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Casey: Endocrine > Handler Lectures > Flashcards

Handler Lectures Flashcards

1
Q

Turns thyroid on/off and binds to receptors of follicular cells

A

TSH

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2
Q

Is essential for manufacture of thyroid hormones

A

Iodine

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3
Q

Significant source of hypothyroidism

A

Iodine deficiency

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4
Q

Of the thyroid hormones, T3 & T4, what primary enters cells and exhibits effects?

A

T3

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5
Q

What is made in the liver and binds 80% of thyroid hormone?

A

Thyroxine Binding Globulin (TBG)

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6
Q

If thyroid hormone is absent at birth it leads to severe mental retardation aka___

A

cretinism

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7
Q

Helps maintain thermogenic and metabolic homeostasis in the adult; essential for normal metabolism, protein synthesis and organ function

A

Thyroid hormone

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8
Q

The most informative tests of thyroid function

A

TSH & free T4

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9
Q

TSH is decreased: Graves, toxic nodular goiter

A

Primary hyperthyroidism

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10
Q

TSH is increased in___

A

Primary hypothyroidism

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11
Q

MC form of hypothyroidism=

A

Hashimoto’s thyroiditis

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12
Q

MC form of hyperthyroidism=

A

Graves disease

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13
Q

Definitive test for evaluating thyroid nodules

A

Fine Needle Aspiration

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14
Q

Lymphocytic infiltration of gland; goiter often present

A

Autoimmune hypothyroidism

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15
Q

Tx of hypothyroidism

A

Levothyroxine

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16
Q

A clinical syndrome associate with excessive levels of thyroid hormone; aka Hyperthyroidism

A

Thyrotoxicosis

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17
Q

MC form of hyperthyroidism:

A

Grave’s Disease

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18
Q

Autoimmune disorder: TSH-R Ab-IgG antibodies directed to TSH receptor: over-activate gland–> hyper secretion, hypertrophy and hyperplasia (goiter common)
8x more common in women

A

Grave’s Disease

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19
Q

Symptoms=hyperactivity, irritability, restlessness, anxiety, HEAT INTOLERANCE, sweating, palpitations, INCREASED APPETITE, WEIGHT LOSS

A

Grave’s Disease

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20
Q

Often presents with VERY LOW TSH

A

Hyperthyroidism

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21
Q

May include Ophthalmology/dermopathy; proptosis/exophthalmos, “lid-lag”, conjunctival inflammation/edema, corneal drying (lymphocytic infiltration of the orbit, muscles, eyelids; may cause diplopia and compression of optic nerve

A

Grave’s Disease

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22
Q

May include non-inflammatory induration and plaque formation of pre-tibial areas leading to edema, thicker skin with “orange skinned” appearance; “pre-tibial myxedema”

A

Grave’s Disease

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23
Q

Complications include cardiac arrhythmias s/a new onset afib*; high output cardiac failure-toxic, dilated cardiomyopathy; thyroid storm and crises (extreme thyrotoxicosis with delirium, high fever, dehydration and death)

A

Hyperthyroidism

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24
Q

Definitive therapy; used to destroy overactive thyroid tissue; Tx of choice for Grave’s

A

Radioactive iodine

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25
Q

May hypersecrete thyroid hormone leading to thyrotoxicosis; Usually a benign adenoma or colloid cyst, but cancer is a possibility

A

Thyroid Nodule

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26
Q

Most thyroid cancers are what kind?

A

Papillary cancers

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27
Q

Outer layer of adrenal cortex secretes this:

A

Aldosterone

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28
Q

Major glucocorticoid secreted by middle and inner adrenal cortex: secretion regulated by ACTH release from pituitary

A

Cortisol

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29
Q

Inhibits insulin secretion; increases hepatic gluconeogenesis, decreases protein stores; dampens defense mechanisms; inhibits production/action of mediators of inflammation

A

Cortisol

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30
Q

Required for production of Angiotensin II; lowers serum calcium; Necessary for normal bodily function

A

Cortisol

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31
Q

Secreted in response to stress, trauma, infection, and major surgery; plays major role in supporting normal circulatory function and hemodynamic stability; “the permissive hormone”

A

Cortisol

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32
Q

Clinical syndrome/disease resulting form excessive systemic corticosteroids; Endogenous (overproduction) from tumors secreting cortisol or ACTH; Exogenous (glucocorticoid administration; superphysiologic)

A

Cushing’s Syndrome/Disease

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33
Q

Most common cause of Cushing’s Syndrome:

