DM Flashcards
Acute presentation
Polydipsia, polyuria, polyphagia, weight loss DKA (type 1) Hyperosmolar coma (type 2)
Unopposed secretion of GH and EPI, exacerbating hyperglycemia
Chronic presentation
Non enzyme glycosylation
1) small vessel disease
2) glucoma
3) nephropathy
4) large vessel atheroscleosis: CAD, PVD gangrene, limb loss and cerebrovascular disease
Osmotic damage (sorbital accumulation in organs with aldose reductase)
5) neuropathy (motor, sensory, autonomic)
6) cataract
Small vessel disease
Diffuse thickening of basement membrane =>
retinopathy: hemorrhage, exudate, microaneurysm, vessel proliferation
Nephropathy
Nodular sclerosis, Progressive proteinuria, Chronic renal failure Arterioscelrosis leading to HTN Kimmselstiel-Wilson nodules
Test:
Tasting serum glucose
Oral glucose tolerance
HbA1c (reflects average over 3 months)
Type 1
Genetic predisposition: weak (50% in twin), polygenic, HDL-DR3,4
Ketoacidosis: common
Classic presentation (polyuria, polydipsia, polyphagia, weight loss): common
Histology: islet leukocytic infiltrate
Type II
Genetic predisposition: relatively strong (90% in twin), polygenic.
Ketoacidosis: rare
B cells: numbers variable with amyloid deposits
Histology: islet amyloid (AIAPP) deposits
Diabetic ketoacidosis
Most important complication of Type I
Usually due to increase insulin requirement from stress (infection)
Excess fat breakdown
Increased ketogenesis from increased free FA
(beta-hydroxybutyrate >acetoacetate)
DKA:
signs
Kussmal repiration (rapid/deep) Nausea/vomoting Abd pain, psychosis/delirium dehydration fruity breath odor
DKA:
lab
Hyperglycemia, low pH, low HCO3- (anion gap metabolic acidosis) high blood ketone Leukocytosis Hyperkalemia (but depleted intracellular due to transcellular shift)
DKA
complication
Life threatening mucormycosis, Rhizupus infection Cerebral edema, cardiac arrhythmia heart failure
DKA
treatment
IV fluid
IV insulin
K+ (replete intracellular store)