Renal Physiology Flashcards

1
Q

osmolarity

A

solute concentration: number of osmoles (Osm) per liter = Osm/L

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2
Q

what is the difference between osmolarity and tonicity?

A

osmolarity refers to both penetrating and non-penetrating solutes, tonicity refers to only non-penetrating solutes

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3
Q

osmosis

A

movement of water from areas of high osmotic pressure (hyperosmotic - more concentrated relative to some other solution) to areas of low osmotic pressure (hypo-osmotic)

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4
Q

isosmotic

A

no difference in osmotic pressure

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5
Q

what is the difference between osmotic regulators and conformers?

A

osmotic regulators maintain a constant blood osmolarity, conformers follow isosmotic line (blood osmotic pressure = ambient osmotic pressure)

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6
Q

ion regulator

A

maintenance of a constant concentration of inorganic ions in blood plasma

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7
Q

ionic conformer

A

allows concentration of a particular ion species in blood plasma to match the concentration in environment

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8
Q

challenges to freshwater regulators

A
  • external environment is hypo-osmotic to internal environment
  • constantly taking in water through osmosis
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9
Q

challenges to marine regulators

A
  • external environment is hyperosmotic to internal environment
  • constantly losing water (faces dessication/constant water loss) - constantly drinking seawater to compensate for water loss (this also causes a load up on ions that needs to be removed)
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10
Q

solutions for challenges faced by freshwater regulators

A
  • copious amounts of dilute urine counters water uptake (leads to ionic loss)
  • active uptake of ions through gills (active transport) to counter ionic loss/dilution
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11
Q

what are the cell types in freshwater gills?

A

1) pavement cells: 90% of gill epithelium, principally responsible for oxygen uptake
2) mitochondria rich cells (MRCs): uptake of chloride, sodium, and calcium; partially under hormonal control, density and type can be changed in varying conditions

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12
Q

density of MRC’s in very “soft” freshwater (low calcium)?

A

this increases osmotic pressure for water to enter fish and dilute ionic concentrations (ion loss), thus MRC density is upregulated to counter challenges of ionic loss

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13
Q

V-type (vacuolar) ATPase

A

located on apical membrane of MRCs in freshwater gills. Transports H+ out of the cell which leaves the cell with a net negative charge

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14
Q

sodium channels

A

located on apical membrane of MRCs in freshwater gills.

-negative charge of MRCs due to V-type ATPase attracts cations into the cell passively

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15
Q

Na+ - K+ pump/ATPase

A

located on the basolateral membrane of MRCs in freshwater gills, pumps 2Na+ out of MRC and 3K+ into MRC

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16
Q

potassium leak channels

A

located on the basolateral membrane of MRCs in freshwater gills, helps maintain negative charge of MRC and low intracellular K+ concentration

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17
Q

electroneutral anion exchanger

A

found on pavement cells and apical membrane of MRC’s, exchanges a bicarbonate ion for a chloride ion (driven by buildup of bicarbonate which causes a driving force for bicarbonate efflux)

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18
Q

cystic fibrosis transmembrane regulator (CFTR)

A

found on pavement cells and basolateral membrane of MRC’s, allows chloride ions to move from cells into the bloodstream

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19
Q

mutations in CFTR

A
  • results in cystic fibrosis
  • reduces chloride clearance from cells, this maintains a higher than normal electronegative potential in the cells
  • this also reduces extracellular removal of cations (cations also build up inside the cells)
  • this causes increased mucosal buildup (higher osmotic pressure causes water to enter cells) - leads to respiratory and digestive difficulties
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20
Q

calcium co-transporter and calcium-ATPase

A

moves calcium out of the cell based on driving force for sodium (sodium influx-attraction to negative charge) or ATP breakdown

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21
Q

what are the effects of drinking seawater?

A
  • water in the gut will be hyperosmotic to blood plasma (will cause water to be drawn out of the blood plasma by osmosis and sodium and chloride ion diffusion into blood plasma)
  • net result is very concentrated blood plasma
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22
Q

what are the adaptations of marine fish for the effects of drinking seawater?

A
  • later parts of the intestine actively transport sodium and chloride ions out of the gut into the blood
  • increases water reabsorption
  • excess ions are removed in the gills (NKCC cotransporter causes chloride buildup in MRC to produce a driving force for chloride to leave the cell, negative charge attracts sodium ions to the apical membrane which enters environment via a paracellular pathway)
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23
Q

challenges faced by marine birds/reptiles

A
  • body is hypo-osmotic to seawater

- results in water loss and salt loading due to ingestion of hyperosmotic water (must remove excess solutes)

24
Q

how do marine birds/reptiles remove excess solutes?

