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Download Pathophysiology Chapter 8 Study Guide- Fluid Compartments, Electrolytes, Osmosis, Tonicity and more Exams Advanced Education in PDF only on Docsity!
{. Intracellular Fluid: 2/3 of body fluid (fluid within the cells) 1, Extracellular Fluid: 1/3 of body fluid (interstitial fluid, plasma, transcellular fluid) 3. Electrolytes: When a substance is added to water, it dissociates into ions, which are charged particles 4 Cations: positively charged ions 5, Anion: Negatively charged ions 6. Nonelectrolytes (provide two examples): Substances that do not dissociate into ions when dissolved in water. Examples: Glucose and Urea 7. Role of Glucose: Providing energy for cells, but not directly involved in electrical activity 8, Urea: waste product formed in the liver, filtered out of the blood by the kidneys, and excreted in urine 9. ECF Highs: SALTY-(Bl)... Sodium, chlroide, bicarbonate 10. ICF highs: PotMa. Potassium and Magnesium {. Normal Value of Sodium: 135-145 mEq/L 1. Normal Value of Potassium: 3.5-5.0 mEq/L 13. Normal Value of Chloride: 98-106 mEq/L 14. Normal Value of Bicarbonate: 21-28 mEq/L 15. Osmosis: Movement of water down its concentration gradient across a semipermeable membrane 16. Result of higher ECF osmolality: water leaves the cell (shrinking) 17. Result of lower ECF osmolality: Water enters the cell (swelling) 18. Tonicity: Tension or ettect a solution with impermeable solutes exerts on cell size due to water movement across the cell membrane 19. Capillary filtration pressure (hydrostatic): pushes water out of capillary and into tissue 10. Capillary colloidal osmotic pressure: pulls water into capillary from tissue 11. interstitial hydrostatic pressure: pushes water out of tissue and into capillary 2. interstitial colloidal osmotic pressure: pulls water into tissue and out of capillary 33. arterial end of capillary: increased hydrostatic pressure pushes fluid into interstitial space 14. venous end of capillary: higher colloidal osmotic pressure, pulling fluid into capillaries. Increased pressure is due to plasma proteins, such as Albumin 35, Lymph Drainage: Excess fluid and plasma proteins not reabsorbed into capillaries can move into lymph system 26. Edema: Palpable swelling produced by an increase in interstitial fluid volume 77. causes of edema: Increased capillary filtration pressure, decreased capillary colloidal pressure, increased capillary permeability, obstruction of lymph flow 4g. Hypodipsia: decrease in the ability to sense thirst (common in elderly, hypothalamic lesions) 4]. Polydipsia: Increased thirst. Real thirst: resolves with fluid intake (vomiting, diabetes) Spurious: false thirst (chronic diseases, dry mouth, meds) Thirst Compulsion: compulsive (schizophrenia) 48. ADH present: collecting duct is highly permeable to water, small volume of concentrated urine 49. No ADH present: Collecting duct is not permeable to water large volume of dilute urine 50. Diseases of the posterior pituitary: SIADH Diabetes Insipidus 51. Diabetes insipidus: Insuflciency of ADH. Leads to excessive urine and thirst. Increased plasma osmolality and hypertonic dehydration 51. Causes of Diabetes Insipidus: Neurogenic: Not enough ADH produced Nephrogenic: kidneys dont respond to ADH (due to drugs like lithium) 53. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Too much ADH. Enhanced water retention. Diluted blood, low sodium levels, low urine output, GI symptoms, dulled senses, mental changes 54. Causes of Isotonic Fluid Volume Deficit: Volume loss -- vomiting, diarrhea, sweating Endocrine disturbances Third Spacing 55. Compensatory mechanisms of Isotonic Fluid Volume Deficit: Increased thirst, in- creased ADH 56. Manifestations of Isotonic Fluid Volume Deficit: Signs of vascular dehydration: decreased skin turgor, dry mucous membrane, sunken eyeballs Decreased vascular volume: postural hypotension, weak, rapid pulse 57. causes of isotonic fluid volume excess: decreased renal elimination (kidney disorders, heart failure, liver failure) 58. manifestations of isotonic fluid volume excess: Increased interstitial fluid volume (edema), increased vascular volume (bounding pulse, venous distention, pulmonary edema) 59. Potassium (K+): major intracellular electrolyte. Essential for normal cellular functions such as osmolality and fluid balance, glycogen and glucose deposition in skeletal muscle and liver, nerve skeletal muscle, and cardiac function 60. mechanisms of potassium regulation: renal regulation and transcellular shifts 61. Potassium and Membrane Potential: Potassium is vital to regulation of resting membrane potentials, opening of sodium channels during action potentials, and the rate of membrane repolarization 62. Hyperkalemia: excessive potassium in the blood, decreases membrane excitability, Can lead to bradycardia