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Integrated Physiology and Pharmacology > Kidneys > Flashcards

Kidneys Flashcards

1
Q

What type of genetic disease is Liddle’s syndrome?

A

Autosomal dominant

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2
Q

What are the primary symptoms of Liddle’s Syndrome?

A

Sodium retention and fluid retention

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3
Q

What are the secondary symptoms of Liddle’s syndrome?

A

Hypokalaemia, metabolic acidosis, low renin and aldosterone in a compensation attempt

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4
Q

What are the subunits of an epithelial sodium channel (ENAC) and the ratio?

A

Alpha, beta, gamma in ration 1:1:1

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5
Q

What are the three channels on the apical membrane of the principal cell and what are their roles?

A

ENaC causes Na to be reabsorbed
RomK causes potassium to leave the cell
Aquaporin 2 causes water to move into the cell

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6
Q

What are the three channels on the basolateral membrane of the principal cells and what are their roles?

A

Sodium potassium ATPase - set up concentration gradient of sodium
Kir2.3 - causes potassium to leave the cell for the negative membrane potential
Aquaporin 3 and 4 - causes water to leave the cell

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7
Q

What is the mutation in ENaC that causes Liddle’s?

A

mutations in the COOH tail of the Bete or Gamma sununits. Deletion of the proline rich motifs which are key for endocytosis

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8
Q

What is the effect of the mutation in ENaC in Liddle’s?

A

It is not pulled out the cell properly when it should be so endocytosis is disrupted. This is because the protein can not be tagged with ubiquitin

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9
Q

How can it be shown experimentally that this mutation in ENaC could cause Liddle’s syndrome?

A

Injection of complementary RNA into xenopus oocyte. Shows that the current in the WT is 3 microamps but in the mutated version it is 6. The channels are removed very slowly

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10
Q

What causes hypertension in Liddle’s?

A

Excess sodium and water reabsortpion

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11
Q

What causes hypokaleamia in Liddle’s?

A

More sodium uptake cause more potassium to be secreted on the apical membrane and is excreted into the urine

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12
Q

How does Liddle’s cause metabolic alkalosis?

A

Recording electrodes show that epithelial cells have a negative membrane potential
The negative charge is a driving for H+ excretion. As more sodium is reabsorbed there is an increase in the negative membrane potential so H+ secretion increases

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13
Q

Normally, what happens when there is low aldosterone and renin in a person?

A

Low levels of aldosterone causes ENaC to be pulled away from the apical membrane of the principal cells. This decreases sodium reabsorption, increases urine flow rate and lowers blood pressure

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14
Q

What is the risk of hypertenstion in a Liddle’s syndrome patient?

A

Increased risk of heart disease and stroke

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15
Q

Which drug can be used to treat the high blood pressure in Liddle’s syndrome and how does it work?

A

Amiloride

It works by blocking ENaC so sodium reabsorption is lower

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16
Q

For a child a blood pressure of 121/67 is very high - true or false?

A

True

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17
Q

Why is spinolactone not effective in trating Liddle’s syndrome?

A

It is a mineralcorticoid receptor antagonist but has no effect as the receptors for aldosterone are not being activated anyway. Normally this can be used to treat high blood pressure

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18
Q

Vasopressin causes what on the apical membrane of principal cells?

A

Binding of vasopressin causes cAMP to be activated, which causes Pka to be activated, causing the shuttling of Aquaporin 2 vesicles onto the apical membrane. This results in increase water reabsorption

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19
Q

Diabetes insipidus is generally categorised as a problem with what?

A

The vasopressin - aquaporin 2 system

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20
Q

What are the 4 types of diabetes insipidus?

A

Primary polydypsia, gestational, central and nephrogenic

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21
Q

What is primary polydypsia?

A

Not an actual condition, polydypsia caused by excessive drinking

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22
Q

What is gestational diabetes insipidus?

A

Can be seen in some pregnant women, the placenta produces enzymes which break down vasopressin so urine flow rate increases causing polydypsia. Will return back to normal after pregnancy

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23
Q

What is central diabetes insipidus?

A

Impaired vasopressin production, can be acquired or congenital

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24
Q

What is nephrogenic diabetes insipidus?

