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Renal SB > Physiology > Flashcards

Physiology Flashcards

1
Q

what is osmolarity

A

concentration of osmotically active particles present in a solution

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2
Q

what is the units of osmolarity

A

osmol/l

mosmol/

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3
Q

what two factors are needed to calculate osmolarity

A

molar concentration of the solution

number of osmotically active particles present

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4
Q

what is another word for osmolarity

A

osmolality

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5
Q

what is the osmolarity of body fluids

A

around 300 mosmol/l

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6
Q

what is tonicity

A

the effect a solution has on cell volume

can be either hypo/hyper/iso tonic

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7
Q

what is the effect of an isotonic solution

A

no change in cell volume

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8
Q

what is the effect of an hypertonic solution

A

decrease in cell volume as the cell is losing water to extracellular environment
cell shrinks

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9
Q

what is the effect of an hypotonic solution

A

increase in cell volume as the cell gains water from the extracellular environment
cell hurts/lysis

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10
Q

what else is taken into consideration in tonicity

A

ability of a solute to cross the cell membrane

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11
Q

effect of urea on RBC

A

RBC very permeable to urea, all urea molecules enter the cell. Leaves behind water; osmotic gradient from outside to inside the cell. Cause cell to burst

Therefore must be hypotonic

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12
Q

effect of sucrose on RBS

A

RBC membrane impermeable to sucrose. Same osmolarity.

Therefore is isotonic

RBC cell membrane is more permeable to urea than sucrose

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13
Q

who has a greater total body water and why

A

Males

Females have more fat cells which hold less water

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14
Q

what are the 2 compartments of total body water and which has more water

A

Intracellular - has higher % of water

Extracellular

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15
Q

what does ECF contain

A

plasma
interstitial fluid (highest % of ECF)
lymph + transcellular fluid

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16
Q

what can we use to measure body fluids compartments

A

through tracers

- obtain the distribution volume of a tracer

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17
Q

what are the useful tracers

A

TBW: 3H2O
ECF: Inulin
Plasma: labelled albumin

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18
Q

how can we measure intracellular water

A

rearrange TBW = ECF + ICF

ICF = TBW - ECF

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19
Q

how can volume of distribution be measured

A

V (in litres) = Dose/sample concentration

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20
Q

how can the distribution volume of a tracer be measured

A

1 - Add a known quantity of tracer X (Qx; mol or mg) to the body
2 - Measure the equilibration volume of X in the body ([X])
3 - V = Qx /[X]

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21
Q

what is essential for water balance/homeostasis in the body

A

input=output

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22
Q

what is the ionic composition of ICF and ECF

A

ECF
- more sodium, chloride and HCO3

ICF

  • more potassium and magnesium
  • -ve charged proteins
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23
Q

what separates the ECF and ICF and helps to maintain the differences between these compartments

A

cell membrane

membrane transport mechanism

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24
Q

what is fluid shift

A

Movement of water between the ICF and ECF in response to an osmotic gradient.

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25
Q

what happens if the osmotic concentration of ECF increases

A

osmolarity increases in ECF
ICF becomes hypertonic
cell looses water and cell volume decreases

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26
Q

what effects fluid homeostasis

A

gain/loss of water
gain/loss of NaCl
gain/loss of isotonic fluid

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27
Q

what is the affect of NaCl gain/loss

A

ECF NaCl gain:ECF ↑ ICF ↓

ECF NaCl loss:ECF ↓ ICF ↑

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28
Q

what does change in isotonic fluid affect

A

only the ECF

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29
Q

what regulates ECF and why is it important to do so

A

Kidney alters composition & volume of ECF

Regulation of ECF volume is vital for long term regulation of blood-pressure

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30
Q

what is > 90% of osmotic concentration of ECF

A

Na+

therefore vital to regulate it

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31
Q

what does K+ play a key role in

A

establishing membrane potential

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32
Q

what can changes in K+ lead to

A

muscle weakness → paralysis

cardiac irregularities → cardiac arrest

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33
Q

how does salt imbalance manifest

A

changes in ECF volume

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34
Q

what is the functional unit of the kidney

A

the nephron

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35
Q

what is the function of the nephron

A

1 - filtration
2 - reabsorption
3 - secretion

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36
Q

what does the Juxtaglomerular apparatus secrete

A

rennin

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37
Q

what are the 2 types of nephron

A

Juxtaglomedullary (around 20%)

