First Pass Miss Flashcards
What effect to catecholamines have on potassium homeostasis via the Beta-2 receptors? What would propranolol do?
B2 receptors promote entry of potassium into primarily skeletal muscle and liver cells -> activate Na/K ATPase
Propanolol would block this B2 receptor effect and may contribute to hyperkalemia
alpha2 agonists blocks insulin release and predisposes to hyperkalemia as well
How does insulin affect K+?
Insulin promotes entry of K+ into skeletal muscle directly by increasing the number of Na/K ATPases
Insulin stimulates Na/H exchanger in liver, bringing Na+ into the cell. Every 3 turns of this leads to 2 K+ brought into the liver cell via the Na/K ATPase
Insulin allows K+ entry into cells passively.
What effect does metabolic acidosis have on potassium homeostasis and why?
Causes hyperkalemia
- > decreased ability to run Na/H antiporter since ECF is already acidic
- > less Na+ inside the cell to run Na/K ATPase -> potassium stays outside of the cells
Is the hyperkalemic effect of metabolic acidosis worse with mineral or organic acids?
Worse with mineral acids, since the anions can’t enter the cell and must stay in the blood
Organic acids can be transported into the cell so the effect of hyperkalemia will be less dramatic. This is because organic acids entering the cell will reduce cellular pH, so Na/H antiporter can still be run to push H+ into ECV, bring Na+ in, and keep K+ balance normal.
What effect will hyperosmolarity have on blood potassium levels and why?
Hyperosmolarity - increased K+ levels
- > Osmotic drag = K+ leaves the cells with water
- > Decreased water inside cells also concentrates K+, passive movement out of cells
How is the majority of the potassium reabsorbed in the kidney?
Majority in proximal tubule
Early proximal tubule - due to solvent drag, from movement of water and sodium into cells, concentrating K+
Late proximal tubule - due to paracellular diffusion, as lumenal potential becomes positive
What is the general underlying problem of the aldosterone paradox?
High K+ levels stimulate aldosterone secretion, which preferentially leads to K+ excretion within minimal Na+ reabsorption
Angiotensin II also stimulates aldosterone secretion, which preferentially leads to Na+ reabsorption with minimal K+ excretion
What justifies the aldosterone paradox?
Angiotensin II - stimulates the WNK kinases and reabsorbs more Na+ via the NCC in the early DCT so less sodium load is delivered to late DCT / principle cells, preventing K+ losses
K+ stimulation of aldosterone - WNK kinases not affected, to K+ is lost more readily, and same amount of Na+ is reabsorbed
What is the function of the WNK kinases? What else are they stimulated by other than Angiotensin II?
They lead to removal of ROMK channels in the distal nephron -> Also stimulated by low blood potassium levels
-> make sense because we want to save potassium from excretion
What effect does pH have on K+ reabsorption and why?
Acidemia - increases K+ reabsorption, can quickly run H/K antiporter -> acidemia is associated with hyperkalemia
Alkalemia - decreases K+ reabsorption, cannot run H/K antiporter -> alkalosis is associated with hypokalemia
What endocrine abnormalities are induced by hypokalemia?
Decreased insulin secretion (already too much K+ in cells)
Increased renin with decreased aldosterone (aldosterone paradox)
-> aldosterone would waste K+
->also remember than WNK kinases are stimulated with hypokalemia -> reduce ROMK levels in collecting duct, preventing K+ wasting
What are the causes of renal K+ loss without HTN?
Vomiting Diuretics - increased Na+ load Bartter syndrome Gitelmans syndrome Renal tubular acidoses types I and II
What is pseudohyperkalemia?
- High K+ due to difficulty with venipuncture which causes local mechanical trauma and muscle K+ release.
- Serum H+ is always higher K+ than plasma K+ when measured in the lab because of clotting process leads to lysis. High WBC / platelet counts can make this effect greater
In what conditions will inadequate urinary excretion lead to hyperkalemia?
- Very late stage renal failure - GFR <20
- Effective circulatory volume depletion - K+ excretion limited by small urine volume
- Hypoaldosteronism - Type IV RTA
What are the clinical ECG manifestations of hyperkalemia? Are these more serious than hypokalemia?
