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urinary Flashcards

1
Q

anatomy urinary tract

A
  1. 2 kidneys either side spine behind caudal rib
  2. ureters for urine kidney -> bladder
  3. bladder stores urine
  4. urethra for urine bladder -> outside

kidneys not always kidney shaped

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2
Q

kidney functions

A
  1. reg fluid vol + electrolyte balance - ECF/blood press, osmolarity, ions, pH
  2. waste excretion (metabolic + foreign)
  3. prod hormones - activate D3, synth renin enz, synth erythropoietin
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3
Q

renal anatomy

A
  1. outer cortex for filtration
  2. inner medulla to collect + excrete urine

w nephrons = functional units

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4
Q

nephron structure

A
  1. renal corpuscle - prods filtrate
  2. proximal convoluted tubule, PCT - unregulated reabsorp water, ions, organic nutrients
  3. loop of henle, LoH - reabsorp ions + water + set up osmotic grad
  4. distal convoluted tubule, DCT - variable secretion + reabsorp water + ions (more reg)
  5. collecting duct - several nephrons join for variable secr + reabsorp water + ions (more reg)
  6. papillary duct delivers urine to renal pelvis

long tube, squished in reality

LoH has descending + ascending limbs
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5
Q

identifying areas kidney histology

A
  1. cortex = mainly tubules w renal corpuscles
  2. medulla = only renal tubules
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6
Q

how much blood to kidneys + where from/to

A

renal arteries directly branch off aorta, giving 20-25% CO -> renal veins
* loads blood so change bp affects kidneys = damaged if high

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7
Q

artery + vein path thru kidneys

A
2 cap beds in series = cap portal sys
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8
Q

where are renal cap beds found

A
  1. glomerular caps in renal corpuscle
  2. peritubular caps around PCT then parallel to LoH
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9
Q

how incr filtration across cap bed

A
  • vasodilate precap arterioles = incr HP
  • constrict efferent to cap (at least relative to afferent)
  • incr permeability = thin + porous mem
  • large SA for filtration
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10
Q

passage of stuff for filtration out glomerular caps

A

in theory osmotic press would balance HP eventually but balance lies above pt where ever actually happens + filtr conts along length caps

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11
Q

histology edge kidney

A

renal capsule = fibrous CT w lots collagen

OLC = outer layer capsule ILC = inner layer capsule
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12
Q

initial filtrate general content

A

approximates prot free plasma w water, ions, gluc, aas, N waste products
* bigger holes but not most prots or bcs

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13
Q

glomerular filtration rate

GFR

A

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

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14
Q

reabsorp + secr in nephron defns

A

reabsorp = returning important substances filtrate -> blood

secr = movement waste mats body -> filtrate

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15
Q

details bulk reabsorp

A

70% filtrate reabbed in PCT
* selective via prot transporters but mostly unregulated (no hormonal control)
* active + passive

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16
Q

path tubular reabsorp

A

filtrate -> renal insterstitium -> renal bvs -> body circulation

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17
Q

tubule cells of PCT specialisations

A
  • microvilli on apical mem incr SA reabsorp (ONLY PCT)
  • lots Na+K+ATPase on basolateral mem
  • lots carbonic anhydrase
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18
Q

types absorp in PCT

A
  1. transcellular = thru tubule cells, AT into cell + out
  2. paracellular = thru tight junctions bet tubule cells, diffusion

diffusion ISF -> blood in peritubular cap

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19
Q

how does transcellular absorp Na+ in PCT work

A
  1. Na+ AT over basolateral mem tubule cell -> ISF
  2. sets up Na+ grad (low conc in cell) so Na+ tubule lumen -> tubule cell

Na+K+ATPase pump

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20
Q

result of Na+ AT out tubule lumen -> blood

A
  • 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

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21
Q

how are substances reabsorbed PCT

A

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)

