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URI > Renal structure and function 3 > Flashcards

Renal structure and function 3 Flashcards

1
Q

How does increased extracellular pCO2 affect renal hydrogen extretion?

A
  • Tubular cells respond directly
  • Respiratory acidosis
  • Increase rate of H+ secretion
  • Hyperventilation
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2
Q

How does a loss in ECF affect renal hydrogen excretion?

A
  • Stimulates sodium reabsorption, increases H+ secretion, increases HCO3- reabsorption
  • Increase angiotensin II, directly stimulate activity of Na+/H+ exchange
  • Increase aldosterone levels, stimulate H+ secretion by cortical collecting tubules
  • Alkalosis due to excess H+ secretion and HC)3- reabsorption
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3
Q

Explain the effect of hypokalaemia on renal hydrogen excretion

A
  • Stimulates H+ secretion in proximal tubule
  • Increased H+ concentration in renal tubular cells
  • Increasig H+ secretion and HCO3- reabsorption
  • Tends to cause alkalosis
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4
Q

Explain the effect of hyperkalaemia on renal hydrogen excretion

A
  • Inhibitis H+ secretion in proximal tubule

- Decreases H+ secretion and HCO3- reabsorption and tends to cause acidosis

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5
Q

Explain the effect of hypochloraemia on renal hydrogen excretion

A
  • Secretion and HCO3- reabsorption
  • Na+ must be absorbed in exchange for H+ and K+ secretion
  • Paradoxical aciduria
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6
Q

Explain how lungs and kidney work together to control plasma pH

A
  • Lungs open system, release CO2 to atmostphere
  • CO2 rises, drop in pH, raise H+, increase resp to remove more CO2 and bring back to normal
  • In kidney: excretion of NH4+ to remove H+ ions, reabsorption of HCO3-
  • Degree of this controlled by pH
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7
Q

What may be an effect of dehydration?

A
  • High urine creatinine, urea and albumin

- Also reduced flow rate through nephrons

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8
Q

What is renal insufficiency?

A

Renal function impairment not severe enough to cause azotaemia, but sufficient to cause loss of renal reserve. May have reduced ability to compensate for dehydration
- Urine concentrating ability may be diminished

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9
Q

Define renal disease

A

Damage or functional impairment of the kidneys. Can var yin severity from very mild, to severe enough to cause uraemia

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10
Q

Define renal failure

A

Renal functional impairment sufficient to cause azotaemia. Urine concentrating ability usually impaired.

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11
Q

How can diet be modified to limit progression of renal failure?

A
  • Low protein diet (reduces production and thus build up of urea)
  • Low sodium diet
  • Low phosphorous diet
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12
Q

How does renal failure cause high blood pressure?

A
  • Decreased perfusion of kidney (likely due to initial damage from hypertension)
  • Increases release of renin
  • Activates angiotensin II = constriction of blood vessels
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13
Q

Why is a low phosphorous diet important in renal disease?

A
  • Can lead to secondary renal hyperparathyroidism

- Calcification of body tissues in high phos (block up nephrons)

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14
Q

How is anaemia caused in renal disease?

A
  • Erythropoeitin produced in kidney

- Damaged kidney produces less EPO

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15
Q

What is azotaemia?

A

The build up of creatinine and urea in the blood (nitrogen compounds)

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16
Q

Outline the ocular manifestations of hypertension in the cat

A
  • Blindness

- High BP leads to thickening of walls of blood vessles to retina, restricts blood flow and leads to retina detaching

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17
Q

Outline appropriate therapy for cats with hypertension

A
  • Low protein, sodium adn phosphorous diet
  • ACE inhibitors, vasodilators (to reduce BP)
  • Fluids not useful as unable to concentrate urine
  • Exogenous EPO to manage anaemia
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18
Q

What is the function of intracellular potassium?

A
  • Maintaining intracellular volume

- Cell growth (needed for enzyme function)

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19
Q

Why is potassium regulation important?

A
  • Cellular depolarisation
  • Threshold potential (point at which sodium influx exceeds potassium efflux)
  • Heart most affected when K goes wrong
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20
Q

What is the effect of hyperkalaemia on cells?