and ventricular fibrillation 63. Hypokalemia: Low potassium levels in the blood, decreases resting membrane potential 64. Causes of hypokalemia: Inadequate intake, excessive losses (GI, renal, and skin), Diuretics, Insulin, Bicarbonate excess, Alkalosis 65. Manifestations of hypokalemia: polyuria, polydipsia, lethargy, muscle weakness, muscle cramps, paralysis, Dysrhythmias, confusion, metabolic alkalosis 66. treatment for hypokalemia: IV replacement -- must be slow, generally given oral route 67. Causes of hyperkalemia: Think MACHINE -- medications (ACE inhibitors) M A -- metabolic and respiratory acidosis C -- Cellular injury (burns and trauma) H -- hypoaldosteronism | -- intake N -- nephrons (renal failure) E -- excretion (impaired potassium removal) 6&. Manifestations of hyperkalemia: Think MURDER -- muscle weakness -- Urinary (oliguria) -- Respiratory distress -- Decreased cardiac contractility -- ECG changes -- reflexes (hyperreflexia) 9. Treatment for hyperkalemia: In emergent situations -- IV insulin (plus glucose to prevent hypo- glycemia), calcium, sodium bicarb Insulin stimulates sodium potassium pump, bring potassium back into cells and out of blood 70. Calcium: 8.5-10.5 mg/dL Functions include... Bone strength and stability membrane potentials and excitability >Pmownce Ss 81. CO2: carbon dioxide is produced by body cells through intracellular metabolism. It can be exhaled 82. Mechanisms of CO2 transport in the blood: 10% dissolved in blood (plasma) 70% transported as bicarbonate dissolved in plasma 20% carried as carbaminohemoglobin 83. CO2 as bicarbonate: Excess CO2 is carried a bicarbonate dissolved in plasma. First carbon dioxide and water combine to form carbonic acid (enzyme called carbonic anhydrase) Carbonic acid dissociates into a hydrogen ion and bicarbonate. RBCs exchange bicarbonate for chloride (chloride shift) Bicarbonate exits the cell and can be dissolved in the plasma 84. How do we regulate pH: Chemical butter systems in body fluids, lungs, and kidneys 8. Chemical Buffer Systems: &. Respiratory control mechanisms of pH: This is a rapid response. Increased ventilation = increased CO2 elimination = decreased co2 levels in the blood = increased pH Decreased ventilation = decreased co2 elimination = increased co? levels in the blood = decreased pH §7. Renal exchange systems: - H+/HCO3- exchange system - K+/H+ exchange Acidosis = increased hydrogen elimination and increased potassium retain Alkalosis = retains hydrogen and increased potassium elimination - Cl-/HCO3- exchange 88 Renal buffer system: generation of new bicarbonate Ammonia butter system and phosphate butter system 8. Ammonia buffer system: glutamine metabolized end products are ammonium and bicarb ammonium ions secreted and bicarb ions reabsorbed 90. Metabolic acidosis: low pH, low HCO3 compensatory mechanism = increased respiratory rate, bone breakdown 91. metabolic alkalosis: high pH, high HCO3 compensatory mechanism = decreased respiratory rate 92. Respiratory Acidosis: low pH, high CO2 93. Causes of Metabolic Acidosis: Increased production of Fixed metabolic acidosis (increased produc- tion or decreased removal of lactic acid via anaerobic metabolism) Ingestion of chemical toxins (asprin, wood alcohol, antifreeze) Decreased renal function (chronic kidney disease) Bicarb losses through the kidneys or the Gl tract (vomiting and diarrhea) Hyperchloremic acidosis (too little bicarb, too much chloride) 94. manifestations of metabolic acidosis: signs and symptoms related to alterations in CV, neuro, Gl, skin, and skeletal muscle function 95. Treatment of metabolic acidosis: correct cause of condition, restore fluid and electrolytes, admin- ister NaHCO3 96. Causes of metabolic alkalosis: ingestion of excess bicarb (too many tums) Loss of fixed acids via Gl 97. manifestations of metabolic alkalosis: Nervous system and Cardiovascular ettects 98. treatment of metabolic alkalosis: Correct cause of condition Treat chloride and pottasium deficit with KCL Replace volume deficit with .9% NS 99. Too much CO2: Hypercapnia or Hypercarbia {00. Causes of Respiratory acidosis: increased CO2 pressure due to conditions that impair alveolar ventilation Acute disorders of ventilation (drug overdose, anesthesia, chest injury) Chronic disorders of ventilation (COPD and pulm fibrosis) {01. manifestations of respiratory acidosis: Vasodilation of cerbral vessels, skin is warm and flushed 10. Treatment of respiratory acidosis: improve ventilation, mechanical ventilation 103. Causes of respiratory alkalosis: Not enough CO2, hyperventilation stimulation of medullary respiratory center (anxiety, pain, pregnancy, fever, sepsis) 14. manifestations of respiratory alkalosis: vasoconstriction of cerebral vessels cardiovascular ettects 105. treatment of respiratory alkalosis: correct underlying cause breathe in paper bag 
