Term
| How is plasma and filtrate filtered/reabsorbed/secreted? |
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Definition
Plasma is filtered non-selectively
Filtrate in the tubule can be selectively reabsorbed back into the peritubular capillary
Molecules in the peritubular capillary can be selectively secreted into tubular lumen --> excreted |
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Term
| What types of transport do not require ATP? |
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Definition
Solvent drag/bulk flow
Transcellular/paracellular
Diffusion
Osmosis |
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Term
| When a substance is secreted into the LUMEN, what happens to it? |
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Definition
| It is in the tubule and is excreted |
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Term
| When a substance is reabsorbed through the basolateral surface into the interstitial space, what happens to it? |
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Definition
| It is reabsorbed into the peritubular capillaries and the blood stream |
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Term
| What is passive diffusion? |
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Definition
Follows concentration gradients without requiring ATP
- Simple - lipid soluble, passes through membrane
- Channel mediated - water soluble, flows through a channel
- Carrier mediated - water soluble,uses a transport protein |
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Term
| What is primary active transport? |
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Definition
Pumps requiring ATP such as the Na/K pump on the renal tubular membrane.
Na gradient is into the cell, so requires ATP to be pumped out of the cell. K wants to leave, requires ATP to be pumped into the cell |
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Term
| How are Na/K pumps responsible for electrical gradients? |
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Definition
| Na/K pumps are NECESSARY for creating the RMP. Pump Na out of the cells allows K to move in. K leaks out, leaving a negative charge. This charge leaves a gradient for sodium to move in. |
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Term
| What are the different types of pumps located on a membrane? |
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Definition
- Symporter - same direction.
- Antiporter - different directions. Na/H
- Uniporter - one substance transported |
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Term
| What is secondary active transport? |
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Definition
| When a molecule binds to a symporter down it's gradient, such as sodium going into the cell, it can drag glucose/amino acids against their gradient using ATP |
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Term
| In the renal tubule, where is sodium reabsorbed? |
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Definition
67% proximal tubule
25% thick ascending limb (site 2)
5% Distal tubule (Site 3)
3 % principal cells in collecting duct (site 4)
0.5% excreted |
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Term
| What is Gradient-time transport |
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Definition
Passive transport that does not exhibit a t-max. Rate depends on
- gradient
- permeability
- time in contact with luminal membrane |
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Term
| What are properties of Gradient-Time sodium reabsorption? |
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Definition
- Greater concentration of sodium = greater reabsorption (glomerulotubular balance
- Slower flow rate (GFR) = higher reabsorption as more fluid comes in contact with the membrane |
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Term
| What are the processes of sodium movement in the proximal tubule? |
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Definition
- Active transport by the Na/K pump on the basolateral surface into the capillary.
- Passive diffusion into the lumen of the tubule with secondary active transport of glucose and amino acids
- paracellular
- transcellular bulk flow |
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Term
| How are other substances reabsorbed in the proximal tubule compared to sodium? |
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Definition
Sodium and water are reabsorbed at a constant rate.
Chlorine is almost reabsorbed as much as Na, but not quite
Urea is not reabsorbed as well as sodium/water.
Creatinine and inulin are neither secreted nor reabsorbed
The majority of bicarbonate is reabsorbed, faster than Na/water
Almost all glucose and amino acids are reabsorbed completely in the proximal tubule |
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Term
| How is sodium handled in the thick ascending limb? |
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Definition
Pump Na out of the cells into the capillary allows K to move in, creating an electrical charge. Na/K/Cl pumps ions out of the lumen.
Na/H antiporter (H moves out into the lumen)
K excreted into the lumen creating a positive charge into the lumen, allows sodium and calcium to move paracellularly through tight junctions |
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Term
| How is sodium handled in the distal convoluted tubule? |
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Definition
Na/K pump on basolateral membrane transports Na into capillary.
Passive transport of Na into luminal membrane with secondary active co-transport of chlorine, reabsorbed. |
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Term
| How is sodium handled in the principal cells of the collecting duct? How does this change in the presence of aldosterone? |
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Definition
Reabsorption of Na in exchange for K on the luminal surface --> K and Cl reabsorption.
