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Guyton Chapter 27

Terms in this set (110)

calculation of tubular reabsorption
reabsorption = filtration - excretion
Filtration calculation
Filtration = GFR x Plasma Concentration

Plasma concentration - Px
Excretion of X equation
Excretion = Ux X V

Ux - Urine concentration of x
V - urine flow rate
Transcellular route
when water and solutes can be transported through the cell membrane
Paracellular route
when water and solutes are transported through the spaces between the cell junctions
Ultrafiltration
Bulk Flow - mediated by hydrostatic and colloid osmotic forces
after absorption across the tubular epithelial cells into the interstitial fluid, water and solutes are transported through the peritubular capillary walls into the blood by this method
Reabsorption energy needs
Active process, requires ATP
Primary Active transport
Transport that is coupled directly to an energy source, such as the hydrolysis of ATP. Importantly, it moves solutes against an electrochemical gradient.
example: Sodium-Potassium ATPase pump
Secondary Active Transport
two or more substances interact with a specific membrane protein and are transported together across the membrane.
Transport that is coupled indirectly to an energy source, such as due to an ion gradient.
Example: Glucose along with Na
Osmosis
the passive reabsorption of water -- diffusion from a region of low solute concentration, to one of high solute concentration
Tight Junctions
hold renal tubular cells together
have lateral intercullular spaces inbetween
Facilitated diffusion
carrier proteins that bind to a solute on the luminal surfance of the membrane and release them inside the cell
Pinocytosis
an active transport mechanism for reabsorption of proteins
Transport Maximum
limit to the rate at which as solute can be transported (reabsorbed or secreted), due to the saturation of the specific transport systems involved , when the amount of solute delivered to the tubule exceeds the capacity of the carrier protein and specific enzymes involved in the transport process.
Transport Threshold
the tubular load at which transport maximum is exceeded in some nephrons, but not all.
Not all nephrons have the same transport max
Glucose transport max
375 mg/min
gradient-time transport
the rate of transport depends on the electrochemical gradient and the time that the substance is in the tubule, which in turn depends on the low rate
Na backleak determinates
1) permeability of the tight junctions
2) the interstitial physical forces, which determine the rate of bulk flow reabsorbtion from the interstitital fluid into the peritubular capillaries
Solvent drag
water moving across tight junctions by osmosis, carrying with it some solutes
ADH
Anti-diuretic hormone
increases the water permeability in the distal and collecting tubules
Proximal tubule reabsorbtion
Na, Cl, HCO3, K, H2O, Glucose, amino acids (almost all glucose and AA reabsorbed)
Proximal tubule secretion
H+, Organic acids & bases -- bile salts, oxalate, urate, chatecholamines, PAH, drugs, toxins
Percentage of Na & H2O reabsorbed by the proximal tubule
65%
Divisions of the Loop of Henle
Thin descending segment, thin ascending segment, thick ascending segment
Descending Thin segment
highly permeable to water, moderatly permeable to urea and sodium
allows simple diffusion
Percentabe of water reabsorbed in loop of Henle
20% -- most in thin descending limb
Ascending thin & thick segment
virtually impermeable to water
(diluting urine)
Ascending thick segment reabsortption
reabsorbs Na, Cl, K, Ca, HCO3, Mg
Mediated primarily by a 1-sodium, 2-chloride, 1-potassium co-transporter
Percent of Na reabsorbed in loop of Henle
25%
mostly in thick ascending limb
Loop Diuretics
Furosemide, ethacrynic acid, butetanide

