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A-BIOL 1191 LECTURE > CH 27 > Flashcards

CH 27 Flashcards

1
Q

what is a body fluid?

A

an aqueous solution produced by the human body containing dissolved solutes

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2
Q

what fraction of body fluid is ICF? ECF?

A
  • 2/3 of body fluids is intracellular
  • 1/3 is extracellular
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3
Q

what fraction of ECF is IF? blood plasma?

A

4/5 of ECF is interstitial fluid
1/5 is blood plasma

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4
Q

what body fluids are interstitial fluid?

A
  • lymph plasma
  • cerebrospinal fluid
  • synovial fluid
  • aqueous and vitreous humour
  • pleural, peritoneal, and pericardial fluids
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5
Q

what are the two barriers that separate ICF from ECF?

A
  1. plasma membrane surrounding cells
  2. blood vessel walls
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6
Q

what type of blood vessel is specialized for exchange btwn blood and IF?

A

capillaries

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7
Q

what structural features specialize capillaries for exchange btwn blood and IF?

A
  • walls are thin and leaky to increase diffusion rates
  • extensively branched to increase SA
  • small diameter to slow blood flow
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8
Q

what is fluid balance?

A

a state comprising water and solutes in the right proportions in the right anatomical locations

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9
Q

why do individuals with higher body fat % have less water?

A

adipose tissue contains only 20% water by mass

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10
Q

what are electrolytes?

A

inorganic compounds that dissociate in aqueous solution

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11
Q

what determines in what direction water will move across barriers?

A

the concentration of electrolytes

*where salt goes,water follows!

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12
Q

why is the ability of the kidneys to adjust water loss by producing dilute/concentrated urine crucial to maintaining fluid balance?

A

fluid and electrolyte intake is rarely equal to body fluid composition

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13
Q

what are the main sources of water gain?

A
  • ingested liquids and moist foods
  • metabolic water
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14
Q

what is metabolic water?

A

water produced from the reduction of oxygen in aerobic respiration (Electron Transport Chain)

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15
Q

what are main sources of water loss?

A
  • urine
  • sweat
  • exhaled water vapour
  • water in feces
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16
Q

what does metabolic water production depend on?

A

entirely on the rates of aerobic respiration in cells

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17
Q

why is more metabolic water formed when we increase our energy expenditure?

A

when more ATP is produced by the body, more metabolic water is produced

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18
Q

what is fluid intake controlled by?

A

thirst centre in hypothalamus

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19
Q

how does hypothalamus sense dehydration?

A

osmoreceptors in hypothalamus detect increased blood osmolarity

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20
Q

what are other receptors in body that sense dehydration and lead to an increase in thirst?

A
  • volume receptors in atria
  • baroreceptors in blood vessels
  • angiotensin II signals increase in blood pressure
  • sensory neurons in mouth that sense low salivary flow
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21
Q

what is a major stimulus that promotes the sensation of thirst?

A

an increase in blood osmolarity

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22
Q

why is it important for Na+ to be reabsorbed at the same time water is also reabsorbed?

A

so the water reabsorbed is not lost again through urinary salt loss, conserving the volume of bodily fluids

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23
Q

why may thirst not act quickly enough to prevent dehydration?

A
  • elderly people/infants may not communicate their needs or understand drives by the body
  • their sensations of thirst may not be strong
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24
Q

what is the main determinant of body fluid volume?

A

urinary salt (NaCl) loss

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25
Q

why is the main determinent of body fluid volume urinary salt (NaCl) loss?

A

Na+ and Cl- are the most abundant ions present in extracellular

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26
Q

what is the main determinant of body fluid osmolarity?

A

urinary water loss

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27
Q

what hormone is the major regulator of water loss?

A

antidiuretic hormone

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28
Q

where is ADH synthesized and stored in the body?

A

synthesis: neurosecretory cells of anterior and periventricular nuclei of hypothalamus

storage: posterior pituitary

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29
Q

what does ADH do to its target cells?

