| 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 |