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22
Q

which substances reabsorbed in PCT by 2AT w Na+

A
  • gluc
  • aas
  • lactate
  • citric acid cycle intermediates
  • phosphate
  • sulphate
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23
Q

how much gluc -> PCT

A

freely filtered - depends plasma conc for rate bc diffusion, but no limit

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24
Q

how much gluc reabsorbed from PCT

A

depends:
* rate filtrate flow
* no. prot transporters - if saturate

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25
Q

is gluc excreted

A

normally no bc all reabsorbed, only if renal threshold reached if overwhelming amount gluc = gluc in filtrate = glucosuria

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26
Q

how is phosphate reabsorbed PCT

A

Na+ co-transport BUT hormonally regged by parathyroid hormone
* PTH reduces reabsorp = incr excretion

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27
Q

adaptations PCT incr reabsorp

A
  • 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
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28
Q

why are environmental toxins lipid soluble

A

= 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

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29
Q

details of secretion

A

always active - substances must be ionised to pump across mem thru channs

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30
Q

secr H+ in PCT

A
  1. 2AT Na+H+ exchanger apical mem
    * some bind non-bicarb buffers + excreted in urine
  2. 2AT NH4+ Na+ antiporter apical mem
    * from aas combined w H+ make NH4+

all unregged

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31
Q

reabsorp bicarb PCT how + why

A

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

works bc CO2 v lipid soluble + can diff into cell HCO3- -> blood = Na+ symport
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32
Q

what else is secreted in PCT

A

ionised organic acids/bases
* e.g. prot-bound organic mols - hormones, drugs, environ pollutants

non-specific organic anion/cation transporters

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33
Q

how much of diff stuff has been reabsorbed by end PCT

A
  • 100% gluc + aas
  • 70% water, Na+, K+
  • 80-90% HCO3-
  • other ions + stuff variable
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34
Q

osmolarity along nephron

A
  1. mostly same along PCT bc loads solutes etc out but also loads water out
  2. DCT = decr vol + diff composition to prot free plasma
  3. urine output varies in vol + osmolarity
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35
Q

renal medulla osmotic grad

A

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

urine can be conced to 1200mOsm/l
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36
Q

what does ability to conc urine depend on

A

relative length LoH + no. juxta medullary nephrons

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37
Q

why have medullary osmotic grad

A

need conc grad to move water by osmosis against

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38
Q

how does LoH make osmotic grad

A
  1. descending no ion pumps but lots aquaporins (v permeable water)
  2. all ascending impermeable to water (= no solvent drag)
  3. AT ions out thick ascending = osmosis water out descending -> ISF (bc ISF hyperosmotic)
  4. water out = incr conc filtrate
  5. fluid flow = higher osmolarity further down tube = more extreme = osmotic grad multiplies down tube

controls conc urine by expression aquaporins

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39
Q

cap network round juxtamedullary LoH

A

= vasa recta (specialised peritubular caps) to supply O2, nutrients -> medulla
* parallel to limbs LoH
* blood flows opp direction to filtrate
* hairpin loop slows Robloodflow

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40
Q

how does countercurrent multiplication LoH work

A

as down takes solutes (= more concd), as up takes water (less concd) - free exchange blood + ISF
* accentuates conc diff bet cortex + medulla

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41
Q

why need countercurrent multiplication LoH

A

if normal cap bed exchange blood + ISF fuck up osmotic grad

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42
Q

how else maintain osmotic grad in medulla

A

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

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43
Q

what does ADH do in urea recycling

A

upregs urea channs in CD = more passive flow -> ISF + descending LoH

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44
Q

how is ADH released

A

antidiuretic hormone released posterior pituitary:
1. made + packaged in neuron
2. vesicles transported down cell
3. stored posterior pituitary
4. released into blood -> circulate

