Renal Flashcards

Question

Why can NSAIDS damage the kidney when renal perfusion is low?

Answer 1

NSAIDs stop the synthesis of prostaglandins that act as a brake to prevent over vasoconstriction in response to low renal perfusion Thus you reduce the blood flow even more and cause more renal damage

Answer 2

1. Transcellular. You transport Na into the cell from the tubule via an apical channel/carrier. Then you move the Na out of the cell through the basolateral side via the Na/K ATPase...this is also the one that's affected by diuretics 2. Paracellular: moves through the tight junctions b/w cells due to a tubular electrochemical gradient

Answer 3

1. Na/H antiport where H is secreted per Na reabsorbed. This proton in the lumen combines with a bicarbonate and forms carbonic acid that breaks down into water and CO2. The CO2 enters the cell again and combines with water to form carbonic acid, which is broken down into bicarbonate ion and a proton by CARBONIC ANHYDRASE. the proton then goes and brings in another Na. Meanwhile, the water from before, goes paracellular into interstitial fluid. 2. You have a Na/Glucose cotransporter

Answer 4

1. you have two antiporters that bring in Na and Cl while kicking out H+ and an anion, respectively. in the lumen, the H+ and the anion combine together and enter the cell, where they dissociate again and bring back another Na and Cl 2. The Cl- gradient favors movement of Cl- from lumen to interstitial fluid. This causes the areas locally around the transporter to be positive. This positive charge is the driving force for the paracellular transport of Na

Answer 5

From the two mechanisms in the early PCT (1. Na/H antiport 2. Na/Glucose cotransport) that bring in Na but leave Cl- in the lumen, causing a negative charge After the PCT, it goes from hyperosmotic to isosmotic

Answer 6

Na and HCO3-

Answer 7

You have a Na/K/2Cl transporter that actively brings in all 3 ions into the cell. Then the K is released back into the lumen to be recycled and ensure that this transport can continually happen. This also creates a net positive charge in the TAL segment, which leads to the paracellular expulsion of Na/K/Mg/Ca from the lumen into the interstitial fluid

Answer 8

Early DCT --> Na/Cl cotransport Late DCT/CD ---> you have an eNaC channel that allows for Na to flow inside the cell. The lack of Cl- coming out causes a huge negative charge in the lumen, which acts as the electrochemical graident for moving Cl- out paracellularly. Also, you have a channel that releases K into the lumen to ensure you still have an electrically negative cell that allows for the Na to move in.

Answer 9

Thiazide block the Na/Cl cotransporter in early DCT Furosemide blocks the Na/2Cl/K in TAL Acetazolamide blocks the Carbonic anhydrase in the early PCT and stop Na reabsorption by reducing the supply of H+ in the cell that can be sent out Amiloride blocks the eNaC channel in the end and is known as a K-sparing diuretic

Answer 10

It's a measure of the efficiency of tissue perfusion by blood...HOW WELL DOES BLOOD CIRCULATE TO THE TISSUES IN THE BODY

Answer 11

Baroreceptors help to regulate ECV. Baroreceptors in the juxtaglomerular apparatus affect renin secretion Low pressure sensors in the pulmonary vein & atria that regulation secretion of ANP High pressure sensors in the carotid sinus & aortic arch that regulate sympathetic activity

Answer 12

Short term CHANGE BP by affecting heart and blood vessels Long term CHANGE SODIUM EXCRETION by affecting the kidneys

Answer 13

1. Increased RPF and GFR will cause increased Na excretion 2. Starling forces at the peritubular capillaries. If you have low hydrostatic pressure or high oncotic pressure, then you favor reabsorption

Answer 14

This is when you favor filtration in the peritubular capillaries, and thus any reabsorbed material in the interstitial fluid goes back into the tubule

Answer 15

Stimulated by LOW BP, sympathetic stimulation, & reduced delivery of NaCl to the macula densa Inhibited by High BP, ANP, and increased delivery of NaCl to the macula densa RAS controls the reabsorption of Na and thus the blood volume

Answer 16

Angiotensinogen by the liver is modified by renin by the kidneys into angiotensin I. This is further cleaved by ACE into angiotensin II. Aliskiren (Tecturna) is a renin inhibitor. Captopril is an ACE inhibitor. Losartan is a AT1 receptor antagonist.

