Pharmacology Exam #5

Front 1

What is the most common cause of iron-deficiency anemia in premenopausal women?

Back 1

menstrual blood loss

Front 2

What is the most common cause of iron-deficiency anemia in post-menopausal women?

Back 2

occult blood loss through GI bleeding

Front 3

Ferrous sulfate tablets are _____ supplements.

Which is the most commonly used form?

Back 3

oral iron;

an immediate release ferrous sulfate generic preparation

Front 4

What is the dosage of Ferrous Sulfate tablets?

What are some common ADRs?

Back 4

325mg TID between meals;

constipation, darkened stools, nasuea, epigastric pain

Front 5

_____therapy darkens stools.

Back 5

oral iron

Front 6

When taking oral iron supplements and al-mg hydroxide antacids, want to take the iron at least ____ hour(s) before or ___ hour(s) after the antacid.

Ferrous ion reacts with hydroxide to form........

Back 6

1;3;

insoluble complexes

Front 7

Antacids or H2RAs cause a _______ in epigastric pH which results in a ________ solubility of iron salts from iron supplements.

Back 7

increased; decreased

Front 8

Iron greatly decreases _____ absorption, through a chelation interaction.

Back 8

tetracycline

Front 9

Iron Dextran is a _______ form of iron supplementation.

It is a ______ molecular weight form of iron.

Back 9

parenteral;

higher

Front 10

When using Iron Dextran, need to be cautious about ________ because it can cause a potentially _____________ reaction. Due to this, _______ is required.

Back 10

hypersensitivity;

fatal anaphylactic;

a test dose

Front 11

ADR's are more common in which form of iron supplementation?

Back 11

high molecular weight iron (iron dextran)

Front 12

Delayed reactions at ____-____ hours after recommended doses of Iron Dextran have been reported.

Back 12

24-48

Front 13

Iron dextran is not recommend for its with ____, ____ or ____.

Back 13

CKD, cancer- or chemo-induced anemia

Front 14

When injecting Iron Dextran, only want to inject it into the _______ of the _______. Never inject it into......

Give by deep injection using the ____ Technique to avoid....

Back 14

muscle mass; upper outer quad of the butt;

the arm or exposed area;

z track; leakage into SC tissue and staining of the skin

Front 15

What are three major causes of folic acid deficiency?

Back 15

alcoholism due to poor nutrition, any condition of rapid cell turnover (malignancy), and malabsorption syndromes

Front 16

What is a contraindication for the treatment of folic acid deficiency?

This is because treating with large doses of folate can reverse the hematologic abnormalities but does nothing to correct the _________ damage associated with the B12 deficiency, and it will continue to progress.

Back 16

treatment of pernicious anemia when B12 is deficient;

neurologic

Front 17

If the folic acid deficiency is caused by a ______ inhibitor, then use __________.

This drug is a form of folic acid that does not require......

Back 17

DHFR; leucovorin calcium (folinic acid);

DHFR for conversion to the active form, bypassing the inhibited DHFR

Front 18

The enzyme __________ is needed to convert dietary or supplemental folic acid to the biologically active forms of folate required for DNA synthesis.

Back 18

dihydrofolate reductase (DHFR

Front 19

Epoetin alfa is a ______ manufactured through recombinant DNA technology and has the same actions as ______.

Indicated for: (3)

Contraindicated in ________

Back 19

glycoprotien;

erythropoietin;

anemia associated with CKD, Anemia related to zidovudine (tx in HIV pts), and chemo-induced anemia;

uncontrolled HTN

Front 20

When hemodialysis pts are on epoetin alfa, _____ iron supplements have been reported to fail to maintain adequate iron stores.

Many CKD pts and almost all hemodialysis pts will require ____ iron supplementation

Back 20

oral;

parenteral

Front 21

FDA recommends a target Hbg in the range of ______ when using Epoetin alfa. When exceeds ____g/dL, risk of serious _______ and ______ increases

Back 21

10-12 g/dL;

12;

CV events and death

Front 22

What are the 4 clinical uses for glucocorticoids?

Back 22

adrenal insufficiency (replacement tx), tx of chronic inflammatory dz such as RA, tx of allergic rxns, and immunosuppression (during transplantation)

Front 23

What are (4) adverse drug reactions of glucocorticoids?

Back 23

osteoporosis, peptic ulceration/gastric bleeding, cataracts, suppression of the HPA axis

Front 24

What is the main glucocorticoid?

Back 24

prednisone

Front 25

Cyclooxygenase 2 (COX2) is an inducible enzyme produced in response to.........

Now known to be involved in normal mechanism for normal ____ function, _____ integrity, and ____ function.

Back 25

external stimuli (tissue damage, inflammation);

renal; GIT; platelet

Front 26

PGE2 is the major PG involved in...

Back 26

the inflammatory process

Front 27

During acute and chronic inflammation, PGE2 is produced by _____ Resulting in ___ and ___

Back 27

COX2; pain, vasodilation

Front 28

PGE2 produced in the gastric mucosa is produced by _____

Back 28

COX1

Front 29

In the renal cortex, _____ and ____ Are both present, but ____ predominates. ____ is needed for normal kidney function.

PGE2 and PGI2 produced in the kidney cause renal ____ and maintain _______.

Back 29

COX1; COX2;

COX1; COX2;

vasodilation; perfusion

Front 30

In platelets, COX1 stimulates....

Back 30

TXA2-induced platelet aggregation.

Front 31

Nonselective NSAIDs inhibit both ____, ____ and ____ causing....(6)

Back 31

COX1, COX2 and thromboxane synthetase;

antiinflammatory, analgesic, antipyretic effects, decrease gastric mucosal protection and increase risk of ulceration, decreased renal perfusion, decreased platelet aggregation and increased bleeding tendency

Front 32

Theoretically, selective inhibition of COX2 would produce ____ and ____ effects with decreased risk of GI ulceration, renal toxicity and bleeding. However, clinically the only real advantage of COX2 selectivity is ________.

Back 32

anti-inflammatory, analgesic;

the decreased GI toxicity

Front 33

If only using a COX2 inhibitor, the risk of heart disease or stroke would not be decreased because COX1 can still induce _______ since _____ and ____are only formed through COX1

Back 33

platelet aggregation; TXA2; PGI2

Front 34

What are 5 therapeutic effects of NSAIDs (nonselective)?

Back 34

anti-inflammatory, analgesics, antipyretic, antiplatelet, relief of dysmenorrhea

Front 35

In the GIT, NSAIDs cause a loss of ________ of PGs resulting in ____, ____ and _____.

