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Physiology Flashcards

1
Q

what is osmolarity?

A

the concentration of osmotically active particles present in a solution

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2
Q

what 2 factors are needed to calculate osmolarity?

A
  1. the molar concentration of the solution

2. the number of osmotically active particles present

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3
Q

what is tonicity?

A

the effect a solution has on cell volume

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4
Q

what will an isotonic solution do to cell volume?

A

no change

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5
Q

what will a hypertonic solution do to cell volume?

A

decrease in cell volume

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6
Q

what will a hypotonic solution do to cell volume?

A

increase in cell volume

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7
Q

what does tonicity take into consideration that osmolarity doesnt?

A

the ability of the solute to cross the cell membrane

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8
Q

compare percentage of total body water to body weight in males and females?

A

males- 60% of body weight

females 50% of body weigh

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9
Q

what are the 2 major compartments that make up total body water? (and the percentage of each)

A

intracellular fluid 67%

extracellular fluid 33%

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10
Q

what are the main 2 compartments that make up the extracellular fluid? (and the percentage of each)

A

plasma 20%

interstitial fluid 80%

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11
Q

what separates the extracellular fluid and the intracellular fluid?

A

plasma membrane

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12
Q

how do we measure body fluid compartments clinically?

A

tracers

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13
Q

what tracer allows us to determine the total body water?

A

3 H20

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14
Q

what tracer allows us to determine the volume of extracellular fluid?

A

inulin

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15
Q

what tracer allows us to determine the volume of plasma?

A

labelled albumin

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16
Q

is sodium higher intracellularly or extracellularly?

A

extracellularly

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17
Q

is potassium higher intracellularly or extracellularly?

A

intracellularly

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18
Q

is chloride higher intracellularly or extracellularly?

A

extracellularly

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19
Q

what separates the plasma from the interstitial fluid?

A

capillary wall

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20
Q

what are the main ions in the ECF?

A

Na+
Cl-
HCO3-

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21
Q

what are the main ions in the ICF?

A

K+
Mg2+
negatively charged proteins

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22
Q

what is the osmotic concentration of the ECF?

A

roughly 300 mosmol/l

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23
Q

what is the osmotic concentration of the ICF?

A

roughly 300 mosmol/l

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24
Q

urea is the biproduct of the breakdown of what substance?

A

protein

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25
Q

bilirubin is the biproduct of the breakdown of what substance?

A

haemoglobin

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26
Q

what hormone is released by the kidney in response to hypoxia?

A

erythropoetin

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27
Q

uric acid if the biproduce of the breakdown of what substances?

A

purines

eg adenosine, guanine

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28
Q

what is the active form of vitamin D?

A

calcitriol

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29
Q

what is the function of calcitriol?

A

promotes Ca++ absorption in the GI tract

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30
Q

how many OH hydroxyl groups are added to vit D in order to convert it to calcitriol?

A

2 hydroxyl groups

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31
Q

where is the first hydroxyl group added to vitamin D? (a step in the conversion to calcitriol)

A

liver

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32
Q

where is the second hydroxyl group added to vitamin D? ( a step in the conversion to calcitriol)

A

kidneys

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33
Q

what percentage of cardiac output goes to the kidneys?

A

25%

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34
Q

what are the 2 types of nephron? (and give percentages of each)

A

cortical 80%

juxtamedullary 20%

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35
Q

compare the loop of Henle’s in the cortical and juxtamedullary nephrons?

A

juxtamedullary nephron loop of Henle is much longer and extends right down into the medulla, cortical nephron is shorter and only extends slightly into the medulla

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36
Q

compare the capillaries which surround the renal tubules of the cortical and juxtamedullary nephrons?

A

juxtamedullary nephron- efferent arteriole becomes a single capillary called the vasa recta
cortical nephron- efferent arteriole becomes a network of capillaries called the peritubular network

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37
Q

compare the diameter of the afferent and efferent arterioles?

