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111: Anatomy/Phys 2 > 7.2 Urinary > Flashcards

7.2 Urinary Flashcards

1
Q

overview of kidney physiology

  • how much fluid does it process
  • how much O2 does it consume
  • what does it form
A
  • process 180-200L flid/day but only product 1.5L of urine
  • kidneys filter bodys entire plasma volume 60 times/day
  • consume 20-25% of oxygen used by body @ rest
  • filtrate (produced by flomerular filtration) -> basically blood plasma minus proteins
  • urine is produced form filtrate
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2
Q

what are the 3 processes involved in urine formation

A
  1. Glomerular filtration: produces cell and protein free filtrate
  2. Tubular reabsorption: selectively retuns 99% of substances from filtrate to blood in rental tubules and collecting ducts
  3. Tubular secretion: selectively move substances from blood -> filtrate in renal tubules and colelcting ducts
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3
Q

describe glomerular filtraiton

A

* step 1 of the three major renal processes

  • passive process -> no metabolic energy required
  • hydrostatic pressure forces fluids and solutes through filtration membrane into glomerular capsule
  • no reabsorption into capillaies of glomerulus occurs
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4
Q

describe the filtration membrane

A
  • determines what gets into the capsule
  • porous mebrane between blood and interior glomerular capsule that allows water and solutes smaller than plasma prteins to pass

contains 3 layers: fenestrated endothelium, basement membrane, foot processes of pdocytes wth filtration slits

  • macromolecules “stuck” in filtration membrane are englufed by glomerular mesangial cells

*allows molecules smaller than 3nm to pass: water, glucose, amino acids, nitrogenous wastes

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5
Q

describe the 3 layers of the filtration membrane

A
  1. Fenestrated endothelium: of glomerular capillaries
  2. Basemen membrane: fused basal laminae of two layers
  3. Foot processes of podocytes with filtraiton slits; slits diaphragms repal macromolecules
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6
Q
A
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7
Q

what maintains bolloid osmotic pressure

A

plasma proteins

*part of filtration membrane

  • prvents loss of al water to capsular space
  • proteins in filtrate indicate membrane problem
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8
Q
A
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9
Q

describe the glomerular capillary endothelium

A
  • fenestrated epithelium allows for solute-rich, virtually protein free filtrate to pass from blood into glomerular capsule

* proteins and cells can get out

*first part of filtration membrane

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10
Q

describe the basement membrane

A
  • second aprt of the filtration membrane
  • restricts all but smallest protteins while letting msot toher solutes pass
  • gel-like membrane with negatively charegd glycoproteins to repel large plasma proteins
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11
Q

describe podocytes

A

basement membrane is surrounded by a layer of podocytes

  • have foot processes (orpedicles) that fit together leaving small filtration slits

*allows for further selectivity

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12
Q

what are the outward pressures that affect filtraiton

A
  • promote filtrate formation
  • hydrostatic pressure in glomerular capillaries HPgc -> essentialy glomerular BP
  • chief force purshing water and solutes out of blood
  • HIGH: 55mmHG (26mmHg seen in most capillary beds)
  • reason is that efferent arteriole is a high resistance vessel w/ diameter smaller than afferent arteriole
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13
Q

what inward pressures affect filration

A
  • forces that inhibit filtrate formation
  • hydrostatic pressure in capsular space (HPcs): filtrate presssure in capsule; 15 mmHg
  • Colloid osmotic pressure in capillaries (OPgc): Pull of protiens in blood (30mmHg)
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14
Q

what is net filtartion pressure

A

sum of inwards and outward forces

  • 55mmHG forcing out - 45mmHg opposing = net outward force of 10 mmHg
  • pressure resposible for filtrate formation
  • main controllable factor in determining glomerular filtration rate (GFR)
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15
Q

what is glomerular filtration rate

A

volume of filrate formed/min by BOTH kidneys

*noraml = 120-125mL/min

  • directly propertional to:
  • > Net Filtration pressue (NFP): primary pressure = glomerular hydrostatic pressure
  • > total surface area available for filtration: glomerular mesangial cells control by contracting
  • > Filtration membrane permeability: much more permeable than other capillaries
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16
Q

why is it important to ahve constant GFR

A

allows kidneys to make filtrate and maintain extracellular homeostasis

*maintinance is the goal of local intrinsic controls (renal autoregulation

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17
Q

how does GFR relate to systemic BP

A
  • increased GFR affects systemic BP
  • increased GFR causes increase urine output -> lowers BP and vice versa
  • goal of extrinsic controls = maintain systemic blood pressure

