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Renal > 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 are the units of osmolarity?

A

osmol/l or mosmol/l

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3
Q

what 2 factors are needed to calculate osmolarity?

A
  • the molar concentration of the solution

- the number of osmotically active particles present

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4
Q

what are the units of osmolality?

A

osmol/kg water

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5
Q

when can the terms osmolarity and and osmolality be used interchangeably?

A

for weak salt solutions including body fluids

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6
Q

what is tonicity?

A

the effect a solution has on a cell volume

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7
Q

what affect does a hypertonic solution have on a cell?

A

fluid moves out of the cell- the cell shrinks

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8
Q

what affect does a isotonic solution have on a cell?

A

there is no change

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9
Q

what affect does a hypotonic solution have on a cell?

A

water moves into the cell, cell bursts

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10
Q

what are the 2 major components of total body water?

A

intra cellular fluid and extracellular fluid

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11
Q

why do males have 60% of body weight made up of water and woman only have 50%?

A

woman have more fat. fat cells dont contain a lot of water

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12
Q

what does extracellular fluid consist of?

A

plasma, interstitial fluid, other (negligible)

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13
Q

what are all body cells bathed in?

A

interstitial fluid

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14
Q

how can we measure body fluid compartments?

A

with ‘tracers’

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15
Q

what is insulin a useful tracer for?

A

ECF

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16
Q

what is a useful tracer of plasma?

A

labelled albumin

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17
Q

useful tracer of total body water?

A

3H20

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18
Q

how do you calculate the distribution volume (in litres)?

A
  1. add a known quantitty of tracer X (Qx: mol or mg) to the body
  2. measure the equilibration volume of X in the body ([X])
    distribution of volume = Qx (mol) / [X] (mol/litre)
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19
Q

what is meant by insensible loss of water?

A

loss of water from somewhere when there is no physiological control over this water loss eg water loss from the skin, lungs

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20
Q

where is there sensible loss of water in the body?

A
  • in sweat
  • faeces
  • urine
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21
Q

3 ways in which water can be put into the body?

A
  • fluid intake
  • food intake
  • metabolism
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22
Q

what changes when there is water imbalance?

A

body fluid osmolarity

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23
Q

are sodium ions more abundant in ECF or ICF?

A

always more sodium on the outside of the cell in the ECF

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24
Q

where is chloride ions more abundant?

A

ECF

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25
Q

where are potassium ions more abundant?

A

in the cell (ICF)

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26
Q

what are the main ions in the ICF?

A

potassium, magnesium

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27
Q

what is the difference in osmotic concentrations of ECF and ICF?

A

they are identical

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28
Q

what is the osmotic concentration of the ECF and ICF?

A

around 300 mosmol/l

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29
Q

what is meant by fluid shift?

A

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

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30
Q

if the ECF loses water, what will happen to its osmolarity?

A

it will go up

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31
Q

an increase in osmolarity in the ECF will cause what?

A

it to become hypertonic and cells are now in hyperotonic solution so they will begin to loss water from the ICF and water will go into ECF to restore volume and osmolarity

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32
Q

if there is a gain of NaCl in the ECF, what is the fluid shift response?

A

ECF goes up and ICF goes down

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33
Q

if there is a loss if NaCl from the ECF, what is the fluid shift response?

A

ECF goes down and ICF goes up

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34
Q

what affect does a gain or loss of isotonic fluid have?

A
  • no change in fluid osmolarity

- change in ECF volume only

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35
Q

what gives rise to electrolyte balance?

A

when the rates of loss equal the rates of gain

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36
Q

what are the 2 reasons why electrolyte balance is important?

A

1- total electrolyte concentrations can directly affect water balance (via changes in osmolarity)
2. the concentrations of individual electrolytes can affect cell function

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37
Q

what is the balance of sodium and potassium particularly important?

A
  1. they are major contributors to the osmotic concentrations of the ECF and ICF, respectively
  2. they directly affect the functioning of all cells
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38
Q

the presence of what makes up >90% of the osmotic concentration of the ECF?

A

sodium salts

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39
Q

what do potassium ions play a key role in?

A

establishing the membrane potential

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40
Q

what percentage of the bodys potassium is intracellular?

A

> 95%

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41
Q

what are the 2 things that can happen if small leakages or increased cellular uptake of potassium occurs?

A
  1. muscle weakness — paralysis

2. cardiac irregularities — cardiac arrest

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42
Q

what does salt imbalance manifest as?

A

changes in ECF volume

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43
Q

what is bilirubin a breakdown of?

