Ch 3: Cell Environment

Question 1

Total body water
* Intracellular fluid (ICF): Inside the cell
* Extracellular fluid (ECF): Outside the cell
* Interstitial fluid
* Intravascular fluid
* Cerebrospinal fluid (CSF)
* Lymphatic, synovial, intestinal, biliary, hepatic, pancreatic, pleural, peritoneal, pericardial, and intraocular fluids
* Sweat
* Urine

Question 2

Osmolality
Osmotic forces
* Sodium for the ECF
* Potassium for the ICF
Aquasporins
* A family of water channel proteins that provide permeability to water

Answer 2

Osmosis: How water moves between the ICF
and ECF compartments
Water crosses cell membranes freely so the
osmolality of TBW is normally at equilibrium.
When ECF osmolality changes, water moves
from one compartment to another until osmotic equilibrium is reestablished.

Question 3

Water movement b/w Plasma and Interstitial fluid?
Starling hypothesis
* Net filtration is equal to the forces favoring filtration minus the forces opposing filtration.
Forces favoring filtration
* Capillary hydrostatic pressure (blood pressure)
* Interstitial oncotic pressure (water pulling)
Forces opposing filtration
* Capillary (plasma) oncotic pressure (water pulling)
* Interstitial hydrostatic pressure

Question 4

Accumulation of fluid in the interstitial
spaces
Causes
* Increased capillary hydrostatic pressure (venous obstruction)
* Decreased plasma oncotic pressure (losses or diminished production of albumin)
* Increased capillary permeability (inflammation andimmune response)
* Lymphatic obstruction (lymphedema)

Answer 4

Manifestations:
Localized vs. generalized
Dependent edema
Pitting edema
“Third space”
Swelling and puffiness
Tight-fitting clothes and shoes
Weight gain

Treatment:
Elevate edematous limbs.
* Use compression stockings or devices.
* Avoid prolonged standing.
* Restrict salt intake.
* Take diuretic agents.

Question 5

A person with hypertension
and heart failure has edema
in the lower legs and sacral
area. The nurse suspects
this condition is due to a(n)
1. increase in plasma oncotic pressure.
2. decrease in capillary hydrostatic pressure.
3. decrease in lymph obstruction pressure.
4. increase in capillary hydrostatic pressure.

Answer 5

ANS: 4
* Heart failure produces salt and water
retention and subsequent volume overload,
which increases capillary hydrostatic
pressure which leads to edema.
* 1. An increase in plasma oncotic pressure
produces movement of fluid from the
interstitial space into the vascular space
which would decrease edema.
* 2. A reduction in capillary hydrostatic
pressure decreases the force for filtration of
fluid from the capillary which would
decrease edema.
* 3. A decrease in lymph obstruction would
not cause edema; an increase in lymph
obstruction would lead to edema.

Question 6

Discuss Na+/Cl- Balance

Answer 6

Sodium
* Is the primary ECF cation.
* Regulates osmotic forces.
* Roles include:
* Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances
* Is regulated by aldosterone and natriuretic peptides.

Chloride
* Is the primary ECF anion.
* Provides electroneutrality.
* Follows sodium.

Renin-angiotensin-aldosterone system
* Aldosterone
* Increases excretion of potassium by the distal tubule of the kidney
Natriuretic peptides
* Decreases tubular resorption, and promotes urinary excretion of sodium
* Atrial natriuretic peptide
* Brain natriuretic peptide
* Urodilatin (kidney)

Question 7

Water Balance Is regulated by thirst perception and the antidiuretic hormone (ADH)
Thirst perception
* Osmolality receptors (osmoreceptors)
* Signal posterior pituitary to release ADH
* Increase water intake

• Baroreceptors
• Stimulated from depleted plasma volume
• Causes release of ADH

ADH (Vasopressin)
* Is released when there is an increase in plasma osmolality or decrease in circulating blood volume.
* Is also called arginine vasopressin.
* Increases water reabsorption.

