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Adult Health > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Type 1 DM: What is it?

A
  • a chronic autoimmune disease of insulin deficiency and secondary hyperglycemia due to destruction of the beta cells in the pancreas
  • most common type of diabetes in those younger than 20
  • may develop as late as 3rd or 4th decade of life
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2
Q

Type 1 DM: Risk Factors

A
  • genetics
  • more common in whites and men
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3
Q

Type 1 DM: Assessment Findings

A
  • polyuria
  • polydipsia
  • polyphagia
  • weight loss
  • confusion
  • blurry vision
  • ketoacidosis
  • paresthesia
  • altered LOC
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4
Q

Type 1 DM: Diagnostic Tests

A
  • fasting plasma glucose (greater than or equal to 126)
  • A1C (greater than or equal to 6.5%)
  • random plasma glucose (greater than or equal to 200 with symptoms or 2-hr plasma glucose greater than or equal to 200 after a 75-gram glucose load)
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5
Q

Type 1 DM: Prevention

A
  • daily exercise
  • maintenance of ideal body weight
  • limit dietary fat intake
  • look at social determinants of health (such as access to healthy foods, fod insecurity, and community support)
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6
Q

Type 1 DM: Non-Pharmacological Management

A
  • multidisciplinary treatment
  • assessments
  • nutrition
  • exercise
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7
Q

Type 1 DM: Glycemic Targets

A
  • A1C for healthy adults less than 7%
  • A1C for older adults less than 8%
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8
Q

Types of Insulin

A
  1. Rapid Acting
  2. Short Acting
  3. Intermediate Acting
  4. Long Acting
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9
Q

Rapid Acting Insulin Medications

A
  1. Lispro (humalog)
  2. Aspart (Novolog)
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10
Q

Rapid Acting Insulin - Onset, Peak, Duration

A

Onset: 15 minutes
Peak: 30-90 minutes
Duration: 3-5 hours
** can be given 10-15 minutes before a meal or right after a meal (this is better for those with erratic eating habits because it can be given right after the meal)

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11
Q

Short Acting Insulin Medications

A
  1. Regular (Humulin R and Novolin R)
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12
Q

Short Acting Insulin - Onset, Peak, Duration

A

Onset: 30-60 minutes
Peak: 2-4 hours
Duration: 5-8 hours
** can be given 30-45 minutes before a meal

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13
Q

Intermediate Acting Insulin Medications

A
  1. NPH (Humulin N or Novolin N)
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14
Q

Intermediate Acting Insulin - Onset, Peak, Duration

A

Onset: 1-3 hours
Peak: 8 hours
Duration: 12-16 hours
** may not need a prandial dose at lunch if NPH given in the morning

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15
Q

Long Acting Insulin Medications

A
  1. Glargine (Lantus, Levemir)
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16
Q

Long Acting Insulin - Onset, Peak, Duration

A

Onset: 1 hour
Peak: peakless (basal dose)
Duration: 20-26 hours
** usually given at night

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17
Q

Type 1 DM: Calculation of Insulin Dosage

A

Start at 0.2-0.5 units/kg/day divided into 50% basal (long acting/intermediate) in the morning and/or at night AND 50% prandial (short acting/rapid acting) before meals

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18
Q

Dawn Phenomenon

A
  • The Dawn phenomenon happens when hormones your body naturally makes in the early morning (cortisol and growth hormone) increase your blood sugar
  • The best way to diagnose this is by using a CGM. If not using a CGM, check blood glucose by fingerstick at bedtime, about 3 AM, and again in the morning when waking up
  • The best way to treat this is by using an insulin pump that automatically adjusts your insulin dose depending on the blood glucose level. If this is not an option, it will take significant time and effort to get the insulin doses, evening exercise routines, and foods right
  • Some options might be to increase the evening exercise and/or increase the protein-to-carb ratio of the evening meal.
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19
Q

Somogyi Effect

A
  • The Somogyi effect also occurs because of a surge in hormones but is actually due to a low blood sugar episode overnight that has rebounded
  • Recent research with CGM devices has shown that it may not actually be a cause of high blood sugar in the morning
  • If the patient does not have a CGM device, get them to check their blood glucose 2 hours after their evening meal or before they go to bed (one or both, depending on when they eat) in the middle of the night and when they wake up
  • Also, ask about what kinds and how much food they eat for the evening meal and what kind of exercise they may do in the evening
  • Possible options for treatment include adjusting insulin dose, adjusting what you eat for your evening meal and/or snack, changing the time of your evening exercise, and/or switching to a CGM device.
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20
Q

Type 2 DM: What is it?