A

haemoglobin

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44
Q

what hormone stimulates the kidney to produce erythropoitin?

A

EPO

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45
Q

what does erythropoitin do?

A

increase red blood cell production

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46
Q

what percentage of the cardiac output does the kidneys receive?

A

20-25%

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47
Q

what kind of appearance does the medulla have?

A

granulated appearance

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48
Q

what kind of appearance does the cortex have?

A

striated

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49
Q

what does the afferent arteriole subdivide to form?

A

the glomerulus

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50
Q

where does blood from the glomerulus pass to?

A

the efferent arteriole

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51
Q

where does blood flow to from the efferent arteriole?

A

into the peritubular capillaries

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52
Q

following the peritubular capillaries, where does the blood go?

A

the renal vein

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53
Q

what are the 2 types of nephron?

A

juxtramedullary and cortical

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54
Q

what percentage of nephrons are juxtamedullary nephrons?

A

20%

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55
Q

what are the 2 differences between juxtamedullary and cortical nephrons?

A
  1. juxtamedullary nephron has a very long loop of Henle compared to cortical nephron
  2. cortical nephron has a network of capillaries, whereas the juxtamedullary only has one vessel
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56
Q

what is the vessel in the juxtamedullary nephron called and what is its flow like?

A

vasa recta, sluggish flow

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57
Q

what is the function of the juxtamedullary nephrons?

A

enable us to make concentrated urine

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58
Q

if the smooth muscle of the afferent arteriole contracts, how will this affect the flow downstream to the glomerular capillary?

A

less blood will flow downstream

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59
Q

what percentage of plasma that flows through the capillary makes up the initial tubular fluid?

A

20%

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60
Q

how does the initial tubular fluid differ from the plasma?

A

almost identical except tubular fluid does not contain large proteins or red blood cells

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61
Q

what do the macula densa cells of the juxtaglomerular apparatus detect?

A

amount of salt in tubular fluid as it passes through this region of the nephron

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62
Q

for any substance: rate of excretion = ?

A

rate of filtration + rate of secretion - rate of reabsorption

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63
Q

for a freely filterable substance: rate of filtration = ?

A

rate of filtration of
X = [X]plamsa x GFR

GFR= glomerular filtration rate

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64
Q

what is the normal GFR in a healthy adult?

A

125 mil/min

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65
Q

how do you calculate rate of excretion?

A

rate of excretion of X:
X = [X]urine x Vu

Vu = urine flow rate

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66
Q

how do you calculate the rate of reabsorption?

A

Rate of reabsoption of X

= rate of filtration of X - rate of excretion of X

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67
Q

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

A

Rate of secretion of X:

rate of excretion of X - rate of filtration of X

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68
Q

what does is mean if the rate of filtration of a substance exceeds the rate of excretion of that substance?

A

net reabsorption of the substance has occured

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69
Q

what are the 3 filtration barriers in glomerular filtration?

A
  1. glomerular capillary endothelium
  2. basement membrane (basal lamina)
  3. slit processes of podocytes
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70
Q

what is the glomerular capillary endothelium a barrier to?

A

to RBC

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71
Q

what is the basement membrane a barrier to?

A

plasma protein barrier

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72
Q

what is the slit processes of podocytes a barrier to?

A

plasma protein barrier

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73
Q

what charge does the basement membrane have and how is the useful?

A

has a net negative charge, this helps to repel negatively charged plasma proteins to prevent filtration of these

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74
Q

what 4 things contribute to net filtration pressure?

A
  1. glomerular capillary blood pressure
  2. capillary oncotic pressure
  3. Bowman’s capsule hydrostatic pressure
  4. Bowman’s capsule oncotic pressure
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75
Q

how is the net filtration pressure calculated?

A

(glomerular capillary BP + Bowman’s Capsule oncotic pressure) - (Bowman’s capsule hydrostatic pressure + capillary oncotic pressure)

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76
Q

what 2 forces that compromise net filtration favor filtration?

A

glomerular capillary BP and Bowmans capsule oncotic pressure

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77
Q

what 2 forces that compromise net filtration oppose filtration?

A

Bowman’s capsule hydrostatic pressure and capillary oncotic pressure

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78
Q

will a build up of fluid in the lumen of Bowman’s capsule act to oppose or promote filtration?

A

oppose filtration

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79
Q

what is another term for oncotic pressure?

A

colloid osmotic pressure

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80
Q

what are the 4 forces that compromise net filtration pressure often known as collectively?

