18. Endocrine Disease Flashcards

1
Q

T4 assay

A

T4 assay (thyroxine test) is elevated in 90% of patients with hyperthyroidism and depressed in 85% of patients with hypothyroidism

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2
Q

T3 test

A

Checks for levels of triiodothyronine and abnormally high level usually indicates Graves’ disease.

T3 is used to detect hyperthyroidism if T4 is measured to be normal, as T3 may be the only hormone in excess.

T3 can be low due to various factors that impair conversion of T4 to T3 (euthyroid sick syndrome)

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3
Q

Gold standard for diagnosis and treatment of thyroid dysfunction and useful in detecting hypothyroidism

A

TSH test

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4
Q

Normal TSH level

A

0.4 to 4.0 mIU/L

In primary hypothyroidism, levels are greater than 20 mIU/L.

During treatment of hypothyroidism, goal of thyroid replacement therapy is to normalize TSH levels.

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5
Q

What is hyperthyroidism

A

Hyperthyroidism is a condition in which the thyroid gland is overactive and exposes the body tissues to excessive amounts of thyroid hormone.

Etiology: multinodular diffuse goiter and Graves’ disease

Manifestations: warm skin, sweating, increased ventricular contractility, tachycardia, elevated systolic BP, weight loss, diarrhea, palpitations, emotional lability, skeletal muscle weakness, restlessness, heat intolerance.

Graves’ disease patients might exhibit exophthalmos from increased volume of retro-orbital fat

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6
Q

What is Graves’ disease?

A

Autoimmune condition which results in hyperstimulation of TSH receptors from autoantibodies produced by the immune system. Most common cause of hyperthyroidism.

Goiters, exophthalmos, and pretipial myxedema.

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7
Q

How is Graves’ disease treated?

A

Antithyroid drugs (reduce production of thyroid hormone)

Other modalities include radioiodine therapy and thyroidectomy.

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8
Q

What is Plummer’s disease?

A

Toxic multinodular goiter

Thyroid contains autonomously functioning thyroid nodules with resulting hyperthyroidism.

Does NOT cause exophthalmos and pretibial myxedema seen in Graves’

Propranolol, radioiodine therapy, thyroidectomy.

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9
Q

What is Thyroid Storm?

A

Acute exacerbation of hyperthyroidism that is life threatening, and occurs most commonly in undiagnosed or undertreated hyperthyroid patient.
- Triggers = stress of surgery, non-thyroid illness
- Hypermetabolic state caused by excessive release of thyroid hormones
- Dysrhythmias, myocardial ischemia, congestive heart failure, hyperthermia, shaking, change in consciousness, nausea, vomiting, diarrhea, and tachycardia. Heart failure and pulmonary edema can rapidly occur and cause death.
- Early sign = very elevated systolic pressure and low diastolic pressure.

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9
Q

Antithyroid drugs

A

Propylthiouracil
Methimazole

Prevent production of T4 and conversion of T3 from T4

Propranolol can also be used to control symptoms of sympathetic activation (palpitations, trembling, anxiety).

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10
Q

How is thyroid storm treated?

A

Less severe: supportive measures such as cooling blankets, IV fluids, electrolyte correction, EKG monitoring, oxygen supplementation, and medicine to manage agitation.

Severe: further medication with sodium iodide (blocks release of stored thyroid hormone), propylthiouracil, hydrocortisone (prevents conversion of T4 to T3) and propranolol.

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11
Q

Patient management with hyperthyroidism

A

Have patient reach euthyroid state and resting HR <85bpm prior to surgery with normal thyroid function tests.

  • Emergency surgeries - beta blocker (propranolol), glucocorticoids (decrease hormone release and reduce peripheral conversion of T4 to T3
  • Avoid sympathomimetic agents such as ketamine, epinephrine, atropine, ephedrine
  • Monitor EKG
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12
Q

What is hypothyroidism?

A

Hypothyroidism (also known as myxedema) is a common condition where the thyroid gland has decreased production of thyroid hormone resulting in inadequate circulating levels of T4 or T3 or both. Disease development can be insidious and patients often have no or only mild symptoms, making diagnosis difficult.