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45
Q

how does ADH work

A
  1. ADH binds specific mem receptor on sensitive principal cells in CD
  2. activates cAMP 2nd messenger sys
  3. cell inserts aquaporins apical mem
  4. water osmosis -> blood (can’t AT water)

endocrine control water balance

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46
Q

Na + K status at start DCT

A

Na = 100% filtered, 70% reabsorb in PCT, 20% in LoH
K = 100% filtered, 70% reabsorb PCT, 30% in LoH

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47
Q

movement Na+ + K+ in DCT + CD

A
  • Na+K+ATPase on basolateral mem maintains grads
  • leak channs on apical mem = passive diffusion bet filtrate + principal cells
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48
Q

principal cells vs tubular cells

A
  1. DCT/CD vs PCT
  2. both have asymmetrical arrangement Na+K+ATPase
  3. no microvilli principal bc lower vol
  4. principal cells impermeable to water w/o ADH = doesn’t always follow Na+ but does in PCT
  5. principal responsive ADH + aldosterone
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49
Q

how does aldosterone work

A
  1. incr activity channs + pumps (K+Na+ATPase, leak channs)
  2. 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

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50
Q

phosphate filtration + reabsorp

A
  • 100% freely filtered
  • reabsorp PCT Na+ co-transport hormonal control
  • no reabsorp DCT/CD
  • dietary excess excreted (lots)
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51
Q

calcium filtration + reabsorp

A
  • 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
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52
Q

how does parathyroid hormone work

A

released in response decr [Ca2+] in blood - decr reabsorp P in PCT, incr Ca2+ in LoH, DCT, CD

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53
Q

kidney cortex histology

A

DCT = cleaner edges bc no microvilli

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54
Q

kidney medulla histology

A

CD = cuboidal epithelium

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55
Q

what has been completely reabsorbed at start DCT

A

K + HCO3- bbut homeostatic mechs can lead secr back -> filtrate

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56
Q

effect renal blood flow on GFR

A

incr = higher, decr = lower, by incr/decr glomerular cap press (regged by afferent/efferent arterioles)

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57
Q

GFR too high/low result

A

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

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58
Q

why autoreg GFR

A

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

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59
Q

2 mechs for autoreg GFR

A
  1. myogenic response - to change in afferent bp
  2. tubuloglomerular feedback - to change in [Na] in LoH, reps filtrate vol
60
Q

myogenic response

A

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

61
Q

juxtamedullary apparatus

A

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

62
Q

histology renal corpuscle

A

JGA = dense grp cells

63
Q

tubuloglomerular feedback

A
  1. macula densa cells detect changes [Na] + so fluid vol
  2. send paracrine signals to adjacent sm myocytes in afferent arteriole
  3. = vasoconstr/dil

macula densa also stim release renin from JG cells for RAAS

slower, indirect response, detecting incr/decr in GFR

64
Q

effects angiotensin II

A
  1. adrenal cortex -> aldosterone -> Na reabsorb
  2. pit gland -> ADH
  3. arterioles vasoconstruct incr TPR
  4. CV centre medulla oblongata incr symp (incr CO)
  5. hypothalamus incr thirst + ADH

all incr bp (some via incr plasma vol)

overrides autoreg of GFR

65
Q

mechanisms for release aldosterone

A

plasma [K+] directly detected in adrenal cortex for neg feedback in release aldosterone asw as RAAS

66
Q

stimuli for renin secr

A
  1. decr bp directly -> JGCs afferent arteriole
  2. decr bp -> decr GFR -> macula densa -> stim
  3. decr bp -> CV control centre -> incr symp -> JCGs secr
67
Q

result vasoconstriction at kidney (from angiotensin II)

A
  1. constrict afferent arteriole = decr blood flow to glom caps = decr HP = decr GFR
  2. 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

68
Q

result incr bp

A

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

69
Q

changes in ureter

A

urine composition stays same bet CD + bladder, except in horse where glands secr mucous (= viscous urine)