A

Starling forces

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81
Q

why is the oncotic pressure of the Bowman’s capsule zero?

A

since there should be no plasma proteins within the lumen

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82
Q

is filtration at the glomerulus active or passive?

A

passive

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83
Q

what is the normal GFR?

A

125 ml/min

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84
Q

what is the major determinant of GFR?

A

glomerular capillary fluid (blood) pressure

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85
Q

what is the extrinsic regulation of GFR?

A

sympathetic control via baroreceptor reflex

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86
Q

other than extrinsic regulation of GFR, what else controls it?

A

autoregualtion (intrinsic) control

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87
Q

what are the 2 parts to the autoregulation (intrinsic) of GFR?

A
  1. myogenic mechanism

2. tubuloglomerular feedback mechanism

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88
Q

how does blood pressure affect GFR?

A

because it affects glomerular filtration pressure

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89
Q

what happen to GFR is there is vasoconstriction of the afferent arteriole?

A

reduced GFR

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90
Q

what affect does an increase in sympathetic activity have on the GFR and urine output?

A

causes constriction of afferent arterioles which causes a reduction in glomerular capillary fluid pressure which causes a fall in GFR and decreased urine volume

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91
Q

what prevents short term changes in systemic arterial pressure affecting GFR?

A

autoregulation

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92
Q

what happens in the myogenic response?

A

if vascular smooth muscle is stretched (ie arterial pressure increased), it contracts thus consticting the arteriole

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93
Q

what is the tubuloglomerular feedback mechanism? what does it do if GFR rises?

A
  • involved the juxtaglomerular apparatus

- if GFR rises, more NaCl flows through the tubule leading to constriction of afferent arterioles

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94
Q

give an example when extrinsic control to the kidneys can override intrinsic control?

A

haemorrhage

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95
Q

what part of the juxtaglomerular apparatus senses NaCl content of tubular fluid?

A

macula densa

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96
Q

how does a kidney stone decrease GFR?

A

blockage increases hydrostatic fluid pressure in Bowman’s capsule which opposes filtration and decreases GFR

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97
Q

what affect does severe diarrhoea have on GFR?

A

decreases it

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98
Q

how does severe diarhhoea decrease GFR?

A

dehydration which increases plasma protein concentration which increases capillary oncotic pressure which opposes filtration: decreased GFR

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99
Q

what affect does severe burns have on GFR?

A

increases GFR

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100
Q

how do severe burns increase GFR?

A

lose plasma proteins from site of burns, decreases plasma protein conc, decreases capillary oncotic pressure which normally would oppose filatration but since it is decreased GFR goes up

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101
Q

how does damage to the kidneys lead to a decreased GFR?

A

makes glomerular membrane less permeable which leads to reduced GFR

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102
Q

what is plasma clearance a measure of?

A

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

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103
Q

what is the plasma clearance equal to?

A

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

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104
Q

what are the units of plasma clearance?

A

ml/min

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105
Q

how do you calculate clearance of a substance?

A

clearance of substance X =

(conc of X in urine) x (rate of urine flow) divided by plasma conc of X

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106
Q

why does inulin clearnance = GFR?

A

it is freely filtered at glomerulus and is neither absorbed nor secreted and not metabolised by kidney

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107
Q

what can measurements of inulin clearance be used to determine?

A

GFR

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108
Q

what is inulin?

A

exogenous compound- a polysaccharide

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109
Q

what else other than inulin can be used as a rough determinant of GFR?

A

creatinine clearance

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110
Q

why is creatine clearance not as reliable as inulin clearnace in determining GFR?

A

undergoes some tubular secretion

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111
Q

what should the clearance of glucose be?

A

should be zero, should be no glucose in urine

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112
Q

how is urea handled in the kidney?

A

filtered, partly reabsorbed and not secreted

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113
Q

should the clearance of urea be higher or lower than GFR?

A

clearance of urea should be lower than GFR

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114
Q

what percentage of filtered urea is reabsorbed?

A

50%

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115
Q

for a substance that is filtered, secreted but not reabsorbed, is its clearance more or less than GFR?

A

more than GFR

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116
Q

what is used clinically to calculate renal plasma flow (RPF)?

A

para-amino hippuric acid (PAH)

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117
Q

what is para-amino hippuric acid?

A

an exogenous organic anion

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118
Q

how is para-amino hippuric acid dealt with in the kidney?

A

freely filterated at glomerulus, secreted into the tubule, not reabsorbed and completely cleared from the plasma

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119
Q

what should the renal plasma flow of a healthy individual be?