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13
Q

Signs and symptoms of hypothyroidism

A

Generalized reduction in metabolic activity, cardiac and respiratory depression, fatigue, slow mental functioning, hyponatremia, constipation, cold intolerance, slow movement, depression, constipation, thinning of the hair, hair loss, weight gain, thickened tongue, thyroid nodule, periorbital edema, bradycardia.

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14
Q

Primary vs. secondary hypothyroidism

A

Primary: thyroiditis (Hashimoto’s disease), medications (iodine, propylthiouracil, methimazole), iodine deficiency, irradiation to neck, hereditary defects in biosynthesis, previous treatment with radioactive iodine, previous thyroidectomy).

Secondary: hypothalamic or pituitary disease

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15
Q

Lab values in Hashimoto’s thyroiditis (T3, T4, TSH)

A

Low T4 and T3
High TSH
Presence of antibodies against thyroid peroxidase (TPO)

Normal level of TSH reliably excludes hypothyroidism

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16
Q

What is myxedema?

A

A state of decompensated hypothyroidism characterized by hypoglycemia, hypercapnia, hypoventilation, hypotension, susceptibility to cardiac dysrhythmias, hypothermia, stupor or coma, delirium, hyponatremia.

Treated with IV T4 or T3, glucocorticoid therapy, airway management, supportive measures.

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17
Q

What is Diabetes Mellitus?

A

DM is a metabolic disorder which results in a defect in insulin secretion, action, or both, resulting in hyperglycemia.

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18
Q

What is Type I diabetes?

A

Type I diabetes mellitus (insulin-dependent diabetes mellitus) is due to impaired production of insulin and occurs early in life.
- Loss of insulin-producing beta cells of the islet of Langerhans in the pancreas due to an autoimmune process and results in low level of circulating insulin.

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19
Q

What is type 2 diabetes mellitus

A

Occurs due to an altered number and affinity of peripheral insulin receptors and generally occurs later in life. May also have features of reduced insulin secretion.
- Etiology primarily lifestyle factors and genetics.

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20
Q

Function of insulin

A

Increase glycogen synthesis, decrease gluconeogenesis, increase potassium uptake, and increase lipid synthesis.
- Elicits a drastic increase in uptake of glucose by cells, especially in skeletal muscle cells.

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21
Q

Diagnostic criteria for DM

A

Fasting glucose >126 mg/dL on 2 or more occasions

Glucose tolerance test (ratings greater than 200mg/dL 2 hours after 75gram glucose load)

HgB A1C of 6.5 or greater

Non-fasting plasma glucose >200mg/dL and symptoms of DM

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22
Q

DM sequelae

A

Peripheral neuropathy
Coronary disease at young age
Silent ischemic episodes due to myocardial neuropathy
Diabetic nephropathy
Diabetic retinopathy
Ischemic heart disease due to glycosylation of LDLs
Diabetic cheiroarthropathy (limited joint mobility of hands).

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23
Q

What is insulin?

Types

A

Insulin promotes the uptake of glucose into muscle, adipose, and liver tissue.
- Fast acting (lispro, aspart)
- Short acting (regular)
- Intermediate acting (NPH, lente)
- Prolonged acting (Glargine, levemir)

  • Combined insulin treatment = Novolog (70% aspart protamine and 30% aspart) and Humolog (75% lispro protamine and 25% lispro)
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24
Q

List some oral hypoglycemics

A
  • Biguanides (Metformin)
  • Sulfonylureas (Glipizide, Glyburide)
  • Thiazolidinediones (Rosiglitazone, Pioglitazone)
  • Meglitinides (Repaglinide)
  • GLP1 agonist (Exantide/Byetta)
  • DPP4 inhibitor (Sitagliptin/Januvia)
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25
Q

How do biguanides (Metformin) work?

A

Biguanides (Metformin): decrease hepatic gluconeogenesis and decrease intestinal glucose absorption. Risk of lactic acidosis in setting of renal insufficiency with usage.

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26
Q

How do sulfonylureas (Glipizide, Glyburide) work?

