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Pharm Exam 3 > ch 57 > Flashcards

ch 57 Flashcards

1
Q

what cox inhibitor can protect against MI and stroke

A

only Aspirin

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2
Q

which is good cox?

A

COX - 1

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3
Q

which is bad COX?

A

COX-2

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4
Q

what does COX1 do

A

housekeeping chores
protect gastric mucosa
support renal function
promotes platelet aggregation

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5
Q

What does COX2 do

A 
mediates inflammation
sensitizes receptors to painful stimuli
mediates fever and perception to pain in brain
supports renal function in kidney
promotes vasodilation
can contribute to colon cancer
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6
Q

where is COX 2 produced

A

mainly at sites of tissue injury

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7
Q

first generation NSAIDs inhibit

A

COx 1 and 2

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8
Q

Second gen NSAIDs inhibit

A

COX2 only

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9
Q

which COX carries an increased risk for MI and stroke

A

COX2

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10
Q

which COX has adverse effect of renal impairment

A

COX2

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11
Q

COX 1 & COX 2 inhibitors

Promotion/Prevention of MI and stroke and why

A

COX1 - protects against MI and stroke secondary to reduced platelet aggregation

COX2 - Promotes MI and stroke secondary to suppressing vasodilation

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12
Q

Drug of choice for rheumatoid arthritis, osteoarthritis and juvenile arthritis

A

Aspririn

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13
Q

Benefits of ASA

A

inhibiting COX 2
-reduce inflammation, pain and fever

inhibiting COX1
-protect against MI and ischemic stroke

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14
Q

adverse effects ASA

A

gastric ulceration, bleeding and renal impairment

from inhibiting COX1

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15
Q

ASA is a ______ inhibitor of __________

A

ASA is an irreversible inhibitor of cyclooxygenase

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16
Q

NSAIDS are a ______ inhibitor of ________

A

NSAIDS are a reversible (competitive) inhibitors of cyclooxygenase

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17
Q

ASA metabolism

A

rapid conversion to salicylic acid (active metabolite)

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18
Q

salicylic acid is extensively bound to

A

plasma albumin (distributes to all body tissue and fluid including breast milk, fetal tissues and CNS)

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19
Q

used in rheumatic fever, tendinitis and bursitis to suppress inflammation

A

ASA

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20
Q

ASA is most active in what kind of pain

A

joint pain
muscle pain
headache

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21
Q

drug of choice for reducing fever in adults

A

ASA

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22
Q

you cannot give ASA to kids, why

A

Reye syndrome

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23
Q

ASA will reduce fever but will not lower ____

A

body temperature or temp that has been elevated in response to physical activity or rise in environmental temps

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24
Q

body temp is regulated by the

A

hypothothalamus

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25
Q

fever occurs when

A

the set point of the hypothalamus becomes elevated which causes hypothalamus to increase heat production and decrease heat loss

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26
Q

the set point of the hypothalamus elevation is triggered by

A

local synthesis of prostaglandins in response to endogenous pyrogens (fever promoting substances_

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27
Q

ASA works on fever

A

lowers the set point by inhibiting Cox 2 and inhibits pyrogen-induced syntheses of prostaglandins

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28
Q

TXA2

A

promotes clotting

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29
Q

ASA suppresses platelet aggregation by causing

A

irreversible inhibition of COX1

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30
Q

COX 1 makes what (platelet aggregation)

A

TXA2

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31
Q

once a platelet has inhibition of COX1

A

platelet cannot make TXA2 to promote platelet aggregation for the life of the platelet (body has to make new) - essentially inactivates this

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32
Q

Daily ASA is recommended for pt with history of

A 
ischemic stroke
TIA
Acute MI
Previous MI
Chronic stable angina
Unstable angina
Angioplasty and other revascularization procedures
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33
Q

ASA dose recommended for prevention of cardiovascular disease

A

75-81mg/day

higher doses offer no greater protection but will increase risk for GI bleeding

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34
Q

ASA decreases risk of ________ cancer due to inhibition of COX ___

A

colorectal

COX2

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35
Q

side effects ASA

A 
gastric distress
heartburn 
nausea
occult GI bleeding (most cases the daily amount is insignificant - with long term use  it can produce
anemia

gastric ulceration, perforation and bleeding due to increased secretion of acid and pepsin
Decreased production of cytoprotective mucus and bicarbonate
decreased submucosal blood flow
direct irritation of ASA on gastric mucosa

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36
Q

increased risk of gastric ulceration - can occur without preliminary signs

A 
advanced age
PUD
previous intolerance to ASA or other NSAIDS
Cigarette smoking
history of alcohol abuse
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37
Q

hemorrhage secondary to gastric ulceration is due to

A

(hemorrhage due to erosion of stomach wall and suppression of platelet aggregation)

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38
Q

how do we prevent ulcers

A

PPI (proton pump inhibitor)

