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Pathophysiology of Diabetes Mellitus Type II

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Precipitating factors:
frequent or chronic infections
eating too much sweets
development of glucose
intolerance during drug
therapy
diet
sedentary lifestyle

Predisposing factors:
1. family history of DM + HTN
2. obesity
3. Age above 40
Insulin resistance

Exhaustion of beta cells

Insulin production/
decrease secretion of
insulin
Degradation of proteins

Absorption of glucose by the cell

Cell starvation

Stimulation of hunger mechanism via hypothalamus

Hunger

Breakdown of fat

POLYPHAGIA

FBS 140 mg/dL

HYPERGLYCEMIA

FBS to 180 mg/dL

Kidney filtration mechanism impaired

Nerve Demyelinization

Capillary basement
membrane thickening

GLYCOSURIA

Acidity of urine

NEUROPATHY

Diffuse glomerular
sclerosis
Urethral flora

Paresthesias &
numbness

NEPHROPATHY

Impaired pain
sensation
NON-HEALING
ULCERS
Gangrene

UTI

Delayed wound
healing

Circulating
blood volume
Hypovolemia

HYPOTENSION &
TACHYCARDIA

Renal failure

POLYURIA &
ALBUMINURIA

End-Stage Renal
Disease

F & E imbalance

Number of solute relative to water

Potassium ion retention

Sodium ions lost

Cardiac arrythmias

Tissue dehydration

DEATH

POLYDIPSIA

Increase viscosity of
blood

Capillary basement
membrane thickening

Thickening of
blood vessel walls

Musculoskeletal effects

Abnormal retinal vascular


permeability

Occlusion of plaque

Impaired glucose absorption in


the muscle tissue

Scarring

RETINOPATHY

Blurring of vision

Blindness
blindness

Blood flow blocked

Blood pressure

HYPERTENSION

Joint contractures
Myocardial
ischemia
Myocardial
infarction

Stroke
Heart Failure

Diminished
peripheral
pulse

FATIGUE

Breakdown of fat

Fatty acids &


glycerol

Fat content of the


blood

Weight Loss

ketone bodies in the


general circulation
hydroxybutyric acid
acetoacetic acid
acetone

Hyperlipidemia

Convulsions

Metabolic acidosis

Formation of fatty
deposits on the
walls of the blood
vessels
Acetone breath
Atherosclerosis

Nausea and vomiting

Abdominal pain

Cellular Potassium

Body attempts to prevent


further decrease in pH

Depressed central
nervous system

Poor appetite

Cardiac arrhythmias

Kussmauls respirations

Headache

Amino acid in the


general circulation

Coma

Mobilization /
degradation of proteins

Hyperaminoacidemia

Decreased urinary
nitrogen

Further sodium ion loss

Potassium ion retention

Dehydration

Cardiac arrhythmias