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Medical Pharmacology Exam 1 > Antihistamines and NSAIDs > Flashcards

Antihistamines and NSAIDs Flashcards

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USMLE® Step 1 flashcards
1
Q

As a class of drugs, disease modifying anti-rheumatic agents target what 2 cytokines?

A

TNF alpha

IL-1

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2
Q

What is infliximab? How does it work? what 2 diseases is it used for?

A

Humanized anti-TNF-alpha
Works by binding up free TNF alpha
Used for RA and Crohns

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3
Q

What is adalimumab? How does it work? what 2 diseases is it used for?

A

Human antibody to TNF-alpha.
Works by binding up free TNF alpha
Used for RA and Crohns

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4
Q

What is Etanercept? How does it work? what 2 diseases is it used for?

A

Fusion protein containing the TNF alpha receptor
Works by binding up free TNF alpha
Used for RA and Crohns

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5
Q

What is Anakinra? What is it used for? What makes it unique among its class of drugs?

A

Antagonist at IL-1 receptor
Used for RA, other anti-inflammatories
Short half life requires daily injections

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6
Q

Proinflammatory lipid mediators are produced by what major enzyme at the plasma membrane? What is its main substrate and main product?

A

Phospholipase A2
Phosphatidyl choline
Arachidonic acid

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7
Q

How do annexins affect PLA2? What notable drug increases synthesis of annexins?

A

Anexins inhibit PLA2.

Their production is induced by glucocorticoids

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8
Q

What is the substrate for the production of prostaglandins and leukotrienes by their respective enzymes?

A

Arachidonic acid

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9
Q

What is the enzyme target of NSAIDs? What about Zileuton?

A

NSAIDs - Cyclo-oxygenase

Zileuton - Lipoxygenase

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10
Q

What is the major enzyme involved in the release of stored mediators like histamine? What are 2 drugs that block this enzyme?

A

PLC (Phospholipase C)

Cromolyn and nedocromil

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11
Q

Glucocorticoids inhibit the production of prostaglandins, leukotrienes and PAF by _

A

Inhibiting Phospholipase A2

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12
Q

Glucocorticoids inhibit the recruitment of leukocytes by _

A

Inhibiting the production of chemotactic factors

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13
Q

By inhibiting COX, NSAIDs reduce the production of _

A

Prostaglandins

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14
Q

By inhibiting lipoxygenase, zileuton inhibits the production of _

A

Leukotrienes

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15
Q

What is the mechanism of action of cromolyn? What is the net effect?

A

Inhibits degranulation, therefore decreases release of histamines and granular proteins

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16
Q

What is the effect of glucocorticoids on COX, PLA2 and Nitric oxide synthase?

A

Inhibits all of them, block their down stream mediators

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17
Q

What is the enzyme responsible for the production of histamine? What is the precursor? Histamine is preformed / induced when needed?

A

Histidine decarboxylase
Histidine
Preformed

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18
Q

What is the major enzyme involved in the break down of histamine? If this enzyme is absent or non-functional, what can result?

A

Diamine Oxidase

Histamine intolerance

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19
Q

How is histamine related to morphine?

A

It is stored with sulfated polysaccharides, can be displaced by morphine, therefore morphine can increase circulating histamine (itching side effect)

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20
Q

What is complexed with histamine in mast cells / basophils? What about fibroblasts?

A

Mast cells - Heparin

Fibroblasts - Chondroitin sulfate

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21
Q

What is the major antibody type associated with histamine release from mast cells? What is the type of hypersensitivity reaction?

A

IgE

Type 1

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22
Q

Within the CNS, where are histamine neurons located? What is its major function in the CNS?

A

Posterior hypothalamus

Mediates arousal

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23
Q

What type of histamine receptor is associated with vascular endothelium? What is the associated G protein, what is the effect of activation?

A

H1 receptor
Gq
Increased Nitric Oxide production, secondary to IP3 and DAG

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24
Q

How many different types of histamine receptors are there?

A

4, H1 - H4

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25
Q

What is the main receptor that mediates histamine’s inflammatory effects? Where is it located? (5)

A

H1

Smooth muscle, endothelium, cardiac muscle, sensory nerve terminals, CNS neurons

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26
Q

In most places, histamine release promotes smooth muscle constriction. Where is the exception and how does this happen?

