Etc. I Flashcards
2 major causes of edema
Changes in the capillary hemodynamics.
Renal retention of dietary Na and water expansion of ECF.
Non-pitting edema is due to:
Swollen cells due to increased ICF
Pitting edema is due to:
Increased interstitial volume.
Crystalloids
Do not cross the PM - remain in the ECF and can easily diffuse between compartments of the ECF. Increase ECF vol.
Colloids
Cannot pass semipermeable membranes and remin in the vessels. Must be given IV and expand the intravascular volume.
Plasma osmolarity equation
Range
2Na + Glc/18 + BUN/2.8
Range is 275-295
Hypotonic/natremic dehydration
Loss of Na is greater than the loss of water.
Fluid shifts from ECF to ICF.
Serum sodium/osm is less than normal.
Hypertonic/natremic dehydration
Loss of water is greater than loss of Na.
Fluid shifts from ICF to ECF.
Serum sodium/osm is greater than normal.
Isoosmotic volume contraction
Acute loss of isoosmotic fluid.
Decrease in ECF, no change in ICF or osm.
Hyper-osmotic volume contraction
Loss of hypotonic fluid (dehydration, diabetes, alcoholism).
Decrease in ECF and ICF, increase in osm.
Isoosmotic volume expansion
Gain of isoosmotic fluid.
Increase in ECF, no change in ICF or osm.
Hypoosmotic volume expansion
Gain of hypoosmotic fluid.
Increase in ECF and ICF, decrease in osm.
Gibbs-Donnan effect
Proteins are largely negative and cannot cross the PM.
This provides both an oncotic and electrical gradient to attract molecules.
3 layers of the glomerular filtration barrier
Capillary endothelium
Glomerular BM
Podocyte epithelium
Filtered load =
[X] x GFR
Urinary excretion =
Filtrate - amt reabsorbed + amt secreted
Reabsorption =
Filtrate - excretion + amt secreted
Urinary excretion rate =
(Ux) x V
Ux is urine conc of X and V is urine flow rate
Renal clearance definition
Vol of plasma completely cleared of a substance by the kidneys per unit time
Cx =
(Ux x V)/Px
Characteristics if glomerular filtrate
Protein free
Cell free
Isoosmotic
20% of RBF
FF =
GFR/RBF
Inulin
Freely filtered at the glomerulus.
Not reabsorbed or secreted.
Not ideal.
Creatinine
Used clinically.
10% secreted.
Used to measure GFR.
Vasocontriction
RAAS
Na/K ATPase
Receptors
a1
B1
a1
Prerenal problem
> 20:1 BUN/creatinine
Hypovolemia, dehydration, high protein diet
Intrarenal problem
<10:1 bun/creatinine
Liver dz
Low protein diet
PAH
Best way to measure GFR, but needs to be administered in an IV
Net filtration =
GPC - piGC - PBC
3 factors influencing GFR
Hydraulic conductivity (Lp) Surface area (Sf) Capillary ultrafiltration pressure (PUF) GFR = Lp x Sf x PUF
PGC is affected by:
Renal BP
Afferent resistance
Efferent resistence
Kf =
Lp x Sf
Function of mesangial cells:
Adjust Sf
Relationship between PUF and piGC
Inverse.
As filtrate leaves the capillary, the oncotic pressure will increase.
Which end of the arteriole is more regulated by symapthetics?
Afferent. More a1 receptors.
Constriction of the afferent arteriole causes:
GFR
RBF
PGC
Decrease in all
Constriction of efferent arteriole causes:
GFR
RBF
PGC
GFR up then down due to RBF.
RBF down
PGC up
Vasodilators
PGs NO Bradykinin DA ANP
Vasoconstrictors
Synpathetics
Angiotensin II
Endothelin
Myogenic reflex
BVs stretch due to increase in BP.
SM contracts.
AA constricts and EA dilates.
Tubuloglomerular feedback with increased renal perfusion pressure (5)
- Increased RBF and GFR
- Increased delivery of NaCl
- Release of adenosine
- Resistance of AA
- Decreased RBF and GFR
Tubuloglomerular feedback with decreased renal perfusion pressure
- Decreased GFR and RBF
- Decreased delivery of NaCl
- Release renin leading to increased EA resistance OR release of NO leading to decreased AA resistance.
Dilation of the AA
RBF, GFR, PGC
All increase
Constrict AA
RBF, GFR, PGC
All down
Dilation of EA
RBF, GFR, PGC
RBF up
GFR down
PGC up
Constriction of EA
RBF, GFR, PGC
RBF down
GFR up
PGC down
NaH exchanger location, function
PCT, reabsorption of Na and bicarb.
AQP-1 is present in:
PCT
AQP-2 is present in:
What is special about them?
CD
They are under the control of ADH
AQP and TJ availability in both regions of the LoH
Many AQP and few TJ in descending loop.
No AQP and many TJ in ascending loop.
SGLT1
SGLT2
And their location
SGLT1 is low affinity and in S3
SGLT2 is high affinity and in S1
How is Glc reabsorbed?
Exchanged for Na against its gradient
What is the diluting segment? Why?
Thick ascending limb of LoH.
Because it sends out a lot of Na and therefore has lots of Na/K pumps.
Where does furosemide act?
Thick ascending limb via blocking Cl- binding on the Na-K-2Cl transporter
What transporter helps reabsorb some Na in the DCT?
Na-Cl transporter
Where do thiazides act?
What else do they do?
DCT on the Na-Cl transporter
Reduce excretion of Ca and reduce risk of kidney stones.
What causes the release of aldosterone? Other than increasing BP, what does it cause?
Increased plasma K+.
Reabsorption of Na and excretion of K.
K+ sparing spirolactone
Inhibits Na/K exchange in the DCT and CD.
Promotes K retention and Na/water loss.