Cortical (around 80%)

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38
Q

what are podocytes

A

visceral epithelial cells

cells in the Bowman’s capsule that wrap around capillaries of the glomerulus

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39
Q

what arteriole takes blood into the bowmens capsule and what takes it out

A

afferent arteriole - in

efferent arteriole - out

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40
Q

what is urine

A

Modified filtrate of the blood

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41
Q

what is the renal tubule

A

‘conveyor belt’

substances are added/removed as urinary filtrate moves from proximal to distal end

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42
Q

how much of the plasma that enters the glomerulus is filtered

A

around 20%

the other 80% is not filtered and leaves through the efferent arteriole

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43
Q

what is the rule for any substance in regards to filtration

A

Filtration (GF) + Secretion (TS) = Reabsorption (TR) + Excretion
Amount filtered = Amount excreted

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44
Q

how can the equation also be written so that ROExcretion is first

A

Rate of excretion = rate of filtration + rate of secretion - rate of reabsorption

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45
Q

how is movements of a substance within the kidney described as

A

in terms of concentration × flow

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46
Q

what is the equation for rate of filtration of a substance

A

Rate of filtration of X = mass of X filtered into the Bowman’s capsule per unit time

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47
Q

how does the equation for rate of filtration of a substance translate into for the body

A

Rate of filtration of X = [X]plasma × GFR

where GFR = glomerular filtration rate

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48
Q

what is the equation for rate of excretion of a substance

A

Rate of excretion of X = [X]urine × Vu

where Vu = urine flow rate

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49
Q

what is the equation for rate of reabsorption of a substance

A

Rate of reabsorption of X = rate of filtration of X – rate of excretion of X

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50
Q

how is rates of secretion of a substance calculated

A

Rate of secretion of X = rate of excretion of X – rate of filtration of X

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51
Q

what do rates of reabsorption and secretion reflect

A

tubular modification of filtrate

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52
Q

6 kidney functions

A

1- water balance
2 - salt balance
3 - acid-base balance
4 - Excretion of metabolic waste products
5 - Secretion of renin (control of arterial blood pressure)
6 - Secretion of erythropoietin (EPO; RBC production)

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53
Q

in glomerular filtration, what are the 3 filtration barriers in the lumen

A

(1) Glomerular Capillary Endothelium (barrier to RBC)
(2) Basement Membrane (basal lamina) (plasma protein barrier)
(3) Slit processes of podocytes (plasma protein barrier)
(Glomerular epithelium)

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54
Q

what are the forces that comprise net filtration pressure

A

Glomerular capillary blood pressure (BPcg)
Bowman’s Capsule hydrostatic (fluid) pressure (HPbc)
Capillary oncotic pressure
(COPgc)
Bowman’s Capsule oncotic pressure (COPbc)

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55
Q

what are the rough values of the 4 forces

A

BPgc - 55mmHg
HPbc - 15mmHg
COPgx - 30mmHg
COPbc - 0mmHg

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56
Q

what forces are going in what direction

A

BPgc and COPgc - into Bowmen’s

HPbc and COPbc - out of Bowmen’s

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57
Q

what is the Net Filtration Pressure

A

(55+0) - (15+30) = 10mmHg

going into Bowmen’s capsule

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58
Q

what are these forces also known as and what is there role

A

Starling Forces

the balance of hydrostatic pressure and osmotic forces

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59
Q

what is GFR

A

rate at which protein-free plasma is filtered from the glomeruli into the Bowman’s capsule per unit time.

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60
Q

how is the GFR calculated

A

GFR = Kf × net filtration pressure

where Kf = filtration coefficient

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61
Q

what is the normal value for GFR

A

125 ml/min

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62
Q

what is the major determinant of GFR

A

Glomerular capillary fluid (blood) pressure (BPgc)

