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74 Cards in this Set
- Front
- Back
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Homeostatsis
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Actively maintained metabolic equilibrium
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Normal blood pH
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7.4
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Where do acids in body come from?
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Metabolism of carbohydrates, proteins, phospholipids
Approx 1 mEq of non-volatile acid and 15K mEq of carbonic acid |
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Buffers in humans
What's the point What are they |
Weak acids/bases that resist change to pH based on H changes
Without them, we would be dead Bicarbonate Phosphate (in bone) Proteins (mostly albumin) |
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How does bicarb work as a buffer
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HCO3 + H = CO2 and H20
The CO2 is breathed off and pH stays the same |
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How does phosphate work as a buffer?
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HPO4 (2-) + H = H2PO4 (1-)
Phosphate mostly comes from the bones so long term acidosis can result in demineralization of bone |
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How does albumin work as a buffer?
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Negatively charged protein
Usually complexed with Ca++ and Na+ In acidemia, these are displaced In alkalemia, free Ca++ can decrease - tetany |
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Anion gap
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Measured anions less than measured cations
Na > Cl + bicarb This is mostly due to albumin Normal gap (with normal albumin level) is 12 |
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What causes an increased anion gap?
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Presence of organic acids
Metabolic acidosis (no matter what pH or bicarb is) |
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What reduces the anion gap?
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Hypoalbuminuria
For every 1 g/dL drop in albumin, anion gap should be 2.5 less Also unmeasured cations (Ca+, Li+, Mg+) at toxic levels Bromine ingestion will falsely increase measure Cl- |
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Osis vs Emia
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Osis - process pushing in a direction
Emia - content of the blood |
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Acidosis
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Process favoring excess acid
Manifest as increase CO2 (showing increased carbonic acid production) or decrease bicarb (H+ is consuming bicarb) or anion gap (organic acidosis) If unopposed, pH falls |
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Alkalosis
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Process favoring excess alkalosis
High HCO3 (metabolic alkalosis) Low CO2 (respiratory alkalosis) If unopposed, pH rises |
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Acidemia and alkalemia
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Acidemia - p<7.4
Alkalemia- pH>7.4 |
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Respiratory acid base disturbances
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Acidosis PCO2 > 40
Alkalosis PCO2 <40 |
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Metabolic acid-base disturbances
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Acidosis HCO3 < 24
or Anion gap >12 Alkalosis HCO3 > 24 |
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Compensation
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Body reacts to decrease change in pH
Metabolic for respiratory and vv Opposite of disturbance Restoration of pH is NEVER complete |
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Appropriate compensation for metabolic acidosis
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Hyperventilation
1.2 fall in CO2 for every 1 of bicarb |
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Simple acid base disturbance
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One disorder with expected compensation
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Mixed acid base disturbance
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Two or more disorders present, as evidenced by lack of compensation or inappropriate degree of compensation
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Consequence of severe acid-base disturbances
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Changes in protein configuration
Disrupts cellular function Respiratory failure--coma--death |
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Chronic acidosis consequences
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Increased protein catabolism and loss of lean body mass
Loss of bone density Acceleration of kidney disease |
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CO2 chemoreceptor locations
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Medulla
Aortic body Carotid body Hypercapnia increases ventilatory rate |
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pH chemoreceptor location
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Carotid body
Stronger effect than the CO2 chemoreceptors Acidemia increases ventilatory rate |
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Acid base regulation of kidney
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Bicarb is freely secreted and 99% reabsorbed
H2SO4 and HPO4 are filtered NH3 is produced by proximal tubule H+ is secreted in distal tubule and buffered by these abses |
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Bicarb handling in kidney
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HCO3 filtered by glomerulus
Carbonic anhydrase converts to CO2 and H20 CO2 freely diffuses back into tubular cells Intracellular carbonic anhydrates regenerates HCO3, which is pumped into blood |
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Making NH3 in kidney
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Deamination of glutamine
Results in NH3 to kidney and 2HCO3 to blood NH3 can be used to trap H in urine because NH4+ cannot diffuse across membranes |
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Major mechanism for dealing with acid loads?
