INDIVIDUAL OUTPUT #1: FLUID AND ELECTROLYTE IMBALANCE

QUESTIONS

1. Function of each cation or anions

2. Electrolyte imbalances
 Risk factors that could alter the
electrolyte. Explain.
 How would you assess electrolyte
imbalance either diagnostic exams and
their implication?
 Implication for each electrolyte if either
too low or too high
3. Cite at least 1 example of condition, that affect
the electrolytes imbalance

HYPONATREMIA
SODIUM
 Low sodium levels in the blood
Sodium (Na+) is the most abundant electrolyte in the
 Severe hyponatremia occurs when levels drop
extracellular fluid. Its concentration ranges from 135-
below 125 meq/l. Health issues arising from
145 mEq/L and it is the primary determinant of ECF
extremely low sodium levels may be fatal
volume and osmolality.

CONTRIBUTING FACTORS
FUNCTION
Loss of sodium, use of diuretics, loss of GI fluids,
 Controls water and other substances
renal disease, and adrenal insufficiency, gain of water,
throughout the body
excessive administration of D5W and water
 Establishes the electrochemical state
supplements for patients receiving hypotonic tube
necessary for muscle contraction and the
feedings; disease associated with SIADH such as head
transmission of nerve impulses
trauma and oat-cell lung tumor; and medications

SODIUM IMBALANCES associated with water retention. Hyperglycemia and

SODIUM IMBALANCES
heat failure can also cause loss of sodium.
The body obtains sodium through food and drink and
loses it primarily in sweat and urine. Healthy kidneys
SIGNS/SYMPTOMS
maintain a consistent level of sodium in the body by
Anorexia, nausea and vomiting, headache, lethargy,
adjusting the amount excreted in the urine.
confusion, muscle cramps and weakness, muscular
twitching, seizures, papilledema, dry skin, elevated
When sodium consumption and loss are not in
pulse, decreased BP
balance, the total amount of sodium in the body is
affected. The amount of sodium in the blood may be
too low (hyponatremia) or too high (hypernatremia).

