Week 8: Bone Disorder Drugs, Anti-Inflammatory, Antipyretic, and Analgesic Agents

All of the following are Non-Selective (COX1 & COX2) Cyclooxygenase Inhibitors.....EXCEPT:

a. Ketorolac (Toradol)

b. Ibuprofen (Motrin)

c. Diclofenac (Voltaren)

d. Celecoxib (Celebrex)

e. Aspirin (ASA)

f. Naproxen (Naprosyn)

d. Celecoxib (Celebrex)

This prostaglandin drug is indicated for: Used to reduce elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension

a. Misoprostol (Cytotec)

b. Iloprost (Ventavis)

c. Alprostadil

d. Latanoprost (Xalatan) and Bimatoprost (Lumigan)

d. Latanoprost (Xalatan) and Bimatoprost (Lumigan)

This drug is prostaglandin drug is indicated for: A PGI ANALOG that  , when inhaled, is a potent pulmonary vasodilator used to treat PULMONARY ARTERIAL HYPERTENSION

a. Misoprostol (Cytotec)

b. Iloprost (Ventavis)

c. Alprostadil

d. Latanoprost (Xalatan) and Bimatoprost (Lumigan)

b. Iloprost (Ventavis)

This prostaglandin drug is indicated for: Used as a PGE ANALOG to treat/prevent peptic ulcer by increasing mucus production and decreasing gastric acid secretion.

(*** also utilized to induce uterine contractions and labor) 

a. Misoprostol (Cytotec)

b. Iloprost (Ventavis)

c. Alprostadil

d. Latanoprost (Xalatan) and Bimatoprost (Lumigan)

a. Misoprostol (Cytotec)

This prostaglandin drug is indicated for: A PGE ANALOG that is used to elicit local vasodilation in maintaining the patency of the ductus arteriosus in newborns with congenital heart conditions. 

( ** Also used in the treatment of erectile dysfunction via urethral suppository) 

a. Misoprostol (Cytotec)

b. Iloprost (Ventavis)

c. Alprostadil

d. Latanoprost (Xalatan) and Bimatoprost (Lumigan)

c. Alprostadil

All of the following are Clinical Uses of Prostaglandins........EXCEPT: 

a. Used to treat Pulmonary Hypertension via their ability to cause bronchodilation (PGI2) 

b. Used to induce childbirth/uterine contraction (PGE2) 

c. Used to maintain patency and prevent closure of the Ductus Arteriosus (PDA) (the blood vessel connecting the pulmonary artery to the proximal descending aorta. It allows most of the blood from the right ventricle to bypass the fetus's fluid-filled non-functioning lungs. Upon closure at birth, it becomes the ligamentum arteriosum.) (PGI2 & PGE2) 

d. Used to prevent Peptic Ulcers ( PGE2 )  

e. Used to treat  Glaucoma / Ocular Hypertension

f. All of the above are clinical uses of Prostaglandins

f. All of the above are clinical uses of Prostaglandins

These osteoporosis drugs have a mechanism of action of: Bipshosphonate drug that inhibits osteoclasts

a. Alendonate (Fosamax)

b. Ibandronate (Boniva)

c. Risedronate (Actonel)

d. Ralozifene (Evista)

e. Denosumab (Prolia)

f. Teriparatide (Forteo)

a. Alendonate (Fosamax), b. Ibandronate (Boniva), c. Risedronate (Actonel)

This osteoporosis drug has a mechanism of action of: Selective Estrogen Receptor Modulator- that has pro estrogen effects on bone by decreasing osteoclast function

a. Alendonate (Fosamax)

b. Ibandronate (Boniva)

c. Risedronate (Actonel)

d. Ralozifene (Evista)

e. Denosumab (Prolia)

f. Teriparatide (Forteo)

d. Ralozifene (Evista)

This osteoporosis drug has a mechanism of action of: A monoclonal Antibody that binds to a RANKL protein needed for the formation and survival of osteoclasts

a. Alendonate (Fosamax)

b. Ibandronate (Boniva)

c. Risedronate (Actonel)

d. Ralozifene (Evista)

e. Denosumab (Prolia)

f. Teriparatide (Forteo)

e. Denosumab (Prolia)

