NURS 5334 MODULE 6-9 REVIEW
NURS 5334 MODULE 6-9 REVIEW
Review Module 6 Pharm
Diagnostic criteria: fasting glucose 126; casual glucose of 200 or greater or A1c 6.5 and greater
Insulin dosing must be coordinated with cho intake
BP140/90 or below
ACE/ARB
Statins
Review Dr. Rippergers Pearls on insulin
4 step approach:
Step 1-initiate lifestyle plus metformin (at diagnosis)
Step 2- Continue lifestyle changes plus metformin, and add a second drug, either a sulfonylurea, a
thiazolidinedione, a dipeptidyl peptidase-4 (DPP-4) inhibitor, a sodium-glucose cotransporter 2 (SGLT-2)
inhibitor, a glucagon-like peptide-1 (GLP-1) receptor agonist, or basal insulin. The choice of agent is made
in light of relative efficacy, hypoglycemia risk, tolerability, weight-related considerations, and cost.
Step 3- Progress from step 2 to a three-drug combination (inclusive of metformin). Again, the choice of
regimen used is determined based on drug- and patient-specific considerations.
Step 4: If three-drug combination therapy that includes basal insulin fails to achieve treatment goals
after 3 to 6 months, it is recommended to proceed to a more complex insulin regimen, usually in
combination with one or more noninsulin medicines.
Insulin is summarized in Dr. Ripperger’s Pearls and also covered in Collaborate
There are rapid onset, short duration, intermediate duration and long acting
Metformin
● GI most common side effect-eating with med and using ER version can help
● Need to titrate
● Lactic acidosis can occur so watch in patients with CKD
● Works by inhibiting glucose production in the liver; reduces glucose absorption in the gut; and
sensitizes insulin receptors in target tissue and increases glucose uptake in response to whatever
insulin is available
● 1-2% A1c reduction
Sulfonylureas
GLyipizide-Liver toxicity
Glyburide-renal toxicity
Glimepiride-Both
● Hypoglycemia and weight gain
● 1.5 - 2% A1C reduction
Meglitinides
o Repaglinide
o Nateglinide
▪ Hypoglycemia
▪ Weight gain
▪ 0.5-1.5% A1C reduction
Thiazolidinediones
● Rosiglitazone (Avandia)
● Poglitazone (Actos)
,NURS 5334 MODULE 6-9 REVIEW
o Reduces insulin resistance and decrease glucose production
o Weight gain
o 0.5-1.4% A1C reduction
Alpha-glucosidase inhibitors
● Miglitol
● Acarbose
o Act in intestine to delay absorption of glucose
o Explosive diarrhea is SE
o Does not cause weight gain or loss
o 0.5-0.8% A1C reduction
DPP-4 inhibitors
● Gliptins
o Sitagliptin Januvia
o Saxagliptin Onglyza
o Linagliptin
o Alogliptin
▪ Side effects UTI
▪ Weight loss
▪ 0.6-0.8 % A1C reduction
SGLT-2 Inhibitors
● Canagliflozin
● Dapagliflozin
o SGLT-2 inhibitors have been shown to block the reabsorption of filtered glucose,
leading to glucosuria Which leads to yeast infections and UTI
o Do not work well with GFR <45 so should not be initiated but if already taking
can give until GFR 30
o Come in combo with metformin
o Weight loss
o 0.7-.99% A1C reduction
Colesevelam
Bromocriptine
Injectables
● GLp-1 receptor agonists (incretin mimetics)
o Exenatide Byetta
o Slow gastric emptying, stimulate glucose-dependent release of insulin, inhibit
postprandial release of glucagon, and suppress appetite
o Increase risk for medullary thyroid cancer
● Amylin mimetics
o Pramlintide
THYROID
The effect of maternal hypothyroidism is limited largely to the first trimester, a time during
which the fetus is unable to produce thyroid hormones of its own. By the second trimester, the
fetal thyroid gland is fully functional, and hence the fetus can supply its own hormones from
,NURS 5334 MODULE 6-9 REVIEW
then on. Therefore, to help ensure healthy fetal development, maternal hypothyroidism must
be diagnosed and treated very early. When women taking thyroid supplements become
pregnant, dosage requirements usually increase—often by as much as 50%. The need for
increased dosage begins between weeks 4 and 8 of gestation, levels off at about week 16, and
then remains steady until parturition
◼ In first trimester can result in permanent neuropsychologic deficits in the child
◼ In infants
Hypothyroidism in newborns may be permanent or transient. In either case, congenital
hypothyroidism can cause delay in mental development and derangement of growth. In the
absence of thyroid hormones, the child develops a large and protruding tongue, potbelly, and
dwarfish stature. Development of the nervous system, bones, teeth, and muscles is impaired. In
all children, replacement therapy should continue for 3 years, after which it should be stopped
for 4 weeks. The objective is to determine whether thyroid deficiency is permanent or transient.