Camila Grace S. Grepalda

BSN 3B
1
DIAGNOSTICS
Lab indicates decreased serum and urine sodium,
decreased urine specific gravity and osmolality
TREATMENT
 Restore blood sodium levels by drinking less
and adjusting or switching medication. In
severe symptoms, hospitalization and
intravenous sodium treatment is required.
 Treat underlying cause. If a person has liver
disease, kidney disease, or heart disease may
require treatment with medications or surgery.
People with thyroid disorder can typically
manage their symptoms and prevent
hyponatremia and other complications with
medications. They may also need to make
certain lifestyle changes such as avoiding
smoking and reducing alcohol consumption.
HYPERNATREMIA
 The level of sodium in blood is too high
 >145 mEq/L
 The body contains too little water for the
amount of sodium. The sodium level in the
blood becomes abnormally high when water
loss exceeds sodium loss.
 Involves dehydration, which can have many
causes, including not drinking enough fluids,
diarrhea, kidney dysfunction, and diuretics
CONTRIBUTING FACTORS
Water deprivation in patients unable to drink at will,
hypertonic tube feedings without adequate water
supplements, diabetes insipidus, heatstroke,
hyperventilation, and watery diarrhea. Excess
corticosteroid, sodium bicarbonate, and sodium
chloride administration, and salt water near-drowning
victims
SIGNS/SYMPTOMS
Thirst, elevated body temperature, swollen dry tongue
and sticky mucous membranes, hallucinations,
lethargy restlessness, irritability, focal or grand mal
seizures. Pulmonary edema, hyperreflexia, twitching,
nausea, vomiting, anorexia, elevated pulse and BP
DIAGNOSTICS
Elevated serum sodium, decreased urine sodium,
increased urine specific gravity anf osmolality
TREATMENT
Hypernatremia is treated by replacing fluids. In all but
the mildest cases, dilute fluids are given intravenously.
The sodium level in blood is reduced slowly because
reducing the level too rapidly can cause permanent
brain damage.
POTASSIUM
Potassium (K+) is the major intracellular electrolyte;
in fact, 98% of the body’s potassium is inside the
cells. The remaining 2% is in the ECF and is important
in neuromuscular function.
FUNCTION
 Maintaining normal blood pressure
 Transmitting nerve signals between organs
 Controlling muscle contractions
 Balancing pH in the body between acidity and
alkalinity
 Regulating proper digestion processes
Camila Grace S. Grepalda
BSN 3B
2
  Sustaining regular heart muscle activity
POTASSIUM IMBALANCES
The body maintains the right level of potassium by
matching the amount of potassium consumed with the
amount lost. A blood potassium level that is too high
(hyperkalemia) or too low (hypokalemia) can have
serious consequences, such as an abnormal heart
rhythm or even cardiac arrest.
HYPOKALEMIA
 The level of potassium in blood is too low
 Serum potassium level below 3.5 mEq/L
 Low potassium level can make muscles feel
weak, cramp, twitch, or even become
paralyzed, and abnormal heart rhythms may
develop
CONTRIBUTING FACTORS
Diarrhea, vomiting, gastric suction, corticosteroid
administration, hyperaldosteronism, carbenicillin,
amphotericin B, bulimia, osmotic diuresis, alkalosis,
starvation, diuretics, and digoxin toxicity
SIGNS/SYMPTOMS
Fatigue, anorexia, nausea and vomiting, muscle
weakness, polyuria, decreased bowel motility,
ventricular asystole or fibrillation, paresthesias, leg
cramps, decreased BP, abdominal distention,
hypoactive reflexes
DIAGNOSIS
 Blood test to measure potassium level in the
blood
 Electrocardiography
 Sometimes, urine test is done to measure the
amount of potassium present in the urine
 ECG: flattened T waves, prominent U waves,
ST depression, prolonged PR interval
TREATMENT
 Usually, potassium can be replaced by taking
potassium supplements by mouth. Because
potassium can irritate the digestive tract,
supplements should be taken in small doses
with food several times a day rather than in a
single large dose.
 To treat hypokalemia more rapidly, potassium
is given intravenously in the following
situations:
o The potassium level is dangerously
low.
o The low level causes abnormal heart
rhythms.
o Supplements taken by mouth are
ineffective
 Alternatively, diuretics that help the kidneys
conserve potassium (potassium-sparing
diuretics), such as amiloride can be used BUT
only if the kidneys are functioning normally.
Camila Grace S. Grepalda
BSN 3B
3