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39
Q

it is recommended that pts with gastric ulcer histories be tested for

A

H.Pylori

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40
Q

taking just 2 (325mg) ASA can double bleeding time for

A

1 week

41
Q

ASA is contraindicated in

use in caution in

A 
Bleeding disorders such as 
hemophilia
Vit K deficiency
hypoprothrombinemia
HTN - increase r/o hemorrhagic stroke - should be 150/90 or preferably lower prior to starting
pregnancy in third trimester
kids who have chickenpox or influenza
infants

caution in older adults
smokers - higher risk for GI ulceration
H.pylori - linked to GI/bleeds

increased risk for renal injury
ASA causes salt and water retention and edema
increased r/o renal injury due to ASA inhibiting cox1 which deprives kidney of prostaglandins needed for normal function
This is for the following:
heart failure -
hepatic cirrhosis - bleeding risk these pt commonly have coagulation disturbances, increased r/o renal injury. . These pt are at increased risk
hypovolemia -
renal dysfunction

can cause an exacerbation (salicylate hypersensitivity)
asthma -
hay fever
chronic urticaria

nasal polyps - risk for bleeding

asthma and nasal polys - at risk for hypersensitivity

history of alcoholism - higher risk of GI ulceration
anticoagulant therapy

42
Q

ASA should be d/c at least ______prior to surgery

A

1 week to minimize blood loss

43
Q

Do you need to stop ASA prior to dental, derm or cataract surgery

A

no

44
Q

ASA impairs renal function by inhibiting

A

COX1 which deprives kidneys of prostaglandins needed for normal function

45
Q

s/s of renal impairment

A

reduced urine output
weigh gain despite use of diuretics
rapid rise in serum creatinine and BUN

46
Q

a syndrome that begins to develop when ASA levels are barely over therapeutic

A

Salicylism

47
Q

s/s of Salicylism

A

tinnitus
sweating
headache
dizziness

48
Q

if salicylism develops, what do you do?

A

withhold ASA until symptoms subside

resume ASA but with a lower dose

49
Q

Tinnitus and ASA

A

when tinnitus occurs - max acceptable dose has been achieved. but may not be appropriate in older adults who may not develop tinnitus even if levels become toxic

50
Q

ASA acts on CNS to affect resp

A

Acts on CNS to stimulate breathing -> increase CO2 loss and causes respiratory alkalosis

51
Q

in response to resp alkalosis the kidneys

A

excrete more bicarbonate -> then there is a buildup of acids which produces metabolic acidosis

52
Q

Ph reflection in salicylate tox

A

mixed acid base imbalance

53
Q

characteristic symptoms of Reye

A

encephalopathy

fatty liver degeneration

54
Q

epidemiologic connection between Reye syndrome and

A

child having active influenza or chicken pox

55
Q

ASA and pregnancy

A

linked to anemia and postpartum hemorrhage and prolonging labor. Can affect fetus.

56
Q

ASA and fetus when taken during pregnancy

A

prostaglandins prevent closure of ductus arteriosus. ASA can block prostaglandin synthesis and may induce closer of the ductus arteriosus.

associated with low birth weight, stillbirth, renal tox, intracranial hemorrhage and death

57
Q

ASA and breastfeeding

A

safe

58
Q

in older adults ASA

A

contribute to elevated BP
precipitate CHF decompensation
renal failure

59
Q

ASA drug interactions

A

Anticoagulants - can intensify effects of Warfarin, heparin and others. Can increase risk of gastric hemorrhage.

Glucocorticoids - both promote gastric ulcers. A PPI or H2RA for prophylaxis

Alcohol - both increase r/o gastric bleeding. Higher if have 3 or more alcoholic drinks every day while using ASA

NSAIDS - can negate ASA benefits. Give ASA 2 hours before other NSAIDS or utilize high dose ASA therapy instead of using in combo

ACE and ARB - can both increase r/o impaired renal function/renal failure. Low dose ASA is fine, but High dose ASA is a problem

Vaccines - ASA and other NSAIDS can blunt the immune response to vaccines. Should not be used routinely to prevent vaccination associated pain and fever

60
Q

Gastric irritation can be minimized when taking ASA with

A

taking it with water or food

61
Q

ASA and Pt/ptt

A

increases bleeding time without affecting PT/PTT

62
Q

ASA and gout

A

competes with uric acid for excretion and can worsen gout

63
Q

ASA overdose treatment

A

Activated charcoal
Bicarb
Vent support

64
Q

NSAIDs and ASA which is irreversible and which is reversible

A

ASA irreversible

NSAIDS reversible

65
Q

NSAIDS and cardiovascular

A

increase risk for thrombotic events

66
Q

highest cardiovascular risk in NSAIDS

A

indomethacin
sulindac
meloxicam

67
Q

NSAIDS should not be used before coronary artery bypass graft surgery (CABG) or for how long after

A

14 days

68
Q

what hypersensitivity reaction is linked to ibuprophen

A

Stevens Johnson syndrome

69
Q

What is Stevens Johnson syndrome

A

hypersensitivity reaction
a severe hypersensitivity reaction that causes blistering of the skin and mucous membranes and can result in scarring, blindness, and even death.

