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Chemistry Exam 2 Flashcards

1
Q

Half-life of Steroids

A

Hours

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2
Q

Half-life of Protein Hormones

A

Minutes

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3
Q

Steroid hormones are made from

A

cholesterol

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4
Q

Master Gland of the Endocrine System

A

Hypothalamus

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5
Q

The Pineal Gland produces

A

melatonin from serotonin

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6
Q

1° Disorder

A

Organ doesn’t respond

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7
Q

2° Disorder

A

Pituitary doesn’t make stimulating hormone

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8
Q

3° Disorder

A

Hypothalmus doesn’t produce releasing hormone

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9
Q

Anterior Pituitary produces

A
  • TSH
  • ACTH
  • Prolactin (PL)
  • FSH/LH
  • Growth Hormone (GH)
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10
Q

GH production is triggered by

A

Growth Hormone Releasing Hormone

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11
Q

Negative Feedback of GH is mediated by

A

Somatostatin

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12
Q

Effects of GH

A
  • Fat cell breakdown
  • Protein anabolism
  • Inc. blood glucose
  • Liver makes IGF-1
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13
Q

Effects of overproduction of GH

A

Before Puberty: giantism
After Puberty: acromegaly

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14
Q

Effects of underproduction of GH

A

Pituitary Dwarfism

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15
Q

Prolactin

A
  • associated with milk production
  • tumors that make prolactin can cause men to produce milk
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16
Q

Posterior Pituitary produces

A
  • Oxytocin
  • ADH
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17
Q

Parts of the Adrenal Gland

A

Cortex, subdivided into:
- Zona glommerulosa
- Zona fasciculata
- Zona reticularis
Medula

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18
Q

Zona glomerulosa produces

A

Aldosterone and other mineral corticoids

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19
Q

Zona fasciculata produces

A

Cortisol and other glucocorticoids

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20
Q

Zona reticularis produces

A

Sex hormones

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21
Q

Adrenal Medulla produces

A

Catecholamines:
- “Fight or Flight” hormones - epinephrine and norepinephrine
- Dopamine

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22
Q

Hirsutism

A

excess facial hair (especially notable in women)

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23
Q

Cushing’s Syndrome etiology

A

Excess adrenal hormones from adrenal tumor or exogenous cortisol

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24
Q

Cushing’s Disease etiology

A
  • more severe than syndrome
  • excess adrenal hormones from pituitary tumor
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25
Q

Adrenal diabetes

A
  • Cushing’s syndrome causes high blood glucose, causes long-term burn out of insulin-producing cells
  • Diabetes insipidus progresses to diabetes mellitus
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26
Q

Symptoms of Cushing’s

A
  • inc cortisol with no diurnal variation
  • inc blood gluc
  • inc aldosterone
  • inc Na+, dec K+
  • acidosis
  • physical symptoms (moon face, striae, buffalo hump)
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27
Q

Addison’s Disease etiology

A

Low adrenal hormones

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28
Q

Symptoms of Addison’s

A
  • dec blood gluc
  • dec Na+, inc K+
  • acidosis
  • physical symptoms (very thin, darkening of skin an mucus membranes)
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29
Q

Dopamine is made from/in

A

Tyrosine, Adrenal Medulla

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30
Q

Adrenal Liver Metabolites

A
  • Metanephrine (from epinephrine)
  • Normetanephrine (from norepinephrine)
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31
Q

Adrenal Urinary Metabolites

A
  • HVA (from dopamine)
  • VMA (from metanephrine)
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32
Q

Neuroblastoma

A
  • undifferentiated tumor
  • all catecholamines increased
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33
Q

Pheochromocytoma

A
  • differentiated tumor of the adrenal medulla
  • increased norepinephrine and epinephrine
  • increased liver metabolites and VMA
  • NORMAL HVA and dopamine
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34
Q

CaPO4

A

Hydroxyapatite

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35
Q

Physiologically active Calcium

A

Ca2+

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36
Q

Elevated Mg

A
  • Mg intoxication
  • Renal failure
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37
Q

Low Mg

A
  • Low intake or absorption
  • Excess renal loss
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38
Q

Parathyroids produce

A

Parathyroid Hormone (PTH)

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39
Q

PTH stimulates

A

Calcium and Phosphorus from bones to blood

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40
Q

Calcitonin stimulates

A

Calcium and Phosphorus from blood to bones

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41
Q

Calcitonin is produced by

A

C-cells of the thyroid

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42
Q

Normal ratio of calcium to phosphorus

A

2:1

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43
Q

Osteoclasts

A

involved in bone resorption

44
Q

Osteoblasts

A

involved in bone formation

45
Q

Vitamin D

A
  • steroid made from cholestrol
  • inc. absorption of calcium and phosphate in GI
  • inc calcium reabsorption and phosphate excretion in kidneys
46
Q

Active form of Vitamin D

A

1,25 Hydroxy Vitamin D

47
Q

Paget’s Disease

A
  • excess activity of osteoclasts and osteoblasts degrades bones in some areas and deposits them irregularly in others
  • Inc. Alkaline Phosphatase
48
Q

EGTA

A

Chelates calcium

49
Q

Total Calcium Assay methodology

A
  • Calcium complexes with o-CPC dye
  • interference removed with 8-hydroxy quinoline
50
Q

Ionized Calcium Assay methodology

A

Ion-selective electrode

51
Q

Ionized Calcium calculation

A

Ca++ = (6x total Ca - 1/3 total protein) / total protein + 6

52
Q

Phosphorus Assay methodology

A

ion complex with molybdate, then reduced with cupric acid to make Molybdenum Blue

53
Q

Magnesium Assay methodology

A
  • Magnesium binds dye (blue -> red)
  • interference removed with cyanide
54
Q

Thyroid hormones are built from

A

Mono- and di-iodated tyrosine (MIT and DIT)

55
Q

T3 is made from

A

MIT + DIT (3 iodines)

56
Q

T4 is made from

A

DIT + DIT (4 iodines)

57
Q

T3 vs T4

A
  • 10x as much T4 made
  • T3 is 5x as biologically active
58
Q

Reverse t3 (rT3)

A
  • liver deactivates T4 (remove an iodine)
  • not biologically active
  • related to energy conservation (inc in severe illness)
59
Q

How do thyroid hormones circulate in the body?

