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BIOL 2420 > Renal system > Flashcards

Renal system Flashcards

1
Q

how much do the kidneys weigh?

A

kidneys represent less than 1% of the body weight

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2
Q

how much of the cardiac output do kidneys receive?

A

receive approx. 20-25% of CO (over 1 L/min)

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3
Q

look at kidney structure

A

fig 19.1b

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4
Q

what are the 7 main functions of the kidney?

A

1) maintenance of water balance in the body
2) regulate body fluid osmolarity and balance of specific ions
3) help maintain proper acid base balance of the body
4) eliminate unwanted materials from the body
5) an endocrine gland that secretes useful hormones
6) conversion of vitamin D into its active form
7) gluconeogenesis

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5
Q

how do the kidneys maintain water balance in the body?

A

by maintaining extracellular fluid volume

-vasopressin, ADH

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6
Q

which ions do the kidneys regulate?

A

Na+, Cl-, K+, Ca++, Mg++, PO4 3-

  • each of these is regulated independently of one another
  • this indirectly maintains plasma volume and hence, blood pressure
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7
Q

how do the kidneys help maintain proper acid base balance of the body

A

adjust urinary output of H+ and HCO3-

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8
Q

how do the kidneys eliminate unwanted materials from the body

A
  • excrete end products of metabolism (urea, creatinine)
  • excrete foreign compounds (drugs, pesticides)
  • also eliminates things that are not produced by your body such as medications
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9
Q

which 4 functions of the kidneys are performed by specialized tubular structures called nephrons?

A
  • water balance
  • body fluid osmolarity and ion balance
  • acid base balance
  • eliminate waste
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10
Q

which useful hormones do the kidneys secrete?

A
  • erythropoietin (stimulates reaction important for RBC production)
  • renin (triggers reaction important for salt conservation a.k.a. angiotensin I - angiotensin II)
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11
Q

why is gluconeogenesis important?

A

important during fasting to help maintain glucose levels

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12
Q

functional unit of the kidney

A

nephron

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13
Q

what are the two components of the nephron

A

1) vascular elements - two sets of arterioles and two sets of capillaries
2) tubular elements - divided into different zones, with each having specific functions/cell types (where urine gets formed an heavily modified)

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14
Q

what are the two categories of nephrons?

A

1) cortical nephrons

2) juxtamedullary nephrons

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15
Q

cortical nephrons

A
  • 80% of nephrons
  • corpuscle originates in outer layer of the cortex
  • loop of Henle is short and ends slightly before or just dips into the medulla
  • important for reabsorption, secretion, filtration
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16
Q

juxtamedullary nephrons

A
  • originate deep in the cortex and extend deep into the medulla
  • both the ascending and descending tubules have thick and thin components
  • important for the production of dilute or concentrated urine by allowing us to keep or get rid of water, regulates salt balance and hence, FLUID VOLUME
  • 20% of nephrons
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17
Q

what are the basic processes of the nephron

A

1) glomerular filtration
2) tubular reabsorption
3) tubular secretion

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18
Q

what is glomerular filtration

A

the passage of near PROTIN FREE plasma from the glomerular capillaries in the lumen of Bowman’s capsule

  • basically forming serum
  • Gives colloid forces drawing fluid back into capillaries after it’s been filtered
  • without this, kidneys wouldn’t work

-20% of plasma is filtered per pass - blood leaving the glomerulus has less volume but higher [protein]

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19
Q

what is tubular reabsorption

A

the SELECTIVE movement of substances from the tubular lumen back into the venous system (drawn to plasma colloid osmotic pressure)

  • via peritubular capillaries
  • 99% of filtrate is typically reabsorbed (unless there are other hormonal signals)
  • filter 180 L/day
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20
Q

what is tubular secretion

A

the SELECTIVE transfer of substances from the peritubular capillaries and tubular cells into the tubular lumen
-mechanism for rapid elimination of unwanted substances

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21
Q

anything filtered or secreted but not reabsorbed is excreted

true or false?

