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92 Cards in this Set
- Front
- Back
Hormones of the anterior pituitary
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TSH • ACTH • FSH • LH • Prolactin • Growth Hormone • MSH • Endorphins • Thyroid • Adrenal Cortex • Testes, Ovaries • Testes, Ovaries • Mammary gland • Liver • Melanocytes in the skin • Opioid receptors |
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TSH • ACTH • FSH • LH • Prolactin • Growth Hormone • MSH • Endorphins • Thyroid • Adrenal Cortex • Testes, Ovaries • Testes, Ovaries • Mammary gland • Liver • Melanocytes in the skin • Opioid receptors |
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10% of cranial lesions • Most common prolactinoma • Present with visual changes due to pressure on optic chiasm • Treat with dopamine agonist and radiation |
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Growth hormone
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Primarily promotes growth indirectly by stimulating liver’s production of somatomedins
– Primary somatomedin is insulin-like growth factor (IGF-1) • Acts directly on bone and soft tissues to bring about most growth-promoting actions • Stimulates protein synthesis, cell division, and lengthening and thickening of bones • GH exerts metabolic effects not related to growth – Increases fatty acid levels in blood by enhancing breakdown of triglyceride fat stored in adipose tissue – Increases blood glucose levels by decreasing glucose uptake by muscles |
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Growth Hormone Deficiency
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Due to pituitary defect or hypothalamic dysfunction – Laron syndrome, or Laron-type dwarfism, is an autosomal recessive disorder characterized by an insensitivity GH caused by a variant of the growth hormone receptor – Hyposecretion of GH in child is another cause of dwarfism • Symptoms: retarded skeletal growth, poorly developed musculature, excess subcutaneous fat |
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African Pygmies
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African Pygmies
• fails to respond to exogenous hormone in the presence of normal serum levels of growth hormone and of somatomedin ... Thus, the 'defect' appears to involve end-organ responsiveness to somatomedin |
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Acromegally
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Pituitary secretes too much Growth Hormone • Due most common from Pituitary Adenoma secreting Growth hormone or rarely from tumors of other glands that secrete growth hormones • Epiphyseal Plates are closed so bones widen |
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Posterior Pituitary
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Posterior Pituitary
• Oxytocin – – stimulates uterine contractions, – milk ejection reflex in the mammary glands – Rise during sexual activity • ADH - antidiuretic hormone, – Released in response to electrolyte changes or fall in BP – stimulates retention of water action – blocked by alcohol and caffeine |
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Diabetes Insipides
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Diabetes- “To pass through” • Polyuria, excessive thirst • Due to tumor, stroke, surgery, trauma, meds (lithium), hemochromosis, sarcoidosis, polycystic kidney disease, sickle cell anemia, destruction of thirst mechanism • Treatment with Vasopressin ( DDAVP in nasal spray or tablet form) |
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Parathyroid - what are the parts of it
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4 compact glands located posterior aspect of the thyroid • Chief cells produce PTH • Oxyphil cells’ function is unknown |
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Function of the Parathyroid hormone
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•Mobilization of calcium from bone: stimulate osteoclasts to reabsorb bone mineral, liberating calcium into blood.