A

Impaired effect of vasopressin at the level of the kidney, can be aquired or congenital

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25
Q

What are common causes of central diabetes insipidus?

A

Acquired: Infection, head trauma, surgery
Congenital: Neurohypophyseal D1, mutations in the vasopressin gene (67 types)

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26
Q

Mutations in vasopressin often affect what?

A

Transport of vasopressin from the hypothalamus to the posterior pituitary. The ability to traffic the vasopressin which is made down the pituitary stalk properly

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27
Q

What are some possible causes of aquired nephrogenic diabetes insipidus?

A

Lithium (taken for bipolar disorder), some antibiotics, antifungals and chemotherapy. hypokalaemia and hypercalcuria, and acute and chronic kidney failure

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28
Q

What are some possible causes of congenital nephrogenic diabetes insipidus?

A

Mutation in vasopressin receptor (more common) or aquaporin 2 genes
The AVPR2 gene (vasopressin receptor) is X linked
AQP2 gene mutation impact on trafficking and function

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29
Q

What are the first symptoms of congenital nephrogenic diabetes insipidus in children?

A

Hypernatrimic dehydration (Increased urine flow rate), Poor feeding, skin dryness and depressed anterior fontanel (dip in front of forehead)

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30
Q

What can be used to treat central DI?

A

Vasopressin can be replaced with desmopressin via a nasal spray at regular intervals

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31
Q

What can be used to treat nephrogenic DI?

A 
more difficult to treat 
Modulator drugs can be used when proteins are misfolded but are still functional to prevent degredatio
Pharmacological chaperones
Cell permeable receptor agonists
cGMP and cAMP pathway agonists
Statins
Prostaglandins
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32
Q

What can pass through the glomerulus?

A

Water and small molecules (not blood cells and proteins)

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33
Q

Small molecular weight proteins in urine indicates a problem with what?

A

The proximal tubule

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34
Q

Large molecular weight proteins in urine indicate a problem with what?

A

The glomerulus

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35
Q

How many litres are filtered a day?

A

180 litres

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36
Q

20% of plasma in the capillary bed moves to where?

A

The bowman’s capsule

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37
Q

What are the three components of the filtration barrier

A

Endothelial cells
Basement membrane
Epithelial cells

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38
Q

What are the properties of endothelial cells?

A 
Make up the wall of the capillary
Have gaps for solutes and ions to move through called fenestrations
Flat cells
Large nuclei
Stop RBCs and proteins moving through
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39
Q

What makes up the epithelial layer?

A

Podocytes

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40
Q

What is the basement membrane?

A

Main barrier
Made up of glycoproteins - collagen, laminin and fibronectin
Filtration based on molecular shape, size and charge

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41
Q

What are trabeculae?

A

Extensions from the cell body

These have pedicels - finger like projections which interdiginate (they do not fully cross over so leave gaps)

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42
Q

What is the role of podocytes?

A

Maintenance and phagocytosis

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43
Q

What properties can determine filtration?

A

Molecular size, shape and charge

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44
Q

What happens when the F/P ratio is 1?

A

The concentration of the molecule in the filtrate = the concentration of the molecule in the bowmans capsule (plasma concentration)

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45
Q

What happens of the F/P ratio is 0?

A

No filtration occurs

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46
Q

What is dextran?

A

Chains of glucose which can be made bigger

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47
Q

If dextran is uncharged what happens?

A

It passes through the barrier more easily

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48
Q

What is the filtration co-efficient?

A

Kf

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49
Q

GFR is proportional to what?

A 
Forces favouring - forces opposing OR
(Pcap + IIBC) - (Pbc + IIcap)
P = hydrostatic pressure
II = oncotic pressure
cap = capillary
BC = bowmann's capsule
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50
Q

What is oncotic pressure determined by?

A

Protein concentration - more protein = higher oncotic pressure

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51
Q

What is IIbc normally and why?

A

0 because no protein is in the bowman’s capsule

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52
Q

What is Pcap usually?

A

60mmHg - decreases slightly down the capillary as some volume is lost

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53
Q

What is IIcap normally?

A

30mmHg - Changes down the capillary (increases) as fluid is lost but protein concentration remains the same so there is an increase in oncotic pressure

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54
Q

What is Pbc normally?

