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Pharmacology for APRN > Diabetes / Endo > Flashcards

Diabetes / Endo Flashcards

1
Q

Sulfonylureas MOA

A

bind to specific receptors on beta cells, causing adenosine triphosphate (ATP)–dependent potassium channels to close. The calcium channels subsequently open, leading to increased cytoplasmic calcium, which stimulates the release of insulin.

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2
Q

Sulfonylureas Indications:

A

DM for <5 yrs
No history of prior insulin therapy or Good glycemic control on less than 40 U/d
Close to normal body weight
FPG <180

Patients who are lean and insulinopenic or who have monogenic forms of DM

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3
Q

Sulfonylureas SE’s

A

Hypoglycemia (older adults, impaired renal function)
Hypoglycemia increases with alcohol abuse or overexertion
Caution in pregnancy (except Glyburide)
Declining efficacy over time

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4
Q

Sulfonylureas Patient Education

A

Signs and symptoms of hypoglycemia. Can cause weight gain 2-3 kg. Do not use it in sulfa allergies. Baseline renal and hepatic function tests. May cause photosensitivity.

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5
Q

Biguanides MOA

A

Inhibit hepatic glucose production and moderately improves peripheral sensitivity to insulin
Gluconeogenesis and glycogenolysis are inhibited in the liver

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6
Q

Biguanides Indications

A

For DMII or Pre-diabetes. Used with diet as first-line monotherapy or in combination with other diabetic drugs (including insulin)
No risk of hypoglycemia or hyperinsulinemia
No weight gain
OK in pregnancy

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7
Q

Biguanides Dosage

A

Metformin (Glucophage):
Immediate release (IR): Taken before meals in the morning and evening
Initial: 500-850 mg QD or BID
Increase: weekly by 500mg until desired blood glucose
Max: 2,550 mg/day
Peak: 2-2.5 H
Duration: 10-16 H
Steady State: 24-48 H

Extended Release (ER): Taken once a day with the evening meal or at bedtime
Initial: 500 mg QD
Max: 2,000 mg QD

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8
Q

Biguanides Contraindications

A

Severe renal impairment GFR <30
Chronic alcohol abuse
Hepatic disease
Heart failure
Children <10 yrs

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9
Q

Biguanides SE’s

A

GI upset (N/V/D/Bloating)
Anorexia
Metallic taste
Lactic acidosis if GI upset late in therapy (with advanced age and worsening renal function)
Vitamin B12 deficiency
Mitigation: start low and go slow

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10
Q

Biguanides Interactions

A

Combination with sulfonylureas, meglitinides, or insulin may cause hypoglycemia

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11
Q

Thiazolidinediones (TZD) MOA

A

Target specifically the TZD proliferated factor gamma in cells which plays a crucial role in regulating BG in cells.
Helps preserve some beta cell function.
Reduce hepatic glucose production lowering fasting BG levels.
Promote differentiation of preadipocytes into mature adipocytes which helps redistribute fat from muscle to subcutaneous tissue
Reduced r/o CVA and MI

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12
Q

Thiazolidiniones (TZD) Indications:

A

Recommended for DM II not controlled by other oral DM agents or when insulin is not preferred

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13
Q

Thiazolidinediones (TZD) Drug Types & Dose

A

Avandia:
Initial: 4 mg/d in single dose
Increase: If response is inadequate after 12 weeks. Increase to 8 mg/d in single dose

Pioglitazone (Actos)
Initial: 15-30 mg/d
Max: 45 mg/d as monotherapy and 30 mg/d as combined therapy

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14
Q

Pioglitazone (Actos) - TZD SE’s

A

Increased r/o bladder cancer with increased dose and duration of therapy
Decreased concentration of oral contraceptives
Not recommended for those in Class III or Class IV HF
Contraindicated in active liver disease
May stimulate weight gain (redistribution of fats into SQ compartments)

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15
Q

Thiazolidinediones (TZD) SE’s

A

Fluid retention, r/o Fx (particularly in women), liver injury/ liver enzyme elevation, macular edema
CXN in pregnancy
Contraindications in breastfeeding women and in children

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16
Q

Thiazolidinediones (TZD) SE’s

A

Strong CYP2C8 inhibitors
CXN when used with digoxin, fexofenadine, midazolam, nifedipine, and warfarin

