Fluid and Electrolyte Balance Flashcards
(139 cards)
1
Q
The body is in a state of ______ flux
A
constant
2
Q
how much fluid and ions do we ingest
A
- ingest ~2L of fluid containing 6-15g of NaCl
- take in varying amounts of other ions
3
Q
Mass Balance
A
- whatever comes in must be excreted if not needed
- kidneys main route
4
Q
How else can fluid be excreted?
A
- small amounts lost in feces and sweat
- lungs lose water and help remove H+ and HCO3- by excreting CO2
5
Q
H2O and Na+ Homeostasis
A
- determine ECF volume and osmolarity
6
Q
K+ Homeostasis
A
- K+ balance can because problems with cardiac and muscle function
7
Q
Ca2+ Homeostasis
A
- is involved in many processes in the body
8
Q
H+ and HCO3- Homeostasis
A
- determines body pH
9
Q
ECF Osmolarity Affects ____
A
cell volume
10
Q
Cells in Hypotonic Solution
A
- lysed
- cell would burst
- more water outside, so water moves into cell
11
Q
Cells in Isotonic Solution
A
- normal
12
Q
Cells in Hypertonic Solution
A
- shrinks
- less water outside cell, so water moves out
13
Q
Independent Mechanisms to Maintain Cell Volume
A
- renal tubule cells are constantly exposed to hypersonic ECF and produce organic solutes such as sugar alcohols and amino acids to match their intracellular osmolarity to ECF
- some cells use changes in cell volume to initiate cellular responses, liver cells beginning protein and glycogen synthesis (swell)
14
Q
Fluid and Electrolyte balance is an _______ process involving…
A
- integrative process
- involves the respiratory, cardiovascular and renal system, also behavioural responses
15
Q
CV and Renal Systems are under _____ control
A
- under neural control
- quite rapid
16
Q
Renal responses occur ___ ____ because…
A
- occur more slowly
- because kidneys are primarily under endocrine and neuroendocrine control
17
Q
T/F: no overlap between processes.
A
FALSE
18
Q
Water Balance
A
- water intake must match excretion
- normal conditions: water loss in urine (regulated mechanism)
- other mechanisms become significant conditions like excessive sweating, diarrhea (drop in blood pressure, increase osmolarity)
19
Q
Kidneys can ____ excess fluid or ____ what is in the body , but ____ replace what is lost to the environment
A
- remove
- conserve
- cannot
20
Q
Volume Gain in Kidneys
A
- will be offset with increase loss
21
Q
Volume Loss in Kidneys
A
- results in reduced flow through the “handle”
- v. loss is reduced in urine
- reabsorption is regulated and can be increased
- v. loss must be replaced through behavioural mechanisms to maintain homeostasis
22
Q
What does the renal medulla create?
A
- concentrated urine
23
Q
How do you measure how much water is secreted by the kidneys?
A
- the concentration or osmolarity of urine
24
Q
Removal of Excess Water Required
A
- kidneys produce large volume of dilute urine
- osmolarity as low as 50 mOsM
25
Diuresis
- removal of excess urine
| - high concentration of diluted urine
26
Need to Conserve Water
- low volume of concentrated urine is produced
| - up to 1200 mOsM
27
How do the kidneys control urine concentration?
- control urine concentration by varying the amounts of water and Na+ reabsorbed in the distal nephron
- distal tubule and collecting duct
28
How to produce Dilute Urine
- the distal nephron must reabsorb solute without allowing water to follow by osmosis
29
How to produce Concentrated Urine
- the distal nephron must reabsorb water and little solute
30
Vasopressin
- control water reabsorption
- AVP
- posterior pituitary hormone
- antidiuretic hormone (ADH)
31
How do the Distal Tubule and Collecting Duct alter permeability to water?
