NURS 615 EXAM IV QUESTIONS WITH ALL CORRECT DETAILED
ANSWERS A+ PASS
1. How will you prescribe lipase, protease, and amylase components?: Pa-
tients with cystic fibrosis are often prescribed enzyme replacement for pancreatic
secretions each replacement drug has amylase, lipase and protease components,
however the drug is prescribed in units of lipase
2. What is the medication of choice for hypertensive crisis with pheochro-
mocytoma?: Surgical resection of the tumor is the first treatment of choice either
my open laparotomy or laparoscopy either surgical option requires prior treatment
of nonspecific irreversible adrenergic adraonoreceptor blocker phenoxybenzamine
or a shorter acting alpha antagonists, prazosin, terazosin, and doxazosin. Mainly
use phenozibenamine in practice. Doing so promotes the surgery to proceed while
minimizing the likelihood of severe intraoperative hypertension which is likely when
the tumor is manipulated.
3. What is the onset of action, peak of action, and duration of action of each
insulin preparation?: (Intermediate Acting) NPH
Onset-60-90 min after administration,
Peak 48 hrs
Duration 10-18 hrs.
(Short Acting) Regular Onset 30-60 min
Peak 2-4 hrs
Duration 6-10 hrs
(Long Acting) Aspart, Lispro, Glulisine
Onset less than 15 min
Peak 1-2 hrs
Duration 3-6 hrs
(Long Acting) Glargine, Detemir
Onset 1-2 hrs
Peak NO PEAK
Duration 24 hrs
4. Identify the symptoms of hypoglycemia, hyperglycemia, and ketoacidosis.-
: Hypoglycemia- dizziness, confusion, diaphoresis, tachycardia
Hyperglycemia- polyphagia, polydipsia, polyuria, blurred vision, and fatigue
Ketoacidosis- hallmark symptoms include acetone breath like nail polish remover or
fruity breath. Also abdominal pain, nausea, vomiting and sob.
5. When changing from NPH to glargine insulin, how will you adjust the
patient's dose?: The initial dose of glargine is reduced by 20% to prevent hypo-
glycemia.
,NURS 615 EXAM IV QUESTIONS WITH ALL CORRECT DETAILED
ANSWERS A+ PASS
6. How does metformin work?: Decreases hyperglycemia by decreasing hepatic
glucose production called hepatic gluconeogenesis. The average person with type 2
diabetes has three times the rate of gluconeogenesis, metformin treatment reduces
this by over 1/3rd. The molecular mechanism of metformin isn't completely under-
stood. In addition to suppressing hepatic glucose production, metformin increases
insulin sensitivity, enhances peripheral glucose uptake by inducing the phosphoril-
ization of glu4 enhancer factor, decreases insulin induced suppression of fatty acid
oxidation, and decreases absorption of glucose from the GI tract. Also of note**
Metformin helps reduce LDL cholesterol and triglyceride levels and is not associated
with weight gain, in some people it helps promote weight loss**
7. What diagnostic testing is required before and throughout therapy with
metformin?: Metformin is not metabolized, it is cleared from the body by tubular
secretion and is secreted unchanged in the urine. Metformin is undetectable in blood
plasma within 24 hrs of a single oral dose the average elimination half-life in plasma
is 6.2 hrs as it is secreted in the urine you should check a serum crt to assess renal
function.
8. What is the action of gliptin?: The mechanism of DDP-4 inhibitors is to increase
incretin levels incretin are GLP1 and GIP which inhibit glucagon release in which in
turn increases insulin secretion, decreases gastric emptying, and decreases blood
glucose levels
9. How do GLP agonists work?: They bind directly to a receptor in the pancreatic
beta cell. These agents work in the same pathway as the DPP-4 inhibitors as
mentioned above but are generally considered more potent.
10. When should exenatide be administered?: 60 minutes prior to the morning
and evening meal
11. How will you assess for granulocytopenia?: Signs of a Cold or flu including
fever and sore throat
12. What are the adverse effects of propylthiouracil?: Agranulocytosis, thrombo-
cytopenia, and fulminant liver failure as stated above, pt's on PTU when they develop
fever or sore throat, it would be important to check a CBC preferably with a smear
and a diff.