Back 35

cytoprotective function; irritation, peptic ulcer disease, bleeding

Front 36

NSAIDS inhibit cyclooxygenase which results in decreased ______ production. Platelet aggregation is then _____ and the bleeding time is _____.

Back 36

thomboxane; decreased; increase

Front 37

PGs in the kidneys help maintain _____ And ______ especially in the presence of circulating vasoconstrictors. With diminished synthesis, ______, ______, ______ and _____ can occur.

Back 37

adequate renal blood flow, glomerular filtration rate;

decreased GFR, ischemia, acute renal failure (renal insufficiency) and salt/water retention (hyperkalemia

Front 38

The risk of CHF in the elderly increases with ______ NSAID dose.

Back 38

increased

Front 39

Aspirin causes irreversible inhibition of both _____ and ____.

Effects include: (4)

Back 39

COX1 and COX2;

antiplatelet, analgesic, antipyretic, antiinflammatory

Front 40

Arthritic doses of aspirin can cause _______. ______ and have a direct action on the _____ center causing ___ and_____.

Contraindicated in kids due to...

Back 40

GI ulceration/bleeding; salicylism; respiratory; hyperventilation, and respiratory alkalosis;

Reyes syndrome

Front 41

Aspirin exacerbated respiratory disease (AERD) is an aspirin _______ and is also known as aspirin-induced ______.

Triad: _____, _____ and_______.

Back 41

sensitivity; asthma

asthma, rhinitis with nasal polyps, aspirin intolerance

Front 42

Aspirin causes an ____ in the anticoagulant effect of warfarin.

Back 42

increases

Front 43

Ibuprofen reduces or negates the _______ effects of ASA but not all nonselective NSAIDS exhibit this effect. _______ selective NSAIDs do not appear to interact.

Back 43

cardioprotective; COX2

Front 44

When ibuprofen is given prior to administration of aspirin, it binds reversibly to the ______ catalytic site in platelets, which ______ access to ASA. This allows ____ of ASA to occur before irreversible binding can take place.

____-specific inhibitors and _____ do not interfere with ASA binding to COX1

Back 44

COX1; blocks; metabolism;

COX2; acetaminophen

Front 45

Avoid _____ when using NSAIDS because it exacerbates _____.

Back 45

alcohol; bleeding

Front 46

Nonselective NSAIDs include:

Back 46

Aspirin, Difunisal (nonacetyl salicylates), 1st gen NSAIDs, ibuprofen, naproxen, indomethacin, piroxicam, meloxicam, phenylbutazone

Front 47

Nonacetyl salicylates have a lower incidence of ______ and ____ compared to ASA.

Back 47

GI toxicity; bleeding

Front 48

Difunisal is a ________. Is 3-4x more potent than ASA as an ____ and _____.

No ____ Activity because...

_____-acting than ASA

Back 48

nonacetyl salicylate;

analgesic; anti-inflammatory;

antipyretic; doesn't cross BBB;

longer

Front 49

First generation NSAIDs are used mainly for _____ effects as first line agents for relief of symptoms in ___________ states.

-Examples of conditions: (3)

Avoid ______ because it exacerbates ____ and ____.

Has cross-sensitivity with _____.

Back 49

anti-inflammatory; chronic inflammatory diseases

RA, acute gouty arthritis, acute ankylosing spondylitis

Alcohol; GI irritation, bleeding

ASA

Front 50

Ibuprofen is a _____ Drug indicated for ___, ____ and ___.

Back 50

OTC NSAID; mild pain, fever, dysmenorrhea

Front 51

Naproxen is a ____ Drug indicated for relief of mild-moderate ___ and ___

___ dosing due to longer half-life than ibuprofen.

Back 51

NSAID; pain, fever;

BID

Front 52

Indomethacin is a ____ drug with a high incidence of ________ including.... (6).

Back 52

NSAID, adverse drug reactions.

GI bleeding and ulcers; HA's, vertigo, confusion, blood dyscrasias (neutropenia, thrombocytopenia)

Front 53

Piroxicam is a ____ drug that allows ___ dosing taken with the ________ because of the serious ____ toxicity.

Back 53

NSAID; daily; largest meal; GI

Front 54

Meloxicam is a ____ drug with ____ dosing. Has ___ incidence of GI toxicity and is described as '___' preferential.

Back 54

NSAID; daily; low; COX2

Front 55

Phenylbutazone is a _____ drug and is the most ____ and ___.

Long-term use has caused _____

Back 55

NSAID; potent; dangerous;

fatal aplastic anemia

Front 56

Ketorolac is a _____ generation NSAID and is administered via _____ route.

Back 56

second; parenteral

Front 57

Acetaminophen is a nonopioid and nonsteroidal ____ and ____.

Is an effective alternative for ______ but is a much weaker ______ Agent (Lacks therapeutic ____ and ____ effects)

Back 57

analgesic; antipyretic;

ASA; anti-inflammatory; anti-inflammatory and antiplatelet effects.

Front 58

Acetaminophen has a narrow therapeutic index because it can cause ___________.

Does have a much lower incidence of ___ and _____ than ASA

Back 58

liver toxicity;

GI and hematologic disorders

Front 59

Hepatotoxiciy are conditions that deplete ________.

Depletion of this allows the _______ to accumulate resulting in _____, _____, _____, _____.

Four causes:

Back 59

hepatic glutathione;

toxic metabolite; hepatic necrosis, jaundice, bleeding and encephalopathy;

chronic high acetaminophen doses, chronic alcohol consumption, AIDS, poor nutrition

Front 60

About 4-6% of pts with ASA hypersensitivity are also intolerant to ______.

Back 60

acetaminophen

Front 61

Chronic ethanol ingestion can cause hepatotoxicity even when normal ____________ doses are taken.

Mechanism involves chronic alcohol-induced induction of _____ which is a major isoenzyme involved in the production of...

Back 61

acetaminophen;

CYP2E1; the toxic metabolite

Front 62

Ketorolac and Tromethamine are administered via _______.

Used for short term (up to ___ days) for treatment of.....

Have a potential ______ to ASA and other NSAIDS in pts who have exhibited symptoms of _____, _____, _____, _____, _____ or ____ after exposure to NSAIDS

Back 62

IV/IM;

5; mod-severe acute pain requiring analgesia at the opioid level

cross-sensitivity;

asthma, rhinitis, urticaria, nasal polyps, angioedema, bronchospasm

Front 63

COX-1 is present in virtually _____ and is ___.

