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PANRE > Endocrinology 6% > Flashcards

Endocrinology 6% Flashcards

1
Q

Hyperparathyroidism, primary

A

↑ PTH usually caused by a PTH secreting parathyroid ADENOMA

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2
Q

Hyperparathyroidism, secondary

A

↑ PTH by a physiologic response to hypocalcemia or vitamin D deficiency.
Chronic kidney disease is the most common cause of secondary hyperparathyroidism.

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3
Q

Hyperparathyroidism, presentation:

A

“stones, bones, abdominal groans, psych moans, fatigue overtones”:
Nephrolithiasis, DI, bone pain, arthralgia, PUD, constipation, depression, fatigue.

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4
Q

Hyperparathyroidism, labs

A

Hypercalcemia ↑ CA+, ↓ phosphorus, elevated ↑ PTH, and moderately elevated urinary calcium.

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5
Q

Hyperparathyroidism, treatment

A

Acute - Saline, calcitonin, bisphosphonates.

Definitive - Surgical correction. Remove overactive parathyroid gland. If all 4, remove 3.5 glands.

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6
Q

Hypoparathyroidism, presentation

A

Tingling, Tetany, cataracts.

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7
Q

Hypoparathyroidism, signs

A

Chvostek’s sign: tap facial nerve illicit cheek twitch.

Trousseau’s sign: BP cuff inflation illicit carpal spasm.

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8
Q

Hypoparathyroidism, labs

A

Hypocalcemia ↓ CA+, low ↓ PTH, hyperphosphatemia, low urinary calcium.

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9
Q

Hypoparathyroidism, etiology

A

Two most common etiologies are postsurgical (damage from neck or thyroid surgery) or autoimmune.

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10
Q

Hypoparathyroidism, treatment

A

Vitamin D and Calcium

Tetany- secure airway, IV calcium gluconate

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11
Q

Hyperthyroidism, etiology

A

Grave’s disease (autoimmune). Toxic adenoma, thyroiditis, pregnancy, amiodarone.

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12
Q

Hyperthyroidism symptoms

A

Heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia.

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13
Q

Hyperthyroidism, Grave’s signs

A

Diffuse goiter with a bruit, exophthalmos, pretibial myxedema.

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14
Q

Hyperthyroidism, Thyroid storm

A

Fever, tachycardia, delirium.

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15
Q

Hyperthyroidism, diagnosis

A

TSH (best test): Decreased in primary disease (↓ TSH and ↑ Free T4), elevated in secondary disease (↑ TSH and ↑ Free T4).
Thyroid radioactive iodine uptake:
Graves: Diffusely high uptake.
Toxic multinodular: Discrete areas of high uptake.
Grave’s - Thyrotropin receptor antibodies (TRAb, also called TSI, TBII, or TBI).

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16
Q

Hyperthyroidism, treatment

A

Beta-blockers (symptomatic), methimazole/propylthiouracil, radioactive iodine, thyroidectomy.

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17
Q

Hypothyroidism, etiology

A

Hashimoto’s (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine ablation, congenital.

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18
Q

Hypothyroidism, symptoms; signs

A

Cold intolerance, fatigue, constipation, depression, weight gain, bradycardia.
Congenital: round face, large tongue, hernia, delayed milestones, poor feeding.

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19
Q

Hypothyroidism, diagnosis

A

TSH is elevated in primary disease. Low T4 (↑ TSH and ↓ Free T4).
Hashimoto’s: Antithyroid peroxidase (TPO), antithyroglobulin antibodies (Tg).

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20
Q

Hypothyroidism, treatment

A

Levothyroxine. Follow up with serial TSH monitoring.

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21
Q

Thyroid neoplastic disease, findings

A

Hoarse voice; cold nodule on thyroid uptake scan.

Most often papillary carcinoma (80%).

