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Diagnostic Medicine Exam 3 > Endocrine Diagnostic Testing > Flashcards

Endocrine Diagnostic Testing Flashcards

1
Q

Endocrine Glands

A 
Ductless glands
Secrete hormone into systemic circulation
Endo = internal
Exo = external
Controlled by feedback loops
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2
Q

Hormones of the Posterior Pituitary

A

Oxytocin: uterine muscles and mammary glands
ADH: kidney tubules

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3
Q

Hormones of the Anterior Pituitary

A 
TSH: thyroid
ACTH: Adrenal cortex
FSH and LH: testes or ovaries
Growth Hormone (GH): entire body
Prolactin (PRL): mammary glands in mammals
Endorphins: pain receptors in the brain
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4
Q

How does a hormone function?

A

Endocrine gland secretes a hormone, it binds with the receptor on the target cell and can have 3 responses:

  1. alters channel permeability by acting on pre-existing channel-forming proteins
  2. acts through second-messenger system to alter activity of pre-existing proteins
  3. activates specific genes to cause formation of new proteins

this sends a physiologic response and the cycle repeats itself

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5
Q

Humoral Stimulus

A

Hormone release caused by altered levels of certain critical ions or nutrients

Stimulus: low concentration of Ca2+ in capillary blood
Response: parathyroid glands secrete PTH which increases Ca2+

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6
Q

Neural Stimulus

A

Hormone release caused by neural input

stimulus: action potentials in preganglionic cympathetic fibers to adrenal medulla
response: adrenal medulla cells secrete epinephrine and norepinephrine

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7
Q

Hormonal Stimulus

A

Hormone release caused by another hormone (tropic hormone)

stimulus: hormones from hypothalamus
response: anterior pituitary gland secretes hormones that stimulate other endocrine glands to secrete hormones.

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8
Q

Hormone Transport

A

Hormones circulate both free and bound to plasma proteins

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9
Q

Bound hormones

A

Binding helps to increase the half-life of the hormone in the circulation
Hormones bound to transport proteins serve as reservoirs, replenishing the concentration of free hormones when they are bound to target tissue receptors or cleared from the circulation

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10
Q

What factors cause levels of plasma-binding proteins to vary?

A

age
disease states
certain drug therapies

Examples include CBG (cortisol binding globulin), SHBG (sex hormone binding globulin) and TBG (thyroid binding globulin)

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11
Q

Free Hormone

A

In most cases the free hormone:
Is the fraction available for binding to receptors and therefore represents the active hormone
Dictates the magnitude of feedback inhibition that controls hormone release
Is the fraction that is cleared from the circulation
Correlates best with clinical states or hormone excess and deficiency

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12
Q

Timing of Hormone Level Testing

A

Certain hormones are secreted in a more pulsatile/episodic manner and have shorter half lives
This leads to the need to measure hormones at particular times of the day or to rely on 24 hour collection methods

Example: circadian rhythm of ACTH and cortisol secretion

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13
Q

Endocrine Gland Regulation

A

The secretion rates of many (not all) hormones rhythmically fluctuate up and down as a function of time
Basal secretion of most hormones is not a continuous process but rather has a pulsatile nature

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14
Q

Examples of Pulsatile Release Patterns

A

Circhoral
Ultradian
Circadian
Diurnal

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15
Q

Circhoral

A

episodic release of about an hour

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16
Q

Ultradian

A

episodic release longer than an hour but less than 24 hrs

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17
Q

Circadian

A

episodic release approximately every 24 hrs

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18
Q

Diurnal

A

episodic activity is expressed at defined periods of the day

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19
Q

Primary Disease

A

involves the organ(s) that produce the hormone

e.g. primary hypothyroidism results from an underactive thyroid gland and ↓ T4

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20
Q

Secondary Disease

A

related to the pituitary which produces trophic hormones
(e.g. secondary hypothyroidism is due to an underactive anterior pituitary which secondarily ↓ thyroid function owing to ↓ TSH and subsequent ↓ T4)