A
  • a complex, chronic, polygenic metabolic disease characterized by progressive beta cell decline and insulin resistance
  • influenced by genetics as well as environmental factors
  • approximately 10% of the U.S. population has type 2 DM
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21
Q

Type 2 DM: Risk Factors

A
  • BMI > 25
  • history of GDM
  • delivery of large infant
  • family history of DM
  • PCOS
  • HDL < 35 and/or triglycerides > 250
  • HTN or CVD
  • physically active less than 3 days/wk
  • more common in Asians, Native Americans, African American, Hispanic, and Pacific Islanders
    ** Affects men and women equally
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22
Q

Type 2 DM: Screening Recommendations

A
  1. Overweight or obese (BMI 25 or above) with one or more risk factors
  2. Prediabetes (A1C 5.7) test yearly
  3. History of GDM requires lifelong testing every 3 years
    ** At age 10 or puberty if overweight or obese with one or more risk factors
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23
Q

Type 2 DM: Assessment Findings

A
  • Similar to type 1 DM
  • obesity
  • glycosuria
  • proteinuria
  • hyperglycemia
  • acanthosis nigricans
  • chronic candidal vulvovaginitis in women
  • may present with hyperosmolar state or coma
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24
Q

Type 2 DM: Diagnostic Tests

A
  • fasting plasma glucose (greater than or equal to 126)
  • A1C (greater than or equal to 6.5%)
  • random plasma glucose (greater than or equal to 200 with symptoms or 2-hr plasma glucose greater than or equal to 200 after a 75-gram glucose load)
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25
Q

Prediabetes Diagnostic Tests

A
  • Fasting glucose of 100-125
    OR
  • A1C 5.7-6.4%
    OR
  • oral glucose tolerance test 140-199
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26
Q

Type 2 DM: Prevention

A

** Same as type 1 but, reach and maintain a normal BMI
- daily exercise
- maintenance of ideal body weight
- limit dietary fat intake
- look at social determinants of health (such as access to healthy foods, fod insecurity, and community support)

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27
Q

Type 2 DM: Non-Pharmacological Management

A
  • weight loss is primary goal for all obese patients with type 2 DM
  • prefer to diabetes educator at diagnosis and annually or more often if needed
  • nutrition plan
  • avoid alcohol
  • assess medication regimen, etc.
  • assess technology use
  • avoid smoking and vaping
  • exercise (150 minutes per week)
  • physical examinations with lab tests
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28
Q

Type 2 DM: Glucose Recommendations

A
  1. A1C 7% or less
  2. Preprandial glucose 80-130
  3. 2-hour post-prandial less than 180
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29
Q

Type 2 DM: Classifications of Medications

A
  1. Biguanides
  2. Thiazolidinediones (tzd)
  3. Alpha-glucosidase inhibitors
  4. Dipeptidyl peptidase-4 inhibitors (DP4-i)
  5. Sodium glucose cotransporter 2 inhibitors
  6. Glucagon-like peptide-1 receptor antagonists (GLP-1)
  7. Sulfonylureas
  8. Combination drugs
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30
Q

Type 2 DM: 1st Line therapy

A

Biguanides (Metformin)

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31
Q

Type 2 DM: When to consider dual therapy

A

If A1C is 1.5% or higher than goal A1C

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32
Q

Type 2 DM: ASCVD History

A

Consider GLP-1 or SGLT2 inhibitors (if adequate GFR)

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33
Q

Type 2 DM: HF or CKD History

A
  • Consider SGLT2 inhibitor (if adequate GFR)
  • If not tolerated or not adequate GFR, add GLP-1 with proven CKD benefit
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34
Q

Type 2 DM: When is insulin considered?

