ds Flashcards

(45 cards)

1
Q

[Q:] How does EPI regulate plasma K+?

A

Increase EPI–> NaK ATPase–> decreases serum K+ by decreasing K+ reabsorption into extrarenal tissues and moveing it in the cell–> while increasing K+ excretion by the kidney.

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2
Q

[Q:] How does insulin regulate plasma K+?

A

High insulin–> + Na/K ATPase–> 3 Na+ out and 2 K+ inside the cell–> decrease plasma K+

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3
Q

[Q:] How does aldosterone regulate plasma K+?

A

Kidneys:

    • aldosterone–> + K+ secretion–> + K+ excretion

Extrarenal tissues

  • +aldosterone–> +K+ secretion–> goes into the intestinal fluids and saliva.
  • Aldosterone also increases acid excretion via production of system alkalosis*
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4
Q

Receptors on afferent*** and efferent arteries –> vasoconstriction

A

alpha-1

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5
Q

Receptors on JG cells that, when stimulated, cause the release of renin–> + RAAS?

A

B1

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6
Q

Receptors on Na/K ATPase that when stimulated, result in

[increased Na+ reabsorption]?

A

alpha-1

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7
Q
A
  • In alkalosis, K+ is exchanged for H+ ions in the cells (K+ enters the cells, H+ ions leave the cells) in order to try and balance H+ concentrations. Therefore, alkalosis can cause hypokalemia.
  • Alpha-catecholamines decrease cell uptake by decreasing the activity of the Na/K ATPase, by reducing cAMP.
  • When cells are damaged, potassium is free to be ejected into the plasma – causing hyperkalemia.
  • Hyperosmolality enhances cell efflux due to a net increase in intracellular K concentration as a result of water leaving the intracellular fluid.
  • Strenuous exercise directs potassium out of cells by an increasing alpha-catecholamines.
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8
Q

How to calculate filtered load

A

Filtered load=

[GFR] * [plasma concentration of x] * [% filterability]

*plasma proteins cannot be filtered. thus, anything bound to plasma proteins will not be filtered.

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9
Q

Characterstics of proximal tubule (4)

A
  • Extensive brush border
  • High SA
  • Many mT to provide NRG for ATPases
  • Where most reabsorption occurs.
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10
Q

PT has a proximal convoluted tubule (early) and a proximal straight tubule (late).

Most reabsorption occurs here and several anions and cations are secreted in the proximal tubule.

What allows the PT to undergo so much reabsorbtion and secretion?

A

Na/K ATPases on the BL membrane.

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11
Q

What role does Na+ play in K+ reabsorption in the proximal tubule?

A

In the PT, K+ reabsorption is similar to Na+ reabsorption.

  • While Na+ reabsorption does not directly regulate K+, the amount of Na+ reabsorbed or excreted changes the environment of the nephron, INDRECTLY affecting K+
  • Changing Na+ and Cl- reabsorption–> alter distal tubular flow and DT Na+ delivery –> later impacting K+
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12
Q

How is K+ reabsorbed in the PT?

A

-K+ reabsorption is driven by +TEPD that is created in the late PT-

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13
Q

What does a + TEPD mean?

What does a - TEPD mean?

A

+ TEPD–> build up of + charges

-TEPD–> build up of - charges

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14
Q

In order for us to be able to secrete K+, the Na/K+ ATPase requires Na+ to be reabsorbed in the distal tubule. How do we make sure enough Na+ arrives at the DT?

A

We must make sure that Na+ does not get reabsorbed too early. To do this, our goal is to increase the amount of K+ in the medulla.

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15
Q

K+ in the late DT and cortical CD

A

Because most of the K+ is reabsorbed in the PCT and the thick ascending limb, the late DT and cortical CD “fines tunes” the concentration of K+ through reabsorption and secretion.

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16
Q

K+ secretion in the late DT and cortical CD occurs via:

A

1. Principal cells

2. B-intercalated cells

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17
Q

K+ reabsorption in the late DT and cortical CD occur via what cells?

