ENDOCRINOLOGY Flashcards

1
Q

Explain the renin aldosterone path–how does this contribute to secondary hypertension

A

Low CO –> low renal perfusion –> high renin –>high angiotensin I –> high angiotensin II –>high aldosterone –> retention of sodium/water (EXCRETION of K)–>high BP

SECONDARY HTN
(1) renal artery fibromuscular dysplasia
- young woman w/ new or difficult to control HTN
- LOW perfusion to kidneys –>so HIGH renin
-systolic abdominal bruits +/- low/normal potassium

(2) Primary hyperaldosteronism
-High aldosterone
-LOW renin (note Cushing syndrome assoc w/suppressed renin)
-low potassium

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2
Q

What are ekg findings of hyperkalemia

A

(1) peaked T waves (also see w/MI, brain hemorrhage)
(2) decreased amplitude p waves

*NOTE: ekg findings for HYPOkalemia –>U wave (also see w/digoxin, amiodarone, bradycardia)

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3
Q

When is RAIU high? Low?

A

RAIU distinguishes Graves from other forms of hyperthyroidism

RAIU HIGH (<30%)
-Graves
-Tx: methimazole, Propylthiouracil (Pregnancy=PTU)

RAIU LOW
-acute thyroditis (painful)
-iodine excess/ amiodarone deficiency (usus geographic change)
-struma ovari
-Tx: BB (atenolol) or prednisone (if tenderness)

NOTE:
1) Thyrotoxicosis describes high levels of circulating thyroid hormones (T4 and T3) from any cause.
2) Thyrotoxicosis is diagnosed with a low TSH and elevated free T4 and/or total T3.
3) Thyroid scintigraphy with RAIU can verify the cause; HIGH w/Graves and LOW in other causes
4) Thyroid-stimulating immunoglobulin (TSI) or thyrotropin (TSH) receptor antibodies (TRAb) measurement can identify Graves disease (with high sensitivity and specificity)

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4
Q

When is thyroglobulin high? low?

A

Thyroglobulin is only high for endogenous hyperthyroid conditions. For all hyperthyroid (ie factitious) will be LOW

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5
Q

What decr levothyroxine absorption (makes hypothyrodism worse)

A

1) CALCIUM
2) IRON
3) Also:
-PPIs
-Binding agents (sucralfate cholestyramine)
-SSRIs, sertraline (esp if started/stopped/dosage change)

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6
Q

What is tx for hyperthyrodisim

A

Three treatment modalities for hyperthyroidism are (1) thionamides (methimazole and propylthiouracil), (2) radioactive iodine ablative therapy, and (3) thyroidectomy; the choice of treatment depends on the cause of the hyperthyroidism and patient preference

-1st line: methimazole
-IF pregnant: Propylthiouracil. Radioactive iodine is contraindicated
-IF thyroid storm: Propylthiouracil (preferred) or methimazole
-IF thyroiditis: NSAIDS
-IF Severe Graves ophthalmopathy: Methimazole or thyroidectomy. Avoid radioactive iodine

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7
Q

Describe testing/diagnosis for thyroid nodules?

A

When a nodule is discovered, assess thyroid function with a serum TSH level.

1) IF Low TSH (hyperthyoidism) → radioisotope scan scintigraphy

2) IF Normal or high TSH (hyPOthyroidism) → obtain ultrasonography.

3) FNAB is indicated after u/s:
- nodules >1 cm w/ suspicious features on u/s
- nodules <1 cm w/ RFs for thyroid cancer or suspicious ultrasound characteristics

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8
Q

Desc metabolic/lab findings with adrenal insufficiency

A

1) LOW aldosterone
* low aldosterone: low Na reabsorption/ low H/K excretion
- hyponatremia/hypotension, hyperkalemia/metabolic acidosis
- glucocorticoid deficiency

2)ELEVATED ACTH (primary only)
-hyperpigmentation (tanned)

3) Anion GAP
-pre-renal state

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9
Q

When do you measure T3

A

ONLY for HYPERthyroidism
-Meas if FT4 normal despite suppressed TSH

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10
Q

How do you diagnose adrenal insufficiency?