A

true

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22
Q

urine formation begins with what?

A

glomerular filtration, which occurs at the interface between the golmerulus and Bowman’s capsule

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23
Q

is glomerular filtration a passive or an active process?

A

this bulk flow of fluid is extracellular and passive

  • extremely leaky
  • follows Starling forces (hydrostatic pressure and protein osmolarity)
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24
Q

how much plasma enters the afferent arteriole during glomerular filtration per day?

A

900 L/day

-20% of plasma is filtered (180L/day)

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25
Q

glomerular capillaries press into Bowman’s capsule, forming a 3-layer glomerular membrane (filtration barrier) what are these 3 layers?

A

1) a single layer of porous endothelial capillary cells
2) an acellular gelatinous glycoprotein/collagen layer termed the basement membrane (basal lamina)
3) a second layer of specialized endothelial tubule cells (podocytes) encircle the glomerular capillaries

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26
Q

describe the single layer of porous endothelial capillary cells that forms the first layer of the 3 layer glomerular membrane

A
  • this is over 100 times more permeable than capillaries elsewhere (but they are wrapped around other cells so really they are only about 40 times more leaky)
  • the large pores allow most solutes to pass between these cells, though physicall blocks platelets, blood cells, and most proteins
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27
Q

describe the acellular gelatinous glycoprotein/collagen layer termed the basement membrane that forms the second layer of the 3 layer glomerular membrane

A

-most glycoproteins here are anionic, thus repelling small anionic plasma proteins; filtration of much smaller anions (ex: Cl-, HCO3-, HPO4(2-) are not affected

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28
Q

describe the second layer of specialized endothelial tubule cells (podocytes) that encircle the glomerular capillaries that form part of the 3-layer glomerular membrane

A
  • octopus like cells with many finger-like projections
  • projections of adjacent cells interdigitate, forming filtration slits for fluid to pass through
  • this barrier makes it less leaky
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29
Q

what is resulting from the 3 layer glomerular membrane when it comes to glomerular filtration?

A

there is complete extracellular filtration of near PROTEIN FREE fluid into the Bowman’s capsule lumen that is isosmotic with the plasma

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30
Q

does glomerular capillary blood pressure favour or oppose filtration?

A

favours filtration

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31
Q

does plasma colloid osmotic pressure favour or oppose filtration?

A

opposes filtration

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32
Q

does Bowman’s capsule hydrostatic pressure favour or oppose filtration?

A

opposes

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33
Q

what is the average magnitude of glomerular capillary blood pressure?

A
  • 55 mmHg, much higher than in systemic capillaries (37 ish)
  • the afferent arterial is bigger than the tap going out
  • resistance to emptying - higher pressure
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34
Q

what is the average magnitude of the plasma colloid osmotic pressure in the glomerulus

A

-33 mmHg
A bit higher than in other capillaries - due to the fact that we get more filtration
-draws water in opposite direction - opposes filtration
-kidney disease - membrane becomes leaky to proteins - can occur during hypertension, damaging capillaries
-this force would decrease (during both liver and kidney disease) - we get more filtration

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35
Q

what is the average magnitude of the Bowman’s capsule hydrostatic pressure?

A

-15 mmHg - reflects a high rate of filtration

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36
Q

does the net filtration pressure of glomerular filtration favour or oppose filtration?

A

favours filtration

  • we get about 180 L/day of filtration - 60 times our plasma volume per day
  • this varies
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37
Q

what are the 3 forces of glomerular filtration?

A

1) glomerular capillary blood pressure
2) plasma colloid osmotic pressure
3) Bowman’s capsule hydrostatic pressure

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38
Q

glomerular filtration depends on mean arterial pressure

true or false?

A

false, to maintain optimal function, the glumerular filtration rate (GFR) is generally maintained within fairly narrow limits despite short and long term changes in mean arterial pressure

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39
Q

GFR is dependent upon what?