A

afferent arteriole has a bigger diameter

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38
Q

how much plasma of the afferent arteriole is filtered into the bowman’s capsule?

A

20%

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39
Q

what cells is renin secreted from?

A

granular cells (juxtaglomerular cells) wichin the juxtaglomerular apparatus

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40
Q

how do you calculate the rate of filtration of a substance?

A

rate of filtration = plasma conc of substance x GFR

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41
Q

what is the normal GFR?

A

125ml/min

0.125l/min

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42
Q

what happens to the rate of filtration of a substance as the concentration of the substance in plasma increase?

A

rate of filtration increases

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43
Q

how do you calculate the rate of excretion of a substance?

A

rate of excretion = urine conc of substance x urine flow rate

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44
Q

how do you calculate the rate of reabsorption of a substance?

A

rate of filtration - rate of excretion

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45
Q

what is the normal urine flow rate?

A

1ml per minute
0.001l per minute
(very variable depending on body conditions)

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46
Q

how do you calculate the rate of secretion of a substance?

A

rate of excretion - rate of filtration

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47
Q

collectively, what is the glomerular capillary endothelium, basement membrane and podocyte layer called?

A

glomerular membrane

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48
Q

what net charge does the basement membrane of the glomerular membrane have?

A

negative charge

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49
Q

what is the function of the negatively changed basement membrane of the glomerular membrane?

A

repels large negatively charged proteins

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50
Q

what are the 4 starling forces that compromise net filtration pressure at the glomerulus?

A

glomerular capillary blood pressure
bowmans capsule hydrostatic pressure
capillary oncotic pressure
bowmans capsule oncotic pressure

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51
Q

which is the starling force which contributes most to the net filtration pressure at the glomerulus?

A

glomerular capillary blood pressure

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52
Q

how do you calculate the net filtration pressure of the glomerulus?

A

(bowmans capsule hydrostatic pressure + capillary oncotic pressure)

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53
Q

why, unlike most capillaries, is the glomerular capillary blood pressure constant from afferent arteriole to efferent arteriole?

A

because as you lose volume the diameter decreases

–> pressure is maintained

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54
Q

what solutes determine oncotic pressure?

A

plasma proteins

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55
Q

since there should be no plasma proteins within the lumen of the bowman’s capsule, what should the bowmans capsule oncotic pressure be?

A

0 mmHg

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56
Q

what is the glomerular filtration rate?

A

the rate at which protein=free plasma is filtered from the glomeruli into the bowman’s capsule per unit time

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57
Q

how do you calculate the gfr?

A

Kf x net filtration pressure

where Kf = filtration coefficient

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58
Q

what is the main determinant of GFR?

A

glomerular capillary blood pressure

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59
Q

what are the 2 main ways of glomerular filtration rate regulation?

A

intrinsic control

extrinsic control

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60
Q

which nervous system is involved in the extrinsic control of GFR and via what reflex?

A

sympathetic control via baroreceptor reflex

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61
Q

what are the 2 types of intrinsic autoregulation of GFR?

A

myogenic mechanism

tubuloglomerular feedback mechanism

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62
Q

what does vasoconstriction of the afferent arteriole do to the GFR?

A

decreases the GFR

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63
Q

what does vasodilation of the afferent arteriole do to the GFR?

A

increases the GFR

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64
Q

explain why a fall in blood pressure might cause reduced GFR? (external regulation)

A

reduced BP detected by baroreceptors
sympathetic activity is increased
generalised arteriolar vasoconstriction (afferent arteriole)
reduced glomerular capillary BP so reduced GFR and urine volume
[helps to compensate for fluid loss]

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65
Q

broadly speaking, why do systemic arterial blood pressure changes not always causes changed in GFR?

A

intrinsic control of the GFR (autoregulation)

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66
Q

what is myogenic autoregulation of GFR?

A

if vascular smooth muscle is stretched (due to increased BP) it contracts thus constricting the afferent arteriole

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67
Q

what is tubuloglomerular feedback autoregulation of GFR?

