Endocrine Labs Flashcards
Diabetes dx
-Random Blood Sugar: 200mg/dL with DM symptoms
-Fasting Blood Sugar: > or = 126mg/ dL after 8 hr fast on an Initial screening test
-Oral glucose tolerance test: glycemic response after a 75g glucose load, if 2 hrs post glucose >200 mg/dL
-HgbA1C: >6.5% -> Also used for monitoring tx
-steroid use can increase sugar
HgbA1C
-4 months
-8-12 week glucose average
-RBC in a sugar bath -> saturated
Criteria for diabetes dx
-1. A1c >= 6.5%
OR
-2. FPG (fasting plasma glucose) >= 126 (7mmol/L) -> 8 hours fast
OR
-3. 2 hour plasma glucose >= 200 (11.1mmol/L) during an OGTT- 75g glucose drink
OR
-4. in a pt with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose >= 200
current guidelines: sugars
-Retest every 3 years when fasting glucose <100mg/dL or A1C <5.7%.
-Retest every 1-2 years when fasting glucose is 100 to 125 mg/dL or 5.7-6.4 %
-Counseling on smoking cessation, diet, exercise.
-Diabetics should have intensive lifestyle counseling
categories of increased risk for diabetes: PREDIABETES
-A1C 5.7 to 6.4%
-FPG 100-125 (5.6-6.9)
-2 hour post load glucose on the 75 OGTT 140-199
screening
-screening for diabetes in adults aged 45 years or older and screening in persons with multiple risk factors regardless of age
point of care glucose
-finger prick
-Monitoring before meals
-Assessing for hypoglycemia or hyperglycemia
-Not used for diagnosis
-under 126 is goal (she said this)
-not used for dx just monitoring
microalbuminuria
-early marker of nephropathy
autoantibodies: type 1 diabetes
-Pancreatic autoantibodies against one or more:
-for type 1 diabetes you test for autoantibodies ***
-dont need to know specifics:
-GAD65,
-IA2
-Insulin
-ZnT8
what you need to know for test
-normal
-pre-diabetes
-diabetes- 6.5 or greater
-diagnosis and target value is different for all
thyroid hormones
-TRH – thyrotropin releasing hormone. Hypothalamus, induces TSH.
-TSH- Thyroid Stimulating Hormone. Anterior pituitary, stimulates thyroid.
-T3- Triiodothyronine. Thyroid gland
-T4- Thyroxine. Thyroid gland (active)
-TGB- Thyroid binding globulin -> Plasma protein for transport
-Free T4**- unbound to protein -> Better indicator of thyroid status
-free T4 is what you typically order
continuous glucose monintor
-prevents hospitalizations
-on your body 247
-monitors glucose every 3 mins
-A1c monitored
-only used for injection therapy as of right now
endocrine hormone pictures
thyroid hormone negative feedback
anti-thyroid antibodies
-Anti- TPO: Anti-thyroid peroxidase antibodies -> Antibodies against a protein in the thyroid gland that produces thyroid hormones -> Autoimmune thyroid disease
-Anti- TG: Anti-thyroglobulin antibodies
-same antibodies cause hypo and hyperthyroidism
hyperthyroidism
-Thryotoxicosis
-Nervousness, palpittions, muscle weakness, heat intolerance, weight loss, perspiration, exophthalmos, fine tremor of hands.
-Low TSH, high free T4
-Graves disease (autoimmune, TSH receptor antibodies), toxic multinodular goiter, toxic adenoma
-thyroiditis
initial screening modality for thyroid abnormality
TSH
-T3, T4, and antibodies -> if TSH is abnormal
hyperthyroid: toxic multinodular goiter, toxic adenoma, thyroiditis, painless thyroiditis
TOXIC MULTINODULAR GOITER
-Less severe
-Normal to high radioactive uptake
-Iodine localized to active nodules
-hot nodule -secreting T3 and T4
TOXIC ADENOMA
-Adenoma that secretes thyroid hormone
-Radioactive uptake local to adenoma
THYROIDITIS
-Viral infection
-Eventual return to normal
-NO radioactive uptake
-Can progress to hypothyroid after inflammation
PAINLESS THYROIDITIS
-Drug reaction
-Low TSH, elevated Free T4 & T3
-LOW radioactive uptake
hypothyroid
-Infants: cretinism
-95% issue in the thyroid
-Increased TSH, low free T4
-High anti-TPO = Hashimoto thyroiditis 90% of hypothyroid cases
-Dry hair, dry skin, cold intolerance
thyroid function tests
-Euthyroid- normal/true thyroid function
-primary hypo- TSH high, T3 and T4 low
-secondary hypo- TSH low, T3 and T4 low
adrenal cortex
-glucocorticoids- Alter carbohydrate metabolism by increasing glucogenesis & decreasing glucose utilization -> CORTISOL
-mineralocorticoids-
-Sodium conservation and potassium loss
-Influence retention or loss of fluid
-ALDOSTERONE & CORTICOSTERONE
-sex steroids
-Androgens
-Progestogens
-Estrogens
-cholesterol based, synthesized by adrenal and gonads
ACTH
-Glucocorticoids and mineralocorticoids regulated by corticotropin (ACTH) secreted by the anterior pituitary gland
-Cortisol- Highest in the morning 4am-8am
-Stress can blunt and reduce circadian rhythm
-stress, hypoglycemia, exercise, infection, trauma -> hypothalamus -> CRH -> pituitary -> ACTH -> adrenal gland -> cortisol -> neg feedback
Renin/Angiotensin 2
-Renin is released in response to decreased blood sodium, volume, and/or pressure.
