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411 > Week 9 Electrolyte Distribution > Flashcards

Week 9 Electrolyte Distribution Flashcards

1
Q

What is the ECF compartment subdivided into ?

A

Plasma

Interstitial fluid

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2
Q

What is equivalence ?

A

Amount of substance dissolved in a solution relative to its molecular weight and stoichiometry

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3
Q

What is osmolality ?

A

Number of solute particles per kg of H2O

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4
Q

What is the importance of osmolality in the body ?

A

Determines the direction of water flow between compartments

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5
Q

What are the most important solutes in extracellular fluids ?

A

Na+
Cl-
HCO3-

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6
Q

What is oncotic pressure ?

A

Pressure generated by large molecules and proteins

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7
Q

What is tonicity ?

A

The effect of a solution on the volume of the adjacent cell.

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8
Q

What percentage of body weight is water ?

A

60% in males

50% in females

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9
Q

What is the distribution of water between extra and intra cellular compartments ?

A

~1/3 ECF

~2/3 ICF

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10
Q

What is the distribution of water in the EC compartment between the plasma and interstitial fluid ?

A

~3/4 interstitial

~1/4 plasma

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11
Q

What determines hydrostatic pressure ?

A

Arterial/venous pressure
Length of capillary
Pre and post capillary sphincters

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12
Q

What determines oncotic pressure ?

A

Permeability of the membrane to protein molecules

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13
Q

What affects the movement of fluid across a membrane ?

A

SA
Permeability to water
Permeability to proteins

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14
Q

What should the response be to immediate large losses of ECF fluid ?

A

Fluid resuscitation with appropriate fluid

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15
Q

What is the response to sustained losses of ECF over time ?

A

Regulation through thirst and kidney

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16
Q

What is the response to immediate and sustained gains of ECF fluid ?

A

Kidney regulation

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17
Q

What is the response to immediate and sustained gains of ECF fluid in the absence of kidneys ?

A

Dialysis

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18
Q

Determinants of effective circulating volume

A 
Volume of ECF 
Volume of vascular space
BP 
Cardiac output
Intact sensors = baroreceptors
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19
Q

What percentage of cardiac output do the kidneys recieve ?

A

20%

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20
Q

What is a nephron ?

A

Functional unit of the kidneys

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21
Q

How many nephrons does each kidney have ?

A

~ 1 million

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22
Q

What is each nephron comprised of ?

A

Renal corpuscle (glomerulus + Bowman’s capsule) and its tubule

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23
Q

The nest of the glomerular capillary between the ______ and ______ _______ allows for precise regulation of the intraglomerular forces governing the GFR

A

Afferent, efferent arterioles

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24
Q

What is the first step in urine formation ?

A

Glomerular filtration

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25
Q

What is GFR the sum of?

A

Individual filtration rates of ~2 million glomeruli

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26
Q

What are podocyte foot processes linked by ?

A

Slit diaphragm

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27
Q

What is the glomerular filtration barrier ?

A

A size and charge selective sieve

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28
Q

What are the principle determinants of GFR ?

A

Starling forces
Glomerular capillary filtration coefficient
Glomerular plasma flow rate

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29
Q

How do Starling forces determine movement of fluid across glomerular capillaries ?

A

Movement occurs because of difference between trans capillary hydrostatic pressure (favours filtration) gradient and the trans capillary oncotic pressure (opposes filtration)

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30
Q

How is the glomerular capillary filtration coefficient determined ?

A

Hydraulic conductivity x SA

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31
Q

How does glomerular plasma flow (QA) effect GFR ?

A

Plasma flow increase —> increase GFR

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32
Q

What happens if glomerular capillary oncotic pressure increases ?

A

Decreases GFR

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33
Q

What is the minute to minute regulation of GFR is mostly by changes in what ?

A

PGC and QA

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34
Q

How are PGC and QA are controlled ?

A

By alterations in afferent and efferent arteriolar resistances

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35
Q

What happens to GFR and renal blood flow when afferent arteriole resistance increases ?

