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phys 2 exam 3
| Question | Answer |
|---|---|
| Glomerular filtration energy consumption | none |
| reabsorption and secretion energy consumption | does consume energy. |
| Things that are reabsorbed | water, Na, Cl, HCO3, glucose, AA, urea, Ca, Mg, phosphate, lactate, citrate. All from tubular fluid |
| things that are secreted | organic acids and bases, K. All secreted into tubular fluid from peritubular capillaries |
| Net reabsorption occurs when | filtered load is greater than excretion |
| New secretion occurs when | filtered load is less than excretion |
| glucose transporter | Na/Glucose co transporter. SGLT. facilitated glucose transport across peritubular mem. limited # transporters so transport max exists |
| Glucoseuria during pregnancy | GFR increased which increases filtered glucose load. |
| what happens when there are abnormalities/defects in Na/glucose co-transporter | decrease max b/c problem w/ transporter. Glc excreted into urine at lower concentration |
| Fancoli syndrome | disorder in renal proximal tubule. issue w/ Glu transporter. acquired or congential. failure to reabsorb glucose, bicarb, phosphates, certain AA (cystine, ornithine, lysine, arginine) |
| positive Na balance | Na excretion less than intake. retaining Na in ECF. increase ECF volume therefore increase BP. |
| negative NA balance | Na excretion greater then intake. Na lost. decrease ECF vol therefore decrease BP |
| Most Na reabsorption occurs where | in the proximal convoluted tubule. water reabsorption linked. |
| early proximal convoluted tubule | Na reabsorbed most w/ bicarb, Glu and AA. use Na to help transport things. |
| late proximal convoluted tubule | Na reabsorbed w/ Cl |
| why is the proximal convoluted tubule the site of glomerulotubular balance? | b/c coupling reabsorption to GFR |
| the highest priority elements to reabsorb are what | Na, glucose, AA, bicarb |
| Na reabsorption in luminal mem | Mostly secondary transport using Na gradient. Co-transport and counter transport mechanisms. |
| What elements have been reabsorbed by mid PCT | 100% of filtered glucose and AA. 85% of filtered bicarb. Most filtered phosphate, lactate, and citrate |
| how is Fancoli Syndrome diagnosed | increased acid in blood. Increase glucose, AA, phosphates |
| Where is NaCl absorbed | in late proximal convoluted tubule |
| Cellular route of Na reabsorption in late PCT | Na/H exchanger (luminal). Cl/formate exchanger (luminal). |
| Paracellular route of Na reabsorption in late PCT | tight junctions lose and permeable to small solutes. Cl diffuses, followed by Na |
| Glomerulotubular balance | major regulatory mechanism in PCT to ensure that a constant fraction of filtered loa is reabsorbed, regardless of changes in GFR |
| Glomerulotubular balance mechanism | increase filtration fraction, filtering more, increase oncotic pressure, increase reabsorption. |
| What happens if you don't have glomerulotubular balance | loose a lot of Na in urine |
| Thin descending limb | permeable to water and small solutes. water out, solutes in |
| Thin ascending limb | permeable to small solutes. Solutes move out, water stays in. |
| Thick ascending limb | Actively reabsorbs filtered Na, load dependent. |
| Main transporter in thick ascending limb | Na/2Cl/ K co transporter |
| Early distal tubule | reaborbs filtered Na. impermeable to water. |
| Late distal tubule and collecting ducts | principal cells and a-intercalated cells. reabsorbs Na. Fine tuning. |
| Transporter in early distal tubule | Na/Cl co transporter |
| Principal cells | Not- co transport. use Na channels and diffusion. |
| Spironalactone | K sparing diuretic. inhibits aldosterone effects. |
| Amiloride and triameterene | K sparing diuretic. Bind luminal Na channel |
| Maintaining K balance is essential for what function | function of excitable tissues. |
| Internal K balance | distribution of K across cell mem. affected by drugs, hormones, pathological states. determines resting mem potential. |
| external K balance | renal mechanisms to manage variations in K intake |
| Hypokalemia does what to AP | hyperpolarization. more neg resting mem potential. harder to depolar. muscle weakness. |
| Hyperkalemia does what to AP | hyperexcitable cells. more pos resting mem potential. |
| How does insulin change internal K balance | increase Na/K ATPase activity. Take up glucose. increase K into cells. prevents hyperkalemia by moving K into cells |
| why is Alkalemia associated w/ Hypokalemia | increase pH in ECF b/c low H. H leaves cells, K enters cells |
