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Microbiology & Pharmacology > Pharmacology - chapter 41 - Anti-inflammatory drugs > Flashcards

Pharmacology - chapter 41 - Anti-inflammatory drugs Flashcards

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0
Q

What is the concentration of prostaglandins in the blood?

A

Next to naut, prostagalndins act locally in the tissues where they are synthesized.

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1
Q

All the NSAIDs act by inhibiting the synthesis of ………………… ?

A

Prostaglandins

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2
Q

What is the primary precursor of prostaglandins, and which enzymes provides it?

A

Archidonic acid is provided by Phospholipase A2 and othr acyl hydrolases.

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3
Q

What three eicosanoids have a ring structure?

A

prostaglandins, thromboxanes and prostacyclins.

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4
Q

What enzyme is responisble for the physiologic production of prostanoids?

A

COX-1

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5
Q

What enzyme is responisble for the elevated production of prostanoids during chronic disease and inflammation?

A

COX-2

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6
Q

COX-2 is constitutively expressed in these three tissues?

A

1 Brain
2 Kidney
3 Bone

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7
Q

What two proinflammatory mediators are particularly associated with COX-2?

A

TNF-alpha and IL-1

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8
Q

Misoprostol?

A

PGE1 analog that is used to protect the mucosal lining of the stomach during chronic NSAID treatment.

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9
Q

Misoprostol and preganancy?

A

Contraindicated, as this drug have the potential to induce abortion.

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10
Q

Iloprost, mechanism and function?

A

Iloprost is a synthetic analog of prostacyclin that binds to IP receptors(prostacyclin receptors) to increase intracellular cAMP. IT is a very potent vasodilator used in treating pulmonary hypertension.

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11
Q

Alprostadil?

A

PGE1 that is naturally produced in tissues such as seminal vesicles and corpus cavernosum. Alprostadil is used to treat erectile dysfunction and to keep the ductus arteriosus open in neonates with congenital heart conditions.

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12
Q

Lubiprostone?

A

PGE1 derivative used to treat chronic idiopathic constipation. Lubiprostone stimulates chloride channels in the intestinal epithelium.

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13
Q

Latanoprost, mechanism and function?

A

PGF2a analog that is used to treat open angle glaucoma. Latanoprost bind to FP receptors and increase uveoscleral outflow - lowering intraocular pressure.

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14
Q

Three major therapeutic actions of NSAIDs?

A

1 anti-inflammatory ction
2 analgesic action
3 antipyretic action

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15
Q

Aspirin, mechanism of action?

A

irreversibly acetylates COX

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16
Q

Antipyretic action of NSAIDs, mechanism?

A

Fever occurs as a result of PGE2 secretion by the perivascular cells in the hypothlamus. So if you lower the PGE2 synthesis you will lower the temperature.

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17
Q

Analgesic action of NSAIDs, mechanism?

A

PGE2 is thought to sensitize nerve endings to the action of bradykinin, histamine and other chemical mediators released by the inflammatory process. Thus, lowering PGE2 desensitizes nerve endings.

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18
Q

Gastrointestinal effects of aspirin, mechanism?

A

Normally, prostacyclin inhibits HCL secretion whereas PGE2 and PGF2a stimulate sythesis of protective mucus in both stomch and small intestine. In the presence of aspirin, HCL secretion is not inhibited and the mucus membrane is impaired = increased risk for ulceration.

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19
Q

NSAID effect on platelets?

A

Low doses of of aspirin can irreversibly inhibit thromboxane production by platelets. Since platelets lack nuclei they cannot synthesize new enzyme, and the lack of thromboxane persists for the lifetime of the platelet(3-7 days).

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20
Q

Aspirin metabolism?

A

aspirin is hydrolysed to salicylate and acetic acid by esterases in tissues and blood.

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21
Q

Effect of NSAIDs on cellular respiration?

A

Salicylates, a product of aspirin metabolism, uncouple oxidative phosphorylation which leads to elevated CO2 and increased respiration.

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22
Q

Co jest Reye syndrome?

A

Reye syndrome is an often fatal condition characterized by fulminant hepatitis and cerebral edema. It occurs when aspirin, or other salicylates, are given during viral infection. Especially encountered in children.

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23
Q

If a child has a viral infection, what NSAID could be given, if antipyretic drugs is needed?