A

Both GFR and RBF decrease

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36
Q

What happens to GFR and renal blood flow as efferent arteriole resistance increases ?

A

GFR increases then decreases

RBF decrease

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37
Q

How does the kidney respond to changes in arterial blood pressure ?

A

Immediate vasoactive response

Mainly alters afferent arteriole resistance in direction that maintains GFR and RBF

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38
Q

What is the myotonic mechanism ?

A

Ability of arterial smooth muscle to contract (or relax) in response to increases (or decreases) in vascular wall tension
Prevents excessive increases in RBF and GFR when arterial pressure increases
Very rapid

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39
Q

Where does auto regulation occur and which part is most important ?

A

Preglomerular resistance vessels

Afferent arterioles

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40
Q

Describe tubuloglomerular feedback

A

Changes in [NaCl] at the end of the thick ascending limb of LOH affect afferent arteriolar resistance
Stabilizes the delivery of volume and solute to the distal nephron
Kidney uses JGA for this

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41
Q

What makes up the JG apparatus ?

A

JG cells

Macula densa

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42
Q

What do JG cells do ?

A

Secrete renin

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43
Q

What is the macula densa ?

A

Specialized cells at the end of thick ascending limb
Sends flow-related changes in NaCl delivery
Sends out vasoconstrictor signal (adenosine) that affects afferent arteriole tone

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44
Q

Describe TGF response to increase in arterial pressure (RBF)

A

Increase GFR —> increase tubular fluid flow rate —> increase Na and Cl delivery to macula densa —> increase vasoconstrictor signals —> increase afferent aretriolar constriction —> decreased RBF

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45
Q

When is TGF less sensitive ?

A

During volume expansion :
Allows for greater delivery of fluid and electrolytes to the distal nephron to allow for the correction of volume expansion

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46
Q

When is TGF more sensitive ?

A

During extracellular volume contraction: help conserve fluid and electrolytes

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47
Q

What mainly synthesizes and secretes renin ?

A

JG cells of AA

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48
Q

What is renin release stimulated by

A

Decreased effective circulating volume (decreased NaCl delivery at macula densa, decreased AA stretch) and increased SNS activity

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49
Q

Where is angiotensinogen synthesized ?

A

Proximal tubules

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50
Q

Where is ACE located ?

A

Proximal tubules

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51
Q

What is Ang II ?

A

A potent vasoconstrictor due to binding at the AT1 receptors especcialy affects the efferent arteriole

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52
Q

What does Ang II directly stimulate ?

A

Proximal tubular sodium absorption

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53
Q

Why does Ang II exert a greater vasoconstrictor on efferent arterioles than the afferent arterioles ?

A

Because vasodilatory prostaglandins dilate the afferent arteriole

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54
Q

What does decreased effective circulating volume and NSAID use often lead to ?

A

Acute kidney injury

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55
Q

Where is angiotensinogen mainly synthesized ?

A

The liver

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56
Q

Where is ACE mostly synthesized ?

A

Vascular endothelium in the lungs

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57
Q

What does Ang II stimulate the release of ?

A

Aldosterone from the adrenal glands
Salt hunger and thirst
—> increase ECF volume and increased arterial blood pressure

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58
Q

What is the effect of aldosterone ?

A

Increase sodium reabsorption by principle cells in distal nephron

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59
Q

What happens when effective circulating volume decreases and you take an ACE inhibitor or ARB ?

A

Acute kidney injury

Loss of Ang II mediated vasoconstriction results in dilation of efferent arteriole —> decreased GFR

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60
Q

What does mild activation of the SNS cause

A

Decreased sodium and water excretion due to renin release

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61
Q

What effect does mild to moderate activation of the SNS have on renal blood flow and GFR

A

Little effect

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62
Q

What happens with strong activation of the SNS ?

A

Constrict renal arterioles

Decrease renal blood flow and GFR

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63
Q

What is the effect if early diabetic nephropathy on GFR ?

