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Fluid, Electrolyte, and Acid- Base Imbalances Gould Chapter 6 Presented by: Mahmoud Kaddoura, PhD, CAGS, MSN, RN 1

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Page 1: Week 2 rsc 325 summer

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Fluid, Electrolyte, and Acid-Base ImbalancesGould Chapter 6

Presented by:

Mahmoud Kaddoura, PhD, CAGS, MSN, RN

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Fluid Compartments

• Continuous exchange of fluids across membranes separating intracellular and extracellular fluid compartments

• Large molecules and those that are ionized less able to cross membranes

• About 60% of adults’ body weight is water• About 70% of infants’ body is water• Females – higher percentage of fatty tissue, lower water

content than males• Older adults and obese – lower proportion of water

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Fluid Compartments (Cont’d)

• Intracellular compartment (ICF)• Extracellular compartment (ECF)

– Intravascular fluid (IVF) or blood– Interstitial fluid (ISF) or intercellular fluid– Cerebrospinal fluid (CSF)– Transcellular fluids

• Present in various secretions• Pericardial cavity• Synovial cavities

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Major Body Fluid Compartments

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Fluid Compartments in the Body

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Intake and Output of Water

• Amount of water entering the body should equal the amount of water leaving the body.

• Control of Water Balance:• Essential for homeostasis• Frequent indications for IV therapy include

imbalances of– Body fluids– Electrolytes– Acid-base

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Sources and Losses of Water

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Movement of Water

• Fluid circulates throughout body via filtration and osmosis.

• Water moves between compartments via– Hydrostatic pressure – Osmotic pressure

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Movements of Water between Compartments

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Control of Fluid Balance• Achieved through complex mechanisms• Most important regulator of fluid intake is thirst• Primary regulators of fluid output : kidneys

– Renin-angiotensin mechanism– Aldosterone– Antidiuretic hormone (ADH)

• Thirst mechanism– Osmoreceptors in the hypothalamus

• Antidiuretic hormone– Promotes reabsorption of water into blood from kidney tubules

• Aldosterone – Determines reabsorption of sodium ions and water

• Atrial natiuretic peptide– Regulates fluid, sodium and potassium levels

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Osmolality

• Concentration of osmotic solution• Dependent on number of dissolved solutes in a body fluid

– Usually sodium, glucose, or urea• Normal osmolality is 275- 295 mOsm/kg• Changes in osmolality can cause water to move to

different compartments– Greatest contributor is sodium– Sodium controlled by hormone aldosterone

• Tonicity is relative concentration of intravenous fluid– General term, not precise measurement

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Osmosis

• Water moves from area of low osmolality to areas of high osmolality

• Hypertonic intravenous fluid– Water moves from interstitial space to plasma

• Hypotonic intravenous fluid– Water moves from plasma to interstitial space

• Isotonic intravenous fluid– No fluid shift

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Movement of fluids and solution tonicity

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Fluid Balance Disorders

• Deficit-fluid-balance disorders– Can cause dehydration or shock– Treated with oral or intravenous fluids

• Excess -fluid- balance disorders– Treated with diuretics

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Fluid Excess – Edema

• Edema – excessive amount of fluid in the interstitial compartment– Causes swelling or enlargement of tissue– May be localized or throughout the body – May impair tissue perfusion– May trap drugs in ISF

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Capillary Exchange

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Causes of Edema

• Increased capillary hydrostatic pressure– Due to higher blood pressure or increased blood

volume– Forces increased fluid out of capillaries into tissue– Cause of pulmonary edema

• Loss of plasma proteins– Particularly albumin– Results in decreased plasma osmotic pressure

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Causes of Edema (Cont’d)

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Causes of Edema (Cont’d)

• Obstruction of lymphatic circulation– Causes localized edema

• Excessive fluid and protein not returned to general circulation

• Increased capillary permeability – Usually causes localized edema

• May result from an inflammatory response or infection• Histamines and other chemical mediators increase capillary

permeablility

– Can also result from some bacterial toxins or large burn wounds and result in widespread edema

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Causes of Edema (Cont’d)

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Effects of Edema

• Swelling – Pale or red in color

• Pitting edema– Presence of excess interstitial fluid– Moves aside when pressure is applied by finger– Depression – “pit” remains when finger is

removed• Increase in body weight

– With generalized edema

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Effects of Edema (Cont’d)

• Functional impairment– Restricts range of joint movement– Reduced vital capacity – Impaired diastole

• Pain– Edema exerts pressure on nerves locally– Headache with cerebral edema– Stretching of capsule in organs (kidney, liver)

• Impaired arterial circulation– Ischemia leading to tissue breakdown

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Effects of Edema (Cont’d)

• Dental practice– Difficult to take accurate impressions– Dentures do not fit well

• Edema in skin– Susceptible to tissue breakdown from pressure

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Fluid Deficit – Dehydration

• Insufficient body fluid– Inadequate intake– Excessive loss – Both

• Fluid loss often measured by change in body weight• Dehydration more serious in infants and older

adults• Water loss may be accompanied by loss of

electrolytes and proteins, e.g., diarrhea.

