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123 Cards in this Set
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What is Plummer's disease? What do you see on thyroid scan? |
Multinodular toxic goiter -causes 15% of hyperthyroidism hyperfunctioning areas that produce high T4 and T3 levels patchy uptake on radioiodide scan |
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Name as many causes of hyperthyroidism as you can. |
Graves (most common) aka diffuse toxic goiter Plummer's aka multinodular toxic goiter Toxic thyroid adenoma Hashimoto's thyroiditis Subacute thyroiditis (granulomatous) Postpartum thyroiditis Iodine induced hyperthyroidism Excessive doses of levothyroxine |
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What are the 3 signs of hyperthyroidism specific to Grave's disease? |
Exopthalmos pretibial myxedema thyroid bruits |
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What are the common clinical features of hyperthyroidism in the elderly? |
weight loss, weakness and/or atrial fibrillation |
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Symmetrically enlarged, non-tender thyroid gland with a thyroid bruit |
Grave's disease |
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Symmetrically enlarged and very tender thyroid gland followed by a viral illness |
Subacute (granulomatous) thyroiditis |
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Asymmetric, bumpy and irregular thyroid gland with complaints of palpitations and weightloss |
Plummer's or Hashimoto's thyroiditis |
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What are the CV effects of hyperthyroidism? |
arrhythmias (sinus tachy, atrial fibrillation, PVCs) and elevated blood pressure |
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What are the neurological effects of hyperthyroidism? |
Brisk deep tendon reflexes, tremor |
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Explain the clinical relevance of the Radioactive T3 uptake test. |
provides information about TBG helps to differentiate between elevations in thyroid hormones due to increased TBG (like in pregnancy) or from true hyperthyroidism (increase in T4) -Radioactive T3 can bind to TBG or to resin if there is no space on TBG -in hyperthyroidism there is no space bc T4 is bound to TBG -so you are measuring how much T3 is taken up by resin,thus T3 uptake will increase in the setting of hyperthyroidism |
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What are some causes for an increase in TBG? |
Pregnancy, liver disease, OCPs, ASA |
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How do you treat hyperthyroidism? |
1) immediate control: beta blocker (propanolol) -Non-pregnant: beta blocker and methimazole for 1-2 years, taper B-blockers after 4-8wks Pregnant: endocrine consult, PTU Radioactive iodine ablation therapy (most common) Thyroidectomy (last resort usually) |
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What are the most common complications of thyroidectomy? |
permanent hypothyroidism hypocalcemia |
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How do you treat thyroid storm? |
supportive therapy -IV fluids, cooling blankets, glucose PTU every 2 hours, followed with iodine to inhibit thyroid hormone release b-blockers for heart rate Dexamethasone to impair peripheral conversion of T3 from T4 and adrenal support |
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What is the most common cause of primary hypothyroidism? |
Hashimoto's disease (chronic thyroiditis) (Iatrogenic is second mos common) |
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What are the clinical features of hypothyroidism? |
fatigue, weakness, lethargy, heavy menstrual periods, slight weight gain, cold intolerance, constipation, slow mentation, inability to concentrate, muscle weaknes, arthralgias, depression, diminished hearing, dry skin, hoarseness, nonpitting edema, bradycardia, goiter etc.. |
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What lab tests should you order initially when you expect thyroid dysfunction |
TSH (most sensitive) CBC (mild normocytic anemia) Lipid profile (may have elevated LDL and decreased HDL) |
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For all patients taking anti-thyroid medication, what should you monitor on a regular basis? |
leukocyte count to check for agranulocytosis |
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What other diseases is Hashimoto's thyroiditis associated with? |
lupus, pernicious anemia also at an increased risk for thyroid carcinoma and thyroid lymphoma |
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What is Riedel's Thyroiditis? |
Fibrous thyroiditis -fibrous tissue replaces thyroid tissue, leading to a firm thyroid |
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What percentage of thyroid nodules are cancer? What are hints that it is malignant? |
4-10% think malignancy if: -fixed, no movement with swallowing, solitary, hx of radiation of the neck, rapid development, vocal cord paralysis, cervical adenopathy, elevated calcitonin, family hx |
