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ACNP REVIEW > endocrine > Flashcards

endocrine Flashcards

1
Q

Type I DM

A

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.

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2
Q

Type II DM

A

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!

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3
Q

S/S of Type I DM

A

Weight loss, los of muscle mass, dehydration, pareshtesias, acetone breath, +/- mental status changes

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4
Q

S/S of Type II DM

A

Subtle: Vascular changes due to chronic hyperglycemia - nonhealing rashes, skin insult, hair loss in extremities. These changes take years to occur.

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5
Q

Diagnosis of DM

A

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.

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6
Q

Management of DKA

A

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!

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7
Q

Most common complication of DM

A

Neuropathy

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8
Q

Somogyi effect

A

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

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9
Q

Dawn phenomenon

A

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

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10
Q

Type II oral agents that cause hypoglycemia

A

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

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11
Q

Type II oral agents that do NOT cause hypoglycemia

A

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

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12
Q

Sulfonylureas

A

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

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13
Q

Non-sulfonylureas (Meglitinides)

A

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

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14
Q

GLP-1 agonist

Exenatide (Byetta)

A

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

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15
Q

Biguanides

A

Insulin sensitizers

Include: Metformin. Do NOT use of creat >1.5 or GFR

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16
Q

Alpha-glucosidase inhibitors

A

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

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17
Q

Thiazolidinediones (TZD)

A

Insulin sensitizers that can cause heart and/or liver failure!

Include: rosiglitazone (Avandia) and pioglitazone (Actos)

Monitor ALT

Do not use with nitrates or insulin

Pioglitazone has increased risk of bladder cancer

18
Q

Dipeptidyl peptidase-4 (DPP-4)

Sitagliptin (Januvia)

A

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

19
Q

Hypothyroidism

A

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

20
Q

Hyperthyroidism

A

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.

21
Q

Thyroid hormone

A

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”.

22
Q

The most sensitive diagnostic marker of thyroid state

A

TSH level

23
Q

Cortisol

A

A glucocorticoid that suppresses inflammation, maintains vascular tone, mobilizes glucose (and other fuel sources), promotes free water clearance

24
Q

Aldosterone

A

A mineralocorticoid that increases renal reabsorption of sodium, subsequent water reabsorption

25
Q

Cushings syndrome

A

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

26
Q

Addison disease

A

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.

27
Q

The most common cause of Addison’s disease

A

Autoimmune destruction of the adrenal gland

28
Q

Pheochromocytoma

A

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.

29
Q

Diabetes Insipidus

A

A condition of insufficient anti-diuretic hormone or decreased renal sensitivity to exisiting ADH

Labs: serum hypernatremia and hyperosmolality; urine hypoosmolality and hyponatremia

30
Q

SIADH

A

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.

31
Q

Cardinal symptom of osteoporosis

A

fracture

32
Q

The most appropriate intervention for acute Addisonian crisis

A

Hydrocortisone and normal saline solution

ADDisons = ADD cortisone

33
Q

Serum fructosamine

A

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.

34
Q

Most common reason for pts. not to convert from an arrhythmia

A

hypokalemia

35
Q

Which lipoprotein is elevated in the presence of DM

A

VLDL (almost totally triglycerides)

36
Q

How does immobility affect urine output in the otherwise healthy young adult

A

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.

37
Q

Treatment of choice for pts. with osteoporosis

A

Bisphosphonates (Fosamx, Actonel, etc)

Calcium and Vit. D are preventative, not treatment

38
Q

DEXA scan

A 
Evaluates bony demineralization
Indicated for:
All people over 65
All women over 60 with risk factors
Men >65 with low testosterone levels
Men >55 with pathologic fractures
39
Q

Two most common causes of hypercalcemia

A

Malignancy and hyperparathyroidism

40
Q

Sodium glucose cotransporter-2 (SGLT2)

A

-gliflozin
Canagliflozin, dapagliflozin, empagliflozin

increases the amount of glucose excreted in urine

Can help with weight loss

SE: genital mycotic infection, UTI, increased urination

Can be used as add on with metformin, sulfonylurea, others

ACNP REVIEW (32 decks)

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