Ms. Rita is a 15 year old female. She is
a known case of poor control of sugar level since one month without
regular medication. When patient was admitted to hospital her random
blood sugar =300mg/dl. She had no history of vomiting, breathlessness,
altered sensorium or bowel trouble. She had a history of weight loss. On
her initial examination she was calm, conscious and cooperative and
well oriented to time, place and person. Her BP was 140/90mmhg, pulse-80
per minute, abdomen soft non- tender and no organomegaly. She had a
history of polyuria and weight loss and increased thirst. Chest
vesicular breathing, no added sound. CVSSI, S2 heard normally.
Investigations:-Urine Color Pale, turbid
Reaction 6.0
Albumin + + +
Sugar + +
Ketones Negative
Glucose (F) 303mg/dl
Hb 8.3gm/dl
TLC 9000/Ul
DLC N-49%L-47%M-2%E-2%
Platelets 4.15 lacs
Total cholesterol 160mg/dl
DHLcholestrol 30mg/dl
LDL 100mg/dl
VLDL 30mg/dl
Triglycerides 150mg/dl
T. Cholesterol ratio 5.33
Glucose (F) 253mg/dl
FINAL DIAGNOSIS:-Type 1 Diabetes mellitus
Diabetes Mellitus type 1 is a chronic
disorder of carbohydrate, fat and protein metabolism. A defective or
deficient insulin secretary response, which translates into impaired
carbohydrate (glucose) use, is a characteristic feature of diabetes
mellitus (Goodman and Gillman’s, 2001).
Type
1 diabetes is also called Insulin Dependent Diabetes Mellitus (IDDM)
and was previously referred to as juvenile onsetdiabetes. It occurs due
to decreased insulin production and unchecked glucose production by the
liver. Insulin enables the sugar to get out of the blood and into the
cells where it is needed for the cells to function.Diabetes results from
a severe, absolute lack of insulin resulting in reduction in beta cell
mass. Beta cells are a type of cell in the pancreas in areas called the
islets of langerhans. These beta cells produce insulin. The function of
insulin is to counter the action of a number of hyperglycemia-generating
hormones and to maintain low blood glucose levels. Due to lack of
insulin sugar will not be able to get into the cells so, there will be a
high concentration in the blood. On the other hand, high amount of
insulin shifts too much sugar into the cells and there will be not
enough sugar left in the blood (Mohan, 2000). Lack of insulin affects
them because insulin allows for the absorption of glucose by cells in
the body and is secreted by the beta cells, in response to elevated
glucose in the blood (Chatterjea, 2000).
To treat the high level of glucose
insulin was given to the patient. Insulin works to lower blood glucose
by promoting the transport of glucose into cells and by inhibiting the
conversion of glycogen and amino acids to glucose (Smeltzer, 2004).
Ms. Rita was suffering from polyuria
which is increased amount of urine (Smeltzer, 2004). When the blood
glucose level is significantly elevated, (it is also mentioned in the
above paragraph) the kidneys are unable to handle the workload and
therefore allow the excess glucose to spill over into the urine. The
glucose in urine acts osmotically means higher concentration to lower
concentration to draw more water into the urine, resulting in polyuria
(Cotran, 2000).
Mrs. Rita’s urine was pale and turbid
color. It occurs because concentration of glucose in the blood rises.
The renal threshold for glucose is, usually 180 to 200mg/dl. When blood
glucose increases, the kidneys may not reabsorb all the filtered glucose
and the glucose than appears in the urine making it pale and turbid
(Smeltzer et al, 2004).
She had a problem of Polydypsia which
means excessive thirst. As explained above glucose in the urine is
increase, rising the osmotic pressure of the urine, this ways pulls the
water along with the glucose in to the urine which leads to excessive
urination called polyuria, causing a lack of overall body fluids making
the blood hypertonic. This hypertonicity provokes the brain to initiate
thirst as a compensatory mechanism of dehydration so that loss of water
can be fulfill (Chaudhuri, 2002).
She was suffering from problem of weight
loss. Loss of tissue mass occurs in the insulin- dependent form of the
disease (the consequence of glycosuria) that characterizes the illness.
Role of insulin is to provide entry of glucose into the cells. Insulin
deficiency result in non utilization of glucose as it cannot enter into
the cells leading to impaired synthesis of protein, fat and
simultaneously cause accelerated breakdown of proteins and fats for
production of energy causing a catabolic state. It means there is
accelerated breakdown of fat and muscle secondary to insulin deficiency
leading to weight loss.
Ms. Rita’s blood pressure was
140/90mmhg. The reasons for the increased blood pressure are
hyperinsulinemia, glucose intolerance and reduced level of HDL
cholesterol. In a normal physiological state nitric oxide synthesis is
stimulated by insulin besides decreased synthesis and responsiveness to
non insulin resistant states have been associated with increased level
of endothelin-1 and potent vasoconstrictor and proarthero sclerotic
vascular hormone associated with hypertension 4ia,, e.of
Pathologrica..outh.within the central nervous system, all these hormonal
changes may play a major role in the gastr(Kumar and Clark, 2005).
Overall management was good and Ms. Rita discharged in satisfactory condition.