Wide QRS with peaked T waves -> arrhythmias
QT intervals are shortened -> rapid repolarization
-> can cause bradycardia
Widened QRS with severe hyperkalemia can lead to loss of P waves and eventual Vfib
More serious than hypokalemia, more likely to cause emergent arrhythmia
What are the clinical muscle and endocrine manifestations of hyperkalemia?
Muscle weakness and paralysis
Endocrine - increased aldosterone and increased insulin secretion, while decreasing renin
aldosterone paradox
How does plasma osmolality relate to plasma Na concentration, conceptually?
Directly proportional. Thus, total body water content can be estimated by Na concentration, but ECF volume cannot be estimated by Na concentration (needs total body Na, a clinical assessment by physical exam or direct intravascular monitoring)
What is the formula for calculating plasma osmolality? Give the normal value?
2*Na + (glucose / 18) + (BUN / 2.8)
Na in mmol/L - because each Na is accompanied by an anion
Glucose in mg/dL
BUN in mg/dL
Normal value is around 290 mOsm / kg water
Plasma osmolality is inversely proportional to total body WATER CONTENT
What is the difference between water depletion and volume depletion? What is dehydration talking about?
Water depletion - depletion of total body water (increased Na concentration / osmolality) -> dehydration refers to this
Volume depletion - depletion of ECF volume / total body Na. Dehydration should not refer to this, but sometimes sloppily applied
What are the two cases when plasma osmolality is NOT proportional to plasma [Na]?
Pseudohyponatremia:
- Artifactual hyponatremia
- > elevated solid components lead to the same volume of blood having less plasma in it -> lower measured sodium per volume of blood drawn
- Hyperlipidemia
- Hypergammaglobulinemia (multiple myeloma - Hyperosmolal hyponatremia
- > caused by diabetes, sugar pulls water out of cells, diluting ECV
- > treated by insulin
- > Na will recover 1.6mM for every 100 mg/dL above 200 mg/dL blood sugar
What area of the brain regulates plasma osmolality? How do they relate to the BBB? how do they work? What are the osmoreceptors type?
Subfornical organ (beneath hippocampus) and organum vasculosum of lamina terminalis (OVLT)
Outside of BBB, have TRPV1 osmoreceptors and angiotensin II receptors
Other than angiotensin II, low BP, low blood volume, and high plasma osmolality, what other factors stimulate ADH release?
Other stress-related stimuli:
Nausea
Hypoxia
Hypercapnia
Pain (nociceptors)
-> keep these all in mind as causes of normal ECV hyponatremia
What effect does ADH have on the kidneys? What receptor does it bind?
Increases solute absorption via TALH (NKCC) and urea absorption by collecting duct to increase medullary osmotic gradient (greater concentrating power)
-> upregulates UT1/UT2 transporters
Binds V2 receptors. Increases Aquaporin 2 expression in collecting duct (cAMP mechanism). Aqp3 also has a minor effect.
Where is urea synthesized, filtered, reabsorbed, and secreted?
Synthesized - liver
Filtered - glomerulus, freely
Reabsorbed - inner medullary collecting duct, taken up by ascending vasa recta
Secreted - proximal straight tubule - after acquisition from ascending vasa recta
Some urea from ascending vasa recta is also transferred to adjacent descending vasa recta
What is the definition of free water clearance? How do you calculate it?
Volume of urine per unit time that is solute free after removal of the volume of urine that is iso-osmotic plasma
Free water clearance = Urine flow rate - Osmolal clearance
Ch20 = V - Cosm
Where Cosm = (Uosm*V)/Posm
What does it mean when free water clearance is positive, negative, or 0?
If Ch20 is 0 -> urine is iso-osmotic to plasma, meaning Uosm = Posm.
If Ch20 is positive -> substract a number which is less than V, Uosm/Posm <1, urine is hypoosmotic to plasma.
If Ch20 is negative -> Uosm/Posm >1 = urine is hyperosmotic to plasma (subtract a number that is greater than V)
What is T(superscriptC)(subH20)? This relates to free water clearance.
Tubular water reabsorption
It is equal to the negative free water clearance (if free water clearance is -1.5L/day then water is being reabsorbed, and TcH20 = 1.5L/day)
How do you calculate the excess TBW for a patient who was ideally 70 kg before coming ill, and who now has a hypoosmotic plasma of 250 mOsm / kg water?
