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FNP boards > Endocrine disorders > Flashcards

Endocrine disorders Flashcards

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Family Nurse Practitioner (FNP) flashcards
1
Q

Diabetes screening recommendations

A

Testing should be considered in adults who are overweight (BMI >25) and have risk factors

  • In the absence of risk factors, testing should begin at age 45 and then every 3 years thereafter
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2
Q

Lab indicators of DM

A
  • Fasting plasma glucose (8 hour fast) = >126
  • Random plasma glucose = >200
  • OGTT at 2 hours = >200
  • Hgb A1c = >6.5%
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3
Q

When is repeat A1c indicated for patients with DM?

A

If asymptomatic, A1c repeated with glucose <200

Repeat not needed in presence of DM symptoms and/or glucose levels >200

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4
Q

DM laboratory tests

A
  • A1c every 3-6 months
  • Fasting blood glucose (as indicated)
  • Lipid profile (annual)
  • Urine microalbumin/creatinine (annual)
  • Serum creatinine with GFR (annual)
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5
Q

DM treatment (lifestyle modifications)

  • Prediabetes
A
  • Target weight loss of 7% body weight
  • Increase physical activity to 150 minutes/week
  • Consider adding metformin
  • Smoking cessation
  • Mediterranean diet
  • Eat frequent, small, high fiber meals and foods with low glycemic index
  • Calorie deficit
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6
Q

Metformin therapy contraindications

A

Can lead to lactic acidosis

  • Renal impairment (GFR <45)
  • Concurrent IV contrast dye use
  • HF
  • Age 80+ years
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7
Q

Sulfonylurea → glipizide, glyburide, glimepiride

  • MOA
  • Comments
A

MOA: insulin secretagogue

Comments:

  • Hypoglycemia risk
    • Caution in ASCVD
  • Require functioning pancreatic beta cells
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8
Q

Metformin MOA

A
  • Reduces hepatic glucose production and intestinal glucose absorption
  • Insulin sensitizer via increased peripheral glucose uptake and utilization
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9
Q

Example of TZDs

A
  • Pioglitazone
  • Rosiglitazone
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10
Q

GLP-1 agonist → eventide, liraglutide, dulaglutide (incretin mimetic)

  • MOA
  • Comments
A

MOA: stimulates insulin production in response to increase in plasma glucose, inhibits postprandial glucagon release, slows gastric emptying

Comments:

  • N/V
  • Contraindicated with gastroparesis
  • Use with caution in patients with mild-moderate renal impairment
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11
Q

DPP-4 inhibitor → -gliptin

  • MOA
  • Comments
A

MOA: increases levels of incretin, increasing synthesis and release of insulin from pancreatic beta cells, decrease release of glucagon from pancreatic alpha cells

Comments:

  • Monitor for development of pancreatitis
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12
Q

SGLT-2 inhibitor → -gliflozin

  • MOA
  • Comments
A

MOA: lowers renal glucose threshold, increased urinary glucose excretion

Comments:

  • Increased risk of ketoacidosis, hyperkalemia
  • Weight neutral
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13
Q

When is insulin therapy indicated for T2DM management?

A
  • At time of diagnosis to help achieve initial control (especially if glucose greater than 250-300)
  • Acutely ill (should be kept at 140-180)
  • When >2 insulin secretagogues (sulfonylureas, GLP-1 agonist, DPP-4 inhibitor) at optimized use are inadequate
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14
Q

What is the somogyi effect in DM management?

A

An insulin-induced hypoglycemia triggers excess secretion of glucagon and cortisol → hyperglycemia

  • Lower dinnertime dose of intermediate acting insulin (NPH, novolin or humuling)
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15
Q

What is the dawn phenomenon in DM management?

A

Result of reduced insulin sensitivity developing between 5-8am

  • Caused by earlier spikes in GH → cortisol release → hepatic glucose secretion → early morning hyperglycemia
  • Split evening intermediate insulin dose between dinner and bedtime OR switch to bedtime dose of basal insulin (glargine)
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16
Q

Clinical presentation of T1DM and associated ketoacidosis

A
  • Severe dehydration
  • Abdominal pain
  • Vomiting
  • Altered LOC
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17
Q

Diagnostic criteria for metabolic syndrome

A

Insulin resistance (T2DM or impaired fasting glucose) plus 2+ of the following:

  • Abdominal/central obesity
  • Hypertriglyceridemia (150 or greater)
  • Low HDL
    • <35 for men
    • <40 for women
  • High BP (>140/90) or documented use of antihypertensives
  • Microalbuminuria (glucose intolerance)
18
Q

True/false: A 10% body weight loss yields nearly immediate improvements of death rates from heart disease and stroke

A

True

19
Q

Obesity labs

A
  • Fasting lipid panel
  • LFTs
  • Thyroid function tests
  • Fasting plasma glucose
  • A1c
20
Q

Obesity pharmacotherapy

A

D/c if patient has not achieved 5% weight loss by week 12 of treatment

  • Orlistat → reduces dietary fat absorption
    • Taken with or within 1 hour of a meal that contains fat
  • Phentermine and topiramate (Qsymia)
    • Need negative pregnancy test before starting b/c of topiramate
  • Naltrexone and bupropion (Contrave)
    • Black box warning for neuropsychological symptoms
  • Liraglutide → GLP-1 agonist
21
Q

How soon after levothyroxine therapy is initiated for hypothyroidism treatment, should TSH levels be checked again?