70
Q

micturition

A

urination

71
Q

how is micturition controlled

A
  1. detrusor musc - sm of bladder wall, controlled ANS
  2. internal urethral sphincter - sm @ exit bladder -> urethra, controlled ANS
  3. external urethral sphincter - sk, controlled somatic NS (conscious control, prevent emptying even when ANS attempts urine discharge)
72
Q

symp vs parasymp motor nerve supply bladder

A

symp = detrusor relax (bladder fill) + internal contract (close sphincter)
parasymp = detrusor contract (eject urine)

73
Q

how are motor messages passed to bladder muscs for filling

A

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

74
Q

how is bladder emptying brought about

A
  1. filling sufficient to stretch sm musc = myogenic reflex contraction detrusor
  2. sensory nerves carry info -> spinal cord for:
  3. activation parasymp motor nerves contract detrusor
  4. = passive press induced relaxation internal sphincter
  5. also inhibit somatic motor drive to external sphincter
75
Q

receptors for bladder emptying

A

parasymp: Ach on muscarinic for contraction detrusor
somatic: inhibition Ach acting on nicotinic to inhibit contraction

76
Q

which motor nerves to bladder muscs + where from

A
  1. hypogastric = symp to detrusor + internal sphincter
  2. pelvic = parasymp to detrusor
  3. pudendal = somatic to external sphincter

hypogastric from L1-L2 on spinal cord
pelvic + pudendal from S1-S2

77
Q

how + why prod erythropoietin (Epo)

A

from interstitial cells kidney to stim erythropoiesis (production rbcs)
* regged by O2 levels in tiss

neg feedback from hypoxia -> Epo -> normoxia -> less Epo

78
Q

how is erythropoiesis caused by Epo

A

hypoxia = Epo proded = spongy bone stimmed release more rbcs = incr rbcs = incr O2 supply :)

79
Q

K homeostasis

A
  • ingested most foods + not stored
  • [K+] in ECF relatively low + important maintaining mem pot
80
Q

hyperkalaemia

A

high [K+] in ECF = decr movement K+ out = mem pot less polarised + less neg = cell more excitable - esp problem for musc cells

81
Q

potassium filtration + reabsorp

A

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+

82
Q

how measure GFR

A

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

83
Q

creatinine

A

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

84
Q

urea to measure GFR

A

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

85
Q

azotaemia defn

A

incr nitrogenous waste products in blood
* urea + creatinine incr above normal levels animal = azotaemic

azotaemia = meausre decr GFR

86
Q

situation HCO3- at start DCT

A
  • freely filtered
  • 80-90% reabsorbed PCT
  • 10-20% reabsorbed LoH
87
Q

situation H+ at start DCT

A
  • freely filtered
  • unregged secr -> PCT via secr NH4+ (2AT)
  • unregged secr -> PCT via secr H+
  1. captured bicarb buffers + recycled for bicarb reabsorp
  2. captured non-bicarb buffers = urinary secr

intercalated cells allow reg H+ secr + synth bicarb

88
Q

transporter prots in DCT for transport H+

A
  1. H+ ATPase for H+ -> filtrate (DCT)
  2. H+K+ATPase for H+ -> urine exchange for K+
89
Q

type A intercalated cells

A

active response to incr [H+] in interstitial space (acidosis) - get rid H+, make HCO3-

in DCT

bicarb exchange = available buffer more prots + take into cell
90
Q

problem w type A intercalated cells in DCT

A

pH homeostasis prioritised over K+ homeostasis (retains K+ to get rid H+) = can lead hyperkalaemia

91
Q

type B intercalated cells

A

active response decr [H+] in intersititial space (alkalosis) = absorb new H+

DCT

exact opposite type A

CA = carbonic acid

92
Q

proton secr intercalated cells vs PCT

A
  1. H+ATPase vs Na+H+ antiport
  2. HCO3-Cl- exchanger vs Na+HCO3- symport (basolateral mem)
  3. PCT: prot secr = net bicarb reabsorp (if binds bicarb buffer in filtrate)
  4. PCT = unregged, DCT = regged in response changes blood pH
  5. DCT = bicarb/prot synth
93
Q

pH is + equ

A

measure conc prots
= -log10[H+]

