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NSAIDS-GCs Flashcards

1
Q

Describe the MOA of tNSAIDS

A

reversible inhibition of COX1 and 2 and subsequent decrease in inflammatory prostaglandins and thromboxanes

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2
Q

Describe the Uses of tNSAIDs

A
  1. Pain (moderate dose)
  2. Fever (moderate dose)
  3. Inflammation (HD)
  4. More effective for acute pain than ASA-acetaminophen
  5. RA (indomethacin)
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3
Q

Adverse reactions of COX1 related

A
  1. GI upset/nausea
  2. Bleeding
  3. Ulceration
  4. Renal dysfunction/failure
  5. Interstitial nephritis
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4
Q

Adverse reactions of COX2 related

A
  1. Renal dysfunction/ failure
  2. Interstitial nephritis
  3. delayed labor/contractions
  4. ductus arteriosus closure
  5. Increase clotting risk
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5
Q

Adverse reactions of tNSAIDs

A
  • similar to ASA
    1. less bleeding (~2 days vs 4-7day of ASA)
    2. GI upset (dyspepsia/ ulceration)
    3. greater risk for renal dysfunction (reversible)
    4. decrease RBF
    5. fluid retention
    6. increase BP (esp. in elderly)
    7. OD: acute renal failure
    8. Avoid in 3rd trimester pregnancy
  • incidence of GI toxicity reduced by concomitant use of PPIs or H2 antagonists
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6
Q

tNSAIDS that are mostly COX-2 inhibitors

A
  1. Meloxicam

2. Nabumetone

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7
Q

Analgesia and anti-inflammatory effects of NSAIDs are due to:

A

inhibition of inducible COX2 at site of TISSUE INJURY (PGE2/PGI2)

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8
Q

Anti-pyretic effects of NSAIDs are due to:

A

inhibition of inducible COX2 in HYPOTHALAMUS (PGE2)

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9
Q

Antithrombogenesis (anti-clotting) effects of NSAIDs are due to:

A

inhibition of constitutive COX1 in PLATELETS

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10
Q

4 Main groups of NSAIDs and their COX selectivity/reversibility

A
  1. tNSAIDs: reversible inhibition of COX1 and 2
  2. COX2 Selective inhibitors: Reversible selective inhibition of COX2
  3. Acetaminophen: reversible inhibition of CNS COX2
  4. Aspirin: irreversible inhibition of COX1 and COX2
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11
Q 
Reversible inhibitor of COX (cyclooxygenase) 1 and 2: 
A.  Aspirin 
B.  Ibuprofen (Motrin®, Advil®) 
C.  Naproxen (Naprosyn®, Aleve®) 
D.  Celecoxib (Celebrex®) 
E.  Acetaminophen (Tylenol®)
A

B.  Ibuprofen (Motrin®, Advil®)

C.  Naproxen (Naprosyn®, Aleve®)

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12
Q 
Which agent should be avoided in hepatic dysfunction? 
A.  Aspirin 
B.  Ibuprofen (Motrin®, Advil®) 
C.  Naproxen (Naprosyn®, Aleve®) 
D.  Celecoxib (Celebrex®) 
E.  Acetaminophen (Tylenol®)
A

E.  Acetaminophen (Tylenol®)

*use w/ caution in pts w/ alcoholic liver dz

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13
Q

What NSAIDs:

  1. inhibits CNS COX only:
  2. does not have anti-inflammatory effects:
  3. has anti-platelet effects
A
  1. inhibits CNS COX only: acetaminophen
  2. does not have anti-inflammatory effects: acetaminophen
  3. has anti-platelet effects: aspirin
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14
Q

Which of the following actions of prostaglandins is INCORRECTLY matched with the form of the cyclooxygenase enzyme (COX-1 or COX-2) that synthesizes the particular prostaglandin?
A.  Fever : COX-2
B.  Inflammation : COX-1
C.  Protection of GI cells : COX-1
D.  Vasodilation in the kidney : COX-2
E.  Activation of platelet aggregation : COX-1
F.   Contraction of uterine smooth muscle : COX-2
G.  Opening of ductus arteriosus : COX-1

