DKA and hyperosmolar hyperglycemic state (HHS)

5.0(1)
Studied by 3 people
call kaiCall Kai
learnLearn
examPractice Test
spaced repetitionSpaced Repetition
heart puzzleMatch
flashcardsFlashcards
GameKnowt Play
Card Sorting

1/31

encourage image

There's no tags or description

Looks like no tags are added yet.

Last updated 9:25 PM on 3/25/26
Name
Mastery
Learn
Test
Matching
Spaced
Call with Kai

No analytics yet

Send a link to your students to track their progress

32 Terms

1
New cards

insulin is released from the pancreatic ____ cells. what effect does it have on blood glucose, blood fatty acid and ketoacid concentration, protein synthesis, and potassium uptake?

beta cells; decreases blood glucose, decreases blood fatty acid and ketoacid concentrations, increases protein synthesis, and promotes uptake of potassium by the cells by activation of the Na/K ATPase

2
New cards

glucagon is released from the pancreatic ___ cells; what effect does it have on lipolysis, glycogenolysis, and gluconeogenesis, and ketoacid formation?

alpha cells; stimulates glycogenolysis and gluconeogenesis, increases lipolysis, and increases ketoacid formation

3
New cards

explain type 1 vs type 2 DM

1: autoimmune t cell mediated destruction of beta cells

2: increased insulin resistance and progressive pancreatic beta cell failure

4
New cards

What is the mechanism of DKA?

insulin deficiency and glucagon excess→ hyperglycemia

5
New cards

briefly explain how stress triggers DKA

stressful event → increase in glucagon, epi, and cortisol → increased glycogenolysis and gluconeogenesis and decreased insulin production and sensitivity → increased blood glucose

6
New cards

increased glucagon with insulin deficiency in diabetes causes what?

hyperglycemia and increased lipolysis (fatty acids shunted towards ketone synthesis)

7
New cards

What are 4 main things we see in DKA?

hyperglycemia, volume depletion, polyuria, and polydipsia

8
New cards

What electrolyte imbalances do we see with DKA?

hyponatremia (high serum osmo causes water to rush into serum), hyperkalemia (K shifts extracellular and no insulin activation of Na/k ATPase), and decreased total body K

9
New cards

what acid base disorder do we see with DKA?

primary anion gap metabolic acidosis with compensatory respiratory alkalosis

10
New cards

What is the anion gap in DKA and how do we calculate it?

high anion gap (>12)

calculation: Na - (Cl + HCO3)

11
New cards

What are some clinical features of DKA? (5)

delirium/psychosis/coma, kussmaul respirations, abdominal pain/n/v, dehydration, fruity odor in breath

12
New cards

What do we expect with DKA: K, Na, glucose, ketones

hyperkalemia, hyponatremia, and serum and urine ketones, and hyperglycemia (250+)

13
New cards

How can we detect serum ketones and urine ketones?

serum: assay of beta-hydroxybutyrate

urine: positive nitroprusside stick test

14
New cards

With what condition do we expect ECG changes? what are the changes and why?

DKA: peaked T waves on ECG from hyperkalemia

15
New cards

What do we expect to see with DKA for BUN/Creatinine?

increased ratio

16
New cards

What do we expect to see on anion gap for DKA?

>12 (normal is 8-12)

17
New cards

How do we treat DKA? (2)

IV normal saline (fixes hypovolemia and electrolyte imbalance) and insulin (only is K 3.3+, if less than 3.3 then fix that first)

18
New cards

Explain bicarb in treating DKA

it is usually not given, but can consider giving bicarb if pH 6.9 or less

19
New cards

What are some complications of DKA? (6)

cerebral edema, cardiogenic shock, cardiac arrythmias, hypokalemia, hypoglycemia, and mucormycosis

20
New cards

What condition is commonly found in type 1 dm vs type 2?

1: DKA

2: HHS

21
New cards

What is the mechanism of HHS?

insulin deficiency and inadequate water intake → hyperglycemia and hyperosmolarity

22
New cards

Explain the slight difference in the pathophysiology of HHS vs DKA

in HHS some insulin is present with enough insulin activity to prevent the pt from going into ketoacidosis

23
New cards

What condition has more neurologic symptoms and what has more GI symptoms?

neuro: HHS

GI: DKA

24
New cards

What are some clinical features of HHS? (6)

polyuria, polydipsia, lethargy, seizures, focal neuro deficits, possible progression to coma

note: no n/v/abdominal pain or kussmaul respirations

25
New cards

If we see Kussmaul respirations what condition should we think?

DKA

26
New cards

if we see abdominal pain, nausea, and vomiting what condition should we think?

DKA

27
New cards

what do we expect with HHS: serum glucose, serum and urine ketones, ABG, ECG

high serum glucose (600+), no/mild serum and urine ketones, normal pH, and normal ECG

28
New cards

What do we expect with HHS: BUN/creatinine, potassium, sodium, anion gap

increased BUN/Creatinine, normal potassium, normal sodium, normal anion gap

29
New cards

How do we treat HHS?

IV fluids and IV insulin

30
New cards

treatment of HHS is carried out until when?

plasma osmolality is less than 315

31
New cards

If we see ECG changes and ABG changes what should we suspect?

DKA

32
New cards

What is the bottom line difference between the pathophysiology of DKA and HHS?

DKA: absolute insulin deficiency

HHS: relative insulin deficiency