A

Hyperfiltration —> increased GFR

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64
Q

Where does sodium intake come from ?

A

Ingested food and fluids

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65
Q

What is typical daily intake of NaCl

A

5-7 g

2-2.8 g Na (86-120 mmol) = output

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66
Q

How is the effective circulating fluid volume monitored/sensed?

A

Low pressure sensors in atria, ventricles and pulmonary circulation
High pressure sensors in arteries (aortic arch, carotid, renal arteries)
Others in CNS and hepatic circulation (not well characterized yet)

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67
Q

Where are low pressure sensors located

A

Areas of lower BP where changes in blood volume don’t cause large changes in BP.
Cardiac atria, right ventricle, pulmonary circulation

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68
Q

What stimulates low pressure sensors ?

A

Increasing pressure/stretch

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69
Q

What is the response when low pressure sensors are activated ?

A

Inhibition of ADH

Release of ANP and BNP

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70
Q

Net effect of low pressure sensor activation

A

Decrease ADH —> increase diuresis (more water excretion)
ANP and BNP —> increased natriuresis
—> shrink blood volume towards normal

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71
Q

What can higher levels of BNP be indicative of ?

A

Congestive heart failure

This test can help differentiate dyspnea from CHF from dyspnea caused by pulmonary problem (pneumonia)

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72
Q

Where are high pressure sensors located ?

A

Carotid artery, aortic arch, arterioles in the kidney

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73
Q

What stimulates high pressure sensors ?

A

Decrease in arterial pressure (more sensitive to pressure than volume)

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74
Q

What is the response when high pressure sensors are activated ?

A

Increase in SNS activity
Stimulation of ADH release
Activation of RAAS
Inhibition of ANP

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75
Q

What are the effects of increased SNS activity ?

A 
Increased HR and CO 
Increased vascular tone 
Decreased GFR 
Increased renin secretion 
Increased renal Na+ reabsorption 
Decreased renal Na+ excretion
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76
Q

What is the renal sensor for effective circulating fluid volume

A

JG apparatus

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77
Q

What happens in initial filtration of sodium by the nephron ?

A

NaCl is in solution and freely filtered across the glomerular basement membrane
[Na+] at start of proximal tubule = serum [Na+]

78
Q

What happens to sodium in the proximal tubule ?

A

Intracellular space is kept almost Na+ free by Na+ K+ ATPase pump
2/3 of filtered Na+ is reabsorbed here mostly via Na+H+ anti porter or Na+ glucose co-transporter, or Na+AA co-transporter

79
Q

What happens further down the proximal tubule ?

A

Cl- gradient established —> passive reabsorption of NaCl

—> water follows as osmoles leave the proximal tubule lumen

80
Q

What has been reabsorbed by the end of the proximal tubule ?

A

~60% if NaCl and ~60% of water reabsorbed

[Na+] is same as plasma

81
Q

What happens to sodium in the loop of Henle ?

A

Important site for reabsorption of ~25% of filtered sodium, but less water
POwered by basolateral Na+K+ ATPase
Na+ K+ 2Cl- symporter allows entry of 1 Na, 1K and 2Cl down the concentration gradient for NaCl

82
Q

What is the site of action for loop diuretics ?

A

NKCC2

83
Q

What happens in the early part of the distal tubule ?

A

NaCl is reabsorbed without any water

NaCl symporter is main channel

84
Q

Where do thiazide type dieuretics act ?

A

NCC symporter

Commonly used to treat hypertension

85
Q

What happens in the collecting duct/tubule

A

Principle cells carry out NaCl reabsorption via Na+ channel (ENaC)

86
Q

Where does aldosterone act ?

A

Collecting duct/tubule

Increase Na+ reabsorption in exchange for K+ excretion

87
Q

What is the overall effect of prostacyclin ?

A

Afferent arteriolar vasodilation and natriuresis

88
Q

How is prostaglandin formed and what signals this ?