A

1. Type A-intercalated cells

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18
Q

What 3 factors stimulate K+ secretion?

A
  1. Increased ECF [K+]
  2. Aldosterone
  3. Increased tubular flow rate
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19
Q

What factors stimulate K+ reabsorption? (4)

A

1. K+ deficiency

2. Low K+ diet

3. Hypokalemia

4. K+ loss through severe diarrhea.

20
Q

K+ secretion via principal cells

21
Q

K+ secretion via B-intercalated cells

A

Type B-intercalated cells are active under alkalotic conditions.

  1. H+ concentration in the ISF is low.
  2. Inside is the type B-intercalated cell, [CO2+H20–> HCO3- + H+], causing a build up of HCO3 and H+.
  3. HCO3-/Cl- exchanger on the apical membrane secetes HCO3- into the urine and reabsorbs Cl-.
  4. H/K ATPase on the BL membrane moves K+ into the cell and reabsorbed H+ into the ISF.
  5. K+ is then secreted via K+leak channels
22
Q

K+ reabsorption via Type A-intercalated cells

A

Type A-intercalated cells are active under acidic conditions. They helps us secrete H+ ions and reabsorb HCO3.

  1. In the ISF, H+ concentrations are high.
  2. [H+ + HCO3- → CO2]
  3. [CO2 then moves inside the intercalated type-A cells]
  4. Inside, we reconvert [CO2+ H20]–> [HCO3 and H+ ions]
  5. H+ ions increase and are secreted via the H/K+ ATPases on the apical membrane which allow H+ to exit and K+ to be reabsorbed into the cell.
  6. As K+ increases in the cell, it is reabsorbed into the ISF via K+ leak channels that are located on the apical membrane.
  7. *HCO3- inside of the cell will be reabsorbed back into the ISF via HCO3-/Cl- exchanger.
23
Q

The most important factors the encourage K+ secretion when it builds up in the ECF are (5)

A
  1. Increase NaK ATPase pumps on the BL membrane of principals cells.
  2. Increase synthesis and insertion K+ channels on the apical membrane
  3. Increase in aldosterone
  4. Increase distal tubule flow rate (increase Na+ delivery to the DT to promote K+ secretion)
  5. Reduced back leakage of K+ from ICF–> renal interstituim (less K+ leaves from ICF through the BL membrane, causing more to make it out of the apical membrane to be secreted)
24
Q

What exactly do we mean by “flow rate”?

Increased flow rate does what?

