DM and DMT2 and DMT1 Flashcards
overt DMT1 presentation
increase thrist, urination
weight loss
bed wetting
hunge
treatment for emergent severe hypoglycemia
glucagon injections
long term microvascular complications of DM
retinopathy
nephropathy
neuropathy
pathogenesis of DM complications (pathways impacted)
accumulation of advanced glycosylation end products
accumulation of sorbitol
disrupt of hexosamine pathway
disrupt of protein kinase C pathway
activation of poly ADP-Ribose polymerase pathway
increased oxidative stress
2 defects of DM2
2 outcomes
Insulin resistance (imp glucose production and uptake)
inadequate insulin secretion
outcomes:
inability to suppress glucose from liver and kidney during fast
inability to appropriately take up glucose
dehydration in ketoacidosis due to
vomiting (due to ketoacids)
anion gap metabolic acidosis > compensatory tachypnea
severe hyperglycemia > glycosuria > water follows
most common insulin regimen
MDI - multiple daily injections
long acting (glargine or detemir) + short acting with meals (lispro or aspart)
electrolyte changes in untreated T1DM
hyponatremia
hypokalemia
low CO2 (bicarb) ketoacidosis
decreased phosphate intake and phosphaturia
Dx of DM
HbA1c >6.5%
OR
fasting plasma glucose >126mg/dL
OR
2 hour plasma glucose >200 ueing 75g oral glucose tolerance test
OR
Random glucose >200
fluid and electrolyte abnormalities in DM due to
osmotic diuresis that results from hyperglycemia
Adipose tissue inflammation pathogenesis in DMT2
changes in stromovascular cells to phenotypic activation of pro-inflammatory state.
adaptive immune cells interact+activate adipose macrophages>
> macrophages and Tcells shift from anti- to pro-inflammatory state
> CD8, Th1, Th17 cells stimulate M1 macrophage poalrization
>chemokines and cytokines promote inflammation and insulin resistance
moderate hypoglycemia in insulin overdose symptoms
treatment
**neurogenic symptoms: **
confusion, combativeness
poor coordination
slurred speech
treat with fast acting carbs
Dx of pre-diabetes
Fasting plasma glucose = 100-125
OR
2 hour plasma glucose 140-199 during 75g oral glucose tolerance test
OR
A1C 5.7-6.4%
patients present DMT1 when
80-90% of beta cells are lost
Dx of T1DM
random blood glucose >200
or
two fasting blood >126
or
positive oral glucose tolerance test
T1DM in adults pathogenesis
5-15% with DM express anti-islet autoantibodies
rapid 3 year progression to T1
HLA alleles associated
eitologic classification of DM
Type1
Type 2
gestational
1 - autoimmune B cell destruction with lack of insulin
2 - insulin resistance with relative insulin deficiency
Gestational - insulin resistance with B-cell dysfunction
long term macrovascular complications of DM
coronary artery disease
peripheral vascular disease
impaired consciousness in ketoacidosis due to
intracellular dehydration due to severe hyperglycemia
2 ketone bodies typically elevated in DKA
Acetoacetate
B-hydroxybuturate
Pathophys DMT1
molecular mimicry > APCs > CD4 differentiation to CD4Th1 cells
>CD4 Th1 INFg and IL 2 > CD8 CTls >
>CD8 attack beta cells > release more contents = more antigen
insulin overdose causes hypoglycemia, which causes mil adrenergic sympoms…
shakiness,
headaches
dizziness
sweating
tachycardia
hunger + fatigue
(due to increased sympathetic tone)
locations and actions of glucagon like peptide 1 GLP-1
liver: reduces hepatic glucose output by inhibiting glucagon release
Stomach - slows gastric emptying
alpha cell - inhibits glucagon secretion
Beta cell - stimulates glucose-dependent insulin secretion and B-cell differentition and proliferation
