1
Pharmacology Exam 3 Review by Dr. Strathman – Transcript
Strathman's Review July 2016
This is the review for exam number three will go week by week and start with the questions from
the study guide let's begin
Week number eight
1. Differentiate between low dose and high-dose colchicine.
Low dose colchicine is 1.2mg followed by 0.6mg one hour later or 1.8 milligrams total
and high dose colchicine is 1.2mg followed by 0.6mg every four to six hours; or 4.8mg
total. The difference between the two is low dose is as effective as high dose with a lower
side effect profile.
2. What lab value should be monitored with gout?
Check renal function test, BUN, Creatine
3. What patient education should you provide when prescribing colchicine?
Always causes seventh degree of diarrhea so make sure that people understand that (some
have said they think he said “severe degree of diarrhea” it is either 7th or severe)
4. What patient teaching will you provide when prescribing febuxostat (Uloric)?
Gout may worsen with therapy initially.
5. What are the adverse effects of corticosteroids if administered for six months or more?
The main thing you want to worry about is osteoporosis it can also worsen diabetic
control and patients should report any tarry black stools or abdominal pain.
6. Why is it important to tapper the corticosteroid?
Tapering must be done carefully to avoid both recurrent activity of the underlying disease
process and possible cortisol deficiency resulting from the hypothalamic-pituitary-adrenal
axis or HPA suppression during the period of steroid therapy
7. What are the black box warnings on NSAIDs?
May cause an increased risk of serious cardiovascular thrombotic events, myocardial-
infarction and stroke which can be fatal. This risk may increase with duration of use.
Patients with cardiovascular disease or with risk factors for cardiovascular disease may
be a greater risk. NSAIDs can also cause an increased risk of serious gastrointestinal
adverse effects including: bleeding, ulceration, and perforation the stomach or intestines
which can be fatal. These events can can occur at any time during use and without
warning symptoms. Elderly patients are at greater risk for serious GI events.
8. What are the recommendations in the treatment of pain?
You want to start with NSAIDs first and then work your way up from there.
9. What's the mechanism of action of ibuprofen?
, 2
Pharmacology Exam 3 Review by Dr. Strathman – Transcript
NSAIDs such as ibuprofen work by inhibiting the cox enzymes cox which is
cyclooxygenase is officially known as the prostaglandin-endoperoxide synthase (PTGS),
which converts arachidonic acid to prostaglandin h2 or PGH2. PGH2 in turn is converted
by other enzymes to several other prostaglandins which are mediators of pain,
inflammation, and fever, and to thromboxane-A2 which stimulates platelet aggregation
leading to the formation of blood clots.
It's a good idea to familiarize yourself with the cox pathway and how blocking one part
of the cox pathway can lead to build up of other different products.
The exact mechanism of action of ibuprofen is unknown. Ibuprofen is a non-selective
inhibitor of cyclooxygenase, its pharmacological effects are believed to be due to
inhibition of cox-2 which decreases the synthesis of prostaglandins in mediating the
inflammation pain, fever, and swelling. Antipyretic effects may be due to action on the
hypothalamus resulting in an increase of peripheral blood flow, basil dilation, and
subsequent heat dissipation. Inhibition of cox-1 is thought to cause some of the side
effects of ibuprofen including GI ulceration like aspirin and indomethacin, ibuprofen is a
non-selective cox-2 inhibitor in that it inhibits two isoforms of psychologic oxygenase
cox-1 and cox-2. The analgesic and antipyretic and anti-inflammatory activity of NSAIDs
appear to operate mainly through inhibition of cox-2. Resident inhibition of cox-1 would
be responsible for the unwanted effects on the GI tract. However, the role of individual
cox isoforms in the analgesic and anti-inflammatory and gastric damage effects of
NSAIDs is uncertain and different compounds cause different degrees of analgesia and
gastric damage. Ibuprofen is also a reversible inhibitor of the cox pathway. On the other
hand, aspirin is a non-reversible inhibitor of the cox pathway.
10. What are serious side effects associated with acetaminophen?
To-date the mechanism of action of acetaminophen is not completely understood. The
main mechanism is performed a proposed is the inhibition of cox. And recent findings
suggest that it's highly selective cox-2. Because of its selectivity for cox-2 it does not
significantly inhibit the production of pro clotting thromboxanes. While it has analgesic
and antipyretic properties compared to those of aspirin or other NSAIDs its peripheral
anti-inflammatory activity is usually still limited by several factors. One of which is the
high level of peroxides present and inflammatory lesions and in some circumstances even
the peripheral anti-inflammatory activity comparable to NSAIDs can be observed. Acute
overdoses of acetaminophen can cause potentially fatal liver damage. In 2011 the FDA
launched a public education program to help consumers avoid overdose, warning it can
cause serious liver damage if more than directed is used. The maximum recommended
dose is 4 grams in 24 hours.