Question 8

A person reports severe diarrhea for 2 days. The nurse understands this stimulates a(n)
1.reduction in aldosterone secretion.
2.reduction in renin secretion.
3.increase in antidiuretic hormone secretion.
4.increase in natriuretic peptide secretion

Answer 8

ANS: 3
* Hypovolemia stimulates volume sensitive
receptors and baroreceptors and results in
secretion of antidiuretic hormone to
increase water reabsorption.
* 1. Volume depletion produces an increase in aldosterone secretion through the activation of the renin-angiotensin-aldosterone system.
* 2. Volume depletion produces an increase in renin secretion and initiates the renin-
angiotensin-aldosterone system.
* 4. Volume depletion results in reduced
secretion of natriuretic peptides. Natriutetic
peptides are diuretics which would make
more loss of fluid.

Question 9

What are 3 Isotonic Alterations in water balance?

Answer 9

*Total body water change with proportional
electrolyte change
* Isotonic fluid loss (dehydration and hypovolemia)
* Isotonic fluid excess (hypervolemia)

Question 10

What are 3 HYPERTONIC alterations?

Answer 10

1. Hypernatremia
   * Serum sodium >145 mEq/L
   * Related to sodium gain or water loss
   * Water movement from the ICF to the ECF
   * Intracellular dehydration
   * Manifestations: Intracellular dehydration, seizures, muscle twitching, hyperreflexia
   * Treatment: Isotonic salt-free fluids
2. Water deficit
   * Dehydration
   * Both sodium and water loss
   * Manifestations: Low blood pressure, weak pulse, and postural hypotension, Elevated hematocrit and serum sodium levels
   * Headache, dry skin, and dry mucous membranes
   Treatment:
   * Oral fluids
   * Hypotonic saline solution (5% dextrose in water)
3. Hyperchloremia
   * Occurs with hypernatremia or a bicarbonate deficit.
   * Is usually secondary to pathophysiologic
   processes.
   * Is managed by treating the underlying disorders.

Question 11

What are some HYPOTONIC alterations?
(decreased osmolality)

Answer 11

1. Hyponatremia or free water excess
   Hyponatremia decreases the ECF osmotic
   pressure, and water moves into the cell.
   Water excess
   * Compulsive water drinking, causing water intoxication
   * Cellular edema
   * Manifestations: Cerebral edema, pulmonary edema
   * Treatment: Fluid restriction; may need hypertonic saline solutions
2. Hypochloremia
   * Is usually the result of hyponatremia or elevated bicarbonate concentration.
   * Some causes are
   * vomiting.
   * metabolic alkalosis.
   * cystic fibrosis.
   * Treat the underlying cause.

Question 12

Tell me about Potassium?

Answer 12

*ECF concentration: 3.5–5.0 mEq/L
*Is the major intracellular cation.
*Aldosterone, insulin, and epinephrine facilitate K+ into the cells.
*Insulin deficiency, aldosterone deficiency,
acidosis, and strenuous exercise facilitate K+
out of the cells.
*The sodium-potassium (Na+ /K+) pump
maintains concentration.
*Is essential for the transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and
smooth muscle contraction.
*Regulates ICF osmolality and deposits glycogen in liver and skeletal muscle cells.
*Kidneys, aldosterone and insulin secretion,
and changes in pH regulate K+ balance.
*K+ adaptation allows the body to accommodate slowly to
increased levels of K+ intake.

Question 13

Hypokalemia
Potassium level <3.5 mEq/L
Causes
* Reduced potassium intake
* Increased potassium entry into cell
* Increased potassium loss
Treatment
* Replace potassium orally and/or
intravenously.

