DKA/HHS

Question 1

DKA involves…

Answer 1

Ketoacidosis + Hyperglycemia

Question 2

HHS involves…

Answer 2

More severe hyperglycemia without ketoacidosis

Question 3

DKA

Answer 3

• More common <65
• Type 1 DM
• Can occur in type 2 under extreme conditions

Question 4

HHS

Answer 4

Mostly Type 2

-More common >65

Question 5

Extracellular concentration of glucose is regulated by?

Answer 5

1. Insulin

2. Glucagon

Question 6

Insulin restores normal glycemic levels by:

Answer 6

1. Diminishing hepatic glucose production
   - Decreases glycogenolysis + gluconeogenesis
2. Inc glucose uptake by skeletal muscle and adipose tissue

Question 7

When serum glucose rises….

Answer 7

Glucose enters pancreas initiating insulin release by Beta cells

Question 8

Hyperglycemia Causes

Answer 8

1. Insulin deficiency and/or resistance
   - More severe in DKA than HHS
2. Glucagon excess
3. increased catecholamines
4. Increased cortisol

Question 9

DKA

Answer 9

Decreased Insulin secretion

-lipolysis + ketogenesis

Question 10

HHS

Answer 10

Ineffective action of insulin

-osmotic duiresis

Question 11

Serum glucose in HHS

Answer 11

Exceed 1000 mg/dL

Question 12

Serum glucose in DKA

Answer 12

Below 800, often 350-450

• often present with symptoms of ketoacidosis rather than hyperosmolality
• Tend to be younger and have higher GFR

Question 13

Ketone Production (DKA)

Answer 13

1. Insulin def and resistance - can’t get glucose into the cells so body uses fat for energy (enhanced lipolysis in DKA)
2. Lipolysis of peripheral fat stores releases FFA’s and glycerol
3. FFAs are transported to liver and become “activated”
4. Activated FFAs are converted to acetyl-CoA and enter ketogenic metabolic pathway forming “ketone bodies”
5. Accumulation of ketone bodies causes a drop in pH (metabolic acidosis)
   - Not seen in HHS due to having a bit more insulin available

Question 14

Anion Gap Metabolic Acidosis

Answer 14

DKA presents with an elevated anion gap metabolic acidosis

Caused by production and accumulation of KETONES

Severity of acidosis and increase of anion gap factors

1. Rate and duration of ketoacid production
2. Rate of metabolism and ketoacids
3. Rate of loss of ketoacid anions in urine

Question 15

Anion Gap Definition

Answer 15

The difference between negative and positively charged electrolytes
-You want to close the gap (balance)

Question 16

Plasma osmolality and sodium

Answer 16

Plasma osmolality is always elevated
-Higher the glucose, the higher the plasma osmolality

Hyperglycemia pulls water out of cells, expands ECF, reducing plasma sodium (dilutional hyponatremia)

Glucosuria causes osmotic diuresis leadings to excretion of NA+, K, water

Question 17

Potassium

Answer 17

DKA + HHS have decreased K+

1. increased urinary loss (with normal kidney function) GLYCOSURIA
2. GI losses
   * don’t treat K+ until pt. is symptomatic

Serum K+ is normal to high due to hyperosmolality and insulin deficiency

• Increased osmolality causes water + K+ to move out of cells
• Insulin normally promotes K+ uptake by the cells, lack of insulin contributes to increased K+ levels (Serum/ECF)

Question 18

DKA: cellular compensation

Answer 18

Increase in [H+] seen in acidosis

1. H+ move into cell
   - More positively charged ions in the cell
2. K+ moves out of cell
3. Electrical neutrality is restored inside of cell
4. a temporary correction in pH

Process will reverse as the pH returns to normal

However, if the kidneys are working, they will excrete the excess K+ (from ECF)

Body can have depletion of K+ (dysrhythmias)

Question 19

Precipitating Factors of HHS + DKA

Answer 19

HHS + DKA
1. Infection (PNA or UTI) without insulin adjustment

2. Acute major illness or inflammatory process (MI, CVA, Sepsis, Pancreatitis)
3. Drugs that affect CHO metabolism (steroids, thiazide diuretics’)
4. Poorly compliance with insulin regimen or faulty sub-q insulin infusion device

DKA

1. Use of SLGT2 inhibitors (treatment for type 1 or 2 DM)
2. Cocaine use
3. New onset of type 1 DM, DKA is often what triggers diagnosis

Question 20

DKA S/S

Answer 20

• Rapid onset (over 24hrs)
• Polyuria, polydipsia
• GI effects (N/V/ abd pain)
• Neurologic effects
• combative
• drunk
• coma
• Volume depletion
• Dec skin turgor
• Dry mucosa
• Tachycardia
• Hypotension
• Fruity odor of breath (acetone)
• Kussmaul respirations

Question 21

HHS S/S

Answer 21

Insidious (several days)

• polyuria
• polydipsia
• weight loss

As glucose continues to increase

• Lethargy
• Obtunded
• Coma

Signs of volume depletion similar to DKA

• Dec skin turgor
• Dry mucosa
• Tachycardia
• Hypotension

Question 22

Treatments for DKA + HHS

Answer 22

1. Fluid replacement
2. Electrolyte imbalances (K+)
3. Infusion of Insulin
4. Sodium Bicarb
   - DKA with Metabolic acidosis <7.2
5. Dextrose added to saline when serum glucose fall below 200 mg/dL (DKA) if pt. still has anion gap (while still on continuous insulin infusion)

Question 23

How do we know when DKA or HHS has resolved?

Answer 23

DKA: ketoacidosis has resolved (the anion gap has closed)

HHS: Patient is mentally alert and plasma osmolality has dropped to 315 mOsmol/kg

-Patent is able to eat and can transition back to SQ insulin (DKA + HHS)

Question 24

DKA wrap up:

Answer 24

DKA is a condition of ketones in the blood, metabolic acidosis leading to anion gap, and usually hyperglycemia associated with insulin deficiency

Mostly affects type 1

Lack of adherence to insulin doses and or physiologic stressors (infection, MI) are common causes of DKA

Treat volume depletion rapidly with 0.9% NS, supplement K+ as needed, IV infusion of insulin

Monitor glucose, electrolytes, anion gap

Question 25

HHS wrap up:

Answer 25

Marked hyperglycemia, dehydration, electrolyte imbalance, and hyperosmolality

Mostly affects type 2

Higher mortality rate

Symptoms of illnesses such as PNA + UTIs, insulin deficiency, inflammatory conditions (MI, Stroke, severe dehydration or use of some drugs can lead to HHS)

Treat volume depletion rapidly with NS, IV insulin, correct electrolyte imbalances