urinary Flashcards
anatomy urinary tract
- 2 kidneys either side spine behind caudal rib
- ureters for urine kidney -> bladder
- bladder stores urine
- urethra for urine bladder -> outside
kidneys not always kidney shaped
kidney functions
- reg fluid vol + electrolyte balance - ECF/blood press, osmolarity, ions, pH
- waste excretion (metabolic + foreign)
- prod hormones - activate D3, synth renin enz, synth erythropoietin
renal anatomy
- outer cortex for filtration
- inner medulla to collect + excrete urine
w nephrons = functional units
nephron structure
- renal corpuscle - prods filtrate
- proximal convoluted tubule, PCT - unregulated reabsorp water, ions, organic nutrients
- loop of henle, LoH - reabsorp ions + water + set up osmotic grad
- distal convoluted tubule, DCT - variable secretion + reabsorp water + ions (more reg)
- collecting duct - several nephrons join for variable secr + reabsorp water + ions (more reg)
- papillary duct delivers urine to renal pelvis
long tube, squished in reality
identifying areas kidney histology
- cortex = mainly tubules w renal corpuscles
- medulla = only renal tubules
how much blood to kidneys + where from/to
renal arteries directly branch off aorta, giving 20-25% CO -> renal veins
* loads blood so change bp affects kidneys = damaged if high
artery + vein path thru kidneys
where are renal cap beds found
- glomerular caps in renal corpuscle
- peritubular caps around PCT then parallel to LoH
how incr filtration across cap bed
- vasodilate precap arterioles = incr HP
- constrict efferent to cap (at least relative to afferent)
- incr permeability = thin + porous mem
- large SA for filtration
passage of stuff for filtration out glomerular caps
in theory osmotic press would balance HP eventually but balance lies above pt where ever actually happens + filtr conts along length caps
histology edge kidney
renal capsule = fibrous CT w lots collagen
initial filtrate general content
approximates prot free plasma w water, ions, gluc, aas, N waste products
* bigger holes but not most prots or bcs
glomerular filtration rate
GFR
vol fluid filtered from glomerular caps -> Bowman’s space per min (both kidneys)
* varies w metabolic mass
* 3ml/kg/min in dogs
measure kidney function
reabsorp + secr in nephron defns
reabsorp = returning important substances filtrate -> blood
secr = movement waste mats body -> filtrate
details bulk reabsorp
70% filtrate reabbed in PCT
* selective via prot transporters but mostly unregulated (no hormonal control)
* active + passive
path tubular reabsorp
filtrate -> renal insterstitium -> renal bvs -> body circulation
tubule cells of PCT specialisations
- microvilli on apical mem incr SA reabsorp (ONLY PCT)
- lots Na+K+ATPase on basolateral mem
- lots carbonic anhydrase
types absorp in PCT
- transcellular = thru tubule cells, AT into cell + out
- paracellular = thru tight junctions bet tubule cells, diffusion
diffusion ISF -> blood in peritubular cap
how does transcellular absorp Na+ in PCT work
- Na+ AT over basolateral mem tubule cell -> ISF
- sets up Na+ grad (low conc in cell) so Na+ tubule lumen -> tubule cell
Na+K+ATPase pump
result of Na+ AT out tubule lumen -> blood
- neg Cl- follows down electrochem grad
- solutes set up osmotic grad = water follows by osmosis
- bulk movement water =:
1. solvent drag as brings other solutes from filtrate -> caps
2. diffusion as sets up conc grads passive diff solutes (bc less water in lumen)
mostly thru prot channels = selective
how are substances reabsorbed PCT
apical symport prot w Na+ filtrate -> tubule cell (2AT)
basolateral fac diff carrier ion exchanger cell -> ISF down conc grad
e.g. Na-gluc symporter + gluc fac diff transporter (+ need Na+K+ATPase)
which substances reabsorbed in PCT by 2AT w Na+
- gluc
- aas
- lactate
- citric acid cycle intermediates
- phosphate
- sulphate
how much gluc -> PCT
freely filtered - depends plasma conc for rate bc diffusion, but no limit
how much gluc reabsorbed from PCT
depends:
* rate filtrate flow
* no. prot transporters - if saturate
is gluc excreted
normally no bc all reabsorbed, only if renal threshold reached if overwhelming amount gluc = gluc in filtrate = glucosuria
