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Pharmacology I > NSAID > Flashcards

NSAID Flashcards

1
Q

What are the Salicylic Acid Derivative NSAID We Need to Know?

A

Acetyl Salicylic Acid (Aspirin) and Diflunisal

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2
Q

What are the Acetic Acid Derivatives NSAID that we need to know?

A

Indomethacin, Etodolac, Diclofenac, Tolmetin, and Ketorolac

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3
Q

What are the Propionic Acid Derivatives NSAID that we need to know?

A

Ibuprofen, Naproxen, Ketoprofen, Oxaprozin

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4
Q

Enolic Acid Derivatives NSAID That are mentioned in Class

A

Piroxicam and Meloxicam

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5
Q

Non Acidic Compound NSAID (Alkanones)

A

Nabumetone

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6
Q

Para amino-phenol Derivative discussed in Class

A

Acetaminophen

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7
Q

What does Celecoxib Inhibit

A

COX-2 EXCLUSIVELY. all the other medication inhibit COX-1 and COX 2

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8
Q
  1. In the stomach is most of Aspirin Ionized or Non Ionized? 2. Is Aspirin ionized or non Ionized in the cells.
A

ASPRIN is ACIDIC
1. In the stomach most of Aspirin is NON-Ionized and can diffuse into the stomach cells easily.

  1. Asprin is mostly IONIZED in the cell.
    (Aspirin and most NSAIDs are Acidic with a Pka of 3.5 (don’t need to know Pka))
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9
Q

What is Asprins mode of action?

A

Aspirin Irreversibly acetylates Cyclooxyrgenase (COX-1 and COX-2) and Inactivates the enzyme.

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10
Q

A patients is about to have surgery and takes aspirin regularly how long must the patient abstain from Aspirin and why?

A

Aspirin Prolongs bleeding time in healthy individuals. The Antithrombin effects are primarliy due to the Irreversible acetylation and inactivation of COX-1 in Platelets and Megakaryocytic cells. (platelets only have COX-1)

Arachidonic acid is catalyzed to TXA2 via COX-1 enzyme (Lack of TXA2 w/o active COX-1)

Patient must abstain for 4-7 days for these Antithrombotic affects to subside

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11
Q

Where is Aspirin mostly absorbed?

A

SMALL INTESTINE
Even though the PH is high (thus medication is mostly ionized) in the small intestine their is high absorption in the the small intestine due to INCREASED SURFACE AREA

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12
Q

Is Aspirin bound or unbound

A

Aspirin and Salicylates are highly bound to plasma protein albumin

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13
Q

Does Aspirin cross the blood brain barrier and placental barrier?

A

Yes Aspirin can cross both placental and blood brain barrier.

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14
Q

How is Aspirin eliminated from the body? What factor will enhance excretion from the body?

A
  1. Excretion is mostly done by the kidneys
  2. Changing Urinary PH from 5 to 8 renal clearance of salicylate increases from 2-3% to the ABOUT 80% (MORE ASPRIN IS IONIZED CAUSING IT to BE EXCRETED) less is reabsorbed.
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15
Q

Why do GI disturbances occur in patients who take Aspirin?

A

Due to inhibition of Prostaglandin production which act in a protective manner in the stomach.

AA covertes to PG but cant since COX is inactive

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16
Q

What are some of the adverse side effects that can occur due to Aspirin?

A

GI
1. Occult bleeding (in stomach)
2. Iron deficiency anemia (1-4.5 g daily) produces and 2-8mL daily blood loss in 70% of pateints which results in anemia.
3. Ulcers

Otic effects
1. Tinnitus can develop from Chronic aspirin/Salicylate use and is REVERSIBLE
1a. development of Tinnitus indicates that adequate plasma concentration have been reached. Initial sign of Chronic Salicylate intoxication.
Hepatic Efects
1. Hepatotoxicity develops after 1-4 weeks of use.
1a. causes acute and REVERSIBLE hepatotoxicity.

Renal Effects.
1. Rare in usual dosage
2. Overdoages can cause renal damage.
2a. Renal Damage caause by reneal medullary ischemia as a result of INHIBITION OF RENAL PROSTAGLANDIN synthesis.
Note: CONSTITUTIVE (always present) COX-2 is in the Kidney (and brain) only two places this is present.

Cardio vascular effects
1. BLACKBOX WARNING: NSAID may cause increased risk of serious cardiovascular thrombotic events, myocardial infarction and stroke

Hematologic
1. daily dose of 3-4 g can decrease hematocrit and plasma iron conc. and reduce erythrocyte lifespan
2. For surgery recommended to discontinued 5-7 says before surgery to prevent excessive bleeding.