A
  • insulin is usually considered only after oral meds have not worked
  • early introduction of insulin IF A1C 8-10%, but is individualized to the patient
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35
Q

Biguanides

A
  • Metformin
  • do not give with those with CKD, liver failure, or alcoholism
  • avoid in pregnancy and children
  • hold meds if doing a test that requires contrast media and restart in 24-48 hours to prevent acute kidney injury
  • may produce weight loss and improve lipid profiles
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36
Q

Biguanides: Lab Tests

A
  • GFR must be at least 45 to start; stop if GFR falls below 30
  • May cause B12 deficiency, so check B12 levels if patient complains of neuropathy symptoms
37
Q

Biguanides: Mode of Action

A
  • decrease production in liver
  • decrease absorption of glucose in intestine
  • improve insulin sensitivity by increasing peripheral glucose uptake and utilization
38
Q

Biguanides: Initial Dose

A

Start with 500 mg at each meal and increase gradually as needed, may use XL version to help with GI side effects

39
Q

Thiazolidinediones (TZD): Mode of Action

A
  • Inhibits gluconeogenesis in liver
  • Improves liver sensitivity in skeletal muscle and adipose tissue
  • Reduces circulating insulin levels in hyperinsulinemic patients
40
Q

Thiazolidinediones (TZD): Who can’t take these medications?

A
  • Class 3 or 4 HF
  • Pregnancy
  • Age less than 18
  • Liver disease
41
Q

Thiazolidinediones (TZD): Medications

A
  1. Pioglitazone (may cause bladder cancer; improves lipid profile)
  2. Rosaglitazone (can increase total cholesterol, LDL, and HDL)
    ** Obtain LFT prior to initiation
42
Q

Alpha-Glucosidase Inhibitors: Mode of Action

A

Delays absorption of carbs after a meal

43
Q

Alpha-Glucosidase Inhibitors: Who can’t take these medications?

A
  • pregnancy
  • children
  • inflammatory bowel disorders
44
Q

Alpha-Glucosidase Inhibitors: Considerations

A
  • may exacerbate or precipitate HF
  • adjust dosage for renal impairment
  • monitor serum transaminases every 3 months during first year
  • usually does not cause hypoglycemia, but if it does use dextrose instead of sucrose
  • flatulence is main side effect
45
Q

Alpha-Glucosidase Inhibitors: Medications

A
  1. Acarbose
  2. Miglitol (do not use for patients with CKD)
46
Q

Dipeptidyl Peptidase-4 Inhibitors: Mode of Action

A
  • increase insulin secretion
  • suppresses glucagon secretion
  • preserve beta cell potential
47
Q

Dipeptidyl Peptidase-4 Inhibitors: Considerations

A
  • low risk of hypoglycemia when used alone
  • renal dosage adjustments needed for moderate-to-severe renal failure
  • may cause or exacerbate HF
  • monitor pulse rate if on digoxin
  • monitor renal function
  • may cause pancreatitis, HA, upper resp infections, severe joint pain
48
Q

Dipeptidyl Peptidase-4 Inhibitors: Who can’t take these medications?

A
  • Pregnant
  • Children
49
Q

Dipeptidyl Peptidase-4 Inhibitors: Medications

A
  1. Sitagliptin
  2. Saxagliptin
  3. Linagliptin
50
Q

Sodium Glucose Cotransporter 2 Inhibitors (SGLT-2): Mode of Action

A
  • block glucose reabsorption in kidney
  • increase urinary excretion of glucose
51
Q

Sodium Glucose Cotransporter 2 Inhibitors (SGLT-2): Who can’t take these medications?

