Etc. I Flashcards

1
Q

2 major causes of edema

A

Changes in the capillary hemodynamics.

Renal retention of dietary Na and water expansion of ECF.

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2
Q

Non-pitting edema is due to:

A

Swollen cells due to increased ICF

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3
Q

Pitting edema is due to:

A

Increased interstitial volume.

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4
Q

Crystalloids

A

Do not cross the PM - remain in the ECF and can easily diffuse between compartments of the ECF. Increase ECF vol.

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5
Q

Colloids

A

Cannot pass semipermeable membranes and remin in the vessels. Must be given IV and expand the intravascular volume.

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6
Q

Plasma osmolarity equation

Range

A

2Na + Glc/18 + BUN/2.8

Range is 275-295

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7
Q

Hypotonic/natremic dehydration

A

Loss of Na is greater than the loss of water.
Fluid shifts from ECF to ICF.
Serum sodium/osm is less than normal.

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8
Q

Hypertonic/natremic dehydration

A

Loss of water is greater than loss of Na.
Fluid shifts from ICF to ECF.
Serum sodium/osm is greater than normal.

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9
Q

Isoosmotic volume contraction

A

Acute loss of isoosmotic fluid.

Decrease in ECF, no change in ICF or osm.

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10
Q

Hyper-osmotic volume contraction

A

Loss of hypotonic fluid (dehydration, diabetes, alcoholism).

Decrease in ECF and ICF, increase in osm.

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11
Q

Isoosmotic volume expansion

A

Gain of isoosmotic fluid.

Increase in ECF, no change in ICF or osm.

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12
Q

Hypoosmotic volume expansion

A

Gain of hypoosmotic fluid.

Increase in ECF and ICF, decrease in osm.

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13
Q

Gibbs-Donnan effect

A

Proteins are largely negative and cannot cross the PM.

This provides both an oncotic and electrical gradient to attract molecules.

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14
Q

3 layers of the glomerular filtration barrier

A

Capillary endothelium
Glomerular BM
Podocyte epithelium

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15
Q

Filtered load =

A

[X] x GFR

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16
Q

Urinary excretion =

A

Filtrate - amt reabsorbed + amt secreted

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17
Q

Reabsorption =

A

Filtrate - excretion + amt secreted

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18
Q

Urinary excretion rate =

A

(Ux) x V

Ux is urine conc of X and V is urine flow rate

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19
Q

Renal clearance definition

A

Vol of plasma completely cleared of a substance by the kidneys per unit time

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20
Q

Cx =

A

(Ux x V)/Px

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21
Q

Characteristics if glomerular filtrate

A

Protein free
Cell free
Isoosmotic
20% of RBF

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22
Q

FF =

A

GFR/RBF

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23
Q

Inulin

A

Freely filtered at the glomerulus.
Not reabsorbed or secreted.
Not ideal.

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24
Q

Creatinine

A

Used clinically.
10% secreted.
Used to measure GFR.

25
Q

Vasocontriction
RAAS
Na/K ATPase
Receptors

A

a1
B1
a1

26
Q

Prerenal problem

A

> 20:1 BUN/creatinine

Hypovolemia, dehydration, high protein diet

27
Q

Intrarenal problem

A

<10:1 bun/creatinine
Liver dz
Low protein diet

28
Q

PAH

A

Best way to measure GFR, but needs to be administered in an IV

29
Q

Net filtration =

A

GPC - piGC - PBC

30
Q

3 factors influencing GFR

A
Hydraulic conductivity (Lp)
Surface area (Sf)
Capillary ultrafiltration pressure (PUF)
GFR = Lp x Sf x PUF
31
Q

PGC is affected by:

A

Renal BP
Afferent resistance
Efferent resistence

32
Q

Kf =

A

Lp x Sf

33
Q

Function of mesangial cells:

A

Adjust Sf

34
Q

Relationship between PUF and piGC

A

Inverse.

As filtrate leaves the capillary, the oncotic pressure will increase.

35
Q

Which end of the arteriole is more regulated by symapthetics?

A

Afferent. More a1 receptors.

36
Q

Constriction of the afferent arteriole causes:
GFR
RBF
PGC

A

Decrease in all

37
Q

Constriction of efferent arteriole causes:
GFR
RBF
PGC

A

GFR up then down due to RBF.
RBF down
PGC up

38
Q

Vasodilators

A
PGs
NO
Bradykinin
DA
ANP
39
Q

Vasoconstrictors

A

Synpathetics
Angiotensin II
Endothelin

40
Q

Myogenic reflex

A

BVs stretch due to increase in BP.
SM contracts.
AA constricts and EA dilates.

41
Q

Tubuloglomerular feedback with increased renal perfusion pressure (5)

A
  1. Increased RBF and GFR
  2. Increased delivery of NaCl
  3. Release of adenosine
  4. Resistance of AA
  5. Decreased RBF and GFR
42
Q

Tubuloglomerular feedback with decreased renal perfusion pressure

A
  1. Decreased GFR and RBF
  2. Decreased delivery of NaCl
  3. Release renin leading to increased EA resistance OR release of NO leading to decreased AA resistance.
43
Q

Dilation of the AA

RBF, GFR, PGC

A

All increase

44
Q

Constrict AA

RBF, GFR, PGC

A

All down

45
Q

Dilation of EA

RBF, GFR, PGC

A

RBF up
GFR down
PGC up

46
Q

Constriction of EA

RBF, GFR, PGC

A

RBF down
GFR up
PGC down

47
Q

NaH exchanger location, function

A

PCT, reabsorption of Na and bicarb.

48
Q

AQP-1 is present in:

A

PCT

49
Q

AQP-2 is present in:

What is special about them?

A

CD

They are under the control of ADH

50
Q

AQP and TJ availability in both regions of the LoH

A

Many AQP and few TJ in descending loop.

No AQP and many TJ in ascending loop.

51
Q

SGLT1
SGLT2
And their location

A

SGLT1 is low affinity and in S3

SGLT2 is high affinity and in S1

52
Q

How is Glc reabsorbed?

A

Exchanged for Na against its gradient

53
Q

What is the diluting segment? Why?

A

Thick ascending limb of LoH.

Because it sends out a lot of Na and therefore has lots of Na/K pumps.

54
Q

Where does furosemide act?

A

Thick ascending limb via blocking Cl- binding on the Na-K-2Cl transporter

55
Q

What transporter helps reabsorb some Na in the DCT?

A

Na-Cl transporter

56
Q

Where do thiazides act?

What else do they do?

A

DCT on the Na-Cl transporter

Reduce excretion of Ca and reduce risk of kidney stones.

57
Q

What causes the release of aldosterone? Other than increasing BP, what does it cause?

A

Increased plasma K+.

Reabsorption of Na and excretion of K.

58
Q

K+ sparing spirolactone

A

Inhibits Na/K exchange in the DCT and CD.

Promotes K retention and Na/water loss.