•Enhancing absorption of calcium from the small intestine:. Parathyroid hormone indirectly stimulates the production of the active form of Vitamin D in the kidney. Vitamin D induces synthesis of a calcium-binding protein in intestinal epithelial cells that facilitates efficient absorption of calcium into blood. •Suppression of calcium loss in urine: Prevents the excretion of calcium in the urine and stimulates loss of phosphate. |
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Hypoparathyroidism
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Results in decreased of calcium and increased phosphorus in blood. • Leads to tetany and convulsions, and can be acutely life-threatening • Causes: surgical removal , autoimmune disorder, Hemochromatosis, Congenital absence, Magnesium Deficiency. • Treatment focuses on restoring normal blood calcium concentrations by calcium infusions, oral calcium supplements and vitamin D therapy. |
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Hyperparathyroid
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Elevated serum calcium • Ademona • Sestamibi Scan - overactive parathyroid glands pick up agent faster than others • Minimally invasive surgery |
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Pseudohyperparathyroidiam
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The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. I • Seen in: – Chronic Renal Failure where kidneys do not convert enough Vitamin D to the active form – Malabsorption- where vitamin D is not absorbed • Result: – Hypocalcemia – Hyperparathyroidism |
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Histology of the Thyroid
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Follicular cells: responsible for secreting the thyroid hormones as well as thyroglobulin, a glycoprotein
Follicle contains Colloid Thyroid hormones are stored extracellularly as part of the thyroglobulin which is the main component of the colloid Parafollicular cells secrete calcitonin |
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Calcitonin
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Produced by parafollicular cells of the thyroid • Acts to reduce calcium opposing the effects of parathyroid hormone – Decreasing Ca2+ absorption by the intestine – Decreasing osteoclast activity in the bones – Decreasing Ca2+ and phosphate reabsorption by the kidneys • Elevated blood calcium levels strongly stimulate calcitonin secretion, and secretion is suppressed when calcium concentration falls below normal. |
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Hypoparathyroidism
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Results in decreased of calcium and increased phosphorus in blood. • Leads to tetany and convulsions, and can be acutely life-threatening • Causes: surgical removal , autoimmune disorder, Hemochromatosis, Congenital absence, Magnesium Deficiency. • Treatment focuses on restoring normal blood calcium concentrations by calcium infusions, oral calcium supplements and vitamin D therapy. |
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Thyroid Hormones
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TSH • Free T4 – amount of active hormone which is available to enter the target organs. • T3- may be normal in hypothyroid, best for hyperthyroid • T3RU uptake- rarely ordered – measures the amount of thyroid binding hormone |
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Hyperparathyroid
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Elevated serum calcium • Ademona • Sestamibi Scan - overactive parathyroid glands pick up agent faster than others • Minimally invasive surgery |
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Thyroid Antibodies
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Thyroid Peroxidase Antibodies
• TPOAB • Hashimoto and Graves – Thyroglobulin Antibodies • TGAB • Hashimoto and Cancer – Thyroid Stimulating Hormone Receptor Antibody • TRAB • Graves |
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Pseudohyperparathyroidiam
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The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. I • Seen in: – Chronic Renal Failure where kidneys do not convert enough Vitamin D to the active form – Malabsorption- where vitamin D is not absorbed • Result: – Hypocalcemia – Hyperparathyroidism |
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thyroid effect on heart
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Chronotropic
Increase number of β receptors Inotropic Enhance response to circulating catecholamines Increase proportion of -myosin heavy chain (with higher ATPase activity). |
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Histology of the Thyroid
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Follicular cells: responsible for secreting the thyroid hormones as well as thyroglobulin, a glycoprotein
Follicle contains Colloid Thyroid hormones are stored extracellularly as part of the thyroglobulin which is the main component of the colloid Parafollicular cells secrete calcitonin |
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thyrodMyxedema