A

650 ml/min

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120
Q

critea for a GFR marker?

A

should be filtered freely, not secreted or reabsobed

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121
Q

critea for a RPF marker?

A

should be filtered and completely secreted

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122
Q

what is filtration fraction?

A

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

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123
Q

how do you calculate filtration fraction?

A

GFR divided by renal plasma flow

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124
Q

what is the normal filtration fraction?

A

20%

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125
Q

how do you calculate renal blood flow?

A

renal plasma flow x (1/1-Hct)

where Hct = haematocritt

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126
Q

what percentage of CO does the kidneys receieve?

A

around 24%

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127
Q

approximately how many times a day is plasma filtered?

A

65 times per day

128
Q

how much of filtered fluid is reabsorbed in the proximal tubule per minute?

A

80ml/min

129
Q

is the fluid that is reabsorbed in the proximal tubule hypo/hyper or iso-osmotic with filtrate?

A

iso-osmotic

130
Q

what is meant by iso-osmotic?

A

salt and water reabsorption is equal

131
Q

what substances are reabsorbed in the proximal tubule?

A

sugars, amino acids, phosphate, sulphate, lactate

132
Q

what is secreted in the proximal tubule?

A

hydrogen ions, hippurates, neurotransmitters, bile pigments, uric acid, drugs, toxins

133
Q

what are the 2 types of reabsorption that can take place in the nephron?

A

transcellular and paracellular

134
Q

when does paracellular reabsorption occur?

A

if the cells dont have such tight junctions

135
Q

what do substances from the filtrate need to go through to get into the peritubular capillary?

A

luminal membrane then tubular epithelial cells then interstitial fluid then the capillary wall (endothelia)

136
Q

what are the 3 types of carrier-mediated membrane transport?

A
  • primary active transport
  • secondary active transport
  • facilitated diffusion
137
Q

primary active transport?

A

energy is directly required to operate the carrier and move the substrate against its concentration gradient

138
Q

secondary active transport?

A

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

139
Q

facilitated diffusion?

A

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

140
Q

how does oxygen and carbon dioxide move into/out of the cell?

A

diffusion through the lipid bilayer

141
Q

how does sodium enter the cell?

A

diffusion through channels

142
Q

how does glucose enter the cell?

A

facilitated diffusion

143
Q

what type of transport occurs at a sodium/potassium pump?

A

primary active transport

144
Q

what type of transport occurs at a sodium/glucose pump?

A

secondary active transport

145
Q

if one ATP is hydrolysed, what affect does this have in the sodium/potassium pump?

A

3 Na are kicked out of the cell and 2 potassium are taken in

146
Q

what is the isoosmotic fluid reabsorption across ‘leaky’ PT epithelium due to?

A
  1. standing osmotic gradient

2. oncotic pressure gradient

147
Q

what percentage of filtrate glucose is reabsorbed at the PT?

A

usually 100%

148
Q

over what membrane can glucose easily pass down its gradient?

A

over basolateral membrane

149
Q

what membrane can glucose not easily diffuse across, what does it need ti help?

A

the cell membrane - needs co-transporter or facilitated diffusion

150
Q

why is there a transport maximum for glucose?

A

co-transport requires conformational changes in the proteins and therefore only so many molecules can be moved per unit time

151
Q

what causes glucose in the urine in DM?

A

high glucose concentration in the plasma leads to high amount of glucose filtered and the transport mechanisms become saturated so not all glucose can be reabsorbed.

152
Q

what is the renal threhold for plasma glucose concentration?

A

10-12 mmol/l

153
Q

what percentage of all salt and water is reabsorbed in the PT?

A

67%

154
Q

what is Na+ reabsorption driven by?

A

the basolateral Na+ - K+- ATPase

155
Q

what does sodium reabsorption drive?

A

chloride reabsorption through the paracellular pathway

156
Q

how is water reabsorbed?

A

by osmosis

157
Q

what is the function of the loop of Henle and what does this enable?

A
  • generates a cortico-medullary solute concentration gradient
  • enables the formation of hypertonic urine
158
Q

what is opposing flow in the 2 limbs of loop of Henle referred to as?

A

countercurrent flow

159
Q

what does the loop of Henle work with to establish a hyper-osmotic medullary interstitial fluid?

A

vasa recta

160
Q

what is being reabsorbed the entire length of the ascending limb of loop of henle?

A

sodium and chloride

161
Q

how is sodium and chloride reabsorbed in the thick (upper) ascending limb?

