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Renal > Physiology 2 > Flashcards

Physiology 2 Flashcards

1
Q

how much of the plasma is initially filtered by bowmans capsule

A

20%

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2
Q

how does the inital filtrate within bowmans capsule compare to the plasma

A

same minus plasma proteins

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3
Q

where does must reabsorption take place

A

within the proximal tubule

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4
Q

how much of what is filtered in reabsorbed

A 
99% of fluid 
99% of salt 
100% of glucose 
100% of amino acids 
50% of urea 
0% of creatinine
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5
Q

is reasborbtion of filtration specific

A

only reabsorbtion is specific (filtration relatively non specific)

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6
Q

what should glomerular filtrate not contain

A

RBCs, large plasma proteins

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7
Q

how mcuh fluid is reabsorbed in the proximal tubule

A

80 ml/min

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8
Q

how does the fluid reabsorbed within the proximal tubule compare to the filtrate

A

is iso-osmotic- no change in osmolarity between bowmans and end of proximal tubule

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9
Q

what is reabsorbed in the proximal tubule

A 
sugars 
amino acids 
phosphate 
sulphate 
lactate
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10
Q

what is secreted in the proximal tubule

A 
H+
hippurates
neurotransmitters
bile pigments 
uric acid
drugs + drug metabolites (atropine, morphine, pencillin) 
toxins
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11
Q

what is the path of transcellular reabsorption

A 
tubular lumen 
luminal membrane (into tubular epithelial cell) 
basolateral membrane (into interstitial fluid) 
endothlium
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12
Q

what is the path of paracellular reabsorption

A

through tight gap junctions inbetween the tubular epithelial cells

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13
Q

what is primary active transport

A

energy directly required to operate the carrier and move the substrate against its concentration gradient (energy from hydrolysis of ATP)

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14
Q

what is secondary active transport

A

when the molecule is transported coupled to the concentration gradient of an ion (usually sodium)

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15
Q

what is facilitated diffusion

A

passive carrier mediated transport of a substance down its concentration gradient

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16
Q

what is the sodium potassium pump

A

a primary active transporter

moves 3 Na out and 2 K in for every 1 ATP hydrolysed against their concentration gradients

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17
Q

what are the types of secondary active transporters

A

symporter- both molecules moving same direction

Anteporters - move in opposite directions

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18
Q

what are the different ways of getting into a cell

A 
diffusion through lipid bi layer 
diffusion through channels 
facilitated diffusion 
primary active transport 
secondary active transport
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19
Q

where are Na+K+ATPase pumps alwats

A

on the basolateral membranes of cells

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20
Q

what is the Na+K+ATPase pump essential for

A

Na+ reabsorption

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21
Q

describe Na+ reabsorption in the proximal tubule

A

ISO-OSMOTIC
net movement of sodium from lumin to blood via transcellular route creates an electrical gradient
water follows this gradient via paracellular route (passive down NaCl osmotic gradient)
(Cl- also follows sodium)

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22
Q

what other than the NaCl osmotic gradient pulls water from the lumen into the capillary

A

oncotic drag of peritubular plasma- plasma proteins more concentrated within the blood pulls water into capillary (increased on= water in)

also follows the con gradient of glucose via a paracellular route

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23
Q

how much of glucose is reabsorbed in the proximal tubule

A

100%

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24
Q

what is glucose reabsorbed in the proximal tubule

A 
co transport (in with Na+) ad luminal membrane 
facilitated diffusion at basolateral membrane
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25
Q

why is there no change in the osmolarity of the tubular fluid at either end of the proximal tubule

A

as solute and water reabsorbed in equal proportions

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26
Q

what is the transport maximum- why is it relevant

A

maximum rate at which we can reabsorb a particular substance that is dependent on the expression of specific membrane proteins

increasing plasma conc of a substance (e.g. glucose) saturates the transporters, that which cant be reabsorbed is excreted in the urine (diabetes)

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27
Q

what does PAH measure

A

renal plasma flow - completely filtered/ secreted

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28
Q

is there a secretion maximum

A

yes- secreting transporters can also be saturated

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29
Q

how much of salt and water are reabsorbed in the proximal tubule

A

67%

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30
Q

how much of glucose and amino acids are reabsorbed in the proximal tubule

A

100%

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31
Q

what drives Na+ reabsorption

A

the basolateral Na+ K+ ATPase

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32
Q

how does Cl- follow Na+

A

via paracellular pathway

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33
Q

how is water reabsorbed

A

osmosis (paracellular pathway)

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34
Q

describe the tubular fluid when it leaves the proximal tubule

A

iso-osmotic (i.e. 300 mosmol/l)

