Laboratory Result Interpretations Flashcards
1
Q
psychogenic polydipsia
A
Overhydration
2
Q
serum sodium is reduced below 135 mEq/L
A
Overhydration
3
Q
Because the consumed water is excreted by the kidneys, the urine is also dilute in this ion.
A
Overhydration
4
Q
In fact, the osmolality of urine will be low—that is, less than 300 mOsm/kg.
A
Overhydration
5
Q
Often accompanying hyponatremia are low values of the hematocrit and low values of BUN
A
Overhydration
6
Q
Urinalysis in the fluid-restricted patient will reveal urinary sodium of less than 25 mEq/L and low osmolalities.
A
Overhydration
7
Q
The potassium may also be low, although it often remains within the reference range.
A
Overhydration
8
Q
Because mainly water is excreted in urine in this condition, the total 24-hour sodium excre- tion will be low
A
Overhydration
9
Q
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.
A
Diuretics
10
Q
Also, because sodium is no longer retained because it follows chloride in the loop, it also is depleted from serum.
A
Diuretics
11
Q
Thus, unlike in overhydration, the total 24-hour sodium excretion is high
A
Diuretics
12
Q
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.
A
Diuretics
13
Q
Combined hyponatremia and hypokalemia with a high uri- nary sodium and potassium 24-hour excretion point to diuretic use.
A
Diuretics
14
Q
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.
A
SIADH
15
Q
This results in depletion of water in the renal tubules, thereby concentrating the urine.
A
SIADH
16
Q
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.
A
SIADH
17
Q
This condition is second- ary to Addison disease and AIDS-related hypoadrenalism.
A
Aldosterone Deficit
18
Q
Without aldo- sterone, the Na+–K+ and Na+–H+ exchange in the distal convoluted tubules and collecting ducts does not occur.
A
Aldosterone Deficit
19
Q
Therefore, serum sodium concentra- tion is reduced, while serum potassium concentration increases, and there is a mild metabolic acidosis.
A
Aldosterone Deficit
20
Q
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.
A
Aldosterone Deficit
21
Q
This rare condition resem- bles diuretic use except that the hyponatremia is not corrected with fluid restriction.
A
Bartter Syndrome
22
Q
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.
A
Bartter Syndrome
23
Q
caused by absence or mutations of the Na-K-2Cl symporter protein (SLC12A2 or NKCC2 gene) or the ROMK/KCNJ1- encoded potassium channel protein.
A
Bartter Syndrome
24
Q
the CLCNKB gene–encoded chloride channel protein is defective.
A
classic Bartter syndrome
25
associated with hearing loss (sensorimotor loss–associated), the BSND gene–encoded accessory chlo- ride channel protein is dysfunctional.
Bartter syndrome
26
the CASR (calcium-sensing receptor) gene–encoded calcium transporter protein is defective, leading to superimposed hypocalcemia.
Bartter Syndrome
27
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
28
In all forms of this disease, as in diuretic use, there is a high 24-hour sodium and potassium excretion.
Bartter Syndrome
29
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
30
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
31
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
32
Thus, the net effect of diabetic hyperosmolar states is a low serum sodium and a high serum potassium.
Diabetic Hyperosmolar State
33
This resembles hypoal- dosteronism, but the presence of abnormally high glucose levels signals the possibility of diabetes mellitus as the cause.
Diabetic Hyperosmolar State
34
This condition is usually caused by the presence of excess lipids in serum.
Pseudohyponatremia
35
No sodium ions are dissolved in lipids, which can take up a considerable volume of serum.
Pseudohyponatremia
36
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
37
However, part of this volume is lipid that has no sodium; thus, a falsely low value of sodium can be obtained.
Pseudohyponatremia
38
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
39
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
40
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
41
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
42
may be central (neurogenic; i.e., due to decreased vasopressin secretion) or nephrogenic (i.e., due to decreased renal response).
Diabetes Insipidus
43
Functionally, this condition is the reverse of SIADH—that is, water retention in the tubules is not adequate.
Diabetes Insipidus
44
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
45
The pat- tern is elevated serum sodium but dilute urinary sodium due to the func- tionally inadequate levels of ADH.