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22
Q

Thyroid neoplastic disease, diagnosis

A

Usually normal thyroid function.
Ultrasound is the best initial screen followed by a thyroid uptake scan.
Microcalcifications, hypoechogenicity, a solid cold nodule, irregular nodule margins, chaotic intranodular vasculature, and a nodule that is more tall than wide.
Fine needle biopsy for definitive diagnosis (all lesions >1 cm should be biopsied).

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23
Q

Thyroid neoplastic disease, treatment

A

Surgical resection with chemotherapy and external beam radiation reserved for anaplastic thyroid cancer.

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24
Q

Thyroiditis

A

Painful vs. Painless may be hypo or hyperthyroid

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25
Q

Hashimoto’s thyroiditis

A

Diffusely enlarged, painless, nodular goiter.

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26
Q

Subacute thyroiditis

A

Young women, after a viral infection.
Painful enlarged thyroid with dysphagia, mild fever.
Aspirin.

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27
Q

Postpartum thyroiditis

A

1-2 months of hyperthyroidism after delivery.

Completely resolves, give propranolol for cardiac symptoms.

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28
Q

Suppurative thyroiditis

A

Fever, pain, redness, fluctuant mass.
↑ WBC.
Antibiotic/surgical drainage.

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29
Q

Corticoadrenal insufficiency (Addison’s Disease)

A

Typically autoimmune. May be due to Tuberculosis in endemic areas.
Destruction of the Adrenal cortex resulting in loss of cortisol production (↓ cortisol).

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30
Q

Corticoadrenal insufficiency (Addison’s Disease), symptoms

A

Nonspecific symptoms: Hyperpigmentation, hypotension, fatigue, myalgias, GI complaints, weight loss.

31
Q

Corticoadrenal insufficiency (Addison’s Disease), diagnosis

A

↓ sodium, ↓ 8 AM cortisol, ↑ ACTH (primary), ↓ ACTH (secondary), ↑ potassium (primary), ↓ DHEA.
High Dose Cosyntropin (synthetic ACTH) Stimulation Test: Blood or urine cortisol are measured after an IM injection of cosyntropin (synthetic ACTH).
Normal response is a rise in blood and urine cortisol levels after synthetic ACTH is given.
Adrenal insufficiency results in little or no increase in cortisol levels (< 20 mcg/dL) after ACTH is given.

32
Q

Corticoadrenal insufficiency (Addison’s Disease), treatment

A

Hydrocortisone/prednisone PO daily.

33
Q

Cushing’s syndrome/disease

A

Cushing’s Syndrome: primary ↑ cortisol secretion from an adrenal tumor or excess glucocorticoids.
Cushing’s Disease: secondary ↑ cortisol caused by a pituitary adenoma resulting in ↑ ACTH secretion - ACTH causes adrenals to secrete cortisol.

34
Q

Cushing’s syndrome symptoms; signs

A

Fat redistribution (buffalo hump, moon facies) pigmented striae, obesity, skin atrophy, weight gain, easy bruising, elevated glucose, infections, cataracts, hirsutism.

35
Q

Cushing’s syndrome, diagnosis

A

↑ Cortisol, ↓ potassium, ↑ BP .
24-hour urinary free cortisol is the most reliable index of cortisol secretion: Urine cortisol excretion of > 125 mg/dL in 24 hrs.
Low dose dexamethasone suppression test → give a steroid (dexamethasone), failure of steroid to decrease cortisol levels is diagnostic, proceed next to high dose dexamethasone suppression test - no suppression = Cushing’s Syndrome.

36
Q

Cushing’s syndrome, treatment

A

Resection of tumor/adenoma.

37
Q

Adrenal neoplastic disease (pheochromocytoma)

A

Adrenal neoplasm - catecholamine secreting adrenal tumor - secretes norepinephrine and epinephrine autonomously and intermittently.

38
Q

Adrenal neoplastic disease (pheochromocytoma), symptoms

A

Recurrent headaches, HTN, sweating, palpitations.

39
Q

Adrenal neoplastic disease (pheochromocytoma), diagnosis

A

24-hour catecholamines including metabolites - metanephrine and vanillylmandelic acid (VMA)
MRI or CT of abdomen to visualize tumor.

