Laboratory Result Interpretations Flashcards
psychogenic polydipsia
Overhydration
serum sodium is reduced below 135 mEq/L
Overhydration
Because the consumed water is excreted by the kidneys, the urine is also dilute in this ion.
Overhydration
In fact, the osmolality of urine will be low—that is, less than 300 mOsm/kg.
Overhydration
Often accompanying hyponatremia are low values of the hematocrit and low values of BUN
Overhydration
Urinalysis in the fluid-restricted patient will reveal urinary sodium of less than 25 mEq/L and low osmolalities.
Overhydration
The potassium may also be low, although it often remains within the reference range.
Overhydration
Because mainly water is excreted in urine in this condition, the total 24-hour sodium excre- tion will be low
Overhydration
block the chloride pump in the loop of Henle, thereby blocking the formation of the ion gra- dients via the countercurrent multiplier, necessary for water conservation. Thus, water is lost.
Diuretics
Also, because sodium is no longer retained because it follows chloride in the loop, it also is depleted from serum.
Diuretics
Thus, unlike in overhydration, the total 24-hour sodium excretion is high
Diuretics
pattern resembles overhydration (dilute serum and urine), except that loop diuretics cause severe potassium deple- tion unless the diuretic is combined with a potassium-sparing diuretic such as triamterene.
Diuretics
Combined hyponatremia and hypokalemia with a high uri- nary sodium and potassium 24-hour excretion point to diuretic use.
Diuretics
In this condition, secondary to head trauma, seizures, other CNS diseases, and neoplastic conditions, espe- cially lung, breast, and ovarian cancers that secrete ADH-like hormones, the serum sodium is depressed due to the excess retention of water in the collecting ducts.
SIADH
This results in depletion of water in the renal tubules, thereby concentrating the urine.
SIADH
Therefore, while the serum is dilute in sodium (hypotonic), the urine is concentrated to levels of over 40 mEq/L and the urine osmolality exceeds 300 mOsm/kg, while the serum osmolal- ity is less than 280 mOsm/kg.
SIADH
This condition is second- ary to Addison disease and AIDS-related hypoadrenalism.
Aldosterone Deficit
Without aldo- sterone, the Na+–K+ and Na+–H+ exchange in the distal convoluted tubules and collecting ducts does not occur.
Aldosterone Deficit
Therefore, serum sodium concentra- tion is reduced, while serum potassium concentration increases, and there is a mild metabolic acidosis.
Aldosterone Deficit
Urinary sodium increases but not to the high levels seen in SIADH, and the osmolality of urine is also not so elevated as in SIADH.
Aldosterone Deficit
This rare condition resem- bles diuretic use except that the hyponatremia is not corrected with fluid restriction.
Bartter Syndrome
This syndrome is actually a complex of diseases, each of which is caused by mutations of genes that encode ion transporter proteins in the thick portion of the ascending loop of Henle.
Bartter Syndrome
caused by absence or mutations of the Na-K-2Cl symporter protein (SLC12A2 or NKCC2 gene) or the ROMK/KCNJ1- encoded potassium channel protein.
Bartter Syndrome
the CLCNKB gene–encoded chloride channel protein is defective.
classic Bartter syndrome
associated with hearing loss (sensorimotor loss–associated), the BSND gene–encoded accessory chlo- ride channel protein is dysfunctional.
Bartter syndrome
the CASR (calcium-sensing receptor) gene–encoded calcium transporter protein is defective, leading to superimposed hypocalcemia.
Bartter Syndrome
In Gitelman syndrome, which parallels this syndrome but is a milder form of disease, mutations in the NCC gene–encoded sodium-chloride symporter protein, also termed the thiazide-sensitive Na+-Cl− cotransporter protein (Ped- ersen et al., 2010), cause malfunction of reabsorption of sodium and chloride ions from the tubular fluid into the cells of the distal convoluted tubule.
Bartter Syndrome
In all forms of this disease, as in diuretic use, there is a high 24-hour sodium and potassium excretion.
Bartter Syndrome
In patients with diabetes mellitus, if they are in a hyperosmolar state—that is, in which the serum glucose is markedly elevated (say, around 700 mg/dL)—the hyperosmolarity of serum causes efflux of cellular water, with a conse- quent osmotic dilution of serum sodium.
