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57 Cards in this Set

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Diabetes Insipidus-Nephrogenic
Nephrogenic- Kidney Malfunction
Diabetes Insipidus- Cerebral
Head trauma or trauma to pituitary. Can result from surgical trauma
Diabetes Insipidus- clinical manifestations-
Increased urine output
Lower specific gravity in urine
Altered thirst mechanism
Dehydration
Diabetes Insipidus resulting from brain trauma- manifestations
Localized swelling blocks the transport of ADH from hypothalamus to pituitary
Diabetes Insipidus- interventions
Administer Fluids
Administer Pitressin (synth ADH)
SIADH (Syndrome Of Inappropriate Diuretic Hormone)
Excessive ADH production
SIADH- causes
Stress
Anesthesia
Surgery
Tumors
Aids
Meds- cytoxin, diabenese, elavil
SIADH- clinical manifestations
Water retention
Decreased urine output
Increased specific gravity of urine (more concentrated)
BUN/Creatinine levels decreased.
SIADH- interventions
Administer diuretics
Treat cause
Allow recovery time
Water Excess- causes
Excess water or excess sodium ingestion
Water Excess- clinical manifestations
Weight gain
Edema
Rales- too much fluid in lungs
Nausea, vomitting, diarrhea
Abdominal cramps
Low H&H (hematocrit and hemoglobin)
Low B.U.N.
Orthostatic hypotension
Water Excess- Treatment
Diuretics
Limit fluid intake
Dialysis
Water excess- causes
Exessive water or excessive ingestion of sodium
Increased levels of ADH
Renal disease
Water deficit- causes
Decreased water intake
Losses (vomitting, diarrhea, NGT)
Fever
Excessive use of diuretics
Hyperglycemia (causes osmotic diuresis)
Water deficit- clinical manifestations
Turgor decreased
Dry mucuous membranes
Weight loss
Lethargy
Change in mental status
Water deficit treatment
IV fluids to restore electrolytes and fluids
Third Spacing
shift of fluid from vascular space to another part of the body (interstitial space)
Third spacing- causes
increased hydrostatic pressure- as seen in CHF
Too much fluid in vessels
Decreased plasma proteins
Liver disease
Increased capillary permeability- sepsis, trauma and burns
Third Spacing- clinical manifestations
Weak right sided pressure
Low albumin levels
Protein levels
Third Spacing- interventions
IV albumin
Lasix after IV treatment
In sepsis, treat cause
Electrolytes
substances which when dissolved in water separate into ions (capable of conducting electricity)
Intracellular Electrolytes
potassium and magnesium
Extracellular
Sodium and Chloride
Sodium
most abundant cation (postitive ion) 135-145 mEq/L
Sodium- function
maintain extracellular volume and water balance
aids to transmit nerve impulses
Hypernatremia- causes
Decreased water intake
Fluid loss
Osmotic diuresis
Hyperglycemia
Salt water intake
Profuse diaphoresis accompanied by low water intake
Hyperaldosteronism-too much sodium in blood.
Diabetes Insipidus
Hypernatremia- Clinical manifestations
Mental status decrease
Decreased turgor
Dry Skin and mucous membranes
Thirst
Hypernatremia- interventions
Administer hypotonic IV (0.455% NSS)
Water
Administer oral hygeine
Hyponatremia- causes
Sweating followed by large plain water intake causes dilution of plasma sodium
Increased ADH
Adrenal Insufficiency (decreased aldosterone so Na levels fall)
Hyponatremia- clinical manifestations
Neurological symptoms due to brain swelling
Weight gain
Edema
Rales
Abdominal cramps
Low hematocrit
Low BUN
Orthostatic hypotension
Hyponatremia- Interventions
Administer hypotonic IV
Diuretics
Potassium
3.5-5 mEq/L
Potassium- function
Cellular metabolism
Transmission of neuromuscular impulses
supports cardiac cycle
Acid base balance
Any condition that increases urinary output decreases potassium
Hypokalemia- Causes
Diuretics
GI Losses
Adrenal Tumor- may cause excess secretion of aldosterone,which then secretes too much Ka
Hypokalemia- clinical manifestations
Malaise
Muscle Weakness
Leg Cramps
Fatigue
Decreased reflexes
Abnormal ECG and disrhythmia
Hypokalemia- interventions
Administer potassium
Oral or IV (NEVER IV PUSH Ka, THIS CAN BE FATAL)
Hyperkalemia- causes
Renal insufficiency
Cellular destruction
Excessive administration of Ka
Adrenal Insufficiency- too little aldosterone.
Hyperkalemia- clinical manifestations
Mental changes
Abnormal ECG
Lethal disrhythmia
Dialysis (#1 cause)
Hyperkalemia- interventions
Glucose and insulin concentrate to move Ka into cells
Sodium Bicarbonate for acidosis
Kayexelate enema or oral
Calcium- function
formation of bone and teeth
blood clotting
myocardial contractility
nerve impulse conduction (suppressant effect)
Calcium
8.5-10.5mEq/L
Calcium- regulation
Vitamin D
Parathyroid
Hypocalcemia- causes
Hypoparathyroid
Pancreatitis
Low dietary Ca
Alkalosis
Renal disease (kidneys activate V-D, Vit D helps absorb Ca)
Hypocalcemia- clinical manifestations
hyperactive reflexes
tingling in face fingers toes
Muscle spasm
tetany
Decreased blood clotting
Bronchospasms
(assess by checking trousseau's signs)
Trousseaus Signs
BP cuff inflated for 3-4 minutes hand claws up.
Hypocalcemia- interventions
Oral or IV calcium (NEVER IM CALCIUM)
Hypercalcemia- causes
Hyperparathyroidism- causes too much Ca to be retained
Malignancies-some cancers produce pth.
Osteoporosis
Prolonged immobility
Decreased renal function
Hypercalcemia- clinical manifestations
Hypotonicity
Lethargy
Increased blood clotting
Extreme thirst
Decreased neuromuscular function
Kidney Stones
Fractures-too much Ca can cause breaks.
Hypercalcemia- interventions
Parathyroidectomy
Steriods (they decrease GI absorption of Ca)
Mitromycin
Calcitonin
Magnesium- function
Nerve impulse conduction
Chemical metabolism
Cardiac conduction
Magnesium
1.5-2.5mEq/L
Hypomagnesemia-causes
Decreased Mg intake
Malnutrition
Alcoholism
Hypomagnesemia-clinical manifestations
tremors
hyperactivity
tetany
positive Trousseau's
Confusion
Agitation
Hypomagnesemia- interventions
Replace Magnesium- IV (Mg salts)IV Mg can cause cardiac arrest if given too quickly.
Oral
IM
Hypermagnesemia- causes
Renal failure- may be exacerbated by meds containing magnesium.
Hypermagnesemia- clinical manifestations
Lethargy
Slow/Weak pulse
Low BP
Decreased tonicity
Brachypnea
Hypermagnesemia- interventions
Dialysis
Stop intake of Mg.