Back 63

all cells; constitutive

Front 64

PG's (prostaglandins) produced from COX-1 are involved in the maintenance of normal _____ functions.

Back 64

physiologic

Front 65

PGs function in the stomach by providing the gastric mucosal barrier through stimulating _____ and _____ secretion and mucosa _______.

Back 65

mucous; bicarb;

mucosal blood flow

Front 66

PG's function in the kidney through _____ and _____.

They are vaso-______ which provide renal _______ by maintaining ____ and ____.

Back 66

PGE2; PGI2;

dilating; hemostasis; renal blood flow and glomerular filtration

Front 67

PG's function in hemostasis through ______ (platelets only contain this). Inhibition of this causes the effects of increased _____ and _____.

Back 67

COX1;

GI bleeding; renal insufficiency

Front 68

COX2 is an inducible form in cells experiencing _________ but is considered to be constitutive in the ____ and _____.

Inhibition results in _____, ____ and ____ actions.

Back 68

inflammation; kidney; brain;

anti-inflammatory, analgesic, antipyretic

Front 69

Specific inhibition of COX2 may be a predisposition to ________.

Inhibition removes the ____ Effects and allows the pro-thrombic effects of _____ to predominated (disrupts the balance).

Back 69

thrombosis;

PGI2; TXA2

Front 70

Celecoxib is a _____-specific inhibitor that was approved by the FDA but since, has concluded that all NSAIDS should be contraindicated in pts who are immediately post-op from ____ surgery.

Back 70

COX2;

CABG

Front 71

Selective COX2 inhibitors are cross-reactive with ___ and _____ so need to avoid if known allergy to these.

Back 71

ASA and all other NSAIDS

Front 72

Selective COX2 inhibitors are contraindicated in pts with the _________.

Back 72

asthma triad

Front 73

Selective COX2 inhibitors have cross-reactivity with ____ drugs. Celecoxib is contraindicated in pts who have demonstrated allergic reactions to ______.

Back 73

sulfa; sulfonamides

Front 74

All NSAIDs have a significant risk of ____ toxicity.

Reserve COX2 inhibitors for pts at highest risk for ____________.

Use with great caution or not at all in pts with ____, ____ and ___.

Back 74

GI;

NSAID-induced gastropathy;

chronic renal failure, severe heart disease, hepatic failure

Front 75

COX2 inhibitor induced nephrotoxicity mechanism involves both direct toxic damage to the _____ and decreased ________ secondary to inhibition of renal ___ synthesis.

Back 75

tubules; renal perfusion; PGs

Front 76

COX2 plays a significant role in maintaining ______ in pts with compromised renal function; Therefore, selective COX2 inhibitors offer ___ advantage over nonselective NSAIDs with regard in renal safety in pts with decreased renal function.

Contraindicated in advanced _______ and use with caution in ____, ____ or ___.

Back 76

renal blood flow; no; renal disease; fluid retention, HTN, HF

Front 77

COX2 inhibitors have a probability of a greater _______ effect compared to nonselective NSAIDS.

Back 77

pro-thrombic

Front 78

Celecoxib is the first drug to be approved for the tx of a hereditary form of colorectal cancer known as __________

Back 78

familial adenomatous polyposis

Front 79

All pts with a low risk of GI complications: ____ COX2 inhibitor.

Back 79

no

Front 80

For pts at high risk of GI bleeding, a nonselective ____ plus a ____ or _____ appears to be beneficial

Back 80

NSAID; PPI; misoprostol

Front 81

For pts on low-dose ASA, the ASA negates any ____ benefit of using a COX2 inhibitor.

Back 81

GI benefit

Front 82

AHA now recommends d/c all NSAIDS except ____ in MI pts and pts hospitalized for MI or UA

Back 82

ASA

Front 83

Pts with AF receiving either ASA or warfarin for stroke prevention should avoid using _________

Back 83

NSAIDS

Front 84

Naproxen is the preferred choice for pts with _____ or at high risk since it is considered to be safer for this system.

Back 84

CV

Front 85

First Generation antihistamines include: (6)

Back 85

diphenhydramine, dimenhydrinate, chlorpheniramine, promethazine, cyproheptadine, hydroxyzine

Front 86

Second generation antihistamine drugs include: (5)

Back 86

terfenadine, fexofenadine, loratadine, desloratadine, catirizine

Front 87

Terfenadine is a ________ drug, specifically a ___-drug, and has no __________ activity itself. Unchanged it can cause fatal _____ (______ and _____) when taken by pts with liver disease or concurrently with inhibitors of the P450 system

Back 87

antihistamine; pro-; antihistaminic; arrhythmias; QT prolongation, torsades

Front 88

Fexofenadine is the primary active metabolite of _______ which is a ____ drug

Back 88

terfenadine; antihistamine

Front 89

Desloratadine is the active metabolite of _____ which is a _____ drug.

Back 89

loratadine; antihistamine

Front 90

Catirizine is compared to ______ (a _____ drug) but has a ____ onset and causes more _____.

Back 90

loratadine; antihistamine; faster; drowsiness

Front 91

Promethazine has the highest ______ and ____ Activity; has high _____ activity, and has very high _____ effects.

Back 91

antihistaminic; sedative; anticholinergic; antiemetic

Front 92

Nonsedating antihistamines have mod/high _____ effects, low/no _____ effects, low-no _____ effects and no ____ effects.

Back 92

antihistamine; sedative; anticholinergic; antiemetic

Front 93

First generation antihistamines have variable amounts of activity with regard to ____ activity, _____, _____ effects, _____ activity and ______ activity (prevention of _____)

Back 93

antihistaminic; sedation, anticholinergic; antipruritic; antiemetic (motion sickness)

Front 94

Non-sedating antihistamines have _____ antihistaminic activity but little to no activity as ___, ____ or ____.

Have a ____ Duration of action, ___ onset, and do not penetrate the ____.

Back 94

high;

sedatives; anticholinergics; antiemetics;

long; slow; BBB

Front 95

Which drug has the highest activity in all respects of antihistaminic drugs?

Back 95

promethazine

Front 96

Diphenhydramine is the _____ most active agent in all respects of antihistaminic drugs.

Back 96

second

Front 97

Hydroxyzine is a strong _____ and _______ antihistamine drug

Back 97

sedative; antiemetic

Front 98

Cyproheptadine has significant _______ Activity.

Back 98

anti-serotonin

Front 99

Which antihistamine can be used as an anti-pruritic?