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What is the next best step in evaluating a solitary thyroid nodule? What do you do with the results after? |
FNA is the test of choice for initial evaluation. 95% sensitivity and specificity Benign--> observe and repeat if persists Malignant-->surgery Intermediate--> thyroid scan-->Cold-->surgery Intermediate-->scan-->hot-->observe closely |
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What is thyroid ultrasound used for? |
to differentiate cystic masses from solid masses. most cancers are solid, but this cannot distinguish between benign and malignant cystic masses >4cm are not malignant |
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What syndromes are associated with papillary cancer of the thyroid? |
Cowden's Syndrome and Gardner's Syndrome |
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What is Hurthle' cell tumor? |
a variant of follicular cancer of the thyroid, but more aggresive spread by lymphatics (reg. follicular spreads hematogenously) does not take up iodine cells contain abundant cytoplasm, tightly packed mitochondria, oval nuclei and prominent nucleoli Tx: total thyroidectomy |
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What is the least aggressive, slowest growing thyroid cancer? |
Papillary carcinoma 70-80% of all thyroid cancers spread via lymphatics but metastases is rare Positive iodine uptake |
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What is a cold nodule? |
A thyroid nodule that does not take up iodine as avidly more commonly malignant (20%) than hot nodules |
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What are the three most malignant thyroid cancers and some defining characteristic of each? |
Follicular: spreads hematognously, assoc. w/ iodine deficiency Medullary:arises from parafollicular C cells, produces calcitonin, associated with MEN type II-always screen for pheo Anaplastic: mostly in elderly, can arise from lonstandin follicular or papillar, death within months |
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What is the treatment for Papillary, Follicular, Medullary and Anaplastic carcinoma of the thyroid? |
Papillary: If >3cm thyroidectomy, otherwise lobectomy
Follicular: thyroidectomy w/post op iodine ablation Medullary: thryoidectomy, if LN also a modified radical neck dissection Anaplastic: Chemo and radiation for modest survival improvement, palliative surery for airway compromise |
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What are the clinical features of a pituitary adenoma? |
-hormonal effects due to hypersecretion of prolactin, GH, ACTH, and/or TSH -Hypopituitarism -Mass effect: headache, bitemporal hemianopsia (compression of optic chiasm |
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How do you diagnose a pituitary adenoma? |
MRI and pituitary hormone levels |
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What is the treatment for a pituitary adenoma? |
Transphenoidal surgery (radiation and medical tx are adjuncts) |
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What is the most common type of pituitary adenoma? causes? |
Prolactinoma causes: psych meds, H2 blockers, metoclopramide, verapamil, estrogen, pregnancy, renal failure, suprasellar mass lesion, hypothyroidism, idiopathic |
breast milk |
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How do you treat hyperprolactinemia? |
treat underlying cause If prolactinoma is causeBromocriptine or Cabergoline for 2 years surgery if sx progress despite meds recurrence rate is high though |
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What is the most common cause of death in patients with acromegaly? |
Cardiovascular disease |
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What is the cause of acromegaly? |
most commonly GH-secreting pituitary adenoma resulting in excessive secretion of GH after epiphyseal closure causing broadening of the skeleton |
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How do you diagnose acromegaly? |
IGF-1(somatomedin C) is elevated If IGF-1 is equivocal, oral glucose suppression test: glucose load fails to suppress GH MRI of pituitary |
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How do you treat Acromegaly? |
transsphenoidal resection of pituitary adenoma radiation therapy after if IG-F stays elevated Octreotide or another analog o suppress GH secretion |
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What is a craniopharyngioma? |
tumor of the suprasellar region that arise from Rathke's pouch calcifications of the suprasellar region on MRI are diagnostic |
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What are the effects of a craniopharyngioma and how do you treat it? |
hyperprolactinemia, DI, or panhypopituitarism tx: excision w/or without radiation |
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What are the first four things on your differential in a patient with polyuria and polydipsia? |
Diabetes Diuretic use Diabetes Insipidus Primary polydipsia |
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What is diabetes insipidus? |
central DI: low ADH secretion by posterior pituitary Nephrogenic DI: tubules do not respond to ADH causes low osmol urine, polyuria and polydipsia , mild hypernatremia |
