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URI > Renal structure and function 2 > Flashcards

Renal structure and function 2 Flashcards

1
Q

What are the different types of nephrons?

A
  • Cortical

- Juxtamedullar

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2
Q

What is the difference between the 2 types of nephrons?

A
  • Cortical have loops of Henle in renal medulla near junction with renal cortex
  • Juxtamedullary have their loops of Henle deep in renal medulla (glomeruli close to medulla but still in cortex)
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3
Q

What is the vascular arrangement of cortical nephrons?

A

Peritubular capillaries

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4
Q

What is the vascular arrangement of the juxtamedullary nephrons?

A

Have the vasa recta

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5
Q

Which of the nephrons concentrate the urine?

A

Juxtamedullary nephrons

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6
Q

What is the function of the loop of Henle?

A

Confer ability to produce concentrated urine

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7
Q

What is the permeability of the descending limb of the Loop of Henle?

A
  • Permeable to water

- Via aquaporin-1

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8
Q

What is the permeability of the ascending limb of the Loop of Henle?

A
  • Permable to solutes

- Impermeable to water

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9
Q

If an animal is dehydrated but is producing iso-osmolar urine what does this suggest and why?

A
  • Proximal tubule carries out bulk removal of volume so start of loop of iso-osmotic
  • If there is no change to the urine but animal is dehydrated, suggests kidney failure
  • Not concentrating the urine even though is dehydrated
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10
Q

Give a general overview of the movement of solutes and water through the Loop of Henle

A
  • Descending limb pumping out water (aquaporin-1), pumping out water -> hypertonic at end of loop
  • Ascending limb impermeable to water, pumping out solutes, becomes dilute again
  • Generates gradient in the interstitium
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11
Q

What is the tonicity of the medullary interstitium and how is this acheived?

A
  • Hypertonic

- Countercurrent multiplier and countercurrent exchange, maintained by vasa recta

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12
Q

Describe the countercurrent multiplier system in the Loop of Henle

A
  • Descending loop permeable to water, not solutes
  • Ascending loop permeable to solutes not water
  • Interstitial osmolarity elevates as go deeper, drawing water out of descending
  • Solute concentration of fluid in ascending limb higher, more ions pumped out
  • Increases interstitial osmolarity more, more water drawn out of descending
  • U-shaped vasa recta prevents dissipation of this gradient
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13
Q

Describe the countercurrent exchange in the Loop of Henle

A
  • Descending limb of vasa recta: as descends through high osmolarity water out of capillary, NaCl in
  • Ascending: up through hypotonic, solutes out, more water in
  • Result is no net change in medullary gradient
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14
Q

What is the function of the counter current mechanism?

A
  • Concentration then dilution as pass through loop
  • Establishes vertical gradient through kidney to enable production of concentrated urine
  • Provides mechanisms for producing dilute urine
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15
Q

Explain how urea acts to support the generation of the renal medullary concentration gradient

A
  • Is a weak osmolite
  • Requires water to be excreted
  • Recycling of urea maintains medullary gradient needed for counter current multiplier
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16
Q

Describe the passage of urea in the collecting duct

A
  • Nephron impermeable to urea until inner medullary portion of collecting duct
  • Tubular urea more concentrated as water removed
  • Lower collecting duct ura passively reabsorbed via urea transporters (ADH sensitive)
  • Diffuses into interstitial fluid if necessary
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17
Q

What are the main water outputs in the body?

A
  • Kidneys (main one)
  • Lungs
  • Faeces
  • Skin
  • Sweat
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18
Q

What are the main water inputs into the body?

A
  • Drinking (main one)

- Metabolic water

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19
Q

What is body water controlled by?

A
  • Thirst (mostly)
  • ADH
  • Aquaporins
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20
Q

What, in general, do the water control systems respond to?

A

Changes in ECF osmolality and changes in blood volume

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21
Q

What is thirst controlled by?