Back 99

hydroxyzine HCL

Front 100

Which antihistamine can be used for the treatment of vertigo?

Back 100

meclizine (antivert)

Front 101

Which antihistamine can be used for the treatment of motion sickness and N/V?

Back 101

dimenhydrinate (dramamine)

Front 102

Oral antihistamines are used for _______ and ______ and for the treatment of a ____ and ____ due to the common cold.

Drug= _________

Back 102

perennial/seasonal allergic rhinitis, vasomotor rhinitis;

runny nose and sneezing;

chlorpheniramine

Front 103

Parenteral antihistamines are used as an adjunct to ___ and other measures in _______.

Drug= __________

Back 103

Epi; anaphylaxis; diphenhydramine

Front 104

Diphenhydramine is used for active and prophylactic treatment of ______.

Also has an anticholinergic effect in _________ disease.

Back 104

motion sickness;

parkinson's

Front 105

Promethazine is used for preop______, as an adjunct to _____ for control of postop pain, and for postop _____ effects.

Back 105

sedation; opioid analgesics; antiemetic

Front 106

Cyproheptadine is used off label to stimulate _________ (antihistamine)

Back 106

appetite

Front 107

Antihistamines may have additive/synergistic effects with CNS ________. Clinically significant for ___ generation agents.

Avoid concurrent use of _____ and Rx/OTC sources of ____ or _____.

______ may be considered minimally sedating.

Back 107

depressants; 1st;

alcohol; sedatives; tranquilizers;

Cetirizine

Front 108

Continuous use of a ____ generation antihistamine is effective for the tx of seasonal and perennial allergic rhinitis.

Back 108

2nd

Front 109

What are the 2 preferred 2nd generation antihistamine agents preferred for the tx of allergic rhinitis? This is because they do not cause _____ at recommended doses.

Back 109

fexofenadine, loratadine and desloratadine;

sedative

Front 110

Which agent/ route of administration is the most effective for controlling all sx of allergic rhinitis?

Back 110

intranasal steroids

Front 111

Which antihistamines are recommended as safe to use during pregnancy?

Back 111

1st and 2nd

Front 112

Antihistamines inhibit ______ reaction only and do not completely stop symptoms since other mediators are involved.

They reduce ____, _____, _____, and ____ but DO NOT reduce ________.

1st gen agents are ____ and cross the BBB causing ______.
2nd gen agents are less able to ______ and are non-_______.

Anticholinergic effects are prominent with ___ generation agents.

Back 112

early phase;

sneezing, nasal pruritis, lacrimation and rhinorrhea; nasal congestion;

lipophilic; sedation; cross the BBB; sedating

1st

Front 113

Intranasal steroids are the DOC for nasal ____ and also considered to be the first line-agents for moderate to severe _____.

Most effective tx for ______, ______, ____, ____ and ____.

No ___ or ___ effects

Back 113

congestion; allergic rhinitis

nasal congestion, discharge, sneezing, post-nasal drip and pruritis;

sedative or anticholinergic

Front 114

For the pharmacologic tx of osteoarthritis, tx is ____ and directed towards providing _______.

____ may be effective in many cases and is usually recommend as initial tx in max adult daily doses (<___g/day)

_____ should be used if inflammatory component is present or if pain relief from above is inadequate

Back 114

empiric; sympathetic;

acetaminophen;

4;

NSAIDS

Front 115

What two drug classes are the most successful for treating fibromyalgia?

Back 115

antidepressants, anticonvulsants

Front 116

Dual MOA antidepressants used for tx of fibromyalgia block reuptake of ____ and ____. (SNRI)

Drugs include: _____ and _____

Back 116

NE; serotonin;

Duloxitine, Milnacipran

Front 117

Anticonvulsant used for fibromyalgia= ______.

Back 117

pregabalin

Front 118

Gout is always preceded by ________

Back 118

hyperuricemia

Front 119

Transient attacks of gouty arthritis are initiated by.......

Back 119

crystallization of urates in and around joints

Front 120

Tophi are...

Back 120

large aggregates of irate crystals and the surrounding inflammatory response

Front 121

Lesch-Nyham syndrome is a _____ disorder affecting only males in which _____ is totally absent

Back 121

X-linked; HGPRT

Front 122

What are the 4 clinical stages of Gout?

Back 122

Asymptomatic hyperuricemia, acute gouty arthritis, inter critical gout, chronic tophaceous gout

Front 123

Acute gouty arthritis (stage 2)= sudden onset of _________ with localized _____, _____ and _____.

Vast majority of first attacks are ______. May last for ___-____ if untreated and will gradually resolve.

Back 123

excruciating joint pain; hyperemia, warmth, extreme tenderness;

monoarticular; hours-weeks

Front 124

Intercritical period of gout (stage 3) is the ____ period between gout attacks.

Without therapy, this becomes ____ and attacks may become ______.

Back 124

asx;

shorter; polyarticular

Front 125

Renal manifestations of gout include: (3)

Back 125

HTN, renal colic, chronic gouty nephrophathy.

Front 126

Renal Colic is......

Back 126

the passage of crystals and stones (uric acid stones)

Front 127

Treatment for chronic gout includes blocking the synthesis of _____ with a ________ inhibitor such as ___ and ____.

Can also use _____ which increases the uric acid secretion (uricosuric agent)

Or can use _______ for chronic gout refractory to conventional meds

Back 127

uric acid; xanthine oxidase; allopurinol and febuxostat;

probenecid;

pegloticase

Front 128

For treatment for acute gout, want to block the entry of ____ into affected joints with a ______ disrupting agent to limit the inflammatory response.

Drug= ___________

Treat associated pain and inflammation with_____ or ______ (orally or intra-articularly)

Back 128

lymphocytes; micrtotubule;

cholchicine

NSAIDs; corticosteroids

Front 129

ASA is contraindicated in acute gout attacks because salicylate competitively inhibits the .....

Back 129

active tubular secretion of irate.

Front 130

Acidic urine ______ urate crystallization. Want to maintain _____ urine through _____ and ______.

Continue this process until.....

Back 130

promotes; alkaline; liberal fluid intake; sodium bicarb

serum uric acid normalizes and tophaceous deposits disappear

Front 131

About ___% of the uric acid that is secreted into the urine gets reabsorbed.

Back 131

80

Front 132

Uricosuric agents prevent ______ of uric acid by blocking the active ____ and enhances _____

Back 132

reabsorption; reabsorption; uric acid excretion

Front 133

Probenecid is a ____ agent. Normal therapeutic doses inhibit the _____ of urate, thereby increasing the urinary _____ of uric acid and _____ the serum uric acid levels.