Answer 17

While both help to reduce BP by affecting the effect of Angiotensin II. Captopril is an ACE inhibitor w/ side effects that are due to ACE's secondary function of degrading bradykinin into its metabolic factors. If ACE is inhibited, then bradykinin builds up and causes vasoconstriction & coughing.

Answer 18

RESISTANCE: Increases resistance in afferent and efferent arterioles that increases FF and reduces RPF. This increases oncotic pressure and decreases hydrostatic pressure in peritubular capillaries. Stimulates reabsorption of Na EXCHANGER: stimulates the Na/H exchanger in early PCT and the eNaC channel in the late DCT/collecting tubule VASOCONSTRICTION (systemic) ALDOSTERONE SECRETION THIRST INDUCTION

Answer 19

This reduces the RPF to the kidney and makes them think that you have reduced blood volume...hence increases renin secretion and increases blood volume...leads to hypertension

Answer 20

Increases the transcription of Na/K ATPases and eNaC channels to increase Na reabsorption in the collecting duct and DCT Also, increases K+ secretion

Answer 21

Constricts afferent and efferent arterioles that leads to increased re-absorption in peritubular capillaries Increases renin secretion Stimulates Na/H antiport & Na/K ATPase in PCT to increase Na reabsorption

Answer 22

1. Increases free-water reabsorption in the collecting tubules ( 2. Increases the activity of Na/K/2Cl transporter in TAL 3. Increases activity of eNaC in the DCT

Answer 23

This is an aldosterone antagonist!

Answer 24

Low perfusion based ARF is due to a fractional excretion below 1% Tubular necrosis causes fractional excretion to be higher than 2%

Answer 25

This is an abnormally large increase in your aldosterone due to increased secretion by the adrenal medulla. it causes your plasma Na to remain unchanged (water also brought in to balance this out), BP to be increased, K excretion increases and decreases plasma K, blood pH becomes more basic, and renin concentrations decrease (negative feedback) secondary is similar to primary in terms of symptoms..instead you have a known cause (usually due to increased renin-angiotensin II)

Answer 26

1. Renal artery stenosis | 2. Hypovolemia

Answer 27

This is a defect in the transporters of the TAL. Type 1 is a defect in the Na/K/2Cl. Type 2 is a defect in the apical K channel. Type 3 is a defect in the basolateral Cl channel. Type 4 is a defect in the barttin subunit of the basolateral Cl channel Plasma K decrease, Urine volume increases, ECF volume decreases, plasma aldosterone increases, blood pH increases/basic, urinary Ca/Mg excretion increases

Answer 28

Defect in the Na/Cl cotransporter in the early DCT and is less severe than barrter syndrome since the DCT only accounts for 7 percent of the Na reabsorption urine volume increases, ECF volume decreases, plasma K decreases due to increased plasma aldosterone, blood pH increases (basic), urinary Ca excretion decreases

Answer 29

Defect in the eNaC that hyperactivates. Na reabsorption increases, ECF volume increases, Plasma K decreases, and Plasma aldosterone decreases Treatment: Amiloride which inhibits the eNaC

Answer 30

This is a defect in the eNaC channels that inactivates them or in the aldosterone receptor that prevents it from recognizing the hormone. Causes hypoaldosterone like symptoms even though you'll have high levels of aldosterone ECF volume decreases, BP decreases, plasma K increases, and ALDOSTERONE INCREASES

Answer 31

This is when you have no ADH and this causes increases urine volume, reduce urine osmolarity, and increased plama Na since you don't have as much water coming back into the cell Treatment: GIVE THEM ADH

Answer 32

Similar symptoms to CDI however, the reason for this is due to LACK OF ADH RECEPTOR or LACK OF AQUAPORIN Treatment: Reduce sodium intake and drink plenty of fluids...can't give them ADH since that won't do anything

Answer 33

This is a condition where you have increased water in the collecting tubules and they can't be taken out. Urine volume increases, Na & K excretion increases b/c increased water in the tubule reduces their concentrations and thus their driving force to move into interstitium, and ECF volume decreases Treatment: Provide patient w/ insulin and fluids with Na & K

Answer 34

These are both SGLT inhibitors that are used in diabetes to prevent the reabsorption of glucose Canagliflozin can also cause dehydration by affecting the uptake of sodium and thus reducing the water intake as well