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is a skin and tissue disorder usually due to severe prolonged hypothyroidism • results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis • Also seen in Grave’s, Hyperthyroidism, Hoshimotos |
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Calcitonin
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Produced by parafollicular cells of the thyroid • Acts to reduce calcium opposing the effects of parathyroid hormone – Decreasing Ca2+ absorption by the intestine – Decreasing osteoclast activity in the bones – Decreasing Ca2+ and phosphate reabsorption by the kidneys • Elevated blood calcium levels strongly stimulate calcitonin secretion, and secretion is suppressed when calcium concentration falls below normal. |
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Myxedema presentation
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Skin thickening • Coarse skin • Change in facial appearance • Thickening nose • Swollen lips • Puffiness around the eyes • Jelly-like infiltrations in subcutaneous tissues • Slow speech • Mental dullness • Lethargy • Mental problems • Dry skin • Yellow skin • Swollen subcutaneous tissue • Weight gain • Thinning Hair • Brittle Hair • Bald Patches • Muscle Pain Deafness • Hearing Impairment • Carple tunnel syndrome • Constipation |
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Thyroid Hormones
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TSH • Free T4 – amount of active hormone which is available to enter the target organs. • T3- may be normal in hypothyroid, best for hyperthyroid • T3RU uptake- rarely ordered – measures the amount of thyroid binding hormone |
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Thyroid Antibodies
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Thyroid Peroxidase Antibodies
• TPOAB • Hashimoto and Graves – Thyroglobulin Antibodies • TGAB • Hashimoto and Cancer – Thyroid Stimulating Hormone Receptor Antibody • TRAB • Graves |
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thyroid effect on heart
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Chronotropic
Increase number of β receptors Inotropic Enhance response to circulating catecholamines Increase proportion of -myosin heavy chain (with higher ATPase activity). |
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thyrodMyxedema
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is a skin and tissue disorder usually due to severe prolonged hypothyroidism • results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis • Also seen in Grave’s, Hyperthyroidism, Hoshimotos |
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Myxedema presentation
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Skin thickening • Coarse skin • Change in facial appearance • Thickening nose • Swollen lips • Puffiness around the eyes • Jelly-like infiltrations in subcutaneous tissues • Slow speech • Mental dullness • Lethargy • Mental problems • Dry skin • Yellow skin • Swollen subcutaneous tissue • Weight gain • Thinning Hair • Brittle Hair • Bald Patches • Muscle Pain Deafness • Hearing Impairment • Carple tunnel syndrome • Constipation |
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Cretinism
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Severely stunted growth due to congenital hypothyroidism
• Assoc with Iodine deficiency |
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Hashimoto
• chronic lymphocytic thyroiditis |
Hashimoto
• chronic lymphocytic thyroiditis • an autoimmune disease where the body's own T-cells attack the cells of the thyroid. • It was the first disease to be recognized as an autoimmune disease. • Antibodies cause gradual destruction of follicles in the thyroid gland. |
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Hyperthyroidism and Thyrotoxicosis
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Term for symptomatic hyperthyroidism
• Hyperactivity,irritability, dysphoria, heat intolerance, sweating, anxiety palpitations, weight loss, diarrhea, tachycardia, atrial fibrillation, goiter • Very low TSH, high free T4 |
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Graves Disease
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Graves' disease is a thyroid-specific autoimmune disorder in which the body makes antibodies to the thyroid-stimulating hormone receptor (TSHR),
• leading to hyperthyroidism • The autoantibodies produced in Graves' disease are not subject to negative feedback, so they continue to be produced and bind to TSHR even when thyroid hormone levels rise too high. • These antibodies act as agonists, stimulating more hormones to be released and thus leading to hyperthyroidism |
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Thyroid Storm
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Thyroid storm is a crisis or life-threatening condition characterized by an exaggeration of the usual physiologic response seen in hyperthyroidism. Whereas hyperthyroidism can cause symptoms such as sweating, feeling hot, palpitations and weight loss - symptoms of thyroid storm are more severe, resulting in complications such as:
• fever • rapid heart rate • nausea/vomiting • diarrhea • irregular heart beat • weakness • heart failure • confusion/disorientation • Fever tends to be one of the hallmarks of thyroid storm and can be as high as 105-106F. The actual diagnosis of thyroid storm is made on the basis of suspicion in patients with symptoms, and in the setting of elevated blood levels of thyroid hormones (T3 and T4 |
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Pancrea s
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ndocrine and exocrine organ
• Endocrine organ: 1% • Islet cells – secretes – glucagon by alpha cells – Insulin by beta cells • Exocrine organ:Ascini – Buffers: controlled by secretin in duodenum – Enzymes:Controlled by CCK in intestines |
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Pancreatic Enzymes
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Amylase which breaks down carbohydrates
• Lipase breaks down fats • Proteases – Tripsin – Chymotrypsin – Carboxypeptidase |
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Pancreatitis
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Blockage of excretory ducts by infection, ischemia or drugs ( alcohol )
• Causes injury of the exocrine cells • Lysosomes in the damaged cells activate the surrounding pancreatic enzymes and digest surrounding cells • 10-15% of patients the process does not stop and the pancreas is destroyed • Pancreaticpseudocyst – collection of enzymes, blood and necrotic tissues – Conservative treatment vs drainage |
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Diabetes Mellitus
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Mellitum means HONEY
• Diabetes is a group of Metabolic Disorders with the common manifestation: HYPERGLYCEMIA • Type 1 :insulin deficiency, autoimmune • Type 2 : insulin resistance, B cell defect • Gestational Diabetes • Polyuria, Polydipsea, Polyphagia |
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Risk Factors for DM
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Obesity
• Impaired Glucose Intolerance • Hypertension • Lack of Exercise • Poor diet • Gestational Diabetes • Smoking • Metabolic Syndrome |
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Who should be screened for DM
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screening with fasting glucose or oral glucose tolerance test recommended for overweight patients > 45 years old (particularly with BMI > 25 kg/m2)
• screening should also be considered in younger adults with – family history of diabetes – low HDL cholesterol – high blood pressure history of gestational diabetes or birth of baby weighing > 9 pounds – polycystic ovary syndrome (PCOS) or other clinical condition associated with insulin resistance (e.g., acanthosis nigricans) – habit of physical inactivity – vascular disease – ethnic group at increased risk (African-Americans, Native Americans, Hispanic Americans/Latinos, Asian American and Pacific Islanders) • recheck every 3 years if normal (fasting plasma glucose < 100 mg/dL [5.6 mmol/L] or 2-hour oral glucose tolerance test < 140 mg/dL [7.8 mmol/L] |
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Diabetic Ketoacidosis
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Diabetic Ketoacidosis
• In solution Ketone bodies dissociate releasing H ions threatening pH • Starvation increases ketones bodies as another form of fuel • Without insulin body cannot utilize insulin and body is in starvation mode • Type 1 and type 2 Diabetes • Treatment consists of hydration to lower the osmolality of the blood, replacement of lost electrolytes, insulin to force glucose and potassium into the cells, and eventually glucose simultaneously with insulin in order to correct other metabolic abnormalities, such as lowered blood potassium (hypokalemia) and elevated ketone levels. Many patients require admission to a step-down unit or an intensive care unit (ICU) so that vital signs, urine output, and blood tests can be monitored frequently. Brain edema is not rare, and so this may suggest intensive monitoring as well. In patients with severe alteration of mental status, intubation and mechanical ventilation may be required. Survival is dependent on how badly-deranged the metabolism is at presentation to a hospital, but the process is only occasionally fatal. • DKA occurs more commonly in type 1 diabetes because insulin deficiency is most severe, though it can occur in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. In a person known to have diabetes and being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis, the flu, or the development of a serious new health problem (e.g., bacterial infection, myocardial infarction). |
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DKA occurs more commonly in type 1 diabetes because insulin deficiency is most severe, though it can occur in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. In a person known to have diabetes and being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis, the flu, or the development of a serious new health problem (e.g., bacterial infection, myocardial infarction). |
