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Flashcards in ABGs,Electrolytes Deck (7)
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1
Q

Role of BONE in Acid base balance

A

An acid load, is associated with the uptake of excess H+ ions by bone which occurs in exchange for surface Na+ and K+ and by the dissolution of bone mineral, resulting in the release of buffer compounds, such as NaHCO3, CaHCO3, and CaHPO4.

at least 40% of the buffering of an ACUTE ACID load takes place in bone.

CHRONIC acidosis can have very adverse effects on bone mineralization due to this process and can result in bone diseases such as rickets, osteomalacia and osteopenia.

2
Q

Bicarbonate absorption in various portions of nephron

process of bicarbonate reabsorption occur predominantly in the proximal tubule (about 90%). The rest occur in the thick ascending limb and in the collecting tubule. All involve hydrogen ion secretion as shown in the diagram below.

To completely reabsorb bicarbonate,the kidney must secrete 4320 meq/day of hydrogen ions in addition to the amount required to exrete the daily acid load.

A

A

1-The primary step in proximal hydrogen secretion is the secretion of H+ by the Na+ - H+ antiporter in the luminal membrane. Hydrogen ions are generated by the intracellular breakdown of H20 to OH- and H+.

2-Hydrogen ions secreted combine with filtered HCO3- ions to form carbonic acid and then CO2 + H2O, which are then passively reabsorbed.
Technically, HCO3- ions reabsorbed in this process are not the same as the ones filtered. Note that a new HCO3-,ion is generated from the intracellular breakdown of H20 to OH- and H+ and subsequent reaction of OH- with CO2 to form HCO3- .

3-This new bicarbonate then crosses the basolateral membrane via a Na+ - 3HCO3- cotransporter.

The net effect is one mol of bicarbonate ion returned to systemic circulation for every H+ ion that is secreted and reabsorption of virtually all filtered bicarbonate.

B

Similar processes occur in the THICK ASCENDING LOOP of Henle and intercalating cells of the COLLECTING DUCT.

In contrast to the proximal tubule, hydrogen ion secretion in the collecting tubule is mediated by a H+ ATPase pump in the luminal membrane and a Cl-HCO3- exchanger in the basolateral membrane as shown in the diagram above. The H+ ATPase pump is influenced by aldosterone, which stimulates increased H+ secretion. Hydrogen ion secretion in the collecting tubule is the process primarily responsible for acidification of the urine, particularly during states of acidosis. The urine pH may fall as low as 4.0.
Proximal reabsorption of bicarbonate can be affected by many factors, in particular, potassium balance, volume status and renin/angiotensin levels. Therefore these factors can have very significant effects on acid base balance. Their specific effects will be discussed later.

3
Q

Henderson equation

A

The H2CO3/HCO3 2 buffer pair is used for assessment of acid-base status by applying the

Henderson equation:

[H+]=24 x PaCO2/[HCO3-]

4
Q

Dlta Anion gap

AG adjustments for Albumin

A

value must be adjusted for

Changes in patient’s serum AG (DAG) are estimated by comparing calculated serum AG to the average reference value of the laboratory.

the patient’s serum albumin concentration (subtract-ing or adding 2.5 mEq/L for each 1 g/dL of serum albumin below or above the average reference value of 4 g/dL, respectively).

5
Q

Increased Delta AG

A

An elevated DAG, particularly if .5 mEq/L, points to the presence of high AG metabolic acidosis. Examination of the relationship between DAG and D[HCO3 2] (D/D) estimates the degree to which retention of fixed acids is responsible for the D[HCO3 2] and assists in the identification of coexisting acid-base disorders.

6
Q

Refeeding syndrome

A

The syndrome is thought to result largely from a sudden shift from fat to carbohydrate metabolism along with a sudden increase in insulin levels after refeeding, which leads to increased cellular uptake of phosphate and other electrolytes. Intracellular movement of electrolytes, most notably phosphate, occurs along with a decrease in serum potassium, magnesium, glucose, and thiamine

increases overall oxygen demand,
Respiratory stimulation weaning from mechanical ventilation more difficult.

Electrolyte and fluid shifts increase cardiac workload and heart rate, which can lead to acute heart

7
Q

Causes of hypo phosphatemia post Transplant

A

Hypophosphatemia in this setting can be multifactorial, including RESIDUAL SECONDARY hyperparathyroidism,

GLUCOCORTICOID used in many transplant protocols, and a
LOW VITAMIN D state.

Moreover, persistence of inappropriately HIGH LEVEL of FGF-23, a recently discovered phosphaturic hormone, also may play an important role in post-transplant hypophosphatemia