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BIOL1191 > Chapter 27 - Fluid, Electrolyte & Acid-base Homeostasis > Flashcards

Chapter 27 - Fluid, Electrolyte & Acid-base Homeostasis Flashcards

1
Q

4 Types of Homeostasis

A
  1. Fluid Homeostasis
  2. Electrolyte Homeostasis
  3. Acid-base Homeostasis
  4. Nitrogen Homeostasis
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2
Q

Interstitial Fluid (6 Types)

A
  1. CSF
  2. Lymph
  3. Synovial Fluid
  4. Aqueous & Vitreous humours
  5. Pleural, Pericardial & Peritoneal Fluids
  6. Endolymph & Perilymph
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3
Q

Extracellular Fluid/ECF (2 Subdivisions)

A
  1. Interstitial Fluid: 80%
  2. Plasma: 20%

*Contains 15 L of the 40 L of total body H2O

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4
Q

Intracellular Fluid/ICF

A
  • Contains 25 L of the 40 L of total body H2O

- ICF & ECF compartments maintain distinctive compositions of Na+ & Cl- as well as K+, proteins, & PO4(-3)

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5
Q

4 Rules for Fluid/Electrolyte Balance

A
  1. Homeostatic mechanisms respond to changes in ECF
  2. ECF receptors respond to changes in plasma volume (via baroreceptors) & osmolarity (via osmoreceptors)
  3. All H2O movements occur passively in response to osmotic gradients (H2O follows solute)
  4. Body content of H2O salts will accumulate if intake > outflow & vice-versa
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6
Q

4 Hormones Involved in Fluid/Electrolyte Balance

A
  1. Antidiuretic Hormone
  2. Angiotensin 2
  3. Aldosterone
  4. Atrial Natriuretic Peptide
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7
Q

Antidiuretic Hormone

A
  • Causes H2O reabsorption in renal CT & CD via aquaporin-2
  • ADH release triggered by osmoreceptors or by a large decrease in blood volume
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8
Q

Angiotensin 2

A
  • Stimulates PCT Na+/H+ antiporters -> Increased NaCl & H2O reabsorption -> Increased BP
  • Also causes vasoconstriction and secretion of aldosterone
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9
Q

Aldosterone

A

-Increases Na+, Cl- & H2O reabsorption in CT & CD

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10
Q

2 Triggers of Aldosterone

A
  1. JGA cells activate renin-angiotensin-aldosterone mechanism
  2. Direct release in response to hyperkalemia
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11
Q

Atrial Natriuretic Peptide

A
  • Inhibits ADH & aldosterone
  • Promotes fluid/electrolyte losses in urine (natriuresis) by causing relaxation of renal mesangial cells
  • Inhibits Na+ & H2O reabsorption by the PCT & CD
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12
Q

Methods of H2O Loss

A
  • Urine, feces, evaporation from skin & lung: 2300 mL

- Sweating: 200 mL

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13
Q

Methods of H2O Gain

A
  • Eating & drinking
  • Production of H2O primarily during oxidative phosphorylation by mitochondria (Metabolic Generation)
  • Also from dehydration synthesis reactions
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14
Q

H2O Loss > H2O Gains

A

Results in dehydration & hypotension

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15
Q

H2O Gains > H2O Loss

A

Results in overhydration, hypertension & hemodilution

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16
Q

Restoration of Osmotic Equilibrium

A
  • If ECF tonicity > ICF tonicity: H2O travels from ICF -> ECF
  • If ECF tonicity < ICF tonicity: H2O travels from ECF -> ICF
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17
Q

2 Types of Fluid Imbalances

A
  1. Excessive ECF -> Overhydration & H2O intoxication

2. Depleted ECF -> Circulatory shock & hypotension

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18
Q

Urinary NaCl Losses

A

Main determinant of total body H2O fluid volume

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19
Q

2 Rules for Na+ and K+ balance

A
  1. Most salt homeostasis problems due to imbalances between Na+ gains & Na+ losses
  2. K+ homeostasis problems are uncommon, but dangerous
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20
Q

Sodium (Na+) Balance

A
  • Na+ is the most abundant extracellular ion in the ECF
  • Inputs come from dietary intake (salt)
  • Outputs done through urine & sweat

