Pathophysiology Diabetes Mellitus

a. Aetiology:
Predisposing Factors
Factors Presence Mechanism/Justification
Genetic Initial decrease in beta cell
mass related to genetic
factors responsible for beta
cell differentiation or
presence of diabetogenic
gene.
Age >40 Pancreas, similar to several
other components of the
body, does not function well
due to old age.
Gender Most frequent in women than
in men, ages 20-40
Race In the report of CDC,
the populations most affected
are native Americans,
particularly in the desert
Southwest, Hispanic-
Americans, and Asian-
Americans

Precipitating Factors
Factors Presence Mechanism/Justification
Over weight/Obesity Obese people have increased
resistance to the action of
insulin and impaired
suppression of glucose by
liver, resulting both
hyperglycemia and
hyperinsulinemia. 85% of all
people with diabetes are
obese.
Environment(intrapartal Initial decrease in beta cell
stage) mass related to presence of
Maternal Diabetes Mellitus
during pregnancy or in uterine
factors such as intrauterine
growth restriction. High
potential that the children of
diabetic mothers will also
 become diabetic in the future.
Virus Infection Mumps, coxsackeivirus
Presence of Toxin Nitrosamines that are found
in smoked and cured meats,
are related to streptozoin that
is used to induce DM in
experimental animals, rat
poison named Vacor that
induces DM when ingested by
Human
Decrease serum potassium Low potassium level impairs
level release of insulin
Development of glucose Some drugs like thiazide
intolerance during drug therapy diuretics, thyroid hormones,
sex hormones, corticosteroids
and lithium has side effects of
glucose intolerance
Gestational Diabetes Mellitus Mother who has GDM has
(GDM) higher chance of having Type2
DM in the near future
Stress Form of stress with
neuroendocrine response
increases gluconeogenesis
and glycogenolysis.

b. Symptomatology

Symptoms Presence Mechanism/Justification

Polyuria (excessive urination) Glucose exceeds the amount
that can be reabsorbed by
renal tubules this results
glycosuria.
Polydipsia (excessive thirst) Excess glucose in the blood
pulls water out of the cell
causing intracellular
dehydration, including those
in thirst center.
Polyphagia (excessive hunger) Results from depleation of
cellular reserves of
carbohydrates, fats and
proteins.
Blurred Vision Lens and retina are exposed
to hyperosmolar fluids
Weakness and fatigue
Paresthesias
Pruritus, vaginitis, chronic skin
infections
Weight loss
Often Asymptomatic
c. Schematic Tracing
Lowered plasma volume
Temporary dysfunction of
peripheral sensory nerves
Hypergycemia and glycosuria
favors growth of yeast
organisms.
Initial loss due to depleation
of water, glycogen, and
triglyceride store; chronic loss
secondary to decrease muscle
mass as amino acid are
diverted to form glucose and
ketone bodies.
The body is able to adopt ta a
slow rise of blood glucose
level to a greater extent than
it can to a rapid rise.
 d. Narrative

