PATHOPHYSIOLOGY (UNCONTROLLED DIABETES MELLITUS TYPE II)

Sources:
Harrison’s Internal Medicine, 19th edition
Pathophysiology of Diabetic Nephropathy by Dr. Carlos Inope
Essentials of Pathophysiology: Concepts of Altered Health States by Carol Porth

Modifiable Factors Non-Modifiable Factors

 Diet:  Age
o high fat, high carbohydrate o 73 years old
o Caffeinated and Carbonated  Gender
Beverages o Male
 Lifestyle  Genetics
o Previously an alcoholic drinker  Race
o No routine exercise  Ethnicity
 Obesity
o “dako ni si Tatay sang una”,
as claimed
 Hypertension
 Smoking
o 33 pack/year history

Dysfunction of the beta Decreased sensitivity of

cells in the pancreas the cells to insulin

Production of impaired Glucose is unable to

insulin enter the cells

Desensitization of the Glucose remains in the

liver and extremities to blood stream
the levels of blood
glucose

Continued release of
glucose by the liver

Hyperglycemia:
↑216 mg/dl
 Diabetes Mellitus
Type 2:
- Diagnosis in 2016
- Maintenance Medications (noncompliant):
 Gliclazide
 Metformin

UNCONTROLLED
DM TYPE II

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 Abnormal retinal
vascular Hardening of the
Urine permeability glomerulus
output
Thirst
Nutrients can’t get
into the retina glomerulosclerosis
Polyuria
Polydipsia
Retinopathy
Nephropathy
Hypotension
Circulating BP= 90/60 mmHg
blood Volume Blurring of vision
Renal related
complications
Weight Loss Blindness UTZ Results (2018)
“Daw naggulpi kupos -Renal Cysts,
lawas niya” Bilateral
 Creatinine:
↑123.44 U/L

Thickening of the Renal failure

walls of the nutrient
vessels supplying the Vessel ischemia
nerve cells 2

1
Peripheral
Neuropathy

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

Lack of insulin decreases

Musculoskeletal available glucose for cell
Effects metabolism

Impaired glucose Body cells use triglycerides for

absorption in muscle energy
tissues
Lipase breaks down
triglycerides into fatty acids Hyperlipidemia
Chief Complaint: and glycerol  Total Cholesterol: ↑8.51 mmol/L
BODY  Triglycerides: ↑4.67 mmol/L
WEAKNESS  LDL: ↑5.09 mmol/L
Fatty acids are converted into  HDL: ↑1.3 mmol/L
ketones in the liver

Elevation of ketones in the

blood
 Decrease in Fruity smell Brain lacks
bicarbonates breath glucose for fuel

Metabolic Decrease in Dizziness Headache

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

Cardiac Death
Respiratory Rate: arryhtmias
↑21 cycles/minute (V-Tach)

Dyspnea
Cardiac Arrest
Respiratory Arrest