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Why Does Acetazolamide Cause Hyperchloremic Metabolic Acidosis

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This video is about Acetazolamide Mechanism

Acetazolamide [tusom | Pharmwiki]

Trade Names: generic, Diamox, Diamox Sequels Drug Class: diuretic (carbonic anhydrase inhibitor) The diuretic effect of acetazolamide is due to its action in the kidney on the reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. The result is renal loss of bicarbonate (HCO3 ion), which carries out sodium, water, and potassium. Alkalinization of the urine and promotion of diuresis are the end result. Alteration in ammonia metabolism occurs due to increased reabsorption of ammonia by the renal tubules as a result of urinary alkalinization. Carbonic anhydrase inhibitors were the forerunners of modern diuretics. Legend. Mechanism of action of carbonic anhydrase inhibitor diuretics. Bicarbonate absorption by the proximal tubule is dependent on the activity of carbonic anhydrase (CA) which converts bicarbonate (HCO3-) to CO2 and H2O. CO2 rapidly diffuses across the cell membrane of proximal tubule cells where it is rehydrated back to H2CO3 by carbonic anhydrase. H2CO3 dissociates to HCO3- and H+ which are transported out of the cell on the basolateral side by different transporters. Bicarbonate absorption is therefore dependent on the activity of c Continue reading >>

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  1. datgirl1

    Sorry for the lengthy post but I have some concept questions that I'm not too sure about. Any explanations would be greatly appreciated!
    1) Why does diabetic ketoacidosis (high serum glucose levels) increase respiratory rate, decrease blood pressure and increase heart rate? I thought that high glucose levels would increase blood pressure but that's not the case.
    2) Notochord (mesoderm derived) forms the vertebral column and skull (or spine), whereas the neural tube develops into the spinal cord. Is this correct?
    3) Is there a difference between blood and plasma osmolarity? For example does aldosterone increase or decrease plasma osmolarity? I read somewhere that ADH is triggered if there is HIGH blood osmolarity, meaning that ADH would lower blood osmolarity. I thought that ADH would increase osmolarity.
    I'm also confused about filtrate osmolarity cause I read that increasing filtrate osmolarity decreases filtration and decreases blood pressure. This doesn't make any sense to me.
    4) Is it true that a ruptured blood vessel (hemorrhage) causes an increase in arterial pressure?
    5) If partial pressure of water vapor increases in the atmosphere, why does partial pressure of oxygen and nitrogen decrease?
    Thanks in advance!!

  2. Dentalco2020

    Question 1.
    DKA is a condition where your insulin cannot take up glucose into the cells from the blood. If your cells cannot utilize the glucose present in the body, then body tries to use fat as a back up source. In the process, it produces acids and it causes a condition called diabetic ketoacidosis.
    Acidosis simply means your serum CO2 level is high, so your body will try to get rid of it by breathing faster, so high respiratory rate.
    Tachycardia and hypotension are listed as common symptoms of DKA, but I don't know the exact mechanism.
    Question 2. I have no clue!
    Question 3
    ADH increases the amount of water reabsorbed in the kindey, consequently, the blood volume goes up. This means that the osmolarity will decrease, not increase. Maybe you were confused between osmolarity vs blood volume? Blood volume goes up, but osmolarity goes down.
    Answering your question about blood/plasma osmolarity causing ADH release, I believe when your blood osmolarity is high, ADH is released. High blood osmolarity means you have lots of solute, but not enough volume, so ADH is released to counteract that. ADH will make the kidney to reabsorb more water back into the blood, so the blood volume goes up, and osmolarity goes down (decreased osmolarity means it's being watered down / diluted)
    Questoin 4
    I think it's the opposite, but I could be wrong.
    Question 5
    Seems like this is a mole fraction concept.
    O2 and N2 are substances in question. When water vapor is mixed into these gases, mole fraction of O2 and N2 decreases.

  3. 68PGunner

    datgirl1 said: ↑
    Sorry for the lengthy post but I have some concept questions that I'm not too sure about. Any explanations would be greatly appreciated!
    1) Why does diabetic ketoacidosis (high serum glucose levels) increase respiratory rate, decrease blood pressure and increase heart rate? I thought that high glucose levels would increase blood pressure but that's not the case.
    2) Notochord (mesoderm derived) forms the vertebral column and skull (or spine), whereas the neural tube develops into the spinal cord. Is this correct?
    3) Is there a difference between blood and plasma osmolarity? For example does aldosterone increase or decrease plasma osmolarity? I read somewhere that ADH is triggered if there is HIGH blood osmolarity, meaning that ADH would lower blood osmolarity. I thought that ADH would increase osmolarity.
    I'm also confused about filtrate osmolarity cause I read that increasing filtrate osmolarity decreases filtration and decreases blood pressure. This doesn't make any sense to me.
    4) Is it true that a ruptured blood vessel (hemorrhage) causes an increase in arterial pressure?
    5) If partial pressure of water vapor increases in the atmosphere, why does partial pressure of oxygen and nitrogen decrease?
    Thanks in advance!!
    Click to expand... 1) DKA increases respiratory rate bc your body is hyperventilating in order to get rid of excess CO2. DKA is basically lipolysis from Type I Diabetes --> hyperglycemia. Therefore, excess glucose is lost through the urine, carrying a lot of water along with it. Water loss --> hypovolemia --> decreased blood pressure. Your body tries to compensate by constricting the vessels and increasing the heart rate
    2) Notochord is the nucleus pulpous of your intervertebral discs
    3) There is a set point in term of serum osmolarity. Higher serum osmolarity above this set point --> increased ADH --> higher water retention at the PCT in your renal system --> serum osmolarity goes back to the normal set point. This regulation system is controlled by your hypothalamus.
    As for aldosterone, that's another regulation controlled by your renal system. Basically, hypovolemia --> low blood flow through the juxtaglomerular cells --> increased renin + Angiotension I + Angiotension II --> increased aldosterone --> up regulate Enac --> increased Na + H20 retention while losing H+ and K+
    4) Depends on the diff stages
    5) Mole fraction concept

