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358 Cards in this Set
- Front
- Back
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What are 6 symptoms of endocrine disease?
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obesity
unintended weight loss abnormal skin pigmentation gynecomastia bone pain/pathologic fractures mental changes |
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How is obesity measured?
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BMI (weight in K/height in meters squared)
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What is normal BMI?
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18.5-24.9
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What is the etiology of obesity?
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sedentary lifestyle
excessive intake genetics 40-70% |
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How can obesity be treated?
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behavior modification
Sibutramine, Orlistat |
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How are 5 conditions that cause unintended weight loss?
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uncontrolled DM
severe diabetes insipidus hyperthyroidism pheochromocytoma Cushing's syndrome |
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What are 3 abnormal skin pigmentations?
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hyperpigmentation (excessive ACTH-->Addison's)
chloasma acanthosis nigricans |
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What causes gynecomastia?
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can be with obesity
abuse of androgens/anabolic steroids hyperprolactinemia adrenal tumors hyperthroidism |
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What are 4 conditions that cause bone pain and pathologic factors with endocrine disease?
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rickets or osetomalacia
osteogenesis imperfecta hyperparathyroidism osteoporosis |
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What can cause mental changes with endocrine disease?
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hypogonadism
PMS/PMDD hyper/hypothyroidism pheochromocytoma Cushing's syndrome |
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What are 14 prevalent endocrine disorders?
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obesity, type II DM, hyperlipidemia, thyroid disease, osteoporosis, hyperparathyroidism, infertility, PCOS, hirsutism, hyperprolactinemia, ED, gynecomastia, Klinefelter syndrome (males), Turner syndrome (females)
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What is the responsibilty of the thyroid gland?
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to control metabolism
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What in the brain controls the normal secretion of thyroid hormones (T3 and T4)?
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hypothalamus (TRH)
anterior pituitary (TSH) |
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What is hypothyroidism?
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insufficiency in the amount of thyroid hormone in the body
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What is primary hypothyroidism?
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thyroid gland failure despite proper stimulation from the pituitary
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What is secondary hypothyroidism?
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failure of the pituitary to produce TSH to stimulate the thyroid gland
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What is tertiary hypothyroidism?
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failure of the hypothalamus to produce TRH for stimulation
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What can cause hypothyroidism?
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trauma to thyroid/pituitary/hypothalamus
Dietary deficiencies Autoimmune disease Radiation exposure Severe infection Neoplasia (pituitary tumor) Drugs |
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What durgs can cause hypothyroidism?
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glucocorticoids, phenobarbital, phenytoin, salicylates (large doses), fluorouracil, androgens
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What are the early S/S of hypothyroidism?
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Fatigue, lethargy, weakness
Arthralgias, myalgias cramping Cold intolerance Dry skin and possible pruritus Brittle nails Thinning hair Poor skin turgor Headache Menorrhagia Sluggish DTRs Depression Loss of libido |
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What are the later S/S of hypothyroidism?
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Slow speech
Constipation Anemia and pallor Hoarseness Peripheral edema Infertility Impaired mentation, psychosis Hypercholesterolemia |
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What are the physical findings of hypothyroidism?
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Possible goiter
Edema of face and eyelids Loss of outer third of eyebrows Orange tone to skin Thickening of the tongue Alopecia Cardiac enlargement Bradycardia Weight gain |
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What are the diagnostic findings of hypothyroidism?
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*Increased TSH
Decreased free T4 Bradycardia on EKG Effusions on CXR possible Possible pituitary enlargement on head CT |
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How is hypothyroidism treated?
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Treat underlying cause if possible
Thyroid replacement |
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What type of thyroid hormone replacement can be used for hypothyroidism?
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Levothyroxine (Synthroid)
-increase slowly (micrograms) -monitor TSH/free T4 for 6 weeks -pregnant women and women taking estrogen may need a higher dose |
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Is Hashimoto's thyroiditis more common in men or women?
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women 15x greater than men
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What is the peak age of Hasimoto's thyroiditis?
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b/t 30 and 40
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What is the most common type of thyroiditis and hypothyroidism?
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Hashimoto's thyroiditis
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What is the pathology of Hasimoto's thyroiditis?
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-Immune mediated destruction of thyroid parenchyma
-May be associated with other autoimmune diseases |
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What are the clinical features of Hashimoto's thyroiditis?
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-euthyroid or hypothyroid
-Thyroid gland may be diffusely enlarged, firm or rubbery, usually nontender -Surface of thyroid may be irregular or nodular -Slow progression to hypothyroidism |
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What 2 diagnositic studies are used for Hashimoto's thyroiditis?
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thyroid function tests
antithyroid antibodies present |
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How is Hashimoto's thyroiditis treated?
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thyroid hormone replacement even if euthyroid if goiter present
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What is De Quervain's Thyroiditis?
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Painful Subacute Thyroditis
Enlargement/inflammation of thyroid -Self-limited disease (initial thyrotoxicosis followed by several months of hypothyroidism) |
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What is the cause of De Quervain's Thyroiditis?
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probably viral (may be preceded by URI)
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What are the clinical features of De Quervain's Thyroiditis?
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-Tender, enlarged thyroid gland (one or both lobes may be affected)
-Pain over thyroid radiating to jaw or ear -Fever, heat intolerance, sweating, malaise, and myalgias -No ophthalmopathy |
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What do the diagnostic studies show for De Quervain's Thyroiditis?
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-Lymphocytosis on CBC and elevated sed rate
-T3 and T4 may be elevated initially -Low thyroid radioiodine uptake (RAIU) |
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How is De Quervain's Thyroiditis managed?
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-Acute illness lasts 3–8 weeks-->may use beta blockers for symptoms
-ASA or NSAIDS -Thyroid hormone during 2nd stage |
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Who does painless thyroiditis (postpartum) occur in?
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women with Hashimoto's
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What are the clinical features of painless thyroiditis?
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-Thyrotoxic stage lasting 2–6 weeks followed by hypothyroid stage
-Malaise, fatigue, weight loss -Nontender thyroid enlargement |
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How is painless thyroiditis managed?
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initial stage usually mild
2nd stage: thyroid replacement |
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What does myxedema accompany?
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severe hypothyroidism
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What are the early S/S of myxedema?
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Severe Fatigue
Lethargy Weakness Constipation Very Dry Skin Headache Menorrhagia Depression |
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What are the late S/S of myxedema?
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Slow speech
Absence of diaphoresis Severe constipation Lymphedema Severe muscle aches/cramping Dyspnea Puffiness of the face pleural/pericardial effusions Hypothermia Pituitary enlargement Amenorrhea Galactorrhea Severe depression possible psychosis |
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What do the diagnostic studies for myxedema show?
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T4 low
TSH is increased Elevated serum cholesterol Elevated liver enzymes Elevated creatine kinase Increased serum prolactin Hyponatremia Hypoglycemia Anemia |
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What are the complications of myxedema?
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mostly cardiac (advanced CAD)
*↑ susceptibility to infection Megacolon Miscarriage Possible adrenal crisis Organic psychosis=Myxedema Madness |
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How is myxedema treated?
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*thyroid hormone replacement (IV then oral)
treat underlying cause treat hyperlipidemia |
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What can further occur with myxedema coma?
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multiple organ abnormalities and progressive mental retardation
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Myxedema coma is very ____, but has a ___ mortality rate.
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rare
high |
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What causes myxedema coma?
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most commonly stressful situations (trauma, surgery, burns, infection)
can occur b/c of coexisting disease states (diabetes, MI, fluid/electrolyte abnormalities) can be precipitated by certain meds. |
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Why does myxedema coma commonly result from stressful situations?
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b/c w/ any trauma/infection, body normally reacts by ↑ metabolism, but this does not happen as well with myxedema
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What are the S/S of myxedema coma?
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Severe hypothermia
Delayed DTR’s Altered sensorium ranging from stupor to coma Hypoxia, CO2 retention Severe hypoglycemia Hyponatremia Puffy face Yellowish skin discoloration Paranoid psychosis |
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How is myxedema coma treated?
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IV thyroid hormone replacement
Treat underlying infection, if present Monitor TSH Monitor glucose/sodium levels |
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What is the prognosis of myxedema coma?