If TSH rises, indicating thyroid hormone production is low, we know the deficiency is permanent,
so replacement therapy should resume. If TSH and T4 normalize, we know the deficiency was
transient, and hence further replacement therapy is unnecessary
◼ May be permanent or transient
◼ Can cause mental retardation and derangement of growth
1.6 -1.8 mcg/kg/day for adult dosing. Less for older patients. Obese dose by ideal body weight.
Underweight dose by actual weight. Older patients with CAD should start on 12.5-25. Start low
and go slow. younger than 3 months, the dosage is 10 to 15 mcg/kg/day; for children aged 3 to
5 months, 8 to 10 mcg/kg/day; for children aged 6 to 11 months, 6 to 8 mcg/kg/day; for
children aged 1 to 5 years, 5 to 6 mcg/kg/day; and for children aged 6 to 12 years, 4 to
5 mcg/kg/day.
16 Thyroid Hormone Preparations
◼ Levothyroxine [Synthroid]
◼ Synthetic preparation of thyroxine (T4) and drug of choice for
hypothyroidism
◼ Conversion to T3
◼ Half-life: 7 days
◼ Used for all forms of hypothyroidism
Liothyronine (Cytomel)- synthetic T3
Liotrix [Thyrolar] is a mixture of synthetic T4 plus synthetic T3 in a 4 :1 fixed ratio. because
levothyroxine alone produces the same ratio of T4 to T3. Liotrix offers no advantage over
levothyroxine for most indications.
◼ Thyroid (Armour Thyroid, others)
Thyroid [Armour Thyroid, others] consists of desiccated animal thyroid glands. Standardization
is based on content of iodine, levothyroxine, and liothyronine. The ratio of levothyroxine to
liothyronine is not less than 5 :1. Thyroid is available in tablets (15–300 mg).
◼ Drug interactions
◼ Drugs that reduce levothyroxine absorption
, NURS 5334 MODULE 6-9 REVIEW
H2 receptor blockers, PPI, sucralfate, cholestyramine, colestipol, Maalox, Mylanta, calcium
supplement, iron, magnesium, orlistat
◼ Drugs that accelerate levothyroxine metabolism
Among these are phenytoin [Dilantin], carbamazepine [Tegretol, Carbatrol], rifampin [Rifadin],
sertraline [Zoloft], and phenobarbital. Accordingly, to maintain adequate levothyroxine levels,
patients taking these drugs may need to increase their levothyroxine dosage.
◼ Warfarin
Levothyroxine accelerates the degradation of vitamin K–dependent clotting factors. As a result,
effects of warfarin are enhanced. If thyroid hormone replacement therapy is started in a patient
taking warfarin, the dosage of warfarin may need to be reduced.
◼ Catecholamines
Thyroid hormones increase cardiac responsiveness to catecholamines, thereby increasing the
risk for catecholamine-induced dysrhythmias. Caution must be exercised when administering
catecholamines to patients receiving levothyroxine and other thyroid preparations.
Levothyroxine can increase requirements for insulin and digoxin
PTU Versus Methimazole
◼ PTU can cause severe liver injury, whereas methimazole does not
◼ PTU has a shorter half-life than methimazole (90 min compared to 6 to 13 hr), so it
requires two or three daily doses rather than one
◼ PTU crosses the placenta less readily than does methimazole, and concentrations in
breast milk are lower
◼ PTU blocks conversion of T4 to T3 in the periphery, whereas methimazole does not
◼ Effects on primary and secondary sex characteristics
◼ Reproductive tract and secondary sex characteristics
◼ Estrogens influence the physiologic processes related to reproduction:
◼ Ductal growth in the breast
◼ Thickening and cornification of the vaginal epithelium
◼ Proliferation of the uterine epithelium
◼ Copious secretion of thickened mucus from endocervical glands
◼ Metabolic actions
◼ Positive effect on bone mass by blocking bone resorption
◼ Favorable effects on cholesterol levels: decreases LDL, raises HDL
◼ Blood coagulation by increasing levels of coagulation factors
◼ Glucose homeostasis: estrogen has been shown to increase insulin sensitivity to
promote glucose uptake.