HYPERKALEMIA
 The level of patassium in blood is too high
 Serum potassium level greater than 5 mEq/L
 A high potassium level has many causes,
including kidney disorders, drugs that affect
kidney function, and consumption of too
much supplemental potassium.
 Usually, hyperkalemia must be severe before
it causes symptoms, mainly abnormal heart
rhythms.
CONTRIBUTING FACTORS
Vague muscular weakness, tachycardia to bradycardia,
dysrhythmias, flaccid paralysis, paresthesias, intestinal
colic, cramps, irritability, anxiety
Muscle cramps, drowsiness, decreased BP, EKG
changes, dysrhythmias, abdominal cramping,
diarrhea, oliguria
DIAGNOSIS
 Blood tests (potassium level greater than
normal
 Electrocardiogram
 Evaluation of medical history and routine lab
test results to determine which drugs people
have been taking, and do additional blood
tests to check for evidence of diabetes
mellitus, acidosis, muscle breakdown, or
kidney disorders.
TREATMENT
 For mild hyperkalemia, reducing consumption
of potassium or stopping drugs that prevent
the kidneys from excreting potassium may be
all that is needed. If the kidneys are
functioning, a diuretic that increases
potassium excretion may be given.
 For moderate to severe hyperkalemia, the
potassium level must be reduced immediately.
Doctors monitor the heart continuously during
treatment.
 If these measures do not work or if people
have kidney failure, dialysis may be necessary
to remove the excess potassium.
CALCIUM
More than 99% of the body’s calcium (Ca++) is
located in the skeletal system; it is a major
component of bones and teeth. About 1% of skeletal
calcium is rapidly exchangeable with blood calcium,
and the rest is more stable and only slowly
exchanged.
FUNCTION
 Formation of bone and teeth
 Muscle contraction
 Normal functioning of many enzymes
 Blood clotting
 Normal heart rhythm
Camila Grace S. Grepalda
BSN 3B
4
 CALCIUM IMBALANCES
The body precisely controls the amount of calcium in
cells and blood. The body moves calcium out of bones
into blood as needed to maintain a steady level
of calcium in the blood. If people do not consume
enough calcium, too much calcium is mobilized from
CONTRIBUTING FACTORS
the bones, weakening them.
Hypoparathyroidism, malabsorption, pancreatitis,
alkalosis, vitamin D deficiency, generalized peritonitis,
To maintain a normal level of calcium in blood without
chronic diarrhea, decreased parathyroid hormone,
weakening the bones, people need to consume at
diuretic phase of renal failure, lactose intolerance
least 1,000 to 1,500 milligrams of calcium a day. Too
little calcium in the blood is called hypocalcemia. Too
SIGNS/SYMPTOMS
much calcium in the blood is called hypercalcemia.
Dry scaly skin, brittle nails, coarse hair, muscle
cramps, confusion, memory loss, delirium, depression,
HYPOCALCEMIA
hallucinations, tingling sensation in the lips, tongue,
 Serum calcium value lower than 8.6 mg/dL
fingers and toes; muscle spasms, seizure, abnormal
 Older adults and those with disabilities, who
heart rhythm, positive Trousseau’s sign and Chvostek’s
spend an increased amount of time in bed,
sign, tetany
have an increased risk of hypocalcemia,
because bed rest increases bone resorption.
DIAGNOSIS
 Routine blood test- to evaluate kidney
function and to measure magnesium,
phosphate, parathyroid hormone, and vitamin
D levels.

TREATMENT
 Calcium supplements may be given orally or
IV depending on the severity of the symptoms
 Taking vitamin D supplements helps increase
the absorption of calcium from the digestive
tract.

