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RENAL II, Test 2 > Random Kidney Review > Flashcards

Random Kidney Review Flashcards

1
Q

blood flow through kidney?

A

renal aa -> arcuate artery - affarent arteriole - glomerular capillaries - efferent arterioles - peritubular capillaries - vasa recta - arcuate v –> renal v.

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2
Q

kidney autoregulation of blood flow?

A
  1. myogenic response: when smooth mm. is stretched it contracts
  2. tubuloglomerular feedback (TGF): increased MAP leads to increase in RBF and GFR. high delivery of sodium ions to macula densa (TAL/DT) –> results in adenosinie and ATP secretion –> vasoconstriction of afferent arteriole –> decreased RBF and GFR
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3
Q

essential HTN? how does that affect the GFR? renal artery stenosis?

A

increased renal artery pressure –> vasoconstriction of affarent arterioles and vasodilation of efferent aa.

—-> high pressure in the JG apparatus –> decreased renin secretion –> low AngII –> vasodilation of efferent arterioles

patient w/ renal artery stenosis has low renal artery pressures –> low pressure at affarent arterioles: vasodilation of affarent arterioles vosconstriction of efferent arterioles (leads to increased renin secretion and increased ANGII)

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4
Q

nephrogenic DI?

A

ADH receptors are functioning and it not possible to increase reabsorption at CD

patient loses free water and develops hypernatremia

tx is reduction of EC volume w/ thiazide diuretic = increases peritubular oncotic pressure, increases water reabosprtion in PT

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5
Q

effects of symp. NS on the kidney?

A

causes vasoconstriction of arterioles, has greater effect on affarent arteriole

thus RPF PGC, PPC and GFR decrease, FF increases

the oncotic pressure of the PC increases
greater forces promote reabsorption in the peritubular capillaries b/c of low peritubular capillary hydrostatic pressure and increase in plasma oncotic pressure (FF increases)

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6
Q

effects of ANG II?

A

ANG II is vasoconstrictor, constricts both affarenent and efferent arterioles, but has bigger effect on efferent arteriole

RPF decreases
PGC increases
GFR increases
FF increases 
PPC decreases
oncotic pressure in PC increases

thus increased forces promototing reabsorption in the peritubular capillaries b/c of lower peritubular capillary hydrostatic pressure and increase in plasma oncotic pressure (FF increases)

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7
Q

kidneys rxn to stress?

A

symp input and ANGII secretion increased –> vasoconstriction of affarent and efferent arterioles –> drop in RPF and only small drop in GFR

results in net increase in FF –> increase in oncotic pressure –> increase in reabsorption in PTs

overall less fluid is filtered and greater percentagle of fluid is reabsorbed in the PT, leading to preservation of volume in volume depleted state

increase in ADH due to low volume state, and increased renin release

net effect of ANGII is to preserve GFR in volume-depleted state (and for it to not be too large of decrease in GFR)

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8
Q

what causes an increase in FF?

A

decrease in glomerular capillary flow –> results in increased oncotic Peritubular capillary pressure and also decreased PPC - resulting in net increase in reabsorption in the peritubular capillaries of fluid

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9
Q

transport mechanisms?

A

simple diffusion = ions movming down EC gradient, no energy reqd

facilitated diffusion = molecule or ion moving across membrane down its concentration attached to specific membrane bound protein - doesn’t req energy

active transport: protein mediated transport using ATP

Uniport: transporter moves molecule down gradient = facilitated diffusion

symport: coupled transport of solutes in same direction

antiport = mvmt of two solutes in opp. dxn

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10
Q

secondary active transport

A

Na/K ATPase establishes low intracelluar sodium concentration, creating large gradient across cell membrane for sodium on the luminal side to transport glucose via secondary active transport

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11
Q

inulin

A

amount filtered = amout excreted

clearance of inulin is independent of plasma concentration - lies on the X axis (rise in plasma concentration results in rise in plasma filtered load)

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12
Q

creatine

A

freely filtered and very small amount is secreted

- thus creatine clearance always parallels inulin and is slightly higher

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13
Q

calculate reabsorption rate

A

= filtered load - excretion rate
= (GFRxPx) - (Ux x V)
= (GFR x Plasma glucose) - (Urine glucose x urine flow)

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14
Q

clearance

A

= theoretical volume of plasma from which a substance is removed over a period of time

= if substance has concentration of 4 molecules/L and excretion is 4 molecules/min = then the volume of plasma cleared of x is IL/min

Clearance = Excretion rate of x / plasma concentration of X 
Clearance = (Ux * V) / Px
Clearance = (urine concentration of X * Urine flow rate) / plasma concentratino of X
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15
Q

measures of GFR

A

would use inulin as gold standard b/c it is freely filtered and not reabsorbed or secreted

clinically use Creatinine b/c its released from skeletal mm. at constant rate protpprtional to mm. mass

creating production = creatine excretion = filtered load of creatinine = Plasm Creatinine x GFR

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16
Q

glucose

A

at low plasma levels, clearance is zero

at high plasma levels glucose appears in urine

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17
Q

PAH

A

at low plasma concentrations the clearance equals renal plasma flow
as plasma concentration rises the carriers hit TM and results in some PAH appearing in renal venous plasma
Plasma concentrations above TM reduce the clearance of PAH

as plasma levels rise further the clearance approaches but never equals GFR b/c some PAH is always secreted

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18
Q

highest to lowest clearance?

