver disease max dose should be <2g/day.

38
Q

What should be done in an APAP overdose situation?

A

Treat with N-acetylcysteine (NAC; Mucomist)

This is a GSH precursor to help regenerate Glutathione to help detoxify NAPQI.

Must be given within 24 Hrs ideally within 6-10 Hrs; Fatal within 72 Hrs

Pharmacology (14 decks)

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