Diabetic Hyperosmolar State
Roughly, for each 100 mg/dL increase in serum glucose, there is a 1.6 mEq/L decrease in the serum Na+ concentration.
Diabetic Hyperosmolar State
Because transport of glucose into cells is accompanied by concurrent transport of potassium into cells, low insulin levels also cause high serum potassium.
Diabetic Hyperosmolar State
Thus, the net effect of diabetic hyperosmolar states is a low serum sodium and a high serum potassium.
Diabetic Hyperosmolar State
This resembles hypoal- dosteronism, but the presence of abnormally high glucose levels signals the possibility of diabetes mellitus as the cause.
Diabetic Hyperosmolar State
This condition is usually caused by the presence of excess lipids in serum.
Pseudohyponatremia
No sodium ions are dissolved in lipids, which can take up a considerable volume of serum.
Pseudohyponatremia
If the absolute amount of sodium in a given volume of serum is determined, as is performed when using such methods of sodium determination as flame photometry, this value is divided by the sample vol- ume to get the concentration.
Pseudohyponatremia
However, part of this volume is lipid that has no sodium; thus, a falsely low value of sodium can be obtained.
Pseudohyponatremia
This artifact is eliminated by the use of ion-selective electrodes that directly determine the concentration of sodium and do not depend on knowledge of the vol- ume of serum.
Pseudohyponatremia
Note that although most modern, high-throughput chem- istry analyzers measure serum sodium using ion-selective electrodes, they perform a predilution (dilution prior to analysis) of the specimen (so-called indirect potentiometry); thus, the measurement is relative to volume and is susceptible to
Pseudohyponatremia
This can be caused by excess renal loss with high positive free water clearance (i.e., loss of water in excess of NaCl), excess sweating, and low water intake.
Dehydration
The serum sodium is ele- vated, as is the hematocrit (possibly masking a true anemia), and the urine sodium is also high due to increased renal excretion of NaCl.
Dehydration
may be central (neurogenic; i.e., due to decreased vasopressin secretion) or nephrogenic (i.e., due to decreased renal response).
Diabetes Insipidus
Functionally, this condition is the reverse of SIADH—that is, water retention in the tubules is not adequate.
Diabetes Insipidus
Although this condition is not completely understood and may be multi- factorial, current research suggests that either mutation and/or changes in protein expression of “water channel molecules” (renal aquaporins) and/ or the vasopressin V2 renal collecting tubule cell receptor may play a role in both pathologic water loss, such as in nephrogenic DI, and pathologic water retention, such as in SIADH
Diabetes Insipidus
The pat- tern is elevated serum sodium but dilute urinary sodium due to the func- tionally inadequate levels of ADH.
Diabetes Insipidus
This condition may result from adrenal hyperplasia, Cushing syndrome, Cushing disease (see endocrine section to come) and Conn syndrome, in which there is hyper- secretion of aldosterone from the zona glomerulosa.
Hyperaldosteronism
The levels of circulat- ing aldosterone are inappropriately high, causing excessive reabsorption of Na+ and excretion of K+ and H+ ions.
Hyperaldosteronism
The patient will be hypernatremic and hypokalemic and exhibit a mild metabolic alkalosis.
Hyperaldosteronism
Many of the causes overlap with those of hyponatremia, including overhydration; use of loop diuretics; SIADH; and Bartter syn- drome, as discussed earlier.
hypokalemia
Infusion of insulin to diabetics.
hypokalemia
This results in rather large influxes of potassium into cells, lowering its concentration in serum.
hypokalemia
Alkalosis.
hypokalemia
Red blood cells are themselves excellent buffers.
hypokalemia
They are capable of exchanging potassium for hydrogen ions.
hypokalemia
Thus, in acidosis, H+ ions enter red cells in exchange for K+ ions.
hypokalemia
Conversely, in alkalosis, H+ ions leave red cells (to neutralize excess base), while K+ ions enter the red cells.
hypokalemia
Vomiting.
Hypokalemia
The major loss is both H+ and K+ from the stomach.
Hypokalemia
Loss of K+ in gastric fluid may be less important than the overall fluid loss, which causes activation of aldosterone and renal wasting of K+.
Hypokalemia
Among the major causes are those that also cause hypernatremia—for exam- ple, dehydration and DI—acidosis and diabetes mellitus (as discussed earlier), and hemolysis.
