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CRRAB 1 > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

3 Body Fluid Compartments

A

1 - plasma
2- interstitial fluid
3 - intracellular fluid

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2
Q

Anion Gap

A

Na+ - (Cl + HCO3)

- index of albumin ~10-14

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3
Q

Osmolarity/Osmolality

A

total free solute concentration measured as millimoles of total free solute/liter or kg

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4
Q

Milliosmoles

A

units of osmolarity

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5
Q

Osmolarity of plasma

A

~300 mOsms/kg (technically 292)

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6
Q

Osmolarity of water

A

0 osOsms/kg

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7
Q

Isosmotic

A

in medicine -> osmolality of 300 mOsms

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8
Q

Isotonic

A

any solution that does NOT change cell volume

ex. ISF

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9
Q

Isoncotic

A

any solution with 1 mM plama albumin or 4.5 g albumin/100 mL

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10
Q

Protein Osmotic Pressure

A

~25 mmHg

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11
Q

Drink water

A
  • Increase Pc (capillary pressure)
  • decrease mOsms of capillary
  • decrease [Alb] of capillary
  • decrease mOsms of ISF
  • water distributes to all 3 compartments proportional to volume of compartment
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12
Q

Normal Saline infusion

A

Normal saline is 0.9% NaCl or 154 mM NaCl ~300 mOsms

  • isotonic and isosmotic
  • increase Pc
  • no effect of mOsms of capillary
  • decrease [Alb] in capillary
  • no change in mOsms of ISF
  • Na/K pump keeps Na out of cells
  • only distributes to Plasma and ISF
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13
Q

Isoncotic infusion (artificial plasma)

A

~1 mM albumin in normal saline

  • increase Pc
  • no change in mOsms in capillary
  • no change in [Alb] in capillary
  • H2O goes into ISF which causes [Alb] to increase which draws water back into plasma
  • this solution brings pressure back up the fastest
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14
Q

5% dextrose solution infusion

A

isosmotic
distributes to all 3 compartments based on proportion of volume just like water
glucose gets metabolized and disappears –> has calories

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15
Q

Important Kidney Functions

A
  1. Homeostasis –> water and solute balance
  2. Waste products
  3. Regulation of MAP
  4. [H+] - acid/base balance
  5. Endocrine organ
    - EPO, active Vit D, Renin
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16
Q

Triple Filtration of glomerulus

A
  1. Capillary endothelium (fenestrations)
  2. Glomerular Basement Membrane
  3. Podocytes with filtration slits
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17
Q

Minimal change disease

A

disease of podocytes –> they are “backed away” from the glomerular capillary and large amounts of albumin get into the urine

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18
Q

GoodPasture syndrome

A

autoantibodies target the GBM –> loss of glomerular filtration

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19
Q

GFR

A

combined rate of fluid movement from glomerular capillary lumen to Bowman’s space for all nephrons in both kidneys

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20
Q

Renal Plasma Flow

A

600 ml/min

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21
Q

Vasoconstricion of Afferent arteriole (NE)

A

decrease Pgc
decrease RPF
decrease GFR

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22
Q

Vasoconstriction of Efferent arteriole (Ang II)

A

increase Pgc
decrease RPF
increase GFR

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23
Q

Vasoconstriction of both Afferent and Efferent

A

no change in Pgc
decrease RPF
no change in GFR

24
Q

Filtered Load of Solute

A

GFR x [free plasma concentration of solute]

25
Q

Excretion Rates of Solute

A

Urine flow rate x [urinary concentration of solute]

26
Q

Creatinine

A

all creatinine and is filtered is excreted!!!
- if creatinine increases in plasma –> GFR is falling
GFR = (urine flow rate x [Cr]u)/[Cr]p

27
Q

Nephron reabsorption

A

substance goes from proximal tubule to peritubular capillaries

28
Q

Nephron secretion

A

substance goes from peritubular capillaries to proximal tubule

29
Q

Na+ reabsorption

A 
basolateral Na/K ATPase coupled with luminal passive Na entry --> transepithelial Na movement
Passive movement 
1. Na/H antiporter
2. Na/Glucose symporter
3. Na/AA symporter
30
Q

Glucose and AA reabsorption

A

Glucose and AA are pumped against their electrochemical gradient into the cell by secondary active transport with Na symporter
- then they go through their respective uniporters via facilitated diffusion

31
Q

Cl- reabsorption

A

Cl- is brought into cell via the Cl/formate antiporter (Cl- gets pumped up its gradient)
Cl- then moves into plasma through channel or K/Cl- symporter
- Formate is moved into lumen of proximal tubule by Cl/formate antiporter –> couples with H+ to form non-ionized formate –> crosses luminal membrane –> dissociates into H+ and formate

32
Q

H2O reabsorption

A

as solutes leave the lumen of proximal tubule, the contents in the lumen become slightly hypoosmotic