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Causes of Dehydration

• Vomiting and diarrhea• Excessive sweating with loss of sodium and

water• Diabetic ketoacidosis

– Loss of fluid, electrolytes, and glucose in the urine• Insufficient water intake in older adults or

unconscious persons• Use of concentrated formula in infants

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Manifestations of Dehydration

• Decreased skin turgor and dry mucous membranes

• Sunken eyes• Sunken fontanelles in infant • Lower blood pressure, rapid weak pulse• Increased hematocrit• Increased temperature• Decreasing level of consciousness• Urine: low volume and high specific gravity

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Attempts to Compensate for Fluid Loss

• Increasing thirst• Increasing heart rate• Constriction of cutaneous blood vessels• Producing less urine• Concentrating urine

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Third-Spacing of Fluid

• Fluid shifts out of the blood into a body cavity or tissue and can no longer reenter vascular compartment– High osmotic pressure of ISF as in burns– Increased capillary permeability as in some gram-

negative infections

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Intravenous Fluid Therapy

• Replaces fluids and electrolytes– Uses crystalloids and colloids

• Causes of water and electrolyte loss– Gastrointestinal fluid loss, vomiting, diarrhea,

laxatives, suctioning– Perspiration, burns, hemorrhage, excessive

diuresis, ketoacidosis

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Crystalloids

• Contain electrolytes• Used to replace fluids and promote urine

output• Capable of leaving plasma and moving to

interstitial spaces and intracellular fluid• Compartment entered depends on tonicity of

intravenous fluid

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Colloids

• Molecules too large to easily cross capillary membrane– Stay in intravascular space– Rapidly expand plasma volume

• Draw water from intracellular fluid and interstitial spaces into plasma– Increases osmotic pressure

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Electrolytes

• Positively or negatively charged inorganic molecules

• Essential to– Nerve conduction, membrane permeability– Water balance, other critical body functions

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Distribution of Major Electrolytes

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Movements of Electrolytes between Compartments

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Sodium

• Essential for maintaining osmolality, water balance, acid-base balance

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Sodium and Water Regulation

• Water travels with or toward sodium• Sodium movement is link between water

retention, blood volume, and blood pressure• Regulated by kidneys and aldosterone• Sodium major electrolyte in extracellular fluid

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Figure 31.3 Renal regulation of sodium and potassium balance

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Sodium Imbalance

• Review of sodium– Primary cation in ECF– Sodium diffuses between vascular and interstitial

fluids– Transport into and out of cells by sodium-potassium

pump– Actively secreted into mucus and other secretions– Exists in form of sodium chloride and sodium

bicarbonate– Ingested in food and beverages

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Hyponatremia

• Sodium level below 135 mEq/L• Caused by excessive dilution of plasma

– Excess antidiuretic hormone (ADH) secretion– Excessive administration of hypotonic intravenous solution

• Vomiting, diarrhea, gastrointestinal suctioning, diuretic use

• Causes– Losses from excessive sweating, vomiting, diarrhea– Use of certain diuretic drugs combined with low-salt diets– Hormonal imbalances

• Insufficient aldosterone• Adrenal insufficiency• Excess ADH secretion

– Diuresis– Excessive water intake

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Hyponatremia and Fluid Shift into Cells

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Symptoms of Hyponatremia

• Early symptoms– Nausea, vomiting, anorexia, abdominal cramping

• Later signs– Altered neurologic function such as confusion,

lethargy, convulsions, coma, muscle twitching, tremors

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Effects of Hyponatremia

• Low sodium levels– Cause fluid imbalance in compartments

• Fatigue, muscle cramps, abdominal discomfort or cramps, nausea, vomiting

• Decreased osmotic pressure in ECF compartment– Fluid shift into cells

• Hypovolemia and decreased blood pressure

– Cerebral edema • Confusion, headache, weakness, seizures

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Treatment of Hyponatremia

• Hyponatremia caused by excessive dilution– Treat with loop diuretics to cause an isotonic

diuresis• Hyponatremia caused by sodium loss

– Treat with oral sodium chloride or intravenous fluids containing salt

• Normal saline• Lactated Ringers

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Hypernatremia• Sodium level above 145 mEq/L• Most commonly caused by kidney disease• Sodium accumulates

– Decreased excretion– High, net water loss (watery diarrhea, fever, burns)– High doses of glucocorticoids or estrogens

• Cause is imbalance in sodium and water– Insufficient ADH (diabetes insipidus)

• Results in large volume of dilute urine

– Loss of the thirst mechanism– Watery diarrhea– Prolonged periods of rapid respiration– Ingestion of large amounts of sodium without enough water

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Physiology of Hypernatremia

• Elevated sodium increases osmolality of plasma– Draws fluid from interstitial space and cells– Causes cellular dehydration

• Signs and symptoms– Thirst, fatigue, weakness, muscle twitching– Convulsions, altered mental status, decreased

level of consciousness

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Effects of Hypernatremia

• Weakness, agitation• Dry, rough mucous membranes• edema• Increased thirst (if thirst mechanism is

functional)• Increased blood pressure

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Treatment of Hypernatremia

• Can be treated with low-salt diet• Acute hypernatremia treated with hypotonic

intravenous fluids or diuretics

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Potassium Balance

• Essential for– Proper nerve and muscle function

• Maintaining acid-base balance• Influenced by aldosterone

– For each sodium ion reabsorbed, one potassium ion secreted into renal tubules

• Imbalances can be serious , even fatal

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Potassium Imbalance

• Review of potassium– Major intracellular cation– Serum levels are low with a narrow range– Ingested in foods– Excreted primarily in urine– Insulin promotes movement of potassium into cells– Levels influenced by the acid-base balance– Abnormal potassium levels cause changes in

cardiac conduction and are LIFE-THREATENING!

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Sodium and Potassium Affect Nerve Conduction

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Causes of Hypokalemia(serum K+ <3.5 mEq/L)

• Potassium level below 3.5 mEq/L• Caused by

– High doses of loop diuretics– Strenuous muscle activity– Severe vomiting

• Excessive losses due to diarrhea• Diuresis associated with some diuretic drugs• Excessive aldosterone or glucocorticoids

– i.e., Cushing syndrome• Decreased dietary intake

– May occur with alcoholism, eating disorders, starvation• Treatment of diabetic ketoacidosis with insulin

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Symptoms of Hypokalemia

• Neurons and muscle fibers most sensitive to potassium loss

• Muscle weakness, lethargy, anorexia, dysrhythmias, cardiac arrest

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Effects of Hypokalemia

• Cardiac dysrhythmias– Due to impaired repolarization > cardiac arrest

• Interference with neuromuscular function– Muscles less responsive to stimuli

• Paresthesias – “pins and needles”• Decreased digestive tract motility• Severe hypokalemia:

