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Block 2; Week 8 > Keef 2 > Flashcards

Keef 2 Flashcards

1
Q

There is a reciprocal movement of what 2 ions in the body?

A

H+ & K+

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2
Q

In metabolic acidosis: what is the pH & K+ levels? Only taking into account the reciprocal relationship

A

Metabolic Acidosis
low pH
High levels of K+

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3
Q

In metabolic alkalosis: what is the pH & K+ levels?

Only taking into account the reciprocal relationship

A

Metabolic Alkalosis:
high pH
Low levels of K+

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4
Q

When you have hypokalemia what is your pH like?

Only taking into account the reciprocal relationship

A

high pH

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5
Q

When you have hyperkalemia what is your pH like?

Only taking into account the reciprocal relationship

A

low pH

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6
Q

When you have metabolic acidosis do you always have hyperkalemia?

A

Absolutely not! This is just the result when you take into account the reciprocal relationship of the 2 ions.

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7
Q

Taking into account normal endogenous acid production…what happens to the following ions in Joe Cell:
H+
K+
Na+

A

The H+ produced in the cell is pushed out of the cell thru the Na+/H+ exchanger.
The Na+ is pumped out of the cell & the K+ is pumped into the cell w/ the sodium potassium pump.

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8
Q

What happens when you add an inorganic acid (like HCl) to the ECF?

A

The HCl is non-permeant so it stays outside of the cell.
However, the Na+/H+ exchanger doesn’t work as well b/c of this buildup.
Therefore you get buildup of endogenous acid inside the cell.
With less Na+ being exchanged into the cell you have less action of the sodium potassium pump.
Therefore, you have a buildup of potassium outside of the cell. Metabolic Acidosis. Hyperkalemia.

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9
Q

What happens in diabetic ketoacidosis to potassium levels? Why?

A

You have a lot more permeant anions…like ketoacids in the ECF.
These are transported inside the cell.
This increases the amount of H+ inside the cell.
It doesn’t change actions of the Na+/H+ exchanger or the sodium potassium pump, however.
Insulin is the determining factor.
Less insulin means less stimulation of the sodium potassium pump.
this causes a buildup of potassium in the ECF.
Metabolic Acidosis. Hyperkalemia.
K+ excreted in urine a bit.
Give insulin & return K+ levels to normal.
If you overshoot with the insulin you could give the patient hypokalemia.

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10
Q

What is the potassium story w/ metabolic acidosis from diarrhea?

A

Diarrhea causes loss of bicarb from the GI.
This causes metabolic acidosis.
this is a hyperchloremic acidosis (inorganic).
Thus, the sodium potassium pump doesn’t work as well & you initially get hyperkalemia.
however, you lose a lot of fluid thru diarrhea & urine…depleting your K+ stores.
Overall: Diarrhea metabolic acidosis–>Hypokalemia

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11
Q

What is the potassium story w/ metabolic acidosis from renal failure?

A

Loss of functioning nephrons.
Difficulty excreting H+ or K+.
Thus, you end up with acidosis & hyperkalemia.

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12
Q

What are the 2 types of renal tubular acidosis & where do they occur in the nephron?

A

Type I RTA occurs in the distal nephron.

Type II RTA occurs in the proximal nephron.

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13
Q

What does RTA do to potassium?

A

Renal tubular acidosis causes spillage of K+ into the urine.
Thus, it causes hypokalemia.

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14
Q

What is the potassium story for diabetic ketoacidosis?

A

hyperkalemia as a result of the lack of insulin. Insulin stimulates the sodium potassium pump & allows for normal K+ levels in the body.

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15
Q

What is the potassium story for lactic acidosis?

A

It usu has normal potassium levels.

This is b/c it is an organic acid. It doesn’t promote the H+/K+ shift.

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16
Q

What are the 2 kidney problems that can promote metabolic acidosis?

A

Renal Failure

Renal Tubular Acidosis

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17
Q

Where specifically does Type I RTA occur?