Hyperkalemia
Hypoadrenalism resulting in low levels of aldosterone
Hyperkalemia
Any kind of cell damage, such as rhabdomyolysis, and especially hemolysis of erythrocytes
Hyperkalemia
In hemolysis, all of the intracellular K+ is extruded into plasma.
Hyperkalemia
Another analyte that is con- centrated in red cells that rises with K+ in hemolysis is LD.
Hyperkalemia
Concomitant elevations of potassium and LD in serum should be taken as indications of hemolysis either artifactually after a blood sample has been taken from the patient or, less commonly, hemolysis from an underlying hemolytic condition.
Hyperkalemia
must be neutralized by counterions, most of which, in blood, are constituted by chloride and bicarbonate ions, and, to a lesser degree, by phosphate, sulfate, and protein carboxylate groups.
sodium ions
Normal serum sodium
140 mEq/L
Normal serum chloride
100 mEq/L
Normal serum bicarbonate
24 mEq/L
defined as Na+ − (Cl− + HCO3−), which, for normal individuals, is around 16
Anion Gap
comprises the other counterions that neutralize sodium but are not measured in serum
16 mEq/L
the acid will be buffered by bicarbonate (converted to H2CO3)
metabolic acidosis (rise in H+ ion concentration is accompanied by a corresponding rise in Cl− ions)
The bicarbonate value will therefore decrease, but there will be a 1 : 1 increase in chloride ion. Thus, there will be no change in the anion gap.
metabolic acidosis (rise in H+ ion concentration is accompanied by a corresponding rise in Cl− ions)
bicarbonate is reduced but there is no corresponding increase in Cl−
metabolic acidosis (acetoacetic acid/lactic acid/non-chloride-containing acid)
there is an increase in the anion gap that can reach values of 25 to 30 mEq/L
metabolic acidosis (acetoacetic acid/lactic acid/non-chloride-containing acid)
diabetic acidosis
acetoacetic acid
sepsis or hypoperfusion
lactic acid
signify the presence of high levels of basic protein, often a monoclonal paraprotein as occurs in plasma cell dyscrasias
Low Anion Gaps (1 to 3 mEq/L)
Basic protein contains ammonium ions, the counterions for which are
chloride and bicarbonate.
Now the “invisible” ion is ammonium, while there is a measurable increase in chloride and bicarbonate ions.
Low Anion Gaps (1 to 3 mEq/L)
serious sign of possible malignancy—for example, multiple myeloma.
Low Anion Gaps (1 to 3 mEq/L)
The four analytes that aid in the diagnosis of this condition are
BUN, creatinine, calcium, and phosphate.
neither is produced in the kidneys, yet both are excellent indicators of renal conditions
BUN or creatinine
Urea nitrogen is generally measured in plasma or serum, but it has historically been referred to as
BUN
The formula for urea is
H2N—CO—NH2.
per mole of urea
two moles of nitrogen
This is the end product of NH3 metabolism in the liver
BUN
is excreted by the renal tubules at a rate that is roughly proportional to the glomerular filtration rate (GFR).
Urea
Note, therefore, that the retained urea—that is, plasma or serum urea or BUN— is approximately inversely proportional to the GFR—that is,
BUN∝1/GFR
is secreted but is also reabsorbed to an approximately equal extent over a rather wide range for the GFR so that the net effect is that the amount filtered is the amount excreted.
Creatinine
The total amount of creatinine filtered then is its urinary concentration, Ucr × the volume of urine, V, over a given time. The total plasma volume that delivered this quantity of creatinine to the glomerulus in a given time period is the GFR and is the total amount of creatinine filtered divided by the plasma concentration, Pcr. This quantity is also the creatinine clearance, Ccr. Thus, the GFR is:
GFR=Ccr=Ucr×V/Pcr
BUN reference range =
10–20 mg/mL
BUN is abnormally high
Prerenal
Renal and Postrenal
renal plasma flow is reduced from such lesions
Pre renal
renal artery stenosis
Pre renal
renal vein thrombosis
Pre renal
↓ GFR = ↑ BUN
Pre renal
Renal and Postrenal
Normal or mildly elevated CREATININE
Pre renal
CREATININE reference range
0.5 to 1.0 mg/dL
↓GFR = ↓ Urine Volume/Flow
Prerenal
NORMAL Pcr and Ucr
Prerenal
disproportionate rise in BUN over creatinine
Prerenal
normal BUN/creatinine ratio
10:1 to 20 : 1
BUN/creatinine ratio above 20 : 1
Prerenal
creatinine filtration will be compromised so that its serum level will rise correspondingly
Renal
both BUN and creatinine rise together, maintaining the BUN/creatinine at 10:1 to 20 : 1
Renal
obstructive uropathy
Postrenal
renal or ureteral stones (nephro- or urolithiasis)
Postrenal
prostatic enlargement from benign prostatic hypertrophy or prostatic carcinoma
Postrenal
urinary tract infection
Postrenal
bladder stasis
Postrenal
urothelial carcinomas
Postrenal
BUN: 60 mg/dL
Creatinine: 3.5 mg/dL
True renal failure
iltration compartment
glomerulus
concentration compartment
renal tubules
to conserve fluids or to concentrate the urine
kidneys
fluid- restricted diet: higher than the osmolality of plasma (Posm)
osmolality of urine (Uosm)
Uosm/Posm normal
higher than 1.2
If a 24- hour urine specimen collection from this patient on a fluid- restricted diet is measured for [?], we can determine where the lesion has occurred.