A
  • Pregnancy
  • Children
52
Q

Sodium Glucose Cotransporter 2 Inhibitors (SGLT-2): Lab Tests

A
  • obtain GFR (do not start with GFR < 45)
  • Lipid panel
  • BMP prior to initiation AND 2 weeks after starting therapy
53
Q

Sodium Glucose Cotransporter 2 Inhibitors (SGLT-2): Considerations

A
  • weight loss side effect
  • cardiac benefits
  • not as effective with CKD patients
  • monitor for hypotension and hyperkalemia
54
Q

Sodium Glucose Cotransporter 2 Inhibitors (SGLT-2): Medications

A
  1. Canagliflozin (increased risk of limb amputation)
  2. Dapagliflozin
  3. Empagliflozin
55
Q

Glucagon-like Peptide-1 Receptor Agonists (GLP-1 RA): Mode of Action

A
  • promote release of insulin from pancreatic beta cells in presence of elevated glucose concentrations
  • decrease glucagon secretion, leading to reduced hepatic glucose production and slowed gastric emptying
56
Q

Glucagon-like Peptide-1 Receptor Agonists (GLP-1 RA): Who can’t take these medications?

A
  • personal or family history of medullary thyroid cancer
  • pregnancy
  • lactation
  • children
  • history of pancreatitis or gastroparesis
  • avoid if GFR < 30
57
Q

Glucagon-like Peptide-1 Receptor Agonists (GLP-1 RA): Considerations

A
  • weight loss side effect
  • may decrease effectiveness of oral contraceptives
58
Q

Sulfonylureas: Mode of Action

A
  • stimulates release of insulin from functioning pancreatic beta cells
59
Q

Sulfonylureas: Who can’t take these medications?

A
  • renal failure
  • hepatic failure
  • pregnancy
  • children
60
Q

Sulfonylureas: Considerations

A
  • weight gain and hypoglycemia
  • use cautiously in those with cardiovascular disease or in elderly patients because of hypoglycemia
  • monitor BG for 1-2 weeks before changing from longer-acting to shorter-acting versions
61
Q

Sulfonylureas: Medications

A
  1. Glimepiride
  2. Glipizide
62
Q

Combination Drugs: Considerations

A

Because of difficulty adjusting dosages of individual medications, these are not recommended

63
Q

Addison’s Disease: What is it?

A
  • a chronic deficiency of cortisol caused by adrenocortical insufficiency
  • uncommon
  • can be drug related
  • most common in women between 30-50
64
Q

Addison’s Disease: Assessment Findings

A
  • fatigue
  • anorexia, weight loss
  • hyperpigmentation
  • salt craving
  • nausea, vomiting
  • vague abdominal pain
  • postural hypotension
  • cold intolerance
  • psychosis
65
Q

Addison’s Disease: Diagnostic Tests

A
  • morning serum cortisol
  • plasma ACTH
  • serum electrolytes
  • CBC with diff
  • ACTH stimulation test if morning serum cortisol tests do not confirm or exclude adrenal insufficiency
66
Q

Addison’s Disease: Non-Pharmacologic Management

A
  • correct precipitating factors
  • include adequate sodium, chloride, and potassium in diet
  • medic alert bracelet
67
Q

Addison’s Disease: Pharmacologic Management

A
  1. Glucocorticoid supplementation (hydrocortisone 15-30 mg PO QD in 2-3 divided doses)
  2. Mineralocorticoid supplementation (fludrocortisone acetate 0.05-0.2 mg PO QD or every other day)
  3. Calcium and vitamin D supplementation
68
Q

The 5 “S” Approach to Addison’s Disease Management

A
  1. Salt
  2. Sugar
  3. Steroids
  4. Support
  5. Search for precipitating illness
69
Q

Cushing’s Syndrome: What is it?

