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
what is the initial screening test for DM?
FPG: fasting blood sugar
- Dx: >=126 mg/dL
- fast for 8h with no calories
IFG:
- 100-125
HgbA1C
-A1C: glycated hemoglobin ->RBC in a sugar bath -> saturated
-4 months
-8-12 week glucose average
Criteria for diabetes dx
- A1c >= 6.5%
OR - FPG (fasting plasma glucose) >= 126 (7mmol/L) -> 8 hours fast
OR - 2 hour plasma glucose >= 200 (11.1mmol/L) during an OGTT- 75g glucose drink
OR - in a pt with classic symptoms of hyperglycemia (requent urination, increased thirst, and unexplained weight loss) or hyperglycemic crisis, a random plasma glucose >= 200
current guidelines: how frequently do you retests pts?
Normal Sugar: Retest every 3 years
- fasting glucose <100mg/dL
- A1C <5.7%
Pre- diabetics: Retest every 1-2 years
- fasting glucose is 100 to 125 mg/dL
- A1C: 5.7-6.4 %
What should you council diabetics on?
- smoking cessation
- diet
- exercise
- 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
Ppl with impaired fasting glucose (IFG) + impaired glucose tolerance (IGT) = PRE-DIABETIC
screening DM
- Adults aged 45 years+
- persons with multiple risk factors regardless of age
point of care glucose
Finger prick: can give different results from blood draw
- not diagnostic just monitoring
- variance
Use: Monitoring before meals for dosing insulin
-Assessing for hypoglycemia or hyperglycemia
-under 126 is goal (she said this)
Hemoglobin A1C: what is it
blood test that measures the % of glucose chemically attached to Hb in RBCs:
- provides an AVERAGE of blood glucose levels over the past 2 to 3 months
- used for monitoring long-term control of blood glucose
Dx:
- HbA1c level >6.5% = diabetes
- 5.7-6.4%: pre- diabetic -> retest every 3 yrs
- use NGSP certified lab + standardized to DCCT assay
What is an early marker of nephropathy?
microalbuminuria
-early marker of nephropathy/early kidney damage
Type 1 diabetics: will have _____ and you should test for it.
Pancreatic AUTOANTIBODIES against one or more:
-for type 1 diabetes you test for autoantibodies ***
Dont need to know specific names:
-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 flow chart
TRH: thyrotropin releasing hormone in Hypothalamus, induces TSH.
TSH- Thyroid Stimulating Hormone, Anterior pituitary, stimulates thyroid
T3: Triiodothyronine, Thyroid gland
- carries out majority of hormone actions
- primary feedback stimulus
T4: Thyroxine, Thyroid gland
-free T4 is what you typically order: not bound to TBG
- prohormone/active form -> T3 has much greater affinity
- T4 converts to T3 and small portion converted into reverse T3 (inactive)
- Free T4**- unbound to protein -> Better indicator of thyroid status
TBG: thyroid binding globulin:
- plasma protein for transport
What is the initial test for thyroid disease
TSH levels!!!
- inverse log-linear relationship between TSH and free T4 levels -> small changes in free T4 levels can cause significant changes in TSH levels
- ex: low t4 = HIGH TSH
Normal TSH: normal function of thyroid
Abnormal TSH:
- prompts further testing with free T4 test
What is a better indicator of thyroid status?
Free T4!!!
- unbound to protein
- not affected by changes in thyroid hormone binding proteins
continuous glucose monintor
-prevents hospitalizations
-on your body 24/7
-monitors glucose every 3 mins
-A1C monitored
-only used for injection therapy as of right now
anti-thyroid antibodies
Anti- TPO:
- Anti-thyroid peroxidase antibodies -> Antibodies against a protein in the thyroid gland that is essential for SYNTHESIZES of thyroid hormones
- indicates autoimmune thyroid disease (hypo/hyper)
- HIGH anti-TPO = HASHIMOTOS thyroiditis (90% of hypothyroid cases)
Anti- TG:
- Anti-thyroglobulin antibodies
- thyroglobulin = storage form of thyroid hormones within thyroid gland
- indicates autoimmune thyroid disease (hypo/hyper)
what is hyperthyroidism? + sx
Definition: A state characterized by excessive amounts of thyroid hormones in the body.
