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216 Cards in this Set
- Front
- Back
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what hormones are produced by kidneys
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erytrhopoietin, vitamin D |
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what do the kidney synthesize |
ammonia, prostaglandins, kinins, glucose |
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2 types of nephrons |
juxtamedullary superfiical cortical
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renal blood flow from renal artery |
renal artery - segmental artery - lobar artery - interlobar - arcuate - cortical radial artery and glomeruli |
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renal microcircuation:
afferent arteriole -->
efferent arteriole --> |
afferent to the glomerular capillaries
efferent to the peritubular capillaries |
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First capillary network in renal microcirculation |
glomerular capillaries: high hydrostatic pressure; large fluid volume filtered into Bowman's capsule |
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second capillary network in renal microcirculation |
peritubular capillaries: low hydrostatic pressure; large amounts of water and solute are reabsorbed |
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at rest, kidneys receive how much of cardiac output |
20-25% 1.0-1.25 l/min |
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sympathetic neurons in the kidneys synapse on: |
smooth muscle: causing arteriolar constriction
granular cells: causing renin secretion in afferent arterioles |
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effects of sympathetic stimulation in kidneys |
powerful vasoconstriction of afferent arterioles: decreases renal blood flow diverts the renal fraction to vital organs stimulates renin release form granular cells: initiates formation of ang II stimulates Na+ reabsorption in proximal tubule, thick ascending limb of loop of Henle, distal convoluted tubule, collecting duct |
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glomerular filtration |
filtration of plasma from glomerular capilaries into Bowmans capsule |
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tubular reabsorption: |
transfer of substances from tubular lumen to peritubular capillaries |
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tubular secretion |
transfer of substances from peritubular capillaries to tubular lumen |
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excretion |
voiding of substances in the urine |
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basic processes of urine formation |
glomerular filtration tubular reabsorption tubular secretion excretion |
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glomerular filtration Rate (GFR) |
volume of plasma filtered into the combined nephrons of both kidneys per unit time |
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filtration rate of any freely filtered substance = |
GFR x plasma concentration of substance |
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urinary excretion rate |
product of urine flow rate x concentration of substance into the urine |
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if excretion < filtration...
if excretion > filtration.... |
net reabsborption
net secretion |
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renal clearance |
the volume of plasma from which a substance is completely removed from the kidneys in a given time period
units : volume/time |
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clearance of substance X = |
(concentration of X in line x urine volume) / concentration of X in plasma |
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requirements for determining GFR from clearance of certain compounds: |
compound must be freely filtered, but neither secreted, reabsorbed, produced, nor degraded by the kidneys
GFR = Ux x V/Px = Cx |
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inulin |
freely filtered, neither reabsorbed, secreted, nor metabolized |
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amount of inulin filtered per unit time =
Inulin clearance = |
amount excreted per unit time
GFR |
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what does PAH clearance estimate |
renal plasma flow |
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PAH |
para-amino hippuric acid: freely filtered avidly secreted in proximal tubule |
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PAH is completely cleared from peritubular capillaries when... |
PAH concentration is low |
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normally, glomerular filtrate is essentially... |
free of blood cells, proteins, but otherwise identical to plasma |
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what passes freely through the glomerular membrane |
free passage of water, small solutes (glucose, AA, electrolytes): concentrations are the same on both sides of membrane |
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passage of large molecules through glomerular membrane |
passage of large molecules (proteins) and formed elements is impeded.
