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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
Q

What is the cation that usually travels with bicarb out of the urine w/ RTA?

A

potassium.

This explains the hypokalemia often present with RTA

26
Q

When you have less bicarb reabsorption & H+ secretion what else do you have less excretion of?

A

Less Cl- excretion.

Cl- & bicarb seem to usu travel in opposite directions.

27
Q

If bicarb rises & Cl- falls in the body…what happens to the anion gap?

A

It doesn’t change.

28
Q

What are the 3 states that Type I RTA promotes?

A

Metabolic Acidosis
Hypokalemia
Hyperchloridemia

29
Q

What are 4 problems that Type I RTA can cause?

A

bone demineralization
urinary stone formation
nephrocalcinosis (deposition of calcium in the kidney)
failure to thrive

30
Q

What condition did poor Tiny Tim have?

A

Type I RTA

31
Q

Which is more common Type I RTA or Type II RTA?

A

Type I RTA

32
Q

Where are the problems of Type II RTA located?

A

proximal convoluted tubule (proximal nephron)

33
Q

What condition is Type II RTA associated with?

A

Fauconi Syndrome: generalized disorder of proximal tubule reabsorption

34
Q

What is the mechanism of Type II RTA?

A

impaired H+ secretion & bicarb reabsorption b/c of issues w/ the Na+/H+ exchanger & the bicarb chloride exchanger.

35
Q

How can you distinguish whether you’re dealing w/ a problem in the proximal nephron or the distal nephron w/ metabolic acidosis?

A

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
Q

What are the 2 main aspects of treatment for renal tubular acidosis?

A

Bicarb replacement: sodium bicarbonate consumption

Potassium replacement: potassium citrate consumption

37
Q

What happens to your body & to your urine pH, urine K+ & urine bicarb after a single episode of vomiting?

A 
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
Q

What happens to your extracellular volume with persistent vomiting?

A

it decreases. You can become dehydrated b/c of loss of fluids thru vomiting & lack of intake of fluids b/c of condition.

39
Q

What are the plasma sodium levels like in a person after persistent vomiting? Why?

A

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
Q

Aside from aldosterone, what else will be high in a person after persistent vomiting?

A

ADH as an attempt to conserve water. Remember: they are dehydrated after vomiting so much!

41
Q

What are the plasma potassium levels like in a person after persistent vomiting?

A

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
Q

What are the plasma chloride levels like in a person after persistent vomiting?

A

They are low.

This makes sense because they have been vomiting out all of their hydrochloric acid.

43
Q

What are the plasma bicarb levels like in a person after persistent vomiting?

A

They are high.

They person is alkalotic, after all.

44
Q

What is the arterial pH in a person after persistent vomiting?

A

High.

45
Q

What is the PaCO2 like in a person after persistent vomiting? Does this make sense?

A

It is high. This makes sense b/c the body caused hypoventilation to compensate for the metabolic alkalosis. This extra acid is helpful.

46
Q

What is your BUN like after persistent vomiting?

A

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
Q

What is the creatinine like after persistent vomiting? Why?

A

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
Q

What is the urine sodium conc’n like after persistent vomiting?

A

Super low.

This makes sense b/c you are trying to conserve your water & sodium. You’re dehydrated.

49
Q

What is your urine potassium conc’n like after persistent vomiting?

A

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
Q

What is the urine chloride conc’n like after persistent vomiting? Why?

A

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
Q

What is the urine pH like after persistent vomiting?

A

On the more acidic side. This is bad for their body, but the desire to retain volume trumps the acid base balance.

52
Q

After persistent vomiting, are you likely to have an anion gap issue?

A

No. b/c the chloride in the body is going down & the bicarb in the body is going up.

53
Q

What is the urine osmolarity after persistent vomiting?

A

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
Q

After a single episode of vomiting, what is the urine pH like?

A

alkalotic.

55
Q

What are the reasons why you still secrete & excrete H+ when your pH is so alkalotic after days of persistent vomiting?

A

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
Q

In addition to acidic urine, what else is found in urine after volume retention beats acid base balance?

A

More titratable acid & ammonium.

57
Q

How would you treat a patient w/ metabolic alkalosis from persistent vomiting?

A

Crush ‘em w/ fluids!!

And give them potassium for their hypokalemia.

58
Q

Why might you still see low chloride conc’n in the urine even after treating the patient w/ metabolic alkalosis?

A

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
Q 
If you have hyperaldosteronemia (either primary or secondary) what happens to the following:
H+
K+
bicarb
Na+
What state results?
A 
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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