A

active transport

162
Q

how is sodium and chloride reabsorbed in the thin (lower) acending limb?

A

passive

163
Q

why does little or no water follow salt reabsorption in the ascending limb?

A

it is relatively impermeabel to water

164
Q

what does the descending limb of loop of Henle absorb?

A

does not reabsorb NaCl and it highly permeable to water

165
Q

what does the selective permeabilities of the ascending and descending limbs of the loop of Henle enable?

A

an osmotic gradient to be established in the medulla

166
Q

what do loop diuretics block?

A

the triple co-transporter

167
Q

what happens at the triple co-transporter?

A

recycling of potassium and NaCl is absorbed into the interstitial fluid

168
Q

where does the triple co-transporter pump solute from?

A

the thick ascending limb of loop of Henle

169
Q

as you move further into the medulla, what happens to the concentration of interstitial fluid?

A

it increases

170
Q

what happens to the concentration of the tubular fluid as it moves down the descending limb and then up the ascending limb?

A

increasingly concentrated as it moves down the descending limb and becomes increasingly dilute as it ascends the ascending limb

171
Q

the tubular fluid is iso osmotic as it leaves the PT, what is it when it enters the DT?

A

hypo osmotic

172
Q

what contributes to approx half of the medullary osmolality?

A

the urea cycle

173
Q

how does urea enter the loop of Henle?

A

diffuses passively

174
Q

what does urea add to the interstitium?

A

adds solute

175
Q

is the distal tubule permeable to urea?

A

no

176
Q

what is the purpose of countercurrent multiplication?

A

to concentrate the medullary interstitial fluid

177
Q

why does a concentrated medullary interstitial fluid enable the kidney to do?

A

to produce urine of different volume and concentration according to the amounts of circulating ADH

178
Q

essential blood flow through the medulla tends to wash NaCl and urea away. what features of the vasa recta minimise this?

A
  1. vasa recta capillaries follow hairpin loops
  2. vasa recta capillaries are freely permeable to NaCl and water
  3. blood flow in vasa recta is low
179
Q

what preserves the medullary gradient?

A

passive exchange across the endothelium

180
Q

what does preservation of the medullary gradient ensure?

A

that the solute is not washed away

181
Q

what does the high medullary osmolarity allow in the presence of ADH?

A

production of hypertonic urine

182
Q

what is the osmolarity of the tubular fluid leaving the Loop of Henle?

A

hypo-osmotic, 100 mosmol/l

183
Q

what causes the osmotic gradient at the end of the loop of Henle/start of distal tubule?

A

tubular fluid is 100 mosmol/l and the surrounding interstitial fluid of the renal cortex is 300 mosmol/l.

184
Q

what is the collecting duct bathed in?

A

progressively increasing concentrations (300-1200 mosmol/l) of surrounding interstitial fluid

185
Q

what is the distal tubule and collecting duct a major site for?

A

the regualtion of ion and water balance

186
Q

what percentage of filtered ions are left by the time it gets to distal tubule?

A

less than 5%

187
Q

what is fluid and NaCl regualtion mainly influenced by?

A

hormomes

188
Q

what parts of the nephron are affected by hormones?

A

only the distal tubule and collecting duct

189
Q

what are the 4 hormones that influence the distal tubules and collecting duct in the regulation of ion and water balance?

A
  1. Antidiuretic hormone (ADH)
  2. Aldosterone
  3. Atrial natriuretic hormone
  4. Parathyroid hormone (PTH)
190
Q

what affect does ADH have on the regulation of water?

A

causes increased water reabsorption

191
Q

what affect does aldosterone have on ion regulation?

A

increased sodium reabsorption and and increased potassium and hydrogen excretion

192
Q

what affect does atrial natriuretic hormone have on ion regulation?

A

decreased sodium reabsorption

193
Q

what affect does PTH have on ion regulation?

A

increased calcium reabsorption and decreased phosphate ion reabsorption

194
Q

what 2 segments can the distal tubule be split into?

A

the early and late

195
Q

what is the function of the early distal tubule?

A

NaCl reabsorption

196
Q

what does the early distal tubule contain that allows it to undertake NaCl reabsorption?

A

the triple co-transporters

Na+-K+-2Cl- transport

197
Q

what is the late distal tubule responsible for?

A
  • calcium reabsorption
  • H+ secretion
  • sodium reabsorption and potassium reabsorption in the basal state but in presence of aldosterone potassium secretion
198
Q

what hormones is the late distal tubule sensitive to?