inhibit the action of the Na-2Cl-K co-transporter
Ascending thick segment Secretion
H+
Via Na-H+ counter transport mechanism
slight backleak of K
Macula Densa
in the first portion of the distal tubule, group of closely packed epithelial cells that is part of the juxtaglomerular complex, and provides feedbac control of GFR and blood flow in nephrom
Characteristics of the early distual tubule
-Functionally similar to the thick ascending loop
-not permeable to water (diluting) unless +ADH
-not permeable to urea
-Actively reabsorbs Na, Cl, K, Mg
-Contains macula densa
Percentage of NaCl reabsorbed in early distal tubule
5%
Thiazide Diuretics
work on early distal tubule
Late distal tubule
-permeable to H2O, depending on ADH
-Not very permeable to urea
-Reabsorbs Na, Cl, HCO3, and K
-Na absorption controlled by aldosterone
-Secrete K & H2
Principal cells of late distal tubules
Reabsorb Na
Secrets K
(depends on concentration gradient)
Potassium sparing diuretics
spironolactone, eplerenone - mineralcorticoide receptor antagonits, compete w/ aldosterone to inhibit Na reabsorption & K secretion
amiloride, triamterene - Sodium channel blockers - directly inhibit the entry of sodium into the Na channels
Intercalated cells of late distal tubule
Secrete Hydrogen
Reabsorb bicarb & potassium
Final site for processing urine
Medullary collecting duct
Reabsorbed at medullary collecting tubules
Na, Cl, Urea, HCO3, if ADH- H2O
Reason for urea transporters
some tubular urea is reabsorbed into medullary interstitum to help raise the osmolaity in this region of the kidney, contributing to the kidney's ability to form concentrated urine
Secreted in Medullary collecting tubules
H+ -- plays role in acid-base balance
glomerulotubular balance
the ability of the tubules to increase reabsorption rate in response to increased tubular load
GFR remains at about 65%, so increased load = increased reabsorption
Peritubular capillary physical forces
hydrostatic and colloid osmotic forces govern the rate of reabsorption across the peritubular capillaries
Hormones that regulate tubular reaborption
aldosterone
angiotension II
antidiuretic hormone
natriuretic hormones
parathyroid hormones
Increased Kf
increases reabsorption
increased Pc
Decreases reabsorption
Increased πc
Increased reabsorption
determinates of peritubular capillar reabsorption directly influenced by renal hemodynamic changes
hydrostatic and colloid osmotic pressure of the peritubular cpillaries
What influences the peritubular capillary hydrostatic pressure
Arterial pressure & resistance of the afferent & efferent arterioles
Increased Arterial pressures on peritubular capillary
raise peritubular capillary hydrostatic pressure and decrease reabsorption rate
Increased resitance in either afferent or efferent arterioles in peritubular capillary
reduces peritubular capillary hydrostatic pressure and tends to increase reabsorption rate
increased filtration fraction
higher the filtration fraction, the greater the fraction of plasma filtered through the glomerulus, and more concentrated the protein becomes in the plasma left behind.
= icnreased in peritubular capillar reabsoption rate
Angiotension II affect on peritublar capillary reabsorption
increases peritubular capillary reabsoprtion by decreases renal plasma flow and increasing filtration fraction
What increases Pc?
Decreased Ra
Decreased Re
Increased AP
What increases πc?
Increased πa
(arterial plasma colloid osmotic pressure)
Increased FF
(filtration fraction)
What forces reduce reabsorption across the peritubular capillary membrane
increased peritubular capillary hydrostatic
decreased peritubular capillary colloid osmotic pressure
What does a peritbular capillary reabsorption cause
increased interstitial fluid hydrostatic pressure
tendensey for greater ammounts of solute & water t backleak
these reduce the rate of net reabsorption
changes create by initial increase in reabsorption by peritubular capillaries
reduce interstitial fluid hydrostatic pressure
raise interstitial fluid colloid osmotic pressure
favor movement into interstitium, reduce backleak, net tubular reabsorption increases
aldosterone
site of action: collecting tubule & duct
effect: increases NaCl & H2O reabsorption
and K secretion (principal cells)
increased H secretion (intercalated cells)
Angiotensin II
Site of Action: proximal tubule, thick ascending loop of Henle, distal tubule, collecting tubule
Effect: Increased NaCl & H2O reabsorption
increased H+ secretion
Antidiuretic hormone
Site of Action: distal tubule/collecting tubule and duct
Effect: increase H2O reabsorption
Atrial Naturetic peptide
Site of Action: distal tubule/collecting tubule and duct
Effect: decreases NaCl reabsportion
Parathyroid hormone
Site of Action: proximal tubule, thick ascending loop of henle, distal tubule
Effect: decreased PO4 reabsorption, increased Ca reabsoprtion
Factors that increase aldosterone secretion
Angiotensin II
Increased K
Adrenocorticotrophic hormone (permissive role)
Factors that decrease aldosterone secretion
Atrial natriuretic factor (ANF)
Increased Na concentration (osmolality)
Angiotensin medications
ACE (-pril) & ARB (-sartan)
decreases aldosterone
directly inhibit Na reabsorption
decreases efferent arteriolar resistance
causes Natriuresis & diuresis = decreased BP
Major renal tubular site of aldosterone action
principal cells of the cortical collecting tubule
Effects of Angiotension II
1) stimulates aldosterone secretion
2) constricts the efferent arterioles - increasing Na & H20 reabsorption
3) directly stimulates sodium reabsorption
Antidiuretic hormone secretion
from posterior pituitary
ADH is an important controller of
extracellular fluid osmolarity
ANP secretion
from cardiac atria cells in response to stretch from increased blood volume
ANP Effects
-directly inhibits Na reabsoprtion
-inhibits remin release & aldosterone formation
-increases GFR
-helps to minimize blood volume expansion
Parathyroid hormone release
released by parathyroids in reponse to decreased extracellular Ca
Parathyroid hormone effects
-increases Ca reabsoprtion by kidneys
-increases Ca reabsorption by gut
-decreases phos phate reabsorption
-helps to increase extracellular Ca
SNS activation
decreases Na and H2O excretion, by inceasing Na reabsoprtion in proximal tubule, thick ascending limb of the loop of Henle.
Also increases renin release & angiotensin II formation
Increased Arterial pressure
Decreases Na Reabsorption (pressure natriuresis)
Increased peritubular capillary hydrostatic pressure
Decreased renin & aldosterone
Increased release of intrarenal natriuretic factors (prostaglandins & EDRF)
Osmotic effects on reabsorption
-Water is reabsorbed by osmosis
-Decreasing the amount of solutes reabsorbed in the tubules decreases water absorption
(e.g DM, osmotic diuretics)
Tubular secretion
-first step is diffusion from peritubular capillaries to interstitial fluid
-enter and exit tubule can be active or passive
Ex: K, H, organic acids & bases, NH3
Secretion equation
Secretion = excretion - filtration
Ways to assess kidney function
-Albumin excretion (microalbuminurea)
-Plasma concentration of waste (BUN,
Creatinine)
-Urine specific gravity, urine concentrating ability
-Image methods (MRI, PET, angiograms)
-Isotope renal scans
-Biopsy
-Clearance methods (24hr creatinine clearance)
Clearance
general concept that describes the rate at which substances are removed (cleared) for the plasma
Renal clearance
the volume of plasma compleatly cleared of a substance per min by the kidneys
Clearance Rate (Cs)
Cs = (Us x V) / Ps