Manifestations
* Membrane hyperpolarization
causes:
* Decreased neuromuscular excitability
* Skeletal muscle weakness
* Smooth muscle atony
* Cardiac dysrhythmias
* U wave on electrocardiogram (ECG)

Answer 13

Hyperkalemia
Potassium level >5.0 mEq/L
Rare as a result of efficient renal excretion
Causes
* Increased intake
* Shift of K+ from ICF to ECF
* Decreased renal excretion
* Hypoxia
* Acidosis
* Insulin deficiency
* Cell trauma
* Digitalis overdose
Mild attacks
* Tingling of lips and fingers, restlessness, intestinal cramping and diarrhea, T waves on the ECG
Severe attacks
* Muscle weakness, loss of muscle tone, paralysis
Treatment
* Calcium gluconate, insulin and/or glucose, buffered solutions, dialysis

Question 14

Calcium and Phosphate
CA: Ionized form is 5.5–5.6 mg/dL.
Most calcium is located in the bone as
hydroxyapatite.
* 99% in bone
* 1% in plasma and body cells
Is necessary for
* structure of bones and teeth.
* blood clotting.
* hormone secretion.
* cell receptor function.
* muscle contractions.
PHOS:
Serum levels: 2.5–4.5 mg/dL (adults)
Similar to calcium, most phosphate (85%) is also located in the bone.
Is necessary for high-energy bonds located in creatine phosphate and adenosine triphosphate (ATP) and acts as an anion buffer and needed for muscle contraction energy.
Calcium and phosphate concentrations are rigidly controlled.
* Ca++ × HPO4= = K (K is a constant)
* If the concentration of one increases, the
concentration of the other decreases.

Regulated by three hormones:
1. Parathyroid hormone (PTH)
* Increases plasma calcium levels via kidney reabsorption.
2. Vitamin D
* Is a fat-soluble steroid; increases calcium absorption from the gastrointestinal (GI) tract.
3. Calcitonin
* Decreases plasma calcium levels.

Question 15

Hypocalcemia:
Calcium levels <9.0 mg/dL
Causes
* Inadequate intake or absorption
* Decreases in PTH and vitamin D
* Blood transfusions
Treatment
* Calcium gluconate, calcium replacement,
decrease phosphate intake
Manifestations
* Increased neuromuscular excitability (partial depolarization)
* Muscle spasms
* Chvostek and
Trousseau signs
* Convulsions
* Tetany

Answer 15

Hypercalcemia:
Calcium levels >10.5 mg/dL
Causes
* Hyperparathyroidism
* Bone metastasis
* Excess vitamin D
* Immobilization
* Acidosis
* Sarcoidosis
Manifestations
* Decreased neuromuscular excitability
* Weakness

Manifestations (cont.)
 Kidney stones
 Constipation
 Heart block
Treatment
 Oral phosphate
 IV normal saline
 Bisphosphonates
 Calcitonin
 Denosumab (Prolia)

Question 16

Hypophosphatemia:
Serum phosphate level < 2.0 mg/dL
Causes: Intestinal malabsorption and renal excretion, vitamin D deficiency, antacid use, alcohol abuse, malabsorption syndromes, refeeding syndromes

Manifestations: Diminished release of oxygen, osteomalacia (soft bones), muscle weakness, bleeding disorders (platelet impairment), leukocyte alterations, rickets

Treatment: Treat underlying condition such as respiratory alkalosis and hyperparathyroidism.

Answer 16

Hyperphosphatemia:
Serum level >4.7 mg/dL
Causes: Exogenous or endogenous addition of phosphate to ECF, chemotherapy, long-term use of phosphate enemas or laxatives, renal failure
High phosphate levels related to low calcium
levels
Manifestations: Same as hypocalcemia with
possible calcification of soft tissue

Treatment: Treat underlying condition,
aluminum hydroxide, and dialysis.

Question 17

Magnesium: (1.5-3.0)
Is an intracellular cation.
Is stored most in the muscle and bones.
Interacts with calcium.
Is a cofactor in intracellular reactions, protein synthesis, nucleic acid stability, and
neuromuscular excitability.

Answer 17

Hypomagnesemia
* From malabsorption
* Associated with hypocalcemia and
hypokalemia
* Neuromuscular irritability
* Tetany, convulsions
* Increased reflexes
Treatment: Magnesium sulfate

Hypermagnesemia
* From renal failure
* Skeletal muscle depression
* Muscle weakness
* Hypotension
* Respiratory depression
* Bradycardia
Treatment: Avoid magnesium; dialysis

Question 18

Acid-Base Balance (pH=potential for Hydrogen) norm: 7.35-7.45
if H+ is high in number, pH is low (acidic).
If H+ is low in number, pH is high (alkaline).