A
  • Osmoreceptors in hypothalamus
  • Stimulate thirst in response to concentrated ECF
  • Degree of stimulus leads to modification of firing of neurons
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22
Q

What does urine specific gravity measure?

A

The weight of solids in water

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23
Q

What is the relationship between USG and osmolality?

A
  • Osmolality is the number of dissolved osmoles in a kg of water
  • USG and osmolality usually change in parallel
  • Diverge when large and heavy molecules (e.g. glucose, proteins) are present in urine
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24
Q

What is hypersthenuria?

A

Concentrated urine - lots of solutes, not much water

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25
Q

What is hyposthenuria?

A

Dilute urine - lots of water, not many solutes

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26
Q

What is isosthenuria?

A

Same as plasma concnetration, nothing being done to the ultrafiltrate

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27
Q

What is suggested by persistent hyposthenuria?

A
  • Increased loss of water without increased loss of solute
  • Polyuria
  • Diabetes insipidus
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28
Q

What is suggested by persistent hypersthenuria?

A
  • Loss of solutes without water

- Dehydration

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29
Q

What is suggested by persistent isosthenuria?

A
  • Fixed and persistent suggest no ability to dilute or concentrate urine
  • Kidney failure
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30
Q

What is ECF volume altered by?

A
  • Water intake
  • Intravenous infusion of solutions
  • Loss from GIT
  • Loss from blood
  • Loss from sweating
  • Loss from kidneys
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31
Q

What is the action of ADH?

A
  • Preserve blood volume
  • Prevent diuresis
  • Prevent natriuresis
  • Increase blood pressure by inducing vasoconstriction
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32
Q

In what situations is ADH increased?

A
  • Hypovolaemia (decreased atrial filling pressure)
  • Hypotension (baroreceptor mediated)
  • Dehydration (osmolarity increases)
  • Angiotensin II
  • Increased sympathetic innervation
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33
Q

How does ADH exert its action?

A
  • Binds to receptors (V1 and V2) in cortical adn distal collecting duct
  • Activates aquaporins to insert in apical membrane of principle cells
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34
Q

What is the function of aquaporins?

A

Allow rapid water transport across cell membranes

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35
Q

Describe the structure of aquaporins

A
  • 4 proteins in epithelial membranes
  • Hydrophilic pore to allow water through
  • 2 important ones: AQP1 and AQP2
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36
Q

Describe aquaporin-1

A
  • Apical and basolateral membrane of proximal tubule
  • Isosmotic removal of water and solutes
  • Main relevant channel in descending loop of Henle (water loss from tubule)
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37
Q

Describe aquaporin-2

A
  • Main relevant channel in collecting duct that is ADH-responsive
  • In presence of ADH, lots of AQP-2 insert on apical membrane
  • Retention of hypotonic fluid entering cortical collecting duct
  • Production of concentrated urine
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38
Q

How is blood volume/pressure maintained?

A
  • ECF volume and osmolarity (Na concentration)
  • Voume affectin g ADH
  • ANP
  • RAAS (blood pressure)
  • Aldosterone (by increasing Na concentration)
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39
Q

What are the reference ranges for water intake, urine volume and urine osmolal for a cat?

A
  • Water intake: 45ml/kg/day
  • Urine volume: 10-28ml/kg/day
  • Urine osmolal: 1.020-1.040 mosmoles
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40
Q

What are the reference ranges for water intake, urine volume and urine osmolal for a dog?

A
  • Water intake: 90ml/kg/day
  • Urine volume: 20-100ml/kg/day
  • Urine osmolal: 1.016-1.060 mosmoles
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41
Q

What are the reference ranges for water intake, urine volume and urine osmolal for a sheep?

A
  • Water intake: 6L/day
  • Urine volume: 10-40ml/kg/day
  • Urine osmolal: 1.015-1.045 mosmoles
42
Q

What are the reference ranges for water intake, urine volume and urine osmolal for a cow?