A

PTH, aldosterone

199
Q

what is the early collecting duct similar to?

A

the late distal tubule

200
Q

what are the properties of the late collecting duct and what is it influenced by?

A

a low ion permeability and permeability to water (and urea). influenced by ADH

201
Q

Where is ADH secreted from?

A

posterior pituitary

202
Q

what kind of peptide is ADH?

A

an octapeptide

203
Q

where is ADH synthesied?

A

by the supraoptic and paraventricular nuclei in the hypothalmus

204
Q

how is ADH transported from the hypothalmus to posterior pituitary and how is it stored?

A

down nerves to terminals where it is sorted in granules in posterior pituitary

205
Q

what triggers the release of ADH?

A

when action potentials down the nerves lead to calcium dependent exocytosis

206
Q

what is the plasma half-life of ADH?

A

10-15 minutes

207
Q

what effect does increased ADH have on the water permeability of the collecting duct?

A

increased water permeability

208
Q

what does ADH bind to in the tubule/collecting duct?

A

type 2 vasopressin receptor

209
Q

where do you find the type 2 vasopressin receptor?

A

basolateral membrane

210
Q

what type of receptor is a type 2 vasopressin receptor?

A

G-protein coupled receptor

211
Q

what does binding of ADH to type 2 vasopressin receptor cause an increase in?

A

in cyclic AMP

212
Q

what does the increase in cyclic AMP cause?

A

increased permeability of the luminal membrane

213
Q

how does the luminal membrane increase its permeability to water?

A

by inserting new water channels (aqauporins)

214
Q

what happens to the aquaporins on the luminal membrane when we are over-hydrated?

A

the become internalized back into vesicles and stored in the cytoplasm

215
Q

how do the aquaporins on the basolateral membrane differ from those on the luminal membrane?

A

the ones of the basolateral membrane are always present (do not internalize) and they are not influenced by ADH

216
Q

in the presence of high ADH, what type of urine is produced?

A

small amounts if hypertonic (concentrated) urine

217
Q

what is the main stimuli for the release of ADH?

A

an increase in plasma osmolarity

218
Q

what senses an increase in osmolarity?

A

hypothalamic osmoreceptors

219
Q

where does the hypothalmic osmoreceptors send signals to and what does the lead to?

A

the hypothalamic neurons, leads to an increased thirst which increases fluid and decreases plasma osmolarity

220
Q

a significant decrease in what can also activate hypothalamic neurons?

A

decrease in ECF

221
Q

what senses a significant drop in ECF ?

A

left atrial volume receptors

222
Q

if the left atrial volume receptors activates the hypothalamic neurons, what does this cause?

A

an increase in ADH, water reabsortion and decreased urine output so increased plasma volume

223
Q

what are the 2 types of diabetes insipidus?

A

central diabetes insipidus and nephrogenic diabetes insipidus

224
Q

main symptoms of DI?

A
  • large volumes of dilute urine

- constant thirst

225
Q

what is the problem in central DI?

A

posterior pituitary unable to produce or secrete ADH

226
Q

what is the problem in nephrogenic DI?

A

ADH production is normal but it does not exert its affects on tubules - problem with the receptors

227
Q

treatment for central DI?

A

ADH replacement

228
Q

what drug has a 25% risk of giving the patient DI?

A

long term lithium

229
Q

what is the most important stimuli for ADH release?

A

hypothalamic osmoreceptors

230
Q

what affect does decreased atrial pressure have on ADH release?

A

increased ADH release

231
Q

what affect does stimulation of stretch receptors in upper GI tract have on ADH release?

A

feed-forward inhibition of ADH

232
Q

what affect does nictotine and alcohol have on ADH release?

A

nicotine stimulates ADH release and alcohol inhibits ADH release

233
Q

most reabsoption happens at proximal tubule so why is there not a change is osmolarity?

A

salt and water is reabsorbed in equal proportions

234
Q

what is aldosterone released in response to?

A

-to rising potassium or falling sodium conc in the blood

235
Q

what system activates aldosterone release?

A

rennin-angiotensis system

236
Q

what does aldosterone cause?

A

stimulates sodium reabsorption and potassium secretion

237
Q

most of potassium is reabsorbed in the proximal tubule, when aldosterone is absent what happens to the rest of it?

A

it is reabsorbed in the distal tubule, no potassium is excreted in urine

238
Q

a change in what ion directly stimulates the adrenal cortex?

A

an increase in potassium

239
Q

how does a decrease in plasma sodium cause aldosterone secretion?