Acids are formed as end products of protein,
carbohydrate, and fat metabolism.
To maintain the body’s normal pH (7.35–7.45) the H+ must be neutralized by the retention of bicarbonate or excreted.

Bones, lungs, and kidneys are major organs
involved in the regulation of acid-base balance.
pH below 6.8 = death.
pH above 7.8 = death.

Answer 18

Normal arterial blood pH
* 7.35–7.45
* Obtained by arterial blood gas (ABG) sampling

Acidosis
* pH is less than 7.35.
* Systemic increase in H+ concentration

Alkalosis
* pH is greater than 7.45.
* Systemic decrease in H+ concentration or excess of base

Question 19

Volitile Acids?

Answer 19

Carbonic acid (H2CO3)
Can be eliminated as carbon dioxide (CO2)
gas via the lungs

Question 20

Non-volatile acids?

Answer 20

Sulfuric, phosphoric, and other metabolic
acids
* Is eliminated by the renal tubules with the
regulation of HCO3−.

Question 21

Sources of H+ ions
* CO2 diffuses into the bloodstream where the following reaction occurs:
Regulated by the Lung Regulated by the Kidney
CO2 + H2O  H2CO3  HCO3− + H+

Question 22

Buffering Systems: Chemical that can bind excessive H+ or OH− without a significant change in pH

Answer 22

Most important plasma buffering systems:
carbonic acid-bicarbonate system and
hemoglobin
Operates in the lung and the kidney.
The greater the partial pressure of carbon dioxide (pCO2), the more carbonic acid is formed.
* At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1.
* Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained.
Lungs can decrease carbonic acid.
Kidneys can reabsorb or regenerate bicarbonate but do not act as fast as the lungs.

If bicarbonate decreases, then the pH decreases and can cause acidosis.
pH can be returned to normal if carbonic acid also decreases.
* This type of pH adjustment is called compensation.
The respiratory system compensates by
increasing or decreasing ventilation.
The renal system compensates by producing
acidic or alkaline urine.

Other types:
Protein buffering
* Proteins have negative charges; as a result, they can serve as buffers for H+; mainly intracellular buffer with hemoglobin.

Respiratory and renal buffering
* Respiratory: Acidemia causes increased
ventilation; alkalosis slows respirations
* Renal: Secretion of H+ in urine and reabsorption of HCO3−; dibasic phosphate and ammonia

Cellular ion exchange
* Exchanges of K+ for H+ in acidosis and alkalosis

Question 23

Acid-Base Imbalances-4 types:

Answer 23

Acid-Base Imbalances (Cont.)
Four categories
1. Respiratory acidosis—elevation of pCO2 as a result of ventilation depression
2. Respiratory alkalosis—depression of pCO2 as a result of hyperventilation
3. Metabolic acidosis—depression of HCO3− or an increase in noncarbonic acids
*causes:
* Lactic acidosis, Renal failure, Diabetic ketoacidosis, Diarrhea, Starvation
* Manifestations:
* Headache
* Lethargy
* Kussmaul respirations
Treatment:
* Buffering solution administration
* Treat the underlying cause(s)
* Base administration
* Correct sodium and water deficits

4. Metabolic alkalosis—elevation of HCO3−, usually as a result of an excessive loss of metabolic acids

Question 24

Metabolic acidosis?

Answer 24

Metabolic acidosis—depression of HCO3 (bicarb)− or an increase in noncarbonic acids
pH drops below 7.35.
* HCO3− drops: less than 24 mEq/L
* Compensation: Hyperventilation and renal excretion of excess acid

*causes:
* Lactic acidosis, Renal failure, Diabetic ketoacidosis, Diarrhea, Starvation
* Manifestations:
* Headache
* Lethargy
* Kussmaul respirations
Treatment:
* Buffering solution administration
* Treat the underlying cause(s)
* Base administration
* Correct sodium and water deficits

Anion gap
* Used cautiously to distinguish different types of metabolic acidosis.
* By rule, anions (−) should equal cations (+).
* Not all normal anions are routinely measured.
* Represents unmeasured negative ions.
* Normal anion gap is 10–12 mEq/L.
* Normal anion gap or elevated anion gap with metabolic acidosis may help determine the cause.

