PHYS: Urine Formation Flashcards
(47 cards)
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
2
Q
tubular reabsorption
A
- materials from filtrate are selectively reabsorbed back into blood via peritubular capillaries (can be active or passive)
- Na+ and glucose are fully reabsorbed, most water follows
- waste products e.g. urea are poorly reabsorbed
3
Q
tubular secretion
A
- solutes move from peritubular capillaries into DCT to be excreted into urine
- e.g. drugs, H+ ions
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)
5
Q
forces that drive and oppose glomerular filtration
A
- FAVOURS filtration: hydrostatic pressure of blood in glomerulus
- OPPOSES filtration: hydrostatic pressure of blood in Bowman’s capsule and plasma osmotic (colloid) pressure - proteins remain in the blood > water wants to stay in the glomerulus
6
Q
net glomerular filtration pressure - what is the formula and what is a normal GFP?
A
- GFP = glomerular hydrostatic pressure - (capsular hydrostatic pressure + plasma oncotic pressure)
- NORMAL = 55 - (15 + 30) = +10 mmHg = positive filtration
7
Q
interpretation of GFR
A
- 90+ = ideal
- 60-90 = normal but not ideal
- 15-60 = CKD
- 0-15 = kidney failure (end stage kidney disease - needs dialysis)
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 uses creatinine (waste product of creatine) - freely filtered and then passes straight into urine (not reabsorbed or secreted) AND not synthesised or metabolised by the kidney
9
Q
two most important determinants of GFR
A
- renal blood flow
- glomerular capillary pressure
10
Q
what two factors determine glomerular capillary pressure?
A
- arterial pressure
- afferent and efferent resistance
11
Q
what pathologies can increase or decrease GFR?
A
- increase: narrowing of efferent arteriole
- decrease: narrowing of afferent arteriole, diarrhoea, increase in plasma proteins, renal calculi, dehydration
12
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 help facilitate stretch
- therefore able to increase in volume without increasing pressure
13
Q
how is the bladder tissue protected from the waste in urine?
A
- urothelium has specialised impermeable apical layer containing tight junctions and glycoproteins
14
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
15
Q
voiding process
A
- bladder fills, stretch receptors activated
- send afferent signals to spinal cord via pelvic splanchnics (parasympathetic)
- periacqueductal grey (PAG) decides whether or not to activate the pontine micturition centre (PMC) - usually inhibits urination until activated
- BUT to avoid instantly urinating, sympathetic nerves inhibit contraction of detrusor muscle and cause internal urethral sphincter to contract
- pudendal n. contracts external urethral sphincter until an appropriate time to void
16
Q
when can we get incontinence?
A
- parasympathetic nerve damage
- reduced bladder compliance = intravesical pressure increases = urge to void faster
- sphincter damage
17
Q
urge incontinence
A
- sudden, intense urge to urinate followed by involuntary voiding
- can be caused by UTI or neurological conditions
18
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)
19
Q
cystocele
A
- bladder prolapses posteriorly and inferiorly due to weakness of pelvic floor muscles
- can cause urinary retention due to compression of bladder
20
Q
what can cause damage/dysfunction to pelvic splanchnics?
A
- damaged during prostatectomy or abdominal surgeries
- pelvic trauma
- excessive compression
- diabetic neuropathy
21
Q
stress incontinence
A
- increased abdominal pressure under stress (weak pelvic floor muscles e.g. childbirth)
- loss of smooth and skeletal muscle tone
22
Q
deafferentation of bladder
A
- interruption of visceral afferents = disruption in transmission of stretch signals from bladder to spinal cord = atonic bladder (flaccid and distended)
- causes OVERFLOW INCONTINENCE (bladder doesn’t know when to empty anymore so will just overflow with a few drops at a time when it reaches the critical threshold)
- can also lead to vesicoureteric reflux, hydronephrosis and AKI
- e.g. neurosyphilis
23
Q
denervation of bladder
A
- interruption of both the afferent and efferent nerves
- UMN damage = spastic neurogenic bladder (UMN usually inhibitory so when damaged you have a hyper-reflexive bladder, detrusor muscle will contract inappropriately) = urge incontinence
- LMN damage = flaccid bladder (bladder becomes hypo-reflexive due to damage of peripheral parasympathetic nerves) = retention, overflow incontinence
- e.g. diabetic autonomic neuropathy
24
Q
what would happen in a spinal cord transection (above the sacral region) to the bladder?
A
- interruption of voluntary pathways in the brain (e.g. MVA)
- initially, everything (including micturition reflex) is suppressed due to spinal shock = bladder is flaccid & unresponsive
- after shock has passed, micturition reflex will return but not under voluntary control from the descending pathways from the brain = neurogenic bladder (urge incontinence)
25
impacts of a dysregulated GFR
- increased GFR = inadequate reabsorption = substances lost in urine
- decreased GFR = too much reabsorption = wastes not excreted
26
what is/isn't autoregulated in the kidneys and by what mechanisms?