A

Acetaminophen or ibuprofen, non-salicylates.

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24
Q

Why should you take aspirin with food?

A

because asipirin is uncharged in the pH of the stomach. In the stomcah aspirin crosses into mucosal cells where it ionizes and becomes trapped, causing direct damage to the cells.

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25
Q

The propionic acid derivatives, like apirin, inhibit ………… ?

A

the synthesis of prostaglandins, but not leukotrienes.

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26
Q

Ibuprofen, naproxen, fenoprofen, ketoprofen, fluriprofen and oxaprozin are all …………. ?

A

propionic acid derivatives.

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27
Q

Prioxicam and meloxicam are both ………………………. with ……… half life that are used to treat …….., ……… and ………… . Meloxicam inhibits both ……. and …….. , with preferential binding to ………..

A

Prioxicam and meloxicam are both Oxicam derivatives with long half life that are used to treat RA, ankylosing spondylitis and osteoarthritis . Meloxicam inhibits both COX-1 and COX-2 , with preferential binding to COX-2

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28
Q

Indomethacin, sulindac and etodolac are all ……………… and act by ……………….

A

Indomethacin, sulindac and etodolac are all acetic acid derivatives and act by reversibly inhibiting COX

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29
Q

arrange from left to right: from COX-1 affinity to COX-2 affinity

Naproxen, meloxicam, aspirin, ibuprofen, celecoxib

A

aspirin - naproxen - ibuprofen - celecoxib - meloxicam

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30
Q

Celecoxib?

A

selective for inhibition of COX-2, allowing the proper managment of chronic inflammatory conditions.

31
Q

Diclofenac and Tolmetin are both ……………… acids

A

heteroaryl acetic acids

32
Q

Acetaminophe, mechnism?

A

Inhibits COXes primarily in the CNS.

33
Q

Celecoxib, metbolism and adverse effects?

A

Extensively metabolized in the liver by CYP2C9.

Headache, dyspepsia, diarrhea and abdominal pain are the most common adverse effects.

34
Q

Therapeutic disadvantage of Diflunisal?

A

No antipyretic effect

35
Q

Therapeutic disadvantage of Indomethacin?

A

Very potent. Should be considered after less toxic agents have proven ineffective. Upper GI disturbances are common.

36
Q

Therapeutic disadvantages of aspirin and Indomethacin?

A

Upper GI disturbances

37
Q

Therapeutic advantage of aspirin?

A

low cost, long history of safety

38
Q

Therapeutic advantage of Diflunisal?

A

Less GI irritation than aspirin

39
Q

Therapeutic disadvantage of Celecoxib?

A

Potential for increasing myocardial infarctions and strokes

40
Q

Therapeutic advantage of Propionic acid derivatives?

A

Lower toxicity and better acceptance in some patients. Naproxen is considered by some to be the safest NSAID.

41
Q

Therapeutic advantage of Celecoxib?

A

Less GI irritation than aspirin

42
Q

Therapeutic advantage of Sulindac, piroxicam and meloxicam?

A

long half life permits daily or twice daily dosing.

43
Q

Acetaminophen, pharmacokinetics?

A

At normal doses acetaminophen reacts with the sulfhydryl group of glutathione forming mercapturic acid - nontoxic. At therapeutic doses acetaminophen have virtually no adverse effects.

At higher doses a portion of acetaminophen is hydroxylated to form NAPQI - a toxic substance

44
Q

DMARD is short for ?

A

Disease-Modyfying Antirheumatic Agents

45
Q

To lower adverse effects of methotrexate, you can….?

A

take leucovorin once daily after methotrexate.

46
Q

Antipyretic/analgesic of choice in children with viral infections or chicken pox?

A

acetaminophen.

47
Q

Leflunomide, pharmacokinetics?

A

extensively bound to albumin, half life of approx 14-18 days.

48
Q

Leflunomide, mechanism?

A

causes cell arrest of autoimmune lymphocytes through activation on dihydroorotate dehydrogenase. DHODH is necessary for pyrimidine synthesis.

49
Q

Azathioprine?

A

immunosuppressive agent. Kidney transplant rejection prophylaxis

50
Q

Leflunomide, contrindications?

A

pregnancy and in woman with child bering potential. Used with caution in patients who have liver disease

51
Q

What is the role of TNF-alpha and IL-1 in rheumatoid arthritis?