Usually in type 2 diabetics
• Plasma glucose level of 600 mg/dL or greater • Effective serum osmolality of 320 mOsm/kg or greater • Profound dehydration (8-12 L) with elevated serum urea nitrogen (BUN)-to-creatinine ratio • Small ketonuria and absent-to-low ketonemia • Bicarbonate concentration greater than 15 mEq/L • Some alteration in consciousness • 10 to 20% mortality • May be due to infection • Name change since Doma in < 10% of patients |
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Hypoglycemia
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Insulin Reaction: inadequate food, exercise, first trimester of pregnancy due to fetus requirements, diabetic gastroparesis, insulin potientated by drugs: ethanol, salicylates, B- blockers
• Hypoglycenic agent overdose • Autoimmune hypoglycemia • Pentamidine induced hypoglycemia- drugs lytic effect on B cells • Pancreatic B cell tumors- insulinoma- an insulin secreting tumor of the islets of langerhans |
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Adrenal Gland - what are it's two parts
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Embedded above each kidney in a capsule of fat
• Composed of two endocrine organs – Adrenal cortex • Outer portion • Secretes steroid hormones – Adrenal medulla • Inner portion • Secretes catecholamines |
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Adrenal cortex
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Adrenal cortex
– Consists of three layers or zones • Zona glomerulosa – outermost layer • Zona fasciculata – middle and largest portion • Zona reticularis – innermost zone |
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Categories of adrenal steroids |
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Mineralocorticoids – Mainly aldosterone – Influence mineral balance, specifically Na+ and K+ balance • Glucocorticoids – Primarily cortisol – Major role in glucose metabolism as well as in protein and lipid metabolism • Sex hormones – Identical or similar to those produced by gonads – Most abundant and physiologically important is dehydroepiandosterone (male “sex” hormone) |
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Aldosterone
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Principal action site is on distal and collecting tubules of the kidney – Increases the reabsorption of sodium and water and the release (secretion) of potassium in the kidneys – Increases blood volume and as a result increases blood pressure – From zona glomerulosa- outer layer, mineralcorticoid – Aldosterone production is regulated partly by corticotropin (secreted by the pituitary gland) and partly through the renin-angiotensin-aldosterone system – Secretion is increased by • Activation of (RAAS) renin-angiotensin-aldosterone system by factors related to a reduction in Na+ and a fall in blood pressure • Direct stimulation of adrenal cortex by rise in plasma K+ concentration – drugs, such as spironolactone lower blood pressure by blocking the aldosterone receptor |
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Aldosterone Hypersecretion - May be caused by...
symptoms .. |
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May be caused by • Hypersecreting adrenal tumor made up of aldosterone-secreting cells – Primary hyperaldosteronism or Conn’s syndrome ( 75%) • Inappropriately high activity of the renin- angiotensin system – Secondary hyperaldosteronism – Symptoms • Excessive Na+ retention and K+ depletion • High blood pressure |
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Primary Aldosteronism
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Primary Aldosteronism
• Presentation: Hypokalemia and Hypertension • Assessment of renin – angiotensin system: • If normal or elevated in a person with no diuretics-no hyperaldosteronism • If low in presence of low K- check urine and serum aldosterone after starting NaCl suppliment- if suppression dx is made |
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endocrine effect of licorice
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Eating large amounts of real licorice can produce all the symptoms of hyperaldosteronism. Real licorice contains a chemical that can act like aldosterone. However, most candy sold as licorice contains little or no real licorice.
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Cortisol
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Cortisol – is a glucocorticoid produced by the Zona fasciculata of the adrenal cortex – Stimulates hepatic gluconeogenesis (liver makes glucose) – Inhibits glucose uptake and use by many tissues, but not the brain – Stimulates protein degradation in many tissues, especially muscle – Increases Blood Pressure – Facilitates lipolysis – Plays key role in adaptation to stress |
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Sex Hormones
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Secretes both male and female sex hormones in both sexes