– Shallow respirations– Failure to concentrate urine – polyuria

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Treatment of Hypokalemia

• Mild- increase dietary intake• Severe – give oral or parenteral potassium

supplements

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Causes of Hyperkalemia (serum K + >5 mEq/L)

• Potassium level above 5 mEq/L• Caused by high consumption of potassium-rich food, dietary

supplements• Risk with client taking potassium-sparing diuretics• Accumulates when renal disease causes decreased excretion• Renal failure• Deficit of aldosterone• “Potassium-sparing” diuretics• Leakage of intracellular potassium into the extracellular fluids

– In patients with extensive tissue damage• Displacement of potassium from cells by prolonged or severe

acidosis

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Relationship of Hydrogen and Potassium Ions

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Symptoms of Hyperkalemia

• Most serious are dysrhythmias, and heart block

• Other symptoms are muscle twitching, fatigue, parasthesias, dyspnea, cramping, and diarrhea

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Effects of Hyperkalemia

• Cardiac dysrhythmias– May progress to cardiac arrest

• Muscle weakness common– Progresses to paralysis– May cause respiratory arrest– Impairs neuromuscular activity

• Fatigue, nausea, paresthesias

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Treatment of Hyperkalemia

• Restrict dietary sources• Decrease dose of potassium-sparing diuretics• Administer glucose and insulin• Administer calcium to counteract potassium

toxicity on heart• Administer polystyrene sulfonate (Kayexalate)

and sorbitol to decrease potassium levels

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Signs of Potassium Imbalance

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Calcium Imbalance

• Review of calcium– Important extracellular cation– Ingested in food– Stored in bone– Excreted in urine and feces– Balance controlled by parathyroid hormone (PTH) and

calcitonin– Vitamin D promotes calcium absorption from intestine

• Ingested or synthesized in skin in the presence of ultraviolet rays

• Activated in kidneys

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Functions of Calcium

• Provides structural strength for bones and teeth

• Maintenance of the stability of nerve membranes

• Required for muscle contractions• Necessary for many metabolic processes and

enzyme reactions• Essential for blood clotting

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Causes of Hypocalcemia

• Hypoparathyroidism • Malabsorption syndrome• Deficient serum albumin• Increased serum pH• Renal failure

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Effects of Hypocalcemia

• Increase in the permeability and excitability of nerve membranes– Spontaneous stimulation of skeletal muscle

• Muscle twitching• Carpopedal spasm

– Tetany • Weak heart contractions

– Delayed conduction– Leads to dysrhythmias and decreased blood pressure

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Causes of Hypercalcemia

• Uncontrolled release of calcium ions from bones– Neoplasms; malignant bone tumors

• Hyperparathyroidism• Demineralization due to immobility

– Decrease stress on bone• Increased calcium intake

– Excessive vitamin D– Excess dietary calcium

• Milk-alkali syndrome

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Effects of Hypercalcemia

• Depressed neuromuscular activity– Muscle weakness, loss of muscle tone– Lethargy, stupor, personality changes– Anorexia, nausea

• Interference with ADH function– Less absorption of water– Decrease in renal function

• Increased strength in cardiac contractions– Dysrhythmias may occur

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Magnesium Imbalances

• Magnesium– Intracellular ion– Hypomagnesemia

• Results from malabsorption or malnutrition often associated with alcoholism

• Use of diuretics, diabetic ketoacidosis, hyperthyroidism, hyperaldosteronism

– Hypermagnesemia • Occurs with renal failure• Depresses neuromuscular function• Decreased reflexes

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Phosphate Imbalances

• Phosphate– Bone and tooth mineralization– Important in metabolism – ATP– Phosphate buffer system – acid-base balance– Integral part of the cell membrane– Reciprocal relationship with serum calcium – Hypophosphatemia

• Malabsorption syndromes, diarrhea, excessive antacids

– Hyperphosphatemia • From renal failure

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Chloride Imbalance

• Chloride– Major extracellular anion– Chloride levels related to sodium levels– Chloride and bicarbonate ions can shift in

response to acid-base imbalances– Hypochloremia

• Usually associated with alkalosis– Early stages of vomiting – loss of hydrochloric acid

– Hyperchloremia• Excessive sodium chloride intake

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Chloride Shift

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The Hydrogen Ion and pH Scale

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Control of Serum pH

• Buffer pairs in the blood respond to pH changes immediately.

• Respiratory system can alter carbonic acid levels to change pH.

• Kidneys can modify the excretion rate of acids and absorption of bicarbonate ions to regulate pH. – Most significant control mechanism– Slowest mechanism

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Changes in Acids, Bicarbonate Ion, and Serum pH in Circulating Blood

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Buffer Systems

• Sodium bicarbonate–carbonic acid system– Major ECFbuffer– Controlled by the respiratory system and the

kidneys• Other buffering systems:

– Phosphate– Hemoglobin– Protein

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Compensation Mechanisms for pH Imbalance

• Compensation is limited and usually short term.

• Does not remove the cause of imbalance• Compensation occurs to balance the relative

proportion of hydrogen ions and bicarbonate ions in circulation:– Buffers– Change in respiration– Change in renal function

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Decompensation

• Occurs when:– Causative problem becomes more severe– Additional problems occur– Compensation mechanisms are exceeded or fail

• Requires intervention to maintain homeostasis

• LIFE-THREATENING!