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21
Q

Tertiary Disease

A

hypothalamic problems

e.g. tertiary hypothyroidism due to ↓ release of TRH which ↓ TSH which ↓ synthesis of T4

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22
Q

Primary Deficiency Disorder

A 
Examples
Hashimoto’s thyroiditis
Addison’s disease
Type 1 DM
Endocrine organ’s trophic (stimulating) hormone level is actually elevated due to normal feedback responses
↑ TSH and ↓ thyroid hormones
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23
Q

Secondary Deficiency Disorder

A

Example
Secondary hypothyroidism
Secondary adrenal insufficiency
Occurs when the trophic (stimulating) hormone for the target organ is deficient
Can develop due to primary hypopituitarism
Underactive anterior pituitary results in ↓ TSH which results in ↓ thyroid hormones

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24
Q

Tertiary Deficiency Disorder

A

Example
Tertiary hypothyroidism
Occurs one step higher than secondary problems
Hypothalamic problem
Impaired function of the hypothalamus results in ↓ TRH which ↓ TSH which ↓ thyroid hormones

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25
Q

Types of Endocrine Hyperfunction

A

As with deficiency syndromes, endocrine excess may occur in primary, secondary, or tertiary forms.
Parathyroid adenomas causing ↑ PTH production
Graves disease which is characterized by antibodies binding to TSH receptors causing ↑ thyroid hormone production
Anterior pituitary adenoma resulting in acromegaly
Anterior pituitary adenoma resulting in hyperthyroidism

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26
Q

How would you measure hormone deficiency?

A

Stimulation test

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27
Q

How would you measure hormone excess?

A

suppression test

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28
Q

Testing Endocrine Function: Capillary puncture

A

Finger stick glucose

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29
Q

Testing Endocrine Function: Venipuncture

A

Blood is obtained directly from the vein

Used for the majority of tests run on blood

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30
Q

Testing Endocrine Function: Arterial Stick

A

Blood is obtained directly from the artery.

Used for blood analysis

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31
Q

Testing Endocrine Function: Urine

A

Urine sample

24 hour urine

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32
Q

Testing Endocrine Function: Tissue

A

Obtained by biopsy

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33
Q

Glucose

A

The simple sugar (monosaccharide) that serves as the chief source of energy in the body.
Glucose is the principal sugar the body makes.
The body makes glucose from proteins, fats and, in largest part, carbohydrates.
Glucose is carried to each cell through the bloodstream.
Cells cannot use glucose without the help of insulin.
Some cells such as brain cells have severely limited storage capacities for either glucose or ATP, therefore the blood must maintain a fairly constant supply of glucose.

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34
Q

Cells cannot use glucose without the help of what?

A

insulin

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35
Q

Describe the brain and glucose

A

Some cells such as brain cells have severely limited storage capacities for either glucose or ATP, therefore the blood must maintain a fairly constant supply of glucose.

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36
Q

Insulin

A

Pancreatic hormone which works to lower blood glucose levels

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37
Q

Glucagon

A

Pancreatic hormone which works to raise blood glucose levels (works opposite to insulin)

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38
Q

Fatty Acids (FA) / Free Fatty Acids (FFA)

A

Source of fuel that is the product of fat breakdown

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39
Q

Triglycerides (TG)

A

Fatty acids packaged for future use

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40
Q

Amino Acids (AA)

A

Source of fuel that is the product of protein breakdown

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41
Q

Glycolysis

A

Breakdown of glucose to make energy (ATP) for the cell

42
Q

Gluconeogenesis

A

Generation of glucose from non-carbohydrate substances (such as glycerol from pyruvate, lipids, amino acids, and lactic acid).

