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
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
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
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
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
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
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
8
Q
What is Cushing’s syndrome?
A
a collection of signs and symptoms due to prolonged exposure to excess cortisol
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
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
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
12
Q
What is the etiology of diabetes mellitus type 1?
A
autoimmune - HLA-DR3/4/O antibodies, islet cell antibodies
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
14
Q
What is the tx of type I DM?
A
insulin
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
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
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
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
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
What are the characteristics of sulfonylureas?
stimulates pancreatic beta-cell insulin release (insulin secretagogue)
- glyburide (diabeta), glipizide (glucotrol), glimepiride (Amaryl)
- side effects: hypoglycemia
- benefits: cheap, rapidly effective
26
What are the characteristics of thiazolidinediones?
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
What are the characteristics of alpha-glucosides inhibitors?
delays intestinal glucose absorption
- acarbose (precose), miglitol (glyset)
- GI side effects, three times a day dosing
28
What are the characteristics of meglitinides?
stimulates pancreatic beta-cell insulin release
- repaglinide (Prandin) and nateglinide (starlix)
- side effects: may cause hypoglycemia
29
What are the characteristics of GLP-1 agonists?
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
What are the characteristics of DPP-4 inhibitors?
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
What are the characteristics of SGLT2 inhibitor?
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
What are the characteristics of insulin?
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
How is the diagnosis of DM made?
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
What is the diagnostic criteria for prediabetes?
- A1C 5.7-6.4
- fasting glucose 100-125
- 2 hour oral glucose tolerance test 140-199
35
What are the glucose goals and basic management for diabetes?
- 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
What is hyperthyroidism?
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
What is the etiology of hyperthyroidism?
grave's disease (autoimmune), toxic adenoma, thyroiditis, pregnancy, amiodarone
38
What is the presentation of hyperthyroidism?
heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia
- graves - diffuse goiter with a bruit, exophthalmos, pretibial myxedema
- thyroid storm - fever, tachycardia, delirium
39
How is hyperthyroidism dx?
- 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
What are the antibodies of hyperthyroidism?
graves: anti-thyrotropin antibodies
41
What is the tx of hyperthyroidism?
- 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
What drug is used during pregnancy and nursing for hyperthyroidism?
- 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
What is the etiology of hypothyroidism?
Hashimoto's (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine ablation, congenital
44
What is the presentation of hypothyroidism?
- cold intolerance, fatigue, constipation, depression, weight gain, bradycardia
- congenital: round face, large tongue, hernia, delayed milestones, poor feeding
45
What are the labs for hypothyroidism?
TSH - elevated in primary disease, low T4 (increase TSH and decreased free T4)
-hashimoto's: antithyroid peroxidase, antithyroglobulin antiboides
46
What is the tx of hypothyroidism?
levothyroxine, follow up with serial TSH monitoring