*Normal range of blood [Na+] = 136 -148 mEq/L of plasma H2O

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21
Q

4 Hormones Controlling Na+ Homeostasis

A
  1. Aldosterone
  2. Angiotensin 2
  3. Antidiuretic Hormone
  4. Atrial Natriuretic Peptide
  • All 4 hormones also control ECF volume to promote fluid homeostasis
  • Decreased ECFV -> 1,2, and 3 are secreted
  • Increased ECFV -> 4 is secreted
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22
Q

Hypernatremia

A

=Excessive Na+ levels

  • If due to dehydration -> thirst, dry skin & decreased blood volume & BP
  • If due to inadequate renal excretion of Na+ or increased dietary Na+ -> increased blood volume, BP & edema
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23
Q

Hyponatremia

A

=Inadequate Na+ levels

  • Leads to muscle weakness, hypotension, dizziness & disturbed CNS function
  • “H2O Intoxication” -> dilutional hyponatremia & possible cytotoxic brain edema
  • Aldosterone deficiency in adrenal insufficiency -> hyponatremia, hypovolemia & decreased BP
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24
Q

Potassium (K+) Balance

A
  • K+ is the most abundant intracellular cation

- Concentration in ECF is controlled by aldosterone

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25
Q

3 Functions of K+

A
  1. Maintain cell fluid volume
  2. Action potential conduction
  3. Helps regulate PH (w/ K+/H+ antiporters)
  • In acidosis, K+/H+ antiporters -> H+ influx & K+ efflux
  • Alkalosis has reverse effect
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26
Q

2 Reasons for Increased K+ Excretion

A
  1. ECF [K+] increases above normal levels

2. Renin-angiotensin-aldosterone pathway activated

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27
Q

Hyperkalemia

A

=Excessive K+ levels

  • Leads to increased neuromuscular excitability
  • Causes cardiac arrhythmias, cardiac arrest & possible death (Heart)
  • Causes muscle twitching & weakness (Skeletal Muscle)
  • Causes CNS irritability (CNS)
28
Q

Hypokalemia

A

=Inadequate K+ levels

  • Leads to decreased neuromuscular excitability
  • Causes cardiac arrhythmias & possible cardiac arrest (Heart)
  • Causes flaccid paralysis & weakness (Skeletal Muscle)
  • Causes hypoventilation (Lungs)
  • Causes mental confusion (CNS)
29
Q

Calcium (Ca+2) Balance

A
  • Ca+2 is the most abundant ion in the body
  • Functions in blood clotting, exocytosis & muscle contractions
  • PTH & calcitriol increase Ca+2 levels
  • Calcitonin decreases Ca+2 levels
30
Q

Hypercalcemia

A

=Excessive Ca+2 levels

  • Occurs in primary hyperparathyroidism, vitamin D3 toxicity, some cancers & chronic Ca+2 overconsumption
  • Leads to decreased neuromuscular excitability; causes excessive membrane splinting, especially affects excitable cells
  • Also leads to confusion, CNS depression, “metastatic” calcification of soft tissues
31
Q

Hypocalcemia

A

=Inadequate Ca+2 levels

  • Occurs in hypoparathyroidism & hypomangesemia
  • Leads to increased neuromuscular excitability; causes insufficient membrane splinting, especially affects excitable cells
  • Also leads to hyper-reflexia, muscle spasms, convulsions, laryngospasm & paresthesias
32
Q

2 Mechanisms for Hypomagnesemia -> Hypocalcemia

A
  1. Mg+2 for Ca+2 “exchange” in bone

2. PTH secretion inhibited

33
Q

Magnesium (Mg+2) Ion

A
  • Primarily an intracellular electrolyte
  • Is an important activator of protein kinase A & C
  • Is a cofactor for ATPases
  • Is required for PTH secretion
34
Q

Hypermagnesemia

A

=Excessive Mg+2 levels

  • Occurs in overdosing w/ magnesium-containing supplements & renal failure
  • Leads to decreased neuromuscular excitability, lethargy, confusion & respiratory depression
35
Q

Hypomagnesemia

A

=Inadequate Mg+2 levels

  • Occurs in poor diet, alcoholism & severe diarrhea
  • Leads to increased neuromuscular excitability, which causes muscle weakness, cramps & cardiac arrhythmias
36
Q