A

20mmHg - stays the same as there is constant flow to the proximal tubule

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55
Q

What is net filtration pressure?

A

10mmHg

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56
Q

What is unique about the glomerulus net filtration pressure?

A

It always stays positive - fluid never moves in

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57
Q

What is the glomerulus filtration rate?

A

125ml/min

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58
Q

What is SNGFR?

A

Single nephron glomerular filtration rate (50nl/min)

59
Q

How long can you live with full kidney failure?

A

3 days

60
Q

What happens if afferent arteriole resistance decreases?

A

RBF increase, Pcap increases and GFR increases

61
Q

What happens if afferent arteriole resistance increases?

A

RBF decreases, Pcap decreases and GFR decreases

62
Q

How is GFR autoregulated if there is an increase in arterial blood pressure?

A 
Increase in renal blood flow
Increase in glomerular filtrate
Autoregulation occurs;
Increased resistance of the afferent arteriole
Decrease in RBF and Pcap
Decrease in GFR
63
Q

What is the myogenic theory?

A

Changes in pressure are detected in the arterial smooth muscle
Increase in blood pressure causes stretch receptors to be activated
This causes arteriole constriction increasing resistance

64
Q

What is the Tubuloglomerular Feeback theory?

A

The distal tubule passes in close proximity to its own glomerulus (juxtaglomerular apparatus)
Macula densa cells detect the rate of flow = release chemicals for afferent arteriole constriction or relaxation

65
Q

What is osmolality?

A

The measure of concentration: higher concentration = higher osmolality

66
Q

What are the units of osmolality?

A

mOsmol/kgH2O

67
Q

What is the equation for osmolality?

A 
Osmolality = concentration of solute x number of particles X dissociates into 
[X]*n = osmolality
68
Q

What is the osmolality for 100mM of NaCl?

A

100 x 2 = 200 mOsmol/kgH2O

69
Q

How many nephrons does each collecting duct drain?

A

6

70
Q

Which are the only species with Loops of Henle and what does this mean?

A

Birds and mammals

They can concentrate their urine, other species can’t

71
Q

Where does the loss of NaCl occur in the Loop of Henle?

A

In the thick and thin ascending limb

72
Q

What happens to osmolality down the descending limb and why?

A

It increases as water is lost

73
Q

What is the ascending limb impermeable to?

A

Water

74
Q

What is the descending limb impermeable to?

A

NaCl

75
Q

Why is the loop of henle important?

A

Counter current multiplication

Maximises osmolality changes which drives water reabsorption at the level of the collecting duct

76
Q

What are the two gradients seen in the Loop of Henle?

A

Transverse and Vertical

77
Q

What is water movement mediated by in the thin ascending limb?

A

Aquaporin 1

78
Q

What protein regulates CLCK?

A

Barttin

79
Q

What are the symptoms of Bartter’s syndrome?

A 
Salt wasting
Polyuria
Hypokalaemia
Metabolic alkalosis
Hypercalcuria
Nephrocalcinosis
80
Q

Mutations in which proteins cause Bartter’s syndrome?

A

NKCC2, ROMK, CLCK and barttin (stops reabsorption in the thick ascending limb = salt wasting)

81
Q

What are the two cells of the collecting duct?

A

Principal cells

Intercalated cells

82
Q

Does ENaC have a direct role in counter current multiplication?

A

No but mutations can cause polyuria

83
Q

What is aquaporin 2 regulated by?

A

Vasopressin

84
Q

Diabetes insipidus is causes by mutations in what?

A

Aquaporin 2 or Vasopressin

85
Q

What is as equally as important as NaCl in counter current multiplication?

A

Urea

86
Q

Where is impermeable to urea and what does this mean?

A

The top of the collecting duct

Water is lost here but not urea so the urea concentration increases

87
Q

Urea permeability is dependent on what?

A

Vasopressin

88
Q

Why does the cortex’s blood supply need to be specialsed?

A

So there is not a wash out

89
Q

What are the capillaries of the medulla and what is their structure

A

Vasa recta

They loop down into the medulla and back up into the cortex

90
Q

What is the relative permeability of the ascending limb and descending limb of the vasa recta?

A

They are both equally permeable to water and solutes

91
Q

How do vasa recta prevent wash out?

A

Down in the medulla there is an increase in osmolality
As plasma moves down the osmotic gradient means NaCl and H20 moves in
In the ascending limb water moves IN and salt moves OUT preventing wash out

92
Q

What is the UT-B urea transporter?

A

Found on the red blood cell membrane
Solutes move into the plasma red blood cell
UT-B mediates the loss of urea from red blood cells - mutations mean urea can’t leave easily so the urea leaves after the vasa recta so patients struggle to concentrate urine = counter current exchange is not working

93
Q

What is respiratory acidosis?

A

As PO2 falls the response to PCO2 is enhanced - translates to drive for ventilation
Involves both central (long term important) and peripheral (first to respond) chemoreceptors -

94
Q

What is Kussmaul breathing?

A

Hyperventilation

95
Q

What are the 3 renal mechansisms to control acid base regulation?

A

HCO3- handling
Urine acidification
Ammonia synthesis

96
Q

What is the principal cell model for HCO3- handling?

A

H+ out of the cell (Via the Na+ H+ exchanger) combines with HCO3- -> H2CO3
The H2O and the CO2 then moves into the cell
Inside the cell carbonic anhydrase works to make H2CO3 -> H+ and HCO3-
H+ is recycled back across the apical membrane
HCO3- is lost via the basolateral membrane through the sodium bicarbonate transporter
Buffer changes with HCO3- as it is retained

97
Q

What is urine acidification?

A

Alkaline phosphatase (Na2HPO4) -> Acid phosphatase (NaH2PO4)
Na is lost and replaced with a H+ and is then secreted in urine
Uric acid and creatine also bind H+
The H+ ions have to be bound to bufferes for excretion to prevent damage to cells

98
Q

What is ammonia production?

A

NH3 is permeable
NH4+ is impermeable
NH3 is formed by glutamate (forms alpha-keto glutarate)
Ammonia goes through the tubular fluid -> ammonium -> excretion
This is called diffusion trapping

99
Q

What can cause respiratory acidosis?

A

CO2 elimination has decreased
Lung disease
Emphysema and chronic bronchitis

100
Q

What is the renal compensation for respiratory acidosis?

A

Increased H+ secretion
Increased reabsorption of HCO3-
Rise in pH but further rise of HCO3-

101
Q

What can cause respiratory alkalosis?

A

CO2 elimination
Hyperventilation
Fear, stress and pain

102
Q

What is the renal compensation for respiratory alkalosis?

A

Decrease in secretion of H+
Decrease in reabsorption of HCO3-
Fall in pH but further drop in HCO3-

103
Q

What can cause metabolic acidosis?

A

Ingestion of acid
Loss of alkaline fluid
Diarrhoea, cholera and diabetic alkalosis

104
Q

What is the respiratory compensation seen with metabolic acidosis?

A

Increase in respiratory rate
Decrease in arterial CO2
Increase in pH and drop in PCO2

105
Q

What is the renal correction seen with metabolic acidosis?

A

Increase in secreted H+

Increase in reabsorption of HCO3-

106
Q

What can cause metabolic alkalosis?

A

Ingestion of alkaline fluid

Loss of acid eg by vomitting

107
Q

What is the respiratory compensation seen in metabolic alkalosis?

A

Decrease in respiratory rate
Increase in arterial CO2
Decrease in pH and increase in pCO2

108
Q

What is the renal compensation seen in metabolic alkalosis?

A

Kidneys do not help with metabolic alkalosis - they actually make it worse

109
Q

How is asthma a mixed disorder?

A

Respiratory acidosis and lactic acidosis due to lack of O2 can show life threatening changes in pH

110
Q

How is alcoholism a mixed disorder?

A

Metabolic acidosis (alcohol breakdown) and metabolic alkalosis (vomitting)

111
Q

How is COPD a mixed disorder?

A

Patients treated with duiretics = respiratory acidosis and metabolic alkalosis (diuretics promote loss of H+)

112
Q

How is salicylate poisoning a mixed disorder?