◼ Adverse effects
◼ Endometrial hyperplasia and carcinoma
◼ Promotes growth of existing breast cancer
◼ Ovarian cancer
◼ Cardiovascular events
NURS 5334 MODULE 6-9 REVIEW
Review Module 6 Pharm
Diagnostic criteria: fasting glucose 126; casual glucose of 200 or greater or A1c 6.5 and greater
Insulin dosing must be coordinated with cho intake
BP140/90 or below
ACE/ARB
Statins
Review Dr. Rippergers Pearls on insulin
4 step approach:
Step 1-initiate lifestyle plus metformin (at diagnosis)
Step 2- Continue lifestyle changes plus metformin, and add a second drug, either a sulfonylurea, a
thiazolidinedione, a dipeptidyl peptidase-4 (DPP-4) inhibitor, a sodium-glucose cotransporter 2 (SGLT-2)
inhibitor, a glucagon-like peptide-1 (GLP-1) receptor agonist, or basal insulin. The choice of agent is made
in light of relative efficacy, hypoglycemia risk, tolerability, weight-related considerations, and cost.
Step 3- Progress from step 2 to a three-drug combination (inclusive of metformin). Again, the choice of
regimen used is determined based on drug- and patient-specific considerations.
Step 4: If three-drug combination therapy that includes basal insulin fails to achieve treatment goals
after 3 to 6 months, it is recommended to proceed to a more complex insulin regimen, usually in
combination with one or more noninsulin medicines.
Insulin is summarized in Dr. Ripperger’s Pearls and also covered in Collaborate
There are rapid onset, short duration, intermediate duration and long acting
Metformin
● GI most common side effect-eating with med and using ER version can help
● Need to titrate
● Lactic acidosis can occur so watch in patients with CKD
● Works by inhibiting glucose production in the liver; reduces glucose absorption in the gut; and
sensitizes insulin receptors in target tissue and increases glucose uptake in response to whatever
insulin is available
● 1-2% A1c reduction
Sulfonylureas
GLyipizide-Liver toxicity
Glyburide-renal toxicity
Glimepiride-Both
● Hypoglycemia and weight gain
● 1.5 - 2% A1C reduction
Meglitinides
o Repaglinide
o Nateglinide
▪ Hypoglycemia
▪ Weight gain
▪ 0.5-1.5% A1C reduction
Thiazolidinediones
● Rosiglitazone (Avandia)
● Poglitazone (Actos)
,NURS 5334 MODULE 6-9 REVIEW
o Reduces insulin resistance and decrease glucose production
o Weight gain
o 0.5-1.4% A1C reduction
Alpha-glucosidase inhibitors
● Miglitol
● Acarbose
o Act in intestine to delay absorption of glucose
o Explosive diarrhea is SE
o Does not cause weight gain or loss
o 0.5-0.8% A1C reduction
DPP-4 inhibitors
● Gliptins
o Sitagliptin Januvia
o Saxagliptin Onglyza
o Linagliptin
o Alogliptin
▪ Side effects UTI
▪ Weight loss
▪ 0.6-0.8 % A1C reduction
SGLT-2 Inhibitors
● Canagliflozin
● Dapagliflozin
o SGLT-2 inhibitors have been shown to block the reabsorption of filtered glucose,
leading to glucosuria Which leads to yeast infections and UTI
o Do not work well with GFR <45 so should not be initiated but if already taking
can give until GFR 30
o Come in combo with metformin
o Weight loss
o 0.7-.99% A1C reduction
Colesevelam
Bromocriptine
Injectables
● GLp-1 receptor agonists (incretin mimetics)
o Exenatide Byetta
o Slow gastric emptying, stimulate glucose-dependent release of insulin, inhibit
postprandial release of glucagon, and suppress appetite
o Increase risk for medullary thyroid cancer
● Amylin mimetics
o Pramlintide
THYROID
The effect of maternal hypothyroidism is limited largely to the first trimester, a time during
which the fetus is unable to produce thyroid hormones of its own. By the second trimester, the
fetal thyroid gland is fully functional, and hence the fetus can supply its own hormones from
,NURS 5334 MODULE 6-9 REVIEW
then on. Therefore, to help ensure healthy fetal development, maternal hypothyroidism must
be diagnosed and treated very early. When women taking thyroid supplements become
pregnant, dosage requirements usually increase—often by as much as 50%. The need for
increased dosage begins between weeks 4 and 8 of gestation, levels off at about week 16, and
then remains steady until parturition
◼ In first trimester can result in permanent neuropsychologic deficits in the child
◼ In infants
Hypothyroidism in newborns may be permanent or transient. In either case, congenital
hypothyroidism can cause delay in mental development and derangement of growth. In the
absence of thyroid hormones, the child develops a large and protruding tongue, potbelly, and
dwarfish stature. Development of the nervous system, bones, teeth, and muscles is impaired. In
all children, replacement therapy should continue for 3 years, after which it should be stopped
for 4 weeks. The objective is to determine whether thyroid deficiency is permanent or transient.