how is phosphate reabsorbed PCT
Na+ co-transport BUT hormonally regged by parathyroid hormone
* PTH reduces reabsorp = incr excretion
adaptations PCT incr reabsorp
- large SA
- single layer epithelial cells
- high conc Na+K+ATPase
- high conc carbonic anhydrase
- peritubular caps high oncotic press (bc just lost loads fluid in corpuscle
why are environmental toxins lipid soluble
= readily cross mems so as fluid -> blood also -> blood down conc grad = hard excrete
this is why liver converts many foreign substances -> water sol = detoxi
details of secretion
always active - substances must be ionised to pump across mem thru channs
secr H+ in PCT
- 2AT Na+H+ exchanger apical mem
* some bind non-bicarb buffers + excreted in urine - 2AT NH4+ Na+ antiporter apical mem
* from aas combined w H+ make NH4+
all unregged
reabsorp bicarb PCT how + why
no prot carrier apical mem = impermeable to bicarb
* reabsorp linked to H+ secr
* need lots carbonic anhydrase enz
bc bicarb super important buffer in bod + don’t want to lose
H+ + HCO3- AT = = v lil change urine pH
if H+ in lumen binds non-bicarb buffer then secreted in urine
what else is secreted in PCT
ionised organic acids/bases
* e.g. prot-bound organic mols - hormones, drugs, environ pollutants
non-specific organic anion/cation transporters
how much of diff stuff has been reabsorbed by end PCT
- 100% gluc + aas
- 70% water, Na+, K+
- 80-90% HCO3-
- other ions + stuff variable
osmolarity along nephron
- mostly same along PCT bc loads solutes etc out but also loads water out
- DCT = decr vol + diff composition to prot free plasma
- urine output varies in vol + osmolarity
renal medulla osmotic grad
osmolarity incr as go into medulla from that of prot free plasma (ISF becomes more hyperosmotic)
* determines limits for urine osmolarity + conc
* varies specied to species
what does ability to conc urine depend on
relative length LoH + no. juxta medullary nephrons
why have medullary osmotic grad
need conc grad to move water by osmosis against
how does LoH make osmotic grad
- descending no ion pumps but lots aquaporins (v permeable water)
- all ascending impermeable to water (= no solvent drag)
- AT ions out thick ascending = osmosis water out descending -> ISF (bc ISF hyperosmotic)
- water out = incr conc filtrate
- fluid flow = higher osmolarity further down tube = more extreme = osmotic grad multiplies down tube
controls conc urine by expression aquaporins
cap network round juxtamedullary LoH
= vasa recta (specialised peritubular caps) to supply O2, nutrients -> medulla
* parallel to limbs LoH
* blood flows opp direction to filtrate
* hairpin loop slows Robloodflow
how does countercurrent multiplication LoH work
as down takes solutes (= more concd), as up takes water (less concd) - free exchange blood + ISF
* accentuates conc diff bet cortex + medulla
why need countercurrent multiplication LoH
if normal cap bed exchange blood + ISF fuck up osmotic grad
how else maintain osmotic grad in medulla
N waste urea freely filtered = incr conc in filtrate bc less water (v high in collecting duct)
* urea channs in medulla allow CD -> ISF -> recaptured in descending LoH
incr osmolarity in medulla (hyperosmotic ISF) = incr conc grad
what does ADH do in urea recycling
upregs urea channs in CD = more passive flow -> ISF + descending LoH
how is ADH released
antidiuretic hormone released posterior pituitary:
1. made + packaged in neuron
2. vesicles transported down cell
3. stored posterior pituitary
4. released into blood -> circulate
how does ADH work
- ADH binds specific mem receptor on sensitive principal cells in CD
- activates cAMP 2nd messenger sys
- cell inserts aquaporins apical mem
- water osmosis -> blood (can’t AT water)
endocrine control water balance
Na + K status at start DCT
Na = 100% filtered, 70% reabsorb in PCT, 20% in LoH
K = 100% filtered, 70% reabsorb PCT, 30% in LoH
movement Na+ + K+ in DCT + CD
- Na+K+ATPase on basolateral mem maintains grads
- leak channs on apical mem = passive diffusion bet filtrate + principal cells
principal cells vs tubular cells
- DCT/CD vs PCT