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35
Q

what is the function of the loop of henle

A

generates cortico-medullary solute concentration gradient (created by the interstitial fluid)

this enables the formation of hypetonic urine

acts as a countercurrent multiplier

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36
Q

what is fluid flow like within the loop of henle

A

countercurrent- opposing flow in the two limbs

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37
Q

what do the loop of henle and vasa recta establish together

A

a hyper osmotic medullary interstitial fluid

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38
Q

what is the role of the descending limb

A

highly permeable to water

does not reabsorb NaCl

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39
Q

what is the role of the ascending limb

A

Na+ and Cl- reabsorption
(thick upper= active transport, thin lower= passive)

relatively impermeable to water

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40
Q

what enables an osmotic gradient to be established within the medulla

A

selective permeabilities of the ascending and descending limbs

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41
Q

what three ions does the triple co transporter on the luminal membrane move into the cell

A

Na+
K+
Cl-

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42
Q

why is the ascending limb not permeable to water

A

gap junctions too tight

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43
Q

what do loop diuretics block

A

the triple co transporter within the ascending limb

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44
Q

in the ascending limb what allows NaCl to be absorbed into the interstitial fluid

A

K+ recycling (moving in and out of both luminal and basolateral membranes)

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45
Q

where is the triple co transporter

A

the thick ascending limb of the loop of henle

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46
Q

describe what happens to tubular fluid as it goes through the loop of henle

A

goes into descending limb
water removes- concentrated tubular fluid, increased omsolarity (300 to 400)
move into ascending limb where salt is removed- decreasing the osmolarity (400-200)

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47
Q

what type of fluid moves from the ascending tubule to the distal tubule

A

hypotonic

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48
Q

what is countercurrent multiplication

A

the process of using energy to generate an osmotic gradient that enables you to reabsorb water from the tubular fluid and produce concentrated urine

As the fluid continues to move through the loop of Henle, the horizontal gradient is multiplied into large vertical gradient, causing the osmotic gradient to steadily multiply until it reaches a steady state. The length of the loop of Henle determines the size of the gradient - the longer the loop, the greater the osmotic gradient

(progressive increase in interstitial fluid osmolarity)

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49
Q

what is the omsolarity of the kidney interstitial fluid

A

peripheries 300, increases to 1200 at centre (near hilum)

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50
Q

what creates the corticomedullary concentration gradient

A

the different interstitial fluid osmolarities of the kidney (isotonic at peripheral, hypertonic at centre)

made from urea and NaCl concentrations

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51
Q

what contributes 50% of medullary osmolarity

A

the urea cycle (adds solute to interstitium)

  • urea diffuses passively into the loop
  • collecting ducts absorb 50 urea
  • distal tubule not permeable to urea
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52
Q

what is the purpose of countercurrent multiplications

A

to concentrate the medullary interstitial fluid

allows kidney to produce urine of different volume and concentration depending on the circulating antidiuretic hormone

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53
Q

what is normal Vu

A

1ml/min

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54
Q

what is the countercurrent exchanger

A

vasa recta- runs along side the loop of henle juxtamedullary nephrons

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55
Q

how does the countercurrent exchanger work

A

capillary blood equilibriates with interstitial fluid across the leaky endothelium

blood osmolarity rises as it dips down into the medulla (water loss, solute gained)

blood osmolarity falls as it rises back into the cortex (water gained, solute lost)

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56
Q

how does the countercurrent system (loop of henle + vasa recta) prevent essential blood flow washing away NaCl and urea

A

vasa recta capillaries follow hair pin bends (slow blood flow)
are freely permeable to NaCl and water
blood flow to vasa recta is low

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57
Q

what is the purpose of the vasa recta (countercurrent system)

A

prevents essential blood flow washing away NaCl and urea

(no net change in blood as it flows through and then passes into renal vein)

Passive exchange across the endothelium preserves medullary gradient - blood equilibrates at each layer.
Ensures that the solute is not washed away

maintain corticomedullary concentration

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58
Q

what does high medullary osmolarity allow

A

the production of hypertonic urine in the presence of ADH

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59
Q

what is the omsolarity of the fluid leaving the loop of henle (distal tubular fluid)

A

hypo-osmotic (100 mosmol/L)

