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86 Cards in this Set
- Front
- Back
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Adrenal Physiology:
Medulla works how? |
secretes epinepherine and norepinepherine into the adrenal veins when stimulated.
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Adrenal Physiology:
Cortex works how? |
secretes steroids regulating vascular tone, metabolism, cardiac contractility, TBW, K, Na, and androgenic function
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Adrenal Physiology:
Cyclic secretion is controlled by: |
time of day
renin-angiotensin system HPA axis (Hypothalmus-Pituitary-Adrenal axis) K+ levels |
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Adrenal Physiology:
Stress equates to: |
increased basal glucorticoid and mineralcortiocoid levels up to 10 fold within minutes.
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Adrenal Failure
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Stress failure results in adrenal crisis
Basal failure results in adrenal insufficiency-leads to insidious wasting Life threatening Tx with glucorticoids is critical! |
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3 Classes of Corticosteroids:
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Glucocorticoids
Mineralcorticoids Adrenal Androgens |
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Glucocorticoids
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Control endothelial and vascular integrity
Maintain vascular tone and cardiac contractility Catecholamine and β adrenergic receptor synthesis Fat, glucose, protein metabolism |
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Mineralcorticoids
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*Regulated by reninangiotensin system and serum K levels
*Decreased GFR leads to stimulates juxtaglomerular apparatus to release pro-renin. *Aldosterone release leads to Na and H20 resorption at distal tubules *Minor increase K can stimulate aldosterone secretion directly |
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Adrenal Androgens
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*Controlled by ACTH
*Diurnal pattern similar to cortisol *In females, major source of androgens |
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Adrenal insufficiency
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*The adrenal cortex secretes Glucocorticoids, Mineralocorticoids, Adrenal androgens and Androgen precursors, such as DHEA (dehydroepiandrosterone).
*In Addison’s disease, disruption of a negative feedback loop caused by Glucocorticoid deficiency produces an over stimulation of ACTH production and by-products of ACTH such as Melanocyte-stimulating hormone which causes skin hyperpigmentation. *In patients with bilateral adrenal hemorrhage, loss of axillary or pubic hair as a result of androgen deficiency. *Both Glucocorticoid and Mineralcorticoid deficiency contribute to Hyponatremiaprobably due to increased plasma ADH concentration, leads to excessive water retention. |
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Addison’s Disease
*Clinical presentation *Onset *Presentation |
*Clinical presentation is variable, depending on the rate and extent of loss of aderenal function, whether mineralocorticoidporduction is preserved, and degree of stress.
*The onset is acute or chronic with symptoms that can be vague. *Should be suspicious of any pt who presents with hypotension, prolonged administration of glucocorticoids or abrupt withdrawal of steroids or critical illness. *Postural hypotension *Neuro: Headache, visual changes,diabetesinsipidus Wt loss, anorexia, and GI complaints-N/V, diarrhea, abdominal pain Cutaneoushyperpigmentation (not always present) *Lack of energy, fatigue, dizziness *Salt craving, dry skin, myalgia, arthralgia; loss of pubic or axillary hair |
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Adrenal Insufficiency
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*Hypoglycemia
*Normocytic anemia *Pallor out of proportion to anemia *Hyponatremia *Primary insufficiency: lack of aldosterone and Na wasting Secondary insufficiency: Vasopressin secretion and H20 loss *Hyperkalemia-only occurs in primary insufficiency |
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Causes of Primary Adrenal insufficiency
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*Autoimmune adrenalitis
80-90% of cases in developed countries *Infectious adrenalitis (TB, fungal, AIDS associated) *Congenital adrenomyeloneuropathy *Bilateral adrenal hemorrhage or infarct (anticoagulants, meningoccal sepsis) *Bilateral tumor infiltration *Bilateral adrenalectomy *Drug induced (Mitotane, Etomidate, Ketoconazole) |
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Secondary Causes of Adrenal failure
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Failure of the HPA axis:
Usually due to exogenous glucocorticoid administration Pituitary failure-infarct |
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Tertiary Causes of Adrenal failure
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Hypothalmic dysfunction
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Confirmation of Suspected Addison Disease
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*Elevated morning baseline Plasma ACTH
*Serum Cortisol below the normal range *Corticotropin test-measures serum cortisol level 30mins before and 60 mins after IV synthetic ACTH 250mcg. In healthy pts, the stimulation leads to an increase in serum cortisol levels with peak concentrations >500nmol/l. In pts with Primary adrenal insufficiency, the adrenal cortex is already maximally stimulated by endogenous ACTH, and addition of further exogenous ACTH will not lead to further increase of circulating cortisol levels. *Elevated baseline renin concentration in the presence of serum aldosterone below the normal range indicates mineralcorticoid deficiency *Abdominal CT to detect enlarged adrenal glands or calcification. CT directed percutaneous fine-needle aspiration to r/o malignancy. |
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Adrenal insufficiency (Addison disease) Treatment
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*Involves Lifelong administration of adrenal-secreted hormones and education to prevent/recognize adrenal crisis.