- both have asymmetrical arrangement Na+K+ATPase
- no microvilli principal bc lower vol
- principal cells impermeable to water w/o ADH = doesn’t always follow Na+ but does in PCT
- principal responsive ADH + aldosterone
how does aldosterone work
- incr activity channs + pumps (K+Na+ATPase, leak channs)
- synth new channs + pumps
intracellular receptor to upreg movement K+ + Na+ - important K+ homeostasis
= incr reabsorp Na+ = more water reabsorp osmosis incr blood vol incr SV
but decr [K+] in blood (also stimmed incr [K+]
fat sol hormone = can enter cell easy
phosphate filtration + reabsorp
- 100% freely filtered
- reabsorp PCT Na+ co-transport hormonal control
- no reabsorp DCT/CD
- dietary excess excreted (lots)
calcium filtration + reabsorp
- 50% bound albumin so only 50% freely filtered
- 70% reabsorb PCT
- selective reabsorp in DCT/CD hormonal control (PTH incr reabsorp)
- relatively small amount excreted
how does parathyroid hormone work
released in response decr [Ca2+] in blood - decr reabsorp P in PCT, incr Ca2+ in LoH, DCT, CD
kidney cortex histology
DCT = cleaner edges bc no microvilli
kidney medulla histology
CD = cuboidal epithelium
what has been completely reabsorbed at start DCT
K + HCO3- bbut homeostatic mechs can lead secr back -> filtrate
effect renal blood flow on GFR
incr = higher, decr = lower, by incr/decr glomerular cap press (regged by afferent/efferent arterioles)
GFR too high/low result
too high: too much filtrate, incr urine (sys no keep up). incr flow rate = no time reabsorp + stuff lost in urine
too low: too little filtrate = decr flow = some waste has time reabsorb, accumulate in bod, not excreted
v important + has be protected
why autoreg GFR
bp up + down w exercise etc but want GFR constant - would damage caps + nephrons + mess up balance in blood
* so afferent arteriole constricts (GFR decr)/dilates (incr)
can’t rectify extreme bp or prolonged - small/moderate changes bp
2 mechs for autoreg GFR
- myogenic response - to change in afferent bp
- tubuloglomerular feedback - to change in [Na] in LoH, reps filtrate vol
myogenic response
stretch-sensitive musc cells detect incr bp = vasoconstrict vascular myocytes afferent arteriole = decr blood flow, decr HP, prevent GFR incr
+ vice versa, v fast bc change where detection
juxtamedullary apparatus
ascending LoH runs bet afferent + efferent bvs + adjacent cells in walls modified form JMA = specialised cels for detection
* arteriole cells -> juxtaglomerular cells
* tubule cells -> macula densa
histology renal corpuscle
JGA = dense grp cells
tubuloglomerular feedback
- macula densa cells detect changes [Na] + so fluid vol
- send paracrine signals to adjacent sm myocytes in afferent arteriole
- = vasoconstr/dil
macula densa also stim release renin from JG cells for RAAS
slower, indirect response, detecting incr/decr in GFR
effects angiotensin II
- adrenal cortex -> aldosterone -> Na reabsorb
- pit gland -> ADH
- arterioles vasoconstruct incr TPR
- CV centre medulla oblongata incr symp (incr CO)
- hypothalamus incr thirst + ADH
all incr bp (some via incr plasma vol)
overrides autoreg of GFR
mechanisms for release aldosterone
plasma [K+] directly detected in adrenal cortex for neg feedback in release aldosterone asw as RAAS
stimuli for renin secr
- decr bp directly -> JGCs afferent arteriole
- decr bp -> decr GFR -> macula densa -> stim
- decr bp -> CV control centre -> incr symp -> JCGs secr
result vasoconstriction at kidney (from angiotensin II)
- constrict afferent arteriole = decr blood flow to glom caps = decr HP = decr GFR
- relatively greater constr efferent = incr HP = preserve GFR (relatively small decr)
* = HP peritubular caps decr, promoting tubular reabsorp = normalise bp
w/o protective mech 2 GFR fall lots = renal function compromised
result incr bp
natriuretic peptides decr bp + incr GFR (less time reabsorp)
* afferent arterioles vasodil
* adrenal cortex decr aldosterone secr
* nephron decr Na + water reabsorp
* hypothalamus decr ADH secr
* medulla oblongata CV centre to decr bp
changes in ureter
urine composition stays same bet CD + bladder, except in horse where glands secr mucous (= viscous urine)