A

both the net filtration pressure (NFP) and the filtration coefficient (Kf) of the glomeruli (the “leakiness”)

GFR = Kf x NFP

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40
Q

how do we calculate the filtration coefficient Kf?

A

Kf = permeability of glomeruli x total surface area

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41
Q

how is GFR primarily controlled?

A

by altering the glomerular capillary blood pressure
-this is largely accomplished by changing the diameter (resistance) of the AFFERENT and efferent arterioles leading to the glomeruli (local resistance) (this is the only thing we can really change)

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42
Q

what are the two modes of intrinsic control (autoregulation) for glomerular filtration

A

1) myogenic response

2) tubuloglomerular feedback

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43
Q

explain how myogenic response controls GFR

A

-stretch response
ex: decreased afferent arteriole pressure induces vasodilation - increases flow and hence GFR
(less Ca++, less cross bridges, more flow)

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44
Q

explain how tubuloglomerular feedback controls GFR

A
  • mediated by specialized tubular (macula densa) cells in the JUXTAGLOMERULAR region of the ASCENDING limb
  • can sense filtrate content - sends info to arterioles
    ex: too much flow? causes less filtration, not enough flow? causes dilation

changes in GFR affect the flow rate, and hence [NaCl] of fluids moving past the macula densa cells (for salt reabsorption)

ex: elevated [NaCl] (=increased flow through tubules) stimulates them to release local chemical messages that vasoconstrict smooth muscle cells encircling the afferent arterioles
- reduced net filtration pressure and GFR

-this is negative feedback

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45
Q

what are the extrinsic factors that regulate glomerular filtration?

A

this is mediated by sympathetic nervous input to a1 receptors on smooth muscle of afferent arterioles in response to changes in blood pressure

ex: baroreceptor reflex - increased sympathetic activity
- afferent arteriole vasoconstriction (GFR drastically reduced)
- THIS REFLEX OVERRIDES THE AUTOREGULATORY RESPONSE (intrinsic)

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46
Q

the contraction of the podocyte foot processes contract due to the stimulation of which division of the ANS? this leads to what?

A

sympathetic, this leads to decreased filtration slit size (which lowers Kf)
-lower pressure and lower permeability of filtration membrane (could happen during a hemorrhage) - net result - REDUCED GFR

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47
Q

what is the magnitude of tubular reabsorption?

A
  • over 99% of the filtered H2O (approx 178.5L)
  • 100% of the filtered sugars - ex: glucose (180g)
  • 99.5% of the filtered salt (625g)
  • 50% of the filtered urea is reabsorbed on a daily basis
48
Q

is tubular reabsorption of Na_ active or passive?

A

with the exception of the thin descending and ascending tubules, Na+ reabsorption is primarily accomplished via energy-dependent Na+/K+ ATPase
-Na+ is actively pumped across the basolateral membrane into the ISF, decreasing tubular cell [Na+] while increasing ISF [Na+]

49
Q

the active tubular reabsorption of Na+ establishes two electrochemical gradients for Na+ diffusion, what are they?

A

1) from the lumen into tubular cells (enter via epithelial Na+ channels (passive channel))
2) from the ISF into the peritubular capillaries

50
Q

80% of the total energy requirement of the kidneys is used for what?

A

Na+ reabsorption, indicating the importance of this process

51
Q

Na+ is reabsorbed to varying extents throughout the nephron, where is it all reabsorbed?

A
  • 65% from the proximal convoluted tubule (PCT) (lots of Na+/K+ pumps and Na+ epithelial channels)
  • 25% from the ascending limb of the loop of Henle (being taken from filtrate to blood)
  • 8-10% from the late DCT and cortical collecting ducts (mostly cortical collecting ducts - we have some control over 2% of reabsorption; this is either filtered or excreted (30g)
52
Q

what are the three roles of Na+ reabsorption

A

1) in the loop of Henle, Na+/K+/2Cl- cotransport plays a critical role in the kidney’s ability to produce urine of varying concentrations and volumes
2) regulation of ECF volume
3) plays a pivotal role in the passive reabsotprion of glucose, amino acids, H2O, Cl-, and urea from the proximal convoluted tubule (bulk flow)

53
Q

how does the reabsorption of Na+ regulate ECF volume?