A

Stimulate beta cells to produce insulin (risk of hypoglycemia with usage)

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27
Q

How do thiazolidinediones work? (Rosiglitazone, Pioglitazone)

A

Work intracellularly to promote insulin sensitivity in adipose, hepatic, and muscle tissue. Also decrease triglycerides and increase HDL. Weight gain is a side effect.

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28
Q

What is diabetic ketoacidosis?

A

DKA is a metabolic condition that occurs secondary to an insulin shortage that results in hyperglycemia, ketonemia, and an anion gap metabolic acidosis.

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29
Q

Signs/symptoms of DKA

A

Vomiting, confusion, polydipsia, polyuria, dehydration, abdominal pain, Kussmaul breathing, hyperglycemia, hyperkalemia, ketotic “fruity” breath, dry mucous membranes, and hypotension

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30
Q

Triggers of DKA

A

CVA, MI, infection (UTI, gastroenteritis, pneumonia), stress, cocaine usage, inadequate insulin administration.

31
Q

Treatment of DKA

A

Fluid rehydration, insulin
Management of hyperkalemia (remember total body potassium may be low with GI losses)
Bicarbonate for treatment of metabolic acidosis.
Identification and treatment of underlying cause

32
Q

Optimal glycemic goals post-prandial (1-2 hours after a meal)

A

120-200mg/dl

33
Q

Why are diabetics more susceptible to infections?

A

Impaired chemotaxis and phagocytosis by monocytes and neutrophils.

34
Q

Which oral hypoglycemics should be held on the day of surgery?

A

Sulfonylureas (hypoglycemia and increased risk of perioperative myocardial ischemia)
Meglitinides
Metformin (associated with lactic acidosis in setting of hypotension, poor perfusion, or hypoxia)

Note that thiazolidediones can be continued due to low risk of hypoglycemia.

35
Q

What does the adrenal cortex synthesize?

A

Three groups of hormones:
- Glucocorticoids (cortisol)
- Mineralocorticoids (aldosterone and 11-deoxycorticosterone)
- Androgens (dehydroepiandrosterone)

36
Q

What does the adrenal medulla produce?

A

norepinephrine
epinephrine

37
Q

____ from the hypothalamus controls the pituitary hormone ____, which in turn manages the secretion of cortisol

A

Corticotropin Releasing Factor (CRF) from the hypothalamus controls the pituitary hormone Adrenocorticotropic Hormone (ACTH), which in tern manages the secretion of cortisol.

38
Q

What is Cushing’s Syndrome

A

Cushing’s syndrome is a disease of excessive free plasma glucocorticoids.

39
Q

How does Cushing’s syndrome occur?

A

Chronic use of glucocorticoid products such as prednisone, dexamethasone, and prednisolone or from increased endogenous production.

Iatrogenic means from chronic steroid use is most common, while endogenous Cushing’s syndrome is a rare disease

40
Q

Endogenous Cushing’s Syndrome causes

A

ACTH independent (primary adrenal) or ACTH dependent (pituitary or ectopic).

  • ACTH-dependent = pituitary tumor, which produces excess ACTH, which causes increased production of cortisol.

Also ectopic cancers such as medullary thyroid cancer, lung cancer, pheochromocytomas, and pancreatic islet tumors

41
Q

Signs and symptoms of Cushing’s syndrome

A

Buffalo hump, weight gain, truncal obesity, plethora, striae, cognitive dysfunction, depression, proximal muscle weakness, osteopenia, hyperglycemia, hypertension

42
Q

How is Cushing syndrome diagnosed?

A
  • Blood cortisol levels
  • 24-hour urine free cortisol levels
  • Dexamethasone suppression test
  • ACTH level

(Goal is focused on locating an etiology for the many causes of Cushing’s syndrome)

43
Q

What is PRIMARY adrenal insufficiency?

A

A rare entity resulting in a decrease of production of glucocorticoids and mineralocorticoid secretion. Caused by anatomic destruction of the gland from various causes, such as tuberculosis or fungal infection. Autoimmune adrenal destruction is responsible for 80% of the cases (Addison’s disease)

44
Q

What is SECONDARY adrenal insufficiency?