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63
Q

what are the regulators of renal blood flow and GFR

A
  1. Extrinsic regulation of GFR
    (a) Sympathetic control via baroreceptor reflex
  2. Autoregulation of GFR (Intrinsic)
    (a) Myogenic mechanism
    (b) Tubuloglomerular feedback mechanism
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64
Q

what happens if BPgc falls

A

GFR decreases

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65
Q

how does GFR increase

A 
1 - increased arterial BP
2 - increases blow flow into the glomerulus via afferent arteriole 
3 - increases glomerular capillary BP
4 - increases net filtration pressure
5 - increases GFR
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66
Q

what would cause GFR to increase/decrease

A

increase - vasodilation

decrease - vasoconstriction

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67
Q

what helps compensate when there is a fall in blood volume

A

decrease urine volume

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68
Q

what is the role of autoregulation

A

prevents short term changes in systemic arterial pressure affecting GFR

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69
Q

what are the mechanisms of auto regulation in the kidneys

A

1 - myogenic i.e. If vascular smooth muscle is stretched (i.e. arterial pressure is increased), it contracts thus constricting the arteriole

2 - Tubuloglomerular feedback i.e. If GFR rises, more NaCl flows through the tubule leading to constriction of afferent arterioles

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70
Q

what cells of the Juxtaglomerular apparatus sense NaCl content of tubular fluid

A

macula densa cells

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71
Q

what diseases could affect GFR

A

↑ HPbc (e.g. kidney stone) = ↓ GFR

↑ COPgc (e.g. diarrhoea) = ↓ GFR

↓ COPgc (e.g. severly burned patients) = ↑ GFR

↓ Kf (change in surface area available for filtration) = ↓ GFR

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72
Q

what is plasma clearance

A

A measure of how effectively the kidneys can ‘clean’ the blood of a substance

Equals the volume of plasma completely cleared of a particular substance per minute

Each substance that is handled by the kidney will have it’s own specific plasma clearance value

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73
Q

what is the equation for clearance of substance

A

Clearance of substance X

= [X]urine x Vurine/[X]plasma

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74
Q

what do the factors of the plasma clearance equation stand for

A 
[X]urine = Urine concentration of substance X
Vurine = urine flow rate
[X]plasma = Plasma conc. of substance X
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75
Q

what are the units for the clearance of substance equation

A

ml/min

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76
Q

what can be measured clinically to determine GFR and why

A

Inulin clearance = GFR

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77
Q

what is inulin

A 
NOT insulin
freely filtered at glomerulus
enters the urine via filtration alone
neither absorbed nor secreted
not metabolised by kidney
not toxic
easily measured in urine and blood
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78
Q

what clearance can be used instead of inulin

A

creatinine clearance

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79
Q

when does clearance = 0

A

For substances which are filtered, completely reabsorbed and not secreted (e.g. glucose)

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80
Q

when does Clearance

A

For substances which are filtered, partly reabsorbed and not secreted (e.g. urea)

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81
Q

when does Clearance > GFR

A

For substances which are filtered, secreted but not reabsorbed (e.g. H+)

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82
Q

what are the general rules to determine if it is tubular reabsorption of secretion

A

If clearance GFR then substance is SECRETED into tubule

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83
Q

what can be used to calculate the renal plasma flow (RPF)

A

using the para-amino hippuric acid (PAH) value (=650 ml/min)

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84
Q

what is PAH

A

exogenous organic anion
freely filtered at glomerulus,
secreted into the tubule (not reabsorbed)
completely cleared from the plasma i.e. all the PAH in the plasma that escapes filtration is secreted from the peritubular capillaries

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85
Q

what properties should any substance used as a clearance marker

A

(1) Non-toxic
(2) Inert (i.e. not metabolised)
(3) Easy to measure

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86
Q

what properties should a GFR marker have

A

should be filtered freely; NOT secreted or reabsorbed

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87
Q

what properties should a RPF marker have

A

should be filtered and completely secreted

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88
Q

what is the filtration factor

A

the fraction of plasma flowing through the glomeruli that is filtered into the tubules

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89
Q

how can FF be calculated

A

GFR/Renal Plasma Flow

125/650 = 0/19 = 20%

90
Q

where does the remaining 80% of plasma that is not filtered move to

A

the peritubular capillaries

91
Q

what is the average values for GFR, RPF and RBF

A

GFR = 125ml/min, 180litres/day

RPF = 650ml/min

RBF = 1200ml/min

92
Q

where is substances reabsorbed

A

GFR = 125ml/min

80ml is in the Proximal tubule
45ml is in the Loop of Henle

93
Q

what is the fluid reabsorbed in the proximal tubule state

A

iso-osmotic with filtrate

94
Q

what is reabsorbed in the PT

A 
sugars
amino acids
phosphate
sulphate
lactate
95
Q

what is secreted in the PT

A 
H+
Hippurates
Neurotransmitters
Bile pigments
Uric acid
Drugs
Toxins
96
Q

what are the 3 types of carrier-mediated membrane transport

A

primary active transport
secondary active transport
facilitated diffusion

97
Q

what is primary active transport

A

Energy is directly required to operate the carrier and move the substrate against its concentration gradient
e.g. energy-dependent Na+-K+ ATPase transport mechanism