A

They stimulate synovial cells to proliferate and synthesize collagenase, thereby degrading cartilage, stimulate bone resorption and inhibiting proteoglycan synthesis.

52
Q

Cyclophosphamide?

A

cytostatika, that produces cytotoxic effects on both B and T cells. Selectively suppress B-lymphocyte activity.

53
Q

TNF inhibitors, adverse effects?

A

Increased risk for infection(tuberculosis and sepsis) and opportunistic fungal infection. Live vaccinations should be avoided. Rarely, demyelinating disorders and bone marrow suppression may occur.

54
Q

Etanerecept, mechanism?

A

binds to TNF-alpha and blocking its interaction with surface TNF receptors.

55
Q

etanercept, adalimumab, infliximab, golimumab and cerolizumab are all ……… ?

A

TNF inhibitors used to treat symptoms of RA

56
Q

Adalimumab, mechanism?

A

recombinant antibody that binds to TNF-alpha. Results in reduction of MMP-1 and MMP-3, C-reactive protein..

57
Q

Golimumab, mechanism?

A

bind to both soluble and transmembrane TNF-alpha which reduces proinflammatory and autoimmune responses.

58
Q

Certolizumab pegol, mechanism?

A

TNF-alpha that contains fragment of humanized antibody without Fc portion - does not fix complement or cause antibody mediated cytotoxicity.

59
Q

Infliximab, mechanism?

A

chimeric immunoglobulin that binds to TNF-alpha and inhibiting formation of ligand-receptor complex

60
Q

What two interactions are required to activate T lymphocytes?

A 
1 APC(macrophage or B cells) must interact with T cell receptor
2 CD80/CD86 protein on APC must interact with CD28 on T cell.
61
Q

What is CTLA4 and how does it relate to Abatacept?

A

A protein on T lymphocytes that compete with CD28 for binding with CD80/CD86 protein. It inhibits inflammation. Abatacept is made up of the extracellular domain of CTLA4 and therefore works as an antiinflammatory drug - inhibiting activation T lymphocyte

62
Q

Name three ways by which B cells can perpetuate the inflammatory process in the synovium of RA patients?

A

1 activating T lymphocytes
2 produce auto-antibodies, such as CCP
3 produce proinflammatory cytokines, such as TNF-alpha and IL-1

63
Q

Anakinra, mechanism?

A

binds to IL-1 receptor.

64
Q

Name four strategies to treat gout?

A

1 interfere with uric acid synthesis(allopurinol)
2 increasing uric acid excretion(probenecid or sulfinpyrazone)
3 inhibit leukocyte entry into the affected joint(colchicine)
4 NSAIDs

65
Q

Why is aspirin contrindicated in gout?

A

it competes with uric acid for the organic acid secretion mechanism in the proximal tubule.

66
Q

Rituximab, mechanism?

A

antibody directed against the CD20 antigen found on the surface of B cells, resulting in B cell depletion.

67
Q

Colchinine, mechanism?

A

Cochinine binds to tubulin, causing its polymerization. This disrupt the mobility of granulocytes, decreasing their migration into the affected area.

68
Q

for colchicine to be effective it must be administered……. ?

A

within 24-48 hours of attack

69
Q

Most common adverse effect of allopurinol?

A

hypersensitivity reactions, especially skin rashes

70
Q

Probenecid and sulfinpyrazone, mechanism?

A

promote renal clearance by inhibiting the urate-anion exchanger in the proximal tubule that mediate urate reabsorption.

71
Q

Three therapeutic dose-ranges of aspirin, and their clinical manifestations?

A

1 <300 mg/day - prevent platelet aggregation
2 300-2400 mg/day - antipyretic and analgesc effects
3 2400-4000 mg/day - used for antiinflammatory effects

72
Q

Most common adverse effect from therapeutic anti-inflammatory doses of aspirin?

A

gastric upse. Chronic use can cause ulceration.

73
Q

colchinine moa?

A

binds with microtubules in cells that mediate inflammation - incapacitating them in propagating the inflammatory process

74
Q

etanerecept moa?

A

recombinant protein that binds to TNF and prevents inflammation.

75
Q

Celecoxib moa?

A

selective inhibitor of COX2

76
Q

allopurinol inhibits ………….. ?

A

xanthine oxidase

Microbiology & Pharmacology (32 decks)

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