A
  • salt glands (secretory cell uses NKCC and paracellular pathway to converge salt ions into lumen of secretory tubule for excretion)
25
Q

marine osmoconformers

A
  • e.g. sharks, rays, skates
  • match blood osmotic pressure to marine environment
  • produces high concentrations of organic solutes (urea and TMAO) to match osmopressure without the issue of water loss
26
Q

humidic animals

A

animals restricted to humid, water-rich environments (e.g. earthworms, slugs, amphibians, crabs)

27
Q

xeric animals

A

animals capable of living in dry, water-poor places (e.g. mammals, birds, reptiles, arachnids, insects)

28
Q

what is the difference between humidic and xeric animals?

A

the rate of water loss in arid environments

  • humidic animals have a much higher integument permeability which results in increased evaporation, must live in areas with high water vapour pressure
  • xeric animals have low integument permeability, thin lipid layers provide barriers for water loss
29
Q

evaporative water loss (EWL)

A

is determined by body size (smaller animals have higher SA:V ratio, higher metabolisms/respiration rates, higher EWL) and phylogenetic group - most abundant source of water loss

30
Q

excretory water loss

A

2nd most abundant source of water loss

31
Q

U/P > 1

A

concentrated urine produced during times of drought/low water in body system

32
Q

U/P < 1

A

dilute urine produced during times of water loading/too much water in body system

33
Q

U/P = 1

A

urine is isosmotic to plasma

34
Q

glomerulus

A

Bowman’s capsule + vasculature surrounding Bowman’s capsule

35
Q

what forms the ultra-filter in Bowman’s capsule?

A
  • capillaries (single endothelial layer with fenestrations)
  • basement membrane
  • podocytes (specialized epithelial cells with branching processes that form a slit diaphgram)
36
Q

what contributes to the large hydrostatic pressure outside the tubule?

A

pressure created by systole

37
Q

primary urine

A

aqueous solution first introduced into kidney tubules, dissolved solutes nearly identical to the blood, does not contain large plasma proteins (blood osmotic pressure is higher than capsular fluid)

38
Q

definitive urine

A

the urine that is excreted, makeup is very different from primary urine

39
Q

filtration pressure

A
  • hydrostatic pressure created by systole pushes water into nephron
  • colloid osmotic pressure created by osmotic difference draws water back into blood plasma
40
Q

glomerular filtration rate (GFR)

A

rate of production of primary urine (120mL/min)

41
Q

chronic hypertension/diabetes mellitus

A

reduces GFR

42
Q

loops of Henle

A

renal component that allows for concentration of urine, max urine concentration correlates with abundance of long loops of Henle

43
Q

descending thin segments

A

highly permeable to water, moderately permeable to most solutes

44
Q

ascending thin segment

A

impermeable to water, moderately permeable to most solutes

45
Q

ascending thick segment

A

impermeable to water, active transport of sodium chloride (into the cell)

46
Q

single effect

A

initial change in pressure because of active transport (what creates the environment that allows for urine concentration) - creates transverse osmotic gradient

47
Q

countercurrent multiplication

A

osmotic pressure differences are multiplied due to fluids moving in opposite directions - creates axial osmotic gradient

48
Q

diuresis

A

excrete excess water to produce dilute urine, results from decreased permeability of collecting duct to water (water cannot be reabsorbed) but urea continues moving out of collecting duct into interstitial

49
Q

antidiuretic hormone (ADH)

A

aka arginine vasopressin, vasopressin

  • produced in hypothalamus and released from posterior pituitary
  • release is stimulated by low levels of blood plasma, detected by baroreceptors and osmoreceptors
  • modulates permeability of collecting ducts to water, causes insertion of an aquaporin
50
Q

baroreceptors

A

detect blood volume, located in pulmonary venous system, cardiac atria, aortic arch, and carotid sinus

51
Q

osmoreceptors

A

detect changes in osmolarity, located in hypothalamus

52
Q

AQWCV

A

aquaporin water channel containing vesicle

1) vasopressin binds to vasopressin receptor (GPCR)
2) initiates 2nd messenger cascade, activates adenylyl cyclase which increases cAMP and PKA
3) increase aquaporin insertion via exocytosis of AQWCV
4) increase fluid movement out of collecting duct to produce concentrated urine

53
Q

urea

A

produced by oxidation of amino acids not used in protein synthesis and as a byproduct of nitrogenous metabolism (ammonia which is then converted to urea)

54
Q

what are areas with low permeability to urea?

A
  • distal convoluted tubule
  • thick ascending segment of Loop of Henle
  • cortical and outer renal medulla
55
Q

what are areas with high permeability to urea?

A

collecting duct in the inner renal medulla, contains UT-A1

56
Q

urea transporter protein UT-A1

A

facilitates diffusion from collecting duct into interstitial fluid, up-regulated by ADH (should increase concentration of urine)

57
Q

vasa recta

A

vasculature that supplies the renal medulla, goes from cortex down into medulla and back up to cortex. does not destroy osmotic pressure gradients in kidney because there it is very little blood flow (compared to total renal blood flow) and it acts as a countercurrent exchanger (minimizes washout of solutes)