98
Q

what is secondary active transport

A

The carrier molecule is transported coupled to the concentration gradient of an ion (usually Na+)

99
Q

what is facilitated diffusion

A

Passive carrier-mediated transport of a substance down its concentration gradient

100
Q

what is essential for sodium reabsorption

A

An energy-dependent Na+-K+ ATPase transport mechanism at the basolateral membrane

101
Q

why does Isoosmotic fluid reabsorption across proximal tubule epithelium happen

A

Standing Osmotic Gradient

Oncotic Pressure Gradient

102
Q

what is the function of the loop of Henle

A

Generates a cortico-medullary solute concentration gradient

Enables the formation of hypertonic urine

103
Q

what is countercurrent flow

A

Opposing flow in the two limbs

Entire loop of Henle functions as a countercurrent multiplier

104
Q

what establishes a hyper-osmotic medullary interstitial fluid

A

loop of Henle and vasa recta

105
Q

which limb of Henle does not reabsorb NaCl and is highly permeable to water

A

Descending Limb (DL)

106
Q

what is the features of the Ascending Limb of Henle

A

Na+ & Cl- are being reabsorbed
relatively impermeable to water
little or no water follows salt reabsorption

107
Q

is the triple co-transporter

A

Na-K-Cl cotransporter (NKCC) is a protein that aids in the active transport of sodium, potassium, and chloride into and out of cells

108
Q

what blocks the triple co-transporter

A

loop diuretics

109
Q

what ensures NaCl is absorbed into the interstitial fluid

A

K+ recycling

110
Q

what is the pathway of reabsorption in the loop of Henle

A
  1. Solute removed from lumen of ascending limb (water cannot follow)
  2. Tubular fluid is diluted and osmolality of interstitial fluid is raised
  3. Interstitial solute cannot enter the descending limb
  4. Water leaves the descending limb by osmosis
  5. Fluid in the descending limb is concentrated
111
Q

how does flow occur in the loop of Henle

A

1 - Fluid enters the descending limb
2 - Fluid that has been concentrated in the descending limb moves onto the ascending limb
3 - Hypotonic fluid moves onto the distal tubule

112
Q

how does pumping resumes in the loop of Henle

A

1 - Solute pumped out of the ascending limb
2 - Osmolality of the interstitial fluid rises
3 - Passive water efflux from the descending limb
4 - Flow occurs moving everything on as before

113
Q

what is the state of the fluid in the loop of Henle

A

Leaving the PT - iso-osmotic

Entering the DT - hypo-osmotic

114
Q

what contributes to half of the medullary osmolality

A

The urea cycle

115
Q

what tubule is not permeable to urea

A

distal tubule

116
Q

what is the purpose of countercurrent multiplication

A

To concentrate the medullary interstitial fluid

117
Q

why do we need countercurrent multiplication

A

To enable the kidney to produce urine of different volume and concentration according to the amounts of circulating antidiuretic hormone (ADH = vasopressin)

118
Q

where are vasa recta

A

run alongside the long loop of Henle of juxtamedullary nephrons

119
Q

what is the countercurrent exchanger

A

Blood osmolality rises as it dips down into the medulla (i.e. water loss, solute gained)

Blood osmolality falls as it rises back up into the cortex (i.e. water gained, solute lost)

120
Q

why is vasa recta needed

A

blood flow through medulla tends to wash away NaCl and urea

121
Q

how does vasa recta minimise this problem

A

1 - Vasa recta capillaries follow hairpin loops
2 - Vasa recta capillaries freely permeable to NaCl and water
3 - Blood flow to vasa recta is low (few juxtamedullary nephrons)