- by adding or removing water pores in the apical membrane under the direction of the posterior pituitary hormone vasopressin (AVP), aka antidiuretic hormone (ADH)
32
Maximal Vasopressin
- collecting duct is freely permeable to water
- water leaves by osmosis and is carried away by the vasa recta capillaries
- urine is concentrated
33
Absence of Vasopressin
- the collecting duct is impermeable to water
| - urine is dilute
34
Vasopressin Receptor
- V2 Receptor
35
Insertion of AQP2
- graded
- depends on the amount of AVP present
- AVP induced AQP2 insertion
- insertion is all or none
36
AQP2 Insertion Process
1. vasopressin binds to the membrane receptor
2. receptor activates cAMP second messenger system
3. cell inserts AQP2 water pores into apical membrane
4. water is absorbed by osmosis into the blood
37
What activates Osmoreceptors
- blood volume, pressure, and osmolarity
38
What is the most potent stimulus of AVP secretion?
- increased osmolarity
39
AVP secretion also shows _____ _____ (____ at night)
- circadian rhythm
| - increase at night
40
Osmolarity Greater than 280 mOsM
1. hypothalamic osmoreceptors
2. interneurons to hypothalamus
3. hypothalamic that synthesize vasopressin
4. vasopressin (released from posterior pituitary)
5. collecting duct epithelium
6. insertion of water pores in apical membrane
7. increased water reabsorption to conserve water
41
Magnocellular Neurosecretory Cells (MNC's)
- produce and release AVP
42
AVP Production and Secretion
- osmolarity is monitored by osmoreceptor neurons
- stretch sensitive neurons that increase firing rate as osmolarity increases (shrink)
- signal to the MNC's, AP's fire in MNC's causing release of AVP vesicles
- baro and atrial receptors also signal to MNC's
43
Process of AVP Production/Secretion
1. AVP is made and packaged in cell body of neuron
2. vesicles are transported down the cell
3. vesicles containing AVP are stored in posterior pituitary
4. AVP is released into blood
44
Loop of Henle
- countercurrent multiplier
45
AVP is important for water _____ out of the _____.
1. reabsorption
| 2. nephron
46
What is necessary to create the concentration gradient for osmotic movement of water out of the collecting duct?
- high osmolarity within the medullary insterstitium
47
What creates the hyperosmotic interstitium
1. Countercurrent Exchange System
| 2. Urea
48
Countercurrent Exchange System
- evolved in mammal and birds to reduce heat loss from flippers, tails, wings that are poorly insulated and have a high surface-area-to volume ratio
- allows warm blood entering limb to transfer heat directly to blood flowing back into body
- kidneys transfer WATER and SOLUTES instead of heat
49
Urea
- contributes to hyperosmotic interstitium
50
Two Components of the Countercurrent Exchange System
1. Countercurrent Multiplier (loop of henle)
| 2. Countercurrent Exchanger (peritubular capillaries)
51
What structures are responsible for high osmolarity deep in the medulla?
- the nephrons and vasa recta of juxtamedullary nephrons that extend deep into the medulla
52
Countercurrent Multiplier
- the descending limb of the loop of Henle
| - the ascending limb of the loop of of Henle
53
The Descending Limb of the Loop of Henle
- allows water to follow its osmotic gradient into the increasingly hypertonic interstitial
- doesn't allow solutes to be transported
54
The Ascending Limb of the Loop of Henle
- actively transports solutes (Na+, Cl-, K+) into the interstitium
- selective reabsorption of solutes
55
Active Transport in Loop of Henle
- majority of reabsorption happens in proximal tubule
| - NKCC2 transporter uses energy stored to move Na+, K+, 2Cl- into epithelial cells
56
About ____% of Na+ and K+ _____ occurs in the _____ limb of the loop of henle
1. 25%
2. reabsorption
3. ascending
57
NKCC2 Transporter
- on apical membrane
- uses energy stored in Na+ concentration gradient to move solutes into epithelial cell
- target of loop diuretic drugs for treatments of hypertension and edema (prevents generation of hyper osmotic medulla)
58
Na+ is _____ transported _____ concentration gradient on _______ membrane.
1. actively
2. against
3. basolateral
59
Vasa Recta
- removes water
| - picks up some solute and loses some water
60
Why doesn't water entering interstitium via descending limb dilute the hypertonic medulla?
