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DT4-Exam 1 > Ped Diabetes-Melissa > Flashcards

Ped Diabetes-Melissa Flashcards

1
Q

What are two things that can cause an elevated white count in a pediatric patient presenting with DKA1?

A

stress and dehydration

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2
Q

What BMP abnormalities might you expect to see in a patient with DKA? (3)

A
  • FALSE HYPOnatremia
  • LOW CO2 (actually a MEASUREMENT of HCO3-)
  • HIGH glucose
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3
Q

Describe abnormal ABG findings in a patient with DKA:

A
  • Acidosis
  • LOW bicarb (metablic)
  • LOW CO2 (respiratory compensation)
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4
Q

Define diabetes:

A
  • Lack of insulin production (type 1) **MOST KIDS

- Decreases responsiveness to insulin (type 2) **Chubby teenagers

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5
Q

Are M or F more likely to get DM1?
Which races are predisposed?
When does the pediatric onset peak?
During what seasons does the initial presentation most often occur?

A
  • M = F
  • More common in whites
  • Onset 10-14yoa most common
  • Initial presentation most common in autumn/ winter (viral?)
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6
Q

What percentage of beta cells must a patient lose to have DM1?
What congenital infection is associated with the disease?
What are the genes associated with this disease?

A
  • Symptoms onset with autoimmune loss +80% beta cells
  • Congenital rubella linked to disease
  • Genetic link: Chrom 6 (DR3-DQ2, DR4-DQ8)
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7
Q

At what blood sugar is insulin release normally stimulated?

Glucagon?

A
  • BS 150–> ^ insulin release –> glycogenesis

- BS 50–> ^ glucagon release–> glycogenOLYSIS

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8
Q

Describe the clinical presentation of a patient with DM1; how long will they typically have symptoms?

A
  • 3 P’s: polyuria, polydypsia, polyphasia
  • weight loss
  • bedwetting/ nocturia
  • DKA often INITIAL PRESENTATION

**Patient’s sx typically less than 1 mos

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9
Q

List the three scenarios that are diagnostic for diabetes:

A
  • Symptoms + hyperglycemia
  • FASTING plasma glucose OVER 126mg/dl
  • 2 hr post challenge or random plasma glucose OVER 200mg/dL
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10
Q

What are the treatment options for patients with DM1 (4)?

A
  • # 1= Insulin (SQ or pump)
  • Nutrition (count carbs/ insulin unit)
  • Exercise
  • Monitoring + Education
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11
Q

What are the acute (2) and long term (4) complicaitons associated with this DM1? How do we avoid them?

A

Acute complications:

  • HYPOglycemia (overshoot insulin)
  • DKA

Chronic complications: Due to HYPERglycemia

  • Microvascular (eyes, kidney, nerves)
  • Macrovascular (Atherosclerosis, stroke, MI)
  • Autoimmune (thyroid, celiac)
  • Growth disturbance
  • **Avoid by monitoring HbA1C
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12
Q

What is the best way to monitor long term blood glucose?

What are two other monitoring methods used day to day?

A 
#1= Monitor HbA1C
- Good HbA1C= 20-50% reduction in risk of complications

Also use glucose meters and continuous sensors

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13
Q

What happens in the Dawn and Somogyi phenomena?

How are they different? How is each one managed?

A

In both phenomena patients wake with HIGH glucose

Dawn: Sugar is HIGH at 3AM
-Increase or begin afternoon or evening insulin dose

Somogyi: Sugar is LOW at 3AM–> ^ Glygogenolyisis to compensate–> wakes with high glucose
- DECREASE or discontinue afternoon/ evening insulin dose

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14
Q

Describe the nutritional modifications made in patients with DM1?

A

Patients should do all common sense healthy things with emphasis on eating COMPLEX carbs, CARB COUNTING, and APPROPRIATE TIMING of meals

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15
Q

What is one thing you should monitor in patients with DM1 beginning an exercise regimine?

A

Monitor for HYPOglycemia

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16
Q

Describe the pathogenesis of DKA.

What are the two important ketone bodies ?

A

Insulin deficiency–> Lipolysis (FFA–> ketones)–> Rapid onset Metabolic acidosis with anion gap!

Two Important Ketone Bodies:

  • Acetoacetic Acid
  • B-Hydroxybuteric Acid
17
Q

What do you see clinically in patients with DKA?