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NH3-->NH4+ in kidney
Respiratory - limited by muscle fatigue Other buffers limited by dietary intake So tubular dysfunction results in acidosis |
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H+ secretion
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Intercalated cells of distal tubule actively secrete
Trapped by NH3/4 Increased gradient for positive charge based on sodium reabsorption Aldosterone increases both sodium reabsorption and H secretion |
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Volume contraction alkalosis
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Loss of non-bicarb containing fluid
Results in an increased bicarb concentration And increased pH Also activates the RAA system, so more H is loss in urine |
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Examples of metabolic alkalosis
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Vomiting/NG suction
Contraction Rena H+ losses (hyperaldosteronism, hypokalemia) Alkali ingestion |
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Examples of respiratory acidoses
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Anxiety -- hyperventilation
Aspirin toxicity High altitude? |
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Respiratory acidosis
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High pCO2, low pH
Failure to adequately ventilate Central respiratory depression Pulmonary problem Respiratory muscle failure |
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Compensation for respiratory acidosis
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Kidney makes and keeps more bicarb
Small change acutely Larger change chronically |
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Appropriate acute compensation for respirator acidosis
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1 bicarb for every 10 mmHg
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Appropriate compensation for chronic respiratory acidosis?
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3.5 bicarbs for every 10 mmHg
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Metabolic acidosis
Causes |
low bicarb, low pH
Generation of acid - keto, lactic Retention of acid - rental tubular Ingestion of acid - aspirin Loss of bicarb - diarrhea, proximal RTA |
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Witter's formula
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Used to calculate respiratory compensation for metabolic acidosis
expected pCO2 is (1.5xbicarb +8) +/-2 |
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Hyperchloremia metabolic acidosis
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No anion gap
Loss of bicarb (and chloride rises to keep balance) - diarrhea, pancreatic drainage Retention of Cl- (RTA, hyperalimentation) |
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Causes of high anion gap acidosis
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Methanol
Uremia DKA Paraldehyde INH Lactic acidosis Ethylene glycol Salicylates |
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How does aspirin cause a metabolic acidosis
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Decouples the respiratory chain so lactic acid is produced
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Osmolar gap
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Measured osmolarity vs
2x[Na+] +glucose/18 + BUN/2.8 Normally <10 If greater, unmeasured osms are present |
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Causes of osmolar gap with acidosis
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Methanol
Ethylene glycol Ketoacidosis Uremia Paraldehyde Lactic acidosis |
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Causes of osmolar gap without acidosis
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Ethanol
Isopropanol Mannitol Diethyl ether Severe hyperlipidemia Hyperproteinemia Severe Li toxicity |
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Is this just alcohol causing the osmolar gap
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Osmolarity goes up 1 for every 4.6 mg/dl of ethanol
If gap is more than that consider a second ingestion |
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Delta delta in acid-base
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Delta anion gap should equal delta bicarb change
If not, second metabolic disorder If anion gap change is greater, then a metabolic alkalosis If anion gap change smaller, then hypercholermic acidosis |
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Is this hypercholoremia metabolic acidosis renal retention or GI loss?
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Has the patient had massive diarrhea?
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How does normal kidney secrete acid?
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NH4Cl
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What can be measured to see how well kidney is responding to acid load?
