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How does increased extracellular pCO2 affect renal hydrogen extretion?

- Tubular cells respond directly
- Respiratory acidosis
- Increase rate of H+ secretion
- Hyperventilation


How does a loss in ECF affect renal hydrogen excretion?

- 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


Explain the effect of hypokalaemia on renal hydrogen excretion

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


Explain the effect of hyperkalaemia on renal hydrogen excretion

- Inhibitis H+ secretion in proximal tubule
- Decreases H+ secretion and HCO3- reabsorption and tends to cause acidosis


Explain the effect of hypochloraemia on renal hydrogen excretion

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


Explain how lungs and kidney work together to control plasma pH

- 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


What may be an effect of dehydration?

- High urine creatinine, urea and albumin
- Also reduced flow rate through nephrons


What is renal insufficiency?

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


Define renal disease

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


Define renal failure

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


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

- Low protein diet (reduces production and thus build up of urea)
- Low sodium diet
- Low phosphorous diet


How does renal failure cause high blood pressure?

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


Why is a low phosphorous diet important in renal disease?

- Can lead to secondary renal hyperparathyroidism
- Calcification of body tissues in high phos (block up nephrons)


How is anaemia caused in renal disease?

- Erythropoeitin produced in kidney
- Damaged kidney produces less EPO


What is azotaemia?

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


Outline the ocular manifestations of hypertension in the cat

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


Outline appropriate therapy for cats with hypertension

- 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


What is the function of intracellular potassium?

- Maintaining intracellular volume
- Cell growth (needed for enzyme function)


Why is potassium regulation important?

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


What is the effect of hyperkalaemia on cells?

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


What may cause hypokalaemia?

- Decreased intake
- Translocation from ECF to ICF
- Increased loss (Gi, urinary, drugs, mineralocorticoid xs)


What may cause hyperkalaemia?

- 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)


Describe Addison's disease

- Hypoaldosteronism
- Low aldosterone = low Na, high K
- Weakness, lethargy, collapse
- Severe bradycardia


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

- Rehydration/support
- Glucose infusion (or insulin) if bradycardic
- Corticosteroids


What are the main sources of potassium?

- Gastrointestinal (passive diffusion in small intestine, active transport in colon)
- Cellular breakdown (haemolysis, tissue damage)


What is teh primary control of K+ and why?

- Excretion
- Most is intracellular


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

- Can serve asrapid source of more K+ (in cases of hypokalaemia)
- Or as overflow site (in cases of hyperkalaemia)


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

- Hormones (insulin and adrenaline, affect beta 2Rc)
- Increase activity of Na+/K+ ATPase


Briefly describe renal control of plasma potassium concentrations

- 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


How is potassium reabsorbed in the early proximal tubule?

- No active transport
- With water by solvent drag
- Transepithelial potential difference is lumen negative