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Disorders of Fluid and Electrolyte Balance lecturer: Dr . Zainab Sajid Al- Shimmari

This lecture by Dr. Zainab Sajid Al-Shimmari focuses on disorders of fluid and electrolyte balance, specifically diabetes insipidus, syndrome of inappropriate antidiuretic hormone (SIADH), hyponatremia, and hypernatremia. Learn about the causes, manifestations, and laboratory values associated with these conditions.

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Disorders of Fluid and Electrolyte Balance lecturer: Dr . Zainab Sajid Al- Shimmari

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  1. Disorders of Fluid and Electrolyte Balancelecturer:Dr. ZainabSajid Al-Shimmari

  2. *Disorders of Fluid and Electrolyte BalanceDiabetesInsipidus1-Diabetes insipidus , which means “tasteless diabetes,” as opposed to diabetes mellitus, or “sweet diabetes,” is caused by a deficiency of or a decreased responseto ADH. 2- Diabetes insipidus is characterized by excessive urination of a dilute urine (polyuria, usually greater than 2 L/day) and polydipsia.

  3. There are two types of diabetes insipidus: • 1-central or neurogenic diabetes insipidus, which occurs because of a defect in the synthesis or release of ADH. • 2-Nephrogenic diabetes insipidus, which occurs because the kidneys donot respond to ADH. Nephrogenic diabetes insipidus is characterized by impairment of urine-concentrating ability and free-water conservation

  4. Manifestations of diabetes insipidus: • 1-Persons with diabetes insipidus are unable to concentrate their urine during periods of water restriction; they excrete large volumes of urine, usually 3 to 20 L/day, depending on the degree of ADH deficiency or renal insensitivity to ADH. • 2-This large urine output is accompanied by excessive thirst. • 3-In such cases, inadequate fluid intake rapidly leads to hypertonic dehydration and increased serum osmolality

  5. Syndrome of Inappropriate Antidiuretic Hormone • 1-The syndrome of inappropriate antidiuretic hormone (SIADH)results from a failure of the negative feedback system that regulates the release and inhibition of ADH. 2-SIADH can be caused by a number of conditions; however,the major causes are neoplasia, neurologic diseases,lung diseases, and a variety of pharmacologic agents. 3-Tumors particularly bronchogenic carcinomas and cancers of the lymphoid tissue, prostate, and pancreas.

  6. Manifestations: • 1-In persons with this syndrome, ADH secretion continues even when serum osmolality is decreased; this causes marked retention of water in excess of sodium and dilutionalhyponatremia . • 2-An increase in the glomerular filtration rate resulting from an increased plasma volume causes further increases in sodium loss by suppressing the renin-angiotensin mechanism. • 3-Urine osmolality is hight, and serum osmolality is low. Urine output decreases despite adequate or increased fluid intake.

  7. Hyponatremia • 1-Hyponatremia represents a decrease in plasma sodium concentrationbelow (135 mmol/L). • 2-Unlike hypernatremia,which is always associated with hypertonicity, hyponatremia may be associated with high, normal, or low tonicity because of the effects of other osmotically active particles in the ECF such as glucose

  8. Causes : 1-Excessive Sodium Losses and Replacement with Tap Water or Sodium-Free Losses. • A-Exercise- or heat-induced sweating and replacement with sodium-free fluids. • B-Gastrointestinal losses :Vomiting, diarrhea. • C-Renal losses ;Diuresis. 2-Excessive Water Intake in Relation to Output. *Excessive administration of sodium-free parenteral solutions. *Repeated irrigation of body cavities with sodium-free solutions. *Irrigation of gastrointestinal tube with distilled water. *Tap water enemas. *Use of non electrolyte irrigating solutions during prostate surgery. *Kidney disorders that impair water elimination. *Increased ADH levels. *Trauma, stress, pain. *Syndrome of inappropriate ADH. *Use of medications that increase ADH. *Psychogenic polydipsia.

  9. Manifestations 1-Laboratory Values • i*Serum sodium level below 135 mEq/L(135 mmol/L). ii*Decreased serum osmolality,*Dilution of blood components, including hematocrit, blood urea nitrogen. 2-Signs Related to Hypo-osmolality of ExtracellularFluids and Movement of Water Into Brain Cells and Neuromuscular Tissue • Muscle cramps,Weakness,Headache,Depression,Apprehension, feeling of impending doom,Personalitychanges,Lethargy,Stupor, coma. 3-Gastrointestinal Manifestations: • Anorexia, nausea, vomiting,Abdominal cramps, diarrhea. 4-Increased Intracellular Fluid. • Fingerprint edema.