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-Mortality rate of 30 – 60%
-Poor prognosis if advanced age, bradycardia and persistent hypothermia |
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What is cretinism?
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congenital hypothyroidism
-1/4000 live births -Hypoplasia or aplasia of the thyroid gland -OR failure of the gland to migrate into normal anatomic location -OR ineffective hormone due to enzyme deficiency |
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What are the clinical features of cretinism?
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Sluggishness
Pale/gray/cool/mottled skin Nonpitting myxedema Constipation Large tongue Poor muscle tone Mental retardation Dry, brittle hair |
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What do the diagnostic studies for cretinism show?
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Low T4
Elevated TSH Delayed skeletal maturation on x-rays |
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How is cretinism treated?
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thyroid hormone replacement
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How can cretinism be prevented?
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-Neonatal screening within first few days of birth
-Improved prognosis with therapy started in first 2 months of life |
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Is hyperthyroidism more common in males or females?
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females
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What is the etiology of hyperthyroidism?
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*Grave's disease (most common)
-Autoimmune caused by TSH receptor-stimulating antibodies -Toxic multinodular goiter -Solitary hyperfunctioning nodule -Exogenous thyroid hormone -Pituitary tumor secreting TSH (rare) |
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What causes Grave's disease?
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thyroid-stimulating immunoglobin
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With hyperthyroidism there is a solitary "___" nodule and an inflammatory process in the thyroid causing leakage of ___ hormones.
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hot
thyroid |
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What are the symptoms of hyperthyroidism?
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Anxiety, irritability emotional lability
Tremor Weight loss, loose stools Dyspnea and palpitations Heat intolerance increased sweating Fatigue, weakness Excessive lacrimation diplopia |
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What does the physical exam for hyperthyroidism show?
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-Appears anxious
-Skin warm, moist, smooth -Exophthalmos/lid lag(Graves disease -Fine tremor of the tongue -Hyperactive DTRs -Goiter may be present (absence of goiter does not rule out hyperthyroidism) |
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What are the characteristics of a goiter with Grave's disease?
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symmetrically enlarged gland, soft or firm, smooth, +/- tenderness
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What are the characteristics of a toxic multinodular goiter?
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asymmetric, firm and irregular, 2 or more distinct nodules
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What are the characteristics of a goiter with subacute thyroiditis?
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gland moderately enlarged, tender, asymmetric
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What are the characteristics of a goiter from a exogenous source?
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may be suggested by lack of goiter
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What do the diagnostic studies for hyperthyroidism show?
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-Increased T3 and T4
-Possibly increased thyroid-binding globulin (TBG) with high estrogen states -TSH suppressed -RAIU can be elevated or low -In Grave’s disease, TSH receptor antibodies and antimicrosomal antibodies are elevated |
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How is hyperthyroidism managed with medical therapy?
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good response with increased RAIU
-*Propylthiouracil, methimazole -Beta-blockers for symptoms -TOC in adults is radioactive iodine therapy |
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When is hyperthyroidism managed with surgical therapy?
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if not responding to medical Tx
large goiters or local symptoms from compression |
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What is a thyroid storm usually precipitated by?
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life-threatening emergency
-stress (surgery, infection, delivery, trauma) -same pathology as hyperthyroidism |
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Even though a thyroid storm is uncommon, it has a ___ mortality rate.
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high
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What are the clinical features of thyroid storm?
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Exaggerated signs and symptoms of hyperthyroidism
-High fever -Delirium -N/V -Dehydration -Tremor and anxiety -Atrial fibrillation with rapid ventricular response -Hypotension -Death |
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What do the diagnostic studies for thyroid storm show?
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Highly elevated T3 and T4
EKG may show sinus tachycardia, a-fib or flutter |
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How is thyroid storm managed?
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-Aggressive use of propylthiouracil
-Oral or IV sodium iodide (decreases thyroid hormone release) -Propranolol for symptoms -Glucocorticoids (inhibits peripheral conversion of T4 to T3 |
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T3 or T4???
We secrete more ___ than ___, but ___ is the active form so ___ has to be converted to ___. :) |
T4
T3 T3 T4 T3 |
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What must be considered in 10-15% of cases with thyroid nodules?
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cancer
-Suspect cancer if rapid growth, fixed in place with no movement on swallowing, hx of neck radiation, male sex, extremes of age |
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What are the clinical features of thyroid nodules?
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most are asymptomatic
may have hyper/hypothyroidism |
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What diagnostic studies are used for thyroid nodules?
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TSH and free T4
Fine needle aspiration/cytology Ultrasound |
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What MUST be excluded with thyroid nodules?
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malignancy
-treated with surgery followed by thyroid radioiodine ablation |
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What is the epidemiology of thyroid cancers?
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uncommon
women>men incidence increases w/ age low mortality rate |
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What is the most common type of thyroid cancer?
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papillary carcinoma
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What are the causes of thyroid cancer?
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-Radiation exposure (increased with exposure to radiation from atomic blasts)
-X-ray therapy to the neck -Genetic factors, especially medullary which has familial predisposition -Excess TSH may stimulate thyroid cancer |
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What are the S/S of thyroid cancers?
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Mass found in thyroid on exam
Possible hoarseness Possible neck pain Possible cervical LAD |
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Only ___% of palpable thyroid nodules are malignant and thyroid function test are usually ___.
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5%
normal |
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What do the diagnostic studies for thyroid cancers show?
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-Usually seen as a “cold” nodule on thyroid scan
-Ultrasound shows solid, well-formed nodule/s |
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How is thyroid cancer treated?
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surgery followed by radioiodine ablation
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With thyroid cancers, papillary is the ___ common with the ___ prognosis while anaplastic is the ___ common with the ___ prognosis.
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most
best least worst |
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What are jobs of the parathyroid glands?
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-Increases osteoclast activity in bone
-Increases reabsorption of Ca in renal tubules -Inhibits absorption of phosphate and bicarb by renal tubules -Stimulates the synthesis of 1,25-dihydroxycholecalciferol by kidneys -net effect is to increase serum Ca |
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What 2 places are the parathyroid glands hydroxylized?
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liver
kidney |
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What are the essentials of diagnosis for hypoparathyroidism?
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-Tetany, carpopedal spasms, tingling of lips and hands, muscle cramps, psychological changes
-Positive Chvostek's sign and Trousseau's phenomenon -Serum calcium low; serum phosphate high; alkaline phosphatase normal; urine calcium excretion reduced -Serum magnesium may be low |
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What is Chvostek's sign?
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tap over facial nerve (in front of tragus) and get spasm
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What is Trousseau's phenomenon?
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spasm/tetany in carpal with BP cuff
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What are the causes of hypoparathyroidism?
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-Post thyroidectomy (usually transient but may be permanent)
-Parathyroid adenoma removal -DiGeorge syndrome: congenital, rare -gland damage -Tumors; infection; or neck irradiation (rare) -Magnesium deficiency |
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What is the most common cause of hypoparathyroidism?
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post thyroidectomy
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How does parathyroid adenoma removal cause hypoparathyroidism?
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due to suppression of remaining parathyroids
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What can cause damage to the parathyroid gland?
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-Heavy metals, eg, copper (Wilson's disease), iron (hemochromatosis, transfusion hemosiderosis)
-Granulomas -Sporadic autoimmunity -Riedel's thyroiditis |
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How does magnesium deficiency cause hypoparathyroidism?
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prevents PTH secretion
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What happens with DiGeorge Syndrome?
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congenital hypoparathyroidism
-certain parts of head/neck do not develop -ex. parathyroid gland, thymus, unusual facial features, heart problems |
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What is pseudohypoparathyroidism?
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Hypocalcemia and high PTH levels due to renal resistance to PTH from mutations in PTH receptor
-genetic |
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How is pseudohypoparathyroidism characterized?
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short stature, round face, obesity, short fourth metacarpals, ectopic bone formation, and mental retardation
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What happens with autosomal dominant hypocalcemia with hypocalciuria (ADHH)?
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-Gain-of-function mutations of the calcium-sensing receptor (CaSR) gene essentially "fool" the parathyroid glands
-Hypocalcemia without elevations in serum PTH -Characterized by hypocalcemic seizures in infancy |
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What are the acute symptoms of hypoparathyroidism?