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Acid-Base Imbalance• Acidosis is excess acid (pH below 7.35)• Alkalosis is excess base (pH above 7.35)• Both symptoms of underlying disorder• Acidosis

– Excess hydrogen ions– Decrease in serum pH

• Alkalosis– Deficit of hydrogen ions– Increase in serum pH

• Both may be fatal if not treated rapidly• Body uses buffers to maintain overall pH within normal limits• Kidneys and lungs collaborate to remove excess metabolic

acid

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Figure 31.4 Acid–base imbalances

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Acidosis

• May be respiratory , caused by hypoventilation

• May be metabolic– Causes: diarrhea, kidney failure, diabetes, excess

alcohol, starvation

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Respiratory Acidosis

• Acute problems– Pneumonia, airway obstruction, chest injuries – Drugs that depress the respiratory control center

• Chronic respiratory acidosis– Common with chronic obstructive pulmonary

disease• Decompensated respiratory acidosis

– May develop if impairment becomes severe or if compensation mechanisms fail

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Metabolic Acidosis

• Excessive loss of bicarbonate ions to buffer hydrogen– Diarrhea – loss of bicarbonate from intestines

• Increased use of serum bicarbonate• Renal disease or failure

– Decreased excretion of acids– Decreased production of bicarbonate ions

• Decompensated metabolic acidosis– Additional factor interferes with compensation

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Effects of Acidosis

• Impaired nervous system function– Headache– Lethargy– Weakness– Confusion– Coma and death

• Compensation – Deep rapid breathing– Secretion of urine with a low pH

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Changes in Blood Gases with Acidosis

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Pharmacotherapy of Acidosis

• Symptoms affect central nervous system– Lethargy, confusion, coma– Deep, rapid respirations in attempt to blow off

excess acid• Goal is to quickly reverse effects of excess acid

in blood• Administration of bicarbonate is appropriate

pharmacotherapy

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Alkalosis

• May be respiratory– Cause: hyperventilation due to asthma, anxiety, high altitude

• May be metabolic– Prolonged constipation, excess sodium bicarbonate, diuretics that

cause potassium depletion, severe vomiting

• Respiratory alkalosis– Hyperventilation

• Caused by anxiety, high fever, overdose of aspirin• Head injuries • Brainstem tumors

• Metabolic alkalosis– Increase in serum bicarbonate ion

• Loss of hydrochloric acid from stomach• Hypokalemia• Excessive ingestion of antacids

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Effects of Alkalosis

• Increased irritability of the nervous system– Causing restlessness– Muscle twitching– Tingling and numbness of the fingers– Tetany– Seizures– Coma

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Pharmacotherapy of Alkalosis

• Symptoms are due to central- nervous- system stimulation– Nervousness, hyperactive reflexes, convulsions– Slow, shallow respirations in attempt to retain acid

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Pharmacotherapy of Alkalosis (continued)

• Treatment– Administration of ammonium chloride (severe

cases)– Administration of sodium chloride with potassium

chloride (mild cases)

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Role of The Healthcare Provider

• Monitor client’s condition• Provide client education• Obtain medical, surgical and drug history• Assess lifestyle and dietary habits• Obtain baseline weight and vital signs, level of

consciousness, breath sounds, and urinary output

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Role of The Healthcare Provider (continued)

• Evaluate electrolytes, CBC, urine specific gravity and urinalysis, BUN and creatinine, total protein and albumin levels, aPTT, aPT or INR, renal and liver function studies)

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Colloid Solutions

• Monitor fluid-volume status (both deficits and excess)

• Assess neurologic status and urinary output• Report hematocrit below 30% to physician

immediately• Teach client to report bleeding,

hypersensitivity, or fluid-volume overload

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Sodium Replacement Therapy

• Assess sodium and electrolyte balance• Be alert for signs of hyponatremia or

hypernatremia• Monitor serum sodium levels, urine specific

gravity, serum and urine osmolarity

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Sodium Replacement Therapy (continued)

• Client should report symptoms that may relate to fluid overload

• Client should drink water or balanced sports drinks to replenish lost fluids and electrolytes

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Potassium Replacement Therapy

• Monitor for cardiac abnormalities• Contraindicated in cases of severe renal

impairment• Do not use with potassium-sparing diuretics• Contraindicated in acute dehydration, heat

cramps, clients with digoxin intoxication with AV node disturbance

• Take with meals to avoid irritating GI tract

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Sodium Bicarbonate Therapy

• Monitor arterial blood gas reports• Use cautiously in clients with cardiac disease

or renal impairment• Clients should use alternative OTC antacids to

prevent excess sodium or bicarbonate from being absorbed into systemic circulation

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Ammonium Chloride Therapy

• Assess pH in arterial blood-gas levels prior to administration

• Contraindicated in presence of liver disease• Infuse slowly to avoid ammonium toxicity, and

decrease irritation to veins

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Fluid Replacement Agents - Colloids

• Prototype drug: dextran 40 (Gentran 40, Hyskon, 10% LMD, Rheomacrodex)

• Mechanism of action: to raise oncotic pressure of blood; expands plasma volume within minutes of administration

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Dextran

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Fluid Replacement Agents – Colloids (continued)

• Primary use: as fluid replacement with hypovolemic shock from hemorrhage, surgery, severe burns

• Adverse effects: hypersensitivity reactions, fluid overload, hypertension

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Electrolytes

• Prototype drug: sodium chloride• Mechanism of action: as electrolyte/sodium

supplement• Primary use: to treat hyponatremia when

serum levels fall below 130mEq/L• Adverse effects: hypernatremia and

pulmonary edema

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Electrolytes (continued)

• Prototype drug: potassium chloride• Mechanism of action: as

electrolyte/potassium supplement• Primary use: to treat hypokalemia• Adverse effects: GI irritation, hyperkalemia;

contraindicated in clients with chronic renal failure or those taking potassium-sparing diuretic

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Potassium chloride

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Acid-Base Agents

• Prototype: sodium bicarbonate• Mechanism of action: to decrease pH of body

fluids• Primary use: metabolic alkalosis caused by

receiving too much bicarbonate ion and hypokalemia

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Sodium Chloride

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders

• Assessment– Obtain a complete health history– Obtain drug history, including allergies and possible

drug interactions– Assess for presence of fluid-volume deficit– Assess for the presence of fluid-volume deficit– Obtain CBC, serum electrolytes, renal function (BUN

and serum creatinine), total protein and albumin levels, aPTT, aPT or INR, and liver function studies

