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Family Medicine EOR > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the characteristics of primary adrenal insufficiency (Addison’s disease)?

A

problem with the adrenal gland

  • decrease cortisol, increase ACTH and no increase in cortisol level after the ACTH stimulation test, as well as decrease aldosterone and high plasma renin activity
  • the most common cause is autoimmune destruction and adrenal metastases
  • worldwide - TB, secondary infections
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2
Q

What is secondary adrenal insufficiency?

A

insufficient pituitary ACTH production

  • decrease cortisol and decrease ACTH, an increase in cortisol after ACTH administration, but no aldosterone deficiency
  • no increase in ACTH after a CRH injection
  • secondary adrenal insufficiency is usually because of a pituitary macro adenoma or a central nervous system tumor, that can be identified on an MRI and removed through transsphenoidal resection
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3
Q

What is tertiary adrenal insufficiency?

A

insufficient CRH production

  • decrease cortisol and normal aldosterone
  • decrease cortisol and decrease ACTH, an increase in cortisol after ACTH administration, but no aldosterone deficiency
  • ACTH levels increase after CRH injection
  • most common cause - sudden withdrawal of glucocorticoid therapy or after the cur of Cushing disease
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4
Q

What is primary adrenal insufficiency?

A

Addison’s disease

  • typically autoimmune, may be due to Tuberculosis in endemic areas
  • destruction of the adrenal cortex resulting in loss of cortisol production (decrease cortisol)
  • nonspecific symptoms: hyperpigmentation, hypotension, fatigue, myalgias, GI complaints, weight loss
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5
Q

What are the lab findings of primary adrenal insufficiency?

A

decrease sodium, decrease 8 am cortisol, increase ACTH (primary), increase potassium (primary), low DHEA

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6
Q

How is primary adrenal insufficiency dx?

A

high dose cosyntropin (synthetic ACTH) stimulation test

  • blood or urine cortisol is measured after an IM injection of cosyntopin (synthetic ACTH)
  • the normal response is a rise in blood and urine cortisol levels after synthetic ACTH is given
  • primary adrenal insufficiency results in little or no increase in cortisol levels (<20 mcg/dL) after ACTH is given
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7
Q

What is the tx of primary adrenal insufficiency?

A

hydrocortisone/prednisone PO daily

  • crisis: hypotension, altered mental status
  • treatment: emergent IV saline, glucose, steroids
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8
Q

What is Cushing’s syndrome?

A

a collection of signs and symptoms due to prolonged exposure to excess cortisol

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9
Q

What are the characteristics of Cushing’s syndrome?

A
  • increase cortisol, buffalo hump, moon facies, pigmented striae, obesity, skin atrophy, hypertension, weight gain, hypokalemia
  • 24-hour urinary free cortisol is the most reliable index of cortisol secretion = elevated urinary cortisol = Cushing’s syndrome
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10
Q

How is Cushing’s syndrome dx?

A

low dose dexamethasone suppression test - give a steroid (dexamethasone) failure of steroid to decrease cortisol levels is diagnostic, proceed next to high dose dexamethasone suppression test - no suppression = Cushing’s syndrome

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11
Q

What is the difference between Cushing’s syndrome and disease?

A
  • Cushing’s syndrome = symptoms from increase cortisol secretion, it doesn’t specify cause or source of excess
  • cushing’s disease: secondary - increase cortisol due to ACTH excess, typically caused by a pituitary adenoma - ACTH causes adrenals to secrete cortisol
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12
Q

What is the etiology of diabetes mellitus type 1?

A

autoimmune - HLA-DR3/4/O antibodies, islet cell antibodies

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13
Q

What is the presentation of diabetes mellitus type 1?

A
  • children
  • polyuria, polydipsia, polyphagis, fatigue and weight loss
  • often first recognized as diabetic keto acidosis
  • symptoms: fruity breath, nausea, vomiting, dehydration
  • treatment: IV regular insulin
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14
Q

What is the tx of type I DM?

A

insulin

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15
Q

What is the dawn phenomenon?

A

normal glucose until 2-8 am when it rises

  • results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting
  • treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snack late at night
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16
Q

What is smogyi effect?

A

nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone
-treat with decreased nighttime NPH dose or give bedtime snack

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17
Q

What is insulin warning?