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-Tetany, with muscle cramps, irritability, carpopedal spasm, and convulsions
-Tingling of circumoral area, hands, and feet |
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What are the chronic symptoms of hypoparathyroidism?
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Lethargy
Personality changes Anxiety Blurred vision due to cataracts Parkinsonism Mental retardation *some symptoms not reversible |
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What are the signs of hypoparathyroidism?
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Chvostek’s sign positive
Trousseau’s phenomenon Thin and brittle nails Presence of cataracts Dry, scaly skin +/- candidiasis Loss of eyebrows Hyperactive DTR’s |
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What is included in the differential diagnosis for hypoparathyroidism?
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*Pseudohypoparathyroidism
*Vitamin D deficiency -Acute pancreatitis -Chronic renal failure -Hypoalbuminemia -Paresthesias or tetany due to respiratory alkalosis *Familial hypocalcemia with hypercalciuria (normal serum PTH) *Hypomagnesemia |
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What is serum calcium bound to?
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albumin
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What do the laboratory tests for hypoparathyroidism show?
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Low serum calcium
Serum phosphate high Alkaline phosphatase normal Urinary calcium low PTH level low Hypomagnesemia frequently accompanies hypocalcemia and may decrease parathyroid gland function |
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What do the imaging studies for hypoparathyroidism show?
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-Skull x-rays or head CT may show basal ganglia calcifications
-X-rays may show increased bone density or cutaneous calcifications |
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What diagnostic procedures are used for hypoparathyroidism?
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-Slit-lamp examination may show early cataract formation
-EKG shows prolonged QT interval and T-wave abnormalities |
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What is the emergency Tx for acute tetany associated with hypoparathyroidism?
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*ensure adequate airway (laryngospasm)
-Ca gluconae (IV slowly until tetany ceases) -oral Ca -vitamin D -MgSO4 IV for hypomagnesemia (immediately) |
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What is the maintenance Tx of hypoparathyroidism?
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-Ca supplement (maintain slightly low to minimize hypercalciuria)
-vitamin D supplement -titrated Calcitrol (for chronic hypocalcemia) -avoid phenothiazines -avoid Furosemide (Lasix) |
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What type of surgery can be done for hypoparathyroidism?
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Transplantation of cryopreserved parathyroid tissue from prior surgery restores normocalcemia in ~23%
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What is the follow-up for hypoparathyroidism?
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-Monitor serum Ca at least every 3 months; keep serum Ca slightly low
-Monitor "spot" urine Ca to keep level < 30 mg/dL if possible -Hypercalciuria may respond to oral hydrochlorothiazide, usually given with a K+ supplement |
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What are the complications for hypoparathyroidism?
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-stridor (vocal cord palsy-->respiratory obstruction)
-Chronic hypoparathyroidism may be associated with autoimmune diseases -Cataract formation and calcification of the basal ganglia occur in long-standing cases; parkinsonism or choreoathetosis occasionally develops -Nerve root compression due to ossification of paravertebral ligaments (radicular pain) -seizure in untreated pts -Nephrocalcinosis and impaired renal function if overtreatment with calcium and vitamin D |
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What is the prognosis for hypoparathyroidism?
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good w/ prompt diagnosis and Tx
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What changes with hypoparathyroidism are permanent?
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dental changes, cataracts, and brain calcifications
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What are the essentials of diagnosis for hyperparathyroidism?
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-Frequently asymptomatic; hypercalcemia detected by screening
-Renal stones, polyuria, hypertension, constipation, mental changes -Bone pain -Serum and urine calcium elevated; urine phosphate high with low or normal serum phosphate; alkaline phosphatase normal or elevated -Elevated or high-normal serum parathyroid hormone (PTH) level |
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What is primary hyperparathyroidism usually due to?
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-parathyroid adenoma, less commonly hyperplasia or carcinoma (rare)
-If age < 30 years, higher incidence of multiglandular disease (36%) and carcinoma (5%) |
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What are 2 causes of secondary/tertiary hyperparathyroidism?
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chronic renal failure
renal osteodystrophy |
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What cause of chronic renal failure causes secondary/tertiary hyperparathyroidism?
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hyperphosphatemia and decreased renal vitamin D production decrease ionized calcium, thus stimulating the parathyroids
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What cause of renal osteodystrophy causes secondary/tertiary hyperparathyroidism?
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bone disease of secondary hyperparathyroidism and renal failure
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What is the epidemiology of hyperparathyroidism?
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-Incidence of primary hyperparathyroidism in adults is 0.1%
-More common in persons age > 50 -Females > males 3:1 |
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What are the S/S of hyperparathyroidism?
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*Symptoms include problems with "bones, stones, abdominal groans, psychic moans, fatigue"
-frequently asymptomatic -pathologic fractures or cystic bone lesions -Bone pain and arthralgias -Polyuria and polydipsia -Calcium-containing kidney stones -Depression, intellectual weariness, and increased sleep requirement -Constipation, fatigue, anemia, weight loss, muscle weakness, pruritus, paresthesias -Anorexia, nausea, and vomiting in severe cases -Hypertension -palpable mass usually a thyroid nodule -Psychosis or even coma in severe hypercalcemia -Calcium phosphate deposition in corneas or soft tissues |
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What may cause pathologic fractures or cystic bone lesions with hyperparathyroidism?
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Chronic cortical bone resorption due to excess PTH (osteitis fibrosa cystica)
-"brown tumors" of jaw |
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What is polyuria/polydipsia with hyperparathyroidism from?
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hypercalcemia-induced nephrogenic diabetes insipidus
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Parathyroid adenomas are ___ palpable; palpable mass is usually a ___ nodule. Parathryoid carcinomas are ___ palpable and pancreatitis occurs in ___% of hyperparathyroidism patients.
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rarely
thyroid often 3% |
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What is included in the differential diagnosis for hyperparathyroidism?
|
**Hypercalcemia of malignancy
-Multiple myeloma *Vitamin D intoxication -Sarcoidosis, tuberculosis -Hyperthyroidism -Vitamin D deficiency (high serum PTH with normal serum calcium) -High-dose corticosteroid therapy in patients taking thiazide diuretics |
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What laboratory test confirms the diagnosis for hyperparathryoidism?
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elevated/normal-high PTH
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What is the most specific and sensitive test for measureing PTH levels with hyperparathyroidism?
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immunoradiometric assay (IRMA)
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What do the labs show for hyperparathyroidism?
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-Serum calcium > 10.5 mg/dL
-Elevated or high-normal PTH -Serum phosphate often low (< 2.5 mg/dL) -Serum phosphate high in secondary hyperparathyroidism (renal failure) -Urine calcium excretion high or normal |
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What is screened for familial benighn hypocalciuric hypercalcemia?
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24-h urine for Ca and creatinin
-discontinue thiazide diuretics before this test |
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What imaging studies are used for hyperparathyroidism?
|
SPECT
neck ultrasound bone densitometry of wrist/hip/spine MEN1/MEN2 |
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In renal osetodystrophy, what are 4 things that may show up on a bone radiograph?
|
Osteopenia
Osteitis fibrosa Osteosclerosis Ectopic calcifications around joints or soft tissue |
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What medications are given or primary hyperparathyroidism?
|
IV bisphosphonates can temporarily treat hypercalcemia and relieve bone pain
-Pamidronate or zoledronic acid (expensive) Propanolol may prevent adverse cardiac effects of hypercalcemia |
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Are oral bisphosphonates are effective for hyperparathyroidism?
|
no only IV
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Is corticosteroid therapy effective for hypercalcemia in hyperparathryoidism?
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no
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When is surgery (parathyroidectomy) considered for symptomatic hyperparathyroidism?
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symptomatic hyperparathyroidism, kidney stones, or bone disease
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When is surgery considered for asymptomatic patients?
|
-Serum Ca 1 mg/dL above normal if urine Ca excretion > 50 mg/24 h
-Urine Ca > 400 mg/24 h -Cortical bone density > 2 SD below normal (osteoporosis) -Age < 50–60 years -Difficulty ensuring medical follow-up -Pregnancy (second trimester) |
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When is minimally invasive parathyroid surgery usually sufficient?