A

Exogenous: superphysiologic doses of glucocorticoids over prolonged time

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34
Q

Endogenous glucocorticoid excess; Pituitary adenoma secreting excessive ACTH

A

Cushing’s disease

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35
Q

Central obesity; “moon facies”, abdominal protuberance, “buffalo hump”, supraclavicular fat; Catabolic effect; thin skin with easy bruising/striae, thin extremities, muscle wasting

A

Cushing’s syndrome

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36
Q

Lab findings: hyperglycemia, glycosuria, leukocytosis; elevated cortisol levels with loss of diurnal pattern (in excess ACTH states, increased mineralocorticoid can lead to hypokalemia)

A

Cushing’s syndrome

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37
Q

Complications if untreated: Significant morbidity from diabetes, HTN, osteoporosis, susceptibility to infections, compression and pathologic fractures, femoral neck aseptic necrosis

A

Cushing’s syndrome

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38
Q

Glucocorticoid deficiency: fatigue, weakness, and hypotension NOT responding to IV fluids

A

Adrenal Insufficiency

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39
Q

Uncommon disease; autoimmune destruction of the adrenal cortex that can develop over time resulting in chronic deficiency of cortisol, aldosterone and adrenal androgens

A

Addison’s Disease

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40
Q

May result in hyper pigmentation of skin

A

Adrenal insufficiency

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41
Q

Dx: Abdominal CT (small non-calcified adrenals)

A

Addison’s; Adrenal insufficiency

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42
Q

High ACTH levels may be seen in:

A

Addison’s

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43
Q

A rare cause of secondary HTN; tumor of adrenal medulla releasing excessive amounts of norepinephrine/epinephrine into the circulation

A

Pheochromocytoma

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44
Q

HTN with paroxysms of severe HA’s, sweating and palpitations; Dx w/ 24H urine for catecholamines & metanephrines

A

Pheochromocytoma

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45
Q

Tx of choice for Pheochromocytoma

A

Laparoscopic removal of the tumor

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46
Q

Maintains calcium homeostasis in body; increases osteoclastic activity in bone resulting in delivery of Ca and PO4 into ciruclation

A

Parathyroid hormone (PTH)

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47
Q

Increases renal tubular reabsorption of Ca and increases PO4 excretion in urine

A

PTH

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48
Q

Regulates and maintains normal levels of serum ionized calcium

A

PTH

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49
Q

Hallmark is low ionized Ca; most common scenario is post-thyroidectomy or post removal of parathyroid adenoma; may develop with chronic magnesium deficiency which can impair PTH release

A

hypoparathyroidism

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50
Q

Muscles cramps, irritability, carpopedal spasm, tetany, seizures, paresthesias of hands and feet; decr cognitive function; Chvostek’s & Trousseaus’s sign; dry, thin nails, hyperactive reflexes

A

hypoparathyroidism

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51
Q

Labs: low serum total and ionized Ca, elevated PO4; ECG: prolonged QT interval

A

hypoparathyroidism

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52
Q

Hyper secretion of PTH, most often a parathyroid adenoma; Hallmark is elevation of serum total and ionized Ca

A

hyperparathyroidism

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53
Q

Increased excretion of Ca and PO4 by the kidney-> hypercalciuria; cortical bone resorption, osteopenia, osteoporosis

A

hyperparathyroidism

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54
Q

Hypercalcemia/hypercalciuria results in nephrogenic DI (decr sensitivity to ADH)

A

hyperparathyroidism

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55
Q

Labs: increased ionized calcium and PO4 often low (enhanced renal excretion)

A

hyperparathyroidism

56
Q

A skeletal disorder characterized by compromised bone strength predisposing to an increased risk of fracture

A

Osteoporosis

57
Q

MC metabolic bone disease; decreased bone matrix and mineral-> “thin bones”

A

Osteoporosis

58
Q

Increased bone resorption, esp. trabecular bone*

A

Osteoporosis

59
Q

Increases dramatically in puberty in response to gonadal steroids; peaks in young adults

A

Bone density (BD)

60
Q

Bone thinning=

A

osteopenia

61
Q

Etiologies include: Sex hormone deficiency, post-menopause, hypogonadism, excess glucocorticoids (Cushing’s), hyperparathyroidism, thyrotoxicosis (incr bone metabolism), Vit D deficiency

A

Osteoporosis

62
Q

Bone mineral density 1-2.5 SD below peak bone density

A

Osteopenia

63
Q

Bone mineral density >2.5 SD below peak bone density

A

Osteoporosis

64
Q

For managing osteoporosis, use in pts with hypogonadism or premature menopause

A

Estrogen replacement for prevention

65
Q

Inhibit osteoclastic bone resorption; Incr bone density (a little), decr fx; Long half life once in bone (10yrs)

A

Bisphosphonates

66
Q

Alendronate (Fosomax): take 30min before AM meal with water and remain upright for 30min to prevent esophagitis

A

Bisphosphonates

67
Q

What is important for patients taking bisphosphonates?