A

If the NaCl increases (happens when GF is raised) within the juxtaglomerular apparatus raises, the macula densa sense it and cause the afferent arteriole to constrict

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68
Q

why might a kidney stone cause reduced GFR?

A

increased hydrostatic pressure which opposes filtration

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69
Q

why might severe diarrohea cause reduced GFR?

A

dehydration leads to increased plasma protein concentration (ie bigger capillary oncotic pressure which opposes filtration)

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70
Q

why might severely burned patients have an increased GFR?

A

plasma proteins are lost from site so leads to decreased plasma protein concentration (ie smaller capillary oncotic pressure)

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71
Q

why might kidney damage cause decreased GFR?

A

might decrease filtration coefficient leading to decreased GFR

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72
Q

what is plasma clearance?

A

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

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73
Q

what are the units of plasma clearance?

A

ml per min

ml/min

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74
Q

how do you calculate clearance of a substance?

A

rate of excretion/ plasma concentration

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75
Q

what is the inulin clearance rate?

A

125ml/min

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76
Q

is inulin absorbed by the renal tubules?

A

no

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77
Q

is inulin secreted by the renal tubules?

A

no

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78
Q

the clearance of which substance is much more convenient to determine GFR from than inulin?

A

creatinine clearance

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79
Q

why is creatinine clearance not as accurate as inulin clearance as an indicator of GFR?

A

because some is secreted in the tubules

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80
Q

what is the rate of glucose clearance?

A

0ml/min

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81
Q

why might the clearance of a substance be 0?

A
  1. filtered, all reabsorbed, no tubular secretion

2. not filtered no tubular secretion

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82
Q

is urea reabsorbed in the renal tubules?

A

partly

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83
Q

is urea secreted in the renal tubules?

A

no

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84
Q

what is the range of values for clearance of a substance which is partly reabsorbed but not secreted?

A

Less than 125ml/min

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85
Q

what is the range of values for clearance of a substance which is secreted but not reabsorbed?

A

> 125ml/min

because clearance is bigger than GFR

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86
Q

is hydrogen reabsorbed in the renal tubules?

A

no

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87
Q

is hydrogen secreted in the renal tubules?

A

yes

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88
Q

if the clearance of a substance is lower than the GFR, what does this indicate?

A

the substance is reabsorbed in the renal tubulres

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89
Q

if the clearance of a substance is the same as the GFR, what does this indicate?

A

the substance is neither reabsorbed or secreted

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90
Q

if the clearance of a substance is the higher than the GFR, what does this indicate?

A

the substance is secreted into the tubules

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91
Q

the clearance of what substance indicates the renal plasma flow?

A

clearance of para-amino hippuric acid (PAH)

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92
Q

why is clearance of PAH used to measure renal plasma flow?

A

filtered freely at glomerulue and is completely secreted in the renal tubules, none is reabsorbed

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93
Q

creatinine a biproduct of the breakdown of what?

A

muscle

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94
Q

what is the clearance of PAH?

A

650ml/min

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95
Q

what is the renal plasma flow?

A

650ml/min

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96
Q

how do you calculate the filtration fraction?

A

GFR/renal plasma flow

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97
Q

what is the filtration fraction?

A

20%

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98
Q

what is haemocrit?

A

packed cell volume

–> volume percentage of red blood cells in blood

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99
Q

how doyou calculare renal blood flow?

A

renal plasma flow / (1-haemocrit)

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100
Q

what is the average renal blood flow?

A

1200ml/min

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101
Q

compare transcellular and paracellular absorption?

A

transcellular- absorption across the cell of the tubular wall
paracelular- absorption across spaces in the cells of the tubular wall

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102
Q

what is required for primary active transport to occur?

A

ATP

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103
Q

what ion is secondary active transport usually coupled to the movement of?

A

Na+ down its conc gradient

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104
Q

what membrane (apical or basolateral) is the Na/K/ATPase pump exclusively found on?

