406 E3 - DKA & HHS

Question 1

what is the major difference between DKA & HHS

Answer 1

DKA involves ketoacidosis & hypergly and HHS has more severe hypergly but do not have ketoacidosis

Question 2

DKA facts

Answer 2

-more common in people under 65
-associated w/ T1DM but can occur in type 2 under extreme conditions
-decreased insulin secretions
-characterized by increased gluconeogensis, lipolysis, ketogenesis and decreased glycolysis

Question 3

HHS facts

Answer 3

-associated w/ T2DM
-more common in people over 65
-ineffective actions of insulin

Question 4

what is glucose normally regulated by

Answer 4

insulin and glucagon

Question 5

in a normal person, how does insulin restore normal glycemic levels

Answer 5

1) diminishing hepatic glucose production (dec glycongenolysis & gluconeogenesis)
2) inc glucose uptake by skeletal muscle and adipose tissue

Question 6

increases in what lead to an increase in hepatic glucose production and impairs glucose utilization in peripheral tissues

Answer 6

increased glucagon, growth hormones, catecholamines and cortisol

Question 7

what causes dehydration and electrolyte abnormalities w/ DKA and HHS

Answer 7

osmotic diuresis caused by glycosuria

Question 8

what are symptoms of ketoacidosis

Answer 8

-SOB
-abdominal pain
-N/v
causes pt to seek treatment earlier so hyperglycemia is less than it is in HHS b/c these sx aren’t present

Question 9

glucose levels for DKA vs HHS

Answer 9

DKA: 350-450
HHS: 1000+

Question 10

if glucose cannot get into cells to be used for energy, what is used for energy

Answer 10

fat by lipolysis -> fatty acids are converted to acetyl CoA and enter ketogenic metabolic path to form ketone bodies which causes a drop in pH
not seen in HHS b/c there is enough insulin to get some glucose into the cells

Question 11

anion gap

Answer 11

the difference between negatively charged and positively charged electrolytes
equation: Na - (chloride + bicard)
will be elevated w/ DKA

Question 12

severity of acidosis and increase of anion gap factors

Answer 12

-rate & duration of ketoacid production
-rate of metabolism of ketoacids
-rate of loss of ketoacid anions in urine

Question 13

how is Na affected by hyperglycemia

Answer 13

hyperglycemia pulls water out of the cells, expands ECF and reduces plasma sodium levels (dilutional hypoNa)
we do not treat low Na b/c correcting glucose levels will fix that

Question 14

go back and look at acid base notes to remember the potassium & hydrogen balance

Question 15

precipitating factors of DKA and HHS

Answer 15

-infection w/o insulin adjustment
-acute major illness or inflammatory process (MI, CVA, sepsis & pancreatitis)
-new on set T1DM (DKA only)
-glucocorticoids & thiazide diuretics
-use of SGLT2
-cocaine or substance abuse
-poor compliance w/ insulin

Question 16

DKA CM

Answer 16

-rapid onset
-polyuria & polydipsia
-GI effects
-neurologic effects
-volume deletion (dec skin turgor, dry oral mucosa, tachycardic, hypotension)
-fruit breath
-kussmaul respirations

Question 17

HHS CM

Answer 17

-insidious onset
-polyuria & polydipsia
-weight loss
-lethargy, obtunded, coma
-volume depletion (dec skin turgor, dry oral mucosa, tachycardic, hypotension)

Question 18

treatment of DKA & HHS

Answer 18

1) fluid replacement
2) correct lyte imbalances if present (usually if hypo)
3) administration of insulin by infusion
4) admin sodium bicarb is pH is <7.2 cautiously
5) dextrose when glucose falls to 200 if pt still has an anion gap

Question 19

how do we know treatment was effective

Answer 19

DKA: ketoacidosis has resolved & anion gap has closed
HHS: pt is mentally alert & plasma osmolality has dropped to 315
pt can eat and transition back to SQ insulin

Question 20

do we treat hyperkalemia w/ DKA

Answer 20

only if sympathetic