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17
Q

Alpha-Glucosidase Inhibitors MOA

A

The enzyme alpha-glucosidase is found on the brush border of the intestine and is necessary for the absorption of starch and disaccharides. Slows the digestion and absorption of carbohydrates in the small intestine minimizing the postprandial rise in BG

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18
Q

Alpha-Glucosidase inhibitors Indications

A

DMII
Not for use in children
Not useful for patients with postprandial hyperglycemia
Does not lower A1c
Often used as adjunct, not monotherapy

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19
Q

Alpha Glucosidase Dosages and Drugs

A

Acarbose (Precose), Miglitol (Glyset)
Initial: 25 mg TID with the first bite of a meal
Increase: by 25 mg at 4-8 week intervals
Max: 300 mg
Take with the first bite of each meal
Peak: 2-3 hours
Maintain movement after meals to minimize buildup of GI gas

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20
Q

Alpha-Glucosidase Inhibitors Contraindications

A

IBD, Colonic ulceration, obstructive bowel d/o, chronic intestinal d/o of digestion or absorption
Acarbose: contraindicated in liver cirrhosis or SCr >2.0 or CrCl <25
CXN during pregnancy
Contraindicated in breastfeeding

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21
Q

Alpha-Glucosidase SE’s

A

GI (flatulence, diarrhea), less effective for fasting BG. dose dependent

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22
Q

Alpha-Glucosidase Interactions

A

May decrease levels of propranolol and ranitidine

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23
Q

Meglitinide Analogs MOA

A

​​Meglitinide analogs work by stimulating the release of insulin from the pancreatic beta cells in response to a meal. They primarily target the adenosine triphosphate-sensitive potassium (KATP) channels on these cells. When these channels are closed, it triggers the release of insulin, helping to lower blood sugar levels.
These medications stimulate the pancreas to release insulin, but their action is shorter in duration compared to sulfonylureas. Meglitinides are particularly effective at controlling post-meal blood sugar spikes.

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24
Q

Meglitinide Analogs Indications

A

DMII
Rapid Onset of action - effective at controlling postprandial BG
Not for use in children
Monotherapy or in combination with other oral agents

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25
Q

Meglitinide Analog Dosages & Drugs

A

Repaglinide (Prandin):
Initial: 0.5 mg before two to four meals daily if patient has never received other tx for diabetes
If previous treatment: 1-2 mg with two to four meals daily
Max: double dose weekly to max of 16 mg/d
Peak: 1 hour
Nateglinide (Starlix)
Initial: 60-120 mg before each meal
Max: 360 mg/d
Peak: 1 hour

Take within 30 min before each meal
Add or skip if a meal is added or skipped

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26
Q

Meglitinide Analog Benefits

A

Rapid Onset of action
Lower r/o prolonged hypoglycemia
Less weight gain

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27
Q

Meglitinide analog SE’s

A

GI upset, URI’s, HA, Diarrhea/Constipation, arthralgias, back/chest pain

Less effective for fasting BG
May induce hypoglycemia
Short duration of action and frequent dosing

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28
Q

Meglitinide Analog Interactions

A

Use with BB or alcohol leads to increased r/o hypoglycemia

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29
Q

Meglitinide Analog Contraindications

A

DKA
Severe infection, surgery, trauma, severe stressors
Possible risk in pregnancy
Contraindicated in breastfeeding women and children

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30
Q

Dipeptidyl Peptidase-4 Inhibitors MOA

A

Inactivates GLP-1, therefore decreasing GLP-1 and glucoregulatory functions. Block the effect against GOP-1 and increase the amount of native circulating incretins

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31
Q

Dipeptidyl Peptidase-4 Inhibitors Indications

A

DM II
Not for use in children

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32
Q

Dipeptidyl Peptidase-4 Inhibitors: Sitagliptin (Januvia)

A

100 mg oral daily
50 mg PO QD CrCl 30-50 mL/min
25 mg PO QD CrCl <30 mL/min

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33
Q

Dipeptidyl Peptidase-4 Inhibitors: Saxagliptin (Onglyza)

A

5 mg QD
2.5 mg QD for CrCl <30 mL/min
Used in combo therapy with sulfonylureas and TZD’s, not insulin

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34
Q

Dipeptidyl Peptidase-4 Inhibitors: Alogliptin (Nesina)

