cortisol/adrenal probs

Cards (46)

  • Cushing's disease

    Specifically pituitary adenoma (elevated ACTH secretion)
  • Cushing's syndrome

    Excess corticosteroids from any cause, can be ACTH dependent or independent. Causes too much cortisol.
  • Causes of Cushing's syndrome
    • Medications (ACTH independent only)
    • Bodily production (less common)
  • Endogenous Cushing's syndrome
    Adrenal adenoma or ectopic ACTH hormone
  • Adrenal insufficiency

    Autoimmune, infectious, metastatic cancer, lymphoma, medications
  • Primary adrenal insufficiency

    Increased ACTH, decreased cortisol, decreased aldosterone
  • Secondary adrenal insufficiency

    Decreased ACTH, decreased cortisol, regular aldosterone
  • Autoimmune mediated destruction of adrenal cortex

    Addison's disease = primary adrenocortical insufficiency (chronic hypocortisolism), adrenal cortex is destroyed
  • Clinical features of Cushing's disease/syndrome
    • Thin hair, red cheeks, acne, moon face, buffalo hump, supraclavicular fat pad, increased body/facial hair, weight gain, purple striae, pendulous abdomen, thin extremities with muscle atrophy, easy bruise, thin skin, slow wound healing
    • Menstrual irregularities, hirsutism, oily face, increased/decreased libido, virilization (due to inhibition of gonadotropin)
    • Fungal infections, hyperpigmentation
    • Glucose intolerance, progressive obesity, sleep apnea
    • Hypertension, increased risk, thromboembolic events, heart failure/dilated cardiomyopathy, proximal muscle weakness/wasting, bone loss
    • Depression, irritable, anxious, panic attacks, mild paranoia/mania
  • Clinical features of Addison's disease
    • Crave salty foods, nausea/vomiting, orthostatic hypotension/hypotensive
    • Decreased cortisol -> decreased glucose in stress -> weakness/tiredness/disorientation
    • Overactive pituitary gland -> makes more melanocyte stimulating hormone (hyperpigmentation/bronzing of skin)
    • Low androgen levels (women) -> loss of armpit/pubic hair, decreased sex drive
    • Crisis symptoms: pain in back, abdomen, legs, vomiting, diarrhea, dehydration, hypotension -> death
  • Managing Addisonian crisis
    1. Give sugar, steroids, salt
    2. Search for cause
    3. IV saline/5% dextrose (sugar/salt)
    4. IV hydrocortisone (steroids)
  • Primary aldosteronism
    Excess sodium in blood makes water go intravascular so increased volume and hypertension, headache, facial flushing, loss of protons in kidney -> metabolic acidosis
  • Expected lab values for Cushing's disease/syndrome
    • Increased glucose, increased triglycerides, increased WBC, glucosuria
    • Tests: salivary cortisol levels (2 nanograms/mL... get abnormal levels x2), 24 hr free cortisol level, dexamethasone suppression test
    • ACTH low in exogenous/adrenal tumor and high in Cushing's disease
    • Imaging: MRI of thorax, abdomen, pelvis (ectopic ACTH secretion), MRI of head (pituitary), CT abdomen (adrenals)
  • Expected lab values for Addison's disease (primary adrenal gland)
    • Hyperkalemia, hypovolemia, hyponatremia, high H (metabolic acidosis), low serum cortisol, high ACTH, low cortisol
  • Expected lab values for adrenal insufficiency
    • ACTH AM levels high, high potassium/renin, low glucose/sodium, cortisol AM levels low (<3mg/dL at 8am is diagnosis)
    • Secondary: CRH stim test, low ACTH, low cortisol
  • Cushing's syndrome occurs when there is excess production or use of cortisol in the body, leading to symptoms such as weight gain, fatigue, and muscle weakness.
  • Addison's disease results from decreased production of adrenal hormones, causing symptoms like fatigue, low blood pressure, and darkening of skin color.
  • The pituitary gland secretes antidiuretic hormone (ADH) which helps maintain water balance in the body.
  • Likely etiologies of SIADH
    • Post-op pts due to admin of hypotonic fluids
    • Drugs
    • Body's response to stress
    • CNS prob (trauma, stroke, hemorrhage, infection, mental illness)
    • Ectopic ADH production (SCLC, pneumonia, TB, CF)
    • Meds
    • Injury/surgical removal of pituitary
    • Acute psychosis
    • HIV infection
  • Signs and symptoms of SIADH
    • Due to hyponatremia/dec ECF osmolality: malaise, N/V, weak, tired, dizzy, confused, lethargic, anorexia, muscle cramps, myoclonus, tremors, seizures
    • Rapid fall in Na→ delirium, confusion, seizures
  • Laboratory findings for SIADH
    • Serum sodium less than 135 mEq/L
    • Serum osmolality less than 275 mOsm/kg
    • Urine sodium greater than 40 mEq/L
    • Urine osmolality greater than 100 mOsm/kg
    • Absence of clinical evidence of volume depletion– normal skin turgor, normal BP
    • Absence of other causes of hyponatremia
    • Correction of hyponatremia by fluid restriction
  • Alarm symptoms associated with SIADH
    • Delirium
    • Confusion
    • Seizures
  • First line treatment for mild/moderate SIADH
    1. Restrict water to <800 mL/day
    2. NaCl tablets/IV saline or loop diuretics (furosemide)
  • First line treatment for severe SIADH
    1. 100 mL bolus of 3% hypertonic saline given in the first 3-4hrs
    2. Severe Persistent- Vasopressin receptor antagonists - Conivaptan (IV) or tolvaptan (oral)
  • Hyperaldosteronism
    Tied to RAAs, producing above normal levels of aldosterone, impacts CV in HTN/resistant HTN
  • Hyperaldosteronism effects
    1. Inc Na absorption in collecting tubule
    2. Inc water
    3. Hypokalemia causes constipation, wake, arrhythmias
    4. Hypernatremia
  • Hyperaldosteronism signs/symptoms