A

Arachidonic acid is released from membrane phospholipids and is metabolized to PGs by cyclooxygenase (COX-1 and 2) in the presence of Na+ conserving and vasoconstricting stimuli

89
Q

What is the main prostaglandin in the kidney?

A

Prostacyclin (PGI2)

90
Q

What happens to prostacyclin in low ECFV states such as CHF or cirrhosis ?

A

PGI2 levels rise to maintain renal perfusion in the setting of high Ang II, SNS activity etc

91
Q

What do NSAIDS do when PGI2 levels are high ?

A

Remove counter regulation —> sodium retention, hypertension, lower GFR

92
Q

What does increasing SNS acitivity of renal sympathetic nerves lead to ?

A

Renin secretion

Increased Na+/H2O reabsorption

93
Q

What are the effects of ANP and BNP ?

A

Increase GFR and natriuresis

Antagonism of most RAAS actions

94
Q

What is uroguanylin ?

A

Produced in intestine in response to salt intake

Reduces renal sodium reabsorption

95
Q

What happens with increased effective circulating fluid volume ?

A 
Increase GFR
Decrease renin secretion 
Decrease aldosterone secretion 
Decrease Na+ reabsorption 
Increase Na+ and H2O excretion
96
Q

What is edema caused by ?

A

Sodium excess

Treat by causing a negative sodium balance

97
Q

What is the most common cause of death in the world ?

A

Volume depletion

98
Q

What does sodium regulation determine ?

A

ECF volume

99
Q

What does water regulation determine ?

A

Body osmolality

100
Q

What is the formula for tonicity ?

A

Tonicity = ECF solute + ICF solute / TBW = 2[Na] + 2[K] /TBW ~ 2[Na]/TBW

101
Q

How is the plasma osmolality estimated ?

A

2 x [Na+K]

Clinically 2x[Na]

102
Q

What are measured disorders of plasma osmolality primarily due to ?

A

Abnormalities in water handling not abnormal sodium handling

103
Q

What are the two ways that nephrons can be classified ?

A

Location within the cortex

Length of their loop of henle

104
Q

What are the primary 3 locations within the cortex ?

A

Superficial
Midcortical
Juxtamedullary

105
Q

Where does the short loop of henle turn into ?

A

Outer medulla or cortex

106
Q

Where does the long loop of Henle turn back into ?

A

Inner medulla

107
Q

Juxtamedullary nephrons have ____ loops

A

Long

108
Q

What are vasa recta ?

A

Major blood vessels that carry blood into and out of the renal medulla

109
Q

What are the two basic requirements for forming concentrated urine ?

A
  1. Hypertonic medullary interstitium
    - generates osmotic gradient necessary for water reabsorption
  2. High levels of ADH
    - increases water permeability of DCT and CD
110
Q

What are the major factors that contribute to excess buildup of solute ?

A
  1. Thick ascending limb of Loop of Henle
  2. Collecting ducts
  3. Passive Urea diffusion/recycling
  4. Diffusion of only a small amount of water from medullary tubules into interstitium
111
Q

How does the thick ascending limb of the loop of Henle contribute to excess buildup of solute ?

A

Active transport of Na+ ions out into the interstitium

Con transport of Cl- ions, K+ ions, and other ions into the interstitium

112
Q

How do the collecting ducts contribute to excess buildup of solute ?

A
  • active transport of ions out of the CD into the interstitium
113
Q

How does passive urea diffusion/recycling contribute to excess buildup of solute ?

A
  • from the inner medullary collecting ducts —> medullary interstitium —> loop of Henle
114
Q

Where in the kidney is ADH particularly active ?

A

Cortical collecting tubule
Inner medullary collecting tubule
Distal tubule

115
Q

Which limb is the concentrating limb ?

A

Descending limb

116
Q

Which limb is the diluting limb ?

A

Ascending limb

117
Q

What is impermeable to urea?

A

Thick ascending limb
Distal tubule
Cortical collecting duct

118
Q

Urea is ______ reabsorbed from the tubule

A

Passively

119
Q

What is urea recirculated between ?