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)

• Diagnoses– Deficient fluid volume– Decreased cardiac output– Fatigue– Activity Intolerance– Deficient Knowledge (drug therapy)

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)

• Diagnoses– Risk for Falls – Risk for Injury (related to hypotension, dizziness

associated with adverse effects)– Risk for Excessive Fluid Volume (related to drug

therapy);– Risk for Ineffective Health Maintenance (regarding

drug effects and dietary needs)

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Drug Therapy for Fluid-Balance, electrolyte, and Acid-Base Disorders

• Planning – patient will– Report effects: itching, shortness of breath,

flushing, cough, heart palpitations– Exhibit signs of normal fluid volume– Demonstrate an understanding of drug’s action

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)

• Implementation– Monitor hemodynamic status every 15 to 60

minutes– Monitor for

• Hypersensitivity reactions• Circulatory overload• Changes in CBC results• IV sites ( potassium)

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)

• Implementation– Teach client to

• Eat foods rich in potassium (hypokalemia)• Avoid foods rich in potassium and salt substitutes

(hyperkalemia)

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)

• Evaluation –client– Experiences increased urinary output and relief of

dehydration, electrolyte values within normal limits).

– Is free from, or experiences minimal adverse effects

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Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)

• Evaluation –client– Verbalizes an understanding of the drug’s use,

adverse effects and required precautions– Demonstrates proper self-administration of the

medication (e.g., dose, timing, when to notify provider).

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Drugs for Nutritional Disorders

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Vitamins

• Organic substances are needed in small amounts– Promote growth– Maintain health

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Vitamins (continued)

• Human cells cannot produce vitamins– Exception: vitamin D– Vitamins or provitamins must be supplied in diet– Deficiency will result in disease

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Vitamins Serve Important Roles in Function of Body

• Vitamin B complex: coenzymes essential to metabolic processes

• Vitamin A: precursor of retinol needed for normal vision

• Vitamin D: regulates calcium metabolism• Vitamin K: needed to produce prothrombin

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Lipid-Soluble Vitamins (A, D, E, K)

• Must be ingested with lipids to be absorbed in small intestine

• Excess stored in liver and adipose tissue– Can be removed from storage areas and used as

needed• Excessive intake can lead to dangerously high

levels

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Vitamin A

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Water-Soluble Vitamins (C, B Complex)

• Absorbed with water in digestive tract• Easily dissolved in blood and body fluids

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Water-Soluble Vitamins (C, B Complex) (continued)

• Excess cannot be stored– Excreted in urine– Must be ingested daily

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Folic Acid

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Page 135: Week 2 rsc 325 summer

Recommended Dietary Allowances (RDAs)

• Minimum amount of a vitamin needed to prevent symptoms of deficiency

• Need for vitamins and minerals varies among individuals

• Supplements should never substitute for healthy diet

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Vitamin Pharmacotherapy

• Indicated for certain conditions– Poor nutritional intake– Pregnancy– Chronic-disease states

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Symptoms of Deficiency

• Usually nonspecific; occur over prolonged period

• Often result of certain factors– Poverty, fad diets– Chronic alcohol or drug abuse– Prolonged parenteral feeding

• Clients often present with multiple deficiencies

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Deficiencies in Lipid-Soluble Vitamins

• Vitamin A (retinol)– Obtained from foods containing carotenes

• Vitamin D– D2 (ergocalciferol)—from dairy products– D3—from ultraviolet light

Page 139: Week 2 rsc 325 summer

Deficiencies in Lipid-Soluble Vitamins (continued)

• Vitamin E (tocopherols)– Found in plant-seed oils, whole-grain cereals,

eggs, certain organ meats– Primary antioxidant

Page 140: Week 2 rsc 325 summer

Deficiencies in Lipid-Soluble Vitamins (continued)

• Vitamin K—mixture of several chemicals– K1 obtained from plant sources– K2 obtained from microbial flora in colon– Needed for clotting

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Deficiencies in Water-Soluble Vitamins

• Vitamin C deficiency can cause scurvy• Thiamine (B1) deficiency can cause beriberi

• Niacin (B3) deficiency can cause pellagra

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Deficiencies in Water-Soluble Vitamins (continued)

• Cyanocobalamin (B12) deficiency can cause pernicious or megaloblastic anemia

• Deficiencies of riboflavin (B2), folic acid (B9), pyridoxine (B6)– Indicate need for pharmacotherapy with water-

soluble vitamins

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Minerals

• Inorganic substances• Very small amounts needed to maintain

normal metabolism• Constitute 4% of body weight• Can be obtained from normal diet• Excess minerals can be toxic

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Magnesium

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Role of the Nurse• Monitor client’s condition• Provide client education• Obtain medical, surgical, drug history• Assess lifestyle and dietary habits• Obtain description of symptomology and

current therapies

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Drug Therapy with Fat-Soluble Vitamins

• Teach client that excessive vitamin intake can be harmful

• Assess for deficiency• Assess for impaired liver function

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Drug Therapy with Fat-Soluble Vitamins (continued)

• Assess for chronic overdose of vitamins• Consider socioeconomic status and culture of

client– Recommend foods that treat deficiency

• Recommend foods that are affordable for and liked by client

Page 148: Week 2 rsc 325 summer

Water-Soluble Vitamin Therapy

• Thiamine administered for hospitalized clients with severe liver disease

• Niacin and pyridoxine may cause severe flushing– Expected reaction for client; no permanent harm– Assess women of childbearing age for folic acid

deficiency– Prior to attempting or during pregnancy

Page 149: Week 2 rsc 325 summer

Water-Soluble Vitamin Therapy (continued)