A

B.  Inflammation : COX-1

G.  Opening of ductus arteriosus : COX-1

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15
Q

Physiological Functions of COX1

A
  1. Protection of GI cells
  2. Activation of platelet aggregation
  3. RBF maintenance
  4. Bone formation and resorption
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16
Q

Physiological Functions of COX2

A
  1. Fever
  2. Pain
  3. Inflammation (enhance edema)
  4. Vasodilation of the kidney
  5. Contraction of uterine Sm.M
  6. Anti-aggregatory platelet effects
  7. Opening of ductus arterosus
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17
Q

Examples of tNSAIDs

A
  1. Ibuprofen (Advil, Motrin)
  2. Naproxen (Aleve, Naprosyn)
  3. Ketoprofen
  4. Indomethacin
  5. Ketorolac (Toradol)
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18
Q

Describe the PK of Ibuprofen including form, absorption, administration, and elimination

A
  • Form: PO and IV
  • Absorption: rapid, complete absorption
  • Administration: t1/2= 3-4hrs, BID-TID
  • Elimination: Hepatic
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19
Q

Safest tNSAID in LD for GI tract: __

Highest risk with __

A

Ibuprofen (acetaminophen is safer but not a tNSAID)

Ketorolac

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20
Q

Describe the PK of Naproxen including form, administration, and elimination

A
  • Form: PO
  • Administration: t1/2= 12-15hrs, BID
  • Elimination: RENAL
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21
Q

Describe the PK of Ketorolac including form and elimination

A
  • Form: PO, IM/IV**, nasal spray

- Elimination: RENAL

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22
Q

Special uses of Ketorolac

A
  1. post surgical pain (IV)

* IM/IV comparable to morphine

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23
Q

Special uses of ibuprofen or naproxen

A
  1. Dysmenorrhea (via inhibition of synthesis of endometrial PGE)
    * PG induced cramping
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24
Q

Adverse effects of Ketorolac

A
  1. GI toxicity –> limit use to 5 days
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25
Q

Relative CI of tNSAIDs

A
  1. pts w/ high risk PUD
    - Advanced age
    - Hx of PUD or prior NSAID gastropathy
    - Concurrent GC use
  2. 3rd trimester pregnancy
  3. HTN
  4. Diabetes
  5. CKD
  6. CHF (lowest risk w/ naproxen, highest w/ ibuprofen and celecoxib)
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26
Q 
Safest pain medication to recommend to patients with gastric ulcers: 
A.  Aspirin 
B.  Ibuprofen (Motrin®, Advil®) 
C.  Naproxen (Naprosyn®, Aleve®) 
D.  Celecoxib (Celebrex®) 
E.  Acetaminophen (Tylenol®)
A

E.  Acetaminophen (Tylenol®)

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27
Q 
Safest anti-inflammatory medication to recommend to patients with gastric ulcers: 
A.  Aspirin 
B.  Ibuprofen (Motrin®, Advil®) 
C.  Naproxen (Naprosyn®, Aleve®) 
D.  Celecoxib (Celebrex®) 
E.  Acetaminophen (Tylenol®)
A

D.  Celecoxib (Celebrex®)

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28
Q

If taking low-dose aspirin for cardioprotective effect – take NSAIDs for acute dental pain ___

A

one hour after

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29
Q 
Safest agent for pain treatment in patients taking oral anticoagulants 
A.  Aspirin 
B.  Ibuprofen (Motrin®, Advil®) 
C.  Naproxen (Naprosyn®, Aleve®) 
D.  Celecoxib (Celebrex®) 
E.  Acetaminophen (Tylenol®)
A

E.  Acetaminophen (Tylenol®)

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30
Q

What tNSAID has higher efficacy but greater toxicity

A

Indomethacin (PO, IV, rectal)- hepatic

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31
Q

MOA of Celecoxib

A

reversible inhibition of COX2

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32
Q

Describe the PK of Celecoxib including form, metabolism and elimination

A

Form: PO

Hepatic metabolism and renal elimination

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33
Q

Uses of Celecoxib

A
  1. Pain (less effective than tNSAIDs for acute pain)
  2. Anti-pyretic
  3. Inflammation (equal to tNSAIDs for osteo- and RA)
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34
Q