Uosm
urine is not being concentrated
Uosm/Posm: <1.2
tubular lesion
Uosm/Posm: <1.2
glomerular lesion
Uosm/Posm: >1.2
Confirmation can be performed by urinalysis
glomerular lesions
The presence of [?] in urine suggests compromise of the filtration function of the glomerulus.
albumin and/or globulins
glomerulonephritis
glomerular lesions pyelonephritis
glomerular lesions lupus nephritis
glomerular lesions crescentic disease such as Goodpasture syndrome
glomerular lesions immune complex disease
glomerular lesions pauci- immune crescentic disease
glomerular lesions/tubular lesions diabetes
glomerular lesions/tubular lesions infarction
tubular lesions pyelonephritis
tubular lesions papillary necrosis
tubular lesions acute tubular necrosis (ATN)
tubular lesions shock
tubular lesions ischemia
glomerular lesions
It is remarkable that from a blood specimen of only [?] and several urine aliquots, not only can we determine the presence of renal failure, but we can localize the lesion, and all of this virtually noninvasively.
100 μL
filtration mechanisms become nonfunctional such that proteins are filtered and consequently are present in urine; urinalysis should reveal elevated protein concentrations.
glomerular disease
Assay of urine for albumin should likewise be performed.
glomerular disease
Albumin = Total Protein = only albumin was filtered in the glomerulus
This condition is termed and has sometimes been termed
nephrosis or the nephrotic pattern /lipoid nephrosis
β- lipoprotein is often concurrently elevated in serum
lipoid nephrosis
This condition is also termed minimal change disease because there is little morphologic change in the glomerulus histopathologically.
lipoid nephrosis
If the albumin level is elevated but is significantly less than that for total protein in urine, then many proteins, besides albumin, pass through the glomerulus, which, in contrast to the glomerulus in [?], is morphologically damaged.
minimal change disease
The presence of multiple proteins in urine is called the
nephritic pattern
can also be diagnosed by observing the patterns of urine protein electrophoresis
nephritic pattern
only albumin is present; if multiple protein bands, that is, albumin and α, and/or β, and/or γ are present
nephrotic pattern; nephritic pattern
can now be diagnosed by ELISA on sera
glomerular disease
Glomerular diseases often have immunological causes that are of two types:
immune complex disease
autoimmune disease
immune complexes are present as subendothelial or subepithelial deposits in the glomerulus
immune complex disease
specific antibodies to components of the glomerulus, such as the glomerular basement membrane, are present
autoimmune disease
can be identified in immunohistochemical studies on renal biopsies
Immune complex
Autoimmune
the same antibodies in the [?] and in [?] are frequently present in the circulation where they can be identified in ELISA in serum.
immune complexes
glomerular tissue
In fact, due to improved ELISA techniques, there is currently a major trend for relying on these assays on patients’ sera to determine the cause of glomerulopathies. This approach has the advantage that it allows avoidance of performing renal biopsies, which are invasive procedures. In addition, there are studies suggesting that assays for specific proteins in urine samples of patients with glomerular and tubular diseases may result in direct diagnosis of these diseases and can be used to monitor progress in disease treatment such as for diabetes mellitus. Here, we focus on serologic markers for specific proteins that have been validated as markers for specific glomerular diseases. While there are numerous conditions for which these assays are now available, we list the most prominent among them.