A

6.25 mg, 12.5 mg, or 25 mg QD
12.5mg for CrCl 30-50 mL/min
6.25 mg for CrCl <30 mL/min

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35
Q

Dipeptidyl Peptidase-4 Inhibitors: Linagliptin (Tradjenta)

A

2.5 or 5 mg QD
No renal dosing is necessary

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36
Q

Dipeptidyl Peptidase-4 Inhibitors: (Vildagliptin (Galvus)

A

50 or 100 mg QD

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37
Q

Dipeptidyl Peptidase-4 Inhibitors: Contraindications

A

Hypersensitivity
CXN in pregnancy
Consider alternative for breastfeeding

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38
Q

Dipeptidyl Peptidase-4 Inhibitors: SE’s

A

URI
UTI
HA
Hypoglycemia when used in combination with sulfonylureas or insulin

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39
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA) MOA

A

GLP-1 RAs work by binding to and activating the GLP-1 receptors on pancreatic beta cells, among other tissues. Their main actions include:
Stimulating Insulin Release: GLP-1 RAs enhance insulin secretion in a glucose-dependent manner, meaning they increase insulin production when blood sugar levels are elevated.
Inhibiting Glucagon Release: These medications reduce the release of glucagon, a hormone that raises blood sugar levels, from the pancreas.
Slowing Gastric Emptying: GLP-1 RAs slow down the emptying of the stomach, leading to a more gradual release of glucose into the bloodstream after meals.
Promoting Satiety: They induce a feeling of fullness and can reduce food intake, leading to potential weight loss.

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40
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA) Indications

A

GLP-1 RAs are known for their glucose-lowering effects, weight management benefits, and cardiovascular benefits.
Indicated for DMII in adults
DM II in adolescents over the age of 10 (Liraglutide)

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41
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Exenatide (Byetta, Bydureon)

A

Only available as an injectable
Monotherapy or conjunction with oral agents, metformin, sulfonylureas, TZD’s, and insulin
Initiate: 5 mcg administered 60 min before morning and evening meals or prior to the largest meals of the day
Space doses 6 hours apart
Dose can be increased to 10 mcg BID within 1 month of initiation
Bydureon = ER. Dosed once weekly without regard to meals

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42
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Liraglutide (Victoza)

A

Once daily at any time
Initial: 0.6 mg/day not effective for glycemic control, start low to reduce GI symptoms
Effective Dose: 1.2 mg daily
Max: 1.8 mg/day for glucose control
Approved for adolescents over the age of 10
Shown to reduce r/o CV mortality and reduce MI and CVA
Reduction in new or worsening albuminuria in addition to reduction in new onset nephropathy

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43
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Dulaglutide (Trulicity)

A

Dose once weekly at any time of the day
0.75 or 1.5 mg dose injector pen
Shown to reduce r/o CV mortality and reduce MI and CVA
Reduction in new or worsening albuminuria in addition to reduction in new onset nephropathy

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44
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Semaglutide (Ozempic)

A

Dose once a week injectable or oral tab (Rybelsus) once daily in the morning
0.5-1 mg dose
Initiate: 0.25 mg and advance to 0.5 mg after 2-4 weeks
Max: 1 mg after 4 weeks of therapy
Reduce the r/o CV death
Reduction in new or worsening albuminuria in addition to reduction in new onset nephropathy

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45
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Benefits

A

Effective Glucose Control: GLP-1 RAs help lower blood sugar levels by stimulating insulin secretion and inhibiting glucagon release.
Weight Loss: Many patients experience weight loss while taking GLP-1 RAs due to reduced appetite and delayed gastric emptying.
Cardiovascular Benefits: Some GLP-1 RAs have been associated with cardiovascular benefits, including a reduced risk of major adverse cardiovascular events (MACE) in high-risk individuals.
Low Risk of Hypoglycemia: GLP-1 RAs have a low risk of causing hypoglycemia when used as monotherapy. However, when combined with other antidiabetic medications, the risk may increase.

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46
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): SE’s

A

Gastrointestinal Side Effects: Common side effects include nausea, vomiting, diarrhea, and abdominal discomfort, especially when starting the medication. These side effects often improve with time.
Injection: GLP-1 RAs are administered via subcutaneous injection, which may be a drawback for some patients.
Pancreatitis: There have been rare reports of pancreatitis (inflammation of the pancreas) associated with GLP-1 RAs.
Thyroid C-Cell Tumors: Long-term use of certain GLP-1 RAs has been associated with an increased risk of thyroid C-cell tumors in animal studies, although the significance of this risk in humans is still being studied.