- Aka: Thyrotoxicosis.
Sx:
-Nervousness, palpitations
muscle weakness, heat intolerance, weight loss, perspiration
- fine tremor of hands
- sx reflect accelerated metabolic rate
-exophthalmos*
- goiter
Hyperthyroidism labs will show vs hypothyroidism labs
Hyperthyroidism:
-low TSH
- HIGH free T4 (thyrotoxicosis)
Hypothyroidism:
-Increased TSH
- LOW free T4
Diagnosis: hyperthyroidism
Initial TSH test:
- LOW TSH
- high free T4 = Primary (T4 thyrotoxicosis)
T3 thyrotoxicosis: low TSH, normal T4
- only T3 is elevated and T4 stays the same
Primary (T4 thyrotoxicosis):
- check for antibodies: GRAVES
- if no sx of graves: radioactive iodine uptake (RAIU) for toxic adenoma vs multiple adenomas vs thyroiditis (low RAIU)
HIGH TSH + HIGH Free T4 = pituitary adenoma
causes of hyperthyroidism
Graves disease: autoimmune TSH antibodies ds - antibodies stimulate the thyroid to produce too much
Toxic multinodular goiter: multiple nodules in thyroid gland
Toxic adenoma: single nodule in thyroid gland
Thyroiditis
initial screening modality for thyroid abnormality
TSH**
- check T3, T4, and antibodies if TSH is abnormal
hyperthyroid: toxic multinodular goiter
multiple nodules in thyroid gland that are independently producing hormones
-Less severe than graves
-Normal to high radioactive uptake
-Iodine localized to active nodules
-hot nodule -secreting T3 and T4
hyperthyroid: toxic adenoma
Single adenoma that secretes excess thyroid hormone in thyroid gland
-Radioactive uptake local to adenoma
hyperthyroidism: thyroiditis vs painless thyroiditis
thyroiditis:
-Viral infection
-Eventual return to normal
-No radioactive uptake
-Can progress to hypothyroid after inflammation
painless thyroiditis:
-caused by drug reaction
-Low TSH, elevated Free T4 & T3
-No radioactive uptake
hypothyroidism: what can it cause in infants; what is the definition and MC presentation?
Infants: cretinism - failure to grow
Definition:
- low free T4, HIGH TSH*
- 95% issue = in the thyroid
- MCC: Hashimoto thyroiditis (90% of cases)
High anti-TPO = Hashimoto thyroiditis 90% of hypothyroid cases:
- HIGH TSH
- low free T4
- TPO+: high anti-TPO
- causes gradual destruction of thyroid gland
Sx of hypothyroidism
-Dry hair
- dry skin
- cold intolerance
- weight gain
hypothyroidism diagnostic algorithm
Measure TSH:
- Normal TSH: consider pituitary function
- elevated TSH: check free T4
Free T4 and elevated TSH:
- normal T4 + high TSH: subclinical hypothyroidism
- low T4: primary hypothyroidism
Further Investigation: TPO antibodes
- + TPO, low T4, high TSH = hashimotos
adrenal cortex hormones
Glucocorticoids:
- Alter carbohydrate metabolism by increasing gluconeogenesis & decreasing glucose utilization
- CORTISOL
Mineralocorticoids:
-Sodium conservation and potassium loss
-Influence retention or loss of fluid
-ALDOSTERONE & CORTICOSTERONE
Sex steroids:
-Androgens
-Progestogens
-Estrogens
produces steroid hormones: cholesterol based
- synthesized by adrenals and modified by liver -> excreted in kidneys
What are glucocorticoids and mineralcorticoids regulated by?
