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105 Cards in this Set

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level of <2.5 of phosphate
hypophospatemia
level of >4.5 of phosphate
hyperphosphatemia
Extreme thrist, tachycardia, low-grade fever, dry, sticky tongue and oral mucuosa, disorientation, hallucinations, lethargy progressing to coma, hyperactive deep tendon reflexes, seixures, coma
Clinical Manifestations of hypernatremia
Level of <1.8 of magnesium
Hypomagnesemia
Level of >2.4 of magnesium
Hypermagnesemia
Level of <3.5 of potassium
Hypokalemia
Level of >5.5 of potassium
Hyperkalemia
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
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
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
Leve of >147 of sodium
Hypernatremia
Tetany
Circumoral paresthesias
Muscle spasm
Seizures
Soft tissue calcification
Clinical Manifestations of hyperphosphatemia
Level of <9.0 of calcium
Hypocalcemia
Prolonged diuretic therapy, excessive diaphosesis, insufficient Na intake, burns, severe GI loss, adrenal insufficiency, SIADH
Causes of Hyponatremia
Sum of fluids within all body compartments
Total Body Weight (TBW)
All fluid within the cells (2/3)
Intracellular fluid (ICF)
Level of <135 of sodium
Hyponatremia
All fluid outside the cells (1/3)
Extracellular fluid (ECF)
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
Headache, faintness, confusion, muscle cramps, muscle twitching, normal or increased weight, convulsions, coma
Clinical Manifestations of Hyponatremia
Space between cells and outside the blood vessels
Interstitial fluid (ISF)
Level of >10.5 of calcium
Hypercalcemia
Blood plasma
Intravascular fluid
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
Deficient water intake, hypertonic parental fluid abdomin, excessive salt ingestion, prolonged high fever, insensible water loss, diarrhea, mojor burns, diabetes inspidus
Causes of hypernatremia
Drinking, ingestion of water from food, water deprived from metabolism
Intake of body water
Renal excretion, stool, vaporization from skin and lungs
Output of body water
Decreased muscle mass, increase fat cells
Decreased ability to regulate sodium and water balance
Decreases TBW
What causes water movement between ICF and ECF?
Potassium
What causes water movement between plasma and interstitial fluid?
Sodium, water and glucose
Plasma proteins (albumin) maintain effective osmolarity (per liter of the solution) by...
generating plasma oncotic (result of sweeling) pressure
Normal range of 135-147 mEq/L
Sodium
Normal range of 3.5-5.5 mEq/L
Potassium
Renal failure
Mg containing antacids
Untreated diabetic ketoacidosis
Hypoadrenalism
Causes of Hypermagnesemia
Normal range of 9.0-10.5 mg/dL
Calcium
Normal range of 2.5-4.5 mg/dL
Phosphate
Normal range of 1.8-2.4 mg/dL
Magnesium
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
Excessive excretion
Inadequate intake of K
Increased cellular uptake from insulin excess, alkalosis, renal renal
Causes of Hypokalemia
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
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
Apathy, confusion
Paresthesias
Abdominal cramps, nausea
Flaccid muscle paralysis
Diarrhea
Oliguria
Bradycardia
Cardiac arrest
Clinical Manifestations of Hyperkalemia
Lethargy and drowsiness, coma
Depressed neuromuscular activity
Depressed respirations
Flushing sensation
Hypoactive DTR
Hypotension, bradycardia
Cardiac arrest
Clinical Manifestations of Hypermagnesemia
What is responsible for the ECF osmotic balance, and potassium maintains the ICF osmotic balance.