~Glucocorticoid replacement (HC 15-30mg daily) ~Mineralcorticoid replacement (Fludrocortisone 0.05-0.20mg Q AM) ~Normalization of Na ,K, and Renin levels, and BP indicate adequate mineralcorticoid replacement. *Pts and relatives need to be instructed on how to increase the glucocorticoid dose in stressful situations and wear an emergency bracelet which contains dx and detailed advice on steroid dosages in case of trauma, surgery, or infection. |
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Adrenal Crisis
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*Life-threatening, may be due to primary or secondary causes. Hypotension often resistant to catecholamine and IVF resucitation.
*A suspected adrenal crisis requires immediate initiation of tx, even before hormone levels have been determined. *HC 100mg IV, followed by continuous infusion of 100-200 mg HC over 24h combined with NS 1 L/h under cardiac/BP monitoring. *Additional glucose administration may be warranted. |
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Thyroid Feedback Mechanism
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*Small gland, weighs <1oz, located in front of neck, below the larynx, consists of 2 lobes joined together by a narrow band of thyroid tissue, known as the isthmus.
*The function of the thyroid is to take iodine, found in many foods, and converts about 80% to thyroxine (T4) and 20% to triiodothyronine (T3). *T3 possesses about 4x the hormone strength as T4. *Both T3 and T4 are bound reversibly to plasma protein thyroxine binding globulin (TBG). Only free (unbound)fractions enter cells. *Thyroid cells are the only cells in the body that can absorb iodine. These cells combine iodine + tyrosine to make T3 +T4, which are then released into circulation where they control metabolism (convert O2 + calories to energy). |
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Thyroid Gland Physiology
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The Thyroid Gland is under
Control of the Pituitary Gland. When T3 + T4 drops too low, the pituitary gland produces TSH, which stimulates the Thyroid to produce and secrete more T3 + T4. |
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Pituitary Gland Physiology
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*The Pituitary Gland senses the increased production of T3 & T4 and responds by decreasing its TSH production.
*The Pituitary Gland is regulated by the Hypothalmus Gland, which produces TSH Releasing Hormone (TRH) which tells the Pituitary Gland to stimulate TSH. |
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One can imagine the Thyroid Gland as a furnace and the Pituitary Gland as the thermostat. Thyroid hormones are like heat. When the heat gets back to the thermostat, it turns the thermostat off. As the room cools, the thyroid hormone levels drop, the thermostat turns back on (TSH increases) and the furnace produces more heat.
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The Hypothalmus is like the person who regulates the thermostat since it tells the pituitary gland at what level the thyroid should be set.
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Plasma TSH
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Plasma TSH is the initial screening test, except when thyroid function is not in a steady state (as in active tx for hyperthyroidism) or known pituitary or hypothalmic disease:
~Normal TSH: 0.4-5mU/L ~TSH 5-10 mU/L: Subclinical hypothyroidism ~TSH increased(>20 mU/L): Hypothyroidism ~TSH decreased: (<0.1 mU/L): Hyperthyroidism |
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Diagnosis of Thyroid disease is based on
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*Clinical findings
*Palpation of the thyroid for size, nodules, tenderness, or thrill *Measurement of TSH and thyroid hormones |
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Causes of Hypothyroidism
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Thyroid:
*Congenital development *Primary Idiopathic-90% of cases *Post ablative (radioiodine, surgery) *Iodine deficiency *Drug-elicited (iodides, lithium, amiodarone) *Chronic thyroiditis *IL2 ~Suprathyroid: Pituitary: *Panhypopituitarism *TSH deficiency ~Hypothalmic: *Congenital defects *Encephalitis *Neoplasm ~Self-limited: *Withdrawal of suppressive thyroid therapy |
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Symptoms of hypothyroidism
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Memory loss
Cold intolerance Weight gain Diminished appetite Hyponatremia (water clearance Hypercapnea Hypoglycemia Decreased muscle strength Bradycardia Constipation Ileus Moon face Tough doughy skin Hypothermia Myxedema coma mortality 30-40% Goiter may be due to antibodies that stimulte growth, but not function vshypersecretion of TSH |
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Hypothyroid Treatment
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Therapy:
~Replete T4 (levothyroxine): Start 100-125mcg po daily. In elderly, start lower, no food 2h before or 1 hr after dose. Check TSH q 6 weeks and adjust T4 by 25mcg until at goal TSH. ~Myxedema coma: Replete T4 200-400mcg IV x1 for 24hrs followed by 75-100mcg IV daily until oral replacement is possible. Need to convert to PO dosing. ~Also, if IV T4 given, also add Hydrocortisone 50mg IV q 8h for possible coexisting adrenal insufficiency. |