Initiate with small doses to avoid.......

Stops urate _____ and promotes ______ of urate deposits (mobilization).

*Maintain adequate ____ and ____ the urine

Back 133

uricosuric agent; tubular reabsorption; excretion; decreases;

dumping large amounts of irate into the urine and having possible stone formation

deposition; reabsorption

hydration; alkalinize

Front 134

Probenecid is contraindicated in pts with a history of _________

Back 134

nephrolithiasis

Front 135

For probenecid, do not want to start until an acute attack has ____. Therapy must be continued if already begun during an acute exacerbation.

Therapy may mobilize irate deposits in tissues and joints dumping large mounts of irate into the urine resulting in _____ formation.

Concurrent use of _______ is contraindicated. Results in a net urate _____.

Back 135

subsided;

uric acid stone;

salicylates; retention

Front 136

Anionic form of probenicid may competitively inhibit the active tubular secretion of other ________

Probenecid has beneficial interactions with ____.

Back 136

organic acids;

beta-lactams

Front 137

Pt information regarding use of probenicid includes:
-Avoid _____
-May take with __ or ___ for GI upset
-Drink plenty of water to prevent....
-Must be taken _____ For therapeutic effect

Back 137

aspirin;

food; antacid;

kidney stones;

continuously

Front 138

Allopurinol is a ______ inhibitor. Is metabolized into its active metabolite _____. They both inhibit ______ which is needed to convert ____ to ____ and then to _____. This reduces the production of ____ without affecting the synthesis of vital purines

Back 138

xanthine oxidase; oxipurinol (alloxanthine); xanthine oxidase; hypoxanthine, xanthine, uric acid;

uric acid

Front 139

Allergic skin reaction is common and can be severe with ____ use. Rash may be followed by .....

Back 139

allopurinol;

severe hypersensitivity reactions

Front 140

Allopurinol may cause acute ______ in early stages probably due to......

Maintenance doses of _____ are gien for this

Back 140

gout attacks; mobilization of uric acid from tissue deposits;

colchicine

Front 141

Fluid intake to achieve urine output of >= ______ daily and avoidance of an acidic urine may prevent ______ during allopurinol use.

Back 141

2L;

renal urate stones

Front 142

Pt should take allopurinol with ___ or ____ to avoid GI upset. Drink ___-___ glasses of fluids per day. Avoid agents which ____ the urine.

Back 142

food; milk;

10-12; acidify

Front 143

Febuxostat is a _____ inhibitor that is selective for ________________.

Back 143

xanthine oxidase; nonpurine XO

Front 144

Febuxostat is indicated for ______ in pts with gout. Has drug interactions with medications metabolized by _____.

Back 144

chronic management of hyperuricemia;

XO

Front 145

______ have occurred when therapy with Febuxostat was started. Prophylactic therapy is recommended with ____ or ____

Back 145

Gout flares; NSAIDs, colchicine

Front 146

Pegloticase is a recombinant ___________ which is a modified mammalian _____ (urate oxidase)

This oxidates uric acid to _____ (which is a water soluble purine metabolite) which results in lowering serum _____ levels.

Indicated for ________ refractory to conventional tx in adults.

Back 146

polyethylene glycole (PGE); uricase;

allatoin; uric acid;

chronic gout

Front 147

When using Pegloticase, need to premeditate with ____ and _____ to prevent infusion related and anaphylactic reactions.

Prophylactic administration of ____ or ____ is recommended starting 1 week before the first infusion and continuing for at least ____ months in order to prevent gout flare.

Back 147

antihistamines; corticosteroids;

NSAID or colchicine

Front 148

Colchicine binds to ____ (protein in microtubules) and prevents its _____ which causes:
-Inhibition of ___________
-Reduced _____ and diminished ____ response in deposited crystals
-Blocks cell division by binding to ________

Back 148

tubulin; polymerization

leukocyte migration;

Phagocytosis; inflammatory

mitotic spindles

Front 149

Cases of ____ have been seen in pts taking standard therapeutic doses of cochicine with interacting medications.

A substantially lower dose of colchicine was as effective as the higher dose previously used and was associated with...

Back 149

fatal colchicine toxicity;

significantly fewer ADR compared to the higher dose

Front 150

In pts with renal or hepatic impairment who are taking colchicine, don't want to give them _________ or _________

Back 150

P-glycoprotin inhibitors; strong 3A4 inhibitors

Front 151

Colchicine is used for relief of _____ with acute gout attacks and for regular ________ between attacks.

Often effective in ______ an attack when taken at the first sign of articular discomfort.

Back 151

pain; prophylactic use;

aborting

Front 152

Colchicine has severe GI effects including:

_____ is the most common and dose-limiting effect. ______ have been used to control this

Back 152

N/V/D and abdominal pain;

diarrhea; opiates

Front 153

Disease-modifying anti-rheumatic drugs (DMARDs) have the potential to ____ or ____ disease progression.

Nonbiological agents are ......

Biological agents are _______.

Back 153

slow; halt;

conventional DMARDs;

anti-cytokines (biological response modifiers)

Front 154

Biological DMARDs that interact with the physiological actions of TNF-alpha= _____ and ______

Back 154

etanercept; infliximab

Front 155

Biological DAMRDs that antagonize actions of IL-1: _______

Back 155

anakinra

Front 156

Biological DMARDs that antagonize actions of IL-6: _________

Back 156

tocilizumab

Front 157

Glucocorticoids have potent ____ effects that diminish ___ and ____ associated with rheumatic diseases.

Usually reserved for _________ of active disease and for _____ tx while waiting for onset of DMARDs

Also used in______ joints that experience flares.

Back 157

antiinflammatory; pain and swelling;

brief periods; bridge;

isolated

Front 158

Conventional DMARDs are ___ Acting and must be started before ______ mechanical damage occurs.

Do not inhibit ___ and have no ____ or ____ activity.

They ____ or ____ the progression of disease;

They do not repair existing damage but may induce ___ and prevent _________.

Have potential for serious _____.

Back 158

slow; irreversible;

Cyclooxygenase; analgesic or primary anti-inflammatory;

halt/slow;

remission; further injury;

toxicity

Front 159

All patents with active RA should be candidates for ______

Also, any pt with signs and symptoms of a poor RA prognosis should receive a ____ as initial therapy since disease progression is most rapid........