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60
Q

what is the osmolariy of the renal cortex

A

300 mosol/L

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61
Q

what is the osmolarity of the interstitial fluid surrounding the collecting duct

A

progressively increases from 300 to 1200 as descends through the medulla

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62
Q

what are the roles of the distal tubule and collecting duct

A

regulate ion and water balance

>95% of ions reabsorbed before they reach it but remaining 5% v important

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63
Q

what do all tubules empty into

A

the cortical collecting ducts

64
Q

what mainly regulates fluid and NaCl regulation

A

hormones

65
Q

where in nephrones do hormones affect

A

the cells of the distal tubule and the collecting duct (dont affect proximal tubule/ loop of henle)

66
Q

what hormone increases water reabsorption

A

ADH (vasopressin)

67
Q

what hormone causes reabsorption of Na+ and H+/K+ secretion

A

aldosterone

68
Q

what hormone causes decreased sodium reabsorption

A

atrial natriuretic hormone (ANH)

69
Q

what hormone causes increased Ca2+ reabsorption and decreased PO43- secretion

A

parathyroidhormone (PTH)

70
Q

what is the distal tubule permeable to

A

low permeability to water and urea- but can by increased with high ADH circulating

71
Q

why must urea be concentrated in the distal tubule fluid

A

as helps to establish osmotic gradient within the medulla

72
Q

what are the two segments of the distal tubule and their role

A

early segment:
-Na+ K+ 2Cl triple co transporter (salt reabsorption)

the late distal tubule:

  • Ca2+ reabsorption
  • H+ secretion
  • Na reabsorption
  • K+ reabsorption ( K+ secretion if aldosterone there)
73
Q

what cells are sensitive to aldosterone

A

later part of distal tubule

74
Q

what is the late collecting duct permeable to

A

low ion permeability

permeable to water (and urea)

75
Q

what is the collecting duct influenced by

A

ADH

76
Q

what are the parts of the collecting duct

A

early and late

77
Q

what is ADH and where is it made

A

(octa)peptide hormone
synthesised by the supraoptic and paraventricular nuclei in the hypothalamus
(is therefore and neuropeptide)

78
Q

what is the path of ADH

A

transported down nerves to terminals where is stored in granules (vesicles within the terminals) in the posterior pituitary gland
released into blood when action potentials down the nerves lead to Ca2+ dependent exocytosis

79
Q

what is the plasma half life of ADH

A

10-15 mins (short like all peptide hormones)

80
Q

how does ADH affect water permeability of the collecting duct

A

when ADH binds it increases intracellular
cAMP
this initiates the insertion of aquamporins into the apical membrane of collecting duct epithelial cells

this increases the collecting ducts permeability to water

81
Q

what happens to collecting duct when ADH decreases

A

the expression of water channels at apical membranes decreases (channels become internalised within vesicles)

82
Q

what happens to water when there is high ADH

A

moves from the collecting lumen along to osmotic gradient into the meduallry interstitial fluid- enables hypertonic (concentrated) urine formation

83
Q

what happens to water when there is low ADH

A

collecting ducts have low permaebility

enables the creation of hyptonic urine (<50mosmol/L)

84
Q

what equilibrates when there is high ADH

A

the tubular fluid equilibrates with interstitium (via aquaporins) as water moves from into interstitium ad concentrated urine (to 1200 mosmol/L)

85
Q

where is impermeable to water

A

the ascending loop of henle

AND
the collecting duct when there is minimal ADH (no water reabsorption)

86
Q

does ADH conc have a direct/ inversely proportion affect on urine volume and osmolarity

A

direct with osmolarity

inversely proportionate with urine volume

87
Q

how does increased plasma osmolarity affect ADH secretion

A 
stimulates hypothalamic osmoreceptors 
these stimulate hypothalamic neurones 
increase thirst 
increases fluid intake 
decreases plasma osmolarity 
increases plasma volume/ABP
88
Q

how does a decrease in ECF volume cause secretion of ADH

A

causes decrease in ABP (usually when large changes in plasma volume)
stimulates left artial volume receptors
stimulates hypothalamic neurones
increases ADH secretion
increases arteriolar vasoconstriction
also increases H20 permeability of distal and collecting tubules
increases H2O reabsorption
decreases urine output
increases plasma volume and decreases plasma osmolarity

89
Q

what are the symptoms of diabetes insipidus

A

large volumes of dilute urine

constant thirst

90
Q

what are the types of diabetes insipidus

A

central- failure to produce/secrete ADH from post pit

nephrogenic- unable to respond to ADH- defect in type II vasopressin receptor/ defect in cell response

91
Q

what is the treatment for diabetes inspidus

A

central- ADH replacement

nephrogenic- dependent on cause (stop possible causative drugs, rehydrate etc)

92
Q

what is the most important stimulus for ADH release

A

hypothalamic osmoreceptors (respond to changes in omsolarity of plasma)

also stimulated by activation of left atrial stretch receptors

93
Q

decreased atrial pressure = increased/ decreased ADH release?

