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69 Cards in this Set

  • Front
  • Back
In the equation, TF/P,
- the Tubular Fluid (TF) is ?
- the P is ?
TF = Urine

P = Systemic Plasma
In the equation, TF/P, which variable is considered to be constant?
Systemic Plasma
When does the following occur:

TF / P = 1.0
NO Reabsorption (of substance)
OR
Reabsorption (of X) PROPORTIONAL to Water Reabsorption
When does the following occur:

TF / P > 1.0
SECRETION (of X) has occurred
OR
Reabsorption (of X) LESS than Water Reabsorption
When does the following occur:

TF / P < 1.0
Reabsorption (of X) is GREATER than Water Reabsorption
In Bowman's space, characteristic of substance if TF/P = 1.0?

(give example)
FREELY FILTERED Substance

(i.e. - Inulin)
What equation is used as a marker for Water Reabsorption along a nephron?
(TF/P)inulin
(TF / P)inulin INCREASES with?
(increases w/) Water Reabsorption
Fraction of Filtered H2O Reabsorbed (Eq.) = ?
1 - [ 1 / (TF/P)inulin]
If 50% of Filtered water is reabsorbed, then (TF/P)inulin = ?
= 2.0
(b/c 0.5 = 1 - (1/x), thus x = 2.0)
If (TF/P)inulin = 3.0, then how much of the Filtered Water has been Reabsorbed?
67%
(b/c 1 - (1/3) = 0.666667 ,thus 0.67%)
Fraction of Filtered LOAD (x) Remaining
@ any point along nephron (Eq) = ?
= [ (TF/P)x ] / [ (TF/P)inulin ]
At the PT, if the
[ (TF/P)k+ ] / [ (TF/P)inulin ] = 0.3,
then what happened to all the Filtered Potassium?
30% of Filtered K+ REMAINS in the TF

70% of Filtered K+ has been REABSORBED in to the blood.
Na+ REABSORPTION

- at the Glomerular Capillary, what is the TF/P = ?

- why ?
= 1

b/c Na+ is FREELY FILTERED at GC,
thus @ GC, the [Na+] in Urine is equal to that of Plasma
Na+ REABSORPTION

- at the PT, what is the TF/P for Na+?

- at the PT, what is the TF/P for Osm?

- why?
= 1

= 1

- Because PT exhibits ISOSMOTIC REABSORPTION due to Glomerulotubular Balance
Na+ REABSORPTION

- at the TAL of Henle, what is the TF/P for Na+?

- at the TAL of Henle, what is the TF/P for Osm?

- why?
< 1

< 1

- b/c the TAL of Henle is IMPERMEABLE to Water
Na+ REABSORPTION

- at the Early DT, what is the TF/P for Na+?

- at the Early DT, what is the TF/P for Osm?

- why?
< 1

< 1

- b/c the Early DT is IMPERMEABLE to Water
Na+ REABSORPTION

- at the Late DT & CD, what is the TF/P for Na+?

- at the Late DT & CD, what is the TF/P for Osm?

- why?
varies

varies

- depends on the amount of ADH-induced Aquaporins
Na+ REABSORPTION

- what % of Na+ is absorbed at the PT?
67%
Na+ REABSORPTION

- what % of Na+ is absorbed at the TAL?
25%
Na+ REABSORPTION

- what % of Na+ is absorbed at the DT & CD combined?
8%

(DT reabsorbs 5%)
(CD reabsorbs 3%)
Na+ REABSORPTION

- Isosmotic Reabsorption of Na+ occurs where?

- Isosmotic Reabsorption is due to what physiological mechanism?
- PT

- Glomerulotubular Balance
Na+ REABSORPTION

- Glomerulotubular Balance occurs where?

- Glomerulotubular Balance affects Reabsorption in what 2 ways?
- PT

Provides
- ISOSMOTIC Reabsorption (Na+ reabsorb = H2O reabsorb)
- CONSTANT FRACTIONAL Reabsorption (always 67%)
Na+ REABSORPTION

- Glomerulotubular Balance matches _____ with _______.

- therefore, if GFR suddenly increases, what is the resulting effect on reabsorption & where?
- GTB matches FILTRATION with REABSORPTION.
(b/c GTB allows Isosmotic & Constant Fractional Reabs.)

- Increased Reabsorption @ PT
Na+ REABSORPTION

- What Properties (& where) Governs the Glomerulotubular Balance allowing for Isosmotic Fluid Reabsorption?
Starling Forces @ PTCC
Na+ REABSORPTION

In describing the Glomerulotubular Balance MOA sequence:

- an increase in GFR will cause what?
- thus causing what change in fluid flow (& to where & via)?
- thus causing what change to [Protein] (& where)?
- thus causing what change to Starling Forces?
- thus causing what effect on the Nephron (& where)?
1. Increased FF

2. Thus, LESS Fluid (to PTCC via EA)

3. Thus, [Protein] increases @ PTCC

4. Oncotic Capillary Pressure (PPc) increases

5. Thus, Increased Reabsorption @ PT
Na+ REABSORPTION

- ECF Volume CONTRACTION has what affect on Reabsorption?