  10. Hypernatremia 1-Hypernatremia implies a plasma sodium level above 145 mEq/L and a serum osmolality greater than 295 mOsm/kg. 2-Because sodium is functionally an impermeable solute,it contributes to tonicity and induces movement of water across cell membranes. 3-Hypernatremia is characterized by hypertonicity of ECF and almost always causes cellular dehydration.

  11. Causes 1-Excessive Water Losses. • Watery diarrhea,Excessivesweating,Increased respirations due to conditions • such as tracheobronchitis,Hypertonic tube feedings, Diabetes insipidus. 2-Decreased Water Intake. • Unavailability of water,Oral trauma or inability to swallow,Impaired thirst ensation • Withholding water for therapeutic reasons, Unconsciousness or inability to express • Thirst. 3-Excessive Sodium Intake. • Rapid or excessive administration of sodium-containing parenteral solutions.

  12. Manifestations 1-Laboratory Values. • i*Serum sodium level above 145 mEq/L(145 mmol/L). • ii*Increased serum osmolality. • iii*Increased hematocrit and blood urea nitrogen. 2-Thirst and Signs of Increased ADH Levels. • Polydipsia,Oliguria or anuria,High urine specific gravity. 3-Intracellular Dehydration. • Dry skin and mucous membranes,Decreased tissue turgor,Tongue rough and fissured,Decreased salivation and lacrimation. 4-Signs Related to Hyperosmolality of Extracellular Fluids and Movement of Water Out of Brain Cells. • Headache,Agitation and restlessness,Decreasedreflexes,Seizures and coma 5-Extracellular Dehydration and Decreased Vascular Volume. • Tachycardia,Weak and threadypulse,Decreased blood pressure,Vascular collapse.

  13. Hypokalemia 1-Hypokalemia refers to a decrease in plasma potassium levels below 3.5 mEq/L (3.5 mmol/L). 2-Because of transcellular shifts, temporary changes in plasma potassium may occur as the result of movement between the ICF and ECF compartments.

  14. Causes 1-Inadequate Intake. Diet deficient in potassium,Inability to eat,Administration of potassium-freeparenteral solutions. 2-Excessive Renal Losses. Diuretic therapy (except potassium sparing diuretics),Diuretic phase of renal failure, Increased mineralocorticoid levels,Primaryhyperaldosteronism,Treatment with corticosteroid drugs. 3-Excessive Gastrointestinal Losses. Vomiting,Diarrhea,Gastrointestinalsuction,Draining gastrointestinal fistula. 4-Transcompartmental Shift. Administration of β-adrenergic agonist ,Administration of insulin for treatment of diabetic ketoacidosis,Alkalosis; metabolic or respiratory.,

  15. Manifestations 1-Laboratory Values. • Serum potassium less than 3.5 mEq/L(3.5 mmol/L). 2-Impaired Ability to Concentrate Urine. • Polyuria,Urine with low osmolality and specific gravity,Polydipsia. 3-Gastrointestinal Manifestations. • Anorexia, nausea, vomiting,Abdominaldistention,Paralytic ileus. 4-Neuromuscular Manifestations. • Muscle flabbiness, weakness, and fatigue,Muscle cramps and tenderness, Paresthesias,Paralysis. 5-Cardiovascular Manifestations. • Postural hypotension,Increased sensitivity to digitalis toxicity,Changes in electrocardiogram,Cardiac dysrhythmias. 6-Central Nervous System Manifestations: • Confusion,Depression. 7-Acid–Base Disorders: • Metabolic alkalosis.

  16. Hyperkalemia 1-Hyperkalemia refers to an increase in plasma levels of potassium in excess of 5.0 mEq/L (5.0 mmol/L). 2-It seldom occurs in healthy persons because the body is extremely effective in preventing excess potassium accumulation in the ECF.

