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41 Cards in this Set
- Front
- Back
What HLAs is Type I DM associated with? |
HLA-DR3 and HLA-DR4 |
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Metabolic ketoacidosis |
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How do insulin levels differ in the disease course of Type II DM? |
Insulin levels are increased early in disease, but later, insult in deficiency develops due to beta cell exhaustion; histology reveals amyloid deposition in the islets |
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Diagnosis of Type II DM |
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Long-term consequences of diabetes |
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How does diabetes result in kidney damage? |
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How does kidney damage result in blindness? |
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Pancreatic endocrine neoplasms |
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Insulinomas |
Present as episodic hypoglycemia with mental status changes that are relieved by administration of glc; diagnosed by decreased serum glc levels, increased insulin, and increased C-peptide |
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Gastrinomas |
Present as treatment-resistant peptic ulcers (Zollinger-Ellison syndrome); ulcers may be multiple and can extend into the jejunum |
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Somatostatinomas |
Present as achlorhydria (due to inhibition of gastrin) and cholelithiasis with steatorrhea (due to inhibition of cholecystokinin) |
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VIPomas |
secrete excessive vasoactive intestinal peptide leading to watery diarrhea, hypokalemia, and achlorhydria |
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How does hyperaldosteronism present? |
As HTN, hypokalemia, and metabolic alkalosis; edema is often absent due to aldosterone escape |
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Primary Hyperaldosteronism |
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Causes of primary hyperaldosteronism |
Bilateral adrenal hyperplasia is most common; adrenal adenoma (Conn syndrome), and andrenal carcinoma are less common causes |
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Secondary hyperaldosteronism |
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Familial hyperaldosteronism |
Can rarely be due to glucocorticoid-remediable aldosteronism (GRA)
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Liddle syndrome |
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Clinical features of Cushing's syndrome (hypercortisolism) |
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Diagnosing Cushing's syndrome |
24 hr urine cortisol level (increased), late night salivary cortisol level (increased), and low-dose dexamethasone suppression test |
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When is used to suppress ACTH production? |
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Most common cause of acute adrenal insufficiency |
Arises secondary to abrupt withdrawal of glucocorticoids (presents as weakness and hypotension) |
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Waterhouse-Friderichsen syndrome |
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Addison disease |
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What helps distinguish primary from secondary adrenal insufficiency? |
Hyperpigmentation and hyperkalemia |
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Pheochromocytoma |
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How is pheochromocytoma diagnosed? |
By increased serum metanephrines and increased 24 hr urine metanephrines and vanillylmandelic acid |
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How is pheochromocytoma treated? |
Surgical excision
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What is pheochromocytoma associated with? |
MEN 2A and 2B, von Hippel-Lindau disease, and neurofibromatosis type 1 |
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Most common iatrogenic cause of Cushing syndrome |
Exogenous glucocorticoids:
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Cushing disease |
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Findings when cause of Cushing syndrome is ectopic ACTH secretion |
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Findings when cause of Cushing syndrome is primary adrenal adenoma, hyperplasia, or carcinoma |
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Congenital adrenal hyperplasia |
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Most common cause of congenital adrenal hyperplasia |
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Classic form of 21-hydroxylase deficiency |
Presents in neonates as hyponatremia, hyperkalemia, and hypovolemia with life-threatening hypotension (due to salt-wasting); females have clitoral enlargement (genital ambiguity) |
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Nonclassic form of 21-hydroxylase deficiency |
Presents later in life with androgen excess leading to precocious puberty (males) or hirsutism with menstrual irregularities (females) |
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11-hydroxylase deficiency |
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17-hydroxylase deficiency |
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Screening for CAH |
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Treatment for CAH |
Glucocorticoids; mineralocorticoids (21-hydroxylase deficiency) or sex steroids (17-hydroxylase deficiency) may also be needed |