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47
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Interactions

A

Do not administer close to drugs that have a therapeutic window
CXN with patients taking warfarin

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48
Q

Glucagon-Like Peptide Receptor Agonist (GLP1-RA): Contraindications

A

Ketoacidosis, allergy, severe GI d/o including gastroparesis and acute gallbladder disease
CXN: not studied in pregnancy
Contraindicated in breastfeeding
Increased r/o Thyroid C-Cell tumors
Individuals with h/o medullary thyroid carcinoma
Association with acute pancreatitis

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49
Q

Dopamine Receptor Agonists MOA

A

Not fully understood
Bromocriptine’s action on dopamine receptors in the brain’s hypothalamus is thought to help regulate glucose metabolism. It may also influence circadian rhythms, which can impact insulin sensitivity.

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50
Q

Dopamine Receptor Agonists: Bromocriptine Mesylate Dosing

A

0.8 mg within 2H after waking with the first meal of the day
Titration: Increased by 0.8 mg weekly
Max: 1.6-4.8 mg

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51
Q

Dopamine Receptor Agonists: Indications

A

DMII to improve postprandial BG
Does not significantly increase plasma insulin concentrations
Used when other treatments have not achieved glycemic control
Monotherapy, or in combination with other antidiabetic meds

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52
Q

Dopamine Receptor Agonists: SE’s

A

nausea, vomiting, fatigue, and dizziness, orthostatic hypotension, headache

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53
Q

Dopamine Receptor Agonists: Contraindications

A

Pregnancy
Breastfeeding
Exacerbation of psychotic disorders
Reduction in the effectiveness of drugs that treat psychosis
Dopamine receptor agonists used for Parkinson’s disease or RLS

54
Q

Bile Acid Sequestrant: MOA

A

Binds to bile acids in the intestine, thus preventing reabsorption. As the bile acid pool is reduced, hepatic enzymes convert circulating cholesterol to bile acids, thereby upregulating hepatic LDL receptors and clearance of LDL-C from circulation
Secondary effect of BG control

55
Q

Bile Acid Sequestrant: Indications

A

DMII
Mitigates CV risk factors by lowering cholesterol

56
Q

Bile Acid Sequestrant: Colesevelam Dosing

A

Tablet: 6 tabs QD or 3 tabs BID. Tab = 625 mg
Suspension: 3.75 g packets QD or 1.875 g BID
Mix suspension with 4 oz liquid, do not take with a meal
Take 4 hours apart from other medications

57
Q

Bile Acid Sequestrant: Contraindications

A

History of bowel obstruction
Motility disorders such as gastroparesis
Major GI surgery
Triglyceride >500 mg/dL
History of triglyceride-induced pancreatitis
CXN in Pregnancy and breastfeeding

58
Q

Bile Acid Sequestrant: SE’s

A

Constipation, bloating, gas, abdominal discomfort, abdominal obstruction, esophageal obstruction, increased transaminases

59
Q

Bile Acid Sequestrant: Drug Interactions

A

Interferes with the absorption of fat soluble vitamins (ADEK), other drugs utilizing lipid absorption

60
Q

Amylin Analog: MOA

A

Three actions as an amylinomimetic agent
1) delay gastric emptying into the small intestine which delays the rise in postprandial glucose release (may last about 3 hours and does not alter nutrient absorption)
2) Alters the release of additional inappropriate glucagon by pancreatic alpha cells
3) Increase in satiety, which decreases the total caloric intake and promotes weight loss

61
Q

Amylin Analog: Pramlintide (Symlin) Dosing

A

Multi-dose injector pen, dosage differs for DMI vs DMII
DM I: 15 mcg prior to any major meal
DM I Titration: 15 mcg increments to total dose of 30-60 mcg
DM II: 60 mcg prior to any major meal
DM II Titration: increase to 120 mcg in 3-7 days if no nausea
Reduce current insulin regimen by 50%
Discontinue if nausea experienced

62
Q

Amylin Analog: Contraindications

A

Not for those with poor adherence to medications
A1C >9%
Those on drugs that increase gastric motility
No effect on renal or liver!