A

basolateral membrane

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105
Q

the Na/K/ATPase requires the hydrolysis of what?

A

ATP

106
Q

why is it important that the Na/K pump keeps pumping Na out of the cells lining the proximal convoluted tubule?

A

keeps intracellular conc of Na low which allows Na to diffuse from the lumen into the cell down a conc gradient

107
Q

the secondary active transporter on the apical membrane of the cells in the proximal convoluted tubule transports what ion across the membrane into the lumen in replace for Na?

A

H+

108
Q

why does Cl- from the lumen of the proximal convoluted tubule follow Na+ into the interstitial fluid of the cells lining the tubule wall?

A

postively charged Na influx sets up an electrochemical gradient for negatively charged Cl- to follow

109
Q

does Cl- get reabsorbed from the proximal convoluted tubule transcellularly or paracellularly?

A

paracellularly

110
Q

why does H2O from the lumen of the proximal convoluted tubule follow NaCl into the interstitial fluid of the cells lining the tubal wall?

A

NaCl sets up an osmotic gradient for water to follow

111
Q

does H2O get reabsorbed from the proximal convoluted tubule transcellularly or paracellularly?

A

paracellularly

112
Q

why has the oncotic pressure of the vasa recta increased since the afferent arteriole?

A

same number of protiens as before but 20% of plasma has gone

–> increased conc of plasma proteins

113
Q

how does glucose get reabsorbed over the apical membrane from the proximal convoluted tubule lumen?

A

Na/Glucose cotransporter

symport

114
Q

how does glucose get across the basolateral membrane of the cells lininc the proximal convoluted tubule?

A

facillitated diffusion

115
Q

what happens when the glucose transporter mechanisms in the proximal convoluted tubule become saturated?

A

not all glucose can be reabsorbed

–> glucose in urine

116
Q

why might there be more glucose present than space on the glucose transporter mechanisms?

A

high blood glucose eg diabetes mellitus

117
Q

the tubular fluid is ‘iso-osmotic’ when it leaves the proximal convoluted tubule, why?

A

because both salt and water (in correlating amounts) have been reabsorbed

118
Q

the tubular fluid is ‘iso-osmotic’ when it leaves the proximal convoluted tubule? what does this mean?

A

same osmolarity as the plasma

300mosmol/l

119
Q

what is reabsorbed in the ascending limb of the loop of henle?

A

Na+ and Cl-

no water

120
Q

compare the thin ascending limb and thick ascending limb of the loop of henle in terms of how the salt is reabsorbed?

A

thick ascending limb: active transport

thin ascending limb: passive transport

121
Q

what is reabsorbed in the descending limb of the loop of henle?

A

water

no NaCl

122
Q

why is the ascending limb of the loop of henle impermeable to water?

A

very tight junctions so H2O can’t follow osmotic gradient (remember it moves paracellularly)

123
Q

what ions does the triple co-transporter found on the ascending limb of the loop of henle reabsorb?

A

Na+
K+
2Cl-

124
Q

what drug blocks the triple co-transporter found on the ascending limb of the loop of henle?

A

loop diuretics

125
Q

why does water reabsorb in the descending limb of the loop of henle?

A

follows the osmotic gradient created by the interstitial fluid
(originally created by the reabsorption of salt from ascending limb)

126
Q

is the fluid leaving the ascending limb of the loop of henle hypo-osmotic, iso-osmotic or hyper-osmotic?

A

hypo-osmotic

127
Q

is urea actively or passively reabsorbed in the loop of henle?

A

passively

128
Q

what is countercurrent multiplication?

A

the reabsorption of NaCl and urea from the ascending loop of Henle followed by the reabsorption of water from the descending loop of Henle making the corticomedullatry gradient

129
Q

what is the purpose of the countercurrent multiplication?

A

to enable the kidney to produce different volumes and concentrations of urine according to the amounts of ADH

130
Q

what happens to the osmolairity of the vasa recta as it dips down into the medulla? and why?