Back 159

DMARD; DMARD; in the first several years of active disease

Front 160

What has been shown to be the most effective DMARD combination therapy?

Back 160

SSZ plus MTX plus HCQ

Front 161

Hydroxychloroquine (HCQ) is a _______ drug. Is a _____ agent which exerts anti-______ activity by inhibiting the release of IL-___.

Most effective in ___ disease

Major-toxicity is a dose-dependent ______

Back 161

DMARD; a anti-malarial; rheumatic; 1;

mild;

retinopathy

Front 162

Gold salts are considered a _____ Drug. Are ingested by ___ and suppress ____ and ____ release and activity.

Most effective in pts with ______ who do no adequately respond to NSAIDs

PO agent= ______

Back 162

DMARD; macrophages; phagocytosis and lysosomal enzyme

mild RA

Auranofin (*AU=gold)

Front 163

Sulfasalazine (SSZ) is an ________, ______ drug. Works by suppressing _______ cytokines (____ and ___)

May be DOC for pts with _____.

Back 163

immunomodulatory, DMARD;

pro-inflammatory; TNF, IL1

mild RA

Front 164

Methotrexate is a _____drug. Its MOA in RA is _____ but is thought to be similar to the anti-______ action (folate antagonist that inhibits synthesis of ____)


Major ADR include:
-GI: (4)
-Elevated serum _______ which if sustained, may have to ________. Can cause a ____ and _____.
-Less common=________

Doses in RA are much lower than the doses used for _____ and severe toxicity is expected to be _________

Back 164

DMARD; unknown; neoplastic; purines;

N/V/D/ stomatitis;

transaminases; D/C and do liver biopsy; rash and pruritis;

bone marrow suppression;

cancer chemo; less frequent

Front 165

Leflunomide is the first oral agent for active ____ that is labeled for slowing disease progression. (______ drug)

MOA is through ________ that inhibits ____ synthesis. Also has ____ and _____ effects.

Contraindications include the potential for immune ______, so is not recommended for pts with ______ or uncontrolled ____. Do not give ____ vaccines.

Back 165

RA; DMARD;

immunomodulatory actions; pyrimidine; antiproliferative; antiinflammatory;

immune suppression; immunodeficiency; infections; live

Front 166

In Anti-cytokine agents, trials demonstrate RA improvement when ____ action is suppressed by agents which target ____ or _____

Back 166

TNF; TNF or IL1

Front 167

Anti-cytokine agents reduce signs and symptoms of ___, inhibit progression of ____ damage, and are more effective when combined with ____.

Back 167

RA; structura; MTX

Front 168

Etanercept is an _____ agent which is a soluble ____ receptor with high binding affinity for _______.

Back 168

anti-cytokine; TNF; circulating TNF

Front 169

Infliximab (anticytokine agent) is a __________ and is a chimeric monoclonal _____ that is directed against ____.

Back 169

neutralizing ab; IgG; TNF

Front 170

TNF inhibitors are recommended for pts with mod-severe disease who cannot tolerate ______ or have not responded to at least 2________

Back 170

MTX; DMARDs

Front 171

Do not use anti-cytokine agents in any pt with ______, hx of _____ or medical conditions predisposing them to infection.

Back 171

active infx; Hx of recurrent infections

Front 172

All three currently approved anti-cytokine agents have boxed warnings for an increased risk of serious _____, ____ and ___

Back 172

infections, TB, sepsis

Front 173

TNF antagonism is associated with an increased risk for reactivation of _____ and possibly other _______ infections. A positive ____ test requires prophylactic treatment before initiating ______ therapy

Back 173

TB; opportunistic; TB skin; TNF antagonist therapy

Front 174

Etanercept is a biologic response ______.

Is a ________ protein that is composed of extracellular ligand-binding portion of the _______ fused with the Fc domain of human _____.

Is a dimeric soluble form of ____ which binds to _____ competitively inhibiting the binding of TNF to .......... When it binds to TNF, it blocks all interactions modulating the _____ and ____ responses induced by TNF.

Back 174

modifier;

recombinant fusion; TNF-receptor; IgG;

TNF-R; TNF; to target cell surface receptors; inflammatory and immune responses

Front 175

Etanercept reduces signs and symptoms, inhibits progression of _____ and improves ______ in pts with mod-severe active _____. Can be sued in combination with _____.

Back 175

structural damage; physical function; RA

MTX

Front 176

Etanercept has some serious side effects including a risk of serious ____ or _____.

Administration during ____ or any ____ infection is contraindicated. Also do not administer ____ vaccines.

Back 176

infections; death

sepsis; active; live

Front 177

Infliximab is a _____ Drug.

Is a chimeric monoclonal _____ antibody that binds with high affinity and specificity to ____.

Indicated for moderate to severe _____. When used in combination with _____, reduces signs and symptoms, inhibits progression of ____ and improves _______ in patients.

Back 177

anti-cytokine;

IgG; TNF;

RA; MTX; structural damage; physical function

Front 178

Infliximab showed a higher incidence in mortality and hospitalization for worsening of _____ in stages ___-___.

Contraindicated to use doses more than _____.

Back 178

HF; III-IV;


5 mg/kg

Front 179

Do not administer infliximab to pts with active ____ and discontinue if a _______ developed. Do not administer concurrent _______.

Worldwide, most serious ADR is ______ and its important to evaluate for this before hand.

Back 179

infection; serious infection;

live vaccines;

TB

Front 180

Concurrent use of etanercept or anakinra with Infliximab has been associated with.....

Back 180

an increased risk of serious infections and neutropenia

Front 181

Anakinra is a ____ receptor antagonist. Binds and blocks the binding of ___ to target cells. This results in a decreased ___, _____ and ______.

Back 181

IL-1; IL-1; inflammation; pannus formation; bone resorption

Front 182

Anakinra is indicated for the reduction in signs and symptoms and to slow the progression of structural damage of mod-severe _____ in pts who have.......

Can be used alone or in combination with...

Do not use concurrently with ______ agents, do not initiate in pts with _____ and d/c if a ______ develops and do not administer ________.

Back 182

RA; failed therapy with >=1 DMARD

DMARD;

TNF neutralizing agents; active infections; serious infections; live vaccinations

Front 183

Abatacept is a _____ modulator which inhibits _______.

Do not use concurrently with ______ due to increased incidences of.......

If a serious infection develops, need to ____ and _______.

Do not give ______ concurrently or within 3 months after D/C use.