A

CD and loop of Henle

120
Q

Where is the urea transport route ?

A

Along the paracellular route in proximal tubule

121
Q

Describe proximal tubule urea reabsorption

A

Na+ is reabsorbed with H2O following.
As H2O leaves tubule, urea is concentrated —> urea gradient across tubule
Urea passively diffuses down this gradient along the paracellular route

122
Q

Describe Urea transport in Loop and collecting duct

A

Tight junctions are tight
Urea is transported along transcellular route via facilitated diffusion (urea uniporter)
Urea levels in renal medulla are very high
-gradient favours secretion into loop
- gradient favours reabsorption from CT

123
Q

Renal handling of urea summary

A

Freely filtered
Reabsorbed from proximal tubule
Secreted into loop of Henle
Reabsorbed again from collecting duct

124
Q

How does the renal medullary blood flow help prevent dissipation of the hyperosmotic medullary interstitium ?

A

Medullary blood flow is low
- accounts for only 1-2% of renal blood flow
Vasa recta serve as countercurrent exchangers
-minimizes wash out of solutes from interstitium

125
Q

What makes the vasa recta highly permeable to solutes ?

A

Fenestrated endothelium

126
Q

What do vasa recta have channels for ?

A

Urea and water (aquaporins )

127
Q

What are the basic requirements for forming concentrated urine ?

A

Hypertonic medullary interstitium

High levels of ADH

128
Q

What two systems is plasma osmolarity regulated by ?

A

Osmoreceptor-ADH system

Thirst mechanism

129
Q

Where does water reabsorption happen ?

A

70% from proximal tubule
15% from descending limb of loop of Henle
0-15% from collecting duct depending on plasma ADH level

130
Q

How much fluid does the glomerulus filter per day from the plasma ?

A

180L

131
Q

Where is ADH synthesized

A

By specilized nuclei in the hypothalamus (magnocellular nuclei)

132
Q

What type of hormone is ADH ?

A

A preprohormone

133
Q

What is ADH released in response to ?

A
  1. Change in plasma osmolality
    - detected by osmoreceptors in the anterior hypothalamus
  2. Change in blood pressure or in the blood volume
    - detected by arterial baroreceptors and arterial stretch receptors
134
Q

Describe the osmotic stimuli for ADH release

A

Increase plasma osmolarity —> osmoreceptors shrink
—> AP —> SON and PVN —> tips of their axons in post pit —> influx of Ca2+ ions —> ADH release from secretory granules —> ADH is carried away in post pit capillaries —> systemic circulation —> ADH increases water permeability of kidney in late distal tubules, cortical collecting ducts and inner medullary collecting ducts
Signals from osmoreceptors induce thirst mechanism

135
Q

Describe the hemodynamic AVP release

A

Late responder
Insensitive (>10% change in volume/pressure)
Baroreceptors are the sensors

136
Q

What 3 receptors coupled to G proteins does ADH bind to ?

A

V1a
V1b
V2

137
Q

Where is the V1a receptor found and what does its activation lead to ?

A

Vascular smooth muscle

Increase intracellular Ca2+, resulting in contraction

138
Q

Where is the V1b receptor found and what does its activation lead to ?

A

Ant pit

Modulates ACTH release

139
Q

Where is the V2 receptor found and what does its activation lead to ?

A

Basolateral membrane of principle cells from the late distal tubule through the entire collecting duct
Coupled by Gs protein to cAMP —> insertion of water channels (aquaporins)

140
Q

Water reabsorption mechanism with ADH

A

ADH binds to membrane receptor
Receptor activates cAMP second messenger system
Cell inserts AQP2 water pores into apical membrane
Water is reabsorbed by osmosis into the blood

141
Q

In the abscense of ADH the collecting duct is ______ to water and the urine is ______

A

Impermeable, dilute

142
Q

What is the obligatory urine volume ?