Answer 35

Glucose reabsorption threshold = 200 mg/dl if you go above this value then you will start to see glucose in your urine b/c of the over saturation of SGLT transporters...thus your clearance is not enough

Answer 36

this is the gradual approach to Tm at high plasma glucose levels

Answer 37

Both are essentially completely reabsorbed by the end of PCT AA: antiport with H Carboxylates: cotransported w/ Na

Answer 38

K+ is the most permeable ion in the cell and it therefore dictates the membrane voltage...having too much K in the extracellular matrix causes depolarization of the membrane and makes you more excitable since you have a more positive voltage than normal due to reduce driving force. Meanwhile, decreasing extracellular K causes hyperpolarization as a large amount of K leave the cell

Answer 39

K+ is the most permeable ion in the cell and it therefore dictates the membrane voltage...having too much K in the extracellular matrix causes depolarization of the membrane and makes you more excitable since you have a more positive voltage than normal due to reduce driving force. Meanwhile, decreasing extracellular K causes hyperpolarization as a large amount of K leave the cell

Answer 40

1. Rapid Method: Where the cells simply take up the k and act as a buffering mechanism 2. Slower method: Increased excretion by kidneys

Answer 41

95% of filtered K is reabsorbed (65% in PCT via paracellular transport; 30% in PCT via Na/K/2Cl and paracellular transport; type A intercalated cells very minor amounts) Secretion (small amount): increased plasma [K+] causes an increase Na/K ATPase activity that increases the K uptake by intercalated cells from the interstitium --> increases secretion (usually this is used to push out reabsorbed Na into the interstitium). Also, high tubular Na causes increased Na reabsorption and this leads to increased K secretion . FINALLY HIGH FLOW RATE INCREASES K SECRETION

Answer 42

F & T = increase the flow rate and thus cause loss of K A & S = retain K (AKA K-sparing)

Answer 43

Cells have a K/H antiport where K exits the cell and H+ enters the cell. When you have hypokalemia, this works in overdrive to restore plasma [K] and in doing so you pull out a lot of protons making it basic Hyperkalemia, you have reduced function of this mechanism and this causes H+ to not be pushed into the cell and rather it collects on the outside

Answer 44

If you decrease calcium extracellularly, then you need smaller and smaller depolarization to activate the Na b/c you depolarize the membrane Thus, with hypocalcemia you can more easily excite the Na ion channels to activate and form an AP

Answer 45

If you decrease calcium extracellularly, then you need smaller and smaller depolarization to activate the Na b/c you depolarize the membrane Thus, with hypocalcemia you can more easily excite the Na ion channels to activate and form an AP

Answer 46

65% of this happens in PCT and is paracellularly. Another 25% occurs at the TAL paracellularly along w/ Mg, Na, & K. Finally, at the DCT 8% reabsorption that is mostly transcellular via plasma membrane Ca ATPase & Na/Ca exchanger PTH regulates reabsorption by the TAL & DCT

Answer 47

You have too much PTH and thus you have high Ca and low phosphate in plasma High Urine [Ca] Can cause bone problems and kidney stones

Answer 48

If this is happening due to increased plasma Ca, then you have a Ca sensing receptor in the tubular cells that directly inhibits the Ca reabsorption TRIES TO LOSE CALCIUM DUE TO HIGH PLASMA LEVELS & OVERRIDES THE HIGHER PTH

Answer 49

It senses the levels and sends the signal to the parathyroid gland, which regulates PTH secretion Can be in the basolateral membrane of tubular cells If you have low plasma Ca, then it increases reabsorption, increases formation of vitamin D3 (HIGHER PTH) If you have high Ca, then decreases PTH secretion and inhibits reabsorption

Answer 50

A mutation that makes the CaSR to always act as if the plasma [Ca] is low...thus continually high PTH, Ca reabsorption, plasma [Ca] HOWEVER, you will have low urine [Ca]

Answer 51

A mutation that makes the CaSR to always act as if the plasma [Ca] is low...thus continually high PTH, Ca reabsorption, plasma [Ca] HOWEVER, you will have low urine [Ca]

Answer 52

Loop diuretics (furosemide): Inhibit the transporters in the TAL and thus reduce the positive charge gradient in the tubular lumen. Causes a reduction in the Ca reaborption paracellularly Thiazide: inhibit Na/Cl cotransporters in early DCT and this causes less Cl- in the cell which hyperpolarizes the cell ---> This increases the driving force for Ca to enter the cell --> increases Ca reabsorption Amiloride: inhibits the eNaC channel in late DCT and increases the driving force for Ca to enter the cell ---> increases Ca reabsorption

Answer 53

filtration with little reabsorption | secretion

Answer 54

The cell has Na-K-ATPase which creates the Na gradient. This sodium gradient is used to drive alpha keto gluterate into the cell. The AKG is then expelled into the blood and the anion (PAH) enters. PAH exits the cell into the lumen via an unknown mechanism.