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How do you treat Diabetes Insipidus? |
Central: DDAVP )nasal, oral or Injection), chlorpropamide, treat underlying cause Nephrogenic: sodium restriction and thiazide diuretic |
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What is the response to water deprivation in normal patients, central DI pts and Nephrogenic DI patients? |
Normal: increase in urine osmol ality above 280mOsm DI patients: no response |
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What is the pathophysiology of SIADH? |
excess ADH secretion from pituitry or ectopic source causing water retention and concentrated urine excretion |
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Why don't you see edema in the setting of SIADH? |
volume expansion occurs due to water retention, but edema is prevented due to natriuresis ( excretion of excess sodium un urine ). Natriuresis happens bc: -Atrial natriuretic pepetide increases due to volume expansion RAAS is inhibited decreasd tubular sodium absorption due to volume expansion |
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What causes SIADH? |
Neoplasms, CNS disorders, TB, Pneumonia, ventilators with PEEP, Medications (Vincristine, SSRIs, chlorpropamide, oxytocin, morphine, despompressin, Post-op |
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How do you diagnose SIADH? |
Diagnosis of exclusion: features: -Hyponatremia -volume expansion without edema -Natriuresis -Hypouricemia and low BUN -Normal or reduced serum creatinine level (bc of dilution) Normal thyroid and adrenal function |
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How do you treat SIADH? |
restrict water intake isotonic saline (DO NOT EXCEED 0.5mEq/L/hr) to avoid central pontine myelinolysis |
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In which patients should Insulin be started on an outpatient basis? |
-all type I diabetics -any pt with DM, A1C>9.0% and sx of complications -Pts who fail max anti-hyperglycemic therapy |
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What are the rapid acting formulations of insulin? |
*acts w/in 15 minutes, peaks at an hour and gone in 3 hours* Insulin aspart Insulin lispro Insulin glulisine given right before a meal |
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What are the short acting and intermediate insulin? |
lasts a few hours, longer than rapid acting *regular insulin *intermediate-acting insulin (NPH) *75/25 , 70/30, 50/50 (novolog, humalog and humilin) (combos of intermediate and regular insulin) |
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What are the long acting insulins and how are they used? |
Insulin detemir Insulin glargine (Lantus) basal level and injected in morning or evening once daily |
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Explain the the 3 Insulin regimens. |
Basal: once daily w/ a long acting (usually also on a anti-hyperglycemic drug also) -or- short acting twice daily (morning and evening- usually 7-/30 in the morning and a 50/50 at night) Basal-Bolus:"prandial", long acting in the morning and a rapid acting before meals Sliding scale: used in hospitals, short acting at scheduled times and dosed based on blood glucose level at the time |
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How do you calculate the daily dosage of insulin? |
0.5 Units/kg Multiply weight (kg) x 0.5= 2/3 of the daily dose taken in the morning 1/3 of daily dose taken in the evening prandial dose should be started at 0.1-0.3 Units/kg before each meal |
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what is the normal level of fasting blood glucose concentration? |
70-120 mg/dL |
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What are the signs of hypoglycemia? |
sympathetic activations: sweating, tremor, tachycardia, palpitations, anxiety, nausea, vomitting, behavior changes, blurred vision, fatigue, LOC |
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What are some of the most common causes of hypoglycemia? |
diabetic related post-prandial hypoglycemia (dumping syndrome in bariatric surgery, galactomsemia AR condition) infection liver disease hypothyroidism ethanol-induced hypoglycemia factitious hyperinsulinism insulinoma |
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What is the normal serum levels for calcium? |
9.0-10.5 mg/dL (If serum albumin is <4.0, use corrected Calcium: Corr Ca= Ca+0.8 (4-Albumin) |
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What does parathyroid hormone do? |
secreted by the parathyroids in response to low calcium overall effect: to increase serum calcium and decreases serum phosophate -increases osteoclast activity -increases conversion of VitD to increase bowel absortion of calcium and phopsphate -Increases calcium reabsorption in kidneys -decreases phosphate reabsorption in kidneys |
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What does calcitonin do? |
released by parafollicular C cells of thyroid in respnsoe to high serum calcium overall effect: decreases serum calcium |