A

the late DCT & collecting duct: distal nephron

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18
Q

What are some things that can cause Type I RTA?

A

genetic mutation, antibiotic effect, autoimmune disease

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19
Q

What are the 2 general effects that can account for Type I RTA–>that is its problems w/ H+ excretion & bicarb reabsorption?

A
  1. leakiness of the apical membrane.
    * *idea is that pH is low (4.4) here b/c it isn’t permeable to H+…if it is leaky there will be back flow of H+ & less excretion of it.
  2. impaired H+ ATPase or H+/K+ATPase or basolateral bicarb/Cl- exchanger.
    * *these things would prevent H+ secretion
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20
Q

Where is acid secreted from in the distal nephron?

A

the alpha intercalated cells

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21
Q

How low can the PCT pH get?

A

~6

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22
Q

How can you tell if your acidosis problem is due to a problem in the distal nephron?

A

Give ammonium chloride.
It will become an acid load for the body after it hits the liver.
If you have Type I RTA your urine pH won’t be able to get lower than about 5.5 in response to the acid load.

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23
Q 
What will Type I RTA do to the following:
urine bicarb levels
urine pH
urine K+
urine Cl-
Plasma bicarb
plasma pH
Plasma K+
Plasma Cl-
A 
urine bicarb levels: up
urine pH: up
urine K+: up
urine Cl-: down
Plasma bicarb: down
plasma pH: down
Plasma K+: down
Plasma Cl-: up
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24
Q

T/F If you don’t secrete H+ you can’t excrete bicarb.

A

False. If you don’t secrete H+ you can’t reabsorb bicarb.

