Renal Physiology Flashcards
1
Q
3 Body Fluid Compartments
A
1 - plasma
2- interstitial fluid
3 - intracellular fluid
2
Q
Anion Gap
A
Na+ - (Cl + HCO3)
- index of albumin ~10-14
3
Q
Osmolarity/Osmolality
A
total free solute concentration measured as millimoles of total free solute/liter or kg
4
Q
Milliosmoles
A
units of osmolarity
5
Q
Osmolarity of plasma
A
~300 mOsms/kg (technically 292)
6
Q
Osmolarity of water
A
0 osOsms/kg
7
Q
Isosmotic
A
in medicine -> osmolality of 300 mOsms
8
Q
Isotonic
A
any solution that does NOT change cell volume
ex. ISF
9
Q
Isoncotic
A
any solution with 1 mM plama albumin or 4.5 g albumin/100 mL
10
Q
Protein Osmotic Pressure
A
~25 mmHg
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
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
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
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
15
Q
Important Kidney Functions
A
- Homeostasis –> water and solute balance
- Waste products
- Regulation of MAP
- [H+] - acid/base balance
- Endocrine organ
- EPO, active Vit D, Renin
16
Q
Triple Filtration of glomerulus
A
- Capillary endothelium (fenestrations)
- Glomerular Basement Membrane
- Podocytes with filtration slits
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
18
Q
GoodPasture syndrome
A
autoantibodies target the GBM –> loss of glomerular filtration
19
Q
GFR
A
combined rate of fluid movement from glomerular capillary lumen to Bowman’s space for all nephrons in both kidneys
20
Q
Renal Plasma Flow
A
600 ml/min
21
Q
Vasoconstricion of Afferent arteriole (NE)
A
decrease Pgc
decrease RPF
decrease GFR
22
Q
Vasoconstriction of Efferent arteriole (Ang II)
A
increase Pgc
decrease RPF
increase GFR
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
Excretion Rates of Solute
Urine flow rate x [urinary concentration of solute]
26
Creatinine
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
Nephron reabsorption
substance goes from proximal tubule to peritubular capillaries
28
Nephron secretion
substance goes from peritubular capillaries to proximal tubule
29
Na+ reabsorption
```
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
Glucose and AA reabsorption
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
Cl- reabsorption
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
H2O reabsorption
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
HCO3 reabsorption
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
Net Reabsorption
Filtered load of substance X - excretion rate of substance X
35
Polar vs. Nonpolar molecules
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
WOA and WOB
polar molecules --> metabolites of drugs, foreign chemicals --> excreted
37
MCAs
lactate, pyruvate, ketone bodies
- cross luminal membrane via secondary active transport with Na+
Diffuse across basolateral membrane and reabsorbed into peritubular capillaries
38
Ketouria
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
Juxtamedullary nephrons
nephrons that send their loops down into the medulla
40
As nephron goes down into medulla, what happens to osmolarity?
Osmolarity drastically increases as you descend medulla, reaches 1400 mOsms
41
Descending limb of loop of henle
Impermeable to solute, only water moves!
42
Thick ascending limb of loop of henle
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
Bartter's syndrome
Loss of function of Na, K, 2Cl is TAL
44
Distal tubule
still impermeable to water
- 5% Na reabsorption
- has NaCl transporter (sensitive to Thiazides)
45
Gitelman's Syndrome
Loss of function of NaCl symporter in distal tubule
46
Principal Cells
- located in distal tubule/collecting duct
- sensitive to aldosterone
- responsible for 0-4.9% of Na reabsorption
47
Aldosterone
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
Type I Pseudo-hypoaldosteronism
loss of function of luminal ENaC channels in principal and collecting duct cells
49
Liddle's Syndrome
gain of function of ENaC channels in principal and collecting duct cells
*Salt sensitive HTN*
50
Angiotensin II functions
1. stimulates aldosterone receptors
2. powerful vasoconstrictor
3. stimulates proximal tubule Na/H exchange
4. stimulates vasopressin
5. increases SNS activity
51
K+ reabsorption
55-65% of K reabsorbed in proximal tubule
| 80-90% of K reabsorbed before fluid arrives at principal cell
52
Principal Cell
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
Low K+ diet
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
Ca balance
regulated by PTH
decrease in [Ca]plasma --> calcium-sensing receptor on surface of parathyroid cell --> increase PTH --> return of [Ca]plasma
55
4 processes of Ca regulation
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
PTH stimulating renal Ca reabsorption
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
Disease kidney affects Ca stores how?
decrease in renal production of active Vit D --> decreased intestinal reabsorption of Ca --> decrease [Ca]plasma --> increased PTH --> bone resorption --> weak bones