If TSH rises, indicating thyroid hormone production is low, we know the deficiency is permanent,
so replacement therapy should resume. If TSH and T4 normalize, we know the deficiency was
transient, and hence further replacement therapy is unnecessary
◼ May be permanent or transient
◼ Can cause mental retardation and derangement of growth
1.6 -1.8 mcg/kg/day for adult dosing. Less for older patients. Obese dose by ideal body weight.
Underweight dose by actual weight. Older patients with CAD should start on 12.5-25. Start low
and go slow. younger than 3 months, the dosage is 10 to 15 mcg/kg/day; for children aged 3 to
5 months, 8 to 10 mcg/kg/day; for children aged 6 to 11 months, 6 to 8 mcg/kg/day; for
children aged 1 to 5 years, 5 to 6 mcg/kg/day; and for children aged 6 to 12 years, 4 to
5 mcg/kg/day.
16 Thyroid Hormone Preparations
◼ Levothyroxine [Synthroid]
◼ Synthetic preparation of thyroxine (T4) and drug of choice for
hypothyroidism
◼ Conversion to T3
◼ Half-life: 7 days
◼ Used for all forms of hypothyroidism
Liothyronine (Cytomel)- synthetic T3
Liotrix [Thyrolar] is a mixture of synthetic T4 plus synthetic T3 in a 4 :1 fixed ratio. because
levothyroxine alone produces the same ratio of T4 to T3. Liotrix offers no advantage over
levothyroxine for most indications.
◼ Thyroid (Armour Thyroid, others)
Thyroid [Armour Thyroid, others] consists of desiccated animal thyroid glands. Standardization
is based on content of iodine, levothyroxine, and liothyronine. The ratio of levothyroxine to
liothyronine is not less than 5 :1. Thyroid is available in tablets (15–300 mg).
◼ Drug interactions
◼ Drugs that reduce levothyroxine absorption
, NURS 5334 MODULE 6-9 REVIEW
H2 receptor blockers, PPI, sucralfate, cholestyramine, colestipol, Maalox, Mylanta, calcium
supplement, iron, magnesium, orlistat
◼ Drugs that accelerate levothyroxine metabolism
Among these are phenytoin [Dilantin], carbamazepine [Tegretol, Carbatrol], rifampin [Rifadin],
sertraline [Zoloft], and phenobarbital. Accordingly, to maintain adequate levothyroxine levels,
patients taking these drugs may need to increase their levothyroxine dosage.
◼ Warfarin
Levothyroxine accelerates the degradation of vitamin K–dependent clotting factors. As a result,
effects of warfarin are enhanced. If thyroid hormone replacement therapy is started in a patient
taking warfarin, the dosage of warfarin may need to be reduced.
◼ Catecholamines
Thyroid hormones increase cardiac responsiveness to catecholamines, thereby increasing the
risk for catecholamine-induced dysrhythmias. Caution must be exercised when administering
catecholamines to patients receiving levothyroxine and other thyroid preparations.
Levothyroxine can increase requirements for insulin and digoxin
PTU Versus Methimazole
◼ PTU can cause severe liver injury, whereas methimazole does not
◼ PTU has a shorter half-life than methimazole (90 min compared to 6 to 13 hr), so it
requires two or three daily doses rather than one
◼ PTU crosses the placenta less readily than does methimazole, and concentrations in
breast milk are lower
◼ PTU blocks conversion of T4 to T3 in the periphery, whereas methimazole does not
◼ Effects on primary and secondary sex characteristics
◼ Reproductive tract and secondary sex characteristics
◼ Estrogens influence the physiologic processes related to reproduction:
◼ Ductal growth in the breast
◼ Thickening and cornification of the vaginal epithelium
◼ Proliferation of the uterine epithelium
◼ Copious secretion of thickened mucus from endocervical glands
◼ Metabolic actions
◼ Positive effect on bone mass by blocking bone resorption
◼ Favorable effects on cholesterol levels: decreases LDL, raises HDL
◼ Blood coagulation by increasing levels of coagulation factors
◼ Glucose homeostasis: estrogen has been shown to increase insulin sensitivity to
promote glucose uptake.
◼ Adverse effects
◼ Endometrial hyperplasia and carcinoma
◼ Promotes growth of existing breast cancer
◼ Ovarian cancer
◼ Cardiovascular events