• Recommend multivitamin to avoid overdose• Caution clients with history of kidney stones

against using vitamin C• Advise clients taking vitamin C to increase

fluid intake• Water-soluble vitamins are not stored in the

body– Must be replenished daily

Page 150: Week 2 rsc 325 summer

Macromineral Therapy

• For mineral deficiencies or eclampsia• Large doses can cause life-threatening adverse

effects• Encourage well-balanced diet

– Eliminates or reduces need for supplements

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Macromineral Therapy (continued)

• If calcium prescribed– Inform health-care provider of use of

glucocorticoids, thiazide diuretics, tetracyclines– Avoid zinc-rich foods, which impair calcium

absorption

Page 152: Week 2 rsc 325 summer

Macromineral Therapy (continued)

• If phosphorus prescribed– Inform health-care provider if on sodium- or

potassium-restricted diet– Immediately report seizure activity; stop drug– Avoid antacids

Page 153: Week 2 rsc 325 summer

Macromineral Therapy (continued)

• If client is taking magnesium sulfate, immediately report– Changes in consciousness, deep tendon reflexes– Thirst, confusion

Page 154: Week 2 rsc 325 summer

Macrominerals

• Seven major (macro) minerals– Calcium, chlorine, magnesium, phosphorous– Potassium, sodium, sulfur

• Must be obtained daily from dietary sources in amounts of 100 mg or greater

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Page 156: Week 2 rsc 325 summer

Microminerals (continued)

• Nine trace (micro) minerals– Include iron, iodine, fluorine, and zinc

• Required daily amount is 20 mg or less

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Undernutrition

• Many causes– Low dietary intake– Malabsorption disorders– Fad diets– Wasting disorders such as cancer or AIDS

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Undernutrition (continued)

• Reasons for low dietary intake vary– Poverty, depression, difficulty eating

• Nutritional consultation is appropriate

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Enteral Nutrition

• Provided orally or through feeding tube• Means of meeting client’s nutritional needs

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Classification of Enteral Products

• Oligomeric (Vivonex, T.E.N., Peptamen)• Polymeric—most common type (Compeat,

Sustacal, Ensure)• Modular—given to supplement single nutrient

(Casec, Polycose, Microlipid, MCT Oil)• Specialized—given for special disease states

(Amin-Aid, Hepatic-Aid II, Pulmocare)

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Total Parenteral Nutrition (TPN)

• Also known as hyperalimentation• Means of supplying nutrition to clients

– Peripheral vein (short term)– Central vein (long term)

• Administered through infusion pump for precise monitoring

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Vitamin Pharmacotherapy — Lipid –Soluble Vitamins

• Prototype drug: Vitamin A• Mechanism of action:

– Essential for general growth and development– Necessary for proper wound healing– Essential for the biosynthesis of steroids, – One of the pigments required for night vision

Page 163: Week 2 rsc 325 summer

Vitamin Pharmacotherapy — Lipid –Soluble Vitamins (continued)

• Primary use: pregnancy, lactation, or undernutrition, night blindness and slow wound healing

• Topical forms are available for acne, psoriasis

Page 164: Week 2 rsc 325 summer

Vitamin Pharmacotherapy — Lipid –Soluble Vitamins (continued)

• Adverse effects: – Acute ingestion, produces serious CNS toxicity-

headache, irritability, drowsiness, delirium, and possible coma.

– Long-term ingestion of high amounts - drying and scaling of the skin, alopecia, fatigue, anorexia, vomiting, and leukopenia

Page 165: Week 2 rsc 325 summer

Vitamin Pharmacotherapy - Water –Soluble Vitamin

• Prototype drug: Folic Acid ( Folacin).• Mechanism of action: administered to reverse

symptoms of folate deficiency– 1 mg/day of oral folic acid often reverses the

deficiency symptoms within 5 to 7 days

Page 166: Week 2 rsc 325 summer

Vitamin Pharmacotherapy - Water –Soluble Vitamin (continued)

• Primary use: during pregnancy to promote normal fetal growth– Patients with inadequate intake, such as with

chronic alcohol abuse. • Adverse effects: uncommon but

– Patients may feel flushed following IV injections. – Allergic hypersensitivity to folic acid by the IV

route is possible

Page 167: Week 2 rsc 325 summer

Mineral Pharmacotherapy - Mineral Supplement

• Prototype drug: Magnesium Sulfate • Mechanism of action:

– Essential for proper neuromuscular function. – Also serves a metabolic role– in activating certain enzymes in the breakdown of

carbohydrates and proteins

Page 168: Week 2 rsc 325 summer

Mineral Pharmacotherapy - Mineral Supplement (continued)

• Primary use: – Severe hypomagnesemia – To prevent or terminate seizures associated with

eclampsia – Oral forms used as cathartics for complete

evacuation of the colon– Use of magnesium sulfate is restricted to severe

magnesium deficiency

Page 169: Week 2 rsc 325 summer

Mineral Pharmacotherapy - Mineral Supplement (continued)

• Adverse effects: – Early signs of overdose include

• Flushing of the skin, sedation, confusion, intense thirst, and muscle weakness

– Extreme levels cause neuromuscular blockade leading to

• respiratory paralysis, heart block, and circulatory collapse.

Page 170: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy

• Assessment– Obtain complete health history and complete

physical examination– Obtain a history of vitamin deficiencies or

hypervitaminosis – Obtain a dietary history noting adequacy of

essential vitamins, minerals and nutrients

Page 171: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)

• Assessment– Note sunscreen use and amount of sun exposure– Obtain weight and vital signs– Evaluate., CBC, electrolytes, hepatic and renal

function studies, ferritin and iron levels– Assess for and promptly report adverse effects

Page 172: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)

• diagnoses– Imbalanced nutrition: less than body

requirements– Impaired Health Maintenance, (related to dietary

habits, deficient knowledge); – Deficient knowledge, related to drug therapy– Readiness for Enhanced Therapeutic Regimen

Management – Risk for Injury (related to adverse drug effects,

hypervitaminosis).