-Circulating renin hydrolyzes angiotensinogen to produce angiotensin I, which is rapidly converted toangiotensin IIby angiotensin-converting enzyme (ACE) in the lung.
-Angiotensin IIthen stimulates the cells of the adrenal cortex to secrete aldosterone.Angiotensin IIis also a potent vasoconstrictor
cortisol testing
24 hr urinary excretion of cortisol is a reliable gauge of excess cortisol secretion by the adrenal cortex
cushing syndrome
-Disorder of excess cortisol production
-Low-dose dexamethasone Suppression Test
-Glucocorticoid given to suppress ACTH and then cortisol -> If Cushing no suppression of ATCH!
-1. Cushing Disease (pituitary adenoma)*- continuous demand to make more ACTH
-2. Adrenal Cushing Syndrome (adrenal tumor)- know why this is diff (low ACTH)
-3. Cushing Syndrome (lung carcinoma)- tumor secretes ACTH
cushing symptoms
-hypertension
-amenorrhea
-fat pad
adrenal insufficiency: ACTH stimulation test
-Bolus of ACTH given
-Lack of rise in cortisol indicates adrenal insufficiency
adrenal insufficiency: CRH stimulation
-Does pituitary respond?
-Used if ACTH stim abnormal to find site of malfunction
-is it coming from pituitary of acceptance of signal from pituitary
-Primary have elevated ACTH but no cortisol
-Secondary have low ACTH and cortisol
hyperaldosteronism and hypoaldosteronism
-Aldosterone is a mineralocorticoid produced in the adrenal gland
-Responsible for sodium retention and water resorption, control of blood volume
-Excretion of potassium
-Hyperaldosteronism: HTN, hypervolemia, low potassium
-Hypoaldosteronism: low blood volume and low sodium
adrenal medulla
-The catecholamine epinephrine produced the greatest in adrenal medulla.
-2-minute half life- cant test this with blood -> urine tests
-Urine catecholamines, pool delivered in preceding hours, degradative products
pheochromocytoma
-RARE! Benign or malignant
-Chromaffin cell tumor, secretes catecholamines
-HTN, palpitations, sweating, palpitations, anxiety
-Measure plasma metanephrines or urinary metanephrines and then find the tumor!
-24 hour urine
parathyroid
-Disorders alter calcium metabolism and have an effect on bone
-Parathyroid hormone (PTH) secreted from parathyroid gland
Regulates calcium in extracellular fluids
-Increase in PTH causes increase in serum calcium and decrease in serum phosphorus
-A normal or elevated Calcium gives feed back to parathyroid to stop PTH production
-calcium and phosphorous are indirect
-no relation to pituitary
primary hyperparathyroidism
-Excess PTH, high Calcium
-Kidney stones, HTn, polyuria, constipation, depression, neuromuscular dysfunction, recurrent pancreatitis, osteopenia
-Parathyroid adenoma
-Hyperplasia
-Carcinoma
-Work Up: Calcium, PTH & phosporus*
-bone (osteoporosis), groans (muscle ache), moans (GI upset), kidney stones, psychiatric undertone
-high vitamin D, Ca reabsorption, bone resorption
secondary hyperparathyroidism
-Chronic hypocalcemia -> compensation with increased PTH.
-Renal disease or Vit D deficiency
-Work Up: High PTH with low calcium*
vitamin D deficiency
hypoparathyroidism
-Most common with unintentional removal of parathyroid with thyroid surgery
-Hypocalcemia produces numbness, tingling, low serum calcium levels, muscle spasms, convulsions
-Work Up: PTH low and Calcium low, elevated phosphorus*
pseudohypoparathyroidism
-Resistance to the action of PTH
-Work Up: High PTH, low Calcium
-No response when given PTH*
osteoporosis
-Decreased bone mass
-Bone Mineral Density Study
-Bisphosphonate treatment
osteomalacia
-Deficient mineralization from disturbance in calcium and phosphorus
-Rickets when before cessation of growth
-cant properly store calcium and phosphorous
ovaries and testes loop
anterior pituitary: GH and somatostatin
growth hormone excess
-children- giantism
-adults- acromegaly -> pituitary adenoma MC
prolactin/anterior pituitary chart
antidiuretic hormone (ADH) / posterior pituitary
ADH/vasopressin
-Triggered by increase in osmolality.
-ADH: binds to receptors on smooth muscle that induce vasoconstriction, increased BP and volume. Increases water retention
-Negative feedback with atrial natriuretic peptide
serum osmolality
Diabetes insipidus, dehydration, SIADH**
-diabetes insipidus- ADH deficient
-SIADH- ADH high
-SIADH- low serum Na, low serum osmo, high urine osmo
-dehydration- high serum Na, high serum osmo, high urine osmo
-diabetes insipidus- high serum Na, high serum osmo, low urine osmo
polyuria diff dx (just the jist)
-solute diuresis- loser concentration so water follows
-water diuresis -losing water volume