– Not high enough conc. to have any effect – Dehydroepiandrosterone (DHEA) • the most abundant androgen (male steroid hormone) secreted by the adrenal glands • Only adrenal sex hormone that has any biological importance • DHEA can also be converted into other steroid hormones, including testosterone and estrogen • DHEA levels decline with advancing age • Physiologically significant in females where it governs – Growth of pubic and axilla hair – Enhancement of pubertal growth spurt – Development and maintenance of female sex drive |
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Cushing Disease
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Cortisol hypersecretion
– Causes • Overstimulation of adrenal cortex by excessive amounts of CRH and ACTH • Adrenal tumors that uncontrollably secrete cortisol independent of ACTH • ACTH-secreting tumors located in places other than the pituitary – Signs and symptoms • Hyperglycemia and glucosuria (adrenal diabetes) • Abnormal fat distributions – “buffalo hump” and “moon face” |
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Diagnosis of Cushing Syndrome
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either a Dexamethasone suppression test.(administration of dexamethasone and frequent determination of cortisol and ACTH level),
• a 24-hour urinary measurement for cortisol offer equal detection rates • Recently cleared by the US FDA, is sampling cortisol in salive over 24 hours, which may be equally sensitive, as late night levels of salivary cortisol are high in Cushingoid patients |
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Adrenal Androgen Hypersecretion
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Adrenogenital syndrome – Symptoms • Adult females – Hirsutism= male pattern hair growth – Deepening of voice, more muscular arms and legs – Breasts become smaller and menstruation may cease • Newborn females – Have male-type external genitalia • Prepubertal males – Precocious pseudopuberty • Adult males – Has no apparent effect |
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Adrenocortical Insufficiency
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Primary adrenocortical insufficiency • Addison’s disease- all layers (zonas) undersecrete • Autoimmune disease – Aldosterone deficiency » Hyperkalemia (too much K+) and hyponatremia (too little Na+) – Cortisol deficiency » Poor response to stress » Hypoglycemia (low blood glucose) » Lack of permissive action for many metabolic activities – Secondary adrenocortical insufficiency • Occurs because of pituitary or hypothalamic abnormality • Only cortisol is deficient – Poor stress response, pigmentation of skin due to similarity with melanin |
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Addison’s Disease
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Chronic Adrenal insufficiency
• Etiology: autoimmune, infection, hemorrhage, metastatic disease , drug induced, (ketoconizole), sepsis, cortisol resistance, and X-linked adrenoleukodystrophy • Clinical Features: – Orthostatic hypotension – Weakness, anorexia, fatigue – Hyperpigmentation of the skin – Salt Craving – GI problemsAddison’s Disease |
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Acute Adrenal Crisis
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People with Addison’s who are exposed to the stress of trauma, surgery or dehydration
• Due to deficient cortisol • Can rapidly lead to death • Treatment: hydrocortisone sodium phosphate • Symptoms: • Hypotension • Shock • Dehydration • N/V and anorexia • Hypoglycemia • Weakness • Depressed mentation |
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Adrenal medula
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Found in the center of the gland
• Modified part of sympathetic nervous system • Chromaffin cells secrete catecholamines epinephrine and norepinephrine into the blood in response to body stressors • Epinephrine – Reinforces sympathetic system in mounting general systemic “fight-or-flight” responses – Maintenance of arterial blood pressure (vasostriction, increased CO) – Increases blood glucose and blood fatty acids |
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Stress Reaction
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Pattern of reactions to a situation that threatens homeostasis
• Stress – Generalized nonspecific response of body to any factor that overwhelms or threatens to overwhelm the body’s ability to maintain homeostasis • Stressor – Any noxious stimulus that brings about the stress response • Physical, emotional, chemical, infectious, social, physiological All the actions are coordinated by the hypothalamus • Generalized stress response – Activation of sympathetic nervous system accompanied by epinephrine secretion • Prepares body for fight-or-flight response – Activation of CRH-ACTH-cortisol system • Helps body cope by mobilizing metabolic resources – Elevation of blood glucose and fatty acids • Decreased insulin and increased glucagon secretion – Maintenance of blood volume and blood pressure • Increased activity of renin-angiotensin-aldosterone system and increased vasopressin secretion |
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pheochromocytoma
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A rare tumor that develops in the core of an adrenal gland.