A

PAH > creatinine> inulin > urea > sodium > glucose = albumin

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19
Q

urea

A

freely filtered but partially reabsorbed

ADH increases reabsorption of urea in medullary CD –> increasing BUN –> decreasing clearance

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20
Q

proximal tubule:

A

Na+: 2/3 reabsorbed here: sympathetic and Ang II stimulate basolateral ATPase and enhance fraction of Na+ absorbed here

Water reabsorbed here, glucose reabsorbed, 80% bicarbonate reabosrbed here

potassium and AAs also absorbed ehre

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21
Q

bicarb reabsorption?

A

bicarb combines w/ luminal H+ and is converted to water and CO2 by luminal carbonic anhydrase

H+ is pumped into the lumen via sodium antiporter along with an H+ ATPase on the luminal membrane

CO2 is very soluble and crosses the luminal membrane where it combines with water to reform H+ and bicarb due to the CA in the cell

H+ is pumped back into the lumen while bicarbonate exits the basolateral membrane

Ang II stimulates the Na+/H+ antiporter, thus in volume depleted states, the amount of bicar reabsorbed in PT increases –> contraction alkalosis

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22
Q

contraction alkalosis?

A

thiazides, sweating in desert, vomiting…

low volume state –> increase in renin/AngII –> activation of sodium/hydrogen exhcnager via AngII –> increased reabsorption of bicarb and metabolic alkalosis ensues f

23
Q

loop of Henle?

A

descending loop = water reabsorption

Thick ascending limb: sodium reabsorption via Na+/K+/2Cl- cotransporter

Increase in K+ concentration in the cells causes back diffusion of K+ into the tubular lumen, allowing a lumen-positive electrical potential to drive reabsorption of cations (Mg2+, Ca2+) via the paracellular pathway

24
Q

Calcium sensing receptor

A

basolateral membrane of cells in ATL contain CaSR, which is influenced by plasma concentration of calcium

when there is high level of blood calcium it inhibits Na/K/Cl- transporter = results in reduction of K+ back diffusion and no positive luminal potential

thus Ca2 not reabsorbed as much in TAL

25
Q

Distal convoluted tubule

A

NaCl crosses membrane due to cotransporter

26
Q

Principal cells in CD

A

This is where aldosterone acts

  • have Epithelial sodium channel (ENaC) thus sodium flow in following its gradient: creates a negative luminal potential
  • K+ has high level in cell and thus moves through a channel into the lumen
  • ALDOSTERONE results in net influx of Na+ and excretion of K+

THUS hypokalemia is seen with metabolic alkalosis due to increased ALDO secretion

Principal cells also express aquaporins which are regulated by ADH and result in water and urea reapsorption

27
Q

Intercalated cells in CD

A
  • involved in acid base regulation
  • luminal membrane has H+ ATPase which pumps H+ into the lumen, combines with ammonia and is excreted as urea
  • for every H+ excreted, bicarb is adde to the body

ALDO stimulates the H+/ATPase of intercalated cells restulting in metabolic alkalosis

28
Q

Proximal Renal tubular acidosis?

A

due to diminished capacity of proximal tubule to rebsorb bicarb

  • see low plasma bicarb and acid urine
  • serum potassium is low, when bicarb is lost in urine, it is lost as sodium bicarb and that pulls water with it creating osmotic diuresis
  • diuresis leads to loss of potassium in urine
29
Q

Distal renal tubular acidosis

A

due to inability of distal nephron to excrete fixed acid
results in metabolic acidosis w/ high urine pH
and hypokalemia

30
Q

what changes rate of potassium excretion?

A

increased flow (diuresis) or ALDO = increased potassium secretion

decreased flow (antidiuresis) or low ALDO = decreased potassium secretion

31
Q

what promotes hyperkalemia?

A

metabolic acidosis
CKD
hypoaldosteronism

consequences: mm. weakness, general fatigue, ventricular fibrillation, metabolic acidosis

32
Q

promoters of hypokalemia?

