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Renal
Anatomy & Physiology: Renal
| Question | Answer |
|---|---|
| Where is renin released from? | Granular (JG) cells of the macula densa |
| Where is the juxtaglomerular apparatus located in the nephron? | afferent arteriole |
| What are the 3 causes of renin release? | 1. stimulation of B receptors by sympathetic nerves 2. reduction in kidney perfusion 3. reduction in Na+ delivery in macula densa |
| Where is the macula densa located? | distal tubule |
| What are the autoregulator methods of renal blood flow? | 1. myogenic response 2. tubuloglomerular feedback |
| What is the myogenic response? | increased RBF is sensed by vascular smooth muscle and causes them to constrict |
| What is the tubuloglomerular feedback response? | increased NaCl to macula densa leads to constriction of afferent arteriole and decreased renin release |
| What is the main effect of administering an isotonic saline solution? | increased extracellular volume |
| What changes in starling forces cause edema? What are some specific causes of each? | 1. ↑ glomerular capilary pressure; hypertension 2. ↑ interstitial oncotic pressure; trauma, burns or infection 3. ↓ capillary oncotic pressure; liver failure, nephrotic syndrome |
| What is the purpose of the lymphatic system? | to return interstitial fluid and proteins to the vascular compartment |
| 1. How does the charge of the glomerular barrier affect filtration? 2. What contributes these charges? | 1. negatively charges barrier repels large negatively charged solutes 2. neg. charged glycoproteins |
| How do starling forces change along the glomerular capillaries? | only capillary oncotic pressure increases |
| What substance is used to clinically measure GFR? | creatinine |
| How does ADH affect BUN? | ADH causes increased BUN reabsorption |
| If the GFR quickly decreases by 1/2, how does the nephron maintain the same excretion rate of a solute? | the solutes plasma concentration increases by 2x |
| What happens to GFR immediately upon dehydration and why? | GFR decreases because of afferent arteriole constriction mediated by sympathetic response (baroreceptors) |
| 1. If arterial pressure increases, how does the nephron maintain constant GFR and RBF? 2. What are these mechanisms called? | 1. autoregulatory mechanisms -- mainly constriciton of afferent arteriole 2. Myogenic response and tubuloglomerular feedback |
| 1. What receptors do vascular smooth muscle cells have that lead to vasoconstriction? 2. What do binding of these receptors cause in coronary vasculature? | 1. A1 receptors for adenosine 2. vasodilation |
| How does GFR affect reabsorption? | a decrease in GFR allows more time for reabsorption to occur |
| How does angiotensin II affect renal vasculature at low levels? At high levels? | 1. constricts efferent at low levels 2. constricts both afferent and efferent at high levels |
| Where in the nephron is water permeable? | 1. proximal tubule 2. descending limb of Henle's loop 3. collecting duct |
| Where does AVP act on in the nephron and how does it affect water reabsorption? | acts on the collecting duct to increase water reabsorption |
| When is ADH (AVP) released? | 1. ↑ plasma osmolality 2. ↓ plasma volume 3. stress, pain 4. ↓ ethanol |
| 1. What is the greatest stimulus for ADH release? 2. Is ADH released at normal osmolality | 1. decreased plasma volume as in hemorrhage 2. Yes |
| How does glomerulonephritis cause hypertension? | 1. decreased GFR causes NaCl and water retention leading to expansion of the vascular volume 2. protein blocks NaCl from filtering at glomerulus |
| Which has a higher permeability per unit area for salts and water: muscle capillaries or glomerular capillaries | glomerular capillaries |
| How do the kidney's respond to increased mean arterial pressure? | autoregulatory responses to constrict afferent arteriole |
| How do the kidney's respond to decreased mean arterial pressure? | 1. renin and AVP release 2. sympathetic response |
| 1. What fraction of water is reabsorbed in the proximal tubule? 2. for solutes in the filtrate that are freely filtered into the tubule, what is their concentration after water reabsorption? | 1. 2/3 2. 3x plasma concentration |
| What is the filtration fraction? | FF = GFR/RBF |
| Which segment of the nephron is the diluting segment? Why? | 1. thick ascending limb and distal tubule 2. Na is reabsorbed but not water |