A

osmolairity increases as the fluid equilibrates with the corticomedullary gradient
water loss
solute gain

131
Q

what happens to the osmolarity of the vasa recta as it ascends back to the cortex? and why?

A

osmolarity decreases as the fluid equilibrates with the corticomedullary gradient
water gain
solute loss

132
Q

why is the vasa recta in a hairpin loop?

A

prevents the washing away of solutes

as on its ascent it losses solutes and gains water

133
Q

compare the osmolairities of the blood entering and leaving the vasa recta?

A

same osmolarity

300mosmol/l

134
Q

what acts as the countercurrent exchanger?

A

the vasa recta

135
Q

what makes up the countercurrent system?

A

countercurrent multiplier and countercurrent exchanger

ie loop of henle plus vasa recta

136
Q

what is the osmolarity of the tubular fluid entering the distal tubule?

A

100mosmol/l

hypo-osmotic

137
Q

what parts of the nephron are within the corticomedullary gradient?

A

loop of henle

collecting ducts

138
Q

what parts of the nephron do hormone influence?

A

distal convoluted tubule

collecting ducts

139
Q

what does ADH cause the reabsorption/secretion of?

A

increased reabsorption of water

140
Q

what does aldosterone cause the reasbsorption/secretion of?

A

increased reabsorption of Na

increased secretion of K

141
Q

what does atrial natriureteric peptide cause the reabsorption/secretion of?

A

decreased reasborption of Na

142
Q

what does parathyroid hormone cause the reabsorption/secretion of?

A

increased calcium reabsorption

decreased phosphate reabsorption

143
Q

how do you calculate pH from [H+]?

A

pH = log (1/[H+])

144
Q

what is the pH of arterial blood?

A

7.45

145
Q

what is the pH of venous blood?

A

7.35

146
Q

what is the average pH of blood?

A

7.40

147
Q

what happens to the pH as [H+] increases?

A

pH decreases

148
Q

compare acidosis and alkalosis in terms of what they do to the nervous system?

A

acidosis can lead to CNS depression

alkalosis can lead to PNS and CNS overexcitability

149
Q

what does increased plasma [H+] do to the amount of K+ secreted in the renal tubules?

A

decreases K+ secretion

retention

150
Q

what are the 3 sources of H+ addition?

A

carbonic acid formation
inorganic acids produced from nutrient breakdown
organic acids produced from metabolism

151
Q

what molecules form carbonic acid?

A

CO2 + H2O

152
Q

what does carbonic acid dissociate into?

A

H+ + HCO3-

153
Q

compare strong and weak acids in terms of dissociation in solution?

A

strong acids dissociate completely in solution

weak acids dissociate partially in solution

154
Q

what is a buffer system?

A

a pair of substances, one can yield free H+ when the [H+] decreases, the other can take free H+ when the [H+] increases in order to maintain pH

155
Q

what is the first line defence to any change in pH/acid status?

A

buffer system

156
Q

within the HA = H+ + A- buffer system, which molecule can yield free H+ when the [H+] decreases?

A

HA

157
Q

within the HA = H+ + A- buffer system, which molecule can mop up free H+ when the [H+] increases?

A

A-

158
Q

if H+ is added to the HA= H+ + A- system, what happens to the equilibrium and levels of each molecule?

A

equilibrium is shifted to the left

[HA] increases
[A-] decreases
[H+] remains the same

159
Q

if base (B-) is added to the HA = H+ + A- system, what happens to the equilibrium and the levels of each molecule?

A

equilibrium shifts to the right

[HA] decreases
[A-] increases
[H+] remains the same

160
Q

how do you calculate the dissociation constant of a weak acid?

A

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

161
Q

how do you calculate pK using the dissociation constant (K)?

A

pK = -log K

162
Q

what is pK?

A

the pH at which a particular chemical reaction will be at equilibrium

163
Q

what does the henderson-hasselbalch equation calculate?

A

the pH

164
Q

what is the henderson-hasselbalch equation?

A

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

165
Q

what is the most important physiological buffer system?