94
Q

why need homeostatic control protons

A

metabolic reactions prod excess H+ + CO2
normally: homeostatic mechs get rid metabolic acid load by breathing

95
Q

pH should be + problem if not

A

ECF (blood plasma) 7.35-7.45
* outside range affects all bod systems = coma, cardiac failure, circulatory collapse…
* homeostatic pH control overrides all else

96
Q

mechs for acid-base balance

A
  1. buffer systems temporarily bind H+/OH- = hide ions until excreted (first line)
  2. change rate + depth breathing = CO2 exhaled/retained - faster = more CO2 + H+ out (subconscious)
  3. kidney excr/reabsorp acidic (H+/NH4+) + basic (HCO3-/OH-) ions to eliminate acids (slow)
97
Q

how buffers work

A

moderate changes in pH v fast by taking up ions
* e.g. HCO3-, prots, Hb, phosphates NH3

98
Q

how resp sys for correction acid-base balance works

A

more CO2 = more H+ + vice versa

breathe shallow + slow = CO2 + H+ build up

99
Q

limitation resp sys for correction acid-base balance

A
  • 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
100
Q

acidosis types

A
  • respiratory when CO2 accumulates due hypoventilation - CO2 never accumulates blood healthy animals
  • metabolic when non-respiratory acids accumulate or bicarb deficient
101
Q

metabolic acidosis

A

= decr [HCO3-] due
* diabetic ketoacidosis
* kidney disease (didn’t reabsorb)
* faecal loss bicarb in diarrhoea

102
Q

homeostatic response metabolic acidosis

A
  1. protons activate chemoreceptors
  2. resp tract incr rate + depth breathing so pCO2 decr + plasma pH -> normal
103
Q

respiratory acidosis

A

lungs remove CO2 at lower rate than being proded due e.g. pneumonia

= incr pCO2

104
Q

homeostatic response to respiratory acidosis

A

alpha intercalated cells incr secr H+ -> filtrate

105
Q

types alkalosis

A
  • respiratory alkalosis when CO2 in deficit - healthy animals = blood CO2 no decr below normal
  • metabolic alkalosis when non-respiratory acids lost or bicarb incr
106
Q

metabolic alkalosis

A

incr [HCO3-] due
* persistent vomiting (lose lots acid)
* upper GI obstruction

107
Q

homeostatic response metabolic alkalosis

A

resp tract decr rate + depth breathing to return plasma pH to normal = pCO2 incr

108
Q

respiratory alkalosis

A

lungs remove CO2 at faster rate than being proded, e.g. due hyperventilation = decr pCO2

109
Q

homeostatic response respiratory alkalosis

A

beta intercalated cells incr secr bicarb -> filtrate + synth H+ to reabsorb -> blood

110
Q

fluid compartment proportions of bod

A
111
Q

fluid loss types

A
  1. normal thru kidneys (1-2ml/kg/hr) = sensible loss
  2. insensible = evap from skin, exhalation from lungs, faeces
112
Q

how is normal fluid intake done

A

50ml/kg/day thru:
* ingestion liquids/moist foods
* metabolic synth water

polydipsia if >100ml/kg/day

113
Q

normal urine output

A

25ml/kg/day

polyuria if >50ml/kg/day

114
Q

how is water + [Na+] detected for regulation

A

receptors respond changes
* osmolarity
* plasma vol
* bp

no sensory receptors directly monitor water/Na+

115
Q

role kidneys in regging blood vol

A

can’t restore lost just reg sensible water loss
* reg ECF vol by adjusting excretion Na+ (+ so water that follows)

116
Q

how reg ADH for reg sensible water loss

A

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

117
Q

what regs ADH

A
  1. osmolarity
  2. blood vol directly - short term failsafe for sudden release lots ADH of whole blood lost so vol decr but osmolarity same
  3. blood vol via angiotensin II
118
Q

Na+ intake

A

not regged so all ingested absorbed

no direct sensor like for K + Ca

119
Q

how does incr diet Na change blood vol

A

extra % Na (e.g. 24% more) + water freely follows Na so blood vol incr by same %

120
Q

incr blood vol/press detected by?