Phosphate (PO4-3)

A
  • Primarily an intracellular ion
  • Required for synthesis of nucleic acids
  • Is important in buffer systems
37
Q

3 Different Forms of Phosphate Ion

A
  1. H2PO4-
  2. HPO4-2
  3. PO4-3
38
Q

4 Hormones that Regulate Phosphate

A
  1. Parathyroid Hormone: Inhibits phosphate reabsorption by kidneys
  2. Calcitriol: Promotes absorption of dietary phosphate
  3. Calcitonin: Inhibits osteoclastic activity
  4. Fibroblast Growth Factor-23: Decreases GI absorption & increases renal excretion
39
Q

Hyperphosphatemia

A

=Excessive PO4-3 levels

  • Occurs in high phosphate intake, renal failure, cancer chemotherapy & hypoparathyroidism
  • Leads to muscular weakness, vomiting, hyperactive reflexes & tetany
40
Q

Hypophosphatemia

A

=Inadequate PO4-3 levels

  • Occurs in poor diet, malabsorption syndrome, some kidney diseases, hyperparathyroidism, vitamin D3 deficiency & overuse of Al+3 containing drugs
  • Leads to dizziness & memory loss
41
Q

Chloride (Cl-) Ion

A
  • Is a major extracellular anion
  • Regulates osmotic pressure
  • Part of stomach acid
  • Important in RBC chloride shift
  • Blood level is indirectly controlled by aldosterone
42
Q

Hyperchloremia

A

=Excessive Cl- levels

  • Occurs in dietary chloride excess, dehydration, aldosteronism & renal failure
  • Caused by hyperkalemia, muscle weakness & metabolic acidosis
43
Q

Hypochloremia

A

=Inadequate Cl- levels

  • Occurs in excessive vomiting, hypokalemia, primary Addison’s disease & diuretic overuse
  • Caused by metabolic alkalosis, anorexia, muscle cramps, tetany & slow/ shallow ventilation
44
Q

Normal pH Range

A

=7.35 -7.45
pH > 7.45 = alkalosis
pH < 7.35 = acidosis

45
Q

3 Types of Acids in the Body

A
  1. Volatile Acids
  2. Fixed Acids
  3. Organic Acids
46
Q

Volatile Acids

A

=Acids able to leave solution & enter the atmosphere

-Example: Carbonic acid (HCO3-)

47
Q

Fixed Acids

A

=Acids that are non-volatile; remain in the body until excreted
-Examples: Sulfuric acid & phosphoric acid

48
Q

Organic Acids

A

=By-products of cellular metabolism

-Examples: Lactic acid & ketone bodies

49
Q

Rapid Regulation of pH

A
  • Acid-base balance is maintained by controlling H+ concentration of body fluids
  • Buffer systems = weak acid & the salt of a weak acid
  • Example: H2CO3/NaHCO3
50
Q

3 Main Buffer Systems

A
  1. Protein Buffer Systems
  2. Carbonic Acid-bicarbonate Buffer System
  3. Phosphate Buffer System
51
Q

Protein Buffer Systems

A
  • Some amino acids can accept or release H+ ions
  • If pH increases, free carboxyl (-COOH) groups of amino acids can dissociate, releasing H+ & becoming -COO-
  • If pH decreases, free amine groups (-NH2) of amino acids can accept an additional H+ -> NH3+
  • Examples: Hemoglobin of RBCs & albumin of plasma
52
Q

Carbonic Acid-bicarbonate Buffer System

A
  • Uses H2CO3/HCO3-
  • Exchange reactions occur (AB +CD -> AD + BC)
  • If plasma becomes too alkaline, H2CO3 becomes HCO3- by releasing an H+ ion
  • If plasma becomes too acidic, HCO3- becomes H2CO3 by binding to an H+ ion
53
Q

Phosphate Buffer System

A
  • Seen in ICF & urine
  • Uses H2PO4-/HPO4-2
  • If plasma becomes too alkaline, OH- is buffered by H+ from H2PO4-
  • If plasma becomes too acidic, excess H+ is bound by HPO4-2
  • Buffering of H+ is “quick-fix”
54
Q