Week Nine
Pharmacology Exam 3 Review by Dr. Strathman – Transcript
Strathman's Review July 2016
This is the review for exam number three will go week by week and start with the questions from
the study guide let's begin
Week number eight
1. Differentiate between low dose and high-dose colchicine.
Low dose colchicine is 1.2mg followed by 0.6mg one hour later or 1.8 milligrams total
and high dose colchicine is 1.2mg followed by 0.6mg every four to six hours; or 4.8mg
total. The difference between the two is low dose is as effective as high dose with a lower
side effect profile.
2. What lab value should be monitored with gout?
Check renal function test, BUN, Creatine
3. What patient education should you provide when prescribing colchicine?
Always causes seventh degree of diarrhea so make sure that people understand that (some
have said they think he said “severe degree of diarrhea” it is either 7th or severe)
4. What patient teaching will you provide when prescribing febuxostat (Uloric)?
Gout may worsen with therapy initially.
5. What are the adverse effects of corticosteroids if administered for six months or more?
The main thing you want to worry about is osteoporosis it can also worsen diabetic
control and patients should report any tarry black stools or abdominal pain.
6. Why is it important to tapper the corticosteroid?
Tapering must be done carefully to avoid both recurrent activity of the underlying disease
process and possible cortisol deficiency resulting from the hypothalamic-pituitary-adrenal
axis or HPA suppression during the period of steroid therapy
7. What are the black box warnings on NSAIDs?
May cause an increased risk of serious cardiovascular thrombotic events, myocardial-
infarction and stroke which can be fatal. This risk may increase with duration of use.
Patients with cardiovascular disease or with risk factors for cardiovascular disease may
be a greater risk. NSAIDs can also cause an increased risk of serious gastrointestinal
adverse effects including: bleeding, ulceration, and perforation the stomach or intestines
which can be fatal. These events can can occur at any time during use and without
warning symptoms. Elderly patients are at greater risk for serious GI events.
8. What are the recommendations in the treatment of pain?
You want to start with NSAIDs first and then work your way up from there.
9. What's the mechanism of action of ibuprofen?
, 2
Pharmacology Exam 3 Review by Dr. Strathman – Transcript
NSAIDs such as ibuprofen work by inhibiting the cox enzymes cox which is
cyclooxygenase is officially known as the prostaglandin-endoperoxide synthase (PTGS),
which converts arachidonic acid to prostaglandin h2 or PGH2. PGH2 in turn is converted
by other enzymes to several other prostaglandins which are mediators of pain,
inflammation, and fever, and to thromboxane-A2 which stimulates platelet aggregation
leading to the formation of blood clots.
It's a good idea to familiarize yourself with the cox pathway and how blocking one part
of the cox pathway can lead to build up of other different products.
The exact mechanism of action of ibuprofen is unknown. Ibuprofen is a non-selective
inhibitor of cyclooxygenase, its pharmacological effects are believed to be due to
inhibition of cox-2 which decreases the synthesis of prostaglandins in mediating the
inflammation pain, fever, and swelling. Antipyretic effects may be due to action on the
hypothalamus resulting in an increase of peripheral blood flow, basil dilation, and
subsequent heat dissipation. Inhibition of cox-1 is thought to cause some of the side
effects of ibuprofen including GI ulceration like aspirin and indomethacin, ibuprofen is a
non-selective cox-2 inhibitor in that it inhibits two isoforms of psychologic oxygenase
cox-1 and cox-2. The analgesic and antipyretic and anti-inflammatory activity of NSAIDs
appear to operate mainly through inhibition of cox-2. Resident inhibition of cox-1 would
be responsible for the unwanted effects on the GI tract. However, the role of individual
cox isoforms in the analgesic and anti-inflammatory and gastric damage effects of
NSAIDs is uncertain and different compounds cause different degrees of analgesia and
gastric damage. Ibuprofen is also a reversible inhibitor of the cox pathway. On the other
hand, aspirin is a non-reversible inhibitor of the cox pathway.
10. What are serious side effects associated with acetaminophen?
To-date the mechanism of action of acetaminophen is not completely understood. The
main mechanism is performed a proposed is the inhibition of cox. And recent findings
suggest that it's highly selective cox-2. Because of its selectivity for cox-2 it does not
significantly inhibit the production of pro clotting thromboxanes. While it has analgesic
and antipyretic properties compared to those of aspirin or other NSAIDs its peripheral
anti-inflammatory activity is usually still limited by several factors. One of which is the
high level of peroxides present and inflammatory lesions and in some circumstances even
the peripheral anti-inflammatory activity comparable to NSAIDs can be observed. Acute
overdoses of acetaminophen can cause potentially fatal liver damage. In 2011 the FDA
launched a public education program to help consumers avoid overdose, warning it can
cause serious liver damage if more than directed is used. The maximum recommended
dose is 4 grams in 24 hours.
Week Nine