A

a progressive rise in glucose from bedtime to morning

-treat with a charge of insulin dose to bedtime

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18
Q

What is DKA?

A

fruity breath, weight loss, rapid respiration, hypotension

  • diabetic keto acidosis (DKA) should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist’s consultation, if appropriate
  • treat with fluids
  • patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline
  • if the corrected serum sodium level is high, this can be reduced to half-normal saline
  • insulin should always be administered by an IV pump to guard against accidental overdose
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19
Q

How is the diagnosis of DM made?

A

One of the following

  • random blood glucose level of >200 mg/dL + diabetic symptoms
  • 2 separate fasting (8 hours) glucose levels of >126 mg/dL
  • 2-hour plasma glucose of >200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
  • hemoglobin A1c of >6.5%
20
Q

What are insulin and C-peptide levels?

A

low or inappropriately normal fasting C-peptide and insulin levels with concomitant hyperglycemia
-high fasting insulin and C-peptide levels suggest T2DM

21
Q

What is insulin, GAD65, and IA-2 antibodies?

A

if one or more of the antibodies are present, and especially if two or more are positive, the patient should be presumed to have type 1 diabetes and should be treated with insulin replacement therapy

22
Q

How do you monitoring/evaluation of glycemic control?

A
  • hemoglobin A1c
  • represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC)
  • useful to gauge the ‘big-picture’ overall efficacy of glucose control in patients (either Type 1 or Type 2) to assess the need for changes in mediation/insulin levels
  • treatment goal of A1c <7%
  • “finger-stick” blood glucose monitoring
  • useful for insulin-dependent (either type 1 or 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activity
  • treatment goals: <130 mg/dL fasting and <180 mg/dL peak postprandial
23
Q

How is the dx of DM type 2 made?

A

random glucose >200 x two or fasting glucose >126 x two

24
Q

What are the characteristics of metformin?

A

decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)

  • side effects: lactic acidosis, GI side effects, initiation is contraindicated with eGFR <30 mL/min and not recommended with eGFR 30 to 45 mL/min, discontinue 24 hours before contrast and resume 48 hours after with monitoring for creatinine, stop if creatinine is >1.5
  • benefits: weight loss, inexpensive
25
Q

What are the characteristics of sulfonylureas?

A

stimulates pancreatic beta-cell insulin release (insulin secretagogue)

  • glyburide (diabeta), glipizide (glucotrol), glimepiride (Amaryl)
  • side effects: hypoglycemia
  • benefits: cheap, rapidly effective
26
Q

What are the characteristics of thiazolidinediones?

A

increases insulin sensitivity in peripheral receptor site adipose and muscle has no effect on pancreatic beta cells

  • pioglitazone (Acots), rosiglitazone (Avandia)
  • contraindications: CHF, liver disease, fluid retention, weight gain, bladder cancer (pioglitazone), a potential increase in MI (rosiglitazone)
27
Q

What are the characteristics of alpha-glucosides inhibitors?

A

delays intestinal glucose absorption

  • acarbose (precose), miglitol (glyset)
  • GI side effects, three times a day dosing
28
Q

What are the characteristics of meglitinides?

A

stimulates pancreatic beta-cell insulin release

  • repaglinide (Prandin) and nateglinide (starlix)
  • side effects: may cause hypoglycemia
29
Q

What are the characteristics of GLP-1 agonists?

A

lowers blood sugar by mimicking incretin - causes insulin secretion and decreased glucagon and delays gastric emptying

  • exenatide (Bydureon, Byetta), dulaglutide (trulicity), semaglutide (ozempic), liraglutide (victoza, saxenda)
  • side effects: requires injection, frequent GI side effects, caution if gastroparesis
  • benefits: weight loss, reduced CV mortality (semaglutide, liraglutide) in patients with CVD
30
Q

What are the characteristics of DPP-4 inhibitors?

A

dipetpidylpetase inhibition - inhibits degradation of GLP-1 so more circulating GLP-1

  • sitagliptin (Januvia), saxagliptin (onglyza)
  • side effects: expensive, possible increased risk of heart failure with saxagliptin
31
Q

What are the characteristics of SGLT2 inhibitor?