A

Bound to proteins, especially Thyroid Binding Globulin (TBG). Inactive in this state.

60
Q

Normal % free T4 (fT4)

61
Q

Normal % free T3 (fT3)

62
Q

Most common Thyroid Antibodies

A
  • Thyroid Peroxidase (TPO) Antibodies
  • Anti-thyroglobulin
  • Anti-TSH Receptor
63
Q

Hashimoto’s Thyroiditis almost always has what antibody?

64
Q

Grave’s Disease almost always has what antibody?

A

Anti-TSH Receptor

65
Q

Papillary carcinoma

A

Hypothyroid neoplasm - firm, solitary nodule

66
Q

Follicular carcinoma

A

Hypothyroid neoplasm - can metastasize

67
Q

Primary Congenital Hypothyroidism

A
  • Creatinism
  • Deficiency of thyroid tissue in newborns
  • Treat with T3 and T4
68
Q

Thyrotoxicosis

A
  • Inc in free and total thyroid hormones
69
Q

Hypothyroidism

A
  • slow metabolism
  • cold intolerance
  • goiter (inflammation)
  • tissue thickening (skin, tongue, vocal cords)
70
Q

Hyperthyroidism

A
  • metabolism in overdrive
  • heat intolerance
  • goiter (excess thyroid tissue)
  • Exophthalmos (eyelid retraction)
71
Q

Latrogenic hyperthyroidism

A
  • Lab numbers look bad, but no symptoms
72
Q

Thyroid Storm

A
  • acute hyperthyroidism
  • tachycardia, heart failure, fever, vomiting
  • 70-80% fatal if untreated
73
Q

Hashimoto’s: hypo or hyper?

A

Hypothyroidism

74
Q

Grave’s: hypo or hyper?

A

Hyperthyroidism

75
Q

Euthyroid Syndromes

A

Thyroid function tests are abnormal in seriously ill patients, but there is no thyroid condition (the body is coping with their illness)

76
Q

Estrogen effect on TBG

A

Inc TBG, T4 inc, normal fT3 and fT4

77
Q

Aldose

A

carbohydrate with 1 aldehyde

78
Q

Ketose

A

carbohydrate with 1 ketone

79
Q

Monosaccharide

A

Sugar with 1 ring

80
Q

Disaccharide

A

Sugar with 2 rings

81
Q

Oligosaccharide

A

Sugar with several rings

82
Q

Polysaccharides

A

Long chain branched carbohydrates (25-2500 rings)

83
Q

Primary polysaccharide of plants

84
Q

Primary polysaccharide of animals

85
Q

Glycogenesis

A

Synthesis of glycogen in the liver

86
Q

Glycogenolysis

A

Breakdown of glycogen

87
Q

Gluconeogenesis

A

Glucose formation from non-carbohydrate sources (fats, etc)

88
Q

Hormones that store glucose

89
Q

Hormones that pull glucose out of storage

A
  • Glucagon
  • Growth Hormone
  • Cortisol
  • Adrenal/Epinephrine
  • T4
90
Q

Insulin is produced by

A

beta cells of the islets of Langerhans in the pancreas

91
Q

Glucagon is produced by

A

alpha cells of the islets of Langerhans in the pancreas

92
Q

Which hormones trigger gluconeogenesis?

A

Glucagon and Cortisol

93
Q

Pre-diabetic Fasting Glucose

A

105-125 mg/dL

94
Q

Diabetic Fasting Glucose

A

> = 126 mg/dL

95
Q

Pre-diabetic 2 hr Glucose Tolerance/Postprandial

A

140-199 mg/dL

96
Q

Diabetic 2 hr Glucose Tolerance/Postprandial

A

> =200 mg/dL

97
Q

How fast is glucose lost on unspun tubes?

A

7% per hour

98
Q

CSF glucose level

A

2/3 of serum glucose. If lower in a septic patient, suggests organism is in the CSF

99
Q

Ketone Bodies

A
  • form when fat is used as the sole energy source
  • indicate the degree of ketosis
  • associated with Type 1 diabetics
100
Q

Ketone Body methodology

A

Sodium nitroprusside - purple when +

101
Q

HBA1C is also called

A

glycated hemoglobins

102
Q

HBA1C methodology

A

Immunoassay (structural difference)

103
Q

Urine Microalbumin

A
  • sensitive test for albumin
  • monitor diabetes associated renal disease
  • 30-300 mg/day = reversible
  • > 550 mg/day = not reversible
104
Q

Type 1 Diabetes

A
  • “absolute”
  • juvenile onset
  • high fasting glucose
  • autoimmune
105
Q

Type 2 Diabetes

A
  • “relative”
  • adult onset
  • can have normal fasting glucose
  • familial association
106
Q

Insulinoma

A

Insulin-producing tumor, causes fasting hypoglycemia

107
Q

Reactive hypoglycemia

A

pancreas over-produces insulin at mealtimes, crashing the blood glucose level

MLS (18 decks)

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