70 kg * 0.6 = 42 L = ideal TBW
M1V1 = M2V2
ideal Posm * ideal TBW = actual Posm * actual TBW
300 mOsm * 42 L = 250 mOsm * actual TBW
actual TBW = 50.4L
Actual TBW - Ideal TBW = Excess TBW
- 4L - 42 L = excess TBW = 8.4 L
- 4 L of solute free water needs to be excreted to correct the plasma osmolality
Typically you use [Na+] rather than plasma osmolality
What are the signs of ECF volume depletion and what causes this?
Loss of Na from ECF (total body Na)
Signs include low blood pressure, increased heart rate, orthostatic vital changes, dry mucous membranes, poor skin turgor
What are the acquired causes of nephrogenic diabetes insipidus?
Hypercalcemia, hypokalemia
-> impairs cAMP mechanisms, abnormal AQP2 number
Remember hypokalemia lecture mentioned impaired renal concentrating ability
Remember hypercalcemic lecture (polyuria)
What are the causes of inadequate water intake?
- Thirst deficiency - usually brain tumor in subfornical area
- Inability to obtain water (infants, unconscious, desert) - most common
- Intake of hypertonic salt without water
- ADH derangements with inadequate water intake
What are the causes of hypernatremia with low ECV?
Loss of both Na and water, but water more than sodium (hence hypernatremia)
- GI losses - diarrhea or vomiting (BEFORE you drink water to replace the water lost)
- Inability to access food or water, with loss of water and salt in sweat
- Diabetic osmotic diuresis
- Drugs that impair water and salt reabsorption (diuretics)
What is the only real cause of hypernatremia with (almost) normal ECV?
Diabetes insipidus - central or nephrogenic (sodium is absorbed fine, just can’t pull the water out of the urine at all)
Normal respiratory or dermal losses of water
-> lost water without loss of total body Na (by clinical assessment)
What are the causes of hypernatremia with high ECV?
Situations where Na is gained in excess of water
- > hypertonic breast milk / formula
- > hypertonic dialysis
- > primary hyperaldosteronism
- > iatrogenic Na bicarbonate injections (hypertonic fluids)
What is the treatment for all types of hypernatremia, and if you are low ECV vs normal or high ECV?
Treatment for all: permit acess to water, and give oral water if patient is awake / alert
Low ECV - BP is most important, give isotonic saline until BP improved, then switch to hypotonic to normalize hypernatremia
Normal / high ECV - Give D5W - basically giving pure water which is isotonic but does not raise sodium concentrations at all (ECV is already okay)
Why do disorders of urinary dilution cause their symptoms?
Plasma becomes hypoosmotic either due to decreased water loss (water retention) or a concomitant increase in solute loss / renal wasting (cannot reuptake solute)
Signs and symptoms are due to brain cell edema (water ends cells) -> skull has only 10% of space not occupied by brain tissue
How can you think of the functional solute problem differences between problems of urinary concentration and urinary dilution? How can loop diuretics contribute to both?
Urinary concentration disorder - solutes are reabsorbed okay, just can’t seem to reuptake water. Loop diuretics can make this worse by not allowing formation of medullary gradient for water reuptake
Urinary dilution disorder - solutes are not reabsorbed well, water is not being lost adequately. Diuretics make this worse by not allowing reuptake of solute (makes blood hypoosmotic by keeping urine too concentrated).
How can ADH contribute to problems with urinary dilution? What things can cause this?
Inappropriate presence of ADH leads to hyperconcentration of urine -> too much water reuptake, retention of water
Things which cause increased ADH, especially heart failure (associated with hypoxia and hypercapnia, which increases ADH), certain drugs, and SIADH
What drug is especially associated with hyponatremia?
Ecstasy - increases ADH levels + makes you ravenously thirsty
Why does congestive heart failure cause hypo-osmolality?
Normal baroreceptors become insensitive overtime to the volume overload - they stop firing, ADH release is disinhibited, exacerbating heart failure
What are some causes of low ECV hyponatremia?
Individuals lost more sodium than water, usually due to drinking water or hypotonic fluids after salt loss
GI losses
Burns: Loss of Na/water
Renal losses - osmotic diuresis, salt wasting nephritis, mineralocorticoid deficit
Hemorrhage
What are the causes of high ECV hyponatremia? Why does each of them cause this?
