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renal term 2 quizzes 1 and 2 > review session 2 > Flashcards

review session 2 Flashcards

1
Q

short-term regulation of BP

A

control of HR, SV and vasomotor tone by autonomic nervous system
MAP = CO x TPR
not good for long term, carotid sinus adapts to continual increase in BP (discharge rate of receptors goes back to normal after a few days of continually high BP)

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2
Q

long-term regulation of BP

A

by regulating cardiac output and by changes in blood volume
increase in CO increase general peripheral resistance
kidneys regulate PV by regulating Na concentration

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3
Q

na output/losses

A 
105 mmol through urine
10 mmol through feces
5 mmol through skin
all routes regulated
if on high na diet, kidney key regulator
if low na diet all routes of Na loss are curtailed
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4
Q

factors that regulate Na balance

A

antinaturetic mechanisms:
RAAS
renal sympathetics

natriuretic mechanisms:
ANP
intrinsic pressure natriuresis

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5
Q

how does body measure na content?

A

senses blood volume
high pressure receptors - those in afferent arteriole most important - don’t adapt
also ones in cardiac sinus and aortic arch but these are less important
low pressure receptors - cardiac atria, vena cava, large pulmonary vessels

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6
Q

carotid sinus/aortic arch

A

cause changes in sympathetic/parasympathetic tone
response mainly direct cardiovascular with no or little renal participation
high pressure receptors

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7
Q

renal baroreceptors

A

changes in renin-angiotensin-aldosterone cascade

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8
Q

P receptors in the atria

A

changes in secretion of ANPs

changes in sympathetic tone (including renal)

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9
Q

effects of renal sympathetic nerves

A

renin secretion increases

na reabsorption in PT increases

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10
Q

main effects of AII in kidney

A

na reabsorption in PT increases
renin secretion decreases
also increases efferent tone a lot
and increases sensitivity of TGF

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11
Q

extrarenal effects of AII

A

huge increase in aldosterone secretion
increase in arteriolar tone (vasoconstrictor)
small increase in thirst

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12
Q

biological activities of aldosterone

A

increases na reabsorption primarily in CD but also in late DT
increases Na reabsorption in sweat glands
increases Na reabsorption in colon
increases K excretion
increases acid excretion

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13
Q

renal effects of ANP

A

in intermedullary CD, decreases NA reabsorption - not very important for this
decreases afferent tone => increased GFR
decreases renin secretion
decreases ADH sensitivity of CD

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14
Q

extrarenal effects of ANP

A

decreases cardiac contractility
decreases venous tone
increases capillary permeability - reduces circulating BV by allowing more of fluid to seem out into interstitium

decreases sympathetic tone
decreases arteriolar tone
decreases aldosterone secretion
decreases ADH secretion

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15
Q

what happens to segmental Na reabsorption if there’s a decrease in Na intake

A 
typically regain 99% of secreted Na
if low na, every segment responds
70% in PT
25% in ascending LH
3% in DT
3% in CD
only excrete about .1% now
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16
Q

what mechanisms are regulated by catecholamines andgiotensin II?

A

Na/H exchange mechanism in early PT

so also bicarbonate

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17
Q

acetezolamide

A

blocks C.A. IV on PT - acts as potent diuretic

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18
Q

loop diuretics

A

target Na/Cl/K+ channels in TALH
can see the same effects from bartters’s disease
get Na, Ca, Mg wasting

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19
Q

thiazide diuretics

A

the Na/Cl cotransporter in the DT is more powerful than the previous ones b/c transports 1 Na for just 1 Cl
same effects as loss of function in Gitelman’s
get hypotension and hypokalemia

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20
Q

ENaC channels

A

most powerful Na collection
3 Na enters cell in CD
driven in due to low intracellular [Na] and because cell is negative inside

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21
Q

aldosterone on CD

A

aldosterone main regulator of CD Na uptake
acts on MR
up regulates abundance of ENaC channels and of the Na/K atpase

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22
Q

k sparing diuretics

A

inhibit Na+ channels in CD
blocking Na channel blocks associated K secretion as well
antagonists for MR receptor also act like this

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23
Q

gain of function mutation in ENaC

A

get hypertension, hypokalemia becuase too many Na channels in membrane - can’t be removed
too much na uptake and too little k excretion

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24
Q

aldosterone deficiency

A

results in severe hypotension and hyperkalemia because can’t increase ENaC channels and so can’t increase amount of Na reabsorbed or K secreted

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25
Q

11beta-HSD

A

MR can’t distinguish between cortisol and aldosterone, and cortisol at much higher concentration in blood, so MRs would always be saturated by cortisol
but 11b-HSD converts cortisol to cortisone which doesn’t bind to MR
can be inhibited by licorice - would bet situation of apparent mineralocorticoid excess - hypertension and hypokalemia