Page 173: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)

• Planning—patient will– Experience maintenance of overall health,

symptoms of previous deficiency are absent.– Be free from, or experience minimal adverse

effects – Verbalize an understanding of the drug’s use,

adverse effects and required precautions– Demonstrate proper self-administration of the

medication (e.g., dose, timing, when to notify provider)

Page 174: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)

• Implementation– Treat the cause: correct the deficiency – Review dietary and supplement history for

hypervitaminosis and adverse drug effects. – Monitor the use of fat-soluble vitamins [A, D, E,

and K] for possible toxic effects– Monitor liver function

Page 175: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)

• Implementation– Encourage adequate intake of vitamin and folic-

acid rich foods prior to conception– Instruct patient to keep pre-natal vitamins out of

reach of children– Ensure adequate hydration if large doses of water-

soluble vitamins are taken.– Encourage client to take medication appropriately

Page 176: Week 2 rsc 325 summer

Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)

• Evaluation– Experiences maintenance of overall health,

symptoms of previous deficiency are absent – Is free from, or experiences minimal adverse

effects – Verbalizes an understanding of the drug’s use,

adverse effects and required precautions– Demonstrates proper self-administration of the

medication (e.g., dose, timing, when to notify provider)

Page 177: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition

• Assessment– Obtain complete health history and complete

physical examination– Obtain a drug history including allergies, and

possible drug interactions– Obtain baseline height, weight and vital signs– Assess for the presence or history of nutritional

deficits

Page 178: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Assessment– Evaluate appropriate laboratory findings (e.g.,

• CBC, electrolytes, glucose, BUN• hepatic and renal function studies• total protein, serum albumin, lipid profile, serum iron

levels

– Assess for and promptly report adverse effects

Page 179: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• diagnoses– Risk for infection– Imbalanced nutrition: less than body

requirements– Risk for imbalanced fluid volume– Deficient knowledge, related to drug therapy

Page 180: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Planning—patient will– Experience maintenance or improvement of

overall health and nutritional status– Be free from, or experience minimal adverse

effects– Verbalize an understanding of the drug’s use,

adverse effects and required precautions – Demonstrate proper self-administration of the

medication (e.g., dose, timing, when to notify provider)

Page 181: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Implementation– Monitor vital signs

• Observe for signs of infection, such as elevated temperature

– Assess patient’s ability to take oral nutrition and encourage small oral feedings if allowed

– Assess all access sites (e.g., gastric tube site, I.V. or port sites) frequently for

• redness, streaking, swelling, or drainage

Page 182: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Implementation– Monitor for signs of fluid overload– Observe for signs of hyperglycemia or

hypoglycemia• Monitor blood-glucose levels

– Monitor renal status – intake and output, daily weight, serum creatinine and BUN

Page 183: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Implementation – Maintain accurate infusion rate with infusion

pump• make rate changes gradually• avoid abruptly discontinuing TPN feeding

– Refrigerate TPN solution until 30 minutes before using

– Assess for appropriate enteral tube placement before administering any feeding.

Page 184: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Implementation – Report any fever, chills, malaise, or changes in

mental status immediately– Use strict aseptic technique with all I.V. tubing or

bag changes, site dressing changes – Instruct patient and/or family in proper self-

administration of drug

Page 185: Week 2 rsc 325 summer

Patients Receiving Parenteral Nutrition (continued)

• Evaluation- patient– Experiences maintenance or improvement of

overall health and nutritional status – Is free from, or experiences minimal adverse

effects – Verbalizes an understanding of the drug’s use,

adverse effects and required precautions– Demonstrates proper self-administration of the

medication (e.g., dose, timing, when to notify provider)

Page 186: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1

Which of the following mechanisms is the most important regulator of fluid intake?

Page 187: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Choices

1. Thirst 2. Electrolytes 3. Renin–angiotensin 4. Kidneys

Page 188: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Answer

1. Thirst 2. Electrolytes 3. Renin–angiotensin 4. Kidneys

Page 189: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Rationale

Rationale: Thirst is the most important regulator of fluid intake.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity

Page 190: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 2

Which of the following nursing interventions is most important when caring for a patient

receiving a plasma volume expander?

Page 191: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 2 – Choices

1. Assess the patient for deep vein thrombosis 2. Observe for signs of fluid overload3. Encourage fluid intake 4. Monitor arterial blood gases

Page 192: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 2 – Answer

1. Assess the patient for deep vein thrombosis 2. Observe for signs of fluid overload3. Encourage fluid intake4. Monitor arterial blood gases

Page 193: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 2 – Rationale

Rationale: Dextran 40, a plasma volume expander, causes fluid to move rapidly from the tissues to vascular spaces, which places the patient at risk for fluid overload.Cognitive Level: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity

Page 194: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4

The patient complains of muscle cramping in the calves, paresthesia of the toes, and the

sensation of the heart skipping a beat. These symptoms may indicate which one of the

following imbalances?

Page 195: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4 – Choices

1. Hypernatremia 2. Hypercalcemia 3. Hypoglycemia 4. Hyperkalemia

Page 196: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4 – Answer

1. Hypernatremia 2. Hypercalcemia 3. Hypoglycemia 4. Hyperkalemia

Page 197: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4 – Rationale

Rationale: Hyperkalemia, a serum potassium level greater than 5 mEq/L, predisposes the patient to cardiac and muscle irregularities such as cramping in the calves, paresthesia of the toes, and palpitations. Cognitive Level: AnalysisNursing Process: DiagnosisPatient Need: Physiological Integrity

Page 198: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5

A patient will be sent home on diuretic therapy and will need to increase the amount of

potassium in the diet. What food choices would the nurse suggest be added?

