Diabetes Flashcards
BG in DKA vs HHS
DKA 300-500
HHS over 1000
Normal glucose metabolism
Glucose inc with diet, insulin is released from the pancreas, dec gluconeogenesis and glycogenolysis and inc glucose uptake by skeletal muscle and adipose tissue
DKA
insulin is less effective because there isn’t it any
- ketoacidosis and hyperglycemia
HHS
Ineffective insulin; have enough to not get ketoacidosis but not enough to control blood glucose
Counterregulatory hormones
Released under bodily stress
- catecholamines, cortisol, glucagon, GH
- causes inc glucose prod and impaired glucose use in peripheral tissues
Why does dehydration occur with HHS?
osmotic diuresis from glycosuria
Ketoacidosis sx
SOB, ab pain, N/V from inc gluconeogenesis, lipolysis, ketogenesis, dec glycolysis
Is DKA or HHS treated sooner?
DKA because get symptoms earlier from ketoacidosis
pH with ketoacidosis and DKA
Under 7.3
How does GFR affect DKA?
Can excrete glucose better, often while younger
s/s HHS
hypotension, hypoperfusion, weakness, n/v, ab pain, hypothermia, inc BUN and crt, neuro sx, FVD, polyuria, polydipsia, wt loss
Potassium with HHS
- early or normal hyperK
- later possible hypoK
Patho of HHS
- relative ins deficiency
- osmotic diuresis
- hyperosmolality
- serum K high or normal and dilutional hypoN
- neuro sx bc dehydration
Tx for HHS
- 0.9% NS
- potassium (if sx or at least 4)
- IV insulin—drive K back into cells
rf for HHS
- mostly type 2, >65 (inadequate ins or infx w/o ins adjustment)
- predisposed to PNA, UTI, MI, sepsis, inflam
- meds that affect carb met like steroids, thiazide diuretics, SGLT2i, cocaine and subs
- nonDM w/ predispose fx like pancreatitis
When is HHS resolved?
- can eat
- can transition back to SQ insulin
- serum osmolality <315
- mentally alert
DKA s/s
- BG 250-450 or over 600
- rapid onset over 24h (dx sooner)
- polyuria, polydipsia
- n/v, abd pain—delayed emptying or ileus from met acid
- AMS, obtunded w/ severe acidosis
- FVD
- fruity breath from exhaled acetone
- compensatory hypervent
- pH<7.3
- coma and death
patho of DKA
- lack ins
- release counterreg hor
- b/d fat into FFAs and glycerol, proteolysis
- ketone bodies accum
- met acidosis
- anion gap
- hyperosmolality
- osmotic diuresis
- electrolyte imbalance
- neuro sx from dehydration
How does met acidosis occur with DKA?
- lipolysis occurs as glucose can’t get into cells
- FFAs form and become acetyl CoA then ketone bodies
- ketone bodies accumulate in blood
- ketones are acidic
- exacerbates K imbalance bc H+ pushes K+ out of cell to balance
What activates FFAs?
hepatocytes of the liver
Anion gap
Difference between negative (Cl- and bicarb) and Na+ ions
How is anion gap measured
with beta hydroxybutyrate—main met product of ketoacidosis
Fx that affect severity of acidosis
- rate and duration of ketone production
- rat of ketone metabolism
- rate of ketones in urine (depend on fluid vol and GFR_
What speeds up the rate of ketoacids lost in urine?
isotonic fluids
Electrolyte imbalance from DKA
K is high or normal and Na is dilutionally low
- osmotic diuresis causes loss of Na, K, and H2O
DKA tx
0.9% NS
- With dextrose if gluc <200 and pt still has anion gap
Potassium (if symptomatic or at least 4)
IV insulin
- Watch for hypoglycemia and frequently monitor VS
Sodium bicarb if pH <7.2 or difficulty breathing
- Careful of overshoot as insulin is given
rf for DKA
- ppl<65 and type 1 mostly (inadequate ins, infx w/o ins adjust)
- t2 extreme conditions
- predisp to PNA, UTI, MI, sepsis, stroke, inflam, infx
- emotional stress
- steroids, thiazide diuretics, SGLT2i, cocaine sub abuse)
How do you know when DKA is resolved?
- anion gap closed
- ketoacidosis fixed
- can eat
- can take SQ ins again
Patho for microvascular comps
- hypoxia and ischemia
- microangiopathy—thick, weak cap membranes
- freq and sever of damage depends on disease duration
Neuropathy
- most common
- ischemia and demyelination of nerves
- lose pain, temp, vibratic sens
- ulcer, infx, amputation
retinopathy
- lead blindness
- hypoxemia, damage to retinal BVs, RBC agg and HTN
- small vessel infarc and death
Nephropathy
- leads to CKD and ESRD
- GBM thick and hard
Macrovascular comps
- athero lead to CAD, PVD, stroke, infx
- inc inflam
- oxidative stress, endothelial dysfxn, alter mineral metab, inc cytokine prod
Patho of infx in diabetics
- tissue hypoxia and impaired skin integ from neuropathy—healthy cells can’t get there
- pathogens feed on excess gluc and fewer WBCs circ