40
Q

Adrenal neoplastic disease (pheochromocytoma); treatment

A

Resect tumor - complete adrenalectomy.

41
Q

Acromegaly/gigantism, etiology

A

Usually caused by a pituitary adenoma that secretes excessive amounts of Growth Hormone.
Rarely, they are caused by non-pituitary tumors that secrete GHRH.

42
Q

Acromegaly/gigantism (Growth Hormone) presentation

A

Gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before closure of the epiphyses.
Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop:
Large hands, feet, nose, lips, ears, jaw, tongue.
Presents as gigantism (excessive height) if occurs before epiphyseal closure.

43
Q

Acromegaly/gigantism (Growth Hormone), diagnosis; treatment

A

Growth hormone (↑GH) test 2 hours after glucose load.
Increased ↑IGF-1.
MRI/CT shows pituitary tumor.
Pituitary tumor removal.

44
Q

Diabetes insipidus

A

Diabetes insipidus (DI) is caused by a deficiency of or resistance to vasopressin (ADH), which decreases the kidneys’ ability to reabsorb water, resulting in massive polyuria.

45
Q

Central diabetes insipidus

A

Deficiency of ADH from posterior pituitary/hypothalamus.
No ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis.

46
Q

Nephrogenic diabetes insipidus

A

Lack of reaction to ADH.
Partial or complete insensitivity to ADH: caused by drugs (Lithium, Amphoterrible), hypercalcemia and hypokalemia affect the kidney’s ability to concentrate urine, acute tubular necrosis.

47
Q

Diabetes insipidus, diagnosis

A

24 hr urine: ↓ urine specific gravity < 1.010 and ↓ urine osmolarity < 200.
Desmopressin (ADH) stimulation test: differentiates nephrogenic from central DI Give ADH:
Central DI - reduction in urine output indicating response to ADH;
Nephrogenic DI - continued production of dilute urine (no response to ADH) because kidneys can’t respond.

48
Q

Diabetes insipidus, treatment

A

Central: desmopressin.
Nephrogenic: indomethacin +/- HCTZ, desmopressin.

49
Q

Pituitary dwarfism (GH deficiency)

A

Pituitary gland does not make enough Growth hormone.

Congenital - achondroplasia (mutation in FGFR3).

50
Q

Pituitary dwarfism (GH deficiency), signs

A

Short stature/limbs, prominent brow, midfacial hypoplasia.

51
Q

Pituitary dwarfism (GH deficiency), diagnosis

A

Labs: ↓ GH, ↓ IGF1
BONE AGE: X-ray the child’s hand to determine the child’s bone age by comparing this to the child’s actual chronological age_

52
Q

Pituitary dwarfism (GH deficiency), treatment

A

Growth hormone - If dwarfism is due to decreased human growth hormone.
Surgery may be necessary to remove a pituitary adenoma if that is the cause of the dwarfism.

53
Q

Pituitary adenoma and neoplasm

A

Most common tumors are microadenomas (<10 mm) that are functional (hypersecretion of pituitary hormones), nonfunctional or compressive.

54
Q

Pituitary adenoma and neoplasm, diagnosis

A

MRI is the study of choice to look for sellar lesions/tumors.
Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH.

55
Q

Prolactinoma (50%)

A

↑ Prolactin.

Secretes prolactin: Galactorrhea, infertility, amenorrhea.

56
Q

Nonsecreting Adenoma (34%)

A

Null Cell - No secretion

57
Q

Somatotroph Adenoma (10%)

A

↑ Growth Hormone/Prolactin.

Secretes GH - Presentation: Acromegaly.

58
Q

Corticotroph Adenoma (5%)

A

↑ ACTH.

Secretes ACTH - Cushing syndrome.

59
Q

Thyrotroph Adenoma (1%)

A

↑ TSH.

Secretes TSH - Hyperthyroidism.

60
Q

Diabetes mellitus type 1, diagnosis criteria

A

Random blood glucose level of > 200 mg/dL AND diabetic symptoms;
2 separate fasting (8 hours) glucose levels of > 126 mg/dL;
2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
Hemoglobin A1c of > 6.5%.