only very small amounts of protein are filtered into the bowman's capsule |
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what does large amounts of protein in urine indicate |
proteinuria often indicates renal disease |
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what factors affect filterability across glomerular membrane |
molecular size and charge |
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3 layers of the glomerular membrane |
1. fenestrated capillary endothelium: highly perm to water, dissolved solutes 2. glomerular basement membrane: collagen, glyocproteins contain anionic charges 3. podocyte epithelium: slit pores between podocytes restrict filtration of large molecules |
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GFR is product of 2 physical factors: |
1. hydraulic permeability of glomerular membrane 2. surface area for filtration product of 1 and 2 = ultrafiltration coefficient Kf 3. capillary ultrafiltration pressure
GFR = Kf x Puf |
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ultrafiltration pressure (Puf) |
driving force for glomerular filtration |
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Ultrafiltration pressure is determined by: |
hydrostatic and colloid osmotic pressures in glomerular capillaries, Bowman's capsule |
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ultrafiltration pressure is the driving force for... |
glomerular filtration |
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mechanisms for altering GFR |
altered Kf (ultrafiltration coefficient): glomerular mesangial cell contraction
altered Puf: changes in Pgc (hydrostatic pressure in glomerular capillaries) |
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Hydrostatic pressure in glomerular capillaries (Pgc) is determined by 3 factors: |
renal arterial BP
afferent arteriolar resistance
efferent arteriolar resistance |
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where are glomerular mesangial cells located |
within glomerular capillary loops |
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effects of contraction of mesangial cells |
shortens capillary loops, lowers Kf, and thus lowers GFR |
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GFR is physiologically controlled by: |
adjusting resistance of afferent and efferent arterioles |
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effect of afferent arteriolar constriction |
greater pressure drop upstream of glomerular capillaries
Pgc falls, which lowers GFR
renal blood flow falls (inc resistance) |
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effect of efferent arteriolar constriction |
pooling of blood in glomerular capillaries
increased Pgc increases GFR
decrease renal blood flow |
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effect of efferent arteriole dilation |
decrease Pgc
decrease GFR
increase renal blood flow |
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effect of afferent arteriole dilation |
increase Pgc
increase GFR
increase Renal blood flow |
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hydrostatic pressure decreases from: |
renal arteries - afferent arteriole - glomerular capillary - efferent arteriole - peritubular capillary - renal veins |
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mechanisms for autoregulating renal blood flow and GFR |
myogenic repsonse to increased systemic arterial pressure
tubuloglomerular feedback responses to: inc GFR dec GFR |
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myogenic mechanism of autoregulation |
intrinsic property of vascular smooth muscle to resist stretch
stretching vascular smooth muscle in interlobular arteries and afferent arterioles --> smooth muscle contraction, narrowing of vessels
inc vascular resistance --> dec renal blood flow
dec Pgc --> dec UP --> dec GFR |
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components of the Juxtaglomerular apparatus |
macula densa
extraglomerular mesangial cells
juxtaglomerular (granular) cells |
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macula densa |
in wall at end of thick ascending limb of loop of henle |
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extraglomerular mesangial cells |
transmit signals from macula dense to JG cells |
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juxtaglomerular (granular) cells |
in afferent arteriolar smooth muscle |
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JGA responds to _____ to maintain ____ |
responds to changes in BP to maintain GFR nearly constant |
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Tubologlomerular filtration response to increased renal blood pressure |
1. increase GFR 2. Increase NaCl deliver to loop of Henle 3. signal generated by macula densa of JGA 4. increase afferent arteriolar resistance (Ra) |
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Adenosine mediates... |
vasoconstriction in response to tubuloglomerular feedback |
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Response to decreased renal BP |
GFR falls; N+Cl- filtered and delivered to macula densa macula densa signals granular cells to secrete renin Increased circulating ang II |
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effects increased circulating ang II |
potent vasoconstrictor --> restores BP
efferent arteriolar vasoconstriction restores GFR |
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function of renal prostaglandins |