A
  • Makes cells hyperexcitable (increased K opens some voltage gated Na channels, charge closer to AP threshold)
  • Slow repolarisation
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21
Q

What may cause hypokalaemia?

A
  • Decreased intake
  • Translocation from ECF to ICF
  • Increased loss (Gi, urinary, drugs, mineralocorticoid xs)
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22
Q

What may cause hyperkalaemia?

A
  • Pseudohyperkalaemia (poor blood sampling technique leading to haemolysis)
  • Increaed intake
  • Translocation ICF to ECF (insulin defic, tumour lysis syndrome, acidosis etc)
  • Decreased urinary excretion (renal failure, rupture, obstruction, Addison’s)
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23
Q

Describe Addison’s disease

A
  • Hypoaldosteronism
  • Low aldosterone = low Na, high K
  • Weakness, lethargy, collapse
  • Severe bradycardia
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24
Q

What are the main points for treating Addison’s disease?

A
  • Rehydration/support
  • Glucose infusion (or insulin) if bradycardic
  • Corticosteroids
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25
Q

What are the main sources of potassium?

A
  • Gastrointestinal (passive diffusion in small intestine, active transport in colon)
  • Cellular breakdown (haemolysis, tissue damage)
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26
Q

What is teh primary control of K+ and why?

A
  • Excretion

- Most is intracellular

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27
Q

Why is the control of flux between intra/extracellular compartments important?

A
  • Can serve asrapid source of more K+ (in cases of hypokalaemia)
  • Or as overflow site (in cases of hyperkalaemia)
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28
Q

How is uptake of K+ into liver and muscle promoted?

A
  • Hormones (insulin and adrenaline, affect beta 2Rc)

- Increase activity of Na+/K+ ATPase

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29
Q

Briefly describe renal control of plasma potassium concentrations

A
  • K+ freely filtered at glomerulus
  • 70% proximal tubule (cellular and paracellular, mainly passive)
  • 10-20% in AL of LoH
  • Net reabsorption or secretion in dista nephron
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30
Q

How is potassium reabsorbed in the early proximal tubule?

A
  • No active transport
  • With water by solvent drag
  • Transepithelial potential difference is lumen negative
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31
Q

How is potassium reasborbed later in the proximal tubule?

A
  • Transepithelial potential difference becomes lumen positive
  • K+ reabsorbed by transcellular route
  • K channel in luminal and basolateral membrane
  • K/Cl cotrasnproter in basolateral membrane
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32
Q

How is potassium reabsorbed in the thick ascending loop of Henle?

A
  • Transepithelial potential difference strongly lumen positive
  • Most K+ reabsorption by transcellular route
  • K+ channels in luminal membrane for paracellular
  • Transcellular route is lumina NaK2Cl cotransporter, K channels, K/Cl cotransporter in basolateral membrane
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33
Q

Describe ion (Na, Cl, K) movements in the distal convoluted tubule

A
  • Na/Cl cotransporter (thiazine sensitive)
  • K/Cl transporter
  • Secretion of K, reabsorption of Na, Cl recycled across luminal membrane
  • Basolateral Na/K ATPase maintains low intracellular Na and high intracellular K (facilitating secretion of K+)
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34
Q

Describe the movement of ions in the connecting tubule and collecting duct

A
  • K secretion (Na/K ATPase)

- High intracellular K to facilitate K secretion down gradient

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35
Q

Describe the role of the principle cells in potassium secretion

A
  • Found in connecting tubule
  • Electrogenic Na channel
  • Makes transepithelial potential difference negative
  • Promote secretion of K through luminal K channels
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36
Q

What are the 2 types of intercalated cells and where are they found?

A
  • Distal nephron
  • Alpha: collecting duct, cortical collecting duct, outer medullar collecting duct
  • Beta: only in cortical collecting duct
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37
Q

How do the alpha-intercalated cells carry out their function?

A
  • H+ ATPase, K-ATPase, Cl/HC)3- counter transporter

- CL and K channels in basolateral membrane

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38
Q

How do the beta-intercalated cells carry out their function?

