endocrine labs Flashcards

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

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
Q

hyperthyroid: toxic adenoma

A

Single adenoma that secretes excess thyroid hormone in thyroid gland
-Radioactive uptake local to adenoma

26
Q

hyperthyroidism: thyroiditis vs painless thyroiditis

A

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
Q

hypothyroidism: what can it cause in infants; what is the definition and MC presentation?

A

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
Q

Sx of hypothyroidism

A

-Dry hair
- dry skin
- cold intolerance
- weight gain

29
Q
A
30
Q

hypothyroidism diagnostic algorithm

A

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
Q

adrenal cortex hormones

A

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
Q

What are glucocorticoids and mineralcorticoids regulated by?

A

ACTH in the anterior pituitary gland
- controls the cortex of adrenal gland: glucocorticoids + mineralcorticoids

33
Q

Cortisol: characteristics + testing

A

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
Q

Renin/Angiotensin 2 (RAAS System)

A

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
Q

When is renin released? in what response?

A

Decreased blood sodium, volume, and/or pressure.

36
Q

Dexamethasone Suppression Tests:

A

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
Q

CRH stimulation test

A
  • 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
Q

ACTH Stimulation Test

A
  • 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
Q

cushing syndrome definition

A

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
Q

Cushing syndrome vs Cushing disease?

A

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
Q

cushing symptoms

A

-hypertension
-amenorrhea
-fat pad
- wt gain
- moon face
- buffalo hump
- osteoporosis

42
Q

hyperaldosteronism and hypoaldosteronism

A

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
Q

adrenal medulla function

A

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
Q

pheochromocytoma

A

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
Q

parathyroid gland

A

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
Q

prolactin/ant pituitary feedback loop

A

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
Q

Testes and Ovaries

A

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
Q

primary hyperparathyroidism

A

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
Q

secondary hyperparathyroidism

A

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
Q

hypoparathyroidism

A

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
Q

pseudohypoparathyroidism

A

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
Q

osteoporosis

A

Definition: Decreased bone mass
-do a Bone Mineral Density Study
-Tx: Bisphosphonate

53
Q

osteomalacia

A

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
Q

growth hormone excess adults vs kids

A

-Excess in children- giantism
-excess in adults- acromegaly -> pituitary adenoma MC

55
Q

Feedback loop for GH

A

Excess in children- giantism
-excess in adults- acromegaly -> pituitary adenoma MC

56
Q

ADH/vasopressin

A

-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
Q

Serum osmolarity calculation

A

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
Q

Diabetes insipidus, dehydration, SIADH**: what is the serum Na+, serum osmo, urine osmo

A

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
Q

polyuria diff dx (just the jist)

A

-solute diuresis- loser concentration so water follows
-water diuresis -losing water volume