A

increased

94
Q

how does the GI tract affect ADH secretion

A

stretch receptors in upper GI tract exerts feed-forward inhibition of ADH (stops secretion of ADH before food as fluid about to be absorbed in meals)

95
Q

what ‘drugs’ stimulates/ inhibit ADH release

A

nicotine stimulates release

alcohol inhibits release

96
Q

summaries the omsolarity of tubular fluid throughout the nephron

A

Tubular fluid at the start of the nephron flows along the proximal tubule (absorption of all filtered water and fluid- in equal proportions so stays same osmolarity) (flow rate reduces as so much absorbed)
When enters descending limb it loses water and osmolarity increases
When enters ascending limb loses salt so osmolarity decreases (when leaves has osmolarity of 100)

Depending on level of ADH when it enters distal tubule and collecting duct will increase in osmolarity (ADH high) or decreases (ADH low)

97
Q

what is aldosterone and where is it made

A

steroid hormone secreted the adrenal cortex (zona glomerulosa)

98
Q

when is aldosterone secreted

A

in response to rising K+ or falling Na+ in the blood

due to activation of the renin-angiotensin system

99
Q

what does aldosterone do

A

stimulates Na+ reabsorption and K+ secretion

100
Q

what does Na+ retention cause

A

increased blood volume and pressure (water follows sodium)

101
Q

where is potassium K+ absorbed

A

90% in the early regions of the nephron (proximal tubules)

when aldosterone is absent the rest is reabsorbed in the distal tubule (no K+ excreted in the urine)

102
Q

what does an increase in K+ conc directly stimulate

A

the adrenal cortex

103
Q

how does sodium affect secretion of aldosterone

A

a decrease in plasma Na promotes the indirect secretion of aldosterone via the juxtaglomerular apparatus (macula densa cells) (activates RAAS system)

104
Q

where does aldosterone affect

A

the cells of the distal and collecting tubule

105
Q

what secretes renin

A

granular cells in the JGA

106
Q

what secretes angiotensin

A

liver

107
Q

what secretes ACE

A

lungs

108
Q

where does angiotensin II stimulate

A

adrenal cortex

109
Q

how does aldosterone affect Cl levels

A

Cl- follows Na+ passively (aldosterone increases Na reabsorption so Cl also increases)

110
Q

what are the affects of angiotensin II (not on the kidney)

A 
arteriolar vasconstriction 
increased thirst 
increased vasopressin (ADH)
111
Q

what causes the release of renin

A

decreased: NaCl/ ECF volume/ ABP

reduced pressure in efferent arteriole
increased sympathetic activity as a result of reduced arterial blood pressure

112
Q

what innervates the granular (renin secreting cells)

A

sympathetic nervous system (increased firing in decreased ABP causes renin release)

113
Q

what senses a decrease in NaCl in the distal tubule

A

macula densa cells in the JGA (decreased NaCl = more renin released)

114
Q

how does aldosterone increase Na+ reabsorption

A

increase number of Na channels in apical membrane

increase number and activity of channels of transporters at the basolateral membranes

115
Q

why do the effects of aldosterone take longer

A

as steroid hormones (alter gene transcription and proteins, have longer half life)

116
Q

how does heart failure cause fluid retention

A

as decreased CO and BP
low BP stimulates RAA system
increased salt and water retention

117
Q

what is the treatment for heart failure

A 
low salt diet 
loop duiretics (target to triple co transporter) 
ACE inhibitor (stop fluid and salt retention and ateriolar constriction)
118
Q

what produces ANP

A

the heart- stored in atrial muscle cells

119
Q

when is ANP released

A

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

120
Q

what does ANP do

A

promotes excretion of Na+ and duiresis (decreases plasma volume)
afferent arteriolar vasodilation
decreased sympathetic stim= decreased CO and total peripheral resistance
(decreased arterial BP)

121
Q

what controls micturation

A 
the mitcuration reflex (involuntary emptying by simultaneous bladder contraction and opening of sphincters) 
voluntary control (tightening of ecternal sphinter and surrounding pelvic diaphragm)
122
Q

describe the steps of the micturition relfex

A 
bladder fills 
stretch receptors
increases parasym 
bladder contracts 
sphintcers open
123
Q

how much can the bladder hold

A

250-400mls

124
Q

what is water diuresis

A

increased urine flow but not increased solute excretion

125
Q

what is osmotic diuresis

A

increased urine floe as a result of primary increase in salt excretion

126
Q

what is the difference between water and osmotic diuresis

A

Any loss of solute in the urine must be accompanied by water loss (osmotic diuresis), but the reverse is not true; water diuresis is not necessarily accompanied by equivalent solute loss.