A

SGLT2 inhibitor lowers renal glucose threshold which results in increased urinary glucose excretion

  • canagliflozin (Invokana or Sulisent)
  • side effects: vulvovaginal candidiasis, urinary tract infections, bone fractures, lower limb amputations, acute kidney injury, DKA, long-term safety not established
  • benefits: weight loss, reduction in systolic blood pressure, reduced cardiovascular mortality in patients with established CVD
32
Q

What are the characteristics of insulin?

A

add if HbA1C > 9

  • follow up: annual - ophthalmologist visit, urine micro albumin
  • complications: neuropathy (most common), retinopathy (a leading cause of blindness), nephropathy
  • normal fasting glucose is between 70 and 100
33
Q

How is the diagnosis of DM made?

A

made by one of the following

  • a random blood glucose level of >200 mg/dL and diabetic symptoms
  • two separate fasting (8 hours) glucose levels of >126 mg/dL
  • 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
  • hemoglobin A1c of >6.5%
34
Q

What is the diagnostic criteria for prediabetes?

A
  • A1C 5.7-6.4
  • fasting glucose 100-125
  • 2 hour oral glucose tolerance test 140-199
35
Q

What are the glucose goals and basic management for diabetes?

A
  • A1C <7.0% check every 3 months if not controlled and 2x per year if controlled
  • preprandial glucose 80-110 (60-90 if pregnant)
  • postprandial blood glucose goal (1.5-2 hours after a meal) is <140
  • annual dilated eye exams, ACEI if microalbuminuria, annual foot examination
  • blood pressure should be maintained at <130/80
  • new statin guidelines: recommend statins in persons with diabetes mellitus who are 40 to 75 years of age with LDL-C levels of 70 to 189 mg per dL but without clinical ASCVD
36
Q

What is hyperthyroidism?

A

the production of too much thyroxine hormone
-can increase metabolism and accelerate the body’s metabolism, causing unintentional weight loss and a rapid or irregular heartbeat

37
Q

What is the etiology of hyperthyroidism?

A

grave’s disease (autoimmune), toxic adenoma, thyroiditis, pregnancy, amiodarone

38
Q

What is the presentation of hyperthyroidism?

A

heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia

  • graves - diffuse goiter with a bruit, exophthalmos, pretibial myxedema
  • thyroid storm - fever, tachycardia, delirium
39
Q

How is hyperthyroidism dx?

A
  • TSH (best test): decreased in primary disease (decrease TSH, increase free T4), elevated in secondary disease (increase TSH and increase free T4)
  • T4: elevated although may be normal
  • thyroid radioactive iodine uptake:
  • graves: diffusely high uptake
  • toxic multi nodular: discrete areas of high uptake
40
Q

What are the antibodies of hyperthyroidism?

A

graves: anti-thyrotropin antibodies

41
Q

What is the tx of hyperthyroidism?

A
  • beta-blockers (symptomatic), methimazole/propylthiouracil, radioactive iodine, thyroidectomy
  • thyroid storm - prompt beta-blockers, hydrocortisone, methimazole/propylthiouracil, iodine
  • thyroidectomy - most likely complication is injury to the recurrent laryngeal nerve (hoarseness)
42
Q

What drug is used during pregnancy and nursing for hyperthyroidism?

A
  • propylthiouracil used to be the drug of choice during pregnancy because it causes less severe birth defects than methimazole
  • experts now recommend that propylthiouracil be given during the first trimester only
  • this is because there have been rare cases of liver damage in people taking propylthiouracil
  • after the first trimester, women should switch to methimazole for the rest of the pregnancy
  • for women who are nursing, methimazole is probably a better choice than propylthiouracil (to avoid liver side effects)
43
Q

What is the etiology of hypothyroidism?

A

Hashimoto’s (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine ablation, congenital

44
Q

What is the presentation of hypothyroidism?

A
  • cold intolerance, fatigue, constipation, depression, weight gain, bradycardia
  • congenital: round face, large tongue, hernia, delayed milestones, poor feeding
45
Q

What are the labs for hypothyroidism?

A

TSH - elevated in primary disease, low T4 (increase TSH and decreased free T4)
-hashimoto’s: antithyroid peroxidase, antithyroglobulin antiboides

46
Q

What is the tx of hypothyroidism?

A

levothyroxine, follow up with serial TSH monitoring

Family Medicine EOR (14 decks)

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