ADR: ______ and ______

Back 183

costimulation; T-cell activation;

TNF antagonists; infections and serious infections;

D/C and test for TB

live vaccines;

serious infections and malignancies

Front 184

Rituximab is a chimeric ____/human recombinant monoclonal Ab directed against the _____ antigen found on the surface of normal and malignant _____.

Net effect is to.......

Indicated in combination with ____ to reduce signs and symptoms of mod-severely active ____ who had an inadequate response to one or more ___________.

Premedicate with _______ 30 min prior to each infusion.

Boxed warnings include (2)

Back 184

murine; CD20; B cells;

deplete the population of immature and mature B cells that have CD20 on their surface;

MTX; RA; TNF antagonists

methylpredinsolone;

fatal infusion reactions; severe mucocutaneous reactions

Front 185

Tocilizumab is a recombinant humanized monoclonal Ab that blocks the ____ receptor.

Indicated for treatment of pts with mod-severe active ____who have had an inadequate response to one or more _____

Back 185

IL-6;

RA; TNF blockers

Front 186

What two types of medications can be used to treat asthma?

Back 186

bronchodilators and antinflammatories.

Front 187

Bronchodilators include ...(3)

Back 187

beta adrenergic agonists, anticholinergics and theophylline

Front 188

What are the 6 types of anti-inflammatory drugs used to treat asthma?

Back 188

phospholipase A2 inhibitors, mast cell inhibitors, lipoxygenase inhibitor, leuktotriene receptor antagonist, monoclonal Ab to IgE, and short-acting beta2 agonists

Front 189

Short acting beta2 agonists are used to relieve ______ symptoms associated with asthma.

Back 189

acute

Front 190

Phospholipase A2 inhibitors are ______ that are used to treat asthma.

Back 190

steroids

Front 191

Mast cell inhibitors used to treat asthma include: (1)

Back 191

cromolyn sodium

Front 192

Lipoxygenase inhibitors used to treat asthma include: (1)

They function to decrease the production of _____ which trigger inflammation and ____.

Back 192

Zileuton; leukotrienes, bronchoconstriction

Front 193

Leukotriene receptor antagonists used to treat asthma include: (2)

They function to.....

Back 193

zafirlukast, montelukast;

block actions of leukotrienes

Front 194

What is the monoclonal Ab to IgE that is used to tx asthma?

Back 194

omalizumab

Front 195

Bronchodilators can either be ______ onset and ____ acting; or _____ onset and ____ acting.

Back 195

immediate; short;

delayed; long

Front 196

Immediate onset and short acting beta2 adrenergic agonists stimulate the beta2 receptors in the lung causing ______

Drugs include: (3)

Back 196

bronchodilation;

epinephrine; isoproterenol; albuterol

Front 197

Epinephrine (as a bronchodilator) is nonselective for _____ and _____

Back 197

beta1; beta2

Front 198

Isoproterenol (as a bronchodilator) is nonselective for _____ and ____

Back 198

beta1; beta2

Front 199

What is the DOC (bronchodilator) for the treatment of asthma? What is it selective for?

Back 199

albuterol; beta2

Front 200

Indications for short-acting beta2 agonists include for acute attacks of ______ including _________. Treat this with _____ and ____.

Also indicated for the prevention of ________ (drug=_______)

Back 200

bronchospasm; status asthmaticus;

albuterol, epi;

exercise induced bronchospasm; albuterol

Front 201

Beta2 agonists can cause ____ if enough systemic absorption occurs (of the short-acting beta agonists) casing ________

Back 201

vasodilation; reflex tachycardia

Front 202

Epi can cause _____ and ______ because it directly stimulates _____ along with beta2.

Back 202

tachycardia and palpitations; beta1

Front 203

Short-acting beta2 agonists can cause tremors because they can stimulate beta2 receptors in the ________

Back 203

skeletal muscle

Front 204

Long acting beta2 agonists are no longer used to treat asthma in adults and children because when they are taken without an inhaled steroid, they have been shown to increase the risk of.....

Back 204

even more severe attacks and death

Front 205

Salmeterol is a ________ and is indicated for the prevention of......

Not indicated for....

Boxed warning: increased __________ was seen in clinical studies when subjects received LABAs in addition to their regular asthma medication

Back 205

long acting beta2 agonist; exercise induced bronchospasm;

tx of acute attacks;

asthma-related deaths

Front 206

Formoterol is a ____ onset _____ drug when compared to salmeterol. Is more convenient for _____ with administration 15 min before ____.

Back 206

faster; LABA; exercise-induced asthma; activity

Front 207

Theophylline is classified as a ________ but may have a more important effect as an ___________ agent affecting the late asthmatic response.

Drug has a narrow therapeutic index requiring.....

Back 207

bronchodilator; anti-inflammatory immunomodulating

monitoring

Front 208

Factors which increase the half-life of theophylline include drug interactions with....

Example drugs include: (3)

Back 208

P450 inhibitors;

cimetidine, erythromycin, ciprofloxacin

Front 209

At therapeutic levels, theophylline can cause ____, ____ and____.

Over 20 mg/L it can cause ____,_____, ____, ____and ____

Over 30 mg/L it can cause ____ and _____

Back 209

nausea, nervousness, anxiety;

nausea, insomnia, tremor, anxiety, tachycardia;

arrythmias, seizures

Front 210

Indications for theophylline inclue moderate to severe ________

Also used as a second line agent in _____ (no firm evidence that increases effects of B2A;s) .IV forms have been considered ineffective in _______.

Back 210

chronic asthma;

acute asthma;

status asthmaticus

Front 211

status asthmatics is....

Back 211

an acute asthma attack that doesn't respond to standard treatments of bronchodilators and steroids

Front 212

Stimulation of parasympathetic muscarinic receptors in the lungs activates _____ which increases ____ and results in ______

This is blocked by ______.

Drug: (1).....

Back 212

guanyl cyclase; cGMP; bronchconstriction;

anticholinergics;

Ipratropium

Front 213

Ipratropium is a _____ drug that is indicated as a ______ for maintenance treatment of ______ associated with COPD. Primary use of this class of drugs is in ____ and ____

Back 213

anticholinergic; bronchodilator; bronchospasm;

chronic bronchitis; emphysema

Front 214

Steroids decrease the synthesis and prevent release of _______, decrease activation of ______ and decrease vascular _____

Back 214

chemical mediators; inflammatory; permeability

Front 215

Systemic steroids should be initiated in any pt requiring ______ for acute asthma.

IV drug= ________

Indicated for the treatment of _______.

