obesity

family history increases

genetics
risk 2-4 times
due to

lack pf physical activity

diet high in refined

sugars

insulin resistance
liver, adipose, and
muscle tissue becomes
less responsive to
insulin

initially pancreas
produces more insulin

beta cell failure to

compensate due to
exhaustion or
desensitization
due to

HLA alleles (genetic

free fatty acids inhibit
component)
insulin
autoimmune processes
relative insulin
environmental
virus theory deficiency HHNK
component pancreatic islet cell
idiopathic due to Type 2
destruction
decreased insulin levels
fatigue
and increased BGL
iatrogenic due to drugs blurred vision
marks the onset of
slow wound healing
symptoms
poor circulation
polyuria absolute insulin increased infections
polydipsia deficiency numbness or tingling
polyphagia
weight loss
lifestyle changes

fatigue symptomatic
progressive as beta
blurred vision (hyperglycaemia) w/ treatment oral medication
cells are destroyed
slow wound healing ~80% destruction
poor circulation
increased infections exogenous insulin
numbness or tingling must include
exogenous insulin
fasting BGL
DKA
pancreatic cell Type 1 Diabetes Mellitus
transplant diagnosis glucose tolerance test
treatment

experimental HbA1c
treatments

heart disease
lifestyle changes

stroke circulatory comprimise

fasting BGL

infection related to elevated BGL

glucose tolerance test diagnosis

poor wound healing

HbA1c

abdominal obestity

increased risk of
elevated triglycerides

Metabolic syndrome 3 or more risk factors elevated fasting BGL

retinopathy elevated BP
microvascular
complications
neuropathy decreased HDL

macrovascular
complications