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Ok, before I go on the reasoning I would like to say that i'm definitely not an expert and I would like it if some of the veterans who understand this better than I correct me so there is a better mutual understanding of the topic.

Two major factors in Salicylate poisoning:

results due to independant or simultaneous Metabolic Acidosis w/ resp alkalosis.
1) Loss of bicarbonate = promoting factor for K+ excretion by the kidneys, thus hypokalemia.

results due to respiratory alkalosis
1) K+ moves from ECF to interstitial fluid.
2) Loss of more bicarbonate due to compensation of dec CO2.

this is what i believe causes Hypokalemia....correct me if i'm wrong please.
 

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Does this explanation make sense?

Initially there is a respiratory alkalosis due to a direct stimulatory effect on the respiratory centre. To compensate for this there is a loss of bicarbonate from the urine with loss of sodium, potassium and water. This eventually results in a metabolic acidosis, with hypokalaemia and dehydration.

I dont' really get the second mechanism.
 

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Lemme go over everything with you, even the second mechanism of metabolic acidosis

Initially there is a respiratory alkalosis due to a direct stimulatory effect on the respiratory centre. To compensate for this there is a loss of bicarbonate from the urine with loss of sodium, potassium and water. This eventually results in a metabolic acidosis, with hypokalaemia and dehydration.

I dont' really get the second mechanism.
Ok as far as I can relate, the metabolic acidosis doesn't just occur because of loss of bicarbonate in urine, it also occurs because of accumulation of organic acids due to the inhibition of TCA cycle enzymes and alterations in lipid and Amino acid metabolism.

you are on the right track, but that mechanism in my opinion does not have such a large impact in HCO3-, because in mild salicylate poisoning you will have initial or acute respiratory alkalosis, in severe salicylate poisoning the biggest factors are Respiratory Alkalosis and Metabolic Acidosis together. The reason why I say this is because in Resp alkalosis the HCO3- does not always HAVE to be excreted out of the proximal tubules, it can be changed into CO2 itself, how? remember this eq?

H2O + CO2 <= H2CO3 <= HCO3- + H+

in resp alkalosis, since there is lack of CO2 this rxn will go from HCO3- (bicarbonate) to carbonic acid and then water and CO2....so it doesn't necessarily mean that there will be a huge bicarbonate loss but there will be some because you are taking protons and releasing them as CO2 and H2O.

Couple that with vomiting, INC organic acids, and small loss of bicarbonate in urine THEN metabolic acidosis (high anion gap) takes over as a major Factor (remember that resp alkalosis could also occur secondary to metabolic acidosis as a compensatory mechanism)

Now in Salicylate poisoning the pathophysiology is: (all of these things are happening right around the same time and/or overlap eachother, if not exactly simultaneously)
1) Resp alkalosis because of hyperventilation (b/c the resp centers are enhanced) thus CO2 DEC.
2) Simultaneously, since salicylates inhibit the Krebs cycle enzymes (leads to Dec glucose availability and INC organic acids****), and uncouple the oxidative phophorylation (INC metabolism => hyperthermia)
3) alterations in lipid and amino acid metabolism enhance metabolic acidosis (protons provided by glutamic acid and histidine carboxyl groups)
4) vomiting, Inc fluid and electrolyte loss through the kidney (HCO3, K+, Na+) cause dehydration, inc anion gap and DEC buffering capacity to acids.

Again I would like for someone who knows more about this to correct me because this is starting to confuse me now too! lol :eek:
 

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Why there is Hypokalemia in Salicylate poisoning.................
Things to keep in mind... metabollic effects of Salicylate poisoning range from Respiratory Alkalosis to Severe Metabolic Acidosis.

Also metabolic effects of Salicylate poisoning are dose related....

In the moderate toxicity

There is respiratory alkalosis, due to direct stimulation of the respiratory centers & uncoupling of oxidative phosphorylation.

In severe toxicity,

There is high anion gap metabolic acidosis due to increased production of organic acids.

Even in severe toxicity the immediate effect is respiratory alkalosis followed by metabolic acidosis.

Now effect of pH on the Potassium Homeostasis....

Different metabolic disorders affect differently on the Potassium Homeostasis. Even there is difference among the acute & chronic conditions of a same metabolic disorder.

Acute Respiratory Alkalosis cause

1) Intracellular shift of Potassium (dec plasma potassium)
2) Inc. loss from the kidneys (potassium depletion)

Chronic Metabollic Acidosis (as synthesis of organic acids would take some time, so the behaviour of acidosis seen in salicylate poisoning is similar to a chronic disorder)

1) Extracellular shift of Potassium (inc. plasma potassium)
2) Inc. loss of potassium from the kidneys due to release of Aldosterone.
(inc loss of potassium & hydrogen in urine)

It is supported by the fact that the pts of severe salicylate poisoning excrete hydrogen & potassium in their urine.

I hope this helps .....:)
 
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Even in severe toxicity the immediate effect is respiratory alkalosis followed by metabolic acidosis.

2) Inc. loss of potassium from the kidneys due to release of Aldosterone.
(inc loss of potassium & hydrogen in urine)

It is supported by the fact that the pts of severe salicylate poisoning excrete hydrogen & potassium in their urine.
Ok, so there is resp alkalosis preceding metabolic alkalosis in severe toxicity also? you sure? cuz i'm kind of confused by this! whether there is resp alkalosis preceding met acidosis in SEVERE poisoning.

But the 2nd point made is Excellent, can't believe i forgot about that! haha *thumbs up*
 

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Ok, so there is resp alkalosis preceding metabolic alkalosis in severe toxicity also? you sure? cuz i'm kind of confused by this! whether there is resp alkalosis preceding met acidosis in SEVERE poisoning.

But the 2nd point made is Excellent, can't believe i forgot about that! haha *thumbs up*
The metabolic respose of salicylate poisoning is dose dependant in high therapeutic dose (moderate toxicity) there is repiratory alkalosis.

In toxic dose (severe toxicity) there is metabolic acidosis.

Source : kaplan Physiology

The cause of the metabolic acidosis is the production of organic acids which would take some time. While the effects on the respiratory centers are more immediate.
 
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Discussion Starter · #10 ·
Thank you guys for all this info...............thats what Harrison says on this issue..........
In Salicylate poisoning there occur a whole range of effects ranging from Alkalosis to Metabolic Acidosis.
Initially Alkalosis occur that will cause the Hypokalemia due to all the above mentioned ways........Increase Potassium loss and Inward movement of potassium in cell.
Acidosis is the terminal stage of toxicity ending up with respiratory failure.....

Correct me if I am wrong in my understanding of text......
 
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