122
Q

what does the kidney not reabsorb

A

creatinine

123
Q

how much urea does the kidney reabsorb

A

50%

124
Q

what is reabsorbed in the PT of the kidney

A 
Sugars
Amino acids
Phosphate
Sulphate
Lactate
125
Q

what is secreted in the PT

A 
H+
Hippurates
Neurotransmitters
Bile pigments
Uric acid
Drugs
Toxins
126
Q

what is the renal threshold for glucose

A

10-12 mmol/l

127
Q

what is transport maximum

A

point at which increases in concentration do not result in an increase in movement of a substance across a membrane

128
Q

how can the amount of substance filtered be calculated

A

plasma concentration of substance x GFR

129
Q

how can excretion be determined

A

(filtration + secretion) - reabsorption

130
Q

what is Na+ reabsorption driven by in the proximal tubule

A

by the basolateral Na+-K+-ATPase

131
Q

what does Na+ reabsorption drive and through which pathway

A

Cl- reabsorption through the paracellular pathway

132
Q

what is being absorbed in the ascending limb of the loop of Henle and not the Descending limb

A

Na+

Cl-

133
Q

which limb of the loop of Henle is highly permeable to water and what is not

A

descending limb - very permeable

ascending limb - impermeable

134
Q

what does the difference of water permeability in the loop of henle cause

A

an osmotic gradient to be established in the medulla

135
Q

what hormones regulate the distal tubule and collecting ducts ion and water balance

A

ADH/Vasopressin
Aldosterone
Atrial Natriuretic hormones (ANH)
Parathyroid hormone (PTH)

136
Q

what does ADH do

A

Increases water reabsorption

137
Q

what does Aldosterone do

A

Na+ reabsorption ↑

H+ / K+ secretion ↑

138
Q

what does Atrial natriuretic hormone do

A

Na+ reabsorption ↓

139
Q

what does PTH do

A

Ca2+ reabsorption ↑

PO43- reabsorption ↓

140
Q

where is urea concentrated and why

A

in the tubular fluid

distal tubule has low permeability to water and urea

141
Q

what is responsible for the synthesis of octapeptide of ADH

A

supraoptic and paraventricular nuclei in the hypothalamus

142
Q

where is the octapeptide stored for ADH

A

posterior pituitary

143
Q

when is ADH released

A

Released into blood when action potentials down the nerves lead to Ca2+-dependent exocytosis

144
Q

what is the action of ADH on the collecting ducts

A

Increases permeability of
luminal membrane to H2O
by inserting new
water channels (aquaporins)

145
Q

what happens in the presence of ADH in the collecting duct

A

water moves from collecting duct into the medullary interstitial fluid

enables hypertonic urine formation

146
Q

summary - what is the physiological state when there is high/low ADH

A

High [ADH]
= high water permeability
= hypertonic urine
i.e. Small volume, Concentrated urine

Low [ADH]
= low water permeability
= hypotonic urine
i.e. Large volume, dilute urine

147
Q

how does the tubular fluid escape to equilibrate with interstitium

A

via aquaporins

148
Q

when is there high ADH

A

when there is a water deficit

149
Q

what are symptoms of Diabetes insipidus and what is the Tx

A

Large volumes of dilute urine Constant thirst

ADH replacement

150
Q

what is the most important stimulus for ADH release and what is also a factor

A

Hypothalamic osmoreceptors - most important

Left atrial stretch receptors - also important

151
Q

what does a decrease in atrial pressure cause

A

increased ADH release

152
Q

what other chemicals can influence ADH

A

Nicotine stimulates ADH release

Alcohol inhibits ADH release

153
Q

what is aldosterone

A

Steroid hormone secreted by the adrenal cortex

154
Q

when is aldosterone secreted

A
  1. In response to rising [K+] or falling [Na+] in the blood

2. activation of the renin-angiotensin system

155
Q

what does aldosterone do

A

Stimulates Na+ reabsorption and K+ secretion

156
Q

what does sodium retention contribute to

A

increased blood volume and pressure

157
Q

how does aldosterone work

A
  • normally, 90% of K+ reabsorbed in PT
  • when aldosterone ABSENT, rest is reabsorbed in distal tubule
  • an increase in K+ directly stimulate adrenal cortex
  • Aldosterone stimulates SECRETION of K+
  • increase Na+ reabsorption in the distal and collecting tubule
158
Q

what does a decrease in plasma Na+ promote

A

indirect secretion of aldosterone by means of the juxtaglomerular apparatus

159
Q

what factors control the release of renin

A
  • reduced pressure in afferent arteriole
  • Macula densa cells sense the amount of NaCl in the distal tubule
  • Increased sympathetic activity as a result of reduced arterial blood pressure
160
Q

where is renin released from

A

granular cells in JGA

161
Q

what does reduced pressure in afferent arteriole cause

A

More renin released, more Na+ reabsorbed, blood vol. increased, blood pressure restored.