Camila Grace S. Grepalda

BSN 3B
5
  Sometimes people with hypoparathyroidism
are given a synthetic form of parathyroid
hormone.
HYPERCALCEMIA
 serum calcium value greater than 10.2 mg/dL
 a dangerous imbalance when severe; in fact,
hypercalcemic crisis has a mortality rate as
high as 50% if not treated promptly
CONTRIBUTING FACTORS
Hyperparathyroidism, prolonged immobilization,
overuse of calcium supplements, vitamin D excess,
oliguric phase of renal failure, increased parathyroid
hormone
SIGNS/SYMPTOMS
Muscular weakness, constipation, anorexia, nausea
and vomiting, polyuria and polydypsia, hypoactive
DTR, lethargy, deep bone pain, calcium stones
DIAGNOSIS
 Routine blood test
 ECG- dysrhytmias
 Double-antibody PTH test
 X-rays - may reveal presence of osteoporosis
 Urine test- amount of calcium
TREATMENT
 If people have mild hypercalcemia and their
kidney function is normal, they are usually
advised to drink plenty of fluids. Fluids
stimulate the kidneys to excrete calcium and
help prevent dehydration.
 If the calcium level is very high or if
symptoms of brain dysfunction or muscle
weakness appear, fluids and diuretics are
given intravenously as long as kidney function
is normal.
MAGNESIUM
Magnesium (Mg++) is an abundant intracellular
cation. It acts as an activator for many intracellular
enzyme systems and plays a role in both carbohydrate
and protein metabolism.
FUNCTION
 helps with muscle and nerve function
 regulates blood pressure
 supports the immune system
 Required for proper growth and maintenance
of bones
MAGNESIUM IMBALANCES
The level of magnesium in the blood depends largely
on how the body obtains magnesium from foods and
Camila Grace S. Grepalda
BSN 3B
6
excretes it in urine and stool and less so on the total
body stores of magnesium. The level of magnesium in
the blood can become too high (hypermagnesemia) or
too low (hypomagnesemia).
HYPOMAGNESEMIA
 Below 1.3 mg/dL serum magnesium
concentration
 Usually, the magnesium level becomes low
because people consume less or because the
intestine cannot absorb nutrients normally.
But sometimes, hypomagnesemia develops
because the kidneys or intestine excrete too
much magnesium.
CONTRIBUTING FACTORS
Chronic alcoholism, hyperparathyroidism, diuretics,
malabsorptive disorders, diabetic ketoacidosis, chronic
laxative use, diarrhea, acute myocardial infarction,
malnutrition
SIGNS/SYMPTOMS
Neuromuscular irritability, positive Trousseasu’s and
Chvostek’s signs, insomnia, mood changes, anorexia,
vomiting, increased tendon reflexes, elevated BP
DIAGNOSIS
 Routine blood test
 ECG
TREATMENT
 Magnesium is given by mouth when the
deficiency causes symptoms or persists.
 If a very low magnesium level is causing
severe symptoms or if people cannot take
magnesium by mouth, magnesium is given by
injection into a muscle or vein.
 When treating hypomagnesemia, doctors also
must correct other electrolyte abnormalities,
such as hypocalcemia and hypokalemia.
HYPERMAGNESEMIA
 serum magnesium level higher than 3.0
mg/dL
 a rare electrolyte abnormality, because the
kidneys efficiently excrete magnesium
CONTRIBUTING FACTORS
Oliguric phase of renal failure, adrenal insuffieciency,
excessive IV magnesium administration
SIGNS/SYMPTOMS
Flushing, hypotension, hypoactive reflexes, depressed
respirations, diaphoresis, muscle weakness, impaired
breathing
Camila Grace S. Grepalda
BSN 3B
7
DIAGNOSIS
 Routine blood test
 ECG findings may include a prolonged PR
interval, tall T waves, a widened QRS, and a
prolonged QT interval, as well as an
atrioventricular block
TREATMENT
 People with severe hypermagnesemia are
given calcium gluconate intravenously to block
the toxic effect of increased levels of
magnesium.
 Diuretics can be given to increase the kidneys’
excretion of magnesium. However, if the
kidneys are not functioning well or if
hypermagnesemia is severe, dialysis is usually
needed.
CHLORIDE
Chloride (Cl−), the major anion of the ECF, is found
more in interstitial and lymph fluid compartments than
in blood. Chloride is also contained in gastric and
pancreatic juices, sweat, bile, and saliva.
FUNCTION
 helps to regulate the amount of fluid and
types of nutrients going in and out of the cells
 maintains proper pH levels
 stimulates stomach acid needed for digestion
 stimulates the action of nerve and muscle
cells
 facilitates the flow of oxygen and carbon
dioxide within cells
CHLORIDE IMBALANCES
Chloride control depends on the intake of chloride and
the excretion and reabsorption of its ions in the
kidneys. Chloride control depends on the intake of
chloride and the excretion and reabsorption of its ions
in the kidneys.
HYPOCHLOREMIA
 serum chloride level below 97 mEq/L
 Usually occurs when sodium is lost because