dampen vasoconstriction by ang II and sympathetic nerves... thus, cause vasodilation |
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where is the bulk filtration of all small molecules |
into Bowmans capsule |
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transcellular transportation |
moves through through the cells |
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paracellular transport |
moves through tight junctions across the tubular membrane |
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simple diffusion |
a mechanism for transcellular solute movement
passive transport; down the electrochemical gradient via lipid binary or aqueous channels |
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facilitated diffusion |
a mechanism for transcellular solute movement
passive transport; 'down' electrochemical gradient, but requires specific carriers |
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primary active transport |
a mechanism for transcellular solute transport
energy dependent; agains electrochemical garden; ATP hydrolysis provides energy |
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secondary active transport |
a mechanism for transcellular solute transport
energy dependent; downhill movement of one substance provides energy for uphill movement of another
cotransport; counter transport |
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endocytosis |
a mechanism for transcellular solute transport
energy dependent;
protein reabsorption |
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proximal tubule reabsorbs: |
mot filtered water, Na+, K+ Cl-,bicarbonate, Ca2+ phosphate
normally reabsorbs all the filtered glucose and amino acids |
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what is secreted in the proximal tubule |
several organic anions and cation s (drugs, drug metabolites) |
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Tubular fluid/plasma concentration ratios provide info on |
tubular handling of substances |
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is PAH absorbed or secreted in the proximal tubule |
secreted |
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is glucose absorbed or secreted in the proximal tubule |
glucose is 100% reabsorbed |
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proximal tubular Na+ reabsorption provides the driving force for |
reabsorption of water and other solutes |
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the polarity of the epithelial cell membranes facilitates... |
net unidirectional transport |
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what is proximal tubular Na+ reabsorption powered by |
Na+, K+ ATPase in the basolateral membrane |
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sodium reabsorption is linked to: |
transcellular transport of other substances |
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how is sodium reabsorbed across the basolateral membrane |
countertransport with K+ powered by Na+k+ATPase |
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transport of sodium across the apical/luminal membrane |
cotransport paired with glucose
counter transport with H+
cotransport with K+, 2Cl- |
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Water reabsorption follows ____ in the PCT |
Na+ reabosorbtion |
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factors promoting fluid movement into the capillaries |
high plasma colloid osmotic pressure
low hydrostatic pressure of blood in these capillaries |
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consequence of high fluid movement into peritubular capillaries |
almost as much fluid is reabsorbed as was initially filtered into the Bowmans capsule |
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filtering of small molecules in the proximal tubule |
small molecules are freely filtered |
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filtering of glucose and amino acids in the proximal tubule |
they are completely reabsorbed in the proximal tubule |
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filtering through the distal segments of the proximal tubule |
no reabsorption in more distal segments |
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what regulates plasma concentrations of glucose, amino acids |
the kidneys DO NOT
they are regulated by liver and endocrine systems |
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How does tubular reabsorption of glucose and amino acids occur |
secondary active trasnport; transcellular ONLY |
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uptake of glucose and amino acids across luminal membrane |
against concentration graient
couplet to Na+ entry down its electrochemical gradient
ultimately dependent on the Na+K+ATPase |
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how do glucose and amino acids exit cell's basolateral membrane? |
facilitated diffusion |
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there are a limited number of ____ cotransporters in the luminal membrane |
Na+ glucose |
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effect of filtered amount of glucose exceeding a critical rate |
capacity of nephrons to reabsorb all the filtered glucose is exceeded
glucose appears in the urine (glucosuria) |
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is glucose reabsorption saturable?