micturition
urination
how is micturition controlled
- detrusor musc - sm of bladder wall, controlled ANS
- internal urethral sphincter - sm @ exit bladder -> urethra, controlled ANS
- external urethral sphincter - sk, controlled somatic NS (conscious control, prevent emptying even when ANS attempts urine discharge)
symp vs parasymp motor nerve supply bladder
symp = detrusor relax (bladder fill) + internal contract (close sphincter)
parasymp = detrusor contract (eject urine)
how are motor messages passed to bladder muscs for filling
symp: noradrenaline acting on β2 receptors on detrusor + α1 receptors on internal sphincter
somatic: Ach acting on nicotinic receptors to excite external sphincter musc for contraction
how is bladder emptying brought about
- filling sufficient to stretch sm musc = myogenic reflex contraction detrusor
- sensory nerves carry info -> spinal cord for:
- activation parasymp motor nerves contract detrusor
- = passive press induced relaxation internal sphincter
- also inhibit somatic motor drive to external sphincter
receptors for bladder emptying
parasymp: Ach on muscarinic for contraction detrusor
somatic: inhibition Ach acting on nicotinic to inhibit contraction
which motor nerves to bladder muscs + where from
- hypogastric = symp to detrusor + internal sphincter
- pelvic = parasymp to detrusor
- pudendal = somatic to external sphincter
hypogastric from L1-L2 on spinal cord
pelvic + pudendal from S1-S2
how + why prod erythropoietin (Epo)
from interstitial cells kidney to stim erythropoiesis (production rbcs)
* regged by O2 levels in tiss
neg feedback from hypoxia -> Epo -> normoxia -> less Epo
how is erythropoiesis caused by Epo
hypoxia = Epo proded = spongy bone stimmed release more rbcs = incr rbcs = incr O2 supply :)
K homeostasis
- ingested most foods + not stored
- [K+] in ECF relatively low + important maintaining mem pot
hyperkalaemia
high [K+] in ECF = decr movement K+ out = mem pot less polarised + less neg = cell more excitable - esp problem for musc cells
potassium filtration + reabsorp
100% filtered, 100% reabsorbed in PCT + LoH
* plasma conc regged by secr -> filtrate in DCT + CD
* aldosterone stims principal cells secr more in filtrate
* reg bp trumps reg K+
how measure GFR
equiv to clearance drug w known amount in plasma if:
* drug freely filteres
* not metabed
* not absorbed/secr
* excreted unchanged in urine
ideally use continual infusion plant polypeptide inulin but not practical so look at conc N waste products in blood
creatinine
N waste product from degradation creatine phosphate
* synthed at continual steady rate
* freely filtered w no reabsorp or secr so urine output good measure GFR (measure it in blood plasma)
GFR decr = less creatinine excr (bc blood moving at same rate so less out -> filtrate = accumulates in plasma = higher reading
urea to measure GFR
main N waste product in animals + freely filtered
* water soluble + so small also partially fat soluble = some reabsorb down conc grad w/o transporters
* normally 50% reabsorbed but GFR decr = more time reabsorp = incr conc blood (where measure)
synthed liver so liver disease can affect result also less reliable
azotaemia defn
incr nitrogenous waste products in blood
* urea + creatinine incr above normal levels animal = azotaemic
azotaemia = meausre decr GFR
situation HCO3- at start DCT
- freely filtered
- 80-90% reabsorbed PCT
- 10-20% reabsorbed LoH
situation H+ at start DCT
- freely filtered
- unregged secr -> PCT via secr NH4+ (2AT)
- unregged secr -> PCT via secr H+
- captured bicarb buffers + recycled for bicarb reabsorp
- captured non-bicarb buffers = urinary secr
intercalated cells allow reg H+ secr + synth bicarb
transporter prots in DCT for transport H+
- H+ ATPase for H+ -> filtrate (DCT)
- H+K+ATPase for H+ -> urine exchange for K+
type A intercalated cells
active response to incr [H+] in interstitial space (acidosis) - get rid H+, make HCO3-
in DCT
problem w type A intercalated cells in DCT
pH homeostasis prioritised over K+ homeostasis (retains K+ to get rid H+) = can lead hyperkalaemia
type B intercalated cells