A

Due to decrease or loss of glucocorticoid secretion only. Suppression of the hypothalamic-pituitary axis by exogenous steroids or endogenous steroids (e.g. tumor). Administration of high doses of glucocorticoids is the most common cause.

45
Q

What is Addison’s disease?

A

Addison disease is a disorder of insufficient adrenocortical synthesis and secretion of glucocorticoids and mineralocorticoids.

46
Q

Addison’s disease signs/symptoms

A

Weakness, anorexia, arthralgia, abdominal pain, hyperpigmentation, hypotension, and disruption of electrolytes (hyponatremia and hyperkalemia)

47
Q

Diagnosis of Addison’s Disease

A

When low morning cortisol levels are detected, a corticotropin stimulation test may be performed. If morning levels are less than 3 mcg/dL, no further testing is required.

48
Q

What is Adrenal crisis?

A

A life threatening physiological state, brought about by major physical stress.
- Severe circulatory collapse, hypotension not responsive to vasopressors.
- Fever, lethargy, flank or abdominal pain, tachycardia, delirium, coma

49
Q

Perioperative glucocorticoid regimen for secondary adrenal insufficiency

A
  • Minor (dentoalveolar) - usual dose of intraoperative steroids. No taper.
  • Moderate (orthognathic) - hydrocortisone 50mg or equivalent preoperatively. Continue 25mg hydrocortisone Q8H for 24 hours, then resume regular dosage.

-Major (free flap) - hydrocortisone 100mg or equivalent preoperatively. Hydrocortisone 50mg Q8H for 24 hours, then taper by half each day to usual dosage.

50
Q

What is the purpose of the parathyroid glands?

A

Produce parathyroid hormone (PTH) in response to circulating calcium levels in the bloodstream.

  • As calcium levels decrease, PTH increases and vice-versa. (CALCIUM HOMEOSTASIS).
51
Q

Where does PTH act?

A

GI system (uptake Ca)
Renal system (retain calcium)
Bone (osteoclastic activity to release calcium)

52
Q

Hyperparathyroidism primary and secondary causes

Maxillofacial manifestations

A

Primary hyperparathyroidism: adenoma or enlargement of one of the four parathyroid glands (overproduction of PTH).

Secondary hyperparathyroidism: hypocalcemia due to other systemic effects leading to release of excess PTH

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

53
Q

Causes of hypoparathyroidism

Dental, neurologic, and muscular manifestations

A

Surgically removed parathyroid glands, irradiated parathyroid glands, autoimmune process, hereditary, hyper-hypomagnesium

DiGeorge’s Syndrome is associated with hypoplasia or aplasia of the parathyroid glands.

Dentition: enamel hypoplasia, malformed roots, missing teeth.

Neurologic: paresthesia of lips and/or tongue

Muscular: facial muscle spasms, muscles of mastication spasms.

54
Q

Hypercalcemia causes

A

HYPERCALCEMIA
- Hyperparathyroidism (most common)
- Medications
- Vitamin supplements
- Cancer
- TB, pneumonia, sarcoidosis

55
Q

Hypercalcemia consequences (CNS, Renal, Musculoskeletal)

A

HYPERCALCEMIA
- CNS: lethargy, fatigue, confusion, seizure, coma
- Renal: increased urination, thirst, nephrolithiasis, renal insufficiency
- Musculoskeletal: decreased strength, osteoporosis (calcium sequestered from bone)
- GI: nausea, vomiting, abdominal pain
- Cardiac: arrhythmia (short QT)

56
Q

Hypocalcemia causes

A

HYPOCALCEMIA
- Hypoparathyroidism (most common)
- GI malabsorption
- Hypophosphatemia
- Magnesium levels
- Vitamin D depletion
- Medications

57
Q

Hypocalcemia consequences

A

HYPOCALCEMIA
- Neuromuscular: paresthesia, muscle spasm
- CNS: seizures, dementia
- Derm: coarse skin, brittle nails, hair loss
- Skeletal: osteoporosis (not enough calcium to be sequestered by the bone)
- Cardiac: arrhythmia (long QT)

58
Q

Effective, objective tool for assessing patient compliance and long-term hyperglycemic status

A

Measurement of glycosylated hemoglobin (HbA1C) level.

