DKA Flashcards by Hannah McMahon

Pathophysiology of Type 1 DM Hint: 2

1) Autoimmune disease → body starts to attack beta cells in our immune system
2) Pancreas is NOT producing any insulin

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True or False:

People can be carriers without actually having type 1 DM

TRUE

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Pathophysiology of type 2 DM Hint: 4

1) Insulin resistant
2) Tend to be above ideal body weight
3) Have HTN
4) Chronic state of inflammation → too much epinephrine & aldosterone

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What does it mean to be insulin resistant?

When the cells do not allow glucose to get in and they get into a hyperglycemic state

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List 4 ways to Dx diabetes mellitus

1) Hgb A1c of 6.5% or > on 2 separate occasions
2) Sx of DM & glucose > 200 mg/dL
3) Fasting BG >/= 126 mg/dL
4) 2 hr postprandial glucose > 200 mg/dL during oral glucose tolerance test

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List 5 common causes of DKA

1) New onset type 1 DM
2) Type 1 diabetics who stop taking insulin, insulin is ineffective, outdated, or not properly stored
3) Drugs affecting carbohydrate metabolism
4) Physical/ emotional stress
5) Infection/ inflammatory response

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List 4 drugs that affect carbohydrate metabolism

1) Glucocorticosteroids
2) Higher-dose thiazide diuretics
3) Sympathomimetic agents
4) Newer “atypical” antipsychotic agents

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List 2 less common causes of DKA

1) Use of SGLT2 inhibitors (mostly used in Type 2 but some off-label use in type 1)
2) Cocaine use → associated w recurrent DKA

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Patho of DKA:

List 3 things that occur when there is no insulin being produced by the pancreas

1) Cells can not use glucose for energy
2) Liver will convert glycogen to glucose
3) leads to hyperglycemia

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Patho of DKA:

The kidneys cause an ____ ____

Osmotic diuresis

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Patho of DKA:

What occurs when kidneys cause an osmotic diuresis Hint: 3

1) Hyperosmolality of ECF stimulates thirst (polydipsia)
2) Causes fluid shift from ICF to ECF
3) Fluid shifting causes low or normal serum Na+ despite water losses w polyuria (pseudohyponatremia)

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Patho fo DKA:

What does lack of insulin cause?

Breakdown of fat (lipolysis) into free fatty acids & glycerol

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Patho fo DKA:

What are free fatty acids converted into?

Ketone bodies by the liver

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Patho of DKA:

What leads to metabolic acidosis in DKA?

The excessive production of ketone bodies

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How does the body compensate for the metabolic acidosis seen in DKA?

Respiratory center is triggered to blow off fits of respiratory acid, leading to rapid deep respirations (Kussmaul’s)

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List 6 ways to Dx DKA

1) Blood glucose > 250 mg/dL
2) Low serum pH (6.8-7.3)
3) Low serum bicarb (0-15 mEq/L)
4) Accumulation of serum & urine ketones (high)
5) Presence of glucose in urine
6) Abnormal levels of Na+, K+, & Cl-

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List 5 clinical manifestations of DKA

1) Polyuria
2) Polydipsia
3) Weakness
4) malaise
5) Blurry vision

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Why do we see blurry vision in DKA?

Due to edema on the lens r/t hyperglycemia → comes from the edema in the macula

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List 8 things we see as a result of volume depletion in DKA

1) Severe drop in BP; orthostatic hypotension
2) Warm, dry skin
3) Decreased skin turgor
4) Dry mucous membranes
5) Anorexia, N/V, Abd pain
6) Acetone (fruity) breath
7) Kussmaul’s resp
8) Mental status changes → Na+

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Electrolyte changes in DKA:

Potassium serum level

Normal or elevated

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Electrolyte changes in DKA:

Potassium total body stores

Depleted

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Electrolyte changes in DKA:

Potassium key clinical points

Drops with insulin → monitor closely

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Electrolyte changes in DKA:

Sodium serum levels

Decreased (pseudohyponatremia)

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Electrolyte changes in DKA:

Sodium total bodys tores

Variable

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Electrolyte changes in DKA: Sodium key clinical points

Calculate corrected sodium

Electrolyte changes in DKA: Chloride serum level

Variable

Electrolyte changes in DKA: Chloride total body stores

N/A

Electrolyte changes in DKA: Chloride key clinical points

May rise with Tx

Electrolyte changes in DKA: Bicarbonate serum levels

Decreased

Electrolyte changes in DKA: Bicarbonate total body stores

Depleted

Electrolyte changes in DKA: Bicarbonate key clinical points

Marker of metabolic acidosis

Electrolyte changes in DKA: Phosphate serum level

Normal → decreased

Electrolyte changes in DKA: Phosphate total body stores

Depleted

Electrolyte changes in DKA: Phosphate key clinical points

Replace if very low or symptomatic

What is priority/ first line Tx for DKA? Why?

ALWAYS fluid resuscitation → b/c it deals with ABCs since the patient's BP is compromised

What are the second & third lines of Tx for DKA?