A

-in the distal portion of the nephron, Na+ reabsorption is variable and under hormonal control

1) atrial natriuretic peptide (ANP)
- secreted by atria when myocardial cells excessively stretched (i.e. increased plasma volume) - causes more Na+ to be reabsorbed, losing fluid volume)
- induces afferent arteriolar vasodilation; increases GFR
- inhibits vasopressin, renin, and aldosterone secretion (decreases H2O and Na+ reabsorption, reduces MAP)
2) aldosterone (released from adrenal cortex)
- stimulates insertion of ENaC and Na+/K+ ATPase pumps in principal cells of the late DCT and early (cortical) collecting duct
- more Na+ reabsorption, leads to increased water reabsorption - smaller urine volume

54
Q

granular cells embedded in the afferent arterioles secrete renin (enzyme) when what?

A

1) intrarenal blood pressure decreases
2) [NaCl] of fluid passing by macula densa decreases
- could occur if blood has low osmolarity (when you want to reabsorb more salt)
3) sympathetic stimulation increases (via non renal baroreceptors) (B1 receptors)

55
Q

renin converts ____ into _____ which is then converted to its active form ______ by _____

A

angiotensinogen, angiotensin I, angiotensin II, ACE

56
Q

does the renin-angiotensin-aldosterone system promote vasodilation or vasoconstriction?

A

vasoconstriction

57
Q

angiotensin II stimulates the secretion of aldosterone and vasopressin

true or false?

A

true

58
Q

explain renin-angiotensin-alsdosterone control

A

ex: a decrease in afferent pressure causes a decrease in NaCl and an increase in sympathetic stimulation
- renin is secreted by granular cells because of this
- renin leads to the activation of angiotensin II which leads to an increase in vasopressin, thirst, and arteriolar vasoconstriction; as well as secretion of aldosterone which leads to increased Na+ reabsorption
- all this leads to an increase in H2O reabsorption and conservation

-this then negatively feedsback to the beginning of the cycle where afferent pressure and NaCl [ ] is back to normal

59
Q

passive tubular reabsorption is indirectly linked to ____ reabsorption

A

Na+

60
Q

what are the 4 things that passively get reabsorbed in tubular reabsorption?

A

1) glucose and amino acids
2) Cl-
3) H2O
4) urea

61
Q

by what mode of transport do glucose and amino acids get passively reabsorbed ?

A

they are co transported form the tubular lumen with Na+ against their concentration gradient by secondary active transport

62
Q

tubular cells posses a limited number of co transport carriers, what does this have to do with glucose and amino acid reabsorption?

A
  • because of this, there is a tubular maximum, and reabsorption has limits
  • the kidneys have 3x more glucose transporters than they need which is good when you’ve just had a meal
  • if there’s too much sugar, a lot of sugar gets filtered, when more gets filtered, co transport carriers become saturated and we can’t pick up any more sugar (in diabetes type 1 and 2 this happens)
63
Q

explain Cl- reabsorption in the kidneys

A

mostly occurs via a paracellular route, following the electrical gradient established by the active transport of Na+

  • EXCEPTION: THICK ASCENDING LIMB where there is a different transport mechanism
  • when Na+ leaves from the lumen into the ISF, is becomes more negative in the lumen so Cl- follows Na+
64
Q

explain the reabsorption of H20 in the kidneys

A

the removal of solutes from the tubular lumen decreases the lumen osmolarity, while increasing the ISF
-by removing salts and amino acids, this creates a water gradient which promotes its movement

65
Q

if tubular epithelia is impermeable to water, how does water cross the membrane in order to follow its gradient?