They have high total sodium, but VERY high TBW
Big four:
- CHF - decreased baroreceptor responsiveness
- Cirrhosis - low BP due to profound splanchnic vasodilation to increase liver blood flow + fluid loss due to oncotic changes
- Renal failure - inability of kidney to excrete water in limited function
- Nephrotic syndrome - low intravascular volume due to oncotic changes
How should you treat a patient with low ECV hyponatremia and why is this easier than high ECV hyponatremia?
low ECV hyponatremia - give isotonic saline. Na levels will normalize in body, and their baroreceptors work fine so they will lose the excess water through their kidneys
high ECV hyponatremia is bad because their baroreceptors are working badly, allowing too much ADH, or their kidneys aren’t working at all. -> kidneys will not allow them to lose water, and treating with isotonic saline would just exacerbate the problem.
Why does glucocorticoid deficiency cause normal ECV hyponatremia?
Cortisol-releasing hormone stimulates ADH release. If cortisol is not feeding back to inhibit CRH, ADH will build up.
If mineralocorticoids are normal, total body Na balance is normal in this situation
-> all normal ECV hyponatremias are caused by situations of too much ADH release when you don’t need it, or you’re just drinking too mush water
What does hypothyroidism cause in hyponatremia?
Normal ECV hyponatremia -> in patients with myxedema
What are the major causes of SIADH?
Ectopic ADH - malignancies, i.e. small cell lung cancer
Pulmonary disease - especially TB, but also asthma and other infections
(hypoxia / hypercapnia / nausea / pain induce ADH release)
CNS disorders / head trauma
(disruption of OVLT)
Certain drugs
How do demeclocycline and lithium treat SIADH?
Demeclocycline - impairs AQP2 insertion into apical membrane
Lithium - prevents cAMP formation, so AQP2 can’t be moved to the membrane
Note: Tolvaptan and Conivaptan are much better but are more dangerous
What is the risk of too rapidly correcting hyponatremia levels? What is most susceptible?
Osmotic demyelination syndrome
- > rush of fluid out of myelin sheaths into extracellular space (there was lack of osmolytes in brain to prevent cerebral edema from all this water) causes damage
- > need to give sodium back to ECF slowly to allow brain cells to generate osmolytes so fluid doesn’t leave the cells too rapidly
- > especially affects pons, can cause locked in syndrome
- > max replacement: 6 mM Na per 24 hours
What is the difference between a volatile and nonvolatile acid? Give some examples of the latter.
Nonvolatile - acids which cannot be evaporated.
Examples:
Sulfur-containing amino acids -> degrade to sulfuric acid
positively charged AA -> HCl
Phosphates also contribute -> phosphoric acid
negatively charged AA and organic anions -> produce bicarbonate, which buffers some of this.
Why do we need to keep making HCO3-? How does the kidney function in this?
We make about 1 mEq/kg/day of nonvolatile acids which need to be buffered by bicarbonate system.
When they are buffered, they rapidly form CO2 gas which is loss (volatile gas). This HCO3- then needs to be replaced. Kidney functions to excrete the sodium salts that are made from this conversion and replenish the HCO3- by secreting acid EXACTLY EQUAL to the nonvolatile acid produced, and reclaim filtered HCO3-.
What is total H+ secretion by the tubules equal to? (sum of other H+ secretions)?
Total H+ secretion = H+(HCO3-) + H+(NH4+) + H+(TA)
H+ total = H+ for reabsorption of bicarbonate + H+ in the form of NH4 + H+ in another titratable acid
What is the net acid secretion then / how is it calculated?
Net acid secretion = [(Excreted NH4 + Excreted TA)] - [Excreted HCO3-]
Excreted HCO3- is bicarbonate which wasn’t reabsorbed
Excretion can be calculated by the urinary concentration of the substance multiplied by the urine flow rate
What are the transporters which help reabsorb bicarbonate in the proximal tubule on both the apical and basolateral membranes?
Apical - H+-ATPase (Vacuolar), Na/H exchanger
Basolateral - 3HCO3/Na cotransporter (driven by relatively positive ECF), HCO3-/Cl- antiporter (AE1)
What is the function of the beta intercalated cell and what transporter does it have at the apical and basolateral membranes?
For secretion of bicarbonate (bases) in the lumen, rarely needed except in vegans who can have base excess. Basically a mirror image of an alpha intercalated cell.
Apical transporter - Pendrin** - functions like AE1/AE2 but not the same. HCO3- out with Cl- in.
Basolateral transporter - V-ATPase, pumps H+ out. Cl- also passively reabsorbed into blood.