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Hyperthyroidism causes
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Graves disease-autoimmune may also cause exopthalmus and pretibialmyxedema
Toxic multinodular goiter-common in older pts Iodine induced hyperthyroidism- usualy drug induced such as with amiodarone or radiographic contrast media Thyroid adenomas Subacutethyroiditis Ingestion of Thyroid hormone (surreptiously) |
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Hyperthyroid Clinical Findings
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Heat intolerance
Weight loss Weakness Palpitations Oligomenorrhea, amenorrhea Anxiety, emotional lability Brisk reflexes Fine tremor Proximal weakness Stare, eyelid lag ST, AFib Exacerbation of CHF or CAD Increased perspiration Urinary frequency Hyperdefecation Men: gynecomastia, erectile dysfunction |
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Differential Dx of Hyperthyroidism
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Diffuse, nontender goiter
Grave’s disease or painless thyroiditis Multiple thyroid nodules Toxic multinodular goiter Single thyroid nodule Thyroid adenoma Tender painful goiter Subacutethyroiditis Normal thyroid gland Grave’s disease, painless thyroiditis, or factituous hyperthyroidism |
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Lab Findings of Hyperthyroisidm
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~Low TSH and high free T4 and T3 : Hyperthyroidism
~T3 Toxicosis: Early in course caused by Grave’s dissease or Nodular goiter have greater increases in T3 than in serum T4. ~T4 Toxicosis: High free T4 and Normal T3 found in pts who have a concurrent nonthyroidal illness that decreases extrathyroidal conversion of T4 to T3. IE. Amiodarone inhibits extrahthyroidal conversion of T4 to T3. |
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Radioiodine UPtake
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24hr Thyroid radioiodine uptake and scan are frequently necessary to confirm the Dx of Graves’ hyperthyroidsm and exclude other causes, especially painless thyroiditis.
~High radioiodine uptake indicates de novo synthesis of hormone ~Low (nearly absent) uptake indicates either inflammation or destruction of thyroid tissue with release of preformed hormone into the circulation, or an extrathyroidal source of thyroid tissue. |
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Treatment of Hyperthyroidism
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~Propylthiouracil (PTU) or methimazole, both of which act by inhibiting new hormone synthesis. PTU has added effect of decreasing peripheral T4 to T3 conversion.
~Beta Blockers to inhibit target activity of thyroid hormone. Propanolol is preferred agent it also blocks peripheral conversion of T4. Atenolol or metoprolol may be used. ~1h after PTU or methimazole, Iodide is given to inhibit further thyroid hormone release. ~Acetaminiphenfor fever. ~Hydrocortisone if pt hypotensive as a result of adrenal insufficiency. |
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Euthyroid Hyperthyroxinemia
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Both T4 and T3 circulate in the blood bound to 1 of 3 binding proteins:
~Thyroxine-binding globulin (TBG) ~Transthyretin (TTR) ~Albumin *Serum total T4 or T3 assays measure bothbound and free hormone. Factors that alter binding protein concentrations can have profound effects on serum total T4 and T3, even though serum free T4 and T3 concentrations do not change and the pt is Euthryoid. |
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Euthyroid Disease
Causes of TBG Excess |
Heredity
Estrogens Hepatitis 5FU,heroin, methadone Acute intermittantporphyria Test: T3 resin uptake |
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Euthyroid Disease:
Causes of Reduced thyroninedeiodination |
Iodinated radiographic contrast agents
Propanolol Amiodarone |
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Euthyroid Disease:
Other causes |
Acute psychosis-mechanism unknown
Hyponatremia Thryoid hormone resistance Niacin Phenytoin Carbamzepine |
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Serum TSH - Normal
Serum Free T4 - Normal Serum T3 - Normal |
Euthyroid
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Serum TSH - Normal
Serum Free T4 - Normal or high Serum T3 - Normal or high |
Euthyroidhyperthyroxinemia
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Serum TSH - Normal
Serum Free T4 - Normal or low Serum T3 - Normal or low |
Euthyroidhypothyroxinemia
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Serum TSH - Normal
Serum Free T4 - Low Serum T3 - Normal or high |
Euthyroid:Triiodothyronine therapy
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Serum TSH - Normal
Serum Free T4 - Low normal or low Serum T3 - Normal or high |
Euthyroid: Thyroid extract therapy
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Serum TSH - High
Serum Free T4 - Low Serum T3 - Normal or high |
Primary hypothyroidism
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Serum TSH - High
Serum Free T4 - Normal Serum T3 - Normal |
Subclinical hypothyroidism
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Serum TSH - Low
Serum Free T4 - Normal or high Serum T3 - High |
