2- Glomerulus, Clearance, Regulation Ca and PO4 Flashcards
Function of the Kidney
Regulation of ions
Excretion of waste
Endocrine: EPO, renin, prostaglandins
Metabolism: active forms of vit D, catabolism of insulin, PTH
What is almost 100% recovered
Water Sodium Chloride Bicarbonate Glucose Amino acids
What substances are actively secreted
H+
How much blood is filtered each day
180L/day
How much urine is produced each day
1.5L
Where is the glomerulus found
Cortex only
What is the filtration fraction
GFR/Renal plasma flow
How much of arriving blood exits unfiltered
80%
What are the two types of nephron
Cortical
Juxtamedullary
What is normal GFR
90-120 mL/min/1.73m2
How is the end product of filtration different from plasma
No large proteins and cells (RBC)
How do podocytes keep proteins out
Negatively charged so repel the neg charged proteins
What allows filtrate to pass through
Fenestrations
What pressures work in bowmans capsule
Hydrostatic of capillary
Hydrostatic of capsule
Oncotic of capillary and tubular lumen
Regulation of renal blood flow and GFR
Myogenic and tubuloglomerular feedback mechanism
Myogenic regulation
Arterial smooth muscle responds to increases and decreases in vascular wall tension
Rapid
Property of predominantly the preglomerular resistance vessels (afferent)
i.e to increase GFR constrict efferent or dilate afferent
to decrease GFR constrict afferent or dilate efferent
Tubuloglomerular feedback with high tubular flow
NaCl conc at macula densa linked with renal arteriolar resistance
The higher the flow of filtrate the higher Na conc
Increased NaCl = vasoconstriction of smooth muscle in afferent to reduce renal plasma flow to reduce GFR
Tubuloglomerular feedback with low BP
Release of prostaglandins reduce constriction of afferent arteriole
Renin released by juxtaglomerular cells in response to
1. sympathetic nerve stimulation
2. decrease stretch of afferent
3. macula densa signals in response to low NaCl
= RAAS
Where does RAAS mainly work
Constrict efferent arterioles = increase GFR
Issue with people on NSAIDs and ACEI
Inhibit prostaglandins and RAAS
What is the equation for excretion
filtration-reabsorption+secretion
What could cause a decreased GFR
Decrease number of nephrons
What is renal clearance
Volume of plasma cleared of substance in a unit of time
Measure of kidney’s ability to remove substance and excrete it
What is the clearance equation
C = conc of substance in urine (mg.mL) x urine flow rate (mL/min) / conc of substance in plasma
What unit is clearance measure in
mL/min
Where is most Ca stored and how is it stored
Calcium phosphate in the bones
What is the difference between diffusible and non diffusible Ca
Diffusible: free ionised Ca, used for cellular processes
Non diffusible: bound to negatively charged proteins
Where is most Ca reabsorbed
65% PCT
Solvent drag
Transcellular
What happens in TAL to Ca
25% reabsorbed
50% trancellularly through Na/K/2Cl- then Na pumped out so lumen becomes positive so Ca repelled = moves between cells (Paracellularly)
What is phosphate essential for and where is most of it found
Structure of bones and teeth
80% bones, 20% interstitial fluid
Where is PO4 reabsorbed mainly
PCT
How is PO4 reabsorbed
2Na for every PO4
What causes itching
Increased PO4
What is the relationship between Ca and PO4
They precipitate to form insoluble calcium phosphate
So if one increases the other is removed
Inversely proportional
What is released in response to low Ca
PTH
What are the effects of PTH
Decrease PO4 reabsorb in PCT
Increase in active Vit D
Increase Ca reabsorb in DCT
Increase bone reabsorb
All = increase plasma Ca
What does low Ca lead to
Increase in neuromuscular excitability = tetany and convulsions, cramps and arrhythmias
Causes of low Ca
Hyperphosphatasemia and low levels of active Vit D
Rickets and osteomalacia - low vit D
Tissue injury- cells die and release PO4
Alkalosis- reduced H to bind to protein so more Ca can bind = reduced free Ca
Treatment of low Ca
Oral or IV Ca
Alfacalcidol
Vit D analogue
What does high Ca cause
Less excitable Slow reflexes Weakness and constipation Polyuria Bone pain and fractures Stones Groans Moans
Causes of high Ca
Hyperparathyroidism Acidosis- release of Ca from protein Too much vit D Bone destruction- malignancy Granulomatous disease Drugs
Treatment of high Ca
Treat underlying cause
Rehydrate
Bisphosphonates
Causes of low PO4
Excessive loss
Hyperparathyroidism- increase Ca so decrease PO4
Reduced GI absorption - alcohol or antacids
Reduced intake
Refeeding- move in to allow glycolysis
DKA- insulin given- big movement in to cell
Resp alkalosis- decrease CO2- shift intracellular- increase Ph cell stimulates glycolysis = lots of PO4 needed in cell
How does
DKA
Resp alkalosis
Refeeding cause low PO4
Refeeding - move in to allow glycolysis
DKA- insulin given- big movement in to cell
Resp alkalosis- decrease CO2- shift intracellular- increase Ph cell stimulates glycolysis = lots of PO4 needed in cell
Signs of low PO4
Stones, mones, bones, groans, psychiatric overtones
Treatment of low PO4
Oral or IV PO4
Gradual refeeding
Causes of high PO4
CKD - low GFR
Pseudohypoparathyroidism- kidneys don’t respond to PTH = low Ca so high PO4
Respiratory acidosis- decrease Ph = inhibits glycolysis
DKA- PO4 not taken out of blood- risk of low when insulin given
Symptoms of high PO4
Only with severe Spontaneous firing of neurons Tetany Involuntary contraction of muscles Calcium phosphate crystals- stones
Treat high PO4
Phosphate binders
Low dietary intake
Forced diuresis