A

in principal cells, increases reabsorption of water by increasing permeability to water

  • increases expression of aquaporin-2 on plasma membranes of principal cells
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30
Q

what stimulates ADH release into blood by the posterior pituitary?

A
  • dehydration (increased blood osmolarity)
  • atrial volume receptors
  • baroreceptors in blood vessels
  • pain, nausea, stress
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31
Q

what hormones control urinary salt loss?

A
  • Aldosterone
  • Atrial Natriuretic Peptide
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32
Q

why do ADH and Aldosterone cooperate to increase blood pressure?

A

both hormones respond to the same signals (low blood volume, low blood pressure)

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33
Q

how does Atrial Natriuretic Peptide control urinary salt loss?

A
  • leads to natriuresis (excretion of Na+ into urine)
  • decreases blood volume, decreases renin release, decreases aldosterone levels
  • increases urinary salt and water loss to decrease blood volume
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34
Q

how does Aldosterone control Na+ excretion?

A
  • increases reabsorption of Na+ in DCT and CD - increased blood osmolarity to promote increased blood volume
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35
Q

what is an osmotic consequence of excreting more Na+?

A

the loss of more water in urine

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36
Q

how does atrial natriuretic peptide inhibit release of aldosterone?

A

an increase in blood volume slows the release of renin from the kidneys, decreasing aldosterone secretion

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37
Q

What effect does alcohol have on ADH secretion?

A

inhibits secretion of ADH and promotes diuresis

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38
Q

why doesn’t a cell normally shrink/swell?

A

the extracellular fluid surrounding the cell and the intracellular fluid inside the cell are isotonic, they have the same osmolarity

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39
Q

what happens if a human cell is placed in a hypertonic environment?

A

shrinks/shrivels

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40
Q

what happens when you eat an excessively salty meal? why is it bad?

A

ECF increases in osmolarity

  • if prolonged, cells shrink, including neurons → confusion
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41
Q

why may confusion be prevented after ECF has increased osmolarity for a prolonged period of time?

A

thirst and urinary system cooperate to prevent hypertonic ECF

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42
Q

why do body cells usually shrink only slightly and only for a short duration in response to an increase in the osmolarity of extracellular fluid?

A

corrective measures (e.g. thirst mechanism and secretion of antidiuretic hormone) increase the amount of body water, reducing the concentration of solutes in extracellular fluid back to normal levels

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43
Q

what will happen if cells are in a hypotonic environment for a prolonged period of time?

A

they swell and lyse

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44
Q

when do decreases in body fluid osmolarity happen?

A
  • drinking excessive volumes of water that is taken faster than the kidneys can excrete it
  • renal function is compromised
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45
Q

what is water intoxication?

A

when water is consumed at a rate faster than the kidneys can excrete it

  • body is flooded with water
  • water intake greater than 15mL/min
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46
Q

what does water intoxication lead to?

A

swelling of body cells, including neurons

  • leads to confusion, coma, and eventually death
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47
Q

how do you treat water intoxication?

A

intravenous rehydration with low concentrations of NaCl salt

(IV drip)

  • kidneys can slowly reabsorb the solutes
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48
Q

Why do solutions used for oral rehydration therapy contain a small amount of table salt (NaCl)?

A

both the salt and water are absorbed in the digestive canal, blood volume increases without a decrease in osmolarity, and water intoxication does not occur.

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49
Q

why do we need electrolytes?

A
  1. maintain osmolarity of body fluids
  2. maintain acid-base balance required for cellular activities
  3. carry electrical current for graded and action potentials
  4. act as cofactors for enzyme catalysis
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50
Q

what is a milliequivalent per litre?

A

charge in one mole of an ion

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51
Q

what electrolytes are abundant in ECF?

A
  • Na+
  • Cl-
  • Ca2+
  • HCO3-
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52
Q

what electrolyes are abundant in ICF?

A
  • K+
  • Mg 2+
  • HPO4 2-
  • SO4 2-
  • protein anions
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53
Q

what is responsible for the blood colloid osmotic pressure exerted by blood plasma?