A

the CO2 - HCO3 buffer

166
Q

what is the CO2 - HCO3 buffer?

A

CO2 + H2O = H2CO3 = H+ + HCO3-

167
Q

formation of carbonic acid from carbon dioxide and water is catalysed by what enzyme?

A

carbonic anhydrase

168
Q

what is the pK for carbonic acid?

A

pH at equilibrium (pK) = 6.1

169
Q

what controls the [HCO3-] of plasma?

A

the kidneys

170
Q

what controls the PCO2 of plasma?

A

the lungs

171
Q

why might the renal vain have a higher [HCO3-] than the renal artery?

A

because the kidneys can add new HCO3- to the blood

172
Q

what does the reabsorption of filtered HCO3- and the addition of new HCO3- to the renal vein depend on?

A

H+ secretion into the renal tubule

173
Q

how does reabsorption of HCO3- occur in the proximal tubule?

A

indirectly
H+ is secreted into tubule, this binds with HCO3- to form carbonic acid which forms carbon dioxide and water. This readily diffuses across the apical membrane into the cell.

174
Q

what happens to the carbon dioxide and water which enters the tubular cell? (formed from H+ and HCO3- in the renal tubule)

A

forms carbonic acid and then dissociates into HCO3- and H+

175
Q

where in the nephron is HCO3- reabsorbed?

A

proximal tubule

176
Q

how does HCO3- leave the basolateral membrane of the tubular cell?

A

Na/HCO3 cotransporter

177
Q

how doe H+ leave the apical membrane of the tubular cell in the proximal tubule in order to bind with HCO3-?

A

Na/H antiporter

178
Q

what drives the secretion of H+ through the apical membrane of the tubular cell? in order to bind with HCO3-

A

CO2 partial pressure

179
Q

what happens to the H+ that is transported across the apical membrane into the tubular fluid when all the HCO3- has already been absorbed?

A

binds to phosphate to form acid phosphate and is excreted

if even more H+
binds to ammonia to form ammonium and is excreted

180
Q

what 2 ways does titratable acid and ammonium excretion increase the pH of the plasma?

A

loss of H+ ions
gain of HCO3-

(simultaneously rids body of acid and regenerates buffer stores)

181
Q

what is the maximum amount of titratable acid that can be excreted and therefore the maximum amount of new HCO3- that can be gained through this way?

A

40mmol/day titratable acid

40mmol/day new HCO3-

182
Q

ammonia is formed from the breakdown of what in the tubular cells?

A

glutamine

183
Q

what enzyme breaks glutamine down to ammonia?

A

glutaminase

184
Q

how is ammonia transported across the apical membrane into the tubular fluid?

A

diffusion

185
Q

for every H+ excreted as acid phospate, how many new HCO3- have been formed?

A

1

186
Q

for every H+ excreted as ammonium, how many new HCO3- have been formed?

A

1

187
Q

in what pH state will titratable acid and ammonium be excretion be increased?

A

acidosis

188
Q

what is the normal range of [HCO3-] of the plasma? (and the usual value?)

A

23-27mmol/l

24mmol/l

189
Q

what is the normal range of PCO3 of the plasma? (and the usual value?)

A

35-45mmHg

40mmHg

190
Q

compare compensation and correction of acid base disturbances?

A

compensation: restoration of pH irresepctive of what happens to [HCO3- ]and PCO2
correction: restoration of pH, [HCO3-] and PCO2

191
Q

why can buffer stores not always completely compensate for acid base disturbances?

A

stores become depleted

192
Q

what organ has a role in restoring free bicarbonates invovled in buffering?

A

kidney

193
Q

respiratory acidosis drives the carbonic equlibrium to which side?

A

to the right

194
Q

what happens to the [H+] and [HCO3-] in respiratory acidosis?

A

both increase

195
Q

what indicates uncompensated respiratory acidosis?

A

pH below 7.35 and CO2 above 45mmHg

196
Q

why is more HCO3- reabsorbed/made in the kidneys in respiratoy acidosis?