Adverse reactions of Celecoxib

A
  1. Renal dysfunction
  2. Delayed labor
  3. close ductus arteriosus
  4. Prothrombotic potential (NO BLEEDING RISK)
    5 increase MI risk and HF
  5. Lower risk of GI toxicity*
  6. hypersensitivity rxn due to sulfa moiety

**Black box warning: increased CV thrombotic events

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35
Q

___ is an option for patients requiring chronic NSAID treatment at high risk for gastric complications (high RF include: ___)

A

Celicoxib

  1. Age >65
  2. use of an anticoagulant
  3. prior GI bleed
  4. active PUD
  5. concurrent use of oral GCs
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36
Q

Side Effects - Platelets No alteration of platelet function or increase in bleeding risk
-No inhibition of COX-1 mediated TXA 2 synthesis in platelets

A

Celecoxib

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37
Q

BLACK BOX WARNING

  • Increased risk of adverse cardiovascular thrombotic events
  • Possibly due to selective inhibition of anti-aggregatory PGI 2 in endothelial cells
A

Celecoxib

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38
Q 
A 64-year-old male presents with mild to moderate musculoskeletal back pain after playing golf. He states he has tried acetaminophen and that it did not help. His past medical history includes diabetes, HTN, hyperlipidemia, gastric ulcer (resolved), coronary artery disease. Which of the following is the most appropriate NSAID regimen to treat this patient’s pain? 
A.  Celecoxib 
B.  Ketorolac and omeprazole 
C.  Naproxen and omeprazole 
D.  Naproxen 
E.  Ibuprofen
A

C.  Naproxen and omeprazole

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39
Q

for naproxen, ibuprofen and celicoxib, compare the GI risk, CVS risk and renal risk

A

GI: naproxen> ibuprofen> celicoxib (COX1>COX2 inhibition)

CVS: celecoxib > ibuprofen = naproxen (COX2>COX1)

Renal: celecoxib = ibuprofen = naproxen (COX2=COX2)

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40
Q

The primary reason for developing drugs that selectively inhibit the COX-2 enzyme (e.g., celecoxib [Celebrex®]) is to:
A.  Decrease the risk of myocardial infarction
B.  Improve anti-inflammatory effectiveness
C.  Lower the risk of gastrointestinal toxicity associated with existing anti-inflammatory agents
D.  Reduce the cost of treatment of rheumatoid arthritis
E.  Selectively decrease levels of thromboxane A2

A

C.  Lower the risk of gastrointestinal toxicity associated with existing anti-inflammatory agents

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41
Q 
Safest agent to treat musculoskeletal pain in patients with kidney dysfunction: 
A.  Aspirin 
B.  Ibuprofen (Motrin®, Advil®) 
C.  Naproxen (Naprosyn®, Aleve®) 
D.  Celecoxib (Celebrex®) 
E.  Acetaminophen (Tylenol®)
A

E.  Acetaminophen (Tylenol®)

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42
Q

Do not use Celebrex in who?

A
  1. 3rd trimester pregnancy (otherwise Category C)
  2. CKD
  3. severe heart disease
  4. Volume depletion
  5. hepatic failure
43
Q

MOA of acetaminophen

A

inhibition of COX2 in CNS (no effect on COX in periphery)

44
Q

Describe the PK of acetaminophen including form, absorption and metabolism, and elimination and phases

A

Forms: PO, rectal, IV
Absorption: faster w/ liquid preps (related to gastric emptying)
Metabolism: hepatic

Phase II–> inactive
Phase I–> hepatotoxic

45
Q

Uses of acetaminophen

A
  1. pain (less effective than tNSAIDs)
  2. fever (as effective or superior to ASA or ibuprofen)
  3. some use in OA
    * *NOT anti-inflammatory
46
Q