Hyperthyroidism
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Serum TSH - Low
Serum Free T4 - Normal Serum T3 - Normal |
Subclinicalhyperthyroidsm
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Serum TSH - Normal or high
Serum Free T4 - High Serum T3 - High |
TSH mediated hyperthyroidism
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Serum TSH - Normal or low
Serum Free T4 - Low or low normal Serum T3 - Low or normal |
Central hypothyroidism
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Hypernatremia
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~Serum Na >145 and represents state of hyperosmolality
~Maintenance of osmotic equilibrium in hypernatremia results in ICF volume contraction and cerebral cell shrinkage. ~May be caused by primary Na gain or Water Defecit ~Appropriate response to hypernatremia is increase water intake by stimulating thirst and minimum excretion of maximally concentrated urine. |
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Causes of Hypernatremia
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~Due to water loss
*Evaporation of skin *Loss from GI tract-diarrhea *Insensible losses due to fever, exercise, heat exposure, severe burns. ~Due to Renal water loss *Osmotic diuresis *Diabeteses Insipidus ~Due to Na gain *DKA-due to osmotic diuresis |
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Hypernatremia Diagnosis
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~Complete hx and Physical
~Assessment of urine volume and osmolality *Appropriate excretion of minimum urine volume 500ml/day of maximally concentrated urine (urine osmolality>800 mOsm/kg ) *These finding suggest extrarenal water loss or hypertonic fluid administration ~CDI and NDI: polyuria and hypotonic urine. Urine osmo<250mOsm/kg |
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Central Diabetes insipidus
is characterized by decreased release of? |
Antidiuretic Hormone (ADH)
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Central Diabetes insipidus Results in:
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Results in variable degree of polyuria
decreased bone mineral density at the LS and femerol neck. |
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Central Diabetes insipidus are caused by disorders that act on site involved in ADH secretion:
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Neurosurgery or trauma to hypothalmus or posterior pituitary
Tumors –hypothalmic or pituitary Idiopathic-50-60% of cases Pregnancy can exacerbate or make apparent Hypoxic encephalopathy-can lead to increased ADH release Anorexia nervosa-due to erratic release ADH |
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Nephrogenic Diabetes Insipidus results from
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resistance to actions of vasopressin
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Is Nephrogenic Diabetes Insipidus congenital, acquired or both?
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May be congenital or acquired
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Is Nephrogenic Diabetes Insipidus more common in males or females?
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More common in males
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Nephrogenic Diabetes Insipidus - Acquired forms seen with:
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pyelonephritis
renal amyloidosis meyloma K depletions chronic hypercalcemia |
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Congenital Nephrogenic Diabetes Insipidus is linked to:
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Congenital linked to a defect in the renal vasopressin receptor
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Signs/Symptoms of DI
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~Onset my be insidious or abrupt, at any age
~Intense thirst ~Enormous quantities of fluid may be ingested, varying from 4-20 L/day ~Very dilute urine, SG <1.0005 ~Hypernatremia-due to renal water loss ~Nocturia ~Dehydration and hypovolemia my develop rapidly if fluids are not replaced. ~Muscular pains |
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Differental Diagnosis of DI
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Compulsive psychogenic water drinking
IV fluid administration CNS sarcoidosis DM Polyuria caused by Cushing’s syndrome |
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To differentiate the diagnosis between Central DI and Nephrogenic DI:
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~Endocrine consult
~Administer vasopressin analog DDAVP (10mcg intranasally) after careful water restriction. *The urine osmo should increase by at least 50% in CDI and does not change in NDI. |
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Treatment Goals of DI
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Stop ongoing water loss
Correct water deficit |
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Calculate Free Water Deficit:
the formula |
Water Deficit = TBW in liters x(serum Na+/ 140) – 1 x Weight in Kg
*TBW=0.6 if male and 0.5 if female |
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How do you correct a water deficit?
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~Rapid correction of hypernatremia is dangerous.