A
  • Water intake: 100L/day
  • Urine volume: 17-45ml/kg/day
  • Urine osmolal: 1.030-1.045 mosmoles
43
Q

What are the reference ranges for water intake, urine volume and urine osmolal for a horse?

A
  • Water intake: 40-50L/day
  • Urine volume: 3-18ml/kg/day
  • Urine osmolal: 1.025-1.060 mosmoles
44
Q

Compare dehydration and hypovolaemia

A
  • Dehydration: specific loss of just water (osmolality increased)
  • Hypovolaemia: loss of blood volume (osmolality stays the same)
45
Q

What may cause primary loss of Na?

A
  • Diarrhoea
  • Vomiting
  • Diuretics
  • Addison’s disease
46
Q

What may cause excess water retention?

A

Increased secretion of ADH

47
Q

What may cause primary loss of water?

A

Inability to produce ADH

48
Q

What may cause excess Na in ECF?

A
  • AME
  • Increased aldosterone
  • Cushing’s disease
49
Q

What is the role of the kdiney in maintenance of the internal (watery) environment?

A
  • Regulation of water, ion and pH levels

- Elimination of organic wastes and excess electrolytes

50
Q

What is the endocrine function of the kidney?

A
  • Production of erythropoeitin
  • Calcitriol
  • Renin
51
Q

How does hydrostatic pressure relate to filtration in the glomerulus?

A
  • higher pressure in efferent than afferent
  • Increases pressure in glomerulus
  • Affects podocytes and gaps between
  • Hydrostatic pressure in glomerulus affects how much is pushed out
52
Q

What facilitates filtration in the glomerulus?

A
  • Fenestrated endothelium
  • Glomerular basement membrane (-ve charge, thick)
  • Podocytes
53
Q

What is the osmolality of the ultrafiltrate?

A

Same as plasma

54
Q

What is azotaemia?

A

Build up of nitrogen compounds (e.g. creatinine and urea) in the blood

55
Q

What is meant by pre-renal renal disease?

A

Changes in body or organ that lead to changes in kdiney function e.g. hypertension

56
Q

What is meant by renal renal disease?

A

Intrinsic problem of the kidney e.g. interstitial fibrosis

57
Q

What is meant by post-renal renal disease?

A

Problem after the kidney affecting its function e.g. urethral bloackage, stenosis

58
Q

What is the most common type of renal disease?

A

Pre-renal

59
Q

What are teh sites of potential renal damage and what is the effect?

A
  • Glomerular: filtration affected
  • Tubular: secretion and reabsorption affected
  • Interstitial: ability to concentrate urine affected
60
Q

What factors determine the glomerular filtration rate in a single nephron?

A
  • Pressure in afferent/efferent arteriole
  • Colloid osmotic pressure
  • Hydrostatic pressure
  • Renal plasma flow
  • Electrical charges across the glomerular basement membrane
61
Q

What is the glomerular filtration rate?

A

The volume of fluid filtered from the glomerular capillaries into the Bowman’s capsule per unit time
- Sum of ultrafiltrate from both kidneys/time

62
Q

What are the limitations to measuring GFR in practice?

A
  • Inferred via serum creatinine (SCr)
  • SCr influences by lean mass, breed, diet
  • Low GFR indicated nephrone loss - shown by high SCr (BUN)
  • Usually measured by creatinine clearance
63
Q

What happens to GFR in renal damage?

A
  • Nephron loss
  • Cannot be regenerated
  • Other nephrons increase in function
  • But GFR will not increase again
64
Q

What exerts the hydrostatic pressure?

A
  • Water in blood
  • Cardiac output generates pressure
  • Afferent and efferent arterioles determine relative pressure difference across glomerulus
  • Concentration of plasma proteins
65
Q

What occurs in proteinuria?