- the opposite direction loop of vase recta
| - creates a gradient allowing much of the water transported from the descending limb to move into vasa recta
61
Main job of the Multiplier
- create the hypertonic interstitium
62
Main job of the Exchanger
- prevent the washout (dilution) of the hypertonic interstitium
63
Urea Contribution Countercurrent Exchange System
- contributes to the osmolarity of the medullary interstitium
64
The high solute concentration in the medulla is only partly due to _____
NaCl
65
About _____ the solute in the medulla interstitium is _____.
1. half
| 2. urea
66
a ____ amount of urea is _______ in the distal portion of the nephron and create a ______ loop.
1. large
2. reabsorbed
3. recycling
67
Water Balance Depends on:
1. hyperosmotic medullary interstitium
| 2. AVP mediated insertion of water pores in collecting duct (AQP2)
68
Na+ is distributed _____ between ____ and _____ fluid thus representing our eCF [Na+]
1. freely
2. plasma
3. interstitial
69
Normal Plasma Na+ concentration
135-145 mOsM/L
70
Affect of adding NaCl and no water
- increase total body osmolarity from 300-307 mOsM
| - would draw water from cells disrupting normal function
71
Our ______ mechanisms maintain mass balance
- homeostatic
72
Homeostatic Responses to Salt Ingestion
- anything extra that enters the body is secreted
- kidneys are responsible for most Na+ excretion
- only Na+ absorption is regulated
- Cl- tends to follow through the electrochemical gradient set up by Na+ movement or co-transported with Na+
73
Aldosterone
- helps control Na+ balance
- steroid hormone
- responsible for altering Na+ reabsorption and K+ excretion
74
Renin-Angiotensin-Aldosterone System
- a complicated endocrine pathway
- where the regulation of blood Na+ levels take place
- aldosterone control Na+ balance
- targets the last third of the distal tubule and the portion of the collecting duct located in the cortex of the kidney
75
Aldosterone acts on ______ cells.
principal cells
76
Early response phase to aldosterone binding
- aldosterone binding receptor apical Na+ and K+ channels increase their open time through an unknown mechanism
77
On apical membrane
- Na+ = ENaCs
| - K+ = ROMK (renal outer medulla K)
78
Cytoplasmic Aldosterone Receptor
- mineralocorticoid receptor
79
Aldosterone binds to what in where?
- binds to cytoplasmic mineralocorticoid receptor in P cells
80
What does aldosterone binding do?
1. increases opening of apical Na+ and possible K+ channels enhancing Na+ reabsorption and K+ excretion
2. hormone ligand complex translocate into the cell nucleus
81
Increased Na+ entry to cell does what?
- speeds up basolateral Na-K pump leading to increased Na+ reabsorption
82
Increase Na-K pump
- increases intracellular K+ leading to increased K+ secretion
83
Hormone Ligand Complex
- translocate into the cell nucleus
- binds to hormone response elements that increase transcription of apical Na+ channels
- basolateral Na/K+ pumps and possibly apical K+ channels further enhancing Na+ reabsorption and K+ excretion
84
What Triggers Aldosterone Secretion
- K+ acts directly on the adrenal cortex protecting the body from hyperkalemia
- decreased blood pressure**
85
Decreased Blood Pressure and Aldosterone Secretion
- controls aldosterone secretion initiating a pathway that results in the production of angiotensin II which triggers aldosterone release
86
2 Additional Modifiers of Aldosterone Release
1. increased osmolarity acts directly on the adrenal cortex during dehydration to inhibit release
2. abnormally large drops in plasma Na+ can directly stimulate aldosterone secretion
87
Renin-Angiotensin-System (RAS)
- a multi-step pathway for maintaining blood pressure
88
RAS Process
1. begins with Renin Secretion
2. Renin converts angiotensinogen into angiotensin I
3. angiotensin I is then converted to angiotensin II
4. ANGII travel to adrenal cortex and stimulates production of aldosterone
89
3 Stimuli for Renin Secretion
1. low blood pressure in renal arterioles causes granular cells to secrete renin
2. sympathetic neurons activated by CVCC when blood pressure decreases terminate on granular cells and stimulate renin secretion
3. paracrine feedback (prostaglandins) from macula densa cells signal to the granular cells to secrete renin
90
Granular cells are also known as...