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17
Q

What is the Aspirin triad?

A

In Asthma patients, patients with aspirin Sensitivity and Nasal polyps may develop Bronchospasm. (Hypersensitivity reaction)

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18
Q

What Hypersensitivity reaction may develop from Aspirin

A
  1. Urticaria and/ or angioadema. invovles IgE antibodies (type 1 hypersensitivity rxn)
  2. Asthma triad.
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19
Q

What is Reye’s Syndrome?

A

illness in children/young adults associated with use of NSAID in children with Varicella infections (Chicken pox) or influenza-like illness. NSAID IS NOT RECOMMENDED IN CHILDREN WITH INFLUENZA AND CHICKEN POX DUE TO THIS ILLNESS.

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20
Q

What is the recommended treatment for Children who have Varicella or Influenza

A

Acetaminophen

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21
Q

Is Aspirin safe for pregnant women or Lactatiing women?

A
  1. No safe level of use of salicylates during pregnancy has been established. CONgentital abnormalities can occur as SALICYLATES CROSS THE PLACENTAL BARRIER.
  2. NSAID has been found in nursing women milk can cause the baby to have platelet function problem.
22
Q

What is Salicylism and what are the effects of it.

A
  1. Salicylism is defined as Chronic salicylate intoxication (high dosage)
  2. Effects can be
    a. Chronic intoxication,
    b. Tinnitus (bc drug crosses blood brain barrier)
    c. Hyperventilation and CNS effects
    d. Metabolic acidosis and respiratory alkalosis
    e. CNS stimulation and depression
    d. Death occurs from respiratory failure
    d. PRINCLE MANIFISTATION IS ACID-BASE AND ELECTROLYTE DISTURBANCES, DEHYDRATION, HYPERPYREZIA AND HYPERGLYCEMIA OR HYPOGLYCEMIA
23
Q

Treatment for Salicylism

A
  1. Intensive symptomatic support and therapy
  2. Removal of salicylate from GI tract via Gastric lavage (MUST BE WITHIN HR) and use of activated charcoal
  3. To enhance salicylate elimination: IV SODIUM BICARBONATE recommended bc alkalinazation of urine ot pH 7.5 or greater enhances salicylate excretion. ( drug is ionized at high PH )
24
Q

Drug Interaction with NSAID

A
  1. Protein-bound drug
  2. Anticoagulants
  3. Thrombolytic agents
    g. Corticosteroid
    e. NSAID (Salicylates not be used in conjunction with other NSAID) NSAIDs SYNERGIZE
25
Q

What is the mechanism of action for Diflusinal.

A

REVERSIBLY inhibits Cyclooxygenase enzyme COX 1 and 2)

26
Q

Diflusinal Half life vs Aspirin Half Life.

A

Diflusinal = 8-12 hours
Aspirin = 3-4 hours

27
Q

Diflusinal Uses
Diflusinal Adverse reactions

A

Uses= Acute or longeterm relief of mild to moderate pain

  1. Milder GI affects as compared to aspirin
  2. Asprin Tirad
28
Q

Acetic Acid, Propionic Acid, Enolic Acid, Anthranilic Acid and Alkanone Derivatives all have what mode of action

A

REVERSIBLE COX 1 and COX-2 inhibitor

29
Q

Which NSAID is used for Rheumatoid and Osteoarthritis

A

ALL NSAID are suitable EXCEPT Ketoroloac and Mefenamic acid

30
Q

What is the treatment for Juvenile rheumatoid arthritis

A

Tolmetin and Naproxen are two agents indicated for this condition

31
Q

General Absorption of NSAID

A

Readily absorbed into the GI
These are ACIDIC drugs

32
Q

What Cardiovascular Adverse reactions occur with NSAID

A

Hypertension in both normotensive and hypertensive individuals

Hypertension can cause fluid retention and peripheral edema which may compromise cardiac function

33
Q

Your patient presented to clinic with strong headaches adter taking indomethacin. Why did the drug cause her to have strong headaches

A

NSAID can cross the Blood brain barrier.

Ketorolac and Indomethacin are known to cause severe headaches.

CNS adverse effect from NSAID caused bc it can cross Blood brain barrier

34
Q

How do NSAID impact elderly differently

A

Increased sensitivity to NSAID and more likely to develop adverse reaction.

SPONTANEOUS FATAL GI events can occur in elderly patients

35
Q

What are GI adverse reaction for NSAID what can put you at higher risk to them?