A

Minimal volume of water needed to excrete ingested and waste produced osmoles

143
Q

Signs of hypoosmolality

A 
Edema 
Hypotension 
Fatigue 
Lethargy 
Anorexia 
Confusion 
Ataxia 
Seizures
144
Q

Hyper osmolarity signs

A 
Thirst 
Polyuria
Fatigue 
Hypotension 
Confusion 
Seizures
145
Q

When is renin secreted ?

A

Decreased BP
Decreased renal arterial pressure
Decreased NaCl at macula densa cells

146
Q

Effect of furosemide on ions

A

Hypokalemia
Metabolic alkalosis
Loss of Mg2+ and Ca2+ reabsorption

147
Q

Indications for furosemide

A

CHF
Acute pulmonary edema
Peripheral edema

148
Q

Adverse effects of loop diuretics

A 
Hyponatremia 
Hypovalemia 
Hypotension 
Hypokalemia 
Metabolic alkalosis 
Ototoxicity
149
Q

Mechanism of action of thiazide diuretics

A 
Block Na+/Cl- symporter at distal tubule 
- increase Na+ secretion 
-decrease blood volume 
—> prevents maximal dilution of urine 
Dilation of arterioles 
- decrease BP
150
Q

Clinical use for thiazide diuretics (hydrochlorothiazide)

A

Hypertension

Edema

151
Q

Main adverse effects of thiazide diuretics

A

Hyponatremia
Hypokalemia
Metabolic acidosis

152
Q

Mechanism of K+ sparing diuretics

A

Interfere with reabsorption of Na+ and secretions of K+/H+ at the cortical collecting tubule

153
Q

Clinical use of spironolactone, amiloride

A

Edema
Heart failure
Primary hyperaldosteronism

154
Q

Main adverse effects of K+ sparing diuretics

A

Hyperkalemia

155
Q

What are the 3 primary purposes of RAAS?

A

maintain extracellular volume
regulate systemic vascular resistance
control cardiac output and arterial BP

156
Q

how is angiotensinogen converted to Ang II?

A

angiotensinogen + renin –> Ang I –> Ang I + ACE –> Ang II

157
Q

characteristics of Renin

A

proteolytic enzyme

primarily synthesized, stored and secreted from the kidney

158
Q

Hypovolemia stimulates renin release via what 3 inputs ?

A
  1. renal sympathetic activation
  2. intrarenal baroreceptors
  3. macula densa
159
Q

what are intrarenal baroreceptors ?

A

JG cells in afferent arteriole walls sensitve to BP

160
Q

How are intrarenal barorecptors stimulated and what is the result ?

A

Low BP –> reduced stretch –> increase renin

161
Q

How is the macula densa stimulated and what is the result ?

A

senses sodium conc in tubular fluid

low sodium beyond renal sympathetic nerves –> reduced GFR –> reduced tubular flow –> further renin secretion

162
Q

what are non-ACE pathways that concert Ang I to Ang II

A

Chymase: produced in heart and vascular tissues
Cathepsins
Limited role under physiologic conditions

163
Q

what do AT1 receptors mediate ?

A

most effects classically associated with RAAS

164
Q

classification of aldosterone

A

Mineralocorticoid

165
Q

where is aldosterone primarily found ?

A

zona glomerulosa adrenal cortex

166
Q

what is the plasma half life of aldosterone ?

A

20 minutes

167
Q

how much aldosterone is secreted daily ?

A

50-200 mg

168
Q

what is aldosterone release stimulated by ?

A

Ang II and Ang III, ADH, endothelin

169
Q

what is aldosterone inhibited by ?

A

ANP dopamine

170
Q

what are the physiological actions of aldosterone ?

A

Na+ and water reabsorption
K+ and H+ excretion
Na+ and water reabsorption from gut, salivary glands and sweat glands

171
Q

how does ang II alter peripheral resistance and what is the end result ?

A

i. direct vasoconstriction
ii. enhancement of peripheral noradrenergic neurotransmission
a. increased NE release
b. decreased NE reuptake
c. increased vascular responsiveness
iii. increased sympathetic discharge
iv. release of catecholamines from adrenal medulla
- -> rapid pressor response

172
Q

how does ang II alter renal function and what is the end result ?