43
Q

Glycogen

A

Long term storage molecule of glucose which is stored and synthesized mainly in the liver and muscles

44
Q

Glycogenesis

A

Formation of glycogen from glucose

45
Q

Glycogenolysis

A

Breakdown of glycogen into glucose for use as fuel

46
Q

Lypolysis

A

Breakdown of triglycerides to fatty acids and further degradation which leads to production of ketones and energy

47
Q

Pancreatic Islets

A 
Pancreatic islets (Islets of Langerhans) comprise 2% of pancreas and produce insulin and glucagon
Other 98% of pancreas cells produces digestive enzymes
48
Q

Insulin Secretion

A

Insulin secreted by beta () cells
Secreted during and after meal when glucose and amino acid blood levels are rising
Stimulates cells to absorb these nutrients lowering blood glucose levels
Promotes synthesis glycogen, fat, and protein
Suppresses use of already stored fuels
Brain, liver, kidneys and RBCs absorb glucose without insulin, but other tissues require insulin
Insufficiency or inaction is cause of diabetes mellitus

49
Q

Glucagon

A

secreted by alpha () cells
Released between meals when blood glucose concentration is falling
In liver, stimulates gluconeogenesis, glycogenolysis, and the release of glucose into the circulation raising blood glucose level
In adipose tissue, stimulates fat catabolism and release of free fatty acids
Glucagon also released in response to rising amino acid levels in blood, promotes amino acid absorption, and provides cells with raw material for gluconeogenesis

50
Q

Hyperglycemia

A

ELEVATED Blood Glucose (> 100 mg/dl)

51
Q

Normoglycemia (Euglycemia)

A

NORMAL Blood Glucose (70-100 mg/dL)

52
Q

Hypoglycemia

A

LOW Blood Glucose (< 70 mg/dL)

53
Q

Diabetes Mellitus Definition

A

Diabetes Mellitus (from ancient Greek)
Diabetes “siphon”
Mellitus “honey sweet flow”
From a time in which tasting a patient’s urine was still part of the physician’s diagnostic repertoire
Sweet taste of the urine, distinguished diabetes mellitus from diabetes insipidus

54
Q

Diabetes Mellitus Pathology

A

Disorder of glucose metabolism in which the action of insulin on body cells is inadequate leading to hyperglycemia
Either because of:
Insulin resistance (Type II diabetes mellitus)
State in which a given concentration of insulin is associated with a subnormal glucose response
Insulin deficiency (Type I diabetes mellitus)
Relative or absolute insulin deficiency

55
Q

Insulin Resistance Type II Diabetes Mellitus

A

State in which a given concentration of insulin is associated with a subnormal glucose response

Adult-onset* diabetes
Older, sedentary, overweight individuals
Family history of diabetes.
Cannot use insulin effectively (insulin resistance) so glucose builds up in the blood

56
Q

Insulin Deficiency Type I Diabetes Mellitus

A

Relative or absolute insulin deficiency

Juvenile-onset diabetes
Children & young adults
Immune system sees its own cells as foreign and attacks and destroys β-cells of the pancreas
In the absence of insulin, glucose cannot enter the cells so blood glucose increases

57
Q

Diabetic Hyperglycemia

A

Insulin deficit / resistance causes:
Rise in blood glucose (hyperglycemia)
Excess glucose spills into urine (glucosuria)
Glucose in urine increases its osmotic pressure resulting in loss of water and electrolytes (polyuria)
Bed-wetting in younger patients
Dehydration results
Thirst mechanism (polydipsia)
Lack of nutrient transport into cells causes large appetite (polyphagia)
Weight loss in patients with type I DM

58
Q

Diabetes Mellitus – Plasma glucose

A

Serum glucose levels must be evaluated according to the time of day they are performed and whether the patient has been fasting
Commonly assessed with:
Metabolic panel (BMP or CMP)
Glucometer (Accu-Chek)

59
Q

Diabetes Mellitus – Hemoglobin A1c

A

Blood test that represents the amount of glycosylated hemoglobin – the average blood sugar level for the 120 day period before the test
Reflects degree of hyperglycemia of the preceding 3 months
Advantageous because it is not affected by short-term variations in glucose
Used to diagnose and monitor DM