162
Q

why does Increased sympathetic activity cause renin release

A

Granular (renin-secreting) cells directly innervated by sympathetic nervous system

163
Q

how is the RAAS system responsible of fluid retention associated with congestive heart failure

A

Failing heart&raquo_space; Decreased CO & BP&raquo_space; Low BP stimulates RAAS&raquo_space; Increased salt + water retention&raquo_space; failing heart

164
Q

Tx of fluid retention

A

low salt diet
Diuretics (loop diuretics)
ACE inhibitors

165
Q

where is ANP produced and where is it stored

A

the heart and is stored in atrial muscle cells

166
Q

when is ANP released and what does is promote

A

when atrial cells are mechanically stretched due to an increase in the circulating plasma volume

promotes excretion of Na+ and diuresis, thus decreasing plasma volume

167
Q

what is the process that empties urine from the bladder

A

micturition a.k.a urination

168
Q

what two mechanisms govern urination

A 
The micturation reflex
Voluntary control (external sphincter and pelvic diaphragm)
169
Q

what is the micturition reflex

A

involuntary emptying of the bladder by simultaneous bladder contraction and opening of both the internal and external urethral sphincters

170
Q

what monitors ECF osmolarity

A

Hypothalamic osmoreceptors

171
Q

what is water diuresis

A

an increased urine flow but not an increased solute excretion

172
Q

what is osmotic diuresis

A

increased urine flow is as a result of a primary increase in salt excretion.

173
Q

what can cause osmotic diuresis

A

failure of normal Na+ reabsorption causes both increased sodium and increased water excretion

174
Q

what is Erythropoiesis

A

making RBC

175
Q

how does an increase in [H+] cause

A

reduced pH

176
Q

what are sources of [H+] in the body

A

Carbonic acid formation
Inorganic acids produced during breakdown of nutrients
Organic acids resulting from metabolism

177
Q

how do strong/weak acids dissociate in solution

A

strong - dissociate completely in the solution

weak - dissociate partially in solution

178
Q

what is the equilibrium equation

A

HA H+ + A-

HA undissociated acid
H+ proton
A- base

179
Q

what cause the equilibrium to shift to the left and what does it cause

A

if acid (H+) is added

[HA] rises, [A-] falls
as protons are ‘mopped up’ by A- making more HA

180
Q

what happens when a base is added to the system

A

equilibrium shifts to the right

[HA] falls, [A-] rises
Base is “tied-up” by combining with H+, allowing more HA to dissociate

181
Q

what is the buffer in these equations

A

HA - either its formation or dissociation

182
Q

at equilibrium what does the dissociation constant equal

A

K = [H+][A-] / [HA]

183
Q

what is the log notation for K (the dissociation constant)

A

pK = -logK

184
Q

what is the Henderson-Hasselbalch equation (used to calculate pH)

A

pH = pK + log ([A-] // [HA] )

185
Q

what is the most important physiological buffer system

A

CO2 - HCO3 buffer

186
Q

what is the buffer equation

A

CO2 + H2O ⇔ H2CO3 ⇔ H+ + HCO3-

187
Q

what enzyme catalyse converting CO2 and water in to Carbonic acid (H2CO3)

A

Carbonic anhydrase (CA)

188
Q

what controls [HCO3-]

A

the kidneys

189
Q

what control Pco2

A

the lungs

190
Q

what is normal plasma pH

A

7.4

191
Q

what is the role of the kidney in control of [HCO3-]p

A

Variable reabsorption of filtered HCO3-

Kidneys can add “new” HCO3- to the blood

192
Q

what is the control of [HCO3-] in the kidneys dependant on

A

upon H+ secretion into the tubule

193
Q

how can the kidneys form ‘new’ HCO3-

A

secreted H+ combines with phosphate

194
Q

what does H+ secretion by the tubule do

A
  • drives reabsorption of HCO3-
  • forms acid phosphate
  • forms ammonium ion
195
Q