  • this is corrected when H2O follows solutes via AQP 1 and simple diffusion across membrane
  • water is then reabsorbed into peritubular capillaries
33
Q

HCO3 reabsorption

A

HCO3 in the lumen of proximal tubule is destroyed by C.A. as its converted to CO2 and H2O
But, intracellularly the CO2 and H2O are being converted back into HCO3 by C.A.
HCO3 then is transported across basolateral membrane along with Na+ into peritubular capillaries

34
Q

Net Reabsorption

A

Filtered load of substance X - excretion rate of substance X

35
Q

Polar vs. Nonpolar molecules

A

Polar molecules become trapped in the proximal tubule and excreted in urine without specific transporters or channels (waste products, toxins)
Nonpolar molecules become reabsorbed in proximal tubule because of ability to diffuse across membrane into peritubular capillaries

36
Q

WOA and WOB

A

polar molecules –> metabolites of drugs, foreign chemicals –> excreted

37
Q

MCAs

A

lactate, pyruvate, ketone bodies
- cross luminal membrane via secondary active transport with Na+
Diffuse across basolateral membrane and reabsorbed into peritubular capillaries

38
Q

Ketouria

A

occurs when person is starving/fasting. Body is breaking down so much fat that there are too many ketone bodies in the urine and the pump becomes saturated –> ketones end up in the urine

39
Q

Juxtamedullary nephrons

A

nephrons that send their loops down into the medulla

40
Q

As nephron goes down into medulla, what happens to osmolarity?

A

Osmolarity drastically increases as you descend medulla, reaches 1400 mOsms

41
Q

Descending limb of loop of henle

A

Impermeable to solute, only water moves!

42
Q

Thick ascending limb of loop of henle

A

Impermeable to water, only solute moves!

  • has Na, K, 2Cl transporter (2nd AT)
  • responsible for 20% of Na reabsorption
  • lasix blocks Na, K, 2Cl transporter
43
Q

Bartter’s syndrome

A

Loss of function of Na, K, 2Cl is TAL

44
Q

Distal tubule

A

still impermeable to water

  • 5% Na reabsorption
  • has NaCl transporter (sensitive to Thiazides)
45
Q

Gitelman’s Syndrome

A

Loss of function of NaCl symporter in distal tubule

46
Q

Principal Cells

A
  • located in distal tubule/collecting duct
  • sensitive to aldosterone
  • responsible for 0-4.9% of Na reabsorption
47
Q

Aldosterone

A

steroid hormone

  • enters and translocates to nucleus and binds SREs –> increased transcription, translation, and insertion of luminal ENaC channels as well as basolateral Na/K pumps
  • end result = more Na reabsorption
48
Q

Type I Pseudo-hypoaldosteronism

A

loss of function of luminal ENaC channels in principal and collecting duct cells

49
Q

Liddle’s Syndrome

A

gain of function of ENaC channels in principal and collecting duct cells
Salt sensitive HTN

50
Q

Angiotensin II functions

A
  1. stimulates aldosterone receptors
  2. powerful vasoconstrictor
  3. stimulates proximal tubule Na/H exchange
  4. stimulates vasopressin
  5. increases SNS activity
51
Q

K+ reabsorption

A

55-65% of K reabsorbed in proximal tubule

80-90% of K reabsorbed before fluid arrives at principal cell

52
Q

Principal Cell

A

During high K+ diet……
secrete K+ into nephron lumen to achieve K+ homeostasis
- ROMK channels = aldosterone sensitive –> K+ excretion
- BK channels = K+ sensitive –> leads to K+ excretion

53
Q

Low K+ diet

A

BK and ROMK channels not expressed
instead, alpha or type A intercalated cells actively reabsorb K+
hypokalemia often accompanied by alkalosis (loss of K+)

54
Q

Ca balance

A

regulated by PTH
decrease in [Ca]plasma –> calcium-sensing receptor on surface of parathyroid cell –> increase PTH –> return of [Ca]plasma

55
Q

4 processes of Ca regulation

A
  1. PTH inhibits osteoblasts and stimulates osteoclasts to reabsorb Ca from bones
  2. PTH stimulates renal activation of Vit D –> increases intestinal Ca reabsorption
  3. PTH stimulates renal Ca reabsorption
  4. PTH reduces renal H2PO4 reabsorption
56
Q

PTH stimulating renal Ca reabsorption

A

PTH binds to PTH receptor on basolateral side on distal convulted tubule –> increased luminal Ca channel expression –> Ca flows into cell from lumen via Calbindin –> Ca pumped into capillaries via Na/Ca antiporter and Ca-ATPase

57
Q

Disease kidney affects Ca stores how?

A

decrease in renal production of active Vit D –> decreased intestinal reabsorption of Ca –> decrease [Ca]plasma –> increased PTH –> bone resorption –> weak bones

CRRAB 1 (18 decks)

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