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Endocrine Laboratory Testing

Terms in this set (66)

overview of endocrine testing
principles: hormone measurement
- negative feedback loops

stimulation test to assess hypofunctioning
(hormone deficiency)

suppression test to assess hyperfunctioning
(hormone excess)
goals of endocrine testing
identify hormone(s) that are being over or under produced

determine which gland(s) are involved

determine the cause of hormone imbalance
diabetes mellitus type I
absolute insulin insufficiency due to destruction of pancreatic islet cells

autoimmune

idiopathic
diabetes mellitus type II
insulin resistance due to obesity & risk factors
DM type I symptoms
polyuria
polydipsia
wt loss
blurred vision
vomiting
lethargy
tachypnea
DM type II symptoms
asymptomatic
polyuria
polydipsia
polyphagia
fatigue
skin changes
recurrent infections
DM lab tests
plasma glucose
- random
- fasting
- oral glucose tolerance test

HbA1c

fasting C-peptide

DM antibody panel

urinalysis
plasma glucose
serum glucose levels must be evaluated according to the time of the day they are performed & whether the patient has been fasting

commonly assessed with:
- metabolic panel
- glucometer

in general, true glucose elevations indicate DM

criteria for dx of DM: FPG >/= 126
hemoglobin A1c
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

not affected by short-term variations in glucose

used to dx & monitor

ADA recommends HbA1c of < 7% for most DM patients
prediabetes
HbA1c 5.7-6.4
DM screening
testing should be considered in all adults who are overweight (BMI > 25) & have additional risk factors

absence of risk factors- testing should begin at 45

if normal results, testing should be repeated at least at 3 year intervals
c-peptide
c-peptide is a byproduct formed when proinsulin is processed into insulin

levels reflect insulin production

low or undetectable levels indicate absence of insulin secretion from pancreatic beta cell

helpful in distinguishing type I from type II (levels are decreased in type I)

insulin & C-peptide are linked when first made by pancreas
antibody panel
up to 90% of individuals with type I dm will have autoantibodies to specific antigens:

- glutamic acid decarboxylase

- insulin (IAA)

- islet cell (ICA)
urinalysis
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 dm

ketones: products of fat metabolism, normally are not found in the urine; positive result (ketonuria) is associated with diabetic ketoacidosis

protein: reagent on most dipstick tests is sensitive to albumin; significant amount of albumin in the urine (proteinuria) in a diabetic patient suggests renal disease (nephropathy)
hypothalamic- pituitary axis
primary disorder: involves target organ

secondary disorder: involves pituitary

tertiary disorder: involves hypothalamus

endocrine system coordinates functioning between different organs through hormones

interaction between hypothalamus & pituitary is a feedback control system
thyroxine (T4)
product of the thyroid gland

93% of metabolically active hormones secreted by the thyroid gland is T4
triiodothyronine (T3)
produced in peripheral organs from deiodination of T4

more potent than T4

much smaller quantities in blood

persists for shorter time
thyroid stimulating hormone (TSH)
produced by the pituitary gland

stimulates the thyroid gland to release the hormones T4 & T3

best thyroid screening test
free thyroxine (T4)
unbound thyroxine hormone, available for uptake by cells (metabolically active)

used along with serum TSH to determine thyroid hyperfunction or hypofunction; initially to dx as well as for monitoring therapy
total triiodothyronine (T3)
amount of bound plus unbound T3 in the blood

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
thyroid antibodies
develop when a person's immune system mistakenly targets components of the thyroid gland or thyroid proteins, leading to chronic inflammation of the thyroid (thyroiditis)

thyroid peroxidase antibody (TPO)

thyroglobulin antibody (TGAb)

TSH receptor blocking antibody (TSHRAb)

thyroid stimulating immunoglobulins (TSI)

thyrotropin binding inhibitory immunoglobulin (TBII)
primary hyperthyroidism
serum TSH low
serum free T4 high
what should all be positive in Graves' disease?
TSH receptor antibody (TRAb)

TSI

TBII
primary hypothyroidism
serum TSH high
serum free T4 low
calcitonin
secreted by thyroid gland
parathyroid disorders
hypocalcemia
hypercalcemia
hypocalcemia
weakness

paresthesias

tetany (chvostec & trousseau signs)

arrhythmia (QT prolongation)
hypercalcemia
moans
bones
stones
abd groans
psychiatric overtones
parathyroid disorders blood tests
PTH
total calcium
phosphate
vitamin D
parathyroid hormone (PTH)
produced by 4 parathyroid glands

acts to increase calcium levels in the body
total calcium
measure of both the free & bound forms of calcium

serum calcium should be corrected for albumin

half is bound to albumin

half is ionized
phosphate
only about 1% of total body phosphate is present in the blood- most combines with calcium & is stored in bones & teeth
vitamin D
help regulate blood levels of calcium, phosphorus, & magnesium

two forms can be measured in the blood: 25-hydroxyvitamin D & 1,25-dihydroxyvitamin D