Adverse effects of acetaminophen

A

*well tolerated, NO GI upset or bleeding

  1. less renal concerns
  2. Hepatoxicity– limit does to 4g/day
  3. Dizziness, excitement disorientation w/ supra-therapeutic acute dose
  4. OD: liver failure
  5. use w/ caution in pts w/ alcoholic liver dz
47
Q

TX of acetaminophen OD

A

N-acetylcysteine: replenishes GSH and inactivates Ac*directly

48
Q

Acetaminophen is an efficacious analgesic and antipyretic agent, but differs from NSAIDs in that it has no anti- inflammatory action. Which of the following reasons explains this unique aspect of acetaminophen?
A.  The distribution of acetaminophen does not reach peripheral sites of inflammation
B.  Acetaminophen is not an inhibitor of the COX enzyme C.  Peroxide formation at sites of inflammation inhibits the activity of acetaminophen
D.  Anti-inflammatory doses of acetaminophen are too high and toxic
E.  Acetaminophen undergoes significant first-pass metabolism

A

C.  Peroxide formation at sites of inflammation inhibits the activity of acetaminophen

49
Q

Describe the elimination and metabolism (phases) of acetaminophen

A

Phase II conjugation: metabolized to inactive sulfate and glucuronide

Small % metabolized to hepatotoxic metabolite (phase I - CYP2E1) - detoxified by GSH conjugation (phase II)

Phase II–> inactive
Phase I–> hepatotoxic

50
Q 
Relative to ibuprofen (Advil®), agents that preferentially inhibit COX-2 over COX-1 will cause a higher incidence of: 
A.  Bleeding side effects 
B.  Gastric irritation 
C.  Clotting-related disorders 
D.  Kidney dysfunction 
E.  Inhibition of labor contractions
A

C.  Clotting-related disorders

51
Q

MOA of Aspirin

A

irreversible inhibition of COX1 and 2

*COX1 selective at low doses (81-325mg)

52
Q

Describe the PK of aspirin including form, absorption, metabolism

A

Form: PO/rectal
Absorption: rapid from stomach and SI
Metabolism: hepatic (hydrolysis-conjugation, zero order at HD)

53
Q

Uses of Aspirin

A
  1. Pain (limited use- MD)
  2. Fever (MD)
  3. Inflammation (HD)
  4. 2ndary prevention of MI (LD)
  5. decreased tendency for clotting (LD)
54
Q

Adverse effects of Aspirin

A
  1. Reyes Syndrome (liver damage encephalopathy)
  2. Asthmatic reaction/bronchospasm (hypersensitivity allergy)
  3. Tinnitus
  4. GI irritation/ulcers
  5. Increased bleeding time
  6. Renal dysfunction
  7. OD: hyperthermia, acidosis
55
Q

Tx of ASA OD

A

IV NaHCO3

cooling blankets or gastric lavage-charcoal-whole bowel irrigation

56
Q

Describe the elimination and metabolism of ASA

A

ASA rapidly hydrolyzed by esterases
LD- 1st order kinetics

SA then conjugated w/ glycine or glucuronide
HD (anti-inflammatory)- zero order kinetics

57
Q

LD ASA is essentially platelet COX1 selective via 2 mechanisms:

A
  1. platelets cannot sythezie new COX1 enzymethus TXA2 synthesis inhibited for life of platelet
  2. Acetylsalicylic acid highest in portal vein prior to hepatic metabolism by esterases thus greater effect on circulating platelet COX1 relative to tissue endothelial cell COX2
58
Q

CI of ASA

A
  1. Ulcer pts (or take PPI too)
  2. alcoholics
  3. on oral anticoagulants
  4. CKD (elderly more susceptible)
  5. avoid in preg. esp. 3rd trimester (delay onset of labor)
  6. caution in asthmatics
  7. children <12 w/ viral infections
59
Q

SX of mild ASA intoxication

A

aka salicylism

  1. HA
  2. dizziness
  3. diarrhea
  4. tinnitus
  5. visual disturbance
  6. mental confusion
  7. drowsiness
  8. sweating
  9. thirst
  10. hyperventilation
60
Q