  17. Causes 1-Excessive Intake • Excessive oral intake,Treatment with oral potassium supplements,Excessive or rapid infusion of potassium containing parenteral fluids. 2-Release From Intracellular Compartment. • Tissue trauma,Burns,Crushinginjuries,Extreme exercise or seizures. 3-Inadequate Elimination by Kidneys. • Renal failure,Adrenal insufficiency (Addison’s disease),Treatment with potassium-sparing diuretics,Treatment with angiotensin-converting enzyme inhibitors.

  18. Manifestations: • 1-Laboratory Values. • Serum potassium above 5.0 mEq/L(5.0 mmol/L). • 2-Gastrointestinal Manifestations. • Nausea and vomiting,Intestinalcramps,Diarrhea. • 3-Neuromuscular Manifestations. • Paresthesias,Weakness, dizziness,Muscle cramps. • 4-Cardiovascular Manifestations. • Changes in electrocardiogram,Risk of cardiac arrest with severe excess.

  19. METABOLIC ACIDOSIS 1-Metabolic acidosis involves a primary deficit in base HCO3− along with adecrease in plasma pH. 2-In metabolic acidosis, the body compensates for the decrease in pH by increasing the respiratory rate in an effort to decrease CO2 and H2CO3 levels.

  20. Causes 1-Excess Metabolic Acids (Increased Anion Gap). • Excessive production of metabolic acids,Lacticacidosis,Diabetic ketoacidosis • Alcoholic ketoacidosis,Fasting and starvation,Poisoning (e.x., salicylate, methanol, • ethylene glycol),Impaired elimination of metabolic acids,Kidney failure or dysfunction. 2-Excessive Bicarbonate Loss (Normal Anion Gap). • Loss of intestinal secretions,Diarrhea,Intestinal suction, Intestinal or biliary fistula • Increased renal losses,Renal tubular acidosis,Treatment with carbonic anhydrase • Inhibitors,Hypoaldosteronism. 3-Increased Chloride Levels (Normal Anion Gap). • Excessive reabsorption of chloride by the kidney,Sodium chloride infusions, Treatment with ammonium chloride,Parenteralhyperalimentation.

  21. Manifestations 1-Blood pH, HCO3−, CO2. • pH decreased, HCO3− (primary) decreased,PCO2 (compensatory) decreased. 2-Gastrointestinal Function. • Anorexia,Nausea and vomiting,Abdominal pain. 3-Neural Function. • Weakness,Lethargy,Generalmalaise,Confusion,Stupor,Coma,Depression of vital functions. 4-Cardiovascular Function. • Peripheral vasodilation,Decreased heart rate,Cardiac dysrhythmias. 5-Skin: Warm and flushed. 6-Skeletal System: • Bone disease (e.x., chronic acidosis). 7-Signs of Compensation. • Increased rate and depth of respiration(i.e., Kussmaul breathing),Hyperkalemia, • Acid urine,Increased ammonia in urine.

  22. METABOLIC ALKALOSIS 1-Metabolic alkalosis is a systemic disorder caused by an increase in pH due to a primary excess of plasma HCO3−ions. 2-It can be caused by a loss of H+ ions, net gain in HCO3− ions, or loss of Cl− ions in excess of HCO3− ions. Causes 1-Excessive Gain of Bicarbonate or Alkali Ingestion or administration of sodium bicarbonate,Administration of hyperalimentation solutions containing acetate,Administration of parenteral solutions containing lactate,Administration of citrate-containing blood transfusions.

  23. 2-Excessive Loss of Hydrogen Ions. Vomiting,Gastricsuction,Binge-purge syndrome,Potassiumdeficit,Diuretictherapy,Hyperaldosteronism,Milk-alkali syndrome. 3-Increased Bicarbonate Retention. Loss of chloride with bicarbonate retention. 4-Volume Contraction: Loss of body fluids,Diuretic therapy.

  24. Manifestations • 1-Blood pH, HCO3−, CO2. • pH increased,HCO3− (primary) increased,PCO2 (compensatory) increased. • 2-Neural Function. • Confusion,Hyperactivereflexes,Tetany,Convulsions. • 3-Cardiovascular Function: • Hypotension,Dysrhythmias • 4-Respiratory Function. • Respiratory acidosis due to decreased respiratory rate. • 5-Signs of Compensation. • Decreased rate and depth of respiration,Increased urine pH.