A

the difference in concentration of protein anions between blood plasma and interstitial fluid

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54
Q

why are there fewer protein anions found in interstitial fluid compared to blood plasma?

A

normal capillary membranes are impermeable to proteins, so only a few plasma proteins leak out of blood vessels into the interstitial fluid

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55
Q

why do Na+ and Cl- move in same direction?

A

they are counterions

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56
Q

what kinds of processes require Na+?

A
  • depolarization of neurons and special sensory structures, like photoreceptors
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57
Q

why is dietary intake of Na+ usually higher than required?

A

because it comprises 90% of cations in ECF and processes that require it are important for normal functioning

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58
Q

level of Na+ during hyponatremia

A

less than 136mEq/L of Na+

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59
Q

level of Na+ during hypernatremia

A

greater than 148 mEq/L

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60
Q

why may hypernatremia occur?

A
  • excess Na+ intake
  • renal dysfunction
  • hyperaldosteronism, which promotes Na+ reabsorption
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61
Q

what occurs during hypernatremia?

A
  • blood osmolarity increases
  • blood volume increases
  • blood pressure increases
  • filtration to tissues increases
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62
Q

what is fluid accumulation in the tissues called?

A

edema

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63
Q

what happens during hyponatremia?

A
  • blood osmolarity decreases
  • excessive water loss
  • hypovolemia
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64
Q

what is hypovolemia?

A

abnormally low volume of blood

65
Q

what can cause hyponatremia?

A
  • aldosterone deficiency
  • diuretic drug overuse
66
Q

what are the consequences of hyponatremia?

A

if neurons are in a hypotonic environment, they will swell and their structure and function changes

  • problems with carrying out nerve impulses, loss of neurological function, confusion
67
Q

why does Cl- move freely between ECF and ICF?

A

plasma membranes contain abundant Cl- leak channels

68
Q

why do plasma membranes contain abundant Cl- leak channels?

A
  • chloride shift helps balance levels of other anions
  • Cl is a component of gastric acid
69
Q

what hormone regulates Cl- excretion

A

ADH

70
Q

why do hormones that affect Na+ also affect Cl-?

A

they are counterions

71
Q

what are counterions?

A

ions that mimic each other’s behaviour when they’re moving in solution

72
Q

what is the most abundant cation in ICF?

A

potassium (K+)

73
Q

what processes require K+

A
  • repolarization of neurons
  • depolarization of hair cells and vestibular structures
74
Q

why is K+ required for acid-base balance?

A

it is often exchanged for H+ by the body

75
Q

what hormone stimulates principal cells to secrete excess K+

A

Aldosterone

76
Q

what is hyperkalemia?

A

abnormally high blood K+

77
Q

why may hyperkalemia be fatal?

A

atrial fibrillation: hyperkalemia interferes with the ability of cardiac muscle cells to depolarize and repolarize at the appropriate times

78
Q

what is the second most abundant anion in the ECF?

A

bicarbonate (HCO3-)

79
Q

why is there a greater [HCO3-] in tissues but decreased [HCO3-] in the pulmonary capillaries?

A

to facilitate CO2’s movement into alveoli for exhalation by respiratory system

80
Q

what is bicarbonate’s role in acid-base balance?

A

it is a blood buffer

81
Q

what do intercalated cells of renal tubule do to HCO3-?

A

if in excess: they can excrete excess HCO3- into urine

if deficient: can form HCO3- when blood levels are low

82
Q

what is the most abundant mineral in the body?

A

calcium (Ca2+)

83
Q

what are some roles Ca2+ has in the body?

A
  • mineralizes bone tissue ECM
  • required for blood clotting
  • required for exocytosis of neurosecretory vesicles and release of NTs
  • maintains muscle tone
  • excites nervous and muscle tissue
84
Q

what endocrine hormone increases bone resorption?

A

PTH: stimulates osteoclasts to break down more bone

85
Q

how does PTH regulate Ca2+ blood levels?