What is different from just DM1 (5)?

A

Everything the same as DM1 without DKA + the following:

  • Kussmaul breathing
  • Acetone breath
  • Abdominal pain
  • Vomiting
  • Possibly obtunded with coma
18
Q

What are the 4 diagnostic criteria for DKA?

What are three additional signs that may be apparent?

A
  • Hyperglycemia (300+)
  • Acidosis (BELOW 7.35)
  • KEtonemia
  • Glucosuria + Ketonuria

May also see leukocytisis, ^ amylase, electrolyte abnormalities

19
Q

At what blood glucose concentration does one begin to spill glucose?

A

BS OVER 180

20
Q

List the 4 items on ones Ddx for DKA:

A
  • Gastroenteritis (rule out bc no fever, infxn signs)
  • Ingestion (attention to hx.)
  • Pancreatitis (will see ^ amylase or lipase)
  • Appendicitis (rule out w/out infeciton signs)
21
Q

What are the two things we do to treat DKA and how do they fix the problem?

A

ALWAYS TREAT SHOCK FIRST!–>

  • Correct hydration + provide Insulin!
  • This combination will correct acidosis and electrolyte imbalances as well!
  • Rarely we add HCO3- (only corrects BLOOD not cellular pH)
22
Q

Describe the treatment of dehydration in DKA.
What is the initial fluid of choice?
How much do we administer?
When do we administer glucose and how is it given?

A
  • Start with normal saline: 10 mL/kilo over an hour w/max of 1L
    (avoid dropping sugar too fast)
  • THEN switch to twice maintenance 0.45% NS
  • Add glucose (DxW) when BS is UNDER 300

**NEVER GIVE JUST GLUCOSE SOLUTION BECAUSE IT IS TOO HYPERTONIC–Always administer in concert with saline and taper dosing

23
Q

What is a maintenance dose of fluid?

A

Maintenance fluid means the amount of fluid requireed by the patient to meet their needs for one day (i.e. produce urine, etc. )

24
Q

When do we give bicarb?

A

RARELY, but it can be given when the pH drops BELOW 7.2-7.1

25
Q

Describe the 3 electrolyte imbalances that can occur when treating DKA and how we can manage them:

A

False Hyponatremia
-Decrease BS–> Na should increase; indicates we are giving too much free H2O

Hypokalemia

  • We gave insulin and that drives K into cells
  • Give K when it drops BELOW 5.5
  • Make first bag K-Phos

Chlorides
- NaCl is in saline soln; too much Cl in IV fluid will not allow Hco3- to increase

26
Q

How do we administer insulin to treat DKA?

A
  • Give REGULAR INSULIN ONLY: 0.1 unit/kg/hr IV

- NEVER STOP INFUSION

27
Q

List 6 important monitoring tools when treating patients with DKA:

A
  • ABG (for bicarb)
  • Beadside glucose
  • BMP
  • EKG (to follow acidosis, K imbalance arrythmias)
  • flowsheet meds (urine production, etc)
  • NEURO CHECKS–keep MANNITOL handy for ^ICP
28
Q

What is the serum osmol equation?

A

Serum osmol = 2Na + glucose/20 + BUN/3

29
Q

What age range will most likely experience complicaitons assocated with DKA?
When do incidences of DKA peak?

A

Kids between 7-11 most likely to have complications;

Most patients with DKA are between 10-14 yoa

30
Q

What are itiogenic osmoles?

A

Glutamine and aspartate created by brain cells during hyperglycemia–> hold onto water/ maintain cellular osmolality

31
Q

Describe how rapid correction of hyperglycemia can lead to ^ ICP:

A

Rapid correction hyperglycemia–> DECREASE blood osmolality + NO CHANGE cellular osmolality–> H2O rush INTO CELLS–> Cerebral edema + ^ICP

32
Q

What is the first sign of cerebral edema on radiographic imaging?

A

Swelling of basillar cystern

33
Q

What are the 2 most salient complications that can occur with DKA?

A
  • cerebral edema (1% of cases = CLINICALLY apparent, occurs at LEAST SUBCLINICALLY 100% of the time)
  • Hypoglycemia
34
Q

How do we treat cerebral edema due to DKA? (3)

A
  • mannitol
  • hypertonic saline
  • ventilation

DT4-Exam 1 (17 decks)

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