ACTH in the anterior pituitary gland
- controls the cortex of adrenal gland: glucocorticoids + mineralcorticoids
Cortisol: characteristics + testing
Cortisol
- Highest in the morning: 4am-8am
- diurnal and pulsatile
- Alter carbohydrate metabolism by increasing glucogenesis & decreasing glucose utilization
Stress: elevates cortisol levels and disrupts circadian rhythm
-stress, hypoglycemia, exercise, infection, trauma -> hypothalamus: stimulates CRH RELEASE in hypothalamus
- increase ACTH -> increase cortisol -> neg feedback on pituitary and hypothalamus
24 hr urinary excretion of cortisol:
- is a reliable gauge of EXCESS cortisol secretion by the adrenal cortex
Renin/Angiotensin 2 (RAAS System)
Renin:
- made by kidney: juxtaglomerular apparatus
- released in response to decreased blood sodium, volume, and/or pressure
-Circulating renin hydrolyzes angiotensinogen to angiotensin I
angiotensin-converting enzyme (ACE):
- converts Ang I to Ang II
- produced in the lung
Angiotensin II:
- stimulates the cells of the adrenal cortex to secrete aldosterone
- potent vasoconstrictor: increases SVR and BP
Aldosterone:
- increase Na+ reabsorption, increase K+ excretion
When is renin released? in what response?
Decreased blood sodium, volume, and/or pressure.
Dexamethasone Suppression Tests:
Function:
- Dexamethasone suppresses CRH and ACTH
- used to determine if the adrenal glands are producing too much CORTISOL
- normal: glucocorticoid should decrease ACTH and decrease cortisol
Administer low dose of dexamethasone:
- NO suppression of cortisol with administration = CUSHING syndrome
CRH stimulation test
- Determines how the PITUITARY gland responds to hypothalamic hormone stimulation
- Test: synthetic CRH is administered, followed by measuring ACTH and cortisol
CRH test Outcome:
- Normal: increased ACTH and cortisol
- primary adrenal insufficiency: HIGH ACTH, normal cortisol
-secondary adrenal insufficiency: LOW ACTH and cortisol
ACTH Stimulation Test
- Evaluates adrenal gland responsiveness to ACTH.
- test: cortisol levels are measured before and after an injection of an ACTH analog
Outcome:
- normal = increase in cortisol levels
- no response = primary or secondary adrenal insufficiency
cushing syndrome definition
Definition: disorder of EXCESS CORTISOL production*
- ACTH dependent = MC
- -Low-dose dexamethasone Suppression Test*
-dexamethasone given to suppress ACTH + cortisol
- If Cushing: no suppression of ATCH!
Causes:
- adrenal origin tumor: ADRENAL cushing syndrome
- non-pituitary tumor: Cushing syndrome (common = lung carcinoma)
- PITUITARY tumor = Cushing DISEASE
Cushing syndrome vs Cushing disease?
Syndrome:
- ds where cortisol levels are too high: could have number of underlying causes
- LUNG carcinoma
- adrenal cushing
Disease:
- caused by a PITUITARY ademona
cushing symptoms
-hypertension
-amenorrhea
-fat pad
- wt gain
- moon face
- buffalo hump
- osteoporosis
hyperaldosteronism and hypoaldosteronism
Aldosterone = mineralocorticoid produced in the adrenal gland
Function:
- sodium retention and water resorption
- control of blood volume
-increases excretion of potassium
Hyperaldosteronism: HTN, hypervolemia, low potassium
Hypoaldosteronism: low blood volume and low sodium
adrenal medulla function
catecholamine production: NE, Epi, dopamine
- epinephrine most produced
-2-minute half life- cant test this with blood -> need urine tests
Urine catecholamines:
- accumulation over several hours - degradative products
- used to assess secretion over time
pheochromocytoma
RARE! Benign or malignant tumor of chromaffin cells
-secretes catecholamines
SX:
-HTN, palpitations, sweating, palpitations, anxiety
Dx:
-Measure free plasma metanephrines: first line
- then find the tumor! CT scan
-24 hour urine test
parathyroid gland
Disorders of parathyroid gland:
- alter calcium metabolism
- have an effect on bone
Parathyroid hormone (PTH) function:
- Regulates calcium levels in the blood
- reduces phosphorus reabsorption in kidneys (more excretion)
-Increase in PTH: increase in serum calcium and decrease in serum phosphorus
-A normal or elevated Calcium gives feed back to parathyroid to stop PTH production
-NO relation to pituitary: controlled by calcium levels
prolactin/ant pituitary feedback loop
Function:
- Stimulates development of the breasts
- promotes milk secretion from the breasts during lactation
- suppresses ovulation
nonpregnant, non lactating females and in males: blood levels of prolactin are low
During pregnancy and lactation, blood levels of prolactin increase, consistent with the hormone’s role in breast development and lactogenesis (milk production)
- stimulated by suckling
- POSITIVE feedback loop
Testes and Ovaries
Testes:
-Germ cells produce spermatogonia
-Sertoli cells synthesize a glycoprotein hormone called antimüllerian hormone
- Leydig cells synthesize testosterone.