60
Q

Pre-Diabetes Diagnosis

A

“Pre-diabetes”, “impaired fasting glucose (IFG)”, or “impaired glucose tolerance (IGT)” recognizes a stage between normal glucose tolerance and overt diabetes mellitus
Symptomatic hyperglycemia may be absent, but there is increased risk for the atherosclerotic complications of diabetes and for the development of overt diabetes in the future
Those who score:
100 to 126 mg/dl on the FBG test, OR
140-199 mg/dl on the OGTT, OR
Hemoglobin A1c between 5.7 – 6.4%

61
Q

Diabetes Mellitus – ADA Screening

A

Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2) and have additional risk factors*
In the absence of criteria (risk factors), testing for diabetes should begin at age 45 years
If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more frequent testing depending on initial results (e.g., those with prediabetes should be tested yearly), and risk status

62
Q

Diabetes Mellitus - Urinalysis

A

Certain components of the dipstick U/A can be used to assess/screen for complications related to DM
Glucose
Glycosuria occurs when the filtered load of glucose exceeds the ability of the tubule to reabsorb it – with the most common etiology being uncontrolled diabetes mellitus
Ketones
Ketones, products of fat metabolism, normally are not found in the urine. A positive result (ketonuria) is associated with diabetic ketoacidosis
Protein
The reagent on most dipstick tests is sensitive to albumin. A significant amount of albumin in the urine (proteinuria) in a diabetic patient indicates renal disease (nephropathy)

63
Q

Anatomy of the Thyroid Gland

A
  • The thyroid gland is located anterior and lateral to the trachea, just below the thyroid cartilage (Adam’s apple). It consists of 2 lobes (one on each side of the trachea). The lobes are connected by a bridge of thyroid tissue called the isthmus, which is located just below the cricoid cartilage.
  • The thyroid gland is barely palpable. Hence, physical examination is a good way to detect thyroid gland enlargement, as could occur either in hyperthyroidism, or in those forms of hypothyroidism characterized by thyroid enlargement (e.g. - iodine deficient hypothyroidism).
64
Q

Important Aspects of Thyroid Physiology

A

About 99.95% of circulating T4 and T3 is bound to thyroid binding proteins.
Functional value of protein binding:
½ life is increased to days rather than minutes
Provides a substantial intravascular reservoir
H-P-T feedback mechanism maintains free T4 and T3 concentrations in normal range
Only the free fraction is biologically active – i.e cross cell membranes.

65
Q

TSH - Thyroid Stimulating Hormone

A

Thyroid-stimulating hormone (TSH) is produced by the pituitary gland
TSH stimulates the thyroid gland to release the hormones thyroxine (T4) and triiodothyronine (T3)
Mechanism is akin to a thermostat that is set to turn on the heater when it senses that the temperature has fallen below a preset range (or, visa versa)
In the early phases of developing thyroid disease, TSH is the first marker to reflect the disorder
TSH is therefore an exquisitely sensitive probe of thyroid status

66
Q

TSH - Thyroid Stimulating Hormone

A

TSH is the best initial or screening test of thyroid function
Evaluates both hyper & hypofunction
Low TSH = hyperfunctioning
High TSH = hypofunctioning
TSH levels can also be effectively used to follow patients being treated with thyroid hormone

67
Q

Free Thyroxine (T4)

A

Unbound thyroxine hormone, available for uptake by cells (metabolically active)
Used along with serum TSH to determine thyroid hyperfunction or hypofunction; initially to diagnose as well as for monitoring therapy

68
Q

Free Triiodothyronine (T3)

A

T3 is more active metabolically than T4
Used when TSH is abnormal, particularly with a normal free T4 result, to further determine thyroid hyperfunction or hypofunction

69
Q

Total T4 and Total T3

A

Measures the free + bound T4 and T3 in serum
Elevated in hyperthyroidism and decreased in hypothyroidism
Total T4 or T3 is an inadequate indicator of thyroid status → not routinely used

70
Q

What can affect the level of thyroid hormone binding proteins (THBP)?