A
  • the diffusion of water from the lumen to the ISF is primarily via osmosis through H2O pores in the luminal and basolateral plasma membranes called aquaporin chanels
  • these are found in the PROXIMAL CONVOLUTED TUBULE ONLY, some water can pass paracellularly (starling forces)

-RECALL, plasma entering peritubular capillaries has an elevated colloid osmotic pressure, thus pulling H2O into the plasma (starling forces)

66
Q

how many different aquaporin isoforms are there? how many are expressed in the kidney?

A

13, 6 types are expressed in the kidney

67
Q

where are aquaporins ALWAYS present?

A

in the proximal convoluted tubule and the thin descending tubules
-75% of filtered H2O is obligatorily reabsorbed via this route

-so water can always go through here

68
Q

which aquaporin channels open up vasopressin release? (anti diuretic hormone) how does this work?

A

levels of a specific aquaporin (AQP2) isoform in principal cells of the late DCT and collecting ducts depend on vasopressin release

-this happens by the binding of vasopressin onto the membrane receptors which activated the cAMP secondary messenger system inserting AQP2 pores into the luminal (apical) membranes

69
Q

a(n) ______ in plasma [vasopressin] leads to an increase in H2O reabsorption

A

increase

70
Q

vasopressin leads to an additional ____% (fully hydrated to over ____% (dehydrated of the remaning H2O being reabsorbed

A

5, 24

71
Q

two stimuli control vasopressin secretion from the posterior pituitary, what are they?

A

1) ECF osmolarity “salt receptors”
- these osmoreceptors in the hypothalamus stimulate vasopressin release if osmolarity rises above 280 mOsM
2) decreased blood pressure and reduced blood volume
- decreased firing of carotid and aortic baroreceptors, and stretch sensitive receptors in the atria stimulate the release of vasopressin

72
Q

diabetes insipidus

A

failure to produce vasopressin or an inhability of principal cells to respond to this hormone

  • children occasionally have problems with vasopressin “bet wetting”
  • not secreting as much vasopressin as they should
73
Q

explain how urea gets reabsorbed in the kidneys

A

solute and H2O reabsorption in the proximal convoluted tubule create a [] gradient for urea (urea here is very concentrated)
-there are no urea channels but ‘leaky’ tight junctions here are moderately permeable to urea (50% reabsorbed)

74
Q

which area of the kidney is impermeable to urea?

A

the tight junctions in the loop of Henle. DCT, and cortical/outer medullary collecting ducts

  • however, membrane urea uniporters in the thin region of Henle’s loop passively secrete an equivalent amount back into lumen
  • half of this waste product is agian reabsorbed by transporters in the distal (inner medullary) collecting ducts
75
Q

how does vasopressin affect urea reabsorption in the kidneys?

A

-vasopressin increases the number of urea uniporters in the thin regions of Henle’s loop, increasing urea reabsorption and thus the medullary vertical osmotic gradient

76
Q

what is tubular secretion?

A

a similar process as reabsorption, but in opposite direction and of much lower magnitude
-everything here is against the [] gradient

77
Q

what are the 4 substances that are SELECTIVELY secreted in the kidneys?

A

1) K+
2) H+ ions
3) waste products such as creatinine and urobilin (urochrome)
4) foreign substances (ex: drugs, penicillin)

78
Q

why is it important that K+ be secreted in the kidneys?

A

-important for normal nerve and muscle function (high levels of K+ inside cells, low levels outside - membrane potential)

79
Q

where is most of the filtered K+ reabsorbed?

A

-most of the filtered K+ is first reabsorbed in the PCT (via leaky tight junctions) and thick ascending tubules (via Na+/K+/2Cl- cotransport)

80
Q

what is tubular reabsorption

A

the process by which the nephron removes water and solutes from the tubular fluid (pre-urine) and returns them to the circulating blood.

81
Q

why is tubular secretion of H+ ions important

A

important for regulating acid base balance

-increased secretion when body fluids become to acidic

82
Q

how fast does it generally take for foreign substances to get secreted?