chloride most frequently bound with sodium
CONTRIBUTING FACTORS
Addison’s disease, reduced chloride intake or
absorption, excessive sweating, severe vomiting,
gastric suction, diarrhea, sodium and potassium
deficiency, metabolic alkalosis
SIGNS/SYMPTOMS
Agitation, irritability, tremors, muscke cramps,
hyperactive DTR, hypertonicity, tetany, slow and
shallow respirations, seizures, dysrhythmias, coma
DIAGNOSIS
 Routine blood test- low serum chloride, low
serum sodium, elevated pH, low urine chloride
level
TREATMENT
 Normal saline (0.9% sodium chloride) or half-
strength saline (0.45% sodium chloride)
solution is given by IV to replace the chloride
Camila Grace S. Grepalda
BSN 3B
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  If the patient is receiving a diuretic (loop,
osmotic, or thiazide), it may be discontinued
or another diuretic prescribed
HYPERCHLOREMIA
 serum level of chloride exceeds 107 mEq/L
 Hypernatremia, bicarbonate loss, and
metabolic acidosis can occur with high
chloride levels
CONTRIBUTING FACTORS
Excessive sodium chloride infusions with water loss,
head injury (sodium retention), hypernatremia, renal
failure, dehydration, severe diarrhea, respiratory
alkalosis, diuretic use
SIGNS/SYMPTOMS
Tachypnea, weakness, lethargy, rapid respiration,
diminished cognitive ability, hypertension, pitting
edema, decreased cardiac output
DIAGNOSIS
 ABG
 Routine blood test
 Urine test
 Labs indicate: increased serum chloride,
increased serum sodium, decreased serum
pH, increased urinary chloride level
TREATMENT
 Hypotonic IV solutions may be given to
restore balance.
 Lactated Ringer solution may be prescribed to
convert lactate to bicarbonate in the liver,
which increases the bicarbonate level and
corrects the acidosis.
 Diuretics may be given to eliminate chloride
as well. Sodium, chloride, and fluids are
restricted
BICARBONATE
The body’s major extracellular buffer system is the
bicarbonate–carbonic acid buffer system, which is
assessed when arterial blood gases are measured.
FUNCTION
 Acts as a buffer to maintain the normal levels
of pH in blood and other fluids in the body
 Bicarbonate levels are measured to monitor
the acidity of blood and body fluids
BICARBONATE IMBALANCES
Normally, there are 20 parts of bicarbonate (HCO3−)
to 1 part of carbonic acid (H2CO3). If this ratio is
altered, the pH will change.
If either bicarbonate or carbonic acid is increased or
decreased so that the 20:1 ratio is no longer
maintained, acid– base imbalance results.
BASE BICARBONATE DEFICIT
 Metabolic acidosis is a common clinical
disturbance characterized by a low pH and a
low plasma bicarbonate concentration
 can be produced by a gain of hydrogen ion or
a loss of bicarbonate
CONTRIBUTING FACTORS
Direct loss of bicarbonate, diarrhea, lower intestinal
fistulas, ureterostomies, and the use of diuretics; early
Camila Grace S. Grepalda
BSN 3B
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renal insufficiency; excessive administration of
chloride; and the administration of parenteral nutrition
without bicarbonate
SIGNS/SYMPTOMS
Headache, confusion, drowsiness, increased
respiratory rate and depth, nausea and vomiting,
peripheral vasodilation, decreased cardiac output, cold
and clammy skin
DIAGNOSIS
 ABG- low bicarbonate level and a low pH
 Routine blood test
 ECG detects dysrhythmias caused by the
increased potassium
TREATMENT
 If the problem results from excessive intake of
chloride, treatment is aimed at eliminating the
source of the chloride.
 In chronic metabolic acidosis, low serum
calcium levels are treated before the chronic
metabolic acidosis is treated to avoid tetany
resulting from an increase in pH and a
decrease in ionized calcium. Alkalizing agents
may be given.
BASE BICARBONATE EXCESS
 Metabolic alkalosis is a clinical disturbance
characterized by a high pH and a high plasma
bicarbonate concentration.
 It can be produced by a gain of bicarbonate
or a loss of H+
CONTRIBUTING FACTORS
Gastric suction with loss of hydrogen and chloride
ions, pyloric stenosis, diuretic therapy that promotes
excretion of potassium, ACTH secretion as in
hyperaldosteronism and Cushing syndrome
SIGNS/SYMPTOMS
Decreased calcium ionization, tingling of the fingers
and toes, dizziness, and hypertonic muscles,
depressed respirations, tachycardia, decreased motility
DIAGNOSIS
 ABG- pH greater than 7.45 and a serum
bicarbonate concentration greater than 26
mEq/L
 Urine test- urine chloride concentrations lower
than 25 mEq/L
TREATMENT
 Sufficient chloride must be available for the
kidney to absorb sodium with chloride
 In patients with hypokalemia, potassium is
given as KCl to replace both K+ and Cl−
losses