- Juxtaglomerular cells (JG cells)
91
Macula Densa Cells
- sense distal tubule flow and release paracrines that affect afferent arteriole diameter
92
Granular Cells Job
- secrete renin
93
Renin
- an enzyme
- involved in salt and water balance
- main role: convert inactive plasma protein angiotensinogen into angiotensin I
94
Angiotensin Converting Enzyme (ACE)
- an enzyme
- produced in blood vessel endothelium ( especially in the lungs)
- converts Angiotensin I to Angiotensin II
95
Effects of ANGII
1. increases vasopressin secretion (ANG receptors in hypothalamus initiate this reflex)
2. stimulates thirst
3. one of the most potent vasoconstrictors in the body
4. ANGII receptors activated in CVCC increase sympathetic output to heart and blood vessels
5. increases proximal tubule Na+ reabsorption (stimulate an apical Na+/H+ exchanger)
- all help to restore blood pressure
96
ACE Inhibitors
- used as a treatment of hypertension
| - prevents conversion of ANGI to ANGII leads to relaxation of the vasculature and lower blood pressure
97
Other Inhibitors
- AT2 receptor antagonists
| - renin inhibitors
98
Atrial Natriuretic Peptide (ANP)
- promotes Na+ and water excretion
- peptide hormone produced and secreted by specialize myocardial cells primarily in the atria of the heart
- increased blood volume causes stretch of atria causing ANP release
99
Natriuresis
- loss of Na+
100
Branin Natriuretic Peptide (BNP)
- a second type of natriuretic peptide produced in ventricles and in some neurons in the brain
101
ANP Receptor
- an enzymatic membrane bound receptor acting through cGMP second messenger system
102
ANP Jobs
1. increased blood volume stretches atrial wall during filling
2. atrial myocytes release ANP in response to stretch
103
ANP in Kidneys
- relaxes afferent arterioles (increases GFR)
- reduces renin release from granular cells (reduces aldosterone)
- reduces Na+ reabsorption at the collecting duct
104
ANP in Hypothalamus
- reduces AVP release
105
ANP in Adrenal Cortex
- inhibits aldosterone release
106
ANP in Medulla
- acts on the CVCC to decrease blood pressure
107
Potassium Balance
- aldosterone also plays critical role in K+ homeostatic (enhances excretion
108
Plasma K+
- needs to be maintained within a narrow range (3.5-5mM)
| - alterations in body K+ levels affects the resting membrane potential of all cells
109
Hyperkalemia
- depolarizes cells
- more dangerous
- initially leads to hyperexcitability
- eventually cells are unable to depolarize and become less excitable
- can lead to life threatening arrhythmias in the heart
110
Hypokalemia
- hyper polarizes cells
- can't reach threshold
- causes muscle weakness because its more difficult to fire AP's (failure of respiratory and cardiac muscles)
111
Disturbances in K+ Balance
- results from kidney disfunction
- eating disorders
- loss of K+ in diarrhea or use of diuretics that prevent kidneys from properly absorbing K+
112
Behavioural Responses
- critical in restoring the normal state, particularly when ECF volume decreases or osmolarity increases
113
Drinking Water
- normally the way to replace lost water
- relieves thirst, doesn't actually need to be absorbed
- unknown receptors in mouth/pharynx respond to water by decreasing thirst and decreasing VP release
114
Behavioural Responses
- critical in restoring the normal state
| - particularly when ECF volume decreases or osmolarity increases
115
Avoidance Behaviours
- helps prevent dehydration
116
Control of Volume and Osmolarity
- CV and Renal systems
- can be kept within narrow range
- can change independently to cause diff. scenarios
117
Increase volume, Increase osmolarity
- when eating salty foods and drinking liquids at same time
- net results = ingestion of hypertonic saline (salt > water)
- need to excrete solute and liquid to match what was taken in
118
Increase volume, no change in osmolarity
- salt and water ingested is equivalent to isotonic solution
119
Increase volume, Decrease osmolarity
- simply drinking pure water without ingesting solute
- kidneys can't excrete pure water
- some solute would be lost