63
Q

Amylin Analog: SE’s

A

Nausea
Vomiting
HA
Anorexia

64
Q

Amylin Analog: Interactions

A

Delay absorption of concomitantly administered analgesics, ABX, and oral contraceptives

65
Q

Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2) MOA

A

SGLT2 inhibitors primarily act on the kidneys. They block the action of SGLT2 proteins in the renal tubules, which are responsible for reabsorbing glucose from the urine back into the bloodstream. By inhibiting SGLT2, these drugs increase the amount of glucose excreted in the urine, leading to reduced blood glucose levels.

66
Q

Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2): Indications

A

Glycemic control for DM II
Weight loss by promoting the excretion of calories in the form of glucose through the urine
CV benefits by reducing major CV events
Renal benefits by reducing the risk of kidney disease progression

67
Q

SGLT2 Empagliflozin (Jardiance) Dosing:

A

10 mg orally in the morning
Max: 25 mg
Discontinue for persistent eGFR <45

68
Q

SGLT2 Canagliflozin (Invokana) Dosing:

A

100 mg before the first meal of the day
Max: 300 mg QD if eGFR >60
Max: 100 mg QD if eGFR 30-60

69
Q

SGLT2 Dapagliflozin (Farxiga) Dosing:

A

5 mg with or without food
Max: 10 mg
Do not initiate or discontinue if eGFR <45

70
Q

SGLT2 SE’s

A

urinary tract infections (UTIs), genital yeast infections, increased urination, and a slightly increased risk of low blood pressure and dehydration.
It is important to maintain hydration

71
Q

SGLT2 Contraindications

A

DKA
Severe kidney disease eGFR <30
Hemodialysis

72
Q

First Line for the Treatment of DM II

A

Metformin and Lifestyle therapy such as physical activity, portion control, weight management

73
Q

Treatment of DM II Recommendation Table

A
74
Q

Sick day guidelines in DM

A

Do not stop medications when ill
Increase fluid to 8 oz water every hour
Monitor BG every 2-4 hours
Test urine for ketones
Seek medical care if BG >300 mg/dL x 2, fever high, and dehydration and ketonuria develop

75
Q

DMII First Line Therapy

A

Monotherapy with metformin and Lifestyle Therapy (physical activity, portion control, weight management)
Goal: achieve A1c <7%
Insulin if A1c >10% or >9% with symptoms of hyperglycemia
First Line: Sulfonylureas
If the patient is thin, older than 40, and has had DM for <5 yrs, and has a BG of >250 mg/dL

76
Q

DMII Second-Line Therapy

A

Failure to achieve optimal BG after 3 mon of monotherapy, add a second oral agent
GLP-1 RA and SGLT-2 for patients with HF, ASCVD, or CKD. Also if weight loss is needed
DPP-4i, GLP-1 RA, SGLT-2i, or TZD for those with a higher risk for hypoglycemia
Sulfonylureas or TZDs if cost is an issue

77
Q

DMII Third-Line Therapy

A

If A1c >9% on 2 agents, add a 3rd oral agent
If A1c is not at goal after 3 mon, insulin therapy is suggested
Intermediate or basal insulin at bedtime added to oral regimen

78
Q

DM I First-Line Therapy

A

Insulin regimen that provides basal insulin coverage and rapid-acting before meals, dose is 0.4-0.5 units/kg/day
Insulin regimen combining intermediate and short-acting insulin. 2 injections per day in the morning and evening

79
Q

DM I Second-Line Therapy

A

Adjustments are made at 1 to 2 units at a time or 10% to 20% twice a week

80
Q

Very rapid-acting insulin

A

Humalog (Insulin Lispro)
Novolog (Insulin Aspart)

81
Q

Short-acting insulin

A

Humalin or Novolin R (Regular Insulin)
Effect: 1 H
Peak effect: 2-4h
Duration: 5 H

82
Q

Intermediate-acting insulin - basal

A

NPH or Humalog N, Novolin N
Effect: 1-2 H
Peak Effect 4-12 H
Duration 12-24 H
Basal insulin coverage

83
Q

Long-acting insulin, basal

A

Insulin Glargine Lantus, Levemir, Trusvia
Onset: Varies
Peak: minimal or no pronounced actual effect
Duration: 12 - 24H or more