1) Give insulin slowly 2) Give potassium

List 3 reasons why we give fluid replacement for DKA TX

1) Maintain tissue perfusion 2) Increases excretion of excessive glucose by the kidneys 3) May need as much as 6-9 L of IV fluid to replace losses caused by polyuria, hyperventilation, diarrhea, & vomiting

Explain the 2 bag protocol for fluid replacement in DKA

1) Start with 0.9% NaCl 2) As sugars begin to reduce more give 50/50 w 0.9% & 0.45% 3) For sugars < 300 give all 0.45%

Give an example patient scenario of giving fluid replacement **Hint: 4**

1) Give 1-2 L for first 1-2 hrs & then 1L/hr for 3-4 hrs, depending on response 2) Once volume restores → change fluid to 0.45% NSS & assess for signs of fluid balance 3) Watch for cerebral edema 4) When sugars reach 250 mg/dL we add dextrose to the IV

How can we reverse the acidosis seen in DKA?

With insulin → inhibits fat breakdown

How should insulin be given to Tx acidosis in DKA?

Regular insulin is added to saline solution & infused via IV at a slow, continuous rate (0.1 U/kg/hr)

List 5 things to remember when giving insulin to Tx acidotic DKA

1) Often, given as a bolus first 2) K+ MUST be > 3.3 mEq/L 3) If BS does not drop by at least 50-70 mg/dL infusion should be doubled 4) Nurse must convert hourly rates of insulin infusion to IV drip rates 5) IV insulin 100 units/ 100 mL NSS = 1 u/ 1 mL

Is it okay to infuse insulin & rehydration solutions together?

NO → should be separate to allow for frequent changes in rate of IV

How long should we infuse insulin for? **Hint: 2**

1) Insulin is infused continuously until SQ admin of insulin can be resumed 2) Even when BS return to normal, insulin drip is not stopped until SQ therapy has been started

Rehydration Tx for DKA can lead to what electrolyte imbalance?

Potassium → can be low, normal, or high

Why might K+ levels be low in DKA?

B/c of renal loss due to osmotic diuresis

Why might K+ levels be normal or high in DKA?

B/c of shifting of K+ out of the cell to accompany the movement of H+ into the cells b/c of acidemia

What is withheld if K+ is elevated (> 5.3 mEq/L) or patient is anuric?

Potassium replacement → until serum levels fall to normal to prevent possibility of cardiac arrest

How can we decrease K+ levels?

Insulin → facilitates movement of K+ back into the cell

What must be assessed prior to starting insulin therapy?

K+ levels → if it's low insulin will cause K+ to move into the cell & cause hyperglycemia

Every ____ mEq of parenteral K+ should increase serum level by ~ ____ mEq/L

10 mEq; 0.1 mEq/L

What should be monitored to prevent hyperkalemia when managing K+ in DKA?

Urine output → to ensure adequate kidney function

What to remember if serum K+ is < 3.5 mEq/L **Hint: 2**

1) Insulin should NOT be administered until > than this value 2) IV KCl: 10-20 mEq/hr → usually requires 10-20 mEq/L added to each L of IV fluid

What to remember if serum K+ values are btwn 3.5 to 5 mEq/L **Hint: 2**

1) If initial serum K+ is 3.5-5 → IV KCl (10-20 mEq) is added to each L of IV fluid 2) Maintain level between 4-5 mEq/L

List 9 clinical manifestations of HYPOkalemia

1) Generalized muscle weakness 2) Fatigue 3) Diminished to absent reflexes 4) Decreased GI motility 5) Vomiting 6) Hypotension 7) Dysrhythmias 8) Prolonged QT intervals 9) Flattened, depressed T waves

List 9 clinical manifestations of HYPERkalemia

1) Impaired muscle activity 2) Muscle pain/ cramps 3) Increased GI motility 4) Oliguria 5) Dizziness 6) Bradycardia 7) Asystole 8) Large, peaked T wave 9) Broad, slurred QRS complex

When Tx DKA, blood glucose levels are corrected before ____ is corrected. What does this mean for Tx?

Blood glucose corrected before **acidosis** corrected **Means IV insulin must be continued until serum bicarb improves to at least 15 mEq/L & anion gap is 12 or <**

What should be measured hourly when Tx DKA?

Blood glucose values → to ensure levels are dropping at a safe decrease

What is the goal when Tx DKA?

Decrease serum glucose by 50-100 mg/dL/hr to prevent complications (i.e. cerebral edema)

How do we prevent rapid drop in blood glucose levels?

Use NSS with higher concentrations of glucose (i.e. D5NS, D5.45NS) when BS levels reach 250 mg/dL

What is normal anion gap?

3-10

Formula for calculating serum anion gap

Serum anion gap = serum Na+ - (serum Cl- + bicarb)

We can see anion gaps at what level in DKA?

> 20 mEq/L

What can an elevated anion gap indicate?

Indicates metabolic acidosis caused by DKA , lactic acidosis, or kidney failure

What can a low anion gap indicate?

Suggests multiple myeloma, alkalosis, hypoalbuminemia, & specific electrolyte imbalances

Can you have a normal anion gap & still be acidotic?

Yes

List 6 sick day rules for diabetic patients to prevent DKA

1) Do NOT eliminate insulin doses when N/V occur 2) Take reg/ rapid insulin ONLY if able to tolerate PO 3) Take usual insulin dose, or previously prescribed "sick day" doses 4) Attempt to consume frequent small portions of carbs 5) Drink fluid every hr to prevent dehydration 6) Blood glucose & urine ketones → assess q2-3h if not using CBM

Sick day rules: When should patient contact their HCP?

If they cannot take fluids w/o vomiting, or if elevated glucose or ketone levels persist

DKA Flashcards

(68 cards)