Flashcards in endocrine Deck (40)
Type I DM
Autoimmune predisposition activated by environmental trigger
Tx: Insulin replacement mimicking physiologic insulin production and release; basal insulin supplemented with premeal short or ultra short acting.
Type II DM
Relative insulin deficiency due to either distended/distorted peripheral receptors or beta cell dysfunction (or both)
Tx: Oral therapy to sensitize insulin receptors (metformin or thiazolidinediones) and/or beta cell stimulation with sulfonylureas or non-sulfonylurea insulin sensitizers. Insulin is used only when 2 or more oral agents are maximized and glucose control still suboptimal. START WITH METFORMIN!
S/S of Type I DM
Weight loss, los of muscle mass, dehydration, pareshtesias, acetone breath, +/- mental status changes
S/S of Type II DM
Subtle: Vascular changes due to chronic hyperglycemia - nonhealing rashes, skin insult, hair loss in extremities. These changes take years to occur.
Diagnosis of DM
S/S of polyuria, polydipsia, unexplained wt. loss PLUS:
Fasting blood sugar (FBS) >126 or a random plasma glucose >200 on two separate occasions.
HbA1C >7% can also be diagnostic.
Management of DKA
Centers around isotonic fluid replacement and IV insulin at doses of 0.1u/kg/h and determining precipitating event.
Typical fluid deficit is 4-5 L upon presentation!
Most common complication of DM
Nocturnal hypoglycemia develops, stimulating a surge of counterregulatory hormones that raise blood sugar, resulting in elevated early morning glucose levels.
Pt. is hypoglycemic at 3am and rebounds wtih elevated blood sugar at 7am.
Tx: reduce or omit the bedtime dose of insulin
Decreased sensitivity to insulin occurs nocturnally owing to the presence of growth hormone, which spikes at night. Blood sugar becomes progressively elevated throughout the night, resulting in elevated sugars at 7am.
Tx: Add or increase the bedtime dose of insulin
Type II oral agents that cause hypoglycemia
Sulfonylureas (glyburide, glipizide, etc) - insulin stimulator
Repaglinide (Prandin) - insulin stimulator
Nateglinide (Starlix) - insulin stimulator
Pramlintide (Symlin) - High risk for hypoglycemia Must be on strict carb intake per day.
Exenatide (Byetta) - *may exacerbate hypoglycemia when administered with insulin or insulin stimulators* Causes N/V
Type II oral agents that do NOT cause hypoglycemia
Biguanides (Metformin) - insulin sensitizer. Do NOT give if creat >1.5. Causes renal failure.
Alpha-glucosidase inhibitors - work in the gut to present the breakdown on glucose so it is not absorbed in your blood. Cause BAD GI side effects.
Thiazolidinediones - insulin sensitizer. Liver and heart SE.
Sitagliptin (Januvia) - people on this drug feel like they have an URI
Insulin stimulators that can cause hypoglycemia
Include: Chlorpropamide, Glyburide, glucotrol, glypizide, glimepiride, tolazamide, tolbutamide
Less effective after >5 years of T2DM, older adults, or presence of severe hyperglycemia
Insulin sitmulators with a more rapid onset. Can cause hypoglycemia.
Include: repaglinide (Prandin) and nateglinide (Starlix)
Take Medication 1-30 minutes prior to meal
Caution in hepatic or renal impairement
Can cause hypoglycemia if used with insulin or insulin stimulators.
Slows gastric emptying, leading to appetite suppression and weight loss
Major adverse effect: N/V, pancreatitis
Contraindicated in gastroparesis
Include: Metformin. Do NOT use of creat >1.5 or GFR
Take with first bite of meal
Work in the gut to block glucose metabolism. Can cause severe GI effects such as diarrhea, flatulence.
Include: Acarbose (Precose) and Miglitol (Glyset)
SE: diarrhea, increased flatus
Avoid in IBD and impaired renal function
Insulin sensitizers that can cause heart and/or liver failure!
Include: rosiglitazone (Avandia) and pioglitazone (Actos)
Do not use with nitrates or insulin
Pioglitazone has increased risk of bladder cancer
Dipeptidyl peptidase-4 (DPP-4)
Inhibits idpeptidyl peptidase-4. Increases insulin synthesis/release, decreases glucagon levels.
Causes pts. to feel as though they have a URI with rhinitis, HA, etc.
Can develop pancreatitis
Results from anti-thyroid antibodies (anti-TPO) blocking TSH receptors.
Have increased TSH and decreased T4.
Hashimotos is another name for this; most common thyroid disorder
Result of autoantibodies (thyroid stimulating immunoglobulins - TSI) acting like TSH and stimulating TSH receptors.
Have decreased TSH and increased T4. Will have very low or undetectable TSH levels.
Graves disease is another name for this.
Sets the rate of gene transcription and metabolism. Excessess and deficiencies of this hormone will manifest in all body systems as a generalized "slow down" or "speed up".
The most sensitive diagnostic marker of thyroid state
A glucocorticoid that suppresses inflammation, maintains vascular tone, mobilizes glucose (and other fuel sources), promotes free water clearance
A mineralocorticoid that increases renal reabsorption of sodium, subsequent water reabsorption
Adrenal excess of cortisol, aldosterone, and androgens.
S/S: fatigue, central obesity, muscle wasting, poor wound healing, purple striae, HTN, hirsutism
Lab triad: hypokalemia, hyperglycemia, leukocytosis
Tx: remove the source of excess or manage manifestations
Adrenal deficiency. The whole gland is affected sot he pt. is deficient in cortisol, aldosterone, and androgens.
S/S: fatigue, hypotension, hyperpigmentation, arthraligias
Triad of findings: hyponatremia, hyperkalemia, and hypotension
TxL replace the deficient hormone, cortisol alone typically adequate, some cases may need addition of aldosterone.
The most common cause of Addison's disease
Autoimmune destruction of the adrenal gland
A condition characterized by a hormone producing tumor of the adrenal medulla
Lab: increased urinary metanephrines and VMA. Need a 24 hour urine to assess for the byproducts of excess catecholamines.
Tx: centers around controlling CV status with alpha blockers and removing the tumor if possible.
A condition of insufficient anti-diuretic hormone or decreased renal sensitivity to exisiting ADH
Labs: serum hypernatremia and hyperosmolality; urine hypoosmolality and hyponatremia
A condition characterized by excess ADH production. Nephron conserves too much water.
Labs: serum hyponatremia and hypoosmolality; urine hyperosmolality and hypernatremia.
Tx: free water restriction; give loop diuretic and 3% saline when neuro symptoms are present secondary to extreme hyponatremia.
Cardinal symptom of osteoporosis
The most appropriate intervention for acute Addisonian crisis
Hydrocortisone and normal saline solution
ADDisons = ADD cortisone
Approximates glycemic control for the preceding 2-3 week period.
Use this measure when you cannot use HbA1C in situations such as with hemoglobinopathies like sickle cell.
Most common reason for pts. not to convert from an arrhythmia
Which lipoprotein is elevated in the presence of DM
VLDL (almost totally triglycerides)
How does immobility affect urine output in the otherwise healthy young adult
Increase followed by decrease
For the first 4-5 days, there is a natural diuresis followed by fluid shifts and a decrease in urine output.
Treatment of choice for pts. with osteoporosis
Bisphosphonates (Fosamx, Actonel, etc)
Calcium and Vit. D are preventative, not treatment
Evaluates bony demineralization
All people over 65
All women over 60 with risk factors
Men >65 with low testosterone levels
Men >55 with pathologic fractures
Two most common causes of hypercalcemia
Malignancy and hyperparathyroidism