GFR Flashcards
Describe the differences between cortical and juxtamedullary nephrons. (6)
Location: C - outer part of cortex, LoH just into medulla; J - inner part of cortex, LoH well into medulla.
Arteriole size: C - AA>EA, 2:1; J - AA=EA.
Drainage: C - peritubular capillaries, J - vasa recta.
Sympathetic innervation: C - high; J - low
Conc of renin: C - high; J - low
Ratio: C - 90%; J - 10%.
What is normal GFR and what 4 factors does it depend on? (2)
125ml/minute.
Gender, age, size, pregnancy.
Why can GFR changes in pregnancy be dangerous for diagnosis AKI? (2)
GFR increases in pregnancy under the influence of progesterone, so creatinine clearance increases. This means that a fall in creatinine clearance as seen in AKI could be missed because it puts the creatinine clearance back in normal range.
Explain the forces acting on the glomerulus that result in filtration. (6)
P(GC) - hydrostatic pressure in the capillaries pushes water from the glomerulus into the Bowman’s capsule. Very big.
P(BC) - hydrostatic pressure in the Bowman’s capsule pushes water from the capsule back into the glomerulus. Very small.
pi - oncotic pressure difference between the capillary and the capsule because all the proteins still exist within the glomerulus. Small.
Explain the autoregulation of P(GC) to maintain GFR levels. Mention Renin, prostaglandins and adenosine. (8)
Autoregulation through glomerular tubular feedback.
If Na+ levels increase at the macula densa (DCT), it means too much is being filtered, so GFR needs to decrease. Adenosine release causes vasoconstriction of the AA and vasodilation of the EA.
If Na+ decreases at the macula densa, it means too little is being filtered, so the GFR needs to increase. Prostaglandin release causes vasodilation of AA, and Angiotension II (produced from the release of renin) causes vasoconstriction of the EA.
Describe the changes that occur to maintain GFR with changing blood pressure. (4)
High BP - AA constriction, EA dilation - lowers P(GC) - lowered glomerular pressure - unchanged GFR.
Low BP - AA dilation, EA constriction - raises P(GC) - raised glomerular pressure - unchanged GFR.
Explain the autonomic innervation of the EA and AA. (4)
Sympathetic fibres normally have a low effect, but in fight or flight, or haemorrhage, or ischaemia, vasoconstriction occurs which reduced GFR.
Parasympathetic release of NO causes vasodilation.
Explain the changes in GFR present in babies, the elderly, and pregnant women. Explain why the changes in pregnancy could be lead to missing diagnosis of AKI. (6)
Babies - premies and LBW babs have a lower nephron number which struggles to catch up. Normal babs have adult GFR by 18 months.
Elderly - GFR begins to decline after 30, with the loss of functioning nephrons.
Pregnancy - GFR increases, but nephron number remains the same. This means creatinine clearance increases, so a lowered creatinine clearance in AKI could put it back into normal range.
What are the 4 necessary characteristics that a substance used to work out GFR must have, and why? (5)
Produced at a constant rate, freely filtered across the glomerulus, not reabsorbed in the nephron, not secreted into the nephron.
Then excretion rate = GFR.
Describe inulin and it’s use in clinical practice. (3)
A polysaccharide that can be used as a substitute for GFR. Not used in clinical practice because it needs an IV drip and a catheter.
Describe 51 Cr-EDTA and it’s use in clinical practice. (2)
A radioactive labelled marker given in timed injections with blood samples being taken. Approx 10% lower clearance than inulin.
Describe creatinine and it’s flaws. (4)
An endogenous substance that is the end point of muscle breakdown. Has issues with exogenous production (meaty meals, exercise), and is secreted into the nephron so overestimates GFR. Measured by collecting urine over 24 hours.
Explain why eGFR is less accurate in mild kidney disease. (4)
The body compensates well for a mildly reduced GFR: reduction in GFR causes increase in blood flow, reduced nephron number causes hypertrophy, reduced filtration fo creatinine leads to higher blood creatinine, so more is secreted into the tubules.
Explain why hypertrophy can keep GFR constant. (2)
Individual nephrons work harder to maintain GFR so the whole kidney hypertrophies. Nephron number does not increase.