A
  • Loss of protein to urine
  • Less protein in plasma
  • more in tubular fluid
  • Less net filtration force, less fluid filtered out of blood
  • Fluid retention leading to oedema
66
Q

Define renal clearance

A

The volume of plasma from which a substrance is completely removed by the kidney in a given amount of time (e.g. a minute)
- Is ameasure of kidney’s ability to remove compounds from teh blood

67
Q

How can GFR be measured?

A
  • Clearance of a substance
  • Usually creatinine
  • Also iohexol, inulin, Tc-99m (radioactive tracer, used for renal split function and in larger animals)
68
Q

Why can creatinine clearance be used as a measure of GFR?

A
  • Is not reabsored or secreted by the kidney
  • Small and free of charge
  • What ends up in the urine is exactly what came from the ultrafiltrate
  • The amount flowing through the nephrons is the amount being produced
69
Q

What are the factors that affect renal clearance?

A
  • GFR
  • Tubular reabsorption
  • Tubular secretion
70
Q

How is creatinine clearance measured?

A
  • Catheterise bladder, remove all urine
  • Collect all urine over given time (e.g. 24 hours)
  • Collect blood sample in middle of this time period
  • At end, measure Cr in urine
  • Measure Cr concentration in blood
  • Compare
71
Q

Where does creatinine come from?

A
  • Creatinine phosphate in muscle
  • Produced at a fairly constant rate by the body
  • Produced daily and is related to muscle mass
72
Q

What is creatinine?

A

A non-protein nitrogenous substance from muscle

73
Q

What information does the ratio of urine to serum creatinine provide?

A
  • Indirect information about glomerular filtration and tubular function
74
Q

What is involved in sedimentary analysis of urine?

A
  • RBC
  • WBC
  • Epithelial cells
  • Micro-organisms
  • Crystals (type, concentration, pH, some found in normal urine)
  • Casts (should be none)
75
Q

What is the role of the kidney in regulation of acid base balance?

A
  • Second biggest control of acid-base after lungs

- Excretes hydrogen ions to maintain constatn concentration of H+ in the body

76
Q

What are the mechanisms of H+ excretion in the kidney?

A
  • Na/H exchange in proximal tubule

- Active H+ ATPase pymp in collecting ducts

77
Q

Why must H+ be excreted?

A
  • Very reactive
  • Reacts with proteins easily even when found at 1 millionth concentration of other electrolytes
  • Avoid detrimental changes in proteins, enzyme structure, cellular structure
78
Q

What is the primary physiological regulator of acid secretion?

A

Extracellular pH

79
Q

How is H+ excreted by the kidneys?

A
  • Must be bound to filtered buffers such as phosphate or ammonia
  • Too reactive to be excreted on its own
  • Na/H exchange in PT, H+ ATPase pump in collecting ducts
80
Q

What are the 4 major factors which control bicarbonate reabsorption?

A
  • Luminal HCO3- concentration
  • Luminal flow rate
  • Arterial pCO2
  • Angiotensin (via decrease in cyclic AMP, alters flow
    through kidney)
  • Increase in each of the above will increase bicarb reabsorption
81
Q

What is the importance of carbonic anhydrase in bicarbonate reabsorption?

A
  • Allows continuous bicarbonate reabsorption by generating the bicarb from H2O and CO2, making a concentration gradient and also producing H+ ions to be secreted
82
Q

Where does the energy for proximal acidification come from?

A

Basolateral Na/K ATPase pump

83
Q

Describe the process of bicarbonate reabsorption in the proximal tubule

A
  • HCO3- cannot cross apical membrane of PCT cell
  • Binds to secreted H+ to produce CO2 and H2O which can cross membrane
  • Converted to H+ and HCO3- using carbonic anhydrase
  • HCO3- crosses basolateral membrane ia Na+/HCO3- symporter
  • 3 bicarb per 1 Na+
84
Q

What is the importance of the basolateral Na/K ATPase pumps in the proximal tubule?