A
  • increases osteoclast activity to increase bone resorption
  • stimulates increased calcium reabsorption by increases early DCT cells permeability to Ca2+
  • stimulates increased calcitriol production, increased dietary Ca2+ absorption in duodenum
86
Q

what are the functions of phosphate in the body?

A
  • part of mineralized bone ECM
  • covalently bound to important molecules (ATP, phospholipids, nucleic acids)
87
Q

what happens to HPO4 2- levels in blood when PTH releases Ca2+ into blood?

A

it decreases as it is released into urine

  • PTH decreases phosphate reabsorption and increases its excretion
88
Q

what hormone promotes absorption of dietary Ca2+ and HPO4 2-?

A

Calcitriol

89
Q

what is fibroblast growth factor?

A

local paracrine hormone
- increases phosphate excretion in urine
- decreases phosphate absorption in duodenum

90
Q

where is most magnesium found in?

A

in bone

91
Q

what are some of magnesium’s roles in the body?

A
  • cofactor for enzymes
  • required for synaptic transmission and myocardial function
  • production of PTH requires Mg2+
92
Q

what are cofactors?

A

inorganic molecules that assist with enzyme catalysis

93
Q

what can lead to increased excretion of Mg2+ into urine?

A
  • hypercalcemia
  • low PTH
  • acidosis
94
Q

who might be vulnerable to electrolyte imbalances?

A
  • elderly and infants cannot communicate their electrolyte needs or cannot understand/sense thirst
  • pregnant women
  • individuals in hot/cold climates
  • elite athletes
  • bed-ridden hospitalized patients
95
Q

what is homeostasis

A

dynamic state of keeping all bodily conditions within a tolerable range

96
Q

how does protein catabolism acidify blood?

A

catabolism of proteins leads to production of ammonia and excess H+

97
Q

what are the three systems that maintain pH of body fluids?

A
  1. buffer systems
  2. exhalation of CO2
  3. urinary excretion of H+
98
Q

how do buffer systems maintain bodily fluid pH?

A

bind excess H+ but do not remove it from body

99
Q

how does exhaling CO2 maintain bodily fluid pH?

A

reduces formation of H2CO3 by carbonic anhydrase to prevent blood acidification

100
Q

how does excreting H+ through urine maintain bodily fluid pH?

A

slowly but physically eliminates excess H+ from body

101
Q

what is the only mechanism that physically removes H+ from body?

A

urinary excretion of H+

102
Q

what is the most abundant intracellular and extracellular buffer in the body?

A

protein buffers

  • Hb
  • albumin
103
Q

what happens to amino acids when pH increases?

A

carboxyl group (-COOH) is ionized (-COO-), releasing H+ into solution

-OH and H+ form H2O, OH removed from solution

104
Q

what happens to amino acids when pH decreases

A

amino group (-NH2) can bind H+ (-NH3+), removing protons from solution

105
Q

what is the buffering function of hemoglobin?

A

deoxyhemoglobin can bind H+, turning into the reduced hemoglobin Hb-H

106
Q

what is the carbonic acid-bicarbonate buffer system?

A
  • CO2 accumulates in blood
  • CO2 + H2O → H2CO3 (by carbonic anhydrase)
  • H2CO3 dissociates
    H2CO3 → HCO3- + H+

HCO3- can recombine with H+ when in excess

107
Q

where does carbonic anhydrase perform the reaction:

H2CO3 → H2O + CO2

A

in the lungs, so that CO2 can be exhaled out

108
Q

what are the extracellular buffer systems?

A
  • carbonic acid-bicarbonate buffer system
  • phosphate buffer system
109
Q

what is the phosphate buffer system?

A

H2PO4 - can act as a weak acid and bind to OH to decrease pH

HPO4 2- can act as weak base and bind H+ to increase pH

110
Q

in what pH does the reaction occur?

OH+ + H2PO4- → H2O + HPO4 2-

A

alkaline solution, where there is an excess of OH+

111
Q

in what pH does the reaction occur?