- compensation is imperfect
120
no change in volume, Increase osmolarity
- eating salty foods without drinking water
- increases ECF osmolarity shifting water from cells to ECF
- triggers intense thirst and kidneys make concentrated urine
121
no change in volume, Decrease osmolarity
- water and solutes would be lost in sweat
- only water is replaced
- can lead to hypoklemia or hyponatremia
- sports drinks help
122
Decrease volume, Increase osmolarity
- dehydration could be due to heavy exercise
- water loss from lungs can double, sweat loss, or diarrhea
- result in inadequate perfusion (decrease blood volume) and cell dysfunction
- increase water intake
123
Decrease volume, no change osmolarity
- hemorrhage
| - need blood transfusion or ingestion of isotonic solution
124
Decrease volume, Decrease osmolarity
- may result from incomplete compensation for dehydration but is uncommon
125
Direct Effects of Decreased Blood Pressure/Volume
- granular cells (renin secretion)
| - glomerulus (decreased GFR)
126
Reflexes of Decreased Blood Pressure/Volume
1. carotid and aortic baroreceptors (CVCC; increased sympathetic output, decreased parasympathetic output)
2. carotid and aortic baroreceptors (thirst stimulation)
3. carotid and aortic baroreceptors (vasopressin secretion)
4. Atrial volume receptors (thirst stimulation)
5. Atrial volume receptors (vasopressin secretion)
127
Direct Effects of Increased Blood Pressure
- glomerulus (increased GFR - transient)
| - myocardial cells (natruieuretic peptide secretion)
128
Reflexes of of Increased Blood Pressure
1. carotid and aortic baroreceptors (CVCC; decreased sympathetic output, increased parasympathetic output)
2. carotid and aortic baroreceptors (thirst inhibition)
3. carotid and aortic baroreceptors (vasopressin inhibition)
4. Atrial volume receptors (thirst inhibition)
5. Atrial volume receptors (vasopressin inhibition)
129
Direct Effects of Increased Osmolarity
- pathological hyponatremia --> adrenal cortex --> decreased aldosterone secretion
130
Reflexes of Increased Osmolarity
1. osmoreceptors (hypothalamus; thirst stimulation)
| 2. osmoreceptors (hypothalamus; vasopressin secretion)
131
Direct Effects of Decreased Osmolarity
- pathological hyponatremia --> adrenal cortex --> increased aldosterone secretion
132
Reflexes of Increased Osmolarity
1. osmoreceptors (hypothalamus; decreased vasopressin secretion)
133
Severe Dehydration
- results in a loss of ECF volume, decrease in blood pressure and increase in osmolarity
134
Compensatory Mechanisms that Restore the 3 Factors
1. conserving fluid to prevent additional loss
2. trigger CV reflexes to increase blood pressure
3. stimulate thirst so normal fluid volume and osmolarity can be restored
135
4 Compensatory Mechanisms with Redundant Overlap Overcome the Symptoms of Dehydration
1. Cardiovascular mechanisms
2. Renin-angiotensin system
3. Renal mechanisms
4. Hypothalamic mechanisms
136
During Severe Dehydration
- decreased ECF volume (blood pressure) would signal to increase aldosterone release but at same time an increased osmolarity inhibits aldosterone release
- osmolarity control wins
137
Aldosterone Release during Severe Dehydration
- would because Na+ reabsorption which would worsen the already high osmolarity
138
Homeostatic Compensation for Severe Dehydration Process
1. Carotid and aortic baroreceptors signal CVCC
2. decreased blood pressure directly decreases GFR
3. paracrine feedback at macula densa cells causes granular cells to release renin
4. Granular cells respond to decreased blood pressure by releasing renin
5. Decreased blood pressure, volume, increased osmolarity, and increased ANGII all stimulate vasopressin and the thirst centers of the hypothalamus
139
Compensation Process Results in:
1. Rapid attempt by the CVCC to maintain blood pressure (depending on volume loss CVCC response may not completely
restore pressure)
2. Restoration of volume by water conservation and fluid intake
3. Restoration of normal osmolarity by decreased Na+ reabsorption and increased water reabsorption and intake