what is titratable acid

A

way to measure amount of H+ excreted

196
Q

how can the amount of acid phosphate made by H+ secretion be calculated

A

Measure the concentration of titratable acid (TA) in the urine ([TA]u

197
Q

how can the amount of ammonium ion made by H+ secretion be calculated

A

Measure [NH4+]u

198
Q

what rids the body of acid load and what else does this process do

A

Excretion of TA and NH4+ simultaneously

regenerate buffer stores

199
Q

what is the normal [HCO3-] range

A

23-27

200
Q

what is compensation

A

normal acid-base balance is disrupted, the first priority is to restore pH to 7.4

i.e. restoration of pH irrespective of what happens to [HCO3-]p and PCO2

201
Q

what is correction

A

restoration of pH and [HCO3-]p and PCO2 to normal

202
Q

what is the Davenport diagram used for

A

describe blood bicarbonate concentrations and blood pH following a respiratory and/or metabolic acid-base disturbance

203
Q

what is respiratory acidosis and what can cause it

A

retention of CO2 by the body

e.g chronic bronchitis, chronic emphysema, airway restriction (bronchial asthma, tumour), chest injuries

204
Q

how does CO2 retention cause acidosis

A

drives equilibrium to the right
[H+]p and [HCO3-]p rise

Increased [H+]p results in acidosis

205
Q

what values would indicate uncompensated respiratory acidosis

A

pH 45 mmHg

206
Q

what drives H+ secretion by the kidney and what does CO2 retention therefore stimulate

A

Pco2

H+ secretion into the filtrate

207
Q

how does renal compensation for resp acidosis work

A

H+ secretion is stimulated

All filtered HCO3- is reabsorbed (i.e. no HCO3- excretion)

H+ continues to be secreted and generates titratable acid (TA) and NH4+

Acid is excreted and “new” HCO3- is added to the blood

208
Q

what is respiratory alkalosis and what can cause it

A

Excessive removal of CO2 by the body

e.g. hyperventilation

209
Q

how does hyperventilation cause respiratory alkalosis and what does this cause

A

Excessive CO2 removal drives equilibrium to the left

[H+]p and [HCO3-]p fall

The decreased [H+]p results in alkalosis

210
Q

what values indicate uncompensated respiratory alkalosis

A

pH > 7.45 and PCO2

211
Q

how does excessive removal o CO2 affect H+ secretion

A

reduces H+ secretion into the tubule

212
Q

how does the kidneys compensate for respiratory alkalosis

A

H+ secretion is insufficient to reabsorb the filtered HCO3-

HCO3- is excreted and urine is alkaline

No titratable acid (TA) and NH4+ is formed, so no “new” HCO3- is generated

Renal compensation further lowers [HCO3-]p

213
Q

what is metabolic acidosis and what can cause it

A

Excess H+ from any source other than CO2
e.g. Excessive metabolic production of H+ (DKA)
Excessive loss of base from the body (e.g. diarrhoea)

214
Q

what values indicate metabolic acidosis

A

pH

215
Q

how does the respiratory system compensate for metabolic acidosis

A

decrease in plasma pH stimulates peripheral chemoreceptors

Ventilation is quickly increased and more CO2 is blown off

216
Q

how is metabolic acidosis corrected

A

Filtered HCO3- is very low and very readily reabsorbed

H+ secretion continues and produces TA & NH4+ to generate more “new” HCO3-

The acid load is excreted (urine is acidic) and [HCO3-]p is restored

217
Q

what is metabolic alkalosis and what can cause it

A

Excessive loss of H+ from the body

e.g. Loss of HCl from the stomach (vomiting)

218
Q

what happens in metabolic alkalosis

A

result of loss of H+ or addition of base, [HCO3-]p rises

219
Q

what values indicate metabolic alkalosis

A

pH > 7.45

[HCO3-]p is high

220
Q

how does the resp system compensate for metabolic alkalosis

A

slows ventilation
CO2 retained, PCO2 rises
[H+]p rises, lowering pH
[HCO3-]p also rises further

221
Q

how is metabolic alkalosis corrected

A

Filtered HCO3- load is so large compared to normal that not all of the filtered HCO3- is reabsorbed

No TA or NH4+ is generated

HCO3- is excreted (urine is alkaline)

[HCO3-]p falls back towards normal

Renal SB (15 decks)

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