127
Q

what regulates erythtopoiesis

A

kidney produce erythropoietin if O2 in tissues too low

erythropoietin stimulates stem cells in bone marrow to produce RBCs which increase O2 supply in tissues

128
Q

what is pH

A

measure of the unbound H+ conc

129
Q

what is a normal pH

A

7.35-7.45

130
Q

which blood is more acidic

A

arterial- 7.45
venous- 7.35
(averages 7.4)

131
Q

what do small changes in pH show

A

big changes in H+ conc

132
Q

what is the pH of ECF

A

7.4 (tightly controlled)

133
Q

what does acidosis cause

A

depression of the CNS (coma)
enzyme activity affected
potassium retention

134
Q

what does alkanosis cause

A

overexcitability of the peripheral NS and central NS (pins and needles, muscle spasms)
affects enzymes

135
Q

what ads to H+ in the body

A

carbonic acid formation
inorganic acids (produced during breakdown of nutrients- e.g. meat proteins)
organic acids resulting from metabolism (fatty, lactic or keto acids)

136
Q

how does DM affect body pH

A

the metabolism of fat produces keto acids= acidosis= DKA

137
Q

what are strong and weak acids

A

Strong acids dissociate completely in solution

Weak acids dissociate partially in solution

138
Q

what makes up a buffer system

A

pair of substances

  • one can yield free H+ of they decrease
  • one can bind free H+ if the H+ increases

HA (undissociated acid) = H+ (proton) + A- (base)

139
Q

what happens if H+ is added to HA = H+ + A-

A

equilibrium shifts to the left as protons are mopped up by A- causing more HA to be made (HA rises, A- falls)

140
Q

what happens if B- is added to HA = H+ + A-

A

base is tidied up by combining with H+ allowing more HA to dissociate
equilibrium shifts to the right (HA falls A- rises)

141
Q

what is the dissociation constant

A

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

shows much much an acid will dissociate

142
Q

what is pK

A

the pH at which the reaction will be at equilibrium

143
Q

how do you calculate [H+]

A

= K x [HA]/[A-}

or

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

144
Q

what forms carbonic acid

A

CO2 and water, catlyzed by carbonic anhydrase

145
Q

what is the carbonic acid buffer system

A

CO2 + H20 = (carbonic anhydrase) = carbonic acid (H2CO3) = H+ + HCO3- (bicarb)

146
Q

what controlls HCO3-

A

the kidneys

147
Q

what controls PCO2

A

the lungs

148
Q

what controls the normal plasma pH at 7.4

A

HCO3- (24mmol/l) from kidneys

PCO2 (40mmHg x 0.03) from lungs

149
Q

what is the role of the kidney in HCO3- concentration

A

variable reabsorption of filtered HCO3-

kidneys can add new HCO3- to the blood

(both these dependent on H+ secretion into the tubule)

150
Q

what drives the reabsorption and secretion of bicarb from the kidneys (HCO3-)

A

H+ secretion

151
Q

how is HCO3- reabsorbed in to the proximal tubule

A

combines with H+ to make carbonic acid which dissociates to make CO2 and water
these move into epithelial cells where via carbonic anhydrase they form carbonic acid again then split into H+ and bicarb
the H+ goes back to apical membrane to join the HCO3- in lumen again, the HCO3- moves out of basolateral membrane with Na+ to get into the interstitial fluid

152
Q

what drives hydrogen ion secretion

A

CO2- CO2 retention will cause H+ ion secretion

153
Q

how does the kidney make new HCO3-

A

(e.g. in order to regenerate buffer stores depleted by an acid load)
when [HCO3-] in tubular fluid is low, secreted H+ combines with phosphate (a waste product of protein metabolism) which forms and acid an is excreted in the urine = net gain of HCO3- and excretion of acid

154
Q

what is titratable acid

A

the amount of H+ excreted as largely H2PO4-

max that can be excreted is 40 mmol/day

155
Q

how else can acid be excrete (other than binding to phosphate)

A

break down glutamine (from liver) to form ammonia - this goes into tubular fluid and forms ammonium ion (NH4+) which is excreted in urine
(generates new HCO3- aswell)

this is done in severe acidosis

156
Q

what does H+ secretion by the tubule do

A

drives reabsorption of HCO3- (to prevent acidosis)
forms acid phosphate (to excrete)
forms ammonium ion (to excrete)

alkanises the body and regenerates buffer stores

Renal (27 decks)

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