Term
| What are the components to metabolic alkalosis for recognition of the simple disorder? |
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Definition
1) elevated pH
2) elevated HCO3
3) adaptive (compensatory rise in PaCO2: 0.6mmHg/1mEq/L HCO3 |
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Term
| How is metabolic alkalosis generated (first step)? |
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Definition
1) bicarbonate load
2) H loss
*will cause initial rise, but will require sustained elevation* |
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Term
| How is increased HCO3 maintained in metabolic alkalosis? |
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Definition
| 1) defect in kidney HCO3 excretion must be present, e.g. increased tubular reabsorption, defective HCO3 excretion. |
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Term
| What are the two types of "maintenance" phases for metabolic alkalosis? Examples? |
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Definition
1) Chloride responsive (ECF + Cl depletion): vomiting, NG suction, diuretics, villous adenoma, post-hypercapnia
2) Chloride resistant (direct stimulus to H secretion): primary aldosteronism, cushings syndrome, steroid admin, ectopic ACTH, adrenogenital syndrome, licorice, bartter's syndrome, severe hypokalemia |
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Term
| Define: contraction alkalosis. |
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Definition
1) disproprtionate Na and Cl loos, leading to an increase in plasma HCO3 due to decreased volume (contraction)
2) pure contraction alkaloses are rare; bleeding leads to contraction but no alkalosis |
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Term
| How is chloride responsive alkalosis initiated? |
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Definition
| 1) loss of ECF disproportionately rich in Cl and usually in H |
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Term
| What are the factors that help result in maintenance of increased plasma HCO3 with chlroide responsive alkalosis? |
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Definition
1) Na reabsorption is upregulated (concomitant inc. HCO3, cotransport)
2) volume depletion -> aldosterone -> inc. H secretion
3) reduction in filtered Cl, decreased HCO3 secretion by type B intercalated cells
4) H secretion by A intercalated cells is Cl dependent, low luminal Cl will facilitate Cl and H movement into lumen.
5) Na-aldosterone reabsorption stimulates H/K secretion |
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Term
| What would urine Cl be for "chloride responsive alkalosis"? What would urine Na be for this condition? What is a notable exception? |
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Definition
1) U_Cl < 25mEq/L
2) U_Na low
3) refractory vomiting (due to HCl, not NaCl in stomach) |
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Term
| How does Chloride resistant alkalosis differ from Chloride responsive alkalosis? |
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Definition
1) Cl deficiency plays no role in accelerated tubular H secretion
2) no loss of Cl rich fluid
3) no volume depletion |
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Term
| What are the two major factors that lead to increased tubular H secretion to maintain the alkalosis |
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Definition
1) mineralocorticoid excess
2) potassium depletion |
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Term
| Describe how mineralocorticoid excess contributes to chloride resistant alkalosis? |
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Definition
1) unregulated production vs. exogenous administration (licorice)
2) distinction: increased level is not dependent on volume deficit
3) CL no avidly reabsorbed (U_Cl > 40mEq/L) |
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Term
| How does potassium depletion contribute to chloride resistant alkalosis? |
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Definition
1) consequence of mineralocorticoid excess (stimulated K secretion)
2) hypokalemia resultant K shift out of cells and H/Na shift into cells (more cellular H for secretion)
3) H/K exchanger in A intercalated cells; activated by K depletion
4) nearly always present in metabolic alkalosis |
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Term
| What are the treatments for chloride responsive metabolic alkalosis? |
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Definition
1) volume, Cl, K repletion
- NaCl
- KCl
- Stop diuretics
- H2 blockers (NG suction)
- K sparing diuretics
- acetazolamide |
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Term
| What are the treatments for chloride resistant metabolic aclkalosis? |
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Definition
1) increase K, block aldosterone
- K sparing diuretics
- resect tumor
- reduce steroid dose
- replace K
- low salt diet
- HCl infusion |
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