Type two Diabetes Mellitus is a heterogeneous condition that describes the presence of
excess serum glucose level in association with relative insulin deficiency. Type 2 Diabetes is
associated with high, normal, low insulin levels. However there is a presence of insulin
resistance thus the insulin cannot function effectively and hyperglycemia will occur. Most
people with this type of diabetes are older and obese, but type 2 Diabetes is becoming a more
common occurrence in obese adolescent. The metabolic abnormalities that contribute in
hyperglycemia in people with type 2 diabetes are impaired beta cell function and insulin
production, peripheral insulin resistance, and increase hepatic glucose production.
Insulin is a anabolic hormone. Without insulin three major metabolic problems occur:
decrease glucose uptake and utilization, increase fat and lipid mobilization and increased
protein and amino acid utilization.
Beta cells chronically exposed to high blood levels of glucose become progressively less
efficient when responding to further glucose elevation. Insulin resistance initially produces an
increase beta cell secretion of insulin as body attempt to maintain normoglycemic state. In
time, however the insulin response declines because of increasing beta cell dysfunction. This
results to postprandial hyperglycemia. Eventually fasting blood glucose level also rise until frank
type 2 Diabetes occurs.
Cells that require insulin as carrier of glucose can take only 25% of glucose they require for
fuel, but nerve tissues, erythrocytes, and cells of intestine, liver, kidney tubules do not require
insulin for glucose transport. However, adipose tissue, along with skeletal and cardiac muscle
requires insulin for glucose transport.
 During severe stress such as hospitalization, the body of a type 2 diabetes patient will turn
fat reserves into glucose for energy production when glucose is not available. Fat and lipid
metabolism cause breakdown products called ketones to form. Ketones accumulate in the
blood and excreted through kidneys and lungs. Ketones interfere with the body’s acid base
balance by producing Hydrogen ions. The pH can decrease, and metabolic acidosis can result. In
addition when ketone is excreted in urine, sodium is also eliminated, causing sodium depletion
and further acidosis. The excretion of ketone also increases osmotic pressure, leading to
increase fluid loss.
In this type of Diabetes Mellitus the onset of clinical manifestation may develop gradually
that clients may notice a few or no clinical manifestations for a number of year. Some of the
manifestations are frequency in urination, increase thirst or fluid intake, and as the disease
progresses, weight loss despite hunger and increased food intake.
Clients with diabetes mellitus are living longer, with an increased risk for development of
chronic complications. Chronic complication are the major cause of morbidity and mortality in
client with diabetes mellitus. Diabetes mellitus-related complications are classified into two
types: macrovascular, including coronary artery diseases, cerebrovascular disease,
hypertension, peripheral vascular disease and infection; and microvascular, including
retinopathy, nephropathy, and neuropathy.
The very-low density lipoprotein and low density lipoprotein level are increased and high
density lipoproteins are decreased, and the most characteristic of lipid abnormality in diabetes
mellitus is an increase triglyceride level. Therefore the influence of diabetes in these disease are
not additive, it is multiplicative. Macrovascular disease tends to occur year before the onset of
clinical diabetes mellitus.
Clients with DM are two to four times more likely to have coronary artery disease than
those who do not have DM. In many clients with DM, often presents atypical or silent CAD, that
often presents as indgestion, or unexplained heart failure, dyspnea or excretions, or epigastric
pain. CAD is common in clients younger than 40 years old, of diabetes mellitus is of long
duration. DM patients with history of myocardial infarction have higher chance of having
second infarct than the patient who does not have DM. The incidence of cerebrovascular
disease is two to three times greater in diabetic client, and is more severe.
Atherothromboembolic infarction manifested by transient ischemic attracts and
cerebrovascular accidents are the most commont incidence of CVD that are the complication of
DM.
Hypertension has increased of 40% occurrence in diabetic population. Hypertension is a
major risk factor for stroke and nephropathy.
Diabetis mellitus augments the process of atherosclerosclerosis by variety of mechanism
thus causing peripheral vascular disease. Hyperglycemia and insulin resistance contribute to
endothelial dysfunction by decreasing available nitric oxide bioavailability and altering the
function of various cell mediators.
Clients with diabetes are susceptible to different type of infection. Three factors may
contribute to the development of infection are impaired polymorphonuclear-leukocyte
function, diabetic nephropathies and vascular insufficiencies. Damaged area heals slowly
because the damaged vascular system cannot carry sufficient amount of oxygen, white blood
cells, nutrients and antibodies to the injured site. Infection increases the need for insulin and
enhances the possibility of ketoacidosis. Urinary tract infection is the most common infection
especially in women. Factors that impairs the polymorphonuclear-leukocyte is the presence of
glycosuria and the development of neurogenic bladder, which results in incomplete emptying
and or urinary stasis.
About 80% of clients with DM have some form of retinopathy, the exact cause of
retinopathy is not understood but it is probably a multifactorial and associated with protein
glycosylation, ischemia, and hemodynamics mechanism that increases the permeability and
decreases the elasticity of capillaries.
About 20% of diagnosed DM type 2 patients have nephropathy 5 to 10 years after diagnosis.
A consequence of microangiopathy, nephropathy involves damage to and eventual obliteration
of the capillaries that supply the glomeruli of the kidney. This damage leads to complex
pathologic changes and manifestations such as intercapillary glomerolonecrosis, nephrosis,
gross albuminuria and hypertension. Unsuccessful treatment of nephropathy will lead to stage
5 chronic kidney disease. Like retinopathy, diabetic nephropathy is irreversible.
Neuropathy, the most common chronic complication of diabetes mellitus. Nearly 60% of
diabetic patients experience it. Because nerve fibers do not have their own blood supply, they
depend on diffusion of nutriens, and oxygen across membrane. When axon and dendrites do
not receive nourishment their transmission of impulses becomes slow. Both temporary and
permanent neurologic problem may develop. The neuropathy might be mild that causing minor
inconveniences or severe that quality of life is affected. Clients might present mononeuropathy
or polyneuropathy and may have motor or sensory impairment, depending on which nerve that
are involved. Mononeuropathy usually involves single or group nerves. It produces sharp,
stabbing pain and is usually caused by an infarction of blood supply. Polyneuropathy also
known as diffuse neuropathy, which involves both sensory and autonomic nerves. Sensory
neuropathy is most common type. It is commonly assed as bilateral, symmetrical and is
affecting the lower extremity. Client may describe tingling, numbness, burning, and mild to
severe sensory loss, a major factor in injuries to the legs.
Autonomic neuropathy affects the nerves that regulate vital functions, including the heart
muscle and smooth muscles. Autonomic neuropathy involves damage to the nerves that run
through a part of the peripheral nervous system. The peripheral nervous system includes the
nerves used for communication to and from the brain and spinal cord (central nervous system)
and all other parts of the body, including the internal organs, muscles, skin, and blood vessels.
Damage to the autonomic nerves affects the function of areas connected to the problem nerve.
Some of the autonomic neuropathy are: autonomic neuropathy of the pupil which interferes
with pupils ability to adapt to dark because pupils dilation is inadequate; autonomic neuropathy
of the cardiovascular system is evidence by abnormal response to exercise, fixed heart maybe
noted; autonomic neuropathy of gastrointestinal, client may have dysphagia, abdominal pain,
nausea, vomiting, diarrhea malabsorption, post prandial hypoglycemia, constipation, or fecal
incontinence and gastroparesis. Bladder hypotonisity of neurogenic bladder is common
manifestation of autonomic neuropathy of genitourinary organs. In male client it can contribute
to erectile dysfunction and retrograde ejaculation. Women may experience painful coitus.
All of these complications can be prevented by good control of blood sugar level,
exercise and diet modification.