PHYS: Filtration and Urination Flashcards

1
Q

glomerular filtration

A
  • blood enters via afferent arteriole
  • high pressure passively and non-selectively pushes small molecules e.g. water, glucose, AAs through very large fenestrations in capillaries = now called filtrate = goes to bowman’s capsule and PCT
  • large molecules e.g. proteins, blood cells do not cross = transported back into general circulation via efferent arteriole
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2
Q

tubular reabsorption

A
  • materials from filtrate are selectively reabsorbed back into blood via peritubular capillaries
  • water, Na+ and glucose are fully reabsorbed
  • waste products e.g. urea are poorly reabsorbed
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3
Q

tubular secretion

A
  • solutes move from peritubular capillaries into DCT to be excreted into urine
  • e.g. drugs, H+ ions
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4
Q

3 layers of glomerular filtration barrier

A
  • simple squamous fenestrated capillary endothelium
  • non-cellular basement membrane
  • simple epithelium of Bowman’s capsule (contains podocytes with filtration slits, bridged by a diaphragm)
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5
Q

forces that drive and oppose glomerular filtration

A
  • FAVOURS filtration: glomerular hydrostatic pressure (in blood)
  • OPPOSES filtration: hydrostatic pressure in Bowman’s capsule and plasma osmotic (colloid) pressure - since there is more proteins and less water in plasma (therefore glomerulus) than bowman’s capsule = water wants to move out of Bowman’s capsule back into glomerulus
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6
Q

net glomerular filtration pressure

A
  • GFP = hydrostatic pressure - (capsular hydrostatic pressure + osmotic pressure)
  • NORMAL = 55 - (15 + 30) = +10 mmHg = positive filtration
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7
Q

interpretation of GFR

A
  • 60-120 = normal
  • 15-60 = kidney disease
  • 0-15 = kidney failure
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8
Q

how is GFR measured?

A
  • renal clearance - volume of plasma that is completely cleared of a substance by the kidney per unit time
  • often measured using clearance of creatinine (waste product of creatine) - freely filtered but not reabsorbed or secreted (i.e. passes straight into urine following lack of reabsorption), AND not synthesised or metabolised by the kidney
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9
Q

two most important determinants of GFR

A
  • renal blood flow
  • glomerular capillary pressure
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10
Q

what pathologies can increase or decrease GFR?

A
  • increase: kidney stones blocking renal pelvis, increase in plasma proteins
  • decrease: blockage/stenosis of efferent arteriole, diarrhoea
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11
Q

how does the bladder pressure remain low during filling?

A
  • highly compliant due to transitional urothelium: 5-7 layers of cuboidal/columnar cells when relaxed and 2-3 layers of squamous cells when stretched
  • rugae (internal folds) also helps facilitate stretch
  • therefore able to increase in volume without increasing pressure
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12
Q

how is the bladder tissue protected from the waste in urine?

A
  • urothelium has specialised impermeable apical layer containing tight junctions and glycoproteins
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13
Q

change in bladder shape during filling

A
  • becomes spherical and then pear-shaped as it fills
  • very full bladder may be palpable above the pelvic brim
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14
Q

guarding reflex + voiding suppression process

A
  • normal involuntary reflex to hold urine (regulated at spinal cord level)
  • afferent signals from stretch receptors travel via spinothalamic and DCML pathways to reach pontine micturition centres
  • when bladder reaches a critical level of distension, brain is alerted: periacqueductal grey (PAG) helps to voluntarily suppress urination via connections with all the nerves
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15
Q

when can we get incontinence?

A
  • parasympathetic nerve damage
  • reduced bladder compliance = intravesical pressure increases = urge to void faster
  • sphincter damage
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16
Q

urge incontinence

A
  • sudden, intense urge to urinate followed by involuntary voiding
  • can be caused by UTI or neurological conditions
17
Q

when can we get urinary retention? what can it result in?

A
  • obstruction of bladder outflow e.g. prostatic hypertrophy, cystocele
  • nerve damage affecting sphincter tone
  • damage of afferent nerves or poor detrusor muscle contractility (rare)
  • can result in overflow incontinence if intravesical pressure gets large enough to overcome increased outflow resistance
  • can also predispose to infection, bladder stones, retrograde flow (hydroureter, hydronephrosis etc)
18
Q

cystocele

A
  • bladder prolapses posteriorly and inferiorly due to weakness of pelvic floor muscles
  • can cause urinary retention due to compression of bladder
19
Q

what can cause damage/dysfunction to pelvic splanchnics?

A
  • damaged during prostatectomy or abdominal surgeries
  • pelvic trauma
  • excessive compression
  • diabetic neuropathy
20
Q

stress incontinence

A
  • increased abdominal pressure under stress (weak pelvic floor muscles e.g. childbirth)
  • loss of smooth and skeletal muscle tone