Pathophysiology: Diabetes Mellitus, HACVD

Host

Agent

55
HPN
DM

Environment

Insulin resistance
Decreased sensitivity to glucose levels

Pancreas compensates by producing more insulin

Decreased glucose utilization of cells

Increased insulin levels in blood

Cell hunger
Gluconeogenesis

weakness

Glycogenolysis

Increased blood
glucose levels
(CBG: 285mg/dL)

Signals hypothalamus
to increase appetite

Insulin induces HMG-CoA reductase activity

HMG-CoA reductase promotes cholesterol synthesis in liver
With increased cholesterol in the liver, LDL receptor synthesis is inhibited

Protein
metabolism

Fat
Increased blood
breakdown glucose levels

Polyphagia
Decreased LDL uptake in plasma
Increased plasma LDL cholesterol

Muscle
wasting

Inc circulation of
fat in blood vessels

Ketone
production

Weakness
& fatigue

Fat adheres to blood

vessel walls

Decrease in
blood pH

Plaque formation

Metabolic
acidosis

Increased cholesterol levels in blood

Plaque formation in blood vessels

*Blood vessels
narrow

Atherosclerosis
*Blood vessel narrows
HACVD (*Highest BP: 210/120mmHg)

DKA
Kussmauls respiration
Fruity or pear-drops like breath
Hyperglycemia

Excretion of excess glucose

by kidney

Increased blood osmolarity

Increased blood
viscosity

Glycation of
ion pumps

Endothelial cells in blood vessels take in more

glucose

Osmotic diuresis

Fluid shift from interstitial space to blood

Poor wound healing

Osmotic stress disrupts

the cells of the eye

Increase surface glycoprotein formation

Polyuria
Weight loss

Dehydration

*Increase BP
Polydypsia

Risk for infection

Cataract formation

Thickening & weakening of basement membrane

of blood vessels

Electrolyte imbalance
Decreased tissue perfusion

Accelerated atherosclerosis
Plaque formation

Kidneys conserve fluid

when water is limited
in the body

Hypovolemia

Decreased tissue perfusion

Weakness

Microvascular complications

Hypovolemic
shock

Inability to meet oxygen demands of body

Neuropathy

Nephropathy

Organs become hypoxic

Nerve
conduction is
disrupted

Kidney function Angiogenesis

is impaired

Decreased
sensation in
extremities

Multiple system Rupture of fragile

failure
blood vessels

Blood vessels narrow

Glucose levels rise

even higher

*Increase in blood pressure

Organ failure

*Damage to endothelial
lining of blood vessels

Retinopathy

Death

Accelerated atherosclerosis

Risk for
infection from
unrecognized
lesions

Vitreous hemorrhage
Light cant pass through

Fibrous scar tissue

formation

Infection

Loss of vision

Retinal detachment

Decreased tissue perfusion

Macrovascular complications
Necrosis of tissue
Coronary artery disease

Stroke

Peripheral vascular disease

Decay of body tissue

Myocardial infarction

Diminished peripheral pulses

(radial pulse)

Gangrene

Loss of vision