A

about 80% are secreted in 3 to 4 hours

83
Q

what is tubular secretion

A

a process by which substances are produced and discharged from a cell, gland, or organ for a particular function in the organism or for excretion

84
Q

it is VERY important to regulate K+ levels within a very narrow range

true or false?

A

true

85
Q

where does K+ secretion happen? How?

A

K+ secretion, via K+ channels in the luminal membrane of the late DCT and cortical collecting duct principal cells, is subject to regulation

  • elevated plasma [K+] (hyperkalemia) stimulates aldosterone release by the adrenal cortex
  • decreased aldosterone also lowers K+ secretion
86
Q

additional K+ can be reabsorbed in exchange for what?

A

in exchange for H+ by TYPE A INTERCALATED CELLS in the collecting ducts during hypokalemia, with little or no K+ excreted, however plasma pH increases

87
Q

explain the mechanism of K+ secretion

A

K+ transport across the basolateral membrane of principal cells is linked with Na+ transport via the Na+/K+ ATPase pump

  • aldosterone stimulated increased Na+ uptake from tubular lumen through ENaC channels
  • K+ diffuses into the lumen down its electrochemical gradient, leading to a net loss of K+ from plasma (to cancel out negative charge)
88
Q

how does acidosis affect K+ secretion?

A

the basolateral pump and K+ channels are inhibited by low pH, thus K+ secretion becomes impaired

89
Q

the ______ possess few K+ channels, thus most K+ diffuses back into the ISF here

A

proximal tubule luminal membranes

90
Q

the osmolarity of body fluids is closely regulated near____ mOsM

A

300

91
Q

what is the range our urine concentration can range from? Why is this such a big range?

A

urine [] can range from 80 to over 1200 mOsM - either 4x saltier or 4x more dilute

-this ability depends on teh presence of a vertical osmotic gradient in the ISF of the renal medulla (cortex ISF always isosmotic with plasma)

92
Q

the 900 mOsM vertical osmotic gradient of urea is created by two equally contributing factors. What are they?

A

1) urea ‘trapping’ in the inner medulla (because there are no urea transporters)
2) operation of a countercurrent multiplier that progressively increases lumen [solute] as tubules descend into the medulla

net result: more NaCl is reabsorbed from Henle’s loop (25% of total) than H2O (10% of total)
-a second countercurrent system (vasa recta) prevent the dissolution of this gradient

93
Q

explain how the osmotic gradient is established in the countercurrent multiplier system (urea gradient)

A

1) prior to the vertical osmotic gradient being established, [ISF] and [tubular lumen] = 300 mOsM which is isosmotic
2) there is active transport of solutes from the thick ascending limb lumen in the ISF - these tubule cells are IMPERMEABLE TO WATER THERE ARE NO AQUAPORIN CHANNELS
3) there is a net diffusion of H2O from the descending tubules into the ISF - there is NO REABSORPTION OF SOLUTES HERE
4) as this stepwise process continues, the filtrate moving down the descending limb becomes more concentrated, while that moving up the ascending limb becomes more dilute

-the longer the loop, the greater the [] gradient

94
Q

how is the medullary osmotic gradient maintained?

A

1) prior to the vertical osmotic gradient being established, [ISF] and [lumen] are 300 mOsM - everything is isosmotic
2) the movement of solutes out of the ascending limb lumen creates a localized 200 mOsM gradients
- but water CANNOT follow
3) there is a net diffusion of water that occurs by osmosis out of the descending limb into the ISF until the osmolarities of the two fluids equilibriate

repeating this process over and over increases [] gradient by 12 fold

95
Q

how is hyperosmotic urine formed?

A
  • when vasopressin is present
  • late DCT and collecting ducts are permeable to H2O
  • this leads to a SMALL VOLUME of concentrated urine (hyperosmotic)

vasa recta also has huge role in how [ ] it is (makes filtrate more [] then less [] keeping gradient)

96
Q

how is hyposmotic urine formed?

