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What 2 factors control body water concentration?
fluid intake and renal excretion
What is the range of urine osmolarity that the kidneys can excrete?
50 mosm / L (very dilute) to 1400 mosm / L (very concentrated)
What is the purpose of excreting a dilute urine?
Get rid of excess water (body fluid osmolarity is reduced)
What is the purpose of excreting a concentrated urine?
Conserve water (body fluid osmolarity is increased)
There is a decrease in what hormone when ECF concentration is low (excess body water in relation to solutes)?
- ADH production and secretion (by post pit) is decreased
- This causes decreased permeability of the DT and CT to water (water is not reabsorbed)
- Water is then excreted
Where are the osmoreceptors that control ADH secretion located?
When ADH secretion is decrease, what happens to cause decreased water reabsorption?
Decreased number of aquaporins in the DT and CT, this causes water to NOT be reabsorbed, but secreted
Explain how a dilute urine is created (differences in tubular reabsorption in the different tubules)
- Tubular fluid remains isosmotic in PCT (solute and water reabsorbed equally)
- Tubular fluid becomes concentrated (water is reabsorbed) in the desc LoH (in the medulla)
- Tubular fluid becomes dilute in the asc LoH as solutes (Na, K, Cl) are reabsorbed, this portion is impermeable to water, so dilution occurs
- More dilution occurs in the DT and CT (solutes reabsorbed, water is NOT reabsorbed)
In the distal and collecting tubules, what affects water reabsorption?
T or F, the ascending LoH is very permeable to water due to the effect of ADH
- F, this area is NOT affected by ADH levels
- Even in the presence of high ADH levels, the ascending LoH is impermeable to water
What is the stimulus for excreting a concentrating urine?
Increased plasma ECF
Obligatory urine volume
- The minimum amount of urine that must be excreted to get rid of waste products from metabolism
- For a 70 kg pt, 600 mosm of waste must be excreted
- Max urine concentration is 1200 mosm/ L
- 600/ 1200- 0.5 L / day
- This is where min UO of 20-30 ml / hr is derived from
What 2 factors allow us to produce a concentrated urine?
- #1- Hyperosmolar medullary interstitial fluid (provides an osmotic gradient to allow water reabsorption)
- #2- High levels of ADH (increase in # of aquaporins to allow increased reabsorption)
What are the vasarecta?
- Blood vessels to the LoH
- Part of the peritubular capillaries
What solutes are key contributors to a hyperosmolar medullary interstitial gradient?
What is the only part of the LoH that's permeable to water?
In the thick ascending LoH, what solutes get reabsorbed (back into blood) and what get excreted?
- Reabsorbed- Na, Cl, K, Ca, bicarb, Mg
- Excreted- H
What factors contribute to the build up of solute in the renal medulla to create a hyperosmolar medullary interstitial gradient?
- Active transport of Na out of LoH and into medullary interstitial
- Co-transport of K, Cl, and other ions with Na
- Facilitated diffusion of urea into medullary interstitial
- Limited diffusion of water from tubules into medullary interstitium
process that allows creation of hyperosmolar medullary interstitial gradient
What is the driving force behind counter current mechanism?
Explain the main activities occurring in counter current mechanism
- Active pump in thick ascending LoH moves Na and Cl into medullary ISF (increased osm in ISF)
- To balance this out, water moves out of desc LoH into medullary ISF
- Solutes keep getting reabsorbed and tubular fluid gets more concentrated, and this process gets repeated
- Concentration gradient established by active transport gets multiplied
- Urine gets very concentrated as water gets reabsorbed to dilute medullary ISF
ADH causes water to be reabsorbed, does it get reabsorbed in the medullary or cortical ISF? Why?
Water gets reabsorbed into the cortical ISF, if it got reabsorbed into the medullary ISF it would dilute it and counteract the hyperosmolar gradient (that serves to allow urine concentration)
When a substance is reabsorbed, where is it going?
Back into the blood
What is the only part of the LoH that allows water reabsorption?
What percent of the hyperosmolar medullary interstitial gradient is urea?
Is urea passively or actively reabsorbed from the tubules?
What is the significance of urea ?
- Urea cycles through the tubules multiple times before excretion
- Urea contributes to the hyperosmolar medullary interstitial gradient (water gets reabsorbed from the collecting ducts and urea is concentrated, this allows facilitated diffusion to move urea from tubules into medullary ISF)
Where does urea reabsorption occur?
medullary collecting duct
What happens after urea is reabsorbed into the medullary collecting ducts?
- Contributes to hyperosmolar medullary interstitial gradient
- Urea then diffuses into thin LoH and passes again thru the distal tubules
- Process repeats a few times, until urea is finally excreted
What 2 features of the renal medially blood flow contribute to preservation of hyperosmolarity?
- 1) Low blood flow, < 5% of total renal BF, this minimizes solute loss from medullary interstitium
- 2) Vasarecta serve as countercurrent exchanges, this minimizes washout of solutes
T or F, the purpose of countercurrent exchange with VR is not to create hyperosm state in medullary interstitium but rather to prevent it from being dissipated?
How does the VR help to maintain medullary hyper osmotic state?
- Desc LoH:
- Solute leaves medullary ISF and goes into VR
- Water goes from blood (VR) into medullary ISF
- Asc LoH:
- Solutes leave VR and go into medullary ISF
- Water leaves medullary ISF and enters medulla
- Both things make the blood less concentrated and the tubular fluid more concentrated
What stimulates ADH secretion?
Plasma osm, BP and BV (both mediated by baroreceptors, N/V, hypoxia, medications (morphine)
What's an easy way to estimate plasma osm?
Na x 2.1
What happens to ADH secretion if plasma osm is increased?