- ECF Volume CONTRACTION has what effects on Starling Forces?
Increases Reabsorption @ PT

Decreased ECF means
- Decreased Pc
- (Increased [Protein]), so PPc also increases

(Decreased Pc & Increased PPc cause reabsorption of isosmotic fluid @ PT)
Na+ REABSORPTION

- ECF Volume EXPANSION has what affect on Reabsorption?

- ECF Volume EXPANSION has what affect on Starling Forces?
- Decreases Reabsorption @ PT

- Increased Pc
- Decreased PPc

(thus decreasing Reabsorption @ PT)
Na+ REABSORPTION

- What areas of the Nephron are IMPERMEABLE to Water?
- TAL of Henle

- Early DT

- possibly Late DT & CD
(depends on presence of ADH)
Na+ REABSORPTION

- @ the Early PT, Reabsorption of Na+ & H2O occurs WITH Reabsorption of what solutes?
- Glucose
- AA, Lactate & Phosphate
- Bicarb
Na+ REABSORPTION

- @ the Early PT, what solutes are completely reabsorbed there?
- Glucose
- AA
- Bicarb
Na+ REABSORPTION

- @ the Early PT uses what Transporter(s)?
- Cotransporter (w/ G ALP)

- Na+/H+ Exchanger (w/ B)
(countertransporter)
Na+ REABSORPTION

- @ the Late PT uses what Transporter(s)?
Na+Cl- Cotransporter
Na+ REABSORPTION

- @ the TAL of Henle uses what Transporter(s)?
NKCC Cotransporter
Na+ REABSORPTION

- @ the Early DT uses what Transporter(s)?
Na+Cl- Cotransporter
Na+ REABSORPTION

- @ the Late DT & CD uses what Transporter(s) for Principal cells?

- @ the Late DT & CD uses what Transporter(s) for alpha-Intercalated cells?
- Na+ channels
- K+ channels

- H+/K+ ATPase
- H+ ATPase
Na+ REABSORPTION

- which transporter is NOT electrically neutral?

- why?

- what does this result in?
- NKCC Cotransporter @ TAL

- Reabsorbed K+ diffuses out to Lumen

- Lumen Positive Potential Difference
Na+ REABSORPTION

- @ the Early PT, Na+ reabsorption via COTransport occurs with what solutes?

- this transporter system is responsible for the Complete Reabsorption of what?
- Glucose
- AA
- Lactate
- Phosphate

- Glucose & AA
Na+ REABSORPTION

- @ the Early PT, Na+ reabsorption via COUNTERTransporter (Na+/H+ Exchanger) is directly linked to complete reabsorption of what solute?

- when H+ get exchanged out to lumen, what reaction does it partake in?

- what is the enzyme involved?
Bicarb

@ Lumen:
HCO3- + H+ ==> H2O + CO2
(where CO2 diffuses back into cell & becomes Bicarb)

- Carbonic Anhydrase
Na+ REABSORPTION

- @ the Late PT, Na+ reabsorption occurs WITH what solute(s)?
Chloride
Na+ REABSORPTION

- which segment is known as the Diluting Segment?

- why?
TAL of Henle

b/c it is Impermeable to water
(so just reabsorbs solutes, diluting urine)
Na+ REABSORPTION

- which segment is known as the Cortical Diluting Segment?

- why?
Early DT

b/c it is in the Cortex & Impermeable to water (so just reabsorbs solutes, diluting urine)
Na+ REABSORPTION

- Lumen Positive Potential Difference is seen where in the Nephron?

- why does this occur?
- TAL of Henle

- the K+ reabsorbed by the non-electrically-neutral NKCC leaks back out into lumen.
Na+ REABSORPTION

- what parts of the Nephron contain Na+Cl- Cotransporter?
Late PT

Early DT
Na+ REABSORPTION

- Principal Cells of the Late DT & CD will reabsorb what?
(with what transporter?)

- will secrete what?
(with what transporter?)
- Na+ & H2O
(via Na+ channels)

- K+
(via K+ channels)
Na+ REABSORPTION

- Alpha-Intercalated Cells of the Late DT & CD will reabsorb what?
(with what transporter?)

- will secrete what?
(with what transporter?)
- K+
(via H+ K+ ATPase)

- H+
(via H+ ATPase)
ALDOSTERONE

- synthesis is stimulated by?