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26
Q

clinical importance of K

A

too much or too little results in arrhythmias

27
Q

effects of exercise on K

A

longer increase in K conductance and short increase in Na conductance
end result is that K is lost from cells
get hyperkalemia

28
Q

catecholamines on K (epi - beta-receptors)

A

epi acts on beta2-receptors
increases activity of Na/K atpase
enhances K uptake into cell
allows prevention of large hyperkalemia associated with exercise
can also be stimulated pharmacologically - asthmatics receive beta receptor agonists - makes them prone to developing hypokalemia
can also use b-receptor agonists to treat acute hyperkalemia

29
Q

catecholamines on K (norepi - alpha-receptors)

A

inhibits Na/K atpase
results in K leaving cell - hyperkalemia
contributes to minimizing rebound hypokalemia after exercise
less important than opposing effect of beta receptors but can become more pronounced in patients taking beta blockers

30
Q

effects of insulin on K

A

enhances activity of Na/K atpase - potent inducer of k uptake into cell
so in diabetes mellitus get hyperkalemia - get significant fall in plasma K following insulin treatment in DM
refeeding with a carbohydrate rich meal following a period of starvation may result in fatal hypokalemia
can be exploited for the correction of hypokalemia due to other causes by giving insulin with glucose

31
Q

effect of hypertonicity on K

A

as there’s hyperosmosis, cell shrinks cause water leaves but k amount stays the same so concentration goes up - k leaves cell
a hyperglycemic, hyperosmolar state contributes to hyperkalemia in DM

32
Q

acid/base balance on K

A

mineral acids: cell behaves as though it has a H/K exchange mechanism (a little more complicated than that, but easier to remember this way) so large effect on K
organic acids: are lipophilic and so can cross the membrane without the charge movement - so small change in K
respiratory acidosis where CO2 can enter the cell in unionized form doesn’t affect K much either

33
Q

sites of K reabsorption and secretion

A 
65% reabsorbed in PT
10% passively tranported in ascending LH
30% reabsorbed in ascending LH
regulated in CT - if k depletion, only about 2% reabsorbed, if K loading, about 20% secreted
mostly regulated in cortical CD though
if k depletion, 2% reabsorbed
if K loading, up to 160% secreted
in medullary CD, if k depletion, 10% reabsorbed, if K loading, 20% reabsorbed

creates buildup of K gradient in medulla so that K isn’t reabsorbed from CD when we want to excrete it

34
Q

ion transport in CD - aldosterone

A

na reabsorbed and k secreted into tubule
because of more na ions reabsorbed for number of k ions secreted, creates negative charge in lumen
cl then goes through paracellular pathway and also creates more favorable voltage for K secretion
if force CD to reabsorb more na by delivering more to it then mechanism of K excretion will be enhanced
aldosterone also upregulates K secretion

35
Q

diuretic action before or after macula densa

A

if diuretic acts proximal to macula densa, more na will be delivered to CD and more K will be secreted
all diuretics that act proximal to macula densa therefore produce K wasting

36
Q

effect of tubular flow rate on K

A

in CD, how much K is in tubular fluid depends on flow rate - if flow is low and equilibirum is reached between the cell and the tubular fluid
if flow is high then k secretion can occur throughout full length of cortical CD

37
Q

ADH and K

A

if flow is high then k secretion can occur throughout full length of cortical CD - creates potential problem with ADH since ADH affects flow in CD - but need to regulate water balance and K balance independently - so in the absence of ADH, have a high flow rate - maintains K secretion
when ADH acts, CD becomes water permeable, H2O reabsorbed, flow is reduced , but ADH also has direct effect on open probability of luminal K channels - allows the effect of slower tubular flow rate to be canceled out and for water to be regulated separately from K

38
Q

pH and K

A

alkalosis increases open probability of K channels on luminal side fo CD
acidosis inhibits opening of channels

39
Q

aldosterone and K

A

hyperkalemia stimulates aldosterone secretion directly

when aldosterone secretion is stimulated by hyperkalemia, the main effect is an increase in K excretion in cortical CD

40
Q

aldosterone and Na

A

na depletion stimulates aldosterone secretion indirectly via renin and AII
when aldosterone secretion is stimulated by Na deficiency, Na delivery to the cortical collecting duct is decreased by enhanced reabsorption in preceding nephron segments - prevents K wasting
get increase in Na reabsorption in PT which results in decreased Na load in cortical CD => K secretion unchanged

41
Q

what generates base?