Diabetes Insipidus
46
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
47
The levels of circulat- ing aldosterone are inappropriately high, causing excessive reabsorption of Na+ and excretion of K+ and H+ ions.
Hyperaldosteronism
48
The patient will be hypernatremic and hypokalemic and exhibit a mild metabolic alkalosis.
Hyperaldosteronism
49
Many of the causes overlap with those of hyponatremia, including overhydration; use of loop diuretics; SIADH; and Bartter syn- drome, as discussed earlier.
hypokalemia
50
Infusion of insulin to diabetics.
hypokalemia
51
This results in rather large influxes of potassium into cells, lowering its concentration in serum.
hypokalemia
52
Alkalosis.
hypokalemia
53
Red blood cells are themselves excellent buffers.
hypokalemia
54
They are capable of exchanging potassium for hydrogen ions.
hypokalemia
55
Thus, in acidosis, H+ ions enter red cells in exchange for K+ ions.
hypokalemia
56
Conversely, in alkalosis, H+ ions leave red cells (to neutralize excess base), while K+ ions enter the red cells.
hypokalemia
57
Vomiting.
Hypokalemia
58
The major loss is both H+ and K+ from the stomach.
Hypokalemia
59
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
60
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
61
Hypoadrenalism resulting in low levels of aldosterone
Hyperkalemia
62
Any kind of cell damage, such as rhabdomyolysis, and especially hemolysis of erythrocytes
Hyperkalemia
63
In hemolysis, all of the intracellular K+ is extruded into plasma.
Hyperkalemia
64
Another analyte that is con- centrated in red cells that rises with K+ in hemolysis is LD.
Hyperkalemia
65
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
66
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
67
Normal serum sodium
140 mEq/L
68
Normal serum chloride
100 mEq/L
69
Normal serum bicarbonate
24 mEq/L
70
defined as Na+ − (Cl− + HCO3−), which, for normal individuals, is around 16
Anion Gap
71
comprises the other counterions that neutralize sodium but are not measured in serum
16 mEq/L
72
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)
73
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)
74
bicarbonate is reduced but there is no corresponding increase in Cl−
metabolic acidosis (acetoacetic acid/lactic acid/non-chloride-containing acid)
75
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)
76
diabetic acidosis
acetoacetic acid
77
sepsis or hypoperfusion
lactic acid
78
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)
79
Basic protein contains ammonium ions, the counterions for which are
chloride and bicarbonate.
80
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)
81
serious sign of possible malignancy—for example, multiple myeloma.
Low Anion Gaps (1 to 3 mEq/L)
82
The four analytes that aid in the diagnosis of this condition are
BUN, creatinine, calcium, and phosphate.
83
neither is produced in the kidneys, yet both are excellent indicators of renal conditions
BUN or creatinine
84
Urea nitrogen is generally measured in plasma or serum, but it has historically been referred to as
BUN
85
The formula for urea is
H2N—CO—NH2.
86
per mole of urea
two moles of nitrogen
87
This is the end product of NH3 metabolism in the liver
BUN
88
is excreted by the renal tubules at a rate that is roughly proportional to the glomerular filtration rate (GFR).
Urea
89
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
90
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
91
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
92
BUN reference range =
10–20 mg/mL
93
BUN is abnormally high
Prerenal
Renal and Postrenal
94
renal plasma flow is reduced from such lesions
Pre renal
95
renal artery stenosis
Pre renal
96
renal vein thrombosis
Pre renal
97
↓ GFR = ↑ BUN
Pre renal
Renal and Postrenal
98
Normal or mildly elevated CREATININE
Pre renal
99
CREATININE reference range
0.5 to 1.0 mg/dL
100
↓GFR = ↓ Urine Volume/Flow
Prerenal
101
NORMAL Pcr and Ucr
Prerenal
102
disproportionate rise in BUN over creatinine
Prerenal
103
normal BUN/creatinine ratio
10:1 to 20 : 1
104
BUN/creatinine ratio above 20 : 1
Prerenal
105
creatinine filtration will be compromised so that its serum level will rise correspondingly
Renal
106
both BUN and creatinine rise together, maintaining the BUN/creatinine at 10:1 to 20 : 1
Renal
107
obstructive uropathy
Postrenal
108
renal or ureteral stones (nephro- or urolithiasis)
Postrenal
109
prostatic enlargement from benign prostatic hypertrophy or prostatic carcinoma
Postrenal
110
urinary tract infection
Postrenal
111
bladder stasis
Postrenal
112
urothelial carcinomas
Postrenal
113
BUN: 60 mg/dL
Creatinine: 3.5 mg/dL
True renal failure
114
iltration compartment
glomerulus
115
concentration compartment
renal tubules
116
to conserve fluids or to concentrate the urine
kidneys
117
fluid- restricted diet: higher than the osmolality of plasma (Posm)
osmolality of urine (Uosm)
118
Uosm/Posm normal
higher than 1.2
119
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
120
urine is not being concentrated
Uosm/Posm: <1.2
121
tubular lesion
Uosm/Posm: <1.2
122
glomerular lesion
Uosm/Posm: >1.2
123
Confirmation can be performed by urinalysis
glomerular lesions
124
The presence of [?] in urine suggests compromise of the filtration function of the glomerulus.