  25. RESPIRATORY ACIDOSIS 1-Respiratory acidosis occurs in conditions that impair alveolar ventilation and cause an increase in plasma PCO2, also known as hypercapnia, along with a decrease in pH. 2- Respiratory acidosis can occur as an acute or chronic disorder. Acute respiratory failure is associated with a rapid rise in arterial PCO2 with a minimal increase in plasma HCO3− and large decrease in pH. 3-Chronic respiratory acidosis is characterized by a sustained increase in arterial PCO2, resulting in renal adaptation and a more marked increase in plasma HCO3-.

  26. Causes 1-Depression of Respiratory Center. • Drug overdose,Head injury. 2-Lung Disease. • Bronchial asthma,Emphysema,Chronicbronchitis,Pneumonia,Pulmonary edema, • Respiratory distress syndrome. 3-Airway Obstruction, Disorders of Chest Wall and Respiratory Muscles. • Paralysis of respiratory muscles,Chest injuries, Extreme obesity,Treatment with paralytic drugs. 4-Breathing Air With High CO2 Content.

  27. Manifestations • 1-Blood pH, CO2, HCO3−. • pH decreased,PCO2 (primary) increased,HCO3− (compensatory) increased. • 2-Neural Function. • Dilation of cerebral vessels and depression of neural function,Headache, • Weakness,Behaviorchanges,Confusion,Depression,Paranoia,Hallucinations, • Tremors,Paralysis,Stupor and coma. • 3-Skin: • Skin warm and flushed. • 4-Signs of Compensation: • Acid urine.

  28. RESPIRATORY ALKALOSIS • 1-Respiratory alkalosis is a systemic acid-base disorder characterized by a primary decrease in plasma PCO2, also referred to as hypocapnia, which produces an elevation in pH and a subsequent decrease in HCO3−. 2-Because respiratory alkalosis can occur suddenly, a compensatory decrease in bicarbonate level may not occur before respiratory correction has taken place.

  29. Causes : • 1-Excessive Ventilation. • Anxiety and psychogenic hyperventilation,Hypoxia and reflex stimulation of • Ventilation,Lung disease that reflexly stimulates ventilation,Stimulation of respiratory center,Elevated blood ammonia level,Salicylatetoxicity,Encephalitis, • Fever, Mechanical ventilation.

  30. Manifestations: 1-Blood pH, CO2, HCO3− • pH increased,PCO2 (primary) decreased,HCO3− (compensatory) decreased. 2-Neural Function. • Constriction of cerebral vessels and increased neuronal excitability,Dizziness, panic, light-headedness,Tetany,Numbness and tingling of fingers and toes. 3-Cardiovascular Function • Cardiac dysrhythmias.

  31. Diabetes Mellitus • 1-The term diabetes is derived from a Greek word meaning“going through” and mellitus from the Latin word for“honey” or “sweet.” • 2-Diabetes is a disorder of carbohydrate, protein, and fat metabolism resulting from an imbalance between insulin availability and insulin need. • 3-It can represent an absolute insulin deficiency, impaired release of insulin by the pancreatic beta cells, inadequate or defective insulin receptors, or the production of inactive insulin or insulin that is destroyed before it can carry out its action. 4-A person with uncontrolled diabetes is unable to transport glucose into fat and muscle cells; as a result, the body cells are starved, and the breakdown of fat and protein is increased.

  32. CLASSIFICATION AND ETIOLOGY. 1-The revised system for the classification of diabetes was continues to include type 1 and type 2 diabetes, but uses Arabic rather than Roman numerals and eliminates the use of “insulin dependent”and “non–insulin-dependent” diabetes mellitus. • Type 2 diabetes currently accounts for about90% to 95% of the cases of diabetes. 2-Included in the classification system are the categories of gestational diabetes mellitus (i.e., diabetes that develops during pregnancy)and other specific types of diabetes, many of which occur secondary to other conditions (e.g., Cushing’s syndrome, hematochromatosis, pancreatitis, • acromegaly).

  33. 3-The revised classification system also includes a system for diagnosing diabetes according to stages of glucose in tolerance . The revised criteria have retained the former category of impaired glucose tolerance (IGT) and have added a new category of impaired fasting plasma glucose(IFG). The categories of IFG and IGT refer to metabolic stages intermediate between normal glucose homeostasis and diabetes, and are labeled together as prediabetes .