A

promotes indirect secretion of aldosterone by means of the juxtaglomerular apparatus

240
Q

what are the 3 ways in which rennin release can be stimulated?

A
  1. reduced pressure in afferent arteriole
  2. macula densa cells sense the amount of NaCl in distal tubule
  3. increased sympathetic activity as a result of reduced arterial BP
241
Q

what affect does reduced pressure in the afferent arteriole have on renin release and what affect does this have on blood volume?

A

more renin released, more sodium reabsorbed, increased blood volume, BP restored

242
Q

what affect does a reduced NaCl conc in the distal tubule have on renin release?

A

more renin release so more NaCl is reabsorbed

243
Q

what can abnormal increases in the R-A-A system cause?

A

hypertension

244
Q

what do loop diuretics target and inhibit?

A

the triple co-transporter found in the ascending limb of loop of Henle

245
Q

where is atrial natriuretic peptide/hormone produced and stored?

A

produced by the heart and stored in atrial muscle cells

246
Q

when is ANP released?

A

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

247
Q

what does ANP promote?

A

excretion of sodium and diuresis, decreasing plasma volume

248
Q

what affect does ANP have on smooth muscle of afferent arteriole?

A

vasodilation

249
Q

what affect does ANP have on sympathetic system?

A

decreases sympathetic activity

250
Q

what affect does ANP have on kidney tubules?

A

decreased sodium reabsorption

251
Q

what 2 mechanisms governs urination?

A
  1. the micturation reflex

2. voluntary control

252
Q

how much urine can the bladder accommodate before stretch receptors within its walls initiates micturation reflex?

A

250-400 ml

253
Q

what happens in the micturation reflex?

A

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

254
Q

how is mictruation reflex over-ridden?

A

by voluntarily tightening the external sphincter and surrounding pelvic diaphragm

255
Q

what is the normal pH of arterial blood?

A

7.45

256
Q

what is the normal pH of venous blood?

A

7.35

257
Q

average pH of blood?

A

7.40

258
Q

what is a pH of 7 in terms of nmol/l?

A

100 nmol/l

259
Q

what is a pH of 7.8 in terms of nmol/l?

A

16 nmol/l

260
Q

what do small changes in pH reflect?

A

large changes in hydrogen ion concentration

261
Q

what affect can acidosis have on the CNS?

A

can lead to depression of the CNS

262
Q

changes in what can influence potassium levels in the body?

A

changes in Hydrogen ions

263
Q

what affect does an increase in hydrogen ions have on potassium ions and where does this happen?

A

renal tubule increase hydrogen ion secretion and have a decrease in potassium ion secretion and this can lead to potassium ion retention

264
Q

hydrogen ions are continually added to the body fluids by what 3 sources?

A
  1. carbonic acid formation
  2. inorganic acids produced during breakdown of nutrients
  3. organic acids resulting from metabolism
265
Q

how do strong acids dissociate in solution?

A

dissociate completely

266
Q

how do weak acids dissociate in solution?

A

partially dissociate

267
Q

what do buffer systems consist of?

A

a pair of substances- one can yield free hydrogen ions as the hydrgen ion concentration decreases and the other can bind free hydrogen ions when the hydrogen increases

268
Q

at arterial PCO2 of 40mmHg what is the solubility coefficient?

A

0.03

269
Q

what is the Henderson-Hasselbalch equation?

A

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

270
Q

what is the normal pK?

A

6.1

271
Q

what is the normal bicarbonate?

A

24 mmol/l

272
Q

how do you work out the rate of filtration of bicarbonate ions?

A

GFR x [HCO3-]plasma

273
Q

what is the normal filtration rate of bicarbonate ions?

A

4320 mmol/day

274
Q

when the concentration of bicarbonate ions is low in tubular fluid, what does secreted hydrogen ions combine with?

A

phosphate

275
Q

what is tritratable acid?

A

the amount of hydrogen ions excreted as (largely) hydrogen phosphate

276
Q

is ammonia a measurement of titratable acid?

A

no - separate ammonium determination is necessary

277
Q

what can increase ammonium excretion in urine?

A

acidosis

278
Q

what 3 things does secretion of hydrogen ions by the tubules do?

A
  1. drives reabsorption of bicarbonate ions
  2. Forms acid phosphate
  3. forms ammonium ion
279
Q

how much hydrogen ions need to be secreted to accomplish a reaborption of 4320 mmol/day of bicarbonate ions?