Back 215

hospitalization;

Methylprednisolone;

status asthmaticus

Front 216

TOC for acute severe asthma exacerbations=

Back 216

early aggressive use of systemic steroids and aerosolized beta2 agonists

Front 217

Inhaled steroids are used for the long-term treatment of ____ in asthma patients. They are used for management of pts progressing to _________ and are NOT indicated for....

Back 217

inflammation;

persistant asthma;

relief of acute bronchospasm

Front 218

Inhaled steroid drugs used: (4)

Back 218

beclomethasone;
Fluticasone/salmeterol (advair);
Budesonide/formoterol (symbicort);
mometasone/formeterol (dulera)

Front 219

Advair diskus (drugs included):

Back 219

fluticasone

salmeterol

Front 220

Symbicort (drugs included):

Back 220

budesonide;

formoterol

Front 221

Dulera (drugs included):

Back 221

mometasone;

formoterol

Front 222

Pt counseling when prescribing steroids for asthma includes that they are to be used for _____ and not _______; as well as not to D/C abruptly because it may cause.....

Back 222

chronic disease; acute attacks;

severe asthma exacerbations

Front 223

Cromolyn sodium is used in the prevention of ________. There is no role for it in the treatment of _____.

Back 223

exercise-induced asthma; acute asthma

Front 224

Cromolyn works by binding to ______, blocking the entry of ____ and stabilizing the membranes. This causes prevention of ____ and ______.

Also causes the opening of ____ channels causing an influx and _ __________. This results in the inhibition of the activation of.......

Back 224

mast cells; calcium ions; rupture and degranulation;

chloride; hyperpolarizaton; several cell types

Front 225

Leukotrienes causes ___ and ____ migration, increase capillary _____, and ____ contraction.

This results in _____, ___ and ____

Back 225

neutrophil; eosinophil;

permeability;

visceral smooth muscle;

inflammation, edema, bronchoconstriction

Front 226

Zileuton is inhibits _____ and inhibits _____ formation.

Indicated for prophylaxis and _____ Treatment of asthma in adults and children >__years.

Is intended for continuous use in chronic therapy and to continue taking during........Also, do not use to treat ______

Back 226

5-lipoxygenase; leukotriene

chronic; 12;

symptom-free periods; acute attacks

Front 227

Zileuton is a ____ inhibitor

Back 227

lipoxygenase

Front 228

Zafirlukast and montelukast are ________ antagonists

Back 228

leukotriene receptor

Front 229

Zafirlukast is a selective and competitive leukotriene receptor antagonist of leukotrienes ____ and ____

Indicated for prophylaxis and chronic treatment of _____ in adults and children > ___ years.

Take on a.....

Intended for continuous use even during _________ and not for ______

Back 229

D4 and E4;

asthma; 5;

empty stomach

asx periods; acute attacks

Front 230

Montelukast selectively inhibits the ______ leukotriene receptor blocking the actions of ______ here with no agonist activity.

Dosing is _________ for asthma or asthma combined with _____, taken with or without ____

Intended for use even during ______ and not for ______

Back 230

cysteinyl; LTD4;

Once daily in the evening; allergic rhinitis; food

asx periods; acute attacks

Front 231

Antileukotriene agents are not useful for ____ and must be taken continuously to.....

Back 231

acute attics; derive benefit

Front 232

Omalizumab is a monoclonal Ab to _____. Binding does not occur at the variable allergen specific Fab site so.....

Administered ____ once every ____.

Indicated for use in pts over ____ with mod-severe persistent ____ whose symptoms have not been adequately controlled with _______.

Back 232

IgE;

all allergen induced responses are inhibited regardless of allergen specificity.

SC; 2-4 weeks.

12; asthma; inhaled steroids

Front 233

Omalizumab carries a risk of _____ which may occur anytime from soon after the first dose to more than a year after the start of regularly scheduled treatments. Need to observe for at least ______ post-dose

Back 233

anaphylaxis; 2

Front 234

Antitussives work centrally to increase the __________ of the medullary cough center by decreasing _____________.

Optiate antitussives include ____ and ____

Nonopiate antitussives include ____

Back 234

threshold for stimulation; sensitivity to afferent impulses

codeine, hydrocodone;

dextromethorphan

Front 235

Antitussives work peripheral to decrease the __________ through a topical local _____ effect.

Drug: (1)

Back 235

sensitivity to irritant receptors; anesthetic;

benzonatate (tessalon perles)

Front 236

Codeine is an effective antitussive at doses that are not ____, do not cause ______ and are not likely to result in _____.

Back 236

analgesics; respiratory distress; abuse

Front 237

Hydrocodone is very similar to _____ but somewhat more ______. Available as antitussive only .......

Back 237

codeine; habituating; in combination with other ingredients

Front 238

Dextromethorphan causes minimal ______, has no ____ effects.

___ Isomer used therapeutically and is structured similarly to ___ but does not......

Elevates the ____ For coughing, should not be _____ at normal doses

Back 238

CNS depresson; analgesia/nonopiate;

D; codeine; interact with opioid receptors;

threshold; addicting

Front 239

____ sensations and ____ can be produced when high doses of Dextromethorphan are ingested.

Back 239

euphoric; hallucinations;

Front 240

"Serotonin syndrome" may result if using dextromethorphan with __________ causing ____, ____ and ______

Back 240

MOA inhibitors; hypotension, fever, muscle regidity

Front 241

Tx of acute cough due to common cold=

_____ antihistamines are ineffective;

Back 241

1st gen antihistamine/decongestant combinations;

nonsedating

Front 242

Tx of a cough due to acute bronchitis=

Back 242

short acting inhaled beta2 agonists if wheezing

Front 243

Tx of a cough due to chronic bronchitis=

Back 243

ipratropium, SABA for bronchospasm and dyspnea, antitussive for persistent cough despite other tx

Front 244

Tx of a cough due to acute exacerbation of chronic bronchitis:

Back 244

ipratropoum, SABA, or combo
oral steroid for 10-15 days

Front 245

Do not use cough and cold medications in children under age _____

Back 245

4

Front 246

Expectorants facilitate the removal of ______ by decreasing ______.

Only currently used agent is _______

Back 246

viscous mucus;

mucus viscosity;

Guaifenesin

Front 247

Mucolytics decrease sputum _____, ______ thickened mucus secretions and facilitates _______.

Drug=_______

Also used as an antidote for ___________

Back 247

viscosity; liquefies; expectoration;

acetylcysteine;

acetaminophen poisoning