 Carbonic anhydrase inhibitors are useful in
treating metabolic alkalosis in patients who
cannot tolerate rapid volume expansion
PHOSPHATE
Bone contains about 85% of the body’s phosphate.
The rest is located primarily inside cells, where it is
involved in energy production.
FUNCTION
 necessary for the formation of bone and teeth
Camila Grace S. Grepalda
BSN 3B
10
  used as a building block for several important
substances, including those used by the cell
for energy, cell membranes, and DNA
PHOSPHATE IMBALANCES
The body obtains phosphate from foods and excretes
it in urine and sometimes stool. . Foods that are high
in phosphate include milk, egg yolks, chocolate, and
soft drinks. The level of phosphate in the blood may
be too high (hyperphosphatemia) or too low
(hypophosphatemia)
HYPOPHOSPHATEMIA
 value below 2.5 mg/dL
 can be caused by an intracellular shift of
potassium from serum into cells, by increased
urinary excretion of potassium, or by
decreased intestinal absorption of potassium.
CONTRIBUTING FACTORS
Malabsorption syndromes, chronic diarrhea,
malnutrition, vitamin D deficiency, chronic alcoholism,
phosphate-binding antacids, diabetic ketoacidosis,
respiratory alkalosis
SIGNS/SYMPTOMS
CNS depression, muscle weakness, polyneuropathy,
seizures, cardiac problems, rickets, irritability
DIAGNOSIS
 Routine blood test- serum phosphorus level is
less than 2.5 mg/dL
 X-ray- may show skeletal changes of
osteomalacia or rickets
TREATMENT
 Adequate amounts of phosphorus should be
added to parenteral solutions, and attention
should be paid to the phosphorus levels in
enteral feeding solutions
 Aggressive IV phosphorus correction is usually
limited to the patient whose serum
phosphorus levels decrease to less than 1
mg/dL and whose GI tract is not functioning
HYPERPHOSPHATEMIA
 a serum phosphorus level that exceeds 4.5
mg/dL
CONTRIBUTING FACTORS
Renal failure, phosphate enemas, excessive ingestion,
tumor lysis syndrome, thyrotoxicosis,
hypoparathyroidism, sickle cell anemia, hemolytic
anemia, hyperthermia
SIGNS/SYMPTOMS
Hypocalcemia, numbness and tingling in extremities
and region around mouth; hyperreflexia, muscle
cramps, tetany, seizures, soft tissue calcification
DIAGNOSIS
 Routine blood test
 X-ray
 Urine test
TREATMENT
 Vitamin D preparations, such as calcitriol,
which is available in both oral and parenteral
forms to decrease serum phosphate level
Camila Grace S. Grepalda
BSN 3B
11
  Restriction of dietary phosphate, forced
diuresis with a loop diuretic, volume
replacement with saline, and dialysis may also
lower phosphorus.
 Surgery may be indicated for removal of large
calcium and phosphorus deposits.
SULFATE
Sulfate is among the most important macronutrients
in cells and is the fourth most abundant anion in the
plasma.
FUNCTION
 Required for proper cell growth and
development
 involved in a variety of important biological
processes, including biosynthesis and
detoxification
 required for cell matrix synthesis and for the
maintenance of cell membranes
SULFATE IMBALANCES
SULFATE DEFICIT
CONTRIBUTING FACTORS
Inadequate sulfur intake, reliance on highly-processed
foods, sulfur intolerance
SIGNS/SYMPTOMS
Acne, arthritis, brittle nails and hair, convulsions,
depression, Eczema, Itchy skin or scalp, Migraine
headaches,memory loss, gastrointestinal issues,
rashes and even slow wound healing.
DIAGNOSIS
 Routine blood test
SULFATE EXCESS
CONTRIBUTING FACTORS
Excessive sulfur intake, polioencephalomalacia (PEM),
gut dysbiosis, problems with detoxification
SIGNS/SYMPTOMS
Diarrhea, intestinal pain, lung irritation, dry skin,
dermatitis, edema, hypotension
DIAGNOSIS
 Routine blood test
ORGANIC ACIDS
Organic acids are categorized in the “weak” acid
group that do not totally dissolve in water, and they
comprise one or more carboxylic acid groups
covalently linked in groups such as amides, esters and
peptides.
There are two types of organic acids. One has the
carboxyl group (COOH group), for example acetic acid
(CH3COOH) which is made by oxidising grain alcohol
or by the fermentation of fruit sugar in cider. The
second type has a phenol group (C6H5OH). Salicylic
acid (OHC6H4COOH) is an example of an organic acid
with both carboxyl and phenol groups.
FUNCTION
 play a role in the regulation of basic cellular
processes such as pH modification, signalling
messengers and modulating transport across
biological membranes
Camila Grace S. Grepalda
BSN 3B
12
  extensively modifies the cellular, subcellular or
extracellular compartments in which they are PROTEINATES
found due to their chemical properties An anion derived from protein.
 can be involved in various biochemical and
physiological processes in vivo FUNCTION
 helps to controls energy production by