This osteoporosis drug has a mechanism of action of: A Parathyroid Hormone ( PTH) analog drug that activates osteoblasts by producing an  intermittant exposure to PTH

a. Alendonate (Fosamax)

b. Ibandronate (Boniva)

c. Risedronate (Actonel)

d. Ralozifene (Evista)

e. Denosumab (Prolia)

f. Teriparatide (Forteo)

f. Teriparatide (Forteo)

The Mechanism of Action for the  Selective Estrogen Receptor Modulator (SERM) drugs, in treating osteoporosis, is related to _____________________________. 

a. its Anti-Estrogenic effects on bone and decreasing osteoclast function

b. its Pro-Estrogenic effects on bone and decreasing osteoblast function

c. its Pro-Estrogenic effects on bone and decreasing osteoclast function

d. its Anti-Estrogenic effects on bone and decreasing osteoblast function

c. its Pro-Estrogenic effects on bone and decreasing osteoclast function

Normally, when taking Tylenol, there is enough of the Glutathione enzyme in the liver to bind to a toxic intermediate (NAPQI) and neutralize it. But, when the dose of tylenol exceeds ____________________, that toxic intermediate (NAPQI) accumulates and can cause hepatoxcicity and cell death in the liver.

a. 2 extra strength tablets / Day

b. 1 extra strength tablet / Day

c. 5 extra strength tablets / Day

d. 8 extra strength tablets / Day

d. 8 extra strength tablets / Day

The Triptan Drugs (Sumatriptin (Imitrex), Rizatriptan (Maxalt), Zolmitriptan (Zomig) used in treating Migraine headaches are highly effective, reducing the symptoms or aborting the attack within 30 to 90 minutes in ___________________of patients. 

a. 100%

b. 70 - 80 % 

c. 50% 

d. 20- 30%

b. 70 - 80 %

All of the following are TRUE with respect to Ustekinumab (Stelara), EXCEPT:

a. Ustekinumab (Stelara) is indicated for Psoriatic Arthritis

b. Ustekinumab (Stelara) is indicated Rheumatoid Arthritis (RA) 

c. Ustekinumab (Stelara) has an initial dosage of 45mg, then 45mg 4 weeks later, then 45 mg every 12 weeks.

d. Ustekinumab (Stelara) is a monoclonal Antibody Drug that targets Iinterleukin IL-12 and IL-23 Cytokines for its anti-inflammatory mechanism of action. 

e. Ustekinumab (Stelara) is indicated for Plaque Psoriasis (Ps)

b. Ustekinumab (Stelara) is indicated Rheumatoid Arthritis (RA)

All of the following are true statements regarding Prostaglandins,......EXCEPT:

a. They are derived from a primary precursor called Arachidonic Acid that is present in all plasma cell membranes.

b. They are produced, in minute quantities, by virtually all the tissues in the body. 

c. In the GI tract, they decrease stomach acid production and help the gut release more protective mucus

d. They are referred to as "mediators of pain and inflammation" 

e. They generally are released into and circulate in the blood to act on tissues throughout the body. 

f. in the Kidney, they regulate renal hemodynamicsa, renin release and salt/water balance.

e. They generally are released into and circulate in the blood to act on tissues throughout the body.

This headache type has these characteristics: Usually Unilateral......Visual Auras.....sesnitivity to light and sound...pale face...Nausea & Vomitting......lasts 2 to 72 hours per episode.....Pulsating & throbbing....females more often than males...family history

a. Migraine headache

b. Cluster headache

c. Tension headache

a. Migraine headache

This headache type has these characteristics: Usually bilateral in band around head.......dull persistent pain....30 minutes to 7 days per episode....females more than males....family history

a. migraine headache

b. cluster headache

c. tension headache

c. tension headache

This type of headache has these characteristics: Behind or around one eye....sweating.....pupillary changes.....lasts 15 - 90 minutes...excruciating sharp and steady pain.......males more than females.....no family history

a. migraine headache

b. cluster headache

c. tension headache

b. cluster headache

All of the following are true regarding why Estrogen Replacement Therapy for postmenopausal osteoporosis is not considered first line therapy, EXCEPT:

a. Estrogen increases factors VII and X

b. stroke

c. hormone dependent breast cancer

d. Estrogen increases ATIII

e. hormone dependent endometrial cancer

f. All of the above are true

d. Estrogen increases ATIII

Arachidonic acid is converted to good "housekeeping' prostaglandins" that promote normal cellular responses by ___________________________, while the the prostaglandins that are responsible for an inflammatory response are converted from arachidonic acid by _____________________________________. 

a. Cyclooxygenase-2 (COX2), Cyclooxygenase-1 (COX1) 

b. Cyclooxygenase-1 (COX1), Cyclooxygenase-2 (COX2) 

b. Cyclooxygenase-1 (COX1), Cyclooxygenase-2 (COX2)

Choose the GI 'protective' prostaglandin associated with: a) decreasing gastric acid secretion and b) increasing gastric mucus secretion.

a. PGF

b. PGE

c. PGI

b. PGE

All of the following Drugs or Drug Classes Contribute to Bone Loss....EXCEPT:

a. Glucocorticoids

b. Proton Pump Inhibitors

c. Selective Serotonin Reuptake Inhibitors (SSRI's) 

d. Anticonvulsants (Phenytoin) 

e. Furosemide (Lasix) 

f. Alcohol

g. All of the above increase Bone Loss and contribute to Osteoporosis. 

g. All of the above increase Bone Loss and contribute to Osteoporosis.

Which drugs for Gout has a mechanism of action of: Inhibits Xanthine Oxidase enzyme needed for uric acid production

a. Allopurinol (Zyloprim)

b. Febouxostat (Uloric)

c. Probenecid

d. Colchicine

a. Allopurinol (Zyloprim), b. Febouxostat (Uloric)

Which drug for Gout has a mechanism of action of: binds to tubulin and microtubule function, which inhibits Neutrophils, Cytokines and Chemokines; serves a dual purpose in gout management: a short course for immediate relief of an existing flare and a longer, low-dose regimen to prevent future occurrences.

a. Allopurinol (Zyloprim)

b. Febouxostat (Uloric)

c. Probenecid

d. Colchicine

d. Colchicine

Which drug for Gout has a mechanism of action of: Increase uric Acid excretion in the kidney (uricosuric) (used more to prevent gouty attacks)

a. Allopurinol (Zyloprim)

b. Febouxostat (Uloric)

c. Probenecid

d. Colchicine

c. Probenecid

All the following are TRUE with respect to the drug Denosumab (Prolia), EXCEPT:

a. It is a Monoclonal Antibody Drug. 

b. It is parenteral drug given ( SQ )  subcutaneously.

c. It is indicated in the treatment of:

- Osteoporosis in Postemenopausal women at high risk of bone fracture

- To increase bone mass in men with osteoporosis

- And in the treatment of bone loss in men receiving androgen deprivation therapy for prostate cancer. 

d. The dosage is 60mg every 6 months.

e. Prolia targets and inhibits the RANKL cytokine protein from binding to the RANKL receptor transmembrane proteins that are vital in the formation, function and survival of osteoblasts. 

f. All of the above are TRUE

e. Prolia targets and inhibits the RANKL cytokine protein from binding to the RANKL receptor transmembrane proteins that are vital in the formation, function and survival of osteoblasts. 

All of the following are true regarding Parathyroid Hormone (PTH), EXCEPT: 

a. PTH regulates serum calcium levels

b. Parathyroid hormone (PTH) is released by the parathyroid glands when blood calcium levels are low to raise them.

c. PTH raises serum calcium levels  via activating osteoblasts to break down bone tissue and release calcium into the bloodstream. 

d. chronically elevated PTH will deplete bone stores of calcium, and bones will ultimately get weaker

e. All of the above are true

c. PTH raises serum calcium levels via activating osteoblasts to break down bone tissue and release calcium into the bloodstream.

True or False: Aspirin, when compared to other Non-selective COX Inhibitors has more of an effect on inhibiting platelet aggregation

true

Which Disease Modifying Anti-Rheumatic Drug (DMARD) has a mechanism of action of: A Tumor Necrosis Factor ( TNF ) Inhibitor, given SQ twice a week, that reduces the ability of TNF to regulate Immune Cells theri role in inflammation. ( warning = increased risk fro developing serious infections )

a. Methotrexate (MTX)

b. Etanercept (Enbrel)

c. Adalimumab (Humira)

d. Tofacitnib (Xeljanx)

e. Abatacept (Orencia)

b. Etanercept (Enbrel)

Which Disease Modifying Anti-Rheumatic Drug (DMARD) has a mechanism of action of: Inhibitor of T-Cell ( T-Lymphocyte ) activation by binding to; a) proteins found on Antigen Presenting Cells, b) proteins found on Activated B-Cells, and c) proteins expressed on T-Cells.

a. Methotrexate (MTX)

b. Etanercept (Enbrel)

c. Adalimumab (Humira)

d. Tofacitnib (Xeljanx)

e. Abatacept (Orencia)

e. Abatacept (Orencia)

Which Disease Modifying Anti-Rheumatic Drug (DMARD) has a mechanism of action of: A Janus-Associated Kinase ( JAK) Inhibitor that disrupts the signaling of cytokines associated with the inflammation of Rheumatoid Arhtritis ( RA) . ( given orally twice daily ) ( warning = increased risk fro developing serious infections )

a. Methotrexate (MTX)

b. Etanercept (Enbrel)

c. Adalimumab (Humira)

d. Tofacitnib (Xeljanx)

e. Abatacept (Orencia)

d. Tofacitnib (Xeljanx)

Which Disease Modifying Anti-Rheumatic Drug (DMARD) has a mechanism of action of:A Monoclonal Antibody, given SQ weekly or every other week, that binds to TNF thereby interfering with its ability to regulate the immune response and inflammatory response ( warning = increased risk fro developing serious infections )

a. Methotrexate (MTX)

b. Etanercept (Enbrel)

c. Adalimumab (Humira)

d. Tofacitnib (Xeljanx)

e. Abatacept (Orencia)

c. Adalimumab (Humira)

Which Disease Modifying Anti-Rheumatic Drug (DMARD) has a mechanism of action of: A 'antimetabolite' anticancer drug used also to treat Rheumatoid Athritis ( but given just once weekly and at much lower doses to minimize adverse effects) . Mechanism of action involves inhibition of enzymes needed for T-Cell expression.

a. Methotrexate (MTX)

b. Etanercept (Enbrel)

c. Adalimumab (Humira)

d. Tofacitnib (Xeljanx)

e. Abatacept (Orencia)

a. Methotrexate (MTX)

In Rheumatoid Arthritis ( RA ), White Blood Cells view the synovium ( tissue that nourishes cartilage and bone) as Non-Self, and this ____________________ the inflammatory response.

a. Inhibits

b. Initiates

b. Initiates

Which Bone Mineral Density T-Score is indicative of the presence of Osteoporosis?

a. - 1.0

b. - 2.0

c. + 1.0

d. + 2.5

e. - 3.0

e. - 3.0

The Mechansim of Action for the BiPhosphonate Drugs is________________________.

a. Stimualtion of Osteoclasts

b. Stimulation of Osteoblasts

c. Inhibition of Osteoclasts

d. Inhibition of Osteoblasts

c. Inhibition of Osteoclasts

Osteoporosis is characterized by an imbalance of cells that break down bone (_____________________) , and cells which deposit new bone ( ________________________).

a. osteoblasts, osteoclasts

b. osteoclasts, osteoblasts

b. osteoclasts, osteoblasts

The decrease in Bone Density and associated Osteoporosis that is  associated with excessive alcohol intake is attributable to all of the following mechanisms, EXCEPT: 

a. Alcohol can lead to increased calcium excretion by the kidneys

b. Alcohol increases cortisol levels, and this reduces osteoblast function and increases osteoclast function. 