A

high PCO2 drives H+ secretion into the tubular fluid which drives HCO3- reabsorption/production

197
Q

how does the kidney compensate for respiratory acidosis?

A

excretes acid

increases [HCO3-] of plasma

198
Q

what mechanism corrects respiratory acidosis?

A

restoration of normal ventilation

199
Q

in respiratory acidosis, what does the renal compensatory system do to [H+] and [HCO3-]?

A

[H+] decreases

[HCO3-] increases further

200
Q

what is respiratory alkalosis?

A

excess removal of CO2 from the body

201
Q

what is respiratory acidosis?

A

retention of CO2

202
Q

what does hyperventilation do to PCO2?

A

decreases it

203
Q

what does respiratory alkalosis do to the carbonic acid equilibrium?

A

shifts it to the left

204
Q

what happens to [H+] and [HCO3-] in respiratory alkalosis?

A

they both fall

205
Q

when is uncompensated respiratory alkalosis indicated?

A

pH above 7.45 and PCO2 below 35mmHg

206
Q

what does respiratory alkalosis do to the rate of H+ secretion from the kidney tubules?

A

decreases it

207
Q

what does respiratory alkalosis do to the rate of HCO3- reabsorption/new production?

A

decreases reabsorption

no new HCO3- is generated

208
Q

in respiratory alkalosis, what does the renal compensatory system do to [H+] and [HCO3-]?

A

[H+] is increased

[HCO3-] is decreased further

209
Q

how does correction of respiratory alkalosis occur?

A

restoration of normal ventilation

210
Q

what does the renal compensatory system do to the pH in respiratory alkalosis?

A

reduces it

due to reducing HCO3- and therefore increasing H+ through buffer system

211
Q

what is the most common of the 4 major acid base disturbances?

A

metabolic acidosis

212
Q

in metabolic acidosis, what happens to the levels of [H+] and [HCO3-]?

A

[H+] increased

[HCO3-] decreased

213
Q

what is uncompensated metabolic acidosis indicated by?

A

pH below 7.35 and [HCO3-] is low

214
Q

how does the respiratory system compensate for metabolic acidosis?

A

ventilation increases to blow off more CO2

215
Q

in respiratory compensation of metabolic acidosis, what happens to the [H+] and the [HCO3-]?

A

[H+] decreases

[HCO3-] further decreases

216
Q

why is respiratory compensation for metabolic acidosis? essential when metabolic correction through the kidneys can occur?

A

respiratory compensation is needed to compensate pH immediately

renal system would take too long to correct

217
Q

how do you correct for metabolic acidosis?

A

kidneys lose H+ and gain HCO3-

218
Q

what happens to the [H+] and [HCO3-] in metabolic alkalosis?

A

[H+] decreases

[HCO3-] increases

219
Q

what is uncompensated metabolic alkalosis indicated by?

A

pH above 7.45 and [HCO3-] is high

220
Q

how does the respiratory system compensate for metabolic alkalosis?

A

ventilation is slowed

221
Q

how do pH changes signal to change lung ventilation?

A

through peripheral chemoreceptors

222
Q

what happens to the [H+] and [HCO3-] in respiratory compensation of metabolic alkalosis?

A

[H+] increases

[HCO3-] further increases

223
Q

how do you correct for metabolic alkalosis?

A

HCO3- is excreted

this also increases [H+] due to buffer system

224
Q

compare correction of resp acidosis/alkalosis to metabolic acidosis/alkalosis?

A

resp: restoration of normal respiratory function
metabolic: mediated by renal system

225
Q

compare compensation of resp acidosis/alkalosis to metabolic acidosis/alkalosis?

A

resp: renal system compensates
metabolic: resp system compensates

226
Q

why is respiratory acidosis harder to compenate for than metabolic acidosis?

A

because renal compensation (for respiratory acidosis) takes far longer than respiratory compensation (for metabolic acidosis)

227
Q

which parts of the nephron are the triple cotransporters found on?