A

Secrete HCO3- ions as their polarity is reversed

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39
Q

Where in the nephron is potassium reabsorbed?

A
  • Proximal tubule
  • Thick ascending loop of Henle
  • Inner and outer medullar collecting duct (even though TEPD is negative)
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40
Q

Where in the nephron is potassium secreted?

A
  • Distal convoluted tubule
  • Connecting tubule
  • Collecting duct
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41
Q

List the factors that influence renal potassium excretion

A
  • Sodium
  • Potassium
  • Aldosterone
  • Hydrogen
42
Q

Explain how sodium influences renal potassium excretion

A
  • High sodium leads to increased K+ excretion
  • Increased Na+ into cells causes increased Na+/K+ ATPase to pump Na+ into peri-tubular renal interstitium
  • Increased cellular uptake of K+, K+ moves down electrochemical gradient into nephron
43
Q

Explain how potassium influences renal potassium excretion

A
  • High K+ = more K+ excretion

- INcreased aldosterone, increased activity of Na/K ATPase, increased secreton of K+ by tubular cells

44
Q

What is the effect of hydrogen on potassium excretion?

A
  • High H+ (acidosis) decreases K+ excretion

- Low H+ (alkalosis) increased K+ excretion

45
Q

What is the role of aldosterone in potassium regulation?

A

Increases potassium excretion

46
Q

Describe the mechanism by which aldosterone regulates potassium

A
  • Binds to cytoplasmic receptors in principle cells of DT
  • Synthesis of proteins for apical Na+ channel and Na+/K+ ATPase
  • Membrane permeability increased, sodium pump activity increased, NaCl cotransporter increased, ENaC increased
  • K+ secretion is result
47
Q

In what endocrine condition can potassim rise to dangerously high levels due to lack of aldosterone?

A

Addison’s disease

48
Q

What stimulates secretion of aldosterone?

A
  • ACTH
  • Angiotensin II (RAAS)
  • K+
49
Q

What inhibits secretion of aldosterone?

A

Atrial natriuretic peptide (ANP)

50
Q

Under what circumstances is ANP released?

A
  • Sodium and or water loading

- Inhibits aldosterone secretion (which would act to retain sodium as well as secrete potassium)

51
Q

How is the regulation of potassium and hydrogen linked?

A
  • Alkalaemia stimulates increased uptake K+ into cells (ECF to ICF)
  • Acidosis: K+ from ICF to ECF
  • K+ exchanged for H+ i.e. in hypokalaemia K+ to ECF, H+ to ICF, increased H+ secretion = alkalosis
52
Q

What stimualtes uptake of K+ into cells?

A
  • Insulin
  • Aldosterone
  • beta-adrenergic receptor stimulation
  • Alkalaemia
53
Q

What causes movement of K+ out of cells?

A
  • Insulin deficiency
  • Aldosterone deficiency
  • beta-adrenergic blockage
  • Acidemia
  • Cell lysis
  • exercise
  • Increased ECF osmolarity
54
Q

Explain how increased tubular flow rate can reduce K+ excretion

A
  • Volume expansion, high sodium and diuretic increase tubular flow rate and K secretion
  • Tubular K increases, reduces gradient for diffusion across luminal membrane
  • Therefore flushed down tubule
  • Helps preserve normal K excretion during high sodium intake
  • decreases aldosterone, decreasing K excretion
55
Q

What are the 3 main pathways by which nitrogenous waste can be excreted

A
  • The urea cycle
  • The uric acid pathway
  • As ammonia
56
Q

Describe the removal of nitrogenous waste as ammonia

A
  • Binds to hydrogen to give ammonia
  • Toxic
  • Excreted directly by some animals e.g. fish
  • Need lots of water
57
Q

Which animals use ammonia for removal of nitrogenous waste?

A

Fish, amphibians

58
Q

Which animals use the uric acid pathway for removal of nitrogenous waste?

A

Birds, reptiles

59
Q

Which animals use the urea cycle for removal of nitrgenous waste?