| What is the osmolality of the proximal tubule? Of the plasma? | both are ~300 mOsm |
| What is TF/P? | ratio of the osmolality of tubular fluid to plasma |
| What is the TF/P in: 1. proximal tubule 2. descending tubule 3. ascending tubule | 1. 1 2. increases b/c water is reabsorbed with solute 3. decreases back to 1 b/c solute reabsorbed without water |
| Lowest tubular osmolarity in a well hydrated subject: | Deep medullary collecting duct |
| 1. Where in the nephron is the Na/K/2Cl symporter? 2. Where in the nephron is the Na/K ATPase in the basolateral membrane? 3. Where in the nephron is the Na/H antiporter? 4. Na/organic solute symporter? 5. electrogenic Na+ channels | 1. ascending limb 2. entire nephron 3. proximal tubule and ascending limb 4. proximal tubule 5. principal cells of collectig duct |
| Where in the nephron can tubular fluid be either hypotonic, isotonic or hypertonic to plasma? | deep medullary collecting duct depending on the levels of ADH |
| Where does Angiotensin II stimulate H+ secretion? | acts on Na+/H+ transporters in the proximal tubule and thick ascending limp of Henle's loop |
| 1. Where in the nephron does aldosterone act to increase H+ secretion? 2. Where does it act upon the Na/K ATPase? 3. What does this lead to? | 1. H+ ATPase in alpha intercalated cells of the collecting duct 2. increases synthesis of Na/K pump in principal cells of collecting duct and late distal tubule 3. increased Na reabsorption and K secretion |
| Which cells of the collecting duct does ADH act upon? | principal cells |
| 90% of HCO3 is reabsorbed where? | proximal tubule |
| What is the most important regulator of aldosterone release? | plasma potassium concentration |
| Tranfusion of 1 liter of whole blood into a normal person will stimulate secretion of ... | atrial natriuretic peptide |
| The substance which makes the greatest contribution to the osmolarity of the deep medullary interstitium is? | urea |
| Changes in the rate of K excretion depend predominantly on changes in the activity of.... | transport through principal cell K+ channels |
| To measure the rate at which the kidney synthesizes new bicarbonate to replace that used in the buffering process, you need to determine... | urinary titratable acid + urinary NH4+ |
| What is the tonicity of ___ compared to plasma: 1. proximal tubule 2. end of the descending tubule 3. early distal tubule 4. collecting duct | 1. isotonic 2. hypertonic 3. hypotonic 4. variable depending on ADH secretion |
| 1. Transport of glucose against its concentration gradient in kidney cells occurs by which mechanism? 2. Which solute does it travel with? | 1. secondary active cotransport (symport) sodium dependent glucose transporter (SGLT-1) 2. sodium |
| Urea is reabsorbed ____ and secreted ____ in the nephron. | 1. inner medullary collecting duct 2. thin ascending limb |
| 1. What is the normal BUN/creatinine ratio? 2. What is BUN/creatinine ratio during renal failure | 1. 15 2. still 15 but both values are high |
| 1. BUN/creatinine ratio during dehydration? 2. How does this differ from renal failure + dehydration? | 1. 30 2. still has ratio of 30 but values are both very high |
| Prerenal failure originates because of... | hypoperfusion of kidney (ie, from plaque buildup) |
| What is the formula for net transport rate? | = Filtered Load - Excretion Rate = (GFR x Px) - (Ux x V) |
| 1. If net transport rate is positive, what can be said about the solute excreted? 2. If net transport rate is negative, what can be said about the solute excreted? | 1. net reabsorption 2. net secretion |
| 1. Total Body Water is approximately? 2. Extracellular Fluid volume is? 3. Intracellular Fluid volume is? | 1. 42L 2. 17L 3. 25L |
| What affect does ANP have on the renal system and circulation? | 1. dilation of afferent arterioles 2. inhibition of aldosterone 3. inhibition of renin |
| Identify how each diuretic acts on the nephron: 1. CA inhibitors 2. Osmotic Agents 3. Loop agents 4. Thiazides 5. aldosterone antagonits 6. ADH antagonist | 1. inhibits Na+ reabsorption 2. inhibits reabsorption of solute 3. inhibits Na/2Cl/K symporter 4. inhibits NaCl cotransporter 5. inhibits action of aldosterone 6. inhibits ADH |
| Identify where each diuretic acts on the nephron: 1. CA inhibitors 2. Osmotic Agents 3. Loop agents 4. Thiazides 5. aldosterone antagonits 6. ADH antagonist | 1. proximal tubule 2. proximal tubule and descending limp 3. ascending limp 4. distal tubule 5. distal tubule/cortical collecting 6. deep medullary collecting |
