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Flashcards in Endocrinology Deck (104)
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1

What is acromegaly?

acromegaly and gigantism are usually caused by a pituitary adenoma that secretes excessive amounts of Growth Hormones; rarely, they are caused by non-pituitary tumors that secrete GHRH
-gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses
-acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop

2

What is the presentation of acromegaly?

-large hands, feet, nose, lips, ears, jaw, tongue
-presents as gigantism (excessive height) if occurs before epiphyseal closure

3

How is acromegaly dx?

-GH test 2 hour after glucose load
-increased IGF-1
-MRI/CT shows a pituitary tumor

4

What is the tx for acromegaly?

pituitary tumor removal

5

What is 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

6

What are the lab findings for Addison's disease?

decreased sodium, decreased 8 AM cortisol, increased ACTH (primary), increased potassium (primary), low DHEA

7

How is Addison's disease dx?

high dose cosyntropin (synthetic ACTH) stimulation test
-blood or urine cortisol is measured after an IM injection of cosyntropin (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

8

What is the tx of Addison's disease?

hydrocortisone/prednisone PO daily
-Crisis: hypotension, altered mental status
-treatment: emergent IV saline, glucose, steroids

9

What is Cushing's syndrome?

a collection of signs and symtpoms due to prolonged exposure to excess cortison
-symptoms from increased cortisol secretion
-it doesn't specify cause or soure of excess

10

What is Cushing disease?

ACTH secreting pituitary microadenoma usually very small on anterior pituitary, F 3x >M
-secondary - increased cortisol due to ACTH excess, typically caused by pituitary adenoma -ACTH causes adrenals to secrete cortisol

11

What are the features of Cushing disease?

-hypercortisolism (increased cortisol) = obesity (buffalo hump, moon facies, supreclavicular pads), HTN, thirst, polyuria, hypokalemia
-proximal muscle weakness, pigmented striae; backache, headache, oligomenorrhea/amenorrhea/ED; emotional lability/psychosis

12

How is Cushing disease dx?

confirming high cortisol with a 24 hr urine free cortisol, late-night serum cortisol, and/or low-dose dexamethasone suppression test
-24-hr urinary free cortisol is the most reliable index of cortisol secretion
-once confirmed, the source of the high cortisol needs to be determined with an ACTH level
-a high ACTH level indicates an ACTH dependent cause, a low ACTH level indicated an ACTH independent cause (plasma or serum ACTH < 20 pg/mL suggest adrenal tumor
-if it is an ACTH dependent cause, an MRI of the brain should be done to look for a pituitary adenoma (Cushing disease)
-if it is an ACTH independent cause, a CT of adrenals should be done to look for an adrenal mass such as an adenoma

13

What is low dose dexamethason suppresion test?

-give a steroid (dexamethasone) = failure of steroid to decrease cotisol levels is diagnostic = proceed next to high dose dexamethason suppression test = no suppression = Cushing's syndrome
-supression < 5 ugs/dL excludes Cushing with some certainty

14

What is the tx for Cushing disease?

trnasphenodial selective resection of pituitary tumor cures 75-90%
-irradiation provides remission in 50-60%
-95% 5-year survival

15

What is diabetes insipidus?

caused by a deficiency of or restance to vasopressin (ADH), which decreases the kidney's ability to reabsorb water, resulting in massive polyuria

16

What is central diabetes insipidus?

deficiency of ADH from posterior pituitary/hypothalamus
-no ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis

17

What is nephrogenic diabetes insipidus?

Lack of reaction to ADH
-partial or complete insensitivity to ADH: caused by drugs (lithium, amphoterrible), hypercalcemia and hypokalemia affect the kidney's ability to concentrate urine, acute tubular necrosis

18

How is diabetes insipidus dx?

serum osmolality (concentration) is high (unable to stop the secretion of water into the kidneys so blood becomes more concentrates) and urine osmolality is low because it is so dilute
-water deprivation test - simplest/most reliable method - continued production of dilute urine despite water deprivation
-desmopression stimulation test:
-central: reduction in urine output indicating a response to ADH
-nephrogenic: continued production of dilute urine (no response to ADH) because kidenyes can't respond

19

How is diabetes insipidus tx?

-central = desmopression/DDAVP
-nephrogenic = sodium and protein restriction, HCTX, indomethacin

20

What is the etiology of diabetes mellitus type 1?

autoimmune - HLA-DR3/4/O antiboies
-Islet cell antibodies

21

What is the presentation os Type 1 DM?

-children
-polyuria, polydipsia, polyphagia, fatigue and weight loss
-often first recognized as diabetic ketoacidosis:
-symptoms: fruity breath, nausea, vomintg, dehydration
-treatment: IV regular insuling

22

What is the the treatment of type I DM?

insulin

23

What is the dawn phenomenon?

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 snak late at night

24

What is the somogyi effect?

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

25

What is insulin waning?

a progressive rise in glucose from bedtime to morning
-treat with a change of insulting dose to bedtime

26

What is DKA?

fruity breath, weight loss, rapid respirations, hypotension
-diabetic ketoacidosis (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! patinets with DKA are always dehydrated and need large-volume IV fluid resucitation, usually isotonic fluids such as normal saline
-if corrected serum sodium level is high, this can be reduced to half-normal saline
-insuling should always be administered by an IV pump to guard against accidental overdose

27

How is the diagnosis of DM made?

-randoma 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%

28

What are the insulin and c-peptide levels with Type I DM?

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

29

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

if one or more 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

30

How you monitor/evaluate glycemic control?

-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 medication/insulin levels
-treatment goal of A1c <7.0%
-"finger-stick" blood glucose monitoring
-useful for insulin-dependent (either type 1 or type 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