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if adenoma identified preoperatively
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What type of surgery is for patients with resistant parathyroid hyperplasia?
|
subtotal parathyroidectomy (3 1/2 glands removed)
-remaining 1/2 is usually enough to function/maintain PTH levels |
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What is advised to patients who have mild, asymptomatic hyperparathyroidism?
|
-Keep active
-Drink adequate fluids -Avoid immobilization -Avoid thiazides, large doses of vitamins D and A, calcium-containing antacids or supplements, and digitalis (hypercalcemia predisposes to toxicity) |
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What should be monitored/checked in hyperparathyroidism?
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-Serum calcium and albumin twice yearly
-Renal function and urine calcium once yearly -Bone density (distal radius) every 2 years |
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What should be done post-operatively for hyperparathyroidism?
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-Monitor serum calcium and PTH
-Oral calcium and calcitriol for 2 weeks helps prevent tetany |
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How is secondary hyperparathyroidism treated?
|
calcium and vitamin D
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What may hyperthyroidism immediately following parathyroid surgery require?
|
short-term propanolol
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What are the complications of hyperparathyroidism?
|
-Forearm and hip fractures
-UTI due to obstruction by stones -Confusion, renal failure, and soft tissue calcinosis from rapidly rising serum Ca -Renal osteodystrophy from hyperphosphatemia -Peptic ulcer and pancreatitis -Pseudogout before or after surgery -Disseminated calcification in skin, soft tissues, and arteries (calciphylaxis) can result in gangrene, arrhythmias, and respiratory failure |
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What is pseudogout?
|
build-up of Ca crystals in joints (not uric acid)
-can be differentiated by examining joint fluid (needle) |
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Does asymptomatic mild hypercalcemia affect survival?
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no
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What does resection of sporadic parathyroid adenoma for hyperparathyroidism generally result in?
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cure
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|
|
What happens to bones if parathyroid tumor is removed due to hyperparathyroidism?
|
heal, despite severe cyst formation or fracture
|
|
|
What may happen to the kidneys even after adenoma is removed?
|
significant renal damage may progress
|
|
|
What can repeat surgical resections and radiation therapy for parathyroid carcinoma (that tends to invade local structures and may metastasize) do?
|
can prolong life
|
|
|
What are the essentials of diagnosis for osteomalacia and rickets?
|
-Painful proximal muscle weakness; bone pain and tenderness
-Decreased bone density from diminished mineralization of osteoid -inc. alkaline phosphatase -dec. 25-hydroxy-vitamin D -Hypocalcemia, hypocalciuria, hypophosphatemia, secondary hyperparathyroidism -Classic radiologic findings |
|
|
What is the definition of osteomalacia?
|
defective skeletal mineralization in adults
|
|
|
What is the definition of rickets?
|
defective skeletal mineralization in children
|
|
|
What is osteomalacia and rickets commonly caused by?
|
deficiency in vitamin D
|
|
|
What are 2 forms of vitamin D?
|
D2 (ergocalciferol) from plants
D3 (cholecalciferol) synthesized in the skin (sunlight) |
|
|
In order to be used by the body, the Vitamin D must be hydroxylized twice, first in the ___, 2nd in the ___.
End product is 1,25[OH]2D3 which is ___. |
liver
kidney 1,25-dihydroxycholecalciferol |
|
|
What is the main action of vitamin D?
|
to increase the absorption of calcium and phosphate form the intestine
|
|
|
What is the etiology of osteomalacia and rickets?
|
Common disorder that is caused by any condition that results in inadequate calcium or phosphate mineralization of bone osteoid
|
|
|
There are common, rare and serious causes of osteomalacia/rickets. What are 6 common causes?
|
-Vitamin D deficiency due to environmental factors
-Dietary vitamin D deficiency -GI causes that reduce absorption of vitamin D (surgery, malabsorption, biliary disease, etc.) -Cirrhosis -Corticosteroid use -Renal disease that leads to defective 1,25-dihydroxycholecalciferol synthesis |
|
|
There are common, rare and serious causes of osteomalacia/rickets. What are 7 rare causes?
|
-Anticonvulsants
-Hypophosphatemia -Systemic acidosis -Intoxication with fluoride, aluminum or diphosphonate -Autonomous hyperparathyroidism -Mesenchymal tumor -Medications |
|
|
There are common, rare and serious causes of osteomalacia/rickets. What are 6 serious causes?
|
Renal disease
Hepatic disease Pancreatic dysfunction Crohn’s disease GI fistulae Mesenchymal tumors |
|
|
What are 7 predisposing factores of osteomalacia/rickets?
|
Lack of sunlight exposure
Institutional care Vitiligo High latitude Dark clothes Poor diet, vegetarianism Alcoholism *older you get, less likely that you are to stabilize vitamin D |
|
|
The epidemiology of osteomalacia/rickets has a prevalence of ___, common in ___ (often w/ osteoporosis), women > men, more common in young ___ and ___ women in India, and ___ socioeconomic class may contribute to poor diet.
|
1/1000
elderly pregnant lactating low |
|
|
What is included in the differential diagnosis for osteomalacia/rickets?
|
**Osteoporosis (may coexist)
Rheumatic joint disease Paget’s disease Neurologic disease Polymyalgia rheumatica Dermatomyositis Polymyositis Muscular dystrophy Malignancy |
|
|
What are the early symptoms of osteomalacia/rickets?
|
fatigue
stiffness skeletal pains |
|
|
What are the later symptoms of osteomalacia/rickets?
|
muscular weakness
hyporeflexia paresthesia |
|
|
What are the signs of osteomalacia/rickets? (16)
|
-Waddling gait (valgus or varus)
-Marked adductor spasm -Proximal muscle weakness -Costochondral swelling -Spinal curvature -Narrowed pelvic outlet -Pathological fractures of pelvis and long bones -Tenderness over pseudofractures and ribs -Signs of hypocalcemia (Chvostek’s and Trousseau’s) -Grand mal seizure -Metastatic calcification seen on x-ray and occasionally palpated -Paleness due to lack of sun exposure -Signs of malnutrition -Abdominal scars/hepatomegaly -Full passive ROM without pain -Normal muscle bulk |
|
|
When is grand mal seizure seen with osteomalacia/rickets?
|
severe cases of hypocalcemia
|
|
|
What diagnostic tests are used for osteomalacia/rickets?
|
-Serum electrolytes (including Ca, phosphate, BUN and creatinine)
-Liver function tests -Serum vitamin D levels (best one to get is 25-hydroxy vitamin D-active form) -Thyroid function tests -PTH -24-hour urine -Plain x-rays of weight-bearing bones |
|
|
What are the goals of therapy for osteomalacia/rickets?
|
-Reduce pain and muscle weakness
-Reverse pathologic changes -Increase mobility and restore skeletal health -Prevent recurrence -Treat any underlying conditions |
|
|
How can simple vitamin D deficiency be replaced for osteomalacia/rickets? (3)
|
oral vitamin D
calcium phosphate add sunlight or UV light as needed |
|
|
Osteomalacia/rickets should be treated until serum alkaline ___ is normal, then start ___ therapy.
|
phosphatase
maintenance |
|
|
What is the treatment plan for patients with malabsorption and liver disease?
|
high dose oral vitamin D2 making sure to monitor serum calcium
|
|
|
What is the 1st choice of treatment in renal disease associated w/ osteomalacia/rickets?
|
1,25-dihydroxy vitamin D
|
|
|
How is hypocalcemic tetany associated with osteomalacia/rickets treated?
|
IV calcium gluconate
|
|
|
What is the clinical pearl of treatment for osteomalacia/rickets?
|
never start a bisphosphonate before correcting vitamin D deficiency (make sure have normal vitamin D first)
|
|
|
With osteomalacia/rickets treatment it is important to educate patients that bone pain may ___ during first 2 weeks of treatment.
|
*INCREASE*
|
|
|
What needs to be monitored in treatment of osteomalacia/rickets?
|
-serum calcium for toxicity
-bony pathology monthly (pseudofracture) -PTH |
|
|
What is the prognosis for osteomalacia/rickets?
|
treatment of simple vitamin D deficiency should lead to dramatic improvement
|
|
|
How can osteomalacia/rickets be prevented?
|
-Encourage sunlight exposure
-Use vitamin-D fortified foods -Use of supplements in at-risk groups -Decrease alcohol use -Long term maintenance therapy for those prone to recurrence |
|
|
When is cortisol the highest?
