B5.001 Big Case Flashcards
what is acanthosis nigricans
velvety, hyperpigmented plaques on the skin
commonly on neck and axilla
non-irritable
pathophys of acanthosis nigricans
elevated levels of insulin may stimulate keratinocyte and dermal fibroblast proliferation via interaction with IGFR1
result in plaque like lesions
associated with multiple disorders characterized by insulin resistance/hyperinsulinemia
what are screening recommendations for diabetes in asymptomatic persons
begin at 45 years of age, every 3 years
screen at any age and more frequently if BMI is >25 or person has additional risk factors
ADA sanctioned risk factors for diabetes
family history high risk race HbA1c >5.7% or impaired glucose levels on previous testing polycystic ovary syndrome HTN HDL < 35, TG > 250 CVD history physical inactivity
what is IFG and how does it manifest
impaired fasting glucose (baseline too high)
fasting plasma glucose 100-125
what is IGT and how does it manifest
impaired glucose tolerance (doesn’t return to baseline very easily)
2 hour post prandial glucose 140-199
test values for normal glucose metabolism
HbA1c <5.7
fasting glucose < 100
OGTT <140
test values for type 2 diabetes
HbA1c <6.5
fasting glucose >126
OGTT >200
best way to reduce the incidence of DM2
lifestyle intervention (exercise and dietary restrictions)
reduced incidence more than metformin alone or placebo
58% vs 31% reduction
3 primary components leading to pre-diabetes and/or DM2
`insulin resistance
relative insulin deficiency
impaired incretin action
how does insulin level change over the natural course of DM2
initially very high levels
at onset of diabetes, begins to decrease to below normal levels and continue to decrease over time
how is obesity implicate din the development of DM2
abdominal adipose more metabolically active than subcutaneous fat
increased release of FFA, TNFa and other hormones can lead to increased insulin resistance
what is central obesity
waist to hip ratio >1
waist > 40 in in med
waist > 35 in in women
definition of metabolic syndrome
any 3 of the following: abdominal obesity TG > 150 HDL <40 for men, <50 for women BP >135/85 fasting glucose >100
normal function of insulin
inhibit lipolysis
inhibit glucose production
stimulate glucose uptake by muscle
what portions of the brain is insulin thought to act on
hypothalamus
prefrontal cortec
discuss the reduction of B cells in DM2
the human pancreas is incapable of renewing B cells after age 30
glucolipotoxicity and amyloid deposition result in B cell apoptosis through oxidative and endoplasmic reticulum stress
discuss the role of a cell dysfunction in DM1
abnormal glucagon release
elevated fasting glucagon (increases glucose production from hepatocytes and contributes to hyperglycemia)
non-suppression after meal ingestion
what is the incretin effect?
oral glucose provides a much greater C-peptide response than IV glucose
what is C-peptide
measure of innate insulin production
only created by the body and longer lasting than insulin
what is incretin
substance released by the gut in response to food that stimulates insulin secretion
two well described incretins
glucagon-like peptide-1 (GLP-1)
glucose-dependent insulinotropic peptide (GIP) (minor, not as potent and GLP-1)
discuss the role of the GI tract in hormonal dysfunction in DM2
meal stimulated levels of GLP-1 are reduced
deficient GLP-1 response contributes to a rise in plasma glucagon secretion and impaired suppression of hepatic glucose production after a meal
deficient GLP-1 response leads to reduction in insulin secretion
discuss the role of the a cell in hormonal dysfunction in DM2
elevated basal glucagon leads to increased rate of hepatic glucose production
possible liver hypersensitivity to stimulatory effect of glucagon in hepatic gluconeogenesis