ORGANIC ACID IMBALANCES controlling sugar levels.

Organic Acid Disorders (OAs) are a group of rare
inherited conditions caused by enzymes that do not
work properly. A number of enzymes are needed to
process protein from the food we eat for use by the
body. Problems with one or more of these enzymes
can cause an organic acid disorder. Each disorder has
different signs and symptoms, but they often include:
SIGNS/SYMPTOMS
Dehydration, dizzy or lightheaded, rapid heartbeat,
 important for bone formation and protein
metabolism
PROTEINATES IMBALANCES
The body needs protein to function and survive and
must get it through food. However, the body cannot
store protein long term for future use, so people need
to consume enough protein every day to ensure the
body gets enough to work correctly.
HYPOPROTENEMIA

dry mouth and lips, lethargy, low blood sugar, low Uncommon in developed countries where most people
body temperature, metabolic acidosis, nausea, eat a well-balanced diet. However, people who have
diarrhea, vomiting, skin rashes or infections, weak certain health conditions or diets lacking in protein
muscles or muscle spasms may develop the condition.

DIAGNOSIS SIGNS/SYMPTOMS
 Routine blood test  fatigue and weakness
 Urine test  recurrent viral or bacterial infections
 thinning, breaking hair
TREATMENT  hair that falls out
 Medications such as Vitamin B12, Biotin,  brittle nails and dry skin
Betaine, L-carnitine  mood changes and irritability
 Food plan such as low-protein diet, low-  cravings for protein-rich foods
leucine diet, low-valine diet
 Regular blood and urine tests-Your child's diet DIAGNOSIS
and medication may need to be adjusted  Routine blood test
based on the results of these tests  Urine analysis
Camila Grace S. Grepalda
BSN 3B
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  Imaging test

HYPERPROTENEMIA
Hyperproteinemia may be seen in dehydration due to
inadequate water intake or to excessive water loss
(eg, severe vomiting, diarrhea, Addison disease, and
diabetic acidosis) or as a result of increased
production of proteins.

SIGNS/SYMPTOMS
 Fatigue and weakness
 Unexplained weight loss
 Swelling in the extremities
 Changes in urine colour or frequency
 Abdominal pain or discomfort
 Loss of appetite

DIAGNOSIS
 Routine blood test
 Urine analysis
 Imaging test

Camila Grace S. Grepalda

BSN 3B
14
BSN3(SECTION)-LAST NAME-GIVEN NAME-
INDV.ASSIGN.
3B – DEADLINE ON WEDNESDAY 11:59 NN Reflection Paper:

1. Reflect on it’s effect on nursing education

2. Reflect on it’s effect on nursing research
3. Reflect on it’s effect on nursing practice

BSN3(SECTION)-LAST NAME-GIVEN NAME-

INDV.ART.
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Camila Grace S. Grepalda

BSN 3B
15