A

4300 mmol/day H+ secretion

280
Q

how much titratable acid is secreted a day?

A

20 mmol/day

281
Q

how much ammonium is secreted per day?

A

40 mmol/day

282
Q

how much titratable acid is excreted each day?

A

20 mmol/day

283
Q

how much ammonium ions are excreted per day?

A

40 mmol/day

284
Q

what is the amount of hydrogen ion excretion equal to?

A

amount of “new” bicarbonate generated

285
Q

what is the vast majority of hydrogen ion secretions used for and why?

A

for bicarbonate ion reabsorption to prevent generation of acidosis

286
Q

what is the difference between compensation and correction of acid-base balance?

A

compensation is the restoration of pH irrespective of what happens to bicarbonate ions and Pco2.
correction of acid-base disturbance is restoration of pH and bicarb and Pco2 to normal

287
Q

what things can cause Co2 retention?

A

-chronic bronchitits, chronic empyhsema, airway restriction, chest injuries, respiratory depression

288
Q

what does co2 retention cause?

A

respiratory acidosis

289
Q

what causes the acidosis in CO2 retention?

A

increased CO2 drives equilibrium to the right and there is an increase in hydrogen ions

290
Q

what values indicates uncompensated respiratory acidosis?

A

pH 45 mmHg

291
Q

have affect does CO2 retention have on the renal tubules?

A

stimulates them to secrete hydrogen ions into filtrate

292
Q

in respiratory acidosis what happens to the bicarb ions in the renal tubules?

A

they are all reabsorbed

293
Q

what does correction of respiratory acidosis require?

A

lowering PCO2 by restoration of normal ventilation

294
Q

what causes respiratory alkalosis and when can this happen?

A

excessive removal of CO2 by the body

  • low inspired P02 at altitude
  • hyperventilation
295
Q

pH is only a measure of what?

A

free hydrogen ions

296
Q

why does excessive CO2 removal cause an alkalosis?

A

drives equilibrium to the left and there is an fall in hydrogen ions and bicarb ions (pH is only a measurement of free [H+]

297
Q

what values indicate a respiratory alkalosis?

A

ph > 7.5 and

PCO2

298
Q

how does the kidney compensate for resp alkalosis?

A

reduces H+ secretion into the tubule

299
Q

what affect does renal compensation for resp alkalosis have on bicarb concentration?

A

further lowers it

300
Q

what causes metabolic acidosis?

A

excess H+ from any source other than CO2

301
Q

examples of things that can cause an increase in H+?

A
  • ingestion of acids or acid-producing foodstuffs
  • excessive metabolic production of H+ (lactic acid)
  • excessive loss of base from the body (e.g diarrhoea)
302
Q

values that indicate metabolic acidosis?

A

ph

303
Q

what does a decrease in plasma pH stimulate?

A

peripheral chemoreceptors

304
Q

how does the respiratory system compensate for metabolic acidosis?

A

ventilation is increased and more CO2 is blown off, [H+]p is lowered raising pH to normal (bicarb ions are also lowered)

305
Q

how does the renal system correct metabolic acidosis?

A
  • filtered bicarb ions are very low and very readily reabsorbed
  • H+ secretion continues and produces TA and NH4+, to generate more “new” bicarb ions
306
Q

why is respiratory compensation essential in metabolic acidosis?

A

acid load cannot be excreted immediately, can take hours/days and even weeks to normalise

307
Q

what causes metabolic alkalosis?

A

excessive loss of H+ from the body

308
Q

in what ways can there be an excessive loss of H+?

A
  • loss of HCl from the stomach (vomiting)
  • ingestion of alkali
  • aldosterone hypersecretion
309
Q

how can aldosterone hypersecretion cause excessive loss of H+?

A

causes stimulation of Na+/H+ exchange at the apical membrane of the tubule: acid secretion

310
Q

what values indicate metabolic alkalosis?

A

ph > 7.45

bicarb ions high

311
Q

in respiratory acidosis is the bicarb high or low?

A

high

312
Q

in metabolic alkalosis is the bicarb high or low?

A

high

313
Q

in metabolic acidosis, is the bicarb low or high?

A

low

314
Q

in respiratory alkalosis , is the bicarb low or high?

A

low

315
Q

what affect does increased pH have on breathing?

A

slows ventilation

316
Q

what is the correction of metabolic alkalosis?

A
  • filtered bicarb load is so large so not all of it is reabsorped
  • bicarb excreted in urine
  • no TA or NH4+ is generated

Renal (10 decks)

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