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41 Cards in this Set

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What HLAs is Type I DM associated with?


Metabolic ketoacidosis

  • Hyperglycemia (>300mg/dL), anion gap metabolic acidosis, and hyperkalemia
  • Presents with Kussmaul respirations, dehydration, nausea, vomiting, mental status changes, and fruity smelling breath (due to acetone)

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

Diagnosis of Type II DM

  • Random glc > 200 mg/mL
  • Fasting glc > 126 mg/dL
  • Glc tolerance test with serum vlc level > 200 mg/dL two hours after glc loading

Long-term consequences of diabetes

  • Nonenzymatic glycosylation (NEG) of vascular basement membranes leads to atherosclerosis (CVD, peripheral vascular disease, kidney damage)
  • Osmotic damage (peripheral neuropathy, impotence, blindness, and cataracts)

How does diabetes result in kidney damage?

  • Neg of small vessels leads to hyaline arteriolosclerosis
  • Involvement of renal arterioles leads to glomerulosclerosis, resulting in small, scarred kidneys with a granular surface
  • Preferential involvemne tof effereent arterioles leads to glomerular hyper filtration injury with microalbuminuria that eventually progresses to nephrotic syndrome; characterized by Kimmelstiel-Wilson nodules in glomeruli

How does kidney damage result in blindness?

  • Glc freely enters into Schwann cells (which myelinate peripheral nerves), pericytes of retinal blood vessels, and the lens
  • Aldose reductase converts glc to sorbitol, resulting in osmotic damage

Pancreatic endocrine neoplasms

  • Tumors of islet cells; account for <5% of pancreatic neoplasms
  • Often a component of MEN 1 along with parathyroid hyperplasia and pituitary adenomas
  • Can be insulinomas, gastrinomas, somatostatinomas, VIPomas


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


Present as treatment-resistant peptic ulcers (Zollinger-Ellison syndrome); ulcers may be multiple and can extend into the jejunum


Present as achlorhydria (due to inhibition of gastrin) and cholelithiasis with steatorrhea (due to inhibition of cholecystokinin)


secrete excessive vasoactive intestinal peptide leading to watery diarrhea, hypokalemia, and achlorhydria

How does hyperaldosteronism present?

As HTN, hypokalemia, and metabolic alkalosis; edema is often absent due to aldosterone escape

Primary Hyperaldosteronism

  • High aldosterone and low renin (increased renal perfusion pressure down regulates renin)
  • First-line treatment is mineralocorticoid receptor antagonist (e.g. spironolactone or eplerenone); adenomas are usually surgically resected

Causes of primary hyperaldosteronism

Bilateral adrenal hyperplasia is most common; adrenal adenoma (Conn syndrome), and andrenal carcinoma are less common causes

Secondary hyperaldosteronism

  • Seen with activation of RAAS system
  • High aldosterone and high renin

Familial hyperaldosteronism

Can rarely be due to glucocorticoid-remediable aldosteronism (GRA)

  • aberrant expression (AD) of aldosterone synthase in the fasciculata
  • presents in children as TNA, hypokalemia, high aldosterone, and low renin
  • responds to dexamethasone, confirmed with genetic testing

Liddle syndrome

  • Mimics hyperaldosteronism
  • Decreased degradation of sodium channels (AD) in collecting tubules
  • Classically presents as HTN, hypokalemia, and metabolic alkalosis in a young patient
  • Low aldosterone and low renin
  • Treatment is potassium-sparing diuretics (e.g. amiloride or triamterene), which block tubular sodium channels; spironolactone is not effective

Clinical features of Cushing's syndrome (hypercortisolism)

  • Muscle weakness with thin extremities
  • Moon facies, buffalo hump, truncal oesity
  • Abdominal striae (due to impaired collagen synthethis)
  • HTN with hypokalemia and metabolic acidosis
  • Osteoporosis
  • Immune suppression

Diagnosing Cushing's syndrome

24 hr urine cortisol level (increased), late night salivary cortisol level (increased), and low-dose dexamethasone suppression test

When is used to suppress ACTH production?