A

metabolic alkalosis
increase in insulin or sympathetic stimulation
diarrhea, vomiting, low potassium diet
diuretics, hyperaldosteronism (adrenal adenoma or renal arterial stenosis)

consequences:
mm. weakness and fatigue, metabolic alkalosis

33
Q

acute renal failure

A

loss of renal function , results in accumulation of waste products (BUN and CR)

34
Q

pre renal

A

decreased renal perfusion due to decreased renal perfusion pressure (hypovolumia, hemorrhage, diarrhea, vomiting, CHF)

see reduced GFR
Na+ reabsorption is increased due to Ang II and catecholamines elevated

elevated BUN:Cr ; both are elevated, the high reabsorption of urea (water reabsorption is elevated and urea through aquaporin channels) - causes BUN elevation more the Cr

35
Q

intrarenal

A

tubular damage occurs resulting in tubular dysfunction
ex: toxins, interstitial nephritis, ischemia, rhabdomyolysis, sepsis

See decreased reabsorption of Na+
See casts/cells in urine
Low plasma BUN:Cr - tubular damage prevents reabsorption of urea

36
Q

Postrenal

A

caused by obstruction of fluid outflow from kidneys
ex: renal calculi, enlarged prostate

Early: characteristics are similar to prerenal - elevated BUN:Cr
Late: build up of pressure results in tubular damage and causes intrarenal failure, so see low plasma BUN:Cr

37
Q

Chronic renal failure

A

see inability to excrete waste products: rise in plasma BUN and Cr

Inability to regulate water and sodium = hyponatermia, volume overload and edema

hyperkalemia and metabolic acidosis

hyperphosphatemia , reduces plasma calcium, cause ing rise in PTH and bone resoprtion (renal osteodystrophy)

inability to excrete EPO –> anemia

38
Q

normal values

A 
pH = 7.4
PCO2 = 40 mm Hg
HCO3- = 24 mEq/L
39
Q

4 primary disturbances?

A

resp acidosis = too much CO2
Met acidosis = addition of H+ or loss of bicarb
resp alkalosis = not enough CO2
met alkalosis = loss of H+ or addition of base

if CO2 and HCO3- go in opposite directions it is probably a mixed disorder

40
Q

measuring anion gap

A

Na+ - (Cl + HCO3-)

normal PAG = 12 +/- 2

41
Q

Isosmotic volume contraction

A

Osmolarity remains the same in ECF & ICF
Only changes ECF volume (ICF remains unchanged)
Examples: vomiting& diarrhea, hemorrhage/

42
Q

Isosmotic volume expansion

A

Osmolarity remains the same in ECF & ICF
Only changes ECF volume (ICF remains unchanged)
ex: infusion of 0.9% NaCl

43
Q

Hyperosmotic volume contraction

A

loss of water
Osmolarity of ECF increases as ECF volume decreases
ICF volume decreases as water shifts from ICF to equilibrate osmolarity
Examples: dehydration; diabetes insipidus

44
Q

Hyperosmotic volume expansion

A

(gain of NaCl):
Osmolarity of ECF increases as ECF volume increases
ICF volume decreases as as water shifts from ICF to equilibrate osmolarity
Examples: excess NaCl intake; mannitol infusion

45
Q

Hyposmotic volume contraction

A

(loss of NaCl):
Osmolarity of ECF decreases as ECF volume decreases
ICF volume increases
Examples: hypoaldosteronism; adrenal insufficiency

46
Q

Hyposmotic volume expansion

A

(gain of water):
Addition of pure water decreases ECF osmolarity
Water proportionately increases ECF and ICF volumes
Examples: SIADH; psychogenic polydipsia

47
Q

body fluid compartments

A 
total = 42 L
ECF = 14 L 
Plasma = 4 L
48
Q

contraction of mesangial cells

A

shortens capillary loops and thus lowers GFR

49
Q

symp stimulation

A

Constriction of afferent and, to a lesser extent, efferent arterioles: ↓RBF, ↓GFR
Diverts the renal fraction to vital organs
Increased renin secretion by granular cells
Angiotensin II thus produced restores blood pressure (systemic vasoconstriction)
Angiotensin II promotes arteriolar constriction (efferent > afferent): raises blood pressure, may stabilize GFR (moderate ang II)
Stimulates Na+ reabsorption in proximal tubule, thick ascending limb of Henle’s loop, distal convoluted tubule, collecting duct

50
Q

clearance

A

creatinine clearance ~ GFR

CL = Ux * V / Px

51
Q

ALDO, ANP, ADH

A

Aldosterone stimulates Na+ reabsorption, K+ secretion, H+ secretion in this segment

Atrial natriuretic peptide inhibits Na+ reabsorption (medullary collecting duct)

Antidiuretic hormone [aka arginine vasopressin (AVP)] stimulates water reabsorption

52
Q

what does ANP do?

A

ANP increases GFR: Afferent arteriolar dilation, efferent arteriolar constriction
ANP inhibits Na+ reabsorption in medullary collecting duct
ANP suppresses renin secretion
ANP suppresses aldosterone secretion
ANP is a systemic vasodilator
ANP suppresses AVP secretion, actions

53
Q

osmolar gap

A

Plasma solute concentration, mOsm/kg H2O =
(2 · Na+, mEq/l) + (glucose, mg/dl / 18) + (BUN, mg/dl / 2.8)

Osmolar gap: Difference between plasma osmolality estimated as above and true plasma osmolality measured with an osmometer. Normally < 10 mOsm/kg H2O

RENAL II, Test 2 (5 decks)

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