A

I. direct effect to increase Na+ reabsorption in proximal tubule

ii. release of aldosterone from adrenal cortex
iii. altered renal hemodynamics
a. direct renal vasoconstriction
b. enhanced noradrenergic neurotransmission in kidney
c. increased renal sympathetic tone
- -> slow pressure response

173
Q

how does ang II alter cardiovascular structure and what is the end result ?

A

i. non-hemodynamically mediated effects
a. increased expression of proto-oncogenes
b. increased production of growth factors
c. increased synthesis of EC matrix proteins
ii. hemodynamically mediated effects
a. increased afterload
b. increased wall tension
- -> vascular and cardiac hypertrophy and remodelling

174
Q

how does Ang II cause vasoconstriction ?

A

acts on AT1 receptor

increases intracellular Ca2+ –> vasoconstriction

175
Q

how does SNS activation cause vasoconstriction?

A

ang ii mediated

increased NE release, decreased NE reuptake

176
Q

____ arterioles are more sensitive than _____

A

efferent, afferent

177
Q

Where in the kidney does aldosterone act ?

A

in distal and collecting duct to simulate Na+ reabsoprtion and K+ secretion

178
Q

aldosterone negative outcomes

A

remodelling (hypertrophy, fibrosis)
arrhythmia
ischemia
volume (Na+ retention)

179
Q

ACE 2 effects

A

AII –> Ang 1-7

opposes Ang II effects

180
Q

side effects of ACE Inhibitor?

A 
renal impairment 
hyperkalemia
hypotension
cough
angioedema 
teratogenicity
181
Q

contradictions to start ACE inhibitor

A 
serum K+>5 mM
serum creatinine > 200 uM
critical aortic stenosis
bilateral renal artery stenosis
history of angioedema
182
Q

how to use ACE inhibitor

A

check renal/electrolytes, initiate, recheck 1 week
up-titrate 2-4 weeks to maximum tolerated dose
recheck renal/electrolytes 7-10 days after increase
recheck renal/electrolytes at 3 months
renal/electrolytes 6 monthly once stable

183
Q

Causes of exercise associated hyponatremia

A

excessive intake of hypotonic fluids
impaired renal water excretion due to ADH/AVP
sweat loss of sodium
inability to mobilize sodium stores

184
Q

incidence of assymptomatic hyponatremia in endurance events

A

13-18 %

185
Q

predisposing factors to exercise induced hyponatremia

A 
exercise duration > 4 hours or slow running / exercise pace
female
low body weight
excessive drinking during the event 
pre-exercise overhydration
abundant avaliabily of drinking fluids at the event 
NSAIDs 
extreme hot or cold
186
Q

Major classes of diuretics

A

carbonic anhydrase inhibitors (acetazolamide)
loop diuretics (furosemide)
thiazide diuretics (hydrochlorothiazide)
potassium sparing diuretics (spironolactone, amiloride)

187
Q

action of acetazolamide (carbonic anhydrase inhibitor)

A

inhibits carbonic anhydrase–> renal loss of Na+ and HCO3-

  1. diuresis of an alkaline urine
  2. mild metabolic acidosis
188
Q

major clinical use of acetazolamide

A

prevention of acute mountain sickness

treatment of open-angle glaucoma

189
Q

how can acetazolamide help prevent acute mountain sickness ?

A

stimulating respiration through renal loss of Na+HCO3- –> metabolic acidosis of cerebrospinal fluid and hyperventilation

190
Q

how can acetazolamide help treat open angle glaucoma ?

A

inhibit action of carbonic anhydrase –> reduce intraocular pressure.
topical application

191
Q

mechnism of action of furosemide

A

inhibits Na+/K+/2Cl- at:
ascending loop of Henle –> reduce Na+ reabsorption, blood volume and BP
macula densa cells: inhibits detection of Na+ at distal tubule
dilates veins –> reduce venous pressure

411 (16 decks)

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