A

Mammals

60
Q

Rank the nitrogenous waste removal pathways by the amount of water needed for excretion (high to low)

A
  • Ammonia: most water
  • Urea: middle amount
  • Uric acid: least water
61
Q

Rank the nitrogenous waste removal pathways by the amount of energy needed for excretion (high to low)

A
  • Uric acid (most energy required)
  • Urea (medium)
  • Ammonia (low amount of energy
62
Q

Describe the excretion of urea (or uric acid) by the kidney

A
  • Urea produced in liver, via plasma to kidney
  • Freely filtered through glomerulus
  • In edullary collecting duct some urea reabsorbed into interstitium
  • Into vasa recta
  • Back to lumen of LoH for excretion
63
Q

Describe the process of urea recycling

A
  • Urea transported into interstitium in medullary collectin gduct
  • Urea enters vasa recta at distal end of hairpin loop of LoH
  • Passes near descending limb of nearby nephrons
  • Urea transporters return urea to lumen for excretion
  • Small amount enters systemic circulation
64
Q

What is the function of urea recycling?

A

Enables urea to be excreted, but also to contribute to hypertonicity at bottom of LoH
- Contributes to ~50% of medullary concentration gradient

65
Q

What will increase urea?

A
  • Decreased GFR
  • Increased nitrogen intake
  • Poor blood flow
66
Q

How does a decreased GFR increase blood urea?

A
  • Slower filtration

- Increased urea reabsorption

67
Q

How does poor blood flow lead to increased blood urea?

A
  • Less put back into descending loop from vasa recta

- More in blood

68
Q

What may cause a decreased GFR?

A
  • Poor renal perfusio (deydration, hypovolaemia, decreased cardiac out put)
  • Too few function nephrons
  • Urinary tract obstruction/rupture
  • I.e. pre-renal, renal, post-renal
69
Q

Why can urea be used as a marker of renal function?

A
  • More affected by poor perfusion than creatinine
  • Due to slow flow rate
  • Creatinine unchanged through tube, urea reabsorbed fom collecting duct (so high urea means low reabsorption)
  • Slow flow rate leads to less in urine
  • Early sign of kidney disease
70
Q

What are the limitations of using urea as an indicator of renal clearance in horses?

A
  • Colonic secretion of urea
  • Metabolised by GI bacteria
  • Use nitrgoen to make proteins and energy
  • Product of this is ammonia
  • Taken up into portal circulation where it is turned into urea again
  • i.e. is constantly cycled round
71
Q

What are the limitations of using urea as an indicator of renal clearance in birds?

A
  • Mostly use uric acid for nitrogen excretion
  • Low urea in blood
  • Urea reabsorption at low flow rates very high
72
Q

What are the limitations of using urea as an indicator of renal clearance in reptiles

A
  • Do not synthesise urea
  • uric acid secreted by proximal convoluted tubule and affected by post-prandial (high protein food leads to increase), pre-renal (dehydration leads to increase), renal and body temperature
73
Q

What happens to the urine that is produced during hibernation?

A
  • Almost all ultrafiltrate reabsorbed
  • Able to reabsorb urine from bladder
  • Do not develop azotaemia
74
Q

Describe protein metabolism during hibernation

A
  • Protein turnover continues at low level
  • Protein synthesis maintained
  • Protein degradation reduced
  • I.e. high synthesis and low degradation = conservation of limited supply
75
Q

Describe urea recycling in bears

A
  • AA degradation leads to production of ammonium (but little taking place)
  • In bears, urease expressing gut bacteria hydrolyse urea to free N which is used to form new AAs to maintain muscle mass
76
Q

Explain how urea recylcing is linked to the generation of fatty intermediates in hibernation

A
  • To reincorporate N into body protein need some carbon
  • Non-protein source of carbon is glycerol
  • Lipolysis -> glycerol -> TCA cycle -> pyruvate -> alanine
  • Also produces water
77
Q

Define oliguria

A

Production of abnormally small amounts of urine

78
Q

Define anuria

A

No urination

79
Q

Why is the tonicity of urine in chronic renal disease and why?

