Medicine (Endocrine Disease) Flashcards

1
Q

What are the two thyroid hormones, which is more active?

A

-T3 and T4
-T3 more active (T4 converts to T3 in liver/kidney)
-T3 must be in unbound form to be active

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2
Q

What is hyperthyroidism?

A

-A condition in which the thyroid gland is overactive, excessive amounts of thyroid hormone exposed to body tissues

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3
Q

What is the most common etiologies of hyperthyroidism?

A

-Graves disease
-Multinodular diffuse goiter

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4
Q

How does hyperparathyroidism present?

A

-Warm skin
-Sweating
-Tachycardia
-Palpitations
-Exophthalmos
-Heat intolerance

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5
Q

What is Graves disease?

A

-Autoimmune condition which results in hyperstimulation of TSH receptors

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6
Q

What is thyroid storm?

A

-Acute exacerbation of hyperthyroidism that is life threatening
-Patient induced into a hypermetabolic state caused by excessive release of thyroid hormones (dysrhythmias, MI, CHF, hyperthermia, high systolic/low diastolic pressure)
-Can be caused from surgical stress or illness
-Treat with supportive measures (cooling blanket, IV fluid, electrolyte correction), propranolol, sodium iodide

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7
Q

What is your patient management for hyperthyroidism patients.

A

-Consult with endocrinologist for optimization (ideally euthyroid state)
-Avoid ketamine, epinephrine, atropine, ephedrine
-Takes 8 weeks for anti-hyperthyroidism medications to take effect

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8
Q

What is hypothyroidism?

A

-Condition where thyroid gland has decreased production (myxedema)

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9
Q

What are the symptoms of hypothyroidism?

A

-Reduced metabolic activity, cold intolerance, weight gain

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10
Q

What are etiologies of hypothyroidism?

A

-Primary: Hashimoto’s thyroiditis, iodine deficiency
-Secondary: Hypothalmic or pituitary disease

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11
Q

What is hashimoto’s thyroiditis?

A

-Most common cause of hypothyroidism, autoimmune process of destruction of the thyroid gland

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12
Q

What is myxedema?

A

-Decompensated hypothyroidism characterized by hypoglycemia, hypercapnia, hypoventilation, hypotension, delirium
-Medical emergency
-Treated with IV doses of T3, T4

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13
Q

What is the patient management for hypothyroidism?

A

-Consult with endocrinologist for euthryoid state
-Consider increasing NPO time
-More prone to hypotension
-More sensitivity to anesthetic drugs

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14
Q

What is diabetes mellitus?

A

-A metabolic disorder which results in a defect in insulin secretion, action or both resulting in hyperglycemia

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15
Q

What is type I DM?

A

-Impaired production of insulin (insulin dependent diabetes)
-Autoimmune destruction of beta islet cells in pancreas

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16
Q

What is type II DM?

A

-Altered number and affinity of peripheral insulin receptors. May have decreased secretions as well.

17
Q

What is the function of insulin?

A

-Increase uptake of glucose by cells
-Increase glycogen synthesis, decrease gluconeogenesis.

18
Q

How is DM diagnosed?

A

-Fasting glucose >126 on 2+ occasions
-HgB A1C 6.5 or greater
-Non fasting glucose >200 with symptoms
-Glucose tolerance test

19
Q

What are sequelae or DM?

A

-Peripheral neuropathy
-CAD
-Diabetic nephropathy
-Diabetic retinopathy
-

20
Q

How does insulin work and what are the types used to treat?

A

-Promotes uptake of glucose into muscle, adipose and liver tissue

-Fast acting: lispro, aspart
-Short acting: Regular
-Intermediate: NPH, lente
-Prolonged acting: Glargine, levemir

21
Q

What is metformin?

A

-Biguanide
-Decrease hepatic gluconeogenesis and decrease intestinal glucose absorption
-Risk of lactic acidosis

22
Q

What is glipizide?

A

-Sulfonylurea
-Stimulate beta cell to produce insulin
-Risk of hypoglycemia

23
Q

What is ozempic?

A

-GLP-1 agonist (exantide)
-Synthetic glucagon like peptide that stimulates insulin secretion and decreases glucagon synthesis

24
Q

What is Januvia?

A

-DPP4 inhibitor
-GLP1 works better when DPP4 is inhibited

25
What is DKA?
-Metabolic condition secondary to insulin shortage. -Hyperglycemia, ketonemia, and anion gap metabolic acidosis
26
How is DKA treated?
-Fluid rehydration -Insulin gtt -Manage hyperkalemia -Bicarb
27
Why are diabetic patients more susceptible to post-op infections?
-Impaired chemotaxis and phagocytosis by monocytes and neutrophils
28
What is the function of the adrenal gland?
-Produces glucocorticoids, mineralcorticoids and androgens -Produces norepinephrine and epinephrine
29
What is Cushing's syndrome?
-Disease of excessive free plasma glucocorticoids -Most common from chronic use of steroids -S/s: Buffalo hump, weight gain, obesity, depression, muscle weakness, osteopenia
30
What is Addison's Disease?
-Disorder of insufficient adrenocortical synthesis and secretion of glucocorticoids and mineralcorticoids -Weakness, anorexia, arthralgia, hyperpigmentation, hypotension, hyponatremia/hyperkalemia
31
What is your patient management of Addison's disease?
-Pre-op antibiotics -Discuss with patient's endocrinologist regarding stress dose of steroids to avoid adrenal crisis -Check serum potassium pre-op
32
What is your patient management of Cushing's syndrome?
-Concern for obesity (OSA, GERD) -Concern for glucose intolerance (may need sliding scale glycemic control) -Frail patient (osteoporosis)
33
What is adrenal crisis?
-A life threatening physiologic state brought about by major physical stress -Severe circulatory collapse and hypotension not responsive to vasopressors
34
What are the causes of hyperparathyroidism?
-Primary: Adenoma or enlargement of the parathyroid gland -Secondary: Hypocalcemia leading to excessive PTH
35
What are maxillofacial manifestations of hyperparathyroidism?
-Browns tumor (giant cell lesion) -Loose teeth, altered eruption, root malformation -Sialolithiasis
36
What are the causes of hypoparathyroidism?
-Surgically removed parathyroid gland, autoimmune process, DiGeorge's syndrome
37
What are the manifestations of hypoparathyroidism?
-Enamel hypoplasia, malformed roots, missing teeth, paraesthesia of lip/tongue, muscle spasms
38
What happens with hypercalcemia/hypocalcemia (cardiac)?
Hypercalcemia: Short QT Hypocalcemia: Long QT