61
Q

Diabetes mellitus type 1, presentation

A 
Children, polyuria, polydipsia, polyphagia, fatigue, and weight loss.
Diabetic ketoacidosis (DKA) is commonly the initial presentation:  Fruity breath, nausea, vomiting, dehydration.
62
Q

Diabetes mellitus type 1, Dawn Phenomenon

A

Normal glucose until 2-8 am when it rises.
Results from decreased insulin sensitivity and nightly surge of counter-regulatory hormones during nighttime fasting.
Treat with bedtime injection of insulin to blunt morning hyperglycemia; avoiding carbohydrate snack late at night.

63
Q

Diabetes mellitus type 1, Somogyi effect

A

Nocturnal hypoglycemia followed by rebound hyperglycemia due to surge in growth hormone.
Treat with decreased nighttime insulin dose or give bedtime snack.

64
Q

Diabetes mellitus type 1, Insulin waning

A

Progressive rise in glucose from bed to morning.

Treat with change of insulin dose to bedtime.

65
Q

Diabetes mellitus type 1, Hemoglobin A1c

A

Represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC).
Treatment goal of A1c < 7.0%.

66
Q

Diabetes mellitus type 1, “finger-stick” blood glucose monitoring

A

Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial.

67
Q

Diabetes mellitus type 1, comorbidities

A

Blood pressure should be maintained at < 130/80.

Statins for 40-50 y/o with LDL-C 70-189.

68
Q

Diabetes Mellitus Type 2, diagnosis criteria

A

Random blood glucose level of > 200 mg/dL AND diabetic symptoms;
2 separate fasting (8 hours) glucose levels of > 126 mg/dL;
2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
Hemoglobin A1c of > 6.5%.

69
Q

Diabetes Mellitus Type 2, prediabetes, diagnostic criteria

A

A1C 5.7-6.4;
Fasting glucose 100-125;
2-hour oral glucose tolerance test 140-199.

70
Q

Diabetes Mellitus Type 2, Medications

A

Metformin - decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss).
Side effects: Lactic acidosis, GI side effects.

Sulfonylureas - stimulates pancreatic beta cell insulin release (insulin secretagogue).

Glyburide, glipizide, glimepiride.
Side effects: Hypoglycemia.

Thiazolidinediones - increases insulin sensitivity in peripheral receptor site adipose and muscle. Has no effect on pancreatic beta cells.

Pioglitazone.
Contraindications: CHF, liver disease.

Alpha-glucosidase inhibitors.
Delays intestinal glucose absorption.

Acarbose, miglitol.
GI side effects.

Incretins - Dipeptidyl peptidase inhibition - inhibits degradation of GLP-1 so more circulating GLP-1.

DDP4- sitagliptin, Incretin mimetics-Exenatide.
Side effects: Hypoglycemia, severe allergy.

Insulin – add if HbA1C >9.

71
Q

Diabetes Mellitus Type 2, Glucose goals and basic management

A

A1C < 7.0 % check every 3 months if not controlled and 2x per year if controlled.
Preprandial glucose 80-110 (60-90 if pregnant).
Postprandial blood glucose goal is < 140.
Annual dilated eye exams, ACEI if microalbuminuria, annual foot examination.
Blood pressure should be maintained at < 130/80.
New statin guidelines: recommend statins in persons with diabetes mellitus who are 40 to 75 years of age with LDL-C levels of 70 to 189 mg per dL but without clinical ASCVD (see guidelines).
Annual- ophthalmologist visit, urine microalbumin.

72
Q

Diabetes Mellitus Type 2, complications

A

Neuropathy (most common), retinopathy (leading cause of blindness), nephropathy.

73
Q

Hypercholesterolemia, four groups most likely to benefit from statin therapy are identified:

A

Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD).
Patients with primary LDL-C levels of 190 mg per dL or greater.
Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL.
Patients without diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%.

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