what about amino acids? |
both amino acid and glucose reabsorption are saturable |
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what is Tmg |
tubular gloucose maximum: max rate of glucose reabsorption by all the nephrons combined |
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would an inhibitor of the renal tubular Na+K+ ATPase affect reabsorption of glucose? |
Yes it would prevent it because you lose the driving force of reabsorption across the basolateral membrane |
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why does urine output increase in diabetes? |
due to increased osmosis. Glucose will old on to some of the water, and it will be harder for reabsorption of water to occur |
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what provides the driving force for solute and water transport in the proximal tubule |
sodium reabsorption |
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renal control of sodium and water balance is crucial for the regulation of: |
BP
ECF solute concentration
concentrations of Na+, K+ in body fluids |
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normal function of renal control of sodium and water balance allows: |
water retention during dehydration
excretion of dilute urine when well hydrated
inc sodium excretion when BP rises
dec sodium excretion with BP falls |
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failure of renal control of sodium and water balance can cause |
edema hyper/hypokalemia (K+) undesireable changes in BP acid/base disorders neurologicla problems (swelling/shrinking brain) |
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sodium reabsorption mechanisms in the proximal tubule |
cotransport with glucose, amino acids, phosphate
counter transport with H+ (Na+/H+ exchange) |
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sodium reabsorption mechanisms in thick ascending limb |
Na+K+,2Cl- cotransport |
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sodium reabsorption mechanisms in early distal convoluted tubule |
Na+Cl- cotransport |
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sodium reabsorption mechanism in late distal convoluted tubule and collecting duct |
luminal membrane channels |
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water reabsorption |
is always passive; can be transcellular or paracellular
follows osmotic gradients established by reabsorption of sodium and other solutes |
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chloride reabsorption |
always linked, either directly or indirectly to Na+ reabsorption (Cl- can balance the + charges on Na+)
specific mechanisms differ in different segments |
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what is the descending limb of Henle permeable/impermeable to |
freely permeable to water
impermeable to Na+, Cl- |
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what is the ascending limb of henle permeable/impermeable to |
always IMPERMEABLE to water
thin segment passive NaCl reaborption thick segment: active Na+, K+, 2Cl- cotransport |
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what does magnesium (Mg2+) transport depend on in the thick ascending limb |
the Na+K+2Cl- cotransporter in the tubule lumen |
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what is the major site of physiological control of salt and water balance |
late DCT and collecting duct |
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function of aldosterone in the late DCT and Collecting duct |
aldosterone stimulates Na+ reabsorption, K+ secretion, H+secretion |
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function of atrial natriuretic peptide in late DCT and Collecting duct |
inhibits Na+ reabsorption (medullary collecting duct) |
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function of Vasopressin in Late DCT and collecting duct |
stimulates water reabsorption |
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what cells secrete K+ in the late DCT and collecting duct |
principal cells |
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what is the driving force for K+ secretion in the late DCT and collecting duct |
Na+K+ATPase counter transport and the large transepithelial potential (-50mV in the lumen, 0 in the blood) |
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what is aldosterones mechanism for increasing Na+ reabsorption in late DCT and collecting duct |
incorporation of Na+ channels in the luminal membrane
incorporation of Na+K+ATPase ion pumps in the basolateral membrane |
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water permeability of the late DCT and collecting duct in well-hydrated individuals |
collecting duct is impermeable to water
water remains in tubular lumen; dilute urine is excreted |
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water permeability of late DCT and collecting duct in dehydrated individuals |
collecting duct is highly permeable to water
water is reabsorbed; low volume of concentrated urine is excreted |
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how does ADH work in the late DCT and collecting duct |
ADH binds to its receptor on the basolateral membrane - guanine nucleotide stimulatory protein - adenylate cyclase - cyclic AMP - cAMP dependent protein kinase - causes incorporation of H20 channels (aquaporins) in the luminal membrane which acts increase water permeability |
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what part of the peritubular interstitium has a very high solute concentration |
inner medullary interstitial fluid |
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function of the countercurrent multiplier system |