A
  • Increased flow rate–> dilutes K+ secreted into the lumen–> increasing K+ concentration gradient between the ICF and tubular fluid–> enhances K+ secretion.
    • Increased flow rate also increases Na+ delivered to the distal tubule for reabsorption–> Na+ reabsorbed via ENaC channels–> causing K+ to be secreted.
25
**What exactly do we mean by "flow rate"?** Decreased flow rate does what?
* Decreased flow rate --\> K+ concentration build up early in the tubule--\> decreasing concentration gradient between tubular fluid and cell (ECF and ICF)--\> slows K+ secretion
26
What happens when we have a **high Na+ diet** (eat something REALLY salty)?
27
What happens when we have a high K+ diet (eat several bananas)?
High K+ diet--\> Insulin will move K+ into the princpal cells--\> Build up of K+ in the cell will increase the concentration gradient--\> --\> K+ will be secreted from the PC--\> urine *This is why we don't become hyper/hypokalemic during times of increased or decreased salt intake.*
28
Why is the relationship between the **distal tubule flow rate** and **K+ secretion** important?
It helps aldosterone to **[regulate K+]** and **[Na+ excretion]**
29
What is the difference between **alkalosis** and **alkalemia**?
1. **Alkalosis--\>** high pH (low H+ ions) in the ECF. 2. **Alkalemia--\>** physiologically high blood pH.
30
**Alkalosis** is typically a problem with ***hypokalemia***. How does this occur? mneumonic: ***alkalosis; k is lo***
**Alkalosis** is typically a problem with ***hypokalemia.*** **Alkalosis**: + activity of Na/K+ ATPase pump *(and adds K+ channels into apical membrane)* --\> increases intracellular K+ concentration--\> K+ passively moves from the cell to the lumen--\> K+ is secreted * Result: **HYPOKALEMIA**
31
What is the difference between **acidosis** and **acidemia**?
1. **Acidosis**--\> increase in H+ ions in the ECF 2. **Acidemia**--\> physiologically low blood pH
32
**Acidosis** typically a problem with **hyperkalemia**. How does this occur?
**Acidosis**: decreases the activity of the Na/K ATPase *(and decreases K+ channels on the apical membrane)* --\> K+ does not move into cell--\> decrease in intrallular K+ concentration--\> decrease diffusion of K+ into the lumen--\> decreases K+ secretion * RESULT: **Hyperkalemia**
33
**_RECAP_**: **Alkalosis** is association with \_\_\_\_\_kalemia, _____ K+ secretion **Acidosis** is associated with \_\_\_\_\_kalemia, \_\_\_\_K+ secretion
_Alkalosis_ is association with **hypokalemia, increasing K+ secretion.** _Acidosis_ is associated with **hyperkalemia, decreasing K+ secretion.**
34
**Chronic acidosis** \_\_\_\_\_\_K+ secretion.
**stimulate** When problems are chronic, our body learns to compensate for these dillemmas. Chronic inhibition of the Na/K ATPase will prevent us from reabsorbing solutes and fluid, which will increase our tubular flow rate. * As a result, more Na+ is delivered to the distal tubule, which will increase K+ secretion. * Also, we will activate the RAAS system--\> aldosterone--\> K+ secretion
35
36
37
How does increased Na+Cl- reabsorption upstream affect Na+ delivery to CNT and CCD and subsequent events?
**[Decrease Na+ delivery to CNT and CCD]** --\> **[decrease lumen-negative potential difference]** --\> **[decrease K+ secretion]**
38
Aldosterone is a kaliuretic hormone, induced by hyperkalemia. However, until certain condition assx with marked induction of aldosternoe, such as dietary Na+ restriction, Na+ balance is maintained without \_\_\_\_\_\_\_\_.
**Effecting K+ (aldosterone paradox)**
39
Diuretics that inhibit Na+ reabsorption--\>
**promote K+, except for K+ sparing drugs.**
40
Low K+ diet
Low K+ diet--\> princpal cells are depleted of K * Intracellular concentration of K+ decreases--\> decreases the driving force for K+ secretion * Alpha-intercalated cells will reabsorb K+ **RESULT: LOW RATES OF K+ excretion**
41
**DISTAL TUBULAR FLOW RAT**E WILL COMPENSATION FOR
changes in **aldosterone**, which affects K+ secretion and absorption
42
What happens in cases of **acidosis**
1. Na/K ATPase pumps will be inhibited 2. Decrease in intracellular K+ 3. K+ will not be secreted to compensate 1. Decrease proximal tubule reabsorption 2. Increase distal tubular flow rate 3. Increase Na in the DT 4 . increase K secretion
43
What happens in cases of volume expansion
Volume expansion: increase in NaCl 1. Decrease in aldosterone 2. Decrease K secretion to compensation; 1. Decrease proximal tubule reabsorption 2. Increase distal tubular flow rate 3. Increase Na in the DT 4 . increase K secretion
44
What happens in cases of high water intake
1. Decrease ADH 2. Decrease distal K+ secretion and decrease distal water absorption 3. Increase distal flow 4. increase distak K secretion
45
What happens in vases of volume contraction
1. Decreased ECF---\> decreased NaCl 2. Renin 2. ANG II 3. Increase aldosterone --\> increase K+ secretion to compensate; 1. Decrease GFR 2. Decrease distal flow 3. decrease K+ secretion