Ovaries also have three cell types
- Germ cells produce oocytes.
- Theca cells synthesize progesterone
- Granulosa cells, synthesize estradiol
primary hyperparathyroidism
Definition: Excess PTH with HIGH CALCIUM
-Parathyroid adenoma
-Hyperplasia
-Carcinoma
Work Up: Calcium, PTH & phosphorus*
- high PTH, High CALCIUM
- low serum phosphate
Sx:
-Kidney stones, HTN, polyuria, constipation, depression, neuromuscular dysfunction, recurrent pancreatitis, osteopenia
“bones (osteoporosis), groans (muscle ache, HTN), moans (constipation + pancreatitis), kidney stones (+polyuria), psychiatric undertone (depression)”
secondary hyperparathyroidism
Caused by: chronic hypocalcemia -> compensation with increased PTH
- parathyroid gland hyperplasia
-MCC: renal disease or vit D deficiency
- often leads to bone disease
Work Up: HIGH PTH with LOW calcium*
- LOW calcium
- high phosphate*
- low vit D
why is phosphate high???
- kidney ds: not properly excreting phosphate
- vit D deficiency: vit d also promotes excreting phosphate
hypoparathyroidism
MCC: unintentional removal of parathyroid with thyroid surgery
Hypocalcemia sx:
- numbness, tingling, muscle spasms, convulsions
Work Up:
- PTH low and Calcium low
- elevated phosphorus*
pseudohypoparathyroidism
Inherited disorder:
-Resistance to the action of PTH
- pt has enough PTH but body doesnt respond
Work Up:
- HIGH PTH, low Calcium
-No response when given PTH**
osteoporosis
Definition: Decreased bone mass
-do a Bone Mineral Density Study
-Tx: Bisphosphonate
osteomalacia
softening of bone
-Deficient mineralization from disturbance in calcium and phosphorus metabolism from vit D deficiency
-can cause Rickets when before cessation of growth
-cant properly store calcium and phosphorous
growth hormone excess adults vs kids
-Excess in children- giantism
-excess in adults- acromegaly -> pituitary adenoma MC
Feedback loop for GH
Excess in children- giantism
-excess in adults- acromegaly -> pituitary adenoma MC
ADH/vasopressin
-Triggered by increase in osmolality.
ADH function:
- binds to receptors on smooth muscle that induce vasoconstriction: increase BP
- Increases water retention in collecting ducts back into bloodstream
-Negative feedback with atrial natriuretic peptide
Serum osmolarity calculation
ex:
Sodium (Na+): 140 mEq/L
Potassium (K+): 4 mEq/L
Glucose: 90 mg/dL
Blood Urea Nitrogen (BUN): 14 mg/dL
Estimated Serum Osmolality:
2 (140+4) + (14/2.8) + (90/18) = 298 mOsm/kg
Diabetes insipidus, dehydration, SIADH**: what is the serum Na+, serum osmo, urine osmo
SIADH:
- ADH HIGH = too much water in blood ->dilute hyponatremia + serum osmolarity
- low serum Na, low serum osmo, high urine osmo
Dehydration:
- high serum Na, high serum osmo, high urine osmo
Diabetes insipidus:
- ADH deficient = DILUTE urine
- 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
