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

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

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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
3 Functions of K+
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
26
2 Reasons for Increased K+ Excretion
1. ECF [K+] increases above normal levels | 2. Renin-angiotensin-aldosterone pathway activated
27
Hyperkalemia
=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
Hypokalemia
=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
Calcium (Ca+2) Balance
- 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
Hypercalcemia
=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
Hypocalcemia
=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
2 Mechanisms for Hypomagnesemia -> Hypocalcemia
1. Mg+2 for Ca+2 "exchange" in bone | 2. PTH secretion inhibited
33
Magnesium (Mg+2) Ion
- Primarily an intracellular electrolyte - Is an important activator of protein kinase A & C - Is a cofactor for ATPases - Is required for PTH secretion
34
Hypermagnesemia
=Excessive Mg+2 levels - Occurs in overdosing w/ magnesium-containing supplements & renal failure - Leads to decreased neuromuscular excitability, lethargy, confusion & respiratory depression
35
Hypomagnesemia
=Inadequate Mg+2 levels - Occurs in poor diet, alcoholism & severe diarrhea - Leads to increased neuromuscular excitability, which causes muscle weakness, cramps & cardiac arrhythmias
36
Phosphate (PO4-3)
- Primarily an intracellular ion - Required for synthesis of nucleic acids - Is important in buffer systems
37
3 Different Forms of Phosphate Ion
1. H2PO4- 2. HPO4-2 3. PO4-3
38
4 Hormones that Regulate Phosphate
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
Hyperphosphatemia
=Excessive PO4-3 levels - Occurs in high phosphate intake, renal failure, cancer chemotherapy & hypoparathyroidism - Leads to muscular weakness, vomiting, hyperactive reflexes & tetany
40
Hypophosphatemia
=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
Chloride (Cl-) Ion
- 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
Hyperchloremia
=Excessive Cl- levels - Occurs in dietary chloride excess, dehydration, aldosteronism & renal failure - Caused by hyperkalemia, muscle weakness & metabolic acidosis
43
Hypochloremia
=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
Normal pH Range
=7.35 -7.45 pH > 7.45 = alkalosis pH < 7.35 = acidosis
45
3 Types of Acids in the Body
1. Volatile Acids 2. Fixed Acids 3. Organic Acids
46
Volatile Acids
=Acids able to leave solution & enter the atmosphere | -Example: Carbonic acid (HCO3-)
47
Fixed Acids
=Acids that are non-volatile; remain in the body until excreted -Examples: Sulfuric acid & phosphoric acid
48
Organic Acids
=By-products of cellular metabolism | -Examples: Lactic acid & ketone bodies
49
Rapid Regulation of pH
- 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
3 Main Buffer Systems
1. Protein Buffer Systems 2. Carbonic Acid-bicarbonate Buffer System 3. Phosphate Buffer System
51
Protein Buffer Systems
- 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
Carbonic Acid-bicarbonate Buffer System
- 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
Phosphate Buffer System
- 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
Respiratory System & Acid-base Homeostasis
- 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
Urinary System & Acid-base Homeostasis
- 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
Acidosis
=When blood pH < 7.35 | -Principal effect: Decreased neuromuscular excitability, can lead to possible coma & death
57
Alkalosis
=When blood pH > 7.45 -Principal effect: Increased neuromuscular excitability, can lead to nervousness, muscle spasms, convulsions & possible death
58
Respiratory Acidosis
=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
Respiratory Alkalosis
=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
Metabolic Acidosis
=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
5 Causes of HCO3- Depletion
1. Deficient renal H+ secretion 2. Excessive production of fixed acids 3. Excessive production of organic acids 4. Chronic diarrhea 5. Nephrotic syndrome
62
Metabolic Alkalosis
=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
Diagnosis of Acidosis & Alkalosis (3 Tests)
1. Systemic Arterial Blood pH 2. Blood PCO2 levels 3. Blood HCO3- levels
64
Age-related Changes in Homeostasis
- 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
3 Other Infantile Problems w/ Homeostasis
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
Elderly Problems w/ Homeostasis
1. Impaired fluid/electrolyte, acid-base homeostasis 2. Respiratory or renal compensations often inadequate 3. Pharmaceuticals may contribute to fluid/electrolyte imbalances
67
4 Elderly Susceptibilities for Homeostatic Imbalances
1. Dehydration & hypernatremia 2. Hyponatremia 3. Hypokalemia 4. Acidosis

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