Page 199: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5 – Choices

1. Liver, red meats, lettuce 2. Apples, pears, celery, onions 3. Bananas, tomatoes, beans, fresh meats 4. Potato chips, licorice, rice, corn

Page 200: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5 – Answer

1. Liver, red meats, lettuce 2. Apples, pears, celery, onions 3. Bananas, tomatoes, beans, fresh meats 4. Potato chips, licorice, rice, corn

Page 201: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5 – Rationale

Rationale: Bananas, strawberries, tomatoes, dried beans, and fresh meats are natural sources of potassium. The other food items have low levels of potassium but may be part of a healthy diet.Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity

Page 202: Week 2 rsc 325 summer

NCLEX-RN ReviewQuestion 6

The nurse weighs the patient and finds that there has been a weight gain of 1.5 kg since the previous day. What would be the nurse’s next

highest priority?

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NCLEX-RN ReviewQuestion 6 – Choices

1. Check with the patient to see if there have been any dietary changes in the last few days.

2. Assess the patient for signs of edema and BP for possible hypertension.

3. Contact dietary to change the patient’s diet to reduced sodium.

4. Request a diuretic from the patient’s provider.

Page 204: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Answer

1. Check with the patient to see if there have been any dietary changes in the last few days.

2. Assess the patient for signs of edema and BP for possible hypertension.

3. Contact dietary to change the patient’s diet to reduced sodium.

4. Request a diuretic from the patient’s provider.

Page 205: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Rationale

Rationale: A weight gain of 1 kg (approximately 2 lb) or more may indicate fluid retention. Signs of fluid retention include hypertension and edema. A complete nursing assessment is needed to determine other signs or symptoms that may be present. Checking dietary history may be considered after the nursing assessment is completed.

Page 206: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Rationale (cont)

Changing diet or medications is part of the collaborative treatment plan with the health care provider.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity

Page 207: Week 2 rsc 325 summer

207

Nutrition Questions

Page 208: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1

An older adult has been diagnosed with pernicious anemia and replacement therapy is

ordered. The nurse will anticipate administering which vitamin, and by what technique?

Page 209: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Choices

1. B6, orally in liquid form

2. K, via intramuscular injection 3. D, by light-box therapy or increased sun

exposure 4. B12, by intramuscular injection

Page 210: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Answer

1. B6, orally in liquid form

2. K, via intramuscular injection 3. D, by light-box therapy or increased sun

exposure 4. B12, by intramuscular injection

Page 211: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Rationale

Rationale: Pernicious anemia results in the inability to absorb vitamin B12 due to the lack of intrinsic factor in the gut. Replacement therapy must be administered via intramuscular injection because oral supplementation will not be absorbed. Pernicious anemia affects vitamin B12 absorption.

Page 212: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 1 – Rationale (cont)

Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity

Page 213: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 3

The nurse is assessing a patient who is exhibiting generalized weakness, cardiac dysrhythmias,

hypertension, loss of deep tendon reflexes, and respiratory distress. What could be the possible

cause of these symptoms?

Page 214: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 3 – Choices

1. Hypocalcemia 2. Hypercalcemia 3. Hypomagnesemia 4. Hypermagnesemia

Page 215: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 3 – Answer

1. Hypocalcemia 2. Hypercalcemia 3. Hypomagnesemia 4. Hypermagnesemia

Page 216: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 3 – Rationale

Rationale: Hypomagnesemia should be assessed. Patients experiencing hypomagnesemia may experience general weakness, dysrhythmias, hypertension, loss of deep tendon reflexes, and respiratory depression.Cognitive Level: AnalysisNursing Process: Assessment Patient Need: Physiological Integrity

Page 217: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4

The patient is a long-time alcoholic. The nurse understands that alcoholism is the most

common cause of which vitamin deficiency?

Page 218: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4 – Choices

1. Vitamin E 2. Vitamin A 3. Vitamin D 4. Thiamine

Page 219: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4 – Answer

1. Vitamin E 2. Vitamin A 3. Vitamin D 4. Thiamine

Page 220: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 4 – Rationale

Rationale: Alcohol is known for its ability to inhibit the absorption of thiamine and folic acid. Alcohol abuse is the most common cause of thiamine deficiency. Cognitive Level: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity

Page 221: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5

The patient is a 12-year-old child with hemophilia. The nurse is aware that this patient will require administration of which vitamin to

improve the function of clotting factors?

Page 222: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5 – Choices

1. Folic acid2. Riboflavin 3. Vitamin K 4. Vitamin A

Page 223: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5 – Answer

1. Folic acid2. Riboflavin 3. Vitamin K 4. Vitamin A

Page 224: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 5 – Rationale

Rationale: Vitamin K should be given to the patient to improve clotting. Without vitamin K, abnormal prothrombin is produced and blood clotting is affected. Cognitive Level: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity

Page 225: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6

Total parenteral nutrition (TPN) has been ordered for a patient with gastric cancer who is

no longer able to maintain oral intake. The nurse notes that the patient has a temperature of 100.4º F. What should the nurse assess first?

Page 226: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Choices

1. The date the TPN was ordered 2. The patient’s last electrolyte levels,

particularly glucose3. The intravenous access site and all IV

equipment and TPN bag 4. The patient’s last chest x-ray report

Page 227: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Answer

1. The date the TPN was ordered 2. The patient’s last electrolyte levels,

particularly glucose3. The intravenous access site and all IV

equipment and TPN bag 4. The patient’s last chest x-ray report

Page 228: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Rationale

Rationale: TPN access sites, tubing, and parenteral nutrition bag are all areas at risk for contamination and for bacteria to enter the patient. The nurse should assess the IV access site for redness, streaking, swelling, or drainage and all tubing and bag for signs of cracks, cloudiness, or precipitate. Glucose levels and TPN orders will be assessed periodically but do not directly contribute to the development of infection.

Page 229: Week 2 rsc 325 summer

Critical Thinking ReviewQuestion 6 – Rationale (cont)

Periodic chest x-ray monitoring may be ordered and should be obtained if adventitious breath sounds are noted. Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity