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Physiology with pharmacology - L1 > Gene models & nephron function > Flashcards

Gene models & nephron function Flashcards

1
Q

What % of plasma is filtered into Bowman’s capsule?

A

20%

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2
Q

What is tubular secretion?

A

movement from peritubular capillary

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3
Q

What is the diameter of the glomerulus?

A

20um

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4
Q

How much plasma is filtered per day?

A

180 litres/day filtrate

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5
Q

Describe the level of energy needed for glomerular filtration to take place

A

High levels of energy

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6
Q

What arteriole carries blood into the glomerular capillaries?

A

afferent arteriole

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7
Q

What arteriole carries blood out of the glomerular capillaries?

A

efferent arteriole

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8
Q

What does the glomerulus permit across its membrane?

A

H20 & small molecules

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9
Q

What does the glomerulus restricts across its membrane?

A

blood cells & proteins

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10
Q

What is ultra-filtrate composed of?

A
  • consists of protein free plasma
  • 1% protein filtered (albumin) - usually reabsorbed by the proximal tubule
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11
Q

What can proteins in urine be a sign of?

A

UTI

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12
Q

What is movement from the lumen of the nephron into peritubular called?

A

transcellular reabsorption

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13
Q

What is movement from the peritubular capillary into the lumen of tubule called?

A

transcellular secretion

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14
Q

What is movement in both directions between the lumen of tubule & peritubular capillary called?

A

Paracellular secretion or reabsorption

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15
Q

What is transcellular reabsorption called?

A

transport using transport proteins, transpiring ion solutes + water into cell across membrane

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16
Q

What does paracellular movement move?

A

Between cell

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17
Q

How many genes does the human genome have?

A

33,000 genes

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18
Q

How many renal genes does a human have?

A

Several hundred

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19
Q

How much reabsorption takes place in the proximal tubule?

A
  • 70% (H2O & Na+)
  • approx 100% glucose & amino acids
  • 90% HCO3 (bicarbonate)
  • high levels of mitochondria to allow energy-requiring processes to occur
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20
Q

What ATPase is found on the proximal tubule basolateral membrane?

A

sodium-potassium ATPase

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21
Q

What membrane are potassium channels found on in the basolateral membrane?

A

basolateral

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22
Q

Describe the intracellular sodium concentration in the proximal tubule

A

low

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23
Q

What cotransporters are involved on the apical surface of the proximal tubule involved in the movement pf sodium & glucose into the cell?

A

SGL T1 & SGL T2

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24
Q

What is the sodium phosphate cotransporter (NaPiII) involved in?

A

The movement of phosphate into cell

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25
Q

What are the results of NaPiII knockout mouse phenotype?

A
  • Less Pi reabsorption
  • More lost in urine
  • Issues renal mineralisation
    (renal mineralisation - renal stone/crystal formation)
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26
Q

What is the importance of phosphate?

A
  • bone formation
  • used for ATP
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27
Q

What staining is used to see the NaPiIIa knockout in a mouse?

A

Von Kossa staining - lots of dark-stained sports indication of mineralisation

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28
Q

What occurs as a result of low intracellular sodium concentration?

A

creates an electrochemical gradient for cotransporter to move sodium into the cell & hydrogen out of the cell

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29
Q

What happens to the hydrogen once it has left the cell?

A

it binds to HCO3 (bicarbonate), forming H2CO3 (carbonic acid). Carbon anhydrase then moves CO2 & H20 into the cell. Intracellular anhydrase then moves bicarbonate out of the cell via the basolateral exit

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30
Q

Why is reabsorption of bicarbonate important?

A

regulates the pH of the body

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31
Q

What is the effect of knocking out the NHE3 gene?

A

struggle to reabsorb plasma bicarbonate (HCO3), and a lower pH due to lack of pH regulation

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32
Q

What is the relationship between plasma glucose concentration & plasma glucose reabsorption?

A

linear relationship

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33
Q

When does plasma glucose concentration not have a linear relationship with plasma glucose reabsorption?

A

when there is no more free carriers for reabsorption

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34
Q

What is the renal threshold?

A

concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine

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35
Q

What is the inherited disease given to those whose sodium-glucose carriers don’t work?

A

diabetes

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36
Q

What 2 systems are used to remove substances from the proximal tubule?

A

organic cations & organic anions

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37
Q

What is the function of the Loop of Henle?

A
  • concentration of the urine
  • reabsorption of Na+, Cl-, H2O
  • reabsorption of Ca2+ & Mg2+
  • site of action of loop diuretics
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38
Q

What are the 3 parts of the loop of Henle?

A
  • descending limb
  • thin ascending limb
  • thick ascending limb
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39
Q

What size diameter is the descending limb?

A

thin

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40
Q

What leaves in the thin descending limb?

A

water

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41
Q

what leaves in the ascending limb?

A

sodium & chloride

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42
Q

What is the purpose for water leaving in the descending limb & sodium & chloride leaving in the thin ascending limb?

A

creates osmotic gradient which allows for water reabsorption

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43
Q

What leaves the thick ascending limb?

A

1 sodium, 1 potassium, 2 chloride ions released into the intracellular compartment

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44
Q

How does sodium leave the body?

A

via a sodium ATPase

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45
Q

What is needed for the CLCK channel to reabsorb chloride?

A

Barttin (beta subunit)

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46
Q

What does ROMK allow?

A

potassium reabsorption

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47
Q

What does Bartter’s syndrome lead to?

A

problem with sodium & chloride reabsorption
- hypotension (due to reduced ECF)
- kypokalaemia
- metabolic alkalosis
- hypercalciuria (calcium in urine)
- nephrocalcinosis - kidney stones

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48
Q

What is the biological effect of inability to produce barttin?

A

faulty CLCK

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49
Q

What do diuretics do?

A

increase urine, therefore reducing high blood pressure

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50
Q

What are people with Barter’s syndrome unlikely to experience?

A

hypertension

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51
Q

What occurs in the early distal tubule?

A
  • reabsorption of Na + Cl
  • reabsorption of Mg2+
  • sensitive to thiazine diuretics
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52
Q

What is Gitelman’s syndrome?

A

salt wasting & polyuria (lots of urine)
- hypotension
- hypokalaemia
- metabolic alkalosis
- hypocalciuria

53
Q

What is the role of NCC?

A

transport of sodium & chloride into early distal tubule, no potassium

54
Q

What occurs in the late distal tubule?

A
  • increasing the concentration of the urine
  • reabsorption of Na+ & H2O
  • secretion K+ & H+
55
Q

What 2 types of cell is the late distal tubule & cortical collecting duct?

A

principal & intercalated cells

56
Q

What occurs in principal cells in the late distal tubule?

A
  • Na & H2O reabsorption
  • K+ & H+ secretion
57
Q

What occurs in intercalated cells in the late distal tubule?

A

a (alpha) IC & b (beta) IC
IC = intercalated
- different levels of A&B cells lead to different levels of hydrogen & bicarbonate secretion & absorption

58
Q

What is the ENaC channel in principal cells?

A

Epithelium sodium channel

59
Q

What does ROMK do in principal cells?

A

secretion of potassium, which is driven by reabsorption of sodium

60
Q

What does aquaporin 2 do?

A

reabsorb water

61
Q

What is lost in the urine?

62
Q

What is the role of the ATPase?

A
  • maintain negative membrane potential
  • maintain low intracellular concentration
63
Q

What diseases can be caused by principal cell?

A

diabetes insipidus - AQP2
Liddle’s syndrome - ENaC

64
Q

What is the effect of amiloride?

A
  • to increase fluid loss - block Na+ channel = lower H2O = decrease blood pressure
65
Q

What is lost in alpha intercalated cells?

A

Hydrogen cells (using ATP)

66
Q

What does the AE1 (anion exchange protein 1) cotransporter do?

A

move chloride (that has been moved out) into cell, while bicarbonate is moved out

67
Q

What happens in B intercalated cells?

A

AE1 cotransporter on apical membrane
- hydrogen removed via ATP in basolateral membrane

68
Q

What is the difference between an alpha intercalated cells & beta intercalated cells?

A

alpha - hydrogen removed from apical & bicarbonate on basolateral
beta - hydrogen removed on basolateral & bicarbonate on apical membrane

69
Q

What will more b cells being present lead to?

A

more hydrogen ion being retained

70
Q

What will more a cells being present lead to?

A

more hydrogen excretion

71
Q

What occurs in the medullary collecting duct?

A
  • Low Na+ permeability
  • High H20 & urea permeability in the presence of antidiuretic hormone
72
Q

What is acute renal failure?

A

reversible impaired fluid & electrolyte homeostasis
- accumulation nitrogenous waste
- lasts 1 week

73
Q

What are the general symptoms of renal failure?

A
  • hypervolaemia
  • hyperkalaemia
  • acidosis
  • high urea/creatinine
74
Q

What is hypervolaemia?

A

lack of urine due to a fall in GFR

75
Q

What is hyperkalaemia?

A

lack of K+ secretion

76
Q

What is acidosis, and its consequence?

A

acidic bodily fluids - leads to depressed central nervous system - stops function of neurones

78
Q

What can high urea/creatinine lead to?

A

impaired mental function, nausea, vomiting

79
Q

What is oliguria?

A

Fall in GFR

80
Q

What is a pre-renal cause of acute renal failure?

A

Rhabdomyolysis - release myoglobin from damaged muscle - toxic effects on kidney tubules

81
Q

What is a renal cause of acute renal failure?

A

High K+ lack of defection & release from damaged cells - tachycardia

82
Q

What can a lack of bicarbonate lead to?

83
Q

What is used to hyperkalaemia?

84
Q

What is used to treat acidosis?

A

increase in bicarbonate

85
Q

What is antidiuretic hormone?

A

vasopressin

86
Q

Where is ADH released from?

A

posterior pituitary gland

87
Q

Where do axons move down?

A

pituitary stalk

88
Q

What type of cells fire action potentials?

A

neuronal cells

89
Q

What does ADH do?

A

regulates body fluid osmolality - conserves H2O

90
Q

What happens if there is an increase in ADH?

A

there is an increase in body fluid

91
Q

What happens if there is a decrease in ADH?

A

there is a decrease in body fluid

92
Q

Other than water, what else does ADH regulate?

A

sodium concentration

93
Q

What detects water levels?

A

hypothalamic osmoreceptors

94
Q

What level of water change do hypothalamic osmoreceptors detect?

A

3 mosmol/kg H2O

95
Q

What occurs if the supra-optic & paraventricular nuclei is stimulated?

A
  1. Release ADH from posterior pituitary
  2. feeling of thirst
96
Q

What occurs following activation of osmoreceptors?

A

activation of neuronal cells. This leads to an increase in ADH released

97
Q

What occurs if ADH levels is increased?

A

increase osmolality plasma

98
Q

What does ecstasy promote?

A

water retention

99
Q

What occurs if ADH levels is decreased?

A

decrease in osmolality plasma

100
Q

Describe the effect of alcohol on ADH release

A

inhibits the release of ADH - high level of water released

101
Q

What is the normal plasma ADH pg/ml?

102
Q

What is the normal plasma osmolality mosm/kgH2O?

103
Q

How is an osmotic force created on principal cells?

A

there are aquaporins present on both the apical & basolateral membrane

104
Q

What is the V2 receptor?

A

receptor for ADH. This activates protein kinase A (PKA), which leads to high levels of aquaporin 2 being inserted into the membrane.

105
Q

What happens if there are a high number of aquaporin 2 in the membrane?

A

high number of aquaporin 2 = high number of channels = high level of water absorption

106
Q

Are aquaporins 3+4 regulated ADH?

A

aquaporin 2

107
Q

What is the net effect of ADH?

A
  • increase in H2O reabsorption
  • fall in body fluid osmolality
108
Q

How many litres of dilute urine do people with diabetes insipidus excrete a day?

109
Q

What is diabetes insipidus caused by?

A

no ADH released - defect in secretory neurones of ADH

110
Q

What can treat diabetes insipidus?

A

nasal spray - desmopressin

111
Q

What is nephrogenic diabetes insipidus?

A
  • defect in V2 receptor
  • H2O channel defect
112
Q

Where is aldosterone released from?

A

cortex of the adrenal gland -zona glomerulosa layer

113
Q

What does mineralocirticoid do?

A

regulates plasma Na+, K+ & body fluid volume

114
Q

When is aldosterone released?

A

released in response to:
- increase in plasma K+ - 01mM
- decrease plasma Na+ - minor concentration maintained by osmoregulation
- decrease volume - via renin-angiotensin

115
Q

What structures does aldosterone act on?

A
  • late distal tubule
  • collecting duct
116
Q

What are the causes of aldosterone release?

A
  • increased reabsorption of Na+
  • increased reabsorption of H2O
  • increased secretion of K+ & H+
116
Q

What is the result of aldosterone on ENaC?

A

aldosterone puts more channels in the membrane & makes the channels stay open for longer

117
Q

What is a Pseudohypoaldosteronism?

A
  • salt loss but high aldosterone
  • loss response to aldosterone
  • mineralocorticoid receptor problem
118
Q

What does renin-angiotensin regulate?

A

body fluid volume, plasma Na & K

119
Q

Where is Renin released from?

A

juxtaglomerular apparatus (JGA)

120
Q

What type of cells within the juxtaglomerular apparatus (JGA)?

A

granular cells

121
Q

What triggers the release of angiotensinogen?

122
Q

What is necessary to allow the conversion from angiotensin 1 to angiotensin 2?

A

ACE (angiotensin cascade enzyme)

123
Q

What does angiotensin 2 release?

A

aldosterone

124
Q

Describe what would occur if you ingested salt?

A
  • increase in plasma Na+ & H2O moves out of ICF
  • increase in extracellular fluid volume & an increase osmolality plasma
125
Q

How does a decrease in ECFV occur?

A
  • decrease aldosterone
  • increase in loss of Na+
  • increase in loss of H2O
  • decrease in ECFV
126
Q

How does an increase in ECFV occur?

A
  • increase in ADH
  • increase in absorption of H2O
  • decrease in osmolality
  • increase in extracellular fluid volume
127
Q

Why is extracellular volume key in integration?

A

blood pressure is most important over water content

Physiology with pharmacology - L1 (17 decks)

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