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 a. Family History ±Grand father of paternal side (there is a strong inheritable genetic connection in type 2 diabetes mellitus) b. Age ± 47 years old (type 2 diabetes mellitus traditionally has been thought to affect individuals 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) Precipitating Factors a. Lack of exercise b. Diet ± high sugar intake c. Noncompliance to medication

Legend: Disease process Medications
Laboratory Values

Insulin resistance Exhaustion of beta cells Insulin production in the beta cells of the pancreas

Signs and symptoms manifested by the patient Surgical intervention

Absorption of glucose by the cells

Look: Cellular starvation

Serum glucose level
1stHgt monitoring: 284 mg/dL

Hyperglycemia Serum osmolarity Blood viscosity Body fluid is pulled out of tissues including lenses of eye or fluid shifts from intracellular to extracellular area since glucose attracts water

Metformin

Blood flow to organs and extremities

Tissue perfusion of the Kidneys

Sluggish blood circulation RBC production

Tissue perfusion

Blood pressure Activation of renninangiotensin- aldosterone system

Removal of wastes from blood

Impaired delivery of blood component (RBCs and WBCs

Nerves Nerve hypoxia Segmental demyelinization

Eyes Deterioration of the blood vessels that nourishes the retina

Release of rennin Formation of angiotensin 1 from angiotensinogen

Inadequate inflammatory response Microorganisms enter the open wound

Inadequate nutritional support

Nerve damage

Ability of lenses to focus is affected Blurred vision

Angiotensin 1 will be converted into angiotensin 2 in the lungs via ACE

Infection Fever
WBC: 21, 600 (N.V: 5,000 ± 10,000/cumm) Co-amoxiclav, clindamycin

Delayed wound healing Presence of necrotic tissues and ulcer at left foot Debridement

Excessive glucose is converted to sorbitol which accumulates in nerves Sorbitol impairs motor nerve conduction ³SOMATIC NEUROPATHY´ Constant trauma to the affected extremity Numbness at affected site

Sympathetic and parasympathetic nervous system dysfunction ³AUTONOMIC NEUROPATHY´ Slowing of nerve conduction or blocked nerve impulse transmission Nausea, vomiting, abdominal pain Domperidone

Powerful vasoconstriction

In the adrenal gland, angiotensin 2 will be converted into angiotensin 3 Aldosterone release Retention of sodium and water

Blood pressure and

blood flow to the kidneys

When glucose levels exceeds renal threshold Impaired renal function

Polyuria

Hypertension Blood pressure: 160 / 90 mmHg

BUN: 55.3 (N. V: 4.6- 23.3 mg/dL), Creatinine in serum: 2.6 (N. V: 0.5-1.1 mg/dL)

Hgb: 9.7 (N.V: 12-16 gms %), Hct: 27.4 (N.V: 37-47 vol%)

Absorption of glucose by the cells Cellular starvation Gluconeogenesis If it worsens: Breakdown of fat stores which is normally stored in the cells Free fatty acids are broken down through beta oxidation pathway Formation of ketone bodies in the liver Amino acids can be converted to glucose (gluconeogenesis) worsening hyperglycemia Amino acids can be converted into energy Ketosis Acid-base balance: decrease pH Metabolic acidosis
Nausea and vomiting, abdominal pain, rapid respirations (RR > 20 cpm)

When fat is broken down in the body, it uses more energy as compared to glucose Body goes in negative calorie effect Fatigue

When the body needs energy, and glucose or fat are not available, proteins are broken down into amino acids

Nausea, vomiting, poor appetite Domperidone

Use of proteins as energy will cause the muscles or other organs to breakdown

Domperidone

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