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endocrine labs Flashcards

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1
Q

Diabetes dx

A

-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

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2
Q

what is the initial screening test for DM?

A

FPG: fasting blood sugar
- Dx: >=126 mg/dL
- fast for 8h with no calories

IFG:
- 100-125

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3
Q

HgbA1C

A

-A1C: glycated hemoglobin ->RBC in a sugar bath -> saturated
-4 months
-8-12 week glucose average

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4
Q

Criteria for diabetes dx

A
  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 (requent urination, increased thirst, and unexplained weight loss) or hyperglycemic crisis, a random plasma glucose >= 200
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5
Q

current guidelines: how frequently do you retests pts?

A

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 %

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6
Q

What should you council diabetics on?

A
  • smoking cessation
  • diet
  • exercise
  • intensive lifestyle counseling
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7
Q

categories of increased risk for diabetes: PREDIABETES

A

-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

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8
Q

screening DM

A
  • Adults aged 45 years+
  • persons with multiple risk factors regardless of age
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9
Q

point of care glucose

A

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)

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10
Q

Hemoglobin A1C: what is it

A

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

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11
Q

What is an early marker of nephropathy?

A

microalbuminuria
-early marker of nephropathy/early kidney damage

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12
Q

Type 1 diabetics: will have _____ and you should test for it.

A

Pancreatic AUTOANTIBODIES against one or more:
-for type 1 diabetes you test for autoantibodies ***

Dont need to know specific names:
-GAD65,
-IA2
-Insulin
-ZnT8

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13
Q

what you need to know for test

A

-normal
-pre-diabetes
-diabetes- 6.5 or greater
-diagnosis and target value is different for all

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14
Q

thyroid hormones flow chart

A

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

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15
Q

What is the initial test for thyroid disease

A

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

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16
Q

What is a better indicator of thyroid status?

A

Free T4!!!
- unbound to protein
- not affected by changes in thyroid hormone binding proteins

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17
Q

continuous glucose monintor

A

-prevents hospitalizations
-on your body 24/7
-monitors glucose every 3 mins
-A1C monitored
-only used for injection therapy as of right now

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18
Q

anti-thyroid antibodies

A

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)

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19
Q

what is hyperthyroidism? + sx

A

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

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20
Q

Hyperthyroidism labs will show vs hypothyroidism labs

A

Hyperthyroidism:
-low TSH
- HIGH free T4 (thyrotoxicosis)

Hypothyroidism:
-Increased TSH
- LOW free T4

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21
Q

Diagnosis: hyperthyroidism

A

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

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22
Q

causes of hyperthyroidism

A

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

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23
Q

initial screening modality for thyroid abnormality

A

TSH**
- check T3, T4, and antibodies if TSH is abnormal

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24
Q

hyperthyroid: toxic multinodular goiter

Study These Flashcards
A

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

25
hyperthyroid: toxic adenoma
Single adenoma that secretes excess thyroid hormone in thyroid gland -Radioactive uptake local to adenoma
26
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
27
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
28
Sx of hypothyroidism
-Dry hair - dry skin - cold intolerance - weight gain
29
30
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
31
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
32
What are glucocorticoids and mineralcorticoids regulated by?
ACTH in the anterior pituitary gland - controls the cortex of adrenal gland: glucocorticoids + mineralcorticoids
33
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
34
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
35
When is renin released? in what response?
Decreased blood sodium, volume, and/or pressure.
36
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
37
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
38
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
39
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
40
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
41
cushing symptoms
-hypertension -amenorrhea -fat pad - wt gain - moon face - buffalo hump - osteoporosis
42
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
43
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
44
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
45
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
46
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
47
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
48
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)"
49
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
50
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*
51
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**
52
osteoporosis
Definition: Decreased bone mass -do a Bone Mineral Density Study -Tx: Bisphosphonate
53
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
54
growth hormone excess adults vs kids
-Excess in children- giantism -excess in adults- acromegaly -> pituitary adenoma MC
55
Feedback loop for GH
Excess in children- giantism -excess in adults- acromegaly -> pituitary adenoma MC
56
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
57
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 ​
58
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
59
polyuria diff dx (just the jist)
-solute diuresis- loser concentration so water follows -water diuresis -losing water volume

Clinical Lab (17 decks)

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