A

Exception is vascular smooth muscle

Indirect vasodilation, because histamine releases NO with then causes the relaxation

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27
Q

What is the effect of H1 receptor activation in endothelial cells?

A

Increased NO release, separation of endothelial cells, therefore hypotension and edema

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28
Q

What are 3 smooth muscle beds where histamine works and what are its effects there?

A

Constriction for all
bronchioles - Increased difficulty breathing,
uterine smooth muscle - premature labor
gastric smooth muscle - diarrhea

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29
Q

What is the effect of H1 receptor activation in sensory nerves, hypothalamus and emetic center?

A

Sensory nerves - pain, itching
CNS - hypothalamus - increased wakefulness
CNS - emetic center - Nausea and vomiting

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30
Q

What is the effect of H2 receptor activation on gastric secretions?

A

Increased acid, pepsin and intrinsic factor secretion

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31
Q

What is the histamine triple response?

A

Wheal and flare reaction

Edema, reddening, swelling

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32
Q

What is the major compound used as an antagonist of histamine? What type of an antagonist is it?

A

Epinephrine

Physiological antagonist

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33
Q

What are 2 major histamine release inhibitors discussed? What disease are they used for?

A

Cromolyn and nedocromil

Asthma

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34
Q

The major effect of H1 receptor antagonists is _. What are they used for clinically (4)?

A

Sedation, mainly with first generation drugs

Allergy, uticaria, motion sickness, emesis

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35
Q

Four non-H1 mediated side effects of H1 receptor antagonists are _

A

Anticholinergic effects- Atropine like
Adrenoreceptor blockade
Serotonin receptor blockade
Local anesthesia (via sodium channel block)

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36
Q

What effects do 1st generation antihistamines elicit by acting at adrenoreceptors? Serotonin receptors?

A

Adrenoreceptors - orthstatic hypotension

Serotonin receptors - Increased appetite

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37
Q

What are the 4 first generation antihistamines that we are responsible for?

A

Diphenhydramine
Dimenhydrinate
Cyclizine
Promethazine

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38
Q

What is a main commonality of the first generation antihistamines?

A

All cause sedation

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39
Q

Beyond allergy and uticaria, 3 other uses of the first generation antihistamines are _

A

Motion sickness
Sleep aids
Antiemetics

40
Q

Second generation antihistamines bind poorly to the cholinergic receptors, true or false? What is their intended receptor target?

A

True, poor binding

H1, high receptor selectivity

41
Q

What are the three second generation antihistamines? What are their improvements?

A

Loratidine
Certirizine
Fexofenadine
Poor CNS penetration, therefore low sedation

42
Q

What is the precursor of both prostanoids and leukotrienes? What enzyme makes prostanoids? Leukotrienes?

A

C-20:4 fatty acid
COX
Lipoxygenase

43
Q

What are the 4 prostanoids with biologic activity? What is their precursor?

A 
PGE  - alpha
PGF-alpha
PGI2
TXA2
PGH is the precursor
44
Q

How are protanoids stored? How are they released?

A

They aren’t stored. They are passively released following synthesis. This makes their activity entirely synthesis dependent

45
Q

What is another name for TXA2? PGI2? Where are they found?

A

TXA1 - Thromboxane - endothelium (vasculature)

PGI2 - Prostacyclin - Platelets and macrophages

46
Q

All of the biologically active prostanoids have a half life of 30 seconds, except for one with a half life of 3 mins. Which is this?

A

Prostacyclin

47
Q

What is the enzyme responsible for the synthesis of the common prostanoid precursor? What is this common precursor? What are the 2 components of the synthesizing enzyme?

A

COX enxymes
PGH2
Cyclooxygenase and peroxidase

48
Q

How do the prostanoids affect blood vessels?

A

PGE and PGI dilates

TXA constrict

49
Q

How do prostanoids affect smooth muscle?

A

PGE and PGI dilates
TXA constrict
** PGE does both based on g-protein associated with**

50
Q

What prostanoids inhibit platelet aggregation? Promote?

A

Inhibit - PGI2

Promote - TXA2

51
Q

Which 2 prostanoids are associated with hyperalgesia?

