Pathophysiology (Diabetes Mellitus Type 2)

Theoretical
Sources: Brunner and Suddarths: 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
Lifestyle
Obesity
Hypertension
Smoking

Non-Modifiable Factors
Age
Gender
Genetics
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
the levels of blood
glucose

Glucose remains in the

blood stream

Continued release of
glucose by the liver

Hyperglycaemia

Diabetes Mellitus
Type 2

1
glucose
concentration

glucose
concentration

glucose in urine/
glucose
reabsorption in the
renal tubules
osmotic
pressure

glucose intake
of the cells

osmotic
pressure in the
blood

production
of ATP

energy for
normal cellular
functions

H2O move from

the cells towards
the blood

Urine
output

Bursting of
arterioles

Polyphagia
Arteriosclerosis

Stimulation of
osmoreceptors

Nutrients cant get

into the retina

Hardening of the
glomerulus

Thirst
Retinopathy

Polyuria

blood pressure
in the arterioles

Formation of scar
tissue

Dehydration
H2O
reabsorption

blood viscosity

glomerulosclerosis

Polydipsia
Blurring of vision

Weight Loss
Blindness

Thickening of the
walls of the nutrient
vessels supplying the
nerve cells

Nephropathy

Renal related
complications
Renal failure

Vessel ischemia
2

Peripheral
Neuropathy
Segmental
demyelination of the
nerves

Slowing of the
conduction system
1

Peripheral
numbness

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

Decrease in
bicarbonates
Metabolic
acidosis
Respiratory
system
compensates
(acid-base buffer
system)
Kussmauls
respiration
(increased RR
and depth)
Dyspnea
Respiratory
Arrest

Fruity smell
breath

Brain lacks
glucose for fuel

Decrease in
cardiac
contractility

Decrease in
levels of
consciousness

Decrease in
cardiac output

Coma

Heart becomes
less responsive to
catecholamines
(epinephrine and
nor-epinephrine)
Cardiac
arryhtmias (VTach)
Cardiac Arrest

2
Death