Proficiency Testbuilder 4th Edition
Proficiency Testbuilder 4th Edition
Proficiency Testbuilder 4th Edition
diabetes mellitus
Anca Bacârea, Alexandru Schiopu
Complications of diabetes mellitus
Acute complications:
Ketoacidosis
The hyperglycemic hyperosmolar nonketotic syndrome
Hypoglycemia
Chronic complications:
Disorders of the microcirculation
Neuropathies
Nephropathies
Retinopathies
Macrovascular complications
Foot ulcers
Diabetic ketoacidosis (DKA)
It occurs when ketone production by the liver exceeds cellular use
and renal excretion.
Most commonly occurs in a person with type 1 diabetes, in whom
the lack of insulin leads to mobilization of fatty acids from adipose
tissue because of the unsuppressed adipose cell lipase activity that
breaks down triglycerides into fatty acids and glycerol.
The increase in fatty acid levels leads to ketone production by the
liver.
Stress increases the release of gluconeogenic hormones and
predisposes the person to the development of ketoacidosis.
DKA often is preceded by physical or emotional stress, such as
infection, pregnancy, or extreme anxiety.
In clinical practice, ketoacidosis also occurs with the omission or
inadequate use of insulin.
Diabetic ketoacidosis (DKA)
The three major metabolic derangements in DKA are:
Hyperglycemia
Ketosis
Metabolic acidosis
The definitive diagnosis consists of hyperglycemia (blood glucose
levels >250 mg/dL), low bicarbonate (<15 mEq/L), and low pH
(<7.3), with ketonemia (positive at 1:2 dilution) and moderate
ketonuria.
Hyperglycemia leads to osmotic diuresis, dehydration, and a critical
loss of electrolytes.
Hyperosmolality of extracellular fluids from hyperglycemia leads to a
shift of water and potassium from the intracellular to the extracellular
compartment. Extracellular sodium concentration frequently is low or
normal despite enteric water losses because of the intracellular-
extracellular fluid shift. This dilutional effect is referred to as
pseudohyponatremia.
Serum potassium levels may be normal or elevated, despite total
potassium depletion resulting from protracted polyuria and vomiting.
Metabolic acidosis is caused by the excess ketoacids that require
buffering by bicarbonate ions; this leads to a marked decrease in
serum bicarbonate levels.
Manifestations
The person typically has a history of 1 or 2 days of polyuria,
polydipsia, nausea, vomiting, and marked fatigue, with eventual
stupor that can progress to coma.
Abdominal pain and tenderness may be present without abdominal
disease.
The breath has a characteristic smell because of the presence of the
volatile ketoacids.
Hypotension may be present because of a decrease in blood
volume.
A number of the signs and symptoms that occur in DKA are related
to compensatory mechanisms:
The heart rate increases as the body compensates for a
decrease in blood volume
The rate and depth of respiration increase (i.e., Kussmaul’s
respiration) as the body attempts to prevent further decreases in
pH.
Treatment
The goals in treating DKA are:
To improve circulatory volume and tissue perfusion