A
  • Provide energy for proximal acidification
  • Are electrogenic in opposite direction to Na/HCO3- symporter
  • Sodium pump keeps intracellular Na+ low, setting up gradient for H+/Na+ antiport on apical membrane
85
Q

What is the main role of distal tubule acidification?

A

Primary role in minimising K+ loss

86
Q

How does distal tubule acidification occur?

A

H+ secreteion in cortical and medullary collecting tubules by active secretion using H+ATPase

87
Q

What is the role of filtered weak acids as buffers?

A
  • Bicarbonate buffer is open system (primary buffer of ECF)

- Buffers of H+ in urine

88
Q

What is a buffer?

A

A compound that can accept or donate protons (H+) to minimise change in pH

89
Q

What is the role of ammonium in the renal tubular cells?

A
  • H+ can be excreted as ammonium
  • Adds flexibility to renal acid base regulation (by regulating NH4+ production)
  • As more is used, more is made
90
Q

How is ammonium produced in the renal tubular cells?

A
  • Glutamine from peritubular capillaries and filtrate
  • Glutaminase to make glutamate and ammonium
  • Glutamate metabolised to produce alpha-ketoglutarate
  • This metabolised to give 2 HCO3- ions and NH4+
  • Also produces glucose
91
Q

Where is the majority of ammonium produced in the nephron?

A

In the proximal convoluted tubule cells

92
Q

What is ammonium cycling in the nephron and how does this occur?

A
  • Ammonium cycled in medulla
  • 75% proximally produced NH4+ removed from tubular fluid in medulla, only small amount into distal tubule
  • Thick AL of LoH important for removal of NH4+
  • Some interstitial NH4+ returns to late proximal tubule and enters medulla again (recycling)
93
Q

How does ammonium aid H+ excretion?

A
  • H+ excreted as part of NH4+ molecule (HCO3- produced by alpha-ketoglutarate metabolism)
  • NH4+ also in equilibrium with NH3, out of cell and binds with H+ in lumen, excretion of H+ bound to NH3 (as NH4+)
94
Q

What increases secretion of ammonium?

A
  • Lower pH (i.e. higher H+ in tubular lumen)

- Increased removal of H+, extracellular pH increased to normal

95
Q

What occurs to ammonium if it is returned to the blood stream?

A

Metabolised in liver to urea by the Krebs-Henseleit cycle

- net production of one H+ per ammonium molecule

96
Q

Briefly describe ammonium excretion in the collecting ducts

A
  • Different to proximal convoluted tubule
  • Less excretion
  • NH3 bids to H+ in lumen, out as NH4+
97
Q

Summarise acid base regulation in the proximal tubular cell

A
  • HCO3- and H+ being produced (carbonic anhydrase)
  • 3HCO3- to blood with 1 Na (symport)
  • H+ antiporter with Na: H+ into lumen, Na into cell
  • H+ bound to NH3 to make NH4+ and excreted, or NH4+ directly from cell
  • NH4+ produced by metabolism of alpha-ketoglutarate, also produced HCO3-
  • NH4+ antiport to put Na into cell
  • NH4+ in equilibrium with NH3
  • NH3 out and binds to H+ for excretion
98
Q

List factors that control renal hydrogen excretion

A
  • Extracellular pH
  • Plasma Cl-, K+ and PO4- concentrations
  • Extracellular pCO2
  • ECF volume
99
Q

What is the effect of increased extracellular pH on renal hydrogen excretion?

A
  • Increased HCO3- in blood, need to excrete HCO3- load (kidneys)
  • Acute buffering (ICF and ECF)
  • ## Body retains CO2 by alveolar hypoventilation (will decreases pH)
100
Q

What is the effect of increased extracellular pH on Cl-, K+ and PO4-? Treatment?

A
  • Those ions decrease
  • Lactate increases
  • Result is maladaptive
  • HCO3- increases more
  • Administer NaCl or KCl solutions

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