A
  • Isosthenuric

- Lost ability to modify (reabsorb or secrete) the ultrafiltrate

80
Q

What is the effect of renal failure on urine volume?

A
  • Polyuria

- Inability to retain water thus dehydration and increased thirst, furthering increased urination

81
Q

List the laboratory methods used to assess renal function and identify renal failure

A
  • GFR
  • Renal clearnace
  • Creatinine/urea clearance
  • Electrolyte/fractional clearance
  • Acid-base balance
  • Urinalysis
  • Haematology
82
Q

How can glomerular function be assessed in the laboratory?

A
  • Urinalysis
  • Look for protein in urine (although can be caused by things at all levls of urinary tract)
  • Protein:creatinine ratio
83
Q

Why is protein:creatinnie ratio used rather than protein alone to assess glomerular function?

A
  • Protein can come from all levels of UT (inflammation)
  • Creatinine should be excreted in consistent way and should match creatinine production
  • By comparing can quantify importance of protein in urine
84
Q

What can be used to assess renal tubular function?

A
  • Electrolyte/fractional clearance
  • Acid-base balance
  • Urinalysis
  • Assessment for presence of casts
85
Q

What is the function of the proximal tubule and how does it carry out this function?

A
  • Regulates pH of filtrate (exchanges H+ in interstitium for HCO3- in filtrate)
  • Secretion of organic acids
  • Reabsorption to peritubular capillaries
  • Na/K ATPase in basolateral memrbane driving reabsorption
86
Q

What is renal fractional clearance?

A
  • the ratio of electrolyte clearance to creatine clearance
  • I.e. the volume of plasma that would have been cleared of the substance to give the amount of that substance found in the urine in the given time period
87
Q

What is suggested by low fractional electrolyte clearance?

A
  • Net conservation
  • More reabsorption than secretion
  • e.g. volume depletion, sodium retained, FC of sodium very low (less is being cleared)
88
Q

What would be expected of the fractional clearance in renal damage?

A
  • High FC
  • Reabsorption has been decreased, more secretion
  • Except phosphate, poorly secreted in damaged situation
89
Q

How can urinalysis be used to asses renal tubular function?

A
  • Urea and creatinine
  • Assess pH, protein, glucose
  • USG
90
Q

What is likely to happen to urea:creatinine in renal damage?

A
  • Increased

- Reduction in ability to reabsorb urea

91
Q

What is likely to happen to USG in chronic renal failure?

A
  • Isosthenuric urine

- Loss of concentrating ability

92
Q

What is the significance of the presence of casts in urinalysis?

A
  • Should be non in urine
  • Formed in lumen of tubules
  • Suggestive of disease/damage
  • Cahnge in type according to duration of urine in tubule
  • Caused by slow flow
93
Q

What are the different types of casts that may be seen in urinalysis?

A
  • Cellular
  • Granular
  • Waxy
  • Hyaline
94
Q

What is likely to be seen on haematology in renal damage?

A
  • Chronic renal disease leads to loss of renal tissue, reduced EPO
  • EPO deficiency
  • Non-regenerative anaemia
  • Inflammation
95
Q

Under what conditions is the clearance equal to GFR?

A
  • If teh substance is filtered, not reabsorbed and not secreted
  • e.g. creatinine
96
Q

Experimentally, GFR can be measured using the clearance of what?

A
  • Inulin
  • Creatinine
  • Plasma clearance markers
97
Q

What may lead to low creatinine levels?

A

Low muscle mass, not as much production of creatinine possible

98
Q

What (other than renal causes) may lead to high urea levels?

A
  • High protein in diet

- Haemorrhage (leading to high protein in gut from blood digestion)

99
Q

What different types of renal damage are there?

A
  • Glomerular (affecting filtration)
  • Tubular (affecting secretion and reabsorption)
  • Interstitial (affecting concentrating ability)
  • Mixed (most cases)
100
Q

What are the non-excretory roles of the kidney?

A
  • Maintain water and composition of plasma
  • Water, ion, pH level regulation
  • Nutrient retention
  • Endocrine function (EPO, calcitriol, renin)

URI (15 decks)

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