A

1) 8 AM Cortisol test
-IF High (>15) –>NOT adrenal insufficiency (AI)
-IF Low (<3) –>AI
-IF equivocal (3-15) –>ACTH Stim Test

2) ACTH Stim test (ONLY if cortisol 3-15)
-IF peak cortisol high (>18) –>NOT AI
-IF peak cortisol low (<18) –> AI

3) MEASURE ACTH (after cortisol test, and +AI)
- IF High –>primary AI
-IF Low –>secondary AI

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11
Q

What is the management for DKA?

A

1) FLUIDS
- Give 0.9% saline IV at 1 L/h
- SWITCH to 0.45% saline if corrected serum sodium level becomes normal or high.

2) GLUCOSE (goal 150-200)
- Give IV insulin
- SWITCH to 5% dextrose (w/ 0.45% saline) if plasma glucose 200 mg/dL (or 300 mg/dL in HHS)

3) POTASSIUM (goal 4-5 range)
-If serum potassium LOW (<3.3 mEq/L), do not start insulin; instead, give IV potassium chloride until level is >3.3 mEq/L. Then Add 20-30 mEq of potassium chloride to each liter of IV fluids to keep serum potassium level in the 4-5 mEq/L range.
-If serum potassium HIGH ( >5.2 mEq/L), do not give potassium chloride; instead, start insulin and IV fluids and check serum potassium level every 2 hours.

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12
Q

What is DKA? What is HHS?

A

HHS
-Hyperglycemic hyperosmolar syndrome
-Occurs with extreme hyperglycemia (>600 mg/dL) in OLDER pts w/ DM2
-Labs: no or low serum levels of ketones, and a relatively normal arterial pH and bicarbonate level.

DKA
-hyperglycemia, ketosis, and hypovolemia.
-Labs: plasma glucose level ≥250 mg/dL, arterial blood pH ≤7.30, bicarbonate level ≤15 mEq/L, increased anion gap, and positive serum ketone levels.

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13
Q

What 3 labs used to diagnose DM2? Do you have to confirm abnl results? What is 1 scenario where abnl results do NOT have to be repeated?

A

Diabetes mellitus can be diagnosed by an abnormal result on one of the following screening tests:
(1) hemoglobin A1c >6.5
(2) fasting plasma glucose >126
(3) oral glucose tolerance test.

** Abnl testing needs to be confirmed 2x.
** A single plasma glucose measurement of
> 200 mg/dL + plus symptoms is also diagnostic for DM2

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14
Q

How do you control triglycerides in DM2?

A

Triglycerides related to glucose control!
-If glucose control poor, triglycerides wil be high
-If triglycerides high and LDL normal in DM2–start statin!

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15
Q

Describe lab values of hypocalcemia caused by LOW PTH

A

-low PTH
-low Calcium
-High Phosphate

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16
Q

What are hormones of anterior pituitary. Dx of excess?

A

“FLAT PIG”
FSH
LSH
ACTH –> cortisol excess, aldosteronism
TSH
Prolactin –>Prolactinoma (decr LH/FSH)
GH –>acromegaly

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17
Q

How do you diagnosis cortisol excess

A

Cortisol excess
-pituitary dependent: Cushing disease
-NOT 2/2 pituitary: Cushing Syndrome

DIAGNOSING CORTISOL EXCESS:
1) First-line: overnight low-dose dexamethasone suppression test, 24-hour urine free cortisol measurement, and late-night salivary cortisol measurement; 2 or 3 tests must be abnormal.
2) Measure ACTH; determine whether the patient has adrenocorticotropic hormone-dependent or -independent Cushings.

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18
Q

How do you treat cortisol excess?

A

Surgical resection is the definitive treatment

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19
Q

How do you dx aldosterone excess?

A

SUSPECT in pts w/resistant HTN +/- low normal K
1) Order plasma renin activity
-plasma aldosterone concentration (PAC)/PRA (plasma renin actvitity)

A plasma aldosterone–plasma renin activity ratio >20, with a plasma aldosterone level >15 ng/dL, strongly suggests primary hyperaldosteronism.

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20
Q

How do you tx aldosterone excess?

A

-Spironolactone or eplerenone is the treatment of choice for adrenal hyperplasia.
-Laparoscopic adrenalectomy is indicated for an aldosterone-producing adenoma (will show on adrenal vein sampling)

21
Q

Desc thyrotoxicosis?

A

*thyrotoxicosis: any cause of thyroid hormone excess.
*Hyperthyroidism is thyrotoxicosis caused by excessive endogenous thyroid hormone production.

22
Q

what are side effects of methimazole, PTU?