Sodium
Acute or chronic renal failure
Vitamin D deficiency
Insufficient dietary intake
Hyperphosphatemia
Alkalosis
Hypoalbuminemia
Hypomagnesemia
Causes of Hypocalcemia
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
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
Metabolism of wastes
Fever and increased respiratory rate
Kidneys, GI tract, skin and lungs
Loss of water movement
Things you can see/measure
Urine and feces
Sensible
Things you can not see/measure
Lungs and skin
Insensible
60% of body weight
Total Body Water (TBW)
40% of body weight
Fat and Fat-Free solids, particularly bone
Pushes water
Arises from heart contraction
Favors movement to plasma water into ISF
Hydrostatic pressure
Helps maintain plasma volume
Colloid osmotic pressure
Pulls water
Movement of water into interstitial space causes accumulation of water into tissue (edema)
Osmotic forces
Limited to site of trauma
Localized
Uniform distribution
Generalized
Loss or trapping of ECF into transcellular space, pericardial sac, peritoneal cavity, pleural cavity
Third-space accumulation
Excessive fluid into the pleural cavity
Hydrothorax
Excessive fluid in the peritoneal cavity
Ascites
Fluid in the serous cavities
Effusion
Capillary hydrostatic pressure
Interstitial oncotic pressure
Filtration
Integrity is key in the movement of water and solutes
Capillary membrane
Movement of particles along a concentration gradient from an area of higher concentration to lower concentration
Diffusion
Movement of water across a semipermeable membrane
Osmosis
Pressure needed to move opposite the movement of water across the membrane
Osmotic Pressure
Osmolar concentration in 1L of solution
Refers to fluids outside of the body
Osmolarity
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
Plasma proteins accumulated into tissue spaces and coagulated
Occurs with local infection or trauma
Nonpitting Edema
Accumulation of interstitial fluid exceeds the absorptive capacity of tissue
Water is mobile and can be translocated with finger pressure
Pitting Edema
the abnormal accumulation of fluid in interstitial spaces of tissues, such as in the pericardial sac, intrapleural space, peritoneal cavity, or joint capsules
Edema
Regulated by Antidiuretic Hormone(ADH) or vasopressin
Water Balance
Hypothalamus
Angiotensin 2
Thirst
Absent thirst sensation
Adipsia
Decrease thirst sensation
Hpodipsia
Excessive thirst
Polydipsia
Water deficit
Sodium excess
Plasma osmolality increases
Plasma osmolality increases
Circulating blood volume decreases and blood pressure drops
ADH and vasopressin
Tasteless diabetes
Deficiency of ADH
Diabetes Insipidus
Decrease ADH synthesis
Kidneys inability to respond to ADH
Deficiency of ADH
Excessive dilute urination(polyuria)
Clinical Manifestations of Diabetes Insipidus
Kidneys do not respond to ADH
Neurogenic Diabetes Insipidus
Defect in pituitary gland
Primary Diabetes Insipidus
Interfere with kidneys response
Drug-related Diabetes Insipidus
Failure to negative feedback system to regulate ADH
Water retention with dilutional hyponatremia
(Decreased osmolarity)
Syndrome of Inappropriate Antidiuretic Hormone(SIADH)
Neoplasia
Neurologic disorders
Lung disease
Medicine
Causes of SIADH
Change in water content resulting in cellular swelling/shrinking
Tonicity
Same concentration of particles as ICF or ECF
Isotonic
Lower concentration of particles/dilute
Hypertonic
Higher concentration of particles
Hypotonic
Gain or loss of ECF resulting in a concentration equivalent to a 0.9% sodium chloride solution:No shrinking or swelling of cells
Isotonic imbalance
Imbalances that result in an ECF concentration more than 0.9% salt solution:Cells shrink
Hypertonic imbalance
Imbalance that results in an ECF less that 0.9% salt solution:Cells swell
Hypotonic imbalance
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
H2CO3 determined by lungs and respiratory capacity
Volatile
Are not eliminated by the lungs, buffered by body proteins such as HCO3 then excreted by the kidneys
Nonvolatile
Respiratory mechanisms that eliminates CO2
Renal mechanisms that conserve HCO3 and eliminate H+ ions
Electrolyte composition
Regulation of pH
Maintain membrane integrity
Speed of metabolic enzyme reactions
Hydrogen ions
Clinical conditions r/t changes in dissolved CO2 and HCO3 concentrations
Sodium bicarbonate is the main alkali in ECF
Disorders of Acid-Base
Produce alterations in bicarbonate concentration and result from addition or loss of nonvolatile acid or alkali from ECF
Metabolic Disorders of Acid-Base
Reduction in pH due to decreased HCO3
Metabolic Acidosis
Elevated pH due to increased HCO3
Metabolic Alkalosis
Involve alteration in PCO2
Respiratory Disorders of Acid-Base
Decreased pH, reflecting a decrease in ventilation and an increase in PCO2
Respiratory Acidosis
Increased pH, reflecting from an increase in alveolar ventilation and a decreased PCO2
Respiratory Alkalosis