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    If a 55 year old woman comes into the clinic with deep breathing, pain of passing urine and loss of consciousness. Blood tests show urea is high, haemoglobin is low, inulin is low, potassium is high, bicarbonate is low.

    Couple of things I was wondering.

    First, surely the low haemoglobin and high urea are most likely unrelated, anaemia and kidney stones? Deep breathing is surely an indication of her low oxygen content.

    Secondly, what type of property of drugs would especially need to be considered for this patient? I wasn't sure what this meant. Cointrindicated with pregnancy? Oedema? How they're metabolised presumably, i.e waste products aren't toxic?

    Finally, does the high K+ and low HCO3- indicate anything specifically?

    Thanks
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    (Original post by That Bearded Man)
    If a 55 year old woman comes into the clinic with deep breathing, pain of passing urine and loss of consciousness. Blood tests show urea is high, haemoglobin is low, inulin is low, potassium is high, bicarbonate is low.

    Couple of things I was wondering.

    First, surely the low haemoglobin and high urea are most likely unrelated, anaemia and kidney stones? Deep breathing is surely an indication of her low oxygen content.

    Secondly, what type of property of drugs would especially need to be considered for this patient? I wasn't sure what this meant. Cointrindicated with pregnancy? Oedema? How they're metabolised presumably, i.e waste products aren't toxic?

    Finally, does the high K+ and low HCO3- indicate anything specifically?

    Thanks
    Are you sure about the haemoglobin and urea being unrelated? Think about the hormone that's involved in red blood cell production and where that is produced. The low haemoglobin could partially account for the deep breathing - but think along the lines of acid-base balance, the potassium and bicarbonate levels are important here. There is one major system that seems to be failing here - knowing this will help a lot with these questions, this applies to the drugs question (think metabolism/excretion).

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    (Original post by Mushi_master)
    Are you sure about the haemoglobin and urea being unrelated? Think about the hormone that's involved in red blood cell production and where that is produced. The low haemoglobin could partially account for the deep breathing - but think along the lines of acid-base balance, the potassium and bicarbonate levels are important here. There is one major system that seems to be failing here - knowing this will help a lot with these questions, this applies to the drugs question (think metabolism/excretion).

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    Deficiency in erythropoeitin? The renal system is failing, low bicarbonate levels can lead to metabolic acidosis,

    Isn't the HCO3- linked to hydrogen. Again however, I can't connect them.

    Metabolic acidosis in the long term can lead to a deficiency in CO2 as CO2 and H2O is converted to H2CO3.

    I don't see the connection to erythropoeitin, haemoglobin or urea?
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    (Original post by That Bearded Man)
    Deficiency in erythropoeitin? The renal system is failing, low bicarbonate levels can lead to metabolic acidosis,

    Isn't the HCO3- linked to hydrogen. Again however, I can't connect them.

    Metabolic acidosis in the long term can lead to a deficiency in CO2 as CO2 and H2O is converted to H2CO3.

    I don't see the connection to erythropoeitin, haemoglobin or urea?
    Erythropoeitin is indeed correct, which in renal failure is likely to be low, resulting in a low haemoglobin. Urea also increases in renal failure due to reduced excretion.

    Metabolic acidosis is indeed correct (also related to hyperkalaemia). In metabolic acidosis you compensate using the respiratory system - increasing ventilation 'blows off' CO2, as the failing kidneys won't be conserving bicarbonate.

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    (Original post by Mushi_master)
    Erythropoeitin is indeed correct, which in renal failure is likely to be low, resulting in a low haemoglobin. Urea also increases in renal failure due to reduced excretion.

    Metabolic acidosis is indeed correct (also related to hyperkalaemia). In metabolic acidosis you compensate using the respiratory system - increasing ventilation 'blows off' CO2, as the failing kidneys won't be conserving bicarbonate.

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    So the deep breathing can also be explained by the hyperventilatory response to metabolic acidosis - fair enough.

    Erythropoeitin levels dropping is normal considering renal failure?

    What about the cointradicator for a 55 year old? Would how the drug is metabolised be the answer?
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    (Original post by That Bearded Man)
    So the deep breathing can also be explained by the hyperventilatory response to metabolic acidosis - fair enough.

    Erythropoeitin levels dropping is normal considering renal failure?

    What about the cointradicator for a 55 year old? Would how the drug is metabolised be the answer?
    Yep, you would expect that to happen in (long-standing) renal failure.

    Well - if the kidneys are failing, think about what would happen if drugs were given that are renally metabolised or excreted.

