ANTI INFLAMMATORIES 1 Flashcards

1
Q

WHAT DOES NSAID STAND FOR

A

NON STEROIDAL ANTI INFLAMMATORY DRUGS

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2
Q

IF YOU HAVE PRE EXISTING HEART ISSUES, IS IT WISE TO TAKE NSAIDS WITHOUT CONSULTING A DR

A

NO

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3
Q

WHAT IS THE HISTORY OF ASPIRIN

A

ORIGINALLY SALICYCLIC ACID FROM THE WHITE WILLOW BUT HAD MANY UNDESIRABLE EFFECTS
WAS THE FIRST SYNTHESISED DRUG IN ITS CONVERSION TO ACETYL SALICYLIC ACID WHICH WE NOW KNOW AS ASPIRIN

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4
Q

HOW DOES ASPIRIN WORK

A

IS A SUICIDE INHIBITOR THEREFORE BINDS TO CYCLOOXYGENASE ON THE SERINE RESIDUE
THIS MEANS THE TIME COURSE FOR ASPIRIN IN THE TIME IS TAKES FOR THE BODY TO MAKE NEW COX ENZYMES

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5
Q

WHAT ARE THE PROPERTIES OF NSAIDS

A

ANTI -INFLAMMATORY
ANALGESIC (REDUCES SOME TYPES OF PAIN)
ANTIPYRETIC (REDUCES TEMPERATURE)

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6
Q

WHAT ARE THE BEST KNOWN NSAIDS

A

ASPIRIN
IBUPROFEN
PARACETAMOL

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7
Q

HOW DOES IBUPROFEN WORK

A

COMPETITIVE INHIBITOR

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8
Q

WHAT CHARACTERISTIC DOES PARACETAMOL NOT HAVE

A

PARACETAMOL IS NOT ANTI INFLAMMATORY PURELY BECAUSE IT ACTS ON THE CENTRAL NERVOUS SYSTEM

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9
Q

WHAT IS THE AIM OF NSAIDS

A

DECREASE THE PRODUCT OF INFLAMMATORY MEDIATORS SUCH EICOSANOIDS

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10
Q

WHAT ARE EICOSANOIDS

A

SIGNALLING MOLECULES DERIVED BY THE OXYGENATION OF ARACHIDONIC ACID

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11
Q

WHAT CLASSES OF EICOSANOIDS ARE THERE

A

PROSTAGLANDINS, LEUKOTRINES AND THROMBOXANES

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12
Q

WHAT CONVERTS PHOSPHOLIPID TO ARACHIDONATE

A

PHOSPHOLIPASE

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13
Q

WHAT ARE PROSTAGLANDINS

A

PARACARINE MEDIATORS INDUCED BY TISSUE DAMAGE THAT DIFFUSE OUT AND ACT ON SURROUNDING CELLS AND THEIR RECEPTORS (GPCR)

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14
Q

WHAT DO PROSTAGLANDINS STIMULATE

A
CHEMOATTRACT OTHER INFLAMMATORY CELLS
INCREASE SENSITIVITY OF NOCICEPTORS
CONSTRICTION OF SMOOTH MUSCLE
PLATELET AGGREGATION
THIS DEPENDS ON WHAT PROSTAGLANDINS IN WHAT TISSUE
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15
Q

ARACHINDONATE IS THEN CONVERTED TO WHAT

A

CYCLIC ENDO PEROXIDES

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16
Q

WHAT DO CYCLIC ENDOPEROXIDES CONVERT TO

A

PROSTAGLANDINS

17
Q

HOW IS ARACHINDONATE CONVERTED TO CYCLIC ENDOPEROXIDES

A

BY CYCLOOXYGENASE

18
Q

HOW DO NSAIDS WORK

A

NSAIDS INHIBIT COX ENZYMES THEREBY PREVENTING RELEASE OF INFLAMMATORY MEDIATORS

19
Q

WHAT COX ENZYMES ARE THERE

A

COX1
COX2
COX3

20
Q

WHERE IS COX1 FOUND

A

IN ALL CELL AND IS ALWAYS ACTIVE (IMPORTANT IN HOMEOSTASIS)

21
Q

WHERE IS COX2 FOUND

A

FOUND IN INFLAMMATORY CELLS AND IS INDUCED

22
Q

WHERE IS COX3 FOUND

A

IS A SPLICE VARIANT OF COX1 AND IS RESTRICTED TO THE CNS

23
Q

WHY IS COX1 NOT THE BEST TARGET

A

IMPORTANT IN HOMEOSTASIS THEREFORE MAY HAVE SIDE EFFECTS

24
Q

WHAT IS THE MOST COMMON SIDE EFFECT OF NSAIDS

A

GUT ISSUES: DYSPEPSIA, DIARRHOEA, NAUSEA, ULCERS

25
Q

WHY DO NSAIDS HAVE SIDE EFFECTS ON THE GUT

A

PROSTAGLANDINS HOMEOSTATICALLY HAVE A ROLE IN ACID SECRETION AND PROTECTION OF THE MUCOSA

26
Q

WHY DO NSAIDS ALSO AFFECT THE KIDNEYS

A

PROSTAGLANDINS HOMEOSTATICALLY HAVE A ROLE IN RENAL BLOOD FLOW THEREFORE THERE IS A CHANCE OF RENAL FAILURE

27
Q

WHAT OTHER ISSUES DO NSAIDS CAUSE

A

LIVER DAMAGE

PARACETAMOL HAS A TOXIC INTERMEDIATE

28
Q

SOME NSAIDS ARE ADVANTAGEOUS FOR OTHER ISSUES LIKE

A

ASPIRIN IS AN ANTI THROMBOTIC FOR COX 1 AND IN SMALL DOSES CAN BE USED TO PREVENT HEART ATTACK/ STROKE