active response decr [H+] in intersititial space (alkalosis) = absorb new H+
DCT
CA = carbonic acid
proton secr intercalated cells vs PCT
- H+ATPase vs Na+H+ antiport
- HCO3-Cl- exchanger vs Na+HCO3- symport (basolateral mem)
- PCT: prot secr = net bicarb reabsorp (if binds bicarb buffer in filtrate)
- PCT = unregged, DCT = regged in response changes blood pH
- DCT = bicarb/prot synth
pH is + equ
measure conc prots
= -log10[H+]
why need homeostatic control protons
metabolic reactions prod excess H+ + CO2
normally: homeostatic mechs get rid metabolic acid load by breathing
pH should be + problem if not
ECF (blood plasma) 7.35-7.45
* outside range affects all bod systems = coma, cardiac failure, circulatory collapse…
* homeostatic pH control overrides all else
mechs for acid-base balance
- buffer systems temporarily bind H+/OH- = hide ions until excreted (first line)
- change rate + depth breathing = CO2 exhaled/retained - faster = more CO2 + H+ out (subconscious)
- kidney excr/reabsorp acidic (H+/NH4+) + basic (HCO3-/OH-) ions to eliminate acids (slow)
how buffers work
moderate changes in pH v fast by taking up ions
* e.g. HCO3-, prots, Hb, phosphates NH3
how resp sys for correction acid-base balance works
more CO2 = more H+ + vice versa
breathe shallow + slow = CO2 + H+ build up
limitation resp sys for correction acid-base balance
- only if resp sys + control centres working normally
- limited by availability bicarb ions (bicarb reserve)
- can’t protect against pH changes bc of incr/decr CO2
acidosis types
- respiratory when CO2 accumulates due hypoventilation - CO2 never accumulates blood healthy animals
- metabolic when non-respiratory acids accumulate or bicarb deficient
metabolic acidosis
= decr [HCO3-] due
* diabetic ketoacidosis
* kidney disease (didn’t reabsorb)
* faecal loss bicarb in diarrhoea
homeostatic response metabolic acidosis
- protons activate chemoreceptors
- resp tract incr rate + depth breathing so pCO2 decr + plasma pH -> normal
respiratory acidosis
lungs remove CO2 at lower rate than being proded due e.g. pneumonia
= incr pCO2
homeostatic response to respiratory acidosis
alpha intercalated cells incr secr H+ -> filtrate
types alkalosis
- respiratory alkalosis when CO2 in deficit - healthy animals = blood CO2 no decr below normal
- metabolic alkalosis when non-respiratory acids lost or bicarb incr
metabolic alkalosis
incr [HCO3-] due
* persistent vomiting (lose lots acid)
* upper GI obstruction
homeostatic response metabolic alkalosis
resp tract decr rate + depth breathing to return plasma pH to normal = pCO2 incr
respiratory alkalosis
lungs remove CO2 at faster rate than being proded, e.g. due hyperventilation = decr pCO2
homeostatic response respiratory alkalosis
beta intercalated cells incr secr bicarb -> filtrate + synth H+ to reabsorb -> blood
fluid compartment proportions of bod
fluid loss types
- normal thru kidneys (1-2ml/kg/hr) = sensible loss
- insensible = evap from skin, exhalation from lungs, faeces
how is normal fluid intake done
50ml/kg/day thru:
* ingestion liquids/moist foods
* metabolic synth water
polydipsia if >100ml/kg/day
normal urine output
25ml/kg/day
polyuria if >50ml/kg/day
how is water + [Na+] detected for regulation
receptors respond changes
* osmolarity
* plasma vol
* bp
no sensory receptors directly monitor water/Na+
role kidneys in regging blood vol
can’t restore lost just reg sensible water loss
* reg ECF vol by adjusting excretion Na+ (+ so water that follows)
how reg ADH for reg sensible water loss
blood plasma osmolarity monitored osmoreceptors in hypothalamus
* incr = incr rate of firing of neurons = incr ADH release
decr below threshold = neurons no fibre = no ADH = dilute urine
incr osmolarity by 3% = stim thirst
what regs ADH
- osmolarity
- blood vol directly - short term failsafe for sudden release lots ADH of whole blood lost so vol decr but osmolarity same
- blood vol via angiotensin II
Na+ intake
not regged so all ingested absorbed
no direct sensor like for K + Ca
how does incr diet Na change blood vol
extra % Na (e.g. 24% more) + water freely follows Na so blood vol incr by same %
incr blood vol/press detected by?