84
Q

Combination or Biphasic insulins: basal and prandial. Recommendations

A

Humalog 75/25 or Novolog 70/30, dosed BID before breakfast and before dinner
⅔ TDD in the morning with a 2:1 ratio of
intermediate to short-acting insulin

⅓ TDD before dinner with a 1:1 ratio of intermediate to short-acting Insulin

Not recommended for intensive insulin regimens
Rapid and Intermediate combo
Increased weight gain associated

85
Q

Inhaled rapid-acting insulin: Afrezza drug facts

A

Onset: 12-90 min
Peak 35-45 min
Duration: 90-180 min
Take at the beginning of each meal
Available in 4U, 8U, and 12U cartridges
Contraindications: COPD, smokers
SE’s: cough, bronchospasm, throat pain, irritation, bronchitis

86
Q

Insulin SE’s

A

Hypoglycemia, hypokalemia, lipodystrophy, local or systemic allergy

87
Q

Somogyi Effect

A

rebound hyperglycemia occurs after an early morning episode of insulin-induced hypoglycemia (unnoticed during sleep)

Symptoms: night sweats, nightmares, sleep disturbances, early morning HA

88
Q

Dawn Phenomenon

A

worsening hyperglycemia that occurs in the early morning hours, caused by growth hormone surges during sleep

89
Q

Insulin drug-to-drug interactions

A

Increase r/o hypoglycemia: ARBS, fibrates, fluoxetine, MAOIs, salicylates, sulfonamide ABX
Decrease glucose-lowering effect of insulin: antipsychotics, corticosteroids, diuretics, estrogens, niacin, thyroid hormones, OCPs

90
Q

Sensitivity Factor Definition

A

Determines how sensitive the patient is to insulin
Divide 1,800 by the TDD of insulin
SF = change in the blood glucose anticipated by injecting 1 U of insulin

91
Q

Basal insulin dosing for DM I

A

0.4-0.5 units /kg / day
40-50% of the TDD in the form of basal insulin
Titrate: up or down by 2-4 U every few days until target glucose levels obtained

92
Q

Basal and bolus insulin dosing for DM II

A

0.1-0.2 U/Kg/Day or 10 U/day
Titrate: 2 U every 3 days until fasting BG at goal without hypoglycemia
Bolus initiation: once basal reaches 0.5 U/Kg/Day if A1c is still above target.
Bolus Dosing: 4 U per meal or 10% of the basal dose.
Bolus Titration: every 3-4 days by 1-2 U or 10-15% until goal glucose achieved or hypoglycemia occurs

93
Q

Insulin dosing for special populations: Adolescents, growth spurts, pregnancy

A

Children / Adolescents:
0.4-1 U/kg/day
Adolescents during a growth spurt:
1.2-1.5 U/kg/day
Pregnancy:
0.7-2 U/kg/day

94
Q

Definition of primary hypothyroidism

A

Elevated TSH and Decreased FT4

95
Q

Definition of secondary hypothyroidism

A

a result of pituitary dysfunction, results in low free T4 and low TSH levels.

96
Q

Definition of tertiary hypothyroidism

A

Results from decreased production of thyroid releasing hormone (TRH) by the hypothalamus.

Distinguished from secondary by imaging of the pituitary and hypothalamus

97
Q

Hypothyroidism Clinical Manifestations

A

Fatigue, weakness, weight gain, cold intolerance, constipation, dry skin and hair, depression, menstrual irregularities, goiter, bradycardia

98
Q

Hypothyroidism Diagnostic criteria

A

Clinical assessment
Elevated TSH >10 mIU/L and low free T4 <0.7 ng/dL

99
Q

Exogenous thyroid Hormone Levothyroxine (LT4) MOA:

A

Bind to thyroid receptors on the cell nuclei to initiate gene transcription and exert metabolic effect in the tissues.