*Nervous system and endocrine mechanisms are main extrinsic controls

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18
Q

what are the two types of renal autoregualtion

A

* intrinsic controls

  • maintains nearly constant GFR when MAP is in range of 80-180 mmHg

*autoregulation ceases if out of that range

  • 2 types of renal autoreg:
  • > myogenic mechanism
  • > tubuloglomerular feedback mechanism
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19
Q

describe the myogenic mechanism

A
  • local smooth muscle contracts when stretched
    • inc bp causes muscle to stretch -> afferetn arterioles constrict
      • Restricts blood flow into glomerulus
      • protects glomeruli from dmaging high BP
    • dec bp causes dilation of afferent arterioles
  • helps maintain nomal GFR desipte normal fluctuations in BP

*helps to rotect nephrons and kidneys

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20
Q

describe the tubualr feedback mechanism

A

*regulation of glomerular filtration

  • flow dependent mechanism directed by macula densa cells
    • responds to filtrates NaCl concentration
  • if GFR increases, filtrate flow rate increases
    • leads to dec reabsorption time -> high NaCl levels in filtrate
    • sensed by macula densa, causes constriction of afferent arteriole which lowers NFP and GFR allowing more time for NaCl reabs
  • opposite echanism for decreased GFR
21
Q

how is GFR regulated extrinsically

A
  • neural and hormonal mechanisms
  • regulates GFR to maintain systemic blood pressure
  • extrinsic controlls will override renal intrinsic controlls if blood volume needs to be increased
22
Q

how deos the sympathetic enrvous system control glomerular filtration

A
  • under normal conditions
    • renal blood vessels dilated
    • renal autoregulation mechanisms prevail
  • Under abnormal conditions (extremely low ECF volume aka low bp)
    • NE is released by SNS, epinephrine by adrenal medulla
      • systemic vasoconstriction: inc BP
      • Constriction of aferent arterioles: dec GFR
      • blood volume and pressure increase
23
Q

how does the renin angiotension aldosterone system regualte glomerular filtration

A
  • method of extrinsic contorl
  • main mechanism for incerasing bloop pressure
  • 3 pathways to renin release by granular cells
  • > direct stimulation of grnaular cells by SNS
  • > stimulation activated macula densa cells when filtrate NaCl concentration is low
  • > reduced stretch of granular cells
24
Q

overview of internal mechanism to regulate GFR

A

*directly regualtes GFR despite moderate changes in blood pressue

  • Dec in bp in afferent arterioles -> dec GFR
    • dec in stretch of smooth uscle walls of afferent arterioles
    • vasodilation of afferent arterioles
    • overall inc in GFR
    • ***myogenic mechanism of autoregualtion
  • Dec in GFR
    • Dec filtrate flow and dec NaCl in ascening limp of nephron loop
    • acts on macula densa cells of juxtaglomerular complex of kidney
    • release of nasoactive chemicals inhibited
    • dilation of afferent arterioles
    • inc in GFR
    • **tubuloglomerular mechanism of autoregulation
25
Q

describe the extrinsic mechanisms

A
  • hormonal (renin-angiotensin-aldosterone mechanism)
    • decrease in systemic BP, sensed by granular cells of juxtaglomerular complex of kidney
    • releases renin
    • catalyzes cascade resulting in formation of angiotensin II
      • Inc aldosterone secreted by adrenal cortex
        • inc Na reabsorption by kidney tubules; water follows
        • increases blood volume
        • overall inc in systemic pressure
  • neural contorls
    • inhibits baroreceptors in blood vessels of systemic circulation
      • activates sympathetic nervous system
        • acts on granualr cells of juxtaglomerular complex and/or vasocontriction of systemic arterioles increasesing peripheral resistance
        • (converges to pathway above)
26
Q

what other factors affect GFR

A
  • renal cells releae a variety of chemicals
  • some act as paracrine factors that affect renal arterioles like adenosine and prostaglandin E2
  • some cells make thier own locally acting angiotensin II
  • reinforces effects of hormonal angiotensin II
27
Q

what is anuria

A
  • abnoramlly low urinary output (less than 50mL/day)
  • may indicate that glomerular blood pressure is too low to cause filtration
  • renal failure and anuria can also result from situations in which nephrons stop functioning
    ex: acute nephritis, transfusion reactions, and crush injuries (injury to kidenys themselves)

*injury to the kidneys themselves

28
Q

what si tubular reabsorption

A
  • quickly recalis most of tubualr contens and return them to blood
  • almost all organic nutrients are reabsorbed
  • water and ion reabsorption is partly hrmonally regualred and adjusted
  • includes active and passive tubular reabsorption, substances can flow trancellularly or paracellularly
29
Q

describe the transcellular route

A
  1. transport across the apical membrane
  2. diffusion through the cytosol
  3. transport across the basolaterial membrane (ofen involved the lateral intercellular spaces bc ions transported into these spaces)
  4. movement thorugh the interstitial fluid and into capillary
30
Q

describe the paracelular route of tubular reabsorption

A
  • movemnt through leaky tight junctions, particularly in PCT
  • movement through the interstitial fluid and into the capillary