albumin and/or globulins
125
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
126
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
127
filtration mechanisms become nonfunctional such that proteins are filtered and consequently are present in urine; urinalysis should reveal elevated protein concentrations.
glomerular disease
128
Assay of urine for albumin should likewise be performed.
glomerular disease
129
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
130
β- lipoprotein is often concurrently elevated in serum
lipoid nephrosis
131
This condition is also termed minimal change disease because there is little morphologic change in the glomerulus histopathologically.
lipoid nephrosis
132
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
133
The presence of multiple proteins in urine is called the
nephritic pattern
134
can also be diagnosed by observing the patterns of urine protein electrophoresis
nephritic pattern
135
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
136
can now be diagnosed by ELISA on sera
glomerular disease
137
Glomerular diseases often have immunological causes that are of two types:
immune complex disease
autoimmune disease
138
immune complexes are present as subendothelial or subepithelial deposits in the glomerulus
immune complex disease
139
specific antibodies to components of the glomerulus, such as the glomerular basement membrane, are present
autoimmune disease
140
can be identified in immunohistochemical studies on renal biopsies
Immune complex
Autoimmune
141
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
142
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.
143
common cause: deposition of polymeric IgA1 in the mesangium of the glomerulus
primary glomerulonephritis
144
The cause of this condition appears to be antibodies to this immunoglobulin.
primary glomerulonephritis
145
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
146
This results in an unexpected antigenic determinant that provokes an immune response.
primary glomerulonephritis
147
However, other antibodies against IgA1 are also required for full expression of this disease.
primary glomerulonephritis
148
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
149
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
150
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
151
A diagnostic serologic finding is depletion of circulating levels of C3.
membranoproliferative glomerulonephritis
152
do not seem to have an immunologic component
minimal change disease and focal segmental glomerulosclerosis
153
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
154
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
155
cytotoxic antibodies to glomerular cells result from [?] that are not confined to the kidneys
autoimmune systemic diseases
156
antinuclear antibodies (ANAs) circulate and cause polysystemic disease, including renal nephropathy
systemic lupus erythematosus
157
It appears that two prominent antibodies that cause direct glomerular damage are ANAs and antinucleosome antibodies.
systemic lupus erythematosus
158
Circulating antibodies against neutrophil cytoplasmic antigen (ANCA)
Wegener granulomatosis
159
serodiagnostic: affecting both lung and kidney, with a specificity for myeloperoxidase (ANCA- MPO)
Wegener granulomatosis
160
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
161
Anti- glomerular basement membrane (anti-GBM) antibody has been identified as a prominent causative factor
Goodpasture syndrome
162
is a systemic disease affecting both kidney and lung
Goodpasture syndrome
163
about 20% of patients who have high titers of anti- GBM antibodies also have high titers of ANCA- MPO.