Metabolic Effect: Energy metabolism, protein synthesis, tissue growth

100
Q

Exogenous thyroid Hormone Levothyroxine (LT4) Dosing:

A

Initiate: 1.6 mcg / kg / d using ideal body weight. I.E: 12.5 → 100 mcg/d
Maintenance dose: 75 → 150 mcg/d
If >75 yrs: 25-50 mcg/d
If ischemic heart disease: 12.5-25 mcg/d
Take consistently at same time each day
Take on empty stomach

101
Q

LT4 response time

A

Within a few weeks to several months
Thyroid function tests such as serum TSH and T4 levels regularly
Check TSH within 6-8 weeks of thyroid replacement therapy, titrate based on TSH level
10-20% change in dose

102
Q

LT4 Contraindications

A

Untreated adrenal insufficiency or thyrotoxicosis. Hypersensitivity to the allergy, not used as sole tx for obesity or weight loss, caution when prescribing to patients with cardiovascular disease

103
Q

LT4 SE’s:

A

Hyperthyroidism: palpitations, weight loss, nervousness, heat intolerance
Cardiovascular: due to increased HR and arrhythmia, exacerbate underlying heart conditions
Prolonged use: affects bone density, r/o osteoporosis

104
Q

Myxedema Coma Definition and Treatment:

A

Decompensated hypothyroidism: Hypothermia, CNS depression, respiratory depression, CV instability, electrolyte imbalances, delirium, and coma
Life threatening condition
Tx with large bolus of thyroid hormone with IV LT4 300-500 mcg followed by maintenance of 75-100 mcg IV
IV hydrocortisone to combat adrenal suppression

105
Q

Thyrotoxicosis Definition

A

Inappropriately high thyroid hormone levels on tissues
Most common cause is Graves’ Disease:

106
Q

Graves Disease symptoms

A

Goiter, bulging eyes, weight loss, nervousness
Graves’ Ophthalmopathy (GO): eye discomfort, excessive tearing, sensitivity to light, exophthalmos, eyelid retraction, lid sagging, periorbital edema due to inflammation of the eyes

107
Q

Primary Hyperthyroidism Causes

A

Graves’ Disease
Toxic multinodular goiter
Toxic adenoma
Thyroid cancer
Excessive iodine

108
Q

Secondary hyperthyroidism causes

A

TSH - secreting pituitary tumors
Trophoblastic (hCG-secreting) tumors
Gestational thyrotoxicosis

109
Q

Thyrotoxicosis without hyperthyroidism causes

A

Subacute thyroiditis
Silent (painless) thyroiditis
Excessive thyroid hormone intake
Drug-induced (amiodarone, cytokine or tyrosine kinase inhibitors, interferon, iodine, lithium)

110
Q

Hyperthyroidism Clinical symptoms

A

weight loss, tachycardia, heat intolerance, tremors, anxiety, muscle weakness

111
Q

Hyperthyroidism diagnostic criteria:

A

Symptoms:
Palpitations / atrial fibrillation
Sweating
Heat intolerance
Weight loss
Fatigue, weakness

Clinical: Confirmed by finding a low or suppressed TSH level (<0.5 mlU/L) with an elevated free T4 level (>1.9 ng/dL)

112
Q

Antithyroid Drug Methimazole (MMI, Tapazole) MOA:

A

Inhibits thyroid hormone synthesis. Inhibit thyroid peroxidase (needed for iodination of tyrosine in the thyroglobulin). Have an immunosuppressant effect in Graves’ disease

113
Q

Antithyroid Drug Methimazole (MMI, Tapazole) Dosing & Effects:

A

Maintenance Dose: 5-15 mg/d
Thyroid hormones drop after 2-3 weeks of therapy
Euthyroid achieved by 6 weeks
Continue for 12-18 months or longer, may experience rebound hyperthyroid after ATD discontinuation

114
Q

Antithyroid Drug Methimazole (MMI, Tapazole) SE’s:

A

Skin rash, fever, arthralgia, transient granulocytopenia
Less common: GI tract upset, abnormalities in taste and smell, arthritis, agranulocytosis, aplastic anemia, thrombocytopenia, vasculitis, systemic lupus-like syndrome, hypoglycemia cholestatic hepatitis

115
Q

Antithyroid Drug Methimazole (MMI, Tapazole) Special Considerations:

A

preferred in the 2nd-3rd trimester of pregnancy

116
Q

Antithyroid Drug Propylthiouracil (PTU, Propyl-Thyracil) MOA:

A

Inhibits thyroid hormone synthesis. Inhibits the conversion of T4 to T3 in the peripheral tissues

117
Q

Antithyroid Drug Propylthiouracil (PTU, Propyl-Thyracil) Dosing & Effects:

A

Dose: 5-150 mg TID
Maintenance dose: 50 mg TID x 12-18 months until euthyroid state achieved
Thyroid hormones drop after 2-3 weeks of therapy
Euthyroid achieved by 6 weeks