*limited by tight junctions in move parts of tubule, but leaky in PCT

water, Ca, Mg, K and some Na

31
Q

describe tubular reabsorption of Sodium

A
  1. Na is tranported across basolateral membrane by Na/K ATPase pump
  2. K+ dissues back across the membrane passively (thu channel
    • K+ leaks out cell into interstitial fluid -> neg charge inside cell
      • helps to pull Na inward across apical membrane
    • Na+ and K+ reutn into circulation via peritubular capillaries
  3. Na reabsoprtion across apical membrane via secondary active tranposrt
    • coupled with other ions, amino acids, glucose and occasionally facilliated diffusion
    • export of Na caues an electrochemical gradietns (lots Na in filtrate, little in tubule cell)
    • Na reabs is main driving force for reabsorption of other nutrients
32
Q

How is water reabsored

A
  • constituative aquaporins in PCT (obligatorry water reabsorption)
  • inducible aquaporins in collecting ducts (faculative, inseted into collecting ducts only if ADH is present
33
Q

how are Fat-soluble substances, some ions, and urea reabsorbed

A
  • as water is reabsorbed, the concentration of solutes remaining in filtrate inc -> forms concentration gradient
  • solutes passively follow concentration gradient (if able)
  • > lipid soluble mol will diffuse directly though tubule cells
  • > ions and urea follow paracellular route

*this is why lipid-solubledrugsand environmental pollutants are reabsorbed even though it is not desirable

34
Q

overview of reabsoroption by PCT

A
  1. At basolateral membrane Na is pumped into interstitial space by Na/K+ ATPase.
    • active Na transport creates conc gradient
  2. Get downhill Na+ entry at apical membrane
  3. Reabsorption of organic nutrients and certain ions by cotransport at apical membrane
  4. reabsorption of water by osmosis via aquaporins.
    • inc conc of solutes that are left behind
    • solutes can be reabsored as they move down gradients
  5. Lipid solubel substances diffuse by transcellular route
  6. ions and urea diffuse by paracellular route
35
Q

what is transport maximum

A
  • transport maximum (Tm) exists for almost every reabsorbed substance

*reflects number of carriers in renal tubules

  • when carriers for a solute are saturated, excess is excreted in urine
    ex: hyperglycemia leads to high blood glucose levels that exceed Tm and glucose spills over into urine
36
Q

summary of abs of sodium ions

A
  • in PCT by primary active transport via basolateral Na+-K+ pump
  • crosses apical memrbane through channels, symptorters or antiporters
37
Q

abs summary of nutrients PCT

A

*glucose amino acids, vitamins and some ions

  • secondary active transport with Na
38
Q

abs summary of ions (Cl, K, Mg, Ca) in pCT

A

passive paracellular diffusion driven by electrochemical gradient

39
Q

abs summart of bicarb

A

HCO3- abs by secondary active tranpodrt in PCT linked to H+ sections and Na+ reabsorption

40
Q

abs of urea in PCT

A

primarily passive paracellular diffusion

~50%

41
Q

reabsorption of water

A

65% in PCT by osmosis (driven by solute reabsorption -> obligatory water reabs)

  • in descening limb: permeable to water

*ascenidn glimb is impermeable to water

42
Q

reabsorption in ascening limb

A

*impermeable to water but permeable to solutes

  • thin segment: passive diffusion of Na+
  • Thick segments ahs secondary active Na+/K+/2Cl sympotrts and Na/J antiporters to transport Na in

*Na, Cl and K by secondary actie transport

*Ca and Mg by passive paracellular diffusion

43
Q

reabsortopn in DCT an collecting duct VD PCT and nephron loop

A
  • PCT and nephron loop handle majority of reabsorption but is not responsive to changing needs of body
  • DCT and collecting duct do fine tuning of reabsorption
44
Q

how are Na and Cl abs in DCT

A

priamry active Na transport at basolateral membrane

secondary active transport at apical membrane via Na/Cl sympotrter

  • aldosterone regulated at distal portion
45
Q

how is Ca abs in DCT

A
  • pasive uptake via PTH modulated channels in apical membrane
  • primary and secondary active transport in basolateral membrane
46
Q

how are Na, K and HCO3, and Cl reabsorbed in collecting duct

A

priamry ctive of Na (req aldosterone)

  • passive paracellular diffusion of some Cl
  • net K= sectetion
47
Q

how is water reabs in colelcting duct

A
  • faculative water reabs, ADH is required
48
Q

describe abs or urea in colelcting duct

A
  • facilitated diffusion in response to conc gradient in deep medulla region
  • contributes to osmotic gradient
49
Q
A

111: Anatomy/Phys 2 (31 decks)

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