|
in the mornings
|
|
|
What are the stresses of the adrenal glands? (4)
|
heat/cold
emotional issues trauma infection |
|
|
What causes the adrenal glands to produce cortisol?
|
CRF (hypothalamus) --> ACTH (anterior pituitary) --> cortisol (adrenal glands)
|
|
|
What are the the 3 layers of the adrenal cortex going from outisde to inside?
|
zona glomerulosa
zona fasciculata zona reticularis |
|
|
What does the zona glomerulosa produce?
|
aldosterone
|
|
|
What does aldosterone do?
|
-body's primary mineralocorticoid hormone
-stimulates renal tubule to reabsorb Na and K -protects against hyponatremia and hyperkalemia |
|
|
What does the zona fasciculata produce?
|
cortisol
|
|
|
What does cortisol do?
|
stress hormone
-Counters insulin effects -Inhibits inflammation -Increases serum Ca by inhibiting Ca uptake by renal tubule and in the gut -Redistributes Ca intracellularly -Elevates RBC/platelet count |
|
|
What does the zona reticularis produce?
|
dehydroepiandrosterone
-women's hair/libido androgens some cortisol |
|
|
What does the adrenal medulla produce?
|
catecholamines
-epinephrine (80%) -norephinephrine |
|
|
What is Conn's syndrome also known as?
|
primary hyperaldosteronism
|
|
|
What are the causes of Conn's syndrome?
|
adenoma 73%
-benign tumor of one adrenal hyperplasia 27% -enlargement of both adrenals |
|
|
Is Conn's syndrome mostly in men or women?
|
women
|
|
|
What are the peak years of occurence for Conn's syndrome?
|
age 30-50
|
|
|
What are the S/S of Conn's syndrome?
|
*Hypertension
*Hypokalemia due to renal loss *Polyuria, polydipsia, nocturia -Muscle weakness, possible paralysis -Fatigue, headache, paresthesias -Possibly metabolic acidosis |
|
|
What do the labs for Conn's syndrome show?
|
increased aldosterone
low/undetectable renin K+ decreased Na+ increased metabolic acidosis? aldosterone/renin ratio>20-25 *significant if >100 |
|
|
How is aldosterone-producing adenoma (Conn's syndrome) managed/treated?
|
low Na+ diet
K+ supplement spironolactone surgical removal able to stop meds. after surgery monitor for life |
|
|
How is bilateral hyperplasia (Conn's syndome) managed/treated?
|
low Na+ diet
K+ supplement spironolactone lifelong monitored for life |
|
|
What are 7 other names for Addison's disease?
|
-Adrenal Hypoplasia
-Adrenocortical Hypofunction -Adrenocortical Insufficiency -Chronic Adrenocortical Insufficiency -Primary Adrenal Insufficiency -Primary Failure Adrenocortical Insufficiency -Adreno Hypoplasia |
|
|
Are men or women more affected by Addison's disease?
|
women
|
|
|
By what age does Addison's disease usually appear?
|
15
|
|
|
What is the etiology of Addison's disease?
|
Originally TB
Currently *autoimmune* Additional causes: -Viral infections – HIV, CMV -Cancer, Lymphoma -Systemic Fungal Infections -Amyloidosis -Trauma -Medications |
|
|
What are the S/S of Addison's disease?
|
*Fatigue and weakness
*Anorexia and/or cravings for salt Weight loss Myalgias/arthritis GI: nausea, vomiting, diarrhea Slowed DTRs Small heart Orthostatic hypotension Hyperplasia of lymph tissues Scant axillary/pubic hair *Hyperpigmentation Oligomenorrhea --> amenorrhea Infertility Mania/psychosis/cognitive impairment |
|
|
Where does hyperpigmentation with Addison's disease show up?
|
only in primary disease when ACTH is elevated
-Body folds, on scars, keloids, around mucous membranes, knees, elbows, knuckles, toes May also “brown” around body pressure areas (belt line, bra-lines) -Increased freckles, spots on gingivae, buccal mucosa, tongue |
|
|
What do the labs for Addison's disease show?
|
hyperkalemia
hyponatremia hypoglycemia hypercalcemia low BUN DHEA levels under 1000/ng/mL mild anemia neutropenia lymphocytosis eosinophilia |
|
|
What type of test is used to test plasma cortisol levels at 8AM drawing?
|
*ACTH stimulating test
-tells adrenals to release cortisol |
|
|
What do small non-calcified adrenals on a CT suggest?
|
autoimmune disease causing adrenal deficiency
|
|
|
How is Addison's disease treated?
|
combo. of glucocorticoids & mineralcorticoids
-Hydrocortisone=DOC (can give Prednisone in PM) -Fludrocortisone Acetate -DHEA (women) *wear medical alert bracelets |
|
|
When should dosage of Hydrocortisone for Addison's disease be increased?
|
stressful times, infections, surgery, trauma
|
|
|
When may dosage of Fludrocortisone Acetate for Addison's disease need to be increased?
|
orthostatic hypotension
hyperkalemia |
|
|
When may dosage of Fludrocortisone Acetate for Addison's disease need to be decreased?
|
edema
hypokalemia HTN |
|
|
What happens if the Addison's disease is not treated or
treated improperly, or there is poor compliance? |
potential for adrenal insufficiency/crisis
-do not ignore low-grade fevers |
|
|
What can potentiate an adrenal crisis?
|
non-compliant patient, extreme stresses, med. dosage not raised enough to compensate, trauma, infection, prolonged fasting, sudden withdrawal of adrenal hormones, adrenalectomy, destruction of the pituitary gland, anticoagulant therapy, thrombolytic event affecting the adrenals
|
|
|
What should not be ignored in Addison's disease?
|
fever (even low-grade)
-could have adrenal crisis |
|
|
What is the epidemiology of an adrenal crisis?
|
women>men
more common in 30s-50s, but can happen at any age (always be suspicious of elderly) |
|
|
What are the S/S of an adrenal crisis?
|
Nausea, Vomiting, diarrhea
Abdominal Pain Confusion, can lead to Coma High Fever HYPOtension Cyanosis Dehydration Shock w/o Tx |
|
|
How is an adrenal crisis treated?
|
acute phase:
draw cortisol level IV Hydrocortisone IV Saline Then: Hydorcortisone Phophate or Hydrocortisone Sodium Succinate broad spectrum antibiotics Recuperation: oral Hydrocortisone Fludrocortisone (after adrenal crisis) *dosage adjusted based on clinical response |
|
|
What do the labs for an adrenal crisis show?
|
hyponatremia/hyperkalemia
hypoglycemia |
|
|
What does the normal serum level of cortisol rise to with a simplified cosyntropin stimulation test for an adrenal crisis?
|
20 ug/dL
|
|
|
What does a patient have if the ACTH is markedly elevated in an adrenal crisis?
|
primary adrenal disease
|
|
|
What are 2 possible results of hypercortisolism?
|
Cushing's disease
Cushing's syndrome |
|
|
What is the exogenous form of Cushing's syndrome caused by?
|
chronic excess of glucocorticosteroids, usually used to treat other diseases
|
|
|
What is the endogenous form of Cushing's syndome caused by?
|
usually because of Cushing’s Disease
|
|
|
What can cause Cushing syndome?
|
glucocorticosteroid excess
Cushing's Disese adrenal tumor non-pituitary ACTH-producing tumor (small cell lung CA) |
|
|
What is Cushing's disease caused by?
|
excess secretion of ACTH by pituitary (often caused by a benign pituitary adenoma)
|
|
|
Who does Cushing's disease most commonly occur in?
|
premenopausal women
|
|
|
Who introduced the blood pressure sphygmomanometer to the US?
|
Dr. Harvey Williams CUSHING
(may be extra credit!!!) |
|
|
What age group is hypercortisolism generally diagnosed?
|
between age 20 and 50
|
|
|
What are the S/S of hypercortisolism? (yowsers there are A LOT!!)