SX of acute intoxication-OD (15-30g) of ASA

A
  1. Vomiting
  2. sweating
  3. fever (uncouples oxidative phosphorylation)
  4. Respiratory alkalosis (stimulation of respiration)
  5. Metabolic acidosis (massive ingestion of organic acid)
61
Q 
Aspirin is often used in low doses to prevent platelet aggregation by inhibiting the synthesis of which substance? 
A. Leukotriene B4
B. Prostacyclin (PGI2)
C. Thromboxane A2
D. Arachidonic acid
E. Phospholipase A2
A

C. Thromboxane A2

62
Q

A 16-year-old girl comes to the emergency department suffering from the effects of an aspirin overdose. Which of the following syndromes is this patent most likely to exhibit as a result of this drug overdose?
A.  Bone marrow suppression and possibly aplastic anemia
B.  Fever, hepatic dysfunction, and encephalopathy
C.  Hyperthermia, metabolic acidosis, and coma
D.  Rapid, fulminant hepatic failure
E.  Rash, interstitial nephritis, and renal failure

A

C.  Hyperthermia, metabolic acidosis, and coma

63
Q 
Aspirin should not be used in children with viral syndromes because of the risk of: 
A.  Hepatotoxicity 
B.  Gastric ulcer 
C.  Reyes syndrome 
D.  Thrombosis
A

C.  Reyes syndrome

64
Q

A 28-year-old patient asks you what the difference is between acetaminophen and ibuprofen. You could her that, in comparison to NSAIDs such as ibuprofen, acetaminophen has:
A.  No clinically significant anti-inflammatory activity
B.  Less risk of GI side effects
C.  Less risk of renal toxicity
D.  All of the above

A

D.  All of the above

65
Q 
Patients at an increased risk for GI bleeding, ulceration and perforation with use of non-selective NSAIDs include those with: 
A.  Previous peptic ulcer disease 
B.  Excessive alcohol intake 
C.  Advanced age 
D.  All of the above
A

D.  All of the above

66
Q 
A 68-year-old man with chronic shoulder pain tells you he has heard favorable things from other patients about the lack of side effects with Celebrex®. You could tell him that compared to non-selective NSAIDs, celecoxib appears to cause: 
A.  Less severe GI toxicity 
B.  An increase in bleeding time 
C.  More cardiac toxicity 
D.  More GI ulceration and perforation
A

A.  Less severe GI toxicity

67
Q

MC adveres effects of mineralocorticoids

A
  1. HTN
  2. Hypokalemia
  3. Metabolic alkalosis
  4. Na-Fluid retention
68
Q

Long-term administration of large doses of prednisone is least likely to cause reductions in the synthesis of which hormone?
A.  Cortisol
B.  Corticotropin (ACTH)
C.  Corticotropin-releasing hormone (CRF)
D.  Aldosterone
E.  Growth hormone

A

D.  Aldosterone

69
Q

Describe the physiologic metabolic effects of Cortisol

A
  1. Carbs: increase gluconeogenesis and blood glucose
  2. Protein: decrease protein synthesis –> increase AA to glucose
  3. Fats: increase lipolysis –> increase FFA
70
Q

Describe the metabolic effects of EXCESS Cortisol

A
  1. Carbs: diabetes like state
  2. Protein: muscle wasting, CT atrophy
  3. Fat: increase lipogenesis (centrally)–> central obesity and moon facies

**iatrogenic cushings disease

71
Q

Upsides and downsides of GCs

A

upside: suppress chronic inflammation mediators and autoimmune rxns

Downside: decrease healing and diminish immunoprotection

72
Q

GCs block what inflammatory mediatiors?

A
  1. COX2
  2. phospholipase A2
  3. Eosinophile mediator release
  4. Mast cell mediator release
  5. cytokine production
  6. T cell activation
73
Q

Adverse effects of acute, short course, HD GCs

A
  1. insomnia
  2. behavioral changes
  3. Predispose to ulcers/GI upset
  4. Glucose intolerance in diabetes
74
Q

Describe the physiological effects of GCs

A
  1. antagonize vit. D effect on Ca2+ absorption

2. Stimulation of acid/pepsin production

75
Q

What GC?