Respiratory System & Acid-base Homeostasis

A
  • Exhalation of CO2 & H2O removes excess H+ from blood
  • If ECF pH decreases, chemoreceptors signal medullary DRG to increase ventilation rate -> decreased PCO2 -> pH increases (vice-versa during pH increase)
  • Change in ventilation rate = respiratory compensation
  • Anxiety can double ventilation rate -> alkalosis
  • Intentional slowing of respiration -> acidosis
55
Q

Urinary System & Acid-base Homeostasis

A
  • Kidneys can vary their rates of H+ secretion, HCO3- secretion and HCO3- reabsorption
  • H+ secretion done by Na+/H+ anitporters in PCT and H+ ATPases of intercalated cells in CT/CD
  • HCO3- secretion done by Cl-/HCO3- antiporter of intercalated cells in CT/CD
  • HCO3- reabsorption done by PCT
56
Q

Acidosis

A

=When blood pH < 7.35

-Principal effect: Decreased neuromuscular excitability, can lead to possible coma & death

57
Q

Alkalosis

A

=When blood pH > 7.45
-Principal effect: Increased neuromuscular excitability, can lead to nervousness, muscle spasms, convulsions & possible death

58
Q

Respiratory Acidosis

A

=Excessive CO2 levels in body fluids

  • Symptoms: Fatigue, confusion, dyspnea & somnolence
  • Seen in hypoventilation, emphysema, airway obstruction & pulmonary edema
  • Renal compensation: Increasing H+ secretion & HCO3- reabsorption, while decreasing HCO3- secretion
  • Renal compensation may be partial or complete
59
Q

Respiratory Alkalosis

A

=Inadequate CO2 levels in body fluids

  • Symptoms: vertigo, numbness &/or muscle spasms in hands & feet
  • Seen in high altitude sickness, stroke, anxiety states
  • Renal compensation: Decreasing H+ secretion & HCO3- reabsorption, while increasing HCO3- secretion
  • Renal compensation may be partial or complete
60
Q

Metabolic Acidosis

A

=Depletion of HCO3- reserve

  • Symptoms: Rapid/shallow breathing, confusion, somnolence, anorexia
  • Respiratory Compensation: Increased ventilation rate to blow off more CO2 & H2O
  • Respiratory compensation may be partial or complete
61
Q

5 Causes of HCO3- Depletion

A
  1. Deficient renal H+ secretion
  2. Excessive production of fixed acids
  3. Excessive production of organic acids
  4. Chronic diarrhea
  5. Nephrotic syndrome
62
Q

Metabolic Alkalosis

A

=Excessive levels of HCO3- in blood

  • Symptoms: Myalgia, polyuria & cardiac arrhythmias
  • Caused by prolonged vomitting or excessive consumption of alkaline substances
  • Respiratory Compensation: Decreased ventilation rate to blow off less CO2 & H2O
  • Respiratory compensation may be partial or complete
63
Q

Diagnosis of Acidosis & Alkalosis (3 Tests)

A
  1. Systemic Arterial Blood pH
  2. Blood PCO2 levels
  3. Blood HCO3- levels
64
Q

Age-related Changes in Homeostasis

A
  • 75% of total bodyweight of newborn = H20 (60% for adults)
  • ICF:ECF volume ratio of premature infants = 1:2 (2:1 for adults)
  • Infants have a 2x faster metabolic rate than adults due to immature kidneys, making acidosis common
65
Q

3 Other Infantile Problems w/ Homeostasis

A
  1. More H2O loss via skin due to having greater ratio of body surface area/volume
  2. More H2O loss via lungs due to high respiration rates
  3. Difficult tubular H+ secretion due to higher K+ and Cl- levels in blood
    - Hyperkalemia: less H+ losses via intercalated cells
    - Hyperchloremia: H+ harder to secrete
    - Leads to higher risk of metabolic acidosis
66
Q

Elderly Problems w/ Homeostasis

A
  1. Impaired fluid/electrolyte, acid-base homeostasis
  2. Respiratory or renal compensations often inadequate
  3. Pharmaceuticals may contribute to fluid/electrolyte imbalances
67
Q

4 Elderly Susceptibilities for Homeostatic Imbalances

A
  1. Dehydration & hypernatremia
  2. Hyponatremia
  3. Hypokalemia
  4. Acidosis

BIOL1191 (13 decks)

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