Increase in ADH secretion and insertion of aquaporins (to increase water reabsorption in DT and CD)
Quantitatively, which has more of an effect on blood volume- blood volume or plasma osm?
Plasma osm- a 1% increase stimulates ADH release vs. a 10% decrease in blood volume
Is most K ICF or ECF?
Normal K concentration in the plasma?
What factors will cause K to move from ECF to ICF?
- Insulin (occurs after a meal)
- Catecholamines (beta 2 mechanism)
- Metabolic alkalosis
What factors will cause K to move from ICF to ECF?
Metabolic acidosis, exercise, cell lysis, increased ECF osmolarity (causes cellular dehydration, water moves out of the cell, so does K)
Why is a diabetic pt at particular risk for hyperkalemia?
Impaired insulin release (insulin causes K to move into the cell), K levels are increased after a meal
What % of K gets reabsorbed in the PCT?
Where does the majority of K secretion (into tubular fluid) occur?
principle cells of the DT and CCT
What are the principle cells?
- Special tubular epithelial cells
- Make up 90% of the tubular epithelial cells in the DT and CCT
How do the principle cells of the DT and CCT secrete K?
- 1) uptake of K into principle cells (Na/K/ATPase pump)
- 2) passive diffusion of K from principle cell to tubular fluid (principle cells have unique channels that allow K diffusion into tubular fluid)
What is the major stimulant for K secretion by the DT and CCT?
Plasma K level
T or F, an increase in plasma K will stimulate aldosterone secretion, that will in term cause K secretion?
Renal K excretion is determined by the sum of….?
- Rate of K filtration (GFR x plasma K concentration)
- minus rate of tubular reabsorption
Plus rate of tubular secretion
What does PTH do?
- Increases plasma Ca levels by bone resorption and vitamin D activation
- Also causes increased Ca reabsorption by the tubules and decreased Phos absorption
What does calcitonin do? Where is it released from?
- Decreases plasma Ca levels
Normal ionized Ca level
What form of Ca can be filtered by the kidneys?
The ionized as the rest is complexed to anions or protein bound
What % of filtered Ca gets reabsorbed? Where does most of the reabsorption occur?
In what 3 locations in the tubules does Ca reabsorption occur? What controls the reabsorption at each site?
- PCT- 65%- volume status
- LoH- 25-30%- PTH
- DT and CT- 4-9%- PTH
How does plasma phos level affect Ca levels?
- Increased plasma Phos causes an increase in PTH
- Ca reabsorption is increased
- Ca excretion is decreased
What effect will metabolic acidosis have on Ca reabsorption?
- Increased reabsorption
- Met alkalosis will do the opposite
What factors cause decreased Ca excretion?
Decreased ECF volume, decr blood volume, incr PTH, metabolic acidosis, incr Phos, vitamin D
What effect does SNS stimulation have on the kidneys?
- VC of renal arterioles
- Decr GFR
- Incr tubular reabsorption on Na
- Increased renin release
- Aldosterone and angio 2 release
Increase in aldosterone causes Na and water retention and increased BP and ECF- pressure natruresis and diuresis occur
- released from atrial stretch receptors
- causes an increase in GFR
- decr Na reabs
- incr water secretion
- substance that can donate a proton
- Bronstead- Lowry theory of acids and bases
- substance that can accept a proton
- Bronstead- Lowry theory of acids and bases
Acid base rxn
rxn where a proton is transferred
an acid that gives up H easily and is completely dissociated in water
an acid that does not give up H easily and is less than 100% dissociated in water
splitting apart of an acid in water to produce an H ion and an anion
Why is regulation of H ion concentration (pH) so important?
- optimal enzyme functioning
- proper electrolyte distribution
- optimize myocardial contractility
- optimal Hgb saturation
2 sources of acid
- volatile (able to be eliminated via the lungs)
- non volatile or fixed (must be eliminated by the kidneys
How much CO2 is produced / day from aerobic metabolism? How much is eliminated via the lungs / day
How much non volatile acid is produced each day?
What processes produce H ions?
- Protein metab
- Lactic acid (aerobic CHO metab)
- Ketone bodies (triglycerides)
- CO2 is hydrated to become carbonic acid
- slow process in the plasma, but in the RBC carbonic anhydrase speeds it up
Henderson- Hasselbalch equation
- pHa= pK + log bicarb / 0.03 x PaCO2
- =kidneys / lungs
0.03 is the solubility coefficient of CO2 in the plasma
any substance that reversibly binds H ions
How do the kidneys contribute to acid / base balance?
- Produce an acid or basic urine depending on our needs
- Balance of removing H and bicarb
Is most bicarb reabsorbed or secreted?
Quantitatively, which is more important- secretion of H ion or reabsorption of bicarb?
Primary ECF buffer
What will the kidneys do in response to acidosis?
Reabsorb all filtered bicarb and produce more bicarb
What will the kidneys do in response to alkalosis?
- There's an excess of bicarb
- Kidneys can't reabsorb all the filtered bicarb, so bicarb is excreted
- This has the same effect as increasing the H ion concentration
In what part of the tubules is H ion secreted?
- PCT (80-90% occurs here)
- thick asc LoH
- early distal tubule
Mechanism for H ion secretion?
Counter transport (a form of secondary active transport)
T or F, slightly more H ions are secreted than bicarb reabsorbed
Where does primary active H ion secretion occur?
- intercalated cells of the late distal tubule
- collecting tubule
T or F, in general, for every H ion secreted a bicarb is reabsorbed?
How can new bicarb be produced by the kidneys?
- By the ammonia and phosphate buffers
- Quantitatively the ammonia buffer is more significant
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