H+ + HPO4 2- → H2PO4 -

A

in acidic solutions, where there is an excess of H+

112
Q

how do rate and depth of breathing affect blood pH?

A

they affect [CO2] in blood

113
Q

what is the stimulus for the negative feedback loop of the exhalation of CO2?

A

increase in [H+] and decrease in blood pH

114
Q

what are the receptors for the negative feedback loop of the exhalation of CO2?

A
  1. central chemoreceptors in MO
  2. peripheral chemoreceptors in aortic + carotid bodies
115
Q

what is the control centre for the negative feedback loop of the exhalation of CO2?

A

Dorsal Respiratory Group in the MO

116
Q

what are the effectors for the negative feedback loop of the exhalation of CO2?

A

diaphragm contracts more forcefully and frequently so more CO2 is exhaled

117
Q

what is the net physiological response for the negative feedback loop of the exhalation of CO2?

A

blood pH increases, [H+] decreases

118
Q

how are acids produced by metabolic reactions other than H2CO3 dealt with?

A

they are dealt with kidneys’ intercalated cells, which transport protons into tubular lumen

119
Q

what proteins found on intercalated cells transport protons into tubular lumen?

A
  1. proton pumps (H+-ATPases)
  2. Cl-HCO3- antiporters
120
Q

what do Cl-HCO3- antiporters on basolateral membranes do?

A

move Cl- into intercalated cells, move HCO3- out of tubules and into peritubular capillaries

121
Q

what do H+-ATPases on apical membranes do?

A

pump H+ into tubular lumen

(H+ + NH3 → NH4+)
(H+ + HPO4 2- → H2PO4-)

122
Q

what do H+-ATPases on basolateral membranes do?

A

reabsorb H+ by pumping H+ into interstitial fluid to be reabsorbed by vasa recta

123
Q

what do Cl-HCO3- antiporters on apical membranes do?

A

excrete excess HCO3- :

move Cl- out intercalated cells, move HCO3- into tubules

124
Q

why are NH4+ and H2PO4- not reabsorbed by cells of collecting ducts?

A

they are impermeable to these ions

125
Q

below what pH constitutes acidosis?

A

pH 7.35

126
Q

what is a major consequence of acidosis?

A

inhibition of synaptic transmission in CNS

  • acidic pH interferes w/ proteins on membranes so signals can’t travel properly
  • can lead to confusion, coma, death
127
Q

above what pH constitutes alkalosis?

A

pH 7.45

128
Q

what is a major consequence of alkalosis?

A
  • hyperexcitability of neurons in CNS and PNS
  • anxiety, muscle spasms, convulsions, and death
129
Q

what are the two types of acidosis/alkalosis?

A

respiratory and metabolic

130
Q

what are respiratory acid-base imbalances?

A

imbalances resulting from changes in partial pressure of CO2 in blood

(outside 35-45 mmHg)

131
Q

what are metabolic acid-base imbalances?

A

imbalances resulting from changes to [HCO3-] in blood

  • outside 22-26mEq/L
132
Q

what is respiratory acidosis?

A

the decrease in blood pH when partial pressure of CO2 in systemic blood is greater than 45mmHg because of increased H2CO3 formation

133
Q

what does respiratory acidosis result from?

A

any disorder or condition that decreases respiratory rate (e.g. obstructive disorders)

134
Q

what is the treatment for respiratory acidosis?

A

ventilation therapy, intravenous HCO3-

135
Q

what is respiratory alkalosis?

A

increase in blood pH when the partial pressure of CO2 is less than 35mmHg

136
Q

what is respiratory alkalosis caused by?

A
  • hyperventilation in response to stress
  • high altitude
  • cerebrovascular accident/stroke
  • disease
137
Q

what is the treatment for respiratory alkalosis?

A

breathing into a paper bag increases delivery of CO2 back into blood

  • you trap CO2 inside bag, inhaling it increases partial pressure of CO2 inside body
138
Q

what is compensation?

A

body’s response to being outside of homeostatic conditions and attempt to restore homeostasis

139
Q

how would you expect the kidneys to compensate during respiratory acidosis?