A

Pregnancy
Estrogen Therapy
Genetic Thryoxine Binding Globulin Excess
Hepatic Disease

Patients may be misdiagnosed as being hyperthyroid or hypothyroid, but have no thyroid problem and need no treatment.

71
Q

Free T4 (FT4) and Free T3 (FT3)

A

Free thyroxine and free T3 are NOT affected by changes in thyroid binding protein concentrations
Conditions such as pregnancy or ERT do not affect FT4 /FT3
Free T4 is more specific than free T3
Free T3 levels can fall because of decreased T4 to T3 conversion in persons with non-thyroidal illness or malnutrition

72
Q

Thyroglobulin (Tg)

A

Thyroglobulin (Tg) levels are low or undetectable with normal thyroid function (note Tg ≠ TBG)
Elevation typically seen in the following settings:
Acute thyroiditis
Graves’ disease
Thyroid cancer
Monitoring of Tg levels is frequently used to evaluate the effectiveness of treatment for thyroid cancer and to monitor for thyroid cancer recurrence
Not routinely measured during initial work up

73
Q

Thyroid Antibodies

A

Several antibodies against thyroid antigens have been described in acute and chronic autoimmune thyroiditis.
These include:
Anti-thyroid peroxidase antibodies (antiTPOAb’s)
Thyroglobulin antibodies (TgAb or antiTGAb)
TSH (thyrotropin) receptor antibodies (TrAb or TSHRAb)
Thyroid-Stimulating Immunoglobulins (TSI)

74
Q

Thyroid Nuclear Medicine Scan

A

aka Thyroid uptake and scan, Thyroid scintigraphy
Thyroid uptake - 123I - given via I.V.
Measurements made 4-6hrs and 24 hours with a gamma counter, and compared to a control capsule.
Used to differentiate*
Graves’ disease
Toxic multinodular goiter
Thyroiditis
Thyroid malignancy
Pt must be on low iodine diet and off multivitamins x 4 weeks leading up to scan
Radioactive iodine scan produces “hot” or “cold” lesions
* Very good modality for evaluating nodule activity

Hypothyroidism – decreased uptake
Hyperthyroid – increased uptake (either diffuse or localized)

75
Q

Thyroid Nuclear Medicine Scan

A

Goiter
Non-specific term for enlargement of the thyroid.
A goiter may be diffuse (as in Graves’ disease or Hashimoto’s thyroiditis) or nodular.
Nodule
Discrete area that is clearly different from the surrounding thyroid tissue.
Usually palpable but may only be seen on a scan or ultrasound.
Imaging of nodules allows normally functioning thyroid tissue to be distinguished from hypofunctioning (“cold”) or hyperfunctioning (“hot”) lesions.
Hyperfunctioning (hot) nodules are unlikely to be cancerous.
Hypofunctioning (cold) nodules are associated with a higher incidence of malignancy.

76
Q

Goiter

A

Non-specific term for enlargement of the thyroid.

A goiter may be diffuse (as in Graves’ disease or Hashimoto’s thyroiditis) or nodular.

77
Q

Nodule

A

Discrete area that is clearly different from the surrounding thyroid tissue.
Usually palpable but may only be seen on a scan or ultrasound.

78
Q

Hyperfunctioning (hot) nodules

A
  • Not cancerous
  • accumlates radioiodine to greater extent than rest of gland
  • May be seen in hyperthyroidism
  • Remainder of gland may be suppressed
  • Less liely to be malignant than ‘cold’ nodule
79
Q

Hypofunctioning (cold) nodules

A

associated with a higher incidence of malignancy.