~Water deficit should be corrected slowly over 48-72hrs, Na should be lowered by 0.5mEq/L/H and by no more than 12 mEq/L over the 1st 24h. Safest route is via NG tube. Alternatively ½ isotonic saline IV. |
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Treatment of Central vs Nephrogenic DI
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Central DI
*DDAVP intranasally Nephrogenic DI *underlying disorder or eliminate the offending drug |
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SIADH
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Syndrome of Inappropriate Antidiuretic Hormone Secretion
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SIADH is:
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Disorder in which H2O excretion is partially impaired because of the inability to suppress the secretion of ADH
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In SIADH, u.o. should be:
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In severe case, urine output does not exceed 1L/day
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Water retention leads to development of:
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Hyponatremia
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SIADH should be suspected in any patient with:
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Hyponatremia
Hypoosmolality Urine osmolality> 100mosmol/kg Urine Na concentration > 40 meq/l Normal acid-base balance Low plasma Uric Acid level |
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Differential diagnosis for hyponatremia
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Pseudohyponatremia
Edematous Euvolemic Dehydration |
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Differential diagnosis for Pseudohyponatremia hyponatremia
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Hyperglycemia
Hyperlipidemia Mannitol Hyperlipidemia |
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Differential diagnosis for Edematous hyponatremia
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CHF
Cirrhosis Nephrotic syndrome ARF |
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Differential diagnosis for Euvolemic hyponatremia
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Psychogenic polydipsia
SIADH |
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Differential diagnosis for Dehydration hyponatremia
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Diuretics
GI loss 3rd spacing Adrenal insufficiency Salt losing nephritis |
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SIADH Etiology
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~CNS disturbances enhance ADH release:
CVA, hemorrhage, infection, trauma, psychosis ~Malignancies can cause ectopic production of ADH by tumor: Small cell lung ca, duodenum, pancreas, head/neck ca ~Drugs which enhance ADH release: chlorpropamide, carbamazepine, oxcarbazepine, cyclophosphamide, Selective serotonin reuptake inhibitors (fluoxetine, sertraline), haloperidol, opiates, amiodarone, ciprofloxacin, etc. ~Major surgery: Abdominal or thoracic ~Pulmonary disease: Pneumonia, TB, Respiratory failure, Pneumothorax ~Hormone deficiency: Adrenal and hypothyroidism HIV ~Hereditary SIADH: result in antidiuresis |
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SIADH Presentation
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*May be asymptomatic (mild hyponatremia)
*Severe hyponatremia: Altered mental status, seizures *Normal extracellular fluid volume |
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SIADH Tests
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Serum:
*Electrolytes: Na < 135 *Osmolality (norm: 280-295) : decreased Urine: *Electrolytes: Na > 40meq/l *Osmolality>100 mosmol |
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Normal Serum Osmolality:
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280-295mosm/kg
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Calculated Serum Osmolality formula
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mosm/kg= 2 (Na meq/l) + (Glucose mg/dl/18) + (BUN mg/dl/ 2.8)
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SIADH Treatment Goals
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~Raise the plasma Na+ by restricting water intake and promoting water loss
~Replace Na+ and K= deficits ~Correct the underlying disorder |
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Treatment of SIADH
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~Rate of correction of hyponatremia depends on the presence of absence of neurologic dysfunction
~The risk of correcting hyponatremiatoo rapidly: *ECF volume excess *Development of osmotic demyelination or central pontinemyelinolysis (flaccid paralysis, dysarthria, dysphagia) |
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Treatment of SIADH in
Nonsymptomatic patient and Na+ > 120 meq/l |
~Discontinue any offending drug
~Water restrict to 500ml-1L/day ~Increase salt and protein intake if fluid restriction not working ~Loop diuretic (lasix) to decrease urine osmolality |
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Free Water Excess Formula
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Free Water Excess (liters) = TBW x (1-(Na+/140))
*Males: TBW (liters) = 0.6 x current body weight (kg) *Females: TBW (liters)= 0.5 x current body weight (kg) |
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Treatment of SIADH in Symptomatic (restless, confused, seizure, coma) and Na+ < 120 meq/l:
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~NS IV with goal of increasing serum Na 0.5 meq/h
*The total change in plasma Na+ (140-measured Na+) divided by 0.5meq/liter/hr will yield the #hrs the correction should take place in. Ex: 140 – 115 = 25 / 0.5 = 50hrs ~The free water excess divided by the time calculated yields the target rate of free water removal in liters/h. Ex: 7.56 L/ 50 hrs= 0.15 liters /h target rate of free water removal *Give lasix 40mg IV and titrate to achieve urine output + to the rate of free water removal. *Replace urine output with NS. Stop treatment when serum Na+ reaches 120 or symptoms resolved. |