A

they increase H+ excretion and HCO3- reabsorption

140
Q

how would you expect the kidneys to compensate during respiratory alkalosis?

A

they decrease HCO3- reabsorption and increase H+ reabsorption

141
Q

what is metabolic acidosis?

A

the decrease in pH when [HCO3-] is less than 22 mEq/L

142
Q

what is metabolic alkalosis?

A

the increase in pH when [HCO3-] is greater than 26 mEq/L

143
Q

what causes metabolic acidosis?

A

severe diarrhea (losing large volumes of bodily fluid), renal dysfunction, or ketosis

144
Q

what causes metabolic alkalosis?

A
  • excessive vomiting and loss of gastric HCl
  • endocrine disorders
  • excessive use of antacids
  • severe dehydration
145
Q

how do you compensate for metabolic acidosis?

A

hyperventilation restores normal blood pH by increasing loss of CO2

146
Q

how do you compensate for metabolic alkalosis?

A

hypoventilation, slows loss of CO2

147
Q

how is metabolic alkalosis treated?

A

administration of fluids containing electrolytes and correcting initial cause

  • move H+ back from urine into blood
148
Q

what is ketosis?

A

accumulation of ketone bodies in blood by excessive production of them during ketogenesis

149
Q

what is ketogenesis?

A

production of ketone bodies during metabolic processes to generate ATP

  • beta oxidation of triglycerides
150
Q

how can ketogenesis be induced?

A

severely limiting carbohydrate intake

151
Q

what is ketoacidosis?

A

blood pH lower than 7.35 due to presence of ketone bodies

152
Q

what are some examples of ketone bodies?

A
  • acetone
  • acetoacetic acid
  • beta-hydroxybutyric acid
153
Q

what is beta oxidation of fatty acids?

A

catabolizing fatty acids by oxidizing them to form Acetyl CoA in mitochondria

154
Q

what organs undergo the compensatory mechanism for respiratory acid-base imbalances?

A

kidneys

155
Q

what allows for continual exchange of water and solutes among body fluid compartments?

A

processes of osmosis, diffusion, filtration, and reabsorption

156
Q

Robin was in the early stages of pregnancy and has been vomiting excessively for several days. She became weak, was confused, and was taken to the emergency room. What do you suspect has happened to Robin’s acid–base balance? How would her body attempt to compensate? What electrolytes would be affected by her vomiting, and how do her symptoms reflect those imbalances?

A

The loss of stomach acids can result in metabolic alkalosis. Robin’s HCO3− levels would be higher than normal. She would be hypoventilating in order to decrease her pH by slowing the loss of CO2. Excessive vomiting can result in hyponatremia, hypokalemia, and hypochloremia. Both hyponatremia and hypokalemia can cause mental confusion.

157
Q

Henry is in the intensive care unit because he suffered a severe myocardial infarction three days ago. The lab reports the following values from an arterial blood sample: pH 7.30, HCO3− = 20 mEq/liter, PCO2 = 32 mmHg. Diagnose Henry’s acid–base status and decide whether compensation is occurring.

A

(Step 1) pH = 7.30 indicates slight acidosis, which could be caused by elevated PCO2 or lowered HCO3−. (Step 2) The HCO3− is lower than normal (20 mEq/liter), so (Step 3) the cause is metabolic. (Step 4) The PCO2 is lower than normal (32 mmHg), so hyperventilation is providing some compensation. Diagnosis: Henry has partially compensated metabolic acidosis. A possible cause is kidney damage that resulted from interruption of blood flow during the heart attack.

158
Q

This summer, Sam is training for a marathon by running 10 miles a day. Describe changes in his fluid balance as he trains.

A

Sam will experience increased fluid loss through increased evaporation from the skin and water vapor from the respiratory system through his increased respiratory rate. His insensible water loss will also increase (loss of water from mucous membranes of the mouth and respiratory system). Sam will have a decrease in urine formation.

A-BIOL 1191 LECTURE (12 decks)

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