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105 Cards in this Set
- Front
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level of <2.5 of phosphate
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hypophospatemia
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level of >4.5 of phosphate
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hyperphosphatemia
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Extreme thrist, tachycardia, low-grade fever, dry, sticky tongue and oral mucuosa, disorientation, hallucinations, lethargy progressing to coma, hyperactive deep tendon reflexes, seixures, coma
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Clinical Manifestations of hypernatremia
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Level of <1.8 of magnesium
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Hypomagnesemia
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Level of >2.4 of magnesium
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Hypermagnesemia
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Level of <3.5 of potassium
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Hypokalemia
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Level of >5.5 of potassium
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Hyperkalemia
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Inadequate dietary P intake,
Severe, prolonged vomiting, Alcoholism and withdrawal, IV glucose or insulin adm (moves P into skeletal muscle), Malabsorption syndromes, Hyperparathyroidism, Severe metabolic acidosis, Respiratory alkalosis, hypokalemia, Hypomagnesemia |
Causes o phosphatemia
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Paresthesias, Profound muscle weakness, Muscle pain and tenderness, Anorexia, Malaise ,Rapid, shallow respirations, Altered LOC, seizures
Nystagmus, Heart failure, Platelet dysfunction |
Clinical mnifestations of hypophosphatremia
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Acute or chronic renal failure
Excessive dietary P intake Excessive Vitamin D use Insufficient dietary intake Hypoparathyroidism Cancer chemotherapy Excessive laxative use |
Causes of hyperphosphatemia
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Leve of >147 of sodium
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Hypernatremia
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Tetany
Circumoral paresthesias Muscle spasm Seizures Soft tissue calcification |
Clinical Manifestations of hyperphosphatemia
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Level of <9.0 of calcium
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Hypocalcemia
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Prolonged diuretic therapy, excessive diaphosesis, insufficient Na intake, burns, severe GI loss, adrenal insufficiency, SIADH
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Causes of Hyponatremia
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Sum of fluids within all body compartments
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Total Body Weight (TBW)
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All fluid within the cells (2/3)
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Intracellular fluid (ICF)
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Level of <135 of sodium
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Hyponatremia
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All fluid outside the cells (1/3)
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Extracellular fluid (ECF)
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Excessive intake of Ca or Vitamin D
Sever GI fluid loss Prolonged, excessive diuretic therapy Prolonged malnutrition/starvation Malabsorption syndromes Hypoparathyroidism Hypoaldosteronism High dose steriod use Burns Sepsis Diabetic ketoacidosis Chronic alcoholism |
Causes of Hypomagnesemia
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Headache, faintness, confusion, muscle cramps, muscle twitching, normal or increased weight, convulsions, coma
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Clinical Manifestations of Hyponatremia
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Space between cells and outside the blood vessels
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Interstitial fluid (ISF)
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Level of >10.5 of calcium
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Hypercalcemia
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Blood plasma
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Intravascular fluid
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Tachycardia, hypotension
Tremors Tetany Hyperactive DTR +Trousseau's signs +Chvostek's signs Memory loss, emotional lability, confusion Hallucinations, seizures, coma Dizziness Anorexia, nausea Hypocalcemia; hypokalemia |
Clinical Manifestations of Hypomagnesemia
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Deficient water intake, hypertonic parental fluid abdomin, excessive salt ingestion, prolonged high fever, insensible water loss, diarrhea, mojor burns, diabetes inspidus
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Causes of hypernatremia
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Drinking, ingestion of water from food, water deprived from metabolism
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Intake of body water
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Renal excretion, stool, vaporization from skin and lungs
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Output of body water
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Decreased muscle mass, increase fat cells
Decreased ability to regulate sodium and water balance |
Decreases TBW
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What causes water movement between ICF and ECF?
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Potassium
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What causes water movement between plasma and interstitial fluid?
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Sodium, water and glucose
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Plasma proteins (albumin) maintain effective osmolarity (per liter of the solution) by...