|
weight gain, weakness, fever (opportunistic infection?), predisposed to glaucoma, HTN, central obesity, wasted extremities, moon face, pigmented striae, poor wound heeling, skin infections (Candidiasis), hirsutism in women (face, neck, chest, abdomen, thighs), peripheral edema?, osteoporosis, vertebral Fx's, increased serum Ca, increase Ca in urine, *nephrolithiasis, *Buffalo Hump (thoracic kyphosis), proximal muscle weakness, back pain, hyperglycemia, polyuria, polyphagia, polydipsia, nocturia, *oligomenorrhea/amenorrhea, decreased libido, impotence, infertility, easy bruising, leukocytosis w/ lymphopenia, difficulty concentrating, agitated, emotional lability (depression, euphoria, frank psychosis)
|
|
|
What are 4 S/S of hypercortisolism that are a big concern to physicians?
|
hyperglycemia (diabetic state)
HTN (cardiac/kidneys/eyes) infections fractures |
|
|
How is hypercortisolism diagnosed?
|
glucose tolerance test
dexamethasone suppression test -cortisol level under 5ug/dL excludes Cushing syndrome |
|
|
What drugs can give you a false-positive for a dexamethasone suppression test?
|
Anti-seizure drugs (Phenytoin, Phenobarbital, Primidone) and Rifampin
|
|
|
What happens if you get an abnormal dexamethosone suppression test?
|
further testing:
24 hour urine -free cortisol or free cortisol to creatinine ratio >95ug confirms hypercortisolism midnight saliva test can also be done |
|
|
With hypercortisolism, what does a normal or slightly low level of ACTH indicate as the cause?
|
adrenal tumor
|
|
|
What are higher levels of ACTH indicative of with hypercortisolism?
|
pituitary or ectopic tumors
|
|
|
What type of diagnostic procedure is done if the cause of hypercortisolism is determined to be pituitary?
|
brain MRI
|
|
|
What is the Tx plan for hypercortisolism caused by the pituitary?
|
selective transphenoidal adenectomy (successful in 80% of surgeries)
-if not successful than can redo transphenoidal adenectomy or use radiation therapy |
|
|
What type of diagnostic procedure is done if the cause of hypercortisolism is determined to be non-pituitary?
|
CT scan of entire chest and abdomen (special attention to lungs for carcinoid and small cell carcinoma)
|
|
|
Are men or women more likely to have a pituiary adenoma causing hypercortisolism?
|
women
|
|
|
Are men or women more likely to have a non-pituiary cause of hypercortisolism?
|
men
|
|
|
What are other sites of ACTH production (ectopic)?
|
*Thymomas
*Pancreatic islet cell tumors Thyroid medullary carcinomas Adrenal Adenoma (rare) Adrenal Carcinoma (least likely) |
|
|
What is the Tx of hypercortisolism dependent on?
|
ID of source
-necessary to eliminate all of the tissue that is secreting ACTH |
|
|
What are the choices of Tx for ectopic sources of ACTH?
|
surgery, radiotherapy, chemotherapy, immunotherapy, or a combination (want to remove tumor)
|
|
|
Is Cushing's disease generally from pituitary or adrenals?
|
pituitary
|
|
|
Is Cushing's syndrome generally from pituitary or adrenals?
|
adrenals
|
|
|
What is the prognosis if hypercortisolism
is left untreated? |
serious morbidity and death
Most likely from complications of: Hypertension Diabetes-Related Disorders Infections Fractures |
|
|
What is a pheochromocytoma?
|
a rare, usually benign, vascular tumor in the medulla of the adrenal glands (or, rarely, the ganglia of the sympathetic nervous system) which secretes excessive amounts of catecholamines, usually epinephrine and norepinephrine
|
|
|
Where is the tumor of pheochromocytoma located?
|
medulla of adrenals
|
|
|
What does a pheochromocytoma secrete excessive amounts of?
|
catecholamines
|
|
|
What men or women more likely to get a pheochromocytoma?
|
males = females
|
|
|
What is the peak incidence of pheochromocytoma?
|
between 20-50 years of age
(30-50 most common) |
|
|
What are the S/S of a pheochromocytoma?
|
*severe HTN, *headache, *palpitations, *diaphoresis, tremor, epigastric pain, flank pain, constipation/ileus, pallor, anxiety (sense of doom), *weight loss), weakness, dyspnea, neurofibomas, tachyarrhythmias, pulmonary edema, cardiomyopathy, postural hypotension, *Cafe au Lait spots (axillae/groin)
|
|
|
What are the lab findings for a pheochromocytoma?
|
hyperglycemia
hypercalcemia erythrocytosis *catecholamines (24hr urine) |
|
|
What are the diagnositc studies that can be done for a pheochromocytoma?
|
*CT
*MRI (preferred) 131-Iodine-scintigraphy |
|
|
What can precipitate a Hypertensive Crisis?
|
Drugs that inhibit catecholamine reuptake, such as tricyclic Antidepressants and cocaine
-Opiates -Cold Medications -Anesthesia induction -Childbirth -Radiographic contrast media |
|
|
What is included on the differential diagnosis for pheochromocytoma? (13)
|
Angina Pectoris
Hyperthyroidism Factitious Disorder Anxiety Disorder Menopause Toxemia of Pregnancy Panic Attacks Insulinoma Carcinoid Tumor PCP, Cocaine, LSD Use MAOI Crisis Tricyclic Antidepressant Overdose Stroke |
|
|
How is pheochromocytoma treated?
|
surgery followed by alpha blocker (*phenoxybenzamine, doxazosin, prazosin, or terazosin) and beta-blocker (propanolol)
|
|
|
How is malignant pheochromocytoma treated?
|
surgery
combo. chemo 24hr urine collection yearly x 5 years |
|
|
What should be administered to pregnant patients as soon as pheochromocytoma diagnosis is made?
|
alpha blocker (phenoxybenzamine)
-grave prognosis during pregnancy w/ pheochromocytoma |
|
|
What are the 2 exocrine cells of the pancreas and what do they produce?
|
pancreatic acini cells
-digestive juices duct cells -NaHCO3 |
|
|
Where are endocrine tissues of the pancreas contained?
|
Islets of Langerhans
|
|
|
What are the 3 endocrine cells of the pancreas and what do they secrete/produce?
|
alpha cells secrete glucagon
*beta cells produce insulin delta cells produce somatostatin |
|
|
What does glucagon do?
|
-Stimulates breakdown of glycogen in the liver
-Activates hepatic gluconeogenesis (makes sugar) |
|
|
What does insulin do?
|
-Facilitates entry of glucose into cells
-Stimulates the liver to store glucose in the form of glycogen -Promotes synthesis of fatty acids in the liver -Inhibits breakdown of fat in adipose tissue -Increases cell permeability to K+, Mg++ & phosphate -Promotes production of amino acids and enzymes -Inhibits catabolism of proteins |
|
|
What is type I diabetes also known as? (2)
|
Insulin Dependent Diabetes Mellitus (IDDM)
Juvenile Diabetes |
|
|
What is type II diabetes also known as? (3)
|
Non-Insulin Dependent Diabetes Mellitus (NIDDM)
Insulin Resistant Diabetes Adult Onset Diabetes |
|
|
What type of destruction is type I diabetes caused by?
|
pancreatic islet B-cell destruction
-90% destruction immune-mediated -remainder idiopathic |
|
|
What is the main age occurence of type I diabetes?
|
10-14 year olds
|
|
|
In the United States, average incidence of type I diabetes is ___ per 100,000. An estimated ___ million Americans have diabetes mellitus, of whom ~1 million have type __ diabetes.
|
15
18.2 I |
|
|
What are the S/S of type I diabetes?
|
*polydipsia
*polyuria *polyphagia *weight loss ***ketoacidosis *recurrent blurred vision paresthesias vulvovaginitis/pruitus nocturnal enuresis postural hypotension |
|
|
What is included in the differential diagnosis for type I diabetes?
|
*type 2 diabetes
-Hyperglycemia resulting from other causes (corticosteroids, Cushing's syndrome, etc.) -Metabolic acidosis of other causes (alcoholic ketoacidosis) -Nondiabetic glycosuria (renal glycosuria) |
|
|
What do the labs for type I diabetes show?
|
*Fasting plasma glucose > 126 mg/dL or > 200 mg/dL 2 h after glucose load
-Ketonemia, ketonuria, or both -Glucosuria *Glycosylated hemoglobin (hemoglobin A1c) reflects glycemic control over preceding 8–12 weeks -serum fructosamine (time of conception among diabetic women) |
|
|
When is a fasting plasma glucose level diagnostic of diabetes?