concentrates solute in medullary interstitium --> enables kidneys to excrete very concentrated urine and conserve water during dehydration |
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the countercurrent multiplier mechanism requires integrated function of 3 components: |
descending, ascending limbs of henle
vasa recta capillaries
collecting ducts |
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vasopressin promotes _____ reabsorption from inner medullary collecting duct |
urea |
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effects of high vasopressin |
antidiuresis
water is reabsorbed, and a low volume, highly concentrated urine is excreted |
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effects of low vasopressin in collecting duct |
water diuresis
a high volume of dilute urine is excreted, collecting duct is impermeable to water
lower solute concentrations in the medullary interstitium |
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what maintains solute gradient in the countercurrent multiplier system |
vasa recta - remove more water and solute form the medulla than they bring in
the difference = the amounts of solute and water reabsorbed by medially tubular segments |
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what does the total body Na+ content determine |
ECF volume |
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effect of increased total body Na+ content |
water osmosis from cells, renal H20 mention --> increase ECF volume --> increases BP |
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body Na+ content = |
Na+ intake (diet) - Na+ excretion (in urine) |
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how is body Na+ intake controlled |
dietary Na+ intake is not regulated in humans
the kidneys control Na+ content by adjusting urinary excretion |
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effects of increased and decreases in ECF volume |
increased ECF volume activates mechanisms that increase Na+ excretion
decreased ECF volume causes Na+ to be conserved |
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where does reabsorption of filtered Na+ load occur |
bulk reabsorption of filtered Na+ in proximal tubule and loop of henle
fine tuning of Na+ handling is exerted in the distal nephron |
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factors that promote Na+ reabsorption |
renal sympathetic nerves
renin/angiotensin system
aldosterone |
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factors that promote Na+ excretion |
atrial, brain natriuretic peptides (ANP, BNP)
urodilatin
intrarenal prostaglandins |
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effects of increased activity of renal sympathetic nerves |
decreased GFR --> dec rate of fluid delivery to macula densa --> inc renin
increased proximal Na+and H2o reabsorption -->dec rate of fluid delivery to macula densa --> inc renin
direct stimulation of granular cells --> inc renin |
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factors that promote renin secretion |
renal sympathetic stimulation: directly stimulates tubuloglomerular feedback: dec NaCl delivery to macula dens --> inc renin secretion intrarenal baroreceptor: afferent arteriolar vasoconstriction --> dec pressure of granular cells --> inc renin secretion |
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angiotensin II stimulates: |
systemic arteriolar constriction (inc BP) renal arteriolar constriction: efferent > afferent Na+ reabsorption: PCT > TAL, DCT, CCD thirst vasopressin secretion from Post Pit aldosterone secretion from adrenal cortex |
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where does aldosterone act |
late distal convoluted tubule, collecting duct |
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effects of aldosterone in late DCT , collecting duct |
stimulates sodium reabsorption
stimulates potassium secretion
stimulates H+ secretion |
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factors controlling aldosterone secretion |
increase plasma K+ conc --> aldosterone sec increase plasma ACTH conc -->aldosterone sec increase plasma angiotensin II concentration --> inc aldosterone sec
atrial natriuretic peptide inhibits aldosterone secretion |
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effects of ANP |
increases GFR: afferent dilation, efferent constriction inhibits Na+ reabsorption in MCD suppresses renin secretion suppresses aldosterone secretion systemic vasodilator suppresses vasopressin |
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urodilatin |
endogenous renal natriuretic peptide
secreted by DCT, collecting duct in response to increased arterial pressure and ECF volume |
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effect of urodilatin |
suppresses Na+ and water reabsorption by medullary collecting duct
*has no effect on systemic circulation |
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effects of intrarenal prostaglandins (PGE2) |
increase Na+ excretion
increase GFR by dilating renal arterioles suppress Na+ reabsorption in thick ascending limb and cortical collecting duct
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where is vasopressin synthesized and secreted |
syntehsized in neuroendocrine cells in the supraoptic and paraventricular nuclei of hypothalamus
stored in nerve terminals in the neurohypophysis, and secreted from posterior pituitary |
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physiological factors that control vasopressin secretion |
osmolality > volume and pressure of vasculature (hemodynamics)