What happens to NH4 in the medullary interstitium / how is it uptaken by the collecting duct?
NH3 / NH4+ is in equilibrium
It is taken up by the alpha-intercalated cell by one of two mechanisms:
1. Na/K ATPase in place of K (as in basolateral surface of TALH)
2. Rhcg channel (protein is in Rh antigen family)
Then is secreted into tubular lumen by Rhcg channel
NH3 will be again protonated by H+ secreted by alpha intercalated cell, finally resulting in a complete loss of acid.
How does systemic pH affect the action of the NH3/NH4 system?
low pH stimulates proximal tubule glutamine deamidase
(remember this and phosphate dependent glutaminase - PDG)
-> also enhanced by hypokalemia
high pH inhibits it
->also inhibited by hyperkalemia (predisposes to acidosis)
-> secrete more acid in the form of NH4+ when you need to.
How all does hypokalemia interfere with acid-base balance?
Hypokalemia - stimulates NH4+ production, increases Rhcg expression, and stimulates H+,K+ ATPase (hypokalemia will predispose to alkalosis)
What is the mechanism of increased or decreased normal (not NEW) bicarbonate reabsorption in response to alkalosis or acidosis?
Acidosis - more bicarbonate reabsorption
Alkalosis - less bicarbonate reabsorption
Mechanism - lower intracellular pH of alpha-intercalated cell favors secretion of H+ (lower cell-to-lumen gradient to push against via ATPase), and thus bicarbonate reabsorption
-> remember the collecting duct controls the pH!
What is the mechanism for contraction alkalosis?
At low blood volumes, AT2 is stimulated, which increases the number of Na/H exchangers in the proximal tubule, increasing bicarbonate reabsorption
Furthermore, aldosterone makes the collecting duct lumen more negative (favors H+ secretion) and directly alpha-intercalated V-type-ATPase -> more alkalosis
How is the compensatory fall in pCO2 for metabolic acidosis calculated?
Fall in pCO2 = 1.0 -1.3 mmHg * (fall in HCO3-)
HCO3- is assumed to be 25 mEq/L at baseline
pCO2 is assumed to be 40 mmHg at baseline
What causes an increased vs a normal plasma anion gap acidosis, conceptually?
Increased - addition or production of an acid which leaves an unmeasured anion in the blood
Normal - caused by addition of HCl (Cl- is measured in blood), or primary loss in HCO3- (excretion of HCO3- is paired with reabsorption of Cl-)
What is the urinary anion gap useful for and how is it calculated? What is a normal urine value?
Useful for the differential diagnosis of normal plasma anion gap metabolic acidosis
Based on the assumption that HCO3- and other unmeasured cations in the urine is negligible, and charges will equal out
0 = ([NH4+] + [Na+] + [K+]) - ([Cl-] + [Unmeasured anions])
Since NH4+ is difficult to measure, we can calculate the anion gap by assuming there are only four cations in the urine. Thus, we can say that
UAG = -[NH4+] = [Na+] + [K+] - [Cl-]
In normal urine, this gap is zero or slightly negative.
How do you calculate the plasma anion gap?
[Na+] - ([HCO3-] + [Cl-])
Normal = 10
How does the urinary anion gap change if the kidney is properly responding to normal plasma anion gap metabolic acidosis and why?
Normal response would be to increase renal tubule acid secretion in the collecting duct. This is done by increasing ammonia excretion. Since ammonia will be excreted as a positive cation, the Cl- in the urine will also increase to counteract this cation in the urine. This will be measured as an increase in urine chloride.
Thus, normal UAG response to metabolic acidosis is:
UAG = normal Na + Normal K+ - HIGH CL-
Urinary anion gap is VERY negative, reflecting high ammonia concentration.
-[NH4+] = UAG
If it is normal or positive in presence of normal anion gap metabolic acidosis -> distal RTA (Type I)
What is the urinary pH in Type I RTA and how does it change with plasma HCO3-? What pathophys mechanism accounts for this?
Distal renal tubular acidosis, associated with pH > 5.5 even with very low plasma [HCO3-], due to impaired ability to secrete H+ by alpha intercalated cells
- > decreased titratable acid and trapping of NH4+ -> decreased net acid secretion
- > impaired reabsorption of HCO3-, urine remains basic
What are the causes of RTA Type I?