Answer 55

Na/K/ATPase creates a concentration gradient and the cation enters the cell via facilitated diffusion. H+ and the cation (excreted) are exchanged at the luminal membrane and using the Na gradient, Na is brought in and H+ is expelled.

Answer 56

PTH increases cAMP production (receptor --> AC --> cAMP). It is found in the urine because of the anion antiporter starts moving it into the lumen because there is too much of it.

Answer 57

PAH is used to measure RRF. Glucuronides help the kidney excrete H2O soluble substances

Answer 58

We give probenicid with penicillin because probenecid will be removed by the same transporter as pencillin. Therefore, penicillin will be able to the stay in the body longer.

Answer 59

HCO3 in the proximal tubule: The luminal membrane has a Na/H exchanger. As you reabsorb Na, H is excreted. It combines with HCO3 in the lumen and forms H2CO3 using carbonic anhydrase. This is broken down into H2O and CO2 and moves back into the cell. There, it uses carbonic anhydrase to go back to H+ and HCO3. H+ is used in the Na/H exchanger again and HCO3 is reabsorbed in the blood using HCO3/ Cl- exchanger or Na/HCO3 cotransporter TAL differs because it has proton pumps.

Answer 60

Alpha cells reabsorb another 10% of filtered load of HCO3 so almost all filtered HCO3 is reabsorbed. It uses two different mechanisms: H-ATPase and H-K ATPase (which is the source of K+ reabsorption in the cell). For each H+ that is secreted, one HCO3 is synthesized and reabsorbed. Beta cells secrete HCO3. Organized in the opposite way of alpha cells.

Answer 61

One way is via titratable acids and the other way is through NH4+. Titratable acids: Done via the alpha intercalated cells. The H+ that is secreted combines with buffers in the blood (PO4, urate, lactate, etc). NH4: In the proximal tubule, glutamine is broken down into the NH3 and glucose. NH3 combines with H to make NH4. This is secreted into the urine via the Na/H exchanger. Glucose goes on to make CO2 and H2O which gives rise to HCO3. Na-HCO3 cotransporter allows the HCO3 to go back into the blood. Remember glutamine transport into the cells is regulated. It increases when plasma pH falls.

Answer 62

carbonic anhydrase inhibitors: inhibits HCO3 reabsorption so alkanize the urine amiloride: inhibit ENaC which makes the lumen more positive and reduces the driving force for H+ into the lumen. Alkanize the urine. Thiazides and furosemide: works on Na/K/2Cl and Na/Cl cotransporters. Causes volume contraction -->RAS--> Aldosterone--> secrete H+ Enhance Na+ delivery to collecting tubules --> ENaC activity increased --> lumen more negative --> H+ pump increases and more H+ secretion K+ wasting --> hypokalemia --> more H+ into tubular cells --> H+ secretion

Answer 63

The detrusor muscle is innervated by parasympathetic nerves and the internal sphincter is innervated by sympathetic nerves. The external sphincter is innervated by somatic nerves. Somatic sensory nerves detect wall stretching and the urge to urinate begins. Pontine centers inhibit the detrusor and keep spinchters closed to prevent urination. When you relax your external spinchter, the pontine centers stop inhibiting parasympathetic nerves to detrusor.

Answer 64

1. Renin Angiotensin System 2. Calcitrol (1,25 diOH vitamin D3): It is made in the liver and the kidneys activate it. The main function is the increase Ca2+ absorption in the intestines. If you have kidney failure, it might cause bone problems. A lack of Vitamin D causes rickets. 3. Erythropoietin: It is made in the kidney and induces the formation of RBCs. Patient in kidney failure are usually anemic.

Renal Flashcards

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