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Clinical Chemistry Practical - Essay Example

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A patient Ms X has been admitted to hospital; she is semi comatose and unresponsive. No medical history is available. She is approximately 40-50 years old, she has a respiratory rate of 31 and a blood Ph of 7.05, her breath has a very distinctive odour.
A blood sample has been obtained, it has been centrifuged and plasma separated for analysis…
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Clinical Chemistry Practical
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Order # 154645 CLINICAL CHEMISTRY PRACTICAL RESULTS AND INTERPRETATION The Case A patient Ms X has been admitted to hospital; she is semi comatose and unresponsive. No medical history is available. She is approximately 40-50 years old, she has a respiratory rate of 31 and a blood Ph of 7.05, her breath has a very distinctive odour.
A blood sample has been obtained, it has been centrifuged and plasma separated for analysis. A urine sample is also available. The reagents and methods are available for GLUCOSE, UREA and KETONE assays. Assay the samples as follows:
GLUCOSE: plasma and urine, UREA: plasma only, KETONES: urine only.
Blood Ph 7.35-7.45
Respiratory rate 16-20
Blood glucose 2.8-6.0mM
Urea 3.3-6.7mM
Calculations and Results
1) Enter below your plasma and urine glucose concentrations, include all your calculations
To calculate the plasma concentration we need to have the following data: (the data were taken from the case study and in the standard)
a] plasma glucose from table = 31.875mM
urine glucose = 120mM
concentration of glucose in mM
C1 = 1 mM
V1= using 0.2 as example
V2 = 1ml
Next is the formula for the calculation of plasma concentration
C1V1 = C2V2
C1= C1V1
C2= 1 x 0.2 = 0.2 Mm
b] Procedure in testing the plasma glucose :
To measure glucose enrichments, plasma samples were deproteinized with an equal volume of 1.2M perchloric acid and centrifuged. The supernatant was neutralized with 3.2M K2CO3. After recentrifugation, the glucose fraction was extracted from the second supernatant by rapid sequential anion and cation exchange chromatography . The fraction containing glucose was dried before derivatization . The 297-to-299 ionic ratio responses were calculated in terms of isotopic enrichments using a standard curve made up from a known enrichment of glucose solutions.
average blank from table 1= 0.047 + 0.048 = 0.0475
To get plasma glucose concentration in 1 in 5 dilution
Diluted plasma supernatant from graph = 0.64 & 0.63
Undiluted plasma supernatant = (0.64 & 0.62) x 5
= (3.2 and 3.15) x 10
= 32 & 35
Average = 31.75
c] table 2
for 1 in 10 dilution
diluted plasma glucose concentration = 0.34 & 0.30
undiluted plasma glucose concentration = (0.34 & 0.30) x 10
average = 24 + 30 = 32 = 34830
Therefore plasma glucose = 31.75 + 32 = 31.875
d] table 3
for urine glucose, diluted plasma supernatant = 0.41 & 0.39
undiluted plasma = (0.41 &0.39) x 10 x 30 = 123 & 117
urine glucose = 123 + 117 / 2 = 120 mM
2 Enter your plasma urea concentration below, include all your absorbance data and calculations

Average blank = 0.039 + 0.025 = 0.032
Plasma urea concentration = A test x 10.4 mM
A standard
=p/q x 10.4
P = (1.175 - 0.032) + (1.249 - 0.032) = 1.415 = 0.7075
2 2
q= (0.728 - 0.032) + (0.751 - 0.032) = 2.36 = 1.18
2 2
Plasma urea concentration = p/q x 10.4 = 1.18 x 10.4 = 17.35 mM
Plasma urea concentration is elevated.
3. Enter your urinary ketones result
+ + 40 - 100 mg/dl (4.0 - 10mmol) - increased
elevated blood acetone and beta-hydroxybutyric acid
4. What is your diagnosis Explain clearly how this accounts for the glucose, urea and ketone results
The diagnosis is diabetic ketoacidosis (DKA). Three key features of diabetic ketoacidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. DKA is defined as an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level of greater than 250 mg/dL (although it is usually much higher),blood pH of less than 7.2, and a bicarbonate level of 18 mEq/L or less. DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis, glycogenolysis, and lipolysis.
Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum free fatty acids. Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results in accumulation of acidic intermediate and end metabolites (ie, ketones, ketoacids). Ketones include acetone, beta hydroxybutyrate, and acetoacetate. Ketones, in particular beta hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA. Moreover, acetone produces the characteristic fruity breath odor of ketotic patients.
Hyperglycemia usually exceeds the renal threshold of glucose absorption and results in significant glycosuria. Consequently, water loss in the urine is increased due to osmotic diuresis induced by glycosuria. This incidence of increased water loss results in severe dehydration, thirst, tissue hypoperfusion, and, possibly, lactic acidosis.
Typical free water loss in DKA is approximately 6 liters or nearly 100 mL/kg of body weight. The initial half of this amount is derived from intracellular fluid and precedes signs of dehydration, while the other half is from extracellular fluid and is responsible for signs of dehydration.
5. How does your diagnosis explain Ms X clinical signs on admission Explain
the mechanism whereby respiration controls blood pH. What would you expect to happen to Ms X respiration rate as her blood pH increases
Upon admission Ms X was being diagnosed to have diabetic ketoacidosis due to the following symptoms. Because of the acetone it produces a characteristic odor which was observed in the patient. The normal blood pH is 7.35-7.45, Ms X blood pH is lowering which may result in metabolic acidosis. Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia. Natural body buffers can buffer ketonemia in its early stages. When the accumulated ketones exceed the body's capacity of extracting them, they overflow into urine (ie, ketonuria). If the situation is not treated promptly, more accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis), with a drop in pH and bicarbonate serum levels. Respiratory compensation of this acidotic condition results in rapid shallow breathing (Kussmaul respirations). Kussmaul's inspiration-The rapid, deep, and labored respiration observed in patients with diabetic ketoacidosis; an involuntary mechanism to excrete carbon dioxide in order to reduce carbonic-acid level. Ms X has a low blood pH resulting in rapid shallow breathing. However if the blood pH was increased the breathing will slow down and the respiration will be normalize. The breathing rate increases when blood is acidic (too much carbon dioxide in the blood) and decreases when blood is too basic (too little carbon dioxide in the blood).
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