Congenital abnormalities:
Obstruction - damages collecting duct
Hereditary mutation in H+-ATPase
Drugs:
Amphotericin B, tenofovir -> nephrotoxic, increase H+ permeability, allowing diffusion of H+ back into the cell (urine cannot be acidified)
What is RTA Type II? What will the urine characteristics be? Include pH and urinary anion gap.
RTA Type II - proximal RTA
Impaired bicarbonate reabsorption in the proximal tubule leads to increased bicarbonate loss in urine
Urine pH will still be low (<5.5) as alpha-intercalated cells are functioning properly and can secrete H+ into urine via increasing ammonia production + increased H+ secretion.
UAG will be very negative (normal response to acidosis) since cells are responding properly
What are the causes of Type II RTA?
Fanconi syndrome - proximal tubule transporters don’t work at all, leading to loss of all types of things in urine
-> caused by drugs like ifosfamide, cisplatin, tenofovir, expired tetracyclines
Carbonic anhydrase inhibitors - i.e. acetazolamide
Cystinosis
What will a mutation in AE1 cause?
Anion exchanger mutation on basolateral surface of alpha-intercalated cell (and proximal tubule, but failed distal acidification takes precedence)
-> Type I RTA
What is the pathogenesis of Type IV RTA?
Hypoaldosteronism leads to hyperkalemia
Hyperkalemia causes impaired NH4+ generation by proximal tubule -> impaired excretion of acid
-> hyperkalemic renal tubular acidosis
What is the definition of increased anion gap and what are the causes of increased anion gap metabolic acidosis?
Increased: Anion gap >12 mEq/L
MUDPILES M: Methanol, METFORMIN U: Uremia D: Diabetic ketoacidosis / ketoacidosis in general P: Paracetamol - acetaminophen I: Isoniazid, Iron tablets L: Lactic acidosis E: Ethylene glycol S: Salicylates
What are the non-renal loss of HCO3- causes which induce a hyperchloremic (normal anion gap) metabolic acidosis?
Diarrhea - Rich in HCO3- and K+. Kidney will compensate well with acid secretion and K+ reabsorption.
Small bowel or pancreatic drainage - loss of HCO3- secretions
Ureterosigmoidostomy / malfunctioning ileal loop
What is dilutional hyperchloremic acidosis? Where does this appear in the mnemonic for normal anion gap metabolic acidosis?
Rapid ECF expansion via NaCl will dilute out the current concentration of HCO3-, making the body relatively acidic
HARDASS Hyperalimentation Addison disease (hypoaldosteronism -> hyperkalemia -> acidosis) Renal tubular acidosis Diarrhea Acetazolamide Spironolactone - Type IV RTA Saline infusion
What are situations where “HCl” could be added to induce hyperchloremic acidosis?
Parenteral nutrition - formulas contain excess cations -> arginine-Cl or lysine-Cl -> chloride rises and arginine / lysine are acid cations which need to be buffered
Eating HCl or NH4Cl -> ammonium chloride used to be used as a diet pill
Why does increased HCO3- worsen alkalosis?
Increased HCO3- delivery to collecting duct -> non-reabsorbable anion -> secrete more K+ -> hypokalemia -> alkalosis due to stimulation of NH4+ production
What is the formula for respiratory compensation of metabolic alkalosis? What is the limitation?
rise in pCO2 (hypoventilation) - limitation of hypoventilation is hypoxemia
Rise in pCO2 = 0.5 to 1.0 * rise in [HCO3-]
What is the differential diagnosis of metabolic alkalosis based off of?
Based on urine [Cl-] -> low concentration of Cl- implies that bicarbonate is being reabsorbed largely because there is a deficit in Cl- to run Na/Cl- cotransporter -> HCO3- transporter goes in its place. -> kidney is focusing on ECF depletion, its #1 priority
What are the two categories of metabolic alkalosis?
- Saline responsive: Urinary [Cl-] < 20 mEq/L
- > ECF depletion is the issue - Saline unresponsive: Urinary [Cl-] > 20 mEq/L
- > ECF is normal or expanded
What are two common causes of saline responsive metabolic alkalosis?
Diuretics (must stop using them, urine will start reabsorbing chloride again, will be saline responsive. Otherwise saline unresponsive), especially loop diuretics -> volume depletion, loss of chloride and sodium(NKCC)
Vomiting -> HCl loss, volume depletion