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What is the most common cause of hypercalcemia? |
#1:hyperparathyroidism also.. malignancy (PTHrP, bone metasteses) Familial hypocalciuric hypercalcemia thiazide diuretics |
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What is the most common cause of hypocalcemia? |
#1: hypoparathyroidism also.. malnutrition malabsorption loop diuretics bisphosphonates |
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What are the clinical features of hypoparathyroidism? |
cardiac arrhythmias osteomalacia/rickets numbness/tingling tetany Chvostek's sign Trousseau's sign Grand mal seizures QT prolongation cataracts basal ganglia calcifications |
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What are the clinical features of hyperparathyroidism? |
nephrolithiasis, mephrogenic DI, osteoperosis, bone demineralization bone pain abdominal pain pancreatitis neuronal hyperactivity-lethargy, confusion, coma |
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What does the 33-1 rule refer to? |
Chloride/ Phosphorous ratio >33 which is diagnostic of primary hyperparathyroidism Chloride is high secondary to renal bicarbonate wasting (direct effect of PTH) |
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What is the most common cause of secondary hyperparathyroidism and how do you diagnose it? |
most common cause is chronic renal failure elevated PTH, low-low normal serum calcium |
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What is Cushing's syndrome?
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hypercortisolism (different from the disease which is a ACTH secreting pituitary adenoma) |
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What are the effects of cortisol?
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impaired collagen production, enhanced protein catabolism anti-insulin effects leading to glucose intolerance impaired immunity, inhibitory effects on PMNs, T cells enhances catecholamine activity (HTN) |
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What are the signs and symptoms of hypercortisolism?
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weight gain/obesity, buffalo hump, moon facies, abdominal striae, menstrual irregularities, acne, hirsutism, hypertension, polyuria and polydipsia
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What lab would you expect in someone with hypercortisolism?
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hypernatremia hypokalemia glucosuria |
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A person with hyperpigmentation and high levels of cortisol has what specifically?
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Cushing's disease
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How do you diagnose Cushing's?
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overnight dexamethasone suppression test -give 1mg of dexamethasone at 11pm, measure cortisol level at 8am if <5, Cushing's is excluded if>5 Cushings is diagnosis can also do 24 hour urine free cortisol level |
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What if the overnight dexamethasone test comes back with morning cortisol levels of 7?
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Cushing's disease, need to determine cause by using a high dose dexamethasone suppression test to determine if it's true Cushing's, Adrenal tumor or ectopic ACTH tumor |
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high cortisol low ACTH |
Adrenal tumor or adrenal hyperplasia
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What will be the expected results of a high dose dexamethasone suppression test on a patient with Cushings?
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decrease, greater than 50%, in cortisol levels
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What can cause a false positive low dose dexamethasone suppression test?
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AEDs Rifampin pts with eating disorders, depressed or in alcohol wothdrawl (if you suspect a possible false positive, confirm with 24 hour urine cortisol test) |
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Tell me the diagnosis: Suppression w/low dose DXM Suppression w/high dose DXM Mild increase w/CRH test Normal cortisol/ normal ACTH |
HEALTHY
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Tell me the diagnosis: High cortisol/ high ACTH No suppression w/low dose DXM Suppression w/ high dose DXM Large increase in cortisol w/ CRH test |
Cushing's disease (next step pituitary MRI) |
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Tell me the diagnosis: High cortisol/ low ACTH No suppression w/ low dose DXM No suppression w/ high dose DXM No change w/CRH test |
Adrenal tumor or hyperplasia (next step adrenal imaging) |
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Tell me the diagnosis: High cortisol/high ACTH No suppression w/ low dose DXM No suppression w/high dose DXM No change w/ CRH test |
Ectopic ACTH producing tumor (next step Chest CT, Abdominal CT, Octreotide scan) |
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What is the treatment for Cushing's ?
