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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 |
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In the equation, TF/P, which variable is considered to be constant?
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Systemic Plasma
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When does the following occur:
TF / P = 1.0 |
NO Reabsorption (of substance)
OR Reabsorption (of X) PROPORTIONAL to Water Reabsorption |
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When does the following occur:
TF / P > 1.0 |
SECRETION (of X) has occurred
OR Reabsorption (of X) LESS than Water Reabsorption |
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When does the following occur:
TF / P < 1.0 |
Reabsorption (of X) is GREATER than Water Reabsorption
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In Bowman's space, characteristic of substance if TF/P = 1.0?
(give example) |
FREELY FILTERED Substance
(i.e. - Inulin) |
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What equation is used as a marker for Water Reabsorption along a nephron?
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(TF/P)inulin
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(TF / P)inulin INCREASES with?
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(increases w/) Water Reabsorption
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Fraction of Filtered H2O Reabsorbed (Eq.) = ?
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1 - [ 1 / (TF/P)inulin]
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If 50% of Filtered water is reabsorbed, then (TF/P)inulin = ?
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= 2.0
(b/c 0.5 = 1 - (1/x), thus x = 2.0) |
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If (TF/P)inulin = 3.0, then how much of the Filtered Water has been Reabsorbed?
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67%
(b/c 1 - (1/3) = 0.666667 ,thus 0.67%) |
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Fraction of Filtered LOAD (x) Remaining
@ any point along nephron (Eq) = ? |
= [ (TF/P)x ] / [ (TF/P)inulin ]
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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. |
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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 |
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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 |
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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 |
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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 |
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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 |
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Na+ REABSORPTION
- what % of Na+ is absorbed at the PT? |
67%
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Na+ REABSORPTION
- what % of Na+ is absorbed at the TAL? |
25%
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Na+ REABSORPTION
- what % of Na+ is absorbed at the DT & CD combined? |
8%
(DT reabsorbs 5%) (CD reabsorbs 3%) |
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Na+ REABSORPTION
- Isosmotic Reabsorption of Na+ occurs where? - Isosmotic Reabsorption is due to what physiological mechanism? |
- PT
- Glomerulotubular Balance |
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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%) |
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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 |
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Na+ REABSORPTION
- What Properties (& where) Governs the Glomerulotubular Balance allowing for Isosmotic Fluid Reabsorption? |
Starling Forces @ PTCC
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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 |
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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) |
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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) |
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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) |
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Na+ REABSORPTION
- @ the Early PT, Reabsorption of Na+ & H2O occurs WITH Reabsorption of what solutes? |
- Glucose
- AA, Lactate & Phosphate - Bicarb |
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Na+ REABSORPTION
- @ the Early PT, what solutes are completely reabsorbed there? |
- Glucose
- AA - Bicarb |
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Na+ REABSORPTION
- @ the Early PT uses what Transporter(s)? |
- Cotransporter (w/ G ALP)
- Na+/H+ Exchanger (w/ B) (countertransporter) |
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Na+ REABSORPTION
- @ the Late PT uses what Transporter(s)? |
Na+Cl- Cotransporter
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Na+ REABSORPTION
- @ the TAL of Henle uses what Transporter(s)? |
NKCC Cotransporter
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Na+ REABSORPTION
- @ the Early DT uses what Transporter(s)? |
Na+Cl- Cotransporter
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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 |
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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 |
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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 |
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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 |
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Na+ REABSORPTION
- @ the Late PT, Na+ reabsorption occurs WITH what solute(s)? |
Chloride
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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) |
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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) |
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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. |
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Na+ REABSORPTION
- what parts of the Nephron contain Na+Cl- Cotransporter? |
Late PT
Early DT |
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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) |
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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) |
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ALDOSTERONE
- synthesis is stimulated by? - synthesis occurs where? |
- Angiotensin II
- Adrenal Cortex |
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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) |
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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 |
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ALDOSTERONE
- Aldosterone affects how much of the Overall Na+ Reabsorption? |
2%
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VASOPRESSIN (ADH)
- ADH affects the cells in what part of the Nephron? |
Principal cells
(of Late DT & CD) |
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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 |
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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) |
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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) |
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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) |
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VASOPRESSIN (ADH)
- an ABSENCE of ADH causes what scenario? |
Late DT & CD become virtually impermeable to water
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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 |
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DIURETICS
- what Diuretic class inhibits NKCC Cotransporter? - give example(s) of this diuretic |
- Loop Diuretics
- Furosemide - BuMetaNide - Ethacrynic Acid |
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DIURETICS
- what Diuretic class inhibits Na+Cl- Cotransporter? - which specific Na+/Cl- Cotransporter? |
- Thiazides
- NC Cotransporter @ Early DT (NOT the one in Late PT) |
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DIURETICS
- what Diuretic class inhibits K+ channels of Principle cells (in Late DT & CD)? - give example(s) |
- K+ Sparing Diuretic
- Spironolactone - Amilioride - Triamterene |
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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) |
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Synthetic Analogue of ADH?
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Desmopressin
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ADH Antagonist @ the Late DT & CD?
This ADH Antagonist will INHIBIT what process? |
Alcohol
Water Reabsorption (at Late DT & CD) |
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ADH is synthesized where?
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(Hypothalamic va-S-o-P-ressin)
- SON - PVN |
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What unique GI hormone can also elicit ADH release?
Which part of the GI does this hormone come from? |
CCK
Small intestine |
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Na+/H+ Exchanger is located where on Nephron?
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Early PT
(this is the Na+ Countertransporter) |
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ANGIOTENSIN II
- renal Vascular effects (& specify where) - thus causing change in what property? |
- VasoCONSTRICTS Efferent Arteriole
- Increasing GFR |
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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 |
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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 |