Random Kidney Review

Question 1

blood flow through kidney?

Answer 1

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

Question 2

kidney autoregulation of blood flow?

Answer 2

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

Question 3

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

Answer 3

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)

Question 4

nephrogenic DI?

Answer 4

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

Question 5

effects of symp. NS on the kidney?

Answer 5

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)

Question 6

effects of ANG II?

Answer 6

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)

Question 7

kidneys rxn to stress?

Answer 7

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)

Question 8

what causes an increase in FF?

Answer 8

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

Question 9

transport mechanisms?

Answer 9

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

Question 10

secondary active transport

Answer 10

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

Question 11

inulin

Answer 11

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)

Question 12

creatine

Answer 12

freely filtered and very small amount is secreted

- thus creatine clearance always parallels inulin and is slightly higher

Question 13

calculate reabsorption rate

Answer 13

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

Question 14

clearance

Answer 14

= 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

Question 15

measures of GFR

Answer 15

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

Question 16

glucose

Answer 16

at low plasma levels, clearance is zero

at high plasma levels glucose appears in urine

Question 17

PAH

Answer 17

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

Question 18

highest to lowest clearance?

Answer 18

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

Question 19

urea

Answer 19

freely filtered but partially reabsorbed

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

Question 20

proximal tubule:

Answer 20

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

Question 21

bicarb reabsorption?

Answer 21

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

Question 22

contraction alkalosis?

Answer 22

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

Question 23

loop of Henle?

Answer 23

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

Question 24

Calcium sensing receptor

Answer 24

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

Question 25

Distal convoluted tubule

Answer 25

NaCl crosses membrane due to cotransporter

Question 26

Principal cells in CD

Answer 26

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

Question 27

Intercalated cells in CD

Answer 27

- 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

Question 28

Proximal Renal tubular acidosis?

Answer 28

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

Question 29

Distal renal tubular acidosis

Answer 29

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

Question 30

what changes rate of potassium excretion?

Answer 30

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

Question 31

what promotes hyperkalemia?

Answer 31

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

Question 32

promoters of hypokalemia?

Answer 32

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

Question 33

acute renal failure

Answer 33

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

Question 34

pre renal

Answer 34

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

Question 35

intrarenal

Answer 35

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

Question 36

Postrenal

Answer 36

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

Question 37

Chronic renal failure

Answer 37

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

Question 38

normal values

Answer 38

``` pH = 7.4 PCO2 = 40 mm Hg HCO3- = 24 mEq/L ```

Question 39

4 primary disturbances?

Answer 39

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

Question 40

measuring anion gap

Answer 40

Na+ - (Cl + HCO3-) normal PAG = 12 +/- 2

Question 41

Isosmotic volume contraction

Answer 41

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

Question 42

Isosmotic volume expansion

Answer 42

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

Question 43

Hyperosmotic volume contraction

Answer 43

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

Question 44

Hyperosmotic volume expansion

Answer 44

(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

Question 45

Hyposmotic volume contraction

Answer 45

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

Question 46

Hyposmotic volume expansion

Answer 46

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

Question 47

body fluid compartments

Answer 47

``` total = 42 L ECF = 14 L Plasma = 4 L ```

Question 48

contraction of mesangial cells

Answer 48

shortens capillary loops and thus lowers GFR

Question 49

symp stimulation

Answer 49

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

Question 50

clearance

Answer 50

creatinine clearance ~ GFR CL = Ux * V / Px

Question 51

ALDO, ANP, ADH

Answer 51

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

Question 52

what does ANP do?

Answer 52

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

Question 53

osmolar gap

Answer 53

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