A

Agranulocytosis and liver dysfunction are rare but serious adverse effects of thionamides.

23
Q

Do you tx subclinical hyperthyroidism?

A

Treatment of subclinical hyperthyroidism is recommended for patients with thyroid-stimulating hormone level less than 0.1 μU/mL (0.1 mU/L) and cardiac risk factors, heart disease, high risk for osteoporosis, or symptoms.

24
Q

Define RAIU for thyroid excess

A

high (above 30%) or inappropriately normal in hyperthyroidism due to Graves disease and low (less than 10%) in other causes of thyrotoxicosis such as destructive thyroiditis.

25
Q

What is treatment for pheochromocytoma? Dx? Sx?

A

TX:
-surgical resection.
-Preoperative α-receptor blockade with phenoxybenzamine before surgery is essential to prevent hypertensive crises during surgery.

DX:
-urine measurements of metanephrines and catecholamines or measurement of plasma metanephrines is preferred.

SX:
-Resistant HTN

26
Q

What conditions is pheochromocytoma associated with?

A

Pheochromocytoma is associated with MEN2, von Hippel-Lindau disease, and neurofibromatosis type 1.

27
Q

What is tx for hyperaldosteronism? Dx? Sx?

A

SX
-resistant HTN

DX
-plasma aldosterone–plasma renin activity ratio >20, with a plasma aldosterone level >15 ng/dL
-HTN, hypokalema

28
Q

What is A1C goal

A

In young, otherwise healthy patients, the American Diabetes Association recommends a hemoglobin A1c target of less than 7% in most nonpregnant adults.

29
Q

Describe incidental:
-pulmonary nodule
-adrenal nodule

A

ADRENAL NODULE
- Surgery recommended for (1) adrenal masses >4 cm OR (2) functioning tumors.

30
Q

Describe incidental:
-pulmonary nodule
-adrenal nodule

A

ADRENAL NODULE
- Surgery recommended for (1) adrenal masses >4 cm OR (2) functioning tumors.

PULMONARY NODULE
LOW-RISK
<6 mm: No follow-up
>8 mm: CT at 3 months, PET/CT, or tissue sampling

HIGH-RISK
<6 mm: CT at 12 months
>8 mm: SAME as above

31
Q

What test to order to assess Vitamin D levels?

A

SERUM 25-HYROXYVITAMIN D

The most appropriate test to assess adequacy of vitamin D levels is measurement of serum 25-hydroxyvitamin D, which reflects dietary and skin-derived vitamin D.

32
Q

With HYPOcalcemia, what other lab value do you need to measure?

A

PHOSPHOROUS
-Can see hyperphosphatemia

**Initial treatment of hyperphosphatemia is reduction of dietary phosphorus but occasionally requires addition of oral phosphate binders if serum phosphorus exceeds the normal range.

33
Q

What labs do you order for newly diagnosed osteoperosis?

A
  • complete blood count & metabolic profile
  • 25-hydroxyvitamin D
    -TSH
    -Urine calcium level
34
Q

HYPERCALEMIA–describe PTH and Phosporus levels for following:
-Primary hyperparathyrodism
-multiple myeloma
-granulomatous dx
-malignancy

A

PRIMARY HYPERPARATHYRODISM
-PTH elevated/inappropriately nl, phosphorus LOW

MULTIPLE MYELOMA
-PTH suppressed, phosphorous ELEVATED
-new kidney injury, anemia

GRANULOMATOUS dx (sarcoird, TB)
-PTH suppressed, phosphorous ELEVATED

Malignancy
-PTH suppressed, phosphorous nl/low

35
Q

What is treatment for osteoperosis

A

(1) Alrendronate or risedronate
(2) denosumab, 2nd line

IV bisphosphonates are contraindicated in patients with severe hypocalcemia and CKD

36
Q

Describe Osteomalacia vs Paget Dx

A

OSTEOMALACIA
- low Vit D; elevated alk phos
-also hypocalcemia, hypophosphatemia
-tx: vit D

PAGET DX
-disorder of bone remodeling
-elevated alk phos
-bone scintography
-Tx: IV zoledronic acid

37
Q

Describe Hyperparathyrodism vs Familial hypocalciuric hypercalcemia

A

HYPERPARTHYRODISM
- HIGH urinary calcium excretion, trying to get rid of CA

FAMILIAL HYPOCALIURIC HYPERCALCEMIA
-problem w/urine CA sensors….
-LOW urinary calcium excretion.