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iatrogenic: taper steroid pituitary: surgery-transphenoidal ablation of the adenoma adrenal adenoma or carcinoma: surgery |
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What is the difference between primary and secondary hyperaldosteronsim?
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primary: increase in aldosterone only; caused by Conn's syndrome: aldo secreting adrenal neoplasia
secondary: increase in renin and aldosterone; caused by b/l renal artery stenosis, Bartter's syndrome and Liddle's syndrome |
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What are the clinical features and labs seen with hyperaldosteronsim?
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HTN (most common) hypokalemia hypernatremia metabolic alkalosis (high bicarbonate) headache, fatigue, weakness polydipsia, nocturnal polyuria (absence of peripheral edema) |
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How do you diagnose hyperaldosteronism?
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urine aldosterone level and plasma renin level If the aldo-renin ratio is greater than 30, need to evaluate further with either a saline infusion test (saline infusion should decrease aldo levels in a normal pt) or oral sodium (high salt diet) loading for 3 days. Aldo should be low in a normal person |
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How do you treat hyperaldosteronism?
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Adenoma: resect b/l hyperplasia: spironolactone |
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What are the causes of primary adrenal insufficiency?
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(affects all adrenal hormones) Addison's disease Waterhouse-Friderichsen syndrome Surgical removal Infectious disease: TB, CMV, Crypto, Toxo, Pneumocystits metastastis (lung or breast) |
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What are the causes of secondary adrenal insufficiency?
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(only affects cortisol usually) long term steroid therapy (most common) pituitary apoplexy Sheehan's syndrome |
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What is the most common cause of Addison's disease worldwide?
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tuberculosis (worldwide) autoimmune (in our population) |
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What is an adrenal crisis?
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acute symptomatic stage adrenal insufficiency characterized by: severe hypotension cardiovascular collapse abdominal pain acute renal failure and death treat: IV hydrocortisone, IV fluids(NS w/5% Dextrose) |
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What is the best initial step in a stable patient with suspected Addison's disease?
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cosyntropin stimulation test (ACTH analog) |
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How do you treat adrenal insufficiency?
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primary: oral glucocorticoid, fludrocortisone secondary: glucocorticoid only |
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What is congenital adrenal hyperplasia?
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AR disease 90% due to 21-hydroxylase deficiency (10% 11-hydroxylase deficiency) |
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Diagnosis? Headache severe HTN profuse sweating palpitations tachycardia apprehension |
Pheochromocytoma until proven otherwise
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Pheochromocytoma is related to what other diseases?
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von Hippel Lindau Neurofibromatosis-1 MEN 2A MEN 2B |
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How do you diagnose pheochromocytoma when very suspicious? (best initial test)
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Plasma metanephrine test quick and sensitive to r/o pheo If stable is patient, get urine screen-looking for metanephrine and VMA, HVA, and NMM) |
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How do you treat pheo?
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surgical ligation with early ligation of venous drainage alpha blocker: phenoxybenxamine 10-14 days before surgery to control BP and a beta blocker for 2-3 days prior to decrease tachycardia |
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Name the MEN syndromes and what they cause.
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MEN I: PPP: parathyroid, pancreatic islet cell tumors, pituitary tumors MEN IIa: MPH: Medullary thyroid carcinoma, Pheochromocytoma, Hyperparathyroidism MEN IIb: MMMP: Medullary thyroid carcinoma, Mucosal neuroma, Marfan's, Pheochromocytoma |
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What is the characteristic lipid profile of insulin resistance and poorly controlled diabetes?
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hypertriglyceridemia with HDL depletion
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What is the Somogyi effect?
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morning hyperglycemia caused by a rebound response to nocturnal hypoglycemia check glucose at 3am and it should be low. this pts evening insulin should be decreased to avoid nocturnal hypoglycemia |
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What is the Dawn phenomena?
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morning hyperglycemia caused by an increase in nocturnal secretion of growth hormone check glucose at 3am, if high, increase evening insulin to provide additional coverage |
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How do you diagnose diabetes?