- synthesis occurs where?
- Angiotensin II

- Adrenal Cortex
ALDOSTERONE

- Aldosterone effects on Principle cells?

- Aldosterone effects on alpha-Intercalated cells?
- Increased Na+ Reabsorption
- Increased K+ Secretion

- Increases H+ Secretion
(by stimulating H+ ATPase)
ALDOSTERONE

- describe onset of action for aldosterone.

- why is this so?
- SLOW
(like most steroids)

- b/c it takes several hours to SYNTHESIZE a NEW PROTEIN from scratch
ALDOSTERONE

- Aldosterone affects how much of the Overall Na+ Reabsorption?
2%
VASOPRESSIN (ADH)

- ADH affects the cells in what part of the Nephron?
Principal cells

(of Late DT & CD)
VASOPRESSIN (ADH)

- ADH receptors where?

- ADH receptors triggered in response to what INCREASED physiological change?

- ADH receptors triggered in response to what DECREASED physiological change?

- ADH is released from where?
- Atrial receptors

- Increased Blood Osmolarity

- Decreased Blood Volume/Pressure

- Posterior Pituitary
VASOPRESSIN (ADH)

- ADH is involved in control of BP under what conditions?
- Conditions of HEMORRHAGE

(ADH not involved in daily minute-to-minute maintenance of BP)
VASOPRESSIN (ADH)

- ADH action on Receptor V1?

- what Secondary Messenger system is used?

- resulting primary physiological function of ADH binding V1 receptors?
(think "A" is 1st letter, so V1)

- Arteriole Vasoconstriction

- IP3/DAG

- Increase TPR
(arterial constriction increases TPR)
VASOPRESSIN (ADH)

- ADH action on Receptor V2?

- what Secondary Messenger system is used?

- resulting primary physiological function of ADH binding V2 receptors?
- Aquaporin insertion
(directly on luminal membrane of Principal cells of Late DT & CD)

- cAMP

- Increased H2O Permeability
(allows H2O reabsorption @ Late DT & CD Principal cells)
VASOPRESSIN (ADH)

- an ABSENCE of ADH causes what scenario?
Late DT & CD become virtually impermeable to water
DIURETICS

- which inhibitory Diuretic does NOT inhibit a Transporter?

- what does it inhibit?

- where at on the nephron does this action take place?
- Carbonic Anhydrase Inhibitors

- Carbonic Anhydrase enzyme

- Early PT
DIURETICS

- what Diuretic class inhibits NKCC Cotransporter?

- give example(s) of this diuretic
- Loop Diuretics

- Furosemide
- BuMetaNide
- Ethacrynic Acid
DIURETICS

- what Diuretic class inhibits Na+Cl- Cotransporter?

- which specific Na+/Cl- Cotransporter?
- Thiazides

- NC Cotransporter @ Early DT
(NOT the one in Late PT)
DIURETICS

- what Diuretic class inhibits K+ channels of Principle cells
(in Late DT & CD)?

- give example(s)
- K+ Sparing Diuretic

- Spironolactone
- Amilioride
- Triamterene
Aldosterone stimulates what transporters?

(specify location of transporters on the nephron)
@ Principal Cells:
- Na+ channels (to incr. Na+ reabs.)
- K+ channels (to incr. K+ secretion)

@ Alpha-Intercalated Cells:
- H+ ATPase (to incr. H+ secretion)
Synthetic Analogue of ADH?
Desmopressin
ADH Antagonist @ the Late DT & CD?

This ADH Antagonist will INHIBIT what process?
Alcohol

Water Reabsorption
(at Late DT & CD)
ADH is synthesized where?
(Hypothalamic va-S-o-P-ressin)

- SON
- PVN
What unique GI hormone can also elicit ADH release?

Which part of the GI does this hormone come from?
CCK

Small intestine
Na+/H+ Exchanger is located where on Nephron?
Early PT
(this is the Na+ Countertransporter)
ANGIOTENSIN II

- renal Vascular effects (& specify where)

- thus causing change in what property?
- VasoCONSTRICTS Efferent Arteriole

- Increasing GFR
ANGIOTENSIN II

- renal Absorption effects (& specify where)

- renal Secretion affects (& specify where)

- how does Angiotensin II cause these Absorption & Secretion affects on the nephron?
- Increases Na+ Reabsorption
(@ Principle cells)

- Increases K+ Secretion
(@ Principle cells)
- Increases H+ Secretion
(@ a-Intercalated cells)

- by stimulating ALDOSTERONE
Na+ REABSORPTION

- is also COUPLED with Reabsorption of what other cation?

- this occurs where?

- is this cation reabsorption an Active or Passive process?
Calcium

- PT
- TAL of Henle

Passive