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Pharm > Chapter 16 > Flashcards

Chapter 16 Flashcards

1
Q

analgesic

A

compound with pain blocking properties

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2
Q

Antiinflammatory agents

A

drug that blocks effects of inflammatory response

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3
Q

antipyretic

A

blocking fever

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4
Q

Chrysotherapy

A

treatment with gold salts; gold is taken up by macrophages, which inhibit phagocytosis. Used in patients with whom other methods failed, can be toxic

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5
Q

inflammatory response

A

the bodys nonspecific response to cell injury resulting in pain, swelling, heat and redness

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6
Q

nonsteroidal antiinflammatory drugs

A

drugs that block prostaglandin synthesis and act as antiinflammatory, antipyretic, and analgesic agents

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7
Q

salicyates

A

salicyate acid compounds used as antiinflammatory, antipyretic, anaglesic agents; block prostoglandin system

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8
Q

salicylism

A

syndrome associated with high levels of salicylates - dizziness, ringing in ears, difficultly hearing, nausea, vomitting, diahrea, confusion

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9
Q

An inflammatory response is designed to protect the body from

A

injury and pathogens

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10
Q

Anti - inflammatory agents generally block or alter

A

chemical reactions associated with inflammatory response to stop one or more signs and symptoms of inflammation

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11
Q

What are corticosteroids used for?

A

systemically to block the inflammatory and immune systems.
*adverse effects - decreased resistance to infection

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12
Q

What are corticosteroids used for?

A

Systemically to block the inflammatory and immune systems.
*adverse effects - decreased resistance to infection

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13
Q

What are antihistamines used for

A

block the action of histamine in the initiation of the inflammatory response

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14
Q

Children & older adults are more susceptible to what effects of anti-inflammatory agents?

A

GI and CNS effects

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15
Q

What are the only salicylates recommended for children?

A

Choline magnesium trisalicylate
Aspirin

*do no use when any risk of Reye syndrome, viral infection, febrile, lethargic and personality changes

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16
Q

What are the NSAIDs approved in children?

A

Ibuprofen, naproxen, tolmetin, meloxicam and in some cases, indomethacin

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17
Q

What is the most used analgesic/antipyretic drug for children?

A

Acetaminophen

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18
Q

Children with arthritis may recieve treatment with

A

gold salts or etanercept
must be monitored closely for toxicity

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19
Q

Salicylates, NSAIDs and gold products have what effect on neonates and possibly the mother?

A

severe adverse effects

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20
Q

Geriatric warnings have been associated with which drugs?

A

Naproxen, ketorolac and ketoprofen bc of reports of increased toxicity

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21
Q

Salicylates are popular anti-inflammatory agetns because?

A

their ability to block inflammatory response, fever-blocking, and pain-blocking properties

**oldest anti-inflammatory used

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22
Q

Salicylates were extracted from where? by ancient peoples?

A

willow bark, poplar trees and other plants

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23
Q

What is the therapeutic action of salicylates?

A

Inhibit the synthesis of prostaglandin, an important mediator of the inflam response

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24
Q

How do salicylates decrease fever

A

-Antipyretic effects may be related to blocking prostaglandin mediator or pyrogens at thermoregulatory center of hypothalamus

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25
Q

How do salicylates effect platelet aggregation & blood clot formation?

A

@low levels - -affects platelet aggregation by inhibiting synthesis of thromboxane A2

@high levels - inhibits synthesis of prostacyclin, a vasodilator that inhibits platelet aggregation

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26
Q

Salicylates are indicated for the treatment of ?

A

Mild to moderate pain, fever, and numerous inflammatory conditions

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27
Q

Rheumatoid arthritis is concerned a ____disease
have high levels of?
which interacts with
what happens to the joint?

A

-Autoimmunse disease
-high levels of rheumatoid factor (RF), an antibody to immunoglobulin G (igG)
- interacts with circulating igG to form immune complexes that deposit in synovial fluid in joints, eye and other vessels
-destroys the joint & fills with scar tissue/ a cycle of inflammation & destruction

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28
Q

What are the pharmacokinetics of salicylates?

A

-readily absorbed directly from the stomach
-reaching peak levels in 5 to 30 mins
-The half-life of 15 mins to 12 hours
-Metabolized in liver & excreted in urine
-Cross placenta & enter breast milk

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29
Q

What are the contraindications & cautions of salicylates?