- measurement of both in parathyroid dz may help with interpretation

25-hydroxyvitamin D only is measured to assess & monitor vitamin d storage status

the 25-hydroxyvitamin D is the major form found in the blood & is the relatively inactive precursor to the active hormone, 1,25-dihydroxyvitamin D

active vit d levels are not accurate reflections of vit d stores & should not be used to dx vit d deficiency in patients with normal renal function
diagnostic approach in hyperparathyroidism
first step: evaluate total calcium; if abnormal, correct for albumin
primary hyperparathyroidism
(hypercalcemia)
calcium high
PTH high
1,25 vit d high
phosphate low

overproduction coming from the parathyroid itself
corrected Ca +2 is equal to
serum Ca +2 + 0.8 (4-serum albumin)
Secondary hyperparathyroidism
decreased calcium

increased PTH

increased phosphate

parathyroid appropriately secretes PTH but there is chronic hypocalcemia due to underlying condition
Tertiary hyperparathyroidism
increased calcium

increased PTH

increased phosphate

state of excessive secretion of PTH after a long period of secondary hyperparathyroidism & resulting in high calcium levels
diagnostic approach in hypoparathyroidism
evaluate total calcium; if abnormal correct for albumin
primary hypoparathyroidism
(hypocalcemia)
calcium low
PTH low
1,25 vit d low
phosphate high
corticotropin-releasing hormone (CRH)
peptide hormone that stimulates both the synthesis & the secretion of adrenocorticotropic hormone (ACTH) in the corticotropin-producing cells (corticotrophs) of the anterior pituitary gland
adrenal disorder- cortisol deficiency
weakness
fatigue
anorexia
nausea
vomiting
skin changes
hyperpigmentation
adrenal disorders- cortisol excess
central obesity
moon facies
dorsocervical fatpad
menstrual irregularities
hirsutism
skin changes (abd striae)
adrenal disorders lab tests
serum total cortisol

plasma ACTH level

ACTH stimulation

24 hour urinary free cortisol

dexamethasone suppression
serum total cortisol
cortisol is a glucocorticoid released from the adrenal cortex that plays a role in multiple metabolic processes

blood should be drawn between 8am & 9am when cortisol levels peak
plasma ACTH level
ACTH is the hormone produced by the pituitary gland that stimulates the production of cortisol

normal diurnal variation (AM > PM)

used to differentiate primary (adrenal) from secondary (pituitary) & tertiary (hypothalamic) causes of cortisol imbalance

**sample should be collected simultaneously with morning serum cortisol for adequate interpretation
ACTH stimulation test
performed to differentiate etiologies of adrenal insufficiency

agent used is synthetic ACTH (cosyntropin)

2 versions:
- short: 60 minute (most common)
- long: 24 hr or 3 days

stimulation test to assess hypofunctioning (hormone deficiency)
rapid (short) test
obtain baseline plasma cortisol level

administer 250 mcg IV injection of cosyntropin over 2 minutes

measure plasma cortisol levels 30 & 60 minutes after cosyntropin administration
cortisol level doubles
adrenal gland is functioning
cortisol level subnormal response
adrenal insufficiency
ACTH should cause the release of
cortisol by the adrenal glands- inadequate cortisol release reflects inadequate adrenal functioning
24-hour urinary free cortisol
urine is collected over 24 hours & tested for cortisol

test of choice for patients suspected of hypercortsolism caused by Cushing syndrome
dexamethasone suppression test
test is performed to differentiate etiologies of excess cortisol production

agent used is a synthetic steroid (dexamethasone)

versions:
- short: overnight (most common)
- long: 48 hours
- low dose/high dose

suppression test to assess hyperfunctioning (hormone excess)

dexamethasone is the only glucocorticoid that does not cross-react or interfere with the measurement of cortisol levels
dexamethasone short test
obtain baseline plasma cortisol levels

administer 1mg of dexamethasone by mouth at 11pm

at 8 am measure serum cortisol levels
cortisol level no change
cushing syndrome
cortisol level suppressed (decreased)
adrenal gland is functioning
normal result of dexamethasone suppression test
decrease in cortisol levels upon administration of low dose dexamethasone

a low dose of dexamethasone suppresses cortisol in individuals with no pathology in endogenous cortisol production
administering dexamethasone should suppress
ACTH & result in decreased cortisol levels
suspect addison disease
obtain:
plasma ACTH
plasma cortisol
ACTH stimulation test
normal
no adrenal insufficiency
low cortisol
high ACTH
primary adrenal insufficiency
low cortisol
low ACTH
secondary or tertiary adrenal insufficiency
Primary adrenal insufficiency
adrenal damage
secondary/tertiary adrenal insufficiency
central issue

intrinsically normal but atrophic adrenal glands that are capable of producing cortisol but fail to do so bc ACTH secretion is deficient
corticotropin-releasing hormone (CRH) test
differentiation between secondary & tertiary adrenal insufficiency can be made by administration of corticotropin-releasing hormone; little or no ACTH response in patients with secondary or pituitary related adrenal insufficiency, whereas patient with tertiary dz due to lack of CRH from the hypothalamus usually have an exaggerated & prolonged ACTH response
diagnostic approach in cushing problem
initial:
- identify excessive cortisol secretion
- 24 hr urine free cortisol
- confirm failure of normal regulation
- failure to suppress on 1mg overnight dexamethasone suppression test

advanced:
- distinguish ACTH dependent from ACTH independent sources
- ACTH level
- high dose dexamethasone suppression
- CRH stimulation
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