diabetes + DKA Flashcards
islet of langerhans in pancreas consist of
α cells: glucagon
ß cells: insulin
delta cells: somatostatin (D cell in gastric mucosa, CNS cells too)
inadequate insulin:
hyperglycemia
diabetes mellitus
symptoms of hyperglycemia in DM
↑ glucose →
polyuria (osmotically active -draws H20 into urine)
polydispia (losing H20)
polyphagia: skeletal muscle + adipose tissue: glucose not used as fuel
weight loss
complication of type 1 DM
diabetic ketoacidosis (DKA) may be first presentation of type 1 DM, esp children! ketosis-prone type 2 DM (
complication of type 2 DM
hyperosmolar hyperglycemic state (HHS)
may be first presentation!
diagnostic testing for diabetes mellitus
1) glucose-based tests: ↑ glucose
fasting serum glucose or
2-hr glucose tolerance test
2) Hb A1C (average glucose over past 3 mo -good for surveillance once dx made): glucose binds to Hb in non-enzymatic rxn (glycosylation), measure % of surface covered by glucose
complications of hyperglycemia in DM
1) nonenzymatic glycosylation:
Hb
leaky small vessels → retinopathy + nephropathy
osmotic damage
vascular disease in large vessels → atherosclerosis: CAD, cerebral vascular disease, PVD (dry gangrene)
2) osmotic damage: sorbitol
retinopathy in DM
early: leaky vessels (non-proliferative retinopathy)
late: new blood vessels form in eye (proliferative retinopathy) → break → hemorrhage → can cause blindness
“dot and blot” + larger flame hemorrhages + yellow blotches (hard exudate) in fundoscopic exam
retinopathy in DM
eye findings in DM
retinopathy: small vessel proliferation “flame, dot hemorrhages”
macular edema
soft exudates: “cotton wool” spots
↑ risk cataracts, glaucoma
cotton wool spots on fudus
DM
HTN
AIDS
diabetic nepropathy
glycosylation of small vessels → leaky vessels → microscopic proteinuria → progressive proteinuria
afferent arterioles
glomerular capillaries
efferent arterioles
tx: ACEi/ARB: reduce progressive proteinuria
kimmelstiel wilson nodules on renal bx
diabetic nephropathy
in glomeruli: pink nodules
osmotic damage in DM
↑ sorbitol in cells
schwann cells: motor neuropathy, sensory neuropathy, autonomic neuropathy (may be asymptomatic neuropathy, numbness in tips of toes → progresses proximally, may lose vibration/proprioception)
neuropathic pain: gabapentin, duloxetine, pregabalin, amitriptyline
treatment of type 1 DM
insulin: still have insulin sensitivity
profound insulin deficiency: no glucose to cells → hyperglycemia
cells think starving →
↑↑↑ glucagon (catabolic):
↑ glucose → polyuria, dehydration
↑ lypolysis: FFA → ↑ ketones (acetoacetic acid, ß hydroxybutyric acid) → acidosis (get sick quickly)
DKA
causes of DKA: put stress on body →
↑ endogenous catecholamines, glucagon, or glucacorticoids →↑ blood sugar
infection: pneumonia, gastroenteritis, URI, UTI missed insulin doses severe illness: MI, CVA, trauma undiagnosed diabetes dehydration alcohol/drug abuse (stimulants)
sx before acute illness:
polyuria/dehydration, polydipsia, weight loss (hyperglycemia sx)
ab pain, N/V
confusion, delerium
signs of ANION GAP metabolic acidosis:
sweet, fruity odor to breath (ketone in breath)
Kussmaul breathing: regular, deep/labored breathing (compensation for acidosis by hyperventilating)
hyperglycemia > 300 (can occur at any glucose level since problem is absence of insulin)
serum + urine ketones
hyperkalemia: compensation for acidosis (H/K countertransporter: keep H+ in cells, remove K+), DEADLY
↑ K+ in urine (→↓ intracellular K+ = low total body K): kidneys remove K+ from blood
DKA
causes of high ANION GAP metabolic acidosis
MUD PILES Methanol Uremia DKA Propylene glycol Iron tables/INH Lactic acidosis Etheylene glycol Salicylates
treatment of DKA
1) IV fluids -dehydrated
2) IV insulin: inhibit lypolysis from glucagon = stop ketones!
3) monitor anion gap (not glucose levels!): continue insulin (stops ketones) until gap closes
4) switch to injected insulin
3) RESTORE K+ +/- Mg AGGRESSIVELY: may have normal or hyperkalemia BUT low total body K+ (excreting excess K+ in urine) → give K+ to replete intracelluar stores
complications of DKA
arrhythmias: due to hyperkalemia, low total body K+ (if low K+, Mg+ may also be low → vtach, Torsades de pointes)
invasive fungal infections (rhizopus infection) due to hyperglycemia (mucormycosis: invade sinuses → brain abscess)
insulin prevents lipolysis - ß oxidation)→ no ketone bodies → NO ketoacidosis → NO Kussmaul breathing
EXTREME hyperglycemia: >800 →↑ serum hyperosmolarity >340 (vs DKA-none)
hyperosmolar hyperglycemic state (HHS)
initial sx: mental confusion, delerium, coma, dehydration, ab pain, N/V (like DKA but more neuro sx initially) ABG: no ketones hyperosmolar glucose >800
hyperosmolar hyperglycemic state (HHS)
treatment of HHS: hyperosmolar hyperglycemic state
1) IV fluids
2) insulin: ↓ serum glucose + correct hyperosmolarity (not to close anion gap)
3) K+