|
126 mg/dL (confirmed on subsequent days)
|
|
|
What are the pharmaceutical treatments for type I diabetes?
|
*regular insulin
*premixed insulins *inhaled insulin rapid-acting insulin (lispro) intermediate-acting (NPH) long acting (glargine) Pramlintide |
|
|
What type of surgeries can be performed for type I diabetes? (3)
|
pancreas/kidney transplant
-pts receiving simultaneous pancreas and kidney transplants have 85% chance of pancreatic graft survival and 92% chance of renal graft survival after 1 year Solitary pancreas transplant -only for recurrent life-threatening metabolic instability Islet transplantation is minimally invasive |
|
|
What type of therapeutic procedures can be done for type I diabetes?
|
*eucaloric healthy diet (limit cholesterol, protein, saturated fat)
*ACE-I *treat HTN & hyperlipidemia (reduce LDL < 100) |
|
|
*What are the complications of type I diabetes?*
|
-Diabetic ketoacidosis
-Hypoglycemia and altered awareness of hypoglycemia -Diabetic retinopathy, cataracts -Nephropathy -Neuropathy -Diabetic atherothrombosis (coronary artery disease, peripheral vascular disease) -Lipodystrophy at injection sites |
|
|
What is the prognosis of type I diabetes?
|
markedly improved by optimal care
patients can have a full life |
|
|
How can an epidsode with type I diabetes be prevented?
|
*ASA (enteric coated)
-reduce risk of diabetic atherothrombosis without increasing risk of vitreous bleeding -Instruction in personal hygiene, in particular, care of *feet, skin, and teeth *Yearly diabetic eye examination -Patient self-management training *Self-monitoring of blood glucose *Exercise |
|
|
What are the essentials of diagnosis for type II diabetes?
|
*Typically > 40 years of age
*Obesity *Polyuria and polydipsia -Candidal vaginitis sometimes an initial manifestation -Often few or no symptoms *Fasting plasma glucose > 126 mg/dL more than once *OGTT > 200 mg/dL 2 h after the oral glucose -Often associated with hypertension, dyslipidemia, and atherosclerosis |
|
|
What are 3 "enhancers" of insulin resistance with type II diabetes?
|
aging
sedentary lifestyle abdominal-visceral obesity |
|
|
Is type II diabetes genetic?
|
it has strong genetic influences
|
|
|
What is tissue resistance to insulin and impaired B-cell response to glucose further aggravated by in type II diabetes?
|
increased hyperglycemia
-both improve with decreased hyperglycemia |
|
|
What are the demographics for type II diabetes?
|
*18.2 million Americans, or > 90% of all diabetics in the United States, have type 2 diabetes
*Traditionally occurred in middle-aged adults but now more frequently encountered in children and adolescents -No gender predominance (males=females) |
|
|
What are the S/S of type II diabetes?
|
*Polyuria
*Polydipsia *Weakness or fatigue Recurrent blurred vision Vulvovaginitis or pruritus Peripheral neuropathy *Often asymptomatic (needs to be picked up on screening) |
|
|
What is included in the differential diagnosis for type II diabetes?
|
*type I diabetes
Endocrinopathies Drugs -Corticosteroids* -Thiazides -Oral contraceptives* Chronic pancreatitis *Gestational diabetes |
|
|
What do the labs for type II diabetes show?
|
*Fasting plasma glucose 126 mg/dL or 200 mg/dL 2 h after glucose load
*Glycosylated hemoglobin (HbA1c) reflects glycemic control over preceding 8–12 weeks *Lipoprotein abnormalities: -High serum triglyceride (300–400 mg/dL) -Low high-density lipoprotein (HDL) cholesterol (< 30 mg/dL) -a qualitative change in low-density lipoprotein (LDL) particles Glucosuria Ketonuria on occasion without ketonemia |
|
|
What types of pharmaceutical treatments can be done for type II diabetes?
|
insulin secretion stimulators (run risk of hyperglycemia):
*Sulfonylureas (glyburide, glipizide) -Meglitinide analogs (repaglinide) -D-phenylalanine derivative (nateglinide) drugs that alter insulin action (give horrible diarrhea): *Metformin/Glucophage *Thiazolidinediones (rosiglitazone, pioglitazone) glucosidase inhibitors (acarbose, miglitol) *drugs that mimic incretin effect: exenatide (Byetta) *combination oral agents Others: pramlintide, insulin |
|
|
What are the *dietary limitation for type II diabetics?
|
-Cholesterol to 300 mg QD
-Protein intake to 10–20% of total calories -Saturated fats to < 8–9% of total calories -Remainder of diet to consist of monounsaturated fats and carbohydrates with 20–35 g of dietary fiber |
|
|
What should be included in the follow-up monitoring of type II diabetic patients?
|
*Self-monitoring of blood sugar
*HbA1c quarterly *Screen for microalbuminuria annually *Serum lipids annually *Feet examination annually+ *Diabetic eye examination annually |
|
|
What are the Tx goals for type II diabetes? (2)
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Self-monitored blood glucose, 80–120 mg/dL before meals
HbA1c < 7.0% |
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What are some of the complications associated with type II diabetes?
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hypoglycemia
*cataracts/retinopathy *nephropathy gangrene of feet *neuropathy skin (xanthomas, necrobiosis lipoidica diabeticorum, *intertrigious candida, vulvovaginitis) |
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How can type II diabetes be prevented?
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*Goal of therapy is to prevent acute illness and reduce risk of long-term complications
-Lifestyle modifications can prevent/slow development of diabetes -Daily vigorous exercise prevents accumulation of visceral fat, which can prevent the development of diabetes *Screen with fasting glucose at 3-year intervals beginning at age 45; screen earlier and more frequently if risk factors present |
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What is insulin resistance also known as?
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syndrome X, Metabolic syndrome
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What is insulin resistance patients at high risk of developing?
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type II diabetes
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What 5 conditions does insulin resistance include?
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Elevated triglycerides & LDL
Low HDL Elevated blood pressure Hyperuricemia Abdominal obesity |
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What 2 meds. should be avoided with insulin resistant patients?
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diuretics and beta-blockers
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How is insulin resistance treated?
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metformin or thiazolidinediones
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What are 3 ocular complications of diabetes?
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diabetic cataracts
*diabetic retinopathy glaucoma |
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What are 2 pathologic changes that may be seen during a fundoscopic exam of diabetic retinopathy?
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cottonwool spots
pinpoint hemorrhages |
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What is the #1 cause of chronic renal failure in US leading to dialysis?
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diabetic nephropahty
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Diabetic nephropathy begins with _____ and 10-15 years of proteinuria can lead to ___ syndrome. Unless treated, the waste materials (toxins) can build up to ___ levels.
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microalbuminuria
nephrotic fatal |
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What is the overall risk of developing diabetic nephropathy?
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10-20% in type II
30-50% in type I |
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Who is diabetic nephropathy more likely to develop in?
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males
Relatives have had kidney disease or HTN Diabetes began in teens Poor glycemic control Patient has HTN |
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What tests can be used for diabetic nephropathy?
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U/A
Serum BUN/creatinine 24 hour urine Renal ultrasound Possibly renal biopsy |
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What is the most common complication of type II diabetes?
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diabetic neuropathy
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What are the 2 types of diabetic neuropahty?
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peripheral (most common)
autonomic |
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What are the S/S of peripheral diabetic neuropathy?
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Stocking-glove pattern
Isolated peripheral neuropathy Painful diabetic neuropathy |
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What are the S/S of autonomic diabetic neuropathy?
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Postural hypotension
Decreased CV response Gastroparesis Diarrhea with constipation Urine retention ED |
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The annual incidence of cardiovascular disease is increased by _____ in diabetic men and by ____ in diabetic women.
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2-3 times
3-4 times |
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What are the risk factors for cardiovascular disease in diabetics?
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Elevated urinary protein excretion
Poor glycemic control Overweight or obesity Abdominal adiposity Blood clotting activity High-fat diet Sedentary lifestyle Smoking |
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What type of testing can be done on the feet of diabetic patients to test for sensation?
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monofilament test
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What are the skin/mucous membrane complication in diabetic patients?