A

Known allergy to salicylates, NSAIDS, tartrazine
Bleeding abnormalities - changes to platelet
Impaired renal function - excreted in urine
Chickenpox or flu - risk of reye syndrome
Surgery or invasive procedures w/in 1 wk - risk of bleeding
pregnancy - adverse effects

30
Q

What are the adverse effects of salicylates?

A

Nausea, heartburn, epigastric discomfort

31
Q

What is salicylism?

A

Can occur with high levels of asprin
dizziness, ringing in ears, difficulty hearing, nausea, vomiting, diahrea, confusion

32
Q

Signs of salicylate toxicity include

A

hyperpnea, tachypnea, hemorrhage, excitment, confusion, pulmonary edema, convulsions, fever, coma, cardio, renal or respiratory collapse

33
Q

Why do salicylates interact with other drugs?

A

because of alterations in absorption, effects on the liver, and extension of therapeutic effect

34
Q

NSAIDS provide what kind of effects?

A

strong anti-inflammatory & analgesic effects w/o adverse effects with corticosteroids

35
Q

What is the black box warning for NSAIDS?

A

increased risk in CV events and increased bleeding in GI tract

36
Q

NSAIDS include:

A

Propionic acids
acetic acids
fenamates
oxicam derivatives
cyclooxygenase-2 (Cox-2) inhibators

37
Q

What are the therapeutic actions of NSAIDS?

A

inhibition of prostaglandin synthese
blocks 2 enzymes COX1 and COX2

38
Q

What does COX1 do?
What does COX 2 do?

A

COX1 - present in all tissues, blood clotting, protecting stomach lining, maintaining sodium water balance in kidney

COX 2 - active @ sites of trauma or injury

39
Q

What are NSAIDS used to treat?

A

Signs and symptoms of rheumatoid arthritis & osteoarthritis
relief of mild to moderate pain
treatment of dysmenorrhea
fever reduction

40
Q

What are the pharmacokinetics of NSAIDS?

A

Rapidly absorbed in GI tract
reaching peak levels in 1-3 hours
Metabolized in liver, excreted in urine
Cross placenta & into breast milk

41
Q

What are the contraindication of nSAID?

A

-allergy to NSAID, salicylate, celecoxib, sulfonamides
-CV dysfunction or hypertension - effects of prostaglandins
-Peptic ulcer or known GI bleed
-Pregnancy
-Caution should be used w/ renal or hepatic dysfunction

42
Q

What are the adverse effects of NSAIDS?

A

nausea, GI pain, constipation, diarrhea, headache, dizziness, fatique
-bleeding, platelet inhibition, hypertension, and bone marrow depression have been reported with chronic use

43
Q

What are the important drug to drug interactions with NSAIDS?

A

Decreased effects with loop diuretics
Decreased antihypertenive with beta blocker
Lithium toxicity with ibprofien

44
Q

What is acetaminophen used to treat?

A

moderate to mild pain & fever

45
Q

What is the therapeutic action of acetaminophen?

A

Acts directly on thermoregulatory cells in the hypothalamus to cause sweating and vasodilation causes release of heat, and lowers fever

46
Q

What are the pharmcokinetics of acetaminophen?

A

Rapidly absorbed from GI tract
reaching peak levels in .5 to 2 hours
MEtabolized in liver and excreted in urine
half life of 2 hours

**Also available for IV for adults & children over 2

47
Q

What are the contraindications of acetaminophen?

A

allergy to acetaminophen
pregnancy
hepatic dysfunction or chronic alcoholism - liver

48
Q

What are the adverse effects of acetaminophen?

A

headache, hemolytic anemia, renal dysfunction, skin rash, fever

49
Q

What is the antidote for overdose of acetaminophen?

A

acetylcysteine

50
Q

What are the drug to drug interactions with acetaminophen?

A

Anticoagulants - increased risk of bleeding
chronic ethanol - toxicity
barbiturates, carbamazepine, hydantoins or rifampin - hepatotoxicity

51
Q

What is the gold salt available for use?

A

auranofin (ridaura)

52
Q

What is the therapeutic action of chrysotherapy?

A

inhibition of phagocytosis which blocks the release of lysosomal enzymes and tissue destruction is decreased

53
Q

What is the pharmacokinetics of gold salts?

