28: Diabetic Emergencies - Dodge Flashcards
(32 cards)
DKA type 1 ___ type 2
> > >
describe pathophysiology of DKA
- due to relative or absolute insulin deficiency
- elevated glucagon, cortisol, growth hormones
increased glucagon:insulin ration
DKA
this causes increased gluconeogenesis, glycogenolysis and ketone body formation
decreased GLUT4 –>
decrease glucose into cell
- decreased glucose metabolism in skeltal muscle and fat
- increased reliance on alt fuel sources
increased glucagon, decreased insulin –>
pyruvate –> gluconeogenesis
increased glycogenolysis
describe ketoacidosis
- increased lipolyiss
- release of FFA
- liver: elevated glucagon leads to increased ketone body formation
- VLDL and triglyceride formation also increased (usual pathway for FFA) but less than ketone bodies
___ beta-hydroxybutyrate: acetoacetate
3:1 ketone body formation
both can be detected by available assays
urine acetoacetate preferentially
key presentations of DKA
abdominal tenderness
kussmaul/tachypnea respirations
tachycardia
decreased urine output
altered mental status
diagnostic criteria for DKA (4)
- serum glucose > 250 mg/dL
- serum bicarb less than 18 mEq/L
- presence of serum ketones (more accurate representation of body ketone levels than urine)
- serum pH less than 7.3
anion gap will be _______ with DKA
normal is 10-12
increased
due to increased ketoacids which neutralized bicarb; potentially from lactic acidosis as well
the work up of DKA is incomplete without…
attempting to determine inciting event, the WHY
ask about: recent sick contact, illnesses, medication compliance, sexual activity (infection, preggers), cough, fever, sweats, diarrhea, chest pain, drug use
the “I”s of DKA
infection infarction/Ischemia Intoxication Impregnation Idiocy - no meds
what will you order when you suspect DKA?
- serum glucose, electrolytes, ketones, ABG
- urinalysis, dipstick for ketones
- EKG (especially if older)
- CBC with diff
- renal function, ELECTROLYTES, liver enzymes
- culture blood urine sputum
- chest xray
3 key DKA treatments
- fluid resuscitation
- insulin treatment
- electrolytes
DKA: replace fluids initially with __
0.9% NaCl solution
initial bolus of 2-3 liters of fluid over the first 1-3 hrs and reassess as you go
will need to change to 5% dextrose in 0.9% of 0.45% NaCl once serum glucose is less than 200 mg/dL
_____ REQUIRED to reverse/treat DKA
insulin
2 options:
- bolus 0.1 unit/kg, then 0.1 units/kg/hr continuous insulin infusion
- 0.14 untis/kg/hr continuous infusion with no bolus
follow serum or fingerstick glucose every hr; once DKA resolved transition to subcutaneous insulin
DKA: potassium levels are _____; sodium levels are _
depleted; low
- replace K before starting insulin if less than 3.3 mEq/L
- sodium levels are falsely diluted from hyperlgycemia [psuedohyponatremia], decreases about 1.6 mEq/L for every 100 mg/dL over 100 blood sugar levels
follow electrolytes and renal function every 3-4 hrs during treatment
DKA considered resolved when (4)
- serum glucose less than 200
- serum bicarb greater than 15
- serum pH greater than 7.3
- anion gap less than 12
can start subcutaneous insulin at this time; restart home or calculate new dose
HHS =
hyperglycemic hyperosmolar syndrome
type 2 _____ type 1 with HHS
> > >
higher mortality than DKA
what is the pathophysiology of HHS/
- due to relative insulin deficiency or inadequate fluid intake
- deficient insulin = increased hepatic glucose production
- hyperglycemia leads to somotic diuresis = dehyrdatation
HHS: believed that _____ _______ deficiency leads to less counter regulator hormones and therefor no ketoacid production
relative insulin
symptoms of HHS
less severe, slower onset
- polyuria, weight loss, decreased oral intake
- altered mental status
- dehyrdation with hypotension, tachycardia
NO nausea, vomiting , kussmaul breathing, and abdominal pain
diagnostic criteria HHS
- serum glucose > 600
- hyperosmolarity: osmolality > 350
- elevated BUN and creatinine often
- no/mild acidosis and ketoacidosis