A

thick ascending limb of the loop of henle

early distal tubule

228
Q

compare the ion permeability of the early and late collecting duct?

A

late collecting duct has a lower ion permeability

229
Q

what is the half life of ADH?

A

10-15 minutes

230
Q

what receptors within the cells of the collecting duct does ADH bind to?

A

type 2 vasopressin receptors

231
Q

what membrane of the cells lining the collecting duct are type 2 vasopressin receptors found on?

A

basolateral membrane

232
Q

what does the binding of ADH to the type 2 vasopressing receptors do?

A

increases expression of aquaporins on the apical membrane

233
Q

where are the aquaporins stored when they are not on the apical membrane?

A

internalised within vesicles and stored in the cytoplasm

234
Q

what does high plasma ADH concentrations do to the tonicity of the urine?

A

makes it hypertonic

235
Q

what does low plasma ADH concentrations do to the tonicity of the urine?

A

makes it hypotonic

236
Q

why does opening more aquaporins increase urine osmolarity?

A

because the fluid within the collecting duct equalises with the corticomedullary gradient meaning lots of water is reabsorbed

237
Q

as ADH concentration within the plasma increases what happens to the urine volume?

A

decreases

238
Q

as ADH concentration within the plasma decreases what happens to the urine volume?

A

increases

239
Q

as ADH concnetration within the plasma increases what happens to the total solute excretion?

A

remains the same

240
Q

what are the 2 main functions of ADH?

A

H2O reabsorption

arterial vasoconstriction

241
Q

what are the 2 stimulators of the hypothalamus to release ADH?

A

hypothalmic osmoreceptors

left atrial volume receptors

242
Q

what is the main form of treatment for central diabetes insipidus?

A

ADH replacement

243
Q

what long term drug side effect can cause diabetes insipidus?

A

lithium

244
Q

what is the main stimulator of the hypothalamus to release ADH?

A

hypothalmic osmoreceptors

245
Q

what causes the feed-forward inhibition of ADH?

A

stimulation of stretch receptors in the upper GI tract

246
Q

what does nicotine do to ADH release?

A

stimulates

247
Q

what does MDMA do to ADH release?

A

stimulates

248
Q

what does alcohol do to ADH release?

A

inhibits

249
Q

what directly stimulates release of aldosterone from the adrenal cortex?

A

increased K+

250
Q

what indirectly stimulates the release of aldosterone from the adrenal cortex?

A

decreased Na+ through RAS

251
Q

how much K+ is usually excreted in the urine in the absence of aldosterone and why?

A

none because it is all reabsorbed

252
Q

from what organ is ACE produced?

A

lungs

253
Q

what are the 4 functions of angiotensin II?

A

promote ADH secretion
thirst
arteriolar vasoconstriction
aldosterone

254
Q

what are the 3 stimulatory factors for renin release from the granular cells in the juxtaglomerular apparatus?

A
  1. reduced pressure in the afferent arteriole
  2. reduced NaCl sensed by the macula densa
  3. increased sympathetic activity (due to low BP)
255
Q

how does aldosterone increase reabsorption of Na?

A

increases expression of apical Na channels
increases number/activity of basolateral Na/K ATPase
(both in distal and colelcting tubules)

256
Q

where is atrial natriureteric peptide secreted?

A

atrial muscle cells

257
Q

what stimulates the secretion of ANP?

A

mechanical stretching of the atrium

258
Q

what are the 2 mechanisms which govern micturation?

A
  1. micturation reflex

2. voluntary control

259
Q

what stimulates the micturation reflex?

A

stretch in the walls of the urinary bladder

260
Q

what is the earliest expression of diabetic nephropathy?

A

microalbuminuria

261
Q

what is the most common reason for proteinuria? (broad)

A

glomerular proteinuria

262
Q

what are the different reasons for proteinuria? (broad sub groups)

A

overflow
glomerular
tubular
secreted

Renal (6 decks)

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