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Urinary Cl
(excreted as NH4Cl) |
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Urinary anion gap
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Na + K - Cl in urine
Useful in acidosis If gap is positive - acidosis is caused by kidney If gap is negative - acidosis is caused by something else (GI loss) and kidney is responding well |
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Type 1 renal tubular acidosis
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Distal
Impaired H+ excretion Or H+ back leak at distal tubule Distal tubule fnc is need to secrete daily acid load |
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Causes of type 1 renal tubular acidosis
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Anything that damages the distal tubular interacalated cells or cell jcts
Lithium Sjogrens Hypercalciuria RA Hyperglobulinemia Ifosfamide AmphotericinB Cirrhosis SLE Sickle cell Obstructive uropathy |
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Labs in type 1 RTA
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Low serum HCO3
Urine pH > 5.5, positive urinary anion gap Confirm diagnosis w/ HCO3 loading Fraction excretion < 3% (not wasting) Urine pH remains stable |
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Treating Type 1 RTA
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Treat any underlying cause
Supplement with bicarb to attempt to avoid bone loss |
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Type II RTA
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Proximal tubule damage
Defect in rate of bicarb reabsorption Biocarb lost in urine Does reach steady state |
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Fanconi syndrome
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Generalized proximal tubular dysfunction
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Labs in type II RTA
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May have other proximal tubular dysfunction - glucose, amino acids, phosphate, bicarb all in urine
Serum bicarb is low Serum pH is <5.5 once steady state is reached Urine anion gap should be negative Confirm with bicarb load -- urinary pH shoots up |
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Causes of type II RTA
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Familial metabolic disorders
(cystinosis, tyrosinemia, others) Multiple myeloma Ifosfamide Carbonic anhydrase inhibitors Amyloidosis Heavy metals VitD PNH |
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Treating type II RTA
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Treat underlying cause
Very difficult to adequately replete bicarb |
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Type III RTA
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Type I + Type II
Spill bicarb and have problem excrete H Mostly seen in kids Not a popular term |
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Type IV RTA
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Lack of aldosterone effect
low levels or resistance Hyperchloremia acidosis with hyperkalemia |
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Causes of type IV RTA
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Low aldosterone levels - adrenal insufficiency, renal failure resulting in low renin, ACEIs, NSAIDs, cyclosporine
Aldosterone resistance Amiloride, spironolactone, triamterene, trimethoprim, pentamide Tubulointerstitial disease Distal chloride shunt |
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How would you support diagnosis of type IV RTA
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Hyperkalemia and low urine K
(with functioning kidneys) |
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Treating type IV RTA
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Low aldosterone - can give fludrocortisone, watch BP
Furosemide will waste K and contract volume (reducing acidosis) |
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Respiratory alkalosis causes
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High pH, low pCO2
Hyperventilation - Anxiety, respiratory stimulants, pregnancy, advanced liver disease, mechanical ventilation |
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Salicylate toxicity
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Elevated anion gap metabolic acidosis
(w/ ventilatory compensation) Superimposed by Respiratory alkalosis by stimulation of respiratory center |
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Phases of metabolic alkalosis
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Generation -- H+ loss or HCO3 gain in serum
Maintenance - Kidney must increase resorption --otherwise its high capacity to filter would fix problem |
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Pathogenesis of vomiting causing metabolic alkalosis
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Loss of H+ in fluid
Increased bicarb Loss of Cl- inhibits renal secretion of HCO3 at distal tubule Volume depletion stimulates aldosterone resulting in more H secretion |
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Pathogenesis of milk-alkali syndrome
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Hypercalcemia inhibits bicarb excretion
So consuming enough calcium carbonate can lead to metabolic acidosis Just eating bicarb really won't do this, the kidneys can normally secrete a lot |
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Mechanism of hypokalemia leading the metabolic alkaosis
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Low serum K results in shift of K out of cells
H+ shifts in to maintain neutrality Intracellular fluid is now acidotic Kidneys are stimulated to secrete acid --pH rises |
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Appropriate respiratory compensation in metabolic alkalosis
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Hypoventilation
0.7 mmHg rise in CO2 for 1 rise in bicarb |
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Treating metabolic alkalosis
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For vomiting, hypokalemia, contraction, repleat volume K+, Cl-
These are considered "chloride responsive" |
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Treating hyperaldosterone metabolic alkalosis
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Giving fluid, K, Cl won't work (chloride unresponsive)
Block receptor (spironolactone) Remove source of hormone |
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Signs of hyperaldosteronism
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Hypokalemia in 80%
Hypertension that is difficult to manage |