    • HTN, HA, facial flushing, metabolic alkalosis (due to loss of protons in the kidneys)
  • Primary hyperaldosteronism
    Adrenal gland problem, Na high, K low, pH high, high aldosterone, low renin
  • Secondary hyperaldosteronism
    Hypersecretion due to something in body, HIGH ALDOSTERONE AND RENIN
  • Causes of secondary hyperaldosteronism
    • Renal artery stenosis
    • DI aka arginine vasopressin disorders
  • Nephrogenic diabetes insipidus
    Deficiency/resistance to ADH, pts on lithium are at a huge risk
  • Nephrogenic diabetes insipidus effects
    1. Dec ability to abs water
    2. High polyuria/dipsia
    3. Dec urine osmolality
    4. Inc plasma osmolality
  • Types of diabetes insipidus
    • Central- problem w secretion of ADH from post pituitary
    • Nephrogenic- kidneys not responding appropriately to ADH
  • Central diabetes insipidus signs/symptoms
    • Polyuria, polydipsia, nocturia, occasional hypovolemia
  • Central diabetes insipidus lab findings
    • High serum osmolality, low urine osmolality, high Na, norm glucose
  • Central diabetes insipidus workup

    Serum electrolytes, urine SG, plasma ADH levels, water deprivation, desmopressin (ADH) stim test, MRI to r/o pituitary adenoma
  • Central diabetes insipidus treatment

    Desmopressin DDAVP, AA sub of ADH
  • Nephrogenic diabetes insipidus treatment

    Diuretics, DDAVP, thiazide diuretics
  • Pheochromocytoma
    Catecholamine secreting tumor from chromaffin cells in adrenal medulla, can excrete norepi/epi
  • Pheochromocytoma signs/symptoms

    • 5P's (paroxysmal, pain/HA, pressure/HTN, palpitations, perspirations), Classic triad: episodic HA, night sweats, tachycardia