Cs- clearance of substance
Us - urine concentration of substance
V - Urine flow rate
Ps - plasma concentration go substance
Using clearance to measure GFR
Use a substance that is freely filtered, but not reabsorbed or secreted, then renal clearance is = to GFR
-Inulin, L=iothalamate, creatinine
GFR= (Uin x V)/Pin
Using clearance to estimate Renal plasma flow
use a substance that is cleared compleatly from the plasma, then clearance = renal plasma flow
-Paraminohippuric acid (PAH)
ERPS= (Upha x V)/Ppha
Calculate actual RPF
correct for incomplete extraction of PAH
Epah = (Apah-Vpah)/Apah
Normally 90% extracted
RPF= ERPF/Epah
Clearance of inulin
125ml/min
Clearance of PAH
600ml/min (estimate effective renal plasma flow)
Clearance of Glucose
0
Clearance of Sodium
0.9
Clearance of urea
70
Clearance of creatinine
140 (estimate GFR)
Free water clearance
Cx <Plasma = reabsorption of x
Cx > Plasma = secretion of x
Free water clearence
CH20 = V - (Uosm x V)/Posm
Uosm > Posm
Ch20 + (urine more dilute than plasma)
Uosm < Posm
CH20 - (Urine more concentrated than plasma
Disorder that causes a failure to produce ADH
Central diabetes insipidus
Disorder that causes a failure to respond to ADH
Nephrogenic diabetes insipidus
-Impaired NaCl reabsorption (loop diuretics)
-drug induced renal damage (lithium, analgesics)
-Malnutrition (decreased urea)
-Kidney disease (pyelonephritis, hydronephrosis, chronic renal failure)
Normal renal excretion per nephron
(2,000,000 nephrons)
Total GFR: 125
GFR per nephron: 62.5
Urine flow rate (ml/min) - 1.5
Volume excreted per nephron - 0.75
Renal excretion with 75% nephron loss
(500,000 nephrons)
Total GFR: 40
GFR per nephron: 80
Urine flow rate (ml/min) - 1.5
Volume excreted per nephron -3
Two things that control extracellular osmolarity
(NaCl concentration)
ADH & Thirst
Thirst osmoreceptor system
increased extracellular osmolarity (NaCl) stiulates ADH release, which increases H2O reabsorption, and stimulates thirst
Osmoreceptor ADH feeback mechanism
Water deficit = increased extracellular osmolarity
increased release of ADH
Increased H20permeability & reabsorption
decresed h20 excretion
Where is ADH synthisized
in the magnocelular neurons of the hypothalmus,
then released by the posterior pituitary
What stimulates ADH secretion
-Increased osmolarity
-Decreased blood volume (cardiopulmonary reflexes)
-Decreased blood pressure (atrial baroreceptors)
-input from the cerebral cortex (fear)
-Angiotensin II
-Nausea
-nicotine
-morphine
-hypoxia
Factors that decrease ADH secretion
-decreased osmolarity
-increased blood volume (cardiopulmonary reflex)
-increased blood pressure (artrial baroreceptors)
-alcohol
-caffine
-clonidine
-haldol
Factors that stimulate thirst
-Increased osmolarity
-Decreased blood volume
-decreased blood pressure
-increased angiotensin II
-dry mouth
Factors that decrease thirst
-decreased osmolarity
-increased blood volume
-increased blood pressure
-decreased antiotensin II
-gastric distention
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