c. Alcohol damages the pancreas, which is a source of lipase enzymes that hep you digest food and absorb Vitamin D, calcium , and other nutrients. 

d. Alcohol interferes with liver enzymes needed to convert inactive Vitamin D to active Vitamin D, which is needed for absorbing calcium from your GI tract. 

e. Alcohol lowers  Parathyroid Hormone ( PTH ) levels

f. Alcohol reduces testosterone hormone levels,----and testosterone is needed for proper osteoblast function.

e. Alcohol lowers Parathyroid Hormone (PTH) levels

All of the following are true with regard to Estrogen effects on bone, EXCEPT:

a. decreases apoptosis of osteoblasts

b. increases apoptosis of osteocytes

c. decreases bone resorption

d. increases apoptosis of osteoclasts

e. All of the above are true

b. increases apoptosis of osteocytes

The Mechanism of Action for synthetic Parathyroid Hormone (PTH) drugs is____________________________________.

a. inhibit osteoclasts by chronically elevated levels of PTH

b. activate osteoclasts by chronically elevated levels of PTH

c. activate osteoblasts by intemittant exposure of PTH

d. activate osteoclasts by intemittant exposure of PTH

c. activate osteoblasts by intemittant exposure of PTH

Gout is associated with elevated levels of ___________________ in the blood, which crystalizes and deposits in joint and tendons.

a. Ascorbic Acid

b. Uric Acid

c. Folic Acid

d. Salacylic Acid

b. Uric Acid

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: a decrease in inflammation

beneficial

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: kidney regulation is lessened

unwanted

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: increase in gastric acid production

unwanted

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: decrease in stomach mucus production

unwanted

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: decreases hyperalgesia

beneficial

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: decreases fever

beneficial

The Non Steroidal Anti-Inflammatory Drugs ( NSAID's)  block the active site for Arachidonic Acid on Cyclooxygenases preventing the conversion into prostaglandins, which produces a variety of effects. Is this effect of prostaglandin inhibition beneficial or unwanted: inhibition of platelet aggregation

beneficial

All of the following are TRUE with respect to Acetaminophen (APAP) (Tylenol)  .....EXCEPT:

a. Has a very weak Anti-inflammatory effect

b. CNS Cyclooxygenase Inhibition occurs to a greater extent than peripheral cyclooxygenase inhibition. 

c. Has Analgesic Effect

d. Inhibits platelet aggregation &  increases bleeding times

e. NOT considered to be an NSAID

f. Has Antipyretic Effect

d. Inhibits platelet aggregation & increases bleeding times

All of the following are EFFECTS of PROSTAGLANDINS..........EXCEPT. 

a. regulate inflammatory mediation

b. act on the thermoregulatory center in the hyppothalamus to produce fever

c. act on the parietal cells in the stomach wall to INHIBIT gastric acid secretion. 

d. Induce labor

e. Act on the cells in the kidney to increase filtration rate

f. sensitize spinal neurons to pain ( hyperalgesia) 

g. act on the parietal cells in the stomach wall to INCREASE mucus secretion.  

h. Decrease Intraocular Pressure

i. All of the above ARE effects of Prostaglandins. 

i. All of the above ARE effects of Prostaglandins.

The mechanism of action for the "Triptan" drug class {Sumatriptin ( Imitrex), Rizatriptan ( Maxalt), Zolmitriptan ( Zomig) } , is due;

a. Their agonistic effects on central serotonin receptors in cranial blood vessels which causes their constriction. 

b. Their agonistic effects on central Dopamine receptors in cranial blood vessels which causes their constriction. 

c. Their influence on Trigeminal Nerve Endings...causing subsequent inhibition of Pro-Inflammatory and Pain transmitter release. ( Substance-P) 

d. Both b & c

e. Both a & c

e. Both a & c

A "Selective" Cyclooxygenase Inhibitor preferentially targets ___________________, which is more associated with producing "inflammatory" prostaglandins vs. "housekeeping" postaglandins. This preferential inhibition will also have no effect on inhibiting platelets which increase bleeding times, will have no effect on mucus production and will not increase gastric acid production.

a. COX3

b. COX1

c. COX2

c. COX2