A

exogenous organic acids

42
Q

sources of endogenous acids

A

incomplete metabolism of carbohydrates => lactic acid
incomplete metabolism of lipids => ketoacids
2 main sources of endogenous acids

43
Q

sources of bases

A

carboxyl group on AA - also generates NH4 - not acidic but can be converted to H+ and urea

44
Q

NH4

A

not generally acidic but cna be converted into urea and H+

45
Q

how body protects itself from dietary acid

A 
physiochemical buffering (instantaneous) - CO2/bicarbonate buffer system
respiratory compensation (seconds to hours) - pH is determined by ratio of bicarbonate to PCO2 - if we alter them both in the same direction, the pH isn't going to change - so in acidosis, we hyperventilate to blow off CO2 and thereby return pH toward normal
renal compensation (days)
46
Q

buffering of acid

A

by HCO3
CO2 can be blown away
but bicarboanate doesn’t buffer respiratory acidosis/alkalosis so ICF and bone must buffer all
renal compensations are slow

47
Q

respiratory acidosis

A

too much CO2 - retention of H2CO2
directe effect on blood = decreased pH, increased PCO2
compensate by increasing HCO3 concentration - kidney does this

48
Q

respiratory alkalosis

A

due too little H2CO3 - if we hyperventilate
direct effect on blood = pH increases, PCO2 decreases
compensate by decreasing HCO3 - kidney does this
can differentiate acute change from chronic change by amount of bicarbonate produced

49
Q

metabolic acidosis

A

due to addition of fixed acid or removal of alkali
causes decreased blood pH and decreased blood HCO3
compensate by decreasing PCO2 - hyperventilate

50
Q

metabolic alkalosis

A

due to addition of alkali or loss of fixed acid
increases blood pH and increases blood HCO3
compensate by increasing PCO2 - hypoventilate

51
Q

at high elevation

A

erythropoietin goes up but won’t change PO2 - will breathe harder - hyperventilate - if chronic kidney will adjust and lower bicarbonate concentration - so kidney generated metabolic acidosis (essentially)
come down to sea level - bicarbonate concentration is still low, so there will be a respiratory response to that - lower PCO2

52
Q

anion gap

A

no true gap
difference between cations and anions that are not measured by this formula
used to detect the presence of organic acid formation

53
Q

general scheme for acid excretion

A

has to be excreted in buffered form
main buffer is phosphate
need to reclaim all of bicarbonate first

54
Q

HCO2 reabsorption along nephron

A

80% from PT
10% from ascending LH
5% from DT
5% from CD

55
Q

alpha ICC

A

cell responsible for regulating acid base balance
acid secreting
has H ion pump - secretes H ions at expense of ATP hydrolysis - electrogenic so sensitive to voltage in lumen
also has electroneutral H/K exchanger - sensitive to luminal K concentration
source of H ions = intracellular carbonic acid - C.A. enzyme combines OH+CO2 to make HCO3 and H+
H+ pumped into lumen
HCO3 pumped into blood through HCO3/Cl exchanger - same exchanger mutated in RBCs

56
Q

phosphate and ammonia

A

buffers H+ that’s excreted but there’s not enough to buffer entire acid load
so liver makes urea and we eliminate ammonia
glutamine converted to alphaketoglutarate and ammonium in kidney - ammonium excreted

57
Q

NH4/NH3 handling in PT

A

in PT K/Na exchanger puts NH4 into filtrate - NH4 substitutes for K - in these cells, glutamine take up from blood - this is converted to alphaketoglutarate which generate bicarbonate which is sent back into blood through HCO3/Na cotransporter

58
Q

NH4/3 handling in ascending LH

A

has Na/Cl/K cotransporter but NH4 can substitute for K
NH4 splits into NH3 and H+
H+ sent back into urine via Na/H exchanger
NH3 can’t get through membrane into urine but can get into interstitium so diffuses into interstitum - get ammonium gradient

59
Q

NH3/4 handling in medulla of CD

A

highly permeable to NH3, but impermeable to NH4
NH3 diffuses into cells and into urine
here it’s combined with H+ that’s pumped out
since the cell is impermeable to NH4, the NH4 is stuck in the urine and can now be excreted

60
Q

k depletion and acid/base balance

A

K depletion creates metabolic alkalosis
potassium ions leave cells in exchange for H+
therefore K exit leads to intracellular acidification
a low intracellular pH stimulates H+ secretino throughout the nephron and also increases NH4 production by the PT
K+ and NH4+ compete with each other on several transporters and therefore hypokalemia also facilitates NH4 excretion

61
Q

Na balance and acid/base balance

A

in PT and LH, Na reabsorption and H+ secretion are directly coupled (via Na/H exchange)
in the CD Na reabsorption and H+ secretion are linked indirectly
because of the coupling of Na reabsorption to H+ secretion, ECFV depletion promotes the development of metabolic alkalosis

62
Q

aldosterone on A/B balance

A

in CD, get increase in Na transport in CD - increases lumen negative voltage - increases H ion secretion by alpha-ICC cells
also directly activates ICC cell pumps
some K secretion increase too from CD cells, so get more K to fuel ICC cell H/K exchanger

63
Q

urinary anion gap

A

Na + K concentrations - cl concentration
looking for cation = ammonium
becomes negative if the gut is the problem

renal term 2 quizzes 1 and 2 (3 decks)

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