25
What is the cation that usually travels with bicarb out of the urine w/ RTA?
potassium. | This explains the hypokalemia often present with RTA
26
When you have less bicarb reabsorption & H+ secretion what else do you have less excretion of?
Less Cl- excretion. | Cl- & bicarb seem to usu travel in opposite directions.
27
If bicarb rises & Cl- falls in the body...what happens to the anion gap?
It doesn't change.
28
What are the 3 states that Type I RTA promotes?
Metabolic Acidosis Hypokalemia Hyperchloridemia
29
What are 4 problems that Type I RTA can cause?
bone demineralization urinary stone formation nephrocalcinosis (deposition of calcium in the kidney) failure to thrive
30
What condition did poor Tiny Tim have?
Type I RTA
31
Which is more common Type I RTA or Type II RTA?
Type I RTA
32
Where are the problems of Type II RTA located?
proximal convoluted tubule (proximal nephron)
33
What condition is Type II RTA associated with?
Fauconi Syndrome: generalized disorder of proximal tubule reabsorption
34
What is the mechanism of Type II RTA?
impaired H+ secretion & bicarb reabsorption b/c of issues w/ the Na+/H+ exchanger & the bicarb chloride exchanger.
35
How can you distinguish whether you're dealing w/ a problem in the proximal nephron or the distal nephron w/ metabolic acidosis?
Give ammonium chloride. once it reaches the liver it becomes an acid load. If it is a problem with the proximal tubule, then the urine pH will be able to get below 5.5. Can still get acidic in the distal nephron!!
36
What are the 2 main aspects of treatment for renal tubular acidosis?
Bicarb replacement: sodium bicarbonate consumption | Potassium replacement: potassium citrate consumption
37
What happens to your body & to your urine pH, urine K+ & urine bicarb after a single episode of vomiting?
``` Lose H+ thru vomiting. Body pH alkalotic. Secrete less H+ into lumen. Reabsorb less bicarb. Urine pH is alkalotic. Lose bicarb in your urine. Lose K+ in your urine b/c it follows the bicarb out. Form less ammonium that goes into your urine. Overall: Lose H+ in vomit. Lose bicarb in urine. You're fine. ```
38
What happens to your extracellular volume with persistent vomiting?
it decreases. You can become dehydrated b/c of loss of fluids thru vomiting & lack of intake of fluids b/c of condition.
39
What are the plasma sodium levels like in a person after persistent vomiting? Why?
They are probably pretty normal. this is only b/c the body is trying really hard to conserve fluid & sodium in the face of dehydration. This is thru the action of aldosterone.
40
Aside from aldosterone, what else will be high in a person after persistent vomiting?
ADH as an attempt to conserve water. Remember: they are dehydrated after vomiting so much!
41
What are the plasma potassium levels like in a person after persistent vomiting?
They are low. They excreted a lot of K+ in their urine at the beginning of their period of vomiting. Now, their stores of potassium are depleted. They are in a state of hypokalemia.
42
What are the plasma chloride levels like in a person after persistent vomiting?
They are low. | This makes sense because they have been vomiting out all of their hydrochloric acid.
43
What are the plasma bicarb levels like in a person after persistent vomiting?
They are high. | They person is alkalotic, after all.
44
What is the arterial pH in a person after persistent vomiting?
High.
45
What is the PaCO2 like in a person after persistent vomiting? Does this make sense?
It is high. This makes sense b/c the body caused hypoventilation to compensate for the metabolic alkalosis. This extra acid is helpful.
46
What is your BUN like after persistent vomiting?
It is super high. This is b/c urea isn't excreted from your body b/c you are conserving water & urea follows water.
47
What is the creatinine like after persistent vomiting? Why?
It is high. This is b/c creatinine isn't being excreted as much. This is indicative of a low GFR. Make sense b/c trying to conserve volume.
48
What is the urine sodium conc'n like after persistent vomiting?
Super low. | This makes sense b/c you are trying to conserve your water & sodium. You're dehydrated.
49
What is your urine potassium conc'n like after persistent vomiting?
super low. Originally, after one episode of vomiting: you excreted your potassium...this was b/c potassium follows bicarb. Now, your stores are so low that your potassium in the urine is low, too.
50
What is the urine chloride conc'n like after persistent vomiting? Why?
It is low. You are already hypochloremic b/c of your vomiting. Plus, you are dehydrated & reabsorbing all the sodium you can & chloride will be reabsorbed along w/ the sodium. Thus, you won't have much chloride in your urine.
51
What is the urine pH like after persistent vomiting?
On the more acidic side. This is bad for their body, but the desire to retain volume trumps the acid base balance.
52
After persistent vomiting, are you likely to have an anion gap issue?
No. b/c the chloride in the body is going down & the bicarb in the body is going up.
53
What is the urine osmolarity after persistent vomiting?
Still hypertonic. This is b/c there is a very small volume of urine & the urea that is present there makes it very concentrated.
54
After a single episode of vomiting, what is the urine pH like?
alkalotic.
55
What are the reasons why you still secrete & excrete H+ when your pH is so alkalotic after days of persistent vomiting?
Seems bad. It is b/c volume retention trumps acid base balance. Aldosterone causes sodium reabsorption (& K+ secretion). It also directly stimulates the H+ATPase that secretes H+. Also when you are experiencing hypokalemia, more K+ will move outside of the cells. This will promote the action of the K+/H+ exchanger. Ultimately, it all favors H+ secretion & excretion.
56
In addition to acidic urine, what else is found in urine after volume retention beats acid base balance?
More titratable acid & ammonium.
57
How would you treat a patient w/ metabolic alkalosis from persistent vomiting?
Crush 'em w/ fluids!! | And give them potassium for their hypokalemia.
58
Why might you still see low chloride conc'n in the urine even after treating the patient w/ metabolic alkalosis?
b/c now you can excrete a bunch of bicarb & Cl- typically goes in the opposite direction. It will take a while for this to become normal again.
59
``` If you have hyperaldosteronemia (either primary or secondary) what happens to the following: H+ K+ bicarb Na+ What state results? ```
``` H+ secretion increases K+ secretion increases bicarb reabsorption increases Na+ reabsorption increases Metabolic Alkalosis results. ```

Block 2; Week 8 (6 decks)

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