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Acetazolamide - Pharmapedia

Acetazolamide, sold under the trade name Diamox, is a carbonic anhydrase inhibitor that is used to treat glaucoma, epileptic seizures, benign intracranial hypertension (pseudotumor cerebri), altitude sickness, cystinuria, and dural ectasia. Acetazolamide is available as a generic drug and is also used as a diuretic. This section may be confusing or unclear to readers. Please help clarify the article; suggestions may be found on the talk page. (June 2009) This drug is a carbonic anhydrase inhibitor. Carbonic anhydrase (CA) catalyzes the forward motion of molecules in the following equation: where CA converts carbon dioxide (CO2) and water (H2O) to carbonic acid (H2CO3), which then dissociates to a hydrogen ion (H+, an acidic proton), and a bicarbonate ion (HCO3-, a basic anion). In some tissues (particularly plants), the equilibrium is such that CA can catalyze the reverse direction of the reaction. Carbonic acid inhibitors, such as acetazolamide, inhibit CA in tissue and fluid, causing less movement of carbonic acid toward CO2 production. In the kidneys, blocking CA leads to bicarbonate wasting in the tubules (alkalizes urine), loss of bicarbonate subsequently leads to a metabolic Continue reading >>

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  1. boobear

    Hi everyone, I've done keto/low carb on/off last few years. Got really keto serious three weeks ago. On the whole last week my husband pretty much wanted to puke every time I spoke near him as he said my breath was soooo bad. I drink tons of water, chew gum etc. It was making me so self conscious that I went off the next day. It's been two days off and Breath is better but I really hate the way I feel eating carbs. Is there any tips for the keto breath, will it pass, and if so after how long??? It is literally the only thing that stops me from going back! Thanks in advance!

  2. Jessica

    They say that burning fat can cause bad breath due to chemicals released in the process. It's metabolic and not hygiene related. It doesn't usually last forever! Don't let it discourage you! Keep drinking lots of water

  3. boobear

    I'm trying really hard not too! I'm going to get back on tomorrow and keep ketoing but I hate being paranoid about my breath :(.

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Symptoms of hyperchloremia and associated nursing actions. Produced at Broome Community College by Prof. J. Houghtalen and Tera Doty-Blance, Instructional Designer.

How Does Acetazolamide Cause Hyperchloremia?

SDN members see fewer ads and full resolution images. Join our non-profit community! how does acetazolamide cause hyperchloremia? I'm trying to figure out why (mechanism). Acidosis makes sense, and so does hypokalemia. Thanks. I think it's because carbonic anhydrase inhibitors prevent HCO3 reabsorption, so more sodium is being excreted as NaHCO3 instead of NaCl. every non-anion gap acidosis has hyperchloremia. it's inevitable, and unimportant It causes a non-anion gap metabolic acidosis. As the negative bicarb is ridded by the kidney, another anion needs to fill its place in the serum, and this is done by Cl. What makes sense to me, but I could be totally wrong is: Acidosis stimulates the release of aldosterone -> increase in activity of NaCl Cotransporter in early DCT-> Hyperchloremia Pretty sure Aldo isn't involved in the NCC. What the others have said is correct. What makes sense to me, but I could be totally wrong is: Acidosis stimulates the release of aldosterone -> increase in activity of NaCl Cotransporter in early DCT-> Hyperchloremia Lol, sorry to pick on you, but you couldn't be more wrong. I don't think there's one correct statement in there. Continue reading >>

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  1. gear2d

    Could anyone explain how this occurs? From my understanding high glucose levels draws K+ out of cells (HypERkalemia), low insulin promotes less shift of K+ in to cells (HypERkalemia), and acidosis causes K+ to shift out of cells (hypERkalemia)....so how does DKA cause hyPOkalemia? From my understanding DK:
    High glucose (hypertonicity which cause the shift of K+ to ECF),
    Low insulin
    Low pH

  2. blade

    USMLE Forums Guru

    Quote:

    Originally Posted by gear2d
    Could anyone explain how this occurs? From my understanding high glucose levels draws K+ out of cells (HypERkalemia), low insulin promotes less shift of K+ in to cells (HypERkalemia), and acidosis causes K+ to shift out of cells (hypERkalemia)....so how does DKA cause hyPOkalemia? From my understanding DK:
    High glucose (hypertonicity which cause the shift of K+ to ECF),
    Low insulin
    Low pH Hypokalemia in DKA???which book is that pls?your analysis above is correct but
    In DKA=hyperkalemia but with low intracellular K+ hence in treatment of DKA,you treat as if hypokalemia to restore the intracellular loss

  3. gear2d

    Quote:

    Originally Posted by blade
    Hypokalemia in DKA???which book is that pls?your analysis above is correct but
    In DKA=hyperkalemia but with low intracellular K+ hence in treatment of DKA,you treat as if hypokalemia to restore the intracellular loss This is from Step to Med 3rd ed on page312 in the flow diagram.

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