Goodpasture syndrome
164
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
165
play an important role in the regulation of calcium levels
kidneys
166
↓ calcium = ↑ phosphate
renal failure
167
calcium is the most abundant cation in the body, most of it stored in bone as a
calcium hydroxyphosphate in hydroxyapatite crystal
168
complexes with phosphate in several different forms, depending on the ionization state of phosphate
Calcium
169
The most insoluble calcium phosphate forms are those with the most
basic phosphates
170
promote calcium deposition in bone
alkaline conditions
171
promote leaching of calcium from bone
acidic conditions
172
alkalosis promote
acidosis promotes
hypocalcemia
hypercalcemia
173
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)
174
The equilibrium constant, Ksp, for this equilibrium is:
Ksp=(Ca)×(P)/(CaP)insoluble
175
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
176
are almost always accompanied by hyperphosphatemic states and vice versa.
Hypocalcemic states
177
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.
178
is in the ionized form
active calcium
179
are considered to be the best measure of hypocalcemia, normocalcemia, or hypercalcemia.
serum levels of ionized calcium
180
stimulates the renal tubules to excrete phosphate.
level must then rise
parathyroid hormone (PTH)
serum calcium
181
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
182
tubular failure = phosphate excretion is inhibited due to the nonresponsiveness of the tubules to PTH.
renal disease
183
phosphate levels rise, while calcium levels fall
renal disease
184
is reduced, lowering absorbed calcium
active vitamin D production
185
in the face of elevated BUN and creatinine, indicative of renal disease, strongly suggest tubular failure.
Hypocalcemia and hyperphosphatemia
186
alkalosis and renal failure
hypocalcemia
187
hypoparathyroidism, also leading to hyperphosphatemia.
hypocalcemia
188
medullary thyroid carcinomas
hypocalcemia
189
amine precursor uptake and decarboxylase (APUD) activity cell tumors
hypocalcemia
190
medullary thyroid carcinomas and other amine precursor uptake and decarboxylase (APUD) activity cell tumors
Hypocalcemia.
191
the elaboration of calcitonin, a well- known calcium- lowering hormone
Hypocalcemia.
192
vitamin D levels may be low, resulting in diminished reabsorption of calcium for the gut
Hypocalcemia.
193
These causes may be encapsulated in the acronym CHARD (Calcitonin, Hypoparathyroidism, Alkalosis, Renal failure, and vitamin D deficit)
Hypocalcemia.
194
Besides acidosis, the possible causes of this condition may be summarized by Bakerman’s CHIMPS mnemonic (Bakerman & Strausbauch, 1994)
Hypercalcemia.
195
Cancer
Hypercalcemia.
196
Hypercalcemia. Multiple myeloma
Hypercalcemia. Hyperparathyroidism
Hypercalcemia. Sarcoidosis.
Hypercalcemia.
197
Hyperthyroidism
Hypercalcemia.
198
Iatrogenic causes
Hypercalcemia.
199
Multiple myeloma
Hypercalcemia.
200
Hyperparathyroidism
Hypercalcemia.
201
Sarcoidosis.
Hypercalcemia.
202
Calcitonin
Hypocalcemia
203
Hypoparathyroidism
Hypocalcemia
204
Alkalosis
Hypocalcemia
205
Alkalosis
Hypocalcemia
206
Renal failure
Hypocalcemia
207
vitamin D deficit
Hypocalcemia
208
Normal albumin
4 g/dL
209
diabetic ketoacidosis
metabolic acidosis
210
lactic acidosis (e.g., from gram- negative sepsis)
metabolic acidosis
211
renal failure
metabolic acidosis
212
diarrhea
metabolic acidosis
213
most common cause: vomiting, with a loss of HCl from the stomach and an attendant rise in bicarbonate
metabolic alkalosis
214
myasthenia gravis, in which there is partial paralysis of the accessory muscles of breathing
Respiratory Acidosis
215
pneumonia
Respiratory Acidosis
216
CNS diseases affecting the brainstem in areas involved in respiratory control
Respiratory Acidosis
217
is due mainly to hyperventilation, often of psychogenic origin
Respiratory alkalosis
218
pain from trauma or underlying disease, especially inflammation
Respiratory alkalosis
219
Here, the PCO2 is reduced because of the rapidity of breathing.
Respiratory alkalosis
220
This condition is seen mainly in the pediatric population when a child swallows multiple aspirin tablets.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
221
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.
222
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.
223
results from the independent action of salicylate anion on respiratory centers in the CNS.
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
224
“Overcompensation” of metabolic acidosis in salicylic acid overdose.