A
  • when vasopressin is absent
  • late DCT and collecting ducts are impermeable to water
  • a LARGE VOLUME of dilute (hyposmotic) urine is formed
97
Q

what is the role of the glomeruli in the formaition of urine

A

-protein free filtrate exiting Bowman’s capsule is isosmotic (300 mOsM) with the plasma

98
Q

what is the role of the proximal convoluted tubule in urine formation

A

1) 2/3 of filtered Na+ is actively re-absorbed here (Na+/K+ ATPase)
2) Cl-, K+, and water follow passively
3) low urea permeability (50% reabsorbed)

-result: 2/3 of filtrate is absorbed, but still isosmotic with the plasma

99
Q

what is the role of the thin descending loop of Henle in urine formation

A

1) no active transport of Na+ (no pumps)
2) many aquaporin channels (always present and always open) - H2O passively enters ISF here
3) some urea is passively secreted (uniporters)

result: filtrate becomes highly concentrated (1200 mOsM)

100
Q

what is the role of the thin ascending loop of Henle in urine formation

A

1) paracellular diffusion of Na+ and Cl- from the lumen to the ISF
2) lack of AQP channels - H2O impermeable
3) some urea passively secreted into tubular lumen

result: filtrate becomes more dilute as it travels up the tubule

101
Q

what is the role of the thick ascending loop of Henle in urine formation

A

1) Na+/K+/2Cl- cotransport from lumen to tubular cell (Secondary active transport)
- there are also K+ pumps pumping K+ into lumen from tubular cell
2) also paracellular diffusion of Na+ to ISF (50% of total)
- this creates a LOCALIZED 200 mOsM lumen to ISF gradient (due to Na+/K+ ATPase which is what creates the gradient)
3) this area is impermeable to urea AND H2O
- filtrate becomes hyposmotic (less than 100 mOsM) to plasma

102
Q

what is the role of the distal convoluted tubule and collecting ducts in urine formation

A
  • MOST THINGS HAPPEN HERE
    1) active reabsorption of Na+ (and K+ secretion) by principal cells (which have aldosterone receptors) IF aldosterone is secreted
  • increased aldosterone [] = increase in Na+ uptake and increase in K+ secretion
    2) water reabsorption by principal cells here is variable and dependent upon vasopressin levels
  • increase in vasopressin [] = increase in water permeability (because vasopressin inserts more water channels) and a decrease in urine volume (increase [urine])
    3) impermeable to urea (which becomes VERY concentrated)
  • urea transport from inner medullary collecting duct back into ISF helps maintain medullary gradient []
  • ‘urea cycling’ - vasopressin increases urea reabsorption here
103
Q

acidosis

A
  • when the pH is lower than 7.35
  • ECF pH is regulated by excreting H+ in the urine and by reabsorbing HCO3- from the filtrate (bicarbonate is a buffer, binds to protons to make CO2) (one way to compensate is to breathe more)
104
Q

alkalosis

A
  • when the pH is over 7.45
  • ECF is regulated by secreting less H+ into the filtrate and excreting excess HCO3- in the urine
  • disturbances to acid base balance may be respiratory or metabolic in origin (these can come from lung diseases, emphysema, or things like diabetes, or diarrhea)
105
Q

if too much CO2 is exhaled, we can get ______, if too little CO2 is exhaled, we get ______

A

alkalosis, acidosis

106
Q

how does breathing rate lead to acidosis/alkalosis?

A

changes in PCO2, brought about by hypo-hyperventilation, cause the pH to change

-Law of mass action - an increase in CO2 leads to an increase in H+ which leads to the decrease in pH

107
Q

is emphysema associated with alkalosis or acidosis? why?

A

emphysema is characterized by the loss of elastic fibers in the lungs, which means it is harder to breathe out, this means that it is associated with acidosis because of the increase in PCO2 in the lungs, meaning there is an increase in H+, decreasing the pH

108
Q

if the underlying cause of pH disturbance (alkalosis/acidosis) is of respiratory origin (breathing in too much, not breathing out enough), how can we compensate?