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generating plasma oncotic (result of sweeling) pressure
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Normal range of 135-147 mEq/L
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Sodium
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Normal range of 3.5-5.5 mEq/L
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Potassium
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Renal failure
Mg containing antacids Untreated diabetic ketoacidosis Hypoadrenalism |
Causes of Hypermagnesemia
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Normal range of 9.0-10.5 mg/dL
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Calcium
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Normal range of 2.5-4.5 mg/dL
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Phosphate
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Normal range of 1.8-2.4 mg/dL
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Magnesium
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Muscle weakness; flaccidity
Personal changes; LOC Coma n/v; anorexia; extreme thirst Constipation Polyuria Urinary calculi Pathologic fractures Metastatic calcifications (cornea and skin) "itching" |
Clinical Manifestations of Hypercalcemia
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Excessive excretion
Inadequate intake of K Increased cellular uptake from insulin excess, alkalosis, renal renal |
Causes of Hypokalemia
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Anorexia N/V
Drowsiness, lethargy Leg cramps Muscle weakness, esp. legs Hyporeflexia Paresthesia Decreased bowel motility (ileus) Hypotension ECG (ST segment depression; U waves; flat T waves) |
Clinical Manifestations of Hypokalemia
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Increased dietary with decreased UOP
K supplement therapy Excessive salt substitutes K-sparing diuretics Hyponatremia Metabolic acidosis Acute or chronic renal failure |
Causes of Hyperkalemia
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Apathy, confusion
Paresthesias Abdominal cramps, nausea Flaccid muscle paralysis Diarrhea Oliguria Bradycardia Cardiac arrest |
Clinical Manifestations of Hyperkalemia
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Lethargy and drowsiness, coma
Depressed neuromuscular activity Depressed respirations Flushing sensation Hypoactive DTR Hypotension, bradycardia Cardiac arrest |
Clinical Manifestations of Hypermagnesemia
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What is responsible for the ECF osmotic balance, and potassium maintains the ICF osmotic balance.
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Sodium
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Acute or chronic renal failure
Vitamin D deficiency Insufficient dietary intake Hyperphosphatemia Alkalosis Hypoalbuminemia Hypomagnesemia |
Causes of Hypocalcemia
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Muscle cramps
Hyperactive DTRs Paresthesias Tetany Trousseau's signs Chvostek's signs Laryngeal spasm Abdominal muscle spasm Confusion, moody, anxiety Memory loss, seizures ECG (prolonged QT & ST) |
Clinical Manifestations of Hypocalcemia
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Ca supplement therapy
Excessive use Ca-containing antacids Prolonged immobility Excessive vitamin D intake Primary hyperparathyroidism Metastatic carcinoma Hypophoshatemia Renal tubular necrosis |
Causes of Hypercalcemia
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Metabolism of wastes
Fever and increased respiratory rate Kidneys, GI tract, skin and lungs |
Loss of water movement
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Things you can see/measure
Urine and feces |
Sensible
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Things you can not see/measure
Lungs and skin |
Insensible
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60% of body weight
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Total Body Water (TBW)
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40% of body weight
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Fat and Fat-Free solids, particularly bone
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Pushes water
Arises from heart contraction Favors movement to plasma water into ISF |
Hydrostatic pressure
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Helps maintain plasma volume
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Colloid osmotic pressure
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Pulls water
Movement of water into interstitial space causes accumulation of water into tissue (edema) |
Osmotic forces
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Limited to site of trauma
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Localized
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Uniform distribution
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Generalized
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Loss or trapping of ECF into transcellular space, pericardial sac, peritoneal cavity, pleural cavity
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Third-space accumulation
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Excessive fluid into the pleural cavity
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Hydrothorax
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Excessive fluid in the peritoneal cavity
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Ascites
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Fluid in the serous cavities
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Effusion
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Capillary hydrostatic pressure
Interstitial oncotic pressure |
Filtration
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Integrity is key in the movement of water and solutes
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Capillary membrane
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Movement of particles along a concentration gradient from an area of higher concentration to lower concentration
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Diffusion
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Movement of water across a semipermeable membrane
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Osmosis
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Pressure needed to move opposite the movement of water across the membrane
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Osmotic Pressure
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Osmolar concentration in 1L of solution
Refers to fluids outside of the body |
Osmolarity
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Osmolar concentration in 1kg. of water