38
Q

Describe adrenal insufficiency.

A

The most common cause of primary adrenal insufficiency is autoimmune adrenalitis leading to progressive mineralocorticoid, glucocorticoid, and adrenal androgen deficiency

Sx: wt loss, orthostatic hypotension, n/v, fatigue
- hyperpigmentation (primary adrenal insufficiency only)

LABS: hypoglycemia,
hyponatremia and hyperkalemia (primary adrenal insufficiency only)
hypercalcemia

DIAGNOSTICS
-LOW 8am cortisol (<3 μg/dL) confirms
-values >18 μg/dL exclude the diagnosis.
-morning ACTH: distinguishes between primary and secondary (ACTH elevated–primary)

TREATMENT
-Both glucocorticoid and mineralocorticoid therapy are required
-glucocorticoid: hydrocortisone
-mineralcorticolid: fluticasone

39
Q

What DM2 meds are associated with weight loss

A

(1) sodium-glucose cotransporter 2 inhibitors (SGLT)
-dapagliflozin

(2) glucagon-like peptide 1 receptor agonist (GLP-1)
-liraglutide

40
Q

Target glucose for hospitalized pt

A

After insulin therapy is started, a target glucose range of 140 to 180 mg/dL (7.8-10.0 mmol/L) is recommended for most critically ill and non-critically ill patients.

41
Q

Myedema coma tx

A

Myxedema coma
-severe hypothyroidism with hemodynamic compromise

Treatment
-streroids for possible concomitan adrenal insufficiency
-BUT if random cortisol >18ug/dl – can d/c

42
Q

Treat secondary hypothyrodism

A

1) do NOT measure THS
-Because secondary hypothyroidism is caused by an inability to produce TSH, measurement of this hormone cannot be used to monitor therapy.

2) Levothyroxine dose should be adjusted based on free T4
-patient’s levothyroxine dose should be adjusted based on the free thyroxine T4 level, regardless of the TSH.

3) Fee T4 level should be maintained in the mid to upper half of the normal range.

43
Q

What is treatment for PCOS

A

IF pregnancy NOT desired:
-OCPs
-spironolactone for hirsutism

IF pregnancy IS desired:
-letrozole&raquo_space;» clomiphene citrate

44
Q

Diagnosis of MALE hypogonadism

A

1) AM testosterone x2
*note free testosterone if BMI elevated
2) Next, LH and FSH

45
Q

GLP-RECEPTOR

A

GLP-RECEPTOR
“glutide”
-wt loss, advanced CKD
-NO: medullary cancer

TZDs
“glitaZone”
-NO: HF, osteoporosis

Safe in ETOH Disorder
-DD4 inhibitor “gliptin”

SGL2 Inhibitor
“gliflozin”
-wt loss
-good w/MI, (early CKD)
-CON: candida infx

46
Q

DM2 drugs responsible for WEIGHT LOSS

A

“GLIT-GLIF”
GLP1- receptor agonist: “Glutides”
SGL2-inhibitors: “Gliflozin”

47
Q

DM2 Drugs overivew

A

-Metformin is a first-line medication for type 2 diabetes.
-Sulfonylureas (e.g. glipizide, glyburide) stimulate insulin secretion and can cause weight gain.
-Meglitinides (e.g. repaglinide, nateglinide) stimulate insulin secretion, but are short-acting.
-DPP-4 inhibitors (e.g. sitagliptin, linagliptin) enhance incretin hormones to increase insulin secretion.

WT LOSS:
-GLP-1 receptor agonists (e.g. liraglutide, semaglutide) enhance incretin hormones to increase insulin secretion and promote weight loss.
-SGLT2 inhibitors (e.g. canagliflozin, dapagliflozin) promote the excretion of glucose in urine and can lead to weight loss.

48
Q

Discuss mechanisms of DM2 drugs responsible for WEIGHT LOSS

A

GLP-1 receptor agonists (ending in “-glutide”) stimulate GLP-1 receptors, which leads to increased insulin secretion and decreased glucagon secretion. They also delay gastric emptying and promote satiety, which can lead to weight loss.

SGLT2 inhibitors (ending in “-gliflozin”) block the action of SGLT2, which is responsible for reabsorbing glucose in the kidneys. This leads to increased urinary excretion of glucose, which can cause weight loss.