13. What are the adverse effects of levothyroxine?: Tachycardia and angina in
the elderly
14. A patient develops a toxic goiter. What is the recommended treatment?: -
Methimazole for one month then radioactive iodine (p. 641)
15. What are the adverse effects of PTU and methimazole?: PTU- Fatal agranu-
locytopenia look for fever and sore throat and TEMPORARY ALOPECIA
16. What is the action of biphosphonates?: Bone undergoes constant turnover
and is kept in balance by osteoblasts creating bone and osteoclasts destroying
,NURS 615 EXAM IV QUESTIONS WITH ALL CORRECT DETAILED
ANSWERS A+ PASS
bone. Bisphosphonates inhibit the digestion of bone by encouraging osteoclasts to
undergo apoptosis or cell death there by slowing bone loss. Oral bisphosphonates
can cause upset stomach and inflammation as well as erosion. Erosions of the
esophagus which is the main problem of oral and containing preparations. This can
be prevented by sitting upright for 30-60 minutes after taking the medication. If the
patient does develop some type of gastric distress, give them oral 30ml of Maalox 3
hrs after taking it. IV bisphosphonates can give fever and flu like symptoms after the
first infusion which is thought to occur because of their potential to activate human
T cells
17. Which infant formula is linked to impairment of thyroxine absorption?: -
Prosobee
18. What are the drug interactions when prescribing poglitazone?: Metabolized
by the CYP 2C8 which induces just like oral contraceptives. Oral contraceptives will
be less effective, which leads to more unintended pregnancies. Council patients to
change to a more reliable method of birth control that is not metabolized by the
liver such as depropravera, long acting reversible contraceptives such as the IED or
implantable contraceptives such as nexplanon
19. What is the drug of choice to treat neurogenic diabetes insipidus?: Clo-
rapropramide
20. What is the dosage schedule for alpha-glucosidase inhibitors?: Take within
the first bite of each meal
21. Describe the pharmacodynamics of meglitinides.: Citagliptan works to com-
patibly inhibit the enzyme dipeptidyl, dipeptide, or called DDP 4 as mentioned before,
this enzyme breaks down the incretins GLP1 and GIP gastrointestinal hormone
released in response to a meal. By preventing GLP1 and GIP inactivation, they are
able to increase secretion of insulin and suppress the release of glucagon by the
alpha cells of the pancreas, this process ultimately drives calcium into the cell, this
drives blood glucose levels towards normal as the blood glucose level approaches
normal, the amount of insulin release in glucagon suppression diminishes thus
tending to prevent an overshoot of subsequent blood sugar hypoglycemia which is
seen in some other oral hypoglycemia agents.
22. Type 1 diabetes results from autoimmune destruction of the beta cells.
Eighty-five to 90 percent of Type 1 diabetics have:
A. Autoantibodies to two tyrosine phosphatases
B. Mutation of the hepatic transcription factor on chromosome 12
C. A defective glucokinase molecule due to a defective gene on chromosome
7p
ANSWERS A+ PASS
1. How will you prescribe lipase, protease, and amylase components?: Pa-
tients with cystic fibrosis are often prescribed enzyme replacement for pancreatic
secretions each replacement drug has amylase, lipase and protease components,
however the drug is prescribed in units of lipase
2. What is the medication of choice for hypertensive crisis with pheochro-
mocytoma?: Surgical resection of the tumor is the first treatment of choice either
my open laparotomy or laparoscopy either surgical option requires prior treatment
of nonspecific irreversible adrenergic adraonoreceptor blocker phenoxybenzamine
or a shorter acting alpha antagonists, prazosin, terazosin, and doxazosin. Mainly
use phenozibenamine in practice. Doing so promotes the surgery to proceed while
minimizing the likelihood of severe intraoperative hypertension which is likely when
the tumor is manipulated.
3. What is the onset of action, peak of action, and duration of action of each
insulin preparation?: (Intermediate Acting) NPH
Onset-60-90 min after administration,
Peak 48 hrs
Duration 10-18 hrs.
(Short Acting) Regular Onset 30-60 min
Peak 2-4 hrs
Duration 6-10 hrs
(Long Acting) Aspart, Lispro, Glulisine
Onset less than 15 min
Peak 1-2 hrs
Duration 3-6 hrs
(Long Acting) Glargine, Detemir
Onset 1-2 hrs
Peak NO PEAK
Duration 24 hrs
4. Identify the symptoms of hypoglycemia, hyperglycemia, and ketoacidosis.-
: Hypoglycemia- dizziness, confusion, diaphoresis, tachycardia
Hyperglycemia- polyphagia, polydipsia, polyuria, blurred vision, and fatigue
Ketoacidosis- hallmark symptoms include acetone breath like nail polish remover or
fruity breath. Also abdominal pain, nausea, vomiting and sob.
5. When changing from NPH to glargine insulin, how will you adjust the
patient's dose?: The initial dose of glargine is reduced by 20% to prevent hypo-
glycemia.