A

we can ONLY compensate via the kidneys

-breathing in supplemental oxygen will not help get rid of the excess CO2

109
Q

what are causes of acidosis that are not of CO2 origin?

A

1) anaerobic metabolism - lactic acidosis (can get this with an extreme burst of exercise, build up of lactic acid)
2) diabetes mellitus - ketoacidosis (getting rid of sugar, body shifts over to fat based metabolism, and produces ketones - during low insulin levels - this can affect K+ levels
3) diarrhea - HCO3- secreted into small intestine not reabsorbed
- body cannot make protons or bicarbonate, it splits them
- need to neutralize acid in small intestine, if you get rid of bicarbonate quickly through diarrhea, only H+ left in small intestine

110
Q

what are some causes of alkalosis that are not of CO2 origin?

A

1) excessive vomiting of acidic stomach contents (vomiting gets rid of all the protons and keeps the bicarbonate)
2) excessive ingestion of antacids (Tums, Rolaids, etc.)

111
Q

If the underlying cause of pH disturbance is of metabolic origin, how can we compensate?

A

BOTH respiratory and renal mechanisms can compensate

112
Q

how do the kidneys compensate for an increase or decrease in pH? (alkalosis, acidosis)

A
  • under acidotic conditions, filtered HCO3- is INDIRECTLY reabsorbed by proximal convoluted tubule cells (because bicarbonate is not permeable to the membrane)
  • bicarbonate crosses as CO2 then turns into bicarbonate and protons
  • tubular lumen impermeable to HCO3- (Na+/H+ exchange through membrane; H2O and CO2 enter membrane)
  • ca transforms H2O and CO2 into bicarbonate and protons, bicarbonate and Na+ are permeable to membrane and go into ISF

Fig 20.17

113
Q

during acidosis, both intracellular and ECF [H+] increase, with excess H+ entering the filtrate in two ways, which are?

A

1) filtration through the glomeruli
- increased plasma H+ [] lead to an increase in H+ filtration and increased excretion
2) active secretion into lumen by H+-ATPase and H+/K+ ATPase transporters in type A intercalated cells of the collecting duct (making either hyposmotic or hyperosmotic urine)

114
Q

acidosis is often accompanied by hypokalemia

true or false?

A

false, it is often accompanied by hyperkalemia

115
Q

explain the function of type A intercalated cells in the collecting duct. How do type B cells differ?

A
  • high H+ and HCO3- in the ISF, these form CO2 to be able to be transported through the membrane of the type A cell
  • once in the cell, ca quickly transforms these back into H+ and HCO3-
  • HCO3-/Cl- antiporter pumps HCO3- out of and Cl- into cell
  • H+ transported into lumen through H+ transporter and through H+/K+ exchanger (to keep electroneutrality) - increasing K+ levels in the blood = hyperkalemia

TYPE B CELLS ARE THE SAME BUT OPPOSITE

116
Q

the nephron cannot produce a urine with a pH that is under 4.5, thus excess H+ must be buffered by other means prior to excretion, what are 2 urinary buffers?

A

1) initially, excess H+ are buffered by excess filtered phosphates that were not reabsorbed
- ex: HPO4 (2-) + H+ — H2PO4- (which is harmless)

2) once phosphate buffers becom e saturated, tubular cells in PCT deaminate glutamine, producing NH3 and HCO3-
- ex: NH3 + H+ — NH4+ (ammonium) - which is excreted in the urine
- HCO3- is transported into blood to combine with H+

117
Q

how do type B intercalated cells in the COLLECTING DUCT help excrete excess HCO3-?

A

the transport proteins of type B cells have opposite polarity to those of type A cells

  • i.e. transport proteins found on the opposite side of the cell (everything moves in the opposite direction)
  • hence, during ALKALOSI, excess HCO3- is secreted while H+ is returned to the blood

fig 20.18b

BIOL 2420 (5 decks)

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