11-OH for GC activity

A

Cortisol

76
Q

What GC?

C1-C2 double bound for increase AI activity

A

prednisolone

77
Q

What GC?

C6 methyl for increase AI activity

A

Methylprednisolone

78
Q

What GC?

C16 methyl to eliminate MC activity

A

Dexamethasone

79
Q

What GC?

Increase MC vs GC activity

A

Fludrocortisone

80
Q

11-Keto forms that are inactive

A
  1. prednisone

2. cortisone

81
Q

Describe clinical uses of Cortisol (hydrocortisone)

A
  1. Physiologic doses–>replacement therapy – emergencies
  2. GC:MC [1:1]
  3. Administered orally and parenterally.
82
Q

Describe clinical uses of Prednisone

A
  1. Most commonly used oral agent for steroid burst therapy 2. GC:MC [15:1]
  2. Activated to prednisolone in liver (no topical activity)
83
Q

Describe clinical uses of methylprednisolone

A
  1. IV and PO for steroid burst

2. minimal MC action

84
Q

Describe clinical uses of Dexamethasone (Decadron)

A
  1. Most potent anti-inflammatory agent**
  2. Use: cerebral edema, chemotherapy-induced vomiting
  3. Minimal mineralocorticoid action
  4. Greatest suppression of ACTH secretion at pituitary
85
Q

Describe clinical uses of Triamcinolone (Kenalog)

A
  1. Potent systemic agent with excellent topical activity

2. No mineralocorticoid action

86
Q 
Corticosteroids are useful in the treatment of all of the following disorders EXCEPT: 
A.  Addison’s disease 
B.  Adrenal gland crisis 
C.  Allergic rhinitis 
D.  Asthma 
E.  COPD 
F.   Rheumatoid arthritis
A

can use for all?

87
Q

Describe the TX of RA

A
  1. Early: NSAIDs
  2. DMARDs (when dx is certain)
  3. LD GCs used as bridge utnil DMARDs take effect and as adjunctive therapy
88
Q 
A child with severe asthma is being treated with high doses of inhaled corticosteroids. Which of the following adverse effects is of particular concern? 
A.  Hyperglycemia 
B.  Oral candidiasis 
C.  Growth suppression 
D.  Cushing syndrome 
E.  Cataract formation
A

B.  Oral candidiasis

C.  Growth suppression**

89
Q

A boy experiences a moderately severe reaction to a wasp sting. Which method of corticosteroid administration is appropriate for this patient?
A.  Continuous high dose therapy for several weeks
B.  Continuous low dose therapy for several weeks
C.  Gradually increasing doses over several days
D.  Gradually decreasing doses over several days
E.  Intermittent every-other-day therapy until symptoms resolve

A

D.  Gradually decreasing doses over several days

90
Q

Compare the MC effects of different GCs

A
  1. Most w/ cortisol
  2. considerably less w/ prednisone
  3. minimal w/ methylprednisolone- dexamethasone
91
Q

Dosing considerations for GCs anti-inflammatory use

A
  1. MC side effects vary with agent (GC SE are unavoidable)
  2. Dosage often by trail and error w/ re-evaluation
  3. consider seriousness of disease, minimal amount for desired effect, duration of therapy
  4. reduce dosage as soon as therapeutic objectives are obtained
  5. terminate administration gradually to minimize disease rebound and AI
92
Q

How can you minimize adrenal suppression w/ GCs

A

alternate day schedule

*Anti-inflammatory actions (~ 48 hrs) outlast HPA suppression (~ 24 hrs)

93
Q

Which of the following is the primary clinical advantage of the alternate day glucocorticoid regimen?
A.  Can be used to directly stimulate growth if used in children
B.  Can be used to treat patients who require elevated and sustained immunosuppression
C.  Can be used to withdraw patients from chronic glucocorticoid treatment by systematically lowering dosage
D.  Minimizes glucocorticoid block of ACTH release which can significantly reduce adrenal atrophy
E.  Allows satisfactory replacement of cortisol in the treatment of Addison’s disease