• Can develop at any age, but most commonly occurs in people between ages 30 and 60. • Increase catacolamines in the body • Symptoms • Rapid heart rate • Forceful heartbeat • Profound sweating • Chest pain • Upper abdominal pain • Severe brief headaches of sudden onset • Shaking (tremors) of your hands • Feeling of anxiety • Feeling of extreme fright • Pale skin |
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Anemia
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Low RBC Count
• Types: – Macrocytic MCV >100 – Microcytic MCV < 80 – Normocytic MCV between 80 and 100 |
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Macrocytic Anemia
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Also called Megaloblastic anemia • Large RBC • Due to B 12 or Folate deficiency • Seen in people with chronic Alcohol abuse |
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Pernicious Anemia
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B 12 deficiency • B 12 usually absorbed by ileum when bound to intrinsic factor made by parietal cells • Shilling test tests for intrinsic factor • Due to gastritis, surgery or tapeworm • Tx: with B 12 injection |
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Microcytic Anemia
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Small RBC • Lab: – MCV < 80 – MCH < 27 pg – MCHC <32 g/dl – Anisocytosis – Poikilocytosis • Causes – Iron Deficiency – Sideroblastic Anemia – Thallessemia – Lead Poisoning |
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Iron Deficiency Anemia
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Low iron in the body so Hgb cannot be formed • Low or normal reticulocyte count • 20% female, 2 % male • Associated with blood loss and parasites • Pallor, Fatigue, hair loss, Pica • Lab: • Decreased ferritin |
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Thallassemia
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Autosomal recessive blood disease • Major and Minor Classification • Reduced synthesis of one of the globin chains of hemoglobin • Alpha • Beta • Normal has 2 alpha chains and 2 beta chains • Lab • MCV is low • Target cells • Nucleated RBC • Anisocytosis • Poikiolcytosis |
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Normocytic Anemia
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Decreased Hemoglobin and Hematocrit • Causes – Decreased Production – Increased Destruction – Increased Plasma volume |
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Increased RBC loss or destruction
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Acute blood loss • Hypersplenism • Hemolytic disorders – Congenital conditions – Disorders of red blood cell membranes – Red blood cell enzyme deficiencies – Acquired conditions • Mechanical • Autoimmune • Paroxysmal nocturnal hemoglobinuria |
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Increased RBC loss or destruction
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Acute blood loss • Hypersplenism • Hemolytic disorders – Congenital conditions – Disorders of red blood cell membranes – Red blood cell enzyme deficiencies – Acquired conditions • Mechanical • Autoimmune • Paroxysmal nocturnal hemoglobinuria |
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Decreased RBC Production
primary and secondary causes |
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Primary causes – Marrow hypoplasia or aplasia – Myelopathies – Myeloproliferative diseases – Pure red blood cell aplasia • Secondary causes – Chronic renal failure – Liver disease – Endocrine deficiency states – Anemia of chronic disease – Sideroblastic anemias |
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Anemia of Chronic Disease
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“Anemia of Inflammation” • Seen with chronic illness • Perhaps a result of HEPCIDIN release in response to cytokines – Stops release of iron – Blunts RBC production – Produces more WBC • Lab – Low reticulocyte index – Normal or high ferritin – Normal TIBC |
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Sickle Cell Anemia
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Abnormal sickle shape
• Decreased movement depriving cells of oxygen • Vasoocclusive crisis causes ischemia and chromic pain • Prone to autoinfarction of spleen and infections • Osteomyelitis and leg ulcers |
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Hemolytic Anemia
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Anemia secondary to RBC breakdown • RBC breakdown cause release of bilirubin then jaundice and dark urine. Also increased LDH. • Coombs test performed – looks for antibodies to RBC on the surface of the cell • Causes: autoimmune diseases, chronic diseases, drugs, Mechanical heart valves |
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Polycythemia Vera
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Increased RBC due to bone marrow problem • Mean age 60 • Asymptomatic to various symptoms such as generalized itch after warm water exposure • Erythromelolgia • Prone to blood clots • TX: blood letting |
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Aplastic Anemia
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Bone marrow failure: • Multi lineage or Single lineage • Etiology: acquired or inherited – Radiation, chemicals, drugs, infections, autoimmune ( Marie Curie) • Presentation: infection, bleeding or anemia • Incidence: peak 20’s and fifth decade of life • Diagnosis: peripheral blood smear |
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Treatment of Aplastic Anemia
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Immunosuppression • Immunostimulating • Antibiotics • Blood Transfusions risk of iron overload • Bone Marrow transplant- risk of host vs. graft reaction *Death within 6 months without treatment |
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Leukemia
