NR 526: PATHOPHYSIOLOGY DISCUSSION WITH
REFERENCES 100% CORRECT DOWNLOAD TO SCORE A
Diabetic ketoacidosis (DKA) is an acute metabolic disorder characterized by markedly increased
circulating ketone bodies leading to ketoacidosis in the presence of prolonged hyperglycemia due
to an absence of insulin. DKA may present in subjects with Type 1 diabetes mellitus (T1DM)
with an absolute or relative insulin deficiency.
Etiology:
Drugs, infection, lack of insulin, other physiologic stress and recurrent illness is common cause
of Diabetic Ketoacidosis.
Pathophysiology:
The pathophysiologic mechanisms for DKA development include two main mechanisms:
substantial insulin deficiency, and increased amount of counter-regulatory. This leads to
increased hepatic glucose production by increased hepatic gluconeogenesis and glycogenolysis.
There is additionally reduced glucose utilization by the peripheral tissues, especially in muscle.
Low insulin causes activation of hormone-sensitive lipase and increases breakdown of
triglycerides into free fatty acids. In the liver, the free fatty acids are oxidized to ketone bodies
which are stimulated by glucagon. The imbalance of insulin and glucagon leads to an increased
glucagon/insulin ratio which lowers the activity of malonyl coenzyme A. Malonyl coenzyme A
modulates movement of free fatty acid inside the hepatic mitochondria and fatty acid oxidation
occurs. There is increased production of ketone bodies. They are mainly acetoacetate and
βhydroxybutyrate which are two strong acids. This leads to reduction of bicarbonate and causes
metabolic acidosis (Andrade et al., 2016).
Hallmark symptoms of Diabetic Ketoacidosis:
• Patients presenting with DKA have a brief clinical course marked by fatigue
and polyuria, polydipsia, and weight loss, which are the classical symptoms of
hyperglycemia.
• Gastrointestinal complaints are often present such as diffuse abdominal pain (46%), and
REFERENCES 100% CORRECT DOWNLOAD TO SCORE A
Diabetic ketoacidosis (DKA) is an acute metabolic disorder characterized by markedly increased
circulating ketone bodies leading to ketoacidosis in the presence of prolonged hyperglycemia due
to an absence of insulin. DKA may present in subjects with Type 1 diabetes mellitus (T1DM)
with an absolute or relative insulin deficiency.
Etiology:
Drugs, infection, lack of insulin, other physiologic stress and recurrent illness is common cause
of Diabetic Ketoacidosis.
Pathophysiology:
The pathophysiologic mechanisms for DKA development include two main mechanisms:
substantial insulin deficiency, and increased amount of counter-regulatory. This leads to
increased hepatic glucose production by increased hepatic gluconeogenesis and glycogenolysis.
There is additionally reduced glucose utilization by the peripheral tissues, especially in muscle.
Low insulin causes activation of hormone-sensitive lipase and increases breakdown of
triglycerides into free fatty acids. In the liver, the free fatty acids are oxidized to ketone bodies
which are stimulated by glucagon. The imbalance of insulin and glucagon leads to an increased
glucagon/insulin ratio which lowers the activity of malonyl coenzyme A. Malonyl coenzyme A
modulates movement of free fatty acid inside the hepatic mitochondria and fatty acid oxidation
occurs. There is increased production of ketone bodies. They are mainly acetoacetate and
βhydroxybutyrate which are two strong acids. This leads to reduction of bicarbonate and causes
metabolic acidosis (Andrade et al., 2016).
Hallmark symptoms of Diabetic Ketoacidosis:
• Patients presenting with DKA have a brief clinical course marked by fatigue
and polyuria, polydipsia, and weight loss, which are the classical symptoms of
hyperglycemia.
• Gastrointestinal complaints are often present such as diffuse abdominal pain (46%), and