Question 25

metabolic alkalosis:

Bicarbonate concentration is increased, usually from excessive loss of metabolic acids (Cl −)
* pH is elevated.
* HCO3− is elevated.

Answer 25

Causes
* Prolonged vomiting
* Gastric suctioning
* Excessive bicarbonate intake
* Hyperaldosteronism with hypokalemia
* Diuretic therapy
Manifestations: Weakness, muscle cramps, and hyperactive reflexes with signs of hypocalcemia

Treatment: Sodium chloride, potassium, chloride IV (chloride replaces HCO3−)

Question 26

Respiratory Acidosis
Occurs with alveolar hypoventilation
* pH is below 7.35.
* CO2 elevates from hypercapnia.
* Compensation: Is not as effective since kidneys take time but conserve bicarbonate and eliminate H+

Answer 26

Causes
* Depression of the respiratory center (brainstem trauma, oversedation)
* Respiratory muscle paralysis
* Disorders of the chest wall (kyphoscoliosis, pickwickian syndrome, flail chest)
* Disorders of the lung parenchyma (pneumonitis, pulmonary edema, and chronic obstructive lung
disease)
Manifestations: Headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma
Treatment: Restore adequate ventilation; may need
mechanical ventilation; oxygen therapy

Question 27

Respiratory Alkalosis
Occurs with hyperventilation and decreased plasma CO2 (hypocapnia).
* pH above 7.45
* CO2 is decreased less than 38 mmHg.

Answer 27

Causes
* High altitudes
* Hypermetabolic states, such as fever, anemia, and thyrotoxicosis
* Early salicylate intoxication
* Anxiety or panic disorder
* Improper use of mechanical ventilators
Manifestations: Dizziness, confusion, tingling of extremities (paresthesias), convulsions, and coma with signs of hypocalcemia

Treatment: Paper bag; treat hypoxemia and hypermetabolic states

Question 28

Mixed-base disorders

Answer 28

Two or more primary acid-base disorders occurring at the same time.
Common in hospitalized individuals.
Degree of compensation is determined.
Renal and respiratory compensation rarely returns the pH to normal.
Can have alterations in PaCO2 and bicarbonate and a normal pH.

Question 29

A person arrives in the
emergency department after a
loss of consciousness and the
development of Kussmaul
respirations. The individual has
a history of diabetes and 2 days
of vomiting and diarrhea. The
nurse practitioner suspects the
person has which of the
following primary disorders?
1.Respiratory alkalosis
2.Respiratory acidosis
3.Metabolic alkalosis
4.Metabolic acidosis

Answer 29

ANS: 4
* Diabetic ketoacidosis results in an
increase in noncarbonic acids and a
decrease in bicarbonate ion which
produces metabolic acidosis.
* 1. Respiratory alkalosis is produced
by alveolar hyperventilation and
reduction in carbon dioxide
concentration.
* 2. Respiratory acidosis is produced
by alveolar hypoventilation and
increase in carbon dioxide
concentration.
* 3. Metabolic alkalosis is produced by
an excess of bicarbonate ion.

Question 30

A person with a history of
chronic lung disease arrives in
the clinic with a 1-week history
of a productive cough,
hypoventilation, and headache.
The nurse practitioner suspects
the person is experiencing
1.respiratory acidosis.
2.respiratory alkalosis.
3.metabolic acidosis.
4.metabolic alkalosis.