A

6-8 weeks after initiation

  • Once levels are stable, check again after 6 months then at 12 month intervals
22
Q

What foods and/or medications should be avoided, or separated by at least several hours, when on levothyroxine therapy?

A
  • Medications
    • Iron
    • Calcium
    • Aluminum containing antacids
    • Rifampin
    • Phenytoin
    • Carbamazepine
    • Phenobarbital
    • Sucralfate
  • Cow or soy milk
23
Q

How should levothyroxine be taken?

A

Same time every day on empty stomach with water only

  • If taken in morning, no food should be eaten for 1 hour
  • If taken after eating, wait 4 hours after eating with 1 hour wait postdose
24
Q

Subclinical hypothyroidism diagnostic testing

A

Add test for TPO antibodies - clinical marker of autoimmune thyroid disease

25
Q

Is treatment necessary for subclinical hypothyroidism?

A

Yes if…

  • TSH levels increase to more than 10
  • Increase in LDL
  • Increased CVD risk
  • Infertility
  • Pregnancy
  • Plans to become pregnant in the near future
26
Q

Hyperthyroidism treatment

A
  • Methimazole and PTU (if pregnant, PTU in first trimester)
    • Hepatotoxicity warning
  • Once euthyroid state achieved, radioactive iodine for thyroid ablation next step
27
Q

Dyslipidemia diagnostic testing recommendations

A

Begin lipid screening (TC, HDL, LDL, TG) for adults ages 20-78 years without ASCVD every 4-6 years

  • If non fasting and TGs are >400, repeat profile in fasting state
28
Q

When is repeat testing of lipid profiles indicated for patients on drug therapy and those focusing on lifestyle modifications?

A

If on drug therapy, check after 6 weeks of therapy

If not on drug therapy, monitor every 3-6 months

29
Q

Four groups for the prevention of ASCVD risk reduction (indication for statin therapy)

A
  • LDL 190 or higher (high intensity)
  • DM who are aged 40-75 years (moderate intensity)
  • Older than 75 years
  • Aged 40-75 years who have LDL between 70-189
30
Q

Statin therapy considerations before initiation

A
  • Check baseline hepatic enzyme levels
  • Causes LDL reduction
  • High intensity statin → atorvastatin 40-80, rosuvastatin 20-40
  • Moderate intensity statin → simvastatin, atorvastatin 10-20, pravastatin, rosuvastatin)
31
Q

When is a repeat lipid profile indicated after statin therapy?

A

After 4-12 weeks then repeated every 12 months

32
Q

Primary vs secondary adrenal insufficiency

A

Primary - adrenal gland is damaged and hinders production of hormones (autoimmune, infection, hemorrhage, tumor, anticoagulant)

Secondary - pituitary gland is diseased, those who have taken systemic corticosteroids for a chronic condition and then abruptly stop taking them

33
Q

Addison’s disease clinical presentation

A
  • GI upset (chronic diarrhea, N/V, loss of appetite)
  • Weight loss
  • Paleness
  • Darkening of skin, patchy appearance
  • Muscle wasting, fatigue
  • Slow or sluggish movement
  • Hypoglycemia
  • Low BP
34
Q

Addison’s disease diagnostic testin

A
  • Serum potassium, sodium, cortisol, ACTH
  • ACTH stimulation test
    • Inject synthetic ACTH and compare level of cortisol before and after
    • Damage to adrenal gland will show no response to synthetic ACTH
  • Abdominal CT scan
35
Q

Addison’s disease treatment and management

A
  • Corticosteroid replacement therapy
  • Increase salt intake before heavy exercise, hot climates, during GI upset (diarrhea)
36
Q

Cushing’s syndrome clinical presentation

A
  • Progressive weight gain
  • Altered fatty tissue deposits (mid section and upper back)
    • Moon face
    • Buffalo hump
  • Pink or purple stretch marks
  • Fragile skin that bruises easily
  • Slow healing cuts
  • Fatigue
  • High BP
  • Glucose intolerance
  • Hirsutism
  • Menorrhagia
37
Q

Cushing’s syndrome diagnostic testing

A
  • Without history of long term corticosteroid use
    • Urine, blood, saliva tests to evaluate cortisol levels
  • MRI or CT scan to determine any abnormality of pituitary
38
Q

Cushing’s syndrome treatment and management

A
  • For endogenous Cushing’s syndrome or Cushing’s disease → surgery
  • Mifepristone for patients with endogenous Cushing’s syndrome and T2DM or glucose intolerance
39
Q

PALM-COEIN classification system for abnormal uterine bleeding (heavy menstrual bleeding or intermenstrual bleeding)

A

PALM (structural)

  • Polyp
  • Adenomyosis
  • Leiomyoma
  • Malignancy and hyperplasia

COEIN (non structural)

  • Coagulopathy
  • Ovulatory dysfunction
  • Endometrial
  • Iatrogenic
  • Not yet classified
40
Q

Abnormal uterine bleeding diagnostic testing

A
  • CBC
  • Pap smear (if due)
  • Pregnancy test
  • Endometrial sampling via biopsy (for hyperplasia or cancer)
  • Thyroid function (hypothyroid)
  • Prolactin (pituitary function)
  • LFT
  • Coagulation studies
  • Pelvic US
41
Q

Abnormal uterine bleeding treatment and management

A
  • Up to age 39 years → COCs, LNG IUD
  • Pre or perimenopause (40+ years) → cyclic progestin therapy, low dose COC, LNG IUD, cyclic hormone therapy

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