A

absorbed at varying rates depending on route
widely distributed but seem to concentrate in the hypothalamix-pituitary adrenocortical system & adrenal and renal cortices
excreted in urine and feces
crosses placenta and breast milk

54
Q

What are the contraindications of gold salts?

A

quite toxic
allergy to gold, severs diabetes. CHF, hypertension, recent radiation , toxic levels of heavy metals, pregnancy

55
Q

What are the adverse effects of gold salts?

A

stomatitis, glossitis, gingivitis, pharyngitis, laryngitis, colitis, diarrhea & other GI inflammation, bone marrow depression, flushing, fainting, dizziness,

56
Q

What are the drug to drug interactions of gold salts?

A

penicillamine, antimalarials, cytotoxic drugs or immunosyppressive drugs - toxicity

57
Q

What are the tumor necrosis factor (TNF) drugs?

A

adalimumab (humira)
certolizumab (Cimzia)
etanercept (enbrel)
golimumab (simponi)
infliximab (remicade)

58
Q

What is the therapeutic action of TNF blockers??

A

decrease local effects of TNF, which slowsa the inflammatory response and joint damage associated with it

59
Q

What are TNF blockers prescribed for?

A

Rheumaotid arthritis
polyarticular juvenile arthritis
psoriatic arthritis
plaque psoriasis

60
Q

What are the pharmacokinetics for TNF blockers?

A

must be given subcutaneously
**except of infliximab - IV
Slow onset, usually peaking in 48-72 hours
Excreted in tissues
Half life - 115 hours to 2 weeks
Cross placenta & breast milk

61
Q

What are the contraindications of TNF blockers?

A

acute infection, cancer, sepsis, TB, hepatitis, demyelinating disorders - bc they block body immune response

62
Q

What are the adverse effects of TNF blockers?

A

Black box - serious to fatal infections and development of lymphomas and other cancers

Demyelinating disorders, MS, MI, heart failure, hypotension

63
Q

What are the drug to drug interactions with TNF blockers?

A

other immune suppressant drugs - increase risk of serious infections & cancer
live vaccines

64
Q

Other DMARDS are?

A

Anakinra (kineret)
Leflunomide (arava)
Sarilumab (kevzara)
tofacitinib (xeljanz)
penicillamine (depen)

65
Q

What are the therapeutic actions of
Anakinra (kineret)
Leflunomide (arava)
Sarilumab (kevzara)
tofacitinib (xeljanz)
penicillamine (depen)

A

*Anakinra -interleukin-1 receptor antagoinst/blocks degradation of cartilage
*Leflunomide - inhibits enzyme, dihydroorotate dehydrogenase, relieving signs of inflam & blocking damage
*Sarilumab - interleukin 6 receptor antagonist - decrease inflam
*tofacitinib- kinase inhibor - blocks signaling pathways within immune cells - oral
*penicillamine - lowers immunoglobin M, relieving inflam *2-3 months

66
Q

What are the pharmacokinetics of
ANAKINRA

A

Anakinra - slowly absorbed in subcut, peak 3-7 hours. Metabolized in tissues excreted in urine
half life - 4-6 hrs
* do not use with other immune suppresants

67
Q

What are the pharmacokinetics of

Sarilumab (kevzara)

A

Subcut injection slowly absorbed
peak 2-4 days
half life 10 days
**risk of TB and development of lymphomas/cancers

68
Q

What are the pharmcokinetics of
Leflunomide (arava)

A

slowly absorbed from GI tract
peak n 6-12 hrs
undergoes hepatic metabolism & excreted in urine
1/2 life 14-18 days
*sever hepatic toxicity - monitor liver closely

69
Q

What is the pharmacokinetics of

penicillamine (depen)

A

oral - reaches peak in 1-3 hrs
extensively metabolized in liver, excreted in urine
1/2ife 2-3 hrs
*fatal myasthenic syndrome, bone marrow depression, assorted hypersensitive reactions
**decreased if taken with iron salts or antacids

70
Q

What are the pharmacokinetics of

tofacitinib (xeljanz)

A

absorbed quickly
peak 5-1 hr
metabolized inliver, excreated in urine
1/2 life 3 hours
*risk of TB and development of lymphomas/cancers
**dont use with other immune supp

71
Q

What are the adverse effects of
Leflunomide (arava)
Sarilumab (kevzara)
tofacitinib (xeljanz)
penicillamine (depen)

A

local irratation at injection sites
increased risk of infection

Pharm (16 decks)

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