A

D.  Minimizes glucocorticoid block of ACTH release which can significantly reduce adrenal atrophy

94
Q

MC route when systemic GCs actions are desired

A

PO, IV, IM

95
Q 
Which of the following corticosteroids can be used for topical dermatological applications? 
A.  Cortisol 
B.  Cortisone 
C.  Prednisone 
D.  Methylprednisolone 
E.  Dexamethasone 
F.   Triamcinolone
A

A.  Cortisol
D.  Methylprednisolone
E.  Dexamethasone
F.   Triamcinolone

*cortisone and prednisone require hepatic conversion to 11-hydroxy

96
Q

Adverse effects of HD longterm GCs (over 2-4 weeks)

A
  • iatrogenic cushing’s syndrome
    1. Hyperglycemia
    2. protein wasting (muscle)
    3. lipid deposition (wt. gain)
    4. Diabetes like state
    5. HPA axis suppression/ insufficient response to stress
    6. euphoria/psychosis
    7. impaired wound healing
    8. susceptibility to infection
    9. Osteoporosis
    10. posterior capuslar cataracts
    11. growth suppression
    12. peptic ulceration (use antacids to minimize risk)
97
Q

There is more hypothalamic-pituitary-adrenal axis suppression with what meds

A

dexamethasone and betamethason

98
Q

hypothalamic-pituitary-adrenal axis suppression w/ GC may cause a decrease in:

A
  1. ACTH
  2. GH
  3. TSH
  4. LH
  5. Sex steroids
99
Q

All of the following are strategies to minimize the development of HPA axis suppression with chronic corticosteroid therapy EXCEPT:
A.  Alternate-day administration of therapy
B.  Administration via topical or inhalation routes where possible
C.  Using the lowest dose of corticosteroid that adequately controls symptoms
D.  Administration of two-thirds of the daily dose in the morning and one-third in the late afternoon

A

D.  Administration of two-thirds of the daily dose in the morning and one-third in the late afternoon

100
Q

Which of the following patients would most likely have suppression of the HPA axis and require a slow taper of corticosteroid therapy?
A.  A patient taking 40 mg prednisone daily for 7 days to treat an asthma exacerbation
B.  A patient taking 10 mg of prednisone daily for 4 months for rheumatoid arthritis
C.  A patient using fluticasone nasal spray daily for 6 months for allergic rhinitis
D.  A patient receiving an intra-articular injection of methylprednisolone acetate for osteoarthritis

A

B.  A patient taking 10 mg of prednisone daily for 4 months for rheumatoid arthritis

101
Q

Risk of osteoporosis w/ GCs ir decreased by use of

A

bisphophonates

102
Q

Growth suppression in children is due to

A

decreased GH secretion and impaired action of IGF-1

103
Q 
Side effects unlikely to occur following steroid “burst” therapy of 2-3 weeks duration include: 
A.  Loss of muscle mass 
B.  Hyperglycemia 
C.  Osteoporosis 
D.  Posterior capsular cataracts 
E.  Mood disturbances 
F.   Insomnia
A

A.  Loss of muscle mass
C.  Osteoporosis
D.  Posterior capsular cataracts

104
Q

A 50-year-old woman, an asthmatic for the past 30 years, presented to the ED with a 2-day history of worsening breathlessness and cough. Chest auscultation revealed bilateral polyphonic inspiratory and expiratory wheeze. Supplemental oxygen, nebulized albuterol and ipratropium, as well as IV methylprednisolone were administered. Which of the following is a pharmacologic effect of exogenous glucocorticoids?
A.  Increased muscle mass
B.  Hypoglycemia
C.  Inhibition of leukotriene synthesis
D.  Improved wound healing
E.  Increased excretion of salt and water

A

C.  Inhibition of leukotriene synthesis

Pharmacology (31 decks)

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