  34. Type 1 Diabetes Mellitus: 1-Type 1 diabetes mellitus is characterized by destruction of the pancreatic beta cells. Type 1 diabetes is subdivided into two types: type 1A, immune-mediated diabetes, and type 1B, idiopathic diabetes. In the United States and Europe, approximately 10% of people with diabetes mellitus have type 1 diabetes, with 95% of them having type 1A,immune-mediated diabetes.

  35. 2-Type 1A diabetes is characterized by autoimmune destruction of beta cells. This type of diabetes, formerly calledjuvenile diabetes, occurs more commonly in young persons but can occur at any age. • 3- Type 1 diabetes is a catabolic disorder characterized by an absolute lack of insulin, an elevation in blood glucose, and a breakdown of body fats and proteins. The absolute lack of insulin in people with type 1diabetes mellitus means that they are particularly prone to the development of ketoacidosis. • 4- One of the actions of insulin is the inhibition of lipolysis (i.e., fat breakdown) and release of free fatty acids (FFAs) from fat cells. In the absence of insulin, ketosis develops when these fatty acids are released from fat cells and converted to ketones in the liver.

  36. 5-Because of the loss of the first-phase insulin (preformed insulin) response, all people with type 1A diabetes require exogenous insulin replacement to reverse the catabolic state, control blood glucose levels, and prevent ketosis. • 6-The rate of beta cell destruction is quite variable, being rapid in some individuals and slow in others. A-The rapidly progressive form commonly is observed in children, but also may occur in adults. B-The slowly progressive form usually occurs in adults and is sometimes referred to as latent autoimmune diabetes in adults (LADA)..

  37. 7-LADA may constitute up to 10% of adults who are currently classified as having type 2 diabetes. A- It has been suggested that type 1A, immune-mediated diabetes results from a genetic predisposition. B-A hypothetical triggering event that involves an environmental agent that incites an immune response ,and immunologically mediated beta cell destruction. C- The inherited major histocompatibility complex (MHC) genes that encode three human leukocyte antigens found on the surface of body cells . In addition to the major susceptibility gene for type 1 diabetes in the MHC region on chromosome 6, an insulin gene regulating beta cell replication and function has been identified on chromosome11

  38. 8-Type 1 diabetes–associated auto antibodies may exist for years before the onset of hyperglycemia. There are two major types of auto antibodies: (i)insulin auto antibodies(IAAs), and(ii) islet cell auto antibodies and antibodies directed at other islet auto antigens, including glutamic acid decarboxylase (GAD) and the protein tyrosine phosphatase . • These people also may have other autoimmune disorders such as Graves’ disease, rheumatoid arthritis, and Addison’s disease.

  39. 9-The term idiopathic type 1B diabetes is used to describe those cases of beta cell destruction in which no evidence of autoimmunity is present. Only a small number of people with type 1 diabetes fall into this category; most are of African or Asian descent. Type 1B diabetes is strongly inherited. People with the disorder have episodic ketoacidosis • due to varying degrees of insulin deficiency with periods of absolute insulin deficiency that may come and go.

  40. Type 2 Diabetes Mellitus and the Metabolic Syndrome: • I-Type 2 diabetes mellitus is a heterogeneous condition that describes the presence of hyperglycemia in association with relative insulin deficiency. In contrast to type 1 • A-diabetes in which absolute insulin deficiency is present, type 2 diabetes can be associated with high, normal, or low insulin levels. However, in the presence of insulin resistance, the insulin cannot function effectively, and hyperglycemia can result. • B-Type 2 diabetes is therefore a disorder of both insulin levels (beta cell dysfunction) and insulin function (insulin resistance). • C- Type 2 diabetes(unlike type 1) is not associated with auto antibodies. • D-Most people with type 2 diabetes are older and over weight; however, type 2 diabetes is becoming a more common occurrence in obese a dolescents.

  41. II-The metabolic abnormalitiesthat contribute to hyperglycemia in people with type 2 diabetes include. (i) impaired beta cell function and insulin secretion. (ii)peripheral insulin resistance. • (iii)increased hepatic glucose production. • Insulin resistance initially produces an increase in beta cell secretion of insulin (resulting in hyperinsulinemia)as the body attempts to maintain a normoglycemic state. • III-In time, however, the insulin response declines because of increasing beta cell dysfunction. (i)This results initially in elevated postprandial blood glucose levels. Eventually, fasting blood glucose levels also rise until frank type 2 diabetes occurs. (ii)During the evolutionary phase, an individual with type 2 diabetes may eventually develop absolute insulin deficiency because of progressive

  42. IV-As with persons with type 1 diabetes, these persons require insulin therapy to survive. Because most persons with type 2 diabetes do not have an absolute insulin deficiency,they are less prone to develop ketoacidosis as compared with people with type 1 diabetes (the presence of circulating insulin in most type 2 diabetics suppresses ketone body formation).