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what are the osmoreceptors |
hypotahlamic (more sensitive) and hepatic osmorecptors |
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what are the baroreceptors |
aortic barorecptors and carotid barorecptors |
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effect of increase in osmolality |
sensed in the osmoreceptors --> send signals to the paraventricular and supraoptic nuclei in the hypothalamus --> synthesis and secretion of ADH stimulated |
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hyperkalemia:
hypokalemia: |
K+ > 5.0 mEq/l = hyper
<3.5 hypo |
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effects of low K+ on RMP of excitable tissues |
low K+ lowers RMP making it harder to reach threshold and fire an action potential |
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effect of high K+ on RMP of excitable tissues |
high K+ raises RMP making it easier to reach threshold and fire an action potential |
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K+ handling in proximal tubule |
67% of K+ reabsorbed |
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K+ handling in the Thick ascending limb |
20% reabsorbed here via Na+K+2Cl- cotransport |
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where is physiological control of K+ handling exerted? |
late distal tubule and collecting duct |
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principal cells |
located in the distal nephron
either reabsorb or secrete K+ depending on body's K+balance |
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5 factors affecting K+ secretion in late DCT and collecting duct |
1. EC K+ concentration 2. Na+ conc in tubular lumen: Na+/K+ exchange across luminal membrane 3. luminal flow rate: more flow dilutes secreted K+ 4. EC pH: K+ and H+ exchange across cell membranes 5. aldosterone: stimulates K+ secretion in late DCT and Collecting duct |
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situations that alter K+ handling |
diuretics
low-sodium diet |
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diuretics |
drugs that inc urine by inhibiting tubular Na+ reabsorption. most classes of diuretics increase Na+ delivery to late distal tubule and collecting duct, which increases K+ secretion |
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effects of a low-sodium diet |
less Na+ deliver to late distal tubule, collecting duct --> less K+ secretion, excretion --> hyperkalemia |
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effects of alkalemia on K+ secretion |
increases K+ secretion at a given plasma K+ concentration |
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effects of acidemia on K+ secretion |
decrease K+ secretion at a given plasma K+ concentration |
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increased plasma K+ concentration stimulates _____ secretion |
aldosterone |
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mechanism of Ca2+ reabsorption in the proximal tubule |
transcellular and paracellular primary active transport Ca2+3Na+ countertransport
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urinary K+ excretion increases with: |
plasma K+ concentration |
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cation exchange in CD principal cells across the tubular lumen |
Na+ into cell through leak channels K+ out of cell through leak chnanel |
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cation exchange in CD principal cell across peritublular interstitium |
Na+K+ counter transport
counter transport of H+ K+ |
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increase in EC H+ causes: |
H+/K+ exchange, which lowers IC K+ concentration and decreases K+ secretion |
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effect of aldosterone in distal tubule and collecting duct |
stimulates K+ secretion |
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importance of EC Ca2+ |
Ca2+ can dampen APs by blocking Na+ channels low EC Ca2+ can produce hypocalcemic tetany Ca2+ is required for neuromuscular transmission EC Ca2+ can effect contractile strength of myocardium |
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what percent of Ca2+ is bound to plasma proteins |
45% (mostly to albumin) |
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H+ compete with _____ for binding sites on plasma proteins |
Ca2+ |
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acidemia in regards to h+ and Ca2+ |
increase H+ concentrateion --> increase in plasma free Ca2+ conc |
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alkalemia in regards to H+ and Ca2+ |
decrease H+ concentration --> decrease in plasma free Ca2+ |
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effect of GI tract on EC Ca2+ |
GI tract produces calcitriol --> increases EC Ca2+ |
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effect of kidneys on EC Ca2+ |
kidneys: PTH and Calcitriol --> increase EC Ca2+ |
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effect of bone on EC Ca2+ |
bone: PTH, VitD3 --> increase EC Ca2=
bone: Calcitonin --> decreases EC Ca2+ |
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effect of PTH on EC Ca2+ |
PTH --> inc EC [H+] and [PO4] --> increases EC Ca2+ |
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organs that control EC [Ca2+] |
GI tract bones kidneys PTH |
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where is most Ca2+ absorbed in the nephron |
70% reabsorbed in PT
20% in TAL
9% in DT
1% CCD |
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mechanism of Ca2+ reabsorption in distal tubule |