| Where is K+ reabsorbed? | 1. proximal tubule 2. ascending limp 3. a intercalated cells (H+/K+ antiporter) |
| What effect do AT II and ANP have on peripheral vasculature? | AT II causes vasoconstriciton ANP causes vasodilation |
| If a hyperosmotic NaCl solution was administered, what would happen to urine flow? | ADH would increase and urine flow would then decrease |
| How does NaCl transport differ in the thin and thick ascending limb? | 1. thin is passive 2. thick is active by the Na/K ATPase |
| How do Diabetes Insipidus and SIADH both cause hyponatremia? | DI causes polydipsia and dilution of Na+ while SIADH causes water retention and thus dilution |
| What transporter does Na+ use to cross the lumen in: 1. proximal tubule 2. thin ascending limb 3. thick ascending limb 4. distal convoluted tubule 5. collecting duct | 1. Na/H antiporter, Na/solute symporter 2. passive channel 3. Na/K/2Cl symporter, Na/H antiporter 4. Na/Cl symporter 5. passive channel |
| How would increased aldosterone affect NH4 output? | increase NH4 excretion by activating the H ATPase on a intercalated cells |
| What effect do loop and thiazide diuretics have on K concentration? | 1. drugs ↓ Na reabsorption in loop or distal tubule 2. ↑ Na to collecting tubules →↑Na/K activity in collecting duct 3. hypokalemia can result |
| Vasopressin binds __ receptor on principal cells and activates __ subunit of the GPCR. | 1. V2 2. Gas |
| What are the causes of increased anion gap metabolic acidosis? | Methanol Uremia Diabetic ketoacidosis Paraldehyde Iron tablets Lactic acidosis Ethylene glycol Salicylates |
| Which renal tubule acidosis is proximal and which is distal? Which influences H+ and which influences HCO3-? | 1. type 1: distal, prevents H+ secretion on alpha intercalated cells 2. type 2: proximal, prevents bicarbonate reabsorption |
| Which adrenoreceptor causes renin release? | β₁ |
| What is the method of acid base analysis? (BRW AIM) | -look at pH -look at HCO3 -look at pCO2 -see if appropriate compensation has occurred |
| What percentage of total body weight is water? | 60% |
| What gives the glomerular basement membrane a negative charge? | heparan sulfate |
| 1. What is a normal adult GFR? 2. Clearance of which substance can be used to calculate GFR? | 1. ~100 mL/min 2. inulin (creatinine is a close estimate) |
| Which substance is the best estimate of: 1. Glomerular filtration rate 2. Renal plasma flow | 1. creatinine 2. PAH |
| How is PAH handled in the kidney? | all PAH entering the kidney is excreted because is is both filtered and actively secreted in the proximal tubule |
| 1. What is the calculation for filtration fraction (FF)? 2. What is the normal FF? | 1. FF = GFR/RPF 2. Normal FF = 20% |
| 1. Which substance controls the blood flow into the afferent arteriole? 2. Which substance controls the blood flow into the efferent arteriole? | 1. prostaglandins dilate 2. Angiotensin II constricts |
| How do the following effect filtration fraction: 1. afferent arteriole constriction 2. efferent arteriole constriction | FF = GFR/RPF 1. FF doesn't change because both RPF and GFR ↓ 2. FF ↓ because GFR ↑ and RPF ↓ |
| How does an increase in plasma protein concentration effect GFR? | decreases GFR |
| What is the greatest stimulus for ADH secretion? | low blood volume |
| How does digitalis effect potassium concentration? | shift K out of cells causing hyperkalemia |
| What effect does acidosis have on K+ concentrations? | ↑K+/H+ exchanger → ↑ plasma K (hyperkalemia) |
| What effect does alkalosis have on calcium concentration? | alkalosis → stronger binding of free Ca2+ to albumin → ↓ free calcium |
| How are the following handled within the renal tubule: 1. creatinine 2. BUN | 1. filtered and neither secreted or reabsorbed 2. filtered and partly reabsorbed in proximal tubule |
| 1. What is azotemia? 2. Cause of prerenal azotemia | 1. increase in BUN and creatinine 2. hypoperfusion of kidney → ↓ GFR (usually from a ↓ in cardiac output) |
| What BUN:creatinine ratio is seen in: 1. prerenal azotemia 2. renal azotemia 3. postrenal azotemia | 1. ratio > 15 2. ratio < 15 3. ratio > 15 |
| Why does renal azotema present with a BUN:creatinine ratio of < 15. | extrarenal loss of urea (GI, skin) |
| What controls blood flow in: 1. afferent arteriole 2. efferent arteriole | 1. PGE2 2. angiotensin II |
Created by:
amichael87
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