A
  • a debilitating endocrine syndrome that results from overexposure of tissues to corticosteroids via exogenous or endogenous sources
  • exogenous corticosteroid exposure is the most common cause
  • an ACTH-secreting pituitary adenoma is the most common cause of endogenous
70
Q

Cushing’s Syndrome: Assessment Findings

A
  • truncal obesity
  • supraclavicular fat pads
  • proximal muscle weakness
  • moon face, Buffalo hump
  • abdominal striae and protuberant abdomen
  • easy bruising
  • premature osteoporosis
  • HTN
  • poor wound healing
71
Q

Cushing’s Syndrome: Diagnostic Tests

A
  • late night salivary cortisol determination
  • overnight dexamethasone suppression test
  • 24 hour urinary free cortisol and creatinine
  • plasma ACTH and plasma DHEA
  • CT of the adrenals
  • MRI of the pituitary gland
72
Q

Cushing’s Syndrome: Prevention

A

Limit corticosteroid use

73
Q

Cushing’s Syndrome: Non-Pharmacologic Management

A
  • treat cortisol-dependent comorbidities
  • surgery
74
Q

Cushing’s Syndrome: Pharmacologic Management

A

Osilodrostat PO BID

75
Q

Hyperthyroidism: What is it?

A
  • AKA thyrotoxicosis
  • excess secretion and synthesis of thyroid hormones by the thyroid gland
  • more common in women
  • usually occurs between 20-40 years old
76
Q

Hyperthyroidism: Causes

A
  1. Grave’s disease
  2. Toxic multinodular goiter and thyroid nodules
  3. Autoimmune thyroiditis
  4. Medication-induced hyperthyroidism (amiodarone, excess iodine, chemo drugs, immune checkpoint inhibitors)
  5. Pregnancy (Hcg secreting trophoblastic tumors [molar pregnancy]
  6. Testicular choriocarcinoma
77
Q

Hyperthyroidism: Assessment Findings

A
  • nervousness, restlessness, palpitations
  • heat intolerance, increased sweating
  • pruritis
  • fatigue, weight loss
  • muscle weakness, muscle cramps, menstrual irregularities
  • frequent bowel movements
  • angina, Afib
  • enlarged thyroid with a bruit
78
Q

Hyperthyroidism: Diagnostic Tests

A
  • TSH (decreased)
  • T3 and Free T3 (increased)
  • T4 and Free T4 (increased)
  • CBC
  • LFT
  • Radioisotope uptake
  • Thyroid ultrasound
79
Q

Hyperthyroidism: Non-Pharmacologic Management

A

Thyroid surgery

80
Q

Hyperthyroidism: Pharmacologic Management

A
  1. Propranolol
  2. Methimazole
    OR
  3. Propylthiouracil (PTU)
81
Q

Hypothyroidism: What is it?

A

Results from a reduction in circulating free thyroid hormone or from resistance to the action of thyroid hormone

82
Q

Hypothyroidism: Causes

A
  • most common cause primary thyroid gland failure resulting from autoimmune destruction (Hashimoto’s)
  • iodine deficiency or excess
  • treatment for hyperthyroidism
  • history of head or neck irradiation
  • family history
  • medications (amiodarone, chemo)
83
Q

Hypothyroidism: Assessment Findings

A
  • weight gain
  • fatigue, lethargy, weakness
  • depression
  • goiter
  • cold intolerance
  • dry skin, thin brittle nails, thinning hair
  • bradycardia
84
Q

Hypothyroidism: Diagnostic Studies

A
  • Serum TSH (increased)
  • T4 (decreased)
  • T3 (decreased)
85
Q

Hypothyroidism: Prevention

A
  • periodic monitoring of thyroid hormone levels for patients treated for hyperthyroidism
  • identification of risk factors
  • newborn thyroid screening at 2-6 days of age
86
Q

Hypothyroidism: Non-Pharmacologic Management

A
  • high fiber diet
  • weight loss if obese
  • annual lipid level assessment
  • educate about need for lifelong thyroid hormone replacement
87
Q

Hypothyroidism: Pharmacologic Management

A
  1. Levothyroxine daily
    - healthy young and middle aged adults start with 1.6 mcg/kg/day
    - patients with stable CAD or those over 60 years old start with 25-50 mcg/day
    - pregnancy may require an increased dose
88
Q

Hypothyroidism: Follow-Ups

A

Measure TSH monthly after starting levothyroxine, then monthly until at goal, then annually

89
Q

Hypothyroidism: Complications

A
  1. Myxedema coma
  2. HF
  3. Infertility
  4. Miscarriage

Adult Health (20 decks)

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