common cause: deposition of polymeric IgA1 in the mesangium of the glomerulus
primary glomerulonephritis
The cause of this condition appears to be antibodies to this immunoglobulin.
primary glomerulonephritis
An important component of this condition is a defect in the posttranslational modification of IgA1 in that there is the absence of O- glycosylation by galactose of the hinge region of this antibody, resulting in galactose- deficient IgA1 (Gd- IgA1).
opathies have high serum titers of circulating antibodies to a membrane receptor for phospholipase A2 on podocytes (glomerular visceral epithelial cells), the so- called PLA- 2 antigen.
primary glomerulonephritis
This results in an unexpected antigenic determinant that provokes an immune response.
primary glomerulonephritis
However, other antibodies against IgA1 are also required for full expression of this disease.
primary glomerulonephritis
Expression in serum of both antiglycan antibodies and of Gd- IgA1 in the presence of proteinuria appear to identify glomerulonephritis at an early stage.
primary glomerulonephritis
high serum titers of circulating antibodies to a membrane receptor for phospholipase A2 on podocytes (glomerular visceral epithelial cells), the so- called PLA- 2 antigen.
membranoproliferative glomerulonephritis
a major finding is subendothelial deposition of immune complexes, containing high levels of C3 from the primary complement cascade that may result from concurrent infectious or other diseases provoking an immune response.
membranoproliferative glomerulonephritis
A diagnostic serologic finding is depletion of circulating levels of C3.
membranoproliferative glomerulonephritis
do not seem to have an immunologic component
minimal change disease and focal segmental glomerulosclerosis
here are elevated serum levels of a soluble (non- membrane- bound) form of the urokinase receptor, called suPAR, suggesting that both conditions are manifestations of the same underlying disease, although this view is not universally accepted.
minimal change disease and focal segmental glomerulosclerosis
A current hypothesis is that binding of suPAR to integrin 3 on the membrane surface of podocytes seems to induce changes in overall cell- cell orientation, resulting in abnormal spacing between cells.
minimal change disease and focal segmental glomerulosclerosis
cytotoxic antibodies to glomerular cells result from [?] that are not confined to the kidneys
autoimmune systemic diseases
antinuclear antibodies (ANAs) circulate and cause polysystemic disease, including renal nephropathy
systemic lupus erythematosus
It appears that two prominent antibodies that cause direct glomerular damage are ANAs and antinucleosome antibodies.
systemic lupus erythematosus
Circulating antibodies against neutrophil cytoplasmic antigen (ANCA)
Wegener granulomatosis
serodiagnostic: affecting both lung and kidney, with a specificity for myeloperoxidase (ANCA- MPO)
Wegener granulomatosis
These antibodies have been identified as occurring in so- called pauci- immune complex disease identified in the immunohistochemistry on renal biopsies on patients with this disease.
Wegener granulomatosis
Anti- glomerular basement membrane (anti-GBM) antibody has been identified as a prominent causative factor
Goodpasture syndrome
is a systemic disease affecting both kidney and lung
Goodpasture syndrome
about 20% of patients who have high titers of anti- GBM antibodies also have high titers of ANCA- MPO.
Goodpasture syndrome
Thus, serodiagnostic markers for renal disease can not only indicate the presence of renal disease but can further identify the location of the disease in the kidneys and further identify the cause of the disease in a virtually noninvasive manner.
Goodpasture syndrome
play an important role in the regulation of calcium levels
kidneys
↓ calcium = ↑ phosphate
renal failure
calcium is the most abundant cation in the body, most of it stored in bone as a
calcium hydroxyphosphate in hydroxyapatite crystal
complexes with phosphate in several different forms, depending on the ionization state of phosphate
Calcium
The most insoluble calcium phosphate forms are those with the most
basic phosphates
promote calcium deposition in bone
alkaline conditions
promote leaching of calcium from bone
acidic conditions
alkalosis promote
acidosis promotes
hypocalcemia
hypercalcemia
Note also that there is an equilibrium between soluble calcium phosphate and insoluble calcium phosphate in bone. We represent this equilibrium as:
where P represents all ionic phosphate forms and where the left side is all soluble calcium phosphate salts and the right side is the insoluble salt forms.