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1.two fasting glucose measurements greater than 125 2. single glucose of 200 w/ sx 3.increased glucose level on oral glucose tolerance testing 4. A1C>6.5% |
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What should you focus on when evaluating a diabetic patient?
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neuropathies retinopathy renal disease infectious disease vascular disease (PVD, CAD) |
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What is the optimal treatment for type II diabetic patients?
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glycemic control BP<130/85 LDL<100 HDL>40 Smoking cessation Daily aspirin |
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What is considered good, fair and poor control of DM related to A1C levels? fasting glucose and peak post prandial? |
poor: >10% fair: 8.5-10% good: 7.0-8.5% ideal:<7% (fasting <130, and peak post prandial <180) |
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What is the definition of microalbuminuria?
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30-300mg/day Albumin/creatinine ratio: 0.02-0.20 |
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How much SSI do you give someone with blood glucose of 334?
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150-200: 2 units 201-250: 4 units 251-300: 6 units 301-350: 8 units 351-400: 10 units >400: call house officer 10-14 units probably |
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How do you prepare a diabetic patient for radiocontrast imaging?
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generous hydration before administering contrast to avoid acute renal failure If on metformin, hold 48 hours after radiocontrast and make sure renal function has returned to baseline |
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What is the progression from hyperglycemia to ESRD (stepwise)?
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hyperglycemia->increased GFR-> microalbuminuria-> proteinuria -> decreased GFR-> ESRD
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What are the key features of DKA?
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HYPERGLYCEMIA Positive serum or urine ketones metabolic acidosis |
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What is on the differential for DKA?
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DKA Alcoholic ketoacidosis Hyperosmolar, hyperglycemic nonketotic syndrome Hypoglycemia Sepsis Intoxication |
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How do you treat DKA?
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Insulin: (if not hypokalemic) give priming dose of 0.1units/kg of IV regular insulin and then infusion of 0.1 units/kg/hour Fluids: normal saline, add 5% once glucose >250 to prevent hypoglycemia Potassium: replace prophylactically within 1-2 hours of insulin (check renal function first and monitor K, Mag and Phos very closely) |
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What are the complications of DKA?
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Cerebral edema if glucose levels decrease too rapidly Hyperchloremic nongap metabolic acidosis to rapid infusion of a large amount of saline |
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What is HHNS?
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Hyperosmolar hyperglycemic nonketotic Syndrome -hyperglycemia>600 -hyperosmolarity>320 serum pH>7.3 dehydration often seen in elderly with comorbid conditions higher mortality rate than DKA, but less common |
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What are you going to measure if a patient presents with hypoglycemia of unknown cause?
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plasma insulin levels C-peptide Anti-insulin antibodies Plasma and urine sulfonylurea levels |
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What can cause hypoglycemia?
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drugs-insulin, sulfonylureas factitious (look for high insulin, low C-peptide) insulinoma ethanol ingestion post-op complications reactive (idiopathic) adrenal insufficiency liver failure critical illness glycogen storage disease |
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How do you treat hypoglycemia?
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can eat: sugary foods can't eat: 1/2-2 ampules of D50 IV Repeat as necessary, but switch to D10W as condition improves and glucose>100 If alcoholic, give thiamine before administering glucose to prevent Wernicke's |
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What is an insulinoma? How do you diagnose and treat it? |
tumor of the beta cells of the pancreas, assoc. with MEN I syndrome Dx: 72 hour fast-insulin levels will remain high despite hypoglycemic state, C peptide and proinsulin levels high also Tx: resection |
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What is Zollinger-Ellison Syndrome? How do you diagnose and treat? |
Pancreatic islet tumor that secretes gastrin, assoc. with MEN I dx: secretin injection testi: normally secretin inhibits gastrin. In ZES pts, gastrin levels rise in response to secretin Tx: high does PPI, resection if possible |
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Diagnosis? necrotizing migratory erythema glossitis stomatitis diabetes hyperglycemia |
glucagonoma tx: resection |
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What is the triad of somatostatinoma
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malignant pancreatic tumor! -gallstones -diabetes -steatorrhea |
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What are the clinical features of a VIPoma?
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watery diarrhea achlorhydria hypercalcemia hyperglycemia |
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