| why is Acidemia associated w/ hyperkalemia | low pH in ECF b/c high H. H enters cells, K leaves cells |
| B2 adrenergic agonists and K | increases activity of Na/K ATPase. increase K in cells. hypokalemia. |
| a-adrenergic angonists and K | shift K out of cell. hyperkalemia |
| Hyperosmolarity and K | shift K out of cell b/c water in ECF. increase concentration of solutes (K) in cell. create driving force to move K out |
| when can exercise cause hyperkalemia | individual w/ renal failure. or if taking B2 adremergic antagonist |
| in which portions of the nephron is K reabsorption relatively constant | proximal convoluted tubule and thick ascending limb |
| K reabsorption in distal tubule and collecting duct | fine tuning. low k=reabsorption w/ a-intercalated cells. high K= secretion of K w/ principal cells. |
| K reabsorption w/ a-intercalated cells uses what pump | H/K ATPase in luminal mem |
| K secretion w/ principal cells uses what pump | Na/K ATPase (blood to lumen) K channels (out of cell) |
| Aldosterone and K | increases K secretion by principal cells. more syn of luminal Na channels. increase synthesis of Na/K ATPase |
| most Phos is reabsorbed where in nephron | proximal convoluted tubule |
| why is it important that 15% of filtered phos is excreted? | acid base buffering. get rid of H+ |
| what phos transporter is found in the proximal tubule cells? | Na/phos co transporter in luminal mem |
| PTH | regulates reaborption of phos in proximal tubule by inhibiting Na/phos co-transporter. |
| Phosphatonins-direct action | induce neg phos balance by inhibiting renal phos reabsorption in proximal tubule |
| Phosphatonins-indirect action | induce neg phos balance by reducing intestinal absorption of pos and inhibiting syn of active vit D3. |
| Function of FGF-23 in phos regulation | 1. acts on kidneys to decrease Na/phos co transporter 2. suppresses 1-a-hydroxylase. inactivate Vit D. impair Ca absorption |
| when is FGF-23 secreted by osteocytes | elevated calcitriol (active vit D) |
| function of calcitonin | inhibits bone reabsorption |
| Where and to what compound is Ca tightly coupled to | Na reabsorption in proximal tubule and loop of henle |
| Ca absorption in thick ascending limb | paracellular route coupled to Na reabsorption. K leaking back into lumen. increase in pos charge in lumen (K leaves) drives Ca reabsorption |
| loop diuretics | inhibit Ca reabsorption similar to Na reabsorption. treat hyperclcemia. |
| Ca and distal tubule | reg of Ca reabsorption. No longer coupled to Na. PTH regulated |
| What is the Ca transporter in the distal tubule | TRPV-5. luminal Ca channel. more Ca enter cell |
| Where is the majority of Mg reabsorbed | thick ascending limb. driven by lumen pos charge (drive reabsorption of cations). |
| where do hormones that alter water reaborption in the kidney work? | Late distal tubule and collecting duct |
| insensible water loss | water loss via sweat and water vapor |
| sensible water loss | urine |
| what cells do ADH bind to increase water reabsorption | principal cells in dital tubule and collecting duct |
| what happens when water reabsorption increases, urine osmolarity increases to volume of urine? | urine volume decreases |
| what mechanisms create the corticopapillary osmotic gradient? | 1.counter current multiplication in loop of Henle 2.urea recycling in the inner medullary collecting ducts |
| what segments of the nephron is urea not transported | 1. thick ascending limb 2.distal tubule 3.cortical and outer medullary convoluted tubule |
| what transporter moves urea | UT1 carrier protein. moves via simple and facilitated diffusion. ADH activated |
| countercurrent exchange | passive process that helps to maintain corticopapillary osmotic gradient. involves vasa recta. |
| Methods of kidney maintaining normal acid-base balance | 1.Rebasorption of bicarb 2. excrete H+ |
| where is bibarb reabsorbed in the nephoron | early proximal convoluted tubule. H constantly recycled |
| interaction of PCO2 and bicarb reabsorption | increase PCO2, increase bicarb reabsorption. renal compensation for chronic respiratory acid base disorders |
| what cell type does excretion of H occur in | a-intercalated cells. |
| what mechanisms are used to excrete H | 1. H+ATPase 2. H/K ATPase |
| where does secreted H originate when going to excrete it? | 1. Carbonic acid dissociation |
| where in the nephron is H excreted as NH4 | Proximal tubule, thick ascending limb, a-intercalated cells of collecting duct |
| what transporter in the thick ascending limb reabsorbs NH4? | Na/K/2Cl transporter. sub-out K for NH4 |
Created by:
ejohnson17
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