  • does not accumulate radioiodine
  • photopenic area on scan
    15-20% likelihood of malignancy
80
Q

Warm Nodule

A

Nodule accumulates radioiodine to same extent as rest of gland

81
Q

Thyroid Ultrasound

A

Used in setting of
Abnormal thyroid function studies
Palpable or visible physical findings
Distinguish between solid vs cystic nodules
Following growth or change over time
Visual guidance for fine needle aspiration biopsy

High resolution U/S can characterize thyroid gland characteristics, masses, regional blood flow and cystic structures
As small as 2 mm in diameter

Thyroid ultrasound refers to the use of high frequency sound waves to obtain an image of the thyroid gland and identify nodules. It tells if a nodule is “solid” or a fluid-filled cyst, but it will not tell if a nodule is benign or malignant. Ultrasound allows more accurate measurement of a nodule’s size and can determine if a nodule is getting smaller or is growing larger during treatment. Ultrasound aids greatly in performing thyroid needle biopsy by improving accuracy if the nodule cannot be felt easily on examination or is very small.

82
Q

Fine-Needle Aspiration (FNA) Biopsy

A

The procedure of choice for evaluating nodules is fine-needle aspiration (FNA) biopsy.
It is the most reliable test to differentiate the “cold” nodule that is cancerous from the “cold” nodule that is benign.
Fine needle aspiration/biopsy is the test of choice for diagnosing the nature of thyroid nodules
~75% will be benign with “high confidence”
~20% will be “indeterminate” (~20-40% of these will be cancer)
~5% will diagnose a malignant lesion
Do not let the term “follicular” mislead you. Follicular cells are malignant until proven other wise

83
Q

Parathyroid Glands

A 
Commonly 4 glands but can vary (2-6) 
Partially embedded in posterior surface of thyroid gland
Can be found from as high as hyoid bone to as low as aortic arch
Function
Secrete parathyroid hormone (PTH)
Increases blood Ca2+ levels
Promotes synthesis of calcitriol
Increases absorption of Ca2+ 
Decreases urinary excretion
Increases bone resorption
Monitor extracellular fluid (ECF) Ca+2
84
Q

Calcium Homeostasis

A 
Calcium (Ca+2) is important for a wide range of intracellular &amp; extracellular biological processes:
Muscle contraction
Exocytosis
Blood clotting
Formation of cardiac action potentials
Enzyme activation
Cell signaling
Bone &amp; tooth structure
Total serum concentration of calcium in human is maintained between 8.5-10.5 mg/dL.  Deviations in either direction are not readily tolerated and, if severe, can be life-threatening.
85
Q

PTH & Ca+2 Regulation

A

PTH effects on bone (direct)
Stimulates existing osteoclast activity
Stimulates new osteoclast production
PTH effects on the kidneys (direct)
Stimulates the reabsorption of Ca+2 in distal convoluted tubules
Stimulates 1-hydroxylation of 25-hydroxycholecalciferol (i.e. activation of Vitamin D)
PTH effects on the intestines (indirect)
Intestinal uptake of Ca+2 is stimulated by “active” Vitamin D
PTH has no directs effect on intestinal absorption of Ca+2

86
Q

Calcitonin (CT)

A

Secreted by thyroid C cells (parafollicular cells)
Counter-regulatory effect of PTH
Little role in calcium homeostasis
Thyroidectomy does not typically cause hypercalcemia
Clinical use → medullary thyroid cancer marker

87
Q

Calcium Imbalances - Hypercalcemia

A

Possible etiologies include:
Hyperparathyroidism
Bone malignancies
Prolonged immobilization
Excess vitamin D and calcium in the diet
Increase in ECF calcium depresses central and peripheral neural excitability, resulting in mental sluggishness, dulling of consciousness, muscle weakness and hypo-reflexia.
Increased concentrations of calcium in blood may cause calcium salts to precipitate out of solution because of their low solubility at physiological pH. “Stones” form, especially in the kidney, where they product severe painful damage (renal colic), which can lead renal failure and hypertension.
If the hypercalcemia is due to excessive bone resorption, an increased incidence of fractures can also occur.

