NCMA 312 LECTURE

PATHOPHYSIOLOGY
I. Give the functions of the given electrolytes

1. Chloride (Cl-)
 Normal level of serum: 96-106 mEq/L
 Major anion of ECF compartment
 Maintains cellular integrity by providing water balance and maintaining acid-base
balance.
 It has two imbalances which is the Hyperchloremia (Chloride Excess) and
Hypochloremia (Chloride Deficit)

2. Magnesium (Mg)
 Normal level of serum: 1.5-2.5 mg/dl
 Acts as an activator for many intracellular enzyme systems and plays a 
 It’s an abundant intracellular cation
 role in both carbohydrate and protein metabolism.
 It also affects the cardiovascular system, acting peripherally to produce
vasodilation and decreased peripheral resistance.
 It has two imbalances which is the Hypermagnesemia (Magnesium Excess) and
Hypomagnesemia (Magnesium Deficit)

3. Phosphorus (Po4)
 Normal level of serum: 2.5-4.5 mg/dl
 It is the primary anion of the ICF
 It is essential to the function of the muscle and RBCs.
 It provides support to bones and teeth
 It has two imbalances which is the Hyperphosphatemia (Phosphorus Excess)
and Hypophosphatemia (Phosphorus Deficit)
 

II. Make a pathophysiology chart of the following electrolyte imbalances

 1) Hyperchloremia

HYPERCHLOREMIA

Increase serum Cl more than 106

mEq/L
Inc. Chloride Intake Dec. Losses
 Excess salt intake  Hyperthyroidism
w/o water Hyperaldosteronism
ETIOLOGY 
 Hypertonic IV fluid  Renal Failure
Admin.
 Metabolic Acidosis
Increase serum Mg more than 2.5
mg/dl

CLINICAL MANIFESTATION

MANAGEMENT Hypernatremia
 Weakness
 Monitor vital signs, ABG values,
 Lethargy
I&O  Deep Rapid Respiration
 Correcting the underlying cause  Diminished cognitive ability
 Restoring electrolyte, fluid, and  Hypertension
acid-based balance
 Hypotonic IV solutions may be
given If Untreated:
 Lactated Ringers Solution may  Dec. Cardiac Output
 Dysrhythmias
be prescribed (convert lactate to
 Coma
bicarbonate in the liver)
 IV sodium may be given to
increase bicarbonates levels
 Diuretics may be given to
eliminate chloride
 Educates the patients about the
diet
2) Hypochloremia

HYPOCHLOREMIA
 Dec. serum Cl less than 98 mEq/L
Inc. Losses
 Diuresis
Dec. Chloride Intake  Excessive
 Low salt dietary  Vomiting (HCL
sources ETIOLOGY loss)
 Water intoxication  Metabolic
Alkalosis
 Fistulas
 Ileostomy
CLINICAL MANIFESTATION  NG suction

Hyper excitability of muscles

 Tetany
 Hyperactive DTRs
 Weakness
 Twitching
 Muscle Cramps

Hypokalemia
 Cardiac Arrhytmias

MANAGEMENT Hyponatremia
 Seizures
 Monitor vital signs, ABG values,  Coma
I&O, and Serum electrolyte
levels
 Report changes in patient’s
level of consciousness and
muscle strength and movement
 Provides and educate about
foods with high chloride content
 Correcting the cause of
hypochloremia

3) Hypermagnesemia

HYPERMAGNESEMIA
 Increase serum Mg more than 2.5
mg/dl

ETIOLOGY CLINICAL MANIFESTATION

Inc. Magnesium Intake Cardiac changes

 hypertension  Bradycardia
 Peripheral vasodilation
 Hypotension
 Myocardial Infarction
Decreased renal excretion of  Cardiac arrest
Magnesium resulting from renal
insufficiency
CNS
 Drowsy
 Lethargic
 Coma

Neuro changes
 Reduce or Absent Deep
Tendon reflex
 Weak skeletal muscles

MANAGEMENT
Respiratory changes
 Monitor vital signs, I&O  Weak Resp. Muscles
 Restrict Mg intake  Resp. failure or death
 Administer fluids an diuretics
 Hemodialysis if severe

4) Hypomagnesemia

HYPERMAGNESEMIA
 Decrease serum Mg less than 1.5
mg/dl

Inc. Mg Excretion by ETIOLOGY Dec. Magnesium

Kidneys Intake

Dec. Mg via GI tract

 Diarrhea
 Malabsorption

CLINICAL MANIFESTATION

Neuromuscular/Nervous System
 Positive Chvostek’s &
Trousseau’s Signs
 Tremor
 Fasciculations
 Tenany
 Headaches
 Seizures
 Fatigue
 Asthenia

MANAGEMENT
Cardiovascular
 AVD/CAD  Monitor vital signs,
 Arrhythmias ABG values, I&O
 Hypertension  Educates the
 CHF patients about the
diet (Green veg.,
nuts, legumes,
Endocrine bananas and
 Altered Glucose Homeostatis oranges)
5) Hyperphosphatemia
 Diabetoc Complication
 Monitor urine output
 Osteoporosis

HYPERPHOSPHATEMIA
 Increase serum PO4 more than 2.5
mg/dl
Inc. PO4 Intake
 Hypervitaminosis
D
 Phosphate ETIOLOGY Inc. Shift of PO4 from
supplementation ICF to ECF
 Phosphate
containing
enemas/laxatives Dec. Excretion
 Renal disease
 Hypoparathyroidism
 Pseudo-hypoparathyroidism
 Acromegaly
 Bisphosphonate therapy

CLINICAL MANIFESTATION
MANAGEMENT
 Monitor vital signs, ABG
values, I&O Neuromuscular/Nervous System
 Restrict PO4 intake  Tetany, hyperreflexia,
 Educates the patients muscular weakness, flaccid
about the diet (Avoid Po4- paralysis
rich foods: hard cheese,
cream, nuts, meats,
whole-grain cereals, dried
fruits, dried Cardiovascular
vege.,kidneys, sardines,  Tachycardia
and dairy foods)

GI
 Nausea, diarrhea, abdominal
cramps

6) Hypophosphatemia
 HYPOPHOSPHATEMIA

Decrease serum PO4 less than 4.5

mg/dl
Dec. PO4 Intake
 Dec. intestinal
absorption
Internal redistribution
 GI surgeries ETIOLOGY
 Inc. insulin
 Vit. D deficiency
secretion
 Acute
respiratory
Inc. Urine Excretion alkalosis
 Hyperparathyroidism  Hungry bone
phenomenon
 Renal displacement

CLINICAL MANIFESTATION
MANAGEMENT
 Monitor vital signs, ABG
values, I&O
Neuromuscular/Nervous System
 Inc. PO4 intake  Muscle weakness, tremors,
 Correcting the underlying paresthesia, bone pain,
cause hyporeflexia, seizures,
 Educates the patients about delirium, hallucinations,
the diet ascending motor paralysis

Cardiovascular
 Weak pulse, hyperventilation,
respi. weakness

GI
 Anorexia
 Dysphagia