118
Q

Antithyroid Drug Propylthiouracil (PTU, Propyl-Thyracil) SE’s:

A

R/o severe liver toxicity. Skin rash, fever, arthralgia, transient granulocytopenia
Less common: GI tract upset, abnormalities in taste and smell, arthritis, agranulocytosis, aplastic anemia, thrombocytopenia, vasculitis, systemic lupus-like syndrome, hypoprothrombinemia, toxic hepatitis

119
Q

Antithyroid Drug Propylthiouracil (PTU, Propyl-Thyracil) Special Considerations:

A

Favored for the 1st trimester of pregnancy

120
Q

Symptom management before radioactive iodine therapy:

A

BB to control adrenergic symptoms
Methimazole to achieve euthyroid state and control symptoms
Must be stopped 2-3 days before RAI, as it can interfere with efficacy

121
Q

Symptom management before Thyroidectomy

A

BB to control adrenergic symptoms.
Methimazole 6-8 weeks before the procedure to achieve euthyroid state and control symptoms
Follow this with an iodine solution for 10-14 days to decrease the vascularity of the thyroid

122
Q

Hyperthyroid adjunctive therapy: Beta Blockers

A

Nadolol (Corgard)
Dose: 40-160 mg/d
Propranolol (Inderal)
Dose: 30-160 mg/d
Helps manage tachycardia, HTN / CV effects of hyperthyroidism
Used temporarily until primary treatment takes full effect
SEs: bradycardia, fatigue, drowsiness, mood changes, dizziness
Contraindications: Hypersensitivity, uncompensated HF, SB, Sick Sinus, Uncontrolled asthma

123
Q

Hyperthyroid adjunctive therapy: Iodine Compounds

A

Potassium Iodide (SSKI)
Dose: 1-2 drops TID
Prior to thyroidectomy or radioactive iodine therapy
10-14 days to prepare the thyroid for surgery or radioactive iodine therapy
Not used for long-term therapy
SE’s: rash, abdominal discomfort, iodism with prolonged use (burning in the mouth, sore teeth, gums, HA, metallic taste, eye swelling, increased salivation, skin lesions)
Contraindication: active TB, nodular thyroid condition with heart disease
Wolff-Shakeoff effect

124
Q

Thyroid Storm Triggers

A

Infection
Trauma
Thyroidectomy
Radioactive iodine treatment
Abrupt discontinuation of anti-thyroid medications

125
Q

Thyroid storm clinical presentation

A

Intensified signs and symptoms of hyperthyroidism
High fever, tachycardia, AF, tachypnea, agitation, delirium, GI disturbance, seizure, coma

126
Q

Hyperparathyroidism Defined

A

The parathyroid gland becomes overactive and overproduces PTH. Hypercalcemia results

127
Q

Hyperparathyroidism Symptoms:

A

Fatigue, muscle weakness, bone pain, bone fracture, kidney stones, GI symptoms.
Many remain asymptomatic and it is detected in routine lab tests

128
Q

Hyperparathyroidism Drug Therapy: Cinacalcet (Sensipar)

A

MOA: Increases the sensitivity of the calcium receptors on the parathyroid gland, thus enhancing the negative feedback loop to signal the gland to decrease PTH release resulting in lower calcium levels. Decreases iPTH, lowers calcium to normal levels in 70-80% of patients
Dose: 30 mg BID, increased every 2-4 weeks until serum calcium reaches normal range. Give with food
Indication: For those not candidates for surgery
SE’s: Hypotension, paresthesia, HA, Fatigue, depression, N/V, constipation or diarrhea, anorexia, anemia, bone fx, muscle spasms, arthralgia, weakness, myalgia, back pain, dyspnea, cough, URI, QT prolongation, GIB, Sz, severe hypocalcemia
Contraindications: Pregnancy

129
Q

Hyperparathyroidism First Line Tx

A

Surgical removal of the affected parathyroid gland
Parathyroidectomy

130
Q

Hyperparathyroidism in Pregnancy

A

Nephrolithiasis, pancreatitis, preeclampsia, hyperemesis gravidarum.
Fetal risks: preterm delivery, miscarriage
Parathyroidectomy is recommended

131
Q
A

Pharmacology for APRN (8 decks)

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