  • Used when ACTH-dependent Cushing's is detected
  • High-dose dexamethasone suppresses ACTH production by pituitary adenomas; it will not suppress ectopic ACTH production

Most common cause of acute adrenal insufficiency

Arises secondary to abrupt withdrawal of glucocorticoids (presents as weakness and hypotension)

Waterhouse-Friderichsen syndrome

  • Classic cause of acute adrenal insufficiency
  • Characterized by hemorrhagic necrosis of the adrenal glands, classically due to DIC in young children with Neisseria meningitidis infection
  • Lack of cortisol exacerbates hypotension, often leading to death

Addison disease

  • Chronic insufficiency due to progressive destruction of adrenal glands (autoimmune, TV, or metastatic carcinoma)
  • Hypotension, hyponatremia, hypovolemia, hyperkalemia, metabolic acidosis, weakness, hyperpigmentation (very high ACTH stimulates melanocytes), vomiting, diarrhea

What helps distinguish primary from secondary adrenal insufficiency?

Hyperpigmentation and hyperkalemia


  • Tumor of chromatin cells leads to increased serum catecholamines
  • Episodic HTN, headache, palpitations, tachycardia, sweating
  • Rule of 10s: 10% bilateral, 10% familial, 10% malignant, 10% located outside of adrenal medulla (e.g. bladder wall or organ of Zuckerkandl at IMA root)

How is pheochromocytoma diagnosed?

By increased serum metanephrines and increased 24 hr urine metanephrines and vanillylmandelic acid

How is pheochromocytoma treated?

Surgical excision

  • Catecholamines may leak into bloodstream upon manipulation of tumor
  • Phenobenzamine (irreversible alpha blocker) is adminstered perioperatively to prevent a hypertensive crisis

What is pheochromocytoma associated with?

MEN 2A and 2B, von Hippel-Lindau disease, and neurofibromatosis type 1

Most common iatrogenic cause of Cushing syndrome

Exogenous glucocorticoids:

  • High cortisol
  • Low ACTH
  • Bilateral adrenal atrophy

Cushing disease

  • ACTH-secreting pituitary adenoma
  • High cortisol
  • No suppression by Low-Dose Dexamethasone
  • High ACTH; androgen excess may be present
  • Suppression by high-dose dexamethasone
  • Bilateral adrenal hyperplasia/pituitary adenoma on imaging

Findings when cause of Cushing syndrome is ectopic ACTH secretion

  • High cortisol
  • No suppression by Low-Dose Dexamethasone
  • Very high ACTH; androgen excess and hyper pigmentation may be present
  • No suppression by high-dose dexamethasone
  • Bilateral adrenal hyperplasia; ectopic source of ACTH (e.g. small cell carcinoma or carcinoid) on imaging

Findings when cause of Cushing syndrome is primary adrenal adenoma, hyperplasia, or carcinoma

  • High cortisol
  • No suppression by Low-Dose Dexamethasone
  • Low ACTH
  • Adenoma/carcinoma with contralateral atrophy or bilateral nodular hyperplasia on imaging

Congenital adrenal hyperplasia

  • Characterized by enzymatic defects in cortisol production
  • High ACTH (due to decreased negative feedback) leads to bilateral adrenal hyperplasia
  • Mineralocorticoids and androgens may be increased or decreased depending on the enzyme defect

Most common cause of congenital adrenal hyperplasia

  • 21-hydroxylase deficiency (90%)
  • Aldosterone and cortisol are decreased; steroiogenesis shunted towards androgens

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)

Nonclassic form of 21-hydroxylase deficiency

Presents later in life with androgen excess leading to precocious puberty (males) or hirsutism with menstrual irregularities (females)

11-hydroxylase deficiency

  • Biochemically similar to 21-hydroxylase deficiency, but weak mineralocorticoids are increased
  • Leads to HTN (sodium retention) with mild hypokalemia)
  • Renin and aldosterone are low

17-hydroxylase deficiency

  • Leads to decreased cortisol and androgens
  • Weak mineralocorticoids are increased leading to HTN and mild hypokalemia; renin and aldosterone are low
  • Decreased androgens (adrenal and gonads) lead to primary amenorrhea and lack of pubic hair in females or pseudohermaphroditism in males

Screening for CAH

  • Involves serum 17-hydroxyprogesterone levels
  • Increased in 11- and 21-hydroxylase deficiency
  • Decreased in 17-hydroxylase deficiency

Treatment for CAH

Glucocorticoids; mineralocorticoids (21-hydroxylase deficiency) or sex steroids (17-hydroxylase deficiency) may also be needed