Prolonged elevation of serum blood glucose causes non-enzymatic irreversible glycosylation of hemoglobin in red blood cells.

Gives an estimate of glycemic control in the past 90-120 days.

HbA1C > 6% is consistent with diabetes
HbA1C > 7% is indicative of poor glycemic control

59
Q

Sulfonylureas (glipizide, glyburide)
Meglitinides (repaglinide, nateglinide)

MOA

A

Stimulate production of insulin by pancreas

60
Q

Glucophage (metformin, biguanides)

MOA

A

Decrease hepatic glucose production by inhibiting gluconeogenesis and glycogenolysis

61
Q

Thiazolidinediones (pioglitazone, rosiglitazone)

MOA

A

Stimulate target cells’ response to insulin

62
Q

Glucagon-like peptide (GLP-1) agonists (exenatide, liraglutide)

MOA

A

Stimulate glucose-dependent insulin secretion, decrease glucagon secretion, slow gastric motility, induce early satiety

63
Q

How does HbA1C guide therapy in type 2 DM?

A

HbA1C 6.5-7.5: monotherapy
HbA1C 7.5-9: dual therapy
HbA1C >9 with symptoms: insulin. Asymptomatic could be treated with triple therapy

64
Q

Rapid acting insulin

A

Lispro (Humalog), glulisine, aspart insulin

65
Q

Short acting insulin

A

regular insulin (Humulin R, Novolin R)

66
Q

Intermediate acting insulin

A

NPH (Humulin N, Novolin N)

67
Q

Long acting insulin

A

Glargine (Lantus), insulin detemir

68
Q

Acute complications of DM

A

Diabetic ketoacidosis
Nonketotic hyperosmolar syndrome
Hypoglycemia

69
Q

Chronic complications of DM

A

Long-term effects of hyperglycemia on vasculature
- Microvascular retinopathy, nephropathy, neuropathy
- Macrovascular disease (accelerated atherosclerosis, CAD, MI, PVD)

70
Q

Treatment of hypoglycemia

A
  • Awake: oral glucose administration
  • Unconscious w/ IV: dextrose in water (D10W or D50W)
  • Unconscious w/o IV: 1mg glucagon IM/SC
71
Q

Diabetes is diagnosed when fasting blood glucose levels exceed ____mg/dl, a random blood glucose level is greater than ____mg/dl, or when HbA1C is ____% or higher

A

126mg/dl
200mg/dl
6.5%

72
Q

Metabolic syndrome = 3 of the following conditions

A

Elevated triglycerides
Low high-density lipoprotein
Abdominal obesity
Fasting glucose level 100mg/dl or higher
HTN

73
Q

Treatment of DKA

A

IV fluid: start with normal saline and subsequently switch to D51/2NS to address dehydration and decrease plasma glucose level by dilution.

Any indication of cardiac instability (peaked T waves, widened QRS complexes, PVCs) due to hyperkalemia should be treated first with calcium gluconate. This is followed by IV insulin drip to gradually decrease serum glucose and osmolarity (rapid decrease in osmolarity = cerebral edema).

Glucose decreased at 100mg/dl per hour

Monitor urine output.
Monitor serum potassium (may precipitously decrease requiring supplementation)
Replenish magnesium and phosphate as needed.
Bicarbonate rarely recommended for acidosis (high risk for cerebral edema) and is reserved for pH below 7.0.

74
Q

DKA vs. nonketotic hyperglycemia

A

DKA: metabolic acidosis and blood glucose level below 500 mg/dl

Nonketotic hyperglycemia coma: blood glucose above 1,000 mg/dl with no acidosis.

75
Q

Most common cause of DKA

A

infection

76
Q

What is HHS

A

Hyperosmolar hyperglycemic syndrome
- Less insidious onset than DKA
- Begins with mild hyperglycemia compensated by glycosuria
- Hyperglycemia worsens, osmotic diuresis wastes more glucose through urine
- If patient maintains adequate hydration, kidneys continue to excrete excess glucose
- Patient becomes confused/incapacitated, oral hydration decreases, kidneys’ ability to excrete glucose is diminished, exacerbating hyperglycemia and causing mental status changes.