If ADH is present, Na/K pump activated on the basolateral side --> reabsorption of sodium and water |
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Term
| What stimulates Na/K exchange in the collecting duct? |
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Definition
- presence of aldosterone or ADH
- Increased Na concentration in the lumen, reabsorption
- Increased water washes lumenal K out, Na/K exchange to replenish gradient |
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Term
| What pumps are on the intercalated cells of the collecting duct? |
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Definition
On the lumenal surface, potassium reabsorbs and H secretes
Reabsorption of potassium into the peritubular capillary |
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Term
| How does Aldosterone affect sodium reabsorption in the collecting duct? |
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Definition
| In principal cells, when aldosterone binds to the MR receptor --> upregulation of Na/K channels in the tubular lumen --> more Na is absorbed and K is secreted. Diuretics that act here are potassium sparing |
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Term
| What is the difference between tubuloglomerular feedback and glomerulotubular feedback? |
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Definition
- Glomerulotubular feedback takes place in the proximal tubule. The more sodium (tubular load) filtered, the more (67%) reabsorbed and excreted, percentages are constant\
Tubuloglomerular feedback - in the distal tubule, macula densa cells sense sodium load. If GFR is too fast, material is not reabsorbed and the macula densa notices more Na, correcting the GFR. IF the GFR is too slow, the macula densa notices less Na , again correcting the GFR |
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Term
| Which two important effects favor reabsorption of sodium in the peritubular capillaries? |
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Definition
- constriction of the efferent arteriole, which decreases Hp. Hydrostatic pressure decrease FAVORS reabsorption
- Constriction of the efferent arteriole also increases osmotic pressure. Op increase FAVORS reabsorption
In both of these, less blood is distal to the efferent arteriole |
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Term
| Other than efferent arteriole constriction, what influences tubular reabsorption? |
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Definition
- the SNS contracts both arterioles, increasing reabsorption by decreasing Hp and increasing Op. Decreased blood flow and GFR
- AngII constricts, decreasing Hp and increasing Op
- Aldosterone increases reabsorption, as does ADH
- ANF causes vasodilation/increased GFR, will increase Hp and excretion of Na/water |
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Term
In a response to high or low blood pressure, what do the Tubuloglomerular
Feedback or Glomerulotubular
Balance mechanisms do? |
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Definition
| Maintain normal GFR and prevent large changes in sodium excretion |
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Term
| How does the renal tubule handle glucose? |
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Definition
| Glucose is filtered and reabsorbed 100% in the proximal tubules. However, glucose has a threshold of 225 mg/min after which it begins to be excreted. The Tmax, or maximum that can be reabsorbed at one time, is 320 mg/min |
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Term
| How does plasma glucose relate to inulin/creatinine when increased? |
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Definition
Inulin/creatinine is neither reabsorbed nor secreted, so is concentration independent.
As more and more glucose enters the plasma, more and more is excreted approaching but not reaching inulin/creatinine |
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Term
| How is PAH handled by the proximal tubules? |
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Definition
| PAH is never reabsorbed, so the amount excreted = filtered + secreted. PAH has a very low Tmax, so secreted is fairly constant. As secretion reaches a constant, approaches the line of inulin |
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Term
| How do the kidneys handle urea? |
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Definition
50% reabsorbed in the proximal tubule
60% secreted by the thin descending and ascending
70% reabsorbed in the collecting duct in the presence of ADH
~40% excreted
- TAL, DCT, CD (without ADH) impermeable to urea
- Urea is continuously absorbed and secreted to maintain gradient in the loop of henle |
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Term
| How is calcium handled in the renal tubule? |
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Definition
Similar to sodium but in smaller concentrations. Majority reabsorbed passively in the proximal tubule. Only a small amount is excreted. PTH can affect rates.
Calcium moves through epithelial channels and paracellularly driven by K charge in TAL and CD |
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Term
| How is calcium important in diuretic function? |
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Definition
Loop diuretics at site 2 prevent a positive charge from forming in the lumen and Ca from moving transcellularly --> calcium excretion
Thiazide diuretics enhance calcium absorption through epithelial channels |
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Term
| How is uric acid handled in the renal tubules? What drugs act on this site? |
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Definition
ENTIRELY in the proximal tubule
Both reabsorbed, secreted, then reabsorbed again. 10% gets excreted
2 drugs:
- Probenecid -enhances excretion by blocking reabsoption (Uricosuric), very few side effects
- ASA - at low doses, blocks secretion which aggravates gout. At high levels, blocks reabsorption and secretion allowing uric acid to be freely filtered. Bad side effects. |
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Term
| How does the renal tubule handle amino acids? Protein? |
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Definition
AA is filtered and reabsorbed 100% in the proximal tubules, just like glucose.
Reabsorption of protein through receptor-mediated endocytosis |
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Term
| How does the renal tubule handle phosphates? |
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Definition
| Mostly reabsorbed in the proximal tubule, some in the distal tubule. Very small Tmax. PTH enhances excretion by lowering the Tmax |
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Term
| How is potassium handled in the renal tubule? |
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Definition
Maintained at an equilibrium by shifting K into and out of cells
- Hypokalemia - K outside the cell is too little, has gone into cells. Caused by insulin, Aldosterone (K loss), beta receptor 2 stimulation, and alkalosis (At a basic pH, H/K pump exchange)
- Hyperkalemia - Too much K outside the cell. Caused by insulin deficiency, aldosterone deficiency, beta blockade, alpha stimulation, Lysis, exercise, osmolarity increase. Acidosis (acidic pH exchanges K for H into the cell) |
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Term
What is the Distal K secretory system?
How is K handled in other places? |
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Definition
The distal tubule determines potassium secretion or absorption, all other areas are constant reabsorption.
- Low potassium - K reabsorbed at DCT and CD. Reabsorption using intercalated cells.
- Normal/high potassium - K secreted at DCT and CD. Secreted using principal cells
- In the proximal tubule - K reabsorbed paracellularly due to charge in the lumen
- In TAL, K reabsorbed through bulk flow and through Na/K/Cl pump |
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Term
| How is potassium excretion regulated? |
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Definition
Na/K pump on basal membrane increases intracellular potassium
- Aldosterone stimulates potassium loss
- increase in filtrate volume washes away lumenal K, K has a gradient to secrete out.
- increased sodium intake - decrease in aldosterone production while increasing flow rate and K gradient. NO net K change.
- Diuretics increase flow rate - potassium depletion |
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