- renal blood flow and GFR are autoregulated by the myogenic mechanism and tubuloglomerular feedback
- urine flow rate is not autoregulated - instead directly proportional to arterial pressure (pressure natriuresis)
27
when will autoregulation of renal blood flow and GFR NOT occur?
- if blood pressure is outside the range of 80-180mmHg
- i.e. below 80mmHg (e.g. haemorrhage), we don't want to lose fluids
- above 180mmHg we don't want to retain fluids
28
myogenic mechanism (renal)
- autoregulation of renal blood flow and therefore GFR
- high BP causes increased shear stress (stretch) on artery walls = Ca2+ channels open = Ca2+ influx = constriction of afferent arterioles
- reduces renal blood flow to ensure that glomerular pressure and GFR don't increase
29
tubuloglomerular feedback
- autoregulation of renal blood flow and therefore GFR
- macula densa senses change in Na+ flow rate and therefore GFR
- sends adenosine signals to cause constriction of afferent/efferent arterioles and increased/decreased secretion of renin by juxtaglomerular cells to maintain GFR WNL
30
two pathways for tubular reabsorption
- paracellular: through tight junctions between epithelial cells
- transcellular: directly through the epithelial cells
31
where are sodium and water reabsorbed
- mostly in the PCT
- some water is reabsorbed in descending loop of henle and CD
- some Na+ is reabsorbed in ascending loop of henle, DCT and CD
32
what is transport maximum?
- why does it occur?
- where does the excess go?
- what is it for glucose?
- the maximum rate at which a substance can be reabsorbed back into peritubular capillaries
- occurs due to saturation of available carrier proteins
- excess secreted in urine
- Tm for glucose = 375 mg/min
33
filtered load and what is it for glucose?
- the amount of a substance filtered by the kidneys per min
- filtered load = plasma conc. x GFR
- glucose = 125 mg/min
34
when do we get glycosuria? what happens in uncontrolled diabetes mellitus?
- normally, glucose is not excreted
- if we have >300mg glucose per 100mL of plasma, we excrete some = glycosuria
- in uncontrolled diabetes mellitus, glucose filtered load > glucose Tm (375mg/min)
35
why does high Na+ lead to high BP?
- sodium in ECF = increased ECF osmolarity
- water moves from ICF > ECF = increased volume of ECF (plasma) = HIGH PRESSURE
- therefore decreased volume and increased osmolarity of ICF
36
pressure natriuresis
- arterial pressure controls excretion of sodium and therefore water in urine
- increased MAP = increased excretion of Na+ and H2O to get rid of fluids = increased urination = decreased plasma volume back to WNL
37
which part of the nephron can sodium reabsorption be modulated?
- only in the late DCT and CD
- 65% is always reabsorbed in PCT
- 30% is always reabsorbed in ascending loop of henle
- the rest in DCT/CD depends on aldosterone
38
aldosterone
- where is it secreted
- what type of hormone is it
- what does it do
- what will happen if aldosterone levels are high?
- zona glomerulosa (outer section) of adrenal cortex
- steroid hormone (mineralocorticoid)
- controls Na+ reabsorption
- high aldosterone > low renin (-ve feedback)
39
how does aldosterone control Na+ reabsorption
- combines with mineralocorticoid receptor in cytoplasm of DCT/CD epithelial cell and migrates to nucleus
- upregulates expression of proteins P1-P4 = increased synthesis of Na+ and K+ channels in the luminal membrane AND Na+/K+ ATPase pumps in the basolateral membrane
- ultimately, increased Na+/H2O reabsorption
40
addison's disease
- adrenal glands produce insufficient aldosterone
- low BP, salt cravings due to hypokalaemia, muscle weakness due to hyperkalaemia
41
aldosteronism
- adrenal glands produce excessive aldosterone
- high BP, hypernatraemia, hypokalaemia
42
RAAS
- renin (secreted by kidneys) causes angiotensinogen (secreted by liver) > angiotensin I (inactive)
- ACE (secreted by pulmonary and renal epithelium) converts Ang I > Ang II = increased Na+/H2O retention
43
5 effects of ang II
- increased renal sympathetic activity
- increased Na+ (and therefore H2O) reabsorption via increased activity of basolateral Na+/K+ pumps
- increased aldosterone secretion
- vasoconstriction
- increased ADH secretion
44
renin
- where is it synthesised
- what does it do
- 3 things that trigger renin secretion
- juxtaglomerular cells
- converts angiotensinogen > angiotensin I
45
3 factors which trigger renin secretion
- decreased renal arterial pressure (sensed by intrarenal baroreceptors/juxtaglomerular cells)
- decreased Na+ in lumen passing macula densa
- increased renal sympathetic drive (want to retain Na+ to maintain BP)
46
why does decreased renal arterial pressure lead to increased renin secretion
- decreased renal arterial pressure = decreased plasma volume and hence stretch of juxtaglomerular cells (intrarenal baroreceptors) = decreased [Ca2+] = increased renin secretion
47
calcium paradox
- usually increased [Ca2+] = increased secretion
- however in juxtaglomerular cells, increased [Ca2+] = decreased renin secretion
