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Oral Board Review Textbook > Medicine (Endocrine Disease) > Flashcards

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
Q

What is DKA?

A

-Metabolic condition secondary to insulin shortage.
-Hyperglycemia, ketonemia, and anion gap metabolic acidosis

26
Q

How is DKA treated?

A

-Fluid rehydration
-Insulin gtt
-Manage hyperkalemia
-Bicarb

27
Q

Why are diabetic patients more susceptible to post-op infections?

A

-Impaired chemotaxis and phagocytosis by monocytes and neutrophils

28
Q

What is the function of the adrenal gland?

A

-Produces glucocorticoids, mineralcorticoids and androgens
-Produces norepinephrine and epinephrine

29
Q

What is Cushing’s syndrome?

A

-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
Q

What is Addison’s Disease?

A

-Disorder of insufficient adrenocortical synthesis and secretion of glucocorticoids and mineralcorticoids
-Weakness, anorexia, arthralgia, hyperpigmentation, hypotension, hyponatremia/hyperkalemia

31
Q

What is your patient management of Addison’s disease?

A

-Pre-op antibiotics
-Discuss with patient’s endocrinologist regarding stress dose of steroids to avoid adrenal crisis
-Check serum potassium pre-op

32
Q

What is your patient management of Cushing’s syndrome?

A

-Concern for obesity (OSA, GERD)
-Concern for glucose intolerance (may need sliding scale glycemic control)
-Frail patient (osteoporosis)

33
Q

What is adrenal crisis?

A

-A life threatening physiologic state brought about by major physical stress
-Severe circulatory collapse and hypotension not responsive to vasopressors

34
Q

What are the causes of hyperparathyroidism?

A

-Primary: Adenoma or enlargement of the parathyroid gland
-Secondary: Hypocalcemia leading to excessive PTH

35
Q

What are maxillofacial manifestations of hyperparathyroidism?

A

-Browns tumor (giant cell lesion)
-Loose teeth, altered eruption, root malformation
-Sialolithiasis

36
Q

What are the causes of hypoparathyroidism?

A

-Surgically removed parathyroid gland, autoimmune process, DiGeorge’s syndrome

37
Q

What are the manifestations of hypoparathyroidism?

A

-Enamel hypoplasia, malformed roots, missing teeth, paraesthesia of lip/tongue, muscle spasms

38
Q

What happens with hypercalcemia/hypocalcemia (cardiac)?

A

Hypercalcemia: Short QT

Hypocalcemia: Long QT

Oral Board Review Textbook (26 decks)

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