transcellular ONLY primary active transport Ca2+3Na+ countertransport |
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transport in the thick ascending limb |
Na+K+2CL- countertransport K+ leak channels Na+K+ATPase K+Cl- cotransport paracellular reabsorption of Ca2+ Mg2+ via tight junction bc +6 mV potential in tubule |
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where is physiological control of tubular Ca2+ reabsorption exerted |
thick ascending limb and DCT |
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what stimulates reabsorption of Ca2+ |
PTH and calcitriol |
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decreased plasma [Ca2+] induces: |
cells in parathyroid to secrete PTH |
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what is the overall effect of PTH |
increase EC [Ca2+] |
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effect of increasing plasma Ca2+ on PTH and calcitonin |
as plasma Ca+ increases:
PTH decreases Calcitonin increases |
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PTH and calcitriol combine to increase: |
EC [Ca2+] |
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where is phosphate reabsorbed in the nephron |
80% in PT
10% Distal tubule |
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mechanism of proximal tubular phosphate reabsorption |
2Na+Pi cotransport across across the luminal membrane (inhibited by PTH)
Na+K+ ATPase
PiA- countertansport across basolateral membrane
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is proximal tubular phosphate reabsorption saturable |
yes |
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PTH inhibits: |
proximal tubular phosphate reabsorption
this increases the mat of phosphate excreted at any given plasma concentrate n |
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K+ secretion in collecting duct is affected by: |
EC [K+], EC [H+]
luminal Na+ and water delivery
circulating aldosterone |
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2 kinds of acids in the body |
volatile and fixed |
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volatile acid |
carbonic acid (H2CO3) |
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what controls H2CO3 (carbonic acid) in body fluids |
pulmonary ventilation |
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fixed acids |
non-carbonic acids generated metabolically (sulfuric, phosphoric acids)
initially neutralized by buffers in body fluids ultimately excreted in urine
cannot be removed from body by ventilation |
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metabolic sources of H+ |
oxidative metabolism
nonvolatile acids |
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alveolar ventilation controls concentration of : |
[CO2] and [H2CO3] |
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3 lines of defense agains pH changes |
chemical buffers
respiration
kidneys |
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chemical buffer systems |
mix of weak acid and its conjugate base in aces solution |
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ability of buffer to minimize pH changes depends on |
concentration of buffer system components
nearness of buffers pKa to pH of solution |
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bicarbonate buffer system |
chemical equilibrium between CO2 (acid) and bicarbonate (base)
CO2 + H2O <--> H2CO3 <--> H+ + HCO3- |
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why is the bicarbonate system so powerful |
components are abundant (HCO3- and CO2)
its an open system : concentration so fHCo3- and CO2 Are readily adjusted by respiration and renal function |
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renal response to excess acid |
all of filtered HCO3- is reabsorbed
additional H+ is secreted into lumen, excited as titratable acid, ammonium |
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renal response to excess base: |
incomplete reabsorption of filtered HCO3-
decreased H+ secretion
Secretion of HCO3- in collecting duct |
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2 types of urinary buffers |
titratable acid
ammonia |
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titratable acid |
conjugate bases of metabolic acids (phosphate, sulfate) accept H+ into lumen |
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ammonia (NH3) |
generated by tubular epithelium, combines with H+ to form ammonium (NH4+) |
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H+ excretion = |
urinary excretion of titratable acid + ammonium - HCO3 |
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excretion of HCO3- has same effect as |
gaining H+ |
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if arterial pH is too high, kidneys respond by |
incompletely reabsorbing HC3- |
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where is filtered HCO3- reabsorbed |
85-90% of filtered HCO3- is reabsorbed in proximal tubule and thick ascending limb |
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alpha intercalated cells |
actively secrete H+ in collecting ducts |
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beta intercalated cells |
secrete HCO3- to eliminate base |
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what is the most important buffer converted to titratable acid |
HPO42- in the lumen |
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chronic acidemia upregulates: |
renal ammonium production, excretion |
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factors controlling renal H+ secretion |
increased plasma aldosterone
decreased K+
Increased PCO2 |