A

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

121
Q

hormonal reg Na+ + Cl-

A

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

122
Q

purpose urinalysis

A

metric for kidney function looking at
1. constituents
2. urine vol
3. urine conc (SG)

123
Q

abnormal constituents urine

A
  • gluc
  • blood
  • prot - only filtered if kidney disease or high bp
  • ketones
  • cells - just occasional bladder epithelial
124
Q

urine vol names for diff amounts

A
  • normal = 1-2ml/kg/hr
  • polyuria = >2ml/kg/hr
  • oliguria = <1ml/kg/hr
  • anuria = no urine
  • isosthenuria = filtrate low SG
125
Q

what is specific gravity

A

measure solutes in urine compared w distilled water

SG distilled water = 1.0000

126
Q

normal urine conc

A

variable bc depends hydration/bp
* dogs = 1.001 - 1.075

127
Q

isosthenuria

A

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

128
Q

what should always have net excretion of

A

phosphate, potassium, protons

129
Q

what should always have net reabsorp of

A

bicarb, glucose

130
Q

classic changes in blood due kidney disease

A
  1. hyperkalaemia bc reabsorbed/not secreted
  2. hyperphosphataemia bc reabsorbed/not secreted
  3. metabolic acidosis - low pH + HCO3- decr (not reabsorbed)

chronic disease can lead excess loss K + hypokalaemia (esp if anorexic + no consume daily K)

131
Q

what azotaemia tells us is wrong + types

A

decr GFR
1. pre-renal azotaemia
2. renal (intrinsic) azotaemia
3. post renal azotaemia

not necessarily marker of damaged kidney

132
Q

post renal azotaemia

A

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

133
Q

pre renal azotaemia

A

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

134
Q

renal azotaemia

A

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

135
Q

reduced kidney function effects on blood biochemistry

A
  • incr conc N waste products
  • incr conc inorganic phosphate
  • incr conc K (anorexic may be hypokalaemic)
  • decr conc bicarb (-> metabolic acidosis)
136
Q

reduced kidney function effects on urine

A
  • lack ability to conc = dilute
  • abnormal vol (too high or low)
137
Q

types kidney disease

acc problem w kidney

A
  1. acute kidney injury (AKI)
  2. chronic kidney disease (CKD)

classic presentation = losing prot in urine (= weight loss)

138
Q

acute kidney injury

A

rapid life-threatening impairment kidney function
* = GFR decr + can’t conc urine (+ stuff reabsorbed all = decr SG)
* urine output zero, incr or decr

139
Q

chronic kidney disease

A

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

140
Q

cell layers in renal corpuscle

A
  • 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

141
Q

histology ureter

A

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)

141
Q

what is juxtaglomerular apparatus between

A

DCT (-> macula densa cells) + afferent arterioles (-> juxtaglomerular cells)

141
Q

renal lobe

A

renal medullary pyramid + associated cortical tiss
* unilobar kidney in cats, dogs, horses, sheep, goats
* bovine + pig = kidneys multilobar

141
Q

what can’t pass through filtration barrier from blood plasma -> filtrate

A
  • neg charged prots
  • cellular components blood
  • big prots
141
Q

LoH histology

A
  1. thick descending limb - structure like PCT (cuboidal)
  2. thin limb - simple squamous epithelium
  3. thick ascending limb - structure like DCT (cuboidal)

NSF (22 decks)

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