Answer 30

ANS: 1
*Respiratory acidosis is produced by alveolar hypoventilation, which is commonly found in individuals with chronic obstructive pulmonary
disease. Headache can be a symptom of elevated carbon dioxide levels produced by hypoventilation.
*2. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration. Symptoms of respiratory alkalosis include dizziness, confusion, paresthesia, convulsions, and coma.
*3. Metabolic acidosis is produced by an increase in noncarbonic acids and/or a decrease in bicarbonate ion. Symptoms of metabolic acidosis include headache, lethargy,
Kussmaul respirations, anorexia, nausea and vomiting, dysrhythmias, and coma.
*4. Metabolic alkalosis is produced by an excess of bicarbonate ion. Symptoms of metabolic alkalosis include muscle weakness, muscle
cramps, hyperreflexia, paresthesias, tetany, and seizures.

Question 31

A 17-year-old boy is admitted to the pediatric intensive care unit after surgery. The teen requires débridement of a wound on his
sacrum (triangular bone at the base of the spine). His mother attributes this to difficulty in repositioning him because of his size. He has been in a persistent vegetative state for almost 4 years after suffering a traumatic
brain injury as a result of a self inflicted gunshot to his head.
The sacral area is
covered with which
type
of tissue?
A. Muscle
B. Neural
C. Epithelial
D. Connective

Answer 31

ANS: C
* Epithelial tissue covers
most internal and external
surfaces of the body.
Muscle tissue is
responsible for movement.
Neural tissue is composed
of highly specialized cells
that receive and transmit
electric impulses.
Connective tissue binds
various tissues and organ
together, supporting them
in their location.

Question 32

A large portion of the area is removed because of ischemia and cell death. The teen suffers from
tissue
A. apoptosis.
B. necrosis.
C. catabolism.
D. metabolism.

Answer 32

ANS: B
* Necrosis is a form of traumatic cell death that results from acute cellular injury. This may be caused by several types of cell injury, such as from repetitive movements against a surface or not being moved from a particular position over a long period of time. Apoptosis is the process of programmed cell death.
Biochemical changes occur within a cell leading to characteristic cell changes and death. Catabolism involves the metabolic breakdown of complex molecules into simpler ones, often resulting in a release of energy.
Metabolism is the set of life-sustaining transformations within cells of living organisms.

Question 33

An 86-year-old frail woman is admitted to the hospital for monitoring after sustaining a
concussion due to a fall in the patient’s home. The nurse practitioner performs the admission
examination on the patient.
The nurse practitioner
notices that the patient has generalized deteriorated muscle
mass and decreased strength in the
extremities. This condition is called
A. senescence.
B. autophagy.
C. apoptosis.
D. sarcopenia.

Answer 33

ANS: D
Sarcopenia, the loss of muscle mass and strength, can occur in old age. The skin of the aged individual is affected by atrophy and wrinkling of the epidermis and by alterations in
underlying dermis, fat, and muscle.
Senescence is a process of permanent
proliferative arrest on cells in response to various stressors and may be an important contributor to
aging and age-related disease. Autophagy, as a “recycling factory,” is a self-destructive process and a survival mechanism. It degrades
cytoplasmic components and organelles in lysosomes (a catabolic function) and salvages key
metabolites to promote metabolic and nutrient homeostasis (an anabolic function).
Apoptosis is an active process of cellular self-destruction—
called programmed cell death (type I)—in both normal and pathologic tissue changes. It depends
on a tightly regulated cellular program for its initiation and execution.

Question 34

The patient dies from an
aneurysm and the nurse
practitioner assesses the
changes occurring in the
patient’s body immediately
after death. The nurse
notices that the patient’s
lower legs are turning purple.
This is referred to as
A. algor mortis.
B. livor mortis.
C. rigor mortis.
D. postmortem autolysis.

Answer 34

ANS: B
After death, gravity causes blood to settle in the most dependent, or lowest, tissues, which develop a purple discoloration called livor mortis. Algor mortis is the postmortem reduction in body temperature. Within 6 hours after death, acidic compounds
accumulate within the muscles because of the breakdown of carbohydrate and the depletion of ATP. This interferes with ATP-
dependent detachment of myosin from actin (contractile proteins), and muscle stiffening, or rigor mortis, develops. Signs of putrefaction—state of decay with foul- smelling odor—are generally obvious about 24−48 hours after death. At a microscopic
level, putrefactive changes are associated with the release of enzymes and lytic dissolution called postmortem autolysis.