70
Q

Nonacetylated salicylates: Magnesium salicylate, sodium salicylate and salsalate similarities to ASA

A

inhibit COX1 and COX 2

treat arthritis, moderate pain and fever

GI disturbances

dont give to children with flu or chickenpox - Reye syndrome

does not protect against MI or stroke

avoid in pt with sodium restricted diet (heart failure or HTN)

dont use in renal insufficiency - toxic levels

71
Q

COX 2 blockers (COXIBS)

A

suppresses inflammation and pain
somewhat lower risk for GI side effects
can impair renal function ->hypertension and edema
increase risk for MI/stroke

72
Q

Celecoxib (Celebrex) is for

A 
osteoarthritis
RA
Juvenile idiopathic arthritis
acute pain
ankylosing spondylitis
dysmenorrhea
73
Q

what rare genetic disorder can Celecoxib (celebrex) be used

A

familial adenomatous polyposis - predisposes a development of colorectal cancer

74
Q

what does Celecoxib (Celebrex) block

A

selective COX 2 inhibitor

75
Q

Celecoxib (Celebrex) binds to

A

plasma proteins

76
Q

adverse effects Celecoxib (Celebrex)

A

GI ulceration - lower because it does not block cox 1 which offers GI protective effects - combining with PPI will reduce the possibility

77
Q

Avoid Celecoxib (Celebrex) in

A 
existing heart disease 
those who have just undergone CABG surgery
HTN
Diabetes
Dyslipidemia
following are at higher risk for renal impairment
HTN
EDEMA
Heart failure 
Kidney disease
78
Q

why is risk of MI and stroke increased in Celecoxib (Celebrex)

A

it causes vasoconstriction and does not inhibit COX 1 which means platelet aggregation is not suppressed.

79
Q

what allergy cant have Celecoxib (Celebrex)

A

sulfa

80
Q

Celecoxib (Celebrex) in pregnancy

A

this and other nsaids can cause premature closure of the ductus arteriosus

contraindicated in 3rd trimester

81
Q

Drug interactions Celecoxib (Celebrex)

A

warfarin - increased bleeding risk by enhancing anticoagulant effects

may decrease the diuretics effects of furosemide

ACEs decrease antihypertensive effects bc it causes HTN

Lithium - increase levels

Levels of Celecoxib (Celebrex) may be increased by fluconazole (antifungal)

82
Q

does acetaminophen have antirheumatic actions

A

no - it does not have antirheumatic or antiinflammatory effects like NSAIDS

83
Q

does acetaminophen suppress platelet aggregation

A

no so it does not cause gastric ulceration or decrease renal blood flow

84
Q

acetaminophen major adverse reaction

A

severe liver injury with overdose

85
Q

what is the difference in acetaminophen and ASA

A

ASA inhibits cyclooxygenase in both CNS and periphery - cox 1 and cox 2
tylenol is only CNS (Cox-2)

86
Q

what enzyme is required to convert the tylenol to nontoxic metabolites

A

glutathione - in liver so in therapeutic doses

in overdose your liver runs out of glutathione so it causes severe liver injury

87
Q

adverse effect of tylenol

A

daily use connected with HTN

Stevens Johnson Syndrome
TEN (toxic epidermal necrolysis)
AGEP (acute generalized exanthmatous pustulosis)

88
Q

SJS
TEN
are

A

medical emergencies and can lead to death

89
Q

AGEP is characterized

A

by pustular lesions that predominately affect the upper trunk and body folds - usually resolves within 2 weeks of onset.
stop tylenol, seek medical attention

90
Q

alcoholics and tylenol

A

increased risk for liver injury
induces synthesis of P450 containing enzyme -> increasing production of tylenol toxic metabolite

stores of glutathione are depleted in chronic alcoholics

chronic alcoholics have preexisting liver damage makes them less able to tolerate injury from tylenol

can increase risk for both liver and kidney damage

91
Q

which meds interact with Warfarin

A

ASA
Tylenol
Celebrex

92
Q

if you are an alcoholic, you should consume no more than ______ mg/day

A

3000 instead of 4000

93
Q

is tylenol useful in treating rheumatic fever

A

no because it has no antiinflamatory properties

94
Q

med for tylenol overdose

A

Mucomyst (acetylcysteine)

95
Q

principal feature of tylenol overdose is

A

hepatic necrosis

96
Q

severe tylenol overdose can progress to

A

hepatic failure
coma
death

97
Q

early symptoms of tylenol overdose

A

n/v/d
sweating
abd pain

98
Q

How does mucomyst work

A

substitutes for depleted glutathione to convert the toxic metabolite to the nontoxic

100% effective within 8-10 hours
even when 24 hours later it can help

Pharm Exam 3 (19 decks)

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