A

Dental care

68
Q

Increase bone density, but less than estrogen (less effective), less risk of adverse effects; Decr bone loss and incr bone density (less than estrogen); blocks estrogen effects on breasts and uterus*

A

SERMS

69
Q

Synthetic analog of PTH; targets bone formation; indicated for post menopausal women with osteoporosis and risk factors for fracture & hypogonadal men with osteoporosis

A

Teriparatide

70
Q

Islets of Langerhans: Beta cells secrete=

A

insulin

71
Q

Islets of Langerhans: Alpha cells secrete=

A

glucagon

72
Q

Major stimulus of insulin secretion is ___ absorbed from food

A

glucose

73
Q

Following a high carb meal, ____ secretion leads to rapid uptake, storage and use of glucose by all tissues, esp the liver, muscle and fat

A

Insulin

74
Q

Following a high carb meal, most absorbed insulin rapidly stored in liver as _____

A

glycogen

75
Q

Once glycogen stores are full–> insulin converts excess glucose to ___

A

fatty acids

76
Q

Inhibits gluconeogenesis in the liver

A

Insulin

77
Q

“spares” fat-inhibits breakdown; inhibits hormone sensitive lipase-> inhibits excessive fat cell breakdown and release of FA

A

Insulin

78
Q

Following a meal ____ promotes synthesis and storage–> stimulates transport of amino acids into cells

A

Insulin

79
Q

Decreases catabolism of protein; decreases gluconeogenesis in liver

A

Insulin

80
Q

Brain is dependent on ___ for energy

A

glucose

81
Q

Is the signal that determines energy source in the body

A

glucose

82
Q

When CHO present and glucose levels increase, ___ is used for energy and requires insulin

A

CHO

83
Q

When glucose (and insulin) levels decrease, ___ is broken down for energy

A

fat (lipids)

84
Q

Absence of insulin leads to excessive fat breakdown and abnormal FFA metabolism

A

Type 1 DM

85
Q

Secreted by alpha cells; increases glucose levels when needed; breaks down glycogen, increases gluconeogenesis; requires glycogen stores for major effects

A

Glucagon

86
Q

A syndrome with disordered metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or a combo of insulin resistance and inadequate secretion to compensate

A

Diabetes Mellitus

87
Q

Primarily autoimmune mediated with presence of islet cell antibodies; destruction of beta cells in pancreas; onset in juveniles; ketosis common if untreated

A

Type 1 DM

88
Q

Catabolic disorder; absence of insulin in response to glucose leads to hyperglycemia, and fat and protein breakdown (ketoacidosis)

A

Type 1 DM

89
Q

Infectious of toxic insult in genetically predisposed individuals; autoimmune response against altered pancreatic B cell antigens

A

Type 1 DM

90
Q

Circulating insulin prevents ketosis, not hyperglycemia; tissue insensitivity to circulating insulin (insulin resistance)

A

Type 2 DM

91
Q

Combination of insulin resistance and defect of B cells to secrete adequate insulin in response to glucose; aggravated by increased hyperglycemia; decreased insulin production develops over time

A

Type 2 DM

92
Q

Insensitivity to insulin contributed to by obesity, central fat distribution, storage of fat in muscle and inactivity; post-receptor defect in insulin action

A

insulin resistance

93
Q

Hepatic insensitivity results in increased gluconeogenesis-hyperglycemia

A

Type 2 DM

94
Q

Chronic hyperglycemia inhibits increase of insulin secretion normally seen in response to elevation of glucose; eventually destroys B cells permanently

A

Glucotoxicity

95
Q

AKA insulin resistance syndrome; constellation of findings that increase risk of atherosclerosis (3x); often associated with T2DM

A

Metabolic syndrome

96
Q

Findings include: (3 of 5 needed)= central obesity, hyperglycemia, HTN, incr TG, decr HDL

A

Metabolic syndrome

97
Q

Polyuria, thirst, wt loss, weakness, dehydration, polyphagia, ketoacidosis, hyperosmolality

A

Type 1 DM

98
Q

Often no sx early; polyuria, thirst, skin infection, vulvovaginitis, central obesity, hyperglycemia

