Chloride Disorders Flashcards

1
Q

Chloride constitutes approximately what percentage of the anions in plasma?

A

2/3rds

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2
Q

What is a normal chloride conc in dogs and cats?

A

Dogs - 110
Cats 120mEq/L

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3
Q

Chloride Metabolism

A
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4
Q

How is chloride absorbed in the jejunum?

A

Follows the absorption of sodium - is paracellular and due to the need to maintain electroneutrality

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5
Q

What percentage of enterally absorbed chloride is absorbed in the colon?

A

90% - is highly efficient.

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6
Q

Of filtered chloride how much is resorbed in the proximal tubules?

A

Of filtered chloride, approximately 50% to
60% is reabsorbed by the proximal convoluted and straight
tubules. Chloride reabsorption occurs transcellularly in
the thick ascending limb of Henle’s loop, leading to the
generation of a lumen-positive transepithelial voltage
Sodium is reabsorbed transcellularly or paracellularly, and
the transepithelial voltage drives the latter process. Chloride ion delivery is the rate-limiting step in this process, and net sodium chloride (NaCl) transport increases directly with fluid [Cl] concentration. Loop diuretics such as furosemide and bumetanide act in the loop of Henle by competing for the chloride site on the Na-K - 2Cl carrier.

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7
Q

Chloride and acid base balance

A
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8
Q

What must be done to correct a hypochloraemic alkalosis?

A

Provision of volume –> but most importantly provision of chloride
The principal mechanisms by which the
kidneys correct metabolic alkalosis probably operate in
the collecting ducts, especially in the cortical segment,
where HCO3
- can either be secreted or reabsorbed.

chloride
alone is essential for correction of the hypochloremic
alkalosis and that it does so by a renal mechanism. Volume
depletion is a common but not essential feature of the
maintenance phase of alkalosis, and its persistence does
not preclude correction of alkalosis. If adequate chloride
is provided, restoration of depleted volume, however,
may hasten correction of alkalosis by increasing the
GFR and decreasing proximal tubular reabsorption of
fluid and bicarbonate.39,40 The manner by which exogenous
Cl

repletion is detected and the kidneys are signaled
to excrete HCO3

, and the cellular mechanisms
by which these events occur in the various nephron
segments, remain to be determined

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9
Q

What is the main way in which chloride is involved in the renal compensation of an acidosis?

A

Enhanced excretion of NH4Cl . This subsequently increases SID

Ultimately Chloruresis, negative chloride balance,
enhanced fractional and absolute bicarbonate reabsorption,
and enhanced net acid excretion typically are
associated with the renal response to chronic respiratory
acidosis

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10
Q

Clinical Approach to Chloride Disorders

A
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11
Q

What is the value of corrected chloride?

A

Allows adjustement of chloride for gain or loss of free water
Corr Cl = Cl- measured x (Na - normal/Na -measured)

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12
Q

Corrected Hypochloremia

A
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13
Q

What acid base abnormality will be seen with corrected hypochloraemia?

A

Alkalosis and an increased SID

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14
Q

What renal physiologic consequence of hypochloraemia may be seen?

A

A decrease in GFR of 15-20% probably as a result of changes
in tubuloglomerular feedback and internal shifts of
fluid out of the ECF
May compound renal consequences of fluid loss too.

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15
Q

What may cause hypochloraemia

A

Gastrointestinal loss
- Vomiting of stomach contents*
- Selected gastrointestinal diseases associated with
hyperkalemia and hyponatremia in dogs without
hypoadrenocorticism (eg, trichuriasis, salmonellosis,
perforated duodenal ulcer)
Renal loss
- Therapy with thiazides or loop diuretics*
- Chronic respiratory acidosis
- Hyperadrenocorticism
- Glucocorticoid administration

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16
Q

How is hypochloraemia treated?

A

Give them chloride

17
Q

Corrected Hyperchloraemia

A
18
Q

What acid base abnormality is hyperchloraemia associated with

A

acidosis and decreased SID

19
Q

What may interfere with all forms of chloride measure?

A

potassium bromide because bromide
and other halides (e.g., iodides) are measured as chloride.
21,29 Bromide interferes with every chloride assay
to some extent, but ion-selective electrodes are the most
vulnerable to bromide interference

20
Q

What are examples of causes of hyperchloraemia ?

A

Excessive loss of sodium relative to chloride
- Diarrhea*
Excessive gain of chloride relative
to sodium
- Exogenous intake
–Therapy with chloride salts (NH4Cl, KCl)
–Total parenteral nutrition
–Fluid therapy (e.g., 0.9% NaCl, hypertonic saline, KCl-supplemented fluids)**
- Salt poisoning
Renal chloride retention
- Renal failure
- Renal tubular acidosis
- Hypoadrenocorticism*
- Diabetes mellitus*
- Chronic respiratory alkalosis
- Drug-induced: acetazolamide, spironolactone

21
Q

Why may DKA cause hyperchloraemia?

A

The ketoacids are
excreted in the urine at low serum concentrations; thus,
a patient with normal or near normal extracellular volume,
renal perfusion, and GFR may excrete the ketoacids
as fast as they are generated. The kidneys retain chloride
in place of ketones in this situation, increasing chloride
concentration

22
Q

Why may TPN cause hyperchloraemia?

A

Parenteral
nutrition can cause hyperchloremia, because some
solutions have high concentrations of cationic amino
acids (e.g., lysine-HCl, arginine-HCl) that release chloride
and generate hydrogen ions

23
Q

How should hyperchloraemia be treated?

A

Treatment of corrected hyperchloremia should be
directed at correction of the underlying disease process.
The effects of fluid therapy on chloride concentration
should be anticipated, especially in patients with diabetes
mellitus or abnormal renal function