DKA and HHS

Question 1

DKA and HHS

Answer 1

2 of the most serious acute complications of DM
DKA = ketoacidosis and hypergly, <800, 350 - 450 (earlier tm)
HHS = more severe hypergly w/o ketoacidosis, >1000

Question 2

rf: DKA

Answer 2

<65, type 1, type 2 under extreme conditions (bc still make insulin; infection, trauma, CV)
tend to be younger and have higher GFR (greater capacity to excrete glucose), often present earlier with s of ketoacidosis (SOB, abd pain, n/v) rather than hyperosmol

Question 3

rf: HHS

Answer 3

mostly type 2
>65

Question 4

normal response to hypergly

Answer 4

extracellular gly [] regulated by insulin and glucagon
glucose -> pancreas -> insulin release
insulin diminishes hepatic glucose production
glycogenolysis and gluconeogenesis decrease
also increase uptake by skeletal muscle and adipose tissue

Question 5

glycogenolysis

Answer 5

glycogen -> glucose

Question 6

gluconeogenesis

Answer 6

non carb (lactate, AA, glycerol) into glucose

Question 7

hypergly patho

Answer 7

insulin def and/or resistance (decreased net effective action to insulin)
DKA > HHS
DKA = decreased secretion; dehydrated and e abn bc osmotic diuresis from glycosuria
HHS = ineffective insulin
glucagon excess

Question 8

DKA patho

Answer 8

increased gluconeogenesis, lipolysis, ketogenesis, decreased glycolysis

Question 9

hypergly patho: other factors

Answer 9

increased catecholamines, increased cortisol
increased hepatic glucose production, impaired glucose utilization in peripheral tissues

Question 10

glucosuria

Answer 10

initially decreased rise in serum glucose via osmotic diuresis -> v depletion and decreased GFR, limits further glucose excretion (more pronounced in HHS)

Question 11

ketone production

Answer 11

insulin def and resistance: cant get glu into cells, so use fat for E -> enhanced lipolysis in DKA
lipolysis of peripheral fat stores releases free FA and glycerol
FA transported to liver (hepatocytes) -> activated
activated FA converted to acetyl coa and enter ketogenic met -> ketone bodies
ketone bodies accumulate -> decrease pH (met acidosis)
not with HHS bc sufficient insulin to decrease lipolysis but not enough to block gluconeogenesis

Question 12

anion gap met acidosis

Answer 12

DKA typically presents with increased anion gap (differences btw - and + ions Na-Cl and bicarb) from production and accumulation of ketones (B hydroxygutyrate - main met product of ketoacidosis)

Question 13

severity of acidosis and increase of anion gap factors

Answer 13

rate and duration of ketoacid production
rate of metabolism of ketoacids
rate of loss of ketoacid anions in urine -> depend on V status and renal function: increase when treated w/ isotonic fluids to correct hypovol

Question 14

plasma osmol and Na

Answer 14

higher with HHN
always elevated
hypergly -> pull H2O out of cells, expand ecf, decreased plasma Na (dilutional hypoNa)
Na, K, H2O loss w/ glycosuria

Question 15

K

Answer 15

both present with hypoK: GI losses, increased urinary loss (with normal kidney function)
serum K normal d/t hyperosmol and insulin def: H2O out of cells, insulin normally promotes K uptake -> may be hyperK initially, only treat if s/s
w/ correction: H ions out of cell, K in

Question 16

cellular compensation: DKA

Answer 16

increase in H [] seen with acidosis: H in, K out, neutral, temp correction of pH
process will reverse with normalization of pH: but, if kidneys working, they will excrete K -> can have depletion

Question 17

precipitating factors

Answer 17

infection w/o insulin adjust
acute major illness or inflam process -> MI, CVA, sepsis, pancreatitis
new onset type 1
drugs that affect carb met (glucocorticoids, thiazide diuretic)
SGLT2I: type 2 but also off label type 1
cocaine or substance abuse
poor compliance with insulin regimen or faulty SQ infusion device -> run A1C

Question 18

DKA cm

Answer 18

rapid onset over 24 hrs
polyuria, polydipsia
GI: n/v, abd pain (delayed gastric emptying or ileus from met acidosis
may have neuro s/s -> obtunded (severe acidosis)
v depletion: decreased turgor, dry oral mucosa, tachy, hypoT, decreased UO
fruity breath (exhaled acetone - nail polish remover)
kussmal resp -> deep resp, comp hypervent

Question 19

HHS: cm

Answer 19

higher mortality
insidious (several days): polyuria, polydipsia, weight loss
as glu continues to increase, more common neuro s/s bc increased hyperosmol: lethargy, obtunded, coma
s of v depletion similar to DKA

Question 20

tm

Answer 20

replace fluids 1st bc need renal function and to pee out excess, CV collapse, worse in elderly
fluids expand ecf, hemodynamic stability, 0.9 NS
correct e imbalance -> K, replace ~4, replace before insulin bc insulin will drive back into cells
insulin infusion
Na bicarb if DKA w acidosis (<7.2), difficulty breathing
dextrose may be added when <200 if anion gap still present: DKA

Question 21

resolved

Answer 21

DKA: anion gap closed, ketoacidosis resolved
HHS: mentally alert, plasma osmol 315
pt can eat and transition back to SQ insulin