  43. V-Beta Cell Dysfunction: Specific causes of beta cell dysfunction in patients with prediabetes and type 2 diabetes may include: (1) an initial decrease in the beta cell mass (this may be related to genetic factors responsible for beta cell differentiation and function, and environmental factors such as the presence of maternal diabetes during pregnancy or in utero factors such as the presence of intrauterine growth retardation), • (2)increased beta cell apoptosis/decreased regeneration, • (3)long-standing insulin resistance leading to beta cell exhaustion, (4) chronic hyperglycemia can induce beta cell desensitization termed glucotoxicity, (5) chronic elevation of free fatty acids can cause toxicity to beta cells. • Termed lipotoxicity. (6)amyloid deposition in the beta cell can cause dysfunction.

  44. VI-Insulin Resistance and the Metabolic Syndrome: • 1-There is increasing evidence to suggest that insulin resistance not only contributes to the hyperglycemia in persons with type 2 diabetes, but may also play a role in other metabolic abnormalities. These include high levels of plasma triglycerides and low levels of high-density lipoproteins • (HDLs), hypertension, systemic, abnormal fibrinolysis, abnormal function of the vascular endothelium, and macrovascular disease (coronary artery,cerebrovascular, and peripheral arterial disease).

  45. 2-A major factor in persons with the metabolic syndrome that leads to type 2 diabetes is central obesity. Approximately80% of persons with type 2 diabetes are over weight. a-Obese people have increased resistance to the action of insulin and impaired suppression of glucose production by the liver, resulting in both hyperglycemia and hyperinsulinemia. • b-The type of obesity is an important consideration in the development of type 2 diabetes. It has been found that people with upper body obesity (central obesity)are at greater risk for developing type 2 diabetes and • metabolic disturbances than persons with lower body obesity.

  46. c-The increased insulin resistance has been attributed to increased visceral (intra-abdominal) obesity detected on computed tomography scan. • d- The new terminology that is emerging for persons with obesity and type 2 diabetes is diabesity. • e-insulin resistance may improve with weight loss, to the extent that many people with type 2 diabetes can be managed with a weight-reduction program and exercise. • It has been theorized that the insulin resistance and increased glucose production in obese people with type 2 diabetes may stem from an increased concentration of free fatty acids (FFAs).

  47. f- Visceral obesity is especially important because it is accompanied by increases in fasting and postprandial FFA concentrations. This has several consequences:- (i)acutely, FFAs act at the level of the beta cell to stimulate insulin secretion, which, with excessive and chronic stimulation, causes beta cell failure (lipotoxicity). (ii)they act at the level of the peripheral tissues to cause insulin resistance and glucose underutilization by inhibiting glucose uptake and glycogen storage through a reduction in muscle glycogen synthetase activity.

  48. (iii) the accumulation of FFAs and triglycerides reduce hepatic insulin sensitivity, leading to increased hepatic glucose production and hyperglycemia, especially fasting plasma glucose levels. Thus, an increase in FFA that occurs in obese individuals (especially visceral obesity) with a genetic predisposition to type 2 diabetes may eventually lead to beta cell dysfunction/failure, increased insulin resistance, and hepatic glucose production.

  49. 3-A further consequence is the diversion of excess FFAs to non adipose tissues, including liver, skeletal muscle, heart, and pancreatic beta cells. The uptake of FFAs from the portal blood can lead to hepatic triglycerideaccumulation and nonalcoholic fatty liver disease. 4-A proposed link to the insulin resistance associated with obesity is an adipose cell secretion (a dipocytokine)called a diponectin. A diponectin is secreted by adipose tissue and circulates in the blood. It has been shown that decreased levels of a diponectin coincide with insulin resistance in animal models and patients with obesity and type 2 diabetes.

  50. Other Specific Types: • The category of other specific types of diabetes, formerly known as secondary diabetes, describes diabetes that is associated with certain other conditions and syndromes.

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