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Cancer of the blood cells or bone marrow causing and elevation in the WBC count • Divided into Acute or Chronic and Lymphocytic or Myelogenous Leukemias |
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Acute vs Chronic Leukemia
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Acute leukemia • characterized by the rapid increase of immature blood cells. • crowding makes the bone marrow unable to produce healthy blood cells • occurs in children and young adults. • Immediate treatment is required in acute leukemias due to the rapid progression and accumulation of the malignant cells, which then spill over into the bloodstream and spread to other organs of the body. ------------------------- Chronic leukemia • distinguished by the excessive build up of relatively mature, but still abnormal, blood cells. • Takes months or years to progress, the cells are produced at a much higher rate than normal cells, resulting in many abnormal white blood cells in the blood. • occurs in older people, but can theoretically occur in any age group. • Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy |
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Acute Lymphoblastic Leukemia
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( more commonly -a disease of children)
• Excess Lymphoblast – overproduction of immature WBC • Peak age 2 to 5, another peak in older • Cure 85% children 50% adults – Worse as patient gets older – Presence of Philadelphia Chromosome- poor prognosis • Treatment- radiation, chemo, bone marrow transplant |
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Chronic Lymphocytic Leukemia
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Most common type of leukemia • Patients > 50, occasional children, M>F • Results from the accumulation of Mature B cells or rarely T cells • Stages 0 to 4 with survival in years • 0 only Lymphocytosis > 15 • I with lymphadema 8 • II with splenomegaly 6 • III with anemia 3 • IV with thrombocytosis 2 |
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Acute Myelogenous Leukemia
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Cancer of the myeloid lines- which give rise to granulocytes, monocytes, RBC and platelets • Auer rods are pathneumonic • Most common leukemia in adults • Five-year survival varies from 15–70% • Presentation – flu like symptoms • Some experience swelling of the gums because of infiltration of leukemic cells into the gum tissue. • Rarely, development of a solid leukemic mass or tumor outside of the bone marrow, called a chloroma |
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Chronic Myelogenous Leukemia
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Hall mark is Philadelphia Chromosome • Presentation: Elevated WBC on routine CBC and splenomegaly with fatigue, occasional platelet elevation. • Blast Crisis -final phase in the evolution of CML – 30 to 40 % of blasts in bone marrow • TX: chemotherapy |
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Hairy Cell Leukemia
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Mature B cell neoplasm • Cells look “Hairy” in lab • 2% of all leukemias mostly men> 50 • Easily goes into remission • Great chance of developing second cancer |
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Lymphoma
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Tumors develop in the Lymph Nodes • Types: – Hodgkins with 5 sub groups – Non- hodgkins with 20 subgroups |
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Hodgkins Lymphoma
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1% of all cancers • Starts in 1 lymph node and spreads to others • Biopsy shows Reed Sternberg cell • 2 age groups: 15 to 35 and > 55 • Etiology ?? Some consider a viral etiology • 98% survival in early stages goes down to 80% in late stages • Symptoms: Night Sweat, pains, fever, enlarged LN, hepatospleenomegally. |
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Multiple Myeloma
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Malignant proliferation of plasma cells • Most common bone cancer in adults • 30% dx as incidental finding on x-ray • Median Survival 3 years • Characteristics: • Calcium elevation • Renal Failure: Bence Jones Proteins in the Urine • Anemia • Bone Lesions • Bone pain esp. sternum and skull, ribs and back |
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Urticaria
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Multiple etiologies • Food and additives • Drugs • Infections • Inhaled Allergens • Internal Disease • Due to physical exposures – cold, heat |
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Barrett’s Esophagus
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Squamous cells of esophagus become columnar cells with intestional characteristics
• Develops into adenocarcenoma • EGD q 2 years with biopsy |
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Esophageal Varices
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Esophageal varices develop when normal blood flow to your liver is blocked. The blood then backs up into smaller, more fragile blood vessels in your esophagus • Mortality rate- 50% • Treatment- • Hemodynamic care • Band ligation • Sclerotherapy • Somatostatin or Octreotide • Vasopressin |
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Stages of Renal Disease
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Stage 1 CKD • Slightly diminished function; Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies • Stage 2 CKD • Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies. • Stage 3 CKD • Moderate reduction in GFR (30-59 mL/min/1.73 m2) • Stage 4 CKD • Severe reduction in GFR (15-29 mL/min/1.73 m2) • Stage 5 CKD • Established kidney failure (GFR <15 mL/min/1.73 m2,) Dialysis • Causes • The most common causes of CKD are DM, HTN, glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy. |