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PATHOPHYSIOLOGY OF DIABETES MELLITUS TYPE 2

Definition: It is a lifelong, heterogeneous condition that describes the presence


of hyperglycemia in association with relative insulin deficiency.

Predisposing Factors Precipitating Factors


a. Family History –Grand father of paternal side (there is a strong inheritable genetic connection a. Lack of exercise
in type 2 diabetes mellitus) b. Diet – high sugar intake
b. Age – 47 years old (type 2 diabetes mellitus traditionally has been thought to affect individuals c. Noncompliance to medication
older than 40 years, it is being recognized increasingly in younger persons, particularly in highly
susceptible racial and ethnic groups and the obese)
c. Sex – Female (more common in women than in men)
d. Race – Filipino (in the study of Cuasi, L., et. al. they found out that Filipinos are at higher risk
for type 2 diabetes than the U.S. non-Hispanic white population)

Legend:
Insulin resistance
Disease process

Medications Exhaustion of beta cells

Laboratory Values
↓ Insulin production in the beta cells of the pancreas

Signs and
symptoms Look: Cellular starvation
↓ Absorption of glucose by the cells
manifested by
the patient

Surgical
intervention
↑ Serum glucose level

1st Hgt monitoring: 284 mg/dL Hyperglycemia

Metformin
↑ Serum osmolarity

Body fluid is pulled out of


↑ Blood viscosity tissues including lenses of eye
or fluid shifts from intracellular
↓ Blood flow to organs and extremities to extracellular area since
glucose attracts water

↓ Tissue perfusion of the Kidneys Sluggish ↓ Tissue perfusion


blood
circulation
Blood pressure Removal of RBC Impaired delivery Nerve Eyes
wastes from production of blood
Activation of rennin- angiotensin- blood component (RBCs Nerve hypoxia Deterioration of the
aldosterone system blood vessels that
nourishes the retina
Segmental
Inadequate Inadequate
Release of rennin demyelinizatio
inflammator nutritional
y response support Ability of lenses to
Formation of angiotensin 1 Nerve focus is affected
from angiotensinogen damage
Microorganisms Blurred vision
enter the open
wound
Angiotensin 1 will be Infection
converted into angiotensin 2
in the lungs via ACE Excessive glucose is Sympathetic and
Fever converted to sorbitol parasympathetic nervous
Delayed wound which accumulates in system dysfunction
WBC: 21, 600
healing nerves
(N.V: 5,000 –
10,000/cumm) Presence of
Powerful In the adrenal “AUTONOMIC
vasoconstrictio gland, angiotensin necrotic Sorbitol impairs NEUROPATHY”
Co-amoxiclav,
n 2 will be converted clindamycin tissues and motor nerve
into angiotensin 3 ulcer at left conduction
Slowing of nerve conduction
Debridemen or blocked nerve impulse
↑ Aldosterone release transmission
“SOMATIC
NEUROPATHY”
Nausea, vomiting,
Retention of sodium abdominal pain
and water Constant trauma
to the affected Domperidone
↑ Blood pressure and ↑ blood flow to the kidneys extremity

Numbness at
When glucose levels exceeds renal threshold affected site

Impaired renal
function Polyuria

Hypertension BUN: 55.3 (N. V: 4.6- 23.3 Hgb: 9.7 (N.V: 12-16 gms %), Hct:
mg/dL), Creatinine in serum: 27.4 (N.V: 37-47 vol%)
Blood pressure: 2.6 (N. V: 0.5-1.1 mg/dL)
160 / 90 mmHg
↓ Absorption of glucose by the cells

Cellular starvation

Gluconeogenesis

If it worsens: Breakdown of fat stores which is When fat is broken down in the body, it uses
normally stored in the cells more energy as compared to glucose

Free fatty acids are broken down Body goes in negative calorie effect
When the body needs energy, and glucose or fat are not
through beta oxidation pathway
available, proteins are broken down into amino acids Fatigue

Formation of ketone
bodies in the liver Nausea, vomiting,
poor appetite
Amino acids can be Amino acids can be
converted to glucose converted into energy Ketosis Domperidone
(gluconeogenesis)
worsening Acid-base balance:
hyperglycemia Use of proteins as decrease pH
energy will cause the
muscles or other
Metabolic acidosis
organs to breakdown
Nausea and vomiting,
abdominal pain, rapid
respirations (RR > 20 cpm)
Domperidone

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