A

Type 2 DM

99
Q

Reflects state of glycemia over 8-12 weeks; measure every 3-4 months in diabetic

A

HbA1C

100
Q

Diabetic dyslipidemia, high TG, low HDL

A

Type 2 DM

101
Q

Growth hormone, Prolactin, ACTH, TSH, LH, FSH

A

Anterior pituitary

102
Q

Arginine Vasopressin (ADH, AVP), Oxytocin

A

Posterior pituitary

103
Q

Prolactin release is inhibited by ____

A

dopamine

104
Q

Abnormal function of the pituitary

A

hypopituitarism

105
Q

Decr in LH/FSH (decr sex hormones)

A

Hypogonadism

106
Q

Lack all of the anterior pituitary hormones:

A

panhypopituitarism

107
Q

Deficiency of AVP/ADH (posterior pituitary)

A

Central Diabetes Insipidus

108
Q

Autoimmune; familial/genetic forms rare; no visual lesions of pituitary on MRI

A

Primary Diabetes Insipidus

109
Q

Damage to pituitary or pituitary stalk by tumor, surgery, anoxia

A

Secondary Diabetes Insipidus

110
Q

Inability of the kidneys to respond to ADH; congenital (lack ADH receptors) and acquired forms

A

Nephrogenic Diabetes Insipidus

111
Q

Excessive GH release, almost always from a pituitary adenoma

A

Acromegaly and Gigantism

112
Q

Tumor develops before closure of epiphyses; very tall=

A

Gigantism

113
Q

Tumor develops after epiphyseal closure; enlargement of hands, jaw, feet, bones of skull enlarge=

A

Acromegaly

114
Q

IGF-I increased 5x nl with=

A

acromegaly

115
Q

A somatostatin analog; suppresses GH secretion/ used in pts who continue to have excessive GH release post-op; shrinks some tumors

A

Octreotide

116
Q

MC cause is pituitary microadenoma

A

Hyperprolactinemia

117
Q

High levels of _____ suppress GnRH which decreases LH/FSH, resulting in hypogonatropic hypogonadism

A

Prolactin

118
Q

Rapid acting insulin

A

Lispro Insulin

119
Q

Intermediate acting insulin; requires 2-3 injections daily for sustained effect

A

Neutral insulin (Humulin N)

120
Q

Long acting Insulin; insulin analog; 24hr coverage with steady-state insulin levels; bedtime dosing

A

Insulin Glargine

121
Q

Insulin with very rapid onset; ideal pre-meal; rapidly deals with glucose load of meal (less post-meal hypoglycemia); Must correlate dose with CHO load; also used with insulin pump

A

Lispro Insulin

122
Q

Short-Acting insulin; take before meals

A

Regular (Humulin R)

123
Q

Incretin mimetics; potentiate insulin secretion; $$$; SubQ injection; suppress post-prandial glucagon; delay gastric emptying, promotes satiety; decr fasting and post meal glucose

A

GLP-1 Receptor Agonists

124
Q

According to data, what is more effective: Metformin + Insulin OR Metformin+ sulfonylurea + pioglitazone

A

Metformin + Insulin (& less expensive)

125
Q

MC complication seen with insulin and sulfonylurea use:

A

HYPOGLYCEMIA (BS

126
Q

What can mask hypoglycemia?

A

Beta blockers (esp non-selectives)

127
Q

Retinopathy, Nephropathy, and Neuropathy=

A

microvascular complications of diabetes

128
Q

Atherosclerosis (CHD, CVD, PAD)=

A

macrovascular complications of diabetes

129
Q

In diabetes, develops as a result of chronic hypErglycemia and contributed to by uncontrolled HTN

A

Diabetic nephropathy

130
Q

Leading cause of ESRD in U.S.

A

Diabetic nephropathy

131
Q

Losing 30-300mg albumin in urine=

A

mircroalbuminuria

132
Q

Initiatie in Type 1 & Type 2 diabetics in presence of microalbuminuria even if BP normal

A

ACE-I

133
Q

Life-threatening medical emergency primarily in T1DM; triggers from infection, trauma, surgery, MI which cause increased insulin requirements

A

Diabetic Ketoacidosis (DKA)

134
Q

Polyuria, polydipsia, abdominal pain, N/V, weakness, fatigue; stupor and coma may occur; Incr Pulse and decr BP; “fruity” breath, rapid breathing

A

DKA

135
Q

Inadequate insulin resulting in increased BS and increased FAT (& PROTEIN) breakdown

A

DKA

136
Q

Lipolysis leads to production of FFA and conversion to acetoacetic (ketoacid) and beta-hydroxybutyric acid leading to acidosis

A

DKA

137
Q

Results in metabolic acidosis with increased anion gap

A

DKA

Casey: Endocrine (5 decks)

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