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    (Original post by Mushi_master)
    Yep, you would expect that to happen in (long-standing) renal failure.

    Well - if the kidneys are failing, think about what would happen if drugs were given that are renally metabolised or excreted.

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    Exactly - what's more likely though? Drugs that can be metabolised into the body without excretion - or non-toxic products of breakdown?
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    (Original post by That Bearded Man)
    Exactly - what's more likely though? Drugs that can be metabolised into the body without excretion - or non-toxic products of breakdown?
    Do you mean the more likely answer? Sorry don't entirely get the question.

    But the property of the drugs that needs to be considered is the metabolism and excretion. If drugs are renally excreted, and the renal system is screwed, then you're going to get inappropriately high drug levels.

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    (Original post by Mushi_master)
    Do you mean the more likely answer? Sorry don't entirely get the question.

    But the property of the drugs that needs to be considered is the metabolism and excretion. If drugs are renally excreted, and the renal system is screwed, then you're going to get inappropriately high drug levels.

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    Okay, fair enough, thanks

    When you mentioned hyperkalaemia - classic sign of a potential cardiac arrythmia. If Hyperkalaemia can be caused by a damage to the Na+/Ka+ atpase. Would excess potassium lead to excess potassium bicarbonate? So create a low pH?

    If chloride, urea and inulin are normal, bicarbonate 20mmol/L (normal 22-28) and Sodium 130mmol/L (normal 135-145) how would you correct this?
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    (Original post by That Bearded Man)
    Okay, fair enough, thanks

    When you mentioned hyperkalaemia - classic sign of a potential cardiac arrythmia. If Hyperkalaemia can be caused by a damage to the Na+/Ka+ atpase. Would excess potassium lead to excess potassium bicarbonate? So create a low pH?

    If chloride, urea and inulin are normal, bicarbonate 20mmol/L (normal 22-28) and Sodium 130mmol/L (normal 135-145) how would you correct this?
    You are getting your terms mixed up. Hyperkalaemia is a potential cause of dysrhythmia; it is not a sign. A sign is an objective clinical finding which helps you make a diagnosis.

    Hyperkalaemia in renal failure is not due to damage to the Na/K ATPase, it is due to a failure to excrete potassium. High potassium can cause metabolic acidosis because it decreases the kidney's production of ammonia, which is an important buffer for H+ excretion. But renal failure in itself will also impair H+ excretion and HCO3- reabsorption and cause a metabolic acidosis.

    Treatment for this lady would depend on how high her potassium is right now, what her pH is, what her ECG looks like and what her creatinine is. You would also need to investigate her properly to work out why she has renal failure - the "pain on urination" history could be stones, could be infection, could be something else - and the treatment would vary depending on what the cause is.

    This is a very weird question for a first year, and to me reinforces why we shouldn't try to push too much clinical stuff before you really understand the physiology.
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    (Original post by Helenia)
    You are getting your terms mixed up. Hyperkalaemia is a potential cause of dysrhythmia; it is not a sign. A sign is an objective clinical finding which helps you make a diagnosis.

    Hyperkalaemia in renal failure is not due to damage to the Na/K ATPase, it is due to a failure to excrete potassium. High potassium can cause metabolic acidosis because it decreases the kidney's production of ammonia, which is an important buffer for H+ excretion. But renal failure in itself will also impair H+ excretion and HCO3- reabsorption and cause a metabolic acidosis.

    Treatment for this lady would depend on how high her potassium is right now, what her pH is, what her ECG looks like and what her creatinine is. You would also need to investigate her properly to work out why she has renal failure - the "pain on urination" history could be stones, could be infection, could be something else - and the treatment would vary depending on what the cause is.

    This is a very weird question for a first year, and to me reinforces why we shouldn't try to push too much clinical stuff before you really understand the physiology.
    Okay thank you, I wasn't aware that K+ affects the ammonium buffer (which as far as I'm aware alongside phosphate allows the bound H+ to be excreted in urine)

    These questions I assume are at the stage of "every symptom is important" no red herrings or anything.

    The advised textbook clinical scenarios are all simply "acute/chronic, metabolic/respiratory/mixed, acidosis/alkylosis" and then simply is it compensated, a potential cause etc. So these questions are just a bit out there.

    On a more interesting note, we learn by multiple choice questions. I'm glad to be avoiding some rote but it's been heavily criticised by many post-grads who say it really is a terrible way to be asked in first year as they basically DON'T learn it.
 
 
 
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