stretch sensitive nerve endings in atria + veins
detect incr bp by baroreceptors
incr bp/blood vol = incr ANP = incr GFR = decr Na absorp = decr ADH, renin, symp output
hormonal reg Na+ + Cl-
reg reabsorp/excretion
* angiotensin II + aldosterone promote reabsorp (+ so water reabsorp by osmosis)
* natriuretic peptides promote excretion Na+ + Cl- followed by water excretion
to incr/decr blood vol
purpose urinalysis
metric for kidney function looking at
1. constituents
2. urine vol
3. urine conc (SG)
abnormal constituents urine
- gluc
- blood
- prot - only filtered if kidney disease or high bp
- ketones
- cells - just occasional bladder epithelial
urine vol names for diff amounts
- normal = 1-2ml/kg/hr
- polyuria = >2ml/kg/hr
- oliguria = <1ml/kg/hr
- anuria = no urine
- isosthenuria = filtrate low SG
what is specific gravity
measure solutes in urine compared w distilled water
SG distilled water = 1.0000
normal urine conc
variable bc depends hydration/bp
* dogs = 1.001 - 1.075
isosthenuria
urine SG as low as initial filtrate (prot free plasma 1.008-1.012)
* suggests kidney pathology disrupting ability concentrate urine (or severe overhydration but that’s rare)
should look for >1.035 cats, >1.030 dogs
what should always have net excretion of
phosphate, potassium, protons
what should always have net reabsorp of
bicarb, glucose
classic changes in blood due kidney disease
- hyperkalaemia bc reabsorbed/not secreted
- hyperphosphataemia bc reabsorbed/not secreted
- metabolic acidosis - low pH + HCO3- decr (not reabsorbed)
chronic disease can lead excess loss K + hypokalaemia (esp if anorexic + no consume daily K)
what azotaemia tells us is wrong + types
decr GFR
1. pre-renal azotaemia
2. renal (intrinsic) azotaemia
3. post renal azotaemia
not necessarily marker of damaged kidney
post renal azotaemia
renal function normal but outflow blocked
* e.g. ruptured bladder (cld be just small)
* = decr GFR bc urine saturated/not moving = N waste reabsorbed/ not filtered
* also other changes fluid + electrolyte balance (bad)
diagnosis usually straightforward
pre renal azotaemia
large systemic decr bp = decr blood flow -> kidney = decr GFR, e.g. due dehydration, heart disease
* pathology upstream of kidney
* animal can still conc urine (still prods ADH etc) = SG normal, indicating not intrinsic disease (for diagnostics)
* = decr rate flow filtrate = incr time reabsorp = N waste in blood
renal azotaemia
due renal disease directly affecting renal function + so GFR
* animal not prodding much urine or can’t conc urine
* = low SG
* may also be abnormal stuff in urine
reduced kidney function effects on blood biochemistry
- incr conc N waste products
- incr conc inorganic phosphate
- incr conc K (anorexic may be hypokalaemic)
- decr conc bicarb (-> metabolic acidosis)
reduced kidney function effects on urine
- lack ability to conc = dilute
- abnormal vol (too high or low)
types kidney disease
acc problem w kidney
- acute kidney injury (AKI)
- chronic kidney disease (CKD)
classic presentation = losing prot in urine (= weight loss)
acute kidney injury
rapid life-threatening impairment kidney function
* = GFR decr + can’t conc urine (+ stuff reabsorbed all = decr SG)
* urine output zero, incr or decr
chronic kidney disease
long term progressive loss kidney function
* GFR decr + loss ability conc urine (water stays in)
* urine output incr - owner won’t notice bc outside but will notice incr drinking
cell layers in renal corpuscle
- caps = porous endothelium
- thick glomerular basement mem (physical barrier = size filter)
- visceral epithelium (podocytes) - part Bowman’s capsule
- capsule space filtered into
- parietal epithelium (simple squamous) w thick basal lamina - other part Bowman’s capsule
1st 3 make up 3 components filtration barrier
mols captured base mem phagocyt by mesangial cells, podocytes phagocyt
histology ureter
ureter + bladder + urethra quite similar
* all transitional epithelium
* wavy mucosa profile allows expand acommodate urine
* sub-mucosa w lamina propria
* muscularis w inner longitudinal, middle circular + outer longitudinal (allow contraction)
* then serosa (loose CT) in peritoneal cavity OR adventitia (loose CT) when embedded in other tiss
bladder has thicker layers sm musc (more contraction)
what is juxtaglomerular apparatus between
DCT (-> macula densa cells) + afferent arterioles (-> juxtaglomerular cells)
renal lobe
renal medullary pyramid + associated cortical tiss
* unilobar kidney in cats, dogs, horses, sheep, goats
* bovine + pig = kidneys multilobar
what can’t pass through filtration barrier from blood plasma -> filtrate
- neg charged prots
- cellular components blood
- big prots
LoH histology
- thick descending limb - structure like PCT (cuboidal)
- thin limb - simple squamous epithelium
- thick ascending limb - structure like DCT (cuboidal)