Bones, stones, abdominal groans, psychic moans, with fatigue overtones”

88
Q

Parathyroid Disorders

A 
Blood Tests
PTH
Total Calcium
Phosphate
Vitamin D
89
Q

Parathyroid hormone (PTH)

A

PTH is produced by the 4 parathyroid glands
PTH acts to increase calcium levels in the body
Used along with other tests, such as calcium and/or vitamin D, to help diagnose and/or monitor treatment of conditions that cause calcium imbalances

90
Q

Total Calcium

A

A measure of both the free and bound forms of calcium
Serum calcium should be corrected for albumin
Used along with other tests, such as those for PTH and/or vitamin D, to help diagnose and/or monitor treatment of conditions that cause calcium imbalances
Commonly assessed with
Metabolic panel (BMP or CMP)

91
Q

Phosphate

A

Only about 1% of total body phosphate is present in the blood – most combines with calcium and is stored in bones and teeth
Used along with other tests, such as those for calcium, PTH, and/or vitamin D, to help diagnose and/or monitor treatment of conditions that cause calcium imbalances

92
Q

Vitamin D

A

The main role of vitamin D is to help regulate blood levels of calcium, phosphorus, and (to a lesser extent) magnesium
Two forms of vitamin D can be measured in the blood, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D
25-hydroxyvitamin D is commonly measured to assess and monitor vitamin D status
Used along with other tests, such as those for PTH, calcium, and/or phosphorus to help diagnose and/or monitor treatment of conditions that cause calcium imbalances

93
Q

Parathyroid Nuclear Medicine Scan

A

Most common radiotracer for parathyroid imaging is 99mTc-sestamibi
Sestamibi is a radionuclide that is taken up by the heart, thyroid, salivary glands, and abnormal parathyroid tissue

94
Q

Glucocorticoids – Cortisol

A

Cortisol secretion is pulsatile, diurnal and under the control of ACTH.

95
Q

Adrenal Lab Tests

A 
Serum total cortisol
24-hour urinary free cortisol
Plasma ACTH
ACTH stimulation
Dexamethasone suppression
96
Q

Serum Total Cortisol

A
  • Cortisol secretion is pulsatile, diurnal and under the control of ACTH
    Diurnal variation (AM>PM)
    Blood drawn between 8 a.m. and 9 a.m.*
  • > 10 mg/dL – unlikely to have adrenal insufficiency
    < 3 mg/dL – very likely to have adrenal insufficiency
    between 3-10 mg/dL – results are inconclusive
97
Q

24-Hour Urinary Free Cortisol

A

24-hour urine collection
Discard the first morning void
Collect for the next 24 hr, including the void at the end of the 24 hr
Record the last voiding time
Keep urine cool during collection. Higher temperatures alter the results.
If any urine is lost, discard the entire specimen and begin collection again the next day
Measures quantity of free cortisol collected
Ideal for suspected hypercortisolism

98
Q

Plasma ACTH

A 
ACTH produced by the pituitary gland
Stimulates cortisol production
Diurnal variation (AM>PM)
Collected with serum cortisol
Utility
Differentiate primary (adrenal) from secondary (pituitary) and tertiary (hypothalamic) source of cortisol imbalance
99
Q

ACTH Stimulation Test

A

Differentiate source of adrenal insufficiency (cortisol deficiency)
Utilizes cosyntropin (synthetic ACTH)
Short (rapid) version MC
Obtain baseline plasma cortisol level
250 mcg cosyntropin administered via IV
Measure plasma cortisol levels at 30 and 60 minutes

If cortisol level doubles = adrenal gland is functioning

if cortisol level has a subnormal response, there is adrenal sufficiency

100
Q

Dexamethasone Suppression Test

A

Confirm abnormal excess production
Utilizes dexamethasone (synthetic steroid)
Short (overnight) version MC
Obtain baseline plasma cortisol level
1 mg dexamethasone administered by mouth at 11 PM
Measure plasma cortisol levels at 8 AM

if cortisol level doesn’t change= excess cortisol production

if cortisol level is suppressed = adrenal gland is functioning

Diagnostic Medicine Exam 3 (1 decks)

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