,NURS 615 EXAM IV QUESTIONS WITH ALL CORRECT DETAILED
ANSWERS A+ PASS
6. How does metformin work?: Decreases hyperglycemia by decreasing hepatic
glucose production called hepatic gluconeogenesis. The average person with type 2
diabetes has three times the rate of gluconeogenesis, metformin treatment reduces
this by over 1/3rd. The molecular mechanism of metformin isn't completely under-
stood. In addition to suppressing hepatic glucose production, metformin increases
insulin sensitivity, enhances peripheral glucose uptake by inducing the phosphoril-
ization of glu4 enhancer factor, decreases insulin induced suppression of fatty acid
oxidation, and decreases absorption of glucose from the GI tract. Also of note**
Metformin helps reduce LDL cholesterol and triglyceride levels and is not associated
with weight gain, in some people it helps promote weight loss**
7. What diagnostic testing is required before and throughout therapy with
metformin?: Metformin is not metabolized, it is cleared from the body by tubular
secretion and is secreted unchanged in the urine. Metformin is undetectable in blood
plasma within 24 hrs of a single oral dose the average elimination half-life in plasma
is 6.2 hrs as it is secreted in the urine you should check a serum crt to assess renal
function.
8. What is the action of gliptin?: The mechanism of DDP-4 inhibitors is to increase
incretin levels incretin are GLP1 and GIP which inhibit glucagon release in which in
turn increases insulin secretion, decreases gastric emptying, and decreases blood
glucose levels
9. How do GLP agonists work?: They bind directly to a receptor in the pancreatic
beta cell. These agents work in the same pathway as the DPP-4 inhibitors as
mentioned above but are generally considered more potent.
10. When should exenatide be administered?: 60 minutes prior to the morning
and evening meal
11. How will you assess for granulocytopenia?: Signs of a Cold or flu including
fever and sore throat
12. What are the adverse effects of propylthiouracil?: Agranulocytosis, thrombo-
cytopenia, and fulminant liver failure as stated above, pt's on PTU when they develop
fever or sore throat, it would be important to check a CBC preferably with a smear
and a diff.
13. What are the adverse effects of levothyroxine?: Tachycardia and angina in
the elderly
14. A patient develops a toxic goiter. What is the recommended treatment?: -
Methimazole for one month then radioactive iodine (p. 641)
15. What are the adverse effects of PTU and methimazole?: PTU- Fatal agranu-
locytopenia look for fever and sore throat and TEMPORARY ALOPECIA
16. What is the action of biphosphonates?: Bone undergoes constant turnover
and is kept in balance by osteoblasts creating bone and osteoclasts destroying
,NURS 615 EXAM IV QUESTIONS WITH ALL CORRECT DETAILED
ANSWERS A+ PASS
bone. Bisphosphonates inhibit the digestion of bone by encouraging osteoclasts to
undergo apoptosis or cell death there by slowing bone loss. Oral bisphosphonates
can cause upset stomach and inflammation as well as erosion. Erosions of the
esophagus which is the main problem of oral and containing preparations. This can
be prevented by sitting upright for 30-60 minutes after taking the medication. If the
patient does develop some type of gastric distress, give them oral 30ml of Maalox 3
hrs after taking it. IV bisphosphonates can give fever and flu like symptoms after the
first infusion which is thought to occur because of their potential to activate human
T cells
17. Which infant formula is linked to impairment of thyroxine absorption?: -
Prosobee
18. What are the drug interactions when prescribing poglitazone?: Metabolized
by the CYP 2C8 which induces just like oral contraceptives. Oral contraceptives will
be less effective, which leads to more unintended pregnancies. Council patients to
change to a more reliable method of birth control that is not metabolized by the
liver such as depropravera, long acting reversible contraceptives such as the IED or
implantable contraceptives such as nexplanon
19. What is the drug of choice to treat neurogenic diabetes insipidus?: Clo-
rapropramide
20. What is the dosage schedule for alpha-glucosidase inhibitors?: Take within
the first bite of each meal
21. Describe the pharmacodynamics of meglitinides.: Citagliptan works to com-
patibly inhibit the enzyme dipeptidyl, dipeptide, or called DDP 4 as mentioned before,
this enzyme breaks down the incretins GLP1 and GIP gastrointestinal hormone
released in response to a meal. By preventing GLP1 and GIP inactivation, they are
able to increase secretion of insulin and suppress the release of glucagon by the
alpha cells of the pancreas, this process ultimately drives calcium into the cell, this
drives blood glucose levels towards normal as the blood glucose level approaches
normal, the amount of insulin release in glucagon suppression diminishes thus
tending to prevent an overshoot of subsequent blood sugar hypoglycemia which is
seen in some other oral hypoglycemia agents.
22. Type 1 diabetes results from autoimmune destruction of the beta cells.
Eighty-five to 90 percent of Type 1 diabetics have:
A. Autoantibodies to two tyrosine phosphatases
B. Mutation of the hepatic transcription factor on chromosome 12
C. A defective glucokinase molecule due to a defective gene on chromosome
7p