Ca+P↔(CaP)
The equilibrium constant, Ksp, for this equilibrium is:
Ksp=(Ca)×(P)/(CaP)insoluble
Because (CaP) insoluble is constant in concentration, the product of soluble Ca × soluble P is a constant, called the (?). Thus, there is an (?) relationship between Ca and P.
solubility constant or Ksp
inverse
are almost always accompanied by hyperphosphatemic states and vice versa.
Hypocalcemic states
Of the soluble calcium, in the numerator of Equation 9.7, there are two forms
calcium bound to albumin and globulin, and small molecules in chelate form, and so- called ionized or nonchelated calcium.
is in the ionized form
active calcium
are considered to be the best measure of hypocalcemia, normocalcemia, or hypercalcemia.
serum levels of ionized calcium
stimulates the renal tubules to excrete phosphate.
level must then rise
parathyroid hormone (PTH)
serum calcium
kidneys are vital to the formation of active vitamin D in the synthesis of (?), which is necessary for the absorption of calcium in the gut.
1,25- dihydroxycholecalciferol
tubular failure = phosphate excretion is inhibited due to the nonresponsiveness of the tubules to PTH.
renal disease
phosphate levels rise, while calcium levels fall
renal disease
is reduced, lowering absorbed calcium
active vitamin D production
in the face of elevated BUN and creatinine, indicative of renal disease, strongly suggest tubular failure.
Hypocalcemia and hyperphosphatemia
alkalosis and renal failure
hypocalcemia
hypoparathyroidism, also leading to hyperphosphatemia.
hypocalcemia
medullary thyroid carcinomas
hypocalcemia
amine precursor uptake and decarboxylase (APUD) activity cell tumors
hypocalcemia
medullary thyroid carcinomas and other amine precursor uptake and decarboxylase (APUD) activity cell tumors
Hypocalcemia.
the elaboration of calcitonin, a well- known calcium- lowering hormone
Hypocalcemia.
vitamin D levels may be low, resulting in diminished reabsorption of calcium for the gut
Hypocalcemia.
These causes may be encapsulated in the acronym CHARD (Calcitonin, Hypoparathyroidism, Alkalosis, Renal failure, and vitamin D deficit)
Hypocalcemia.
Besides acidosis, the possible causes of this condition may be summarized by Bakerman’s CHIMPS mnemonic (Bakerman & Strausbauch, 1994)
Hypercalcemia.
Cancer
Hypercalcemia.
Hypercalcemia. Multiple myeloma
Hypercalcemia. Hyperparathyroidism
Hypercalcemia. Sarcoidosis.
Hypercalcemia.
Hyperthyroidism
Hypercalcemia.
Iatrogenic causes
Hypercalcemia.
Multiple myeloma
Hypercalcemia.
Hyperparathyroidism
Hypercalcemia.
Sarcoidosis.
Hypercalcemia.
Calcitonin
Hypocalcemia
Hypoparathyroidism
Hypocalcemia
Alkalosis
Hypocalcemia
Alkalosis
Hypocalcemia
Renal failure
Hypocalcemia
vitamin D deficit
Hypocalcemia
Normal albumin
4 g/dL
diabetic ketoacidosis
metabolic acidosis
lactic acidosis (e.g., from gram- negative sepsis)
metabolic acidosis
renal failure
metabolic acidosis
diarrhea
metabolic acidosis
most common cause: vomiting, with a loss of HCl from the stomach and an attendant rise in bicarbonate
metabolic alkalosis
myasthenia gravis, in which there is partial paralysis of the accessory muscles of breathing
Respiratory Acidosis
pneumonia
Respiratory Acidosis
CNS diseases affecting the brainstem in areas involved in respiratory control
Respiratory Acidosis
is due mainly to hyperventilation, often of psychogenic origin
Respiratory alkalosis
pain from trauma or underlying disease, especially inflammation
Respiratory alkalosis
Here, the PCO2 is reduced because of the rapidity of breathing.
Respiratory alkalosis
This condition is seen mainly in the pediatric population when a child swallows multiple aspirin tablets.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
Since aspirin is salicylic acid, the first manifestation of this condition is metabolic acidosis with a partially compensated reduced PCO2 and an increased anion gap.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
However, salicylate anion induces increased respiratory rates, causing lowering of the PCO2 to levels significantly lower than those in the normal compensatory process, resulting in a respiratory alkalosis that masks the fundamental metabolic acidosis.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
results from the independent action of salicylate anion on respiratory centers in the CNS.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