A

PGE and PGI

52
Q

There are types 1, 2 and 3 prostanoids, based on the number of double bonds. Which one is usually most effective? What is the precursor for type 2 prostanoids?

A

Type 2

Arachidonic Acid

53
Q

PGH is the common precursor for the biologically active prostanoids. What enzymes make it? Where are they found?

A

COX1 - All cells except RBC

COX2 - All cells except RBC and platelets

54
Q

Which of COX1 and COX2 is constitutively expressed? Which is inducible? Which can be blocked by corticosteroid and cytokines?

A

COX 1 - Constitutive
COX 2- Inducible
COX 2, blocked by corticosteroids and cytokines

55
Q

At baseline, which COX isotype produces most of the prostanoids found In most tissues? What major tissue is an exception?

A

COX 1 makes most baseline prostanoids

Kidney is exception, where COX 2 plays role

56
Q

Most prostanoids associated with inflammation are produced by what enzyme?

A

COX 2

57
Q

How are the COX enzymes associated with pain? What class of drugs can interfere with this process?

A

During inflammatory injury, COX 2 is made in sensory terminals. They produce PGE and PGI.
NSAIDs block the COX enxymes

58
Q

How are the COX enzymes associated with fever? What class of drugs can interfere with this process?

A 
COX 2 (mediated by IL1 and TNF-alpha) and PGE in the vascular organ of the lamina terminalis cause increase in core body temp.  
Blocked by NSAIDs
59
Q

What is the only COX isotype found in platelets? What is the main product? What is its effect?

A

COX 1
TXA (from arachidonate and PGH)
Stimulates platelet aggregation

60
Q

How do NSAIDs and aspirin differ in their interactions with COX 1?

A

NSAIDs reversibly inhibit while aspirin permanently inhibits COX 1 (approx 1 week platelet lifespan)

61
Q

Regarding platelets, how does PGI affect TXA activity? In what context does COX 2 contribute to PGI synthesis? What is the net effect of COX 2 inhibition?

A

PGI counters TXA, reduces platelet aggregation
COX 2 involved in PGI synthesis in endothelial cells
Inhibit COX 2, reduce PGI, increase clotting

62
Q

What is the major COX isotype in the GI tract? What are the major prostanoids and their locations? What are their net effects?

A

COX 1
PGE - epithelium
PGI - Blood vessels
Decrease acid, increase mucus

63
Q

What is the effect of COX 1 inhibition on the epithelium? What drug is protective against this? How does it work?

A

Causes lysis of epithelium - ulcers

Misoprostol is protective, a PGE analogue

64
Q

Under what circumstances is COX 2 induced in the GI?

A

Following GI infections

65
Q

What major organ expresses both COX 1 and 2 constitutively? What are their functions?

A

Kidney

Maintain renal blood flow

66
Q

What COX isotype is expressed in the uterus? Which prostanoids contract the uterine smooth muscle? Which relaxes it?

A

Both COX 1 and 2
PGE and PGF contract
PGI relaxes

67
Q

What are the 2 notable effects of COX inhibitors on uterine function?

A

Delay premature labor

Can reduce dysmenorrhea (menstrual cramps)

68
Q

Aspirin (Acetylsalicylic acid, ASA) is metabolized to _

A

Salicylic acid

69
Q

How do aspirin and salicylic acid differ in their activities on the COX enzymes?

A

ASA - Irreversible acetylation of both enzymes

Salicylic acid - Reversibly acetylates both enzymes

70
Q

What does the selectivity ratio (Cox 2/ Cox1) of 4.4. tell you about aspirin?

A

It indicates that 4.4 times more aspirin is needed to inhibit Cox 2 than Cox 1. i.e. by the time you are inhibiting Cox 2, Cox 1 already inhibited

71
Q

Among the mixed NSAIDs, what are the preferred target enzymes of ketorolac and indomethacin (Relatively)? What is each used for?

A

Both COX 1 selective (mainly ketotolac, 395 fold selective)
Ketorolac - post-surgical analgesic
Indomethacin - Arthritis, anti-inflammatory

72
Q

Among the mixed NSAIDs, what are the preferred target enzymes of diclofenac, etodolac and meloxicam? What are they used for?