Refers to fluids inside the body Controls the distribution and movement of water between body compartments E.g. kidneys ability to produce a concentrated or dilute urine |
Osmolality
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Plasma proteins accumulated into tissue spaces and coagulated
Occurs with local infection or trauma |
Nonpitting Edema
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Accumulation of interstitial fluid exceeds the absorptive capacity of tissue
Water is mobile and can be translocated with finger pressure |
Pitting Edema
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the abnormal accumulation of fluid in interstitial spaces of tissues, such as in the pericardial sac, intrapleural space, peritoneal cavity, or joint capsules
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Edema
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Regulated by Antidiuretic Hormone(ADH) or vasopressin
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Water Balance
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Hypothalamus
Angiotensin 2 |
Thirst
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Absent thirst sensation
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Adipsia
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Decrease thirst sensation
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Hpodipsia
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Excessive thirst
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Polydipsia
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Water deficit
Sodium excess |
Plasma osmolality increases
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Plasma osmolality increases
Circulating blood volume decreases and blood pressure drops |
ADH and vasopressin
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Tasteless diabetes
Deficiency of ADH |
Diabetes Insipidus
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Decrease ADH synthesis
Kidneys inability to respond to ADH |
Deficiency of ADH
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Excessive dilute urination(polyuria)
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Clinical Manifestations of Diabetes Insipidus
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Kidneys do not respond to ADH
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Neurogenic Diabetes Insipidus
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Defect in pituitary gland
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Primary Diabetes Insipidus
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Interfere with kidneys response
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Drug-related Diabetes Insipidus
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Failure to negative feedback system to regulate ADH
Water retention with dilutional hyponatremia (Decreased osmolarity) |
Syndrome of Inappropriate Antidiuretic Hormone(SIADH)
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Neoplasia
Neurologic disorders Lung disease Medicine |
Causes of SIADH
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Change in water content resulting in cellular swelling/shrinking
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Tonicity
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Same concentration of particles as ICF or ECF
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Isotonic
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Lower concentration of particles/dilute
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Hypertonic
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Higher concentration of particles
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Hypotonic
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Gain or loss of ECF resulting in a concentration equivalent to a 0.9% sodium chloride solution:No shrinking or swelling of cells
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Isotonic imbalance
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Imbalances that result in an ECF concentration more than 0.9% salt solution:Cells shrink
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Hypertonic imbalance
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Imbalance that results in an ECF less that 0.9% salt solution:Cells swell
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Hypotonic imbalance
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Maintained by mechanisms that generate, buffer and eliminate acids and bases
pH 7.35 to 7.45 Acids are continuously generated as byproducts of metabolism |
Acid-Base Balance
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H2CO3 determined by lungs and respiratory capacity
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Volatile
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Are not eliminated by the lungs, buffered by body proteins such as HCO3 then excreted by the kidneys
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Nonvolatile
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Respiratory mechanisms that eliminates CO2
Renal mechanisms that conserve HCO3 and eliminate H+ ions Electrolyte composition |
Regulation of pH
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Maintain membrane integrity
Speed of metabolic enzyme reactions |
Hydrogen ions
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Clinical conditions r/t changes in dissolved CO2 and HCO3 concentrations
Sodium bicarbonate is the main alkali in ECF |
Disorders of Acid-Base
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Produce alterations in bicarbonate concentration and result from addition or loss of nonvolatile acid or alkali from ECF
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Metabolic Disorders of Acid-Base
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Reduction in pH due to decreased HCO3
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Metabolic Acidosis
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Elevated pH due to increased HCO3
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Metabolic Alkalosis
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Involve alteration in PCO2
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Respiratory Disorders of Acid-Base
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Decreased pH, reflecting a decrease in ventilation and an increase in PCO2
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Respiratory Acidosis
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Increased pH, reflecting from an increase in alveolar ventilation and a decreased PCO2
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Respiratory Alkalosis
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