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Chronic pyogenic infections
Eruptive xanthomas Shin spots Repetitive candida infection |
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What is the *Somogyi Effect*?
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rebound
*Swing to a high level of glucose in the blood from an extremely low level, usually occurring after an insulin reaction during the night -Caused by stress hormones -Occurs in Type I diabetics -If blood glucose levels are falling or low, adjustments in evening snacks or insulin doses may be recommended |
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What is the *Dawn Phenomenon*?
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*Reduction in tissue sensitivity to insulin between 5:00 and 8:00 am
-May be evoked by spikes of growth hormone which are released at the onset of sleep -May produce only mild hyperglycemia in early morning, but when associated with Somogyi effect, hyperglycemia may be more severe -Affects 75% of Type I patients and can occur in Type II as well |
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What are the essentials of diagnosis for diabetic ketoacidosis?
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Hyperglycemia > 250 mg/dL
Acidosis with blood pH < 7.3 Serum bicarbonate < 15 mEq/L Serum positive for ketones |
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What may commonly be the initial manifestation of type I diabetes?
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diabetic ketoacidosis
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What is a common serious complication of insulin pump therapy?
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diabetic ketoacidosis
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What are the S/S of diabetic ketoacidosis?
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*May begin with a day or more of polyuria, polydipsia, marked fatigue, N/V and, finally, mental stupor that can progress to coma
-Dehydration, possible stupor *Rapid deep breathing and a "fruity" breath odor of acetone *Hypotension with tachycardia indicates profound fluid and electrolyte depletion *Mild hypothermia usually present; elevated or even a normal temperature may suggest infection -Abdominal pain and tenderness in the absence of abdominal disease |
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What is included in the differential diagnosis for diabetic ketoacidosis?
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*Lactic acidosis in type 1 diabetics, including the use of metformin
*Alcoholic ketoacidosis Hypoglycemia *Hyperglycemic hyperosmolar state Uremia Starvation ketoacidosis Salicylate poisoning |
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What do the labs for diabetic ketoacidosis show?
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*4+ glycosuria, hyperglycemia
*Anion-gap ketoacidosis **Serum potassium often elevated despite total body potassium depletion *Leukocytosis up to 25,000/L w/ a left shift may occur w/ or w/out associated infection -Strong ketonuria and ketonemia -Elevated serum amylase -- not specific for acute pancreatitis |
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How is diabetic ketoacidosis treated?
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regular insulin (begin with loading dose of 0.1 unit/kg as IV bolus)
fluid deficit is usually 4-5L (in first hour give at least 1 L of 0.9% saline to reexpand contracted vascular volume) electrolytes (use NaHCO3 only for pH < 7.1) K+ replacement is rarely required (Initial serum potassium is usually normal or high because of extracellular shifts from acidosis...polyuria/vomiting) |
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What are the complications of diabetic ketoacidosis?
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*Acute MI and infarction of the bowel following prolonged hypotension
*Renal failure, especially with prior kidney dysfunction -Cerebral edema occurs rarely |
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What is the prognosis of diabetic ketoacidosis?
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Life-threatening medical emergency with a mortality rate just under 5% in individuals younger than 40 years, but with a more serious prognosis in the elderly, who have mortality rates over 20%
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What are the essentials of diagnosis for hyperglycemic hyperosmolar state?
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serum glucose > 600 mg/dL
Serum osmolality > 310 mOsm/kg No acidosis; blood pH > 7.3 Serum bicarbonate > 15 mEq/L Normal anion gap (< 14 mEq/L |
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What does hyperglycemic hyperosmolar state frequently occur with?
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*mild or occult diabetes mellitus
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What is hyperglycemic hyperosmolar state often precipitated by? (4)
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infection
MI stroke recent surgery |
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What meds. can precipitate hyperglycemic hyperosmolar state?
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phenytoin, diazoxide, corticosteroids, and diuretics
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What does renal insufficiency in hyperglycemic hyperosmolar state develop from?
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hypovolemia, leading to increasingly higher blood glucose concentrations
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What 2 conditions are common with hyperglycemic hyperosmolar state and the presence of either worsens the prognosis?
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CHF
renal insufficiency |
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Is diabetic ketoacidosis or hyperglycemia hyperosmolar state more common?
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diabetic ketoacidosis
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What age group is generally affected with hyperglycemic hyperosmolar state?
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middle-aged to elderly
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What are the S/S of hyperglycemic hyperosmolar state?
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*Onset may be insidious over days/weeks, w/ weakness/polyuria/polydipsia
-lack of features of ketoacidosis may retard recognition until dehydration becomes more profound than in ketoacidosis *Fluid intake usually reduced from inappropriate lack of thirst, nausea, or inaccessibility of fluids to bedridden patients *Physical examination shows profound dehydration, lethargy, or coma without Kussmaul respirations -Lethargy and confusion -Coma can occur if osmolality exceeds 320–330 mOsm/kg |
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What is included in the differential diagnosis for hyperglycemic hyperosmolar state?
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*Diabetic ketoacidosis
*Sepsis Cerebrovascular accident/head trauma Hypoglycemia Diabetes insipidus |
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What do the labs for hyperglycemic hyperosmolar state show?
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*severe hyperglycemia
*ketosis/acidosis usually absent/mild *Prerenal azotemia with blood urea nitrogen elevations > 100 mg/dL *Rhabdomyolysis? -As dehydration progresses, serum Na can exceed 140 mEq/L |
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What is the treatment for hyperglycemic hyperosmolar state?
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saline
insulin potassium phosphate |
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Is more insulin required in diabetic ketoacidosis or hyperglycemic hyperosmolar state?
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diabetic ketoacidosis
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What is the goal of fluid/saline theraphy in hyperglycemic hyperosmolar state?
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-fluid replacement to correct fluid deficits of 6–10 L
-restore urinary output to 50 mL/h |
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Is the mortality rate in diabetic ketoacidosis or hyperglycemic hyperosmolar state higher?
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hyperglycemic hyperosmolar state
-higher incidence of older patients and greater dehydration |
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What plasma glucose level do the symptoms of hypoglycemia begin?
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~60 mg/dL
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When plasma glucose level does brain function impairment begin?
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~50 mg/dL
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What are the 2 types of spontaneous hypoglycemia?
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Fasting: Often subacute or chronic; usually presents with neuroglycopenia
Postprandial: Relatively acute, with symptoms of neurogenic autonomic discharge (sweating, palpitations, anxiety, tremulousness) |
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What can cause fasting hypoglycemia?
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*endocrine disorders (hypopituitarism, Addison's, myxedema)
-liver malfunction (acute alcoholism, liver failure) -hyperinsulinism -alcohol-related (gatritis/vomiting) *factitous (surreptitious administration of insulin or sulfonylurea) |
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When does postprandial/reactive hypoglycemia occur?
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either early (2-3h after a meal) or late (3-5h after a meal)
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Why does early/alimentary hypoglycemia occur?
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-rapid discharg of ingested carbohydrate into the small bowel followed by rapid glucose absorption and hyperinsulinism
-dumping syndrome after gastrectomy |
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What type of patients does late hypoglycemia occur in?
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occult diabetes mellitus
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What are the S/S of hypoglycemia?
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*Whipple's triad
weight gain from overeating *neuroglycopenia personality changes *convulsions/coma if ignored |
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What does Whipple's triad associated with hypoglycemia consist of?
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-Hx of hypoglycemic symptoms
-associated fasting blood glucose of 40 mg/dL -Immediate recovery on administration of glucose |
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*When do the symptoms for hypoglycemia often develop? (3)
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early morning
after missing a meal occasionally after exercise |
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What are the symptoms of neuroglycopenia associated with hypoglycemia?
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Blurred vision or diplopia
Headache Feelings of detachment Slurred speech Weakness |
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What do the labs for hypoglycemia show?
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glucose <40mg/dL
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How can endocrine tumors associated with hypoglycemia be treated?
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surgical treatment
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How is postprandial/reactive hypoglycemia treated?
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Frequent feedings with smaller portions of less rapidly assimilated carbohydrate combined with more slowly absorbed fat and protein
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How is functional alimentary hypoglycemia treated?
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-Support and mild sedation are mainstays of therapy
-Dietary manipulation is an adjunct: reduce proportion of carbohydrates in the diet, increase the frequency and reduce the size of the meals |
