Type 1 Diabetes Management

Running head: TYPE 1 DIABETES MANAGEMENT
TYPE 1 DIABETES MANAGEMENT
Name of the student:
Name of the university:
Author note:

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TYPE 1 DIABETES MANAGEMENT
Introduction:
Type-1 Diabetes can be described as an auto-immune disorder which takes place when
the immune system of the body attacks and destroys its own insulin-producing beta cells present
in the pancreas (Danne et al., 2019). Diabetic ketoacidosis (DKA) might also follow when the
symptoms of type-1 diabetes is not managed successfully. The present case study show a patient
named Bill suffering from type-1 diabetes along with (DKA). This assignment would show how
nursing professionals can undertake proper interventions, strategies and medication management
to help the patient overcome the disorders successfully.
Pathophysiology of type 1 diabetes and diabetic ketoacidosis:
Type 1 diabetes can be described as the culmination of the two actions – lymphocytic
infiltration as well as destruction of the insulin secreting cells beta cells of the islets of
Langerhans in the pancreatic region. Researchers are of the opinion that when beta cell mass that
are responsible for secreting insulin gets decreased, insulin secretion also falls down below the
required level. This occurrence takes place until the available insulin is no longer found to be
appropriate for maintaining normal blood glucose levels (Farsani et al., 2017). The condition of
hyperglycemia results when almost about 80 to 90% of the beta cells undergo destruction. In
such situations, patients are seen to require exogenous insulin for reversing the catabolic
conditions as well as prevention of the ketosis and even for the decrease of the hyperglycemia
along with normalization of lipid and protein metabolism. This disorder is actually a chronic
autoimmune disorder which is seen to take place in mainly genetically susceptible individuals
which might be precipitated by the number of environmental factors. Studies are of the opinion
that in susceptible individuals, the immune system gets triggered to develop an auto-immune

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response against that of the altered pancreatic beta cell antigens or the molecule in the beta cells
which resemble to that of the viral proteins. It has been found that about 85% of the affected
patients have exhibited circulating islets cell antibodies. It has been found that the majority
numbers of affected individuals are also found to have detectable anti-insulin antibodies. Burns
et al. (2018) had clearly stated that most of these islet cells antibodies are seen to get directed
against that of the glutamic acid decarboxylase (GAD) within pancreatic beta cells. Another
model had been also put forward by many studies. It states that environmental triggers can result
in inducing islet autoimmunity and beta-cell death in the different susceptible and vulnerable
individuals. This actually results in initiating a series of pre-diabetic stages that ultimately sets
forth the clinical onset of that of the disorder.
Diabetic ketoacidosis can be described as the life-threatening problem that can affect
people with diabetes. This situation is seen to take place when the body starts to break own fat at
a rate that is much faster. The liver in this situation is seen to process the fat in ways that it gets
turned to fuel called the ketones that ultimately make the blood acidic in nature (Duca et al.,
2017). This situation is mainly seen to happen when signal from that of the insulin in the body
becomes so low that glucose cannot get into the cells to be used as the fuel source, when the liver
makes huge amount of the blood sugar level and when the fat gets broken down much faster than
for the body to process. It is seen that these fat gets broken down in the liver into the fuels and
this is often called ketones which are actually produced when the body breaks down fat after a
longer period of time between the meals (Peters et al., 2016). It has been found that when
ketones are produced quickly and are built up in the blood as well as the urine, they can be found
to become toxic by making the blood acidic. Researchers have termed this condition is known to
be ketoacidosis.

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Tachypnea or deep, rapid breathing is one of the symptom of DKA which was also
observed in the patient called Bill. It has been found that when the body is seen to produce or
ingest a much higher amount of acid or when the kidneys and lings are seen to fail, blood acid
levels rises. In cases of type-1 diabetes, ketones become higher in amount in the blood resulting
in the increase of the blood acid level. When the blood is seen to become too acidic, acidosis is
seen to take place and therefore, the body tries its best in restoring the imbalance (Robinson et
al., 2016). The body tries to take deeper as well as longer breaths where the lungs try to expel
more acidic carbon disoxide than that of the normal. Hence, rapid breathing s seen in this
disorder often called the Kussmaul breathing which was also observed in Bill. Another symptom
is the fruity smell in the breath of the patient which was also observed in Bill which comprised of
acetone smell in the breath. As the lungs try to expel more acetone-containing carbon dioxide,
the smell of his breath can also be found to be fruity. Another symptom that is also observed is
the flushed face which was also observed in Bill. Decrease in alertness and increase of confusion
is another symptom that was also observed when patient named Bill was admitted. This can be
contributed to a number of reasons (Gard et al., 2017). Because of the increased concentration of
the acids in the blood from that of the breakdown of the fats, the body is seen to urinate in excess
for removing these compounds from that of the blood. Excessive of the urination in the setting of
the continuous production of the keto acids can result in dehydration resulting in a general
feeling of illness, fatigue. Headache and slowed mental capacity. Excessive urination can also
result in huge loss of the potassium causing symptoms of nauseas and vomiting, fainting and
drowsiness, muscle cramps and others which were also seen in the patient (Semenkovich et al.,
2019).