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Pathophysiology - Diabetes Mellitus Type 2

This document provides an overview of the pathophysiology of type 2 diabetes mellitus. It lists modifiable and non-modifiable risk factors and describes the dysfunctional processes involved, including decreased insulin production and sensitivity leading to hyperglycemia. It also outlines the potential long-term complications affecting multiple organ systems like the eyes, kidneys, nerves and blood vessels that can result from prolonged hyperglycemia, as well as diabetic ketoacidosis, a life-threatening complication caused by lack of insulin.

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Francis Kevin Sagudo
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12K views3 pages

Pathophysiology - Diabetes Mellitus Type 2

This document provides an overview of the pathophysiology of type 2 diabetes mellitus. It lists modifiable and non-modifiable risk factors and describes the dysfunctional processes involved, including decreased insulin production and sensitivity leading to hyperglycemia. It also outlines the potential long-term complications affecting multiple organ systems like the eyes, kidneys, nerves and blood vessels that can result from prolonged hyperglycemia, as well as diabetic ketoacidosis, a life-threatening complication caused by lack of insulin.

Uploaded by

Francis Kevin Sagudo
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX or read online on Scribd
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Pathophysiology (Diabetes Mellitus Type 2)

Theoretical
Sources: Brunner and Suddarth’s: Textbook of Medical-Surgical Nursing 11th Ed
Black and Hawks: Medical-Surgical Nursing 7th Ed
Pathophysiology of Diabetic Nephropathy by Dr. Carlos Inope
Essentials of Pathophysiology: Concepts of Altered Health States by Carol Porth

Modifiable Factors
 Diet Non-Modifiable Factors
 Lifestyle  Age
 Obesity  Gender
 Hypertension  Genetics
 Smoking  Race
 Ethnicity

Dysfunction of the beta


cells in the pancreas Decreased sensitivity of
the cells to insulin

Production of impaired
insulin Glucose is unable to
enter the cells

Desensitization of the
liver and extremities to Glucose remains in the
the levels of blood blood stream
glucose

Continued release of
glucose by the liver

Hyperglycaemia

Diabetes Mellitus
Type 2
1

glucose glucose glucose intake blood viscosity


concentration concentration of the cells

blood pressure
glucose in urine/ osmotic production in the arterioles
pressure in the of ATP
glucose blood
reabsorption in the Bursting of
renal tubules arterioles
energy for
H2O move from
normal cellular
the cells towards
functions
osmotic the blood
pressure Formation of scar
tissue
Dehydration Polyphagia
H2O
reabsorption Arteriosclerosis
Stimulation of
osmoreceptors
Nutrients can’t get
into the retina Hardening of the
Urine
glomerulus
output
Thirst
Retinopathy
glomerulosclerosis
Polyuria
Polydipsia
Blurring of vision
Nephropathy
Weight Loss
Blindness
Renal related
complications

Renal failure
Thickening of the
walls of the nutrient
vessels supplying the Vessel ischemia
2
nerve cells

1
Peripheral
Neuropathy

Segmental Peripheral
demyelination of the Slowing of the numbness
nerves conduction system
1

Lack of insulin decreases


available glucose for cell
metabolism

Body cells use triglycerides for


energy

Lipase breaks down


triglycerides into fatty acids
and glycerol

Fatty acids are converted into


ketones in the liver

Elevation of ketones in the


blood

Diabetic Keto Acidosis

Fruity smell
Decrease in Brain lacks
breath
bicarbonates glucose for fuel

Decrease in
Metabolic Decrease in
levels of
acidosis cardiac
consciousness
contractility
Respiratory
system Decrease in Coma
compensates cardiac output
(acid-base buffer
system)
Heart becomes
less responsive to
2
Kussmaul’s catecholamines
respiration (epinephrine and
(increased RR nor-epinephrine)
and depth)

Cardiac Death
Dyspnea arryhtmias (V-
Tach)

Respiratory
Arrest Cardiac Arrest

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