A

Respiratory alkalosis (stimulation of respiratory centre) and metabolic acidosis (increase in acid)

113
Q

What is the normal pH for the majority of cells?

A

Between 7.35 and 7.45

114
Q

Fluctuations in pH have a profound effect on what?

A

The excitability of muscle and nerve
Enzymes
K+ levels (change in nernst potential due to an increase in K+ can have a cardiac and nevous impact)

115
Q

What do cells release in an acidotic state?

A

Potassium

116
Q

What is the pH value for:

a) gastric secretions
b) cerbrospinal fluid
c) pancreatic secretions
d) final urine

A

a) 0.7
b) 7.8
c) 8.1
d) 5.4

117
Q

What are the sources of acid

A

15 moles per day of CO2 from the lungs

Western diet gives an excess of H+ from protein breakdown

118
Q

What are the sources of alkali?

A

Fruit in diet

119
Q

What three mechanisms are used to control pH in the body?

A

1) Blood and tissue buffers - work in seconds
2) Respiration - works in minutes
3) Renal - hours/days

120
Q

Where are buffers present?

A

Blood, ECF, ICF and urine

121
Q

Give four examples of buffers

A

Haemoglobin
HCO3-
Inorganic phosphate
Weak acids/bases on proteins

122
Q

What is the CO2 equilibrium equation?

A

CO2 + H20 H2CO3 H+ + HCO3-

123
Q

What is pK at 37 degrees?

A

6.1

124
Q

What is the Henderson-Hasselbach equation?

A

pH = pK + log [HCO3]/[H2CO3]

125
Q

H2CO3 concentration is roughly the same as what?

A

The concentration of CO2

126
Q

If a patient shows low pH and low HCO3- what are they suffering from?

A

Metabolic Acidosis

127
Q

If a patient shows a high pH and high HCO3 what does the patient have?

A

Metabolic Alkalosis

128
Q

If a patient shows High pH and low HCO3- what does the patient have?

A

Respiratory alkalosis

129
Q

If a patient has low pH and high HCO3- what does the patient have?

A

Respiratory acidosis

130
Q

What can cause an increase in ventilation?

A

Hypoxia
Hypercapnia
Acidosis

131
Q

Where are peripheral chemoreceptors found?

A

The carotid body and the aortic arch

132
Q

What is the main stimulus for peripheral chemoreceptors?

A

Hypoxia

133
Q

What do peripheral chemoreceptors send signals to?

A

The sinus nerve, vagus nerve and the glosso-pharyngeal nerve = changes in breathing
Goes to the medulla and respiratory center

134
Q

What are glomus cells?

A

Have a neural phenotype
Anoxia causes the membrane to depolarise so action potentials are fired
Found in the carotid bodies

135
Q

What are the type II cells of the carotid bodies?

A

Supporting role ie do not fire any action potentials

136
Q

What are the mechanisms leading to afferent nerve fibre stimulation

A 
Decrease in PO2 and pH, Increase in PCO2
Inhibition of BK K channels
Depolarisation
Action potential firing
CaV channels open
Increase in Cai
Neurotransmitter release - Ach, Dopamine, NA, 5HT, Substance P and ANP
Afferent nerve fibre stimulation
137
Q

Some SIDs babies have what?

A

An increased concentration of dopamine in carotid body so their ventilation is abnormal

138
Q

What is the main activator of central chemoreceptors?

A

Hypercapnia

139
Q

A change in CO2 from 40 to 45mmHg causes what?

A

Ventilation to double (The same effect would only be seen with oxygen if it fell by 50%)

140
Q

What did Isodore Leusen do?

A

In 1950s perfused cerebral ventricles with acidic solution = observed hyperventilation

141
Q

Where are central chemoreceptors located?

A

Within the brain parenchyma

142
Q

What can and can’t move across the blood brain barrier easily?

A

CO2 can move across

H+ and HCO3- can’t

143
Q

What is not present in the BECF?

A

Less non-bicarb buffering power (fewer proteins) so the effect of increased CO2 is to give a bigger change in pH

144
Q

What are the two neuronal populations in the ventrolateral medulla?

A

Acid activated - serotonin

Acid inhibited - GABA

Integrated Physiology and Pharmacology (17 decks)

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