A
  1. Gastric or duodenal ulcer with bleeding or perforation.
  2. Intestinal ulceration
  3. Gingival ulcer

Higher risk in patients who smoke and Alcohol

36
Q

What is Autoimmune hemolytic anemia and why does it occur? What Antibiotic causes it

A

Tolmetin

Anemia b/c IgG cells lyce RBC that have NSAID bound to them.

it is REVERSIBLE upon discontinuation of Tolmetin.

37
Q

Why are the NSAID platelet aggregation effects milder for other NSAID compared to Aspirin (antithrombic effects)

A

REMEMBER PLATELETS ONLY HAVE COX-1

The effects are milder because the other NSAID are a REVERSIBLE inhibitor of COX-1 and COX-2. compared to Aspirin which is a IRREVERSIBLE inhibitor of those enzymes.

38
Q

NSAID Hypersensitivity

A

Asthma and anaphylaxis; acute respiratory distress

Ibuprofen has severe reaction w/ fever, rash and abdominal paint

Tolmetin was already mentioned.

39
Q

Renal effects of NSAID include Acute Renal Insufficiency, Interstitial nephritis, Hyperkalemia, Hypernatremia,
and Papillary Necrosis.

What is the cause of these adverse effects?

A

Kidney expresses Constitutive COX-2

AA—>PG via catalytic activity of COX2 in kidney

Kidney damage is done by lack of Prostaglandin (PG) production
NSAID inhibit COX-2 thus PG is unable to be produced in adequate conc.

40
Q

What is fetal Ductus Arteriosus what is the treatment

A

In Fetus Normal passage between pulmonary artery and aorta allow deoxy blood to pass through to aorta

Normally closes at birth but abnormality occurs and doesn’t close.

PG is what allows the duct to stay open

Indomethacin or ibuprofen is used to treat this condition. NSAID block prostaglandin production and induces closure of the duct.

41
Q

Should NSAID be given to pregnant women?

A

NO NSAID can prolong labor and should be avoided especially during the THRID trimester.

42
Q

Why is Celecoxib significant.
where is it metabolized

A

bc it is the only antibitoic that is a COX-2 EXCLUSIVE inhibitor
doesn’t do anything to COX-1

Mechanism is inhibition of prostaglandin via COX2

metabolized in the liver.

43
Q

Compared to other NSAID what are GI side effects of acetaminophen

A

Mild GI side effects compared to NSAID

44
Q

What are the Hypersensitivity reactions associated with Celecoxib

A

patients who have demonstrated allergic rxn to SULFONAMIDES should avoid the drug . (Skin rash occurs through out face chest)
Patient must avoid Celecoxib

Aspirin triade Celecoxib must be avoided

45
Q

Why can COX-2 inhibitors like Celecoxib serious adverse cardiovascular side effects?

A

BC inhibition of COX 2 inhibits vasodilation (lack of prostacyclin PGI2) and declumping is inhibited.

Since COX-1 is not inhibited vasoconstriction and and aggregation still occurs.

All this promotes thrombic events as declumping is inhibited by cox-2 and cox-1 is still active so aggregation still occurs.

46
Q

What does Acetaminophen act on to regulate fever?

A

Hypothalamic heating regulating center.

47
Q

What is the mechanism of action for acetaminophen?

A

WEAKLY inhibits COX-1 and COX-2 primarily affects cells in the brain!!!

48
Q

What is the maximum dose for an alcoholic for acetaminophen and what is the does for normal individuals?

A

Alcoholic = 2 grams MAX
Normal people = 4 grams MAX.

KNOW FOR EXAM

49
Q

Why does acetaminophen cause hepatoxicitiy. how is it normally metabolized?

A

Acetaminophen metabolized by hepatic enzyme to acetaminophen sulfate and acetaminophen glucuronide. These aren’t the problem these inactive metabolites are excreted out in urine.

Small amount is metabolized by CYP 450 to form N-acetyl-p-benzoquinoneime WHICH IS REACTIVE and toxic to liver and kidney. NORMALLy this is further reacts with Glutathione (GSH) and is inactivated from that rxn. HOWEVER if large doses of acetaminophen are given then GSH cant keep up and and the reactive molecule binds to hepatocytes proteins and causes cell hepatic cell death. REFER to slide 76 for visual.

THIS is the result of OVERUSAGE

50
Q

What is the treatment for Acetaminophen overdose.

A
  1. Gastric Lavage
  2. Oral N-Acetylcysteine which is and ANTIDOTE for acetaminophen toxicity.
    RESTORES GSH levels so that it may neutralize the reactive metabolite. (acts as an alternate substrate for conjugation.)

can be given oral or iv

NOTE: critical to begin treatment ASAP must be given within roughly an 8 hour window. from when patient took acetaminophen.

Pharmacology I (12 decks)

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