A

All COX 2 selective

All used for arthritis

73
Q

What is the mechanism by which NSAIDs exert their anti-inflammatory effects?

A

Block COX production of all prostanoids

74
Q

WHat is the mechanism by which NSAIDs exert their anti-pyretic effects?

A

Reduced IL1 and TNf- alpha induced increase in PGE2 production in the CNS

75
Q

What are the major prostanoids (2) responsible for inflammatory pain targeted by NSAIDs?

A

PGE2 and PGI2

76
Q

What is the effect of NSAIDs on platelet aggregation? What is the physilogical manifestation? Which of the NSAIDs will produce the longest lasting effect on platelets?

A

Blocks aggregation
Increased bleeding
Aspirin, because of irreversible inhibition

77
Q

What is the effect of NSAIDs on gastric function? What are the prostanoids targeted?

A

Reduces protection, Increases ulcers

PGE2 and PGI2

78
Q

Which NSAIDs provide cardiovascular benefits if taken daily?

A

Aspirin ALONE!

79
Q

What is salacylism? What are the associated symptoms (5)

A

Hypersensitivity to aspirin.
Hyperventilation (MAJOR)
tinnitus, vertigo, emesis and sweating

80
Q

What is reyes syndrome? What are to major symptoms?

A

Syndrome associated with giving aspirin to children with viral illnesses
Acute encephalopathy
Fatty liver degeneration

81
Q

Dyspepsia, ulcers and GI bleeding can be associated with NSAID use. What class of drugs can be used to prevent the effects (3)?

A

Histidine (H2) receptor antagonists
Proton pump inhibitors
Misoprostol

82
Q

In addition to GI effects, what other systems are associated with NSAID toxicity (2)?

A

Renal

Clotting

83
Q

Analgesic, antipyretic and anti-inflammatory. Which of these attributes is not associated with tylenol? Why?

A

Anti-inflammatory

Effects blocked by peroxides, elevated at sites of peroxides

84
Q

While tylenol is generally well tolerated, what organ is usually affected following overdose?

A

Liver

85
Q

Analgesic, antipyretic and anti-inflammatory. Which of these attributes are associated with COX 2 specific NSAIDs? What organ system is at risk with chronic use?

A

All three

Kidneys

86
Q

What is the major use of COX2 selective NSAIDs?

A

Osteoarthritis

Rheumatoid arthritis

87
Q

What are the 4 examples of COX2 selective NSAIDs provided? Which 2 are most specific for COX2? What is their advantage?

A

Meloxicam, celecoxib, rofecoxib, valdecoxib
rofecoxib, valdecoxib
No GI side effects

88
Q

True or false: Only the COX 2 NSAIDs are associated with adverse cardiovascular effects?

A

False, all NSAIDs except aspirin are associated with adverse cardiovascular effects

89
Q

What is the proposed mechanism by which NSAIDs increase cardiovascular risk?

A

Block the COX2 dependent reduction of platelet aggregation

90
Q

What enzyme is reponsible for making leukotrienes from arachidonic acid?

A

5-lipoxygenase

91
Q

What are the leukotriene receptors antagonists that block LTD 4? (2) What are they used for?

A

Zafirlukast
Montelukast
Reduce broncho-constriction and edema in lungs

92
Q

What is the mechanism of zileuton? What are 2 things to be aware of when using this drug?

A

Blocks 5-lipoxygenase

  • increase liver toxicity
  • CYP inhibitor, blocks other drugs metabolism
93
Q

What are the side effects associated with infliximab? How must it be administered?

A

Increased frequency of infections (upper respiratory, urinary).
Must be administered parenterally

94
Q

What is tofacitinib? What disease is it used for? How is it administered? What is its mechanism?

A

Jak kinase inhibitor
Rheumatoid arthritis
Administered orally (only antibody like that)
Inhibits the signalling of cytokines (IL2, IL4 and IL6) that require Jak kinases to signal

95
Q

What are 2 processes that glucocorticoids directly affect? What is an inflammation related process that glucocorticoids don’t directly affect?

A

Directly anti inflammatory and immunosuppressive

Don’t directly affect histamine release

Medical Pharmacology Exam 1 (15 decks)

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